SRB's Surgery For Dental Students - 1st Ed. (2008)

SRB’s Surgery for
Dental Students
SRB’s Surgery for
Dental Students
Sriram Bhat M MS (General Surgery)

Associate Professor
Department of Surgery
Kasturba Medical College, Mangalore
Karnataka, India
e-mail: [email protected]
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SRB’s Surgery for Dental Students
© 2008, Jaypee Brothers Medical Publishers

All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by
any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the author and
the publisher.
This book has been published in good faith that the material provided by author is original. Every effort is made to ensure
accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s). In case of
any dispute, all legal matters are to be settled under Delhi jurisdiction only.
First Edition: 2008

ISBN 978-81-8448-401-4
Typeset at JPBMP typesetting unit
Printed at Ajanta Press
Dedicated to
My Beloved Father—Mr Sri Krishna Bhat
and also to
My Father-in-Law—Late Dr Krishna Karath
Foreword
I am delightful to write a foreword for this book entitled SRB’s Surgery for Dental Students by Dr Sriram
Bhat.
It is a manual of surgery covering all general surgical topics for dental students with clinical
methods in brief. All topics are discussed in detail as needed for dental students with adequate
diagrams, photos and illustrations. This book will be very useful to all the students of BDS as well
as MDS. The book deals comprehensively with basic general surgery and topics like wounds, shock,
trauma, vascular diseases, burns, thyroid, basic orthopedics, basic ENT topics and instruments.
A comprehensive manual of this standard can be best compiled only by a person with in depth
knowledge of the subject and teaching experience to understand the requirements of the dental
students. It is very apt that Dr Sriram Bhat a person whom the above description applies to has
come out with this book.
I wish Dr Bhat the very best in this and all his other professional endeavors.
Dr. V Surendra Shetty

Dean
Manipal College of Dental Sciences
Mangalore 575 001
Preface
My first book SRB’s Manual of Surgery is well accepted by medical students in our country. But
I felt, it will be much comprehensive for dental undergraduate (BDS) students and it should be
condensed and be selective. Keeping the surgery subject syllabus of BDS students in mind I wrote
SRB’s Surgery for Dental Students mainly concentrating on general surgery, head and neck, oral cavity
and maxillofacial injuries. I also included Basic Orthopedics, Neurosurgery, Adjuvant Therapy,
Sterilization and Instruments in the book. Miscellaneous chapter contains clinical examination of
swelling/hernia/hydrocele/arterial diseases/varicose veins/thyroid/oral cavity/salivary gland to
complete the fulfillment of the clinical surgical university examinations so that it will be easier for
students to get required subject in a single text. I essentially eliminated gastrointestinal and urology
topics. Adequate diagrams, photos, tables and illustrations are added wherever needed. I also
discussed about the topics with staff members of few dental colleges. I hope the book will be
appreciated by the dental faculty and students. Any suggestions and criticisms are well accepted.
Sriram Bhat M
Acknowledgments
I acknowledge Dr V Surendra Shetty, Dean, Manipal College of Dental Sciences, Mangalore for
writing foreword to this book. I acknowledge helps given by Dr Rajendra Prasad, Dean, AB Shetty
Institute of dental sciences, Mangalore; Dr Sripathi Rao, Dean, Yenepoya Dental College, Mangalore;
Dr Sureschandra, Dean, AJ Shetty Institute of Dental Sciences, Mangalore; Dr Moksha Nayak, Dean,
KVG Dental College, Sullia. I also thank all staff members of different dental colleges who have
given me proper guidance to bring out this book.
I extremely thank Dr Raghuveer, Dean, Kasturba Medical College, Mangalore for his
encouragement for all academic activities.
I appreciate our beloved, Head of Surgery Department, KMC, Mangalore, Dr Thangam Verghese
Joshua for her guidance and help.
Heads of all departments in KMC, Mangalore and colleagues from my department always stood
with me for all my works. I remember all of them always for their kind heart.
I thank district surgeon for providing enough clinical materials from Government Wenlock
Hospital, Mangalore where I am working.
I thank to Professor Kishorechandra Prasad and to Sampath, Assistant Professor in ENT
Department for this all kind half.
I thank Dr Ganapathy, Director, Mangala Hospital, Mangalore for his encouragement.
I thank my dear friend Dr Ashok Pandith, Mch (Urology) for his constant guidance to me in
all my endeavors.
I thank Dr Jagadishchandra, MDS, Associate Professor and Dr Veena Jagadischandra, MDS, for
their affectionate help. Dr Jagadish has provided photos, X-rays and syllabus for dental students.
Dr Ragavendra Bhat and Dr Ravichandra, radiologists, Balmatta Diagnostic Center, Mangalore
have helped me a lot by giving necessary X-rays/CT scans/MRI pictures. I remember them a lot.
I acknowledge Dr Achaleshwar Dayal, MS from KMC, Mangalore, Assistant Professor, Surgery
Department for his all help for this work.
I appreciate Dr Ishwarkeerthi, MBBS, who has helped me by sketching diagrams needed for this
book. My beloved daughter, Ananya did many diagrams beautifully and helped me to reduce my
work. My wife, Dr Meera Sriram, MD (ObG), has done the corrections in the script and I owe her
a lot. I thank all my patients and all who have directly or indirectly helped me in bringing out this
book. I thank a lot Shri JP Vij, Chairman and Managing Director of M/s Jaypee Brothers Medical
Publishers (P) Ltd, New Delhi for his constant help and guidance. In spite of his busy schedule
he is always in touch with authors for any needed help. I appreciate him for his scintillating active
approaches.
I thank every production staff of M/s Jaypee Brothers for bringing out this book more effectively.
Contents
1. Wounds, Sinus Fistula and Ulcer ................................................................................................ 1

Wound 1; Compartment syndrome 4; Crush syndrome 4; Keloid (like a claw) 4; Hypertrophic
scar 5; Sinus 6; Fistula 6; Median mental sinus 8; Ulcer 9; Trophic ulcer 12; Pressure sore
(bedsore/decubitus ulcer) 13; Diabetic ulcer (diabetic foot) 14; Meleney’s ulcer 14; Lupus
vulgaris 15; Ulcer due to chilblains 15; Ulcer due to frostbite 15; Clinical examination of an
ulcer/sinus 15
2. Infectious Diseases ....................................................................................................................... 17
Cellulitis 17; Erysipelas 18; Pyogenic abscess 19; Boil (furuncle) 22; Carbuncle 22; Pott’s puffy
tumor 23; Pyogenic granuloma (Granuloma pyogenicum) 24; Pyemia 24; Tetanus 25; Gas
gangrene 27; Tuberculosis 28; Leprosy (Hansen’s disease) 29; Syphilis (great pox, French
disease) 30; Actinomycosis 31; Madura foot (Mycetoma pedis) 31; Rabies (hydrophobia) 32;
Anthrax 35; Nosocomial infection (hospital acquired infection) 35; Opportunistic infections
36; Necrotizing fasciitis 36; Acute pyomyositis 37; HIV infection and AIDS (acquired
immunodeficiency syndrome) 38; Gonorrhea 41
3. Swellings ......................................................................................................................................... 43
Lipoma 43; Papilloma 44; Cysts 46; Dermoids 46; Sebaceous cyst (Wen, epidermal cyst) 48;
Glomus tumor 49; Lymph cyst (lymphatic cyst) 50; Neuroma 50; Neurofibroma 51;
Neurilemmoma (schwannoma) 52; Fibroma 52; Ganglion 53; Bursae 53; Adventitious bursa
54; Morran baker cyst 55; Calcinosis cutis 55; Epignathus 56
4. Arterial Diseases ............................................................................................................................ 57
Surgical anatomy of 57; Thoracic outlet 57; Arteries of upper limb 58; Upper limb ischemia
58; Raynaud’s phenomenon 61; Acrocyanosis 62; Subclavian steal syndrome 62; Arteries of
lower limb 63; Arterial diseases 63; Thromboangiitis obliterans (TAO) syn. Buerger’s disease
68; Acute arterial occlusion 72; Compartment syndrome 73; Embolism 73; Caisson’s disease
or decompression disease 75; Aneurysms 75; Gangrene 79; Diabetic foot and diabetic gangrene
81; Ainhum 82; Hamartomata 82; Hemangioma 82; Cirsoid aneurysm 84; Arteriovenous
fistula (AVF) 85
5. Venous Diseases ............................................................................................................................ 88
Anatomy of veins of lower limb 88; Physiology of venous blood flow in lower limb 89; Deep
vein thrombosis (DVT) 89; Varicose veins 91; Venous ulcer 97; Thrombophlebitis 98;
Anticoagulants 98
6. Lymphatics .................................................................................................................................... 101
Lymphangiography 101; Isotope lymphoscintigraphy 102; Lymphedema 102; Lymphomas
106; Hodgkin’s lymphoma (HL) 106; Non-Hodgkin’s lymphoma (NHL) 109; Burkitt’s
lymphoma (Malignant lymphoma of Africa) 110; Tuberculous lymphadenitis 110
xii SRB’s Surgery for Dental Students
7. Shock and Hemorrhage ............................................................................................................. 113
Shock 113; Central venous pressure (CVP) 117; Pulmonary capillary wedge pressure (PCWP)
118; Systemic inflammatory response syndrome (SIRS) 118; Oxygen therapy 119; Hyperbaric
oxygen 119; Cardiac arrest 120; Mechanism of blood coagulation 122; Hemorrhage 123; Blood
transfusion 126; Blood fractions 126; Massive blood transfusion 127; Blood substitutes 128;
Tourniquets 128
8. Burns .............................................................................................................................................. 130
Burns 130; Management of burns 133; Eschar 134; Burns contracture 135; Electrical burns
135; Inhalation burns 136; Chemical burns 136
9. Reconstruction and Transplantation ........................................................................................ 138
Skin grafting 138; Flaps 140; Transplantation 141; Renal transplantation 142; Liver
transplantation 143; Bone marrow transplantation 143; Graft rejection 143; Cimino fistula
144
10. Fluids, Electrolyte and Nutrition .............................................................................................. 145
Water loss 145; Water intoxication 146; Hyponatremia 146; Hypernatremia 147; Hypokalemia
147; Hyperkalemia 147; Acid-base balance 148; Anion gap 149; Nutrition 149; Gastrostomy
150; Jejunostomy 151; Total parenteral nutrition (TPN) 151; Obesity 152
11. Nerves and Tendon .................................................................................................................... 153
Peripheral nerve injuries 153; Brachial plexus injuries 155; Causalgia 155; Median nerve
injuries 156; Carpal tunnel syndrome 156; Ulnar nerve injuries 157; Claw hand 158; Radial
nerve lesions 158; Common peroneal nerve 159; Axillary nerve injury 160; Long thoracic nerve
(nerve of bell) 160; Trigeminal neuralgia 160; Tendon 160; Tendon repair 161; Tendon transfer
161; Tendon graft 161
12. Hand and Foot ............................................................................................................................. 162
Surgical anatomy of the hand 162; Hand infections 163; Acute paronychia 164; Chronic
paronychia 164; Terminal pulp space infection (FELON) 165; Infection of webspaces 165;
Deep palmar space infection 166; Acute suppurative tenosynovitis 167; Hand injuries 168;
Compound palmar ganglion 168; Dupuytren’s contracture 169; Syndactyly 170; Mallet finger
(base ball finger) 170; Heberden’s nodes 170; Spina ventosa 170; Callosity 170; Corn 171;
Plantar fasciitis (Policeman’s heel) 171; Ingrowing toe nail (Onychocryptosis) 171
13. Trauma ........................................................................................................................................... 173
Triage 173; Spinal injury 176; Neck injuries 176; Bullet injuries 176; Blast injuries 177;
Penetrating injury 177; Abdominal trauma 177; Duodenal injury 178; Pancreatic injury 179;
Small bowel injury 179; Colonic injury 179; Liver injury 179; Splenic injury 180; Renal injury
180; Urinary bladder injury 180; Abdominal compartment syndrome 180
14. Neoplasm and Soft Tissue Tumors ........................................................................................ 181
Neoplasm 181; Spread of malignant tumors 183; Paraneoplastic syndromes 183;
Investigations for neoplasm 184; Soft tissue tumors (sarcomas) 186; Kaposi’s sarcoma 191
Contents xiii
15. Skin Tumors ................................................................................................................................. 193
Classification of skin tumors 193; Skin adnexal tumors 193; Dermatofibroma 194;
Dermatofibrosarcoma protuberance 194; Keratoacanthoma (Molluscum sebaceum) 194;
Rhinophyma (potato nose) 195; Premalignant conditions of the skin 195; Squamous cell
carcinoma (epithelioma) 195; Marjolin’s ulcer 197; Basal cell carcinoma (Rodent ulcer) 197;
Nevi 199; Melanoma 200
16. Neck ............................................................................................................................................... 204
Anatomy of lymphatics of head and neck 204; Branchial cyst 205; Branchial fistula 206;
Pharyngeal pouch 206; Laryngocele 207; Cystic hygroma (cavernous lymphangioma) 208;
Ludwig’s angina 209; Parapharyngeal abscess 210; Retropharyngeal abscess 210; Carotid
body tumor (potato tumor, chemodectoma, non-chromaffin paraganglioma) 211; Torticollis
(wry neck) 212; Sternomastoid tumor 212; Subhyoid bursitis 213; Secondaries in neck lymph
nodes 213
17. Thyroid ........................................................................................................................................... 219
Development 219; Anatomy 219; Congenital anomalies 221; Thyroid function tests 223;
Classification of goiter 223; Diffuse hyperplastic goiter 224; Nodular goiter 224; Solitary thyroid
nodule 225; Retrosternal goiter 226; Thyrotoxicosis (hyperthyroidism) 226; Thyroid neoplasm
234; Papillary carcinoma 234; Follicular carcinoma 235; Anaplastic carcinoma 236; Medullary
carcinoma of Thyroid (MCT) 236; Malignant lymphoma 237; Hashimoto’s thyroiditis 237;
deQuervain’s subacute granulomatous thyroiditis 238; Reidel’s thyroiditis (0.5% common)
238; Thyroidectomy 238; Emil theodor kocher 240; Hypothyroidism 241
18. Parathyroid .................................................................................................................................... 242
Anatomy of parathyroid 242; Hyperparathyroidism 243; Acute hyperparathyroidism (Crisis)
243; Tetany 245; MEN syndrome (MEA syndrome) 245
19. Salivary Glands ............................................................................................................................ 246
Anatomy 246; Sialography 248; Salivary calculus 248; Sialosis 250; Sialectasis 250; Parotid
abscess (acute suppurative sialadenitis of parotid) 250; Parotid fistula 251; Sjögren’s syndrome
251; Mikulicz disease 252; Salivary neoplasms 252; Management of malignant salivary tumors
256; Minor salivary gland tumors 257; Frey’s syndrome (auriculo-temporal syndrome,
gustatory sweating) 258; Parotidectomy 259;
20. Oral Cavity .................................................................................................................................... 260
Ranula 260; Sublingual dermoids 261; Leukoplakia 261; Erythroplakia 262; Oral submucosal
fibrosis 262; Cancrum oris (NOMA) 262; Carcinoma cheek 263; Neoplasm of lip 268;
Carcinoma of lip 269; Tongue 271; Carcinoma tongue 272; Nasopharyngeal carcinoma 276;
Maxillary tumors 277; Carcinoma hard palate 280
21. Laryngeal Tumors ....................................................................................................................... 282
Benign papilloma 281; Malignant tumors 281; Total laryngectomy 284; Care after total
laryngectomy 285
22. Tonsils ............................................................................................................................................ 286
Anatomy of the tonsils 286; Acute tonsillitis 287; Chronic tonsillitis 287; Peritonsillar abscess
(QUINSY) 288; Tonsillectomy 288; Acute pharyngitis 290
xiv SRB’s Surgery for Dental Students
23. Cleft Lip, Cleft Palate and Jaw Tumors ................................................................................. 291
Cleft lip and cleft palate 291; Diseases of the palate 296; Orthopentomogram (OPG) 296;
Preauricular sinus 296; Jaw tumors 296; Epulis 297; Ameloblastoma 298; Dentigerous cyst
(follicular odontome) 299; Dental cyst (radicular cyst, periapical cyst) 300; Alveolar abscess
(dental abscess) 300; Cherubism 301
24. Tracheostomy ................................................................................................................................ 302
Tracheostomy 302; Tracheostomy tubes 302
25. Esophagus ...................................................................................................................................... 306
Anatomy 306; Lower esophageal sphincter (LES) 308; Dysphagia 308; Achalasia cardia;
Gastroesophageal reflux Disease (GERD) 311; Barrett’s esophagus 312; Hiatus hernia 312;
Reflux esophagitis 313; Corrosive stricture of esophagus 313; Plummer-Vinson syndrome
(Patterson-Kelly syndrome) 314; Mallory-Weiss syndrome 314; Boerhaave’s syndrome 315;
Tracheoesophageal fistula 315; Carcinoma esophagus 316
26. Basic Orthopedics ........................................................................................................................ 319
Anatomy of the bone 319; Fracture 320; Plaster of Paris (POP) 324; Arthrodesis 326;
Arthroplasty 326; Osteotomy 328; Infections of the bone 328; Paget’s disease of bone 330;
Rickets 330; Bone disease of hyperparathyroidism 331; Osteoporosis 331; Scurvy 331;
Osteogenesis imperfecta 331; Achondroplasia 331; Tendinitis 332; Diaphyseal achalasia
(multiple exostoses) 332; Enchondromatosis (Ollier’s disease) Arthritis 332; Rheumatoid
arthritis 333; Osteoarthrosis 333; Ankylosing spondylitis 334; Kyphosis 334; Scoliosis 334;
Spondylolisthesis 335; Intervertebral disc prolapse (IVDP) 335; Bone tumors 336
27. Maxillofacial Injuries .................................................................................................................. 340
Primary care (early care) in maxillofacial injuries 341; Fracture middle third area 342; Fracture
mandible 349; Complications of maxillofacial injuries 357
28. Neurosurgery ................................................................................................................................ 358
Head injuries 358; Extradural hematoma 363; Subdural hematoma 364; Depressed skull
fracture 365; Subarachnoid hemorrhage 366; Intracranial abscess 366; Intracranial aneurysm
367; Hydrocephalus 368; Intracranial tumors 369; Pituitary tumors 371; Spina bifida 372
29. Adjuvant Therapy ....................................................................................................................... 373
Radiotherapy 373; Chemotherapy 376; Immunosuppression 377; Hormone therapy 377;
Immunotherapy 378; Hybridoma 378; Gene therapy 378
30. Instruments and Suture Materials ........................................................................................... 380
Instruments 380; Suture materials 391
31. Sterilization and Disinfection ................................................................................................... 394
Sterilization 394; Disinfection 394; Antisepsis 394; Asepsis 394; Halogens 395
32. Cautery, Laser, Cryosurgery and Day Care Surgery ........................................................... 398
Diathermy (electrocautery) 398; Lasers in surgery 399; Cryosurgery 399; Day care surgery
400
33. Advanced Imaging Methods ..................................................................................................... 401
Ultrasound 401; Doppler 402; CT scan 403; Magnetic resonance imaging (MRI) 404
Contents xv
34. Anesthesia ..................................................................................................................................... 406
Preoperative assessment 406; General anesthesia 407; Muscle relaxants 407; Reversal agents
408; Instruments in anesthesia 408; Complications in general anesthesia 409; Postoperative
care 409; Regional anesthesia 410; Spinal anesthesia 411; Epidural anesthesia 412; Caudal
anesthesia 412
35. Miscellaneous ............................................................................................................................... 413
A. History of Surgery .................................................................................................................. 413
B. Laboratory Values .................................................................................................................. 415
C. Clinical Methods for Dental Students ................................................................................ 418
Examination of a swelling/lump 418; Examination in arterial disease (arterial system) 422;
Examination of varicose veins 428; Examination of thyroid gland 432; Examination of inguinal
hernia 438; Hernioplasty 444; Examination of hydrocele 444; Examination of oral cavity 446;
Examination of salivary gland 446
Index ................................................................................................................................................ 449
Wound, Sinus, Fistula and Ulcer 1
1 Wound, Sinus,
Fistula and Ulcer
WOUND
 Wound
 Compartment syndrome DEFINITION
 Crush syndrome Wound is a break or discontinuity in the
integrity of skin or tissues. It can be a simple
 Keloid wound or a complex wound.
 Hypertrophic scar
CLASSIFICATION
 Sinus
a. Tidy wounds
 Fistula They are wounds of surgical incisions and
 Median mental sinus caused by sharp objects.
Usually primary suturing is done. Healing is
 Ulcer
by primary intention.
 Trophic ulcer b. Untidy wounds
 Pressure sore (bedsore/decubitus ulcer) They are:
• Crushed
 Diabetic ulcer (diabetic foot) • Tear
 Meleney’s ulcer • Avulsion
 Lupus vulgaris • Devitalized injury
• Vascular injury
 Ulcer due to chilblains • Multiple irregular wounds
 Ulcer due to frostbite • Burns, etc.
 Clinical examination of an ulcer/sinus Fracture may be present.
Wound dehiscence, infection, delayed
healing are common.
Worry does not empty tomorrow of its sorrow. It empties today of its strength.
2 SRB’s Surgery for Dental Students
9. Crush injury—Is caused by war wounds,
road traffic accidents, and tourniquet.
It leads on to—
– Compartment syndrome
– Muscle ischemia
– Gangrene, loss of tissue.
Fig. 1.1: De-gloving injury, thigh and leg. It is extensive and
needs regular dressing, debridement and later skin grafting 10. War wounds and gunshot injuries.
11. Injuries to bones and joints may be open or
Liberal excision of devitalized tissue and closed.
allowing to heal by secondary intention is the 12. Injuries to nerves, either clean cut or crush.
management. 13. Injuries to arteries and veins (major vessels).
14. Injury to internal organs may be penetrating
OTHER CLASSIFICATION or non-penetrating (blunt) injuries.
1. Clean incised wound—It is a wound caused
by sharp objects like knife, glass or blades. CLASSIFICATION OF SURGICAL WOUNDS
Primary suturing is done and it heals by 1. Clean wound
first intention leaving a thin, linear scar. • Herniorrhaphy
2. Lacerated wound—Wound edge is devita- • Excisions
lized, crushed and wide. It is treated by • Surgeries of the brain, joints, heart,
wound excision and delayed primary transplant.
suturing. Scar formed is wide and prone for • Infective rate is less than 2%.
hypertrophic scar formation. 2. Clean contaminated wound
3. Bruising, contusion. • Appendicectomy
4. Hematoma. • Bowel surgeries
5. Closed blunt injury. • Gallbladder, biliary and pancreatic
6. Puncture wounds and bites. surgeries.
7. Abrasion—It is superficial, and is due to • Infective rate is up to 30%—high.
shearing of skin in which surface is rubbed 3. Contaminated wound
off. It heals by epithelialization. • Acute abdominal conditions
8. Traction and avulsion injury. • Open fresh accidental wounds.
Factors Affecting Wound Healing

Local factors General factors
1. Infection. Age.
2. Presence of necrotic tissue and foreign body. Malnutrition.
3. Poor blood supply. Vitamin deficiency (Vit C).
4. Venous or lymph stasis. Anemia.
5. Tissue tension. Malignancy.
6. Hematoma. Uremia.
7. Large defect or poor apposition. Jaundice.
8. Recurrent trauma. Diabetes.
9. X-ray irradiated area. HIV and immunosuppressive diseases.
10. Site of wound, e.g. wound over the joint and Steroids and cytotoxic drugs.
back has poor healing.
4. Dirty infected wound • If it is a lacerated wound then the wound is
• Abscess drainage excised and primary suturing is done.
• Pyocele • If it is a crushed or devitalized wound, there
• Empyema gallbladder will be edema and tension in the wound.
• Fecal peritonitis. Wound debridement is done by excising all the
devitalized tissues and the edema is allowed
WOUND HEALING to subside in 5-6 days. Then, delayed primary
Stages suturing is done.
• Stage of inflammation. • If it is a deep devitalized wound, after wound
• Stage of granulation tissue formation and debridement it is allowed to granulate comp-
organization. Here as the result of fibroblastic letely. Later, if the wound is small, secondary
activity, synthesis of collagen and ground suturing is done. If the wound is large, a split
substance occurs. skin graft (Thiersch graft) is used to cover the
• Stage of epithelialization—It occurs in 48 defect (Fig. 1.1).
hours. • In a wound with tension, fasciotomy is done
• Stage of wound contraction and connective so as to prevent the development of compart-
tissue formation. ment syndrome.
• Stage of scar formation and resorption. • Vascular or nerve injuries are dealt with
• Stage of maturation. accordingly. Vessels are sutured with 6-zero
polypropylene nonabsorbable suture mate-
Types of wound healing rial. If the nerves are having clean-cut
Healing by primary intention (First intention): wounds it can be sutured primarily with
It is healing in a clean incised wound, which polypropylene 6-zero or 7-zero suture
leads into thin, linear scar. material. If there is difficulty in identifying
Healing by secondary intention (Second cut ends of nerves or if the cut ends of nerves
intention): It is healing in an infected wound, are crushed then a marker stitch using silk
which leads into wide poor scar. is placed at the site and later secondary
repair of the nerves are done.
MANAGEMENT OF WOUNDS • Internal injuries have to be dealt accordingly
• Wound is inspected and classified as per the (intracranial by craniotomy, intrathoracic by
type of wound. intercostal tube drainage, intra-abdominal by
• If it is in the vital area, then— laparotomy). Fractured bones also should be
– The airway should be maintained. identified and properly dealt with.
– The bleeding if present should be • Antibiotics, fluid and electrolyte balance,
controlled. blood transfusion, tetanus toxoid or anti-
– Intravenous fluids are started. tetanus globulin injection (ATG).
– Oxygen, if required may be given. Wound Debridement (Wound toilet, or wound
– Deeper communicating injuries and excision) is liberal excision of all devitalized
fractures, etc. should be looked for. tissues at regular intervals (of 48-72 hours) until
• If it is an incised wound, then primary healthy, bleeding, vascular tidy wound is
suturing is done after thorough cleaning. created.
Always look at what you have left. Never look at what you have lost.
Primary suturing means suturing the wound CRUSH SYNDROME

immediately. It is done in clean incised It is due to crushing of muscles causing extrava-
wounds. sation of blood and release of myohemoglobin
Primary suturing after wound excision is done into the circulation, leading to acute tubular
within 6 hours when wound edges are ragged, necrosis and acute renal failure.
devitalized or if wound contains foreign
bodies. Proper irrigation and excision of CAUSES
devitalized tissues is done and sutured.
Delayed primary suturing means suturing the • Earthquakes
wound in 48 hours. It is done in lacerated • Mining and industrial accidents
wounds, wound with edema, hematoma or • Air crash
contamination. This time is allowed for the • Tourniquet
edema to subside. Wound excision may be Initially tension increases in the muscle
added whenever required. compartment commonly in the limb, which itself
Secondary suturing means suturing the wound impedes the circulation and increases the
in 10-14 days. It is done in infected wounds. ischemic damage. In 3 days, urine gets discolored
Secondary suturing is done once the infection and scanty. Patient becomes restless, apathy and
is controlled and healthy granulation tissue delirious with onset of uremia. Crush syndrome
appears. is often life threatening.
TREATMENT
COMPARTMENT SYNDROME
• Tension in the muscle compartment is relieved
It is common in calf and forearm. Closed injury by placing multiple, parallel, deep incisions in
causes hematoma leading to increased pressure. the limb so as to prevent further damage.
It is often associated with fracture, which • Rheomacrodex, or Mannitol is given to
compresses the major vessel further aggravating improve the urine output by improving the
the ischemia causing pallor, pulseless, pain, renal function.
paresthesia, diffuse swelling and cold limb. • Alkalization of the urine is done using
If allowed to progress it may eventually lead sodium citrate or sodium bicarbonate.
on to gangrene or chronic ischemic contracture • Hemodialysis is done sometimes as a life
with deformed, disabled limb. saving procedure.
Muscle necrosis releases myoglobulin, which • Other measures:
is excreted in the urine damaging kidneys • Bladder catheterization
leading into renal failure. • Oxygen therapy
• Antibiotics
TREATMENT • Blood transfusion.
• These patients require longitudinal lengthy,
deep incisions i.e. fasciotomies to relieve the
KELOID (LIKE A CLAW)
pressure and prevent compression. • Keloid is common in blacks. Common in
• Antibiotics. females.
• Bladder catheterization. • Genetically predisposed. Often familial.
• Mannitol or diuretics to create diuresis so as • There is defect in maturation and stabili-
to flush the kidney. zation of collagen fibrils.
• Fresh blood transfusion. • Keloid continues to grow even after 6 months,
• Hyperbaric oxygen. may be for many years.
• It extends into adjacent normal skin.
• It is brownish black in color, painful, tender
and sometimes hyperesthetic.
Sites: Common over sternum (Figs 1.2 and 1.3A).

Other sites are upper arm, chest wall, and lower
neck in front.
Differential diagnosis: Hypertrophic scar.
Treatment: Controversial.
Modes of treatment—
• Excision and skin grafting.
• Irradiation.
• Excision and irradiation. Fig. 1.2: Keloid over sternal region,
• Steroid injection – Triamcinolone is given which is a common site
intrakeloidally, at regular intervals, may be
once in 7–10 days, of 6–8 injections.
• Steroid injection → Excision → Steroid
injection.
• Methotrexate and vitamin A therapy into the
keloid.
Recurrence rate is very high
HYPERTROPHIC SCAR
• Occurs anywhere in the body (Fig. 1.3B).
• Not genetically predisposed. Not familial
• Growth usually limits up to 6 months.
• It is limited to scar tissue only. It will not
extend to the normal skin.
• It is pale brown in color, not painful, non-
tender.
• Often, self-limiting also. It responds very well
for steroid injection
• Recurrence is uncommon.
Complication Figs 1.3A and B: Keloid over sternum and hypertrophic
scar over thigh
• Repeated breakdown of the scar often occurs
causing infection and pain. It is controlled by pressure garments or often
• After repeated breakdown it may turn into revision excision of scar and closure, if required
Marjolin‘s ulcer. with skin graft.
Faith is the basis of every act. You do not run away from the barber though
he is armed with sharp scissors.
Differences between keloid and hypertrophic scar (Fig. 1.4)

Keloid Hypertrophic scar
a. Genetic predisposition Yes No
b. Site of occurrence Chest wall, upper arm, Anywhere in the body,
lower neck, ear. Common in flexors.
c. Growth Continues to grow without Growth limits for 6 months.
time limit.
Extends to normal skin. Limited to scar tissue only.
d. Treatment Poor response Good response to steroids.
e. Recurrence Very high Is uncommon.
f. Collagen synthesis 20 times more than 6 times more than normal skin
normal skin
g. Relation of size of injury No relation. Small healed Related to size of injury
and lesion scar can form large keloid and duration of healing.
h. Age Adolescents, middle age Children
i. Sex Common in females Equal in both
j. Race More in blacks No racial relation
surrounding tissues. Sinus sprouts outside and

it does not have a floor clinically. Discharge can
be seen on the mouth of the sinus.
FISTULA (FIG. 1.6)

It is an abnormal communication between the
lumen of one viscus to another or the body
surface or between the vessels.
Fistula means “flute” or “a pipe or tube”
TYPES
Congenital Acquired
Pre-auricular sinus Ruptured abscess
Branchial fistula Tuberculosis—common.
Tracheo-esophageal Actinomycosis
fistula
Congenital AV fistula Chronic osteomyelitis
Fig. 1.4: Diagrammatic representation of linear scar,
Fistula in ano
hypertrophic scar and keloid Acquired AV fistula.
Median mental sinus
SINUS (FIG. 1.5)
“Sinus” means “hollow” or “a bay” (Latin). CLINICAL FEATURES
It is a blind track lined by granulation tissue • Discharge from the opening of sinus. No
leading from an epithelial surface into the floor.
Fig. 1.5: Sinus Fig. 1.6: Fistula
• Raised indurated edge, indurated base, non- TREATMENT

mobile. • The cause is treated—Sequestrectomy,
• Often sprouting granulation tissue is seen over foreign body removal, control of tuberculosis.
the sinus opening. • Excision of sinus or fistulas. Always specimen
should be sent for histology.
Causes of persistence of a sinus or fistula
• A foreign body or necrotic tissue underneath,
e.g. suture, sequestrum.
• Insufficient or non-dependent drainage.
• Persistent obstruction in the lumen, e.g. in
fecal fistula, biliary fistulas (distal obstruc-
tion).
• Lack of rest.
• Walls become lined with epithelium or
endothelium.
• Dense fibrosis prevents contraction and
healing.
• Specific infections: Tuberculosis, actinomy-
cosis.
• Presence of malignant disease.
INVESTIGATIONS (FIG. 1.7)

• Fistulogram/sinusogram using ultra fluid
lipidol or water-soluble iodine dye.
• Discharge for culture and sensitivity, AFB,
cytology, staining Fig. 1.7: X-ray femur showing osteomyelitis of the femur
• Biopsy from the edge, chest X-ray, ESR. with sequestrum and sinus
Commitment is what transforms a promise into reality.

Different discharges in a sinus/fistula

• Purulent—bacterial infection
• Caseous—tuberculous
• Sulfur granules—actinomycosis
• Mucus—branchial fistula
• Saliva—parotid fistula
• Feces—fecal fistula (Fig. 1.8A and B)
• Bile—biliary, duodenal fistula
• Bone—osteomyelitis sinus
Fig. 1.9: Median mental sinus. Note the origin of the

sinus from the root/roots of the lower incisor/incisors
teeth forming root abscess, which eventually

tracks down between two halves of the lower jaw
in midline, presenting as discharging sinus on
the point of chin in midline (Fig. 1.9).
Clinical Features
• Usually painless discharging sinus in the
midline on the point of chin.
• Often infection in incisor may be revealed (in
many patients clinically tooth looks normal,
even though root is infected invariably).
• It is often mistaken for infected sebaceous
cyst.
• Osteomyelitis of the mandible is the possible
complication.
Differential Diagnosis
• Infected sebaceous cyst.
• Tuberculous sinus.
• Osteomyelitis.
Investigations
• Dental X-ray is diagnostic. (Plain X-ray
mandible may not reveal the disease).
• Discharge study—culture and sensitivity,
Figs 1.8A and B: Fecal fistula with discharging fecal mat- cytology, AFB.
ter through the fistulous wound. Note the tension sutures in
one of the pictures Treatment
• Antibiotics after doing discharge study
MEDIAN MENTAL SINUS (culture and sensitivity).
It is a chronic infective condition, wherein there • Lay opening and excision of the sinus track
is infection of roots of one or both lower incisor with extraction of incisor tooth/teeth.
ULCER
DEFINITION
An ulcer is a break in the continuity of the cover-
ing epithelium, either skin or mucous membrane
due to molecular/cell death.
PARTS OF AN ULCER (FIG. 1.10)
Margin: It may be regular or irregular. It may be

rounded or oval.
Edge: Edge is the one, which connects floor of
the ulcer to the margin. Fig. 1.11: Ulcer edges
Different edges are (Fig. 1.11)—

Sloping edge. It is seen in healing ulcer. Its inner
part is red because of red, healthy granulation
tissue.
Undermined edge is seen in tuberculous ulcer
(Fig. 1.12).
Punched out edge is seen in gummatous (syphi-
litic) ulcer, trophic ulcer and pressure sores. It is
due to endarteritis.
Raised and beaded edge (pearly white) is seen in
rodent ulcer (BCC).
Everted edge (rolled out edge): It is seen in
carcinomatous ulcer.
Floor: It is the one, which is seen. Floor may Fig. 1.12: Tuberculous ulcer over the foot. Note the
contain discharge, granulation tissue, or slough. undermined edge
Base: Base is the one where ulcer rests. It may

be bone or soft tissues.
CLASSIFICATION I (CLINICAL)
Spreading ulcer: Here edge is inflamed and
edematous.
Healing ulcer (Fig. 1.13): Edge is sloping with
healthy pink/red granulation tissue with serous
Fig. 1.10: Parts of an ulcer discharge.
Let our advance worrying become advance thinking and planning.

Fig. 1.13: Healing ulcer with healthy granulation tissue Fig. 1.15: Callous ulcer in the leg. Note the slough on the
surface of ulcer with no signs of healing
Non-specific Ulcers
• Traumatic ulcer: It may be due to mechanical,
physical, chemical injury.
• Arterial ulcer: Atherosclerosis, TAO.
• Venous ulcer (gravitational ulcer, post-
phlebitic ulcer).
• Trophic ulcer.
• Infective ulcers: Pyogenic ulcer.
• Tropical ulcers: It occurs in tropical countries.
It is callous type of ulcer, e.g. Vincent‘s ulcer.
• Ulcers due to chilblains and frostbite (cryopathic
ulcer).
Fig. 1.14: Non-healing ulcer foot with unhealthy/pale • Martorell‘s hypertensive ulcer: It occurs due to
granulation tissue obliteration of end arteries. It is observed in
Callous ulcer: Floor contains pale unhealthy skin over the back of calf region. Ulcer is severely
granulation tissue with indurated edge/base painful with deep, non-healing ischemic look.
(Fig. 1.14). Ulcer has no tendency to heal. It lasts • Bazin’s ulcer: It is seen exclusively in the legs
for many months to years. It is due to callous and ankles of young females, as erythematous
attitude of the patient (Fig. 1.15). purplish nodules and non-healing ulcers. It
may be due to ischemic (Fig. 1.16)/hyper-
CLASSIFICATION II (PATHOLOGICAL)
Specific Ulcers
• Tuberculous ulcer (See Fig. 1.11).
• Syphilitic ulcer: It is punched out, deep ulcer,
with ‘wash-leather’ slough in the floor and
with indurated base.
• Actinomycosis.
• Meleney’s ulcer.
Malignant Ulcers
• Carcinomatous ulcer.
• Rodent ulcer. Fig. 1.16: Ischemic ulcer foot is due to poor blood supply
• Melanotic ulcer. due to either, atherosclerosis, TAO, diabetes mellitus
sensitive/tuberculous etiology. It is treated Unhealthy, pale, flat granulation tissue: It is seen
with antituberculous drugs, dressings, in chronic nonhealing ulcer (callous ulcer).
vasodilators and often by sympathectomy. It Exuberant granulation tissue (Proud flesh): It
is also called as Erythrocyanosis frigida. occurs in a sinus wherein granulation tissue
• Diabetic ulcer. protrudes out of the orifice of the sinus like a
• Ulcers due to leukemia, polycythemia, proliferating mass. It is commonly associated
jaundice, collagen diseases, lymphedema. with a retained foreign body in the sinus cavity.
• Cortisol ulcers are due to long time application Pyogenic granuloma: It is a type of exuberant
of cortisol(steroid) creams to certain skin granulation tissue. Here granulation tissue
diseases. These ulcers are callous ulcers, last protrudes out from an infected wound or ulcer
for long time and requires excision with skin bed, presenting as well localized, red swelling,
grafting. which bleeds on touch.
GRANULATION TISSUE Treatment: Antibiotics, excision and biopsy.
It is proliferation of new capillaries and Induration
fibroblasts intermingled with RBC‘s and WBC‘s • Induration is a feel of hardness in the edge/
with thin fibrin cover over it. base or surrounding area of an ulcer/ lesion.
• It is observed in squamous cell carcinoma.
TYPES
• It can also be seen in chronic ulcers like
Healthy granulation tissue: It occurs in a healing venous ulcer due to long standing fibrosis.
ulcer. It has a sloping edge with serous dis- • Brawny induration is typical of an abscess.
charge. It bleeds on touch. Skin grafting takes up • Induration is absent in malignant melanoma/
well with healthy granulation tissue. Streptococci poorly differentiated carcinomas.
• It can be seen in chronic sinus, syphilitic
Different discharges in an ulcer (as well as hard chancre.
from a sinus): • Induration is usually absent in tuberculosis.
Serous: in healing ulcer.
Purulent: in infected ulcer. Induration in an ulcer is due to carcinoma or due
Staphylococci—yellowish and creamy. to fibrosis in a long-standing ulcer.
Streptococci—bloody and opalescent.
Investigations for an Ulcer
Pseudomonas—greenish color.
Bloody: malignant ulcer, healing ulcer from • Study of discharge: Culture and sensitivity,
healthy granulation tissue. AFB study, cytology.
Sero-purulent. • Edge biopsy: Biopsy is taken from the edge be-
Sero-sanguinous: serous and blood. cause edge contains multiplying cells. Usually
Serous with sulfur granules: actinomycosis. two biopsies are taken. Biopsy from the center
may be inadequate because of necrosis.
Yellowish: tuberculous ulcer.
• X-ray of the part.
growth in culture should be less than 105/gram • FNAC of the lymph node.
of tissue before skin grafting. • Chest X-ray, Mantoux test is done in
suspected case of tuberculous ulcer.
Unhealthy granulation tissue: It is pale with
purulent discharge. Its floor is covered with Treatment of an Ulcer
slough. Its edge is inflamed and edematous. It is • Treat the cause like diabetes, anemia, and
a spreading ulcer. malnutrition. Often needs blood transfusion.
A mistake in judgment is never fatal, but too much anxiety about judgment is.
• Antibiotics are given depending on the Dressing of an ulcer
culture and sensitivity. • To keep ulcer moist
• Regular dressings using EUSOL (Edinburgh • To keep surrounding skin dry
University Solution containing calcium • To reduce pain
hydroxide, boric acid, sodium hypochlorite), • To soothen the tissues
H2O2, povidone iodine. • To protect the wound
• Wound excision/slough excision/debride- • As an absorbent of the discharge.
ment of the wound at regular intervals.
• Once wound granulates well, split skin
grafting is done to cover the defect. TROPHIC ULCER
• If there is no adequate blood supply, or if bone It is due to —
is exposed then flap is needed depending on • Impaired nutrition
the location of ulcer, either groin flap, • Defective blood supply
pectoralis major flap, etc. • Neurological deficit.
It usually occurs —
Management of an ulcer • Over the heel
• Cause should be found and treated. • In relation to heads of metatarsals
• Correct the deficiencies like anemia, protein • Buttocks
deficiency, vitamins. • Over the ischial tuberosity
• Transfuse blood if required. • Sacrum
• Control the pain. • Over the shoulder
• Investigate properly. • Occiput.
• Control of infection and rest to the part. Because there is neurological deficit, trophic
• Care of the ulcer by debridement, ulcer cleaning ulcer is also called as neurogenic ulcer/neuropathic
and dressing. ulcer.
• Removal of the exuberant granulation tissue. Due to repeated trauma and pressure, it
• Topical antibiotics for infected ulcers only like initially begins as callosity which suppurates
Framycetin, Silver sulphadiazine, Mupirocin, and gives way through a central hole extending
etc. into the deeper plane as perforating ulcer
• Antibiotics are not required once healthy (penetrating ulcer).
granulation tissues are formed. Neurological causes
• Once granulates, defect is closed with • Diabetic neuropathy
secondary suturing, skin graft or flaps. • Peripheral neuritis
• Tabes dorsalis
• Spina bifida
Debridement of an ulcer
• Leprosy
• It is removal of devitalized tissue.
• Spinal injury
• Small ulcers are debrided in ward.
• Paraplegia
• Large ulcers are debrided in operation theater
• Peripheral nerve injury
under general anesthesia.
• Syringomyelia.
• All dead, devitalized, necrotic tissues are
Bedsores are trophic ulcers.
removed.
• Slough should be separated adequately before Clinical Features
debridement. • Painless ulcer, which is punched out.
• Often devitalized tissue separates on its own • Ulcer is nonmobile with base formed by
by autolysis. underlying bone.
• Enzymes like collagenase are used for Investigations Study of discharge, biopsy from
debridement. the edge, X-ray of the part, X-ray spine, blood sugar.
Treatment Predisposing Factors
• Cause should be treated. • Malnutrition, anemia, sensory loss, pressure,
• Nutritional supplements. moisture.
• Rest, antibiotics, slough excision, regular • Incontinence makes skin moist and septic, so
dressings. 5 times more prone for pressure sore.
• Once ulcer granulates well, flap cover or skin • Excessive sweating, edema body.
grafting is done. • Friction due to foreign body, thick bed sheets,
• Excision of the ulcer and skin grafting. hard rough cot.
Superficial bedsores are common (75%). They
PRESSURE SORE are painful and heal slowly by itself.
(BEDSORE/DECUBITUS ULCER) Deep bedsores are painless but covered with
Bedsore/pressure sore is a trophic ulcer with slough. It requires antibiotics, grafting or flaps
underlying bone as the base. to cover it later.
It is nonmobile, deep, punched out ulcer.
It is common in— Treatment
• Old age. • Change of positions should always be encou-
• Bedridden individuals. raged.
• Tetanus. • Use of waterbed, ripple bed is advised. Bed
• Patients with orthopedic and head injuries. should be smooth and free from wrinkles and
• Diabetic. unevenness. Air rings or air cushions are also
• Paraplegic. useful.
• Comatose. • Moisture has to be avoided. Skin must be kept
• Emaciated patient. clean and dry. It should be washed with soap
• Anemia. and water and dried properly. A soothening
• Prolonged immobilization. powder may be beneficial.
Sites of bedsore are occiput, heel, sacrum (Fig. 1.17), • Ripple bed has an alternate pressure point
ischium, scapula, greater trochanter, spinous pad under the bottom sheet of ordinary mat-
process, elbows, and buttocks. tress. It provides regular automatic frequent
redistribution of pressure areas. The pad
consists of vinyl plastic pad with alternating
sets of air cells. To control the air, an air
pump is also present.
• In a patient with urinary incontinence,
special silicone bedclothes are used to attain
waterproof covering to skin. Indwelling
Foley‘s catheter is placed to drain urine.
Thorough washing of the back and drying
twice daily is essential. Disposable soft inco-
pads are used repeatedly as required.
• Bowker-Davidson special pressure cushions
contain foamed cushion with a waterproof
Fig. 1.17: Bedsore over sacral region. polyvinyl chloride bag containing 5 liters of
It is a trophic ulcer the thixotropic gel.
Every exit is an entry somewhere else.

• Soaking by urine, sweat, pus, and feces has
to be taken care off.
• Good nursing, regular dressing, good
nutrition are necessary.
• Antibiotics, blood transfusions are very
essential.
• Excision of dead tissue followed by skin
grafting or local rotation flaps may have to
be done.
DIABETIC ULCER (FIG. 1.18)

(DIABETIC FOOT)
Patients with diabetes are more prone for foot
problems like cellulitis, abscess formation, gangrene,
osteomyelitis of foot. It is due to neuropathy, more
susceptibility for infection, clawing of toes, loss of Fig. 1.18: Ulcer foot in diabetic patient
functioning of foot arch, microangiopathy, bacterial
resistance, and decreased body immunity. TREATMENT
• Control of diabetes using insulin. Sliding scale
Causes
insulin is used depending on the color seen
• Increased glucose in the tissues precipitates
in urine test. Human insulin is the preferred
infection.
type of insulin. When there is ketosis, intra-
• Diabetic microangiopathy, which affects venous insulin is used in normal saline.
microcirculation. • Antibiotics.
• Increased glycosylated hemoglobin decrea- • Nutritional supplements.
ses the oxygen dissociation. • Regular cleaning, debridement, dressing.
• Increased glycosylated tissue protein • Abscess drainage, toe amputation (Ray
decreases the oxygen dissociation. amputation), below-knee/above-knee ampu-
• Diabetic neuropathy involving all sensory, tations.
motor and autonomous components. • Once granulates, the ulcer is covered with
• Associated atherosclerosis. skin graft or flap.
• Patient is prone for septicemia, ketosis,
SITES electrolyte imbalance, silent myocardial infarction
• Foot-plantar aspect—Is the commonest site. and often all these can be fatal.
• Leg.
• Upper limb, back, scrotum, perineum. MELENEY’S ULCER
Diabetic ulcer may be associated with • It is commonly seen in postoperative wounds
ischemia. Ulcer is spreading and deep. in abdomen and chest wall like empyema
drainage or after surgery for peritonitis.
INVESTIGATIONS • It is common over abdomen and thorax. It
• Blood sugar both random and fasting. begins in wound margin and spreads
• Urine ketone bodies. rapidly. It can also occur in other areas of
• Discharge for culture and sensitivity. skin.
• X-ray of the part. • Infection is severe, often with endarteritis of
• Arterial Doppler of the limb. the skin leading to ulcer and destruction.
• It causes severe toxicity and extensive Site—If ulcer is on the toes, fingers or distal
necrosis of the skin and deeper plane, which aspect of the foot, it could be ischemic or diabetic
often needs debridement, antibiotics and later ulcer.
skin grafting. If the ulcer is over medial malleolus, it is venous
ulcer due to long saphenous vein varicosity. If it is
LUPUS VULGARIS over lateral malleolus, it is venous ulcer due to short
saphenous vein varicosity.
• It is cutaneous tuberculosis, which occurs in Floor—Inspect the floor of an ulcer. Floor of
young age group. an ulcer is the part, which is seen. Floor may
• Commonly seen on face, starts as typical contain discharge like blood, serous, pus,
apple-gelly nodule with congestion of face caseation. It may be covered with slough, pale
around. Eventually ulceration occurs with granulation tissue or healthy pink granulation
scarring, necrosis and undermined edge. tissue. It may be pigmented like in melanoma or
• Long standing lupus vulgaris can turn into with wash-leather slough like in syphilitic ulcer.
squamous cell carcinoma. Margin—It is at the junction of edge and
Investigation normal skin or mucosa. It may be well or ill-
defined or may be regular or irregular.
ESR, discharge study, biopsy, chest X-ray. Edge—Is between floor and the margin.
Treatment Sloping edge is seen in healing ulcer, undermined
in tuberculous ulcer, raised and everted in squa-
• Antituberculous drugs. mous cell carcinomatous ulcer (epithelioma),
• If complete healing does not occur, then punched out edge in trophic ulcer, raised and
excision and skin grafting is required. beaded in rodent ulcer (BCC).
Surrounding area should be inspected for
ULCER DUE TO CHILBLAINS redness, edema, pigmentation, ischemic features
It is due to exposure to intense cold causing and for scars.
blisters, ulceration in the feet. These ulcers are
superficial. The condition is also called as Palpation
perniosis.
It may be warm or cold over the lesion.
ULCER DUE TO FROSTBITE Surrounding area should be checked using back
• It is due to exposure of the part to wet cold of the hand and should be compared to normal
below the freezing point. area.
• It leads to gangrene of the part. Ulcers, here Tenderness, its location and extent should be
are always deep. assessed.
Mobility of the ulcer should be checked in
CLINICAL EXAMINATION OF two directions. If mobile, then it is superficial or
AN ULCER/SINUS easy to treat. If nonmobile, base is formed by bone
and it is difficult to treat.
INSPECTION Edge of the ulcer is tender or not/indurated
Inspection of an ulcer/sinus is done after taking or not/friable or not. Induration is seen in epithe-
and documenting detailed history. Lesion is lioma ulcer. Friability is observed in malignancy
inspected after proper exposing the area. or in acute inflammation.
Every oak tree started out as a couple of nuts who stood their ground.
Base of the ulcer is one where ulcer rests on. Joint movements are assessed. Plantar and
Base may be bone, muscles or soft tissues. It is dorsiflexion for ankle joint, inversion and
checked by mobility of the ulcer and also by eversion for subtalar joint is checked.
contracting the muscle/tendon underneath. Base Regional lymph nodes like in groin (inguinal
is also palpated for induration.
node vertical/horizontal group), axilla or neck
Bleeding on palpation signifies either
carcinoma or healthy granulation tissue. depending on the location of primary lesion
Induration and tenderness in surrounding should be examined. Tender node is observed in
area should be checked for. inflammatory condition, non-tender hard node
Bone thickening is looked for by running finger in malignancy, and matted nodes in tuber-
over the bone. It is an evidence of periostitis. culosis.
Palpation of peripheral pulses like dorsalis Look for varicose veins or other relevant
pedis artery, posterior tibial artery should be
findings in relation to the ulcer.
done which gives the idea about the wound
healing. Relevant systemic examinations like of
Sensation of the part like vibration, sense of abdomen, respiratory system or cardiovascular
position, touch should be checked in order. system should be done.
Infectious Diseases 17
2 Infectious Diseases
 Cellulitis CELLULITIS
 Erysipelas It is spreading inflammation of subcutaneous and
 Pyogenic abscess fascial planes.
 Boil Infection may follow a small scratch or
 Carbuncle wound or incision.
 Pott’s puffy tumor
 Pyogenic granuloma Causative Agents
 Pyemia Commonly due to Streptococcus pyogenes and
 Tetanus other gram +ve organisms.
 Gas gangrene Often gram –ve organisms like Klebsiella,
pseudomonas, E. coli are also involved. (Usually
 Tuberculosis
gram –ve organisms cause secondary infection).
 Leprosy
 Syphilis Sequelae
 Actinomycosis
• Infection can get localized to form pyogenic
 Madura foot
abscess.
 Rabies • Infection can spread to cause bacteremia,
 Anthrax septicemia, pyemia.
 Nosocomial infection • Often infection can lead to local gangrene.
 Opportunistic infections
 Necrotising fasciitis Clinical Features (Fig. 2.1)
 Acute polymyositis • Fever, toxicity (tachycardia, hypotension).
 HIV infection and AIDS • Swelling is diffuse and spreading in nature.
• Pain and tenderness, red, shiny area with
 Gonorrhea
stretched warm skin.
What the caterpillar calls the end of the world the master calls a butterfly.
Clinical Features
Diffuse swelling, redness, tenderness, induration
in the floor of the mouth and submandibular
region.
Difficulty in opening of the mouth (trismus),
dysphagia.
Toxic features like fever, tachycardia and
tachypnea.
Severe laryngeal edema (presents with
respiratory distress, stridor and cyanosis). It may
require emergency tracheostomy.
Complications
• Septicemia.
• Spread of infection into the parapharyngeal
space leads to thrombosis of internal jugular
vein, which may extend above into the
sigmoid sinus, which may be fatal.
Fig. 2.1: Cellulitis face. Note the diffuse swelling
Treatment
• Cellulitis progresses rapidly in diabetic and
immunosuppressed individuals. • Antibiotics.
• Early surgical intervention (decompression)
Management is required under general anesthesia. Hori-
zontal incision is placed in submandibular
• Elevation of limb or part to reduce edema so
region extending on both sides, deepened to
as to increase the circulation.
include deep fascia. Mylohyoid muscles on
• Antibiotics.
both sides are cut. It releases the tension,
• Dressing (often glycerin dressing is used as
preventing laryngeal edema and so further
it reduces the edema because of its hygro-
spread of infection is prevented. Antibiotics
scopic action).
should be continued (Fig. 2.2).
• When the infection gets controlled comp-
ORBITAL CELLULITIS
letely, the incised wound is closed by secondary
Cellulitis in orbit causes proptosis, leading to suturing (not earlier). Occasionally loose
impairment of ocular movements and blindness. sutures are placed with placement of a drain
It can spread through ophthalmic veins into into the wound.
cavernous sinus causing cavernous sinus throm-
bosis. It requires hospitalization and immediate ERYSIPELAS
aggressive treatment with higher generation
It is a spreading inflammation of the skin and
antibiotics (Penicillins, Cephalosporins).
subcutaneous tissues due to infection caused by
Streptococcus pyogenes. There will be always
LUDWIG’S ANGINA cutaneous lymphangitis (Fig. 2.3), with develop-
It is cellulitis of upper part of the neck involving ment of rose pink rash and cutaneous lymphatic
submandibular region and floor of the mouth edema. Vesicles form, which eventually ruptures
along the fascial planes. producing serous discharge.
Treatment
Penicillin, amoxicillin or cloxacillin.
PYOGENIC ABSCESS
It is localised collection of pus in a cavity lined by
granulation tissue, covered by pyogenic
membrane. It contains pus in loculi. Pus contains
dead WBC‘s, multiplying bacteria, toxins and
necrotic material (Fig. 2.4).
Fig. 2.2: Incision for draining—Ludwig’s angina
Fig. 2.3: Lymphangitis of the leg.

Note typical redness over the lesion
Fig. 2.4: Pyogenic abscess—Parts
Sites Modes of Infection

• Orbit.
• Direct.
• Face.
• Hematogenous.
• Scrotum.
• Lymphatics.
In the face and orbit, it causes severe edema.
• Extension from adjacent tissues.
Clinical Features
Bacteria Causing Abscess
• Toxemia is always a feature
• Rash is fast spreading and blanches on • Staphylococcus aureus
pressure. It is raised with sharp margin. • Streptococcus pyogenes
• Discharge is serous (in cellulitis discharge is • Gram-negative bacteria (E. coli, Pseudo-
purulent) monas, Klebsiella).
• Milian’s ear sign is a clinical sign used to • Anaerobes.
differentiate erysipelas from cellulitis wherein Factors Precipitating Abscess Formation
ear lobule is spared. Skin of ear lobule is
adherent to the subcutaneous tissue and so • General condition of the patient: Nutrition,
cellulitis cannot occur. Erysipelas being a anemia, and age of the patient.
cutaneous condition can spread into the ear • Associated diseases: Diabetes, HIV, immuno-
lobule. suppression.
• Disease is common in poor hygienic debili- • Type and virulence of the organism.
tated individuals. • Trauma, hematoma, road traffic accidents.
..Persist and persevere, and you will find most things that are attainable, possible.
Clinical Features
• Fever often with chills and rigors.
• Localized swelling which is smooth, soft and
fluctuant.
• Visible (pointing) pus.
• Throbbing pain and pointing tenderness.
• Brawny induration around.
• Redness and warmth, with restricted move-
ment if around a joint.
(Commonly cellulitis occurs first which
eventually gets localized to form an abscess).
Visible (pointing) pus, tenderness, fluctuation are
the features of formed abscess.
Differences between cellulitis and pyogenic abscess

Cellulitis Pyogenic abscess
Diffuse (no edge) and Well-localized
spreading
Pus is not present, only Pus is present
inflammatory fluid
Not fluctuant Fluctuant
Should not be incised Should be incised and
and drained drained
Sites of Abscess
External sites (Figs 2.5 and 2.6)
Figs 2.5A and B: Abscess in the forehead region and face,
• Fingers and hand.
near right nasolabial groove. Note the well-localized lesion
• Neck.
• Axilla.
• Breast.
• Foot, thigh—here it is deeply situated with
brawny induration.
• Ischiorectal and perianal region.
• Abdominal wall.
• Dental abscess, tonsillar abscess and other
abscesses in the oral cavity.
Internal abscess
• Abdominal: Subphrenic, pelvic, paracolic,
amebic liver abscess, pyogenic abscess of
liver, splenic abscess, pancreatic abscess.
• Perinephric abscess.
• Retroperitoneal abscess.
• Lung abscess.
• Brain abscess. Fig. 2.6: Abscess in suboccipital region, which is a
• Retropharyngeal abscess. common site in diabetic patient
Investigations Procedure
• Total count is raised. Hilton‘s method of draining an abscess (Fig. 2.7).
• Urine sugar and blood sugar, to rule out Initially broad spectrum antibiotics is started
diabetes. (depending on severity, extent and site of the
• USG of the part or abdomen or other region abscess).
when required. Under general anesthesia or regional block
• X-ray in case of lung abscess. anesthesia*, after cleaning and draping, abscess
• Gallium isotope scan is very useful. is aspirated and presence of pus is confirmed.
• CT scan or MRI in cases of brain and thoracic Skin is incised adequately in the line parallel
abscess. to the neurovascular bundle, in the most
• Investigations relevant of specific types: Liver dependent position.
function tests, PO2 and PCO2 estimation, Next, pyogenic membrane is opened using
blood culture. sinus forceps** and all loculi are broken up. Pus
Complications of an Abscess is cleared from the abscess cavity and washed
with saline.
• Bacteremia, septicemia, and pyemia. A drain (either gauze drain or corrugated
• Multiple abscess formation (Metastatic rubber drain) is placed.
abscess). Wound is not closed. Wound is allowed to
• Destruction of tissues. granulate and heal. Sometimes secondary suturing
• Antibioma (common in breast abscess). or skin grafting is required.
• Sinus and fistula formation. Pus is sent for culture and sensitivity.
• Large abscess may erode into adjacent vessels Antibiotics are continued.
and can cause life threatening torrential
hemorrhage. For example, As in pancreatic
abscess.
• Abscess in head and neck region can cause
laryngeal edema, stridor and dysphagia.
Specific complications of internal abscess:
• Brain abscess can cause intracranial hyper-
tension, epilepsy, and neurological deficit.
• Liver abscess can cause hepatic failure,
rupture, and jaundice.
• Lung abscess can lead on to bronchopleural
fistula or septicemia or respiratory failure or
ARDS.
Treatment of an Abscess
Abscess should be formed before draining.
Fig. 2.7: All loculi should be broken with finger or sinus
Exceptions for this rule are— forceps while draining an abscess
Parotid abscess.
Breast abscess. * Local anesthesia is not used as it is not effective, because
Axillary abscess. pus is acidic and L /A will not act.
Thigh abscess. ** Sinus forceps do not have lock and has got serrations in
the tip. It is called as sinus forceps because it was initially
Ischiorectal abscess. designed and used to pack sinuses.
..Success is the ability to go from failure to failure without losing enthusiasm.

Treating the cause is important. CARBUNCLE
Counter incision is necessary in breast
Word meaning carbuncle is charcoal.
abscess and it is placed in upper quadrant.
• It is an infective gangrene of skin and subcu-
Deeper incision is necessary while draining
taneous tissue.
pus in radial and ulnar bursae, palmar spaces
• Staphylococcus organism is the main culprit.
and tenosynovitis.
• Common site of occurrence is back and nape
of neck (Fig. 2.8).
Problems in Drainage
• It is common in diabetics and after forty years
• Improper drainage. age.
• Bleeding. • It is common in males.
• Residual abscess or sinus formation.
Differential Diagnosis for an Abscess

Aneurysm, especially in popliteal, femoral and
axillary regions. So aspirating with a needle and
confirming the pus is important.
Soft tissue tumors Sarcomas may be smooth,
soft and warmer.
BOIL (FURUNCLE)
It is an acute staphylococcal infection of a hair
follicle with perifolliculitis, which usually
proceeds to suppuration and central necrosis.
Often boil opens on its own and subsides.
Treatment
• Antibiotics. Patient will be toxic, and in diabetic they are
• Drainage of boil. ketotic.
Complications Investigations
• Cellulitis. • Urine sugar and ketone bodies.
• Lymphadenitis. • Blood sugar.
• Hydradenitis (Infection of group of hair follicles). • Discharge for culture and sensitivity.
Differences between pyogenic abscess and cold abscess
Pyogenic abscess Cold abscess
Red, warm, tender, with signs of acute inflammation. No signs of acute inflammation.
Pyogenic bacteria are nonspecific organisms. Tuberculous bacteria.
(Strepto, Staphylo)
Dependent incision is used for drainage Nondependent incision is used.
Suturing of the wound is not done. Wound is sutured and curetted.
Drain is placed. Drain is not placed.
(Otherwise sinus will form which
is difficult to treat).
Clinical Features
• Pain and swelling in frontal region which is
warm, tender.
• Toxicity and drowsiness.
Complications
• Osteomyelitis of frontal bone.
• Spread of infection into intracranial cavity
leading to intracranial abscess (Extradural or
subdural abscess). So may present with
features of raised intracranial tension like
headache, coning and convulsions.
Investigations
• Total leukocyte count.
• ESR.
Fig. 2.8: Carbuncle is an infective gangrene of skin and • X-ray skull.
subcutaneous tissues. Typical site is nape of the neck • CT scan.
Treatment
• Proper control of diabetes.
• Antibiotics like penicillins, cephalosporins or
depending on culture and sensitivity.
• Drainage is done by a cruciate incision and
debridement of all dead tissues is done.
Excision is done later.
• Once wound granulates well, skin grafting
may be required.
POTT’S PUFFY TUMOR

It is formation of diffuse external swelling in the
scalp due to subperiosteal pus formation and scalp
edema (Fig. 2.9).
It originates commonly in frontal region and
may extend into other regions.
Fig. 2.9: Pott’s puffy tumor
Causes
• Chronic frontal sinusitis which eventually
suppurates and extends into subperiosteal Secondaries in skull or in brain.
region.
• Trauma causing frontal subperiosteal Treatment
hematoma. • Antibiotics and drainage under general anes-
• Chronic otitis media—occasionally. thesia before it spreads into cranial cavity.
..Learning patience takes a lot of patience!

• Once it extends into cranial cavity, it is treated Treatment
accordingly by formal neurosurgical decom- Excision.
pression, often using Dandy‘s brain cannula. Tissue is sent for histopathological study.
• Osteomyelitic skull bone often needs radical
removal with proper reconstruction. BACTEREMIA
It is presence of bacteria in blood.
PYOGENIC GRANULOMA SEPTICEMIA

(GRANULOMA PYOGENICUM) It is presence of overwhelming and multiplying
bacteria in blood with toxins.
• It is a common condition, which occurs in
face, scalp, fingers and toes.
• It may be due to minor trauma or minor
PYEMIA
infection. It is presence of multiplying bacteria in blood as
• Infection leads to formation of unhealthy emboli, which spread and lodge in different
granulation tissue, which protrudes through organs in the body like liver, lungs, kidneys,
the wound. spleen, brain causing metastatic abscess. This may
lead to Multi Organ Dysfunction Syndrome
Clinical Features (MODS). It may endanger life if not treated
• Usually single, well-localized, red, firm, properly.
nodule, which bleeds on touch (Fig. 2.10).
• May or may not be tender. Clinical Features
• Fever with chills and rigors.
Sites • Jaundice, oliguria, drowsiness.
• Face. • Hypotension, peripheral circulatory collapse
• Scalp. and later coma with MODS.
• Fingers.
• Toes. Common Causes
• Urinary infection (most common).
• Biliary tract infection.
• Lower respiratory tract infection.
• Abdominal sepsis of any cause.
• Sepsis in diabetic and immunosuppressed
individuals like HIV, steroid therapy.
Investigations
• Total leukocyte count.
• Pus culture.
• Blood culture.
• Urine culture.
• Blood urea and serum creatinine.
Fig. 2.10: Pyogenic granuloma in the nose • LFT.
Differential Diagnosis Treatment

• Hemangioma. • Monitoring of vital parameters.
• Papilloma. • Antibiotics, (Ceftazidime, Cefoperazone,
• Skin adnexal tumors. Ceftriaxone sodium).
• IV fluids, maintenance of urine output. Pathogenesis
• Hydrocortisone.
• Blood and plasma transfusion.
• Nasal oxygen, ventilator support, monitoring
of pulmonary function.
TETANUS
It is an infective condition caused by Clostridium
tetani organisms leading to reflex muscle spasm,
often associated with tonic-clonic convulsions.
Organism
Clostridium tetani is a gram-positive, anaerobic,
motile, noncapsulated, organism with peritrichous
flagella, with terminal spores (Drum stick
appearance).
Spore is the infective agent. They are found
in soil, manure, dust, etc.
Spore can gain entry through any wound,
prick injuries, injuries resulting from road traffic
accidents, penetrating injuries, foreign body,
anaerobic condition, etc. • Tonic-clonic convulsions.
• Abdominal wall rigidity often with hema-
Clinical Features toma formation.
Symptoms • Severe convulsion may often lead to fractu-
• Jaw stiffness, pain and stiffness in the neck res, joint dislocations and tendon rupture.
and back muscles. • Fever and tachycardia.
• Anxiousness, sweating. • Retention of urine (due to spasm of urinary
• Headache, delirium, sleeplessness. sphincter), constipation (due to rectal spasm).
• Dysphagia. • Rarely features of carditis are seen due to
involvement of the cardiac muscle, which is
• Dyspnea.
dangerous, as it often leads to cardiac arrest
Signs and death. Here steroids are very useful.
• Trismus, due to spasm of masseter and • Symptoms will be aggravated by stimuli like
pterygoids. light, noise.
• Risus sardonicus (smiling face), due to spasm Incubation period
of the facial muscle—zygomaticus major. • Time between the entry of spore and appearance
Looks as if patient is smiling. of first symptom.
• Neck rigidity. • Usually 7–10 days.
• Spasm and rigidity of all muscles. • Shorter the incubation period worser the
• Hyperreflexia. prognosis and more severe the course of
• Respiratory changes. disease.
..Perceive....Conceive....Believe....Achieve!!
Period of onset Staging of tetanus
• Time between appearance of first symptom • Mildly ill: Rigidity, spasm, trismus and
and appearance of first sign. different postures.
• Shorter the period of onset worser the • Seriously ill: Spasm, rigidity, severe
prognosis and vice versa. respiratory infections.
Effects on respiratory system • Dangerously ill: Cyanosis with respiratory
Diaphragm and other muscles of respiration failure and tonic-clonic convulsions.
undergo spasm causing tachypnea, respiratory
distress, respiratory infections, aspiration, Differential Diagnosis
cyanosis, and respiratory failure with altered PO2
and PCO2 levels. • Strychnine poisoning.
• Trismus due to other causes like—Dental,
Types of Tetanus oral, tonsillar sepsis, oral malignancy.
• Meningitis.
• Early tetanus: It is a severe form with a short • Hydrophobia.
incubation period and poor prognosis.
• Convulsive disorders.
• Latent tetanus: Wound is healed and
Culture media for Clostridium tetani are RCM
forgotten. After a long incubation period,
media and nutrient agar.
may be years later, under favorable
environment, spores release bacteria and
cause tetanus. It carries better prognosis. Treatment
• Late tetanus: Disease develops many months Patient is admitted and isolated in a dark, quiet
after injury. room.
• Ascending tetanus: Symptoms and signs Antitetanus globulin (ATG), 3000/units IM
progress from below upwards. stat. Test dose is not required. (It is human
• Descending tetanus: Symptoms and signs
immunoglobulin).
progress from above downwards.
Antitetanus serum (ATS). When ATG is not
• Cephalic tetanus: Facial muscles are involved
available or when patient cannot afford it, as it
first (3rd, 4th, 6th and 7th cranial nerves can
get involved) is expensive ATS is given. After IV test dose (1000
• Localized tetanus. units of ATS), full dose of ATS, i.e. 1, 00,000 units,
• Bulbar tetanus: Muscles of deglutition and half of it IM and half of it IV, is given. It is a
respiration are involved. Highly fatal. horse serum, and so possibility of anaphylactic
• Tetanus neonatorum: Tetanus occurring in reactions should be kept in mind.
neonates. Spread is through umbilical cord. Wound debridement, drainage of pus,
• Urban tetanus. Due to repeated injections in injection of ATG 250-500 units locally to reduce
IV drug abusers. the toxin effect.
Ryle‘s tube is passed, initially to decompress,
Different postures in tetanus and so as to prevent aspiration, but later for
• Opisthotonus: Posterior muscles are acting feeding purpose.
more, so backward bending. Catheterization.
• Orthotonus: Straight posture. Both front and IV fluids and electrolyte balance has to be
back muscles are acting equally. maintained.
• Emprosthotonus: Forward bending as front Tetanus toxoid should be given as disease
muscles are acting more. will not give immunity against further infections.
• Pleurosthotonus: Lateral bending, as lateral To start—first dose; second dose after one month,
muscles act more. third dose after six months.
IV Diazepam 20 mg 4th or 6th hourly. Dose Various strains include—A,B,C,D,E.
is adjusted depending on severity and ‘A’ strain is commonest.
convulsions.
IV Phenobarbitone 30 mg 6th hourly. Exotoxins
IV Chlorpromazine 25 mg 6th hourly. • Lecithinase is important toxin, which is
Injection crystalline penicillin 20 lacs 6th hemolytic, membranolytic and necrotic
hourly, injection gentamicin and metronidazole
causing extensive myositis.
to prevent secondary infection.
• Hemolysin causes extensive hemolysis.
Regular suction and clearance of respiratory
• Hyaluronidase helps in rapid spread of gas
tract.
gangrene.
Nasal oxygen.
• Proteinase causes breaking down of proteins
In severe cases, patient is curarised and placed
in the infected tissue.
in ventilator (IPPR).
Endotracheal intubation or tracheostomy are
often life saving.
Good nursing care—Change of position,
prevention of bedsores, prevention of DVT
(which is common in tetanus and often requires
heparin injection).
Chest (respiratory) physiotherapy during
recovery period.
Steroids to be given when carditis is suspected.
Following treatment, patient often gets spasm of
different muscles (ticks) for a long period of time
which can be prevented by giving Methocarbamol for Effects
6 months to one year. • Extensive necrosis of muscle with production
of H2S gas, which stains brown or black.
GAS GANGRENE • Usually involves muscle from origin to
It is an infective gangrene caused by clostridial insertion.
organisms involving mainly skeletal muscle. • Often may extend into thoracic and abdo-
Earlier it was called as malignant edema. minal muscles.
• When it affects the liver it causes necrosis
Organisms
with frothy blood—foaming liver, is
• Clostridium welchii (Perfringens): Gram- characteristic.
positive, central spore bearing, nonmotile,
capsulated organisms.
• Clostridium oedematiens. Clinical Features (Fig. 2.11)
Clostridium septicum. Incubation period is 1–2 days.
• Clostridium histolyticus. • Features of toxemia, fever, tachycardia,
Clostridium welchii produce toxins— pallor.
Alpha (Commonest). • Wound is under tension with foul smelling
Beta. discharge.
Epsilon. • Khaki brown colored skin due to hemolysis.
Iota. • Crepitus can be felt.
Perfection is the best excuse.

• Jaundice may be ominous sign and oliguria • Electrolyte management.
signifies renal failure. • In severe cases amputation has to be done as
a life saving procedure.
Clinical Types • Often ventilator support is required.
• Fulminant type—causes rapid progress and • Once a ward or operation theater is used for a
often death due to toxemia, renal failure or patient with gas gangrene, they should be
liver failure or MODS. fumigated for 24-48 hours properly to prevent the
• Massive type—infection involving whole of risk of spread of infection to other patients.
one limb containing fully dark colored gas
filled areas. TUBERCULOSIS (FIG. 2.12)
• Group type—infection involving one group
of muscles. Extensors of thigh, flexors of leg. It is commonly caused by Mycobacterium tuber-
• Single muscle type—affecting one single culosis; occasionally by Mycobacterium bovis,
muscle. M. kansasii, M. fortuitum, M. marinum, M. ulcerans.
• Subcutaneous type—of gas gangrene M. tuberculosis is gram neutral, acid-fast and
involves only subcutaneous tissues (i.e. alcohol-fast, straight or slightly curved rod.
Superficial involvement). It is prevalent in most of the developing
countries and has made its resurgence in the
Investigations developed countries with the advent of AIDS.
X-ray shows gas in muscle plane or under the skin. Pathogenesis
Liver function tests, blood urea, serum
The characteristic lesion here is ‘tubercle’, which
creatinine, total count, PO2, PCO2.
is an avascular granuloma composed of a central
zone containing giant cells, with or without
caseation necrosis, surrounded by a rim of
epithelioid cells, lymphocytes and fibroblasts.
It can occur in almost all organs in the body.
Presentation may vary depending on the
Fig. 2.11: Gas gangrene of forearm and hand after an individual sites.
axe injury. Patient underwent above-elbow amputation and
survived
Treatment
• Injection Benzyl penicillin 20 lacs 4th hourly
+ Injection Metronidazole 500 mg 8th hourly
+ Injection Aminoglycosides (if blood urea
is normal).
• Fresh blood transfusion.
• Polyvalent antiserum 25,000/units given
intravenously after a test dose and repeated
after 6 hours. Fig. 2.12: Tuberculous lymphadenitis with tuberculous ulcer
• Hyperbaric oxygen is very useful.
• Liberal incisions are given. All dead tissues General Features
are excised and debridement is done until • Low grade fever with evening rise of
healthy tissue bleeds. temperature.
• Rehydration and maintaining optimum urine • Loss of appetite.
output (30 ml/hour) {0.5 ml/Kg/hour}. • Weight loss.
Investigations • Borderline lepromatous.
• ESR is raised; peripheral smear—lympho- • Borderline.
cytosis. Paucibacillary types
• AFB (Acid fast bacillus) staining using Ziehl- • Borderline tuberculoid
Neelsen stain. • Tuberculoid leprosy: Here strong host
• Chest X-ray to rule out pulmonary tuber- resistance is observed. The disease is more
culosis. localized, but it causes more deformities due
• Culture of the organism—Löwenstein-Jensen to early involvement of nerves. Bacilli are
media. scanty in the lesion and so infectivity is
• Mantoux skin test. minimal.
• Guineapig inoculation.
• Relevant investigations depending on the site Investigations
of the tuberculosis. • Regular checking of sensation of the
suspected area.
Treatment • Split skin smear from lesion or ear lobule.
• Antituberculous drugs are given for 6 months • Nerve biopsy—sural nerve.
to one year.
• Specific treatment is given depending on the Treatment
site of the tuberculosis. Dapsone 100 mg daily.
(Please refer individual chapters for details Rifampicin 600 mg once a month.
about tuberculosis at different locations and also Clofazimine 50 mg daily + 300 mg once a
chapter drugs for Antituberculous therapy). month.
For paucibacillary types treatment is for 6
LEPROSY (HANSEN’S DISEASE) months.
For multibacillary types treatment is for 2 yrs
It is caused by Mycobacterium leprae. It is a gram- or more
positive, acid-fast bacillus.
It mainly involves skin, nasal mucosa and Surgical Complications in Leprosy
peripheral neural tissues. Primary deformities
It involves only the cooler parts of the body. • Leonine facies.
(So axilla, gluteal region are not involved). • Collapsed nasal bridge.
Testicular involvement is seen but not the ovary. • Upper branch facial nerve palsy (causes
It does not involve the vital organs. Though not lagophthalmous).
• Keratitis and blindness.
acutely fatal, the disease leaves the victim
• Claw hand either ulnar or combined ulnar
severely deformed and crippled for life.
and median nerves.
• Radial nerve palsy—wrist drop (1%)
Types
• Clawing of toes due to involvement of
Multibacillary types posterior tibial nerve.
• Lepromatous leprosy: Denotes little or no • Foot drop due to involvement of lateral
host resistance. Bacilli are seen in large popliteal nerve.
numbers in the superficial nodular lesions • (Medial popliteal nerve, which supplies the
and the patient is highly infective. tibialis posterior nerve is never involved).
..Positive attitudes create a chain of positive thoughts.

Secondary deformities • Painless, punched out, gummatous ulcers are
• Anesthesia of the part makes it prone to seen with ‘wash leather base’ and silvery tissue
trauma, infection, infective gangrene, des- paper scar. It is a hypersensitivity reaction.
truction, autoamputation and functionless • Neurosyphilis.
parts. • Cardiovascular syphilis—dissecting thoracic
• Trophic ulcers in the foot are common. aortic aneurysm is common.
Treatment Investigations
Reconstructive surgeries—
• VDRL test; Kahn test.
• Release of contractures.
• Treponema pallidum hemagglutination test
• Tendon transfers.
(TPHA).
• Arthrodesis. • Treponema pallidum immobilization test (TPI).
• Ulcer management.
• Physiotherapy and rehabilitation. Treatment
• Penicillin for 15 days is the drug of choice.
SYPHILIS (GREAT POX, FRENCH • Doxycycline 100 mg can be given thrice daily
DISEASE) for 15 days.
• Others: Erythromycin, Tetracycline, Cephalo-
It is a venereal infection caused by Treponema sporins.
pallidum. Jarisch-Herxheimer reaction is commonly seen
Early syphilis: It lasts for 2 years and the patient after penicillin, which often requires steroid
therapy.
is infective during this period.
Primary syphilis: It presents as a ‘Hunterian CONGENITAL SYPHILIS
chancre’. It is a shallow, painless, indurated, non- Here the infection is transmitted from the
bleeding ulcer usually seen in the genitalia and mother to fetus through placenta.
often on the lips. It occurs in 3–4 weeks after the Early congenital syphilis: It is seen in newborn.
infection. It is confirmed by dark field micro- Features are—
scopic study of the discharge for the organism. • Rash, syphilitic snuffles.
• Nasal discharge, weight loss.
Secondary syphilis: It occurs in 6–12 weeks.
• Periostitis, meningitis, hepatosplenomegaly.
It presents as:
• Pneumonia alba.
– Cutaneous coppery rashes.
– Snail-track oral ulcers. Late congenital syphilis:
– Painless, shotty lymphadenopathy.
Hutchinson‘s triad:
– Moth eaten alopecia.
– Interstitial keratitis.
– Hepatitis, arthritis, iritis.
– 8th nerve deafness.
– Syphilitic osteitis with ‘ivory’ sequestrum.
– Hutchinson‘s teeth: Peg-shaped upper
– Meningitis. incisors, moon‘s molar, molars with cusps.
Latent syphilis: It lasts between 2 years to life
time. Serum tests are positive. • Hutchinson’s triad.
• Congenital neurosyphilis.
Late (tertiary) syphilis: • Cutaneous, skeletal or visceral gummas.
• Here vasculitis and obliterative endarteritis • Saddle nose.
occurs. • Sabre tibia, Clutton‘s joint.
• Perforated palate. • Through blood it may cause pyemia and
Congenital syphilis is treated with penicillins. endanger life.
ACTINOMYCOSIS Investigations
It is caused by Actinomyces israelii. • Pus under microscopy shows branching
It is an anaerobic gram-positive fungal like filaments.
bacterium, which is a branching filamentous • Gram‘s staining shows gram-positive mycelia
organism. It is called as ‘Ray fungus’ because of in center with gram-negative radiating peripheral
sun-ray appearance. filaments. These clubs are due to host reaction,
which are lipoid material.
Clinical Types • Cultured in brain heart infusion agar and
thioglycolate media.
Faciocervical: Infection is either from tonsil or
from adjacent infected tooth. Initially an indu- Differential Diagnosis
ration develops. Nodules form with involvement
of skin of face and neck. It softens and bursts • Chronic pyogenic osteomyelitis.
through the skin as sinuses which discharge pus • Carcinomas at the site.
containing sulfur granules (60%). • Tuberculous disease.
Thorax: Lungs and pleura get infected by direct Treatment

spread from pharynx or by aspiration. Empyema • Penicillins for longer period (4–6 weeks).
develops. Later nodules appear over the chest • Tetracyclines and lincomycin.
wall leading to discharging sinuses (20%). • Dapsone and iodides.
In right iliac fossa, it presents as a mass • Antifungals are often given because it is
abdomen with discharging sinus. From the fungal like bacteria.
intestine organisms migrate across into the • Surgical debridement is occasionally requi-
pericecal region causing inflammatory reaction red.
and later gets adhered to the anterior abdominal
wall causing multiple discharging sinuses.
Liver is infected through portal vein. MADURA FOOT (MYCETOMA PEDIS)
• It is a chronic granulomatous condition of the
Pathogenesis
foot causing multiple discharging sinuses in
Organism enters through deeper plane of the the foot (Fig. 2.13).
tissue, causes subacute inflammation with • It was first identified in Madurai by Gill.
induration and nodule formation. Eventually • It is common in India and Africa.
discharging sinus forms at the surface. Pus • It is common in Tamil Nadu.
collected in a swab or sterile tube will show
sulfur granules.
Organisms
Clinical Features • Nocardia madurae, (commonest).
• Discharging sinus with induration and • Nocardia brasiliensis
nodules. • Nocardia asteroides
• No lymph nodal involvement. • Actinomyces israelii.
..Positive attitudes create positive people.

Regional lymph nodes are not involved.
Condition deteriorates by secondary bacterial
infection.
Clinical Features
• Painless diffuse swelling in the foot of long
duration.
• Later multiple discharging sinuses develop
in the skin.
• Lymph node involvement will not occur
unless there is secondary bacterial infection.
• Significant limb disability is common.
• Chronic osteomyelitis.
• Tuberculous osteomyelitis.
• Carcinoma.
Fig. 2.13: Madura foot. Note the multiple sinuses Investigations

• Discharge study shows branching fila-
mentous appearance.
Pathogenesis
• Culture in Sabourad‘s dextrose agar medium.
• Gram stain for actinomycosis shows sun-ray
appearance with gram +ve center and gram
–ve clubs.
• X-ray of the foot to look for osteomyelitis.
Treatment
• Antifungal drugs—Amphotericin.
• Long-term penicillins.
• Dapsone.
• Iodides.
• In severe cases amputation may be required.
If infection occurs in the hand it is called as
Discharging granules may be black, red, yellow. Madura hand.
In black type of Madura foot, infection is
mainly subcutaneous. RABIES (HYDROPHOBIA)
In red and yellow types, it burrows into the
deeper plane including the underlying bone It is an acute fatal encephalomyelitis caused by
causing bone necrosis (osteomyelitis). Eventually Lyssavirus type 1.
gross swelling of the limb with multiple It is rare in developed countries. It is common
discharging sinuses with disability occurs. in developing countries. It is common in India.
Muscles and bones are involved. Only country where rabies is not seen is
Tendons and nerves are affected. Maldives.
Pathogenesis Local application of antirabies serum into the
It is commonly due to dog bite. Other animals, wound at the earliest is effective in reducing the
which often can cause rabies are cat, jackal, wolf, infection rate.
bat, mongoose, monkey, horse, sheep, goat. Antibiotics: The dog is observed for 10 days.
Transmission is through saliva of the animals. If dog shows symptoms then antirabies vaccine
It is commonly through bite or lick. is advised.
Asymptomatic carrier stage can occur in Vaccination: Antirabies serum.
animals but they are unlikely to be infective
during carrier stage. Classification of Wounds
It is considered that only symptomatic Class I: Touching the diseased animal, lick over
animals are infective. intact skin or scratches without oozing of blood.
Street virus of the Lyssavirus type 1 is the
infective one. Class II: Licks on broken skin, scratches with
(Fixed virus is noninfective and is used for blood ooze, all bites except head, face, palm and
vaccine). fingers.
Virus passes through the peripheral nerve Minor wounds less than five in number.
into the central nervous system and develops Class III: All bites over head, face, palm and
Negri bodies in the brain leading to fatal fingers. Lacerated wounds, wounds more than
encephalomyelitis. five in number, wild animal bites.
It also involves the salivary glands to get
secreted in the saliva to cause infection. Indications for antirabies vaccination
• All rabid animal bites.
Clinical Features • If animal is killed or dies during 10 days of
observation period.
• Incubation period is 3–6 weeks.
• Bite by an unidentified animal.
• Prodromal symptoms like fever, headache.
• If lab tests in animal show positive for rabies.
• Hyperexcitability and irritability.
• All wild animal bites.
• Hydrophobia (fear of water).
• Aerophobia (fear of air).
• Mental instability. Vaccines for Rabies
• Once disease starts, patient dies in 72 hours. 1. BPL inactivated vaccine: It is nervous tissue
Fear of water is seen only in affected human beings vaccine.
not in animals. It is 5% emulsion of the infected brain of the
sheep containing the inactivated fixed virus.
Prophylaxis
Dosage: (as recommended by Pasteur Institute,
Postexposure prophylaxis
Coonoor)
The wound is cleaned initially with running
water and soap for 5 minutes, and later with Adult Children
povidone iodine or alcohol (40–70%). Class I 2 ml 1 ml 7 days.
Suturing of the wound should not be done. Class II 3 ml 3 ml 10 days.
Because suturing hastens the spread of virus into Class III 5 ml 3 ml 10 days.
the deeper plane.
..Praise loudly and blame softly.

Mode of administration: Into the abdominal (maximum up to 3000/units). Half is given into
wall, subcutaneously using long needle. the wound and another half given into the gluteal
Antibody develops in 7–30 days. Protection muscle(IM). Single dose.
lasts only for 6 months.
Human rabies immunoglobulin (HRIG): Dose is
Booster doses are given when used along
20 units/Kg body weight. Part is injected into
with antirabies serum.
the wound remaining part into the muscle (IM).
Side effects Single dose.
• Headache, palpitation, allergic reactions. Patient should be immunized actively along
• Redness, tenderness and swelling at the site with serum with additional booster doses.
of the vaccination.
Side effects: Serum sickness, anaphylaxis.
• Post-vaccinal neuroparalysis—a dangerous life
threatening complication. Pre-exposure prophylaxis is given to veteri-
• During therapy patient should avoid alcohol narians, animal handlers.
and steroids. Dose: 1 ml of cell culture vaccine IM or 0.1
2. Nervous tissue vaccine derived from ml intradermally on 0, 7, 28 days.
suckling mouse brain. Booster doses are given once in every 2 years.
3. Duck embryo vaccine (DEV) has got less Post-exposure vaccination is done if individual
neuroparalytic side effects. It is not available in has been vaccinated earlier: Doses on 0, 3, and
India. 7 days are given. Passive immunity is not given
4. Cell culture vaccines: They are more potent in individuals who had vaccination earlier.
and safer.
Human diploid cell vaccine (HDCV): Safest RABIES IN DOGS
vaccine. But it is costly. It is available in India.
Incubation period: 10 days to 8 weeks.
Second-generation tissue culture vaccines: They are
potent and cost effective. They are derived from Types
nonhuman base sources. Examples are chick Furious type: Here dogs are aggressive.
embryo fibroblast, fetal bovine kidney, hamster
kidney cells, vero cells. Dumb type: Dog is paralytic and sleepy.
Once symptoms of rabies develop in a dog
Dosage: 2.5 IU in one ml One ml is given daily it rarely survives more than a week.
IM into the deltoid on 0, 3, 7, 14, 28 and 90 Dog brain is sent for study in 50% glycerol-
(optional) days. saline solution.
Side effects: Headache, redness at the site, fever. Lab tests to confirm rabies in dogs/animals:
No other serious side effects. Fluorescent antibody test (FRA test): It is reliable
Second generation tissue culture vaccine can also test.
be given intradermally. Intradermal dose is one Microscopic examination of the brain of the
fifth of the intramuscular dose (0.1 ml). infected dead animal to look for NEGRI bodies.
Mouse inoculation test is very sensitive test.
Passive Immunity Corneal test is simpler but negative result
It is used in all severe exposures and in all wild does not rule out the possibility of infection.
animal exposure.
Immunization in Animals
Types BPL inactivated nervous tissue vaccine: Single
Horse antirabies serum (ARS): It is given on first dose 5 ml to dogs. 3 ml to cats. Second dose after
day with a dose of 40 IU/Kg body weight 6 months. Then once a year regularly.
Modified live virus vaccine: Dose—3 ml Sources
single dose which is repeated once in 3 years. • Contaminated infected wounds.
Control of stray dogs and immunization of • Urinary tract infections.
all dogs will reduce the incidence of rabies. • Respiratory tract infections.
• Opportunistic infection.
ANTHRAX • Abdominal wounds with severe sepsis.
It is caused by Bacillus anthracis, which is a gram- Spread can occur from one patient to another,
positive, aerobic, spore forming, capsulated, non- through nurses or hospital staff who fail to
motile, non acid-fast bacillus. It is resistant to heat practice strict asepsis.
and antiseptics. It
is more common in—
Disease is common in cattle and seen in • Diabetics.
people who handle carcasses, wool, and hairs. • Immunosuppressed individuals.
It is often used in biological war. • Patients on steroid therapy and life sup-
porting machines.
Types • Instrumentations (indwelling catheter, IV
Cutaneous Type cannula, tracheostomy tube).
It is the commonest type and occurs within • Patients with artificial prosthesis.
3–4 days after infection.
Indurated papule with black slough sur- Organisms
rounded by vesicles—malignant pustule. Itching Staphylococcus aureus is the commonest organism
is common in papule. causing wound infection. Others are pseudomo-
Regional lymph nodes are involved. nas, klebsiella, E. coli, proteus.
Toxemia is common. Streptococcus pneumoniae, Haemophilus,
Woolsorter‘s disease is respiratory type, and Herpes, Varicella, Aspergillus, Pneumocystis
is due to inhalation of spores causing pneumonia. carinii are the commonest pathogens involved
It is more dangerous and life threatening. in respiratory tract infection, which spreads
Alimentary type is due to ingestion of spores. through droplets.
Klebsiella is the commonest pathogen
Diagnosis involved in hospital acquired UTI, which is
Culture of fluid shows medusa head appearance. highly resistant to drugs.
It shows positive M‘Fadyean reaction and
positive Ascoli‘s thermoprecipitation test. Management
Most of the time, organisms involved are multi
Treatment drug resistant, virulent and hence, cause severe
Penicillins. sepsis.
Ciprofloxacillin. • Antibiotics.
• Isolation.
• Blood, urine, pus for culture and sensitivity
NOSOCOMIAL INFECTION to isolate the organisms.
(HOSPITAL ACQUIRED INFECTION) • Blood transfusion, plasma or albumin
It is an infection acquired because of hospital therapy.
stay. • Ventilator support.
..Not in time, place and circumstance, but in man lies success...

• Maintaining optimum urine output. Fungal: Candida, aspergillus, yeast.
• Nutritional support.
Protozoal: Cryptosporidia (causes diarrhea),
Pneumocystis carinii.
Prevention
Because there is poor defence mechanism,
• Isolation of patients with badly infected open infection is severe and often life threatening.
wounds, severe RTI\UTI.
• Following strict aseptic measures in OT and Investigation
in ward by hospital attendents.
• Swab culture.
• Proper cleaning and use of disinfectant
• Blood culture.
lotions and sprays for bedpans, toilets, floor.
• Pus culture.
• The precipitating cause has to be identified
and treated, along with taking care of proper Treatment
nutrition and improving the anemic status
by blood transfusion. • These infections are difficult to treat as they
are often multi drug resistant.
• Combination of broad-spectrum antibiotics—
OPPORTUNISTIC INFECTIONS Cephalosporins, aminoglycosides, metro-
They are normally of low pathogenicity, occur nidazole is given.
through therapeutic invasive procedures and are • Depending on culture and sensitivity appro-
common in immune deficiency. priate antibiotics are given.
Immune deficiency may be due to— • Often ventilatory support and critical care are
• Diabetes. required.
• HIV.
• Steroid therapy. NECROTIZING FASCIITIS
• Radiotherapy. It is spreading inflammation of the skin, deep
• Immunosuppressive therapy in trans- fascia and soft tissues with extensive destruction,
plantation. and toxemia commonly due to Streptococcus pyo-
• Cytotoxic chemotherapy. genes but often due to mixed infections like
• Starvation and old age. anaerobes, coliforms, and gram-negative organis-
Therapeutic invasive procedures may be in ms.
the form of IV cannula, bladder catheterization, It is common in old age, diabetics, immuno-
tracheostomy and other minor surgical suppressed, malnourished, obesity, steroid
procedures, which permit the skin organisms therapy and HIV patients.
like Streptococcus epidermidis to penetrate the skin It can occur in limbs (Fig. 2.14), lower
and invade the deeper tissues. abdomen (Meleney‘s infection), groin, and
perineum.
Organisms
Muscle is usually not involved in necrotizing
Bacteria: fasciitis.
• Gram-negative: E. coli, Pseudomonas,
Klebsiella, Proteus, Serratia. Types
• Gram-positive: Staph. epidermidis, Streptococcus Type I—It is due to mixed infection. It is usually
pneumoniae. not precipitated by injury.
Viruses: Herpes, CMV, varicella zoster, may Type II—It is due to Streptococcus pyogenes,
cause fatal pneumonia. usually due to minor trauma like abrasions.
• Rapid spread in short period (in few hours).
• Features of SIRS, MODS with drowsy, ill
patient.
• Condition may be life threatening if not
treated properly.
Management
• IV fluids, fresh blood transfusion.
• Antibiotics depending on culture and sensi-
tivity or broad spectrum antibiotics. High
dose penicillins are very effective. Clinda-
mycin, third generation Cephalosporins,
Aminoglycosides are also often needed.
• Catheterization and hourly urine output
monitor.
• Hematocrit, serum creatinine assessment.
• Pus culture, blood culture.
• Electrolyte management and monitoring.
• Control of diabetes if patient is diabetic.
• Oxygen, ventilator support, dopamine, dobu-
tamine supplements whenever required.
• Radical wound excision of gangrenous skin
and necrosed tissues at repeated intervals.
• Once patient recovers and healthy granu-
lation tissue appears, spilt skin grafting is
done. As it commonly involves large area,
mesh graft (meshing of SSG) is needed.
ACUTE PYOMYOSITIS
It is infection and suppuration with destruction
Figs 2.14A to C: Necrotizing fasciitis of the leg in different of skeletal muscles, commonly due to Staphylo-
patients. Note the extensive involvement of the legs coccus aureus and Streptococcus pyogenes,
occasionally due to gram-negative organisms.
Clinical Features It is common in muscles of thigh, gluteal
• Sudden onset of swelling and pain in the part region, shoulder and arm.
with edema, discoloration, necrotic areas, Precipitating factors are similar to necrotizing
and ulceration. fasciitis.
• Foul smelling discharge. Creatine phosphokinase will be very high
• Features of toxemia with high-grade fever and signifies acute phase.
and chills, hypotension. Renal failure is common.
• Oliguria often with acute renal failure due MRI is useful.
to acute tubular necrosis. Treatment is antibiotics, wound excision and
• Jaundice. compartment release often with hemodialysis.
..Prefer a loss to dishonest gain; the one brings pain at the moment; the other for all the time.
HIV INFECTION AND AIDS • Blood transfusions, organ transplantations.

(ACQUIRED IMMUNODEFICIENCY Disease is common in Africa and Asian
countries.
SYNDROME)
HIV mainly harbors in semen, genital
HISTORY secretions, blood, pus, sputum, saliva and other
• 1983: Discovery of the virus. First case of body fluids.
AIDS detected in UK.
• 1984: Development of an antibody test. Anti-HIV Antibody
• It appears about 3 weeks to 3 months after
Definition of AIDS exposure.
Confirmed HIV infection with CD4 T-lympho- • It always indicates infection.
cyte count < 0.2 × 10 6/1 with symptoms. • It has got weak neutralizing capacity.
• It persists throughout the HIV infection.
Human Immunodeficiency Virus
It was discovered by Barre-Sinoussi and Tests for HIV
Montagnier in 1983.
• ELISA test (screening test).
Types • Western blot test (diagnostic test).
• Polymerase chain reaction (PCR).
• Human T-lymphocyte Virus I
• Anti-HIV detection.
• Human T-lymphocyte Virus II
• Viremia quantification—to start treatment and
• Human T-lymphocyte Virus III.
to see the response of antiviral drugs (useful
They are retroviruses.
if it is within 0.5 log10).
• CD4+ count.
Clinical classification of HIV infection
Normal value >500/mm3.
I: Acute infection.
Values between 200–500/mm3 is seen in
II: Asymptomatic but positive HIV.
Kaposi’s sarcoma, Candida infection,
III: Persistent generalized lymphadenopathy.
Mycobacterium tuberculosis.
IV: AIDS (HIV related diseases).
Values between 50–200/mm 3 is seen in
Constitutional diseases like weight loss,
Pneumocystis carinii and Toxoplasma
fever, diarrhea.
infections.
Neurological diseases—Dementia, neuro-
Values < 50/mm3 is seen in atypical myco-
pathy, myelopathy.
bacteria, cytomegalovirus, lymphomas.
Opportunistic infections.
After HIV infection, there is a time gap for
Malignancies—Kaposi‘s sarcoma, non-
the patient to become reactive to tests. This time
Hodgkin‘s lymphomas, primary cerebral
gap is called as ‘Window period’. This period is
lymphomas.
variable. But during this period, the individual
Other diseases attributable to HIV infection.
is infective.
Mode of Transmission
PATHOGENESIS
• Sexual intercourse—vaginal or anal.
• Needle pricks—Using unsterilized needles Envelope glycoprotein of HIV binds with the
for injections, in IV drug abusers, careless surface molecule CD4 of T-lymphocytes, mono-
handling. cytes, macrophages, cutaneous Langerhan‘s
• Mother-to-child—During birth through cells, dendritic cells of all tissues.
vaginal secretion, transplacental, through CD4 of lymphocytes—T-helper cells induce
breast milk. and control the normal immune response.
HIV completely suppresses immune res- • CNS lymphomas.

ponse directly by suppressing ‘T’ cell, indirectly • Anogenital squamous cell carcinoma.
by suppressing ‘B’ cell. Finally it dismantles/ • Testicular tumors (Germ cell types).
destroys the immune system making the indi- • Lung cancer.
vidual prone for opportunistic infections. • GIT lymphomas and adenocarcinomas.
After HIV infection, antibodies develop to
virus envelope and core proteins which persists
Pulmonary Problems in HIV Infection
throughout life.
• Pneumonia.
General features in HIV • Tuberculosis.
• Weight loss more than 10%. • Fungal infections.
• Fever more than 1 month. • Pneumocystis carinii pneumonia.
• Diarrhea more than 1 month. • Cytomegalovirus pneumonia.
• Neuralgia, arthralgia, headache.
• Lymphadenopathy.
• Cutaneous rashes, dermatitis, fungal
(candida), bacterial, viral (herpes simplex
1 and 2).
• Dental infection, gingivitis, candidiasis of
oral cavity and esophagus.
• Varicella zoster infection.
• Opportunistic infections.
• Poor healing after surgery, trauma, infection
with more complications. Cold abscess with
a discharging sinus in HIV patient can be
seen in Figure 2.15
Tumors in HIV Infection

• Kaposi’s sarcoma.
• Lymphomas (NHL common).
Fig. 2.15: Cold abscess with a discharging
• Cervical cancer. sinus in HIV patient
..Problems are only opportunities in work clothes.

GI Problems in HIV Infection Counseling of HIV patients and their families.
Life expectancy after initial HIV infection is
• GIT infections—bacterial, protozoal, viral.
8–10 years.
• Kaposi‘s sarcoma, lymphomas, adenocarci-
nomas. Prevention
• Hepatitis (‘C’ virus), cholestasis.
Continues to be our best weapon in combating
• Anorectal diseases.
the menace of HIV infection.
• Abdominal tuberculosis.
• Safe sex.
• Condom usage reduces the risk of trans-
Neurological Problems in HIV Infection
mission.
• Encephalitis, aseptic meningitis, myelitis. • Health education.
• Neuropathies with demyelination. • Use of disposable needles to prevent
• Opportunistic infections like toxoplasma, infections.
cryptococcus causing severe meningitis.
• Primary CNS lymphomas. Universal precautions against HIV
• CNS tuberculosis (tuberculomas). • Care in handling sharp objects like needles,
• Visual problems. blades.
• All cuts and abrasions in a HIV patient
Management should be covered with waterproof dressing.
Investigations • Minimal parenteral injections.
• Tests for HIV. • Equipments and areas, which are conta-
• Tests for specific and opportunistic infec- minated with secretions, should be wiped
tions. with a sodium hypochlorite solution or 2%
• Tests relevant for associated tumors. glutaraldehyde.
• Contaminated gloves, cottons should be
Treatment incinerated.
Antiviral therapy • Equipments should be disinfected with
Nucleoside reverse transcriptase inhibitor (NRTI)— glutaraldehyde.
Zidovudine, Didanosine, Abacavir, Lamivu- • Disposable equipments (drapes, scalpels,
dine, Stavudine. etc) should be used for whenever possible.
Non-nucleoside reverse transcriptase inhibitor • Walls and floor should be cleaned properly
(NNRTI)— with soap water.
• Separate operation theater and staff to do
Nevirapine, Delavirdine.
surgeries to HIV patients is justifiable.
Protease inhibitors— • Avoid shaving whenever possible before
Ritonavir, Indinavir, Amprenavir. surgery in HIV patients.
Treatment of opportunistic infections. • All people inside the theater should wear
Treatment of tumors. disposable gowns, plastic aprons, goggles,
Immunotherapy overshoes and gloves (Fig. 2.16).
Alpha and gamma interferons. • Surgeons, assistants and scrub nurse should
Interleukins. wear in addition double gloves.
Bone marrow transplantation. • Suction bottle should be half filled with
Anti-CD3 or IL-2 after HAART (Highly Active freshly prepared glutaraldehyde solution.
• Spilled body fluids should be diluted with
Anti-Retroviral Therapy).
glutaraldehyde.
Psychotherapy.
HIV, Hospital and Surgeon
• Isolation per se of HIV patient is not required.
• Proper care should be taken to prevent trans-
mission of the virus.
• Open wounds, disposal of excreta, fluids,
discharge, pus and other infective materials
should be taken care of properly.
• Risk of HIV infection through needle prick
is very less (0.03%).
Following measures should be taken while
managing HIV patients:
• Wearing double gloves.
• Wearing proper spectacles (as HIV can get
transmitted through eyes directly).
• Wearing proper head mask, theater shoes,
and apron.
• Measures to prevent spread of infection from
patient to patient in the hospital.
• Disposal of needles through a sharp
disposing container.
Disinfection
• Autoclave is ideal.
• Boiling.
• Hypochlorite solution.
• 2% glutaraldehyde solution.
GONORRHEA
• It is a sexually transmitted disease caused by
Neisseria gonorrhoeae.
• It is a gram-negative intracellular diplococcus.
It mainly affects epithelium of the urogenital
tract, rectum, conjunctivae, pharynx and
anterior urethra (in male).
Figs 2.16A and B: HIV kit should be used while doing any • Incubation period is 2–14 days.
procedure to HIV infected patients. Note the wearing of
masks, spectacles, and shoes
Features
• Accidental puncture area in surgeon or scrub • Dysuria and urethral discharge.
nurse should be immediately washed with • In women, vaginal discharge, dysuria, bila-
soap and water thoroughly. teral salphingitis and infertility are common.
• Theater should be fumigated after surgery to • After chronic infection Gonococcal urethritis
HIV patient. causes urethral stricture, usually in the bulbar
..Prosperity begins with the state of mind.

urethra. It is the commonest cause of stricture • Ampicillins, Clotrimoxazoles, Ciprofloxacin,
urethra along with traumatic cause. Ceftriaxone (single dose IM), Cefixime and
• It also causes recurrent epididymoorchitis,
Spectinomycin (2 g IM single dose) are also
prostatitis and proctitis.
• Gram staining and culture of urine is used.
diagnostic. • Gonorrhea is more difficult to diagnose and
• Patient is asked to pass urine in two glasses. treat in females than men.
Haziness in first glass signifies infection with • In complicated gonorrhea, prostatic massage,
pus whereas second glass urine is clear. local irrigation, treatment for stricture
Treatment urethra, Doxycycline and Gentamicin
• Penicillins are the antibiotics of choice. therapy are indicated.
Swellings 43
3 Swellings
 Lipoma • It can be diffuse or localized.

 Papilloma • Diffuse lipomas are not encapsulated, not
 Cysts well-localized. Common in palm, sole, head
 Dermoids and neck region (Fig. 3.1), difficult to be
 Sebaceous cyst removed.
 Glomus tumor • It can be single or multiple. Multiple lipomas
 Lymph cyst are often associated with many syndromes
 Neuroma like MEN Syndrome (multiple endocrine
 Neurofibroma neoplasia syndrome).
 Neurilemmoma
 Fibroma Types
 Ganglion • Painful lipomas are called as neurolipomas.
 Bursae Dercum‘s disease is tender deposition of fat
 Adventitious bursa especially on the trunk, is also called as
 Morran baker cyst adiposis dolorosa. It is basically multiple
 Calcinosis cutis neurolipomatosis.
 Epignathus • Fibrolipoma.
• Nevolipoma.
LIPOMA Lipomas attain large size in thigh, shoulder,
• It is a benign tumor arising from yellow fat. retroperitoneum, back and often may turn into
• Tumor arising from brown fat is called as sarcoma.
hibernoma.
• It is called as universal tumor as it can occur Sites
anywhere in the body (except in brain). 1. Subcutaneous.
• It is the commonest benign tumor. 2. Subfascial.
..Pursue one great decisive aim with force and determination.

3. Intramuscular.
4. Intermuscular.
5. Parosteal.
6. Subserosal.
7. Submucosal.
8. Extradural (not intradural).
Fig. 3.2: Pedunculated lipoma

Fig. 3.1: Large lipoma over nape of the neck
Clinical Features
• Localized swelling, which is lobular, non-
tender, semifluctuant, mobile, with edge
slipping between the palpating fingers, with
Fig. 3.3: Gross feature of specimen of lipoma
free skin.
• Lipomas may be pedunculated at times
(Fig. 3.2). Liposarcoma
• It is not transilluminant. • Rapid growth (Commonest type of sarcoma).
• Gross features of a specimen of lipoma are • Warm and vascular.
shown in Figure 3.3. • Dilated veins over the surface.
• Infiltration into deeper plane with restriction
Differential Diagnosis of the mobility.
• Skin fixation and fungation.
• Neurofibroma. • Blood spread to lungs.
• Cystic swellings.
Treatment
• Excision: Small lipoma is excised under local
Complications
anesthesia and larger one under general
• Sarcomatous changes—liposarcoma. anesthesia.
• Myxomatous changes. PAPILLOMA
• Saponification. It is warty swelling from the skin or often from
• Calcification. the mucous membrane.
• Submucosal lipoma can cause intussus- It has got a central axis of connective tissue,
ception and so intestinal obstruction. blood vessels and lymphatics.
Swellings 45
TRUE PAPILLOMA (FIG. 3.4) True papilloma may turn into squamous cell
It is a benign tumor with localized overgrowth carcinoma occasionally. There will be sudden increase
of the epidermis. It is commonly pedunculated in size, bleeding or ulceration.
but rarely can be sessile.
Pedunculated papilloma is villous with a
central axis of connective tissues, blood vessels Amelanotic melanoma, pedunculated lipoma,
and lymphatics. carcinoma.
Infective papilloma is a warty lesion due to Papilloma can occur in the breast called as
infection (Fig. 3.5). For example Condyloma duct papilloma, which is the commonest cause of
acuminata. bloody discharge from the nipple.
Papilloma may be single/multiple. Papilloma can occur in mucous membrane
Papilloma may be pigmented/non-pigmented. like in oral cavity (Fig. 3.6), urinary bladder
(transitional papilloma), in the rectum(columnar),
in the larynx, in the gallbladder (cuboidal).
Treatment
True papilloma is excised with its base and
surrounding 1 cm skin margin.
Infective warts can be treated by excision or
CO2 snow or diathermy coagulation.
Complications of papilloma
• Bleeding.
• Malignant transformation.
• Ulceration.
• Mechanical disability like voice change when
it occurs in vocal cord.
Fig. 3.4: Pedunculated papilloma

with its pedicle
Fig. 3.6: Papilloma tongue. Note: papilloma can also occur

in mucous membrane like oral cavity, urinary and gallblad-
Fig. 3.5: Papilloma right waist. Note the warty surface der, rectum
..Real leaders are ordinary people with extraordinary determination.

CYSTS • Distention cyst: Lymph cyst, ovarian cyst,

Cyst is a collection of fluid in a sac lined by colloid goiter.
epithelium or endothelium. • Exudation cyst: Bursa, hydrocele.
Word meaning of cyst is ‘bladder’ (Greek). Cystic tumors: Dermoid cyst of ovary,
cystadenomas.
TRUE CYST Traumatic cyst: Due to trauma, hematoma
occurs usually in thigh, loin, and shin. It even-
• Cyst wall is lined by epithelium or endo- tually gets lined by endothelium containing
thelium. brown colored fluid with cholesterol crystals.
• If infection occurs cyst wall will be lined by Degenerative cyst: Due to cystic degeneration
granulation tissue. of a solid tumor (due to necrosis of tumor).
• Fluid is usually serous or mucoid derived Parasitic cyst: Hydatid cyst, trichinosis,
from the secretion of the lining. cysticercosis.
FALSE CYST Clinical Features of a Cyst
• It does not have epithelial lining. • Hemispherical swelling which is smooth,
• Fluid collection is as a result of exudation or fluctuant, nontender, well-localized. Some
degeneration. cysts are transilluminant. Presentation varies
Example: depending on its anatomical location.
1. Pseudocyst of pancreas.
2. Wall of cystic swelling in tuberculous Effects of a Cyst
peritonitis. • Compression to adjacent structures: Chole-
3. Cystic degeneration of tumor. dochal cyst compressing over the CBD.
4. In a hematoma after hemorrhage, RBC‘s are • Infection.
lysed and get absorbed and fluid remains as • Sinus formation.
a false cyst. • Hemorrhage.
‘Apoplectic Cyst’ is formed in brain as a • Torsion, e.g. ovarian cyst.
result of ischemia causing collection of fluid. • Calcification.
• Cachexia: In malignant ovarian cyst patient
Classification presents with severe cachexia.
Congenital cyst
• Dermoids: Sequestration dermoid. Swellings that are brilliantly transilluminant
• Tubulodermoids: Thyroglossal cyst, posta- • Ranula.
nal dermoid, ependymal cyst, urachal cyst. • Cystic hygroma and lymph cyst.
• Cysts of embryonic remnants: Cysts from • Hydrocele.
paramesonephric duct and mesonephric • Epididymal cyst (Chinese-lantern pattern).
duct. Cysts of urachus and vitello-intestinal • Meningocele.
duct.
Acquired cysts: DERMOIDS
• Retention cysts: They are accumulation of TYPES
secretion of a gland due to obstruction of a 1. Sequestration dermoid
duct.
It occurs at the line of embryonic fusion due to
For example Sebaceous cyst, Bartholin cyst,
inclusion of epithelium beneath the surface,
cyst of pancreas, cyst of parotid, breast, and which later gets sequestered forming a cystic
epididymis.
swelling in the deeper plane.
Swellings 47
Common sites are— which is smooth, soft, nontender, fluctuant
• Forehead. (Paget‘s test positive, i.e. swelling is fixed with two
• External angular dermoid. fingers and summit is indented to get sensation
• Root of nose. of yielding due to fluid), nontransilluminating,
• Sublingual dermoid. with free skin often adherent into the deeper
• Anywhere in midline or in the line of fusion. plane (Fig. 3.8). There will be resorption and
Dermoids occurring in the skull may extend indentation of the bone beneath.
into the cranial cavity. When it occurs as external
Differential diagnosis
angular dermoid, it extends into the orbital
• Sebaceous cyst.
cavity. Or it can extend into any cavity in relation
• Lipoma.
to its anatomical location (e.g. thorax, abdomen).
Dermoid cyst contains putty-like desqua-
mated material. It is lined by both dermal and
epidermal components.
Types of angular dermoid (Fig. 3.7)
• External angular dermoid: It is a sequestration
dermoid situated over the external angular
process of the frontal bone. Outer extremity
of the eyebrow extends over some part of the
swelling. This typical feature differentiates
it from the swelling arising from the lacrimal
gland. It may extend into the orbital cavity
also.
• Internal angular dermoid: It is a sequestration
dermoid cyst near central position at the root
of the nose.
Fig. 3.8: Postauricular dermoid
Investigations
• X-ray skull or part.
• CT scan head or part.
Treatment
• Excision is done under general anesthesia.
Often, formal neurosurgical approach is
required by raising cranial a osteocutaneous
flaps.
2. Tubulodermoids
Fig. 3.7: Types of angular dermoid (A) External angular It arises from the embryonic tubular structures.
dermoid (B) Internal angular dermoid
Examples includes:
Clinical features • Thyroglossal cyst.
Painless swelling in the line of embryonic fusion, • Ependymal cyst.
presents in the second or third decade onwards, • Postanal dermoid.
..Money is like manure, if you spread it around it does a lot of good.

But if you pile it up in one place, it stinks like hell.
3. Implantation dermoid (Fig. 3.9) 4. Teratomatous dermoid
• Due to minor pricks or trauma (often • It arises from all germinal layers ecto, meso
forgotten), epidermis gets buried under the and endoderms.
deeper subcutaneous tissue, which causes • It occurs in ovary, testis, retroperitoneum,
reaction and cyst formation. mediastinum.
• It is common in fingers (common in tailors), • It contains hairs, teeth, cartilage, muscle.
toes and feet. • It can be benign or malignant.
Clinical features
• Swelling which is painless, observed after
SEBACEOUS CYST
minor trauma, slowly progressing in fingers (WEN, EPIDERMAL CYST)
or toes. • It is a retention cyst that occurs due to
• It is smooth, soft, mobile, tensely cystic, non- obstruction to the mouth of a sebaceous duct.
transilluminating and is adherent to skin. • It is common in face, scalp, and scrotum
(Figs 3.10 and 3.11).
• It is not seen in palms and plantar aspect of foot
(sole) as there are no sebaceous glands.
• Sebaceous cyst contains yellowish material
with fat, and epithelium, has putty-like
consistency, with a parasite in the wall—
demodex folliculorum. It is lined by only
epidermal layer of squamous epithelium.
Clinical Features
• Painless swelling, which is smooth, soft, non
tender, freely mobile, adherent to skin
especially over the summit, fluctuant (positive
Paget‘s test), nontransilluminating with
punctum over the summit.
Fig. 3.9: Implantation dermoid in

(A) Hand (B) Foot
• Lipoma.
• Bursa.
Treatment Figs 3.10A and B: Sebaceous cyst (A) Scalp
• Excision. (B) Infected sebaceous cyst
Swellings 49
Fig. 3.11: Large sebaceous cyst in face
• It moulds on finger indentation.

• In 70% of cases, punctum is present over the
summit because here the sebaceous duct that Fig. 3.12: Incision for sebaceous cyst is elliptical
which includes punctum
directly opens into the skin is been blocked.
Punctum is depressed black colored spot
over the summit of the sebaceous cyst.
Because of the denuded squamous epi-
thelium (keratin) it is black in color. In 30%,
sebaceous duct opens into the hair follicle and
so punctum is not seen.
Multiple sebaceous cysts may be associated with
syndromes like Gardner’s syndrome.
Fig. 3.13: Sebaceous horn scalp
Complications
• Infection and abscess formation.
• Surface gets ulcerated with discharge and is GLOMUS TUMOR
called as Cock‘s peculiar tumor—often • It is also called as glomangioma.
resembles epithelioma. • It arises from a cutaneous glomus composed
• Sebaceous horn (Fig. 3.12). of a tortuous arteriole that communicates
directly into the venule and these vessels
Treatment (Fig. 3.13)
being surrounded by network of small
• Excision including skin adjacent to punctum. nerves.
• Incision and avulsion. • They are often seen in limbs and common in
• If abscess is formed, then initially drainage, nailbeds.
later excision. • They are regulate the temperature of the skin.
• The cyst recurs if capsule is not removed • The tumor is commonly seen under the nail-
properly. bed, 2–3 mm in size.
..Victory has thousand fathers but defeat is an orphan.

—John F Kennedy
• Tumor consists of a mixture of blood spaces, Differential diagnosis
nerve tissues, muscle fibers derived from the Cold abscess, dermoid cyst.
wall of the arteriole, with large cuboidal
glomal cells—angiomyoneuroma. Treatment
• It does not turn into malignancy.
Excision.
Clinical Features
• Severe burning sensation and pain, out of NEUROMA
proportionate to the size. Two types of neuromas are found.
• It is compressible and pain aggravates when • False neuroma.
the limb is exposed to sudden changes of • True neuroma.
temperature.
FALSE NEUROMA
Treatment
• It occurs due to injury to a nerve either
• Excision. following a trauma or amputation, which
presents as a tender swelling.
LYMPH CYST (LYMPHATIC CYST) • It arises from the connective tissues of nerve
It is an acquired type of distension cyst wherein sheath.
lymphatics form a localized swelling with a • It contains fibrous tissue with coiled nerve
capsule around it. fibers.
It usually occurs in subcutaneous plane, • It can be end neuroma, commonly seen in
which is smooth, soft, nontender, mobile, and amputation stump as a tender, localized, firm
brilliantly transilluminant (Fig. 3.14). It is not swelling often adherent to the stump scar. It
usually adherent to the skin. can cause neuralgia in the stump. It prevents
proper usage of the prosthesis. So during
Common sites—are neck and limbs. amputation, nerve should be pulled down
It can get infected and form an abscess. and cut so as to make the cut end retract more
proximally there by preventing it to form
neuroma.
• It can be lateral(side) neuroma that is
observed after partial nerve injury usually
after trauma. It presents as a tender, firm
swelling along the line of a peripheral nerve.
TRUE NEUROMA
• It is rare tumor.
• It occurs in connection with sympathetic
system.
Types
Ganglioneuroma
• It contains ganglion cells and nerve fibers.
• It occurs in connection with sympathetic
Fig. 3.14: Lymph cyst, which is transilluminant. chain. So, it is observed in neck, thorax,
It is an acquired condition retroperitoneum and adrenal medulla.
Swellings 51
• It is relatively benign, symptomless and often Sites
attains a large size. • Cranial.
• Early complete excision can give a cure. • Spinal.
• Peripheral.
Neuroblastoma
• It is poorly differentiated, aggressive, em- Types
bryonic type of tumor.
• It is seen in infants and children. • Nodular neurofibroma presents as a single
• It spreads through blood but can go for smooth, firm, tender(often) swelling, which
spontaneous remission occasionally. moves horizontally or perpendicular to the
direction of the nerve, but not in the direction
Myelinic Neuroma of the nerve. There is pain and hyperesthesia
• It contains only nerve fibers. in the distribution of the nerve.
• Ganglion cells are absent. • Plexiform neurofibroma commonly occurs
• It occurs in spinal cord or pia mater. along the distribution of 5th cranial nerve in
the skin of the face. It often occurs in the
NEUROFIBROMA cutaneous distribution of the peripheral
• It is tumor arising from connective tissues of nerve. It attains enormous size with thicken-
the nerve. ing of the skin, which hangs downwards
• It can be single or multiple. Neurofibromas (Fig. 3.15). It causes erosion into the bone, orbit
may be associated with pheochromocytomas, and deeper structure. It may also cause myxo-
hypertension and few syndromes. matous degeneration. It causes cosmetic problem.
Fig. 3.15: Plexiform neurofibroma in the

(A) Face and neck (B) Buttock
..You will live once; but if you live it right, once is enough.
—Adam Marhshall
• Generalized neurofibromatosis (von Reckling- Treatment
hausen‘s disease): Excision
• It is an inherited autosomal dominant Indications:
disease wherein there are multiple neuro- • Symptomatic neurofibroma.
fibromas in the body. • Cosmetically problematic lesion.
• It may be cranial, spinal or peripheral. • Recent increase in size.
• It is associated with pigmented spots • Malignant transformation.
(coffee colored) in the skin, commonly
seen on the back, abdomen, and thigh (café
NEURILEMMOMA (SCHWANNOMA)
au lait spots) (Fig. 3.16).
• Elephantiatic neurofibromatosis It is arises from schwann (neurilemmal). They
It is of congenital origin. Skin of the limb is are lobulated, encapsulated, soft, and whitish in
greatly thickened and coarse. appearance. They displace the nerve from which
they arise and can be removed. They are
common in acoustic nerve but can also occur in
a peripheral nerve. Often they are multiple.
Presentation is pain along the distribution of
the nerve, hyperesthesia, and tenderness.
Treatment
Excision.
Recurrent schwannoma could be malignant.
FIBROMA
It is a benign tumor arising from fibrous tissue.
It is capsulated.
Classification of True Fibroma

1. Soft fibroma—contains immature fibrous
tissue. Common in face, presents as a soft
Fig. 3.16: Multiple neurofibromas with brown swelling.
café au lait spots in the skin 2. Hard fibroma—contains well-formed fibrous
tissue.
Complications Note: True fibroma is rare and cannot be diagno-
1. Sarcomatous changes: When it occurs it shows sed clinically. It is mostly combined with meso-
rapid enlargement, warmness, and more dermal tissues like nerve sheath (neurofibroma),
vascularity with dilated veins. Secondaries fat(fibrolipoma), muscle (fibromyoma).
in lungs occur through blood spread.
Treatment of true fibroma is excision.
2. Hemorrhage into the tissues.
An entity called aggressive fibromatosis is
3. Spinal and cranial neurofibromas can cause
known to occur as unencapsulated proliferation
neurological deficits.
of fibrous tissue, common in abdominal wall and
4. Erosion into deeper planes, bone, and orbit.
chest wall. It is considered presently as locally
Note: Familial type of neurofibroma may be associated malignant. It does not spread through lymphatics
with scoliosis. or blood. But recurrence is common.
Swellings 53
Desmoid tumor is a variant of aggressive illuminant (Fig. 3.18), swelling which is mobile
fibromatosis seen in females, often associated but mobility is restricted when tendon is
with Gardner’s syndrome. (Desmos = tendon, contracted against resistance.
eidos = appearance). Occasionally it is communicating with joint
Recurrent Fibroid of Paget’s is a rare type capsule.
of fibrosarcoma occurring in scar tissue after Often pain, tenderness and restricted joint
many years. movement may be the presentation (but rare).
GANGLION
It is a cystic swelling occurring in relation to
tendon sheath or synovial sheath or joint capsule.
It contains clear gel-like fluid.
Common Sites
• Dorsum of wrist (Fig. 3.17).
• Flexor aspect of wrist.
• Around ankle joint—occasionally.
Pathogenesis
• Cystic degeneration of the tendon sheath.
• Leakage of synovial fluid through joint Fig. 3.18: Ganglion wrist, which is transilluminant
capsule.
• There are small islets of microspaces in Differential Diagnosis
synovial sheath, which often fuses together • Lipoma.
or one of them get enlarged to form ganglion. • Lymph cyst.
Small ganglion is often mistaken for sesa- • Sebaceous cyst.
moid bone or exostoses.
Treatment
Clinical Features
• Excision, usually under local anesthesia
Well-localized, smooth, soft, cystic, or tensely
(lignocaine plain 2%).
cystic, (Paget‘s test is + ve), nontender, trans-
• Patient should be explained of high recurrence
rate (30%).
• After excision it should always be sent for
histopathology.
BURSAE
Bursa is a sac-like cavity containing fluid within,
which in normal location prevents friction
between tendon and bone.
Minor injuries and pressure leads to bursitis,
Fig. 3.17: Ganglion over the wrist which will present as a swelling at the site.
..Those who don’t study the past will repeat its errors.
Those who study it, will find other ways to err!!
—Charles Wolf
Inflammation of this bursa due to friction
causes bursitis, which commonly presents as
swelling, pain, and restricted movements.
Different Types
• Anatomical.
• Adventitious.
Anatomical
• Subhyoid bursa—an horizontally oval
swelling situated below the hyoid bone, in
front of the thyrohyoid membrane.
• Subacromial bursitis—located in front and
lateral to humeral head in relation to
supraspinatus tendon between acromion and
greater tuberosity of humerus (Fig. 3.19).
• Bicipitoradial bursitis.
• Olecranon bursitis (Student’s elbow) (Miner’s Fig. 3.19: Bursa near elbow joint
elbow) (Fig. 3.20).
• Psoas bursa—a tensely cystic swelling beneath
and below the inguinal ligament in the lateral
aspect of the femoral triangle. But it will not
extend above the inguinal ligament into the
iliac region (unlike in psoas abscess which
extends above and is cross fluctuant).
• Prepatellar bursitis (housemaid’s knee) (Fig. 3.21).
• Infrapatellar bursitis (Clergyman’s knee) (Fig. 3.21).
• Semimembranosus bursitis.
• Bursa anserina—located under the tendons of
Guy ropes (sartorius, gracilis and semi-
tendinosus tendons—goose’s foot).
Fig. 3.20: Adventitious bursa over lateral
• Retrocalcaneum bursitis—between calcaneum aspect of foot—a common site
and tendoachilis.
ADVENTITIOUS BURSA
Occurs in an unusual site like in hallux valgus
(bunion) (Fig. 3.22), over first metatarsal, over
lateral malleolus (tailor’s bursa) (Fig. 3.23),
between tendoachilis and skin (retroachilis
bursitis) or over gluteal tuberosity. It occurs due
to friction or pressure.
• Soft tissue tumor.
Management
• X-ray of the part and often FNAC are required. Fig. 3.21: Prepatellar (housemaid’s knee) and
• Excision of the bursa. infrapatellar bursae (Clergyman’s knee)
Swellings 55
• Swelling does not communicate into knee
joint cavity.
• Knee joint is normal.
Treatment
• Ultrasound of popliteal fossa shows the cystic
swelling under semimembranosus tendon.
• X-ray knee joint is normal.
• Excision is done under general anesthesia
using tourniquet. Complete excision of the
sac is needed to prevent recurrence.
MORRAN BAKER CYST

Fig. 3.22: Olecranon bursa location (Student’s elbow) It is a cystic swelling containing gel-like fluid in
the lower midline of the popliteal fossa. It occurs
due to herniation of the synovial membrane of the
knee joint as a result of chronic arthritis.
Clinical Features
• It is common in middle-aged individuals.
• It is smooth, soft and cystic, often tender
swelling located below and midline of the
popliteal fossa.
• On flexion swelling increases and on exten-
sion swelling decreases in size.
• Pain and tenderness are present in knee joint
Fig. 3.23: Common site of adventitious bursa (BUNION)
with effusion showing positive patellar tap.
• The knee joint movements are painful and
restricted.
SEMIMEMBRANOSUS BURSA
It is a cystic swelling in the upper medial aspect Management
of the popliteal fossa under the semimem- • X-ray of joint shows arthritic changes.
branosus tendon. It is said to be due to friction • MRI may be needed occasionally.
under the tendon causing bursitis.
Treatment
Clinical Features
Arthritis is treated and Baker’s cyst is excised
• Common in young individuals. under general anesthesia in prone position.
• Soft, smooth, cystic, often transilluminant
and nontender swelling located in upper and
CALCINOSIS CUTIS
medial aspect of the popliteal fossa.
• On flexion of knee the swelling disappears • It is circumscribed foci of calcification
and on extension it becomes more prominent. (dystrophic) in or under the skin.
..A lifetime of happiness! No man alive could bear it; it would be hell on earth.
—Bernard Shaw
• Commonly seen in females. Common site is

in the waist (Fig. 3.24).
• Usually bilateral.
• It is said to be due to friction causing
degeneration of skin and immediate deeper
structure with increased local alkalinity of the
tissues causing precipitation of the calcium
leading to solid, hard, swelling in the skin.
Cut section shows hard, yellowish material.
• It may mimic calcified lipoma or neuro-
fibroma.
Fig. 3.25: Epignathus
Treatment
Excision and closure of defect often with local
flaps.
EPIGNATHUS (FIG. 3.25)

This is a type of anomaly seen in neonates
Fig. 3.24: Calcinosis cutis near waist is a common site. It wherein growth from the base of skull protrudes
is common in females through the mouth.
Arterial Diseases 57
4 Arterial Diseases
rib laterally. At the superior aperture of thorax

 Surgical anatomy of thoracic outlet
subclavian vessels, brachial plexus traverse the
 Arteries of upper limb
 Upper limb ischemia cervicoaxillary canal to reach the upper limb.
 Raynaud’s phenomenon Cervicoaxillary canal is divided into proximal
 Acrocyanosis costoclavicular space and distal axilla (divided by
 Subclavian steal syndrome first rib).
 Arteries of lower limb Costoclavicular space is bounded superiorly
 Arterial diseases by clavicle, inferiorly by first rib, anteromedially
 TAO by the costoclavicular ligament, and posterolate-
 Acute arterial occlusion rally by scalenus medius muscle along with long
 Embolism thoracic nerve.
 Compartment syndrome
Scalenus anticus muscle divides the costo-
 Caisson’s disease
clavicular space into two compartments, the
 Aneurysms
 Gangrene anterior one containing subclavian vein and the
 Diabetic foot and diabetic gangrene posterior one containing subclavian artery and
 Ainhum brachial plexus.
 Hamartomata This posterior compartment is called as
 Hemangioma scalene triangle bounded by scalenus anticus
 Cirsoid aneurysm anteriorly, scalenus medius posteriorly, and the
 A-V fistula first rib inferiorly.
Cervical rib narrows this triangle and causes
SURGICAL ANATOMY OF compressive features of C8, T1 nerve roots and
THORACIC OUTLET subclavian artery. Anything that narrows
Thoracic outlet is bounded by manubrium costoclavicular space causes Thoracic outlet
sternum in front, spine posteriorly, and the first syndrome.
..Nothing succeeds like success.

ARTERIES OF UPPER LIMB Causes

Right subclavian artery begins from brachio- • Cervical rib.
cephalic trunk (innominate artery) whereas left • Long C7 transverse process.
• Anomalous insertion of scalene muscles.
subclavian artery directly from the arch of aorta.
• Scalene muscle hypertrophy.
From underneath the sternoclavicular joint,
• Scalene minimus.
subclavian artery arches over the pleura and
• Abnormal bands and ligaments.
apex of lung about 2.5 cm above the clavicle and
• Fracture clavicle or first rib.
then reaches the lateral border of first rib to • Exostosis.
continue as axillary artery. • Tumors in the region.
Subclavian artery is divided into three parts • Brachial plexus trauma and diseases.
by scalenus anterior muscle.
Axillary artery is divided into three parts by Differential diagnosis of TOS
pectoralis minor muscle. • Carpal tunnel syndrome.
At the lower border of teres major muscle, • Cervical spondylosis.
it enters the arm and continues as brachial artery. • Spinal canal tumors.
About 2.5 cm below the crease of the elbow • Shoulder myositis.
joint, it bifurcates into radial and ulnar arteries, • Angina.
which run in the forearm. • Raynaud’s disease.
Ulnar artery forms the superficial palmar • Spinal stenosis.
arch, which is completed by superficial palmar • Ulnar nerve compression.
branch of radial artery. • Epicondylitis.
Radial artery after passing through the
anatomical snuffbox enters the dorsum of hand Clinical Features
and first intermetacarpal space to form deep
palmar arch. It is completed by deep palmar Neurological
branch of ulnar artery and is 1 cm proximal to • Paresthesia.
• Pain in shoulder, arm, forearm and fingers.
superficial palmar arch.
• Occipital headache as referred pain from
tight scalene muscles.
UPPER LIMB ISCHEMIA • Limb weakness in forearm, hand.
THORACIC OUTLET SYNDROME (TOS) Vascular
It is syndrome complex due to compression of • Claudication, ischemic ulcers, gangrene.
neurovascular bundle in the thoracic outlet.
Signs
Thoracic outlet has got two main spaces: • Scalene muscle tenderness.
Scalene triangle is bound by scalenus anterior, • Pulsatile swelling in supraclavicular region
scalenus medius and first rib. It contains with thrill and bruit (25%).
subclavian artery and brachial plexus. • Bony mass above clavicle.
• Positive Adson’s test.
Costoclavicular space is bound by clavicle, first rib, • Positive Roos test.
costoclavicular ligament and scalenus medius. • Positive elevated arm stress test.
It contains subclavian artery and vein and • Costoclavicular compression maneuver—
brachial plexus. radial pulse becomes feeble or absent
• Hyperabduction maneuver—radial pulse Types
becomes feeble or absent. 1. Complete bony: Cervical rib is radiopaque,
• Poor capillary refilling anteriorly ends over the first rib or
• Absence or feeble pulse. manubrium.
2. Fibrous: Cannot be demonstrated radiolo-
Investigations gically.
• X-ray neck and cervical spine. 3. Combined: Partly bony partly fibrous.
• Doppler. 4. Partial bony: With free end expanding as bony
• Subclavian angiogram, CT angiogram, CT mass.
neck.
• Nerve conduction studies, electromyo- Pathology
graphy.
Treatment
• Conservative.
• Surgical.
Conservative treatment for TOS
Exercises—neck stretching, postural and
breathing exercises.
Drugs—analgesics, muscle relaxants, anti-
depressants.
Avoid weight lifting.
Physiotherapy.
Surgical treatment of TOS
Transaxillary (ROOS)—mainly for first rib
excision and also cervical rib.
Supraclavicular approach for cervical rib and
soft tissue excision, scalenotomy, neurolysis,
arterial reconstruction.
Cervical sympathectomy may be needed.
CERVICAL RIB Compression of C8 and T1 will cause tingling and

Definition numbness along its distribution, i.e. in the little finger,
• It is an extension of transverse process of C7 medial side of hand and forearm.
vertebra more than 2.5 cm (normal).
• Syndrome caused by it, is called as cervical Clinical Features (Fig. 4.1)
rib syndrome, thoracic inlet syndrome, thoracic • Majority of patients are asymptomatic.
outlet syndrome, scalene syndrome. Vascular manifestations:
• It is 0.46% common, common in females, Pain is due to ischemia in the muscle. It is
more frequently seen on right side. aggravated by work, exercise and is relieved by
• It can be unilateral or bilateral; can be rest.
asymptomatic or symptomatic. • Roos test is raising the arm above the shoulder.
..Obstacles are those frightful things you see, when you take your eyes off your goals.
• Adson’s test: The hand is raised above after
feeling the radial pulse. The patient is asked
to take a deep inspiration and turn the head
to the same side. Any change in pulse, i.e.
either becoming feeble or absent is noted.
• Modified Adson’s test is same as Adson’s, but
neck is turned towards the opposite side.
Wasting of thenar, hypothenar and forearm
muscles.
Often digital gangrene.
Limb is colder and paler than the opposite side.
Neurological features: Is due to compression
of T1 and C8 causing tingling and numbness in
the little finger, medial side of hand and forearm.
Features in the neck:
a. Hard, fixed, bony mass in the supraclavicular
region.
b. Palpable thrill above the clavicle in the
subclavian artery.
c. Bruit on auscultation.
1. Cervical spondylosis—to differentiate, X-ray
neck—lateral view should be taken.
2. Carpal tunnel syndrome.
3. Tumors or swellings compressing over the
vessel or nerves in the neck.
Investigations
• Chest X-ray—PA-view and lateral view
including neck—only (radiopaque) bony rib
Figs 4.1A to C: Anatomy of cervical rib and its relation to can be identified.
subclavian artery and vein and brachial plexus. Note the • Nerve conduction studies to confirm neurolo-
Eddie’s current, poststenotic dilatation due to arterial gical compression and also to rule out carpal
compression by cervical rib. X-ray picture shows left sided tunnel syndrome or cervical spondylosis.
complete cervical rib
• Arterial Doppler of subclavian artery and of
the upper limb.
• Subclavian angiogram.
The side where cervical rib is present, patient
cannot continue and so drops the hand down. Treatment
• EAST—Elevated Arm Stress Test (Modified Roos 1. In symptomatic cervical rib without arterial
test): Arm is elevated above the shoulder, compression (subclavian artery), along with
with elbow stretched fully. Rapid movements scalenotomy (cutting scalenus anterior
of fingers cause fatigue on the side where muscle), extraperiosteal resection of cervical
cervical rib is present. rib and often resection of first rib is done to
increase the thoracoaxillary channel and 4. Local gangrene: If spasm persists more than
therefore to reduce arterial compression. ischemic time (more than one hour in upper
2. In symptomatic cervical rib with significant limb), then digits go for ulceration and
subclavian artery compression along with gangrene. Does not occur regularly but is an
scalenotomy, extraperiosteal resection of occasional phenomenon in the cycle.
cervical rib, resection of first rib, subclavian
artery reconstruction with or without a graft
has to be done. Causes for Raynaud’s Phenomenon
3. Along with scalenotomy, extraperiosteal Raynaud’s disease:
resection of cervical rib, resection of first rib, It is seen in females, usually bilateral.
reconstruction of subclavian artery, cervical It occurs in upper limb with normal
sympathectomy has to be done to improve peripheral pulses.
the circulation to the ischemic upper limb. It is due to upper limb (hand) arteriolar
spasm due to abnormal sensitivity to cold.
Approaches Patient develops blanching, cyanosis and later
1. Supraclavicular approach—mainly when flushing as Raynaud’s syndrome. Occasionally
there is need for vascular reconstruction. if spasm persists it result in gangrene. Symptoms
2. Transaxillary approach—through axillary can be precipitated and observed by placing
crease, rib is approached and removed. hands in cold water.
3. Thoracotomy approach. Working with vibrating tools: Like pneumatic
road drills, chain saws, wood cutting, fishermen
RAYNAUD’S PHENOMENON traveling in machine boats.
It is an episodic vasospasm, i.e. arteriolar spasm. Collagen vascular diseases: Like scleroderma,
It leads to sequence of clinical features called as rheumatoid diseases causing vasculitis (all auto-
Raynaud’s syndrome.
immune diseases).
Raynaud’s Syndrome: It is sequence of clinical Other causes: Cervical rib, Buerger’s disease,
features due to arteriolar spasm. scalene syndrome.
1. Local syncope: It is due to vasospasm, causing
white and cold palm and digits along with It is often associated with CREST syndrome.
tingling and numbness. (Calcinosis cutis, Raynaud’s phenomenon,
2. Local asphyxia: It is due to accumulation of Esophageal defects, Sclerodactyly, Telangiec-
deoxygenated blood as the result of tasia).
vasospasm causing bluish discoloration of
palm and digits with burning sensation (due Types of Raynaud’s Phenomenon
to accumulated metabolites). 1. Vasospastic
3. Local recovery: It is due to relief of spasm in the 2. Obliterative.
arteriole, leading to return of blood to the
Type is identified by angiogram of palm,
circulation causing flushing and pain in
Doppler, Duplex scan.
digits and palm (pain is due to increased
Other investigations required are X-ray of the
tissue tension).
part, specific tests for autoimmune diseases.
..One man with courage makes the difference.

Treatment
• Treat the cause.
• Avoid the precipitating factors.
• Vasodilators, Pentoxiphylline,
• Small dose of Aspirin (100 mg daily),
• Cervical sympathectomy.
Cervical Sympathectomy
Indications
• Cervical rib with vascular manifestations—
Useful.
• Raynaud’s phenomenon—Useful. Fig. 4.2: Ptosis right eye in Horner’s syndrome
• Hyperhydrosis—Very useful.
• Upper limb vasospasm due to other causes—
ACROCYANOSIS
Useful.
• Acrocyanosis—Useful. It is persistent, painless cyanosis seen in fingers
• Causalgia—Very useful. and often in legs with paresthesia and chilblains
• Sudeck’s osteodystrophy. affecting young females.
It is chronic persistent arteriolar constriction
Approaches with slow rate of blood flow.
Trophic changes, ulcerations are not seen.
a. Supraclavicular approach: Through a inci-
Cyanosis, which is persisting may aggravate
sion in supraclavicular region, sternomas-
by exposure to cold.
toid, omohyoid, scalenus anterior muscles are
It may be associated with endocrine dys-
divided. Phrenic nerve is displaced medially;
function.
subclavian artery is pushed downwards;
suprapleural membrane is depressed, stellate Treatment
ganglion is identified in the neck of the first • Vasodilators.
rib. All rami communicanting from second • Cervical sympathectomy (effective).
and third ganglia are divided. Gray ramus
from second ganglion to first thoracic nerve Raynaud’s phenomenon Acrocyanosis
called as Kuntz nerve is also divided. Persistent. Episodic.
Complications (Fig. 4.2)— Painful. Painless.
• Bleeding. Acute arteriolar spasm. Chronic constriction.
• Injury to subclavian artery and nerves. Ischemic changes are Ischemic changes are
• Pneumothorax and hemopneumothorax. common not seen.
• Horner’s syndrome with ptosis, miosis,
anhydrosis, enophthalmos. SUBCLAVIAN STEAL SYNDROME
b. Transthoracic approach: This gives better Following obstruction of the first part of subcla-
visibility and easier removal of rami, vian artery, vertebral artery provides collateral
compared to supraclavicular approach. circulation to the arm by reversing its blood flow.
c. Endoscopic sympathectomy is the choice, This causes cerebral ischemia with syncopal attacks,
and popular approach at present. Advan- visual disturbances, diminished blood pressure in the
tages are better visibility with magnification, affected limb (Fig. 4.3).
less trauma of access (wound), faster reco- Symptoms will be aggravated by arm
very, and precise (Thoracoscopic). exercise.
Superficial femoral artery at the hiatus in the
adductor magnus, continues as popliteal artery
up to the inferior angle of the popliteal fossa
where it divides into anterior and posterior tibial
arteries.
Anterior tibial artery supplies anterior
compartment of leg and ankle, continues as
dorsalis pedis artery, which forms dorsal arterial
arch of the foot.
Posterior tibial artery supplies posterior
compartment of leg and ends as medial and
lateral plantar arteries, which forms plantar
arterial arch of the foot.
Fig. 4.3: Subclavian steal syndrome
Posterior tibial artery gives peroneal artery,
which runs close to fibula supplying calf
muscles.
Investigations
Duplex scan and angiogram. DSA is useful. ARTERIAL DISEASES
1. Stenosis due to trauma, atherosclerosis,
Treatment emboli.
It may be:
• Transluminal balloon angioplasty.
• In the brain causing transient ischemic
• Endarterectomy or bypass graft. attacks,
• In the limbs causing claudication and rest
ARTERIES OF LOWER LIMB pain,
• In the abdomen causing pain, bloody
Abdominal aorta bifurcates at the level of fourth stool,
lumbar vertebra, (corresponds to the level of the • In the kidney causing hematuria.
umbilicus in anterior abdominal wall) into two 2. Dilatations are aneurysms.
common iliac arteries. 3. Arteritis.
Common iliac artery is about 5 cm in length 4. Small vessel abnormalities.
passes downward and laterally, and at the level
of lumbosacral intervertebral disc, anterior to INTERMITTENT CLAUDICATION
sacroiliac joint, it divides into external and Claudio means ‘I limp’ a Latin word. It is a
internal iliac arteries. Internal iliac artery crampy pain in the muscle seen in the limbs. Due
supplies pelvic organs. to arterial occlusion, metabolites like lactic acid
External iliac artery continues as common and substance P accumulate in the muscle and
femoral artery at the level of inguinal ligament. cause pain.
About 5 cm below the inguinal ligament The site of pain depends on site of arterial
common femoral divides into superficial femoral occlusion.
and deep femoral (Profunda femoris) arteries. • Commonest site is calf muscles.
Deep femoral provides collateral circulation • Pain in foot is due to block in lower tibial and
around the knee joint and also communicates plantar vessels.
above with gluteal vessels to maintain collateral • Pain in the calf is due to block in femoro-
circulation around the gluteal region. popliteal site.
..One ought, every day at least, to hear a little song, read a good poem,
see a fine picture, and if possible to speak a few reasonable words.
• Pain in the thigh is due to block in the CRITICAL LIMB ISCHEMIA
superficial femoral artery. It is persistently recurring ischemic rest pain or
• Pain in the buttock is due to block in the ulceration or gangrene of the foot or toes with
common iliac or aortoiliac segment, often an ankle systolic pressure < 50 mmHg or toe
associated with impotence and is called as systolic pressure < 30 mmHg.
Leriche’s syndrome.
Pain commonly develops when the muscles Pregangrene
are exercising. Cause for pain is accumulation
It is the changes in tissues, which indicates that
of substance ‘P’ and metabolites. During exercise
blood supply is inadequate to keep the tissues
increased perfusion and increased opening of
alive and presents with rest pain, color changes,
collaterals wash the metabolites away.
edema, hyperesthesia with or without ischemic
ulceration.
BOYD’S CLASSIFICATION OF
CLAUDICATION
Gangrene
Grade I: Patient complains of pain after It is macroscopic death of tissue in situ with or
walking, and distance at which pain develops without putrefaction.
is called as ‘claudication distance’. If patient
continues to walk pain subsides because the Dry Gangrene
metabolites causing pain are washed away in It is dry, desiccated, mummified tissue caused
the circulation due to increased blood flow in by gradual slowing of bloodstream. There is a
the muscle and also by opening of collaterals. line of demarcation and is localized.
Grade II: Pain still persists on continuing walk;
but can walk with effort. Wet Gangrene
Grade III: Patient has to take rest to relieve the It is due to both arterial and venous block with
pain. superadded putrefaction and infection. It
Grade IV: Pain persists in spite of taking rest. spreads proximally and there is no line of
Here collaterals are also affected. demarcation. It spreads faster.
Organs where gangrene can develop—
appendix, bowel, gallbladder, testis, and
REST PAIN pancreas.
It is continuous ache in calf or feet and toes or Necrosis It is microscopic cell death.
in the region depending on site of obstruction.
It is ‘cry of dying nerves’ due to ischemia of the Sequestrum is dead bone in situ.
somatic nerves. It signifies severe decompen- Slough is dead soft tissue.
sated ischemia. Pain aggravates by elevation and
is relieved in dependant position of the limb. Line of Demarcation
Pain is more in the distal part like toes and feet. It is a line between viable and dying tissue indi-
It aggravates with movements and pressure. cated by a band of hyperemia. It also indicates
Hyperesthesia is common association with rest that disease is well-localized. Final separation
pain. between healthy and gangrenous tissues occurs
Claudication is not that common in upper by development of a layer of granulation tissue
limb but can occur during writing or any upper in between. It is hyperesthetic due to exposed
limb exercise. nerve endings.
Type of separation— Delayed capillary filling Blanched nails or pulp
• Separation by aseptic ulceration, seen in dry of fingers on pressure, shows delay in refilling
gangrene. (to turn pink) after release of pressure.
• Separation by septic ulceration. Seen in
Delayed venous refilling Two fingers are placed
infected cases and wet gangrene.
over the vein. Finger nearest to heart is moved
away so as to empty the vein. Distal finger is
Features of ischemia (Fig. 4.4)
released to observe the venous refilling. Delay
• Marked pallor, purple-blue cyanosed
in filling is called as Harvey’s sign, signifies
appearance.
ischemia. Venous filling will be increased in AV
• Thinning of skin.
fistulas.
• Diminished hair.
• Loss of subcutaneous fat. Paresthesia over the skin of the foot is due
• Brittle nails, with transverse ridges. to shunting of blood from the skin to muscles
• Ulceration in digits. in deeper plane.
• Wasting of muscles. Sensation in gangrenous area is absent, but
• Tenderness and reduced temperature (cold). the skin is hyperesthetic at the line of
demarcation.
• Disappearing pulse syndrome: After feeling
the pulse the limb is exercised. Pulse dis-
appears once patient develops claudication.
It is because of vasodilatation and increased
vascular space occurring due to exercise
wherein arterial tension cannot be kept
adequately and so pulse will disappear
(unmasking the arterial obstruction).
• Buerger’s postural test: Patient lying down
Fig. 4.4: Leg showing muscle wasting and other features of
early ischemia such as loss of hair, loss of normal luster of
on his back is asked to raise the leg up. In
skin, etc. normal individuals limb (plantar aspect of
foot) remains pink even after raising above
Aortoiliac block causes claudication in buttocks,
90°. Ischemic limb, when elevated shows
thighs, and calves; absence of femoral and distal
marked pallor and empty veins. The angle
pulses, bruit over aortoiliac region. Impotence
in which pallor develops is called as Buerger’s
occurs due to defective perfusion through internal
iliac arteries and so into the penis causing erectile angle of vascular insufficiency. If it is less than
dysfunction (Leriche’s syndrome). 30° it indicates severe ischemia.
Iliac artery obstruction causes claudication in • Systolic bruit: It may be heard over stenosed
thigh and calf; bruit over iliacs with absence of artery like subclavian artery, femoral artery,
femoral and distal pulses. carotid artery, iliacs, renal artery.
Femoropopliteal obstruction causes claudication
in calf muscles with absence of distal pulses but Adson’s Test (Scalene Maneuver)
with palpable femoral. In a patient sitting on a stool, the radial pulse
Distal obstruction shows absence of ankle pul- is felt. The patient is then asked to take a deep
ses with palpable femoral and popliteal pulses. breath (to allow the rib cage to move upwards
..Only those who dare to fail greatly, can ever achieve greatly.
so as to narrow the cervicoaxillary channel) and Abdomen should be examined for the
turn the face to same side (to contract scalenus presence of abdominal aortic aneurysms. It
anterior muscle so as to narrow the scalene presents as pulsatile mass above the umbilicus,
triangle). If the radial pulse disappears or become vertically placed, smooth, soft, nonmobile, not
feeble it signifies cervical rib or scalenus anticus moving with respiration, resonant on percussion.
syndrome. Expansile pulsation is confirmed by placing the
patient in knee-elbow position.
Elevated Arm Stress Test
(EAST; Modified Roos test) Palpation of Blood Vessels
With both arms kept in position of 90° abduction Dorsalis pedis artery is felt against the navicular
and external rotation, patient is asked to make
and middle cuneiform bones, just lateral to the
a fist and release repeatedly for 5 minutes.
extensor hallucis longus tendon at the proximal
Patient continues to do the maneuver in normal
end of first web space. It is absent in 10% cases.
side, whereas in diseased (Thoracic outlet
syndrome) side patient gets pain and paresthesia Posterior tibial artery is felt against the
with difficulty in continuing the maneuver. calcaneus just behind the medial malleolus,
Patient drops the arm down to get relieved from midway between it and tendoachilles.
the symptoms. Anterior tibial artery is felt in the midway
anteriorly between the two malleoli against the
Costoclavicular Compression Maneuver lower end of tibia just above the ankle joint lateral
Radial pulse becomes absent when patient draws to extensor hallucis longus tendon.
his shoulders backwards and downwards in Popliteal artery is difficult to feel. It is palpated
excessive military position. This is because at this better in prone position with knee flexed about
position, subclavian artery is compressed 40°–90° to relax popliteal fascia. It is felt in the
between first rib and clavicle, leading to feeble lower part of the fossa over the flat posterior
or absent radial pulse. surface of upper end of tibia. In upper end of
the fossa, artery is not felt, as there is no bony
Hyperabduction Maneuver (Halsted Test) area in intercondylar region.
When affected arm is hyperabducted, radial Femoral artery in the groin is felt just below
pulse becomes absent or feeble due to compres- the inguinal ligament midway between anterior
sion of artery by pectoralis minor tendon. superior iliac spine and pubic symphysis. Often
hip has to be flexed for about 10°–15° to feel it
Allen’s Test properly.
Radial artery is felt at the wrist on the lateral
It is done to find out the patency of radial and
aspect against lower end of the front of radius.
ulnar arteries. Both the arteries are compressed
Ulnar artery is felt at the wrist on the medial
near the wrist and allowed to blanch completely
in one minute. (In the mean time patient closes end against lower end of the front of ulna.
and opens the fist several times for further Brachial artery is felt in front of the elbow just
venous outflow). Palm appears pale and white. medial to biceps brachii tendon.
One of the arteries is released and color of hand Axillary artery is felt in apex of the axilla
is noted. Normally hand becomes pink and against head of the humerus.
flushed in no time; where as in obstruction, the Subclavian artery is felt against first rib just
area still remains pale. Other artery is also above the middle of the clavicle.
released and looked for changes in hand. Often Facial artery is felt against body of mandible
test has to be repeated to get proper information. at the insertion of masseter.
Common carotid artery is felt medial to sterno- is injected. X-rays are taken to see the block, and
mastoid muscle at the level of thyroid cartilage its extent in the affected limb.
against carotid tubercle (Chassaigne tubercle) of In TAO, corkscrew appearance is charac-
6th cervical vertebra (in carotid triangle). teristic. Distal run off through collaterals is also
Superficial temporal artery is felt just in front important.
of the tragus of the ear against temporal bone. If catheter is passed still proximally angio-
gram of opposite side is possible.
INVESTIGATIONS FOR ARTERIAL DISEASES Seldinger technique can also be used (to
Blood tests: Hb%, blood sugar, lipid profile, study) to do renal angiogram, to detect renal
peripheral smear, platelet count. artery stenosis, renal carcinomas, and renal
Doppler to find out the site of block. anomalies(vascular).
Duplex scan: To study the site, extent,
severity of block, and also about collaterals. Complications of retrograde angiogram
Plethysmography. • Bleeding.
• Dissection of vessel wall.
Ankle-brachial pressure index: Normally it is • Hematoma formation.
1. If it is less than 0.9, it means ischemia is present. • Thrombosis.
If it reaches 0.3 or less, then it signifies severe • Infection.
ischemia with gangrene. • Anaphylaxis.
Angiography Direct aortic angiogram, practiced earlier, is

discouraged at present because of the risk of
1. Retrograde transfemoral Seldinger angiography
aortic dissection and paraplegia due to blockage
It is the commonly done procedure. It is done
of anterior spinal artery.
only when femorals are felt. If femoral pulsation
is not felt then angiogram is done either Digital Substraction Angiography (DSA)
transbrachially (left brachial artery), or transaortic.
Here vessel(artery) is delineated in a better way
by eliminating other tissues through computer
Indications for angiogram
system. A-V fistulas, hemangiomas, lesion in
• TAO.
circle of Willis, vascular tumors, and other
• Atherosclerosis.
vascular anomalies are well made out.
• Raynaud’s phenomenon.
Dye is injected either to an artery or vein.
• A-V fistulas.
Injecting into a vein is technically easier but
• Hemangiomas.
larger dose of dye is required. Injecting into an
• Thoracic outlet syndrome (e.g. cervical rib).
artery is technically difficult but small dose of
• Aneurysms.
dye is sufficient.
• Neoplastic conditions.
Advantages: Only vascular system is visualized;
Other angiograms are carotid angiogram, other systems are eliminated by computer
celiac angiogram, superior mesenteric angio- substraction. Small lesion, its location and details
gram, and coronary angiogram. are better observed with greater clarity.
Femoral artery is cannulated with a guide
wire. Through that Seldinger arterial catheter is Disadvantages: Cost factor and availability.
passed proximally in retrograde direction and Complications: Anaphylaxis, bleeding, thrombo-
water-soluble iodine dye (Sodium diatrizoate) sis.
..Opportunity....Often it comes disguised in the form of misfortune, or temporary defeat.

Ultrasound Abdomen Pathogenesis
To see abdominal aneurysm or nature of aorta
and other vessels.
DISEASES OF THE ARTERIES

1. Atherosclerosis:
Risk factors
• Hypercholesterolemia, hypertriglyceri-
demia and hyperlipidemia.
• Cigaret smoking.
• Hypertension.
• Diabetes mellitus.
• Age—elderly.
• Common in males.
• Sedentary life.
• Family history.
2. Thromboangiitis Obliterans (TAO; Buerger’s

disease).
3. Raynaud’s disease.
4. Conditions causing Raynaud’s phenomenon:
Like scleroderma, rheumatoid arthritis, SLE,
granulomatosis, vasculitis of other causes.
5. Embolus.
6. Aneurysms.
Smoking index (SI) =
Number of packs of cigarettes Number of years
THROMBOANGIITIS OBLITERANS smoked per day × of smoking
(TAO) SYN. BUERGER’S DISEASE SI > 300 is a risk factor.
It is a disease exclusively seen in males of young Pack years index (PYI) =

age group. (Not seen in females due to genetic Number of years Number of packets of
of smoking × cigarettes per day
reason). Seen only in smokers and tobacco users.
Always starts in lower limb, may start on one PYI > 40 is a risk factor
side and later on the other side. Upper limb
involvement occurs only after lower limb is • Cork screw appearance of the vessel—
diseased (Fig. 4.5). collaterals.
• Distal run off is amount of dye filling in
Investigations the main vessel distal to the obstruction
1. Hb%. Blood sugar. through collaterals. If distal run off is
2. Arterial Doppler and Duplex scan (Doppler good then ischemia is compensated. If
+ B mode ultrasound). distal run off is poor then ischemia is
3. Transfemoral retrograde angiogram through decompensated.
Seldinger technique: 4. Transbrachial angiogram: If femorals are not
• Shows blockage. felt, then transbrachial angiogram (Through
Surgery:
1. Lumbar sympathectomy to increase the cuta-
neous perfusion so as to promote the ulcer
healing.
2. Omentoplasty to revascularize the affected
limb.
3. Profundaplasty is done for blockage in pro-
funda femoris so as to open more collaterals
across the knee joint. (It often makes better
perfusion to the knee joint and flap of below
knee amputation).
4. Amputations are done at different levels
depending on site, severity and extent of
vessel occlusion. Usually either below-knee
or above–knee amputations are done.
TREATMENT OF ARTERIAL DISEASES
Fig. 4.5: Bilateral TAO in a young male with large ischemic
ulcers. Patient underwent amputation of both limbs a. Medical:
(Below knee) • General measures.
• Stop smoking.
left side brachial artery—left subclavian • Reduction of weight.
artery – and so to descending aorta) should • Change in life style.
be done. • Exercise.
5. Ultrasound abdomen. • Care of feet.
6. Arterial biopsy usually of dorsalis pedis • Control of diabetes and hypertension.
artery. • Buerger’s position and exercise.
Drugs: Nifedipine, Praxilene, Pentoxiphyl-
Treatment line, small dose of Aspirin, Prostacycline,
Stop smoking. Opt for either cigarett or limb but not Dipyridamole, Ticlopidine.
both. b. Surgery:
Drugs 1. Transluminal balloon angioplasty: Through
• Vasodilators, e.g. Nifedipine. transfemoral Seldinger approach, initially
• Pentoxiphylline increases the flexibility of angiogram is done. Then under guidance
RBC’s and helps them reach the micro- (fluoroscopic) stenosed area is approached.
circulation in a better way so as to increase Balloon of the angioplasty catheter is inflated
the oxygenation. at stenosed area for one minute and repeated
• Small dose of Aspirin. if required. Catheter is withdrawn. It is useful
• Prostacyclins, Ticlopidine, Praxilene. in cases of localized stenosed areas.
All drugs act at the collateral level than at Complications: Thrombosis, bleeding, sepsis.
the diseased vessel. 2. Atherectomy: It is removal of atheroma from
Buerger’s exercise, Buerger’s position, heel raise, the wall of medium sized vessels either
analgesics, care of feet (Chiropady), proper footwear through open surgery or by percutaneous
are advised. route.
..Paralyze resistance with persistence.

3. Thrombectomy: It is removal of thrombus the femoral artery and below to popliteal
from larger vessels through an arteriotomy. segment so as to bypass the blood through
Done in aortoiliac, femoropopliteal region. reverse saphenous vein graft. Saphenous vein
4. Endarterectomy: It is removal of thrombus is reversed to nullify the action of valves so
along with diseased intima through an as to allow easy flow of blood.
arteriotomy. 8. In situ saphenous vein graft: It is arteria-
5. Intraluminal stent placement. lization of saphenous vein. Saphenous vein
6. Profundaplasty: It is done when there is intact in same position is sutured above and
localized block in opening of profunda below the blocked femoropopliteal region to
femoris (deep femoral). Profunda femoris is bypass the blood across. Venous valves are
opened, thrombus if present, is removed. removed through valvulotomy instrument so
Opening is widened using either venous or as to allow the blood to pass.
synthetic (Dacron or PTFE) grafts. This
9. Arterial/venous grafts (Fig. 4.7):
procedure allows collaterals across the knee
Synthetic:
joint to open through profunda femoris and
• Dacron woven graft.
so gives good blood supply to below knee
• Dacron knitted graft.
level and may prevent patient going in for
• PTFE—Polytetrafluoroethylene graft.
above knee amputation (Fig. 4.6).
Natural:
(May be able to save knee joint with below
• Internal mammary artery.
knee amputation and better prosthesis).
• Long saphenous vein either reverse or
in situ.
Grafts of different length and size are available.
Different procedures (Fig. 4.8)
• Aortofemoral bypass graft.
• Ileofemoral bypass graft.
• Femorofemoral bypass graft.
• Femoropopliteal graft (Fig. 4.9).
• Femorodistal graft.
Problems with grafts: Leak, infection, throm-
bosis, cost factor, availability, re-block.
Fig. 4.6: Profundaplasty for deep femoral block
7. Reverse saphenous vein graft: In case of

femoropopliteal block, saphenous vein is
dissected out, reversed and sutured above to Fig. 4.7: Bypass graft
10. Lumbar sympathectomy
Indications:
• Peripheral vascular disease like TAO.
• To promote healing of cutaneous ulcers.
• To change the level of amputation and make
flaps to heal better after amputation.
• Causalgia of lower limb (it is common in
upper limb).
• Hyperhidrosis.
Principle: It increases the cutaneous blood supply
and so healing of ulcer and skin flaps in ampu-
tations is better.
Procedure: Under general or spinal anesthesia,
ganglia are approached through a transverse
incision in the loin at the level of umbilicus.
Through extraperitoneal approach, by dividing
Fig. 4.8: Aortofemoral bypass graft (end to side) external oblique, splitting internal oblique and
transverse abdominis muscles, inferior vena cava
on right side, aorta on left side are identified.
Sympathetic chain is identified by its rami L2-
L5 ganglia are removed. L2 is identified by its
size (larger) and more number of rami. L1 is
retained on one side in bilateral cases. If it is
removed it leads to failure of ejaculation and so
sterility.
Complications:
• Injury to IVC or aorta.
• Bleeding lumbar veins.
• Spinal vessel spasm and so ischemia of spinal
cord and paraplegia.
• Injury to bowel and ureter.
• Wound infection and abscess formation.
• Its effects are only temporary (3–4 wks).
Long-term results are doubtful. It can be
combined with omentoplasty.
• It can also be done along with below-knee
amputation to increase the blood supply of
skin flap so as to have better healing.
• Limb will become warmer immediately after
sympathectomy.
11. Chemical sympathectomy: It is done in
Fig. 4.9: Femoropopliteal bypass graft lateral position using a long spinal needle
..Our greatest glory is not in never falling, but in rising every time we fall.
under local anesthesia. Position is confirmed Procedure: Under general anesthesia, abdomen
by injecting dye under fluoroscopy. Later 5 is opened with upper midline incision. Omental
ml of phenol in water or absolute alcohol is vessels are identified. Omentum with its blood
injected lateral to the vertebral bodies of supply is carefully mobilized to get an adequate
fourth and second lumbar vertebrae. Care length. Lengthened, mobilized omentum is
should be taken to see that the needle does brought into the subcutaneous plane through
not enter IVC or aorta. abdominal wall, lateral to the lower part of rectus
Procedure is contraindicated in patients with muscle. Later this pedicle is mobilized in the
bleeding disorders and in patients who are on subcutaneous tunnel across the leg, burried in
anticoagulants. the deep fascia.
12. Omentoplasty 13. Other treatment methods: Amputations is

Indications: done at different levels depending on extent of
1. Peripheral vascular disease—to improve gangrene, site of block, amount of collaterals.
circulation.
2. For lymphedema, it helps by providing ACUTE ARTERIAL OCCLUSION
lymphatics and so to drain lymph from the
Causes
limb.
3. It is also tried for revascularization of • Trauma.
pharynx, cranial cavity. • Embolism.
Omentum is supplied by omental vessels.
TRAUMATIC ACUTE ARTERIAL OCCLUSION
Causes
• Thrombus due to trauma.
• Subintimal hematoma.
• Acute compartment syndrome.
• During femoral or brachial arterial catheteri-
zation, either diagnostic or therapeutic
procedures.
Four layers of omentum have omental Clinical Features

arcades of vessels. Omentum is also rich in History of trauma, pain, swelling at the site,
lymphatics. It has adhesive property. By retain- pallor, pulselessness, cold limb.
ing one of the pedicles, omentum can be mobi-
lized so as to reach the limb to maintain the circu- Investigation
lation. It can also be mobilized up to the ankle. Duplex scan, angiogram.
It promotes ulcer healing, reduces the pain, and
controls the features of ischemia. It can be used Treatment
in upper limb ischemia. But if patient continues Wound is explored and tear in the artery is
to smoke, disease spreads to these omental identified. It is sutured by using nonabsorbable
vessels also. Often it can be used for both limbs. monofilament material, polypropylene 6-0.
Complications of omentoplasty: Often venous or dacron graft is required for
• Abdominal sepsis. interposition.
• Incisional hernia, where omental pedicle is Proper antibiotics and heparin are required
tunneled into the limb from the abdomen. to prevent thrombosis of the vessel. Later patient
• Adhesions and intestinal obstruction. is advised to take oral Warfarin for maintenance.
COMPARTMENT SYNDROME 3. Blockage at mesenteric vessels causes
intestinal gangrene.
It is common in anterior compartment of leg and
4. Blockage at renal artery leads to hematuria,
in front of forearm. Because of the closed com-
loin pain.
partment, pressure increases here following
5. Blockage at limb vessels cause pain, pallor,
fracture and hematoma, which compresses over
pulseless, paresthesia, paresis, ulceration,
the vessel. It leads to blockade of vessel causing
gangrene.
acute ischemia of the limb presenting with severe
Commonest site of arterial emboli is common
pain, pallor, pulselessness.
femoral artery.
Treatment
Investigations for Arterial Embolism
Immediate decompression by longitudinal fasciotomy,
• Emergency Doppler, ECG and echocardio-
is the treatment of choice, where in deep fascia
graphy, angiogram.
is cut adequately to relieve the compression.
• Relevant tests for origin of emboli.
Otherwise it may lead to severe limb ischemia,
gangrene and may land with amputation.
Treatment
Associated fractures, hematoma, vessel tear
has to be managed accordingly. 1. Embolectomy (Fig. 4.10):
Done as early as possible as an emergency
operation. Under fluoroscopic guidance, Fogarty
EMBOLISM catheter (interventional radiology) is passed
It is due to a solid material which is floating and beyond the embolus and balloon is opened.
travelling in the bloodstream, eventually Catheter is pulled out gently with embolus.
blocking the vessel on its pathway. Procedure has to be repeated until embolectomy
• Arterial emboli:
Source—due to mural thrombus following:
• Myocardial infarction.
• Mitral stenosis.
• Atrial fibrillation.
• Aortic aneurysms.
• Cervical rib causing poststenotic dilata-
tion of subclavian artery.
Venous emboli are due to DVT causing
pulmonary embolism.
• Fat embolism.
• Air embolism.
Effects of Arterial Embolism

1. Brain: Blockage at middle cerebral artery
causes hemiplegia, transient ischemic attacks
(TIA), visual disturbances.
2. Blockage at central retinal artery causes
amaurosis fugax, or permanent blindness. Fig. 4.10: Embolectomy technique
..Our chief want in life is somebody who will make us do what we can.
is completed and bleeding occurs. Angiogram • Aortic angiogram.
is repeated to confirm the free flow. • Ultrasound abdomen.
Postoperatively initially heparin and later
oral anticoagulant are used. Procedure is done Treatment
under general anesthesia. • Initially, heparin is given intravenously—
Open arteriotomy and embolectomy can be done 10,000/units and later 5,000 units/sub-
by direct approach and later the arteriotomy has cutaneously 8th hourly.
to be sutured. Postoperatively, anticoagulants, • Embolectomy can be done using Fogarty
antibiotics should be given. catheter.
2. Intraarterial thrombolysis using fibrino- • Open arteriotomy and embolectomy can also
lysins: be tried.
After passing arterial catheter, angiogram is • Antibiotic prophylaxis has to be given to
done and agents are injected intraarterially prevent infection.
through the arterial catheter. Drugs used are:
• Streptokinase—lysis occurs in 48 hours.
• Urokinase.
• Tissue plasminogen activator (TPA)—lysis
occurs in 24 hours.
• TPA pulse-spray method – lysis occurs in 6
hours.
Contraindications for thrombolysis:
• Stroke.
• Bleeding diathesis.
• Pregnancy.
Heparin should not be used concomitantly
with fibrinolysins.
Fig. 4.11: Saddle embolus blocking the bifurcation of
SADDLE EMBOLUS abdominal aorta
It is an embolus blocking (Fig. 4.11) at the
bifurcation of aorta. FAT EMBOLISM
Causes It is commonly seen after fracture femur, tibia, or
multiple fractures and occasionally following
• Mural thrombus after myocardial infarction.
electroconvulsive therapy.
• Mitral stenosis with atrial fibrillation.
Usually occurs in 24–72 hours.
• Aortic aneurysm.
It is due to aggregation of chylomicrons,
The embolus, which blocks at aortic bifur-
derived from bone marrow, causing fat embo-
cation, is usually large.
lism.
Clinical Features It is often a fatal condition.
• Features of ischemia in both lower limbs.
Clinical Features
• Gangrene of both lower limbs.
• Associated infection and its features. 1. Cerebral: Drowsy, restless, disoriented,
constricted pupils, pyrexia, coma.
Investigations 2. Pulmonary: Cyanosis, tachypnea, right heart
• Arterial Doppler. failure, froth in mouth and nostrils, fat
droplets in sputum, eventually respiratory • Malignancies like renal cell carcinoma,
failure. hepatoma.
3. Cutaneous: Petechial hemorrhages in the skin. • Craniovascular problems.
4. Retinal artery emboli is the earliest sign to appear, • To arrest hemorrhage from GIT, urinary and
causing striae hemorrhages, fluffy exudates— respiratory tract.
confirmed on fundoscopic examination. In bleeding duodenal ulcer or gastric ulcer,
5. Kidney: Blockage in renal arterioles results in embolization is used to occlude gastroduodenal
fat droplets in urine. artery or left gastric artery respectively.
It is also useful in bleeding esophageal
Treatment varices, liver secondaries (mainly due to carci-
• Oxygen. noids), hepatoma.
• Heparinization.
• Low molecular weight dextran. Materials used
• Ventilator support and ICU management. - Blood clot. - Human dura.
- Gel foam. - Plastic
AIR EMBOLISM microspheres.
- Balloons. - Ethyl alcohol.
Causes - Quick setting plastics. - Wool.
• Through venous access like IV cannula. - Stainless coils.
• During artificial pneumothorax.
• During surgeries of neck and axilla. CAISSON’S DISEASE OR
• Traumatic opening of major veins sucking air
DECOMPRESSION DISEASE
inside, causing embolism.
• During fallopian tube insufflation. It occurs due to rapid decompression from high
• During illegal abortion. altitude, aircraft, compressed air chambers
Amount of air required to cause air embolism causing bubbling of nitrogen which blocks the
is 50 ml. small vessels, resulting in—
When the air enters the right atrium, it is • Excruciating pain (bends) in joints and
churned up into foam, which enters the right muscles.
ventricle, later blocking the pulmonary artery. • Spinal cord ischemia causing neurological
deficits.
Treatment • Choking with chest pain, tightness and dry
Patient has to be placed in Trendelenburg cough when lungs are affected.
position. By passing a needle, the air has to be Treatment
aspirated from the right ventricle. Often requires
life saving open thoracotomy to aspirate the • Oxygen therapy.
excess air causing the block. • Recompression and gradual decompression.
THERAPEUTIC EMBOLIZATION ANEURYSMS

It is dilatations of localized segment of arterial
Indications system.
• Hemangiomas. True aneurysm contains all three layers of
• A-V fistulas. artery (Fig. 4.12).
..Our aim should be service, not success.

False aneurysm contains single layer of • Femoral.
fibrous tissue as wall of the sac and it usually • Popliteal.
occurs after trauma. • Subclavian.
• Cerebral, mesenteric, renal, splenic arteries.
Commonest type is true, fusiform, atherosclerotic,
aortic aneurysms.
Berry’s aneurysms are multiple aneurysms
occurring in circle of Willis.
Clinical Features of Aneurysms

• Swelling at the site which is pulsatile
(expansile), smooth, soft, warm, compressible,
with thrill on palpation and bruit on
Fig. 4.12: True and false aneurysms. In true type all layers
auscultation. Swelling reduces in size when
are intact. In false type all layers breached with hematoma pressed proximally.
having a false capsule • Distal edema due to venous compression.
• Altered sensation due to compression of
Types (Fig. 4.13) nerves.
• Fusiform. • Erosion into bones, joints, trachea or eso-
• Saccular. phagus.
• Dissecting. • Aneurysm with thrombosis can throw an
embolus causing gangrene of toes, digits,
often extending proximally.
• Pyogenic abscess: Abscess has to be always
confirmed by aspiration; especially in axilla,
popliteal region, groin.
• Vascular tumors.
• Pulsating tumors—Sarcomas, pulsating
secondaries.
• Pseudocyst of pancreas mimics aortic
aneurysm.
• A-V fistula.
Fig. 4.13: Fusiform and saccular types of aneurysms Investigations

• Doppler study, duplex scan, angiogram,
Causes DSA.
• Atherosclerosis. • Tests relevant for the cause, like blood sugar,
• Syphilis. lipid profile, echocardiography.
• Traumatic.
• Collagen diseases like Marfan’s syndrome. Treatment
• Reconstruction of artery using arterial grafts.
Sites • Arterial endoaneurysmorrhaphy—MATA’s.
• Aorta. • Therapeutic embolization.
• Clipping the vessel under guidance(e.g. Endoluminal stent graft procedure using inter-
cranial aneurysms). ventional radiology with Seldinger tech-
nique.
ABDOMINAL ANEURYSMS Adequate amount of blood is required for
Abdominal aortic aneurysm is the commonest surgery.
aortic aneurysm. 2% incidence. 3. Symptomatic ruptured aortic aneurysm: Risk
of rupture is 1%, if diameter is within 5.5 cm
Causes in size. Risk increases to 20% once the
diameter = 7 cm.
• Atherosclerosis: 95%. It may be anterior rupture (20%) into the
• Others: Syphilis, dissecting, traumatic, free peritoneal cavity causing severe shock
collagen diseases. and very early death; or posterior rupture (80%)
forming a retroperitoneal hematoma of large
Classification I size causing severe back pain, hypotension,
• Infrarenal—Commonest. 95%. shock, absence of femoral pulses and with
• Suprarenal 5%. palpable mass in the abdomen.
Classification II Management
1. Asymptomatic: Found incidentally either on • Immediate diagnosis by ultrasound.
clinical examination or on angiography or on • Resuscitation.
• Massive blood transfusions (10–15 bottles).
ultrasound. Repair is required if diameter is
• Emergency surgery is the only life saving
over 5.5 cm on ultrasound.
procedure in these cases.
2. Symptomatic without rupture: Present as back
Patient has to be shifted to the operation
pain, abdominal pain, mass abdomen which is
theater. Abdomen is opened. Vascular clamps or
smooth, soft, nonmobile, not moving with
bulldog clamps are applied to the aorta above and
respiration, vertically placed above the
below the aneurysm. Adventitia is opened and
umbilical level, pulsatile both in supine as
the clot is removed. Aneurysm is excised and
well as knee-elbow position with same
the arterial graft either PTFE (Polytetrafluoro-
intensity, resonant on percussion. GIT,
ethylene), knitted dacron graft, or woven dacron graft
urinary, venous symptoms can also occur.
is placed. The graft is sutured to the vessel above
Hypertension, diabetes, cardiac problems
and below using monofilament, nonabsorbable
should be looked for and dealt with.
suture material, polypropylene 5-zero.
Investigations
• Blood urea, serum creatinine. Complications
• Ultrasound, aortogram. • Hemorrhage.
• DSA, CTscan, MRI. • Colonic ischemia.
Treatment • Renal failure.
If aneurysm is more than 5.5 cm then surgery • Sexual dysfunction.
is the choice. • Aortoduodenal fistula.
Options are— • Graft leak, graft thrombosis, graft failure.
Open surgical aneurysm repair using PTFE • Aortovenacaval fistula.
or dacron graft (Fig. 4.14). • Spinal cord ischemia.
..Our aspirations are our possibilities.

DISSECTING ANEURYSM
It is the dissection of media of the aorta after
splitting through intima creating a channel in the
media of the vessel wall (Fig. 4.15).
Causes
• Hypertension (It is associated in 80% of
dissecting aneurysms).
• Cystic medial necrosis.
Fig. 4.14: Infra renal aortic aneurysm repair. It is the • Trauma.
commonest site of aortic aneurysm • Weakening of the elastic layers of the media
due to shear forces.
PERIPHERAL ANEURYSMS
Features
Popliteal Aneurysm It is always seen in thoracic aorta, common in
• Is commonest (70%). ascending aorta (70%).
• 65% are bilateral. It is uncommon in other parts of aorta or other
• 25% cases are associated with abdominal vessels.
aortic aneurysm. It can occur in aortic arch or thoracic
• 75% causes complications in 5 years. descending aorta.
This dissected aortic channel gets lined by
endothelium, often reopens distally into the
Presentations
aorta causing double-barreled aorta, which in fact
1. Swelling in popliteal region, which is smooth, prevents complications.
soft, pulsatile, well-localized, warm, com- It is commonly associated with aortic
pressible, often with thrill and bruit. It may insufficiency.
mimic a pyogenic abscess. Dissecting aneurysm is a misnomer. It is only
2. Thrombosis and emboli from popliteal aortic dissection.
aneurysm can cause distal gangrene which Atherosclerosis is not an usual cause for
may be spreading proximally and may lead dissecting aneurysm.
to amputation.
3. Rupture may cause torrential hemorrhage.
Investigations
• Duplex scan.
• Angiogram.
• CT scan.
• MRI.
Treatment
• Aneurysmorrhaphy.
• Repair with arterial graft using PTFE, dacron.
• Endoluminal stenting. Fig. 4.15: Dissecting aneurysm
Classification (Debakey’s) Indications for surgery:
Type I: Dissection begins in ascending aorta • Progressive disease.
extends into descending thoracic aorta (70%). • Significant ischemia.
• Impending rupture.
Type II: Dissection origins and extends only up
to the origin of the major vessels. It is safer type
GANGRENE
with less complications.
It is macroscopic death of tissue in situ (in
Type III: Dissection begins in the descending continuity with adjacent viable tissue) with or
thoracic aorta beyond the origin of the left without putrefaction.
subclavian artery. It can occur in — limbs (Fig. 4.16)
Dissecting aneurysm can be— — appendix
• Acute. — bowel
• Chronic. — testes
• Healed dissecting aneurysm which commu- — gallbladder.
nicates distally again to lumen of aorta
forming a double barreled aorta. Causes
• Secondary to arterial obstruction like athero-
Complications sclerosis, emboli, diabetes, TAO, Raynaud’s
• Acute: Rupture into the pericardium or disease, ergots, etc.
pleura. Dangerous type. • Infective: Boil, carbuncle, gas gangrene,
• Chronic: Blockage of coronary vessels, major Fournier’s gangrene, cancrum oris.
vessels like carotid, subclavian arteries. • Traumatic: Direct, indirect.
Aortic insufficiency. • Physical: Burns, scalds, frostbite, chemicals,
irradiation, electrical.
Clinical Features • Venous gangrene.
• Pain in the chest, and back, which is of
excruciating type. Clinical Features
• Features of ischemia due to blockage of Color changes: Pallor, grayish, purple, brownish
different vessels. black discoloration due to disintegration of
Investigations hemoglobin to sulfide.
• Chest X-ray shows mediastinal widening.

• Arterial Doppler.
• Angiogram.
Treatment
• Antihypertensives.
• Surgery: Using dacron graft, reconstruction
of aorta has to be done with cardio-
pulmonary bypass. Fig. 4.16: Gangrene leg and foot
..Participating in pleasures and pressures of life and keeping one’s own self,
leads to true happiness.
Absence of pulse, loss of sensation, loss of function, Investigations
Line of demarcation is visible between viable and • HB%, blood sugar.
dead tissue by a band of hyperemia and • Arterial Doppler, angiogram(Seldinger
hyperesthesia with development of a layer of technique).
granulation tissue. • Ultrasound abdomen to find out the status
of aorta.
In dry gangrene separation occurs by aseptic
ulceration with minimum infection. Gangrene is Treatment
dry, and mummified. Limb saving methods:
• Drugs: Antibiotics, vasodilators, Pentoxi-
In moist gangrene separation occurs by septic phylline, Praxilene, Dipyridamole, small
ulceration. Often demarcation is vague with skip dose of Aspirin, Ticlopidine.
lesions more proximally and so ending with • Care of feet and toes:
higher level of amputations. Even after ampu- • The part has to be kept dry.
tation skin flap may show die back process, • Any injury has to be avoided.
leading to failure of take up of amputation flap • Proper footwear is advised (Microcellular
and so requires still higher level of amputation. rubber footwear, MCR).
• Measures for pain relief is taken.
Proximal ischemic features may be present with rest • Nutrition supplementation is done.
pain, color changes, hyperesthesia—pregang- • The limb should not be heated.
rene. • Pressure areas has to be protected.
• Localized pus has to be removed.
Types of Gangrene • Cause has to be treated.
• Diabetes has to be controlled.
Dry gangrene is due to slow and gradual loss of • Surgeries to improve the limb perfusion:
blood supply to the part causing dry, desiccated, Lumbar sympathectomy, Omentoplasty,
wrinkled, mummified part with proper line of Profundaplasty, Femoropopliteal thrombec-
tomy or Endarterectomy, Arterial graft
demarcation (Fig. 4.17).
bypass are done according to the need.
Wet gangrene is due to infection with
putrefaction, causing proximally spreading, Life saving procedures: Amputations may have to
edematous, swollen, discoloration, with vague be done occasionally.
line of demarcation. Level of amputation is decided based on skin
changes, temperature, line of demarcation,
Doppler study.
1. Below knee amputation is a better option as BK
prosthesis can be fitted better and also the
movements of knee joint are retained. There
is no need of external support and limp is
absent.
2. In above knee amputation ranges of movements
are less, limp is present, and often requires
third (stick) support to walk.
Different amputations done are Ray amputa-
tion, below knee amputation (Burgess amputa-
Fig. 4.17: Dry gangrene leg. Patient needed above tion), Gritti-Stokes transcondylar amputation,
knee amputation above knee amputation.
DIABETIC FOOT AND • Increased glycosylated hemoglobin in blood
causes defective oxygen dissociation leading
DIABETIC GANGRENE (FIG. 4.18)
to more hypoxia. At tissue level there will
Foot is a complex structure with many layers of be increased glycosylated tissue protein,
muscles, ligaments, joints, arches, fat, thick which prevents proper oxygen utilization
plantar fascia, vascular arches, neurological and so aggravates hypoxia.
system which maintains weight bearing, gravity,
normal walk (swing and stance phases).
Problems in Diabetic Foot
• Callosities, ulceration.
• Abscess and cellulitis of foot.
• Osteomyelitis of different bones of foot like
metatarsals, cuneiforms, calcaneum.
• Diabetic gangrene.
• Arthritis of the joints.
Meggitt’s classification of diabetic foot

Grade 0: Foot symptoms like pain only.
Grade 1: Superficial ulcers. Fig. 4.18: Gangrene 3rd and 5th toes in a diabetic. Patient
Grade 2: Deep ulcers. already underwent amputation of 4th toe earlier for gangrene
Grade 3: Ulcer with bone involvement.
Grade 4: Forefoot gangrene. Clinical Features
Grade 5: Full foot gangrene. • Pain in the foot.
• Ulceration.
Pathogenesis of Diabetic Foot/Gangrene
• Absence of sensation.
• High glucose level in tissues is a good culture • Absence of pulsations in the foot (posterior
media for bacteria. So infection is common. tibial and dorsalis pedis arteries).
• Diabetic microangiopathy causes blockade of • Loss of joint movements.
microcirculation leading to hypoxia. • Abscess formation.
• Diabetic neuropathy: Due to sensory neuro- • Change in temperature and color when
pathy, minor injuries are not noticed and so gangrene sets in.
infection occurs. Due to motor neuropathy,
dysfunction of muscles, arches of foot and Investigations
joints, and loss of reflexes of foot occurs
causing more prone for trauma, abscess, etc. • Blood sugar, urine ketone bodies.
Due to autonomic neuropathy, skin will be • Blood urea and serum creatinine.
dry, causing defective skin barrier and so • X-ray of part to see osteomyelitis.
more prone for infection. • Pus for culture and sensitivity.
• Diabetic atherosclerosis itself reduces the blood • Doppler study of lower limb to assess arterial
supply and causes gangrene. Thrombosis can patency.
be precipitated by infection causing infective • Angiogram to see proximal blockage.
gangrene. Blockage occurs at plantar, tibial, • Ultrasound abdomen to see status of abdo-
and dorsalis pedis vessels. minal aorta.
..Participation is an achievement in itself.

Treatment mature specialized cells or tissue indigenous
Foot can be saved only if there is good blood supply. to the particular site is called as hamartomata.
• Antibiotics—decided by pus C/S. • It is tumor-like overgrowth of tissue or tissues
• Regular dressing. proper to that part.
• Drugs: Vasodilators, Pentoxiphylline, Dipyri- • It may be single lesion or multiple lesions.
damole, small dose of Aspirin. • Hemangiomas, lymphangiomas, A-V malfor-
• Diabetes has to be controlled by insulin only. mations, neural malformations are the
• Diet control, control of obesity. examples.
• Surgical debridement of wound.
• Amputations of the gangrenous area. If blood Problems with Hamartomas
supply is not present, then below-knee or • Pressure symptoms locally.
above-knee amputation may be required. • Bleeding.
Level of amputation is decided by skin and • Infection.
temperature changes or Doppler study.
• Gigantism.
• Care of feet in diabetic:
• Cosmetic problem.
• Any injury to feet has to be avoided.
• MCR foot wears must be used.
Treatment
• Feet have to be kept clean and dry,
especially the toes and clefts. • Depends on site, type, extent.
• Hyperkeratosis has to be avoided. • Cryotherapy, ligation of feeding vessels,
sclerotherapy, excision.
AINHUM
HEMANGIOMA
• Commonly affects males (can also occur in
females). • It is the commonest Hamartoma (a congenital
• Common in blacks, in Negroes. malformation).
• History of running barefoot in childhood is • They are not true tumors.
common. • Commonly seen in skin and subcutaneous
• Fifth toe is commonly affected. tissue, but can occur anywhere in the body
• A fissure develops in interphalangeal joint, like in liver, brain, lung or other organs.
which becomes a fibrous band, that encircles
the digit causing necrosis (Gangrene of little Classification
toe). 1. Capillary.
• Often it can be bilateral. 2. Cavernous (venous).
3. Arterial: is a type of congenital arteriovenous
Treatment fistula.
Is early ‘Z’ Plasty.
Amputation is often required later. Most often CAPILLARY HEMANGIOMA
autoamputation occurs. Types
1. Salmon patch (Fig. 4.19): Present at birth.
HAMARTOMATA Usually on face, scalp, limb. Often involves
Hamartano means ‘I miss’ (Greek). Or ‘fault’ or wide area of skin. With age it goes for
‘misfire’ or ‘error’. spontaneous regression and disappears
• It is a benign lesion with aberrant differen- completely. Hence, masterly inactivity is
tiation producing a mass of disorganized but adviced.
Treatment
• Allow for spontaneous regression.
• Otherwise by laser therapy.
• CO2 snow therapy.
• Sclerosant therapy.
Associated Syndromes
• Klippel-Trenauny-Weber syndrome: Nevus
flammeus + osteohypertrophy of extremities
+ A-V fistula.
• Kasabach-Merritt syndrome: Capillary
hemangioma + DIC (Disseminated intra-
vascular coagulation).
• Sturge-Weber syndrome: Hemangiomas +
hemiplegia and epilepsy (Calcified vascular
cerebral and meningeal deposits) +
glaucoma.
• Maffucci syndrome: Cavernous heman-
Fig. 4.19: Capillary hemangioma—Salmon patch in
gioma + dyschondroplasia.
an infant
CAVERNOUS HEMANGIOMA
2. Port-wine stain (Nevus flammeus): Present • It is present at birth and consists of a multiple
at birth and persists throughout life without venous channels.
any changes. No spontaneous regression. It • Its size increases gradually and may cause
presents as reddish blue, warm area com- problems.
• It often contains feeding vessels which is of
monly on face. Often it is nodular. It requires
surgical importance.
cosmetic coverage, excision and grafting or laser
ablation. Sites
3. Strawberry hemangioma: Child is normal at Face, limbs, liver and other internal organs
birth. Between 1-3 weeks it appears as red (Figs 4.20 and 4.21).
mark which rapidly increases in 3 months to
form strawberry or raspberry hemangioma Clinical Features
which contains immature vasoformative tissues. Smooth, bluish, well-localized, soft, compres-
• It is clinically warm, compressible, and sible, warm swelling from skin and subcu-
taneous tissue.
bluish in color.
• History of bleeding after minor trauma. Complications
• It involves skin, subcutaneous tissue and • Hemorrhage.
often muscle also. • DIC.
• After one year of age, it slowly involutes • Thrombosis.
and by 7–8 years it disappears completely • Infection and septicemia.
(commonly). • Erosion into the adjacent bone.
..Pay attention to the small things, the kite flies because of its tail.
Fig. 4.20: Cavernous hemangioma over (a)Tongue (b) Knee
• If small in accessible area then excision.

• Sclerosant therapy.
• Laser ablation.
CIRSOID ANEURYSM
• It is a rare variant of capillary hemangioma
occurring in skin, beneath which abnormal
artery communicates with the distended
veins.
• Commonly seen in superficial temporal artery
and its branches.
• Often the underlying bone gets thinned out
due to pressure.
• Sometimes extends into the cranial cavity.
• Ulceration is the eventual problem which will
lead on to uncontrollable hemorrhage.
Fig. 4.21: Hemangioma in a child involving
face extensively Clinical Features
Pulsatile swelling in relation to superficial
Investigations temporal artery, which is warm, compressible,
• Ultrasound. with arterialization of adjacent veins and with
• Doppler. bone thickening (due to erosion).
• Angiogram to find out feeding vessel.
• Platelet count. Investigations
• Doppler study.
Treatment • CT scan.
• Ligation of feeding artery. • Angiogram.
• Therapeutic embolization. • X-ray of the part.
Treatment
• Ligation of feeding artery and excision of
lesion, often requires preliminary ligation of
external carotid artery.
• Intracranial extension requires formal
neurosurgical approach.
ARTERIOVENOUS FISTULA (AVF)

It is a type of Arteriovenous Malformations.
Types
• Congenital.
• Traumatic.
Fig. 4.22: Hypertrophic changes due to A-V malformation
CONGENITAL AVF
Complications
During developmental period A-V communica-
tions occur. • Hemorrhage.
• Thrombosis.
Sites • Cardiac failure.
• Limbs either part or whole of the limb. Part Investigations
may be in toes or fingers.
• Lungs. • Angiogram (Fig. 4.23).
• Brain in circle of Willis. • Doppler study.
• Other organs like bowel, liver. • X-ray of the part.
Clinical Features
Structural changes in the limb:
• Limb is lengthened due to increase blood flow
since developmental period (Fig. 4.22).
• Limb girth also increased.
• Limb is warm.
• Continuous thrill and continuous machinery
murmur all over the lesion.
• Dilated arterialized varicose veins are seen due
to increased blood flow and due to valvular
incompetence.
• Often there will be bone erosion or extension
of AVF into the bone as such.
Physiological changes: Because of the hyper-
dynamic circulation, there will be increased
cardiac output and so often congestive cardiac Fig. 4.23: MR angiogram of A-V malformation
failure. in cranial cavity
..People forget how fast you did the job, but they remember how well you did it.
Treatment vein causing diversion of most of the blood.
• Avoid injury. Between the artery and vein, at the site of
• Ligation of feeding artery. fistula, dilatation develops with fibrous sac
• Sclerosant therapy. formation called as aneurysmal sac. This
• Therapeutic embolization. presents as warm, pulsatile, smooth, soft,
• Amputation when required (only) as life compressible swelling at the site with
saving procedure. continuous thrill and continuous machinery
murmur. It is warm at the site.
ACQUIRED AVF (FIG. 4.24)
Changes below the level of the fistula:
Causes
Because of diversion of arterial blood distal
1. Trauma in— part becomes ischemic. Because of high
a. Femoral region. pressure veins become arterialized, with
b. Popliteal region.
valvular incompetence causing varicose veins.
c. Brachial region.
d. Wrist. Changes proximal to the fistula: Hyper-
e. Aorta venacaval. dynamic circulation causing cardiac failure.
f. Abdomen—It may be following road If pressure is applied to the artery proximal
traffic accidents, penetrating wounds, to the fistula, swelling will reduce in size,
cock-fight injury ! (common in South thrill and bruit will disappear, pulse rate and
India). pulse pressure becomes normal. This is called
2. After vascular surgical intervention for major
as Nicoladoni’s sign or Branhan’s sign.
vessels.
Cardiac failure may be very severe in trau-
3. Therapeutic: For renal dialysis, AVF is crea-
ted (cimino fistula) to achieve arterialization matic AVF (Often resistant to drug therapy).
of veins and also to have hyperdynamic
circulation. So as to have easy adequate Investigations
venous assess for long time hemodialysis. • Doppler.
Common sites are wrist, brachial, and femoral • Angiogram.
region.
Fig. 4.24: A-V fistula
Pathophysiology
• Physiological changes: Cardiac failure due to
hyperdynamic circulation.
• Structural changes:
Changes at the level of fistula: Blood flows
from high pressure artery to low pressure Fig. 4.25: Reconstruction of A-V fistula using graft
Treatment
• Excision of fistula and reconstruction of
artery and vein with graft (Fig. 4.25).
• In emergency situation, quadruple ligation,
i.e. both artery and vein above and below
should be ligated without touching the fistula
and sac. Patient recovers well from cardiac
failure (Fig. 4.26).
• Therapeutic embolization may be tried.
Hunter’s ligation should be avoided: It is used
as life saving measure because it invariably
causes limb ischemia and gangrene even though
Fig. 4.26: Quadruple ligation of A-V fistula patient recovers from cardiac failure. It is ligation
of both artery and vein proximally so as to make
• Electrocardiogram. cardiac function normal. But it invariably steals
• Echocardiography. the blood from the limb leading to gangrene.
..People seldom improve when they have no other model but themselves to copy after.
5 Venous Diseases
 Anatomy of veins of lower limb

 Physiology of venous blood flow in
lower limb
 Deep vein thrombosis (DVT)
 Varicose veins
 Venous ulcer
 Thrombophlebitis
 Anticoagulants
ANATOMY OF VEINS OF LOWER LIMB

Deep Veins
1. Tibial, popliteal, femoral veins are called as
‘veins of conduits’ which drain blood into
iliac veins and then to IVC.
2. Pumping veins: They are venous sinuses
existing in the calf muscles, which pump
blood towards major veins. They are better
termed as musculovenous pumps. They are also
called as the peripheral heart.
Superficial Veins (Fig. 5.1)

• Long saphenous vein: It is a subcutaneous
Fig. 5.1: Anatomy veins of lower limb
vein over the inner aspect of the leg and thigh,
joins into femoral vein at fossa ovalis. anterolateral vein, posteromedial vein and
Tributaries of long saphenous vein are sometimes accessory saphenous vein. It has
posterior arch vein, anterior vein of leg, got 15–20 valves.
Venous Diseases 89
• Short saphenous vein: It is over the lateral 2. Calf musculovenous pump: During contrac-
and posterior aspect of the leg, enters the tion phase of walking, pressure in the calf
deep fascia in the upper calf region and later muscles increases to 200-300 mmHg. This
joins popliteal vein at variable distance. It has pumps the blood towards the heart. During
got 10–15 valves. relaxation phase of walking, pressure in the
Superficial veins have got multiple valves, calf falls and so it allows blood to flow from
which facilitates blood flow towards heart. superficial to deep veins through perforators.
Superficial veins usually drain about 10% of Normally while walking, pressure in the
lower limb blood, i.e. from skin and subcu- superficial system at the level of ankle is
taneous tissues. 20 mmHg
3. During walking, foot pump mechanism
Perforator Veins
propels blood from plantar veins into the leg.
They are the veins, which connect superficial to 4. Gravity.
deep veins at various levels. They travel from
superficial fascia through an opening in the deep Factors responsible for venous return
fascia before entering the deep veins. The • Negative pressure in thorax.
direction of flow of blood here is from superficial • Peripheral pump—calf muscle.
to deep veins. These perforators are also guarded • Vis-a-tergo of adjoining muscle.
by valves so that the blood flow is unidirectional, • Non-refluxing valves in course of veins.
i.e towards deep veins. Reversal of flow occurs
due to incompetence of perforator, which will DEEP VEIN THROMBOSIS (DVT)
lead to varicose veins.
Etiology
Types Factors—
1. Ankle perforators.
2. Lower leg perforators. Virchow’s triad— a) Stasis.
3. Gastrocnemius perforators (of Boyd). b) Hypercoagulability.
4. Mid thigh perforators. c) Vein wall injury.
5. Hunter’s perforator in the thigh.
Causes
PHYSIOLOGY OF VENOUS BLOOD 1. Following childbirth.
FLOW IN LOWER LIMB 2. Trauma.
Veins are thin-walled vessels with collapsible 3. Muscular violence.
walls that assume an elliptical configuration in 4. Immobility.
collapsed state and circular configuration in the 5. Debilitating illness, obesity, immobility, bed
filled state. rest, pregnancy, puerperium, oral contra-
Venous valves are abundant in the distal ceptives, and estrogens.
lower extremity and the number of valves 6. Postoperative thrombosis: Common after
decreases proximally, with no valves in superior the age of 40 years. Incidence following
and inferior vena cava. surgeries is 30%. In 30% of cases both legs
are affected. Usually seen after prostate
Venous Return surgery, hip surgery, major abdominal
1. Arterial pressure across the capillary surgeries, gynecological surgeries, and
increases the pumping action of vein. cancer surgeries. Bedridden for more than
..Take time to read; it is the foundation to wisdom.

3 days in the postoperative period increases • Positive Homan’s sign: Passive forceful
the risk of DVT. dorsiflexion of the foot with extended knee
7. Spontaneous thrombosis is common in causes tenderness in the calf.
visceral neoplasm like carcinoma pancreas • Mose’s sign: Gentle squeezing of lower part
or carcinoma stomach. It is often migrating of the calf from side to side is painful. Gentle-
type. ness is very important otherwise it may
8. Thrombus may start in a venous tributary, dislodge a thrombus to form an embolus.
which eventually may extend into the main • Most often, DVT is asymptomatic and presents
vein causing DVT. suddenly with features of pulmonary embolism
9. Axillary vein thrombosis can occur like chest pain, breathlessness and hemoptysis.
spontaneously, following compression by
cervical rib, by various causes of thoracic Investigations
inlet syndrome, or arm being in the hyper • Venous Doppler.
abduction state for prolonged period (e.g. • Duplex scanning.
painting the ceiling), after axillary lymph • Venogram.
node block dissection, after radiotherapy to • Radioactive I125 fibrinogen study.
axilla, occasionally as a complication of • Hemogram with platelet count.
venous cannulation.
10. Polycythemia vera, thrombocytosis. Treatment
11. Deficiencies of antithrombin III, protein C,
• Rest, elevation of limb, bandaging the whole
protein S.
limb with crepe bandages.
• Anticoagulants: Heparin, warfarin, phenin-
Sites
dione.
1. Pelvic veins—Common • For fixed thrombus: Initially high dose of
2. Leg veins—Common in femoral and heparin of 25,000 units/ day for 7 days has
popliteal veins. (Common on left side). to be given. Then later patient is advised to
3. Upper limb veins —Not uncommon. continue with warfarin for 6 months. Low
(Axillary vein thrombosis). molecular heparin can also be used. Dose is
Phlegmasia alba dolens It is DVT of femoral vein controlled by assessment of Activated Partial
(deep femoral vein commonly) causing painful Thromboplastin Time (APTT). Duration of
congestion and edema of leg, with lymphangitis, heparin treatment is usually for 5 days.
which further increases the edema and worsens • For free thrombus: Fibrinolysins—Strepto-
the situation (White leg). kinase or urokinase or tissue plasminogen
activator are used to dissolve thrombus (It
Phlegmasia cerulea dolens: It is extensive DVT should not be given when patient is on
of iliac and pelvic veins causing blue leg with either heparin).
venous gangrene or areas of infarction. • Venous thrombectomy is done using Fogarty
venous balloon catheter.
Clinical Features • Thrombotic emboli is prevented from
• Pain and swelling in the calf and thigh (often). reaching the heart by filtering it at IVC level
Commonly associated with fever. Pain is using Kim ray Greenfield filter, suture sieve
often so severe that the patient finds difficult plication, stapler plication, vena caval
to flex (or move) the leg. ligation, Mobin Uddin umbrella filter.
• Leg is tense, tender, warm, pale or bluish with Note: Streptokinase is derived from Streptococci.
stretched and shiny skin. Urokinase is derived from human urine.
Venous Diseases 91
Prevention of DVT
• Care to be taken to see for proper positioning
of legs with no pressure on the calf muscles.
• Pressure bandage to the legs has to be applied
during major surgeries, and laparoscopic
surgeries. During postoperative period,
elevation, massaging, pressure bandage,
early ambulation, maintaining hydration are
essential measures.
• Low dose heparin is given in suspected cases,
in major surgeries and continued during
postoperative period till the patient is
ambulated. 5000 units is given subcutaneous
2 hours before surgery.
• Various measures like graduated static
compression, elastic stockings, electrical
stimulation of calf muscles, pneumatic
compression are used to prevent sluggish
flow of blood.
• Dextran 70, intravenously 500 ml during
surgery and another 500 ml postoperatively
in 24 hours can also be used to prevent DVT.
Effects and sequelae of DVT Fig. 5.2: Varicose veins in lower limbs.
• Pulmonary embolism. Note the bilateral long saphenous vein varicosity
• Infection.
• Varicose veins due to perforator incompe-
• Venous gangrene.
tence.
• Partial recanalisation, chronic venous
• Thread veins (or dermal flares): Are small
hypertension around the ankle region
varices in the skin usually around ankle,
causing venous ulcers.
which look like dilated, red or purple net-
• Recurrent DVT.
work of veins.
• Reticular varices: Are slightly larger varices
VARICOSE VEINS than thread veins located in subcutaneous
They are dilated, tortuous, elongated veins in the region.
leg (Fig. 5.2). There is reversal of blood flow • Combinations of any of above.
through its faulty valves. Pathogenesis
Types Theories
• Long saphenous vein varicosity (Fig. 5.3). 1. Fibrin cuff theory
• Short saphenous vein varicosity (Fig. 5.4). 2. White cell trapping theory
..Observation is the best teacher.

Inappropriate activation of trapped leuko-

cytes release proteolytic enzymes, which causes Fig. 5.3: Long saphenous Fig. 5.4: Short saphenous
cell destruction and ulceration—White cell vein varicosity vein varicosity
trapping theory. Fibrin deposition, tissue death,
scarring occurs together, called as lipodermato- • Obstruction to venous return like abdominal
sclerosis. tumor, retroperitoneal fibrosis, lymphade-
nopathy.
Etiology of Varicose Veins • Pregnancy (due to progesterone hormone).
Varicosities are more common in lower limb • A-V malformations—congenital or acquired.
because of erect posture and long column of • Iliac vein thrombosis.
blood has to be supported which can lead to
weakness and incompetence of valves. Sites where varicosities can occur
• Lower limb.
Primary varicosities • Pampiniform plexus of veins in scrotum.
Due to— • Vulva.
• Congenital incompetence or absence of • Sites of portosystemic anastomosis.
valves.
• Weakness or wasting of muscles.
• Stretching of deep fascia. Clinical Features
Secondary varicosities It is more common in females (10:1). It is much
• Recurrent thrombophlebitis. more common in females with a family history.
• Occupational—standing for long hours. Often it is familial. Familial varicose veins begins
Venous Diseases 93
in younger age group, seen bilaterally, involves • Perthe’s test: The affected lower limb is
all veins including deep veins. wrapped with elastic bandage and the patient
• Visible dilated veins in the leg with pain, dis- is asked to walk around and exercise.
tress, nocturnal cramps, feeling of heaviness, Development of severe cramp like pain in the
pruritus. calf signifies DVT.
• Pedal edema, pigmentation, dermatitis, • Modified Perthe’s test: Tourniquet is tied just
ulceration, tenderness, and restricted ankle below the sapheno-femoral junction without
joint movement. emptying the vein. Patient is allowed to have
• Bleeding, thickening of tibia occurs due to a brisk walk, which precipitates bursting pain
periostitis. in the calf and also makes superficial veins
• Positive cough impulse at the sapheno- more prominent. It signifies DVT.
femoral junction. DVT is contraindicated for any surgical
• Brodie-Trendelenburg test (Fig. 5.5) intervention of superficial varicose veins. It
Vein is emptied by elevating the limb and a is also contraindicated for sclerosant therapy.
tourniquet is tied just below the sapheno- • Three-tourniquet test: To find out the site of
femoral junction (or using thumb, sapheno- incompetent perforator, three tourniquets are
femoral junction is occluded). Patient is asked tied after emptying the vein.
to stand quickly. When tourniquet or thumb • At saphenofemoral junction.
is released, rapid filling from above signifies • Above-knee level.
saphenofemoral incompetence. This is • Another below knee level.
Trendelenburg test I. Patient is asked to stand and looked for
In Trendelenburg test II, after standing filling of veins and site of filling. Then
tourniquet is not released. Filling of blood tourniquets are released from below upwards
from below upwards rapidly can be observed to again see for incompetent perforators.
within 30-60seconds. It signifies perforator • Schwartz test: In standing position, when
incompetence. lower part of the vein in leg is tapped,
impulse is felt at the saphenous junction or
at the upper end of the visible part of the vein.
It signifies continuous column of blood due
to valvular incompetence.
• Pratt’s test: Esmarch bandage is applied to
the leg from below upwards with a
tourniquet at saphenofemoral junction. After
that the bandage is released to see the ‘blow
outs’ as perforators.
• Morrissey’s cough impulse test: The varicose
veins are emptied. The leg is elevated and then
the patient is asked to cough. If there is
saphenofemoral incompetence, expansile
impulse is felt at saphenous opening.
• Fegan’s test: On standing, the site where the
perforators enter the deep fascia bulges and
Fig. 5.5: Brodie-Trendelenburg test. Note the reversal of this is marked. Then on lying down, button
blood flow while releasing the tourniquet like depression in the deep fascia is felt at the
..A good head and an industrious hand are worth gold in any land.
marked out points, which confirms the site functional and anatomical information, and
of perforator. also color map. Examination is done in
• Examination of the abdomen is done to look standing and lying down position and also
for pelvic tumors, lymph nodes, etc. which with valsalva maneuver. Hand held Doppler
may compress over the veins to cause probe is placed over the site and visualized
varicosity. for any block and reversal of flow. DVT is
very well-identified by this method.
Clinical tests for varicose veins • Venography: Ascending venography was very
• Cough impulse test. common investigation done before Doppler
• Brodie-Trendelenburg test. period. A tourniquet is applied above the
• Modified Perthe’s test. malleoli and the vein of dorsal venous arch
• Three-tourniquet test. of foot is cannulated. Water-soluble dye
• Fegan’s test. injected, flows into the deep veins (because
of the applied tourniquet). X-rays are taken
Investigations below and above knee level.
• Venous Doppler Any block in deep veins, its extent,
It is done with the patient standing; the perforator status can be made out by this.
Doppler probe is placed at saphenofemoral It is a good reliable investigation for DVT.
junction and later wherever required If DVT is present, surgery or sclero-
(Fig. 5.6). Basically by hearing the changes in therapy are contraindicated.
sound venous flow, venous patency, and Descending venogram is done when
venous reflux can be very well-identified. ascending venogram is not possible and also
to visualize incompetent veins. Here contrast
material is injected into the femoral vein
through a cannula in standing position. X-
ray pictures are taken to visualize deep veins
and incompetent veins.
• Plethysmography.
• Ambulatory venous pressure.
• Arm-Foot venous pressure (Foot pressure is
not more than 4mmHg above the arm
pressure).
• Ultrasound abdomen, peripheral smear,
platelet count, other relevant investigations
are done depending on the cause of the
varicose veins. If venous ulcer is present, then
the discharge is collect for culture and
sensitivity, biopsy from ulcer edge is taken
to rule out Marjolin’s ulcer, plain X-ray of the
Fig. 5.6: Doppler machine. Doppler is good investigation
part is done to find out periostitis.
for venous diseases
• Duplex scan is a highly reliable ultrasound Treatment

Doppler imaging technique (Here high 1. Conservative treatment
resolution B mode ultrasound imaging and • Elastic crepe bandage application from
Doppler ultrasound is used) which along below upwards or use of pressure
with direct visualization of veins, gives the stockings to the limb (Fig. 5.7).
Venous Diseases 95
Usually injection is started at the ankle region
and then proceeded upwards along the length
of veins at different points. Later pressure
bandage is applied for three weeks. Often
injection may have to be repeated after a week.
Microsclerotherapy
Fig. 5.7: Crepe bandages applied to both legs in Very dilute solution of sclerosing agent like
bilateral varicose veins STDS, polidocanal is injected into the thread
veins and reticular veins followed by application
• Diosmin therapy, which increases the of compression bandage (30-G needle). Dermal
venous tone. flare disappears well by this method.
• Elevation of the limb.
2. Injection—sclerotherapy (Fegan’s technique). Advantages
By injecting sclerosants into the vein, comp- 1. It can be done as an outpatient procedure.
lete sclerosis of the venous walls can be achieved. 2. It does not require anesthesia.
Disadvantage
Indications Inadvertent subcutaneous injection can cause
1. Uncomplicated perforator incompetence. skin necrosis or abscess formation.
2. In the management smaller varices.
3. Recurrent varices. Contraindications for sclerotherapy
• Sapheno-femoral incompetence.
Sclerosants used are
• Varicose veins with venous ulcer.
• Sodium tetradecyl sulphate 3%(STDS).
• DVT.
• Sodium morrhuate.
• Ethanolamine oleate.
• Polidocanal. 3. Surgery
a. Trendelenburg operation: It is juxtafemoral
Mechanisms of action flush ligation of long saphenous vein (i.e.
• Causes aseptic inflammation leading to flush with femoral vein), after ligating named
thrombosis.
(superficial circumflex, superficial external
• Causes perivenous fibrosis leading to block.
pudendal, superficial epigastric veins) and
• Causes approximation of intima leading to
unnamed tributaries. All tributaries should
obliteration.
After emptying, with the patient sitting down be ligated, otherwise recurrence will occur
and the leg horizontal, a 23-gauge needle is (saphena varix) (Fig. 5.8).
inserted into the vein. 0.5 ml of sclerosant is injec- b. Stripping of vein: Using Myer’s stripper vein
ted into the vein and immediately compression is stripped off. Stripping from below
is applied on the vein (to prevent the entry of upwards is technically easier. Immediate
blood which may cause thrombosis, which in application of crepe bandage reduces
turn gets recanalized later, thereby further the chance of bleeding and hematoma
worsening the condition), so as to allow the formation (Figs 5.9 and 5.10).
development of sclerosis and proper endothelial Complication is injury to saphenous
apposition. nerve causing saphenous neuralgia.
..A man who is proud of this money rarely has anything else to be proud of.
Stripping is not usually done for the veins Complications of varicose vein surgery
in the lower part of the leg. • Infection.
• Hematoma formation.
• DVT.
• Saphenous neuralgia.
• Recurrence.
Fig. 5.8: Incision for juxtafemoral flush ligation of long

saphenous vein (Trendelenburg operation)
Fig. 5.10: Picture showing stripping of the vein

using a stripper
Fig. 5.9: Photo of Myer’s stripper with olive tips
c. Subfascial ligation of Cockett and Dodd

Perforators are marked out by Fegan’s
method. Perforators are ligated deep to the
deep fascia through incisions in antero-
medial side of the leg (Fig. 5.11).
d. Ligation of short saphenous vein at sapheno-
popliteal junction.
e. Removal of superficial varicose veins by hook
phlebectomy.
Fig. 5.11: Cockett and Dodd subfascial ligation of
Contraindication for surgery: DVT. perforators using multiple small horizontal incisions
Venous Diseases 97
Complications of varicose veins Pathogenesis
• Hemorrhage: Venous hemorrhage can occur
from the ruptured varicose veins or sloughed
varicose veins, often torrential, but can be
controlled very well by elevation and
pressure bandage.
• Eczema and dermatitis.
• Periostitis causing thickening of periosteum.
• Venous ulcer.
• Marjolin’s ulcer.
• Lipodermatosclerosis.
• Ankylosis of the ankle joint.
• Talipes equino varus.
• Deep venous thrombosis.
• Calcification.
VENOUS ULCER
It is the complication of varicose veins or deep
vein thrombosis.
Due to regular walking on toes so as to relieve

the pain causes contraction and extra articular
fibrosis of Achilles tendon. Proper exercise is the
remedy – talipes equino varus.
Fig. 5.12: Venous ulcers in the lower limb
Area where venous ulcer commonly develops is Investigations

around and above the medial malleoli (Fig. 5.12) • Discharge from the ulcer for culture/
because of presence of large number of sensitivity.
perforators, which transmit pressure changes • X-ray of the area to look for periostitis.
directly into superficial system. This area is • Biopsy from the ulcer edge to rule out
called as Gaiter’s zone. It can also be on both Marjolin’s ulcer.
malleoli.
Ulcer is often large, nonhealing, tender, Treatment
recurrent with secondary infection. Vertical
group of inguinal lymph nodes are usually Bisgaard method
enlarged and tender. • Foot elevation.
Often it leads to scarring, ankylosis, • Massage of the indurated area and whole calf.
Marjolin’s ulcer formation. Slough from the ulcer • Passive and active exercise.
bed may give way causing venous hemorrhage. • Pressure bandage (crepe bandage).
Periostitis is common which also prevents ulcer • Care of ulcer by regular cleaning with
from healing. povidone iodine, H2O2.
..Many people worry a lot today about tomorrow because they didn’t worry a little yesterday about today.
• Dressing with EUSOL. seen in visceral malignancy like pancreas,
• Antibiotics depending on culture and stomach of affected veins.
sensitivity of the discharge.
Once ulcer bed granulates well, split skin Clinical Features
grafting (SSG) is placed (Thiersch Graft). Pain, redness, tenderness, cord-like thickening
Specific treatment for varicose veins should be of veins, fever.
undertaken—Trendelenburg operation, strip- It can be seen either in upper limb or lower
ping of veins, perforator ligation. limb.
50% of venous ulcer occur as a result of
recanalization of DVT, and the leg is commonly Complications
called as postphlebitic limb (leg). It presents with
all complications of venous diseases like eczema, • Destruction of venous valves resulting in
ulceration, lipodermatosclerosis, and venous varicose veins.
ulcers. • DVT.
Here surgery for superficial varicose veins • Embolism.
is contraindicated. Venous valve repair (valvulo- • Infection.
plasty) or drugs like Stanazolol that reduces the
fibrous tissue in turn increases the oxygenation Treatment
are beneficial. • Elevation.
• Anti-inflammatory drugs, antibiotics.
Complications of venous ulcers • Application of crepe bandage.
• Hemorrhage.
• Marjolin’s ulcer. ANTICOAGULANTS
• Infection.
• Talipes equino varus. HEPARIN
• Periostitis is common over the tibia. It is a natural anticoagulant, a mucopoly-
• Disability. saccharide.
• Calcification. It prevents clotting of blood both in vivo and
in vitro by acting on all three stages of
(EUSOL is Edinburgh University solution of lime coagulation. It prolongs clotting time and activated
containing boric acid, hypochlorite, calcium thromboplastin time in specific (by 1.5 – 2.0 times
hydroxide). the control).
Heparin also causes hyperkalemia.
THROMBOPHLEBITIS Commercial heparin is derived from lung
It is the inflammation of veins, usually superficial and intestinal mucosa of pigs and cattle.
veins due to different causes. The onset of action is immediate after
administration lasting for 4 hours.
Types It is metabolized in the liver by heparinase.
1. Acute: Due to IV cannulation, trauma, minor It does not cross placental barrier and not
infections, hypercoagulability. secreted in breast milk.
2. Recurrent:
3. Spontaneous: Polycythemia vera, polyarteritis, Indications
Buerger’s disease. • As prophylaxis in major surgeries, post-
4. Thrombophlebitis migrans (Trousseau’s sign): It operative period, puerperium.
is spontaneous migrating thrombophlebitis • As therapy in DVT.
Venous Diseases 99
Dose Types
• For prophylaxis: 5,000 units/SC 8th hourly. 1. Coumarin derivatives
• For therapy: 10,000 units/IV 6th or 8th • Bishydroxycoumarin (Dicoumarol)—
hourly. Later change to subcutaneous dose. First coumarin drug derived from sweet
• In severe cases, 5000 units to 20,000 units is clover.
given daily through IV infusion at a rate of • Warfarin sodium—Commonest oral anti-
1000 units per hour. Daily dose should not coagulant used.
exceed 25,000 units. 2. Indandione derivative
Heparin should not be given intramuscularly • Phenindione.
and should not be combined with streptokinase • Anisindione.
or urokinase. Heparin is not given orally.
Heparin administration should always be Modes of action of oral anticoagulant therapy
monitored with APTT. • By suppressing synthesis of prothrombin,
factors VII, IX, and X.
Complications • By inhibiting carboxylation of glutamic acid
Allergy, bleeding, thrombocytopenia. through Vit K.
• Oral anticoagulant does not have in vitro
LOW MOLECULAR WEIGHT HEPARIN action.
(LMWH). • They are slow acting and long acting.
It is a commercially prepared with a • Control of oral anticoagulant therapy is by
molecular weight of 4000 to 6500. monitoring prothrombin time.
• PT becomes normal only 7 days after
Advantages cessation of the drug.
• They are absorbed more completely. • They cross placental barrier and known to cause
• Have a longer duration of action. teratogenicity when given in 1st trimester.
• Have a better anticoagulant effect. • They are secreted in breast milk.
• Less interaction with platelets.
• Less antigenic. Indication
• Usage is easier and acceptable. In DVT, after cessation of heparin for main-
tenance therapy.
Disadvantages After valve replacement surgery.
They are expensive. Presently LMWH are
becoming very popular. Enoxaparin, Dalteparin, Side Effects
Parnaparin, Reviparin. 1. Bleeding—It may require blood transfusion
to control.
Heparin Antagonist 2. Cutaneous gangrene.
50 mg of 1% Protamine sulfate solution is given 3. Fetal hemorrhage and teratogenicity.
slow intravenous. 4. Alopecia, urticaria, dermatitis.
5. Drug interactions: With NSAIDs, Cimetidine,
Omeprazole, Metronidazole, Cotrimoxazole,
ORAL ANTICOAGULANTS Erythromycins, Barbiturates, Rifampicin,
They are given orally and are slow acting. Griseofulvin.
..One cannot love what he cannot respect, whether it be himself or another.

WARFARIN SODIUM (Wiskonian Alumini surgery like tooth extraction and prothrombin
Research Foundation + coumARIN derivative) time should return to normal level. During
is the commonest drug used. It has got lesser side surgery if excess bleeding occurs blood
effects. It has got cumulative action and so given transfusion may be given.
in tapering dose.
In vitro anticoagulants: Oxalates, citrates,
Dose is 5 mg per day.
EDTA.(Ethylene diamine tetraacetic acid).
It should be discontinued 7 days before any
Differences between oral anticoagulants and heparin

Oral anticoagulant Heparin
Slow acting. Immediate.
Long acting. Short acting.
Only in vivo action. Both in vitro and in vivo action.
Monitored by: Prothrombin time. Partial thromboplastin time.
Crosses the placental barrier. Does not cross the placenta.
Secreted in milk. Not secreted in milk.
Administration: Orally. Intravenously.
Lymphatics 101
6 Lymphatics
 Lymphangiography visualized clearly. After making incision, one of

 Isotope lymphoscintigraphy the lymphatic vessels is dissected and 30-G
 Lymphedema needle is passed. Ultrafluid lipiodol, which is an
 Lymphomas oily contrast medium, is injected slowly using
 Hodgkin’s lymphoma (HL) pressure pump at a rate of 1 ml in 8 minutes (total
 Non-Hodgkin’s lymphoma (NHL) quantity is 7 ml). Slowly in 24 hours, it passes
 Burkitt’s lymphoma (Malignant through the lymphatics and reaches the iliac and
lymphoma of Africa) paraaortic lymph nodes. Radiographs taken,
helps to visualize both lymphatic vessels as well
 Tuberculous lymphadenitis
as lymph nodes.
Secondaries in lymph nodes cause filling
LYMPHANGIOGRAPHY defects. Lymphomas show enlarged nodes,
Indications which have foamy or reticular appearance.
• Congenital lymphedema like aplasia, Disadvantages
hypoplasia, hyperplasia.
• Lymphomas, it shows reticular pattern. It is • Technically difficult.
also useful to assess the response to treat- • Extravasation of dye can occur.
ment. • Dye might not have reached the required
• Secondaries in lymph nodes, especially iliac area.
and paraaortic lymph nodes as irregular • Time consuming and invasive procedure.
filling defects.
Lymphangiographic
Technique Classification of Lymphedema
Patent blue dye or 1 ml Isosulphan blue is • Congenital hyperplasia (10%).
injected subcutaneously between toes. Dye will • Distal obliteration (80%).
be taken up by lymphatics,which will be • Proximal obliteration (10%).
..In the field of observation, chance favors only the prepared mind.
ISOTOPE LYMPHOSCINTIGRAPHY primarily due to defective lymphatic drainage.

It is protein rich interstitial fluid.
Radioactive Technetium labeled antimony
sulfide colloid particles are injected into the web Classification
space using fine needle. These particles are Kinmoth classified lymphedema as—
specifically taken up by lymphatics. Using • Primary without any identifiable lymphatic
gamma camera, limb and inguinal region are disease.
exposed to visualize the lymphatics and inguinal • Secondary is acquired due to definitive cause.
lymph nodes. In 3 hours it reaches paraaortic Most common form.
lymph nodes, other abdominal lymph nodes and
liver. Later thoracic duct also can be visualized. Causes of secondary lymphedema
It can be compared to the take up on the other limb. • Trauma.
• Surgery—inguinal block or axillary block
Advantages dissection.
• Filarial lymphedema due to Wuchereria
• It is more sensitive. bancrofti. Common cause in coastal region.
• Technically easier and faster compared to • Tuberculosis.
lymphangiography. • Syphilis.
• Thoracic duct, other lymph nodes and liver • Fungal infection.
can be visualized. • Advanced malignancy—Hard, fixed lymph
nodes in axilla or in inguinal region.
LYMPHEDEMA • Postradiotherapy lymphedema.
It is accumulation of fluid (lymph) in extra- • Bacterial infection.
cellular and extravascular fluid compartment, • Rare causes: Rheumatoid arthritis, snake and
commonly in subcutaneous tissues. It is insect bites, DVT, chronic venous insufficiency.
Primary type
It affects commonly females.
It is common in lower limb and left side.
It can be—
• Familial.
• Syndromic.
It can be—
• Lymphedema congenita — Present at birth.
— Familial type is called as Milroy’s disease.
• Lymphedema praecox — Present at puberty—up to 35 years.
— Familial type is called as Meige’s disease.
• Lymphedema tarda —present in adult life—after 35 years.
It can be radiologically (lymphangiography)—
• Hypoplasia 70%
• Aplasia 15%
• Hyperplasia(varicose lymphatics) 15%
It can be lymphangiographically and clinically—
• Distal obliteration — Here proximal part is normal. It is common in young females.
• Proximal obliteration — Common type 85%. Common in both sexes.
— With distal hyperplasia
— With distal obliteration.
• Congenital hyperplasia—It shows dilated incompetent megalymphatics.
Lymphatics 103
Pathology (commonly in filarial lymphedema)
Rarely it causes protein losing diarrhea,

chylous ascites, chylothorax, chyluria, lymphor-
rhea. Recurrent lymphadenitis occurs in the
region, which aggravate the condition.
Disease in the limb is confined to skin and
subcutaneous tissue, i.e. often, only superficial
lymphatics are involved by the disease, deep
lymphatics are not. Superficial and deep
lymphatics are not communicating with each
other (Unlike the veins in the limb where super-
ficial and deep veins are freely communicating Fig. 6.1: Picture showing elephantiasis left leg with skin
with each other). thickening and fissuring
..Our worst misfortunes never happen, and most miseries lie in anticipation.
Sites of lymphedema Clinical features

1. Lower limb—commonest. • Swelling in the foot, extending progressively
2. Upper limb. into the leg.
• Buffalo hump in the dorsum of the foot.
3. Scrotum, penis (Ram’s horn penis)
• Squaring of toes.
(Figs 6.2A and B).
• Skin over the dorsum of foot cannot be
4. Breast—requires reduction mammoplasty. pinched because of subcutaneous fibrosis-
5. Labia. Stemmer’s sign.
6. Eyelid. • Initially pitting edema, which later becomes
7. Localized lymphedema. nonpitting.
• Eczema, fissuring, papillae formation, ulcera-
tion, lymph ooze, elephantiasis are other
features.
Brunner’s grading of lymphedema

Latent subclinical: No clinically apparent
lymphedema.
Grade I: Pitting edema which more or less
disappears on elevation of the limb is due to
excess deposition of interstitial fluid.
Grade II: Nonpitting edema which does not
reduce on elevation.
Grade III: Edema with irreversible skin
changes like fibrosis, papillae, fissuring.
• Cardiac causes, hypoproteinemias, malnutri-
tion, nephrotic syndrome.
• Myxedema.
• Trauma.
• Venous diseases like DVT, etc.
• Lipodystrophy and lipoidosis.
• Arterial diseases including A-V malforma-
tions.
• Gigantism.
• Drug induced—Steroids, estrogens, nifedipine.
Investigations
• For the cause.
• ESR, peripheral smear.
• Lymphangiography.
• Isotope—lymphoscintigraphy.
Figs 6.2A and B: Ram’s horn penis
Lymphatics 105
Complication Omentoplasty (Omental pedicle): As
• Skin thickening. omentum contains plenty of lymphatics,
• Recurrent cellulitis with non-healing ulcers, omental transfer with pedicle will facilitate
morbidity and disability. lymph drainage.
• Lymphangiosarcoma. c. Combined
Both excision + creation of communication
Treatment between superficial and deep lymphatics.
• Sistrunk operation.
Conservative • Thompson’s operation.
• Elevate the limb. • Kondolean’s operation.
• Massaging and avoiding prolonged stan- d. Bypass procedure
ding. Skin bridge across the thigh and abdomen.
• Diuretics to reduce the edema are contro- • Nodovenous shunt.
versial. It more often causes electrolyte • Lymphovenous shunt using microscope.
imbalance than being beneficial. • Ileal mucosal patch.
• Benzopyrones are proteinolytic agents e. Limb reduction surgeries
• Sistrunk operation: Along with excision
(Lympedin).
of lymphedematous tissue, window cuts
• Daily wearing of below knee stockings.
in deep fascia is done, so as to allow com-
• Avoid trauma and infection.
munication into normal deep lymphatics.
• Intermittent pneumatic compression devices. • Homan’s operation: Excision of lymph-
• Antibiotics—Flucloxacillin, Erythromycins, edematous tissue after raising skin flaps.
long acting Penicillins. Later skin flaps are trimmed to required
• Topical antifungal 1% clotrimazole and size and sutured primarily.
systemic Griseofulvin 250-1000 mg. • Thompson’s operation: Lymphedema-
• Regular washing and keeping the limb clean tous tissue is excised under the skin flaps.
is very important. Epidermis and part of the dermis of one
• Diethyl carbamazine citrate (DEC) 100 mg tid of the skin flaps is shaved off using
for 3 weeks. Humby’s knife. It is buried under oppo-
site flap, deep to the deep fascia like a
Surgery swiss roll(Swiss roll operation or buried
Surgeries for lymphedema has been classified as: dermal flap operation).
a. Excisional Problems here are epidermal cysts and
• Charle’s operation. sinus formation.
• Homan’s operation. • Kondolean’s operation: Along with excision
b. Physiological of lymphedematous tissue, vertical strips of
• Omentoplasty. deep fascia are removed so as to open the deep
• Nodovenous shunt. lymphatics, which creates communication
• Lymphovenous shunt. between superficial and deep lymphatics.
• Ileal mucosal patch. • Charle’s operation: Done in severe lymph-
Here either communication between edema with elephantiasis. Along with
superficial and deep lymphatics is created or excision of lymphedematous tissues, skin
new lymphatic channels are mobilized to the grafting is done. It reduces the size and weight
site. of the limb. Patient becomes ambulatory.
..Pleasure in the job puts perfection in the work.

In severe type, amputation may be required
occasionally.
LYMPHOMAS
They are progressive neoplastic condition of
lymphoreticular system arising from stem cells.
WHO modified REAL (Revised European

American Lymphoma) classification of lymphoma:
1. B-cell neoplasms
I. Precursor B-cell neoplasm—ALL, LBL.
II. Peripheral B-cell neoplasm—It includes Fig. 6.3: Enlarged, bilateral rubbery
all B-cell related NonHodgkin’s lympho- neck nodes—lymphoma
mas.
2. T-cell and putative NK cell neoplasms Rye’s classification
I. Precursor T-cell neoplasms—ALL and 1. Lymphocytic predominance. Has got good
LBL T-cell related. prognosis.
II. Peripheral T-cell and NK cell neoplasm— 2. Mixed cellularity.
It includes all T-cell related Non- 3. Nodular sclerosis.
Hodgkin’s lymphomas. 4. Lymphocytic depletion. Has got bad
3. Hodgkin’s lymphoma prognosis.
I. Predominant HL—Nodular lymphocyte
type. Reed-Sternberg cells are also seen occa-
II. Classical HL. sionally in certain other conditions like glandular
Nodular sclerosis. fever.
Lymphocyte rich.
Clinical Features
Mixed cellularity.
Lymphocyte depletion. • It is more common in males.
• It has got bimodal presentation. It is seen in
Types young and adolescents (20–30 yrs) as well as
in elderly (> 50 yrs) (Fig. 6.4).
• Hodgkin’s lymphoma (HL).
• Painless progressive enlargement of lymph
• Non-Hodgkin’s lymphoma (NHL).
nodes. They are smooth, firm, nontender,
typically India rubber consistency.
HODGKIN’S LYMPHOMA (HL)
Site
• It is the commonest type of lymphoma. • Cervical lymph nodes commonest. 82%
• Grossly lymph nodes are fleshy, pinkish gray, (lower deep cervical group in posterior
and rubbery in consistency (Fig. 6.3). triangle).
• Microscopically contains cellular infiltration • Others include axillary, mediastinal,
with lymphocytes, reticulum cells, histio- inguinal, abdominal.
cytes, fibrous tissue and Reed-Sternberg cells.
(Reed Sternberg cells are giant cells with two Specific Features
large mirror image nuclei). • Nodular sclerosis is most common type.
Lymphatics 107
Ann-Arbor clinical staging
Stage1: Confined to one group of lymph node.
Stage 2: More than one group of lymph nodes
on one side of the diaphragm.
Stage 3: Nodes involved on both sides of the
diaphragm.
Stage 4: Extra nodal involvements like liver,
bone marrow.
Suffix ’S’—Spleen involved, suffix ‘B’—
Presence of constitutional symptoms,
Suffix ‘A’—Absence of constitutional
symptoms.
• Chronic lymphatic leukemia.

• Nonspecific lymphadenitis.
• Sarcoidosis.
Fig. 6.4: Hodgkin’s lymphoma in young boy • Secondaries in lymph nodes (Fig. 6.5).
with typical look of neck nodal involvement.
HL is common in young and elderly patients
with bimodal representation
• Consecutive group of lymph nodes are

involved.
• Splenomegaly is very common (45%).
• Hepatomegaly with jaundice—jaundice is
due to hemolysis or due to diffuse liver
involvement.
• Constitutional symptoms like fever, malaise,
pruritus, weight loss may be present, which
signifies stage ‘B’, and has got poor
prognosis. Stage ‘A’ is absence of these
symptoms, which signifies better prognosis.
• Mediastinal lymph node involvement may
cause compression features like SVC
obstruction. Fig. 6.5: Secondaries in neck is hard, often fixed mass.
• Occasionally bone may get involved, like It is a differential diagnosis for lymphoma
vertebrae. But it is not common in NHL.
• Anemia, pancytopenia. Investigations
• Blood: Hb%, ESR, peripheral smear, blood
Differential Diagnosis urea, serum creatinine.
• Tuberculosis. • FNAC of lymph nodes.
• NHL. • Excision biopsy of lymph nodes. Full lymph
• HIV. node has to be excised to retain the archi-
..The remedy for injuries is not to remember them.

tecture of the lymph node. It is important to
grade the tumor.
• Chest X-ray to see mediastinal lymph nodes,
pleural effusion (Fig. 6.6).
• Ultrasound abdomen—to look for the
involvement of liver, spleen, and abdominal
lymph nodes.
• CT scans of mediastinum and abdomen
(Fig. 6.7).
• Lower limb lymphangiography to see the
pelvic and retroperitoneal lymph nodes.
• Bone marrow biopsy to stage and also to see
the response to treatment.
• Staging laparotomy:
• After opening the abdomen, splenectomy
is done mainly to remove the tumor bulk, Fig. 6.6: Chest X-ray showing mediastinal lymphoma
as spleen is commonly involved and also
to avoid irradiation to splenic area, which
often causes unpleasant pulmonary
fibrosis (due to damage to lower lobe of
left lung). Biopsies are taken from both
lobes of the liver (needle biopsy) from
paraaortic, mesenteric, iliac nodes. In
females ovaries are fixed behind the
uterus to prevent radiation oophoritis
(oophoropexy). It is done in suspected
stage I and II cases. Presently it is not
commonly done as availability of better
modalities of staging like ultrasound, CT
scan, MRI, etc. Advanced radiotherapy Fig. 6.7: CT scan showing mediastinal tumor
technique makes it safer to irradiate suggestive of mediastinal lymphoma
splenic area without causing much
damage to left sided lung. Mustine. M. (Mechloroethamine) 6 mg/sq m
Oncovine. O. (Vinca alkaloids) 1.4 mg/sq m
Treatment for HL
Procarbazine. P. 100 mg orally for 10 days
• Stage I and II: of the cycle.
1. Mainly radiotherapy—external high Prednisolone. P. 15–45 mg for first 10 days.
cobalt RT. Other regimens available —MVPP, ABVD.
• Above the diaphragm—‘Y’ field
therapy, covering cervical, axillary, Prognosis: 5-year-survival rate is 80%.
mediastinal lymph nodes.
Prognostic factors
• Below the diaphragm, mantle or inver-
1. Stage I and II has got better prognosis.
ted ‘Y’ field therapy, covering paraaortic
2. Lymphocytic predominance has got better
and iliac nodes.
prognosis.
2. Chemotherapy.
3. Stage ‘A’ without constitutional symptoms
• Stage III and IV: Mainly chemotherapy.
has got better prognosis.
Drugs used includes—
Lymphatics 109
Causes of death in lymphoma Types
• Disseminated diseases like liver involve- • Nodular (Follicular).
ment (liver failure). • Diffuse lymphocytic.
• Stage IV lymphoma with bone marrow • Undifferentiated.
involvement. • Histiocytic type.
• Recurrent severe opportunistic respiratory
tract infection.
• Spine involvement with paraplegia and Rappaport classification Working classification
pathological fracture. 1. Nodular a. Low grade
• Immunosuppression—septicemia. 2. Diffuse b. Intermediate grade
c. High grade
NON-HODGKIN’S LYMPHOMA (NHL)
Treatment
• It occurs in middle-aged and elderly. It is
more aggressive than HL. Mainly chemotherapy.
• It involves asymmetrical group of lymph Various regimens available include:
nodes. • ChOPP—Chlorambucil, Oncovin, Procar-
• General condition is poor. bazine, Prednisolone.
• Inner Waldeyer ring, epitrochlear lymph • ABVD—Adriamycin, Bleomycin,
nodes, peripheral lymph nodes are com- Vincristine, Dacarbazine.
monly involved. • ABVP—Adriamycin, Bleomycin, Vincristine,
• Spleen is not commonly involved. Prednisolone.
• Hepatomegaly is common. • Combinations of above.
• Vertebral involvement is common; para-
plegia can occur. Role of radiotherapy in NHL: When vertebra is
• Secondary infection, cachexia and immuno- involved.
suppression is more common. Prognosis is poor compared to HL.
Differences between HL and NHL

HL NHL
Age: Young and elderly. Middle age and elderly.
Pattern of involvement: Symmetrical and consecutive. Asymmetrical.
Cervical lymph node: Commonly involved. Any group can be involved.
Splenomegaly: Common. Not common.
Peripheral lymph node
involvement Not common. Common.
(e.g. epitrochlear nodes).
Treatment: Mainly radiotherapy. Mainly chemotherapy.
Chemotherapy.(MOPP regime).
Prognosis: Better. Poor.
..Following the happiness is like chasing the wind or clutching the shadow.
BURKITT’S LYMPHOMA Treatment

(Malignant Lymphoma of Africa) Radiotherapy.
Chemotherapy: Cyclophosphamide, Metho-
• It is common in South Africa and New
trexate, Orthomelphalan.
Guinea.
Surgery is usually not indicated unless it is
• Epstein Barr virus may be the etiological agent.
localized or in case of involvement of ovaries.
It is common in children.
Prognosis is good.
• It is associated with infectious mononuc-
leosis. TUBERCULOUS LYMPHADENITIS
• It is common in malaria endemic area.
• The tumor is multifocal, rapidly growing, Causative organism—Mycobacterium tuberculosis
painless. (not M. bovis).
• Different groups of lymph nodes can also be Site
affected.
Common in neck lymph nodes.
Microscopy Common in upper deep cervical (jugulodigastric—
54%) lymph nodes.
Primitive lymphoid cells with large clear histio- Next common is posterior triangle lymph nodes
cytes—starry night(starry sky) pattern. (22%).
Site Mode of infection
It is common in jaw—either lower or upper. Usually through the tonsils, occasionally through
Abdominal presentation and renal involve- blood from lungs.
ment is common (75%). It may be associated with pulmonary tuber-
Renal involvement often may be bilateral. culosis or renal tuberculosis.
In females ovaries are commonly affected.
Stages of tuberculous lymphadenitis (Fig. 6.8)
Investigation 1. Stage of infection. and lymphadenitis.
2. Stage of periadenitis with matting.
• FNAC and biopsy confirms the diagnosis. 3. Stage of caseating necrosis and cold abscess
• X-ray jaw shows osteolytic lesions. formation (Fig. 6.9).
• Ultrasound abdomen to see involvement of 4. Stage of formation of collar stud abscess.
kidneys. 5. Stage of formation of sinus which discharges
• Blood urea and serum creatinine estimation yellowish caseating material.
is done.
Types
Hyperplastic Caseating
a. 20% common 80% common.
b. Discrete, firm or hard. Matted due to periadenitis.
c. Occurs in the cortex of lymph node. Involves medulla with periadenitis.
d. Host immunity is good. Body resistance is not adequate.
e. Drugs act better. Drugs do not reach in proper concentration
and may not be effective.
f. Drug resistance is uncommon. Drug resistance is common.
g. No cold abscess or sinus formation. Cold abscess or sinus are common.
h. Blood spread. From tonsils.
Lymphatics 111
nodes, mesenteric lymph nodes, and inguinal
lymph nodes.
Disease may be associated with HIV
infection, and lymphomas.
Clinical Features
• Swelling in the neck, which is firm, matted.
• Cold abscess is soft, smooth, nontender,
fluctuant, without involvement of the skin
• As a result of increased pressure, cold abscess
ruptures out of the deep fascia to form collar
stud abscess which is adherent to the overlying
skin.
• Once collar stud abscess bursts open,
discharging sinus is formed.
• Tonsils may be studded with tubercles and so
clinically should always be examined.
• Associated pulmonary tuberculosis should
also be looked for.
Fig. 6.8: Stages of tuberculous lymphadenitis
Often fibrosis and calcification can occur with

or without treatment.
Gross pathology. Firm, matted, lymph node, with
cut section showing yellowish caseating material. Fig. 6.9: Cold abscess in the neck which has formed collar
stud abscess. It eventually leads in to sinus formation
Microscopic. Epithelioid cells with caseating
material are seen along with Langhan’s type of
giant cells.
Disease can also occur in other lymph nodes 1. Nonspecific lymphadenitis.
like, axillary lymph nodes, paraaortic lymph 2. Lymphomas.
..A long life may not be good enough but a good life is long enough.
3. Secondaries in the neck. 3. Ethambutol 800 mg OD. It is bacteriostatic.
4. Branchial cyst mimics cold abscess. It causes GIT intolerance, retrobulbar neuritis
5. Lymph cyst mimics cold abscess. (green color blindness).
6. HIV with lymph node involvement. 4. Pyrazinamide 1500 mg OD or 750 mg BD. It
7. When there is discharging sinus—actinomy- is bactericidal. It is hepatotoxic, also causes
cosis. hyperuricemia and increases psychosis.
Duration of treatment is usually 6–9 months.
Investigations When there is cold abscess, initially it has to
be aspirated. (Needle is introduced into the cold
1. Hematocrit, ESR. abscess in a nondependent site along a ‘Z’ track
2. FNAC of lymph node. (in zigzag pathway) so as to prevent sinus for-
3. HIV test. mation).
4. Open biopsy when FNAC is inconclusive. But if it recurs, then it should be drained.
5. Chest X-ray to look for pulmonary tuber- Drainage is done through a nondependent incision.
culosis. After draining the caseating material, wound is
closed without placing a drain.
Treatment Surgical removal of tubercular lymph nodes are
Antituberculous drugs has to be started— indicated when—
1. Rifampicin 450 mg OD in empty stomach. It • There is no local response to chemotherapy
is bactericidal. It discolors urine red. It is also • When sinus persists.
hepatotoxic. It is done by raising skin flaps and removing
2. INH—300 mg OD. It is bactericidal. It causes all caseating material and lymph nodes. Care
intolerance, neuritis, hepatitis (INH). should be taken not to injure major structures.
Shock and Hemorrhage 113
7 Shock and Hemorrhage
It may be due to—

 Shock
 Central venous pressure (CVP) a. Hemorrhage
 Pulmonary capillary wedge pressure (PCWP) — external from wounds, open fractures.
 Systemic inflammatory response — internal from injury to spleen, liver,
syndrome (SIRS) mesentery or pelvis.
 Oxygen therapy b. Severe burns, which results in loss of
 Hyperbaric oxygen plasma.
 Cardiac arrest c. Peritonitis, intestinal obstruction.
 Mechanism of blood coagulation d. Vomiting and diarrhea due to any cause.
 Hemorrhage 2. Cardiac causes –
 Blood transfusion
a. Acute myocardial infarction, acute
 Blood fractions
 Massive blood transfusion carditis.
 Blood substitutes b. Acute pulmonary embolism, wherein
 Tourniquets embolus blocks the bifurcation of pulmo-
nary artery or one of the major branches.
SHOCK Air embolism (50 ml of air) also can cause
shock due to pulmonary embolism.
Shock is a state of poor perfusion where there
is circulatory failure along with impaired cellular c. Drug induced.
metabolism manifesting with severe patho- d. Toxemia of any causes.
physiological abnormalities. e. Cardiac surgical conditions like valvular
diseases, congenital heart diseases.
CAUSES OF SHOCK f. Cardiac compression causes—
1. Hypovolemic shock—due to reduction in i. Cardiac tamponade due to collection
total blood volume. of blood, pus, fluid in the pericardial
..Nothing stands in front of a willing heart and strong determination.

space, which prevents the heart to
expand leading to shock.
ii. Trauma to heart.
3. Septic shock—It is due to bacterial infections,
which release toxins leading to shock.
4. Neurogenic shock—due to sudden anxious
or painful stimuli causing severe splanchnic
vessel vasodilatation. Here, patient either
goes for cardiac arrest and dies or recovers
fully spontaneously.
5. Anaphylactic shock—It is due to Type 1
hypersensitivity reaction.
6. Respiratory causes:
a. Atelectasis(collapse) of lung.
b. Thoracic injuries.
c. Tension pneumothorax.
d. Anesthetic complications.
7. Other causes:
a. Acute adrenal insufficiency (Addison’s
disease).
b. Myxedema
Pathophysiology of Shock
Cellular changes occur in persistent shock due
to release of lysosomal enzymes, which alters the
cell membrane permeability causing cell death—
sick cell syndrome.
Sympathetic overactivity alters the micro-
circulation leading to capillary dysfunction.
Brain perfusion once decreases and the patient
Effects of Shock becomes drowsy. Brain is the last organ to get
Heart: Low perfusion → low venous return → underperfused in shock.
decreased cardiac output → hypotension → Kidneys: GFR decreases and tubular reabsorp-
tachycardia. Persistent shock causes hypoxia and tion of salt and water increases for compensatory
release of myocardial depressants leading to response. But in severe cases tubular necrosis sets
further cardiac damage. in leading to irreversible damage.
Lung: Interstitial edema → decreased gaseous Blood: Alteration in cellular components includ-
exchange → pulmonary arteriovenous shunting ing platelets leads to Disseminated Intravascular
→ tachypnea → Adult Respiratory Distress Thrombosis (DIC). It causes bleeding from all
Syndrome (ARDS) and pulmonary edema. organs.
Metabolic: Shock leads to hypoxia, which Gastrointestinal tract: Mucosal ischemia
activates anaerobic metabolism leading to lactic develops causing bleeding from GIT with hema-
acidosis. Antidiuretic hormone (ADH) is temesis and melena. It is aggravated by DIC.
released which increases the reabsorption of Hepatic ischemia leads into increased enzyme
water from renal tubules. Other hormones levels.
released are ACTH, prostaglandins, histamine,
bradykinin, serotonin to compensate the effects Types of Hypovolemia
of shock to increase the perfusion of vital organs
a. Covert compensated hypovolemia—When
like heart, brain, and lungs.
blood volume is reduced by 10–15%, there
Stages of Shock will not be significant change in heart rate,
..Nothing is impossible to a willing heart.

cardiac output and splanchnic blood com- Common organisms involved are E. Coli,
pensates for the same. Klebsiella, Pseudomonas, Proteus.
b. Overt compensated hypovolemia: Here
patient has cold periphery, tachycardia, a Septic shock
wide arterial pressure, tachypnea, confusion, • Common causes are biliary, urinary, GIT
hyponatremia, metabolic acidosis, but sepsis (peritonitis, strangulation)
systolic pressure is well-maintained. • Common bacteria are E.coli, Klebsiella,
c. Decompensated hypovolemia: Here all Pseudomonas.
features of hypovolemia is present. Hypo-
• Common pathophysiologies are release of
tension, tachycardia, sweating, tachypnea,
toxins, neutrophil activation, cytokine
oliguria, drowsiness, eventually features of
release, sick cell syndrome, SIRS, MODS.
SIRS appears, and often if not treated on time
leads to MODS, i.e. irreversible shock. • Clinical stages are hyperdynamic and
hypodynamic.
Septic Shock • Find out the source of the infection by
ultrasound CT scan.
Also called as endotoxic shock. It occurs due to
• Do pus/blood/urine culture.
gram-negative bacterial infections, often seen in
• Start antibiotics of high generations like
cases of strangulated intestines, peritonitis, GIT
fistulas, biliary sepsis, urinary sepsis, etc. Ceftazidime, Amikacin, Cefoperazone.
• Dopamine/dobutamine infusion(slow).
Stages of Septic Shock • Monitoring by pulse, BP, respiration, urine
output, level of consciousness.
1. Hyperdynamic (warm) shock: This stage is
• Ventilator support, ICU management.
reversible stage. Patient is still having inflam-
matory response and so presents with fever, • Treat the cause like peritonitis, abscess drainage.
tachycardia, tachypnea, etc. Pyrogenic Anaphylactic shock
response is still intact. Patient should be Injections—Penicillins, anesthetics, stings,
treated properly at this stage. Based on blood shellfish, etc. may be having antigens which
culture, urine culture (depending on focus of combines with IgE of mast cells and basophils,
infection), combination of higher antibiotics releasing histamine and large amount of SRS-
like third generation cephalosporins, amino- A (Slow Releasing Substance of Anaphylaxis).
glycosides, metronidazole, etc. are started.
They cause bronchospasm, laryngeal edema,
The underlying cause is treated like draining
respiratory distress, hypotension and shock.
the abscess if any, laparotomy for peritonitis,
etc. Ventilatory support with proper ICU Mortality is 10%.
monitoring may prevent the patient going for Anaphylactic shock
the next cold stage of sepsis. • Sudden onset.
2. Hypodynamic hypovolemic septic shock (Cold • Distributive shock.
septic shock): Here pyrogenic response is lost.
• Bronchospasm, laryngeal edema.
Patient is in decompensated shock. It is an
• Generalized rashes and edema.
irreversible stage along with MODS(Multi
• Hypotension, feeble pulse.
organ Dysfunction Syndrome) patient
• Mortality 10%.
presents with anuria, respiratory failure
(cyanosis), jaundice (liver failure), cardiac • To start Adrenaline 100μg IV, steroids,
depression, pulmonary edema, hypoxia, IV fluids, oxygen with foot end elevation.
drowsiness. Eventually coma and death • Ventilator in severe cases.
occurs. • Cardiac massage, defibrillation.
Clinical Features of Shock • Nasal oxygen to improve oxygenation or
• In early stage tachycardia, sweating, cold monitoring in intensive care unit with
periphery, hypotension, restlessness, air ventilator support has to be done.
• CVP line to perfuse adequately and to
hunger, tachypnea, oliguria, collapsed veins.
monitor fluid balance. TPN can be given
• In late stage, cyanosis, anuria, jaundice,
when required. Brain perfusion can also be
drowsiness occurs. improved by using Trendelenburg position
(Fig. 7.1)
Investigations • PCWP to monitor very critical patient.
• Regular monitoring of BP, pulse. • Hemodialysis may be necessary when
• Heart rate. kidneys are not functioning.
• Respiratory rate.
• CVP line (Central Venous Pressure).
• PCWP (Pulmonary capillary wedge pressure).
• Measurement of urine output.
• Arterial PO2 and PCO2 analysis.
• Serum electrolyte estimation.
Treatment
Guidelines—
- To treat the cause. Fig. 7.1: Trendelenburg position is used in all patients in
shock to improve the brain perfusion
- To improve cardiac function.
- To improve tissue perfusion.
• Treat the cause, e.g. Arrest hemorrhage, drain CENTRAL VENOUS PRESSURE (CVP)
pus. It is a method to measure the right atrial pressure
• Fluid replacement: Plasma, normal saline, by placing a venous catheter (20cm) into the SVC.
dextrose, Ringer lactate, plasma expander Commonly for CVP monitoring, a venous
(Haemaccel—maximum 1 liter can be given catheter is passed through right internal jugular
vein or infraclavicular subclavian vein to the SVC
in 24 hours).
(used for TPN purpose). Or occasionally a long
• Inotropic agents: Dopamine, Dobutamine, catheter (60cm) can be passed through basilic
Adrenaline infusions. vein (not commonly done). Under radiological
• Correction of acid base balance. guidance, initially a needle is passed 3 cm above
• Steroids is often life saving. 500–1000 mg of the medial end of the clavicle, in the hollow
hydrocortisone can be given. It improves the between the two heads of sternomastoid
perfusion, reduces the capillary leakage and muscles, directing towards the suprasternal
systemic inflammatory effects. notch into the right internal jugular vein. Then
through a guidewire, a venous catheter is passed
• Antibiotics in patients with sepsis; proper
into the SVC through right internal jugular vein,
control of blood sugar and ketosis in diabetic which can also be confirmed by changes in flow
patients. during inspiration and expiration.
• Catheterization to measure urine output Catheter is connected to saline manometer,
(normal output—30-50 ml/hour or > 0.5 taking manubriosternal angle (angle of Louis) as
ml/Kg/hour). zero point (Fig. 7.2).
..A misty morning does not signify a cloudy day.

Normal value is 2–10 cm of saline. PULMONARY CAPILLARY WEDGE
If less than 2 cm, more fluid is infused. PRESSURE (PCWP)
If more than 10 cm, fluid infusion should be
restricted. It is a better indicator of circulating blood volume
and left ventricular function.
Complications of CVP Catheter used is Swan Ganz triple channel
• Pneumothorax. pulmonary artery balloon catheter.
• Hemothorax. It is used to differentiate right and left ventri-
• Injury to brachial plexus and vessels. cular failure, pulmonary embolus, and septic
• Bleeding. shock. To measure cardiac output, to monitor
• Sepsis. fluid therapy, inotropic agents, vasodilators.
• Catheter displacement.
Procedure (Fig. 7.3)
Under strict aseptic precaution, using cannula
and guidewire, catheter is passed through inter-
nal jugular vein, into the right atrium. Balloon
is inflated by 1.5 ml of air and then negotiated
into pulmonary artery, until it reaches a small
branch and wedges it. Pressure at this point is
called as pulmonary capillary wedge pressure.
PCWP normally is 8–12 mmHg, considering
mid axillary point as zero reference point.
After that balloon is deflated to get pulmo-
nary artery pressure which is normally 25 mm
Hg systolic and 10 mmHg diastolic.
PCWP catheter can be kept in situ only for
72 hours.
Complications of PCWP
• Arrhythmias.
• Pulmonary artery rupture. Balloon rupture.
• Pulmonary infarction.
• Pneumothorax.
• Hemothorax.
• Bleeding, sepsis, thrombosis.
SYSTEMIC INFLAMMATORY
RESPONSE SYNDROME (SIRS)
• It is final common pathway in shock due to
any cause (trauma, sepsis, endotoxemia,
burns.), where there is failure of inflam-
matory localization with vasodilatation,
Figs 7.2A and B: Central venous pressure (CVP) is used to
increased endothelial permeability with
monitor the patient. Note the location of the central venous damage, thrombosis, leukoctye migration
catheter and activation.
Differences between CVP and PCWP
CVP PCWP
Technically easier Requires skilled experts.
Normal pressure is 2–10 cm of saline. 8–12 mmHg.
Gives gross idea about fluid balance. Better and specific.
Left ventricular function is not assessed. Left ventricular function is very well assessed
Not used to differentiate between right and Very well-differentiates.
left ventricular function.
Can be kept in situ as long as required. Cannot be kept in situ for more than 72 hours
Catheter tip is in SVC. Catheter tip is in pulmonary capillary with wedging
Plain tip catheter. 1.5 ml air filled balloon tip.
Can be used for TPN, fluid infusion, etc. Cannot be used for TPN, or fluid infusion
Complications are easy to tackle. Often difficult to tackle.
Not as sensitive and specific as PCWP. Sensitive and specific.
• SIRS carries poor prognosis.
OXYGEN THERAPY
Indications
• Chest injuries, any severe hemorrhage.
• Gas gangrene with toxic hemolysis.
• Coal gas poisoning.
• Over morphinization.
• Pulmonary embolism and fat embolism.
• Spontaneous pneumothorax, pulmonary
edema, cardiac infarction, pneumonia, cor
pulmonale.
• Cardiogenic shock and acute bronchitis.
27% oxygen is delivered through ventimask
Fig. 7.3: Pulmonary capillary wedge pressure (PCWP) is
(disposable polythene mask) at a rate of 4–6 liters
better index of shock. But it is technically difficult and cannot per minute. Oxygen is also given along with
be kept for more than 72 hours. It cannot be used for perfusion positive pressure ventilation.
purpose unlike CVP line
HYPERBARIC OXYGEN
• It is associated with release of free radicals,
abnormal arachidonic acid release, cytokine It is administration of oxygen 1 or 2 atmospheres
release, neutrophil sequestration, abnormal above the atmospheric pressure in a compression
NO synthesis, complement activation, and chamber. It increases the arterial oxygen
DIC. saturation so that oxygen perfusion of tissues
• It is a part of severely decompensated will be increased.
reversible shock which eventually leads to
MODS means Multiorgan Dysfunction Indications
Syndrome, a state of irreversible shock wherein • Carbon monoxide poisoning.
patient is anuric, drowsy, cold and terminally • Tetanus, gas gangrene infections.
ill. • Bedsores, frostbites.
..Not in time, place, or circumstance, but in the man lies success.....

• Drenching in paralytic ileus to reduce the
nitrogen gas in distended bowel.
• As a radiosensitiser in the treatment of
cancer.
Complications of hyperbaric oxygen: CO2
narcosis, respiratory depression.
CARDIAC ARREST
It is the cessation of the heart. Heart stops contracting.
Causes: All causes for shock.
Features of cardiac arrest

• No palpable pulse.
• Heart sounds not heard.
• Cessation of respiration—cyanosis occurs.
• Development of unconsciousness.
• Pupils start dilating.
Critical Period
Once heart and lungs stop, brain death occurs in
3 minutes.
Fig. 7.4: Technique of cardiac massage
Immediate measures
• Airway.
• Breathing.
• Cardiac compression.
• Drugs and Defibrillator.
• ECG, Endotracheal tube and monitor.
• External cardiac compression (massage)—
Patient is laid flat on a hard surface (never on
soft surface). Manual compression is exerted
over the lower sternum, using both hands
one over other without bending the elbow
at a rate of 60 to 70 per minute. Rib cage Fig. 7.5: Technique of mouth-to-mouth respiration. Note
damage during procedure can very well be patient’s nose should be held closed with right hand of the
doctor/ assistant and with left hand lower jaw should be
ignored. (Heel of right hand is placed over pushed forward
the sternum 8 cm above xiphoid process and
left hand is placed over it) (Fig. 7.4).
• At the same time, another person should give • Endotracheal intubation and ventilator
mouth-to-mouth breathing at a rate of 20 to 30 support.
per minute after clearing the airway by • Injection of 1:10,000 adrenaline and 10%
removing froth, dentures if present. A bag calcium chloride intravenously.
with mask can be used to ventilate using air • Sodium bicarbonate 8.4% injection, hydro-
or oxygen (Fig. 7.5). cortisone injection.
• Defibrillation, if there is ventricular
fibrillation.
• Analysis of blood gas (PCO2 and PO2), and
serum electrolytes assessment at repeated
intervals.
• Urinary catheterization, Ryle’s tube insertion
• Monitoring the patient with BP, pulse,
respiration, and temperature chart.
Observations to be made are

• Groin pulse.
Fig. 7.6: Left thoracotomy for open internal cardiac massage
• Respiration and breath sounds.
• Blood pressure.
• Pupillary reaction. Defibrillation Technique (Fig. 7.7)
• ECG activity. Gelly is applied to the site of electrodes. One
electrode is placed at the base of heart to the right
Once patient recovers, the cause and sequelae of the sternum, other over the estimated area of
has to be managed properly.
Sequelae are due to hypoxia and circulatory

collapse
• Cerebral edema and permanent brain
damage.
• ARDS (Adult Respiratory Distress Synd-
rome)
• Renal failure.
Internal Open Cardiac Massage (Fig. 7.6)

This method is used when cardiac arrest occurs
in the operation theater during surgery, acute
tamponade, and acute bilateral pneumothorax.
Left side thorax is opened through a lengthy
incision along 4th or 5th intercostals space.
Initially heart with intact pericardium is
rhythmically compressed and relaxed using left
hand against sternum. Mean time costal
cartilages above and below are cut with a knife
to have a better exposure. Pericardium is opened
in front of the phrenic nerve. Direct cardiac
massage is undertaken until heart regains its
function and later shifted to ventilatory support
and critical care. Fig. 7.7: Defibrillator used in case of cardiac arrest
..Kindness is the golden chain by which society is bound together.

the apex of the heart. Ensure that nobody is in VII, IX and X are vitamin K dependent for their
contact with the patient. The defibrillator is synthesis in liver (carboxylation of glutamic
activated. Ventilation and ECG monitoring is acid). In the process of coagulation each factor
resumed immediately. After that continuous gets activated to an enzyme by partial proteolysis
monitoring is done, the acidosis is corrected, which in turn activates other needed coagulation
bladder is catheterized and urine output is factors. Eventually fibrinogen gets converted
observed. Patient is kept in ICU. into soluble fibrin and later into insoluble fibrin.
Two types coagulation system are there—
• Intrinsic pathway
MECHANISM OF BLOOD
• Extrinsic pathway
COAGULATION In vitro coagulation occurs by intrinsic
Hemostasis is the spontaneous arrest of bleeding. coagulation system. Cascade gets activated by
When an injury occurs platelet adhesion occurs vessel wall injury, shear stress of vessel or other
to injured vessel/capillary wall which activates factors. It activates the cascade to get final
the release of ADP (Adenosine diphosphate) result—prekallikreine, kinninogen
which makes more platelet to aggregate (platelet Hemophilia and von Willebrand’s disease are the
aggregation). These activated platelets release two most common inherited bleeding disorders
thromboxane A2 which further increases the due to deficiency of factor VIII.
adhesion and aggregation of platelets. Factor VIII has two components; smaller
Circulating fibrinogen binds to an activated one—factor VIII C is needed for activation of
platelet receptors glycoprotein IIb and IIIa and factor X in intrinsic coagulation pathway; its
fibrinogen gets converted into fibrin. deficiency leads to classic hemophilia. It is
Clotting factors are proteins synthesized by inherited as an X-linked recessive trait, thus it
the liver which with a series of cascade method occurs in males and homozygous females. The
activates clotting factors and achieves blood larger component of factor VIII called von
coagulation by a complex mechanism. Factor II, Willebrand’s factor, facilitates the adhesion of
Coagulation Cascade System

Intrinsic Extrinsic
Blood Clotting Factors Hemophilia B also called as Christmas disease
Factor no. Common name is due to factor IX deficiency is inherited as
X- linked autosomal recessive trait.
I Fibrinogen
II Prothrombin
III Thromboplastin
HEMORRHAGE
IV Ionic calcium Classification I
V Hereditary labile factor, activator
(AC)globulin, proaccelerin a. Arterial: Is bright red in color, spurting like
VI Accelerin,supposed to be active form of jet along with pulse of the patient.
Factor V b. Venous: Is dark red, steady and continuous
VII Proconvertin; serum prothrombin—conversion flow. Blood loss may be severe and rapid
accelerator (SPCA)
VIII Antihemophilic factor(AHF)
when bleeding is from femoral vein, jugular
IX Plasma thromboplastin component vein, other major veins, varicose veins, portal
(PTC; Christmas factor) vein, and esophageal varices.
X Stuart-Prower factor Note—Pulmonary arterial blood is dark red
XI Plasma thromboplastin antecedent(PTA)
in color and pulmonary venous blood is
XII Hageman factor
XIII Fibrin stabilizing factor, Fibrinase bright red in color.
XIV Prekallekreine c. Capillary: Here bleeding is rapid and bright
XV Kallekreine red. It is often torrential due to continuous
XVI Platelet factor ooze.
platelets to subendothelial collagen, hence Classification II

crucial for hemostasis, its absence leads to von 1. Primary
Willebrand’s disease. Occurs at the time of injury or operation.
Classic hemophilia is called hemophilia A is 2. Reactionary
caused by deficiency of factor VIII C with X - It occurs within 24 hours after surgery or after
linked recessive trait. It occurs in males or injury (commonly in 4–6 hours).
homozygous females. Recurrent hemarthroses Precipitating factors Causes
is common presentation. Petechiae and Coughing Thyroid surgery
ecchymoses are absent. Bleeding time is normal Vomiting Cholecystectomy
but coagulation time is prolonged. Treatment is Straining Major abdominal surgeries
Rise of blood pressure Circumcision
factor VIII hemophilic factor replacement. In Restlessness Hydrocele surgery
dental extraction if not known patient may go Venous refilling during
for a life threatening bleeding. recovery from anaesthesia. Tonsillectomy
Slipping of ligature
von Willebrand’s disease is deficiency of larger Clot dislodgement.
component (99%) of the factor VIII- vWF. It is
autosomal dominant disease with normal 3. Secondary
bleeding time and normal platelet count. It occurs in 7-14 days after surgery.
Common presentations are spontaneous bleed- Factors Causes
ing from mucous membrane, excessive bleeding Infection Erosion of carotid artery by cancer
from wounds and severe menorrhagia. Hemar- (secondaries in the neck)
throses is not common in von Willebrand’s Pressure by Hemorrhoidectomy
disease. Treatment is replacement of specific drain or bone
Malignancy Inguinal block dissection
factors.
Everything takes practice, except being born.

Classification III
Revealed hemorrhage Concealed hemorrhage Initially concealed
but later revealed
It is visible external It constitutes internal hemorrhage. Hematemesis
hemorrhage Liver injury Melena
Spleen injury Hematuria
Fracture femur
Ruptured ectopic gestation
Cerebral hemorrhage
Hemothorax
Classification IV chronic anemia with hyperdynamic cardiac

1. Acute hemorrhage failure. They are in a state of chronic hypoxia.
It is corrected by packed cell transfusion not by
It is sudden, severe hemorrhage after trauma,
whole blood itself. Cause has to be treated
surgery. accordingly.
2. Chronic hemorrhage 3. Acute on chronic hemorrage
It is chronic repeated bleeding for long time It is more dangerous as the bleeding occurs
like in hemorrhoids, bleeding peptic ulcer, in individuals who are already hypoxic,
carcinoma cecum, etc. They present with which may get worsened faster.
Pathophysiology of Hemorrhage
Classification of Hemorrhagic Shock (circulatory failure)
Class Blood loss Features
I. Up to 15% (< 750 ml). Normal.
II. Blood loss 15–30% (750–1500 ml). Pallor, thirsty, tachycardia.
III. Blood loss 30–40% (1500–2000 ml). Hypotension, tachycardia, oliguria, confusion.
IV. Blood loss > 40% (>2000 ml). Rapid pulse, low BP, anuria, unconsciousness, MODS.
Effects of hemorrhage Measurement of Blood Loss

• Acute renal shut down. • Clot size of a clenched fist is 500 ml.
• Liver cell dysfunction. • Blood loss in a closed tibial fracture is 500–
• Cardiac depression. 1500ml; in a fracture femur is 500–2000 ml.
• Hypoxic effect. • Weighing the swab before and after use is
• Metabolic acidosis. an important method of on-table assessment
• GIT mucosal ischemia. of blood loss.
• Sepsis.
• Interstitial edema, A-V shunting in lung— Rains factor
ARDS. Total amount of Blood Loss =
• Hypovolemic shock MODS. Total difference in swab weight × 1.5
or
Total difference in swab weight× 2
Clinical Features of Hemorrhage (For larger wounds and larger operations)
• Pallor.
• Cyanosis. • Hb% and PCV estimation.
• Tachycardia. • Blood volume estimation.
• Tachypnea. • Measurement of CVP or PCWP.
• Cold clammy skin due to vasoconstriction. • Investigations specific for cause: ultrasound
• Dry face, dry mouth and goose skin appea- abdomen, Doppler study in vascular injury
rance (due to contraction of errector pilorum) and often angiogram, chest X-ray in hemo-
• Rapid thready pulse. thorax, CT scan in major injuries, CT head
• Oliguria. in head injuries.
• Features related to specific causes.
• Hypotension. Treatment
• Restoration of blood loss: By blood trans-
Signs of significant blood loss fusion, albumin 4.5%, SAG-M blood, saline,
• Pulse > 100/minute. Haemaccel (Gelatin), dextran, plasma
• Systolic BP< 100 mmHg. infusions.
• Diastolic BP drop on sitting or standing > 10 • Catheterisation, foot end elevation, moni-
mmHg. toring.
• Pallor/ sweating. • Pressure and packing.
• Shock index > 1. • Wound exploration and proceeding, i.e.
ligation of the small vessel, suturing the part,
..Most problems have either many answers or no answer. Only few problems have a single answer.
vessel suturing (anastomosis), excision of the stored in special refrigerators at 4°C. CPD blood
tissues. lasts for 3 weeks.
• Absolute rest, analgesics, morphine 10–20 mg
IM/IV to relieve pain, sedation. In stored blood
• ICT placing for hemothorax. • RBC’s last for 3 weeks.
• Laparotomy for liver or spleen or mesentery • WBC’s are destroyed rapidly.
or bowel injuries. • Platelets also get reduced in 24 hours.
• Topical applications for local ooze —Oxycel, • Clotting factors are labile and so their levels
gauze soaked with adrenaline, bone wax for fall quickly.
oozing from bone and other local hemostatic
agents. BLOOD FRACTIONS
• In venous hemorrhage limb elevation, a. Packed cells
ligation of vein or suturing of venous wall • It is obtained by centrifuging whole blood
in case of large vein, pressure bandaging, and at 2000–2300 g for 15–20 minutes.
packing will be helpful. • It is used in chronic anemias, in old age,
• Tourniquet is often useful in operation in children.
theater to control of hemorrhage in limbs. But
• It minimizes the cardiac overload due to
it is not advisable as a first aid measure.
transfusion.
• TPN, CVP monitoring, electrolyte manage-
b. Plasma:
ment are all equally important.
• This is obtained in the same way as
• Steroid injection, antibiotics, ventilator
packed cells by centrifugation.
support is often required.
• It is indicated in burns, hypoalbuminemia,
severe protein loss.
BLOOD TRANSFUSION • It can be fractionalized into different
Indications fragments:
• After trauma with severe blood loss, e.g. liver, c. Human albumin 4.5% is obtained after
spleen, kidney, GIT injuries, fractures, repeated fractionations and can be stored for
hemothorax, perineal injuries. several months in liquid form at 4°C.
• During major surgeries: Abdominoperineal d. Fresh frozen plasma: Fresh plasma obtained
surgery, thoracic surgery, hepatobiliary is rapidly frozen and stored at –40 °C. It
surgery. contains all coagulant factors and is the
• Following burns. choice for severe liver disease with abnormal
• In septicemia. coagulation function.
• Packed cells are given in chronic anemia, e. Cryoprecipitate: When fresh frozen plasma
blood fractions are given in ITP, hemophi- is allowed to thaw at 4°C, visible white
lias. supernatant layer develops and is called as
• As a prophylactic measure prior to surgery. cryoprecipitate, which is rich in Factor VIII
and fibrinogen. It is stored at –40°C.
Donor Criteria f. Fibrinogen is obtained by organic liquid
• Donor should be fit without any serious fractionation of plasma and is stored in dried
diseases like HIV I/HIV II/hepatitis. form. It is very useful in DIC and afibrino-
• Weight of donor should be more than 45 Kg. genemia. It has got risk of transmitting
hepatitis.
Collection of Blood g. Platelet rich plasma: It is obtained by
Blood is collected in a sac containing 75 ml of centrifugation of freshly donated blood at
CPD (Citrate Phosphate Dextrose) solution and 150–200 g for 15–20 minutes.
h. Platelet concentrate: It is prepared by • Sensitization to leukocytes and platelets.
centrifugation of platelet rich plasma at 1200– • Immunological sensitization.
1500 g for 15–20 minutes. 3. Infections—
• Serum hepatitis.
SAG-M Blood • HIV infection.
A proportion of donations will have plasma • Bacterial infection.
removed and will be replaced by crystalloid • Malaria transmission
solution of SAG-M. • Epstein Barr virus infection.
S—Sodium chloride. • Cytomegalovirus infection.
A—Adenine. • Syphilis, Yersinia
G—Glucose anhydrate. • Babesia microti infection.
M—Mannitol. • Trypanosoma cruzi infection.
4. Air embolism.
Advantages 5. Thrombophlebitis.
• This allows good viability of cells. 6. Coagulation failure.
• But it is devoid of any protein. • Dilution of clotting factors
• It is very useful in anemias. • DIC.
7. Haemochromatosis in repeated transfusions
Precautions like in chronic renal failure.
• For every four units of SAG-M blood, one 8. Citrate intoxication causing bradycardia and
whole blood has to be given. hypocalcemia
• Later for every two units of SAG- M blood,
one unit (400ml) of 4.5% human albumin has MASSIVE BLOOD TRANSFUSION
to be given. • It is defined as replacement or transfusion of
• Coagulation status and platelet count should blood equivalent to patient’s blood volume
be checked regularly. in 24 hours corresponding to that particular
After grouping and cross matching, 540 ml of age or single transfusion of blood more than
blood is transfused in 4 hours (40 drops per minute), 2,500 ml continuously. (In adult it is 5-6 liters,
using a filtered drip set. in infants it is 85 ml /kg body weight).
• Massive transfusion causes severe electrolyte
Complications of Blood Transfusion imbalance (hypocalcemia, hyperkalemia).
1. Congestive cardiac failure. altered platelet and coagulation factors.
2. Transfusion reactions— They require proper monitoring and mana-
• Incompatibility—Major and minor reac- gement.
tions with fever, rigors, pain, hypoten- • Massive transfusion is used in severe trauma
sion. associated with liver, vessel, cardiac,
• Pyrexial reactions due to pyrogenic pulmonary, and pelvic injuries. Often it is
ingredients in the blood. required during surgical bleeding (primary
• Allergic reactions. hemorrhage on table) of major surgeries.
..The specialist learns more and more of less and less, finally he knows everything about
nothing about nothing; whereas generalist learns less and less about more and
more until, finally he knows nothing about everything.
Massive transfusion TOURNIQUETS

• Transfusion of blood in 24 hours equiva- Uses
lent to patients blood volume.
• To attain blood less field in limb surgeries—
• Single transfusion of blood of 2,500 ml or
more in 6 hours. upper and lower limbs, orthopedic surgeries,
• Indicated in class IV hemorrhages like soft tissue tumors, amputations.
injuries to major vessels, liver and spleen • It is used (rubber tourniquet) to get assess
• Causes citrate toxicity, hyperkalemia, to veins for IV injections and IV sampling.
hypocalcemia, thrombocytopenia, sepsis, • Tourniquet is used in diagnostic tests for
DIC, etc. varicose veins, purpura (ITP), etc.
• It is used as a first aid in bleeding conditions
BLOOD SUBSTITUTES of limbs, snake bite (it is controversial).
• Human albumin 4.5% • Tourniquets are also often used for small
There is no risk of transmitting hepatitis. procedures in fingers and toes.
• Dextrans—are useful to improve plasma
volume. They are polysaccharides of varying Types
molecular weights. • Rubber tourniquet—Simple red rubber
a. Low molecular weight dextran (40,000 mol
catheter is used for drawing blood, to have
wt) (Dextran 40, Rheomacrodex): Dextran
assess to veins.
40 is very effective in restoring blood
volume immediately. But small molecules • Pneumatic tourniquet—Used in limbs, will
are readily excreted in kidney and so give the arterial pressure and also acts as a
effect is transitory. It may be useful in tourniquet. (Sphygmomanometer cuff is a
prevention of sludging in kidney and simple and easily available type).
hence renal shut down. • Esmarch rubber elastic bandage tourniquet
b. High molecular weight dextran (Dextran 110 (Fig. 7.8).
and Dextran 70): Less effective, but long • Specialized sophisticated tourniquets are
acting and so useful to have prolonged available, which gauge pressure, timing
effect.
accurately.
Precautions
Contraindications
1. Blood samples for blood group and cross
matching should be taken before giving In all peripheral vascular diseases and athero-
dextrans as it interferes with rouleaux sclerosis.
formation of red cells.
2. Dextrans also interfere with platelet function
and so may precipitate abnormal bleeding.
3. Total volume of Dextrans should not exceed
1000ml.
• Gelatin—in a degraded form of mol.wt.
30,000S, is used as a plasma expander. Up
to 1000ml of 3.4–4% solution containing
anions and cations is given intravenously -
Haemaccel. Fig. 7.8: Esmarch rubber tourniquet
Complications • Forgetting the removal of tourniquet or using
• Crushing effect on muscles in thigh may lead more time to release may compromise the
to crush syndrome. blood supply of the limb leading to severe
• Tourniquet palsy in upper limb. ischemia and gangrene.
• Infection.
• Improper application of tourniquet leads to Tourniquet time for upper limb is one hour and
more bleeding. for lower limb is two hours.
..His heart cannot be pure whose tongue is not clean.

8 Burns
 Burns Burns, which are not involving eyes, ears,

 Management of burns face, hand, feet, and perineum.
 Eschar Major (Severe): Second degree burns more than
 Burns contracture 25%in adults, more than 20% in children.
 Electrical burns All third degree burns of 10% or more.
 Inhalation burns Burns involving eyes, ears, feet, hands,
 Chemical burns perineum.
All inhalation and electrical burns.
BURNS Burns with fractures or major mechanical
trauma.
Types
Extensive burns, more than 50% are shown in
• Thermal injury. Figure 8.1.
• Electrical injury.
• Scald injury. Rule of Nine (Wallace’s rule of ‘9’) (Fig. 8.2)
• Chemical burns. • Head and neck 9%.
• Cold injury—Frostbite. • Front of chest and abdominal wall—9×2=
• Ionising radiation. 18%.
• Back of chest and abdominal wall— 9×2= 18%.
Classification of Burns • Lower limb each is 18% and so both—
1. Depending on the Percentage of Burns 18×2=36%.
Mild (Minor): Partial thickness burns < 15% in • Upper limb each is 9% and so both—9×2= 18%.
adult or <10% in children. • Perineum 01%.
Full thickness burns less than 2%. 2. Depending on Thickness of Skin
Can be treated as outpatient basis. Involved (Fig. 8.3)
Moderate: Second degree of 15-25% burns. (10- • First degree: Epidermis looks red, painful, no
20% in children). blisters, heals rapidly in 5–7 days by epi-
Third degree between 2-10% burns. thelialization without scarring.
Burns 131
Fig. 8.1: Extensive burns more than 50%
Fig. 8.3: Degree’s of burn
Fig. 8.4: Second degree burns with blisters
• Second degree: Mottled red, painful, with

blisters, heals by epithelialization in 14–21
days (Fig. 8.4).
- Superficial second degree burn heals,
causing pigmentation.
- Deep second degree burn heals, causing
scarring, and pigmentation.
• Third degree: Charred, parchment like, with
thrombosis of superficial vessels, painless
and insensitive surface. It requires grafting.
Charred, denatured, insensitive, contracted
Fig. 8.2: Percentage of burns in (a) Adults (b) Children full thickness burn is called as eschar.
..There is something wrong if you are always right.

—Arnold Glasow
• Partial thickness burns: It is either first or Cardiac dysfunction is due to—
second degree burn which is red and painful, • Hypovolemia.
often with blisters. • Release of cardiac depressants.
• Full thickness burns: It is third degree burns • Hormonal causes like catecholamines,
which is charred, insensitive, deep involving vasopressin, angiotensins, etc.
all layers of the skin. Renal changes are due to—
• Release of ADH from posterior pituitary to
Clinical Features cause maximum water reabsorption.
• History of burn (Fig. 8.5). • Release of aldosterone from adrenals to cause
• Pain, burning, anxious status, tachycardia, maximum sodium reabsorption.
tachypnea, fluid loss. • Toxins released from the burn wound and
• In severe degrees, features of shock. also sepsis cause acute tubular necrosis.
• Myoglobin released from muscles in case of
electric injury or often from eschar, which is
most injurious to kidneys.
Pulmonary changes are due to—
• Altered ventilation-perfusion ratio.
• Pulmonary edema due to burn injury, fluid
overload, inhalation injury.
• ARDS.
Fig. 8.5: Burns in a child • Aspiration.
• Septicemia.
GIT changes are due to—
• Acute gastric dilatation, which occurs in 2–4
days.
• Paralytic ileus.
• Curling’s ulcer in the stomach in burns more
than 35%.
• Cholestasis and hepatic damage.
Metabolic changes—
• Hypermetabolic rate(BMR).
• Negative nitrogen balance.
• Electrolyte imbalance.
• Deficiencies of vitamins, essential elements,
etc.
• Metabolic acidosis due to hypoxia and lactic
acid.
Common infections are—
Staphylococci and streptococci.
Pseudomonas.
Candida albicans.
Pathophysiology Causes of Death in Burns

Tolerable temperature to human skin is 40° for • Hypovolemia.
brief period. • Renal failure.
Massive edema in the body is due to altered • Pulmonary edema and ARDS.
pressure gradient because of the injury to • Septicemia.
basement membrane. • Multiorgan failure.
Burns 133
Effects of burn injury
1. Shock due to hypovolemia.
2. Renal failure.
3. Pulmonary edema, respiratory infection, adult respiratory distress syndrome (ARDS),
respiratory failure.
4. Infection by Staphylococcus aureus, beta hemolytic streptococcus, pseudomonas, klebsiella
results in bacteremia, septicemia, etc. Fungal and viral infections of dangerous types can
also occur.
5. GIT: Hypovolemia, ischemia of mucosa, erosive gastritis – Curling’s ulcer.
6. Fluid and electrolyte imbalance.
7. Post burn immunosuppression predisposes to severe opportunistic infection of different
bacterial, fungal and viral types.
8. Eschar formation and its problems like defective circulation, ischemia.
9. Electrical injuries often cause fractures, major internal organ injury, and convulsions.
10. Development of contracture is a late problem. It can cause ectropion, microstomia, disability
of different joints, defective hand functions, and growth retardation causing shortening.
11. Inhalation burn causes pulmonary edema, respiratory arrest, ARDS.
12. Chemical injury causes severe GIT disturbances like erosions, perforation, stricture
esophagus (alkali), pyloric stenosis (acid), mediastinal injury.
13. Other problems like DVT, pulmonary embolism, urinary infection, bedsores, severe
malnutrition with catabolic status.
14. Complications of burn contracture itself like hypertrophic scar, keloid formation.
15. Toxic shock syndrome: It is a life threatening exotoxin mediated disease caused by Staph.
aureus, is common in children with rashes, myalgia, diarrhea, vomiting, and multiorgan
failure with high mortality.
16. Other problems like catheter induced infections, bedsores, respiratory infection.
MANAGEMENT OF BURNS • Keep the patient in a clean environment.

• Sedation.
First Aid Fluid Resuscitation
• Stop the burning process and keep the patient Parkland regime
away from the burning area. 4ml/% burn/Kg body weight/24 hours.
• Cool the area with tap water by continuous Maximum percentage considered is 50%.
irrigation for 20 minutes. (not cold water Half the volume is infused in first 8 hours,
which can cause hypothermia). rest given in 16 hours.
Muir and Burclay regime
Definitive Treatment % BURNS × Body weight in Kg.
= 1 Ration
• Admit the patient. 2
• Maintain airway, breathing, circulation. 3 Rations in first 12 hours.
• Assess the percentage, degree, and type of 2 Rations in second 12 hours.
burn. 1 Ration in third 12 hours.
..If a thing is done wrong often enough, it becomes right.

—Richard A. Leahy
Fluids used are normal saline, Ringer lactate, anticlostridial and it penetrates well into the
Hartmann fluid, plasma, etc. Blood is used in tissues but it is an irritant. Silver nitrate causes
later period (after 48 hours). staining of burn area.
In first 24 hours crystalloids should be given. Regular culture and sensitivity for bacteria
(Crystalloids are one which can pass through is required—To see streptococcal growth, which
capillary wall) like saline—either hypo, iso or should be less than 1,00,000/-. (10 5) per gram of
hypertonic, dextrose saline, Ringer lactate. tissue.
Sodium is assessed by formula: 0.52 mmol × • Once the area granulates well, in 3 weeks
Kg body weight × % body burns given at a rate usually, split skin grafting is done (SSG,
of 4.0 to 4.4ml/Kg/hour. Thiersch graft).
After 24 hours up to 30–48 hours, colloids • For wider area MESH split skin graft is used.
should be given to compensate plasma loss. • If there is Eschar, Escharotomy is required
to prevent compression of vessels.
(Colloids are one, which retain in intravascular
• In certain areas like face and ear full thickness
compartment). Plasma, haemaccel{gelatin},
graft (Wolfe graft) or flap is required.
dextrans, hetastarch are used. Usually used at
a rate of 0.35-0.5 ml/kg/% burns in 24 hours.
Treatment of burns
• Urinary catheterization to monitor urine
• Fluid management and resuscitation.
output ; 30–50 ml /hour should be the urine
• Cleaning the wound and debridement.
output. • Open method using silver sulfadiazine
• Monitoring the patient: Hourly pulse, BP, ointment.
PO2, PCO2, electrolyte analysis, blood urea, • Closed method after applying ointment
serum creatinine. dressing and bandaging.
• Nasal oxygen, often intubation is required. • Tangential excision and skin grafting (Split
• IV Ranitidine 50 mg 8th hourly. skin graft/mesh graft).
• Ryle’s tube initially for aspiration purpose
later for feeding purpose (Enteral feeding).
• Antibiotics: Penicillins, minoglycosides, ESCHAR
Cephalosporins, Metronidazole. It is charred; denatured, full thickness deep
• In burns of oral cavity tracheostomy may be burns with contracted dermis.
required to maintain the airway. It is insensitive, with thrombosed superficial
• Total Parenteral Nutrition (TPN) is required veins.
for faster recovery using carbohydrates, Circumferential eschar in the upper limb,
lipids, vitamins (Through a CVP line). lower limb, neck, thorax can cause more edema
which initially causes venous compression but
Local Management later arterial compression causing ischemia,
• Dressing at regular intervals under GA using gangrene of the distal part. So distal area should
paraffin gauze, hydrocolloids, plastic be monitored for circulation.
films. If required deep tangential full thickness
• Slough excision is done regularly. incisions are made in different areas so as to
• After cleaning with povidone iodine, Silver prevent collection of edema fluid and also to
sulfadiazine ointment is used. It is an antiseptic prevent compression over the vessels. This is
and soothening agent. Other agents used are called as escharotomy.
Sulfamylon (Mafenide acetate) and Silver Early rapid separation of eschar indicates
nitrate. Sulfamylon is antipseudomonal, severe sepsis underneath.
Burns 135
Eschar should be excised eventually, the area
is allowed to granulate and later skin grafting
should be done.
BURNS CONTRACTURE
During healing process of burns, if skin grafting
or coverage is not done, healing takes place with
Fig. 8.7: Hypertrophic burn scar with contracture
fibrosis. This leads to development of contrac- neck in a female
ture, thereby different deformities and complica-
tions depending on the location of burns.
8. Pain and tenderness in the scar contracture.
Complications of Burns Contracture 9. Marjolin’s ulcer: It is a very well-differen-
tiated squamous cell carcinoma occurring in
1. Ectropion of eyelid causing keratitis and
a scar ulcer due to repeated breakdown. It
corneal ulcer.
is locally malignant. As there are no
2. Disfigurement of face.
lymphatics in the scar, there is no spread to
3. Narrowing of mouth opening— microstomia
lymph nodes. It is painless as there are no
4. Contracture in the neck causes restricted neck
nerves in the scar.
movements (Fig. 8.6).
5. Disability and nonfunctioning of joints due Treatment for Contracture
to contracture (Fig. 8.7).
Release of contracture surgically and use of Z
6. Hypertrophic scar and keloid formation.
plasty or skin grafting or different flaps.
7. Repeated breaking of scar, infection, ulcer,
Proper physiotherapy and rehabilitation is
and cellulitis. essential.
Prevention of Development of
Contracture
• Encourage joint exercise in full range during
recovery period of burns.
• Use of pressure garments for long period.
• Topical silicon sheeting.
• Saline expanders for scars.
ELECTRICAL BURNS
• It is always a deep burn (Always a major
burn).
• There will be wound of entry (Fig. 8.8) and
wound of exit.
• Patient may be having major internal organ
Fig. 8.6: Elbow contracture due to burns injury, GIT, thoracic injuries.
An ounce of application is worth a ton of abstraction—Unknown.

• Inhaled carbon monoxide binds with Hb
immediately to form carboxyhemoglobin
causing severe anoxia and death.
• Smoke contains hydrocyanide, which causes
tissue hypoxia and profound acidosis.
• Laryngeal edema and laryngospasm.
• Bronchial edema and bronchospasm.
Later Problems
• ARDS.
Fig. 8.8: Wound of entry in an electric burn
• Pneumonia.
• Atelectasis.
• Pulmonary embolism
• Often convulsions can develop. • Pulmonary edema.
• Death may occur due to cardiac arrhythmias. • Pneumothorax.
(Instant death due to ventricular fibril-
lation). Clinical Features
• Gas gangrene is common after electric injury. • They will have low oxygen saturation.
• Release of myoglobin can cause renal tubular • Charring of mouth, oropharynx with facial
damage and renal failure. burns.
• Patient should always be admitted and should • Carbon sputum.
be assessed by ECG, cardiac monitor, • Change in the voice with singed facial and
Ultrasound abdomen, chest X-ray, sometimes nasal hair.
even CT scan head. • Decreased level of consciousness with stridor
• Depending on the injury it is managed or dyspnea.
accordingly.
• Fractures and dislocations are common in Management
electric injuries, which is treated accordingly.
• Mafenide acetate is better agent as it penetrates • Replacing the patient from the site earliest.
well and it is useful against clostridial • Ventilator support.
infection. • Antibiotics.
• Mannitol should be used to prevent myo- • Bronchoscopy.
globin induced renal failure. • Tracheostomy whenever required.
INHALATION BURNS CHEMICAL BURNS

It
occurs after major fire burns. • In chemical burns, tissue destruction is more
It
is due to— and progressive. It is always a deep burn.
• Inhalation of heat. • Acid burn occurs in skin, soft tissues and GIT.
• Noxious gases and incomplete products of In GIT, it is common in stomach due to either
combustion. nitric acid or sulfuric acid, which may lead
• At the site of fire, oxygen concentration is less to severe gastritis or pyloric stenosis. Acids
than 2%, which can cause death in 45 seconds commonly involved—Formic acid, hydro-
due to hypoxia. fluoric acid, nitric acid, and sulfuric acid.
Burns 137
They cause metabolic acidosis, renal failure, • Neutralization with antidote should never be done
ARDS, hemolysis. Acidemia should be at initial phase of treatment as it creates
corrected by IV sodium bicarbonate. exothermic reaction, which aggravates the
• Alkali burns occur in oral cavity and oeso- tissue damage. Neutralizing agents are used
phagus, which leads to multiple esophageal later.
strictures. Common alkalis involved are— • Treatment should be always with hospitali-
Sodium hydroxide, lime, potassium hydro- zation.
xide and bleach. They cause saponification • Mannitol diuresis, hemodialysis, IV calcium
of fat, fluid loss, release of alkali proteinates gluconate, pain relief, serum electrolyte
and hydroxide ions which are toxic. management, TPN, ventilator support are the
• External chemical burns are always deep and initial systemic management required.
cause extensive disfigurement with cosmetic • Late treatment is reconstruction of the face,
problems. esophageal dilatation or colonic transposition
• Initial treatment is dilution with water for esophageal alkali burn, gastrojejunostomy
(Hydrotherapy). for acid induced pyloric stenosis.
Anybody can win—unless there happens to be a second entry.

—George Ade
9 Reconstruction and
Transplantation
 Skin grafting SKIN GRAFTING

 Flaps It is transfer of skin from one area (donor area)
 Transplantation to the required defective area (recipient area).
 Renal transplantation It is an autograft.
 Liver transplantation
 Bone marrow transplantation TYPES
 Graft rejection
Partial Thickness Graft (Split skin graft—SSG)
 Cimino fistula
Also called as Thiersch graft. It is removal of full
FLAPS—Are transfer of tissues from one area epidermis + part of the dermis from the donor
to another with their blood supply (With area.
pedicle). Depending on the amount of thickness of
dermis taken, it may be—
GRAFT—It is transfer of tissues from one area
• Thin SSG.
to another without its blood supply or nerve
• Intermediate SSG.
supply.
• Thick SSG.
Autograft is transfer of tissue from one Indications
location to another on the same patient.
• Well-granulated ulcer.
Isograft is transfer of tissue between two • Clean wound or defect, which cannot be
genetically identical individuals, i.e. between apposed.
two identical twins. • After surgery to cover and close the defect
Allograft is transfer of tissue between two created. For example
genetically different members, e.g. Kidney After wide excision in malignancy.
transplantation. After mastectomy.
After wide excision of squamous cell
Xenograft is transfer of tissue from a donor
carcinoma, etc.
of one species to a recipient of another
Graft can survive over periosteum or
species.
paratenon or perichondrium.
Reconstruction and Transplantation 139
Pre-requisite fixed and tie-over dressing is placed. If graft is
1. Healthy granulation area. near a joint, then the part is immobilized to
2. Streptococci load <105 per gram of tissue, prevent friction, which may separate the graft.
otherwise graft failure occurs. On 5th day dressing is opened and observed for
graft intake.
Contraindications: SSG cannot be done over
bone, tendon, cartilage, joint. Stages of Graft Intake
1. Stage of plasmatic imbibition: Thin, uniform,
Donor area: Commonly thigh, occasionally arm, layer of plasma forms between recipient bed
leg, forearm. and graft.
Knife used is Humby’s knife. Blade is 2. Stage of inosculation: Linking of host and graft,
Eschmann blade. which is temporary.
3. Stage of neovascularization: New capillaries
proliferate into graft from the recipient bed,
which later attains circulation.
Fig. 9.1: Humby’s knife with Eschmann blade to

Disadvantages of SSG
take split skin graft 1. Contracture of graft.
Two types:
• Primary contracture means SSG contracts
Using Humby’s knife graft is taken from the
significantly once graft is taken from
donor area. Punctate bleeding from the graft is
donor area (20-30%). Thicker the graft
observed which says that proper graft has been
more is the primary contracture.
obtained (Figs 9.1 and 9.2). • Secondary contracture occurs after graft has
been taken up to recipient bed during
healing period, due to fibrosis. Thinner
the graft more is the secondary contrac-
ture.
2. Seroma and hematoma formation will
prevent graft take up.
3. Infection.
4. Loss of hair growth, blunting of sensation.
5. Dry, scaling of skin due to nonfunctioning
of sebaceous glands. So after healing oil
(coconut oil) should be applied over the area.
6. Graft failure.
Advantages
Fig. 9.2: Harvesting a skin graft
1. Technically easier.
2. Wide area of recipient can be covered. To
Donor area is dressed and dressing is opened cover large areas like in burns wound, graft
after 10 days, not earlier than that. size is increased by passing the graft through
Recipient area is scraped well and graft is a Mesher which gives multiple openings to
placed after making window cuts in it in order the graft which can be stretched over the
to avoid the development of seroma. Graft is wider area like a net (Fig. 9.3).
..People will believe anything if you whisper it.

• Tendon graft.
• Bone graft.
• Nerve graft.
• Venous graft.
• Corneal graft.
FLAPS
It is transfer of donor tissue with its blood supply
to the recipient area.
Parts of flaps: Base, pedicle, tip of flap. Vasculature
is usually through the pedicle in the center of
Fig. 9.3: Mesh graft. Split skin graft is passed through a
the flap. Tip is the place where often flap goes
mesher to get a wide mesh graft which can be used over to
cover a wider area like of burns for necrosis (Figs 9.4 and 9.5).
3. Graft take up is better.

4. Donor area heals on its own.
Full Thickness Graft (Wolfe graft)

It includes both epidermis + full dermis.
It is used over the face, hands, fingers, and
over the joints.
It is removed using scalpel blade. Deeper raw
area is closed by primary suturing. If a large full
thickness graft is taken, then that donor area has
Fig. 9.4: Anatomy and blood supply of a skin flap
to be covered with SSG, which is a disadvantage
in full thickness graft.
Common sites of donor area:
1. Postauricular area.
2. Supraclavicular area.
Advantages
• Color match is good. Especially for face.
• No contracture (Unlike in SSG).
• Sensation, functions of sebaceous glands, hair
follicles are retained better compared to SSG.
Disadvantages
• Only for small area it can be used.
• Wider donor area has to be covered with SSG
to close the defect.
• Cannot be used to cover ulcers.
Other Grafts
• Composite graft where skin+ fat + other Fig. 9.5: Raising the skin flap. Note the different parts—
tissues like cartilage. base/pedicle/tip
Indications 8. Free flaps: Vascular pedicle of the flap, both
• To cover a wider, deeper defects. artery and vein are anastomosed to
• To cover over bone, tendon, cartilage. recipient vessels using operating binocular
• If skin graft repeatedly fails. microscopes.
9. Omental flaps.
Types 10. Island flap.
1. Random pattern flaps: Here vascular basis is Areas where commonly flaps are used: Oral
subdermal plexus of blood vessels. cavity, neck, breast, limbs(leg), buttock,
2. Axial pattern flaps: Here superficial vascular bedsores, etc.
pedicles pass along their long axes, e.g. Flaps mobilized from donor area with its
forehead flap, deltopectoral flap, groin flap. pedicle is placed and sutured to recipient area.
Anatomical types depending on the types of Once flap gets taken up usually in 3–6 weeks,
tissue in the flap: base of the flap is cut and sutured to recipient
1. Cutaneous flap: Forehead flap, deltopectoral area.
flap. Saltatory flap is mobilizing the flaps in
2. Faciocutaneous flap: Radial forearm flap, stages from distant donor area towards recipient
scapular flap, lateral arm flap. area. It requires many staged surgeries and long-
3. Muscle flap: Gluteus maximus muscle flap, term hospitalization.
gracilis flap, tensor fascia lata muscle flap.
4. Myocutaneous flap: Pectoralis major myo- Advantages
cutaneous flap, latissimus dorsi flap (Fig. 9.6). • Good blood supply, good take up.
• Gives bulk, texture, color to the area.
• Allowing the required movements in the
recipient area, e.g. jaw movements following
pectoralis major flap after wide excision with
hemimandibulectomy for carcinoma cheek.
• Cosmetically better.
Disadvantages
• Long-term hospitalization.
• Infection.
• Kinking, rotation and flap necrosis.
• Staged procedure.
• Positioning of the patient for long time is
important to have a good flap take up which
is a real discomfort to the patient.
Fig. 9.6: Pectoralis major myocutaneous flap
5. Osteomyocutaneous flaps: Radius with TRANSPLANTATION

brachioradialis and skin, rib with intercostal Preoperative evaluation of the patient for
muscles and skin. transplantation.
6. Local rotation flaps. • General evaluation about pulmonary,
7. ‘Z’ plasty. cardiac, GIT, renal and cancer screening.
..The universe is not only stranger than we imagine, it is stranger than we can imagine.
—JBS Haldane
• Immunologic evaluation, serology for
hepatitis, HIV, cytomegalovirus.
Placing the organ in the same position is
called as orthotopic transplantation, e.g liver.
Placing the organ in new position is called
as heterotopic transplantation.
Donor Criteria
Cadaver donor.
Individuals with severe brain injury resulting
in brain death.
Brain death is defined as ‘Complete irreversible
cessation of all brain functions’ along with—
• Absence of reflexes.
• Absence of spontaneous movements.
• Unresponsiveness. Fig. 9.7: Renal transplantation
Other criteria for cadaver donor—
• Normothermic patient. to internal iliac artery (end to end); renal vein
• No respiratory effort by the patient. to external iliac vein (Fig. 9.7).
• No depressant drugs should be there while
evaluating the patient. Postoperative Management
• Individual should not have any sepsis, 1. Immunosuppression: By Cyclosporine,
cancer. Azathioprine, Prednisolone, Antithymocytic
Living donor globulin and antilymphocytic serum.
• Living unrelated donor. 2. Proper fluid balance has to be taken care off.
• Living related donor. Complications
• Individual should have normal health. 1. Acute tubular necrosis.
Requirements 2. Rejection.
• ABO typing. 3. Obstruction of the collecting system.
• Serology tests. 4. Infection.
• Angiogram. 5. Urine leakage.
• Intravenous urography. 6. Secondary hemorrhage.
• HLA typing. 7. Renal infarction.
8. Hazards of immunosuppression—
a. Infection by unusual organisms like
RENAL TRANSPLANTATION cytomegalovirus, herpes, pneumocystis
Two types of donors— carinii, varicella and other bacterial
• Living related donors. infections, candidial infection.
• Cadaver donors. b. Changes in the cellular component of
Compatibility should be checked by tissue blood.
typing, i.e. ABO blood group system and major c. Uncommon malignancies of CNS and
histocompatibility complex. skin.
Usually left kidney is taken for transplantation d. Nephrotoxicity, GIT bleeding and perfo-
because of long left renal vein. ration.
It is placed in right iliac fossa with ureter e. Hirsutism, delayed wound healing,
connected to the urinary bladder; renal artery cataract formation.
CYCLOSPORIN-A heterotopic liver transplantation. Success rate
• It is a fungal metabolite, a potent immuno- in liver transplantation is better.
suppressant used to prevent transplant
rejection. BONE MARROW TRANSPLANTATION
• It is initially given intravenously 4 mg/kg in Indication
500 ml saline and later orally 12 mg/kg daily.
• Leukemias.
After few weeks dose is reduced to 5
• Aplastic anemias.
mg/kg orally daily.
• Immune deficiencies, etc.
• Regular cyclosporin estimation (twice
Recipients are initially treated with total body
weekly), as well as blood urea, serum creati- irradiation. As bone marrow is an active immune
nine, and hematocrit is essential. system, proper tissue typing is essential. Infant bone
• Oral therapy is required for a long time.
marrow is better marrow as a donor. Marrow
• It is commonly given along with Prednisolone
aspirated from donor’s bone is transplanted by
and Azathioprine.
intravenous injection to the recipient.
Toxic Effects Immunosuppression with Cyclospoin-A is
always needed. It will take few weeks to show
• Nephrotoxicity
the response.
• Infections, (CMV, candida, pneumocystis,
secondary infections). Problems
• Hirsutism.
1. Graft rejection.
• Often lymphomas and malignancies of skin 2. Graft-Versus-Host disease (GVH) is more
and CNS. dangerous.
LIVER TRANSPLANTATION GRAFT REJECTION
INDICATIONS Types
• Primary biliary atresia. 1. Hyperacute rejection is due to antibody
• Cirrhosis. reaction, which occurs within minutes of
• Malignant diseases of the liver. vascularization of the graft.
Children respond better for liver trans- 2. Acute rejection results due to cell-mediated
plantation. Tissue typing and cross matching are immunity, occurring in a few days to first 3
not that necessary as they do not influence the months of transplant. It responds well to
results. steroids and immunosuppressants.
If the transplantation is done at the same 3. Chronic rejection occurs in 12 months after
place after doing hepatectomy, it is called as transplant. It is not very common. It is due
orthotopic liver transplantation. If it is placed to late vasculitis. When it occurs, it responds
in a different place it is called as ectopic or very poorly to steroids or other drugs.
..He travels fast who travels alone-----but he hasn’t anything to do when he gets there.
—Finagle
CIMINO FISTULA with hyperdynamic circulation. At the ankle,

fistula is created between posterior tibial artery
It is an arteriovenous fistula created for and saphenous vein or in the thigh between
hemodialysis. Usually at wrist, radial artery is femoral artery and long saphenous vein. Distal
gangrene is not common.
anastomosed side-to-side to cephalic vein. A
good created fistula shows continuous thrill and Complications
bruit, with increased venous engorgement along Infection, bleeding, hyperdynamic circulation.
Fluids, Electrolyte and Nutrition 145
10 Fluids, Electrolyte
and Nutrition
 Water loss Ion ICF ECF and plasma

 Water intoxication Sodium 10 mmol/l 140 mmol/l
 Hyponatremia Potassium 150 mmol/l 4.5 mmol/l
 Hypernatremia Chloride Trace only 105 mmol/l
 Hypokalemia
 Hyperkalemia
 Acid-base balance WATER LOSS
 Anion Gap It is decrease in the whole body fluid volume—
 Nutrition both ECF and ICF.
 Gastrostomy
 Jejunostomy Causes
 Total parenteral nutrition • Poor intake.
 Obesity • Diabetes insipidus.
Drop in ECF is balanced by drop in ICF. So
Normal Physiology clinically patient is not dehydrated even though
Total body water is 60% of body weight in males, there is water drop.
50% of body weight in females, i.e. 30 liters. Thirst, confusion and hypothermia are the
Intracellular water—20 liters (2/3). clinical features.
Extracellular water—10 liters (1/3).
Investigations
Plasma (1/4) (2.5 liters)
Interstitial fluid (7.5 liter). Rise in plasma sodium and urea.
Three hormones—Aldosterone, ADH, atrial
natriuretic hormone, control ECF volume and Treatment
regulates osmolality. Oral water or IV isotonic fluid, 5% dextrose.
..The wind of anger blows out the lamp of intelligence.

WATER INTOXICATION ECF EXCESS

• There is only ECF excess without any ICF
Causes
excess.
• Excessive infusion of intravenous dextrose • Due to excessive infusion of saline with
5%. impaired excretion.
• If water is used instead of saline for colorectal • Raised JVP, cardiac failure and peripheral
bowel wash, at the time of preparation for edema.
surgery of large bowel, especially in children. • Treatment is fluid restriction and diuretics
• In TURP(Transurethral resection of prostate) like Frusemide.
when excess irrigating fluid, water or glycine
is used (commonly used). HYPONATREMIA
• In syndrome of inappropriate antidiuretic Sodium level less than 130 mEq/liter.
hormone (SIADH) which is commonly
associated with lobar pneumonia, empyema, Causes
oat cell carcinoma and head injury. • Intestinal obstruction.
• Fistulas—Intestinal, biliary, duodenal,
Clinical Features gastric, pancreatic.
Drowsiness, weakness. • Gastric outlet obstruction with severe
Convulsions and coma. vomiting.
Nausea, vomiting. • Ryle’s tube aspiration.
Passage of dilute urine. • Severe diarrhea due to viral cause, colitis,
colorectal polyps.
Investigations • Syndrome of inappropriate antidiuretic
Hematocrit, serum electrolytes, blood urea. hormone (SIADH).
(shows fall in serum Na+, low K+ and low blood • Immediately after surgery and trauma,
sodium depletion occurs.
urea).
Treatment Clinical Features
Dry coated tongue.
1. Water restriction and observation.
Sunken eyes.
2. ICU monitoring with proper management of Dry wrinkled skin.
fluid and electrolyte balance. Hypotension.
3. Infusion of hypotonic sodium chloride. Dark scanty urine.
Administration of diuretics and hypertonic Irritability, disorientation, neurological
saline should be avoided. As it may cause rapid manifestations.
changes in serum sodium and water level which Hypothermia, reduced tendon reflexes.
in turn leads to neuronal demyelination and fatal
outcome. Investigations
Serum electrolytes, low urinary sodium.
ECF LOSS
Here only ECF loss is present with normal ICF. Treatment
It is seen in vomiting, diarrhea, and intestinal By IV Normal saline, or double strength saline
obstruction. or Ringer lactate IV.
Treatment is infusion of normal saline. Treat the cause.
HYPERNATREMIA • After trauma or surgery.
• Pyloric stenosis with gastric outlet obs-
Excess infusion of normal saline causing
overload in circulating salt and water. truction.
• Duodena fistula, ileostomy.
Causes • After ureterosigmoidostomy.
• Renal dysfunction. Clinical features:
• Cardiac failure. • Slurred speech.
• Drug induced like NSAID, corticosteroids.
• Muscular hypotonia.
It may be either primary sodium excess or
• Depressed reflexes.
primary potassium excess or primary water
• Paralytic ileus.
deficit.
• Weakness of respiratory muscles.
Clinical Features • Cardiac arrhythmias.
ECG shows prolonged QT interval, depress-
• Pitting edema.
ion of the ST segment and inversion of T wave.
• Puffiness of face.
Often hypokalemia is associated with alkalosis.
• Increased urination.
• Often dilated jugular veins. Serum potassium is decreased.
• Features of pulmonary edema.
Treatment
Investigations • Oral potassium 2 g 6th hourly.
Serum electrolytes. • IV KCl 40 mmol/liter given in 5% dextrose
or normal saline slowly—often under ECG
Treatment monitoring (Total dose is 40 mmol. Maxi-
Restriction of saline and sodium. mum dose per hour is 20 mmol).
Pulmonary edema has to be treated. • Hypokalemic alkalosis which occurs in pyloric
Hypernatremia should be corrected slowly stenosis should be treated carefully by IV
as follows— potassium as there will be severe potassium
Initially normal saline is infused followed loss.
by infusion of half strength saline and later with
5% dextrose, i.e. gradual controlled correction. HYPERKALEMIA
Otherwise cerebral edema and hyperglycemia
can develop. Normal range of potassium is 4.0–4.5 mEq/ liter.
Hyperkalemia manifests when potassium
HYPOKALEMIA exceeds 6 mEq/liter.
Sudden hypokalemia—occurs in comatose
diabetic patient treated by insulin and saline Causes
infusion. • Renal failure.
• Rapid infusion of potassium.
Gradual hypokalemia— • Transfusion of stored blood.
Causes: • Diabetic ketoacidosis.
• Diarrhea of any cause, villous tumor of the Potassium excess is a dangerous condition,
rectum, ulcerative colitis. which can cause sudden cardiac arrest.
..Words that enlighten are more precious than jewels.

Investigations • Tetany due to alkalosis. More often it is latent
Low serum potassium level. Peak ‘T’ wave in tetany, which is revealed by Trousseau’s sign.
an ECG. Investigations
Treatment Serum electrolytes, arterial blood gas analysis.
• IV administration of 50% of 50 ml of glucose Treatment
with 10 units of soluble insulin, given slowly.
• Infusion of 10% calcium gluconate (as IV infusion of normal saline or double strength
saline, with slow IV Potassium chloride 40
cardioprotection) intravenously.
mmol/liter in saline—under ECG monitoring.
• Diuresis using Frusemide injection.
• Hemodialysis when required. RESPIRATORY ALKALOSIS
• Continuous ECG monitor is a must.
Arterial PCO2 is below normal.
• Polyesterene sulfonate ion exchange resin 30
g/hour as an enema. Causes
• Salbutamol/Albuterol nebulization. • Hyperventilation during anesthesia.
• IV sodium bicarbonate. • High altitude.
• Hyperpyrexia.
ACID-BASE BALANCE
• Encephalitis, hypothalamic tumors, drugs
Normal pH (– log10 of H+) is 7.36–7.44. like salicylates.
• Hysteria.
Factors which control the pH It may lead to tetany.
• Buffer system. Respiratory suppression due to alkalosis is
— Bicarbonate buffer. treated by CO2.
— Protein buffer.
— Phosphate buffer. METABOLIC ACIDOSIS
• Renal control of pH. It is an excess acid or base deficit. Standard
• Respiratory control of pH. bicarbonate is below 21 mmol/liter.
METABOLIC ALKALOSIS Causes

It is primary base excess, i.e. HCO3–. Standard Increase in fixed acid—
bicarbonate is above 27 mmol/liter. • Diabetic ketoacidosis.
• Starvation.
Causes • Hypoxia.
• Repeated vomiting due to any cause. • Renal insufficiency.
Commonly seen in pyloric stenosis. Here • Cardiac arrest.
hypokalemic alkalosis occurs, which is • Excessive exercise.
important for managing the patient. • Intestinal strangulation. Here anion gap is
• Excess alkali ingestion, e.g. antacids. increased.
• Cortisol excess either due to over administra-
tion or Cushing’s syndrome. Loss of base—
• Diarrhea.
Clinical Features • Ulcerative colitis.
• Cheyne-Stokes breathing with period of • Gastrocolic fistula.
apnea of 5–30 seconds. • Intestinal fistula.
• Ureterosigmoidostomy causes hyperchlorae- Increased anion gap is Normal anion gap is
mic hypokalemic acidosis. Here anion gap is seen in seen in
normal. Metabolic acidosis due Diarrhea.
to ketoacidosis.
Features Lactic acidosis. GIT fistulas.
Poisoning. Hyperchloremic
• Rapid, deep, noisy breathing (air-hunger). acidosis.
• Cold clammy skin, tachycardia, right heart Renal failure.
strain, altered level of consciousness.
• Capillary stasis. NUTRITION
• Urine is strongly acidic.
• Low standard HCO3 level. Caloric Requirement
• Base deficit. • Neonates 100 kcal/kg/day.
• Adults 40 kcal/kg/day.
Treatment • Adult with catabolism 60 kcal/kg/day.
• Correction of hypoxia. It is given as—
• 50 mmol of 8.4% Sodium bicarbonate Carbohydrates 50%.
infusion IV. Fat 30–40%.
Sodium bicarbonate required in mEq/liter = Protein 10–15%.
Body weight in kg × 0.3 × Base deficit. Caloric values—
Carbohydrate 4 kcal/g.
RESPIRATORY ACIDOSIS Protein 4 kcal/g.
Fat 9 kcal/g.
It is a feature of respiratory failure with high
arterial PCO2 causing fall in pH. Indications for Nutritional Support
• Preoperative nutritional depletion.
Causes
• Postoperative complications: Sepsis, ileus,
• During and after anesthesia. and fistula.
• Chronic bronchitis. • Intestinal fistula: High type wherein output
• Emphysema. is >500 ml/day. It may be duodenal, biliary,
• Thoracic diseases. pancreatic, intestinal, etc.
• Upper abdominal surgeries and diseases. • Pancreatitis, malabsorption, ulcerative colitis,
• Respiratory airway obstruction. pyloric stenosis.
• Myasthenia gravis. • Anorexia nervosa and intractable vomiting
• Poliomyelitis. • Trauma—Multiple, fasciomaxillary, head
ANION GAP and neck.
• Burns.
• It is calculated estimation of the undeter- • Malignant disease.
mined or unmeasured anions in the blood. • Renal and liver failure.
• It is (Na+ + K+)—(HCO3– +Cl– ). • Massive bowel resection causing small bowel
• Normal anion gap is 10–16 mmol/liter. syndrome.
..All things must change to something new and strange.

Assessment GASTROSTOMY
• Body weight. It is done if feeding is required for more than
• Upper arm circumference. one month.
• Triceps skin fold thickness.
• Serum albumin. Indications
• Lymphocyte count.
• Severe malnutrition.
Nutritional requirements: Carbohydrates, fat, • Major surgeries.
proteins, vitamins (includes fat soluble vitamins • Severe sepsis.
also), minerals, trace elements. • Trauma.
• Head and neck surgeries.
Methods of Feeding
• Enteral.
• Paraenteral.
ENTERAL:
By mouth: Requires
• Common sense.
• Cleanliness.
• Compassion.
By nasogastric tube:
Tube end in the stomach is confirmed by
injecting 5 ml of air down the tube and listening
through a stethoscope for its bubbling entry into
the stomach.
Problems with tube feeding are—
• Blockage. Fig. 10.1: Gastrostomy tube in place for enteral feeding
• Nausea and vomiting.
• Aspiration. Types
• Hyperosmolarity. Based on duration of use:
• Diarrhea. • Temporary.
• Tube discomfort. • Permanent.
• Cholestasis. Based on lining:
By enterostomy: • Mucus lined (Permanent).
• Gastrostomy. • Serosal lined (Temporary).
• Jejunostomy. Based on technique:
1. Stamm’s temporary gastrostomy—After open-
Complications of enteral feeding
ing the abdomen, anterior wall of the stomach
• Aspiration.
is opened. Feeding tube (Malecot’s catheter)
• Wound infection and leak.
is placed in position. Two layers of purse
• Diarrhea due to rapid feeding or hyperos-
string sutures are put around the tube.
molarity.
Wound is closed.
• Hyperglycemia.
2. Kader-Senn temporary gastrostomy.
• Hypokalemia.
3. Percutaneous endoscopic gastrostomy.
• Refeeding syndrome due to severe hypo-
4. Janeway’s mucus lined permanent gastrostomy
kalemia and hypophosphatemia.
by creating tunnel in stomach wall.
Problems in gastrostomy: TOTAL PARENTERAL NUTRITION (TPN)
• Leak. About 5% of hospital admissions require TPN.
• Infection.
• Aspiration and pneumonia. Indications
1. Failure or contraindication for any enteral
Contraindications nutrition.
• Previous gastric surgeries. 2. High output abdominal fistulas—Duodenal,
• Intestinal obstruction. biliary, pancreatic.
• Gastric outlet obstruction. 3. Major abdominal surgeries of liver, pan-
creas, biliary, colonic.
4. Septicemia,
JEJUNOSTOMY
5. Multiple trauma.
Jejunostomy for enteral nutrition becoming more
popular because of— Technique
— Its comfort. Using a needle and guidewire a subclavian vein
— Easy to do. catheter is passed just below the clavicle and fixed
— Can be kept for long time. securely to the skin.
— Lesser complication than gastrostomy. TPN is given through central vein and not
Indications are same as gastrostomy. through a peripheral vein.
Components used in TPN
Carbohydrates.
Fat and amino acids.
Vitamins and trace elements.
The patient should be monitored at regular
intervals with body weight, fluid balance, blood
glucose, electrolytes, blood urea, LFT, serum calcium,
magnesium, phosphate, etc.
Complications
Technical:
• Air embolism
• Pneumothorax.
• Bleeding.
• Catheter displacement, sepsis, blockage.
• Infection, thrombosis.
Fig. 10.2: Needle jejunostomy Biochemical:

• Electrolyte imbalance: hyponatremia, hypo-
kalaemia, hypophosphatemia.
Types • Hyperosmolarity.
Witzel jejunostomy: Site of placing jejunostomy • Hyperglycemia.
is 30 cm from duodenojejunal junction. • Dehydration.
Needle jejunostomy (Fig. 10.2) using catheter of • Altered immunological and reticuloendo-
small gauge. thelial function.
..We need men who dream of things that never were.

Others: Classification
• Dermatitis.
• Anemia and increased capillary per- Normal BMI is 20–25.
meability. BMI 25–30 pre-obesity.
• Cholestatic jaundice—It is quiet common. BMI 30–35—mild—class I obesity.
• Severe hepatic steatosis. BMI 35–40—moderate—class II obesity.
• Metabolic acidosis. BMI more than 40—morbid obesity—class III
obesity.
• Candida infection.
Weight more than the double the expected
Contraindications weight to that age and height of the individual
Cardiac failure. is called as morbid obesity.
Blood dyscrasias.
Altered fat metabolism. Complications of obesity
General: Difficulty in work, fatigue, depres-
Anabolic steroid Durabolin 25 mg IM weekly is sion, back pain, arthritis and gout.
given to improve nitrogen balance. Cardiovascular: Hypertension, stroke, throm-
Home parenteral nutrition bophlebitis, pulmonary embolism.
• It is becoming popular. Pulmonary: Hypoventilation, poor respira-
• It is commonly used in western countries. tory effort.
• It is indicated in short bowel syndrome or any GIT: Hiatus hernia with reflux, changes in
other conditions wherein enteral feeding is liver, pancreatitis, gallstones.
not possible but patient can be sent home Endocrine: Diabetes mellitus.
with provision for home parenteral nutrition.
• Patient himself uses the TPN fluids as Obesity and Surgery
advised at home. He will be with TPN • Hernia is more common in obese individual.
catheter. • Gallstones are more common.
• Patient should attend TPN clinic weekly for • Burst abdomen, incisional hernia are more
follow up or immediately whenever common with obesity.
complications arise. • Delay in recovering from anesthesia.
• Patient will be comfortable psychologically • Infertility is more common.
and often can attend his job also. Treatment for Obesity
• Diet restriction.
OBESITY • Exercise.
• Vertical banded gastroplasty.
Definition • Gastric bypass.
Weight more than 20% above the normal. • Laparoscopic gastroplasty or gastric bypass.
Body Mass Index is weight in kilogram divided • Jaw wiring.
by height in meters squared (wt in kg/Ht in • Biliopancreatic diversion.
meters)2. • Jejunoileal bypass.
Nerves and Tendon 153
11 Nerves and Tendon
 Peripheral nerve injuries

 Brachial plexus injuries
 Causalgia
 Median nerve injuries
 Carpal tunnel syndrome
 Ulnar nerve injuries
 Claw hand
 Radial nerve lesions
 Common peroneal nerve
 Axillary nerve injury
 Long thoracic nerve (nerve of Bell)
 Trigeminal neuralgia
Fig. 11.1: Cross-section of a nerve
 Tendon
 Tendon repair
tion. Cross-section of an intact nerve is shown
 Tendon transfer
in Figure 11.1.
 Tendon graft
• Axonotmesis: It is division of nerve fibers or
axons with intact nerve sheath. There is
PERIPHERAL NERVE INJURIES reaction of degeneration distally with near
Seddon’s Classification complete recovery. Patient can present with
sensory loss, paralysis of muscles or
• Neuropraxia: It is temporary physiological causalgia.
paralysis of nerve conduction. Here recovery • Neurotmesis: Here complete division of nerve
is complete. There is no reaction of degenera- fibers with sheath occurs. Degeneration
..The best antiques are old friends.

occurs proximally up to the first node of Debridement of the area is done. If injury is
Ranvier as well as distal to the injury. incised type, then nerve is sutured with 8–0 or
Recovery is incomplete even after nerve 10–0 nonabsorbable interrupted sutures
suturing. There is complete loss of motor and (polypropylene).
sensory functions with loss of reflexes. If the
nerve is mixed type rather than pure motor Types of Nerve Suturing
or sensory recovery is still poorer. Usually operative microscope or loup is used for
Injuries may be incised or lacerated or nerve suturing.
crushed one. i. Epineurorrhaphy: Only epineurium is
Cut end of the nerve forms neuroma proxi- sutured using interrupted sutures.
mally and glioma distally. ii. Epiperineurorrhaphy: Initially perineural
Neuromas may be— sheath and then epineurium is sutured.
• True neuroma or False neuroma. If nerve is lacerated, marker stitches (using silk)
• End neuroma or Side neuroma. are placed at the cut end site to identify the nerve
for suturing at a later period.
Sunderland’s classification If nerve suturing fails or if could not be done,
I: Conduction block—temporary neuronal then tendon transfer is done at a later period after
block. 4–6 months.
II: Axonotmesis but endoneurium is preser- Incomplete injury usually does not require any
ved. suturing.
III: Axonotmesis with disruption of endo- 6 zero polypropylene is usually used.
neurium but perineurium is preserved. Easier suturing is achieved by following
IV: Here there is disruption of endo and methods:
perineurium but epineurium is intact. • Relaxing incisions.
V: Neurotmesis with disruption of endo, peri • Transpositioning of the nerve.
and epineurium. • Shortening of the bone.
• Nerve graft—usually sural nerve is used for
Clinical Features nerve graft.
• Positioning of the limb.
• Loss of sensory, motor, autonomous and • Initially neurolysis (release of the scar tissue
reflex functions. adjacent to injury) is done in case of secon-
• Secondary changes in the skin and joint. dary suturing.
Primary nerve suturing is done if it is a clean
incised wound. Prognostic factors in healing of the nerve
Secondary nerve suturing is done after 3 injury
weeks if it is a crushed wound. • Higher the lesion worser the prognosis.
• More the gap between the cut ends worser
Management the prognosis.
• Associated injuries like fracture, vessel injury, • Associated injuries alter the prognosis.
injuries in other systems should be looked • Children do better with nerve injury.
for. • Type of the injury also decides the prognosis.
• Checking sensation, muscle power, and
reflexes assesses nerve injury. TINEL’S SIGN
• Nerve conduction studies. It is the clinical sign (prognostic indicator) used
• Investigations relevant to associated injuries. to assess the level of regeneration. It is elicited
• Exploration of the wound. 3 weeks after the nerve injury (Regeneration
begins after the completion of nerve degenera- It can be—
tion).
Preganglionic injury Postganglionic injury
Tapping is done over the course of the nerve Avulsion injury. Usually less severe.
from distal to proximal end to elicit a sensation of More dangerous. Better recovery.
‘pins and needles’ or hyperesthesia. If sensation is Extends into the spinal cord.
felt at the site as well as distally along the
distribution of the nerve that means good Investigations
recovery can be expected. If sensation is felt only • Nerve conduction studies.
at the site of tapping, then result is equivocal. • CT/MRI.
If no sensation is felt it means no recovery can
• Electromyogram.
be expected.
• X-ray cervical spine and part.
Causes of peripheral nerve lesions
Treatment
• Traumatic: Either closed or open injury.
• Inflammatory: Leprosy, Herpes zoster, • Conservative.
diphtheria. • Nerve repair.
• Compression neuropathies. • Tendon transfer.
• Lead poisoning. • Physiotherapy.
• Arsenical poisoning.
• Alcoholism. CAUSALGIA
• Diabetes mellitus.
It is severe burning pain in the distribution of
• Vitamin B1 deficiency.
a peripheral nerve due to incomplete injury to the
• Porphyria.
• Neurofibroma and other neural tumors. peripheral nerve.
• Idiopathic. Sites
Common in upper limb, seen in brachial plexus
BRACHIAL PLEXUS INJURIES
or median nerve injuries.
Types In the lower limb it can be seen in distribution
It can be— of sciatic nerve or tibial nerve.
• Supraclavicular injury 65%. Clinically, there will be hyperesthesia and
• Infraclavicular injury 25%. severe, disabling burning pain along the
• Combined 10% distribution of the nerve.
It can be—
Upper plexus injury (Erb-Duchenne paralysis) Lower plexus injury (Klumpke’s paralysis)
It is due to depression of shoulder by trauma. Forcible hyperabduction causes this injury.
In newborn after difficult labor. In newborn due to difficult breech delivery.
Here C5 and C6 roots are injured. Here C8 and T1 roots are injured.
Muscles affected are deltoid, biceps, Intrinsic muscles of the hand are involved.
brachioradialis and supinator
Effects are: 1) Combined median and ulnar claw hand.
Elbow will be extended, pronated and 2) Horner’s syndrome.
upper limb is internally rotated.
(Policeman receiving tip).
..Difficulties come not to obstruct, but to instruct.

Management supplied by the deep branch of ulnar nerve.
• Nerve conduction studies. As all other thenar muscles are paralysed,
• Sympathectomy—cervical for upper limb, thumb lies in the same plane of the
lumbar for lower limb. metacarpals.
• ‘Pen test’: In median nerve injury, pen held
MEDIAN NERVE INJURIES in front of the hand cannot be touched by
thumb, as abduction is not possible due to
• Median nerve arises from lateral(C 5,6,7) and paralysis of the abductor pollicis brevis.
medial cord (C8 and T1) of the brachial plexus.
It lies initially lateral to the axillary artery and In low median nerve palsy
becomes medial in the lower part of the arm Profundus is not paralysed and so pointing index
and in the cubital fossa. It passes through the is not seen.
pronator teres, descends in relation to flexor
muscles and enters the palm through the Investigations
carpal tunnel at the wrist. • Nerve conduction studies.
• It supplies pronator teres, flexor carpi • X-ray of the part in case of fracture.
radialis, palmaris longus and flexor digi- • Electromyogram.
torum superficialis. Anterior interosseous
branch of the median nerve supplies pronator Treatment
teres, lateral half of the flexor digitorum • Nerve suturing or nerve graft.
profundus, flexor pollicis longus and • Tendon transfer.
pronator quadratus. • The condition is treated like carpal tunnel
• In the wrist, it supplies abductor pollicis syndrome.
brevis, flexor pollicis, opponens pollicis of
thenar eminence and lateral two lumbricals.
It gives sensory supply to lateral three and CARPAL TUNNEL SYNDROME
half fingers of the hand. • It is the compression neuropathy of median
nerve in the carpus, deep to flexor retina-
Median nerve is affected in culum.
1. Injuries • Flexor retinaculum (transverse carpal
a. Supracondylar fracture of the elbow. ligament) maintains the concavity of wrist
b. Fracture-dislocation of the elbow. and extends laterally from trapezium and
c. Direct cut injuries. scaphoid to pisiform and hook of the hamate
2. Leprosy. medially.
3. Carpal tunnel syndrome. Carpal tunnel is formed by carpal bones
4. As a part of brachial plexus injury. behind and flexor retinaculum in front. It
contains median nerve and long flexor tendons
Clinical Features of Median Nerve Palsy of fingers and thumb. Ulnar nerve lies super-
In high median nerve palsy ficially, not within the carpal tunnel. Median
• Wasting of the thenar eminence. Loss of nerve gets compressed if space of the carpal
sensation in lateral three and half fingers. tunnel gets reduced.
• Ochsner’s clasping test shows pointing index
because of the inactivity of lateral two Causes
divisions of the profundus. • Lunate dislocation.
• ‘Ape or Simian thumb deformity’ is due to over • Mal united Colles’ fracture.
action of the adductor pollicis, which is • Radiocarpal arthritis.
• Flexor tendon tenosynovitis. middle of the arm. Then it enters the posterior
• Myxedema. compartment in relation to triceps muscle.
• Acromegaly. After passing behind the medial epicondyle
• Pregnancy. and through two heads of flexor carpi ulnaris,
it runs in front of the flexor digitorum
Clinical Features profundus(FDP) in the forearm. It reaches the
• Common in females. hand in front of the flexor retinaculum
• Tingling, numbness, paresthesia and burning through Guyon’s canal. Here it divides into
sensation in the lateral three and half fingers superficial and deep branches.
• Ulnar nerve supplies flexor carpi ulnaris,
supplied by median nerve. Burning sensation
medial half of flexor digitorum profundus,
gets aggravated at night.
all muscles of the hypothenar eminence
• Ape thumb deformity, wasting of thenar
(palmaris brevis, abductor digiti minimi,
muscles, weakness of opponens pollicis and
opponens digiti minimi, flexor digiti minimi),
abductor pollicis brevis, i.e. features of low
adductor pollicis of the thenar eminence and
median nerve palsy.
all interossei of the hand. It also gives sensory
• When BP cuff is inflated patient feels the
supply to medial part of the hand, medial one
typical pain in the fingers.
and half fingers.
• Tapping the median nerve at the distal end
of forearm with the wrist held in extension
Ulnar nerve is affected in
aggravates the symptoms. • Supracondylar fracture.
• Condition is often bilateral. • Injury to the medial epicondyle.
• Tardy ulnar palsy.
Differential Diagnosis • Leprosy.
• Cervical spondylosis. • Cubitus valgus deformity.
• Cervical rib syndrome.
Clinical Features
Diagnosis • Claw hand deformity.
Nerve conduction studies. • Weakness of all the muscles supplied by the
ulnar nerve.
Treatment • ‘Card test’: A card is placed between the two
• Surgical decompression of median nerve by fingers of the patient to grasp. In weak
cutting both superficial and deep part of palmar interossei, patient cannot grasp.
flexor retinaculum completely, by ’S’ shaped (palmar interossei are adductors of the
incision. fingers (PAD)).
• Postoperatively good physiotherapy is • Abduction of fingers is checked. (Dorsal
required. interossei are abductors (DAB)).
• Condition is permanently curable. • Froment’s sign: A book is placed to grasp
between fingers and thumb of the patient.
Normally thumb will be straight because of
ULNAR NERVE INJURIES the action of adductor pollicis muscle. As it
• After arising from the medial cord of the is paralyzed in ulnar palsy, grasp is achieved
brachial plexus (C8 and T1), it runs on the by the action of flexor pollicis longus and
medial aspect of the axillary artery up to there will be flexed thumb.
..Circumstance do not make man, they reveal him.

• Loss of sensation over medial one and half Clinical Features
fingers and hand. • Typical claw hand.
• Loss of sensation along the distribution of the
Investigations nerve.
• Nerve conduction studies. • Inability to grasp card between the fingers.
• Electromyogram. • While holding the book between the thumb
and fingers, thumb will be flexed in ulnar
Treatment claw hand (positive Froment’s test).
• Nerve suturing or nerve grafting.
Types
• Tendon transfer.
1. Ulnar claw hand: Only medial two fingers are
Intrinsic minus deformity: It is due to loss of involved.
intrinsic muscle power, i.e claw hand. a. Low ulnar palsy: Here lesion is in the wrist
(at Guyon’s canal). Here deformity is more
Intrinsic plus deformity: It is due to muscle
because of the over action of the FDP.
contracture and fibrosis.
b. High ulnar palsy: Here as FDP is also para-
Ulnar paradox: In ulnar palsy higher the lesion, lysed, there is no over action. Deformity
lesser the deformity, lower the lesion more the is less.
deformity. In higher lesion, FDP is also Ulnar paradox: Higher the lesion lesser the
paralyzed. In lower lesion, FDP is intact and so deformity, lower the lesion more the
FDP causes more flexion (overaction) and so the deformity.
claw hand is aggravated. 2. Median claw hand: only lateral two fingers are
involved. It is less common.
3. Combined median and ulnar claw hand: Here all
CLAW HAND four fingers of the hand are involved.
• It is the hyperextension of the metacarpo-
phalangeal joint with flexion of the inter- Investigations
phalangeal joints of the hand. • Electromyogram.
• Extension of MCP joint is due to action of • Nerve conduction studies.
extensor digitorum.
• Flexion of MCP joint and extension of Treatment
interphalangeal joints are by extensor hood • Paul Braund’s operation: Extensor carpi
of interossei and lumbricals. So extensor hood radialis longus or brevis (ERCB) is transferred
is functioned mainly by ulnar nerve and also with a graft to the extensor hood through the
by median nerve. In ulnar or median nerve lumbrical canal. Graft is taken from palmaris
palsies, these actions are paralysed and so longus or plantaris muscle.
patient develops claw hand. • Stye-Bunnell’s operation: Flexor digitorum
• It is actually intrinsic minus deformity. superficialis of index finger is used(only in
ulnar claw hand) to transfer to extensor hood.
Causes • Anterior transpositioning of the ulnar nerve in
• Leprosy. case of tardy ulnar palsy.
• Trauma.
• Entrapment neuropathies. RADIAL NERVE LESIONS
• Tardy ulnar palsy.
• Klumpke’s palsy. • Radial nerve is derived from the posterior cord
of the brachial plexus (C 5,6,7,8 and T1). It
descends behind the axillary artery in front • Fracture of the shaft of the humerus.
of the subscapularis, latissimus dorsi and teres • Rarely intramuscular injection of drugs can
major. It passes through the medial and lateral cause radial nerve palsy.
heads of the triceps muscle, winds round the
humerus through the radial groove and enters In the elbow
the forearm in front of the lateral epicondyle • Dislocation or fracture neck of the radius.
in relation to brachioradialis, brachialis and
extensor carpi radialis longus muscles. Clinical Features
• In the arm it supplies triceps, anconeus, • Wrist drop because of inability to extend the
brachioradialis, extensor carpi radialis longus wrist.
and part of the brachialis. It gives posterior • Inability to extend metacarpophalangeal
and lower lateral cutaneous nerves of the arm joint, but extensions of the interphalangeal
and posterior cutaneous nerve of he forearm. joints is normal.
• Superficial branch of the radial nerve from the • Inability to extend the forearm.
elbow runs in the forearm in relation to • Inability to extend the thumb.
supinator and brachioradialis and ends by • Flexion of the elbow against resistance with
forming 5 digital nerves which gives sensory forearm in mid-prone position is difficult
supply to lateral three and half fingers on the because of the weakness of the brachio-
dorsal aspect. radialis muscle.
• Deep branch also called as posterior interos- • Loss of sensation in back of the arm, forearm,
seous nerve winds round the radius
hand and lateral three and half fingers.
supplying supinator and extensor carpi
Posterior interosseous nerve is purely motor
radialis brevis. It gives 3 short branches to
and so sensation is intact when it gets injured.
extensor digitorum, extensor digiti minimi
and extensor carpi ulnaris. It also gives two
Investigations
long branches—One to abductor pollicis
longus and extensor pollicis brevis; another • X-ray of the part.
to extensor digitorum, extensor carpi ulnaris • Nerve conduction studies.
and extensor digiti minimi.
Treatment
Conditions where radial nerve is affected • Nerve suturing or nerve graft.
In the axilla • Tendon transfer.
• Crutch palsy—It is neuropraxia.
• Fracture upper end of the humerus.
• Bony or soft tissue growth. COMMON PERONEAL NERVE
This nerve supplies the extensor and peroneal
In the radial groove group of muscles; and sensory supply to the skin
• Pressure on the arm from the edge of the
over the front and lateral aspect of the leg and
operating table.
dorsum of the foot.
• Saturday night palsy—An individual with
excessive alcohol consumption compresses Common peroneal nerve is affected in
his arm over the chair or by fall. It is • Fracture neck of the fibula.
neuropraxia. • Leprosy.
• Prolonged tourniquet application—Tourni- • Lead poisoning.
quet palsy. • Iatrogenic.
..Tolerance is another word for indifference.

Clinical Features Causes
• Foot drop with high stepping gait. • Postherpetic (zoster).
• Talipes equino-varus deformity. • Malignancy.
• Loss of sensation in the lateral side of the leg
and dorsum of the foot. Features
• Paroxysmal, shooting, sharp, sudden, short
Management pain.
• Treating the foot drop. • It is usually unilateral.
• MCR chappals. • Second and third division of 5th cranial nerve
• Tendon transfer using tibialis posterior is affected.
muscle. Tendon of the muscle is detached • Sensory or motor loss will not be present.
from the navicular insertion and with a • Touching/washing/shaving face or brush-
tendon graft (from plantaris) it is transferred ing are triggering factors.
to cuboid and cuneiform bones to get • It begins behind the ear and spreads towards
dorsiflexion and eversion. orbit, ear/chin.
• Often it begins below the orbit and spreads
AXILLARY NERVE INJURY to nose, upper lip or to cheek.
Axillary nerve supplies the deltoid and teres Treatment
minor muscle and also sensory supply to the skin
• Carbazepine tablets 100 mg three times a day.
over the upper lateral aspect of the arm.
• Peripheral neurectomy.
Axillary nerve is affected in • Injection into gasserian/trigeminal ganglion
• Fracture neck of the humerus. using alcohol/lignocaine.
• Dislocation of humeral head. • Intracranial decompression of trigeminal
• Following IM injection into the deltoid. ganglion pathway or intramedullary
Clinically there will be loss of abduction of trigeminal tractotomy is done only in severe
the shoulder and anesthesia of the skin over the intolerable intractable cases (rarely).
lateral part of the arm.
TENDON
LONG THORACIC NERVE • Tendon is the continuity of the muscle to have
(NERVE OF BELL) its action at the site especially in hand, foot
It supplies serratus anterior muscle. It arises from and digits.
C5,6,7 cervical roots. • It is covered by synovial sheath with a thin
The nerve is injured commonly in malig- layer of fluid in between which allows
nancy, during breast, axillary or chest wall smooth gliding of the tendon.
surgeries. • Tendon injuries may be cut wound,
Clinically, when outstretched (elbow exten- lacerations, injury associated with nerve or
ded) arm is pushed against the wall, the inferior vessel injury.
angle of the scapula becomes prominent After injury tendon heals by—
(Winging of the scapula). 1. Intrinsic healing method—occurs through
synovial fluid when tendon is not under
TRIGEMINAL NEURALGIA stress.
It is the excruciating pain and hyperesthesia 2. Extrinsic healing method—occurs through
along the distribution of the trigeminal nerve. proliferation of fibroblasts across epitenon.
It occurs when tendon is under stress. It forms Suture material used is monofilament non-
a mass of fibrous tissue at the site called as absorbable suture material (polypropylene, 3 or
‘tenoma’. It may interfere with the proper 4 zero).
gliding of the tendon. • Continuous sutures are used for suturing.
• Epitenon can be later apposed with
Stages of Tendon Healing interrupted sutures.
1. By 21 days weak healing occurs and contrac- • Post-operative immobilization is required for
tion of muscle possible. 3–4 weeks.
2. At 6 weeks, mild traction can be applied to • Later passive and active exercise is required
the tendon. with the help of a physiotherapist.
3. At 3 months, moderate stress may be used. Complications of tendon suturing are
4. By 8 months, full tensile strength is recove- infection, adhesion, stiffness and failure.
red.
TENDON TRANSFER
TENDON REPAIR • It is the transfer of one tendon from its
1. Primary repair is done within 24 hours. existing site to another site to have a function
2. Delayed repair within a week after 24 hours. required at the newer site.
3. Secondary repair anytime after one week. • Other tendons should maintain function of
the transferred tendon.
Types of Suturing the Tendon (Fig. 11.2) • Tendon should able to acquire the function
at the newer site properly.
a. Goldner method: Here knot comes away from
• E.g. flexor digitorum superficialis (FDS)
the cut ends of the tendon.
(of index finger) tendon transfer in ulnar claw
b. Kessler method: Here knot comes in the cut
hand to lumbrical canal of the digits to have
part of the tendon.
flexion at MCP joint and extension of
proximal IP joint.
TENDON GRAFT
When tendon suturing or transfer is not possible
because of inadequate length, tendon of a
muscle, which is not much helpful functionally,
is taken as a graft to obtain required length.
Common grafts used are—
• Palmaris tendon in forearm.
• Plantaris tendon in leg.
For example extensor carpi radialis brevis
(ECRB) is lengthened using tendon graft to
transfer to lumbrical canals in claw hand.
Fig. 11.2: Types of tendon suturing (a) Goldner method Problems in tendon graft: Infection, adhesions,
(b) Kessler method graft failure, and stiffness of the part.
..Determination is the wake-up call to the human will.

12 Hand and Foot
 Surgical anatomy of hand trapezium crest as strong fibrous band so as to

 Hand infections bridge carpus to create carpal tunnel.
 Acute paronychia Ulnar nerve and vessels, palmar cutaneous
 Chronic paronychia branches of median and ulnar nerves, palmaris
 Terminal pulp space infection (FELON) longus muscle are superficial to the carpal
 Infection of webspaces tunnel.
 Deep palmar space infection Median nerve, tendons of flexor digitorum
 Acute suppurative tenosynovitis superficialis, profundus and pollicis longus,
 Hand injuries radial and ulnar bursa are deep to flexor
 Compound palmar ganglion retinaculum.
 Dupuytren’s contracture
 Syndactyly Palmar Aponeurosis
 Mallet finger (Baseball finger) It is thickened, modified deep fascia in the palm
 Heberden’s nodes with its apex pointing proximally (as continua-
 Spina ventosa tion of palmaris longus) and base towards distal
 Callosity part with four parts. They extend over deep
 Corn transverse ligament into lumbrical tunnel.
 Plantar fasciitis (Policeman’s heel)
 Ingrowing toe nail (Onychocryptosis) Blood Supply of the Hand
Superficial palmar arch mainly formed by ulnar
artery and is completed by superficial palmar
HAND branch of radial artery. It gives four digital
SURGICAL ANATOMY OF THE HAND branches to medial three fingers.
Deep palmar arch is formed by radial artery
Flexor Retinaculum and is completed by deep branch of ulnar artery.
It extends medially from pisiform and hook of It gives three palmar metacarpal arteries, which
hamate laterally to scaphoid tubercle and communicate with superficial palmar arch. It
Hand and Foot 163
also gives communicating, perforating branches General Features of Hand Infection
to dorsal metacarpal arteries. Infection spreads faster in all areas.
Muscles of the Hand Causes edema over the dorsum of hand due
to lax skin and more lymphatic network even
Thenar muscles: Abductor pollicis brevis, flexor
though infection per se is more over the volar
policis brevis, opponens pollicis and adductor
aspect. It looks like frog hand.
pollicis.
Restricted movements of fingers and hand.
Hypothenar muscles: Palmaris brevis, abductor The hand functions like hook, pinch, grip, grasp
digiti minimi, flexor digiti minimi and opponens are lost.
digiti minimi. Severe pain and tenderness, with fever.
Lumbricals are four in number—named from Tender palpable axillary lymph nodes are
lateral to medial. often present.
Four palmar interossei. Different Types of Hand Infections
Four dorsal interossei. • Acute paronychia.
Nerve Supply • Chronic paronychia.
• Terminal pulp space infection (felon).
Abductor pollicis brevis, flexor pollicis brevis, • Subungual infection.
opponens pollicis and 1st and 2nd lumbricals are • Web space infection.
supplied by median nerve. (5 muscles). • Mid palmar space infection.
Rest of the muscles (15 muscles) in hand are • Thenar space infection.
supplied by ulnar nerve. • Deep palmar abscess.
HAND INFECTIONS • Acute suppurative tenosynovitis.
• Chronic tenosynovitis of flexor tendon sheath
Hand is a compact actively functioning unit. It
of palm and forearm—Compound palmar
contains neurovascular bundles, muscles, bones
ganglion.
and ligaments.
• Lymphangitis of the hand.
Infection can occur due to minor injuries,
hematogenous spread.
Investigations
Precipitating causes • Pus for culture and sensitivity.
• Diabetes. • Blood sugar.
• Immunosuppression. • Urine sugar and ketone bodies.
• Trauma. • X-ray of the part.
• HIV infection.
• Steroid therapy. General Principles of Managing Hand
Infections
Common organisms
• Staphylococcus. Antibiotic Therapy
• Streptococcus. Position of rest with wrist slightly abducted and
• Gram-negative organisms like E. Coli, extended, thumb and index fingers away (Glass
Klebsiella, Pseudomonas. holding position). Position of function is where
• Occasionally fungal infection causing thumb and index fingers are pinching firmly
chronic paronychia, Madura hand due to with wrist extension.
Nocardia group of fungi, viral infection like Elevation of hand reduces the edema, increases
ORF can occur perfusion, and promotes healing.
..Failure is the condiment that gives success its flavor.

Early recognition of localized pus. Once visible under the nail root (Fig. 12.1). Nail on
localized, incision and drainage must be done touch is very tender (paronychia means ‘run
ideally under general anesthesia or regional around’).
block (not local anesthesia). Draining incision
should not cross the palmar crease. Incision Treatment
should have adequate length and adequate • Pus is send for culture and sensitivity.
depth (deep to palmar fascia, otherwise evacua- • Antibiotics like Cloxacillin, Amoxicillin
tion of pus is inadequate). Care should be taken • Analgesics.
not to injure neurovascular bundles. Pus should • The pus is drained by making an incision
be sent for culture and sensitivity. Slough if over the eponychium.
present should be excised thoroughly. Gauze • If there is a floating nail, then the nail is dead,
drain is placed. Regular dressings are done with it has to be removed.
continuation of antibiotics. Communications into • Recovery is fast.
other areas of hand should also be drained.
Bloodless field (using tourniquet) is better to
drain pus from hand.
Proper car must be taken after treatment.
Initial rest, elevation of hand, later proper physio-
therapy and regular exercise of hand and fingers
should be done to restore normal function.
Complications of hand infections

• Stiffness of digits and hand (ankylosis).
• Deformity and disability.
• Bacteremia and septicemia. Fig. 12.1: Paronychia showing pointing pus
• Osteomyelitis of bones depending on
location of abscess like metacarpal bones,
terminal phalanx. CHRONIC PARONYCHIA
• Suppurative arthritis of joints. It is commonly due to fungal infection.
• Paralysis of median nerve.
Clinical Features
ACUTE PARONYCHIA • Itching in the nailbed.
• It is the most common hand infection. • Recurrent pain.
• It occurs in subcuticular area under the • Discharge.
eponychium. • Secondary bacterial infection may supervene.
• Minor injury to finger is the common cause.
• Suppuration occurs very rapidly. Investigations
• It tracks around the skin margin and spreads
under the nail causing hang nail or floating nail. Culture of scrapings for fungus and other
• Organisms are Staphylococcus aureus and causative agents.
Streptococcus pyogenes.
Treatment
Clinical Features • Long-term antifungal therapy.
Presents with severe throbbing pain and • Antibiotics for secondary infection.
tenderness (dependent throbbing), with pus • In severe cases removal of nail is required.
Hand and Foot 165
TERMINAL PULP SPACE INFECTION Causes of collar - stud abscess
(FELON) • Tuberculous cold abscess.
• It is the second most common hand infection • Terminal pulp space infection (Felon).
(25%). • Deep palmar space infection.
• Index and thumb are commonly affected.
• Usually by a minor injury like finger prick. Investigation
X-ray of the part is often required to rule out
Surgical Anatomy (Fig. 12.2) osteomyelitis of terminal phalanx.
Terminal pulp space contains fat and is Pus for culture and sensitivity.
partitioned by septae, which is attached from
periosteum of terminal phalanx to skin. Treatment (Fig. 12.3)
Antibiotics and analgesics.
Drainage of pus from terminal pulp space by
an oblique deep incision.
If osteomyelitis sets in, then the terminal
phalanx may have to be amputated.
Fig. 12.2: Anatomy of the terminal pulp space
Proximally deep fascia is attached to the

periosteum distal to the base of terminal phalanx
i.e. distal to the attachment of flexor tendon.
So, terminal space is a closed compartment
which causes increased pressure when there is
infection, compresses terminal artery leading to
thrombosis resulting in osteomyelitis of terminal
phalanx.
Bacteria
• Staphylococcus. Fig. 12.3: Incision for pulp space drainage
• Streptococcus.
• Gram-negative organisms. Complications
• Osteomyelitis of the terminal phalanx.
Clinical Features • Septicemia.
• Pain, tenderness, swelling in the terminal
phalanx. INFECTION OF WEBSPACES
• Fever.
• Tender axillary lymph nodes. Surgical Anatomy
Often suppuration is severe, forming collar There are three triangular webspaces filled with
stud abscess, which eventually may burst. fat between the dorsal and volar skin. When the
..The most vital test of a man’s character is not how he behavies after success,
but how he sustains defeat.
space is filled with pus it straddles the deep sensitivity. If other webspaces are involved
transverse ligament. Even though pus is on volar they should be drained through a separate
aspect, it points out dorsally. incision. Edges of the wound are cut to leave
a diamond shaped opening in front. Often
It originates from— counter-incision over dorsal skin of web is
• Abrasion. needed.
• Infection of proximal volar space of finger.
• Callosities.
DEEP PALMAR SPACE INFECTION
• Infection of proximal spaces.
Surgical Anatomy
Bacteria Two deep palmar spaces are present
• Staphylococcus. — Midpalmar Space
• Streptococcus. — Thenar Space.
• Gram negative organisms. Midpalmar space is bound in front by palmar
aponeurosis, behind by medial three meta-
Clinical Features carpals, laterally by a vertical line from lateral
margin of the middle finger. It contains flexor
• Fever. tendons, neurovascular bundles and lumbricals.
• Pain and tenderness. It is the common site of the infection.
• Edema of dorsum of hand. Thenar space is located anterior to lateral two
• Maximum tenderness is on the volar aspect. metacarpals. Infection here is usually due to
• ‘V’ sign—Separation of fingers. extension from midpalmar space.
• If untreated, infection may spread into other
webspaces and hand spaces. Causes
• Trauma.
Treatment • Spread from infection of finger spaces and
• Elevation of hand webspaces.
• Antibiotics and analgesics • Hematogenous spread.
• Drainage of pus under regional or general • Spread from tenosynovitis.
anesthesia. A horizontal incision is made on
volar skin of the web, and deepened to reach Clinical features
the space by dividing fibers of palmar fascia • Pain and tenderness in the palm.
(Fig. 12.4). Pus has to be sent for culture and • Edema of dorsum of hand (frog hand).
• Loss of concavity of palm.
• Painful movement of metacarpophalangeal
joint(but movements of interphalangeal joint
are normal and painfree).
• Fever.
• Palpable tender axillary lymph nodes.
• Eventually pus may come out of palmar
aponeurosis forming collar-stud abscess and
later with formation of sinus.
X-ray of the part is required.
Treatment
Fig. 12.4: Incision for webspace drainage • Elevation of the affected limb.
Hand and Foot 167
• Antibiotics and analgesics. Kanavel signs
• Drainage of pus under general anesthesia. A • Swollen finger held in flexion.
horizontal incision is placed on the volar • Exquisite pain on passive extension.
aspect without crossing the palmar crease • Tenderness precisely over the tendon sheath.
and should be extended deep to palmar • Area of greatest tenderness is over the part of ulnar
aponeurosis. A drain is placed. Pus should bursa lying between transverse palmar creases.
be sent for culture and sensitivity and
appropriate antibiotics are continued. In infection of radial bursa, thumb is swollen
with pain and tenderness over the sheath of the
Complications flexor pollicis longus along with inextensibility
of interphalangeal joint.
• Osteomyelitis of metacarpals. Swelling just above the flexor retinaculum is
• Stiffness of hand. common.
• Suppurative arthritis.
• Extension of infection into other spaces. Treatment
• Elevation of the affected limb.
• Antibiotics and analgesics.
ACUTE SUPPURATIVE • Position of rest.
TENOSYNOVITIS Drainage of pus under general anesthesia.
It is the bacterial infection of flexor tendon Incisions are placed over the site of maximum
sheaths. tenderness and flexor sheath should be opened
up. Many a times multiple incisions are required.
Surgical Anatomy Complications
Radial bursa is flexor sheath of flexor tendon • Spread of infection proximally into forearm.
of thumb, which extends to the digit. • Stiffness of fingers and hand.
Ulnar bursa is flexor sheaths of medial four • Suppurative arthritis.
flexor tendons, which extends into the digit of • Osteomyelitis.
the fifth (little) finger. • Median nerve palsy.
• Bacteremia and septicemia.
Common bacteria: Staphylococcus aureus, Strepto-
coccus pyogenes. In HAND
DO’S. DONT’S.
Examine hand Incise every infected
Clinical features carefully. digit.
• Symmetrical swelling of entire finger. Think of other Make puncture
• Flexion of finger—Hook sign. diagnosis. incisions or over pads.
• Severe pain on extension. Wait for abscess to Injure the digital
• Tenderness over the sheath. localize. nerves or vessels.
Place adequate length Place incisions
• Edema of whole hand, both palm and
and depth of incisions. crossing the crease line.
dorsum (due to lymphatic spread). Immobilize, elevate Close human bites or
• As ulnar bursa extends into the little finger, the hand. lacerated wounds.
pain and tenderness extends into little finger Give antibiotics and Forget to send pus for
but not much to other fingers. proper dressings. culture and sensitivity.
..The will to win the desire to succeed, the urge to reach your full potential....
will unlock the door to personal excellence.
Parona’s space is space in the forearm to which structures like muscles, vessels and bones
infection can occur as extension from the hand. without coverage. It needs proper debridement
and later skin coverage by skin grafting or flaps.
HAND INJURIES (FIG. 12.5) It may cause extensive tissue loss; infection,
neurological deficit; gas gangrene etc.
Classifications
Indetermined injuries, which could not be
Tidy injuries: They are clean incised wounds and assessed.
are usually treated by primary suturing; depend
on the tissues involved like nerves, tendons and Assessment of injury: Should include—
muscles. Number, extent, depth, deformity and
disability, neurovascular injuries, tendon
Untidy injuries: They are lacerated wounds and injuries, muscle injuries, bone and joint injuries.
are treated by debridement and later by delayed
primary or secondary suturing. Principles of treatment
Compartment injuries: It is deep injury causing • Hemostasis.
increased pressure within the deep fascia causing • Use of tourniquet.
vascular compromise of muscles leading to • Wound debridement and cleaning.
arterial block; muscle necrosis and Volkmann’s • Antibiotics and antitetanus treatment (toxoid
ischemic contracture as a late effect. Often it may and antitetanus globulin).
cause renal failure due to myoglobulinuria and • Primary suturing if it is incised wound or
septicaemia. It may be life threatening unless delayed primary suturing if there is edema.
immediate surgical intervention is done. • Skin grafting or flaps for skin loss.
• Tendon suturing or tendon graft.
Degloving injuries: It is avulsion of the large part • Rest and elevation of the affected parts.
of skin and fascia exposing wide part of deeper • Management of fractures by splint, wiring.
• Nerve repair.
• Immobilization up to 21 days.
• Later physiotherapy with warm, exercise,
active movements.
• Microsurgical restoration of digits.
Complications and morbidity of hand

injuries
• Infection.
• Osteomyelitis.
• Arthritis of joints.
• Stiffness.
• Loss of function due to disability.
COMPOUND PALMAR GANGLION

It is chronic tenosynovitis of flexor tendon
sheaths due to tuberculosis (tuberculous
Fig. 12.5: Hand injury. Note the severity of injury. Hand tenosynovitis) or rheumatoid arthritis.
injuries are tidy/indeterminate/untidy injuries It can be unilateral or bilateral.
Hand and Foot 169
Pathology
• Flexor tendon sheath on either side of the
wrist is involved, i.e. both in the volar surface
of palm and lower forearm.
• Swelling contains fluid with typical melon
seed bodies.
• Condition is often bilateral in case of
rheumatoid arthritis.
Clinical Features
• Swelling in the palm and lower forearm,
which is smooth, soft, nontender, non-
transilluminating, fluctuant and cross Fig. 12.6: Dupuytren’s contracture in the hands. Note the
fluctuant across flexor retinaculum. involvement of the ring finger
• Wasting of hand and forearm muscles.
• Matted axillary lymph nodes may be There is thickening and nodule formation in
palpable. the palm with adherent skin.
• Primary focus may be there in lungs. It is often familial and bilateral.
Pads(of fat) develop in knuckles and are
Investigations called as Garron’s pads.
• ESR. Condition often is associated with—
• Chest X-ray. • Plantar fasciitis.
• FNAC of axillary lymph node and swelling • Mediastinal and retroperitoneal fibrosis.
itself. • Peyronie’s disease of penis.
• Nodules in the face and ear.
Treatment Etiology
Start antituberculous drugs: INH, Rifampicin, • Repeated minor trauma.
Ethambutol and Pyrazinamide for 9 months. • Cirrhosis.
Excision of flexor tendon sheath with • Epileptics on treatment with phenytoin
caseating material, tubercles, melon seed bodies. sodium.
Care should be taken not to injure median
• Diabetics.
and ulnar nerves.
• Other metabolic conditions.
• Familial.
DUPUYTREN’S CONTRACTURE
It refers to localized thickening of palmar Complications
aponeurosis and later formation of nodules with • Restriction of hand function and so disability.
severe permanent changes in metacarpopha- • Arthritis of MCP and IP joints.
langeal and interphalangeal joints (Fig. 12.6).
It starts in ring and little fingers, with flexion Treatment
of ring and little fingers. Later involving all • Fasciotomy of palmar aponeurosis and later
fingers. physiotherapy (Fig. 12.7).
..When work is a pleasure a joy! When work is a duty life is slavery.

Fig. 12.9: Syndactyly and polydactyly of

both hands and both feet
If bony type is suspected X-ray of the part

Fig. 12.7: Z plasty done for Dupuytren’s contracture should be taken.
Treatment
• If cutaneous, release of web is done as staged
procedure with ‘Z’ plasty or skin grafting.
• If fibrous release can be done.
• If bony type release is difficult because blood
supply can be compromised which will lead
on to gangrene of digit.
MALLET FINGER (BASE BALL FINGER)

The terminal phalanx cannot be extended
because of tear at insertion of extensor tendon
Fig. 12.8: Syndactly in both hands.
It can be bony or fibrous
or avulsion fracture of the base of the terminal
phalanx.
• In severe cases fasciectomy. HEBERDEN’S NODES

• Treatment for the cause.
These are seen in osteoarthritis occurring behind
SYNDACTYLY the distal interphalangeal joints of index, middle,
little and ring fingers.
It is webbing or fusion of fingers (Fig. 12.8).
Causes SPINA VENTOSA

• Congenital and hereditary—common. Refers to phalangeal tuberculosis (tuberculous
• Traumatic like burns. dactylitis). It is called as spina ventosa because
of its appearance as ‘air filled balloon’.
Types
• Cutaneous. FOOT
• Fibrous.
• Bony. CALLOSITY (FIG. 12.10)
It can be unilateral or bilateral. It is a hard, thickened skin occurs as a protective
Often there will be webbing of toes also measure seen in wider area usually over heel and
(Fig. 12.9). heads of metatarsals.
Hand and Foot 171
Soft Corn
It usually occurs between 4th and 5th toes due
to friction of bases of adjacent proximal
phalanges.
PLANTAR FASCIITIS
(POLICEMAN’S HEEL)
It occurs due to friction of the ossified posterior
insertion of the plantar fascia, which is common
Fig. 12.10: Callosity in the foot in people who stand or walk for long time.
CORN (FIG. 12.11) Treatment

Analgesics, rest, steroid injections to the site.
Types
• Hard corn. INGROWING TOE NAIL (FIG. 12.12)
• Soft corn. (ONYCHOCRYPTOSIS)
Hard Corn It is also called as embedded toenail.
It is due to curling of side of the nail inwards
• It is localized area of thickening over bony
causing it to form a lateral spike, which results
projections like heads of metatarsals.
in repeated irritation and infection of over-
• Histologically it differs from callosity by
having severe keratoses with a central core hanging tissues in the nail fold.
of degenerated cells and cholesterol.
• It presses over the adjacent nerves causing Causes
pain. It can get infected causing severe pain Tight shoes.
and tenderness with inability to walk. Improper cutting of nails (very short and
• Treatment: Excision. convexly curved).
Fig. 12.11: Corns in the plantar aspect of the foot Fig. 12.12: Ingrowing toe nail. Note the granuloma caused
by repeated infection and inflammation
..Hardwork doesn’t guarantee success, but improves its chances.

Clinical Features
• It is common in great toe and is often
bilateral.
• Both medial and lateral sides of the toe can
be involved.
• Pain, tenderness, swelling of margins of the
toe, often with foul smelling discharge.
Treatment (Fig. 12.13)

• Regular dressing and packing.
• Antibiotics.
• Discharge should be sent for culture.
• Nails should be cut concavely without Fig. 12.13: Zadik’s or Fowler’s operation
leaving lateral spikes.
tissues with pus and germinal matrix of ingrown
Zadik’s or Fowler’s operation: Skin in lateral part are excised.
margin and root is incised so as to expose the Often excision of entire nail with its root is
lateral spike and germinal matrix. Infected required.
Trauma 173
13 Trauma
 Triage
 Spinal injury
 Neck injuries
 Bullet injuries
 Blast injuries
 Penetrating injury
 Abdominal trauma
 Duodenal injury
 Pancreatic injury Fig. 13.1: Crush injury leg due to road traffic accident
 Small bowel injury
 Colonic injury Triage was a system to attend patients with
 Liver injury trauma formulated by a committee of Trauma of
 Splenic injury the American College of surgeons.
 Renal injury
 Urinary bladder injury Assessing Four Components
 Abdominal compartment syndrome i. Physiologic response.
ii. Anatomical injury.
Trauma is the major public health problem in iii. Biomechanical injury.
all countries (Fig. 13.1). iv. Co-morbid factors.
TRIAGE ALGORITHM
TRIAGE STEP ONE (Assess physiological impact)
Triage means ‘To sort’ in French. Measure vital signs and level of consciousness—
..Nobody is worth your tears and the one who is, will never make you cry.
• By Glasgow Coma Scale.

Tag the patient accordingly
• Systolic blood pressure.
Red color: Immediate treatment is required.
• Respiratory rate.
Yellow color: Urgent treatment is required.
• Revised trauma score. It is based on airway,
laryngeal injury, spine injury, maxillo-facial Green color: Delayed treatment is required.
injury. Blue color: Expectant treatment is required.
Black color: Deceased.
STEP TWO (Assess anatomical impact)
All penetrating injuries to head, neck, thorax,
major burns, fracture bones, pelvic fractures, I. PRIMARY MANAGEMENT
paralysis. Air-way management.
STEP THREE (Assess mechanism) Breathing.
Automobile accidents, crash or blast injuries, Circulation.
high-energy injuries, fall from more than 20 feet. Disability and assessment of level of
Bullet injury. consciousness by Glasgow coma scale.
Exposure of the patient from head to toe for
STEP FOUR (Assess history)
• Patient’s age below 5 years or age more than final assessment.
55 years. Fingers and tubes: Finger evaluation, foley’s
• Cardiac diseases, respiratory and metabolic catheterization.
diseases.
• Pregnancy. GOALS
• Patients with bleeding disorders. • Identify life-threatening conditions.
• Immunosuppressed individuals. • Decide and implement appropriate treatment
BASED ON THE STEP CONSIDER TO SHIFT to the area of trauma.
THE PATIENT TO TRAUMA CENTER AND • First think of salvage of life, then think of
TRAUMA TEAM SHOULD BE KEPT ALERT. salvage of limb.
(It is important in multiple and mass casualities • Rapid assessment, rapid resuscitation, rapid
(fire, blasts, automobile accidents, train accidents). stabilization.
• Optimum, complete care.
MANAGEMENT • Transport efficiently to higher trauma center.
• Initial evaluation of the patient.
• Physiologic stabilization. Categorize the patient—
• Control of hemorrhage. I: Deceased.
• Management of thoracic and abdominal II: Walking wounded.
injury. III: Immobile wounded.
• Management of cranial injury. IV: Trapped wounded.
Trauma 175
Airway Breathing
Chin lift. 100% oxygen.
Jaw thrust. Assess bilateral chest raise.
Nasal airway. Assess breath sounds.
Oral airway. Use pulse oximetry.
Endotracheal intubation. Treat flail chest, pneumothorax.
Tracheostomy. Intercostal tube drainage.
[assess airway patency].
Circulation Disability Evaluation

Monitor vitals. Neurological examination.
Heart sounds. Glasgow Coma Scale.
ECG. Pupillary reaction.
IV fluids
Blood transfusion.
Treatment of shock.
Control of external bleed.
Use two IV lines-14G/16G].
Expose the patient fully Fingers and Tubes

Undress the patient Examine all orifices like P/R,P/V, etc.
Hypothermia assessment Use required tubes like catheter, Ryle‘s tube.
Assess injuries.
Examine joints, bones, abdomen,
and other systems.
Look for identification marks.
II. INVESTIGATIONS
• X-ray spine, chest, pelvis, extremities.
• CT scan.
• Blood group and cross matching.
• Arterial blood gas analysis.
• Serum electrolytes.
• U/S abdomen.
III. SECONDARY SURVEY
Re-evaluate the patient completely again.

Fig. 13.2: Hand injury involving all fingers
IV. DEFINITIVE CARE (Figs 13.2 and 13.3)
Definitive care means management of individual thoracic by chest tube insertion or thoracotomy;
trauma in detail like abdomen by laparotomy; cranial injury by carniotomy etc.
..Life is not always as it appears, you have the power to alter yours and make the difference.
Indications for Exploration in Neck Injuries
• Expanding hematoma.
• Uncontrolled external hemorrhage.
• Decreased carotid pulse.
• Stridor, hoarseness, dysphonia, hemoptysis.
• Severe dysphagia, odynophagia.
• Blood in oropharynx.
Treatment
• Explore the neck with adequate incision
under general anesthesia.
• Suture the injured structure like carotid,
esophagus, trachea, muscles, etc.
Fig. 13.3: Degloving scalp trauma and exposed
bone is granulating well • Antibiotics.
• Blood transfusion as required.
• Ryle’s tube for 5–7 days.
SPINAL INJURY
Other injuries like of head, thorax, maxillo-
• Assess the type, extent and severity of the facial region are discussed in respective chapters.
injury.
• Careful first aid and transfer to prevent
further damage to the spinal cord. BULLET INJURIES
• Assess the sensory loss or motor loss Bullet injury has got wound of entry and wound
properly. of exit. Extent of damage is not related to the
• Assess fractures clinically, by X-ray and MRI. external wound. It is related to the travel of bullet
• Central cord syndrome is common and is due inside, extent of blast or cavitation effect inside
to hyperflexion or hyperextension of the neck caused by the bullet. It causes burn damage.
in an injured patient causing ischemia of It can damage vessels, organs like liver,
spinal column due to interfering of spinal spleen, kidneys, bowel, lungs, heart, cranial
artery blood flow. structures, soft tissues, bone and joints.
• Brown-Séquard syndrome: It is due to partial
transection of the cord causing ipsilateral Management
motor function loss and contralateral sensory
• The wound is explored properly under
function loss.
general anesthesia.
• High dose of steroid is very useful to prevent
further damage. • All dead tissues and dead muscles are
• Rest, traction to neck. excised.
• Decompression of spinal canal surgically is • Skin is incised generously and adequately.
useful by removing bone, disk, hematoma. • Injured nerves are cleaned and silk marker
• Spinal stabilization. stitches are placed to identify for later
secondary suturing (Should not be closed
primarily).
NECK INJURIES • All foreign bodies are removed.
Neck is divided into zones for managing neck injuries. • Tendon repair should not be done primarily.
Zone I—from clavicle to cricoid cartilage. • Wound should not be closed. It should be left
Zone II—from cricoid cartilage to angle of the open.
mandible. • Adequate blood transfusion and antibiotics
Zone III—above the angle of the mandible. coverage is given.
Trauma 177
• Major artery or vein should be sutured. Vein Management
graft can be used. But synthetic graft should • Critical trauma care.
never be used. • Management of shock and triage primary
• Thorough inspection, irrigation and debride- management.
ment of injured joints is done. • Urgent surgeries like laparotomy, thoraco-
• Immobilization. tomy, craniotomy.
• Tetanus toxoid, antitetanus globulin (3000 • Massive blood transfusion.
units IM), antigas gangrene serum is given. • Antibiotics.
• Second look surgeries are done at a later • Ventilator support.
period once patient has been stabilized. • Management of specific organs like eye, ear.
• Delayed primary closure in 7 days or
secondary closure in 14 days is done. PENETRATING INJURY
• Depending on extent of defect skin grafting
• It can occur in abdomen, thorax, cranial
or flaps is used.
cavity (Fig. 13.4).
• Laparotomy, thoracotomy, craniotomy is
• It causes hemorrhage, damage to internal
done depending on the site of the injury.
organs like liver, bowel, vessels, lung,
pericardium and heart, brain, etc.
BLAST INJURIES • It is life threatening and immediate surgical
Here extent of damage is much more than bullet intervention is the only treatment (Fig. 13.5).
injuries. Patient requires adequate number of blood
It creates complex blast wave, which contains transfusion, antibiotics, and shock
blast pressure wave and mass movement of management.
air.
ABDOMINAL TRAUMA
This explosion pressure wave is more than
1000 pounds per square inch. This pressure wave It can be—
has got incident pressure and reflected pressure. • Blunt trauma.
• Stab injury.
Both will cause severe damage.
• Abdominal wall injury.
Factors causing the damage
• High pressure wave.
• Mechanical injury.
• Chemical injury.
• Thermal injury.
• Inhalation of toxic gases and smoke.
Organs effected —
• Ear drums.
• Lungs.
• GIT.
• Brain.
• Skeletal system.
Individual becomes deaf after blast and so
rescue work may be delayed. Fig. 13.4: Traumatic hemoperitoneum
..Love means sharing the same road, wherever it leads.

One of the criterias signifies the positive

lavage
• 10 ml or more of gross blood.
• RBC count more than 1,00,000/ cu mm.
• WBC count more than 500/ cu mm.
• Amylase level in the fluid more than 175 IU/
dl.
• Presence of bile, bacteria, food particles or
Fig. 13.5: Penetrating injury. Pole missed all the major
foreign body.
vessels. Miraculously the patient survived, after a Marathon
surgery to tell her tale to her Children. Contraindications for DPL
• When laparotomy is definitely indicated.
Types • Previous laparotomy.
• Liver injury. • Pregnancy.
• Spleen injury. • Obesity.
• Gastric/small bowel/colonic injuries. CT scan is indicated in assessing retroperito-
• Duodenal injuries. neum, solid organ injuries. It is noninvasive and
• Pancreatic injuries. highly specific.
• Injuries to kidney/bladder/urethra.
• Mesenteric injury. Treatment
• Vascular injuries. Emergency laparotomy.
• Associated injuries like of diaphragm, lungs. Indications:
• Abdominal compartment syndrome. • Frank hemoperitoneum.
• Gunshot or blast injuries. • Significant diagnostic peritoneal lavage.
• Hemodynamically unstable patient.
General Clinical Features
• Ultrasound or CT scan shows significant
• Features of shock—pallor, tachycardia, hypo- intraabdominal injuries.
tension, cold periphery, sweating, oliguria.
• Abdominal distension.
• Pain, tenderness, rebound tenderness, DUODENAL INJURY
guarding and rigidity, dullness in the flank Its severity depends on the type and extent of
on percussion. the injury.
• Respiratory distress, cyanosis depending on It can be hematoma or lacerations.
the amount of blood loss. Lacerations can be duodenal disruption
• Bruising over the skin of the abdominal wall. which may be < 50% or > 50% or 75% or more.
• Features specific of individual organ injuries. Laceration may extend into the ampulla,
distal CBD, pancreas or with duodenal devas-
Investigations cularization.
• Ultrasound abdomen.
• Diagnostic peritoneal lavage (DPL): It is Management
done in case of blunt injury abdomen. • CT scan is more relevant investigation.
Through a subumbilical lavage catheter one • Associated other injuries should be managed
liter of normal saline is infused into the accordingly.
peritoneal cavity. Patient is changed to • Hematoma without extension is managed
different positions. Fluid content is aspirated conservatively with nasogastric aspiration,
from the abdomen for assessment. antibiotics and IV fluids.
Trauma 179
• Lacerations are sutured surgically with • Presentation is like hemoperitoneum or with
stenting or often with bypass like gastro- features of peritonitis.
jejunostomy. • Monks localizing zones in the abdomen signify
• ERCP stenting or CBD bypass is also often the location of the small bowel injury.
required. • Site and the ‘pattern’ bruising over the
abdominal wall signifies the small bowel
Complications injury and its site. It is called as London’s sign.
• Infection.
• Duodenal leak. Management
• Peritonitis. • Plain X-ray abdomen shows gas under
• Hemorrhage. abdomen with ground-glass appearance.
• Ultrasound abdomen is useful.
PANCREATIC INJURY • Laparotomy and closure of the perforation
is done if it is small.
It can be in the head or body and tail of the • If there is extensive bowel injury or multiple
pancreas. injuries, then resection and anastomosis is
It may be associated with injury to duo- done.
denum or portal or superior mesenteric veins. • Any associated injuries should be dealt with
It can be contusion or severe lacerations. accordingly.
Management COLONIC INJURY
• High resolution CT scan is diagnostic. • Left sided injury, if it is small is treated with
• Distal pancreatectomy is done for distal proximal colostomy with closure of the
injuries. wound or resection and anastomosis if wider
• Conservative treatment is useful with area. Closure of colostomy is done at later
antibiotics, IV fluids. stages after 3–6 months.
• Whipple’s operation or total pancreatectomy
• Small wound over right-sided colon can be
is done as a last resort.
sutured primarily.
• Drainage of the pancreatic bed is simple and
• Ileostomy alone or ileostomy with ileo-
often useful method.
transverse anastomosis or right hemicolec-
Complications tomy with ileostomy is indicated in following
situations—
• Pancreatitis.
- Extensive peritoneal contamination.
• Septicemia.
- Colonic vascular injuries.
• Pancreatic fistula.
- Hemodynamically unstable patients.
• Pancreatic abscess formation.
- Long-term hypotension after trauma.
Pancreatic injury has got high mortality
(> 45%). LIVER INJURY
It can be subcapsular hematoma, lacerations,
SMALL BOWEL INJURY deeper injuries, and lacerations with disruption
• It can be blunt injury or stab injury. of hepatic lobes or segments or liver injury with
• Blunt injury causes disruption of either vascular injuries like of inferior vena cava or
duodenojejunal region or ileo-cecal region. hepatic veins.
..In life, let us from the past, to profit by the present, and to live better for the future.
Presentation is of hemorrhagic shock, Complications of splenectomy
distension of the abdomen, tenderness, rebound • Left lung atelectasis.
tenderness, guarding, rigidity. • Overwhelming post splenectomy infection.
Management (OPSI).
• Pancreatitis and pancreatic fistula.
• Small tear is sutured.
• Gastric bleeding.
• For larger tears—
• Subphrenic abscess.
- Deep sutures.
- Packing.
- Debridement. RENAL INJURY
- Hemocoagulants.
• Liver resection is not done (not advisable) • It is often managed conservatively.
usually for injuries. • IVU is the investigation of choice in renal
• Pringle maneuver is compressing the porta injury.
near foramen of Winslow. • Surgery is indicated when there is hilar
• Blood transfusions. injury, progressive bleeding, failure of
• Treatment of associated injuries like of conservative treatment or perinephric
diaphragm, lung, duodenum, colon. abscess formation.
• Antibiotics.
Complications of liver injury URINARY BLADDER INJURY
• Hemorrhage.
Intraperitoneal bladder injury occurs in
• Septicemia.
• Bile leak. distended bladder. It is treated always by
• Liver failure. surgical exploration through transabdominal
• Hemobilia. approach. Bladder tear is sutured with keeping
• Subphrenic abscess. a suprapubic cystostomy using Malecot’s
• CBD stricture. catheter.
Extraperitoneal injury can be treated
SPLENIC INJURY conservatively by placing a Foley’s catheter for
2–3 weeks.
It can be subcapsular hematoma, laceration or
hilar injury.
It can be associated with other organ injuries ABDOMINAL COMPARTMENT
like left kidney, left lobe of the liver, splenic SYNDROME
flexure of the colon or pancreas. • There is sudden increase in intra-abdominal
It can cause torrential hemorrhage and shock.
pressure which causes decreased venous
Management return to heart.
• Ultrasound abdomen, diagnostic peritoneal • It causes increased respiratory pressure,
lavage are the investigations. hypoxia, hypotension and decreased venous
• Blood transfusions. return.
• Splenorrhaphy in selected patients so as to • Measurement of bladder pressure is
save the spleen. diagnostic.
• Splenectomy. • Rapid decompression by opening the
• Management of associated injuries. abdominal wound is the treatment of choice.
Neoplasm and Soft Tissue Tumors 181
14 Neoplasm and
Soft Tissue Tumors
 Neoplasm Neoplasia is
 Spread of malignant tumors Progressive.
 Paraneoplastic syndromes Persistent.
 Investigations for neoplasm Purposeless.
 Soft tissue tumors (Sarcomas) Pervasive.
 Kaposi’s sarcoma Perverted.
Proliferative mass of tissue.
NEOPLASM
Definition Components
Willis defined neoplasm as ‘it is an abnormal mass Parenchyma: It contains proliferating neoplastic
of tissue, the growth of which exceeds and is cells.
uncoordinated with that of the normal tissues and
persists in the same excessive manner even after Stroma: It contains supporting connective tissues
cessation of the stimuli‘. and blood vessels.
Classification
Benign Malignant
Well-differentiated. Lack of differentiation.

Structures are typical of tissue/cell of origin. Atypical structure with anaplasia.
Smooth, slow, progressive rate of growth. Erratic, rapid growth
Normal mitotic figures. Abnormal mitotic activity.
Well-localized and capsulated. Not localized. Not capsulated.
Do not infiltrate surrounding normal tissues. Infiltrate the surrounding tissues.
No metastasis. Metastasize to lymph node or blood.
Curable. May not be completely curable.
Few benign tumors after long time may turn into malignancy.
Treatment is simple. Treatment is complex and complicated.
..A friend is your second identity.

Sarcoma Carcinoma
Arising from mesenchymal tissues. Arising from epithelial cells derived from any
of the three germ layers.
Sar means flesh-[Greek]. Oma means tumor Carc means crab-like.
Smooth, firm or hard swelling. Hard, proliferative, with everted edge.
Warm and vascular with dilated veins over the surface.
Spreads mainly through blood commonly to lungs, Spreads through lymphatics as well as blood.
e.g. liposarcoma, fibrosarcoma, etc. squamous cell carcinoma, renal cell carcinoma,
adenocarcinoma.
Features of anaplasia EtiologicAL Factors
• Lack of differentiation. Age: It is more common in elderly. But it is variable.
• Pleomorphism—variation in size and shape. Heredity
• Hyperchromatism—dark staining nuclei. • Familial: Familial polyposis of colon.
• Anisocytosis. • MEN syndrome.
• Anisonucleosis. • Neurofibromatosis.
• Abnormal mitotic activity. • von Hippel-Lindau syndrome.
• Familial breast and ovarian cancers.
Neoplasm which are only locally malignant: Genetic
No blood spread. No lymph node spread– • Xeroderma pigmentosa.
Marjolin’s ulcer, rodent ulcer, verrucous • Ataxia telangiectasia.
carcinoma, adamantinoma. • Fanconi anemia, bloom syndrome.
Neoplasm which are locoregionally malig- Acquired causes
• Chronic atrophic gastritis.
nant: Regional lymph node spread is
• Solar keratosis.
observed–Squamous cell carcinoma,
• Leukoplakia of oral cavity.
papillary carcinoma thyroid. • Ulcerative colitis.
Neoplasm which are systemic and spreads Chemical carcinogens
through blood and often also to lymph node– • Alkylating agents.
Melanoma, carcinoma breast. • Hydrocarbons.
• Amides, Azo dyes.
Features of malignant tissues • Aflatoxin B1.
• Altered differentiation, anaplasia. • Arecoline, collagenases and tannins
• Rapid rate of growth. (present in betel nuts)
• Local invasion. • Nitrosamines, vinyl chloride, insecticides.
• Metastasis. Radiation carcinogens
• Not capsulated. • U-V rays, ionising radiation.
Microbial carcinogens
Dysplasia: Means ‘disordered growth’. It is loss • Human papilloma virus – carcinoma cervix.
in the uniformity of the cells with pleomorphism • Epstein-Barr virus—Burkitt’s lymphoma,
and hyperchromatism as well as loss in their nasopharyngeal carcinoma.
architectural orientation. • Hepatitis ‘B’ virus.
Carcinoma in Situ: When dysplasia involves • Human T-cell Leukemia virus Type I.
• Helicobacter pylori can cause carcinoma of
entire thickness of the epithelium, which is
stomach and is associated with lymphomas.
preinvasive, it is called as carcinoma in situ.
(Mucosa Associated with Lymphoid Tissue
Basement membrane is intact in carcinoma in {MALT}).
situ.
SPREAD OF MALIGNANT TUMORS 2. Recurrence in the scar after surgery for
malignancy, e.g. Deposition of malig-
1. Local spread: Into adjacent structures like
nancy in the scar of SPC from bladder
soft tissues, vessels, bone.
tumor.
2. Lymphatic spread
3. Seedling in the peritoneal cavity from
• By permeation: Here malignant cells abdominal malignancy is common
proliferate through lymphatic vessels up causing intractable ascites.
to lymph node level, e.g. In carcinoma 5. Transcoelomic spread: Due to spillage or
breast malignant cells permeate into dislodge of malignant cells from primary site
axillary lymph nodes. causing seedling in other organ, e.g. In
• By embolization: Here cells get dislodged carcinoma stomach secondaries in ovary is
from lymphatic vessels and freely travel caused by transcoelomic spread (Krukenberg
to spread into further level of lymph tumor). Here cells get deposited onto the raw
nodes. In carcinoma breast, spread occurs surface of ovary during ovulation. (So it
from axillary lymph node to supracla- occurs in menstruating age group only).
vicular lymph node by embolization. Advanced malignancy can be associated with
• Retrograde lymphatic spread occurs once severe cachexia (Fig. 14.1).
malignant infiltration blocks lymph
vessel. In carcinoma breast retrograde
spread occurs to opposite breast, opposite
axilla, or to mediastinum. In melanoma
through dermal lymphatics and retro-
grade spread ‘in transit nodules’ occur in
the skin.
3. Blood spread: Occurs through veins, as veins
Fig. 14.1: Typical malignant cachexia in an
are thin and infiltration is easier. (Arteries advanced GI malignancy
contain elastic fibers which resist malignant
infiltration.).
PARANEOPLASTIC SYNDROMES
Both by permeation (e.g. permeation
through renal vein is common in renal cell Certain symptom complexes, which are not
carcinoma) and by embolization (in other specifically explained by the tumor, but are
malignancies). relevant, often problematic and life threatening
Blood spread is commonly to lungs, bone are called as paraneoplastic syndromes.
(upper end of femur and humerus, ribs, Incidence: Seen in 10% of patients.
skull), liver, brain, adrenals, and other Grading of Tumor
organs. It signifies aggressiveness of tumor.
In carcinoma prostate, due to increased It is based on differentiation of tumor cells and
pressure and venous block, retrograde mitotic activity.
venous spread occurs through vertebral Staging of the Tumor
venous plexus, which causes osteoblastic It is based on the size of the primary tumor, nodal
secondaries in pelvic bones and vertebrae. spread and blood spread.
4. Seedling, e.g. It is called as ‘TNM’staging.
1. From lower lip cancer to upper lip as kiss ‘TNM’ staging is more relevant than grading
cancer. in managing and predicting prognosis.
..Beware of the little expenses; a small leak can sink a great ship.
Syndrome Cause Types of tumor
Cushing‘s syndrome. ACTH or ACTH like substance. Small cell carcinoma lung.
Neural tumor.
Pancreatic tumour.
Syndrome of inappropriate ADH. ADH Small cell carcinoma lung.
Brain tumor.
Carcinoid syndrome. Serotonin, bradykinin. Bronchial adenoma.
Gastric and pancreatic cancer.
Hypoglycemia. Insulin. Fibrosarcoma.
Insulin like substance. Hepatoma.
Hypercalcemia. PTH related peptide. Renal cell carcinoma.
Carcinoma breast, SCC lung.
Ovarian cancer, leukemia.
Polycythemia. Erythropoietin. Renal cell carcinoma, hepatoma.
Cerebellar hemangioma.
Myasthenia. Immunologic Carcinoma lung.
Acanthosis nigricans. Epidermal growth factor. Lung cancer, uterine cancer,
gastric cancer.
Dermatomyositis. Immunologic Lung cancer, breast carcinoma.
Clubbing and hypertrophic Carcinoma lung.
osteoarthropathy of fingers.
Migrating thrombophlebitis. Tumor product mucin Carcinoma pancreas, lung.
[Trousseau phenomenon]. It activates clotting.
Broder’s grading of squamous cell carcinoma: INVESTIGATIONS FOR NEOPLASM

Based on keratin/epithelial pearls.
Grade I: Well-differentiated—more than 75% I. BIOPSY
epithelial pearls. ‘Bio’ means life or tissue. ‘Opsis’ means vision
Grade II: Moderately differentiated—50% - or microscopy.
75% epithelial pearls.
Biopsy means study of tissues using micro-
Grade III: Poorly differentiated—25%
scopy.
epithelial pearls.
or life by vision
Grade IV: Dedifferentiated.
or vision for life (to save life).
Types of Biopsies
Incision biopsy. FNAC. Excision biopsy. Frozen section biopsy.
Trucut biopsy. Punch biopsy. Pap smear. Ultrasound guided biopsy.
CT guided biopsy. Laparoscopic biopsy. Thoracoscopic biopsy.
Endoscopic biopsy (gastroscopic or colonoscopic or through ERCP or through cystoscopy).
Proctoscopic biopsy.
Open biopsy either laparotomy or thoracotomy or craniotomy using Dandy’s brain cannula.
Incision Biopsy Disadvantage: Negative result cannot rule out
It is done from the edge of the lesion like an ulcer. malignancy.
It is not taken from the center, as there will be
central necrosis. Frozen Section Biopsy
Incision biopsy is contraindicated in It is done in carcinoma breast or in follicular
melanoma where excision biopsy is preferred. carcinoma of thyroid when FNAC fails.
Excision Biopsy II. IMMUNOHISTOCHEMISTRY

In small lesions excision biopsy is done. Lymph 1. To categorize leukemias or lymphomas. Either of
node biopsy is done in case of lymphoma. ‘T’ cell or ‘B’ cell.
2. To find out site of origin of metastatic tumors,
FNAC (Fine Needle Aspiration Cytology) e.g. by assessing levels of prostate specific
It is cytological study of tumor cell to find out antigen in prostate cancer or levels of
the disease and also to confirm whether it is thyroglobulin in thyroid carcinomas.
malignant or not. 3. Detection of receptors or molecules: For example
estrogen receptors in breast cancer. ER +ve
Procedure: It is done using 23 or 24 gauge needle
has got better prognosis. Presence of
with specialized syringes, which creates negative
oncoprotein product c—erbB2 in breast
pressure by aspiration and contents are smeared
cancer signifies poor prognosis.
in the slides. Dry slides as well as 100% methanol
are used for study.
III. TUMOR MARKERS
• It is done in parotid, thyroid, lymph node,
breast and all other surface lesions. Tumor markers are biochemical indicators of
• In follicular carcinoma of thyroid it is not very presence of a tumor. They are not used for
useful as angioinvasion and capsular primary pathological diagnosis. They are of
invasion which are specific cannot be prognostic value.
detected. Presence of tumor marker signifies
• In lymph node it is useful for secondaries and recurrence or residual tumor.
tuberculosis.
• Ultrasound guided or CT guided FNAC are Malignancies which are curable
popular at present. • Basal cell carcinoma.
It is absolutely contraindicated in testicular • Adamantinoma.
tumor. Because the tough tunica albuginea • Verrucous carcinoma.
usually prevents tumor spread and once FNAC • Marjolin’s ulcer.
disrupts it, spread can occur. • Papillary carcinoma of thyroid.
• Carcinoma colon.
Advantages
• Very sensitive. Sarcomas which spread to lymph nodes also
• Done on OP basis. • Synovial sarcoma.
• Least invasive. Safer. • Ewing’s sarcoma.
• Anesthesia is not required. • Lymphosarcoma.
• Tumor dissemination through the track is not • Kaposi’s sarcoma.
there (except in testicular tumor where it is • Rhabdomyosarcoma.
not done).
..One cannot make a slave of a free person, for a free person is free even in a prison.
—Pluto
Category 1
Hormonal
Human chorionic gonadotrophin [HCG]. Trophoblastic tumor, non seminomatous testicular tumor.
Calcitonin. Medullary carcinoma thyroid.
Catecholamines and VMA. Pheochromocytoma.
Ectopic hormones. In tumors of paraneoplastic syndromes.
Category 2
Isoenzymes
Prostatic acid phosphatase. Carcinoma prostate.
Neuron specific enolase. Small cell carcinoma lung, neuroblastoma.
Category 3
Oncofetal antigens
Alfa fetoprotein. Liver cancer, nonseminomatous germ cell tumor.
Carcinoembryonic antigen [CEA]. Carcinoma colon [common].
Carcinoma pancreas, lung, stomach and breast.
Category 4
Mucin and other glycoproteins
CA-125. (Carbohydrate antigen) Ovarian cancer.
CA-15-3. Breast cancer.
CA-19-9. Pancreatic and colon cancer.
SOFT TISSUE TUMORS (SARCOMAS) • Commonest sarcoma of bone is osteo-

sarcoma (Fig. 14.3).
FEATURES • Commonest soft tissue sarcoma is lipo-
• Sarcomas are much lesser in incidence sarcoma.
compared to carcinomas. • Usual clinical features are: Diffuse swelling
• It occurs in younger age group compared to which is smooth, hard, warm and very
carcinomas. vascular.
• They can arise from bone (osteosarcoma) or
Important features of sarcoma
from any soft tissues (soft tissue sarcomas)
(Fig. 14.2) (Mesenchymal tissue). • More aggressive.
• They are much more aggressive compared • Rapidly spreading.
to carcinomas. • Not very much radiosensitive.
• They are rapidly growing tumors with fleshy • Blood spread.
appearance. • Painless soft tissue mass is the presentation.
• They are not encapsulated but are having • Very vascular.
pseudocapsule.
• They spread through blood especially to Soft tissue sarcoma
lungs often also to other organs. • 1 % of adult malignancies.
• Lymphatic spread is not common with • 15 % of pediatric malignancies.
certain exceptions. • Incidence—
• They are not radiosensitive. • 35% occur in lower limb (commonest site).
• Main method of treatment is surgery, i.e. • 15% upper limb, 15% retroperitoneum.
wide excision, amputation. • 10% trunk, 10% viscera, 10 % other areas.
• In inoperable cases debulking is the accepted
• Soft tissue tumor > 5 cm size should be
method of treatment.
biopsied to rule out sarcoma.
• Chemotherapy is the adjuvant therapy.
Investigations
• Incision biopsy is the main method of
diagnosis.
• Excision biopsy is done if the tumor size is
< 3 cm.
• CT scan or MRI of the part to see the extent
Fig. 14.2: Soft tissue sarcoma foot. Note the vascularity and invasion.
• MRI is the investigation of choice as it deter-
mines the vascularity, relation to vessel and
fascial planes (Fig. 14.4).
• Chest X-ray is done to look for secondaries.
• CT chest is ideal to see early lung secondaries.
It is done in all deep-seated, high grade and
tumor more than 5 cm in size.
• Angiogram may be required to find out the
tumor vascularity.
• Radionuclide scintigraphy (Gallium-67).
Fig. 14.3: Osteosarcoma of the upper end of humerus in
an adolescent boy • -p-MRS (p-Magnetic Resonance Spectroscopy
and FDG (Fluor-2-Deoxy Glucose) PET are
Etiology done to assess the metabolic activity of tumor.
• Genetic—
• von Recklinghausen disease. Incision biopsy for soft tissue sarcoma
• Gardner’s syndrome. • It is the ideal tool to conclude sarcoma
• Tuberous sclerosis. histologically.
• Basal cell nevus syndrome. • Incision should be placed in such a way that
• Li-Fraumeni syndrome. it can be included in wide tumor excision at
• Chemicals—PVC, tetrachlorodibenzodioxin, later period.
arsenic. • Incision should be longitudinal in limbs
• Viral—HIV in Kaposi’s sarcoma. • Injury to vessels and nerves should be
• Ionizing radiation—Malignant fibrous histio- avoided.
cytoma(p53).
• Flaps should not be undermined.
• Adequate hemostasis is needed, as tumors
Clinical Features of Soft Tissue Sarcoma are vascular.
• Painless swelling of short duration with • Immunohistochemistry and cytogenetics are
progressive increase in size—soft tissue mass. possible and often essential.
• Compression of adjacent structures.
• Smooth, hard, warm and vascular. FNAC is less useful for sarcomas. Core/ Trucut
• Features of secondaries in lung—cough, biopsy can be done but not equal to incision
hemoptysis and chest pain. biopsy.
..Conflict is the primary engine of creativity and innovation.

—Ranold Heifetz
Staging of the soft tissue tumor is done depending on the tumor size, nodal status, metastasis and histological
grading of the tumor. (GTNM staging).
TNM staging of soft tissue sarcoma

Grade (G)Tumor (T)
Gx Cannot be assessed Tx Cannot be assessed
G1 Well-differentiated T0 No primary
G2 Moderately differentiated T1 Size < 5 cm or 5 cm (maximum dimension)
G3 Poorly differentiated T1a: Superficial T1b: Deep tumor
G4 Undifferentiated T2 Size > 5 cm
T2a: Superficial T2b: Deep tumor
Regional lymph nodes (N) Distant spread (M)

Nx Nodes cannot be assessed Mx Cannot be assessed
N0 No nodes M0 No distant spread
N1 Nodes present M1 Distant spread present
Malignant fibrous
histiocytoma,
Extraosseous
chondrosarcoma.
Undetermined Fibrosarcoma,
Leiomyosarcoma.
Differential diagnosis for soft tissue sarcoma

• Hematoma.
• Abscess.
• Aneurysm.
• Myositis.
• Recurrence of sarcoma (Fig. 14.5)
Fig. 14.4: MRI picture of the soft tissue tumor thigh encasing
vessels partially and eroding the bone. Patient needed high
level above knee amputation
Note: Superficial tumor is outside the superficial

fascia. Deep tumor is deep to superficial fascia or any ‘
tumor invading the superficial fascia.
Grading of sarcomas
Low Desmoid,
Dermatofibrosarcoma,
Liposarcoma.
High Synovial,
Fig. 14.5: Recurrent chest wall tumor, could be secondary
Rhabdomyosarcoma,
as patient was earlier amputated for soft tissue tumor hand
Angiosarcoma, (forearm amputation)
Treatment
• Wide excision is the treatment of choice with
3–5 cm clearance with adequate depth.
• Compartment resection is a radical limb
saving procedure. Here muscle group of one
compartment (anterior, posterior or medial)
is resected entirely from its origin to insertion
with the tumor. It is done only when tumor
is intracompartmental. It is not suitable when
tumor is extracompartmental or many
compartments are involved or encased to Fig. 14.6: Osteosarcoma upper tibia
with tumor fungation
major neurovascular bundle.
• Amputation is done in large tumors of upper • Primary radiotherapy alone (radical) is of less
or lower limbs. beneficial in soft tissue sarcoma.
• Chemotherapy drugs VAC are (Vincristine,
Indications for amputations in soft tissue
Adriamycin, Cyclophosphamide) commonly
sarcoma
used. Other drugs used are Ifosamide,
• Major neurovascular encasement.
Dacarbazine in combination with above
• Bone involvement (Fig. 14.6).
drugs. Mesna is used as a protection for
• Multiple compartment involvement.
hemorrhagic cystitis. Chemotherapy is used
• Limb itself is diseased like lymphedema.
when tumor is more than 5 cm or high grade.
• Recurrence with multicentricity.
Usually postoperative chemotherapy is
• Debulking surgery is useful in large advan-
given.
ced tumors like retroperitoneal sarcomas.
• Neoadjuvant chemotherapy is used to make the
• Preoperative radiotherapy or chemotherapy primary tumor better operable.
followed by wide excision. • Isolated limb perfusion using cytotoxic drugs and
• Postoperative radiotherapy is commonly tumor necrosis factor with hyperthermia is also
used because of less tumor burden and less often used.
wound problems. During surgery titanium • Pulmonary metastasis can be treated with
clips are placed at high-risk areas to identify wedge resection, segmentectomy, lobectomy,
the sites to concentrate proper RT. pneumonectomy. Surgery is done only when
— Brachytherapy is very effective in local primary is well-controlled. Radiotherapy and
control of the tumor. Initially precise map- chemotherapy are also tried. Metastases in
ping of the area is done in the operation lung more than 3 number signifies poor
theater. After loading catheters are placed in prognosis.
surgical field peroperatively. Later these
catheters are loaded with iridium 192. Prognostic factors
— Permanent radioactive sources also can • Size > 5 cm.
be placed to the area. • High grade.
— Palliative external radiotherapy can be • More than one compartment involvement.
given to prevent bleeding, fungation and • Deep tumors and multicentric.
to reduce pain in advanced cases. It is also • Neurovascular invasion.
• Lung secondaries.
used in secondaries in brain and bone.
..To strengthen your heart, forgive yourself and others.

LIPOSARCOMA Clinically it is smooth, hard, warm, localized
It is the commonest type of soft tissue sarcoma tumor.
arising from the fat cells (of primitive mesen- It compresses or infiltrates the adjacent
chymal cells). structures like neurovascular bundle.
It can occur as de novo or from a pre-existing
lipoma.
Common Sites
• Retroperitoneum.
• Thigh.
• Back.
• Shoulder.
Types
• Well-differentiated.
• Myxoid.
• Round cell.
• Pleomorphic has got poor prognosis.
Microscopically it contains lipoblasts with
’signet ring’ malignant cells. It is low grade type.
Spread is to lungs.
Treatment is wide excision or radiotherapy
Fig. 14.7: Dermatofibrosarcoma protuberance
with surgical debulking in places where comp- over left chest wall
lete removal of tumor is not possible like in
retroperitoneal liposarcoma.
MALIGNANT HISTIOCYTOMA
FIBROSARCOMA
It arises from histiocytes.
• It can arise from the bone or from soft tissues
(Fig. 14.7). LEIOMYOSARCOMA
• It is the next common soft tissue malignancy
after liposarcoma. • It arises from smooth muscle. Cut section
• It is arising from fibroblasts. shows whorled appearance.
• Commonest site is thigh. • It is of undetermined grade.
• Spindle fibroblasts with ‘herring bone’ pattern • It is common in retroperitoneum and viscera,
is typical feature on microscopy. but can occur in limbs and skin.
• Recurrence is common. It has got poor
Types prognosis.
• Well-differentiated.
• Poorly differentiated. RHABDOMYOSARCOMA
• Dermatofibrosarcoma protuberance. It is
common in trunk. It arises from striated muscle. It is common in
• Aggressive fibromatoses are variant of head and neck, upper thigh and arm.
fibrosarcoma, which are locally malignant in
Types
which desmoid tumor is also included.
Fibrosarcoma are slow growing tumor, 1. Pleomorphic—commonest type of rhabdo-
which attains large size. myosarcoma.
2. Embryonal—common in infants and children. It produces pain, tenderness and pares-
3. Botryoidal. thesia.
4. Alveolar.
It is more aggressive tumor with poorer KAPOSI’S SARCOMA
prognosis (High grade).
It is malignant blood vessel tumor of multicentric
It also metastasizes to lymph nodes.
origin arising from vascular smooth muscle or
pericytes.
CHONDROSARCOMA
It is seen commonly in HIV patients due to
• It arises from chondroblasts. immunosuppression.
• It attains large size with slow growing nature. Primary tumor commonly occurs in skin,
• Common sites are ribs, flat bones. mucous membrane, lymph nodes or viscera.
It is linked with Human Herpes Virus 8
HEMANGIOSARCOMA (HHV8) as causative agent.
It originates from blood vessel endothelium.
Types
Types • European Kaposi’s sarcoma: It is common in
• Malignant hemangioendothelioma. old age. Kaposi first described it in 1862. It
• Malignant hemangiopericytoma. mainly involves skin especially of lower
extremity. Visceral involvement is rare.
LYMPHANGIOSARCOMA • African Kaposi’s sarcoma: It occurs com-
monly in children and young individual. It
It arises from lymph vessel endothelium.
commonly involves skin and lymph nodes.
It commonly occurs after radical lymph node
It resembles lymphoma.
dissection.
• Transplant associated Kaposi’s sarcoma: It is
due to drug- induced immunosuppression.
SYNOVIAL SARCOMA
It involves mainly skin and often regresses
• It originates from synovial cells. once immunosuppression is discontinued.
• It is common in thigh, leg, shoulder, hand • AIDS associated Kaposi’s sarcoma: It occurs
and foot. in 30–40% of AIDS patients. It is common in
• Occasionally it can occur in the abdominal homosexuals. It has got wide, disseminated
wall and retroperitoneum. involvement with metastases. It is very
• It is common in young individuals. aggressive. It is often associated with
• It occurs adjacent to joint but uncommon to lymphoma and other malignancies.
involve the synovial sheath of the joint.
• It spreads both through blood as well as Clinical Features
through lymph nodes (20%). • Multiple reddish-blue nodules in the skin
• It is very aggressive soft tissue sarcoma (High with ulceration over the nodule.
grade). • Lymph node enlargement.
• Koebner phenomenon is common in areas of
MALIGNANT NEURILEMMOMA trauma.
It is commonly associated with multiple
neurofibromatosis of von Recklinghausen’s Differential Diagnosis
disease. • Lymphomas.
..Modern man lives increasingly in the future and neglects the present.
• Cutaneous angiomatoses. • Antiretroviral therapy.
• Mycobacterial infection of skin. • Interferons.
Investigations Sarcomas, which also spread through lymph

nodes
• Biopsy from the skin lesion. • Synovial sarcoma.
• Tests for HIV infection. • Lymphangiosarcoma.
• Rhabdomyosarcoma—alveolar type.
Treatment • Ewing’s sarcoma.
• Irradiation. • Angiosarcoma.
• Chemotherapy. Drugs used are Adriamycin, • Epithelioid sarcoma.
Bleomycin and Vinblastine. • Carcinosarcoma of uterus.
Skin Tumors 193
15 Skin Tumors
 Classification of skin tumors Dermal

 Skin adnexal tumors • Neurofibroma.
 Dermatofibroma • Dermatofibroma.
 Dermatofibrosarcoma protuberance Malignant
 Keratoacanthom (molluscum sebaceum)
• Squamous cell carcinoma.
 Rhinophyma (Potato nose)
• Basal cell carcinoma.
 Premalignant conditions of the skin • Melanoma.
 Squamous cell carcinoma (epithelioma) • Malignant skin adnexal tumor.
 Marjolin’s ulcer • Secondaries in the skin—Sister-Joseph
 Basal cell carcinoma (Rodent ulcer) nodules around umbilicus.
 Nevi
 Melanoma SKIN ADNEXAL TUMORS
• They are tumors arising from accessory skin
CLASSIFICATION OF SKIN TUMORS structures like sebaceous glands, sweat
glands, hair follicles, etc.
Benign • It is not uncommon. It may be benign or
malignant.
Epidermal • It presents as protruding well-localized
• Seborrheic keratosis. swelling in the skin.
• Trichilemmal tumor. • Malignant skin adnexal tumor forms a
• Sebaceous adenoma. nodular, hard, indurated swelling in the skin,
• Sebaceous epithelioma. often with involvement of hard, nodular
• Hydrocystoma, syringoma, spiradenoma. regional lymph glands.
..A man with one watch knows what time it is; a man with two watches is never sure.
—Unknown
• It mimics squamous cell carcinoma of
skin.
• Squamous cell carcinoma of skin.
• Dermatofibrosarcoma protuberans.
Diagnosis
• Biopsy.
• FNAC of lymph node.
Fig. 15.1: Dermatofibrosarcoma
Treatment
• Excision of benign tumor. • Rarely it spreads into lungs through blood.
• Wide excision and regional lymph node block • It mimics squamous cell carcinoma of skin,
dissection when required. and skin adnexal tumor.
Diagnosis
DERMATOFIBROMA • Biopsy of the lesion.
(Sclerosing angioma or subepithelial benign • Chest X-ray, CT scan chest.
nodular fibrosis). • FNAC of the lymph node.
• It is a benign tumor arising from skin.
• It is formation of firm, single or multiple Treatment
nodules occurring commonly in extremities • Wide excision and follow up.
(limbs). • Recurrence is common.
• It can be red, brownish yellow (due to lipid), • Prognosis is good.
or bluish black (due to hemosiderin).
KERATOACANTHOMA
Differential Diagnosis (Molluscum Sebaceum)
• Squamous cell carcinoma of skin. • It is an overgrowth and subsequent spon-
• Melanoma. taneous regression of hair follicle commonly
• Basal cell carcinoma. seen in adults.
• Skin adnexal tumor. • Cause is unknown. It may be self-limiting
benign neoplasm of viral origin.
Treatment • It presents as a rapidly growing, painless,
Excision. single swelling in the skin with central brown
area.
• It grows usually for 4 weeks and later shows
DERMATOFIBROSARCOMA
spontaneous regression in 4 months.
PROTUBERANCE • During regression phase, central area
• It is a low-grade fibrosarcoma, which grows separates from the lesion leaving a deeply
slowly but persistently. seated scar.
• Occurs in the limb, abdominal wall, and back • Mobile, hard, painless, nontender, lump with
(Fig. 15.1). a central brownish area.
• It is not a rare entity, often attains a large size • No lymph nodes are enlarged.
with multiple, nodular, hard, swelling with • It is a benign condition. It mimics squamous
often involvement of lymph nodes. cell carcinoma.
Skin Tumors 195
• Treatment is excision. Always specimen • Radiodermatitis.
should be sent for histopathological study • Chronic scars develop into Marjolin’s ulcer.
after excision. • Xeroderma pigmentosa wherein there is
defective DNA excision repair mechanism.
It turns into malignant melanoma.
RHINOPHYMA (Potato Nose)
• Chronic lupus vulgaris.
• It is a glandular form of acne rosacea causing • Prolonged irritation of skin by various
immense thickening of distal part of skin of chemicals like dyes, tar, soot, etc.
nose with visible openings of sebaceous
follicles. Nose is bluish red in color with SQUAMOUS CELL CARCINOMA
dilated capillaries (Fig. 15.2). (EPITHELIOMA) (FIGS 15.3 AND 15.4)
• It occurs in premalignant conditions like
Bowen’s disease, chronic scars, chemically
induced chronic irritation, radiodermatitis,
senile keratosis.
For example Khangri cancer in Kashmir,
Chimney scrotal cancer, Kang cancer of
Tibetans.
• It is arising from squamous layer of the skin.
Etiology of SCC
• Bowen’s disease.
• Chronic scars and sinuses.
• Lupus vulgaris.
• Solar keratosis.
• Chemically induced chronic irritation.
Fig. 15.2: Typical rhinophyma
• Radiodermatitis.
• Kangri cancer is due to constant placing of the
PREMALIGNANT CONDITIONS hot charcoal pot(kangri) over the abdominal
OF THE SKIN wall to control cold. Seen in Kashmir.
• Bowen’s disease of skin: It is an intradermal • Kang cancer is seen in buttocks and heel of
precancerous condition. It presents as Tibetians due to sleeping over oven bed to
brownish induration with a well-defined control cold.
edge. Microscopically it contains large clear • Chimney sweep cancer is observed in
cells. Eventually it turns into carcinoma. scrotum due to constant irritation by tar.
• Paget’s disease of nipple. SCC is more common in immunosuppressed
• Leukoplakia. individuals.
• Senile or solar keratosis: It is multiple, dry,
hard, scaly, lesions in face and back of hands
due to exposure to sunlight, occurs after Clinical Features
middle age. Squamous cell carcinoma occurs • An ulcerative or ulceroproliferative lesion.
later. • Raised and everted edge.
..Time does not heal, it merely tucks the pain away into the recesses of memory.
—Maureen Murari
Figs 15.3A and B: Squamous cell carcinoma in (A) Foot (B) Hand
• Indurated.
• Bloody discharge from the lesion.
• Regional lymph nodes are commonly
involved with hard, nodular features, initially
mobile but eventually fixed to underlying
structures.
• Usually no blood spread.
Variants
• Marjolin’s ulcer, which occurs in chronic scar,
is a type of squamous cell carcinoma
without lymph node spread.
• Verrucous carcinoma is a squamous cell
carcinoma, commonly occurs in mucous
membrane or mucocutaneous junction
without lymph node spread. It is dry
exophytic, warty, indurated growth. It has
got good prognosis. It is curable malignancy.
Fig. 15.4: Squamous cell carcinoma in the plantar aspect
of the foot. Note the proliferative cauliflower like lesion
Histology
Whorls of malignant squamous cells with • Keratoacanthoma.
epithelial or keratin pearls are characteristic. • Skin adnexal tumors.
Broder’s classification Investigations

I: Well-differentiated. 75% keratin pearls. • Edge biopsy.
II: Moderately differentiated: 50% keratin • FNAC from lymph node.
pearls.
III: Poorly differentiated: 25% keratin pearls. Treatment
• Radiotherapy using radiation needles
Differential Diagnosis moulds, etc.
• BCC. • Wide excision.
• Melanoma. — Amputation with one joint above.
Skin Tumors 197
— When lymph nodes are involved, block Biopsy from the edge: Confirms the diagnosis.
dissection of the regional lymph nodes
(like of ilioinguinal dissection, axillary Treatment
dissection or neck node dissection • Wide excision.
depending on the location of primary • If ulcer is large, amputation is required.
tumor and site of secondaries) is done. • Radiotherapy should not be given as it may
• In advanced disease with fixed lymph nodes, turn into poorly differentiated squamous cell
palliative external radiotherapy is given to carcinoma.
palliate pain, fungation and bleeding. • It is curable malignancy.
• Chemotherapy is given using Methotrexate,
Vincristine, Bleomycin, Cisplatin or 5-
fluorouracil.
BASAL CELL CARCINOMA
(RODENT ULCER) (FIG. 15.6)
MARJOLIN’S ULCER (FIG. 15.5) It is a low grade, locally invasive, carcinoma
• It is a well-differentiated squamous cell arising from basal layer of skin or muco-
carcinoma, which occurs in chronic scars like cutaneous junction. It does not arise from
burn scar, scar of venous ulcer. mucosa.
• As it develops in a scar due to chronic It is more common in white skinned people
irritation and as there are no lymphatics in than blacks. Common in places where exposure
scar tissue, it will not spread to lymph nodes. to UV light is more (Australia). It is common
• Because scar is relatively avascular it grows in males, in middle-aged and elderly.
slowly. As scar does not contain nerves, it Common site of occurrence is face (Fig. 15.7)–
is painless. above the line drawn between angle of mouth
• Once it reaches the normal skin it may behave and ear lobule. It is called as tear cancer because
like any other squamous cell carcinoma, i.e. it is commonly seen in area where tears roll
it will spread to lymph nodes. down. Often can occur in mucocutaneous
junctions.
Clinical Features
• History of pre-existing venous ulcer or burn.
• Indurated, painless, nontender, ulcer with
raised and everted edge.
Fig. 15.5: Marjolin’s ulcer in a long standing ulcer over elbow Fig. 15.6: Basal cell carcinoma
..A = x+y+z; A = success, x = work, y = play, z = keep your mouth shut.

—Albert Einstein
Fig. 15.7: Note the common site of BCC—in the face Fig. 15.8: Rodent ulcer lateral aspect of the eyebrow. Note
above the between angle of mouth and ear lobule the typical beaded edge
It is only locally malignant. It does not • Morphia type.

spread through lymphatics or through the blood. It contains malignant cells arranged as outer
But it erodes deeply into local tissues including palisading columnar cells with central poly-
cartilages, bones causing extensive local hedral cells without prickle cells or keratinization.
destruction (Fig. 15.8). Hence the name ‘rodent
ulcer’. Clinical Features
• Slowly growing ulcer on the face in a middle-aged
Types man, which is nontender, dry, and nonmobile,
• Nodular. with raised and beaded edge and central scab.
• Cystic. • Site of beading signifies the area of active
• Ulcerative. proliferating cells. In between beaded areas
• Multiple, often associated with syndromes dormant nonactive cells are present.
and other malignancies. • No lymph node or blood spread.
• Pigmented BCC—mimics melanoma.
• Geographical or field fire or forest fire BCC Differential Diagnosis
is wide area involvement with central • Squamous cell carcinoma.
scabbing and peripheral active proliferating • Melanoma.
edge. • Keratoacanthoma.
• Basisquamous BCC—behaves like squa-
mous cell carcinoma with spread into lymph Investigations
nodes. BCC, which has not been treated for Edge biopsy, X-ray of the part.
long time can turn into basisquamous
carcinoma. Treatment
It is radiosensitive. If lesion is away from vital
Microscopic Types structure (like away from eyes), then curative
• Superficial type. radiotherapy can be given.
Skin Tumors 199
Radiotherapy is not given once it erodes
cartilage or bone.
Surgery: Wide excision (with 2 cm clearance)
with skin grafting or flap is the procedure of
choice.
Laser surgery.
Cryosurgery.
MOHS (Microscopically Oriented Histo-
graphic Surgery).
Indications for surgery:
• Rodent ulcer eroding into cartilage or bone.
• BCC close to the eye.
• Recurrent BCC.
NEVI
It is a hamartomata of melanocytes due to
excessive stimulation.
It may present during birth or appear later
in life.
Types (Fig. 15.9)

• Hairy mole is a mole with a hair growing on
its surface.
• Nonhairy mole.
• Blue nevus—It is seen in children. It is located
deep in the dermis, hence appears blue. It is Fig. 15.9: Different types of nevi
common over buttock (Mongolian spot),
hand, feet.
• Junctional nevus—It is centered in the • Juvenile melanoma—It is appearance of
junctional layer (basal layer) of the epidermis junctional like mole before puberty. It is seen
as clusters. It is immature, unstable and in children over the face.
premalignant. Microscopically there is • Hutchinson’s freckle—It is seen in elderly
proliferation of melanocytes at the epidermal with large area of dark pigmentation. In the
junction. Features of malignant transfor- macular stage, it is smooth and brown. In the
mation are—change in the size, color, tumor stage, it is dark and irregular. It
bleeding, ulceration, crusting, satellite spots. commonly turns into melanoma.
• Compound nevus—It is combination of
intradermal and junctional nevus. Treatment
Intradermal part is inactive but junctional Excision. The tissue always should be sent for
part is potentially malignant. histopathology.
..The vehicle in front of you is always traveling slower than yours.

MELANOMA Classifications
• It is a malignant tumor arising from the
epidermal melanocytes. Breslow’s classification: Based on thickness
of invasion measured by optical micrometer.
• Its incidence is equal in both sexes. Its
I: Less than 0.75 mm.
incidence is increasing over the years.
II: Between 0.76 to 1.5 mm.
• It is the most aggressive malignant cutaneous III: 1.51 mm to 4 mm.
tumor. IV: more than 4 mm.
Sites (Figs 15.10 to 15.12) Clark’s levels (Fig. 15.14)

• In females leg is the commonest site. Level 1: Only in epidermis.
• In males it is front or back of the trunk. Level 2: Extension into papillary dermis.
• In the Bantu tribe, sole is the commonest site. Level 3: Filling of papillary dermis completely.
• Other sites—Eyes, mucocutaneous junction, Level 4: Extension into reticular dermis.
Level 5: Extension into subcutaneous tissue.
meninges, anus and mouth.
Clinical Types
Risk Factors
1. Lentigo maligna melanoma: 7–15%. Least
• Exposure to sunlight. common, least malignant. Occurs in old age and
• Ethnic factors, socioeconomic status, life style, common in face. (Hutchinson’s melanotic
climate. freckle).
• Albinism, family history. 2. Superficial spreading: Most common. 64%.
• Xeroderma pigmentosa (Fig. 15.13). Occurs in any part of the body with
• Junctional nevus. variegated irregular look.
Figs 15.10A and B: Oral melanoma in (A) Lip (B) Tongue
Fig. 15.11: Large melanoma in the sole. Note the pigmentation

Skin Tumors 201
Figs 15.12A and B: (A) Melanoma foot (B) LN secondaries
Fig. 15.14: Clark’s level
5. Amelanotic melanoma: This is the worst form.

Because of the undifferentiation, tumor cells
loose their capacity to synthesize melanin. It
presents as pinkish fleshy growth which is
rapidly progressive. It may mimic soft tissue
sarcoma.
Clark’s concept: Initial radial growth phase that
Fig. 15.13: Xeroderma pigmentosa with BCC in the nose. occurs horizontally and later vertical growth
Such patients are prone for other malignancies of phase with invasion.
skin like melanoma also. There is defective DNA excision
repair Clinical Features
• It can start in a pre-existing nevus (commonly
junctional nevus)—90% or as de novo in a
3. Nodular melanoma: 12–25%. more malignant normal skin—10%.
than the above two. It is common in younger • Melanoma is unknown before puberty.
age group, occurring in any part of the body. • Pigmentation with irregular surface and
4. Acral lentiginous melanoma: Occurs in margin with rapid growth.
palms, soles and subungual region. Common • Ulceration, bleeding, itching, changes in the
in Japan. It has got a poor prognosis. color.
..Smart people speak from experience. Smarter people, from experience do not speak.
• When a mole becomes malignant following
changes should be observed.
— Major signs: Change in size, shape and
color.
— Minor signs: Inflammation, crusting,
bleeding, itching, diameter more than
5mm, halo around a mole.
• No induration in melanoma.
Spread
• Through lymphatics it spreads to regional
lymph nodes either by permeation or by
embolization.
Intransit nodules or satellite nodules in the skin
between primary and regional lymph node Fig. 15.15: Secondaries in inguinal lymph nodes from a
area is often seen due to retrograde spread primary in the leg
to dermal lymphatics.
• Through blood: To lungs (cough with hemo- Staging of malignant melanoma
ptysis), liver (massive enlargement of liver), IA: Thickness less than 0.75 mm.
brain (convulsions, raised intracranial IB: Thickness between 0.76 to 1.5 mm.
pressure), skin, bones (paraplegia if spine IIA: Thickness between 1.51 to 4.0 mm.
is involved, pathological fracture, bone pain). IIB: Thickness more than 4.0 mm.
Secondaries are typically black in color. IIIA: Any of the above+ nodes less than 3 cm.
Extensive visceral involvement causes III B: ,, + nodes more than 3 cm.
melanuria. IV: ,, + any node + M1 (distant spread).
• Sometimes primary is very small and so
unnoticed (in anus, subungual region). They Investigations
present with features of secondaries only
(Fig. 15.15). • No incision biopsy: Incision biopsy may
accelerate the blood spread.
Melanoma • Excision biopsy of the primary.
• Incidence —5% of all skin cancers. • FNAC of lymph node.
• 20 times more common in whites than blacks. • Ultrasound abdomen to see liver secondaries
• Mucosal melanoma has got poor prognosis. (usually huge hepatomegaly occurs).
• Chest X-ray to see secondaries.
• Can spread from mother to fetus.
• Other relevant methods depending on site
• Multiple melanomas are 1% common.
and spread.
• Melanoma in retina will not cause lymph
• Urine for melanuria.
node involvement, as retina has no lymphatic
• Sentinel lymph node biopsy (SLNB).
drainage.
• 10% of melanomas are familial. Treatment
• Satellite nodules are secondary skin nodules
Surgery: Is the main treatment.
within 2 cm of primary.
• Intransit nodules are secondary skin nodules For Primary
beyond 2 cm of primary any where up to • Wide excision, with a clearance margin of 3–
lymph node region. 5 cm. (Presently extent of margin of clearance
is controversial).
Skin Tumors 203
• If wider area is involved, then amputation For Locoregional recurrent melanoma:
with one joint above. • Isolated limb perfusion using cytotoxic agents
• In fingers and toes, disarticulation is required. like DTIC, Melphalon.
• Melanoma in anal canal may require • Laser ablation of multiple small cutaneous
abdominoperineal resection. lesions.
• Enucleation of eye in case of melanoma in eye.
For lymph node secondaries Chemotherapy
• In a clinically palpable lymph node, FNAC Indications:
of lymph node is done, the spread is • In secondaries in lungs, liver, bones.
confirmed and then regional block dissection • Postoperatively after surgery for melanoma.
is done, i.e. Ilioinguinal or axillary or neck. Usually it is given intravenously.
• In a fixed lymph node, only chemotherapy Drugs are: DTIC: Diethyl Trimethyl Immino
is the treatment because it is inoperable. Carbazine.
• Lymphatic mapping and sentinel node biopsy: Melphalon (Phenyl alanine mustard).
Radioactive colloid is injected around (Melphalon for Melanoma).
primary site and lymphoscintigraphy is done
using hand held gamma camera to visualize Immunotherapy
the micrometastasis in the nodal field. If there BCG and specific tumor antibodies through
is micrometastasis then regional block melanoma antigens are beneficial.
dissection is done. Radiotherapy has no role, as melanoma is
• Prophylactic regional block dissection, which radioresistant.
was previously advocated is now contro- Prognosis is not good since it is very
versial. But still used in many centers. aggressive tumor.
..Make sure you have finished speaking before your audience has finished listening.
—Dorothy Sarnoff
16 Neck
 Anatomy of lymphatics of head and neck

 Branchial cyst
 Branchial fistula
 Pharyngeal pouch
 Laryngocele
 Cystic hygroma
 Ludwig’s angina
 Parapharyngeal abscess
 Retropharyngeal abscess
 Carotid body tumor
(Potato tumor, chemodectoma,
non-chromaffin paraganglioma)
 Torticollis (Wry neck)
 Sternomastoid tumor Fig. 16.1: Inner and outer Waldeyer’s ring
 Subhyoid bursitis
 Secondaries in neck lymph nodes
ANATOMY OF LYMPHATICS OF Facial nodes are

HEAD AND NECK a. Superficial—
• Upper-infraorbital.
Inner Lymphatic Ring (Inner Waldeyer’s Ring)
• Middle-buccinator.
It consists of adenoids above, lingual tonsils • Lower-supramandibular.
below and two palatine tonsils laterally, one on b. Deep groups—in relation to pterygoids.
each side (Fig. 16.1).
Submandibular lymph nodes drain
Outer Circular Chain of Nodes
(Outer Waldeyer’s Ring) (Fig. 16.2) • The side of the nose.
It consists of occipital, postauricular, preauri- • The cheek.
cular, parotid, facial, submandibular, submental, • Angle of the mouth.
superficial cervical and anterior cervical nodes. • Entire upper lip.
Neck 205
• Outer part of the lower lip. BRANCHIAL CYST (FIG. 16.3)
• The gums. It arises from the remnants of second branchial
• Side of the tongue. cleft. Normally 2nd, 3rd, 4th clefts disappear to
Submental lymph nodes drain from the central form a smooth neck. Persistent 2nd cleft is called
part of the lower lip, floor of the mouth and apex as cervical sinus, which eventually gets
of the tongue. sequestered to form branchial cyst.
Superficial cervical nodes. They lie on outer
surface of the sternomastoid around the external Clinical Features
jugular vein. They drain the parotid region and • Swelling in the neck beneath the anterior
lower part of the ear. border of upper third of the sternomastoid
Deep cervical lymph nodes. muscle.
• Upper deep cervical lymph nodes—jugulo- • It is smooth, soft, and fluctuant, often
digastric nodes. transilluminant.
• Lower deep cervical lymph nodes—jugulo- • It contains cholesterol crystals.
omohyoid nodes.
They drain ipsilateral half of head and neck;
finally form a jugular lymph trunk from lower
deep cervical to join thoracic duct on the left side;
junction of right subclavian and right jugular
vein on right side.
Fig. 16.2: Lymphatic drainage in the neck Fig. 16.3: Branchial cyst
..In order to succeed, your desire for success should be greater than your failure.
—Bill Cosby
Histologically, it is lined by squamous PHARYNGEAL POUCH
epithelium.
It is a protrusion of mucosa through Killian’s
Differential Diagnosis dehiscence, a weak area of the posterior pharyn-
geal wall between thyropharyngeus (oblique fibers)
• Cold abscess. and cricopharyngeus (transverse fibers) of the
• Lymph cyst. inferior constrictor muscle of the pharynx.
It may get infected to form an abscess.
FNAC shows cholesterol crystals.
Treatment
Excision under G/A.
Cyst is in relation to carotids, hypoglossal
nerve, glossopharyngeal nerve, spinal accessory
nerve, and posterior belly of digastric, and
pharyngeal wall. Medially it is close to the
posterior pillar of tonsils. During dissection, all
these structures should be taken care off.
BRANCHIAL FISTULA
It is a persistent second branchial cleft with a
communication outside to the exterior. It is
commonly a congenital fistula. Occasionally the
condition is secondary to incised, infected
branchial cyst. Often it is bilateral. Fig. 16.4: Pharyngeal pouch (Zenker’s diverticulum)
External orifice of the fistula is situated at the
lower third of the neck near the anterior border of Imperfect relaxation of the cricopharyngeus
the sternomastoid muscle. increases the pressure in the pharynx, mainly
Internal orifice is located on the anterior aspect during swallowing which leads to protrusion of
of the posterior pillar of the fauces, just behind mucosa through the Killian’s dehiscence causing
the tonsils. pharyngeal pouch (Fig. 16.4).
Sometimes fistula ends internally as blind The protrusion is usually towards left.
end.
Track is lined by ciliated columnar epithelium Stages
with patches of lymphoid tissues beneath it, 1. Small diverticulum.
causing recurrent inflammation. 2. Large, globular diverticulum causing
Discharge is mucoid or mucopurulent. regurgitation, cough, dysphagia, respiratory
infection.
Investigations: Discharge study, fistulogram.
3. Large pouch, which is visible in the neck as
Treatment: Always surgery. a globular swelling often tender, smooth and
Under G/A after passing a probe, fistula is soft. They present with dysphagia, features
excised across its full length, up to its internal of respiratory infection like pneumonia and
opening. Care should be taken to safeguard lung abscess, weight loss and cachexia. Pouch
carotids, jugular vein, hypoglossal nerve, may get infected and may form an abscess.
glossopharyngeal nerve, and spinal accessory Often the pouch descends downward and
nerve. Track should be excised fully. enters the superior mediastinum.
Neck 207
Clinical Features • Pharyngeal fistula.
Pain, dysphagia, recurrent respiratory infection, • Abscess in the neck.
swelling in the neck on the left side, which is
smooth, soft and tender. LARYNGOCELE
• It is a unilateral narrow necked, air containing
Investigations
diverticulum resulting from herniation of
Barium swallow—Lateral view shows pharyngeal laryngeal mucosa (Fig. 16.6).
pouch (Fig. 16.5). • It is situated in the anterior third of the
Chest X-ray shows pneumonia. laryngeal ventricle, between the false cords
and thyroid cartilage, herniates through the
thyrohyoid membrane.
• It occurs in professional trumpet players, glass
blowers, and in people with chronic cough.
Fig. 16.6: Diagrammatic representation of laryngocele

Fig. 16.5: Barium swallow showing pharyngeal pouch
Clinical Features
Treatment • Swelling in the neck in relation to larynx
adjacent to thyrohyoid membrane, which is
Antibiotics has to be started. smooth, soft, and resonant and is more
Pharyngeal pouch is excised by an oblique neck prominent while blowing (Fig. 16.7).
incision (approach from neck). As there is • Infection is quite common in the sac of
cricopharyngeal spasm, cricopharyngeal myotomy laryngocele, leading to the blockade of
(i.e. cutting of cricopharyngeal circular muscle opening of the sac causing an abscess.
fibers without opening mucosa) is done to • Pus often may be discharged into the pharynx
prevent the recurrence. repeatedly.
Complications Diagnosis
• Infection either mediastinitis or lung infection Clinical features, X-ray neck, laryngoscopy, CT
(Pneumonia or lung abscess). scan.
..Discussion is an exchange of knowledge; argument is an exchange of ignorance.

—Unknown
Treatment
Excision through neck incision. Neck of the sac
should be ligated.
CYSTIC HYGROMA (CAVERNOUS

LYMPHANGIOMA) (FIG. 16.8)
It is a cystic swelling due to sequestration of a
portion of jugular lymph sac from the lymphatic
system, during the developmental period in utero.
Present during birth and so may cause
obstructed labor. Occasionally present in early
infancy.
Sites
• Posterior triangle of the neck—commonest site.
Eventually may extend upwards in the neck.
• Cheek.
• Axilla.
• Tongue—lymphangiogenetic macroglossia.
• Groin.
• Mediastinum.
• Often multiple sites.
Figs 16.7A to C: Laryngocele in a patient which increases

in size after nasal blowing. X-ray picture of same patient Fig. 16.8: Cystic hygroma
Neck 209
Pathology Extension of infection into parapharyngeal space
It contains aggregation of cysts looking like soap may lead to dreaded internal jugular vein
bubbles. Cysts have mosaic appearance with larger thrombosis.
cysts near the surface and smaller cysts in the As the infection is deep to the deep fascia in
deeper planes. Each cyst contains clear lymph a closed fascial plane, it spreads very fast causing
with endothelial lining. dangerous complications.
Clinical Features
Clinical Features
Fever, toxicity, diffuse swelling, dysphagia,
• Swelling is present since birth in the posterior
dyspnea, trismus.
triangle of neck causing obstructed labor.
• Swelling is smooth, soft, fluctuant (cystic). Treatment
compressible, and brilliantly transilluminant.
• Antibiotics.
• Swelling may rapidly increase in size causing
• IV fluids.
respiratory obstruction—dangerous sign.
• Making a deep incision extending into the deep
• It may get infected forming an abscess, which
fascia and also cutting both the mylohyoid
is a tender, warm, soft swelling. It may cause
muscles, decompression of the submandibular
septicemia, which may be life threatening.
region is done. Either it is left open and delayed
suturing is done, (better option) or it is loosely
Treatment
sutured (Fig. 16.9).
• Aspiration of the contents. Later once the sac
or capsule gets thickened by fibrous tissue, Complications
it is excised. • Laryngeal edema and respiratory distress,
• When it causes respiratory obstruction, may require tracheostomy.
aspiration and tracheostomy has to be done. • Septicemia.
• Under proper antibiotics coverage, drainage • Extension of infection into parapharyngeal
of abscess is done. Later sac is excised. space.
Complications
• Respiratory distress.
• Infection → Abscess → Septicemia.
• Surgery itself may cause torrential hemorr-
hage.
LUDWIG’S ANGINA
It is an inflammatory edema of submandibular
region and floor of the mouth, commonly due
to streptococcal infection.
It causes diffuse swelling and brawny edema
of the submandibular region.
It is common in severely ill and in advanced
malignancy, causing trismus, laryngeal edema, Fig. 16.9: Incision for draining Ludwig’s angina
..There’s only one way you can fail, and that’s to quit.
PARAPHARYNGEAL ABSCESS Types (Fig. 16.10)

It is infection of pharyngomaxillary space. • Acute.
This is a cone-shaped space; base is formed • Chronic.
by base of the skull, apex is formed by the greater
cornu of hyoid bone, medial wall by the superior
constrictor, lateral wall is formed by the internal
pterygoid, angle of mandible and submandi-
bular salivary gland.
Usually infection arises from the tonsils, after
tonsillectomy and from the submandibular
space.
Clinical Features
It causes diffuse swelling in the upper neck,
trismus, fever, toxicity.
Complications
1. Thrombosis of internal jugular vein.
2. Erosion into the internal carotid artery
causing torrential bleeding.
3. Septicemia.
Fig. 16.10: Note acute and chronic retropharyngeal abscess.
Treatment Normal anatomy is also shown. Acute is eccentric and is
due to suppuration of retropharyngeal lymph nodes. Chronic
Under G/A, drainage is done by making incision is central, midline and is due to tuberculosis of the cervical
(deep incision) between angle of the mandible vertebra
and hyoid bone. Early drainage is needed. a. Acute Retropharyngeal Abscess
Antibiotics are given.
It is infection and suppuration of retropharyn-
geal lymph nodes due to staphylococci or
RETROPHARYNGEAL ABSCESS streptococci organisms.
Surgical Anatomy Commonly from tonsils or pharynx.
Common in infant and children.
The wall of the pharynx has got 5 layers. Mucosa,
submucosa, pharyngobasilar fascia, muscular Clinical features
layer (contains 3 constrictors and stylopharyn- • It presents as lateral (paramedian, eccentric)
geus, salpingopharyngeus, palatopharyngeus smooth, tender swelling in the pharynx with
muscles), and buccopharyngeal fascia which dysphagia, dyspnea, cough, toxic features
covers outer part of constrictors and extends over and neck rigidity.
buccinator. Buccopharyngeal fascia is adherent • Diagnosis is obvious on proper clinical
to prevertebral fascia posteriorly in the midline. examination.
Retropharyngeal lymph nodes are located bet- Treatment
ween buccopharyngeal fascia and prevertebral • Intravenous antibiotics.
fascia in paramedian (eccentric) position (not • Drainage is done usually through per oral inci-
midline). sion under careful anesthesia. Occasionally
Neck 211
drainage may be required through a neck Blood supply to the tumor is from external
incision. Pus should be sent for culture. carotid artery. Tumor does not secrete epi-
nephrine or any endocrine substances.
b. Chronic Retropharyngeal Abscess They can be familial.
It is invariably due to tuberculosis of cervical Clinical Features (Fig. 16.11)
spine.
• Usually unilateral, more common in middle
Abscess is in the midline behind the
age.
prevertebral fascia. There is destruction of the
• Swelling in the carotid region of the neck,
body of the vertebra due to tuberculosis.
which is smooth, firm, pulsatile (due to
Clinical features pulsatile vessel overlying its surface) and
• It is midline swelling in the posterior pharyngeal moves only side to side but not in vertical
wall, which is smooth and non-tender. direction.
• Features of tuberculosis of cervical spine will • Features of transient ischemic attack due to
be observed. compression over the carotids.
• Often abscess may point in the neck in • Thrill may be felt and bruit may be heard.
relation to sternomastoid. Often tumor may extend into the cranial
• Neurological manifestations may occur in cavity along the internal carotid artery as dumb-
severe disease. bell tumor.
Investigations Investigations
X-ray spine, chest X-ray, ESR, MRI of cervical • Doppler.
spine are essential investigations. • Angiogram to see the ‘tumor blush’.
Treatment
• Antitubercular drugs.
• Drainage of the abscess should be done
through neck approach (never intraoral approach).
• Decompression of the vertebra and stabili-
zation is also often required.
CAROTID BODY TUMOR

(Potato Tumor, Chemodectoma,
Non-chromaffin Paraganglioma)
It arises from the carotid body, which is located
at the bifurcation of the carotid artery.
Cells of the carotid body are sensitive to the
changes in pH and temperature of the blood.
Often they are locally malignant tumors, but
in 20% cases spread can occur to the regional Fig. 16.11: Note the site and location of carotid body
lymph nodes. tumor. Splaying of the carotid is common
..Don’t be discouraged; it’s often the last key in the bunch that opens the lock.
• CT scan.
• No FNAC: No partial excision.
Widening/splaying of the carotid artery with
tumor blush in an angiogram is called as Lyre
sign.
Shamblin classification of carotid body

tumor
• Type I- Localized easily resectable (26%).
• Type II- Adherent, partially surrounding the
carotids (46%).
Fig. 16.12: Torticollis neck. Note the side of the neck
• Type III- Adherent, encased carotids flexed with chin pointing opposite side
completely (27%).
Differential Diagnosis Clinical Features

• Carotid aneurysm. • Restricted neck movements.
• Soft tissue tumor (sarcoma). • Chin pointing towards opposite side.
• Lymph node enlargement. • Squint.
• Features relevant of the causes.
Treatment Treatment
If it is small, it can be excised easily as the tumor Treat the cause.
is in the adventitia.
When it is large, as commonly observed, STERNOMASTOID TUMOR
complete excision has to be done followed by placing It is due to birth injury to the sternomastoid
a vascular graft. muscle.
Carotid body tumor is not radiosensitive. It is a misnomer. It is not a tumor.
TORTICOLLIS (Wry Neck) (Fig. 16.12) Pathogenesis

It is turning of the neck to one side with chin During childbirth, injury to sternomastoid
pointing towards opposite side. muscle causes hematoma in the muscle, which
gets organized to form sternomastoid tumor.
Causes Clinical Features
• Sternomastoid tumor. • It is seen in infants of 3–4 weeks age.
• Traumatic—spinal injury, disk prolapse, • Swelling in the sternomastoid muscle, which
spondylosis. is smooth, hard, nontender and adherent to
• Inflammatory: Lymphadenitis either tuber- the muscle.
culous or suppurative. • Chin pointing towards opposite side. Head
• Spasmodic. tilted towards same side (Scoliosis capitis.)
• Reflex. • In later age groups, it causes hemifacial atrophy
• Rheumatic. because the external carotid artery is
• Burns. compressed by sternomastoid tumor leading
• Ocular causes. to decreased blood supply.
Neck 213
DIFFERENTIAL DIAGNOSIS FOR NECK LYMPH NODE ENLARGEMENT
Tuberculous lymphadenitis. Secondaries in lymph nodes.
HIV infection. Lymphomas.
Chronic lymphatic leukemia. Nonspecific lymphadenitis.
Infectious mononucleosis. Sarcoidosis.
• Compensatory cervical scoliosis.

• Compensatory squint.
Other causes for torticollis.
Treatment
Division of the lower end of the sternomastoid
muscle or excision of the muscle.
SUBHYOID BURSITIS
Subhyoid bursa is space between posterior Fig. 16.13: Sagittal and front view showing location and
surface of the body of hyoid bone and thyro- relation of subhyoid bursa
hyoid membrane (Fig. 16.13). It lessens friction
between these two structures during SECONDARIES IN NECK LYMPH NODES
swallowing.
Due to constant friction, inflammatory fluid Levels in Neck Nodes (Memorial Sloan–
collects in the bursa leading to bursitis, which Kettering Cancer center leveling of neck
presents like a horizontally placed midline nodes) (Fig. 16.14)
swelling between lower part of the hyoid bone Level I—Submandibular lymph nodes and
and thyrohyoid membrane. submental lymph nodes.
Features Level II—Lymph nodes in upper deep cervical
• Smooth, soft, cystic, fluctuant, non-trans- region. (It extends from base of skull to hyoid
illuminating swelling, which moves upwards bone and from lateral margin of sternothyroid
to posterior margin of sternomastoid muscle.
with deglutition but not while protruding the
tongue out. Level III—Lymph nodes in middle cervical
• It should be differentiated from thyroglossal region. (From hyoid bone to omohyoid muscle
cyst and pretracheal lymph nodes. or cricothyroid membrane).
• It contains turbid fluid, often gets infected to
Level IV—Lymph nodes in lower cervical region.
make swelling tender or to form an abscess. (from omohyoid muscle to clavicle).
Treatment Level V—Lymph nodes in posterior triangle
• Excision under general anesthesia. including supraclavicular region.
..Success is dependent upon the glands—sweat glands.

Fig. 16.14: Levels of neck nodes Fig. 16.15: Secondaries in the neck nodes
from laryngeal carcinoma
Level VI—Lymph nodes in the midline neck— • Secondaries from papillary carcinoma of thyroid
pretracheal and prelaryngeal. can be soft, cystic and contains brownish
black fluid.
Level VII—Lymph nodes in the mediastinum.
• Secondaries can infiltrate into carotids, ster-
nomastoid, posterior vertebral muscles,
Common sites of primary
spinal accessory nerve (shrugging of shoul-
1. Oral cavity, tongue, tonsils.
der is affected), hypoglossal nerve (tongue
2. Salivary glands.
deviates towards the same side), cervical
3. Pharynx – nasopharynx.
sympathetic chain (Horner’s syndrome).
4. Larynx.
• Secondaries spread into adjacent soft tissues
5. Esophagus.
and also to the skin causing fungation and
6. Lungs.
ulceration. Often because of tumor necrosis,
7. GIT.
softer area develops in the hard node.
8. Thyroid.
• In advanced cases tumor may infiltrate into
the major vessels like carotids, or branches
It is commonly from squamous cell carcinoma,
of external carotid artery causing torrential
but can be from adenocarcinoma, or melanoma.
hemorrhage.
Squamous cell carcinoma is mainly from oral
cavity, pharynx. Adenocarcinoma is usually Types of Secondaries in the Neck
from GIT, commonly involving left supracla-
vicular lymph nodes. Secondaries in the Neck with
known Primary
Features of Secondaries in Neck • Here secondaries are present and primary
(Figs 16.15 to 16.20) has been identified clinically in the oral
• Nodular surface and is hard, often fixed cavity, pharynx, larynx, thyroid, or other
when it is advanced. areas.
Neck 215
Fig. 16.18: Large secondaries in neck with nodularity with

platysma involvement below. In second photo bilateral
secondaries are observed
Figs 16.16A and B: Advanced secondary carcinoma neck

with ulceration and fungation
Fig. 16.19: Secondaries in neck with ulcer over the summit
Fig. 16.20: Secondaries in neck with nodules and ulceration.

Fig. 16.17: Large secondaries in neck with Note the deviation of tongue towards same side due to
extensive fungation hypoglossal nerve involvement
..Luck is when opportunity knocks and you answer.

• Biopsy from the primary and FNAC from the • Once primary is revealed it is confirmed by
secondaries has to be taken. biopsy and treated accordingly, either by
• Primary is treated accordingly either by curative radiotherapy or by wide excision
curative radiotherapy or by surgery (wide depending on location of revealed primary.
excision). • This type is usually less aggressive and has
• Secondaries when mobile are treated by got better prognosis. Primary branchiogenic
radical lymph node block dissection in the carcinoma may be a differential diagnosis for this.
neck.
Occult primary sites, which can cause
Secondaries in the Neck with Clinically secondaries in neck
Unidentified Primary • Fossa of Rosenmüller.
• Hard, neck lymph nodes are the secondaries, • Lateral wall of pharynx.
but primary has not been identified clinically. • Posterior third of the tongue.
• FNAC of the neck node has to be done and • Thyroid.
secondaries have to be confirmed. Then • Paranasal sinuses.
search for the primary has to be done by • Bronchus.
various investigations. • Esophagus.
They are—
a. Nasopharyngoscopy. Investigations for Secondaries in Neck
b. Laryngoscopy. • FNAC of secondary.
c. Esophagoscopy. • Biopsy from primary.
d. Bronchoscopy. • Blind biopsies from suspected areas.
e. Blind biopsies from the fossa of Rosen- • Nasopharyngoscopy, laryngoscopy, bron-
müller, lateral wall of pharynx, pyriform choscopy, esophagoscopy.
fossa, larynx. • CT scan.
f. FNAC of thyroid and suspected areas.
g. CT scan. Nodal staging in secondaries
Once the biopsy confirms the primary, it is N0—nodes not detected
treated either by surgery or by curative radio- N1—single node same side < 3 cm.
therapy. N2a—single node same side 3–6 cm.
Secondaries in the neck is treated by radical N2b—multiple nodes same side < 6 cm.
neck dissection. N2c—bilateral/contralateral nodes < 6 cm.
N3—node > 6 cm.
Secondaries in the Neck
with an Occult Primary Differential Diagnosis
• Here secondaries in the neck lymph nodes • Lymphomas.
are confirmed by FNAC, but primary has not • Tuberculous lymphadenitis.
been revealed by any available investigations. • Nonspecific lymphadenitis.
• When all the investigations mentioned above
are done does not show any evidence of Treatment
primary, only then it is called as occult • Primary has to be treated depending on the
primary. site, either by wide excision (surgery) or by
• Initially the secondaries in the neck are curative radiotherapy. Then the secondaries
treated by radical neck dissection, then regular have to be treated.
follow up is done (at three monthly intervals) • Secondaries when are mobile are treated by
until the primary reveals. radical neck dissection.
Neck 217
• When fixed it is inoperable. Palliative external
radiotherapy has to be given to palliate the
pain and to prevent the anticipated bleeding.
• Sometimes initially, external radiotherapy has
to be given to downstage the disease so that
it becomes operable and later classical block
dissection can be done.
Types of Block Dissection
Classic Radical Neck Dissection
It is resection of lymph nodes, fat, fascia, sterno-
mastoid muscle, strap muscles, internal jugular
vein, accessory nerve, submandibular salivary
gland, lower part of parotid - ‘enbloc (Criles‘
operation).
Incision that is commonly made is McFee
incision, which are two parallel incisions, one at
submandibular region, another at supraclavi-
cular region. Blood supply of the flap remains
intact and so healing will be better without flap
necrosis (Figs 16.21 and 16.22). Fig. 16.21: Mc’fee incision for radical neck dissection. Upper
incision is from mastoid process along the line of digastric to
Conservative Functional Block Dissection hyoid bone point then upwards to chin. Lower incision is
parallel to clavicle 2 cm above from anterior margin of
(Modified radical neck dissection—MRND) trapezius to midline
It is done only in selected cases where tumor is
very well-differentiated and less aggressive.
Structures preserved here are sternomastoid
muscle, internal jugular vein and spinal
accessory nerve.
• Only spinal accessory nerve is preserved—
MRND type I.
• Accessory nerve and internal jugular vein are
preserved—MRND type II.
• Accessory nerve, sternomastoid and internal
jugular veins are preserved—MRND type III.
Supraomohyoid Block
Only fat, fascia, lymph nodes, muscles,
submandibular salivary gland, with dissection
above the omohyoid muscle is done. Done only
in selected individuals with well-differentiated
tumor and involvement of few submandibular Figs 16.22A and B: Other incisions used in neck block
lymph nodes. (Levels I,II, III are removed). dissection. (A) Schobinger incision (B) Hocky stick incision
..The road to success is lined with many tempting parking places.

Bilateral Neck Dissection
Internal jugular vein has to be preserved on one
side. Always the side where the vein is preserved is
operated first. (If both the jugulars are ligated,
cerebral congestion occurs leading to cerebral
edema which is dangerous. If it occurs during
surgery, the patient has to be kept in propped
position; antibiotics, diuretics, steroids are given,
repeated CSF taps are done to control the
cerebral edema).
Commando Operation (Combined
mandibular dissection and neck
dissection)
It is enbloc removal, which includes wide excision
of primary tumor with hemimandibulectomy
and neck block dissection (e.g. in tongue).
Fig. 16.23: Ligation of external carotid artery should be done
Lateral Neck Dissection when needed distal to the origin of the superior thyroid artery
It is done in laryngeal and pharyngeal primaries
with clinically negative nodes. Levels II, III, IV • Doppler and angiogram should be done to
are removed bilaterally. confirm site of arterial catheter. Drug is
usually administered through an arterial
Anterior (central) Dissection pump. Other method is to increase the height
Level VI (pre, paratracheal) nodes are removed of the drip stand to get a pressure above the
level of the systolic pressure of the patient.
Posterolateral Dissection (i.e. more than 13 ft).
• Drugs can also be given IV or orally.
Levels II, III, IV, V are removed for cutaneous
malignancies. Note
To control hemorrhage in head and neck cancers
Extended Radical Dissection and during head and neck surgeries (like radical
Additional nodes in the mediastinum are cleared parotidectomy, commandos operation, maxillec-
(level VII). tomy) often ligation of external carotid artery is
required. Ligation should be done distal to the
Complications of Block Dissection origin of the superior thyroid artery (Fig. 16.23).
• Hemorrhage. It should never be ligated below the origin of
• Infection. the superior thyroid artery as this will lead to
• Lymph ooze. formation of Eddy current and thrombus at the
• Carotid blow out. carotid artery bifurcation and later to intracranial
embolism. Ligation of ECA to control bleeding
Other Treatment is usually done in continuity.
Carotid blow out—is most dangerous
Chemotherapy complication. It is due to sepsis, wound
• Drugs used are—Methotrexate, Vincristine, breakdown, arterial adventitious stripping and
Bleomycin, Adriamycin. necrosis and drying of the artery. Ligation of the
• It can be given by intraarterial route, through carotid is done to save the life of the patient but
external carotid artery. (Never through internal procedure itself has got 20% mortality and 50%
carotid as it will cause cerebral damage). morbidity (hemiplegia).
Thyroid 219
17 Thyroid
 Development floor between the first and second pharyngeal

 Anatomy pouches (subsequently marked by the foramen
cecum of the tongue).
 Congenital anomalies
The canalized column becomes the thyro-
 Thyroid function tests
glossal duct, which is displaced forward by the
 Classification of goiter
developing hyoid bone and then lies slightly to
 Nodular goiter one side below the hyoid, more commonly to
 Solitary thyroid nodule the left. The duct bifurcates to form the thyroid
 Retrosternal goiter lobes and a portion of the duct forms the
 Thyrotoxicosis (hyperthyroidism) pyramidal lobe.
 Thyroid neoplasm
 Papillary carcinoma ANATOMY
 Follicular carcinoma
 Anaplastic carcinoma It is located in the anterior triangle of the neck.
 Medullary carcinoma of thyroid (MCT) It weighs about 20 grams (Fig. 17.1).
 Malignant lymphoma
Parts
 Hashimoto’s thyroiditis
 de Quervain’s Subacute granulomatous Right and left lateral lobes located in a space
throiditis (thyroid fossa) between trachea and esophagus
 Reidel’s thyroiditis medially and carotid sheath laterally. Each lobe
 Thyroidectomy is 5 × 3 × 1.5 cm in size, extends from the middle
 Emil Theodor Kocher of thyroid cartilage to 6th tracheal ring.
 Hypothyroidism Isthmus is the connecting part between two
lateral lobes in midline extending from 2nd to
4th tracheal rings.
DEVELOPMENT
Pyramidal lobe is upward extension as fibrous
The thyroid gland develops from a median down strands or muscular strands from the junction
growth of a column of cells from the pharyngeal of the isthmus and left lateral lobe.
..How a person masters his fate is more important than what his fate is.
Venous Drainage
Superior thyroid vein.
Middle thyroid vein is short and drains into
the internal jugular vein. It is first to be ligated
in thyroidectomy.
Inferior thyroid veins are many in number.
Kocher’s vein may be present which drains
lower or middle thyroid.
Lymphatic Drainage (Fig. 17.2)

Primary: Tracheoesophageal nodes.
Prelaryngeal nodes.(Delphian nodes).
Mediastinal nodes.
Secondary: Deep cervical nodes.
Supraclavicular nodes.
Occipital nodes.
Fig. 17.1: Relations of the thyroid gland
Gland is invested by pretracheal fascia.

Berry’s ligament is a strong condensed
vascular connective tissue between the lateral
lobe and cricoid cartilage on each side.
Blood Supply
Superior thyroid artery, a branch of external
carotid artery enters the gland near superior pole Fig. 17.2: Lymphatic drainage of thyroid
as a larger anterior superficial branch and a
smaller posterior branch. Important Relations of Thyroid Gland
Inferior thyroid artery, a branch of thyrocervi-
Recurrent laryngeal nerve lies in the tracheo-
cal trunk of subclavian artery passes behind the
esophageal groove, in relation to Berry’s
carotid sheath running medially reaching the
posterolateral aspect of the gland. ligament.
Thyroidea ima artery, a branch of aorta or Superior laryngeal nerve, which gives a
brachiocephalic artery enters the isthmus or branch as external laryngeal nerve supplies
lower pole of one of the lateral lobes. cricothyroid muscle. It accompanies superior
Tracheal and esophageal branches, serve as thyroid artery.
blood supply to the retained thyroid gland after Parathyroid glands – four in number, two on
thyroidectomy. each side embedded in thyroid.
Thyroid 221
Fig. 17.4: Ectopic sites of thyroid
b. Speech impairment.
c. Respiratory obstruction.
d. Hemorrhage.
Any disease, which can occur in normal
thyroid, can also occur in lingual thyroid. i.e.
nodularity, toxicity, malignancy.
Diagnosis
Fig. 17.3: Anatomy of thyroglossal duct showing its pathway
Radioisotope study shows the uptake of iodine by
the lingual thyroid and also says the status of
CONGENITAL ANOMALIES the thyroid in normal fossa.
ECTOPIC THYROID (FIGS 17.3 AND 17.4) Ultrasound neck has to be done to see the
absence of thyroid in normal location.
Ectopic thyroid tissue may lie any where along
the line of descent. Whole of the thyroid gland
Treatment
or residual thyroid lies in an abnormal position
either in the posterior part of the tongue, or in L-Thyroxine is given daily orally.
the upper part of the neck in midline, or Often requires surgical excision and is
intrathoracic region. Radioisotope scan, CT scan technically easier.
for intrathoracic thyroid confirms the diagnosis. Radioisotope therapy for ablation is also
given.
LINGUAL THYROID
It is a thyroid swelling in the posterior third of THYROGLOSSAL CYST (Fig. 17.5)
tongue, at the foramen cecum, presenting as
rounded swelling. It may be the only existing Thyroglossal cyst is a swelling occurring in the
thyroid tissue, which may cause— neck in any part along the line of thyroglossal
a. Dysphagia. tract.
..A goal is a dream with a deadline.

Investigations
• Radioisotope study.
• Ultrasound neck.
• FNAC from the cyst.
Treatment
Sistrunk operation—Excision of cyst along with
entire tract upto the foramen cecum is done along
with removal of part of the hyoid bone as the
tract passes through it.
If there is no normal thyroid gland after the
surgery, maintenance dose of L-thyroxine 0.1 mg
Fig. 17.5: Thyroglossal cyst OD is given life long.
If tract is not completely excised, it results
in thyroglossal fistula.
Possible sites for thyroglossal cyst
THYROGLOSSAL FISTULA (Fig. 17.6)
Beneath the foramen cecum.
In the floor of mouth. It is not a congenital condition.
Suprahyoid. It either follows infection of thyroglossal cyst,
Subhyoid—commonest site. which bursts open or after inadequate removal
On the thyroid cartilage. of the cyst.
It is lined by columnar epithelium, discharges
It is usually congenital wherein there will be mucus, and is a seat of recurrent inflammation.
degeneration of a part of the tract causing cystic ‘Hood sign’ is characteristic.
swelling. Normal thyroid may be present in the
normal location(fossa). Sometimes, thyroid may Investigations
not be present in the normal site but may be
Radioisotope study and fistulogram.
present in the wall of the thyroglossal cyst.
Clinical Features
• Swelling in the midline, towards the left.
• Moves with deglutition as well as with the
protrusion of tongue. Patient is asked to open
the mouth and keep the lower jaw still.
Examiner holds the cyst between the thumb
and forefinger. When the patient is asked to
protrude the tongue, a ‘tugging sensation’ can
be felt.
• Swelling is smooth, soft, fluctuant, (cystic),
nontender, mobile, often transilluminant.
• Thyroid fossa is empty, if there is no thyroid
in normal location.
• Thyroglossal cyst can get infected and may
form an abscess.
• Malignancy can develop in thyroglossal cyst.
(papillary carcinoma). Fig. 17.6: Thyroglossal fistula
Thyroid 223
Treatment 7. RA I123 scan can show either cold nodule,
Sistrunk operation. hot nodule, or warm nodule.
(Note: One more sistrunk operation is done in 8. TRH (thyrotrophin releasing hormone test):
case of lymphedema). After IV TRH (200 mg), TSH level is
estimated.
LATERAL ABERRANT THYROID TSH level is below 2.5 m units /L in hyper-
• It is at present considered as a misnomer. thyroidism and it is exaggerated in hypo-
• It is the metastasis into cervical lymph node thyroid patient (more than 20 m units/L).
from a papillary carcinoma of thyroid. 9. Serum creatinine is increased in hyper-
• FNAC has to be done and treated as papillary thyroidism; decreased in hypothyroidism.
carcinoma of thyroid. 10. Serum cholesterol is increased in hypo and
decreased in hyperthyroidism.
AGENESIS 11. BMR is increased in hyperthyroidism.
12. Thyroid autoantibodies are also useful to
Total agenesis of one thyroid lobe may occur.
evaluate the function.
This is rare but can be clinically important. It
13. T3 suppression test.
leads to confusion in diagnosis, especially in the
toxic gland, where it could be diagnosed as a
CLASSIFICATION OF GOITER
secreting nodule. (FIGS 17.7 AND 17.8)
DYSHORMONOGENESIS 1. SIMPLE NONTOXIC
a. Diffuse hyperplastic—
It is an autosomal recessive condition wherein
1. Physiological—
there is either deficiency of thyroid enzymes
a. Puberty.
(either peroxidase or dehalogenase) or inability
b. Pregnancy.
to concentrate or to bind or to retain iodine.
2. Primary iodine deficiency (Endemic;
It may be familial and patient presents with
dietary intake less than 100ug/day).
large diffuse vascular goiter involving both
3. Secondary iodine deficiency
lobes. - Goitrogens of Brassica family, e.g.
They respond very well to L-thyroxine and cabbage, soyabean
may not require surgery at any time. - Excess dietary fluoride.
Condition may be associated with congenital - Drugs: PAS, Lithium, Phenyl-
deafness which is being called as Pendred’s butazone, thiocyanates.
syndrome. - Dyshormonogenetic goiter.
b. Colloid goiter
THYROID FUNCTION TESTS c. Nodular goiter (Multinodular).
1. T3 (Serum triiodothyronine): 1.2–3.1 nmol/ d. Solitary nontoxic nodule.
liter. e. Recurrent nontoxic nodule.
2. T4 (Serum thyroxin): 55–150 nmol/liter. 2. TOXIC
3. TSH 0–5 IU/ml of plasma. a. Diffuse (Primary)—Graves’ disease.
4. PBI (Protein bound iodide)—8 mg%. b. Multinodular (Secondary)—Plummer’s
5. Free T3 is 0.3% (3–9 pmol/liter). It is the best disease.
single test in assessing hyperthyroidism. c. Toxic nodule (solitary) (Tertiary).
6. Free T4 is 0.03%.(8–26 pmol/liter). d. Recurrent toxicosis.
..Those who wish to sing always finds a song.

many follicles become inactive get filled with
colloid and it is called as colloid goiter.
As diffuse hyperplastic goiter is a reversible stage,
L-thyroxine is beneficial.
NODULAR GOITER
Pathogenesis
Fig. 17.7: Note the goiters in a male and a female patient
3. NEOPLASTIC
a. Benign—Adenomas: Papillary, follicular, Other factors involved are growth stimulating
Hurthle cell, colloid. immunoglobulins and growth prone cell clones.
b. Malignant—Carcinomas: Papillary, folli-
cular, medullary, anaplastic, lymphomas.
4. THYROIDITIS
Hashimoto’s autoimmune thyroiditis.
de-Quervain’s autoimmune thyroiditis.
Reidel’s thyroiditis.
5. RARE CAUSES: Bacterial (suppurative),
amyloid.
DIFFUSE HYPERPLASTIC GOITER

Initial persistent increase in TSH level causes
diffuse active lobules. In late stages of diffuse
hyperplasia, TSH stimulation decreases and Fig. 17.8: Multinodular goiter
Thyroid 225
Clinical Features Types
It is a slowly progressive disease with many 1. Toxic solitary nodule.
years of history. 2. Nontoxic solitary nodule.
Multiple nodules of different sizes are formed Based on radioisotope study:
in both lobes, also in isthmus, which is firm, 1. Hot—Means autonomous toxic nodule.
nodular, nontender, moves with deglutition. 2. Warm—Normally functioning nodule.
Recent increase in size signifies malignant 3. Cold—Nonfunctioning nodule; may be
transformation or hemorrhage. malignant (need not be always).
Complications of MNG Clinical Features

• Secondary thyrotoxicosis (30%). • Single nodule palpable in one or other lobes
• Follicular carcinoma of thyroid. of the thyroid, which is usually smooth and
• Hemorrhage in a nodule. firm.
• Tracheal obstruction. • Lahey’s test does not show any other nodules
• Cosmetic problem. in posterior part of the gland.
Investigations Investigations
T3, T4, TSH, ultrasound neck, FNAC, X-ray neck Ultrasound neck (very useful).
shows ring or rim calcification. FNAC.
T3, T4, TSH.
Treatment Radioisotope study (I123).
Nodular goiter is an irreversible stage and so surgery
is the treatment. Treatment
Partial or subtotal thyroidectomy is done If it is a nontoxic nodule due to any cause,
depending on the amount of gland involved, hemithyroidectomy with complete removal of
amount of normal gland existing, and location lateral lobe and whole of the isthmus is done.
of nodules. If it is papillary carcinoma thyroid, then near total
Postoperatively L-thyroxine is often given to thyroidectomy is done along with suppressive
prevent further fluctuation in TSH level. dose of L-thyroxine given 0.3 mg OD daily.
If it is a toxic nodule, radioiodine therapy, I131
SOLITARY THYROID NODULE – 5 milli curie is given orally, if the age of the
It is a single palpable nodule in thyroid on clinical patient is more than 45 years.
examination, in an otherwise normal gland. If age is less than 45 years, then initially
toxicity has to be controlled by antithyroid drugs,
Causes always followed by surgery—Hemithyroi-
dectomy.
1. Thyroid adenomas—a) Papillary b) Colloid
c) Hürthle cell d) Follicular.
2. Papillary carcinoma of thyroid. DOMINANT NODULE
3. Only one nodule may be palpable in an It is palpable nodule in an enlarged thyroid
underlying multinodular goiter. gland.
..Happiness is not a matter of events; it depends upon the tides of the mind.
RETROSTERNAL GOITER Treatment

Usually arises from the lower pole of a nodular • Surgical removal of retrosternal thyroid is
goiter. done.
Common in short neck individuals. Commonly it can be removed through an
Due to negative intrathoracic pressure, incision in neck (as blood supply of retro-
nodule gets drawn into the superior media- sternal goiter is from neck), but in case of
stinum. Sometimes it may also be an ectopic large retrosternal extension or malignant type
thyroid. median sternotomy is required.
• Radioiodine therapy is not accepted in retrosternal
Types goiter.
1. Substernal type: Part of the nodule is palpable
in the lower neck.
2. Plunging goiter: An intrathoracic goiter is THYROTOXICOSIS (Hyperthyroidism)
occasionally forced into the neck by increased It is a symptom complex due to raised levels of thyroid
intrathoracic pressure.
hormones.
3. Intrathoracic goiter itself.
Types
Clinical Features
1. Dyspnea at night. 1. Diffuse toxic goiter (Graves’ disease,
2. Cough and stridor (stridor is harsh sound on Basedow’s disease, Primary thyrotoxicosis)
inspiration). (Fig. 17.9).
3. Dysphagia. 2. Toxic multinodular goiter (Secondary
4. Engorgement of neck veins and superficial thyrotoxicosis, Plummer disease).
veins on the chest wall. 3. Toxic nodule.
5. Pembertones‘ sign is positive. The patient is 4. Hyperthyroidism of rare causes:
asked to raise the arm above the shoulder a. Thyrotoxicosis factitia—drug induced. Due
level. Dilated veins are seen over neck and to intake of L-thyroxine more than
upper part of chest wall. Stridor and rarely normal.
dysphagia may occur. When patient raises b. Jod Basedow thyrotoxicosis—because of
the arm above the shoulder level, retrosternal large doses of iodides given to a
goiter compresses over the easily compres- hyperplastic endemic goiter.
sible structures like SVC and trachea causing c. Autoimmune thyroiditis or de Quervain’s
dilated veins and dyspnea respectively). thyroiditis.
6. Dull note over the sternum on percussion. d. Occasionally carcinoma thyroid.
7. Retrosternal goiter can be either nodular,
e. Neonatal thyrotoxicosis. It subsides in 3–4
toxic or malignant.
weeks as TsAb titers fall in the baby’s
Differential Diagnosis serum.
Mediastinal tumor. Clinical Features
Investigations • It is eight times more common in females.
• Chest X-ray shows soft tissue shadow under • Occurs in any age group.
the sternum. • Primary type is seen commonly in younger
• I123 study is diagnostic. age group.
• CT scan is useful. • Secondary is common in older age group.
Thyroid 227
Genitourinary system
• Oligoor amenorrhea.
• Occasional urinary frequency.
Integument
• Hair loss.
• Pruritus.
Psychiatry
• Irritability.
• Nervousness.
• Insomnia.
Sympathetic overactivity causes dyspnea,
palpitation, tiredness, heat intolerance, sweating,
nervousness, increased appetite and decrease in
weight. Because of the increased catabolism they
show weight loss in spite of having increased
appetite, and so also increased creatinine level,
which signifies myopathy (due to more muscle
catabolism).
Fine tremor is due to diffuse irritability of gray
Fig. 17.9: Thyrotoxicosis(primary). matter.
Note the exophthalmos Thrill is felt in the upper pole of the thyroid
and also bruit on auscultation. It is because in
upper pole, superior thyroid artery enters the
Symptoms of Hyperthyroidism gland superficially, and so thrill and bruit can
Gastrointestinal system easily be assessed. In lower pole inferior thyroid
• Weight loss in spite of increased appetite. artery enters the gland from deeper plane and
• Diarrhea (due to increased activity at so thrill cannot be felt.
ganglionic level).
Signs of Hyperthyroidism
Cardiovascular system
• Palpitations. Eye Signs in Toxic Goiter
• Shortness of breath at rest or on minimal
Eye signs are common in primary thyrotoxicosis. Lid
exertion.
lag, lid spasm can occur in secondary thyrotoxicosis
• Angina.
also.
• Cardiac irregularity.
• Cardiac failure in the elderly (CCF). von Graefe’s sign: Lid lag sign is visible white sclera
above the corneal margin during lid lag.
Neuromuscular system
• Undue fatigue and muscle weakness. Dalrymple’s sign: Upper eyelid retraction, so
• Tremor. visibility of upper sclera.
Skeletal system Stellwag’s sign: Absence of normal blinking—so
• Increase in linear growth in children. starring look. First sign to appear.
..Happiness is in the taste, not in the thing.

WAYNE’S DIAGNOSTIC INDICES (CLINICAL)

Symptoms Present Absent
1-Dyspnea on effort +1
2-Palpitation +2
3-Tiredness +2 –5
4-Preference for heat
5-Preference for cold (Heat intolerance) +5
6-Excessive sweating +3
7-Nervousness +2
8-Appetite increased +3
9-Weight decreased +3
Signs Present Absent
1-Bruit over thyroid +2
2-Exophthalmos +2
3-Lid retraction +2
4-Lid lag +1
5-Hyperkinetic movements +4 –2
6-Fine finger tremors +1
7-Hands Hot +2 –2
Moist +1 –1
8-Atrial fibrillation +4
9-Pulse rate 80/minute –3
80–90/minute 0
More than 90/minute +3
10-Palpable thyroid +3
< 11 points—nontoxic 11–19 –equivocal > 19 points –toxic goiter
Joffroy’s sign: Absence of wrinkling on forehead Cowen’s sign: Jerky pupillary contraction to
when patient looks up (frowns). consensual light.
Moebius sign: Lack of convergence of eyeball. Kocher’s sign: When clinician places his hands on
Defective convergence is due to lymphocytic patient eyes and lifts it higher, patients upper
infiltration of inferior oblique and inferior rectus lid springs up more quickly than eyebrows.
muscles in case of primary thyrotoxicosis. There
Nafziger’s sign: With patient in sitting position
will be diplopia. It may be an early sign of
and neck fully extended, protruded eyeball can
eventual ophthalmoplegia.
be visualized when observed from behind.
Jellinek’s sign: Increased pigmentation of eyelid
margins. Order of appearance of signs
Stellwag’s sign - Mild. First sign to appear.
Enroth sign: Edema of eyelids and conjunctiva.
von Graefe’s Sign - Mild.
Rosenbach’s sign: Tremor of closed eyelids. Joffroy’s sign - Moderate.
Moebius sign. - Severe.
Gifford’s sign: Difficulty in everting upper eyelid.
Differentiates from exophthalmos of other
causes. EXOPHTHALMOS
• It is proptosis of the eye, caused by infiltration
Loewi’s sign: Dilatation of pupil with weak
of the retrobulbar tissues with fluid and
adrenaline solution.
round cells, with lidspasm of upper eyelid (Lid
Knie’s sign: Unequal pupillary dilatation. spasm is spasm of levator palpebrae
Thyroid 229
superioris muscle which is partly innervated 7. Paroxysmal atrial fibrillation.
by sympathetic fibers). 8. Persistent atrial fibrillation (not responsive
• Sclera can be seen clearly above the limbus to digoxin).
of the eye.
• Proptosis can be measured by ophthalmometer. Myopathy
• Exophthalmos is often self-limiting, but not • Weakness of proximal muscles occurs, i.e. the
always. Sleeping in propped up position and front thigh muscles, or arm muscles.
lateral tarsorrhaphy will help to protect the • Weakness is more when muscle contracts
eye. isometrically either while getting down steps,
or lifting a filled bucket.
Severe exophthalmos • Often when it is severe it resembles myasthe-
• Eyelid edema, chemosis, conjunctival injec- nia gravis. Once hyperthyroidism is control-
tion. led recovery occurs.
• Diplopia, ophthalmoplegia (complete weak-
ness of all extraocular muscles and so no Pretibial Myxedema
movements possible).
Pretibial myxedema is often a feature of primary
• Corneal ulceration.
thyrotoxicosis.
• Papilledema soon develops.
Is usually symmetrical, red, shiny, thickened
• Finally it may also cause loss of vision.
skin, with coarse hair.
It is called as malignant exophthalmos.
In severe cases skin of whole leg below the
(eventhough it is not malignant nor related to
knee with foot and ankle is involved.
any malignancy).
It is due to deposition of myxomatous tissues
It needs emergency treatment, i.e. Large (mucin like deposits) in skin and subcutaneous
doses of systemic steroids (Prednisolone) are plane.
given along with orbital decompression, systemic It might or might not regress completely after
antibiotics, steroid drops, antibiotic drops. treatment for toxicity.
It is associated with exophthalmos with high
Cardiac Manifestations levels of thyroid stimulating antibodies.
1. Tachycardia is common.
As per Crile’s grading. Thyroid Acropachy
Pulse rate Thyroid acropachy is clubbing of fingers and
Grade I—90—100 toes in primary thyrotoxicosis.
Grade II—100—110
TOXIC NODULE
Grade III—>110.
Is a solitary overactive nodule.
Sleeping pulse rate is usually checked for three There is an autonomous hypertrophy and
consecutive nights and average is taken as the hyperplasia of the part of the gland where there
value. is a nodule (It is not due to thyroid stimulating
2. Ectopic. antibody (TsAb)).
3. Pulsus paradoxus. Here high levels of circulating thyroid
4. Wide pulse pressure. hormones suppress TSH secretion, and so
5. Multiple extrasystoles. normal thyroid tissue surrounding the nodule
6. Paroxysmal atrial tachycardia. is itself suppressed and inactive.
..The man who has no inner life is a slave to his surroundings.

Differentiating points between Primary and Secondary hyperthyroidism

Primary thyrotoxicosis Secondary thyrotoxicosis
1. Symptoms appear first, then swelling. Swelling appears first.
2. Goiter is diffuse, smooth, firm or soft, Swelling is large nodular, obvious.
both lobes are involved.
3. There is thrill and bruit. Symptoms appear after long time,
4. Features are much more severe compared which is less severe and slowly progressive
to that of secondary toxicosis. compared to primary toxicosis.
5. Eye signs and exophthalmos are common. Cardiac features are more common.
6. As it is an autoimmune disease, there may be Eye signs are not common.
hepatosplenomegaly.
Histologically, there is hyperplasia of acini, lined by
columnar epithelium, often containing vacuolated
colloid.
Once patient becomes euthyroid by drugs, TRH estimation.

surgery (hemithyroidectomy) or radioactive ECG—To look for cardiac involvement and
iodine therapy I 131 in a therapeutic dose of if required opinion from cardiologists is taken
5mcurie is given orally. and cardiac problems are managed.
Because normal gland is inactive, radioactive Total count and neutrophil count are very
iodine affects only the autonomous nodule, essential base line investigations before starting
allowing the normal gland to remain intact, antithyroid drugs (as it may cause agranulo-
which later gets activated, and functions cytosis).
normally.
Drugs are used initially, only for a temporary Treatment
period to make the patient euthyroid.
1. Antithyroid drugs.
Investigations 2. Surgery.
3. Radioiodine therapy.
Thyroid function tests:
1. ANTITHYROID DRUGS
Type of disease T4 T3 TSH Indications for Antithyroid drugs:
Conventional increased increased undetectable • Toxicity in pregnant women—Propylthiou-
hyperthyroidism racil is preferred.
T3 hyperthyroidism → increased undetectable • Toxicity in children and young adults.
Subclinical → → undetectable • Before subtotal thyroidectomy, to make the
hyperthyroidism patient euthyroid.
• After radioactive I 131 therapy for 6 to 12
Serum T3 and T4 levels are very high. TSH weeks. (Effects of radiotherapy starts only in
is very low or undetectable. Some times, only 6 to 12 weeks).
T3 level is increased and is called as T3 toxicosis.
Here in T3 toxicosis, free T3 estimation is important. a. Carbimazole
Radioisotope study by I131 (Diagnostic dose • Is the commonest drug used.
-5 microcurie is used) shows more up take, i.e. • Dose is 5–10 mg, exactly 8th hourly, (as T1\2
hot nodules or hot areas. This is very useful in of carbimazole is 8 hours).
autonomous solitary toxic nodule. • Usually given for 12–18 months.
Thyroid 231
• Peak plasma level should be maintained in Advantages of antithyroid drugs
optimum concentration to have a proper • Avoids surgery and its complications
benefit. • Avoids radiotherapy.
• Often triiodothyronine 20 microgram 4 times
Clinical improvement occurs in 2 weeks.
daily or thyroxine 0.1 mg daily is given in
Biochemical improvement occurs in 6 weeks.
combination with antithyroid drugs, to
prevent iatrogenic thyroid insufficiency or to
prevent the increase in size of goiter. Disadvantages:
• It acts by blocking thyroid hormone syn- Prolonged course of treatment for 18 months and
thesis. Carbimazole also suppresses the auto- in spite of this cannot predict the remission or
immune process in thyroid in Graves‘ relapse. Relapse rate is 40%.
disease. Size of swelling may not regress.
b. Methimazole: Similar like carbimazole. Dose It may lead to agranulocytosis and thrombo-
is 5 to 20 mg daily. cytopenia, liver damage, hair loss.
c. Propylthiouracil: Sore throat is the earliest presentation of
• It acts by blocking thyroid hormone synthesis agranulocytosis. If it is so, drug has to be
as well as by blocking peripheral conversion stopped; total count has to be done. If it is less,
of T4 to T3.
agranulocytosis is confirmed. High doses of
• It also decreases the thyroid autoantibody
levels. injection benzyl penicillin 10–20 lacs, 6th hourly,
• It can be given in hyperthyroidism in children IV has to be started to prevent infection. If
and pregnancy. required, blood transfusion has to be done.
• Dose is 200 mg 8th hourly. Patient usually recovers by this. To control
Antithyroid drugs are continued during and toxicity, Tab Propranolol 40 mg tid has to be
after surgery, for 7–10 days and after radioactive started. Rarely they need bone marrow
iodine therapy for 6 weeks to 12 weeks. transplantation.
Studying HLA status and TsAb level can
assess response to treatment and possibility of 2. SURGERY
relapse in primary thyrotoxicosis. Indications
1. Failure of drug treatment in primary thyro-
Propranolol
Dose is 40 mg tid. toxicosis in young patients.
It reduces the cardiac problems and also 2. Autonomous toxic nodule.
blocks the peripheral conversion of T4 to T3, as 3. Nodular toxic goiter.
it is the T3 which is the principle active agent 4. When malignancy cannot be ruled out.
in periphery. Surgery done is subtotal thyroidectomy—Both
Contraindications are bronchial asthma, lobes with isthmus are removed and a tissue
heart block, cardiac failure. equivalent to pulp of finger is retained in lower
Lugol’s iodine (5% iodine + 10% potassium pole of the gland on both sides – 8 grams.
iodide): In autonomous nodule, hemithyroidectomy is
It decreases the vascularity of the gland and done—Entire lateral lobe with whole of isthmus
makes it more firmer and easier to handle during is removed.
surgery. Dose is 10–30 drops/day (minims) for
10 days prior to surgery. Potassium iodide tablets Advantages: Rapid cure and high cure rate.
60 mg tid also can be given instead of Lugol’s Patient should be euthyroid before under
iodine. But its use at present is disqualified. going surgery (It should be confirmed by
(One minim= one drop. One ml = 16 drops). repeated estimation of T3 and T4 levels).
..Life shrinks and expands in proportion to one’s courage.

Disadvantages • To give therapeutic dose, patient should
1. Recurrent thyrotoxicosis (5%). be admitted and isolated for 7 days (Half
2. Thyroid insufficiency 20–45%. It is revealed life) to prevent irradiation. It is given
in 6 months to 2 years and confirmed by orally soon after getting from the
doing T 3 and T 4 and TSH estimation. manufacturer without much delay to
Hypothyroidism is better than recurrent have optimal efficacy.
thyrotoxicosis. It is treated by tab. L- Advantages
thyroxine 0.1mg daily (OD) for life long. 1. No surgery.
3. Complications of thyroid surgery itself. 2. No prolonged drug therapy.
3. RADIOIODINE THERAPY Disadvantages
Indications 1. Availability of facilities.
1. Primary thyrotoxicosis after 45 years of age. 2. Proper follow up is essential.
2. In autonomous toxic nodule.
3. In recurrent thyrotoxicosis. TOXIC THYROID IN PREGNANCY
• Radioiodine destroys the cells and causes
• Radioiodine therapy is an absolutely contra-
the complete ablation of thyroid gland. indicated in pregnancy (High risk to fetus).
It is given only after the age of 45 yrs, as • Antithyroid drugs can be administered
the chances of genetic mutation (damage), carefully.
leukemia, carcinomas are high in younger • But, the problem here is that both TSH and
individual. antithyroid drugs crosses the placental
• Usual dose is 5 to 10 millicurie, or 160 barrier and baby born may be hypothyroid
microcurie/gm of thyroid. and goitrous.
• It takes 3 months, to get full response, and • Propylthiouracil is preferred in pregnancy.
so until then, the patient has to take • Subtotal thyroidectomy can be done in
antithyroid drugs. Often additional one second trimester.
or two doses of radioiodine are required
to have complete ablation. Eventually
TOXIC THYROID IN CHILDREN
they go for hypothyroidism and so
require maintenance dose of L-thyroxine Radioiodine therapy is absolutely contraindicated
0.1 mg daily. in children because of high risk of developing
Choice of Therapies
Condition Age Treatment
Diffuse toxic goiter
a. Small goiter Antithyroid drugs for 18 months.
b. Large goiter Over 45 years Radioiodine therapy.
Under 45 years Surgery [Subtotal thyroidectomy].
Toxic nodular goiter Surgery:[ Subtotal thyroidectomy]
Initially antithyroid drugs are given to make
the patient euthyroid before surgery.
Toxic solitary nodule Under 45 years Radioiodine.
Over 45 years Surgery: [Hemithyroidectomy].
Recurrent thyrotoxicosis Under 45 years Antithyroid drugs.
after surgery Over 45 years Radioiodine therapy.
Failure of antithyroid drugs
or radioiodine therapy Surgery.
Thyroid 233
thyroid carcinoma. Recurrence rate is also very and later released into circulation as protein
high after surgery. So proposed treatment is, bound iodide (PBI). Normal value of PBI is
initially antithyroid drugs are given until ado- 8 mg%.
lescent period and then subtotal thyroidectomy • Using Gieger Muller’s gamma ray counter
is done. scanning of thyroid gland is done to visualize
gland.
THYROCARDIAC • Hot area suggests more uptake.
Severe cardiac damage resulting from hyperthy- • Warm area suggests normal uptake.
roidism (may be partly or wholly due to same), • Cold area suggests no uptake.
usually secondary type, requires proper opinion I 123 Radioisotope can be safely used in
from cardiologists and treatment with Propra- children and pregnancy for only diagnostic
nolol. Subtotal thyroidectomy is the treatment. purpose (5 microcurie) as the dose is low.
In a patient with thyrotoxicosis, with recent
onset of proptosis, early thyroidectomy has to Indications for diagnostic radioactive iodine
be avoided. Because early surgery may study
precipitate malignant exophthalmos. Here the a. Doubtful toxicity.
b. Ectopic thyroid.
patient has to be treated initially with antithyroid
c. Autonomous toxic nodule.
drugs and if required with steroids, until the
d. After total thyroidectomy, to look for
proptosis has remained static for six months.
secondaries in follicular carcinoma thyroid.
Then subtotal thyroidectomy is done. e. Retrosternal thyroid.
Since half life of L-thyroxine is 7 days,
Propranolol and antithyroid drugs has to be Radioisotope study is done to see the secon-
continued for 7 days after thyroidectomy. daries by doing whole body scanning (Total
T3 THYROTOXICOSIS should be suspected body scintigraphy). For diagnostic radioactive
if the clinical picture is suggestive of toxicosis, study Technetium 99 pertechnetate can also be
but routine tests for thyroid function are within used but it is not as good as I123.
normal range. Therapeutic Uses
RADIOACTIVE IODINE • In primary thyrotoxicosis after 45 years.
• In autonomous toxic nodule after 45 years, it is
It is used both as a diagnostic as well as a useful as remaining gland still will function
therapeutic agent. adequately after radiotherapy. (as during
1. I131—is used for radioactive iodine therapy. radiotherapy radioisotope will not be taken
2. I123—is used for diagnostic studies. up by this retained normal gland as it is
• For diagnostic purpose I123 is given orally on suppressed in the presence of toxic nodule
previous day. (Dose- 5microcurie;T 1\2 (half life) which will function later adequately).
of I123 is 13 hours and so it is suitable for • In follicular carcinoma of thyroid, after total
diagnostic purpose). thyroidectomy, if there are secondaries else-
• Patient should not take L-thyroxine for 7 days where in the body, as in bone or lungs, then
prior to radioisotope study. radioiodine therapy is given. I131 is given as
• Thyroid treats this I123 similar to inorganic its half life is 8 days. Patient should be isolated
I127. This I123 enters the thyroid from the for this period. It is given orally in a dose of 5
circulation and gets incorporated into T3, T4 milli curies (160 microcurie/gm of thyroid).
..It takes 26 muscles to smile, and 62 muscles to frown.

Half life. Etiology

I123 13 hours. • Radiation either external or radioactive
I131 8 hours. iodine therapy.
I132 2.3 hours. TSH levels in the blood of these patients are
Tc 99 scan 6 hours. high and so it is called as hormone dependent
tumor.
It is a slowly progressive and less aggressive
THYROID NEOPLASM
tumor.
A. Benign It is commonly multicentric.
• Follicular adenoma. It spreads within the gland through intra-
• Hurthle cell adenoma. thyroidal lymphatics to other lobe, comes out of
• Colloid adenoma. the capsule and spreads to lymph nodes.
• Papillary adenoma. Usually there is no blood spread.
B. Malignant (Dunhill classification).
a. Differentiated Types
Papillary carcinoma (60%)
Follicular carcinoma (17%). i. Occult (< 1.5 cm).
Papillofollicular carcinoma behaves like ii. Intrathyroidal.
papillary carcinoma of thyroid. iii. Extrathyroidal.
Hurthle cell carcinoma behaves like
follicular carcinoma. Gross
b. Undifferentiated It can be soft, firm, hard, cystic. It can be solitary
Anaplastic carcinoma (13%) or multinodular. It contains brownish black fluid.
c. Medullary carcinoma (6%).
d. Malignant lymphoma (4%). Microscopy
e. Secondaries in thyroid (rare).
It shows cystic spaces, papillary projections with
psammoma bodies, malignant cells with ‘Orphan
Etiology of Thyroid Malignancy
Annie eye’ nuclei (intranuclear cytoplasmic
1. Radiation either external or radioiodine can inclusions).
cause papillary carcinoma thyroid. There is
increased incidence of thyroid carcinoma Clinical Features
among children following exposure to ioni-
1. Soft or hard or firm, solid or cystic, solitary
zing radiation after the Chernobyl nuclear
disaster in Ukraine in 1986. Earlier radio- or multinodular thyroid swelling.
therapy was the treatment for acne, tonsillar 2. Compression features are uncommon in
diseases, adenoids, thymus enlargement or papillary carcinoma thyroid.
hemangiomas which in turn predisposed 3. Often discrete lymph nodes in the neck are
papillary carcinoma of thyroid. palpable.
2. Pre-existing multinodular goiter. It turns into
follicular carcinoma of thyroid. Diagnosis
3. Medullary carcinoma thyroid is often • FNAC.
familial. • Radioisotope scan shows cold nodule.
• TSH level in the blood is higher.
PAPILLARY CARCINOMA
• It is 60% common. Treatment
• Common in females and young age group. • Near total thyroidectomy.
Thyroid 235
• Suppressive dose of L-thyroxine 0.3 mg OD life
long.
• Block dissection (Functional block) is required
if lymph nodes are involved.
• Occasionally if small lymph nodes are
present, ‘Berry picking’ may be done (not
accepted now).
Prognosis
Prognosis is good and it is one of the curable
malignancies.
AMES scoring
A: Age. Age less than 40 years has got better
prognosis.
M: Distant metastasis.
E: Extent of the primary tumor.
S: Size of the tumor. Size less than 4 cm has
got better prognosis.
AGES scoring Fig. 17.10: Follicular carcinoma thyroid
with skull secondaries
A: Age less than 4 cm has got better prognosis.
G: Pathologic grade of the tumor.
E: Extent of the primary tumor. • It spreads mainly through blood into the
S: Size of the primary tumor. Size less than 4 lung, bones, and liver.
cm has got better prognosis. • Bone secondaries are typically vascular,
warm, pulsatile, localized, commonly in
Psammoma bodies are seen in skull, long bones, ribs.
• Papillary carcinoma thyroid. • It can also spread to lymph nodes in the neck
• Meningioma. occasionally.
• Serous cystadenoma of ovary.
Clinical Features
Berry’s in thyroid 1. Swelling in the neck, firm or hard and
• Berry ligament. nodular.
• Berry sign. 2. Tracheal compression and stridor.
• Berry picking. 3. Dyspnea, hemoptysis, chest pain when there
are lung secondaries.
4. Recurrent laryngeal nerve involvement
FOLLICULAR CARCINOMA (FIG. 17.10) causing hoarseness of voice, +ve ‘Berry’s sign’
• It is 17% common. signifies advanced malignancy (infiltration
• It is common in females. into the carotid and so absence of carotid
• It can occur either de novo or in a pre-existing pulsation).
multinodular goiter. 5. Pulsatile secondaries in the skull, and long
• It is a more aggressive tumor. bones (Fig. 17.11).
..The most important thing that you wear is the expression on your face.
abundant oxyphill cells. It spreads more
commonly to regional lymph nodes than folli-
cular carcinoma of thyroid.
ANAPLASTIC CARCINOMA (FIG. 17.12)

• It is a very aggressive tumor of short
duration, presents with a swelling in thyroid
region which is rapidly progressive
Fig. 17.11: X-ray skull showing secondaries causing—
from follicular carcinoma thyroid i. Stridor and hoarseness of voice.
ii. Dysphagia.
iii. Fixity to the skin.
Investigations
• Swelling is hard, with involvement of
• Most often FNAC is inconclusive, because isthmus and bilateral lateral lobes.
capsular and angioinvasion which is the main • FNAC is diagnostic.
feature in follicular carcinoma cannot be • Tracheostomy and isthmectomy has got a
detected by FNAC. role to relieve respiratory obstruction tempo-
• Frozen section biopsy is very useful. rarily.
• Ultrasound abdomen, Chest X-ray, X-ray • Treatment is external radiotherapy.
bones are the other investigations required. • However prognosis is poor.
Treatment
Total thyroidectomy is done, along with block
dissection whenever lymph nodes are enlarged.
Maintenance dose of L-thyroxine 0.1 mg OD
is given life long.
Follow-up
It is by radioisotope I123 scan done at regular
intervals (6months) to look for secondaries.
Thyroglobulin estimation is a good follow-
up method to decide for radioisotope study.
Further Treatment
If secondaries are detected therapeutic dose Ra
I131 is given. L-thyroxine has to be stopped 7 days
prior to RT, and then required dose of Ra I131 Fig. 17.12: Anaplastic carcinoma of thyroid
is given.
Secondaries in bone are treated by external
radiotherapy. Internal fixation should be done MEDULLARY CARCINOMA OF
whenever there is pathological fracture. THYROID (MCT)
There is no role of chemotherapy for follicular • It is uncommon (5%) type of thyroid malignancy.
carcinoma thyroid. • It is arises from the parafollicular ‘C’ cells
Hurthle cell carcinoma is a variant of which is derived from the ultimobronchial
follicular carcinoma of thyroid which contains body (Fig. 17.13).
Thyroid 237
Types
1. Sporadic.
2. MCT with MEN II syndrome.
3. Familial MCT.
Investigations
1. FNAC: shows amyloid deposition with
dispersed malignant cells and ‘C’ cell
hyperplasia.
2. Tumor marker: Calcitonin level will be higher.
3. Ultrasound neck-thyroid region.
Treatment
1. Total thyroidectomy + central node dissection
Fig. 17.13: Note the parafollicular cells. + Maintenance dose of L-thyroxine.
Cell of origin of medullary carcinoma thyroid 2. Neck lymph node block dissection whenever
lymph nodes are involved.
• It contains characteristic ‘amyloid stroma’ 3. Adriamycin is drug used for chemotherapy
wherein malignant cells are dispersed. (But benefit)??.
• In these patients blood levels of calcitonin both 4. No role of suppressive hormone therapy or
basal as well as that following calcium or radioactive iodine therapy.
pentagastrin stimulation is high, a very useful All family members of the patient should be
tumor marker. evaluated for serum calcitonin and if it is high they
• Tumor also secretes 5-HT (serotonin), should undergo prophylactic total thyroidectomy.
prostaglandin and vasoactive intestinal (Can also be assessed by genetic evaluation).
polypeptide (VIP).
• It spreads mainly to lymph nodes. Prognosis
• It may be associated with MEN II syndrome Sporadic MCT and MCT with MEN II are
and pheochromocytoma with hypertension. aggressive.
• There may be mucosal neuromas in lips, oral Familial MCT not associated with MEN II has
cavity. got better prognosis.
Clinical Features
MALIGNANT LYMPHOMA
1. Thyroid swelling often with enlargement of
neck lymph node. It is NHL type. Occurs in a pre-existing
2. Diarrhea, flushing. Hashimoto’s thyroiditis (Not proved well).
3. Hypertension, pheochromocytomas and FNAC is useful to diagnose the condition.
mucosal neuromas when associated with Chemotherapy is the main treatment.
Often total thyroidectomy is done to enhance
MEN II syndrome.
the results.
4. Sporadic and familial types occur in
adulthood whereas conditions associated
with MEN syndrome II occur in younger age HASHIMOTO’S THYROIDITIS
groups. • Also called as diffuse nongoitrous thyroiditis
..Love means making the other happy, even from a distance.

• It is an autoimmune thyroiditis, common in Clinical Features
women. Presents with diffuse pain, swelling in thyroid
• There is hyperplasia initially, then fibrosis, which is tender.
eventually infiltration with plasma cells and Commonly seen in females.
lymphocytic cells. Initially there will be transient hyperthy-
roidism with high T3 and T4 but poor radioiodine
Clinical Features uptake.
1. Painful, diffuse, enlargement of usually both It is usually a self-limiting disease.
lobes of thyroid which is firm, tender and
smooth (occasionally one lobe is involved). REIDEL’S THYROIDITIS
2. Initially they present with toxic features but (0.5% common)
later, they manifest with features of • A very rare benign entity wherein thyroid
hypothyroidism. tissue is replaced by fibrous tissue which
Hyperplasia Hyperthyroid interestingly infiltrates the capsule into
Euthyroid muscles, paratracheal tissues, carotid sheath.
Fibrosis Hypothyroid • It is often associated with retroperitoneal and
3. There may be hepatosplenomegaly. mediastinal fibrosis. (‘Woody Thyroiditis’,
4. It is often associated with other autoimmune ‘Ligneus Thyroiditis’).
diseases.
5. In 85% cases significant rise in the thyroid Clinical Features
antibodies (microsomal, thyroglobulin, or Hard, fixed, swelling with stridor, often Berry’s
colloid antibodies) is observed. sign may be positive, i.e. absence of carotid
6. Often condition may be associated with or pulsation.
may predispose to malignant lymphoma. It is
at present not well-proved. Differential Diagnosis
Anaplastic carcinoma of thyroid.
Investigations
FNAC, T3, T4, TSH. Thyroid antibodies assay. Investigations
Usually ESR is very high (over 90 mm/hour). T3, T4 may be low due to hypothyroidism.
Radioisotope scan will not show any uptake.
Treatment FNAC to rule out carcinoma.
1. L-thyroxine therapy.
2. Steroid therapy often is helpful. Treatment
3. If goiter is large and causing discomfort, then Isthmectomy is done to relieve compression on
subtotal thyroidectomy is done. the airway. They require L-thyroxine replace-
ment later, as hypothyroidism is common.
DE QUERRIANIN’S SUBACUTE
GRANULOMATOUS THYROIDITIS THYROIDECTOMY
It is due to viral etiology either mumps or cox- Types
sackie viruses causing inflammatory response 1. Hemithyroidectomy: Along with removal of
with infiltration of lymphocytes, neutrophils, one lobe, entire isthmus is removed. It is done
multinucleated giant cells. in benign diseases of only one lobe.
Thyroid 239
2. Subtotal thyroidectomy commonly done in Skin and platysma are incised—upper flap
toxic thyroid either primary or secondary and raised upto thyroid cartilage, lower flap up to
also often for nontoxic multinodular goiter. sternoclavicular joint. Deep fascia is opened
Here about 8 grams, or a tissue size of pulp vertically in the midline. Strap muscles are
of finger is retained on lower pole, on both retracted or cut in between two Kocher’s forceps.
sides and rest of the thyroid gland is Pretracheal fascia is opened to mobilize the
removed. thyroid. First, short stout middle thyroid vein
3. Partial thyroidectomy is removal of the gland is ligated, then superior thyroid pedicle is ligated
in front of trachea after mobilization. It is close to the gland so as to avoid injury to external
commonly done in nontoxic multinodular laryngeal nerve. Inferior thyroid artery is ligated
goiter. away from the gland so as to avoid injury to
4. Near total thyroidectomy: Here both lobes recurrent laryngeal nerve. Mobilized gland is
except the lower pole which is very close to removed. Bed is sutured with catgut so as to
recurrent laryngeal nerve and parathyroid is prevent bleeding. Drain is placed. The wound
removed. It is done in case of papillary is close in layers (Fig. 17.15).
carcinoma of thyroid.
5. Total thyroidectomy: Entire gland is removed.
It is done in case of follicular carcinoma of
thyroid, and medullary carcinoma of thyroid.
Procedure
Position: Under general anesthesia patient is put
in supine position with neck extended by placing
a sand bag under shoulder—with table tilt of 15°
head up to reduce venous congestion.
Incision: Horizontal crease incision is done, two
finger breadth above the sternal notch, from one
sternomastoid to the other (Fig. 17.14).
Fig. 17.15: Note the relation of recurrent laryngeal nerve
Thyroid steal: Patient is taken to operation

theater for few days before doing surgery so as
to reduce the anxiety of the patient.
Complications of Thyroidectomy
Hemorrhage: May be due to slipping of ligatures
either superior thyroid artery or other pedicles.
Fig. 17.14: Note the incision for thyroid surgery It will cause tachycardia, hypotension, breath-
..We do not remember days, we remember moments.

lessness, and compression over the trachea may parathyroid glands, occurs in 2–5th post-
cause severe stridor, respiratory obstruction. As operative day. Present with weakness, +ve
a first aid, immediate release of sutures including Chvostek’s sign, carpopedal spasm, convulsions.
that of deep fascia has to be done and pressure Serum calcium estimation has to done and then
over the trachea is released. Then patient is 10 ml of 10% Calcium gluconate is given IV
shifted to operation theater, and under general eighth hourly, and later supplemented by oral
anesthesia exploration is done and bleeders are calcium 500mg 8th hourly. After 3–6 weeks,
ligated. Blood transfusion may be required. patient is admitted, drug is stopped and serum
calcium level is repeated (Fig. 17.16).
Respiratory obstruction: It may be due to
hematoma (if it is so, the hematoma has to be Thyrotoxic crisis (Thyroid storm): occurs in a
evacuated), or due to laryngeal edema. For thyrotoxic patient inadequately prepared for
thyroidectomy and rarely a thyrotoxic patient
laryngeal edema, immediate emergency endo-
presents in a crisis following an unrelated
tracheal intubation is done along with steroid
operation or stress. They present in 12–24 hours
injections. Often emergency tracheostomy may
with severe dehydration due to circulatory
be required as a life saving procedure. collapse, hypotension, hyperpyrexia, and often
Recurrent laryngeal nerve palsy: It can be transient cardiac failure.
or permanent. Transient is 3% common. They Treatment is injection hydrocortisone, oral
usually recover in 3 weeks to 3 months. Often antithyroid drugs, tepid sponging of whole
they require steroid supplement and speech body, beta blocker injection, oral iodides, large
therapy. Permanent paralysis is rare. amount of IV fluids for rehydration, digitoxin,
cardiac monitor, often ventilator support, and
Hypoparathyroidism is rare 0.5% common. Mostly observation. It has got high mortality rate with
it is temporary due to vascular spasm of critical period of 72 hours. Fluid and electrolyte
management, cardiac management are impor-
tant aspects to be monitored and treated.
Injury to external laryngeal nerve causes weak-
ness of cricothyroid muscle leading to alteration
in pitch of voice.
Hypothyroidism: Revealed clinically after 6
months.
Wound infection, stitch granuloma forma-
tion.
Keloid formation.
EMIL THEODOR KOCHER

He was the first surgeon to get Nobel Prize.
He did extensive work on thyroid surgeries
and designed present technique of thyroid
surgeries. He was from Switzerland.
He was the founder of:
• Kocher’s vein.
• Kocher’s forceps (has got tooth in the tip).
Fig. 17.16: Note the location of parathyroid glands • Kocherization (duodenal mobilization).
Thyroid 241
• Kocher’s incision, (Right subcostal for Clinical Features
cholecystectomy). • General: Tiredness, weight gain, cold intole-
• Kocher’s thyroid incision. rance, goiter, hyperlipidemia.
• Kocher’s test. • Cardiovascular: Bradycardia, angina, cardiac
• Kocher’s method for reduction of failure, pericardial effusion.
shoulder dislocation. • Hematological: Anemia,
He died in 1917. • Dermatological: Dry skin, vitiligo, alopecia,
Other surgeons who got nobel prizes are erythema.
ALEXIS CARRELL, (for his work on vascular • Reproductive: Infertility, menorrhagia, galac-
anastomosis), CHRISTIAN BERNARD, (for torrhea, etc.
heart transplantation), CHARLES HUGGINS • Gastrointestinal: Constipation, ileus.
(Urologist, for management of carcinoma • Developmental: Growth and mental retar-
prostate). dation, delayed puberty.
• Other features: Carpal tunnel syndrome,
myalgia, hoarseness, deafness, ataxia, dep-
HYPOTHYROIDISM ression, psychosis (myxedema madness).
Causes Investigations
1. Agenesis or dysgenesis. T3, T4 estimation.
2. Enzyme deficiency. TSH level estimation which is higher.
3. Iodine deficiency.
4. Hashimoto’s thyroiditis. Treatment
5. Antithyroid drugs. Replacement with L-thyroxine 100 to 150 ug/
6. Radioiodine. day. In old patients with ischemic heart disease
7. Drugs: Lithium, amiodarone. initial therapy is with 25–50 ug/day and then
8. After thyroidectomy. gradually increased up to the required dose.
..One joy scatters a hundred grieves.

18 Parathyroid
 Anatomy of parathyroid Two upper glands are constant in position.

Hyperparathyroidism Superior is behind recurrent laryngeal nerve.

They develop from 4th pharyngeal pouch hence
 Acute hyperparathyroidism (CRISIS)
called as parathyroid IV.
 Tetany
Two lower glands are variable in position.
 MEN syndrome (MEA syndrome)
They develop from endoderm of 3rd pharyngeal
pouch hence called as parathyroid III. It is usually
ANATOMY OF PARATHYROID in front of the lower part of recurrent laryngeal
Parathyroids are endocrine glands situated nerve.
behind the thyroid gland. They are four in Each gland weighs 50 gm. It is brownish
number two on each side (Fig. 18.1). (khaki colored) firm gland, which sinks in the
fluid unlike fat, which floats. It is usually adjacent
to the anastomosis between superior and inferior
thyroid arteries posteriorly.
Glands (chief cells) secrete parathormone
(PTH), which controls the calcium metabolism.
PTH
• Increases absorption of the calcium from the
gut.
• Mobilizes calcium from the bone.
• Increases the calcium reabsorption from the
renal tubules.
DiGeorge’s syndrome
• Absence of parathyroids.
• Thymic aplasia with immunodeficiency.
Fig. 18.1: Anatomical location of parathyroids
• Cardiac defects.
Parathyroid 243
HYPERPARATHYROIDISM • They are more prone for skin necrosis, band
keratopathy, pseudogout, myalgia, arthral-
Types: gia, polyuia, glycosuria, and hypertension.
1. Primary
2. Secondary
ACUTE HYPERPARATHYROIDISM
3. Tertiary.
(CRISIS)
Primary is unstimulated inappropriate high
It is rare but dangerous presentation (crisis)
PTH secretion due to hyperplasia or adenoma.
wherein patient presents with severe, acute
Secondary is due to chronic renal failure or due abdominal pain, vomiting, dehydration, oliguria
to malabsorption, i.e. due to chronic hypo- and death.
calcemia. Serum calcium is very high.
Tertiary is due to autonomous hyperplasia. Treatment
• Adenoma 75–90% • Rehydration.
• Hyperplasia 20–24% • Steroids.
• Carcinoma, rare 1%. • Clodranate sodium.
Carcinoma of parathyroid is one of the most • Drugs to reduce calcium level, i.e. Mithramy-
aggressive tumor known but fortunately rare. cin, Calcitonin, Prednisolone, Biphosphonates.
May present as a nodule and can have blood born Biphosphonates like disodium Pamidronate
metastasis. 60 mg is given slow intravenously as single
dose, which prevents mobilization of calcium
Clinical Features from the bone and so controls hypercalcemia.
Clinical vignette of hyperparathyroidism— • Condition has got high mortality rate.
“Bones, stones, abdominal groans and psychic Investigations
moans.”
• Hyperparathyroidism is common in middle- • High serum calcium — > 10 mg\100 ml.
aged women. • Decreased serum phosphorus.
• Presentation may be asymptomatic hypercal- • Increased urinary calcium — > 250 mg\24
cemia. (Commonest—50%) hrs.
• Nonspecific symptoms and psychiatric symptoms • Increased serum alkaline phosphatase.
with behavioral problems (They are most • Increased PTH level in the serum is
often named as neurotics). diagnostic — > 0.5 pg\L.
• The bone presents with osteitis fibrosa cystica • X-ray skull shows salt-pepper appearance
(von Recklinghausen disease), which shows (Fig. 18.2).
single or multiple cysts or pseudotumor in • X-rays phalanges and jaw are specific.
the jaw, skull or middle phalanges. • Ultrasound abdomen to find out problems
• The first bony change seen in lamina dura in kidney, pancreas.
of tooth. • Ultrasound neck and CT scan neck and
• In the kidney, there may be bilateral multiple mediastinum.
renal stones (25%) or nephrocalcinosis (may go • Selective venous sampling for PTH is also
for renal failure). very useful.
• It may be associated with the peptic ulcer, • Thallium–Technetium scan shows hot spots,
pancreatitis, MEN I syndrome. which is diagnostic of parathyroid adenoma.
..Those who can’t hear the music think the dancer’s mad.
Indications for parathyroidectomy

• Severe symptoms.
• Young age group.
• Markedly reduced bone density.
• Serum calcium more than 11 mg %.
• Urinary calculi.
• Neuromuscular presentations.
• Urinary calcium more than 400 mg /24
hours.
Medical treatment of primary hyperparathyroi-
dism is usually ineffective and not popular.
However occasionally as initial therapy and in
acute crisis it is being advocated. Estrogens,
Progestogens, Raloxofene (estrogen receptor
Fig. 18.2: Plain X-ray skull. Note the characteristic Salt- modulator), Mithramycin, Calicitonin are the
Pepper appearance of the skull bones few drugs used. Mithramycin is used once a
week but it is hepatotoxic and causes thrombo-
cytopenia.
• Technetium-99m labeled Sestamibi isotope scan
is better and sensitive (80%) than Thallium- Surgical aspects in parathyroidectomy
Tc scan. As it is very expensive it is used in • Single adenoma—Excision
parathyroid re-exploration. It is often • Carcinoma—Removal of entire four glands
combined with single photon emission with thyroidectomy.
computerized tomography (SPECT). • Hyperplasia—All four glands are removed
• Urinary cAMP level increases in 90% cases. with autotransplantation of 1/3rd of one
Note: Serum albumin should also be assessed to gland over sternomastoid muscle in the neck
get accurate calcium level. or over brachioradialis muscle in the forearm.
Corrected serum Ca in mmol/l = Measured • Postoperative follow up by doing regular
serum ca + (40 –Albumin) × 0.02. estimations of serum calcium and parathor-
mone.
Differential diagnosis • Parathyroidectomy is technically difficult.
Parathyroid glands are dark-brown in color,
• Secondaries in the bone. which should be confirmed by frozen section
• Multiple myeloma. biopsy. It should be differentiated from fat
• Vit D intoxication. and lymph nodes. Fat is yellow in color and
• Sarcoidosis. floats in water. Lymph node is light brown
• Functioning carcinoma. or pale in color.
Treatment Problems in parathyroidectomy
• Surgical removal of the glands and implan- • Permanent hypoparathyroidism.
tation of fragments of the gland in forearm • Recurrent hyperparathyroidism-hypercal-
muscle mass (brachioradialis or sterno- cemia 12 months after parathyroidectomy.
mastoid) or neck. • Recurrent laryngeal nerve injury.
• If it is carcinoma, additional hemithyroidec- • Often needs additional thyroidectomy.
tomy with postoperative radiotherapy is • Variations in positions of the gland especially
required. lower, may be in mediastinum.
Parathyroid 245
• Sudden drop in calcium level after surgery pressure of the patient for three minutes can
due to increased absorption of calcium by demonstrate carpal spasm (Trousseau’s sign).
bones—hungry bone syndrome. There is • Stridor and difficulty in breathing due to
sudden drop in serum calcium level with paralysis of respiratory muscles.
features of severe tetany. It should be treated • Generalized weakness and twitching all
initially by continuous slow intravenous over the body in severe cases mimicking
calcium infusion usually for 2–4 days later convulsions.
with oral calcium supplements.
Management
TETANY • Serum calcium estimation is done. It will be
Decreased level of calcium in blood causing its less than 7 mg%.
effects. • IV calcium gluconate 10%, 10 ml sixth to
eighth hourly is given slowly over 10
Causes minutes.
• Later oral calcium with vitamin D supple-
• After thyroidectomy (It is decreased level of
parathormone in the blood causing hypo- mentation.
calcemia). It is usually temporary lasting for • Follow up at regular intervals by doing
4–6 weeks. It is the commonest cause of serum calcium level.
hypoparathyroidism. Other causes of hypo-
parathyroidism are neck dissection, hemo- MEN SYNDROME (MEA syndrome)
chromatosis, Wilson’s disease, DiGeorge’s
syndrome. • Commonly inherited as autosomal dominant.
• Severe vomiting, hyperventilation associated • Cells involved have got common features of
with respiratory alkalosis. APUD cells (Apudomas). (Amine Precursor
• Metabolic alkalosis like in pyloric stenosis. Uptake and Decarboxylation).
• Rickets, osteomalacia.
• Chronic renal failure. Types
• Acute pancreatitis. • Type I: Parathyroid hyperplasia or adeno-
Decreased PTH causes decrease in calcium level in mas; pituitary tumor; pancreatic tumor
the blood leading to— (Endocrine -(Insulinoma, gastrinoma,
• Circumoral paresthesia, paresthesia of neck, glucagonoma, vipoma)). It is also called as
fingers and toes. Wermer’s syndrome.
• Twitching and weakness of tongue muscles, • Type II: Also called as Sipple’s disease:
muscles of forearm, hand, foot and digits— 1. II A includes medullary carcinoma of
carpopedal spasm. thyroid + pheochromocytoma + para-
• Chvostek’s sign Tapping above the angle of thyroid hyperplasia (50%).
the jaw to stimulate branches of facial nerve 2. II B includes medullary carcinoma of
causes the twitching of the angle of mouth thyroid + phechromocytoma + mucosal
and eyelids. neuromas in lips and eyelids with
• Applying the sphygmomanometer to the arm bumpy-lumpy lesions, with marfanoid
and inflating the pressure more than systolic face, megacolon.
..For every minute you are angry you lose sixty seconds of happiness.
19 Salivary Glands
 Anatomy Parotid duct (Stensen’s) is 2–3 mm in

 Sialography diameter, begins behind the angle of the
 Salivary calculus mandible, passes through the buccinator muscle,
 Sialosis and opens into the oral mucosa opposite upper
 Sialectasis second molar tooth.
 Parotid abscess (acute suppurative Facial nerve emerges from the stylomastoid
foramen lying between external auditory meatus
sialadenitis of parotid).
and mastoid process. It passes around the neck
 Parotid fistula
of the condyle of mandible and becomes
 Sjögren’s syndrome
superficial, later dividing into temporofacial and
 Mikulicz disease
cervicofacial branches, which in turn divides into
 Salivary neoplasms many branches. Some of these may be inter-
 Management of malignant salivary tumor connected as pes anserinus.
 Minor salivary gland tumors
 Frey’s syndrome (auriculotemporal SUBMANDIBULAR SALIVARY GLAND
syndrome, gustatory sweating)
Parts (Fig. 19.2)
 Parotidectomy
Superficial part: Lies in submandibular triangle,
superficial to mylohyoid and hyoglossus muscles,
ANATOMY between the two bellies of digastric muscles.
PAROTID GLAND Deep part is in the floor of the mouth and deep
(PARA—AROUND, OTIS—EAR) to the mylohyoid.
Submandibular duct (Wharton’s) (5 cm),
Parts of the Parotid Gland (Fig. 19.1) comes from the deep part of the gland, enters
• Superficial part—lies over the posterior part the floor of the mouth, on a papilla beside the
of the ramus of mandible. frenum of the tongue.
• Deep part—lies behind the mandible and Lingual nerve and submandibular ganglion
medial pterygoid muscle. are attached to upper pole of the gland.
Accessory parotid is prolongation of the Facial artery emerges from under surface of
gland along the parotid duct. the stylohyoid muscle, enters the gland from
Salivary Glands 247
Fig. 19.1: Anatomical relations of the parotid gland
Fig. 19.2: Anatomical relations of the submandibular gland
..Kindness is a language which the dumb can speak, the deaf can understand.
posterior and deep surface reaching its lateral SALIVARY CALCULUS
surface crossing the lower border of mandible
to enter the face. • 80% submandibular.
Venous drainage is to anterior facial vein. • 80% radiopaque.
• It is commonly calcium phosphate and
calcium carbonate stones.
SIALOGRAPHY (FIG. 19.3) • Calculi are more common in submandibular
Indications gland, because the secretion of the gland is
viscous, contains more calcium and also its
• Salivary fistulas.
drainage is nondependent, leading to stasis.
• Sialectasis.
• Secretion from parotid is serous, contains less
• Congenital conditions.
calcium and so stones are not common.
• Extraglandular masses.
Dye used is Lipiodol or sodium diatrizoate
Presentation
(Hypaque).
24 gauge cannula is passed into either Acute features
Stensen’s duct or Wharton’s duct and X-ray is • Pain, swelling, tenderness is seen in sub-
taken after injecting 1ml of the dye into the duct. mandibular region and floor of the mouth.
• Duct is inflamed and swollen.
Findings Features in chronic cases
• Narrowing, (Stricture). • Pain is more during mastication due to
• Grape-like cluster appearance (Sialectasis). stimulation.
• Dilatations. • Salivary secretion is more during mastication
• Communications (Fistulas). causing increase in gland size.
• Mass lesions. • Firm, tender swelling is bi-digitally palpable.
Sialography should never be performed in acute • When stone is in the duct, it is palpable in
inflammation. Only one ml of dye is injected, if the floor of the mouth as a tender swelling
more dye is injected it will cause extravasation, with features of inflammation in the duct. Pus
and chemical sialadenitis. exudes through the duct orifice.
• In submandibular salivary gland, the stones
are multiple, associated with inflammation
of gland (sialadenitis) (Fig. 19.4).
Fig. 19.3: Sialogram X-ray done to visualize the ductal Fig. 19.4: Submandibular sialadenitis in a young boy who
pattern in parotid required excision of gland
Salivary Glands 249
• Submandibular lymphadenitis.
• Salivary neoplasm.
Investigations
• Intraoral X-ray (dental occlusion films) to see
radiopaque stones (Fig. 19.5).
• FNAC of the gland to rule out other pathology.
• Total count and ESR in acute phase.
Treatment
• If it is a ductal stone, removal of the stone
is done intraorally, by making an incision on
the duct. Incised duct is not sutured as it may
Fig. 19.6: Incision for excision of submandibular salivary
result in stricture. gland. It should be 2 cm below the margin of the mandible to
• If stone is in the gland, excision of submandi- avoid injury to marginal mandibular nerve
bular gland is done.
Approach is from submandibular region taken care off. Mylohyoid is retracted so as to
(outside). Skin incision is made in submandi- remove the deep portion of the gland. Drain is
bular region, about 5–8 cm length, parallel to and placed after removal of the gland.
2–4 cm below the mandible (Fig. 19.6). Incision
is deepened through the deep fascia until the COMPLICATIONS OF SURGERY
gland is visualized without raising the flaps (so • Hemorrhage.
as to avoid injury to marginal mandibular nerve, • Infection.
branch of facial nerve). Facial artery is ligated • Injury to marginal mandibular nerve, lingual
twice. Lingual nerve and hypoglossal nerves are nerve, hypoglossal nerve.
Rule of two in submandibular salivary gland
• Two parts divided by myelohyoid muscle.
• Two conditions affect it—tumor and stone.
• Two superficial nerves—cervical and mandi-
bular branch of facial nerves.
• Two deep nerves—lingual and hypoglossal
nerves.
• Incision—2 cm below the mandible.
• Ligate facial artery at 2 places.
Salivary calculi
Submandibular gland Parotid
80% common. 20% incidence (Rare).
80% radiopaque Radiolucent.
Seen in plain X-ray Not seen in plain X-ray.
(intraoral)
Fig. 19.5: X-ray showing large stone in duct of submand-
Sialogram is not Identified by sialogram.
ibular salivary gland, which is radiopaque (By Dr Jagadish
Mangalore) needed.
..Human beings, by changing the inner attitudes of their minds, can change the
outer aspects of their lives.
Calculi are common in submandibular Causes of Acute parotitis (Differential

salivary gland diagnosis of suppurative parotitis)
• Viscous nature and mucin content. • Viral—Mumps.
• Calcium content. • Bacterial—Staphylococcus aureus.
• Nondependent drainage. • Allergic.
• Stasis. • HIV infection.
• Radiotherapy.
• Specific infections like syphilis.
SIALOSIS
It is enlargement of the salivary gland due to Clinical Features
fatty infiltration as a result of various metabolic • Pyrexia, malaise, pain and trismus.
causes like diabetes, acromegaly, obesity, and • Red, tender, warm, well-localized, firm
liver disease. swelling is seen in the parotid region.
• Tender lymph nodes are palpable in neck.
Clinical features: Bilateral diffuse enlargement • Features of bacteremia are present in severe
of parotids, which is smooth, firm, nontender. cases.
Treatment: The cause is treated. • Pus or cloudy turbid saliva may be expressed
from the parotid duct opening.
SIALECTASIS
Investigations
• It is an aseptic dilatation of salivary ductules • Ultrasound of parotid region.
causing grape-like (cluster-like) dilatations. • Pus collected from duct orifice is sent for
• It is a disease of unknown etiology with des- culture and sensitivity.
truction of gland parenchyma a ccompanied • Needle aspiration from the abscess to confirm
by stenosis and cyst formation in the ducts. the formation of pus.
• It is common in parotids; often bilateral. Sialogram is contraindicated in acute phase, as
• Presents as a smooth, soft, fluctuant, non- it causes retrograde infection leading into
transilluminating swelling, which increases bacteremia.
in size during mastication. It is tender
initially. It lasts for many days with a long Treatment
symptom free period of the disease. • Antibiotics are started depending on culture
• Sialogram is diagnostic. report.
• Treatment is conservative (nonsurgical). • When it is severely tender, localized, incision
and drainage has to be done under G\A. Skin
PAROTID ABSCESS (ACUTE SUPPURA- is incised in front of the tragus vertically and
then parotid sheath is (pyogenic membrane)
TIVE SIALADENITIS OF PAROTID)
opened horizontally. Pus is drained using
It is a result of an acute bacterial sialadenitis of sinus forceps and sent for C/S. Antibiotics
parotid gland. continued (Blair’s incision) (Fig. 19.7).
It is an ascending bacterial parotitis, due to Complications of suppurative parotitis and
reduced salivary flow and poor oral hygiene. abscess:
Causative organism are Staphylococcus aureus, • Septicemia.
Streptococcus viridans, and often other gram- • Severe trismus.
negative and anaerobic organisms. • Rupture into the external auditary canal.
Salivary Glands 251
SJÖGREN’S SYNDROME
It is an autoimmune disease causing progressive
destruction of salivary and lacrimal glands,
leading to keratoconjunctivitis sicca (dry eyes), and
xerophthalmia (dry mouth).
Types
1. Primary.
2. Secondary.
Secondary Sjögren’s Syndrome

• Dry mouth.
• Dry eyes.
Fig. 19.7: Blair incision used to drain the parotid abscess
• With association of connective tissue dis-
orders like.
Note: In suppurative parotitis patient may develop • Primary biliary cirrhosis (near 100%).
severe laryngeal or pharyngeal edema and may require • SLE (30%).
steroids, tracheostomy and critical care. • Rheumatoid arthritis (RA) (15%).
Primary Sjögren’s Syndrome

PAROTID FISTULA
• Severe dry mouth.
Causes • Severe dry eyes.
• After superficial parotidectomy. • Widespread dysfunction of exocrine glands.
• After drainage of parotid abscess. • Incidence of developing lymphomas is high.
• After biopsy. • There is no association of connective tissue
• Trauma. disorders.
• Malignant recurrence of tumor.
Clinical Features
Clinical Features • It is common in middle-aged females who
• Discharging fistula in the parotid region of present with dry eyes, dry mouth, enlarged
face. parotids and enlarged lacrimal glands.
• Tenderness and induration. • Often they are tender.
• Trismus. • Super added infection of the mouth, with
Candida albicans is common.
Diagnosis Investigations
• Fistulogram. • Autoantibody estimation—Rheumatoid
• Discharge study. factor, antinuclear factor, salivary duct
• MRI. antibody.
• Sialography.
Treatment • Estimation of salivary flow.
Initial radiotherapy and then exploration. • Slit-lamp test of eyes.
..Great people talk about ideas; average people talk about things;
small people talk about other people.
• Schirmer test—to detect lack of lacrimal b. Nonepithelial
secretion. Hemangioma—commonly seen in infants,
• FNAC of parotids and lacrimal glands. usually in parotid. Spontaneous regression
• 99Technetium pertechnetate scan for gland is common.
function. Lymphangioma
Neurofibromas and neurilemmomas.
Treatment is Conservative c. Malignant lymphomas.
• Artificial tears.
• Artificial saliva. Clinical features of parotid tumor
• Frequent drinking of water. • Raised ear lobule (Figs 19.8A and B, 19.9).
• Treat the cause. • Cannot be moved above the zygomatic bone.
• Deviation of uvula and pharyngeal wall
towards midline in case of deep lobe.
MIKULICZ DISEASE • Facial nerve, masseter, skin, lymph node and
• It is a clinical variant of Sjögren’s syndrome bone involvement in case of malignancy.
• It is autoimmune disorder of salivary and
lacrimal glands, resulting in infiltration of the Incidence
glands with round cells. • 75-80% salivary neoplasms are in the parotids
(Fig. 19.10) of which 80% are benign.
Triad • 80% of these are pleomorphic adenomas
• Symmetrical enlargement of all salivary (Fig. 19.11).
glands. • 15% of salivary tumors are in the submandi-
• Narrowing of palpebral fissures due to bular salivary gland of which 60% are benign.
enlargement of the lacrimal glands. • 95% of these are pleomorphic adenomas.
• Parchment like dryness of the mouth. • 10% of salivary neoplasms are in the minor
salivary glands—palate, lips, cheeks, and
SALIVARY NEOPLASMS sublingual glands. Of these only 40% are
benign.
Classification
a. Epithelial PLEOMORPHIC ADENOMAS (FIG. 19.12)
1. Adenomas (MIXED SALIVARY TUMOR)
- Pleomorphic adenoma.
- Monomorphic adenomas • Commonest of the salivary gland tumor. It
- Adenolymphoma (Warthin’s tumor) . is 80% common.
- Oxyphil adenomas. • More common in parotids.
2. Carcinomas • It is mesenchymal, myoepithelial and duct
- Mucoepidermoid carcinoma—Com- reserve cell origin.
monest malignancy. Grossly it contains cartilages, cystic spaces, and
- Acinic cell carcinoma. solid tissues.
- Adenoid cystic carcinoma—Very
aggressive. Histologically it shows ]
- Adenocarcinoma. — Epithelial cells.
- Squamous cell carcinoma. — Myoepithelial cells.
- Carcinoma in ex. Pleomorphic adenoma. — Mucoid material with myxomatous changes.
- Undifferentiated carcinoma. — Cartilages.
Salivary Glands 253
Figs 19.8A and B: Typical parotid swelling with earlobe raise. Facial nerve should be tested by clenching the teeth
Fig. 19.9: Parotid tumor showing typical raise in earlobe Fig. 19.10: Neoplasm of parotid gland
Fig. 19.11: Typical parotid tumor—a pleomorphic adenoma Fig. 19.12: Pleomorphic adenoma
..If the only tool you have is a hammer than treat everything like a nail.
Even though it is capsulated, tumor may
come out as pseudopods and may extend
beyond the main limit of the tumor tissue.
When disease occurs in parotid, commonly
it involves superficial lobe or superficial and
deep lobe together.
But sometimes only deep lobe is involved and
then it presents as swelling in the lateral wall
of the pharynx, soft palate and posterior pillar
of the fauces.
There may not be any visible swelling in the
preauricular region—Dumbbell tumor.
This tumor is in relation to styloid process,
mandible, stylohyoid, styloglossus, stylopharyn-
geus muscles.
Fig. 19.13: Recurrent pleomorphic adenoma. Facial nerve
Clinical Features palsy, skin involvement, rapid recent growth, soft tissue
spread and neck nodal involvement are features of malignant
• 1:1 male to female ratio. 80% common. transformation
• Occurs in any age group. Usually unilateral.
• Present as a single painless, smooth, firm
Investigations
lobulated, mobile swelling in front of the
parotid with positive curtain sign (As the deep • FNAC is very important and diagnostic.
fascia is attached above to the zygomatic • CT scan to know the status of deep lobe.
bone, it acts as a curtain, not allowing the Treatment
parotid swelling to move above that level.
• Surgery—1st line of treatment.
Any swelling superficial to the deep fascia
• If only superficial lobe is involved, then
will move above the zygomatic bone).
superficial parotidectomy is done wherein
• The ear lobule is lifted.
parotid gland superficial to facial nerve is
• When deep lobe is involved, swelling is com-
removed.
monly located in the lateral wall of pharynx,
• If both lobes are involved, then total conser-
posterior pillar and over the soft palate.
vative parotidectomy is done by retaining
• Facial nerve is not involved. facial nerve.
Long standing pleomorphic adenoma may turn • Enucleation is avoided, as the recurrence is
into carcinoma (carcinoma in ex. pleomorphic high.
adenoma).
Its features are: ADENOLYMPHOMA (WARTHIN’S TUMOR,
• Recent increase in size. PAPILLARY CYSTADENO- LYMPHOMATOSUM)
• Pain and nodularity. It is a benign tumor that occurs only in parotid,
• Involvement of skin. usually in the lower pole.
• Involvement of masseter. Common in males. It is often bilateral.
• Involvement of facial nerve (Fig. 19.13)— It is said to be due to trapping of jugular lymph
Lower facial nerve palsy –(Difficulty in sacs in parotid during developmental period.
closing eyelid, difficulty in blowing and It composed of double layered columnar
clenching teeth). epithelium, with papillary projections into cystic
• Involvement of neck lymph node. spaces with lymphoid tissues in the stroma.
Salivary Glands 255
It presents as a slow growing, smooth, soft, Low grade.
cystic, fluctuant swelling, in the lower pole, often High grade.
bilateral, and is nontender. Facial nerve involvement is rare or very late
It is common in males. It is 10% common. in mucoepidermoid carcinoma of parotid.
Clinical Features
Investigations
Swelling in the salivary (parotid or submandi-
• Adenolymphoma produces a ‘hot spot’ in bular) region, slowly increasing in size, even-
99 Technetium pertechnetate scan—it is
tually attaining a large size, which is hard,
diagnostic. nodular, often with involvement of skin and
• FNAC. lymph nodes.
Adenolymphoma does not turn malignant. Facial nerve is usually not involved.
Treatment ADENOID CYSTIC CARCINOMA

Superficial parotidectomy. It is common in minor salivary glands.
It consists of myoepithelial cells and duct
MUCOEPIDERMOID TUMOR (FIG. 19.14) epithelial cells with cribriform or lace like
It is the commonest malignant salivary gland appearance.
tumor (in major salivary glands). It involves facial nerve very early, spreads
It is slowly progressive, often attains a large through the perineural sheath and infiltrates into
size, and spreads to neck lymph nodes. the perineural tissues over a long distance more
It contains malignant epidermoid and mucus proximally.
secreting cells. It also invades periosteum and bone medulla
early and spreads extensively.
Prognosis is poor.
ACINIC CELL TUMOR

It is a rare, slow growing tumor that occurs
almost always in parotid and is composed of cells
General features of malignant

salivary tumors
• Fixation.
• Resorption of adjacent bone.
• Pain and anesthesia in the skin and mucosa.
• Muscle paralysis.
• Skin involvement and nodularity.
• Involvement of jaw and masticatory muscle.
• Nerve involvement (facial nerve in parotid
or hypoglossal nerve in submandibular
salivary gland).
Fig. 19.14: Mucoepidermoid tumor
..Others can stop you temporarily...you are the only one who can do it permanently.
alike serous acini. It is more common in women.
It occurs in adult and elderly.
It can involve facial nerve or neck lymph
nodes.
Clinically it is of variable consistency with
soft and cystic areas.
SUBMANDIBULAR SALIVARY
GLAND TUMORS
Benign tumors, commonly pleomorphic adeno-
mas are smooth, firm or hard, bi-digitally
palpable, without involving adjacent muscles or
hypoglossal nerve or mandible bone.
Diagnosis is by FNAC, Orthopentomogram
(OPG), and CT scan.
Excision of both superficial and deep lobes
of the gland is done. Fig. 19.16: Incision for parotid tumor. Note the lazy S incision
Malignant tumors of submandibular salivary with involving the skin over the tumor within the incision
gland (Fig. 19.15):
They are hard, nodular, often get fixed to
skin, muscles, hypoglossal nerve, and mandible.
Diagnosis is by FNAC of primary tumor and
of lymph nodes when involved, CT scan and
OPG.
Treatment (Fig. 19.16 and 19.17)
Wide excision, with removal of adjacent muscle,
soft tissues, and mandible.
If lymph nodes are involved, block dissection
of neck (Classical neck dissection) is done.
Fig. 19.17: On table exposure of facial nerve branches
after superficial parotidectomy for a benign tumor
MANAGEMENT OF MALIGNANT
SALIVARY TUMORS
Specific investigations
• FNAC.
• CT scan to see the deep lobe of the parotid;
to look for the involvement of bone, extension
into the base of the skull; relation of tumor
to internal carotid artery, styloid process.
• OPG.
• Blood grouping and cross matching; required
Fig. 19.15: Submandibular salivary gland tumor which is quantity of blood is keep ready.
malignant. Patient underwent wide excision • FNAC of lymph node.
Salivary Glands 257
• MRI shows better soft tissue definition than Complications of surgery
CT scan. • Hemorrhage.
Sialogram is not useful in assessment of • Infection.
tumor. • Fistula.
• Frey’s syndrome.
TNM staging of malignant salivary tumors • Facial nerve palsy.
T—Tumor.
Tx—Tumor cannot be assessed. Postoperative radiotherapy is quiet useful to
T0—No primary tumor evidence. reduce the chances of relapse. Usually external
T1—Tumor < 2 cm without extra parenchymal radiotherapy is given. It is given in all carcino-
spread. mas, but more useful in adenoid cystic and
T2—Tumor 2–4 cm. squamous cell carcinomas.
T3—Tumor 4–6 cm. Chemotherapy is also given. Drugs given
—or with extraparenchymal spread. here depend on tumor type. Intra-arterial chemo-
—but no facial nerve spread. therapy is beneficial.
T4—Tumor > 6 cm. Preoperative radiotherapy is given in large
tumors to reduce the size and make it better
—or facial nerve spread.
operable, i.e. to down stage the disease.
—or base of skull spread.
If lymph nodes are involved, which is con-
N—Lymph node. firmed by FNAC, radical neck dissection is done.
Nx—Nodes not assessed. In submandibular salivary gland: Wide
N0—Regional nodes not involved. excision is done, with removal of mandible, and
N1—Single ipsilateral node< 3 cm. soft tissues around. If lymph nodes are involved,
N2a—Single ipsilateral node 3–6 cm. then block dissection of the neck is done.
N2b—Multiple ipsilateral nodes < 6 cm.
Indications for radiotherapy in malignant
N2c—Bilateral or contralateral nodes < 6 cm.
salivary gland tumors:
N3—Single node spread > 6 cm.
• All adenoid cystic and adenocarcinomas.
M—Metastases. • T3 and T4 tumors.
M0—No blood spread. • Recurrent tumors.
M1—Blood spread present. • Poorly differentiated tumors.
• Tumors with lymph node involvement.
Treatment • As preoperative radiotherapy.
• Recurrent benign pleomorphic adenomas.
In parotid.
• Spillage during surgery in case of pleomor-
Surgery: phic adenomas.
Radical parotidectomy is done which includes
removal of both lobes of parotid, soft tissues, part MINOR SALIVARY GLAND TUMORS
of the mandible with facial nerve. • It is 10% of salivary tumors.
Facial nerve is reconstructed using greater • It is common in - palate (40%).
auricular nerve, or sural nerve. - lip
Often lateral tarsorrhaphy or temporal sling - cheek
reconstruction is done. - sublingual glands.
..Positive attitudes create a chain reaction of positive thoughts.

• Palate is the commonest site. • It is due to injury to the auriculotemporal
• 40% are benign—commonly pleomorphic nerve, where in postganglionic parasympa-
adenomas. thetic fibers from the otic ganglion become
• 60% are malignant—commonly adenoid cystic united to sympathetic nerves from the
carcinomas. superior cervical ganglion (Pseudosynapsis).
• They present as swelling with ulcer over the
summit. Causes
• If it is malignant, then extension into the
palate, maxilla, pterygoids can occur often • Surgeries or accidental injuries to the parotid.
with involvement of lymph node. • Surgeries or accidental injuries to temporo-
mandibular joint.
Differential Diagnosis • Rarely birth trauma.
Squamous cell carcinoma of oral cavity.
Clinical Features
Investigations
• Flushing, sweating, pain and hyperesthesia
• Incision biopsy.
in the skin over the face innervated by the
• CT scan.
auriculotemporal nerve, whenever salivation
• X-ray maxilla.
is stimulated (i.e. during mastication).
• FNAC of lymph node.
• Involved skin is painted with iodine and
Treatment dried. Dry starch applied over this area will
• Wide excision often with palatal excision or become blue due to more sweat in the area
maxillectomy is done. in Frey’s syndrome—Starch iodine test.
• Reconstruction by dental plates, skin • Condition causes real inconvenience to the
grafting, or flaps are done. patient.
• Lymph node block dissection of the neck is
done if involved. Treatment
Initially conservative and reassurance. Most of
Points to be remembered the time they recover.
• Salivary gland tumors are usually benign in Occasionally they require surgical division
an adult. of the tympanic branch of the glossopharyngeal
• It is rare in children but when it occurs, it is nerve below the round window of middle ear.
commonly malignant. (i.e. Intratympanic parasympathetic neurec-
• Clinical and FNAC are diagnostic methods. tomy).
• Open biopsy is contraindicated.
• Sialogram is not useful in salivary tumors.
Treatment of Frey’s syndrome
• CT or MRI is often needed.
• Reassurance.
• Nerve should be preserved in benign lesions.
• Jacobsen neurectomy (tympanic).
• Nerve can be sacrificed to achieve clearance
• Injection of botulinum toxin to the affected
in malignancies.
skin.
• Antiperspirants like aluminium chloride.
FREY’S SYNDROME (AURICULO- • Syndrome can be prevented on table by
TEMPORAL SYNDROME, GUSTATORY placing muscle (sternomastoid) or fascial
SWEATING) (temporalis) flaps or artificial membranes
• Occurs in 10% of cases. over parotid bed.
Salivary Glands 259
PAROTIDECTOMY FACIAL NERVE PALSY
• Facial nerve palsy after parotidectomy is
Types lower facial nerve palsy.
1. Superficial parotidectomy: It is the removal of • Features are inability to close eyelid,
superficial lobe of the parotid (superficial to exposure keratitis, difficulty in clinching
facial nerve). Done in case of benign diseases teeth and blowing air, master weakness and
of superficial lobe of the parotid (Fig. 19.18). drooping of the angle of the mouth.
2. Total conservative parotidectomy: It is done in • Often it could be due to neuropraxia due to
benign diseases of parotid involving either handling of the nerve during surgical
only deep lobe or both superficial and deep technique. In such occasion, steroids will be
lobes. Here both lobes are removed with beneficial.
preservation of facial nerve. • Classic nerve injury if identified immediately,
3. Radical parotidectomy: Both lobes of parotid nerve repair is done immediately. Nerve can
is removed along with facial nerve, fat, fascia, be reconstructed using nerve grafts like sural
muscles, lymph nodes. It is done in case of
nerve, great auricular nerve.
carcinoma parotid.
• Nerve cross suturing is done often by
Later facial nerve reconstruction is done
suturing hypoglossal/spinal accessory/
using hypoglossal or greater auricular nerve.
phrenic nerves to distal branches of the facial
Complications of Parotidectomy nerve.
• Facial nerve injury. In late cases either static or dynamic
• Hemorrhage. procedures are done.
• Salivary fistulas.
Surgeries for facial nerve palsy
• Infection.
• Frey’s syndrome. Static
• Flap necrosis is common. • Suspension surgeries (of lip, cheek and angle
• Sialocele and numbness over the face and ear. of mouth using temporal fascia, palmaris
Conservative surgeries are becoming longus or synthetic materials.
popular for malignancy but they are not • Correction of medial canthus to reduce
universally accepted. epiphora.
• Lateral tarsorrhaphy to treat exposure
keratitis.
• Upper lid weights.
Dynamic
• Muscle transfer-temporal to masseter with
nerve and vessel.
• Free muscle graft.
• Cross facial nerve transplant using sural
nerve from normal facial to paralyzed facial
nerve.
• Nerve grafts.
• Neurovascular gracilis muscle graft using
Fig. 19.18: ‘S’ shaped incision towards parotidectomy
microscope.
..Never let yesterday use up too much of today.

20 Oral Cavity
 Ranula
 Sublingual dermoids
 Leukoplakia
 Erythroplakia
 Oral submucosal fibrosis
 Cancrum oris (NOMA)
 Carcinoma cheek
 Neoplasm of lip
 Carcinoma tongue
 Nasopharyngeal carcinoma
 Maxillary tumors
 Carcinoma hard palate
RANULA
(Rana = Frog, Ranula looks like belly of frog,
hence the name). Fig. 20.1: Ranula
Ranula is an extravasation cyst arising from
sublingual gland or mucus glands of Nuhn or glands It often extends into the submandibular
of Blandin in the floor of the mouth. region through the deeper part of the posterior
margin of mylohyoid muscle and is called as
Clinical Features (Fig. 20.1) plunging ranula.
Present as a bluish smooth, soft, fluctuant, Ranula has a delicate fibrous capsule and is
brilliantly transilluminant swelling in the lateral lined by a layer of macrophages.
aspect of the floor of the mouth. It contains clear fluid.
Oral Cavity 261
Clinical features of Ranula Types
• Bluish swelling in the floor of the mouth. 1. Homogenous.
• Laterally placed, Nontender. 2. Nodular—more potentially malignant.
• Fluctuant and cross fluctuant. 3. Speckled—more potentially malignant.
• Brilliantly transilluminant. Clinically the lesion appears as white or
grayish colored, well-localized patch in the
Treatment cheek, tongue, palate or other areas of the oral
Initially marsupialization can be done and later cavity (Fig. 20.2).
when the wall of the ranula gets thickened it is
Common Causes
excised. If ranula is small it can be excised
directly. • Smoking.
• Spirit.
Differential Diagnosis • Sepsis.
• Lymph cyst. • Superficial glossitis.
• Sublingual dermoid. • Syphilis.
• Spices.
SUBLINGUAL DERMOIDS • Sharp tooth.
They are sequestration dermoids lined by • Susceptibility.
squamous epithelium containing keratin. • Pan chewing using areca, tobacco, slaked
lime.
Types • Chronic hypertrophic candidiasis (long
1. Median sublingual dermoid: It is derived standing candidial infection).
from epithelial cell rests at the level of fusion of Incidence of leukoplakia in those who smoke
two mandibular arches. It is located between two or chew pan is 20%, where as incidence in non-
genial muscles, above the level of mylohyoid smokers is 1%.
muscle. It is a midline swelling which is smooth, Incidence of it turning into malignancy is 2-
soft, cystic, nontender, nontransilluminant. 4%. It increases with age, duration of the pan
Treatment is excision through per oral chewing, smoking.
approach.
Histology: Parakeratosis with widening of rete pegs.
Complication is abscess formation.
2. Lateral sublingual dermoid: It develops in
relation to submandibular duct, lingual nerve
and stylohyoid ligament. It is derived from first
branchial arch. It forms a swelling in the lateral
aspect of the floor of the mouth.
Treatment: Small dermoids are removed per
orally; larger one, through submandibular
incision.
LEUKOPLAKIA
It is a white patch in the mucosa of the oral cavity
that cannot be characterized clinically or
pathologically to any other disease. It is a pre- Fig. 20.2: Leukoplakia cheek. Note the typical white patch.
malignant condition. It is a premalignant condition
..Money is a good servant, but a dangerous master.

Histological staging Treatment

• Acanthosis. Precipitating factors has to be avoided.
• Parakeratosis. Surgical excision when required followed by
• Widening of retepegs. skin grafting has to be done.
• Dyskeratosis.
RETROMOLAR TRIGONE is the anterior
• Dysplasia.
surface of the ascending ramus of the mandible.
• Carcinoma in situ.
It is triangular in shape with the base being
Biopsy confirms the diagnosis as well as rules superior and apex inferiorly behind the third
out the carcinoma. molar tooth.
Treatment Premalignant conditions of oral cavity

• Leukoplakia.
• Pan chewing and smoking has to be stopped.
• Erythroplakia.
• Excision, if required skin grafting has to be
• Chronic hyperplastic candidiasis.
done.
• Oral submucosal fibrosis.
• Regular follow up is necessary.
• Syphilitic glossitis.
• Sideropenic dysphagia.
ERYTHROPLAKIA • Oral lichen planus.
• It is red velvety appearance of the mucosa, • Discoid lupus erythematosus.
which cannot characterize any recognized • Dyskeratosis congenita.
condition.
• It is 17–20 times more potentially malignant
CANCRUM ORIS (NOMA)
than leukoplakia.
• Histologically parakeratosis with severe • It is an infective gangrene, a severe form of
epithelial dysplasia is the typical feature. Vincent’s acute ulcerative gingivitis and
• Diagnosis is by biopsy.
stomatitis.
Treatment • Seen in poorly nourished, ill child due to
Borrelia vincentii and Fusiformis bacteriae.
Biopsy and surgical excision.
• It starts in gums, spreads into cheek, bone,
soft tissues and skin causing extensive tissue
ORAL SUBMUCOSAL FIBROSIS
loss with severe toxemia.
• It is a progressive fibrosis deep to the mucosa • There will be other secondary infection also.
of the oral cavity, which causes trismus and
ankyloglossia.
Treatment
• The mucosa of cheek, gingivae, palate and
tongue shows a mottled/marbled pallor. • Systemic antibiotics, high dose Penicillins,
• It is common in Asians and Indians. Metronidazole.
• High protein and vitamin rich diet, through
Etiology nasogastric tube.
Hypersensitivity to chilli, betelnut, tobacco and • Wound irrigation and liberal removal of the
vitamin deficiencies probably alter the collagen dead tissue.
metabolism leading to juxtaepithelial fibrosis, • Blood transfusion, TPN.
epithelial atrophy and dysplasia. • Later patient requires flaps to cover the
30-33% of oral submucosal fibrosis can turn defect.
into malignancy. It has got high mortality.
Oral Cavity 263
CARCINOMA CHEEK Premalignant conditions
Squamous cell carcinoma is the most common type • Leukoplakia.
of carcinoma of the cheek (Fig. 20.3). • Erythroplakia.
Occasionally it can be adenocarcinoma • Submucosal fibrosis.
arising from the minor salivary glands or • Hyperplastic candidiasis.
mucous glands. Rarely it can also be melanoma.
Betel nut chewing (Pan, with pan quid kept
Sites of carcinoma in oral cavity in order in cheek pouch for a long time) is an important
In India In Western countries causative factor of carcinoma cheek.
• Cheek—commonest • Tongue
• Floor of the mouth • Floor of the mouth Types
• Palate • Lip 1. Ulcerative.
• Lips • Cheek 2. Proliferative (exophytic).
3. Verrucous.
Verrucous carcinoma:
Malignancies of the oral cavity
• It occurs as a superficial proliferative
• Squamous cell carcinoma—commonest.
exophytic lesion with minimal deep invasion.
• Minor salivary gland tumors.
• Lesion has got white, dry, velvety or warty,
• Melanomas.
keratinized surface.
• Adenocarcinomas—rare.
• It is of low grade, very well-differentiated
• Sarcomas—rare.
squamous cell carcinoma, which is locally
malignant without any lymphatic spread.
Precipitating factors:
• It is a curable malignancy.
All ’S’—Smoking, Spirit, Syphilis, Sharp tooth,
• After biopsy, treatment is wide excision.
Sepsis, Spices.
Radiotherapy is not given as it may lead to
anaplastic transformation.
Biological Behavior of Carcinoma Cheek

(Figs 20.4A and B)
• Carcinoma cheek is more common in
posterior half of cheek than anterior.
• It spreads into the deeper plane to involve
buccinator, pterygoids; into the retromolar
trigone, base of the skull, pharynx.
• It spreads outwards to involve the skin
causing fungation, ulceration, orocutaneous
fistula formation.
• Mandible is commonly involved either by
direct extension or through subperiosteal
lymphatic plexus, which communicates
Fig. 20.3: Recurrent carcinoma cheek (postsurgical) freely with oral lymphatics.
..Wisdom in the man, patience in the wife, brings peace to the house and a happy life.
here communicate freely with the pharyngeal
lymphatics.
• Everted edge, induration are the typical features
of the ulcer. Induration occurs in the edge and
base.
• Bidigital examination of mandible is done to
look for thickening, tenderness, and sites of
fracture.
• Trismus and dysphagia signifies involvement
of pterygoids, or posterior extension.
• Occasionally it may extend into the upper
alveolus and to the maxilla causing swelling,
pain and tenderness.
• Submandibular lymph nodes and upper deep
cervical lymph nodes are involved which are
hard, nodular, initially mobile but later get
fixed to each other and then to deeper
structure.
• Once lymph nodes get fixed it may
infiltrate into hypoglossal nerve (tongue
deviates towards the same side), spinal
accessory nerve (defective shrugging of
shoulder) and cervical sympathetic chain
(Horner’s syndrome).
• Compression over external carotid artery
Figs 20.4A and B: Advanced carcinoma cheek in two causes absence of superficial temporal
different patients. In first male patient there is fungation with
artery pulsation.
oro-cutaneous fistula
• Eventually it causes fungation and
• Lymph nodes commonly involved are bleeding from major vessels—carotid
submental, submandibular, and deep cervi- blow out.
cal and often lateral pharyngeal groups. Staging
• Infection of the tumor area and soft tissues TNM Staging.
around is common; causing fever, foul T1 — Tumor size < 2 cm.
smelling ulcer, and halitosis. T2 — Tumor size 2–4 cm.
• Respiratory infection is common in these T3 — Tumor > 4 cm.
patients. T4 — Tumor of any size involving bone, soft
• Dysphagia occurs when tumor extends into tissues, muscles.
the retromolar region, soft palate, pharynx,. N1 — Lymph node size < 3 cm
Clinical Features N2 — Lymph node size 3–6 cm and single
(N2a) or multiple lymph nodes 3–6 cm
• Ulcer in the cheek which gradually increases size on same side (N2b)
in size in a patient with history of chewing or bilateral or opposite side nodes up
pan or smoking. to –6 cm size (N2c)
• Pain occurs when it involves the skin, bone N3 — Lymph node spread more than 6 cm
or if secondarily infected. Referred pain into size.
the ear signifies involvement of lingual nerve. M0 — No distant spread
• Involvement of retromolar trigone indicates that M1 — Distant spread
it is an advanced disease, as the lymphatics
Oral Cavity 265
Features of advanced carcinoma cheek (Fig. 20.5)
• Involvement of retromolar trigone.
• Extension into the base of skull and pharynx.
• Fixed neck lymph nodes.
• Extension to the opposite side.
Investigations
• Edge biopsy usually taken from two sites.
Biopsy has to be taken from the edge as it
contains active cells; not from the center as
Fig. 20.6: Orthopantogram showing secondaries in mandible
it is the area of necrosis.
Malignant squamous cells with epithelial
Treatment
pearls (Keratin pearls) are the histological
Treatment may be curative or palliative.
features.
Treatment strategy:
• Surgery (Fig. 20.7): Wide excision, hemi-
Broder’s histological grading mandibulectomy, neck lymph nodes block
1) Well-differentiated — > 75% Epithelial pearls. dissection.
2) Moderately — 50-75% Epithelial pearls. • Radiotherapy: Curative or palliative; external
differentiated
or brachytherapy.
3) Poorly differentiated— 25-50% Epithelial pearls.
• Chemotherapy: Intraarterial, IV or orally.
4) De-differentiated — < 25% Epithelial pearls.
a. Early growth without bone involvement:
• FNAC from lymph nodes. (No biopsy from • Curative radiotherapy using Caesium137
lymph nodes). needles or Iridium192 wires, i.e. Brachy-
• CT scans—to assess the extension of tumor therapy.
and its secondaries. Advantages are that—
• Orthopentamogram to look for the involv- • Surgery is avoided.
ement of mandible—destruction and fracture • No surgical mutilation and parts are
sites (Fig. 20.6). retained.
Fig. 20.5: Advanced stage 4 carcinoma cheek Fig. 20.7: Resected specimen after Hemimandibulectomy.
(By Dr. Jagadishchandra MDS)
..Every man is the master of his own fortune.

• As it is a squamous cell carcinoma,
primary is radiosensitive.
• Other option is wide excision with 3 cm
clearance. Often, the approach to the tumor
is by raising the cheek flap (outside). After
the wide excision, the flap is placed back
(Patterson operation).
• Presently advanced technology in
radiotherapy, facilitates the use of
external radiotherapy also. The incidence
of dreaded complication like osteoradio-
necrosis of mandible has reduced due to
better RT methods. Fig. 20.8: Marginal mandibulectomy
b. Growth with mandible involvement
(Figs 20.8 to 20.10): Here along with wide
excision of the primary tumor, hemimandi-
bulectomy or segmental resection of the
mandible or marginal mandibulectomy
(using rotary electric saw) is done.
c. Operable growth with mandible involv-
ement and mobile lymph nodes on same side:
(confirmed by FNAC): Along with wide
excision of the primary, hemimandibulec-
tomy and radical neck lymph node dissection
is done (Commando like operation) (Fig. 20.11).
d. Operable growth with mandible involvement;
mobile lymph nodes on same side and opposite Fig. 20.9: Segmental resection of the mandible
side:
Along with wide excision of the tumor,
hemimandibulectomy, radical neck lymph
node dissection on same side and functional
block dissection on opposite side are done,
retaining the internal jugular vein, sterno-
mastoid, spinal accessory nerve.
e. Operable primary tumor with mobile lymph
nodes on same side but without mandibular
involvement: Wide excision of primary
tumor and radical neck lymph node
dissection on same side are done. Mandible
is not removed (Fig. 20.12).
f. Fixed primary tumor or advanced neck
lymph node secondaries: Only palliative
external radiotherapy is given to palliate pain,
fungation and to prevent anticipated
torrential hemorrhage. Fig. 20.10: Hemimandibulectomy
Oral Cavity 267
reduce the recurrence and to improve the
prognosis.
i. Prophylactic block dissection has become
popular.
Reasons are—even though clinically, lymph
nodes are negative there may be microscopic
involvement of lymph nodes (25-65%).
Clinically detectable disease in lymph nodes
of the patient signifies extracapsular spread,
which has got poor prognosis. Recurrence rate
is less after prophylactic block compared to
block dissection with clinically positive nodes
because there is no extracapsular spread in the
former even if there is microscopic spread of
tumor in many cases. Block dissection is an
acceptable surgery as there is negligible
Fig. 20.11: Carcinoma cheek, on table wide excision.
mortality and less morbidity.
It requires pectoralis major myocutaneous flap for
reconstruction j. If growth is extending to upper alveolus:
Partial maxillectomy or total maxillectomy
may be required.
k. Role of chemotherapy: Drugs used are
Methotrexate, Vincristine, Bleomycin,
Adriamycin.
Often it is given intraarterially through
external carotid artery using arterial pump or
by increasing the height of the drip more than
13 ft so as to attain a pressure more than
systolic pressure. Chemotherapy can also be
given IV or orally.
Reconstruction after surgery (Figs 20.13 to 20.16):

• Split skin graft.
• Deltopectoral cutaneous flap-based on 2nd
perforator of internal mammary artery.
• Forehead flap-based on anterior branch of
Fig. 20.12: Radical neck dissection for secondaries in superficial temporal artery.
neck through Mc fee incision
• Pectoralis major myocutaneous flap-based
g. Preoperative radiotherapy is often used in on thoracoacromial artery.
fixed lymph nodes to downstage the disease • Mandible reconstruction by cortical bone
so as to make it operable. graft or rib, fibula or synthetic material.
h. Postoperative radiotherapy is given in T3 • Free flaps (microvascular).
and T4 tumors; N2 and N3 nodal status to
..A man who does nothing nerver has time to do anything.

Fig. 20.16: Reconstruction of the mandible after hemi-

Fig. 20.13: Forehead flap is used after wide excision mandibulectomy using plate and opposite rib fixation (By
of carcinoma cheek. It is based on anterior branch of Dr. Jagadishchandra MDS)
superficial temporal artery
Problems with surgery

• (Surgical) mutilation.
• Anesthesia complications.
• Requirement for reconstruction.
• Mortality.
• Morbidity.
Problems with radiotherapy
• When mandible is irradiated, chances of the
Fig. 20.14: Deltopectoral flap used to cover defect after dreaded problem, osteoradionecrosis are
surgical clearance in carcinoma cheek. It is based on 2nd high which requires the removal of mandi-
perforator, a branch of internal mammary artery ble.
• Loss of taste and dryness.
• Infection.
• Skin excoriation.
• Trismus may get aggravated.
• Can itself cause dysphagia, laryngeal edema.
Problems with chemotherapy

• Bone marrow suppression.
• Megaloblastic anemia.
• GIT symptoms.
• Hepatotoxicity and renal toxicity.
• Alopecia.
NEOPLASM OF LIP
Minor salivary gland tumors are common in upper
Fig. 20.15: Carcinoma cheek operated with radical neck
lip. They are usually pleomorphic adenomas.
dissection of same side lymph nodes. Reconstruction done In lower lip, squamous cell carcinoma is
using pectoralis major myocutaneous flap common.
Oral Cavity 269
CARCINOMA OF LIP Causes
• Incidence is 10% (Fig. 20.17). • Ultraviolet rays, smoking.
• It is more common in men (90%). Common • Leukoplakia.
• Agriculturists who are commonly exposed to
in lower lip (90%).
sunlight get carcinoma lip more often and so it
• Commonly due to exposure to sunlight
is called as countryman’s lip.
(ultraviolet rays).
• Khaini chewers (tobacco+ lime).
• Initially starts as a red, granular dry lesion,
It spreads to submental nodes and later to
which eventually gets ulcerated and forms
other neck nodes on both sides.
an ulceroproliferative lesion. Occasionally it Usually it is a well-differentiated squamous cell
occurs at the angle of mouth. Verrucous carcinoma.
carcinoma also can occur in lip.
Clinical features of carcinoma lip
• Nonhealing progressive ulcer, painless to
begin with.
• Everted edge with indurations.
• Growth moves with the lip.
• Submental, submandibular and upper deep
neck nodes may get enlarged.
• In half of the cases lymph nodes are enlarged
due to infection or as reactive.
• Fungation, bleeding.
• Keratoacanthoma.
• Minor salivary gland tumors.
Often carcinoma of lip is an extension from
carcinoma of cheek.
Diagnosis
Edge biopsy, FNAC of lymph nodes.
Treatment
• If lesion is less than 2 cm, then curative
radiotherapy is given, either brachytherapy or
external beam radiotherapy. It gives a good
cure. Dose: 6000 cGy units.
• If tumor is more than 2 cms, wide excision is
Figs 20.17A and B: Carcinoma lip. Note the proliferative
done. Excision up to one-third of lower lip can
lesion. Lower lip is commonly involved by squamous cell be sutured primarily in layers keeping
carcinoma vermillion border in proper apposition
..To read without reflecting is like eating without digesting.

without causing any microstomia. Excision of inferior labial vessel. It is used for defects
more than one-third of the lip requires recons- in the upper lip after wide excision of
truction using different flaps (Fig. 20.18). upper lip tumor (Fig. 20.20).
Methods • Lymph nodes are dealt by radical neck
1. Estlander’s rotating flap (Modified lip-switch
dissection on one side and functional block
flap) from the upper lip based on upper
labial artery. It is used for the defect after or suprahyoid block dissection on other
wide excision of the tumor of the lower side.
lip near the angle (Fig. 20.19). • Postoperative radiotherapy is given if tumor
2. Fries‘ modified Bernard facial flap-recons- is large or if lymph nodes are involved.
truction using lateral facial flaps.
3. Abbe lip-switch flap using entire thickness Prognosis
of V-shaped lower lip part based on Good. 5-year survival is 70%.
Fig. 20.18: Primary repair of lip after wide excision of small tumor. One-third of the lip can be sacrificed. Lip is sutured in
layers. First layer with absorbable sutures for mucomuscular layer. Second layer is skin with non-absorbable monofilament
sutures like polypropylene
Fig. 20.19: Lower lip tumor after excision when primary suturing is not possible, the upper lip flap based on
upper labial artery can be used
Oral Cavity 271
Fig. 20.20: For upper lip tumor when primary repair is not possible, then lower lip flap based on
inferior labial artery can be rotated to upper lip
TONGUE
LYMPHATIC DRAINAGE OF THE TONGUE
Tip drains into submental lymph nodes.
Lateral margin drains to submandibular
lymph nodes and then into upper deep cervical
lymph nodes. Many lymphatic vessels pass as
subperiosteal lymphatics of mandible. So
carcinoma can involve the bone through this
route.
Lymphatics in the midline of tongue freely
cross communicate with each other and so,
spread of malignancy can occur to bilateral neck
lymph nodes.
Lymphatics from posterior third of tongue
drain into pharyngeal group of lymph nodes, as
well as to the upper deep cervical lymph nodes.
Early spread to the pharyngeal lymph nodes
from carcinoma of posterior third of tongue has
a poor prognosis (Fig. 20.21).
Lymphatic vessels are named as—
• Apical vessels.
• Central vessels.
• Marginal vessels. Figs 20.21A and B: Anatomy and lymphatic
• Basal vessels. drainage of tongue
..Diseases of the soul are more dangerous than those of the body.
DEVELOPMENT AND Macroglossia
NERVE SUPPLY OF THE TONGUE It is painless diffuse enlargement of tongue
• Anterior two-third develops from first bran- Causes
chial arch through two lingual swellings and 1. Lymphangioma—soft, painless enlarged
one tuberculum impar. It is supplied by tongue with ulcers.
lingual nerve for general sensation and by 2. Hemangioma—soft, fluctuant, compressible,
chorda tympani for taste sensation. bleeding, red/blue lesion.
• Posterior one-third develops from third arch i. Both are treated by sclerotherapy
from cranial half of hypobranchial eminence. (ethonalamine oleate)/partial excision.
It is supplied by glossopharyngeal nerve for ii. Angiogram/MR angiogram must be
both general and taste sensations. done in hemangioma.
• Posterior most part develops from the fourth iii. Ligation of lingual artery/ECA on both
arch. It is supplied by vagus nerve (internal sides may be needed in large lesions.
laryngeal nerve). 3. Neurofibroma—partial excision is done.
• Muscles of the tongue are derived from occipital 4. Tongue muscular hypertrophy—partial
myotomes and are supplied by hypoglossal excision is done.
nerve except palatoglossus, which is supplied
by cranial part of accessory nerve.
CARCINOMA TONGUE
Differential diagnosis for tongue ulcers
• Dental ulcers. Incidence is equal in both sexes. Presently its
• Aphthous ulcers (Fig. 20.22). incidence is increasing in females due to increase
• Ulcers in lichen planus. in number of female smokers.
• Syphilitic ulcers.
• Tuberculous ulcers. Etiology
• Malignant ulcers.
• Leukoplakia.
• Erythroplakia.
Benign tumors of the tongue
• All’S’s.
1. Papilloma.
2. Fibroepithelial polyp.
• Premalignant conditions mentioned earlier.
3. Hemangioma and lymphangioma.
4. Neurofibroma. Types (Fig. 20.23)
5. Lipoma. Gross: 1) Papillary.
6. Granular cell myoblastoma. 2) Ulcerative or ulceroproliferative.
3) Fissure with induration (Fig. 20.24).
4) Lobulated, indurated mass.
Histologically:
1. Squamous cell carcinoma—commonest.
2. Adenocarcinoma may be from minor salivary
glands or mucous glands.
3. Melanomas.
Sites:
1. Lateral margin—Commonest—47–50%.
2. Posterior third—20%.
Fig. 20.22: Aphthous ulcer lower lip. It is painful, self-limiting 3. Dorsum—6.5%.
ulcer. It can occur in tongue, lip, cheek and other parts of the
oral mucosa
4. Ventral surface—9%.
Oral Cavity 273
Clinical Features
1. Pain in the tongue due to infection or
ulceration or due to the involvement of
lingual nerve (pain is referred to ear). Pain
on swallowing, in case of carcinoma of
posterior third of tongue.
2. Excessive salivation.
3. Dysphagia either due to fixed tongue or due
to the involvement of genioglossus or
growth in the posterior third of the tongue.
4. Visible ulcer in anterior two-thirds of tongue.
Growth or ulcer in posterior third, is usually
not visible.
5. Ankyloglossia.
6. Inability to articulate.
7. Foetor (Halitosis). Due to infection and
necrosis in the oral cavity.
8. Change in voice: Occurs in posterior third
tumors. Tumor in posterior third area is
more aggressive.
9. Palpable lymph nodes in the neck which are
hard, nodular and may get fixed in advan-
ced stages.
10. Features of bronchopneumonia.
Figs 20.23A and B: Carcinoma tongue. Spread of Carcinoma Tongue

Commonest site is lateral margin
Local spread: In case of growth in anterior two
thirds of tongue, the spread occurs to genio-
glossus muscle, floor of the mouth, opposite side
and mandible. In case of growth in posterior
third of tongue it spreads locally to tonsil, lateral
side of pharynx, soft palate, epiglottis, larynx and
cervical spine.
Lymphatic spread: From tip of tongue it spreads to
submental nodes. From lateral margin it spreads
to submandibular lymph nodes and later to deep
cervical lymph nodes. Lymphatics in the tongue
are freely communicating, and so involvement of
bilateral neck lymph nodes is common. From
Fig. 22.24: Fissure in the anterior aspect of posterior third it spreads to pharyngeal nodes and
the tongue midline. It is a premalignant condi- upper deep cervical lymph nodes.
..The mill gains by going, not by standing still.

Investigations
• Edge biopsy: Biopsy from posterior third
growth should be done under general
anesthesia.
• FNAC of lymph nodes.
• Indirect and direct laryngoscopy to see
posterior third growth.
• CT scan to see the extension of posterior third
growth or to see the status of advanced
secondaries.
• Chest X-ray to see bronchopneumonia.
Treatment
Surgery, Radiotherapy, Chemotherapy. Fig. 20.26: Tumor between 1–2 cm size is treated by
partial glossectomy with 2 cm clearance
Surgery:
• Early growth < 2cm in size requires, wide
excision and growth >2cm in size requires
hemiglossectomy (Figs 20.25 and 20.26).
• Larger primary tumor can be given preope-
rative radiotherapy, and then later hemi-
glossectomy is done (Fig. 20.27).
• Same side palpable, mobile lymph nodes are
removed by radical neck block dissection.
• Bilateral mobile lymph nodes are dealt with one
side radical block and other side functional block
dissection with essentially retaining internal
jugular vein (on opposite side) to maintain the
cerebral venous blood flow. Other option is
Fig. 20.27: Tumor larger than 2 cm requires

hemiglossectomy
same side radical neck dissection and on

opposite side suprahyoid block dissection
can be done.
• Wide excision when growth is in the tip.
• Posterior third growth can be approached by
lip split and mandible resection, so as to have
total glossectomy.
• When mandible is involved hemimandibulec-
tomy is done.
• The procedure that involves wide excision
or hemiglossectomy, hemimandibulectomy
Fig. 20.25: Wide excision is done in small lateral margin and radical neck dissection together is called
tumor of 1cm size with 1 cm clearance as Commando Operation.
Oral Cavity 275
• Reconstruction of tongue and other area after It is given either intraarterially, as regional
surgery: chemotherapy through external carotid artery
— By deltopectoral flap, forehead flap, using arterial pump or through IV. It can also
pectoralis major muscle flap, skin be given orally.
grafting.
Complications:
• Prophylactic block dissection is becoming
• Megaloblastic anemia,
popular at present.
• Bone marrow suppression.
Postoperative management: • Alopecia.
• Control of infection. • Sepsis.
• Edema. For melanoma, melphalan and DTIC are
• Regular mouthwash. used.
• Maintaining the airway.
• Prevention of aspiration. Terminal events
1. Inhalational bronchopneumonia.
Radiotherapy:
2. Hemorrhage from erosion of lingual artery.
• In small primary tumor—Curative radio-
In posterior third of the tongue, erosion into
therapy (Brachytherapy using caesium or
internal carotid artery can occur.
iridium needles).
3. Cancer cachexia.
• Large primary tumor—Initial radiotherapy
4. Asphyxia due to pressure on air passages or
is given to reduce the tumor size so that the
due to edema glottis.
later resection will be better.
• Advanced primary as well as secondaries in
Prognosis
the neck can be controlled by palliative
external radiotherapy. 5-year survival for females is 50%, for males is
• Postoperative radiotherapy is given in large 25%.
tumors to reduce the chances of relapse.
• In case of growths in the posterior third of Nodal prognostic factors
tongue, radiotherapy is of curative as well • Positive histology in node reduces the
as palliative mode. survival.
• Level III and IV has poor prognosis.
Complications of radiotherapy • Bilateral/ contralateral nodes carry poor
• Loss of sensation like taste. prognosis.
• Trismus and ankyloglossia. • Extracapsular spread/size > 3 cm carry poor
• Infection. survival.
• Pharyngeal and laryngeal edema. • > 3 in number of nodes involved is poor sign.
• Dermatitis and skin infection.
Prognostic Factors
Chemotherapy: Given in postoperative period
and also for palliation. • Size of the tumor > 4 cm carries poor
Price-Hill regimen is commonly used. Drugs prognosis.
are Methotrexate, vincristine, adriamycin, • Site of tumor (Posterior third has got poor
bleomycin and mercaptopurine. prognosis).
..Fire proves gold, adversity proves men.

• Tumor crossing the midline has poor therapy is needed if it is a poorly differen-
prognosis. tiated type or nodal status is more than N1.
• Lymph nodes status. • Advanced lesions need palliative radio-
• Differentiation. therapy or chemotherapy.
• Bone involvement. • T4 lesions are often treated by total glossec-
tomy with laryngectomy and neck dissection
CARCINOMA OF POSTERIOR ONE-THIRD/ but overall outcome is not good.
BASE OF THE TONGUE • In many centers primary curative radio-
• Lesion may remain asymptomatic for long therapy is used.
time. • Lymphoepithelioma and transitional cell
• Clinically may be missed easily. carcinoma can occur in posterior third tongue
• Earlier symptoms are features mimicking (rarely).
sore-throat and throat discomfort.
• Dysphagia and change in voice (hot potato
NASOPHARYNGEAL CARCINOMA
voice) occurs later.
• Referred pain in the ear, bleeding from • Nasopharynx lies above the level of the soft
mouth, visible mass in posterior third of palate which divides it from oropharynx
tongue are late local features. below.
• Induration on palpation in posterior third is • It is also called as postnasal space or
diagnostic of the carcinoma. epipharynx. Eustachian tube opens on its
• As posterior third tongue has got abundant anterolateral wall. Fossa of Rosenmüller is
located above and behind the opening of the
lymphatics which cross-communicate on
Eustachian tube as a small depression.
either side, lymph node spread is common
• It is common in China but rare in India.
(70%). Bilateral nodal spread is common.
• Squamous cell carcinoma is commonest type
Massive nodal involvement and involvement
(85%). Lymphoma, lymphoepithelioma,
of jugulodigastric node are also common.
melanoma, rhabdomyosarcoma can occur
• Infiltration into the tongue muscles like
rarely.
genioglossus, epiglottis, pre-epiglottic space,
• Grossly it can be proliferative, ulcerative or
tonsillar pillars and hypopharynx are
infiltrative type.
common.
• Carcinoma posterior third of the tongue is
Features
commonly poorly differentiated and so
carries poor prognosis. • Epistaxis, nasal speech, postnasal discharge
• Blood spread can occur into bones, liver and and nasal obstruction.
lungs in posterior third cancers. • Pain in the ear, with unilateral deafness due
• Palpation under anesthesia will give better to compression of Eustachian tube along with
idea about the tumor, its spread and also fluid collection in the middle ear.
allows the biopsy. • Elevation and immobility of soft palate on the
• CT scan is always needed to plan the staging same side.
and therapy. • Pain in the area of distribution of trigeminal
• T1, T2, N0 and N1 diseases are treated by nerve due to direct infiltration of the nerve
surgical wide excision often total glossec- at foramen lacerum.
tomy using midline mandibulotomy incision • Palpable secondaries in upper deep cervical
(mandible split) with neck dissection on both lymph nodes (70%)—Most common presen-
sides (MRND one side). Postsurgery radio- tation.
Oral Cavity 277
• It is most common in China and Taiwan.
• Its incidence in China is 18–25%. In India it
is only 0.5%. Male to female ratio is 3:1.
• Vitamin C deficiencies, burning of wood,
salted fish use and Epstein-Barr virus are the
common etiological factors.
• VI cranial nerve palsy is most common palsy
in nasopharyngeal carcinoma.
Trotter’s triad
• Unilateral deafness (conductive deafness).
• Immobile elevated soft palate.
• Pain in the distribution of trigeminal nerve.
• Lymphoma.
• Lymphoepithelioma.
Fig. 20.28: Carcinoma maxillary antrum. Note the
• Minor salivary gland tumor. involvement of nostril, palate and skin over the maxilla
Investigations
Types
• Biopsy from the primary site.
1. Squamous cell carcinoma (80%).
• FNAC from the neck lymph nodes.
2. Adenocarcinoma.
• X-ray of the skull to visualize erosions.
3. Transitional cell carcinoma.
• CT scan skull.
4. Salivary gland tumors.
• MRI to confirm intracranial extension.
5. Sarcomas and melanoma.
Histological type: Squamous cell carcinoma. 6. Burkitt’s lymphoma.
Treatment BEHAVIOR AND PRESENTATION

• External irradiation for primary. • Initially may be asymptomatic, or may
• Radical block dissection of cervical lymph present with epistaxis or features of chronic
nodes. sinusitis.
• Systemic chemotherapy using Methotrexate, • When it spreads to the floor, loosening of the
Vincristine or Adriamycin or Bleomycin. teeth, necrosis, antrooral fistula can occur.
• Extension medially causes nasal block,
MAXILLARY TUMORS fungation, bloody nasal discharge, blockage
• Maxillary sinus is the commonest site for of nasolacrimal duct(Epiphora).
malignancy of paranasal sinuses. Ethmoids, • Extension anteriorly causes pain, anesthesia
frontal and sphenoids are next in order. and swelling in the cheek, ulceration and
• It is common in people working in furniture fungation in the skin of cheek.
industries, mustard gas industries, and • Spread above into the orbit causes ocular
leather industries. It is common in Bantus in pain, epiphora, diplopia, proptosis.
South Africa where snuff with nickel and • Posterior spread is most dangerous as it is not
chromium is commonly used (Fig. 20.28). revealed easily. It causes postnasal discharge,
..An error gracefully acknowledged is a victory.

pain, trismus, limitation of movement of
temporo-mandibular joint. Extension into
base of skull can occur.
• Involvement of upper deep cervical lymph
nodes in later stage is common.
Classification
1. Ohngren’s classification (Fig. 20.29)
An imaginary plane is drawn extending between
medial canthus of eye and the angle of mandible.
Growth situated above this plane is called as
suprastructural which has got poor prognosis.
Growth below this plane is called as infrastruc-
tural. It has got better prognosis.
2. Lederman’s classification (Fig. 20.30)
Two horizontal lines are used, one passes
Fig. 20.30: Diagrammatic representation of
through the floor of the orbit, another passes Lederman classification
through the floor of the antra. These lines are

called as line of Sebileau.
1. Suprastructure type: In this type olfactory area
of nose, ethmoidal, sphenoid, and frontal
sinuses are involved.
2. Mesostructural type: This involves maxillary
sinus and nasal respiratory part are involved.
3. Infrastructural type: This type involves
alveolar process.
Lederman’s classification is further divided
by two vertical lines over medial walls of the
Fig. 20.29: An imaginary plane is drawn extending between
medial canthus of eye and the angle of mandible and line in orbit to separate ethmoid sinuses and nasal fossa
this plane is called as Ohngren’s line from maxillary sinuses.
TNM staging Staging

• T1, Tumor limited to antral mucosa Stage I T1 N0 M0
• T2, Tumor causing bone erosion/destruction including extension Stage II T2 N0 M0
into hard palate or middle meatus of nose. Stage III T3 N0 M0,
• T3, Tumor invading bone of posterior wall of maxillary sinus/ T1/T2/T3 N1 M0
skin of cheek/medial wall of orbit/infratemporal fossa/ Stage IVA T4 N0 M0, T4 N1 M0
pterygoid plates/ethmoid sinuses. Stage IVB Any T N2 M0,
• T4, Tumor invading orbital contents beyond the floor or medial Any T N3 M0
wall including orbital apex/cribriform plate/base of skull/ Stage IVC Any T Any N M1
nasopharynx/sphenoid or ethmoidal sinuses.
Oral Cavity 279
Chronic sinusitis.
Diagnosis
• X-ray of the part-opacity of the involved sinus
with destruction of bony walls is seen
(Fig. 20.31A).
• CT scan (Fig. 20.31B).
Fig. 20.32: Incision for Caldwell-Luc operation which is used
for taking biopsy from maxillary tumor. Incision is not used
for definitive therapy for carcinoma maxilla. Incision is also
used in benign conditions to approach maxillary sinus.
Gingivo-buccal mucosa is incised and mucoperiosteum is
raised. Bone of canine fossa is cut to reach the maxillary
antrum
• Biopsy is done through nasal/oral or on early

stage through Caldwell-Luc operation
(Fig. 20.32).
• Sinus endoscopy for detailed examination of
sinus and for biopsy.
Treatment
• Preoperative megavoltage radiotherapy is given.
After six weeks, total maxillectomy is done.
Reconstruction of maxilla along with dental
reconstruction is required (Fig. 20.33).
Figs 20.31A and B: X-ray picture showing haziness and

irregularity in the maxillary sinus suggestive of carcinoma. Fig. 20.33: Weber-Fergusson incision used for
CT picture shows extensive involvement of the maxilla. total maxillectomy
..A fault once denied is twice committed.

• When lymph nodes are involved radical neck Treatment strategy for oral malignancies
lymph nodes dissection is done. • Wide excision with adequate clearance.
• Postoperative radiotherapy and chemo- • Hemimandibulectomy when bone is involved.
therapy is given as an adjuvant therapy. • Proper reconstruction after surgery.
• Overall prognosis is 30–40%. • Maintenance of functions like swallowing,
CARCINOMA HARD PALATE speech.
• Neck nodal dissection radical/modified
• Minor salivary gland tumors are more
radical.
common in palate.
• Adjuvant therapy—chemotherapy/radio-
• In males in reverse smokers squamous cell
therapy.
carcinoma is seen in palate due to repeated
• Curative radiotherapy for early cases,
thermal injury.
palliation in late cases, and in postsurgery
• Malignant tumors may spread to periosteum,
cases.
bone, maxilla, sinus, or nose.
• Regular follow up with clinical methods along
• Salivary gland tumors are commonly malig-
with investigations.
nant and are of adenoid cystic type. Other
types also can occur. It presents as a single Prognostic factors in oral carcinomas
solid smooth swelling with ulcer over the • Stage of the disease—Stage I and II has got
summit. 80% 5-year survival.
• Squamous cell carcinoma is ulcerative with • Stage III and IV has got less than 20% 5-year
raised and everted edge (Fig. 20.34). survival rate.
• Upper deep cervical lymph nodes are • T3 and T4 lesions has got poor survival rate.
involved in 25% of patients. • Carcinoma lip has got best prognosis.
• Investigations are edge biopsy, FNAC lymph • Carcinoma posterior 1/3rd tongue has got
node and CT scan to see extensions. worst prognosis.
• Treatment is wide excision with removal of • Cheek, floor of the mouth and palate has got
the underlying palatal bone. Often partial or intermediate prognosis.
total maxillectomy (Weber-Fergusson incision) • Histologically positive nodes decrease the
may be required. Myocutaneous flap with survival rate by 50%.
dental prosthesis is essential to reconstruct • Level III and IV, node > 3 cm, bilateral nodes
after surgery. Postoperative radiotherapy extracapsular nodal spread are poor
and neck block dissection are often required. prognostic factors.
• Grading (differentiation) of the tumor.
• Tumor thickness > 6 mm has got poor
prognosis.
• Exophytic tumor is better than infiltrating
type.
Problems with oral carcinomas

• Upper airway obstruction and broncho-
pneumonia.
• Feeding difficulties and severe malnutrition.
• Immunosuppression.
• Secondary sepsis, uncontrollable bleeding.
• Fixity of secondaries, fungation and
disability.
• Psychological trauma.
Fig. 20.34: Carcinoma hard palate extending laterally
Laryngeal Tumors 281
21 Laryngeal Tumors
 Benign papilloma Treatment

 Malignant tumors • Endoscopic removal.
 Total laryngectomy • Application of podophyllum.
 Care after total laryngectomy • Cryosurgery, Laser surgery.
BENIGN PAPILLOMA MALIGNANT TUMORS

• Epithelial tumors can be papilloma, vocal
Etiology
nodule or vocal polyp.
Papilloma is usually single in adult, • Smoking, tobacco.
multiple in children. • Alcohol intake.
• Connective tissue tumors like fibroma, • Occupational/industrial exposure to chemi-
myxoma, angioma. cals like mustard gas, asbestos, benzopyro-
Indirect laryngoscopy (ILS) or direct laryn- nes, petroleum products.
goscopy confirms the diagnosis. • Previous radiation.
Childhood papilloma Adult papilloma

Multiple of viral origin (Papova). Single of neoplastic origin.
Can occur in glottic, supra and infraglottic region. Glottic only.
Not premalignant. Premalignant.
Recurrence common. Not common after complete excision.
Excision is difficult. Easier removal.
Causes more dyspnea, stridor, cough. Hoarseness only.
May require tracheostomy.
Note: Stridor can be inspiratory, expiratory or biphasic.
..The eyes sees only what the mind is prepared to comprehend.

Types
• Ulcerative.
• Proliferative.
Anatomical Types (Fig. 21.1)
• Supraglottic (25%): It arises from infrahyoid
part of epiglottis, ventricles, and arytenoids.
It spreads to neck lymph nodes early (40%)
due to rich lymphatics in this area. Throat
pain, dysphagia, palpable neck nodes and
referred pain are common features. Hoarse-
ness of voice, loss of weight, respiratory
obstruction, halitosis are late features.
Carcinoma in epiglottis causes bilateral nodal
spread. Local spread occurs to vallecula, base
of tongue and pyriform fossa.
• Glottic (65%) (Fig. 21.2): It is the commonest
type. It begins from upper part or free edge
of vocal cords (mid or anterior) often
Fig. 21.1: Anatomy of larynx showing supraglottic, glottic, extending 10 mm below. Lymphatic spread
subglottic regions
is slow (only 4%) as this area has got least
lymphatics. Opposite vocal cord can involve
as kiss cancer. Vocal cord mobility is
unaffected in early cases. Vocal cord fixation
signifies thyroarytenoid spread which is a
poor prognostic sign. It presents very early
due to early hoarseness of voice. Eventual
cord fixation causes stridor. Locally it spreads
anteriorly to anterior commissure,
posteriorly to vocal process and arytenoids,
above to ventricle and false vocal cords,
below to subglottis.
• Subglottic (2%) is less common involving
undersurface of true vocal cords and sub-
glottic space. It spreads to deep cervical and
paratracheal nodes (20%). Upward spread is
Fig. 21.2: View of larynx as seen through a rather late and so hoarseness is not an early
laryngoscope
symptom in this type. It can spread through
cricothyroid membrane or thyroid gland.
• Genetic—Russians develop familial
Note (Fig. 21.3)
laryngeal cancers.
In Indian subcontinent supraglottic tumors are
• Papilloma, virus, keratosis, malnutrition.
more common than glottic. Glottic type is
Squamous cell carcinoma is commonest (95%). common in Western countries.
Common in males (10:1). Fixation of cords is due to involvement of
Common in 5th/6th decade. thyroarytenoid muscle or cricoarytenoid joint.
Fig. 21.3: Types of laryngeal carcinoma. Note the typical sites. Glottic is the commonest site.
Next is supraglottic. Subglottic is rare
Clinical features Investigations

• Hoarseness of voice. • ILS (Indirect laryngoscopy) (Fig. 21.4).
• Pain and discomfort. • Direct laryngoscopy and biopsy.
• Cough. dyspnea, stridor, dysphagia in late • CT neck-very useful investigation.
cases. • Chest X-ray.
• Bloody sputum. • FNAC of lymph node.
• Palpable neck nodes, which eventually get • Microlaryngoscopy in small lesions to
fixed. identify and to have proper biopsy.
• Absence of laryngeal crepitus. • Toluidine blue staining to stain early
• Common in males—10:1. superficial cancers which facilitate the
accurate biopsy.
• Hopkin’s endoscopy.
• Flexible, fiberoptic laryngoscopy.
STAGING Nodal staging is similar to any other oral

Tumor carcinomas.
T1—Tumor confined to one anatomical site in TREATMENT
larynx with normal cord mobility. • Supraglottic: Stage I –Curative radiotherapy
T 2—Tumor confined to one anatomical region is the choice. In stage II and III total laryn-
within larynx. gectomy and block dissection of neck nodes.
T 3—Tumor spreads beyond one anatomical • Glottic: Radiotherapy is the choice as nodes
region within larynx with cord fixation. are commonly not involved. Endoscopic laser
T4—Tumor spreads beyond larynx—thyroid surgery or open partial laryngectomy can be
cartilage/neck soft tissues/pharynx/esophagus. done.
..Art is long, life short, judgement difficult, opportunity transient.

• Subglottic: Total laryngectomy is the treat-
ment of choice with nodal block dissection
when needed.
• In advanced stage IV carcinomas surgery and
radiotherapy both are not possible. Here
chemotherapy is given using Cyclophos-
phamide, Cisplatin and Methotrexate.
• In advanced resectable tumors, induction
chemotherapy for 3 cycles with Methotrexate and
Cisplatin 100 m/sq meter BSA (at 0, 22, 43 days)
and total laryngectomy is under trial. Concurrent
Fig. 21.4: Indirect laryngoscopy to visualize chemotherapy and radiotherapy are also under
larynx and its parts trial in these cases.
Conservative laryngeal surgery

Indications Advantages
• Early growth without fixation especially glottic • Permanent tracheostomy is avoided.
type. • Voice is retained.
Types Disadvantages
• Cordectomy through laryngofissure—excision • Inadequate clearance.
of vocal cord after splitting of larynx. • Recurrence of the disease.
• Partial frontolateral laryngectomy—excision of
vocal cord and anterior commissure.
• Partial horizontal laryngectomy—excision of
supraglottis (epiglottis, aryepiglottic folds, false
vocal cords and ventricle).
TOTAL LARYNGECTOMY
(FIGS 21.5A AND B)
Indications Technique (Fig. 21.6)
• T3 lesions with cord fixation. • Entire larynx with hyoid bone, pre-
• All T4 lesions. epiglottic space, strap muscles, one or more
• Bilateral arytenoids spread. rings of trachea are removed.
• Thyroid/cricoid spread. • Pharyngeal wall is repaired.
• Transglottic cancers involving ventricle with • Lower tracheal stump is sutured to the skin
fixation of the cord. as permanent tracheostomy.
• Posterior commissure disease. • Often laryngoesophagectomy is done when
• Failure of conservative surgery or RT. pharyngeal spread is present. Gastric pull-
Problems up is done to maintain GI continuity.
• Mortality of surgery. • Technique may be combined with neck
• No speech. nodal dissection both sides.
• Having permanent tracheostomy and its
problems.
Figs 21.5A and B: Carcinoma larynx, patients underwent total laryngectomy with permanent
tracheostomy
• In subglottic extension, fixed growths, nodal

spread stage, radiotherapy is less effective.
CARE AFTER TOTAL

LARYNGECTOMY
• Speech therapy by creation of pseudoglottis,

aphonic lip speech, battery operated artificial
larynx (electrolarynx), transoral pneumatic
device, esophageal speech prosthesis.
Tracheoesophageal speech prosthesis
(TOSP) is ideal (Singer-Blom prosthesis,
Fig. 21.6: Gluck-Sorenson’s laryngectomy incision.
Extension lines sideward can be used for adding radical neck Panje prosthesis).
dissection • Social and job rehabilitation.
• Care of permanent tracheostomy by avoi-
ROLE OF RADIOTHERAPY IN ding immersion in the water, care during
LARYNGEAL CANCER bath and shower use and swimming. Shower
covers are available for this purpose.
• In early growth with no impairment in
• Often along with total laryngectomy, total
motility, curative RT is very useful with 90%
thyroidectomy and removal of parathyroid
cure rate with preservation of voice.
glands are required. Patient then needs
• It is commonly used in superficial exophytic
lesions, growth in tip of epiglottis and supplementation with thyroxine and
aryepiglottic folds. calcium for life time.
..Liberty means responsibility; that is why most men dread it.

22 Tonsils
 Anatomy of the tonsils It is supplied by tonsillar branch of facial

 Acute tonsillitis artery. Ascending pharyngeal, ascending
 Chronic tonsillitis palatine and descending palatine arteries also
 Peritonsillar abscess (Quinsy) supply the tonsil.
 Tonsillectomy Tonsil drains into upper deep cervical
 Acute pharyngitis nodes—jugulodigastric lymph nodes.
ANATOMY OF THE TONSILS

It is a mass of lymphoid tissue, situated on each
side of oropharynx. The medial surface exposed
to the pharynx is pitted by crypts. It forms a part
of Waldeyer’s ring. It is located between anterior
and posterior pillars. Laterally it is covered by
a well-defined capsule which is on the tonsillar
bed (Fig. 22.1).
Tonsillar bed is formed by (from medial to
lateral) pharyngobasilar fascia, superior
constrictor muscle and styloglossus, bucco-
pharyngeal fascia, glossopharyngeal nerve and
stylohyoid ligament, paratonsillar vein and
tonsillar artery. Paratonsillar vein drains into
common facial vein and pharyngeal plexus.
Upper pole extends into soft palate with
supratonsillar fossa in between. Lower pole
extends as anterior tonsillar space which is
separated from tongue. Fig. 22.1: Anatomy of oropharynx
Tonsils 287
ACUTE TONSILLITIS Precipitating Factors
It is generalized inflammation of the tonsils, • Malnutrition.
accompanied by inflammation of fauces and • Exposure to cold.
pharynx. • Pollution.
• Immunodeficiency status.
Causative Agents
Clinical Features
• Viral(Rhino, adeno).
• Bacterial (streptococcus hemolytics, stap- • Sore throat.
hylococcus, pneumococcus, H. influenzae). • Pyrexia, headache, malaise.
• Difficulty/painful swallowing.
• Earache.
• Tonsils are enlarged, congested, become
studded with yellow spots over the crypts,
which coalesce to form a patch on the tonsil.
• Tongue is coated with foul breath.
• Cervical lymph nodes (jugulodigastric) are
enlarged.
Complications
• Chronic tonsillitis.
• Peritonsillar abscess.
• Parapharyngeal/retropharyngeal abscess.
• Laryngeal edema.
• Acute otitis media.
• Septicemia, subacute bacterial endocarditis.
• Rheumatic fever, acute glomerulonephritis.
Treatment
• Patient is confined to bed.
• Analgesics (NSAIDs) for pain.
• Antipyretics.
Fig. 22.2: Acute follicular tonsillitis • Antibiotics—Penicillin is the drug of choice.
Alternatively Amoxycillin/Ampicillin/Ery-
thromycin can be given.
Types
• Fluids and soft diet are advised.
Acute catarrhal tonsillitis is seen along with
• Warm antiseptic gargle for smoothening can
generalized pharyngitis due to viral infection.
be given.
Acute follicular tonsillitis (Fig. 22.2) is of
bacterial origin with pus filled crypts.
Acute parenchymatous tonsillitis involves CHRONIC TONSILLITIS
tonsil parenchyma which is red and inflamed. It occurs as a complication of acute tonsillitis with
Acute membranous tonsillitis is formation of microabscesses walled off by fibrous tissue seen
membrane due to exudates from crypts. in tonsillar lymphoid follicles. It also can occur
..Once you learn to quit, it becomes a habit.

in chronic sinusitis/caries teeth/recurrent sub- spreading towards the peritonsillar space
clinical tonsillitis. leading to abscess formation. It may be
sequelae of acute tonsillitis or de novo to begin.
Types • Streptococcus pyogenes, Staphylococcus aureus
• Chronic follicular tonsillitis is chronic and anaerobics are the causative organisms.
inflammation wherein yellowish, cheesy • Usually unilateral.
materials are present in the crypts.
• Chronic parenchymatous tonsillitis is chronic Clinical Features
infection of tonsils with enormously • Common in adults.
enlarged tonsils which interfere with speech, • Severe pain the throat.
swallowing and breathing. It causes sleep • High temperature.
apnea also. • Dysphagia and otalgia on the same side.
• Chronic fibroid tonsillitis is chronic fibrotic • Dribbling of saliva, voice change (hot potato
inflammation of the gland which is small, voice).
firm and fibrotic. • Trismus, torticollis.
• There is marked edema, bulging of the
Clinical Features tonsillar, peritonsillar and palatal region on
• Recurrent sore throat, chronic cough, throat the affected side, with the uvula being
irritation. pushed to the opposite side.
• Halitosis, change in voice, dysphagia. • Cervical lymph nodes are enlarged and
• Difficulty in breathing at night. tender.
• Yellowish beaded pus with cheesy material
and congestion over the surface. Treatment (Fig. 22.3)
• Palpable jugulodigastric lymph nodes in the • Antibiotics—Inj. Penicillin 5L 8th hourly IM
neck. started.
• Analgesics, antipyretics, IV fluids, warm
Treatment of chronic tonsillitis saline gargling of the mouth.
• Conservative treatment using antibiotics,
mouthwash, oral hygiene, diet, therapy for Incision and drainage: Incision is made on the most
causes like sinusitis. fluctuant bulged out area on the palate (just
• Tonsillectomy. above the upper pole of tonsil). It should be done
under general anesthesia as aspiration or
bleeding may occur.
Complications Pus is drained. Antiseptic mouthwash is
• Peritonsillar/intratonsillar abscess given. Tonsillectomy is advised after 4–6 weeks
• Tonsillolith—stone in tonsil usually due to once the acute phase subsides.
chronic infection. It causes foreign body
sensation and gritty feeling is typical on TONSILLECTOMY
palpation. Tonsillectomy is needed.
• Focus of infections like rheumatic fever, Indications
glomerulonephritis. • Recurrent attacks of tonsillitis.
• Following an attack of peritonsillitis.
• Chronic tonsillitis, with recurrent exacer-
PERITONSILLAR ABSCESS (QUINSY) bation.
• Recurrent attacks of tonsillitis causes oblite- • Enlarged tonsil causing mechanical obstruc-
ration of the clefts resulting in infection tion.
Tonsils 289
Fig. 22.4: Operative position for tonsillectomy (Guillotine

method of tonsillectomy is now obsolete. {Not used})
Monitoring of BP, PR, RR is done. Any

Fig. 22.3: Peritonsillar abscess drainage excessive swallowing, especially in children
are noted, as it indicates a possibility of
postoperative bleeding from the tonsillar bed.
• Enlarged tonsil suspicious of malignancy. • After 4–5 hours the patient is encouraged to
• Persistent carrier of streptococcus hemo- take fluids. So earlier the patient uses the
lyticus. muscles of pharynx, easier it becomes and
more rapid is the recovery.
Procedure (Fig. 22.4) • Analgesics and sedatives.
Tonsillectomy is now done by dissection method • Normal diet can be advised from the day 2.
under general anesthesia. The patient is laid in Patient is asked to do antiseptic gargle after
supine position with head extended; sand bag any food intake.
being placed under the shoulder. A Boyle-Davis • Antibiotics are given to prevent any infection.
mouth gag is used to open and fix the jaw • Patient should be ambulant from the 2nd day.
including the tongue. A pack is placed in the • There may be earache in the postoperative
larynx to prevent aspiration. The tonsil are period due to referred otalgia. A white slough
grasped with tonsil holding forceps and may be seen over the tonsillar bed due to the
stretched medially. The mucosa is incised over healing process. The patient should be
the upper pole, anterior pillar and part of reassured regarding these aspects.
posterior pillar. Using blunt dissection the tonsil
is separated from its bed. Finally the lower pole Complications
of the tonsil is separated with a snare. The
bleeding vessel is ligated or cauterized. 1. Reactionary hemorrhage: Commonly seen in
the first 5–6 hours of postoperative period. It
NURSING CARE occurs mainly due to failure to ligate all bleeding
• Postoperatively the patient is placed in points or slipping of ligatures. It is more
‘tonsillar position’, i.e. made to lie on one side dangerous in children as it goes unnoticed until
with knee and hips flexed. A pillow is placed hematemesis sets in. The child looks pale with
behind him to prevent rolling on the back. tachycardia and features of shock.
..Children, like animals use all their senses to discover the world.
Management • Acute otitis media
• The airway is cleared and the tonsillar fossa • Palatal injury.
is inspected. • Sepsis.
• The clots are removed and a swab is held
firmly against the fossa for few minutes, ACUTE PHARYNGITIS
which usually controls the bleeding. If
bleeding continues the bleeding points are It is acute inflammation of the pharynx com-
ligated under anesthesia. monly associated with common cold, viral
• Blood transfusion may be necessary. infections (measles, influenza).
2. Secondary hemorrhage: Occurs after 24 hours Clinical Features
of postoperative period, usually between 5th-
10th day; in the form of mild bleeding to frank • Sore throat, fever, headache.
ooze. It mainly occurs due to secondary infection. • Cough and odynophagia.
Slough or infected clot may be seen in the • Pharyngeal mucosa, tonsils, palate are
tonsillar fossa. congested, uvula is edematous.
Management
Investigations
• Patient is asked to have H2O2 gargle, which
removes the clots/slough and bleeding Throat swab for C/S.
usually stops.
• Systemic antibiotics are started. Treatment
• If bleeding persists, then the tonsillar pillars • Bedrest.
are sutured over a gauze as it is very difficult • Analgesics.
to ligate the bleeding points due to edema. • Antibiotics—Benzathine penicillin 24L. IM or
3. Others Erythromycin/Cephalosporin.
• Aspiration pneumonia. • Warm saline gargle.
• Lung collapse. • Antiseptic lozenges for soothening.
Cleft Lip, Cleft Palate and Jaw Tumors 291
23 Cleft Lip, Cleft Palate

and Jaw Tumors
 Cleft lip and cleft palate • Rubella infection.

 Diseases of the palate • Radiation.
 Orthopentomogram (OPG) • Chromosomal abnormalities.
 Preauricular sinus
Classification
 Jaw tumors
 Epulis I. Cleft lip alone: Unilateral.
 Ameloblastoma Bilateral.
 Dentigerous cyst (Follicular odontome) Median.
 Dental cyst (Radicular cyst, II. Cleft of primary palate only:
Periapical cyst) a. Complete - means absence of pre-
 Alveolar abscess (Dental Abscess) maxilla.
 Cherubism b. Incomplete - means rudimentary pre-
maxilla.
i. Unilateral.
CLEFT LIP AND CLEFT PALATE ii. Bilateral.
Development of Face iii. Median.
III. Cleft of secondary palate only:
Face is developed from median nasal process,
a. Complete.
lateral nasal process, maxillary process,
b. Incomplete.
mandibular arch, globular arch, olfactory pit and
c. Submucous.
eye. Any changes in the development or fusion
It can be
of these arches leads to formation of different
- Cleft with soft palate involvement.
types of cleft lip or cleft palate.
- Cleft without soft palate involvement.
IV. Cleft of both primary and secondary palates.
Etiology
V. Cleft lip and cleft palate together.
• Familial. Defect is often associated with other conge-
• Protein and vitamin deficiency. nital anomalies of cardiac, gastrointestinal,
neurological system, Pierre-Robin syndrome, LAHS classification of cleft disorders
Klippel-Feil syndrome, trisomy. • ‘L’ for lip, ‘A’ for alveolus, ‘H’ for hard palate,
’S’ for soft palate.
Cleft lip • Capital‘LAHS’ for ‘complete’ type
• Central—rare in upper lip. Between two • Small letters ‘lahs’ for ‘ incomplete types’.
median nasal processes (Hare lip) (Fig. 23.1). • Asterisks ‘lahs’ for microclefts.
• Lateral—maxillary and median nasal • ‘LAHSHAL’ for bilateral clefts.
process. Commonest. Can be unilateral or
bilateral (Fig. 23.2). Incidence
• Incomplete cleft lip does not extend into nose
• Common in Caucasians.
• Complete cleft lip extends into nasal floor.
• In 75% of cases it is unilateral. Commonly
• Simple cleft lip is only cleft in the lip.
occurs on the left side.
• Compound cleft lip is cleft lip with cleft of
• In 50% of cases it is combined cleft lip and
alveolus.
palate.
• In 25% of cases it is cleft lip alone.
• In 25% of cases it is cleft palate alone.
Problems in Cleft Disorders (Figs 23.3 to 23.6)

• Difficulty in sucking and swallowing. This
is commonly observed in cleft palate than in
cleft lip.
• Speech is defective especially in cleft palate
mainly to phonate B, D, K, P, T and G.
• Altered dentition or supernumerary teeth.
• Recurrent upper respiratory tract infection.
• Chronic otitis media, middle ear problems.
• Cosmetic problems.
Fig. 23.1: Central cleft lip (Hare lip, Type I cleft lip—It is rare) • Hypoplasia of the maxilla.
• Problems due to other associated disorders.
Fig. 23.2: Lateral type of cleft lip (Type II variety—it is

commonest). It is due to imperfect fusion of maxillary process
and median nasal process. It can be unilateral or bilateral Fig. 23.3: Bilateral cleft lip
Fig. 23.4: Unilateral cleft lip, lateral type which is the Fig. 23.6: Cleft palate only. Lip is normal
commonest type
a. Millard cleft lip repair by rotating the local
nasolabial flaps.
b. Management of associated primary or
secondary cleft palate deformity.
c. Proper postoperative management like
control of infection, training for sucking,
swallowing and speech.
d. Tenninson’s ‘Z’ plasty. (Tenninson-Randall
triangular flap).
Fig. 23.5: Bilateral cleft lip with involved palate
Treatment for Cleft Lip (Fig. 23.7)

Fig. 23.7: Steps of cleft lip repair
Millard criteria is used to undertake surgery for
cleft lip.
Principles of cleft lip repair
Millard criteria (Rule of 10). • “Rule of 10’ should be fulfilled.
• 10 pound in weight. • Infection should not be there.
• 10 weeks old. • Millard advancement flap is commonly used
• 10 gm Hb%. for unilateral cleft lip repair.
..A clear conscience can bear any trouble.

• Bilateral cleft lip repair can be done either as

single or two staged (with 6 months gap in
each stage) procedure.
• One stage bilateral cleft lip repair is done
using Veau III method/Millar’s single stage/
Black method.
• Proper markings are made prior to surgery
and incision should be over full thickness lip
• Often 1:2, 00,000 adrenaline injection is used
to achieve hemostasis.
• Three layer lip repair should be done
(mucosa, muscle and skin).
• Cupid’s bow should be horizontal.
• Continuity of white line should be repaired.
• Vermilion notching should not be there. Fig. 23.8: Complete cleft palate Type I
Cleft palate
• It is due to failure of fusion of the two palatine
processes.
• Defect in fusion of lines between premaxilla
(developed from median nasal process) and
palatine processes of maxilla one on each side.
• When premaxilla and both palatine processes
do not fuse, it leads into complete cleft palate
(Type I cleft palate) (Fig. 23.8).
• Incomplete fusion of these three components
can cause incomplete cleft palate beginning
from uvula towards posteriorly at various
Fig. 23.9: Cleft palate Type II a—bifid uvula
lengths. So it could be Type II a –Bifid uvula
(Fig. 23.9), Type II b—bifid soft palate (entire
length) (Fig. 23.10) or Type II c –bifid soft
palate and posterior part of hard palate (but
anterior part of hard palate is normal)
(Fig. 23.11).
• Small maxilla with crowded teeth, absent/
poorly developed upper lateral incisors.
• Bacterial contamination of upper respiratory
tract with recurrent infection is common.
• Chronic otitis media with deafness may
occur.
• Swallowing difficulties to certain extent and
speech problems can occur.
• Cosmetic problems can occur (Figs 23.12A Fig. 23.10: Cleft palate type II b—bifid soft palate (entire soft
and B show cleft lip and palate in an adult). palate) Cleft palate II c-bifid soft palate and cleft post hard
palate
Fig. 23.11: Cleft palate II c—bifid soft palate entire length

with cleft of posterior hard palate (anterior palate is normal) Figs 23.12A and B: Cleft lip and cleft palate in an adult
Treatment for Cleft Palate • Often staged surgical procedure is done,

whenever complicated problems are present.
Criteria for surgery • Wardill- Kilner push back operation—by raising
• 10 kg weight. mucoperiosteum flaps based on greater
• 10 months of age (10–18 months). palatine vessels.
• 10 gm Hb%.
Principles of palatoplasty (Fig. 23.13)
• Cleft palate is usually repaired in 12–18
• Timing is between 10-18 months
months. Early repair causes retarded
• Mucoperiosteum flap is raised
maxillary growth (probably due to trauma • Palatal defect is closed using 3 layers—nasal,
to growth center and periosteum of the muscle and oral layers.
maxilla during surgery if done early). Late • Hook of pterygoid hamulus is fractured to
repair causes speech defect. relax tensor palate muscle to relieve tension
• Both soft and hard palates are repaired. on suture line.
• Abnormal insertion of tensor palati is
released. Mucoperiosteal flaps are raised in the
palate which is sewed together. If maxillary
hypoplasia is present then osteotomy of the
maxilla is done. With orthodontic help teeth
extraction and alignment of dentition is
done.
• Regular examination of ear, nose and throat
during follow up period.
• Postoperative speech therapy. Fig. 23.13: V-Y palatoplasty
..The important thing in life is to have a great aim, and the determination to attain it.
DISEASES OF THE PALATE Differential Diagnosis

• Cleft palate. • Cold abscess.
• Torus palatinus—a bony hard swelling in the • Sebaceous cyst.
center of the hard palate.
• Nasopalatine cysts. Treatment
• Epstein’s pearls at the junction of soft and hard Excision of the sinus with complete track.
palates in the midline in infants due to retained
developmental cell rests. Treacher-Collins Syndrome
• Apical cyst or abscess. • Mandibulofacial dystosis.
• Minor salivary gland tumor—commonest • Hypoplasia of the zygomatic bone and
site is palate. mandible.
• Maxillary tumor extending into the palate. • Antimongoloid slant to the palpebral fissure.
• Squamous cell carcinoma of the palate. • Coloboma of lower eyelid.
• Gummatous perforation in the middle of the • Low ear lobule with deficient middle ears.
palate seen in congenital syphilis. • Familial—3rd arch syndrome (Mandibulo-
• Perforation of the palate anywhere in facial dystosis).
carcinoma palate.
ORTHOPENTOMOGRAM (OPG) JAW TUMORS

It is a plain X-ray of the mandible which shows Classification (Fig. 23.14)
the whole of mandible in a single plane. It is
better than X-ray mandible lateral view as it I. Swelling arising from the gums (Epulis)
highlights proper dentition, inner and outer • Congenital epulis.
plates of mandible and joints. • Fibrous epulis.
• Pregnancy epulis.
Indications • Giant cell epulis.
• Jaw tumors—Adamantinoma, dental cyst, • Myelomatous epulis.
dentigerous cyst, osteoclastoma. • Sarcomatous epulis.
• Osteomyelitis of the mandible.
• Fracture mandible.
PREAURICULAR SINUS
• It is due to failure of fusion of anterior tuber-
cles of the auricle creating a sinus.
• Often sinus opening gets sealed forming a
preauricular cyst which gets infected forming
an abscess.
• Sinus can get infected repeatedly discharging
pus through its opening.
• It is often multiple.
Investigations
• Sinusogram. Fig. 23.14: Jaw tumor arising from mandible. It could be
• Discharge study. adamantinoma/osteoclastoma/dentigerous cyst
II. Swelling arising from the dental epithelium: Clinical features
(Odontomes) Well-localized swelling from the gum which is
• Ameloblastoma. firm and bleeds on touch.
• Compound odontome.
Treatment
• Enameloma. Excision.
• Cementoma.
• Dentinoma. b. Fibrous Epulis
• Odontogenic fibroma and myxoma.
• It is a benign condition, can occur in any indi-
Cysts arising in relation to dental epithelium: vidual with caries tooth.
• Dental cyst. • It is seen in the gum, adjacent to the caries
• Dentigerous cyst. tooth.
• It is fibroma arising from periodontal mem-
III. Swelling arising from the mandible or brane.
maxilla • It is the commonest type.
• Osteoma and osteoblastoma.
• Torus palatinus and mandibularis. Clinical features
• Fibrous dysplasia. • Painful, well-localized, hard, tender swelling
• Osteoclastoma. in the gum which bleeds on touch.
• Osteosarcoma. • Caries tooth adjacent to the lesion.
• Secondaries. Differential diagnosis
IV. Surface tumors Squamous cell carcinoma from the gum.
Tumors from the surface, which extend into the Investigations
jaw. • X-ray jaw.
• Ossifying fibroma. • Orthopentomogram.
• Osteofibrosis of maxilla. • Biopsy from the lesion.
• Ivory osteoma of jaw.
Treatment
• Leontiasis osea (diffuse osteitis).
Excision with extraction of the adjacent tooth.
• Carcinoma extending into the jaw.
c. Pregnancy Epulis
EPULIS • It occurs in pregnant women due to inflamma-
It is a swelling arising from the mucoperiosteum of tory gingivitis usually during 3rd month of
gums. pregnancy.
• Clinically it resembles fibrous epulis or pyogenic
a. Congenital Epulis granuloma.
• It usually resolves after delivery. Otherwise
• It is a benign condition seen in a newborn arising it should be excised.
from gum pads.
• It is a variant of granular cell myoblastoma d. Myelomatous Epulis
originating from gums. • It is seen in leukemic patients.
• It is more common in girls. It is more common • Investigated for leukemia by peripheral
in upper jaw. smear, bone marrow, biopsy.
• It is not a malignant condition. • Treatment: For leukemia.
..Happiness sneaks through the door you didn’t know you left open.
e. Granulomatous Epulis • It arises from the dental epithelium probably
It is a mass of granulation tissue in the gum from the enamel.
around a carious tooth. • It occurs commonly in mandible or maxilla.
• Occasionally it is seen in the base of the skull
f. Giant Cell Epulis in relation to Rathke’s pouch or in tibia.
Osteoclastoma causing ulceration and hemorr- • Histologically it is a variant of basal cell
hage of gum. carcinoma.
• It is a locally malignant tumor.
g. Carcinomatous Epulis • It neither spreads through lymph node nor
Squamous cell carcinoma of the alveolus and through blood. Hence it is curable.
gum presenting as localized, hard, indurated • It is usually unilateral.
swelling with ulceration. • It can occur in a pre-existing dentigerous cyst.
h. Fibrosarcomatous Epulis Clinical Features
Fibrosarcoma arising from fibrous tissue of the • Swelling in the jaw usually in the mandible
gum. near the angle which attains a large size
extending into vertical ramus—Eggshell
Epulis crackling.
• Congenital. • It is gradually progressive, painless, smooth
• Fibrous—commonest. and hard with intact inner table (enlarges
• Granulomatous. externally with outer table expansion).
• Pregnancy. • Lymph nodes are not enlarged.
• Carcinomatous.
• Myelomatous. Differential Diagnosis
• Fibrosarcomatous. • Osteoclastoma of the mandible: Here inner
table is not intact.
Odontogenic tumors • Dentigerous cyst.
Epithelial • Dental abscess.
• Ameloblastoma.
• Calcifying odontogenic tumor. Investigations
• Odontogenic adenomatoid tumor. • Orthopentomogram(OPG) shows multi-
• Composite odontoma, which may be either loculated lesion—Honeycomb appearance
complex or compound. It is odontogenic (Fig. 23.15).
hamartoma contains all 4 layers, dentin, • Biopsy from the swelling.
enamel, cementum and pulp.
Mesodermal tumor Treatment
• Odontogenic fibroma, myxoma. • Segmental resection of the mandible. OR
• Cementoma, dentinoma. • Hemimandibulectomy with reconstruction of
Malignant odontogenic tumors the mandible.
• Malignant ameloblastoma. Note:
• Fibrosarcoma. - Curettage and bone grafting should not
be done.
AMELOBLASTOMA - It is a curable condition.
(Adamantinoma, Eve’s disease, Multilocular - Recurrent adamantinoma can spread
cystic disease of the jaw). through blood (to lungs).
Fig. 23.16: Dentigerous cyst
Clinical Features
• Painless swelling in the jaw which is smooth
and hard.
Figs 23.15A and B: X-ray (two different X-rays) showing • Adamantinoma.
typical honeycomb/multiloculated features of adamantinoma • Dental cyst.
(By Dr Veena Jagadish MDS) • Osteoclastoma.
Complication
DENTIGEROUS CYST (FIG. 23.16)
(FOLLICULAR ODONTOME) • It can turn into adamantinoma.
• It is a unilocular cystic swelling arising in Investigations
relation to the dental epithelium from an un-
erupted tooth. • Orthopentomogram shows tooth within the
• Common in lower jaw, but can also occur in cyst, which is well-defined (Fig. 23.17).
upper jaw.
Treatment
• It occurs over the crown of unerupted tooth.
Commonly seen in relation to premolars or • If it is small, excision of the cyst is done.
molars. • If it is large, initial marsupialization and later
• It causes expansion of outer table of the excision is done.
mandible. • Unerupted tooth should be extracted.
..The universe is not hostile, not yet is it friendly. It is simply indifferent.

Clinical Features
As a smooth, tender swelling in the jaw in
relation to caries tooth which causes expansion
of the jaw bone.
Complication
It can cause osteomyelitis of the jaw.
Fig. 23.17: Orthopentomogram showing dentigerous cyst
Dentigerous cyst.
DENTAL CYST (FIG. 23.18) (RADICULAR
CYST, PERIAPICAL CYST) Investigation
• It occurs under the root of the chronically Orthopentomogram.
infected dead erupted tooth.
• It is lined by squamous epithelium derived Treatment
by epithelial debris of Malassez. • Antibiotics.
• Drainage or excision of the cyst with
extraction of the infected tooth is done.
Curable malignancies
• Adamantinoma.
• Verrucous carcinoma.
• Papillary carcinoma thyroid.
• Marjolin’s ulcer.
• Carcinoma colon.
ALVEOLAR ABSCESS
(DENTAL ABSCESS)
It is due to spread of infection from root of the
tooth into the periapical tissue. Initially it forms
periapical abscess which later spreads through
the cortical part of the bone into the soft tissues
Fig. 23.18: Dental cyst around forming an alveolar abscess.
Differences between Dental cyst and Dentigerous cyst

Dental cyst Dentigerous cyst
Site of occurrence Erupted tooth under the root Over the crown of an unerupted
tooth
Infection Common Not common
Complication Osteomyelitis Adamantinoma
Treatment Excision and extraction of tooth Marsupialization, excision and
then extraction of tooth
Bacteria: Staphylococci, Streptococci, anaerobic CHERUBISM
bacteria and gram-negative organisms.
It is an autosomal dominant condition occurs in
first year of life.
Clinical Features
• Deep, throbbing pain in the jaw and adjacent Pathology
oral cavity with diffuse swelling over the
• Giant cell granuloma with fibrous tissues in
cheek. the jaw.
• Tender soft tissue swelling in the jaw which • It is commonly bilateral.
eventually bursts spontaneously leading to • Commonly seen in angles of the mandible and
sinus formation. also in maxilla.
• Edema, pain and tenderness in the floor of
the mouth. Clinical Features
• Trismus and dysphagia.
• Diffuse enlargement of maxilla and both
• Fever and features of toxemia. sides of the mandible.
• Tender palpable lymph nodes in the neck. • Bulging of the cheek causes pull of the lower
Investigations eyelid. Hence child appears like, as if looking
upwards.
• X-ray of the mandible or maxilla. • Interference of the development and eruption
• Discharging pus for culture study. of the teeth.
Complications Treatment
• Septicemia. It is a self-limiting disease. Often requires dental
• Spread of infection into other spaces like care and treatment for proper dentition.
parapharyngeal spaces.
• Chronic osteomyelitis of the jaw with Pierre-Robin syndrome
discharging sinuses. • Congenital condition.
• Cleft palate.
Treatment • Mandibular hypoplasia.
• Antibiotics. • Cyanotic episodes.
• Deficiency in transforming growth factor.
• Drainage of the abscess under general
• Defective sucking and tongue falling
anesthesia.
backwards in infants.
• Extraction of the tooth at a later period.
• Cryptorchidism.
• Excision of the sinus whenever required.
..Discovery consists of seeing what everybody has seen and thinking what nobody has thought.
24 Tracheostomy
 Tracheostomy
 Tracheostomy tubes
TRACHEOSTOMY
Tracheostomy is making an opening in the
anterior wall of trachea and converting it into
a stoma on the skin surface.
TYPES
• Emergency tracheostomy.
• Elective tracheostomy.
• Permanent tracheostomy.
High tracheostomy—above the level of isthmus.
It can cause tracheal stenosis. It is above 2nd ring. Fig. 24.1: Tracheostomy tube with inflation part and
syringe (Inflated with air)
Midtracheostomy—ideal and commonly used.
It through 2nd and 3rd rings behind isthmus.
It is approached by dividing thyroid isthmus. 2. Jackson’s tracheostomy tube: It has got outer
tube, inner tube and an obturator.
Low tracheostomy—below the isthmus level. It
is deep and impinges the suprasternal notch. It 3. Red-rubber tracheostomy tube.
can cause torrential bleed which is difficult to 4. PVC tracheostomy tube.
control. Modern tracheostomy tubes are made of
plastic. They are soft, least irritant and dis-
TRACHEOSTOMY TUBES (FIG. 24.1) posable. They have inflatable cuff which makes
1. Fuller’s bivalved tracheostomy tube: It has it easier to give assisted ventilation. Cuff should
got a outer tube and a inner tube. Outer tube be deflated at regular intervals to prevent
is biflanged and so insertion is easier. Inner tracheal pressure necrosis. (For assisted venti-
tube is longer with an opening on its posterior lation, endotracheal tube can be kept for 7 days.
aspect. Inner tube can be removed and re- Beyond that period patient needs tracheostomy
inserted easily whenever required. for further ventilation).
Tracheostomy 303
Indications for Tracheostomy Indications for tracheostomy
• In head, neck and facial injuries. Respiratory obstruction due to—
• Tetanus. • Acute infections causing edema laryx.
• Tracheomalacia after thyroidectomy or • Trauma.
bilateral recurrent laryngeal nerve palsy. • Neoplasms- benign/malignant.
• Laryngeal edema/spasm. • Foreign body.
• Major head and neck surgeries like
• Bilateral abductor palsy.
Commando’s operation, block dissection.
• Congenital causes.
• Acute laryngitis as in diphtheria.
• Carcinoma larynx (Fig. 24.2), foreign body Respiratory secretions due to—
larynx, burns mouth, pharynx, larynx. • Inability to cough—tetanus, head injury,
• Respiratory paralysis like bulbar palsy. neurological causes, strychnine poison.
• Respiratory failure due to asthma, ARDS. • Painful cough in chest injuries, pneumonia
• Aspiration of secretions.
Technique of Tracheostomy (Fig. 24.3)
Neck of the patient is hyper extended by placing Respiratory insufficiency due to chronic lung
sand bags under the shoulder. Vertical (midline) diseases like emphysema, chronic bronchitis,
or horizontal incision is made. Deep fascia is bronchiectasis.
opened. Strap muscles are retracted laterally.
Isthmus is divided or retracted upwards. A few
drops of lignocaine are instilled into the trachea
to suppress the cough reflex. Trachea is fixed
Fig. 24.3: Figure showing the position of tracheostomy tube
with tracheal hook. 2nd and 3rd or 3rd and 4th

tracheal rings are opened and circular opening
Fig. 24.2: Advanced secondaries in neck with is made. Tracheostomy tube is placed. It is tied
tracheostomy tube to control respiratory stridor around the neck (Fig. 24.4).
..Conduct has the loudest tongue.

• Prevention of infection.
• Decannulation of tracheostomy should be
done with care especially in children as
sudden respiratory distress can occur and in
such occasion emergency reinsertion of the
tube should be done.
• Flexible bronchoscopy may be needed to clear
the lower airway through the tracheostomy
tube.
Functions of the tracheostomy

• Alternate pathway for respiration bypassing
the upper airway.
Fig. 24.4: Vertical midline or transverse incisions are used • It decreases the dead space by 50% and
for tracheostomy. Vertical midline incision extends from reduces the resistance to airflow so as to
cricoid cartilage to sternal notch. It is used in emergency
and often elective tracheostomy. It gives rapid access with
improve the ventilation.
less dissection but leads into poor scar. Transverse incision • It prevents aspiration in bulbar palsy, coma,
can be used in elective tracheostomy. It is placed two finger hemorrhage from larynx/pharynx.
breadths above the sternal notch with a length of about 5 cm
transversely. It gives a better cosmetic scar
• In injuries of head, chest, abdomen, in
respiratory paralysis lower airway is kept
Note clean and patent by doing suction of the
• First tracheal ring should never be used to do secretions through the tracheostomy tube.
tracheostomy as perichondritis of cricoid cartilage • Tracheostomy is better and ideal for inter-
with stenosis can occur.
mittent positive pressure ventilation (IPPR).
• Skin should not be sutured or loosely sutured to pre-
vent development of subcutaneous emphysema. • To give general anesthesia when endo-
• Cautery should be used during tracheostomy as tracheal intubation is not possible.
much as possible to prevent oozing/bleeding from
places like muscles, tracheal cut edge. Often Complications of Tracheostomy
torrential hemorrhage known to occur which may
need a re-exploration to control bleeding. • Bleeding.
• Aspiration, sudden apnea.
Tracheostomy Care • Pneumothorax.
• Regular suctioning of the tube. • Surgical emphysema in the neck.
• Cleaning of tracheostomy tube. • Mediastinal emphysema.
• Humidification of the inspired air using • Injury to adjacent structures like esophagus,
normal saline/Ringer lactate/acetylcysteine, recurrent laryngeal nerve, thyroid gland.
(mucolytic agent) to liquefy secretions or • Tracheal stenosis.
crusts so as to prevent blockage. • Laryngeal stenosis due to perichondritis of
• Constant observation of the patient for block, cricoid cartilage.
bleeding. • Tracheitis/tracheobronchitis.
• Periodic deflation of the cuff of the tube for • Displacement/blockage of the tube or
short period to prevent pressure necrosis of erosion of the tube into major vessels.
tracheal mucosa. • Tracheoesophageal, tracheoarterial fistula.
Tracheostomy 305
Nursing care • Tracheal dilator and additional tracheo-
• Consent should be taken. stomy tube should be kept ready at bedside
• Materials like tracheostomy tubes (8.5 size), in case of blockage of existing tube/balloon
sterile gown, drapes, gloves, cap, mask, tra- not getting inflated to replace with a new
cheostomy sterile set, gauze, local anesthetic one.
agent, suction apparatus and tubes, con- • Absolute asepsis like scrubbing hands, using
necting tubes to ventilator, sterile syringes sterile equipments are essential.
should be kept ready. • Sterile suction tubes should be used.
• During procedure the patient is monitored • Care of inner tube is essential in case of metal
for vital signs. tracheostomy tube.
• Proper nursing care of the tracheostomy tube • Regular dressing of the wound is needed.
is done like, humidifying, cleaning, suction, Antibiotics are required to prevent pulmo-
care of the wound, checking of cuff pressure. nary sepsis.
..Charm strikes the sight, but merit wins the soul.

25 Esophagus
 Anatomy It lies anterior to vertebral column and

 Lower esophageal sphincter (LES) posterior to the trachea. It lacks serosal layer but
 Dysphagia is surrounded by a layer of loose fibroareolar
 Achalasia cardia adventitia.
 Gastroesophageal Reflux Disease
(GERD)
 Barrett’s esophagus
 Hiatus hernia
 Reflux esophagitis
 Corrosive stricture of esophagus
 Plummer-Vinson syndrome
(Patterson-Kelly syndrome)
 Mallory-Weiss syndrome
 Boerhaave’s syndrome
 Tracheoesophageal fistula
 Carcinoma esophagus
ANATOMY
Esophagus begins at the lower edge of the cricoid
cartilage (C 6 vertebra) and ends at eso-
phagogastric junction (T1 vertebra). Upper end
is closed by cricopharyngeus muscle which is
18 cm from upper incisors. Lower end is 40 cm
from the upper incisors. (Upper jaw is fixed and
so is used as the landmark to measure, but not
the lower jaw which is mobile) (Fig. 25.1). Fig. 25.1: Anatomical relations of esophagus
Esophagus 307
Parts
1. Cervical esophagus: It extends from crico-
pharyngeus. It is part of inferior constrictor
muscle which is located as lower horizontal
part. Upper oblique part is called as
thyropharyngeus. Gap between two is called
as Killian’s dehiscence which is a site of
occurrence of pharyngeal pouch. Cervical
esophagus is related to trachea and recurrent
laryngeal nerve.
2. Thoracic esophagus: Lies initially towards
the right side. In lower third it deviates
towards the left and continues as abdominal
esophagus. It is related to azygos vein,
thoracic duct (which crosses the esophagus
Figs 25.2A and B: (A) Arterial supply and (B) Venous
posteriorly from right to left), aorta, pleura drainage of esophagus
and pericardium.
3. Abdominal esophagus is 2.5 cm long and Lymph nodes are—
grooves behind the left lobe of the liver. • Paraesophageal groups in the wall of the
esophagus and are cervical, thoracic,
Three areas of anatomic narrowing:
paraesophageal and paracardial nodes.
1. Cervical constriction—occur at the level of
• Periesophageal groups located immediately
cricopharyngeal sphincter—narrowest point
adjacent to esophageal wall. They are deep
of GIT.
cervical, scalene, paratracheal, mediastinal,
2. Bronchoaortic constriction—located at the
diaphragmatic, gastric and celiac lymph
level of T4.
nodes.
3. Diaphragmatic constriction—occurs where
• Lateral esophageal groups receive lymph from
esophagus traverses the diaphragm.
para and peri esophageal lymph nodes.
Arterial supply of esophagus: By inferior Esophagus is innervated by vagus. There is
thyroid artery, oesophageal branches of the both sympathetic and parasympathetic
aorta, gastric arteries and inferior phrenic innervation.
arteries (Fig. 25.2A). Meissner’s plexus of nerves is located in the
submucosa, Aurbach’s plexus lies between the
Venous drainage of esophagus: By inferior
longitudinal and circular layer of muscle.
thyroid veins, brachiocephalic vein, left hemi-
azygos vein, azygos vein, coronary vein, splenic
Three types of contractions in the esophagus
vein and inferior phrenic vein. Veins are longi-
1. Primary—progressive, triggered by swal-
tudinal and they lie in submucosal plane in lower
lowing.
third and in muscular plane above (Fig. 25.2B).
2. Secondary—progressive, generated by
Lymphatic drainage: Lymphatics in esophagus distention or irritation.
are longitudinal and so spread of carcinoma 3. Tertiary—nonprogressive.
occurs to distant lymph nodes occurs early.
..An unspoken word never does harm.

LOWER ESOPHAGEAL Investigations for dysphagia

SPHINCTER (LES) Barium swallow.
Esophageal manometry.
It is a high physiological pressure zone located
Ultrasound abdomen.
in the lower end of the esophagus in terminal
Esophagoscopy.
4 cm region (4 cm in length), with a pressure of
pH study of esophagus.
10–25 mmHg.
MRI study.
LES prevents reflux of gastric and duodenal
CT scan.
contents.
Endosonography.
It is influenced by food, gastric distension, gas-
tric pathology, smoking, GI hormones, alcohol.
BARIUM SWALLOW X-RAY (FIG. 25.3)
Normally there is a transient relaxation period
wherein reflux (physiological) occurs but then It is done in cases of dysphagia which may be
immediately gets cleared by esophageal due to carcinoma esophagus, achalasia cardia,
clearance mechanism. stricture esophagus, hiatus hernia; to look for
So pathological reflux or GERD can occur due external compression, esophageal spasm,
to decreased LES tone, altered relaxation time, pharyngeal diverticula, esophageal webs.
and reduced esophageal clearance mechanism, Varices can also be visualized. While screening
or other altered mechanical factors. motility of esophagus can be visualized.
Esophageal clearance mechanism is due to
primary esophageal peristalsis which carries
saliva with high bicarbonate content which
neutralizes and clears the transient physiological
reflux. Manometry with special microtrans-
ducers is used to measure the LES pressure.
DYSPHAGIA
It is difficulty/inability to swallow.
Causes for dysphagia
• Gastroesophageal reflux disease (GERD).
• Carcinoma esophagus.
• Achalasia cardia.
• Foreign body in esophagus.
• Plummer-Vinson syndrome.
• Hiatus hernia.
• Esophageal diverticula.
• Corrosive strictures. Fig. 25.3: Barium swallow showing irregular filling defect
• Esophageal candidial infection. and shouldering sign in middle third esophagus
• Carcinoma post 1/3 of the tongue.
• Carcinoma pharynx. ESOPHAGOSCOPY
• Diffuse esophageal spasm. Indications
• Boerhaave’s syndrome.
• To identify the lesion (Fig. 25.4) and to take
• Drug induced dysphagia (KCl, Quinine,
biopsy in carcinoma esophagus (Fig. 25.5).
NSAID).
• For diagnosing other esophageal conditions.
• Congenital anomalies of esophagus.
• To remove foreign body.
Esophagus 309
geal opening. This is the most difficult part
in esophagoscopy. After that procedure,
negotiation through the esophagus is easier.
The lesion is identified and biopsy is taken
if required.
Complications are perforation, bleeding.
2. Fiberoptic flexible esophagoscope: It can be
done under local anesthesia. Reflux and
hiatus are well-identified. Stomach also can
be visualized. Easier to pass and perforation
is unlikely.
But tissue taken for biopsy is smaller and
removal of foreign body is also difficult.
Esophageal endosonography
Fig. 25.4: Esophageal candidiasis—Note the
multiple lesions It is a useful method of finding and assessing
different layers of esophagus especially in
• To dilate stricture. carcinoma esophagus. It shows all layers clearly
• To place endostents for inoperable carcinoma and distinctly and so invasion can be better made
esophagus. out and so operability can be decided.
• To inject sclerosants for varices.
ACHALASIA CARDIA
Types It is failure of relaxation of cardia (esophago
1. Rigid esophagoscope (Negus type): It is gastric junction) due to disorganized esophageal
done under general anesthesia. Head is peristalsis, as a result of integration of
extended and head end of the table is tilted parasympathetic impulses causing functional
upwards, scope is passed behind the epi- obstruction.
glottis and cricoid through the cricopharyn-
Etiology
• Stress.
• Vit B1 deficiency.
• Chaga’s disease.
There is pencil-shaped narrowing of cardia
(O-G junction) with enormous dilatation of
proximal esophagus, which contains foul
smelling fluid and is more prone for aspiration
pneumonia (Fig. 25.6).
Achalasia cardia is a precancerous condition.
Clinical Features
• Common in females between 20–40 years age
Fig. 25.5: Esophagoscopic view of carcinoma esophagus group.
..Self-respect—that a corner-stone of all virtue.

Fig. 25.6: Diagrammatic representation of achalasia cardia
• Present with progressive dysphagia, which Fig. 25.7: X-ray picture of achalasia cardia
is more for liquid than to solid food.
Regurgitation and recurrent pneumonia are Treatment
common. 1. Modified Heller’s operation: Esophagocardio-
myotomy (Fig. 25.8).
Triad Either through thoracic or through abdo-
• Dysphagia. minal approach, thickened circular muscle
• Regurgitation. fibers are cut longitudinally for about 8–10
• Weight loss. cm, 2 cm proximal to the thickened muscle
to 1 cm distal to O-G junction. Care should
Malnutrition and general ill health. be taken not to open the mucosa.
Investigations 2. Nissen’s fundoplication is done along with the
above procedure to prevent reflux.
• Barium swallow is diagnostic—shows
(Fig. 25.7).
- Pencil-like smooth narrowing of lower
esophagus.
- Dilatation of proximal esophagus.
- Absence of fundic gas bubble.
• Chest X-ray shows patches of pneumonia.
• Esophageal manometry shows unrelaxed
lower sphincter of esophageal sphincter.
• Esophagoscopy is done to confirm the
diagnosis and to rule out carcinoma eso-
phagus.
Fig. 25.8: Heller’s cardiomyotomy for achalasia cardia. Only
• Carcinoma esophagus. circular muscle layer is cut longitudinally in O-G junction until
• Stricture esophagus. mucosa protrudes out without perforating the mucosa
Esophagus 311
3. Rarely Negus hydrostatic dilatation is done to • Laryngeal symptoms.
dilate O-G junction. It is not very well- • Dysphagia occurs once complications begin.
accepted method as chances of perforation • Symptoms are more with change of position.
are high. • Chronic cough, shortness of breath and
hoarseness.
GASTROESOPHAGEAL REFLUX
DISEASE (GERD) Complications
• Reflux esophagitis.
It is a pathological reflux from the stomach into
• Sliding hiatus hernia.
the lower esophagus.
• Stricture lower end esophagus.
• Esophageal shortening.
Anatomical Factors
• Barrett’s esophagus.
• Obesity. • Carcinoma (Adeno) esophagus.
• Altered length of intraabdominal esophagus.
• Altered obliquity of O-G junction. Investigations
• Reduced pinching action of crus of dia- • Barium study in head down position.
phragm. • Endoscopy and biopsy.
• Esophageal manometry.
Physiological Factors • 24 hour esophageal pH monitoring.
• Reduced LES pressure.
• Altered transient relaxation period in LES. Differential Diagnosis
• Reduced oesophageal clearance mechanism. • Achalasia cardia.
• Delayed gastric emptying due to diabetes, • Carcinoma esophagus.
neuromuscular block, gastroparesis, medi- • Peptic ulcer.
cations. • Gallstones.
• Increased gastric distension and gastric acid • Pancreatic diseases.
hypersecretion. • Gastritis.
Other Factors Treatment of Uncomplicated GERD

Alcohol, smoking, stress, lifestyle. • Control of obesity.
• Stop smoking and alcohol.
Types • Avoid tea, coffee.
• Propped up position.
• Symptomatic uncomplicated GERD. • H2 antagonists.
• Symptomatic, complicated GERD. • Proton pump inhibitors (PPI’S)-
Omeprazole 20 mg
Clinical Features Lansoprazole 30 mg
• Fatty dyspepsia Pantoprazole 30 mg
• Odynophagia. Esomeprazole 20 mg.
• Appearance of symptoms within seconds of
ingestion of food is typical. Indications for Surgical Treatment
• Chest pain and heartburn (pyrosis). • Failure of drug treatment.
..God gives every bird its food, but he does not throw it into the nest.
• Sliding hernia. • Squamous epithelium of lower end of the
• Barrett’s ulcer. esophagus is replaced by diseased columnar
epithelium (columnar metaplasia).
Surgeries • There is macroscopic visible length of
1. Total or partial Nissen’s fundoplication columnar mucosa with microscopic features
(Fig. 25.9) wherein after narrowing the crus of intestinal metaplasia.
of the diaphragm, mobilized fundus is • If the length of metaplasia is more than 3cm.
wrapped around the O-G junction area either it is called as long segment Barrett’s esophagus.
totally or partially. • If the length is less than 3 cm it is called as
short segment Barrett’s esophagus.
• This diseased columnar epithelium is more
prone for malignant transformation, i.e. when
there is intestinal metaplasia, the risk of
malignant transformation increases that too
when there is more amount of dysplasia.
Clinical Features
• Features of GERD.
• Hematemesis.
Management
• Regular endoscopic biopsy.
• Ablation of Barrett’s esophagus by laser.
• Photodynamic therapy.
• Argon beam coagulation.
Fig. 25.9: Nissen’s fundoplication
• Proton pump inhibitors.
2. Laparoscopic fundoplication is safe and a • Antireflux treatment by surgery.
popular alternate approach. • Resection.
3. Belsey-Mark—4 operation is plication of
esophagus to the diaphragm through many HIATUS HERNIA
sutures and so as to push the lower end of It
may be (Figs 25.10 and 25.11):
esophagus downwards and make it • Sliding hernia (85%).
intraabdominal. • Rolling hernia (10-12%).
4. Placement of Angelchik prosthesis in lower end • Combined.
of esophagus also prevents the reflux. Sliding hernia is commonly associated with
5. Collis‘ vertical gastroplasty is done using GERD (Should be discussed like GERD).
fundus of stomach (by giving vertical cut and
suturing fundus) for esophageal shortening
(a complication of GERD).
6. Esophagogastrectomy may be required in
severe cases. (Lower end of esophagus and
part of stomach).
BARRETT’S ESOPHAGUS
• It is metaplastic changes in the mucosa of the
esophagus in response of GERD. Fig. 25.10: Types of hiatus hernia
Esophagus 313
Pathology
There is bleeding granulation tissue in lower
esophageal mucosa with spasm of longitudinal
muscle which pulls the adjacent gastric area
upwards into the esophagus causing sliding
hernia.
Clinical Features
Fig. 25.11: Different types of hiatus hernia—sliding, • It is a part of GORD, pain and burning
rolling and combined sensation in retrosternal area often referred
to shoulder, neck, arm, etc.
ROLLING HERNIA • Heartburn is common.
(PARAESOPHAGEAL HERNIA) • Dysphagia, anemia.
It is herniation of stomach or rarely other
abdominal contents through a hiatus usually Diagnosis
towards left side. • Barium meal X-ray.
• Gastroscopy and biopsy.
Clinical features Complications
Pain Gangrene of stomach. Barrett’s ulcer is an ulcer with gastric (columnar)
Hiccough Perforation into the metaplasia in lower esophagus.
mediastinum.
Regurgitation Perforation into the Treatment
peritoneum.
Cardiac abnormality Gastric volvulus. • H2 blockers: Ranitidine, Famotidine, etc.
• Proton pump inhibitors:
Investigations Omeprazole 20 mg OD one hour before
Plain X-ray. food (Morning).
Barium meal study. Lanzoprazole 30 mg
ECG. Pantoprazole 40 mg
Esomeprazole 20 mg
Treatment Rabeprazole 20 mg
Treatment is always surgical. • Treating GERD and associated causes. By
Excision of sac and repair of the defect. fundoplication and other surgeries.
If it is gangrenous, gastrectomy is required. • Resection in severe cases.
REFLUX ESOPHAGITIS CORROSIVE STRICTURE OF

Types ESOPHAGUS
1. Acute: Following burns, trauma, infection, • Mainly due to alkali sodium hydroxide,
peptic ulcer. occasionally due to acid (sulfuric acid, nitric
2. Chronic: Reflux of acid in sliding hernia, after acid, etc). Acid commonly damages the
gastric surgery. stomach.
Reflux is quiet common in pregnancy. • It causes extensive inflammation of the
Site is always in lower esophagus. mucosa with periesophagitis which if not
..Habit is either the best of servants or the worst of masters.

treated leads to multiple strictures in esopha- • Once anemia comes under control, webs will
gus. clear and patient can swallow.
• Sometimes it causes severe life-threatening Follow up endoscopy is a must.
necrotizing lesion which requires immediate
surgical intervention. MALLORY-WEISS SYNDROME
Management • It is seen in adults with a severe prolonged
• Careful gentle endoscopy. vomiting causing longitudinal tear in the
• Steroids for 3 weeks. mucosa of stomach at and just below the
• Antibiotics. cardia, leading to severe hematemesis.
• Later regular esophageal dilatation is done • Violent vomiting often may be due to
for stricture. migraine or vertigo.
• In multiple strictures, treatment is esophageal • Presents with severe vomiting and later
resection with colonic transposition. hematemesis, with features of shock.
Colonic transposition bypass without
resection of esophagus can also be done. Investigations
Gastroscopy, Hb%, PCV, blood grouping.
PLUMMER-VINSON SYNDROME
(PATTERSON-KELLY SYNDROME) Differential Diagnosis (Fig. 25.12)
1. Esophageal webs seen in uppermost portion of • Bleeding peptic ulcer.
esophagus with spasm of circular muscle • Esophageal varices.
fibers. It is a premalignant condition. • Erosive gastritis.
2. Iron deficiency anemia. • Carcinoma stomach.
3. Superficial glossitis, cheilitis, kolionychia.
4. Splenomegaly.
In esophageal webs, mucosa is hyperkera-
totic, friable, desquamated and causes severe
dysphagia.
Esophagoscopy and biopsy is required to rule
out malignancy.
Treatment
• Oral iron—Ferrous sulfate 300 mg tid with
vitamins.
• Blood transfusion is given when there is
severe anemia (Transfusion of packed cells). Fig. 25.12: (A) Mallory-Weiss syndrome,
• IV or IM iron therapy. (B) Boerhaave’s syndrome
Presentations Differential diagnosis Complications

Sudden onset of symptoms Myocardial infarction Mediastinitis
Severe chest pain Pancreatitis Septicemia
Pain abdomen
Shock
Esophagus 315
Treatment
• Conservative, as tear is only mucosal.
• Blood transfusion, IV fluids, sedation.
• Hemostatic agents like Vasopressin.
• Endoscopic injection therapy if required.
• Surgery is rarely required.
BOERHAAVE’S SYNDROME
It is a tear in the lower third of the esophagus Fig. 25.13: Types of tracheoesophageal fistula (A) H type
(B) Lower end blind, upper end connected to trachea (C)
which occur when a person vomits against a closed Both ends blind (D) Upper end blind, lower end connected
glottis, causing leak into the mediastinum, to stomach
pleural cavity and peritoneum.
Clinical Features
Investigations • TEF should be recognized within 24 hours
• Chest X-ray and MRI. of birth.
• Total count. • Newborn baby regurgitates all feeds and
there is continuous pouring of saliva from the
Treatment
mouth, which is a diagnostic feature.
• Nil by mouth. • It is commonly associated with maternal
• Antibiotics. hydramnios.
• IV fluids.
• TPN. Investigations
• Feeding by jejunostomy. • Obstruction while passing nasogastric tube.
• Often surgery with resection may be • Contrast study reveals fistula and obstruc-
required. tion.
• When severe mediastinitis occurs, condition • Look for other anomalies.
has high mortality. • Chest X-ray.
• Echocardiography.
TRACHEOESOPHAGEAL FISTULA
Treatment
Types (Fig. 25.13) Surgery
In 85% cases it is a blind upper end with lower Through right sided thoracotomy (opposite to
end communicating with trachea. the side of aortic arch), fistula is identified and
It may be associated with VACTER ano- resected. Lower segment is anastomosed to the
malies. blind upper segment. If the length is inadequate
then, colonic interposition has to be done.
• V—Vertebral defects. Complications of surgery

• A—Anal atresia. - Pneumonia.
• C—Cardiac defect (PDA\VSD). - Leak from anastomotic site.
• TE—Tracheoesophageal fistula. - Reflux.
• R—Radial hypoplasia and renal agenesis. - Dysphagia.
..You cannot strengthen the weak by weakening the strong.

CARCINOMA ESOPHAGUS phagus away from the main tumor. Above in

the neck it spreads to left supraclavicular lymph
Etiology nodes.
Diet, deficiencies 5% common In the thorax it spreads to paraesophageal,
Mycotoxin Common after 45 years tracheobronchial lymph nodes to subdiaphrag-
Alcohol and tobacco Common in men matic lymph nodes.
Achalasia cardia Common in China–Henan In the abdomen it spreads to celiac lymph
Esophageal webs province nodes.
Blood spread occurs to liver.
Pathology
Site Clinical Features
Common in middle third • Recent onset of dysphagia is the commonest
Lower third feature. For the dysphagia to develop two-
Upper third third of the lumen should be occluded.
Incidence • Regurgitation.
> 50% • Anorexia and loss of weight (severe)
33% (cachexia).
17% • Pain—substernal or in the abdomen.
• Liver secondaries.
Type • Bronchopneumonia.
Squamous cell carcinoma. • Features of bronchoesophageal fistula in
Adenocarcinoma and SCC carcinoma of upper third esophagus.
Squamous cell carcinoma • Supraclavicular lymph nodes may be
palpable.
Lower 3 cm of esophagus is lined by
columnar epithelium, and so adenocarcinoma is Investigations
common here. Barrett’s columnar metaplasia
• Barium swallow: Shouldering sign and
which occurs in lower third esophagus is also
irregular filling defect (Fig. 25.14).
more prone for adenocarcinoma.
Gross
• Annular.
• Ulcerative.
• Fungating—cauliflower-like.
Spread
Direct: In upper third it spreads through
muscular layer and get adherent to left main
bronchus, trachea, and left recurrent laryngeal
nerve (causes hoarseness), aorta or its branches
(causes fatal hemorrhage, but rare).
It may perforate and cause mediastinitis.
It may get adherent to pleura also.
Lymphatic spread: It spreads both by lymphatic
permeation and lymphatic embolization. It can Fig. 25.14: Barium study showing shouldering sign and
cause satellite nodules elsewhere in the eso- irregular filling defect—carcinoma lower esophagus
Esophagus 317
• Esophagoscopy to see the lesion, extent and Through right side neck approach, esophagus
type. with growth is removed. Anastomosis between
• Biopsy for histological type and confir- pharynx and stomach is done in the neck.
mation.
• Chest X-ray to see pulmonary infection. Middle Third Growth
• Bronchoscopy, to see invasion in upper third Ivor Lewis operation: After laparotomy stomach
growth. is mobilized. Pyloroplasty is done. Through right
• Esophageal endosonography to look for the 5th space thoracotomy is done and growth with
involvement of layers of esophagus. tumor is mobilized. Partial esophagectomy and
• CT scan to look for local extension and status esophagogastric anastomosis is done in the
of tracheobronchial tree in case of upper third thorax. Intercostal tube drainage is placed during
growth. closure.
• Ultrasound abdomen to look for liver and If growth is inoperable, palliative radio-
lymph nodes status in abdomen. therapy is given.
• Endoscopic esophageal staining with labeled
Lower Third Growth
iodine results in normal mucosa being
stained brown, but mucosa remains pale in Here through left thoracoabdominal approach,
carcinoma. (In carcinoma mucosa will not partial esophagogastrectomy is done with
take up iodine). esophagogastric anastomosis. Often jejunal Roux
–en –Y loop anastomosis is done.
Treatment Orrhinger and Orrhinger approach, i.e. Trans-
hiatal blind total esophagectomy (Fig. 25.15) with
Curative treatment
anastomosis in the left side of the neck—Through
Indications:
laparotomy, stomach and lower part of the
• Early growth, when patient is fit for surgery.
esophagus are mobilized. Through left sided
• When there is no involvement of lymph
neck approach, upper part of the esophagus is
nodes, bronchus, and liver.
mobilized using finger. Blind dissection is
completed by meeting both fingers above and
Postcricoid Tumor
• It is treated mainly by radiotherapy.
• Often pharyngolaryngectomy is done along with
gastric or colonic transposition. But complica-
tions are more in this procedure.
Upper Third Growth

• Treated mainly by radiotherapy.
• Commonly it is advanced with left recurrent
nerve palsy and bronchial invasion.
If it is early and operable, Mc Keown three
staged esophagectomy and anastomosis is done
in the neck.
Initially laparotomy is done to mobilize the
stomach. Then thoracotomy through right 5th Fig. 25.15: Transhiatal blind esophagectomy on table
space is done and esophagus is mobilized. surgical specimen
..You cannot help men permanently by doing for them what they could and should do for themselves.
below in the thorax. Later esophagus is pulled • Souttar tube.
up out through the neck wound and removed. • Mousseau-Barbin tube—cheaper, but
Continuity is maintained in the neck. It is a requires laparotomy to pass.
palliative surgery. Expanding metal stents are passed through
Thoracoscopic—Laparoscopic esophagectomy is endoscope under C-arm guidance.
practised in a few centers. Endoscopic laser is used to core a channel
When interposition is required, mobilized through the tumor to improve dysphagia.
stomach or jejunum or colon(left) are used.
Commonly it is placed in the thorax. Often it can Complications of major surgeries: Infection,
be placed in substernal space or in front of the leak, bleeding.
sternum in subcutaneous plane (especially
colon). Terminal events in carcinoma esophagus
• Cancer cachexia.
Palliative Treatment • Sepsis.
Gastrostomy should not be done as a palliative • Immunosuppression.
procedure. • Malignant tracheoesophageal fistula (causes
• Palliative radiotherapy severe respiratory infection and death. Here
• Intraluminal brachytherapy (Radiation expansile endoluminal stents are used at the
intraluminally). site of fistula to have temporary benefit).
Chemotherapy: Cisplatin, Methotrexate, 5-FU.
Prognosis
Intubation Not good because of early spread due to longi-
• Atkinson tube. tudinal lymphatics, aggressiveness, difficult
• Celestin tube. approach, late presentation.
Basic Orthopedics 319
26 Basic Orthopedics
 Anatomy of the bone  Ankylosing spondylitis

 Fracture  Kyphosis
 Plaster of Paris (POP)  Scoliosis
 Arthrodesis  Spondylolisthesis
 Arthroplasty  Intervertebral disc prolapse (IVDP)
 Osteotomy  Bone tumors
 Infections of the bone
 Paget’s disease of bone
 Rickets ANATOMY OF THE BONE
 Bone disease of hyperparathyroidism Human skeleton has got 206 bones. It may be
 Osteoporosis long, short, flat, irregular, pneumatic (maxilla,
 Scurvy ethmoid, mastoid), sesamoid bones.
 Osteogenesis imperfecta Bone can be–compact lamellar bone which
 Achondroplasia is hard and has got bone marrow. It can be
 Tendinitis spongy cancellous bone like ends of long bones
 Diaphyseal aclasia and flat bones. It can be membranous bone or
 Enchondromatosis (Ollier’s disease) cartilaginous bone (Fig. 26.1).
 Arthritis
 Rheumatoid arthritis CARTILAGE
 Osteoarthrosis It is hard connective tissue which contains
chondrocytes and matrix.
..Idleness rusts the mind.

Types Or it may be formed after formation of cartilage
It may be— from the mesenchymal rudiment and is called
a. Hyaline (articular cartilage, costal, nose, as cartilaginous ossification.
larynx (except epiglottis, cuneiform, corni- Primary and secondary ossification centers
culate, trachea, bronchi). It is avascular and develop during bone formation.
insensitive.
b. White (intervertebral disk, semilunar, cartila- FRACTURE
ges, symphysis pubis, acetabular and ‘Fracture’ is defined as break in the bone.
glenoidal labrum). It is vascular but insensi-
tive. Causes of Fracture
c. Elastic cartilage (ear, eustachian tubes, • Trauma—commonest cause.
external auditory meatus, epiglottis, corni- • Pathological—It is due to underlying patho-
culate, cuneiform cartilages). It is avascular logy like malignancy, secondaries in bone,
and insensitive. osteoporosis, osteomyelitis, multiple
Microscopically bone contains Haversian myeloma, hyperparathyroidism, rickets.
• Stress fracture—It is due to repeated minor
canal, lacunae, lamellae, canaliculi, osteoblasts,
trauma leading to repetitive stress to the bone
osteocytes, osteoclasts.
causing fracture. It is common in second
Bone is covered by metatarsal of foot, occurs due to repeated
thick two layered struc- marching and stamping. It is also called as
ture called as periosteum. It ‘march fracture’. It is treated by rest, immo-
protects the bone, gives bilization with plaster slab of the foot.
nutrition, allows bone
formation by osteogenic Types of Fracture
activity, and provides • Greenstick fracture—is seen in children
attachments to muscles, wherein bone breaks incompletely and
tendons, ligaments. It is partially keeping cortex intact. It is treated
very sensitive due to by rest, immobilization.
plenty of nerve networks. • Closed fracture and simple fracture (Fig. 26.2)—
Bone has got three wherein fracture does not communicate
parts—epiphysis, meta- outside.
physis, diaphysis. Bone • Open fracture (Fig. 26.3)—wherein fracture
gets its blood supply from communicates outside to skin through soft
tissues exposing the bone, and allowing
nutrient artery, metaphy-
infection to get in. It is also called as
seal vessels, epiphyseal
‘compound fracture’.
and periosteal vessels.
• Transverse fracture (Fig. 26.4)
The process of bone for- • Oblique fracture
mation which is gradual is • Spiral fracture (Fig. 26.5)
called as ossification. It • Comminuted fracture –here bone is broken into
may be formed directly more than two fragments (Fig. 26.6).
from mesenchymal rudi- • Stellate fracture begins at one point and
Fig. 26.1: Anatomy of
bone showing epiphysis, ment and is called as radiates towards periphery as a star. It is
metaphysic, diaphysis membranous ossification. common in patella and skull.
Fig. 26.2: Simple fracture Fig. 26.3: Open fracture communicating externally
Fig. 26.4: Transverse fracture Fig. 26.5: Spiral fracture
..You cannot build character and courage by taking away a man’s initiative and independence.
Fig. 26.6: Comminuted fracture Fig. 26.7: X-ray showing compression fracture spine with
wedging of the vertebra
Clinical features of fracture

• Avulsion fracture occurs due to powerful
• Pain.
contraction of muscle.
• Deformity.
• Impacted fracture.
• Swelling.
• Depressed fracture is common in skull.
• Local bony tenderness.
• Complicated fracture is fracture associated with
• Shortening of the limb.
injuries to vessels, nerves, joints.
• Abnormal mobility.
• Compression fracture (Fig. 26.7)
• Crepitus.
Mechanism of injury in fracture • Loss of function.
• Direct violence. • In fractures of femur, tibia there will be
• Indirect violence. features of shock.
• Torsion forces. • Features of associated injuries.
Stages of healing of fracture (Fig. 26.8) Factors affecting fracture healing

• Stage of hematoma formation. • Improper immobilization.
• Stage of granulation tissue formation. • Infection.
• Stage of fibrocartilaginous callus. • Interposition of soft tissues.
• Stage of callus formation. • Inadequate blood supply.
• Remodeling phase. • Old age.
• Deficiencies of vitamin C, proteins.
• Anemia.
• Diabetes, HIV, steroid therapy.
Delayed—
• Fat embolism—Due to fracture microscopic
fat globules from the bone marrow enters the
circulation and reaches the lung, brain and
skin causing respiratory distress, drowsiness
and petechial hemorrhage. Often it is life-
threatening.
• Infection.
• Delayed nerve injury.
• Volkmann’s contracture.
• ‘Myositis ossificans’, is common in elbow
causing stiffness due to hematoma forma-
tion—organization—calcification in front of
the elbow joint.
• Disability.
Late—
• Malunion—common in Cole’s fracture.
• Nonunion.
• Osteomyelitis of the bone.
• Stiffness and contracture.
• Osteoarthritis of the joint.
Principles of Management of Fracture

• Immediate splinting and first aid.
• Safe transport.
• Assessment of shock, associated injuries,
vessel and nerve involvement, type of
fracture.
• Resuscitation with blood transfusion,
antibiotics, IV fluids, analgesics, splinting,
wound debridement.
• X- ray of the part to see fractures. Often MRI
is required in spine, hip injuries.
• Proper documentation and case sheet
Fig. 26.8: Stages of healing of bone after injury maintenance.
• Reduction of fracture either by closed or by
open method (Fig. 26.9).
Complications of Fracture • Immobilization.
Immediate— • Physiotherapy.
• Shock. • Rehabilitation.
• Injury to other structures. • Check X-ray to confirm the proper union of
• Compartment syndrome. fracture segments.
..A bone to the dog is not charity. Charity is the bone shared with the dog,
when you are just as hungry as the Dog.
Fig. 26.9: Different methods of interlocking used in fracture shaft of femur
Principles Open Reduction by Surgical Method

• Reduction. Indications—
• Rest until recovery. • Compound fracture.
• Restoration of function. • Distracted fracture.
• Fracture within the joint like fracture neck
Reduction—means restoration of anatomical of femur.
alignment. It is done under general anesthesia • Fracture near a joint.
with muscle relaxation. Simple fractures can be • Multiple fractures.
reduced by closed method. Compound fracture • Pathological fracture.
requires open surgical method of reduction. • Fracture with vascular compression.
Immobilization—Once reduced it should be Methods of open reduction—

maintained by proper immobilization using Screws, screws and plates, wires, intra-medu-
plaster cast. Upper limb fracture unites in 8 llary nails (Figs 26.10 to 26.13).
weeks. Lower limb fracture unites in 12 weeks. Beware of infection of bone in open reduction.
Fracture union is diagnosed by check X-ray.
PLASTER OF PARIS (POP)
United fracture site is stiff due to immobi-
lization. Stiffness should be corrected by proper POP is made up of hemihydrated calcium sulfate.
physiotherapy and rehabilitation. When water is added, solid hydrated calcium
Fig. 26.10: Oblique screw placed to an oblique fracture Fig. 26.11: Method of nailing a bone (tibia upper end)
Fig. 26.12: Diagram showing method of Fig. 26.13: Diagram showing external fixation in
compression plate and nail fracture tibia and fibula
..To be effective means doing the right thing. To be efficient means doing the thing right.
• Both limbs should be positioned properly
before placing the skeletal traction.
• Groin rings and pressure points should be
taken care of in skeletal traction.
• Care of arthroplasty patient.
ARTHRODESIS
Fig. 26.14: POP cast placed to leg with knee flexion
• It is a method used to relieve pain and to
achieve stable mechanical system (Fig. 26.15).
sulfate forms due to exothermic reaction. POP • But it permanently restricts the mobility.
powder can be impregnated with roller bandage. • Joint surfaces are excised and raw bony ends
Usually 12–16 layers are required. Now ready are fused together to eliminate the existing
made POP bandages and slabs are available. It joint.
is dipped in water until air bubbling stops, and • It is useful in chronic disabled joints like
then extra water is squeezed gently. POP is thus osteoarthrosis, rheumatoid arthritis and
ready for use as decided. Over that, roller other degenerative diseases.
bandage is placed and moulded as required • It is commonly used in spine, toes, hip, and
before it sets and solidifies (Fig. 26.14). knee joints.
• Patient may not be able to squat and sit on
Precautions the floor.
After applying the patient is observed for any • Technique may be intraarticular or extra
severe pain and tenderness, numbness, pallor, articular fixation.
duskiness, edema distally. It signifies that POP is
compressing the vessel and requires immediate
removal and application of a new POP.
POP is maintained until fracture unites. If
external wound has to be inspected small
window cut in the POP over wound area is made
to visualize the wound.
Nursing Care
• Nurse should observe the limb for edema,
skin color, pulse.
• Weight for the skin traction should be noted.
• Care of bedsore in bedridden patients is
important.
• Proper exercise to non-injured limb is
essential to prevent stiffness in it.
• Sponge bath, hygiene, nutrition of the patient
should be taken care of.
• Soakage and soiling of the dressing or POP
Fig. 26.15: Types of arthrodesis—extraarticular,
should be noted. intraarticular
• Arranging for dressing as required is
essential.
• Care of POP. ARTHROPLASTY
• Care of splints. Splints may press certain It is repair of bone so as to achieve mobile,
points in the body and can cause ulceration. functioning, painless joint.
TYPES
a. Excision arthroplasty (Fig. 26.16)
• Both surfaces of the joint are excised and gap
is allowed to develop fibrous tissue. It is
commonly used in hip, metatarsophalangeal
joint.
• Joint becomes freely mobile and painless. But
joint becomes unstable with shortening.
• Hip—Girdlestone’s excision arthroplasty.
• Great toe—Keller’s operation.
b. Hemiarthroplasty
Here one of the articular surfaces is excised and
replaced with prosthesis. Other normal articular
surface is left behind. It is commonly done in hip
joint wherein femoral head is removed and
prosthesis is placed (Fig. 26.17).
c. Total replacement arthroplasty (Fig. 26.18)
Here both the articular surfaces are excised and Fig. 26.17: Figure showing hemiarthroplasty of hip joint
replaced with metal and high-density poly-
ethylene. It is held in place using acrylic cement.
It is commonly used in hip joint. Often used in
knee and other joints. Absolute care should be
taken against sepsis. Good asepsis, proper
sterilization like autoclaving, proper prepara-
tion, hypersterile laminar OT is extremely
Fig. 26.18: Diagram showing Total Hip Replacement

Fig. 26.16: Girdlestone excision arthroplasty Arthroplasty (THRA)
..The important thing is not to stop questioning. Curiosity has its own reasons for existing.
important in preventing infection. If infection ACUTE OSTEOMYELITIS
occurs, prosthesis has to be removed and It is acute bacterial infection of the bone.
problem will still persist. DVT is a common
problem. It can be prevented by elevation, Causes
exercise, crepe bandaging the limbs, and
Gram-positive bacteria like staphylococci, strepto-
anticoagulants.
cocci, gram-negative bacteria like klebsiella,
OSTEOTOMY pseudomonas.
It is therapeutic cutting of the bone to correct or
Mode of Infection
stabilize the joint (Fig. 26.19).
• Direct—through the traumatic wounds.
Indications • Hematogenous—from an infective focus
• Correction of angulations, bowing, rotation from different parts of the body, like skin
deformity. infections.
• Correction of discrepancies in the limbs.
• To correct or compensate mal alignment of Mode of Spread
the joint. Bacteria spread through metaphyseal vessels into
• To correct instability of joint. the metaphysis of the bone and multiply there
• To control and relieve pain. releasing toxins and evoking inflammation. These
It is useful in vagus or varus deformity, vessels being end arteries get compressed by
osteoarthritis of the joint.
increased pressure in the metaphysis causing pus
Multiple drills are made in the cortex of the
formation and suppuration. This pus can spread
bone. Bone is divided and necessary corrections
are made. Fragments are fixed using nail and longitudinally into the diaphysis or across the
plate. Patient should be immobilized in POP cast joint capsule into the joint causing arthritis. It
or splints for 6 weeks or until fracture are united. can spread outward into the soft tissues (muscles
and fascia) and reach the subcutaneous plane
Problems: Improper correction, infection.
causing a swelling. It eventually bursts through
the skin forming discharging sinuses. Periosteum
lays new bone eventually, as a reaction.
Clinical Features
• Common in young boys.
• Fever, toxicity.
• Pain in the bone. Tender swelling at the site.
• Effusion in adjacent joint.
• Inability to move the limb.
Fig. 26.19: Osteotomy of femur Investigations

• X-ray shows no changes for 2 weeks. Later
INFECTIONS OF THE BONE it shows widening of cortical margin with
Bone gets infected by gram-positive and gram- new bone formation. Often joint effusion may
negative bacteria, tuberculosis, brucellosis, be visualized.
typhoid, syphilis. • Total count and ESR may be increased.
Infection of the bone along with bone marrow • Blood culture.
is called as osteomyelitis. It can be acute or chronic. • MRI bone.
Treatment
• Antibiotics—Erythromycin, Cefotaxime,
Cefadroxyl.
• Rest and immobilization.
• Often drainage of pus from the bone is
required. Bone is drilled to reach the marrow
with pus, which is drained and sent for
culture and sensitivity.
Sequelae
• Septicemia can develop.
• Chronic osteomyelitis.
• Limb shortening, disability.
• Recurrent infection.
• Chronic discharging sinus formation.
• Malignancy—squamous cell carcinoma from
the skin.
Nursing Care
Fig. 26.20: Diagram showing osteomyelitis
• Adequate rest and maintenance of hygiene.
• Immobilization using proper splints.
• Observation of joint fullness and pain. Investigations
• Later physiotherapy and rehabilitation. • X-ray of the part shows sequestrum and new
bone formation with sinus (Fig. 26.21).
CHRONIC OSTEOMYELITIS • Culture and sensitivity of discharge.
It is chronic, recurrent bacterial infection and • MRI of bone.
inflammation of bone and bone marrow usually
of long bones. There is new bone formation Treatment
called as involucrum (like envelope) with • Surgical exploration of the wound and
discharging sinus with bone spicules in the sinus. removal of the sequestrum with laying open
It occurs either due to trauma or as sequelae of of the sinus cavity.
acute osteomyelitis. Dead part of the bone within • Antibiotics—often are given for long dura-
the infected bone is separated by granulation tion of 3–6 weeks.
tissue and is called as sequestrum (Dead bone in
situ) (Fig. 26.20). Problems
• Deformity.
Clinical Features • Malignant change—Squamous cell carci-
• Discharging sinus with swelling. noma.
• Bone pain and tenderness. Thickening of the • Amyloid deposition.
bone. • Recurrence.
• Shortening, restricted mobility and defor- • Pus can get localized in the metaphysis to
mity. form an abscess called as Brodie’s abscess.
..Never complain and never explain.

—Benjamin Disreali.
• Thickening and increase in visible size of the
bone like in skull causing requirement of
larger sized caps.
• Dull continuous pain in the bone with often
pathological fracture.
• Due to increased vascularity of bone there
is hyperdynamic circulation leading to
congestive cardiac failure.
• Bending (bowing) of leg bones. Paraplegia
due to vertebral involvement.
• Deafness due to middle ear sclerosis.
• The involved bone is more prone for
osteosarcoma than normal bone.
Investigations
• Raised serum alkaline phosphatase.
• Elevated urinary excretion of hydroxy-
proline.
• X-ray shows dense sclerotic bone.
• Bone scan confirms the diagnosis.
Fig. 26.21: X-ray showing chronic osteomyelitis of femur
Treatment
It can cause pain, tenderness and swelling in • Diphosphonates, calcitonin.
the bone. It can lead to pathological fracture. • Correction of pathological fracture.
It requires open drainage and curettage.
RICKETS
Nursing Care
Formed bone matrix is not calcified leading to
• Care of the limb and regular physiotherapy
rickets. Bones contain uncalcified bone matrix
and exercise.
called as osteoid.
• Care of the splint and plaster cast whenever
used. Causes
• Regular dressing of the wound. • Dietary deficiency of vitamin D prevents
• Psychotherapy and counseling to the patient. calcium absorption from the gut.
• Excessive excretion of calcium in the kidney
PAGET’S DISEASE OF BONE
leading to less available calcium for bone
It is also called as Osteitis deformans wherein there calcification—Renal rickets.
is increased blood supply to the bone, causing
bone to enlarge more than normal because of Clinical Features
more vascularity and laying of coarse fibered • Seen in infants.
abnormal bone. This is thick but not strong and • Ricketic rossary in costochondral junction.
is vulnerable for pathological fracture. Common • Bosselated frontal bone.
bones involved are long bones like femur and • Tri-radiate pelvis.
tibia, spine, skull. This bone is more prone to • Bowing of long bones.
develop osteogenic sarcoma. • Stunted growth.
• X-ray confirms the disease.
Clinical Features • Serum calcium and serum phosphatase level
• Common in elderly male. estimation.
Treatment Causes
• Vitamin D supplementation. • After menopause in women.
• Osteotomies to correct the bone deformity. • In old age (elderly).
OSTEOMALACIA is vitamin D deficiency • Disused due to lesser activity.
seen in adults (features are like rickets).
Treatment is also same. Problems
These individuals are more prone for fracture
BONE DISEASE OF by minor trauma, which is often unnoticed.
HYPERPARATHYROIDISM Commonly observed fractures are Colle’s
Increased parathormone secretion by hyperfunc- fracture, fracture neck of femur, compression
tioning parathyroid glands or by parathyroid fracture of vertebrae, intertrochanteric fracture.
adenoma causes calcium resorption from the Treatment is of fractures wherever occurs.
bone replacing the bone with fibrous tissue often
with cystic spaces. It is called as osteitis fibrosa SCURVY
cystica. Bone becomes friable and leads to Deficiency of vitamin C causes defective
pathological fracture. endochondral ossification with more unossified
cartilages leading to hemorrhages and swelling
Features in the epiphyseal region.
• Common in phalanges, jaw bones and skull They present with hemorrhages, swelling,
bones. pathological fracture.
• Pathological fracture can occur.
• Serum calcium is high. Serum phosphorus is
lowered. Serum alkaline phosphatase is OSTEOGENESIS IMPERFECTA
increased. It is a congenital inherited disease with defective
• Serum PTH is raised. Thallium scan shows collagen synthesis leading to brittle bones which
hyperfunctioning parathyroids. CT neck or are prone for multiple fractures in multiple
MRI shows the nodule in parathyroid. bones.
• X-ray of skull, hand, jaw shows salt and
pepper lesion. Features
• Multiple fractures.
Treatment • Sclerosed ear (otosclerosis).
• Correction of hypercalcemia by Calcitonin, • Blue eyes (blue sclerotics).
Glucagon, Mithramycin, Diphosphonates. • Ligament laxity.
• Surgical removal of parathyroids. • Blood chemistry normal.
• Bone histology normal.
• Treatment for fracture.
OSTEOPOROSIS ACHONDROPLASIA
It is reduction in total skeletal bone mass leading It is a familial congenital disease where there is
to thinning of the cortical margins, less dense failure of normal ossification of long bones and
cancellous bone. skull bones.
..Never insult an alligator until after you have crossed the river.
Features Complications
• Long large head, normal trunk. • Bursitis.
• Short proximal part of the limb. • Compression of neurovascular bundle and
• Lumbar lordosis. tendons.
• Trident hand and wide pelvis side-by-side. • Restriction of joint movements.
• Mental impairment is not present. • Turning into chondrosarcoma (5%).
Treatment
TENDINITIS Usually excision is done once epiphysis fuses,
not earlier. Cosmetic complications are indica-
Inflammation of the tendon is called as tendinitis.
tions for excision.
It is commonly due to friction, trauma, and
calcification. Common sites are supraspinatus
ENCHONDROMATOSIS
tendon, patellar tendon, Achilles tendon in the
(OLLIER’S DISEASE)
foot, plantar fasciitis.
It causes painful movements of the tendon, There is abnormal proliferation of cartilage cells
with stiffness,and restricted function. of the growth plate into the metaphysis of long
Supraspinatus tendinitis causes painful arc bones. It is commonly seen in bones of fingers,
syndrome with restriction of mid 60° of abduction toes and other long bones. It also can turn into
of the shoulder. chondrosarcoma (5%).
Treatment ARTHRITIS
• Powerful contraction of the muscle and ACUTE PYOGENIC ARTHRITIS
tendon is avoided. It is acute infection of a joint caused by
• Rest. staphylococcus, streptococcus, pneumococcus
• Steroid injection locally. organisms either through hematogenous spread
• Analgesics and physiotherapy. from distant focus or trauma. Exudates may be
• Rarely surgical removal of calcification in the serous, serofibrinous or purulent depending on
tendon and decompression is done. But the severity of infection. Pus formation in the
results are not fully assured. joint leads to destruction of articular cartilage;
it may track through the soft tissues and skin
causing abscess and sinus. Often severe virulent
DIAPHYSEAL ACHALASIA infection causes septicemia and if not treated
(MULTIPLE EXOSTOSES) properly death may ensue.
It is a growth disorder due to defective endo- Clinical Features
chondral ossification with failure of remodeling
• Pain and swelling in the joint.
of bone ends.
• Restricted joint movement, tenderness, warm-
ness, redness, and fullness over the joint.
Features
• Joint is in maximum ease position.
• It is commonly familial. • Spasm of the muscles adjacent to the joint.
• Common in lower end of femur, upper end
of tibia, humerus. Investigations
• Dwarfism is common. • Total count is increased.
• Exostosis is peduncle with cartilage as cap • Pus aspirated is sent for culture and
with a bursa in between. It grows away from sensitivity.
the joint surface. • X-ray of joint shows widened joint space.
Treatment • Flexion deformity of fingers and toes occurs
• Broad spectrum antibiotics. often with buttonhole or swan neck defor-
• Immobilization of the joint. mity.
• Analgesics. • In severe cases patient may be permanently
• Aspiration of the pus and immobilization. crippled.
• Arthrotomy and drainage of pus with saline • Symmetrical joint involvement is seen.
wash and later immobilization. • Patient may present with carpal tunnel
• Later physiotherapy. syndrome, tennis elbow, plantar fasciitis,
• If there is destruction of joint surfaces, it leads rheumatoid subcutaneous nodules, vasculitis
to bony ankylosis (fusion of joint). with ischemia or gangrene of fingers or toes,
Arthritis can occur in infants, in patients with pleural effusion, pericardial effusion, muscle
gonococcal infection and also syphilis. wasting.
CHRONIC PYOGENIC ARTHRITIS Investigations

It is due to chronic recurrent infection of the joint • X-ray shows narrowed joint space with
by gram-positive or other bacteria. It causes subchondral cystic areas.
deformity, disability and eventually bony • High ESR.
ankylosis of the joint. • IGM rheumatoid factor is positive.
• Synovial fluid shows high cell count
RHEUMATOID ARTHRITIS (> 10,000) and high protein (> 5 gm%).
It is an autoimmune connective tissue disorder • Synovial biopsy is diagnostic.
involving many systems including skeletal • Arthroscopy is very useful.
system. In joints, it causes inflammation of the
synovial membrane which gets thickened, Treatment
edematous, and vascular. Eventually articular • Rest, analgesics (Aspirin, Indomethacin,
cartilage also gets involved in inflammatory
Ibuprofen), Chloroquine, Prednisolone.
process leading to formation of granulation
• D-penicillamine, gold therapy(sodium
tissue called as pannus. Pannus eventually
aurothiomalate).
extends to capsule, periarticular tissue and
• Splint and immobilization.
deeper bone surfaces. Finally joint ankylosis,
• Later physiotherapy.
muscle atrophy occurs.
• Intraarticular injection of hydrocortisone.
Clinical Features • Wax bath therapy.
• Cytotoxic drugs like Cyclophosphamide,
• Common in women.
Methotrexate, Azathioprine.
• It has got different phases with remissions
• Synovectomy, capsulotomy, osteotomy,
and exacerbations.
arthrodesis, arthroplasty.
• Small joints of hand and feet are involved
first. Later proximal joints are involved.
• Morning stiffness and pain are typical.
OSTEOARTHROSIS
• Restricted painful joint movements with It is a degenerative disease of the joint. There
effusion and swelling of the joint occur. is degeneration of articular cartilage due to wear
..The three grand essentials to happiness in this life are: something to do; something to love;
and something to hope for.
—Joseph Addison
and tear. There is low grade or no inflammatory ANKYLOSING SPONDYLITIS
process. There is fragmentation and fibrillation.
Cartilage once gets thinned out, bone surface is • It is a chronic, progressive disease of spine
exposed. Reactive hypertrophy is observed in and sacroiliac joints, which is genetically
peripheral margins of the bone surfaces which predisposed as HLA-B-27.
forms osteophytes. Ankylosis of joint is not • There is progressive restriction of movements
common. As there is not much of inflammatory of all joints in the spine. Patient cannot bend
reaction it is better called as osteoarthrosis not with total stiffness and calcification of
as osteoarthritis. ligaments of the spine(Bamboo spine).
• Costovertebral ankylosis causes poor chest
Types
expansion (< 5 cms) leading to pulmonary
• Primary osteoarthrosis occurs in weight complications.
bearing joints like knee, hip and spinal joints. • Eventually ankylosis of hip, knee, temporo-
It is common in old age, women, and obese
mandibular joints occur.
individuals.
Condition is diagnosed by clinical features,
• Secondary osteoarthrosis is due to other
diseases in the joint like avascular necrosis, X-ray, ESR, positive HLA-B-27, negative
trauma and so on. It is due to mechanical rheumatoid factor.
incongruity of the articular surfaces.
Common joint involved is knee, then hip. Treatment
• Hard bed with a single pillow is used for
Clinical Features
sleeping.
• Pain, stiffness, difficulty in squatting. • Correction of anemia.
• Muscle wasting, position of ease. • Chest and spine physiotherapy.
• Restricted movements, disability.
• Total hip/knee replacement.
• Joint effusion and swelling.
• Lumbar spinal osteotomies.
• Crepitations over the joint.
X-ray reveals narrowed joint space with
subchondral sclerosis and osteophytes over the KYPHOSIS
margins of the articular surfaces. It means there is an exaggerated anterior
Treatment curvature of thoracic spine with obliteration of
lumbar lordosis.
• Rest, skin traction, analgesics, physiotherapy,
exercise, weight reduction.
Causes
• In severe cases intraarticular hydrocortisone
injections may be useful. • Tuberculosis of spine—angular –Gibbus type.
• Osteotomy, arthrodesis, arthroplasty are • Adolescent kyphosis.
surgical treatment required. • Trauma, osteoporosis.
• Osteoarthritis is a morbid condition.
Types
Types of arthritis • Angular—only one or two vertebrae are
• Rheumatoid arthritis.
involved.
• Osteoarthritis(osteoarthrosis).
• Rounded—many vertebrae are involved.
• Hemophilic arthritis.
• Gouty arthritis.
• Reactive arthritis. SCOLIOSIS
• Tuberculous arthritis. It is lateral curvature of the spine. It is common
• Psoriatic arthritis. in thoracic spine.
Causes
• Idiopathic is the commonest. It is common
in girls. Main primary convex curve is
towards one side with secondary compensa-
tory curves above and below towards
opposite side.
• Postural in young people.
• Neuropathic like polio, cerebral palsy.
• Myopathic due to muscular dystrophies.
• Osteopathic due to hemivertebrae, fusion
vertebrae.
Commonly patient presents with respiratory
difficulties.
Scoliosis may be mobile or rigid.
X-ray is diagnostic.
Fig. 26.22: Intervertebral disc prolapse posterolateral
Treatment
• Spinal exercises and breathing exercises.
• Heel and sole raise.
• Spinal braces.
• Spinal fusion using different types of rods
and bone graft.
SPONDYLOLISTHESIS
It is defined as slipping forward of one vertebra
over the next lower vertebra, usually seen in L4-
L5 or L5-S1 junction. It causes sudden severe pain
with lumbar lordosis and step like depression
over the sacrum. X-ray is diagnostic. It is treated
by exercises, physiotherapy, often by lumbo-
sacral fusion.
INTERVERTEBRAL DISC Fig. 26.23: MRI is the ideal investigation for IVDP
PROLAPSE (IVDP)
It is herniation of the nucleus pulposus of the X-ray shows findings only at late stage.
disk through the nucleus fibrosus of the disc, Myelogram, MRI are diagnostic (Fig. 26.23).
commonly posterolateral direction in one or both
sides (Fig. 26.22). Features
It is common in L4-L5 or L5-S1 region. Prolapse • It is the commonest cause of back pain.
of L4-L5 disk compresses the lower nerve root • Always possible neurological deficits should
–L5. Prolapse of L5-S1 compresses the S1 nerve be looked for.
root. • SLR test will be positive.
..The best bridge between despair and hope is a good night’s sleep.
—E. Joseph Cossman
Treatment
• Absolute bedrest, analgesics, pelvic traction,
avoiding weight lifting for 6 months.
• Laminectomy and discectomy is the surgical
procedure done.
BONE TUMORS
It is either benign or malignant. Malignant can
be either secondaries or primary. Secondaries are
the commonest malignant bone tumor. Osteo-
chondroma is the commonest benign bone
tumor.
Benign Bone Tumors

• Osteoma.
• Osteochondroma.
• Chondroma.
• Osteoblastoma. Fig. 26.25: Chondroma types. Enchondroma grows from
within. Ecchondroma grows outwards
OSTEOMA
It is a benign tumor arising from the surface of Only if it is cosmetically troublesome it can
a long/flat/skull bone (Fig. 26.24). be excised. But it should be differentiated
from other swellings in the scalp like dermoid
Types (Fig. 26.25) cysts or secondaries. Frontal bone osteoma
may rarely extend into frontal sinus or orbital
1. Ivory osteoma is hard compact. It usually cavity and if it is so after doing CT scan it
occurs in skull bone like frontal bone/parietal needs surgical excision.
bone. It presents like bony hard localized 2. Cancellous osteoma is usually arising from
swelling which is nontender, nonmobile, spongy bone with a localized swelling.
with free skin over the surface. It does not Features are similar to ivory osteoma.
turn into malignancy. It can be left alone.
CHONDROMA
It is a tumor arising from cartilage.
Types (Fig. 26.25)

1. Ecchondroma grows outwards from the bone.
It is common in flat bones like scapula/ilium
or bones of hands and feet. In flat bones they
often reach large size. It may turn into
malignancy occasionally as chondrosarcoma.
2. Enchondroma is more common in bones of
hands and feet. The affected bone expands
from within leading to thinning of the bone
Fig. 26.24: Osteoma in the skull. Frontal bone is the cortex. Pathological fracture can occur. If this
common site is not troublesome it can be left alone.
3. Multiple chondromas in major long bones is after completion of the development of the
called as dyschondroplasia/multiple chon- bone.
dromatosis or Ollier’s disease. It usually Complications
begins in childhood as enchondromatosis in • It often can compress neurovascular bundle.
the region of the growing epiphyseal carti- It presents with painless swelling.
lages of many bones. So there will be inter- • Only cartilaginous component turns into
ference of the growth of the epiphyseal plates malignancy—chondrosarcoma. Osseous part
which causes shortening and deformity. will not turn into malignancy.
OSTEOCHONDROMA OSTEOCLASTOMA
• It is commonest benign tumor of the bone. • Osteoclastoma often termed as giant cell
• It begins in childhood from the growing tumor. It occurs in ends of long bones from
epiphyseal cartilage plate. As the bone grows epiphyses, often extends into the joint cavity.
tumors is left behind and so appears like It also occurs in jaw either mandible or
migrating towards the shaft of the bone. It maxilla (Fig. 26.27).
grows outwards from the bone like a • It can be benign/intermediate or malignant
mushroom. Its stalk and proximal part is (10%). Malignant osteoclastoma spreads into
bony but distal part is cartilaginous like a cap lungs through blood.
often with a bursa in between (Fig. 26.26). • It forms an expanding tumor with localized
• Usually it is single but it can be familial. swelling which is bony hard. It has got typical
Multiple osteochondromas involving several loculated appearance. Histologically it
long bones is called as diaphyseal, aclasis/ contains spindle cells (typical) with osteo-
multiple exostoses. clastoma giant cells. It can cause pathological
• Osteochondroma should be excised only fracture.
Fig. 26.26: Osteochondroma Fig. 26.27: Osteoclastoma
..Hope puts our feet on the path when our eyes cannot see it.
SECONDARIES IN BONE
Common primaries causing secondaries in bone Common bones involved
are • Vertebral bodies.
• All sarcomas. • Ribs and sternum.
• Carcinoma kidney (RCC). • Pelvis.
• Carcinoma breast—70% cases in females. • Upper end of femur and humerus.
• Follicular carcinoma thyroid. Types
• Carcinoma prostate. • Osteolytic—common.
• Carcinoma lung. • Osteosclerotic—carcinoma prostate.
• Combined osteosclerotic and
osteolytic.
• X-ray/incision biopsy and CT/MRI are the Investigations

needed investigations. • X-ray shows tumor in the end of the long
• Treatment is wide excision/hemimandibu- bone with cortical destruction, Codman’s
lectomy. Partial removal/curettage is not triangle, ’sun-ray’ appearance, pathological
advisable because recurrence is likely. fracture.
Malignant Bone Tumors • Open incision biopsy.
• MRI of the lesion.
Secondaries is the commonest malignant tumor
• CT chest to look for secondaries.
of the bone.
Treatment
Primary malignant bone tumors
• Osteosarcoma. • Amputation above the level of the lesion.
• Chondrosarcoma. • Wide local excision if possible to salvage the
• Fibrosarcoma of bone. limb.
• Ewing’s tumor. • Radiotherapy/chemotherapy (Adriamycin,
• Multiple myeloma. cis-platin, Methotrexate) as sandwich therapy
along with surgeries.
OSTEOSARCOMA • Condition has got poor prognosis.
• It is common primary malignant tumor of the
bone (Fig. 26.28). EWING’S SARCOMA
• It is common in children/adolescence. • It is highly malignant endothelial sarcoma of
• Common sites are lower end of femur/upper bone arising from bone marrow. It begins in
end of tibia/upper end of humerus. diaphysis (Fig. 26.28).
• It arises from metaphysis.
• It is soft, vascular tumor arising commonly
• It expands outwards, extends into adjacent
from shafts of femur/tibia/humerus.
soft tissues.
• It expands outwards with successive layer by
• It spreads into lungs commonly through
layer formation of new bone.
blood.
• It is very aggressive tumor. • It commonly spreads through blood into
• It causes extensive destruction of bone with lungs.
rising of the periosteum with new bone • It commonly occurs in children.
formation. • Soft, vascular, firm, fusiform swelling in the
• Pathological fracture is common. shaft of long bones with warm skin over the
• Localized pain, swelling which is warm, tumor.
hard, and vascular are the features. • X-ray has typical ‘onion-peel’ appearance.
phamide), surgery (amputation) and radio-
therapy (tumor is radiosensitive)
MULTIPLE MYELOMA
• It is malignant aggressive tumor arising from

plasma cells of the bone marrow.
• It mainly involves spine, skull, flat bones and
ends of long bones.
• Generalized pain and illness, anemia, bone
pain, pathological fracture, neurological
deficits often with paraplegia are the features.
• X-ray shows multiple radiolucent areas in
spine, pelvic bones, and skull bones.
• Blood smear shows cart-wheel shaped
plasma cells.
Fig. 26.28: Showing osteosarcoma and
Ewing’s sarcoma
• Bence Jones proteins are positive in urine of
the patient.
• Specific immunoglobulin will be elevated
• Open biopsy, MRI bone, chest CT are the and is diagnostic.
investigations needed. • Bone marrow biopsy is essential.
• It should be differentiated from osteoid • Radioisotope study of bone is useful.
osteoma, osteomyelitis. • Treatment is chemotherapy (Melphalan and
• Treatment is chemotherapy (Actinomycin D, Cyclophosphamide) and radiotherapy.
Vincristine, Adriamycin, Cyclophos- • It carries poor prognosis.
..Be strong enough to face the world each day.

Be weak enough to know you cannot do everything.
—Nabil Mourad.
27 Maxillofacial Injuries
 Primary care (early care) in

maxillofacial injuries
 Fracture middle third area
 Fracture mandible
 Complications of maxillofacial injuries
Maxillofacial region is a complex bony struc-

ture made up of many bones. Often injury invol-
ves not just one bone but multiple bones in the
complex. Structure is related to the complex and
complicated functions of the face, mastication,
breathing, and speech and swallowing. So any
injury in this region will alter these functions in
one way or other (Fig. 27.1).
Fracture in maxillofacial region can be grouped

as— Fig. 27.1: Maxillofacial injuries regions
• Fracture lower third that comprises mandible. Maxillofacial fracture also can be grouped as—
• Fracture middle third that comprises maxilla, • Fracture of the face which do not involve the
zygoma and nose. dental occlusion—fractures of zygoma and nose.
• Fracture upper third of the face involving • Fracture which involves the dental occlusion-
part of the orbit, frontal bones. fracture mandible and maxilla.
Maxillofacial Injuries 341
Treatment of these fractures always involves which also improves the breathing. Placing
restoration and maintenance of correct dental the patient on his back supine position flat
occlusion otherwise it leads into permanent should be avoided as much as possible.
irreversible deformity. • Tracheostomy should be done when needed
without delay as it will be life-saving by
facilitating the easy airway and breathing.
PRIMARY CARE (EARLY CARE) IN
MAXILLOFACIAL INJURIES Control of Pain
Injury can be isolated single bone fracture or Analgesics like NSAIDs are used to control pain.
multiple bone fractures. Any real primary care Morphine and analogues are not used as they
is usually not required except when there is may suppress the respiration. They may mask
mechanical respiratory block causing airway the pain of alarming severe injury in chest,
obstruction. abdomen or other areas, or they may interfere
with pupillary reaction and neurological signs
Respiratory Obstruction in the presence of intracranial injuries.
Causes
Control of Infection
• Oronasal airway block can occur by blood,
Antibiotics are needed. Tetanus toxoid and often
clot, vomitus, foreign body, dentures, teeth,
antitetanus globulin (ATG 3000 units IM) are
saliva, bone pieces, etc.
required.
• Backwards falling of tongue can cause obs-
truction of the nasopharynx and oropharynx.
Hemorrhage in Maxillofacial Injuries
It is common in bilateral mandibular fracture.
• Occlusion of the nasopharynx and oro- Hemorrhage in maxillofacial injuries is usually
pharynx can occur in fracture maxilla with not life-threatening. But it should be identified
posterior and inferior displacement. and controlled properly. In association with
other internal injury, such hemorrhage may be
• Hematoma in floor of the mouth or posterior
important to cause the circulatory failure.
oral cavity can cause airway block.
• Laryngeal/pharyngeal edema. Hemorrhage may be due to—
• Surgical emphysema. • Soft tissue bleeding.
• Bleeding from inferior alveolar artery,
Treatment palatine vessels.
• Cleaning of the oral and nasal cavities to • Nasal bleeding.
remove obstructing agents like clot, dentures, Control of bleeding—
teeth or bone. Gauze swabbing and suction. • Blood transfusion, IV fluids, resuscitation.
• Fallen tongue should be placed forward • Nasal packs.
using finger and often temporary alignment • Fracture correction.
of the occlusion may be needed. • Ligation of the bleeder.
• Maxillary disimpaction is done when needed • Cauterization.
in fracture maxilla. • Packing the area.
• Positioning of the patient is important. Prone • Under running the bleeding field.
position with head towards one side is the • Embolization.
safest position. If this is not possible then • External carotid artery ligation above the level
patient may be placed in sitting position of the origin of the superior thyroid artery.
..Reading make a full man, conference a ready man, and writing an exact man.
Associated Injuries
All associated injuries should be assessed
properly and individually. On priority basis it
should be treated.
• Soft tissue injuries.
• Cranial injuries.
• Orbital injuries.
• Intraabdominal/thoracic/pelvic injuries.
FRACTURE MIDDLE THIRD AREA

Surgical Anatomy of Middle Third Area
It includes—
• Maxillae, zygomatic bones, palatine bones,
nasal bones, lacrimal bones, inferior conchae Fig. 27.2: Relation between middle third and
(one on each side). cranium in 45° plane
• The vomer, ethmoid and its attached con-
chae, pterygoid plates of sphenoid.
Features
• Middle third articulates with frontal bone
and body of the sphenoid at an angle of 45°.
It forms an inclined plane inferiorly and
posteriorly. It is displaced along the inclined
plane in middle third fracture. It can also
force mandible downwards producing
posterior gagging of the teeth and an anterior
open bite (Figs 27.2 and 27.3).
• In nasoethmoid fracture or LeFort II or III
fractures, communition fractures of ethmoid
occurs which in turn break the region of cribri-
form plate of ethmoid leading into CSF
rhinorrhea. Fig. 27.3: Posterior gagging of occlusion due to displace-
• Infraorbital nerve injury can occur in fracture ment backwards of fracture segment in middle third fracture
of zygomatic bone leading into anesthesia in
the area supplied by the nerve. Classification of Fracture Middle Third Area
• Fracture of orbital floor results in herniation
• Nasoethmoid complex fracture.
of the orbital contents into the maxillary sinus
• Zygomatic complex fracture.
which causes diplopia due to restriction of
the movements of the inferior rectus and • Maxillary fracture.
inferior oblique.
• Change in the position of the eye globe/ LE FORT CLASSIFICATION
injury to eye globe/optic nerve tear can occur (Rene Le Fort – French surgeon classified these
in injury of zygomatic prominence. fractures by dropping rocks on the face of the
Fracture middle third includes fracture cadavers and later dissecting the area for study
maxilla, zygoma and nasal bones. and research and published paper in 1911).
Fractures not involving occlusion Fractures involving occlusion
Central Dentoalveolar.
• Fracture nasal bones and/or nasal septum. Subzygomatic.
• Fracture of frontal process of maxilla. • Le Fort I—low level either
• Fractures of above two extending into ethmoid- unilateral or bilateral.
nasoethmoid. • Le Fort II—pyramidal either
• Fractures above three which extends into frontal unilateral or bilateral.
bone – fronto-orbito-nasal dislocation. Suprazygomatic Le Fort III —high level
Lateral • Craniofacial disjunction—unilateral
• Fractures involving zygomatic bone, arch and or bilateral.
maxilla excluding the dentoalveolar component.
Types (Fig. 27.4) Features

Le Fort I (Guerin’s fracture-low level) (floating • Bleeding from nose.
fracture, horizontal fracture of maxilla) • Posterior gagging of occlusion.
It runs horizontally above the floor of the nasal • Upper lip swelling.
cavity involving lower third septum, palate, • Palatal ecchymosis.
alveolar process of maxilla and lower third of • Occlusion derangement.
pterygoid plates of maxilla. • Floating maxilla.
Le Fort II (pyramidal fracture) • Edema of middle third face.

From the nasal bones at topmost, fracture runs • Both sides circumorbital and subcon-
laterally towards lacrimal bones, medial wall of junctival ecchymoses.
orbit, infraorbital margin, through or medial to • Nasal bleeding/obstruction/deformity.
infraorbital foramen and backwards below the • Deformity of face (dish face), diplopia.
zygomaticomaxillary area through lateral wall • Retroposition of maxilla with posterior
of maxillary sinus and pterygoid plates. gagging.
Zygoma is intact with skull base. • Limitation of ocular movements, CSF
rhinorrhea.
• Tenderness and separation of infraorbital
margin.
Le Fort III (craniofacial disjunction, high level) • Lengthening of face.

Here fracture runs parallel to skull base. • Enophthalmos, ocular level depression.
It passes through the nasal bone, lacrimal bone, • Hooding of eyes, occlusal plane tilting.
ethmoid bone, optic foramen, inferior orbital • Entire facial skeleton moves as a single
fissure, pterygomaxillary fissure and lateral block.
orbital wall with frontozygomatic suture with • Tenderness and separation of suture line.
zygomatic arch. • Diplopia.
• Trismus, teeth malalignment.
Guerin sign: Hematoma at greater palatine
foramen.
..Better alone than in bad company.

Figs 27.4A to D: Le Fort classification—different types and also dentoalveolar fracture (Refer table for details)
NASOETHMOID COMPLEX FRACTURE • Head-on-violence causing backward displace-

Classification ment and splaying of nasal bones creating
collapse of nasal bridge and saddle deformity.
• Isolated nasoethmoidal and frontal bone
fracture/injury without other facial bone Features
injuries, which can be unilateral or bilateral. • Pain, tenderness in nasal and frontal region.
• Combined nasoethmoidal and frontal bone • Swelling in the region with deviation and
injury with fracture of other bones in middle displacement.
third face, which can be unilateral or bilateral. • Bleeding from the nose.
• Subconjuctival hemorrhage.
Mode of Injury in Nasal Bone Fracture • Crepitus over nasal bridge.
• Lateral violence on the nose causing nasal bone • CSF rhinorrhea.
fracture with deviation, displacement and • X-ray nasal bone shows fracture.
fracture nasal septum. • CT is done to see other injuries.
Treatment • Step in the margin of the bony orbit at the
Fracture is treated on the basis of the clinical infraorbital foramen.
examination. • Sensory loss over the supply of the branches
Walsham’s forceps is used to reduce the of the superior orbital nerve—teeth on the
fractured nasal bone. Asch’s forceps is used to affected area is anesthetic on percussion.
reduce the nasal septum. Procedure is done • Sensory loss over the supply of the infra-
orbital nerve usually over infraorbital region,
under general anesthesia. Alignment is main-
upper lip and alar region of the nose.
tained by nasal packs from inside and nasal
• Enophthalmos is due to herniation of the
plaster from outside.
orbital fat across the fracture floor of the orbit
into the antrum.
ZYGOMATIC COMPLEX FRACTURE
• Diplopia is due to entrapment of the inferior
Classification (Fig. 27.5) rectus muscle preventing upward rotation of
• Simple fracture which is stable and undisplaced— the eyeball while looking up.
here fracture line passes across the infra- • Trismus with marked restriction of the lateral
orbital foramen downwards over anterior movements.
• Epistaxis, lowering of pupil level.
wall of the antrum.
• Infraorbital ecchymosis of the orbit is called
• Simple fracture which is displaced medially. It
as Panda sign.
may be associated with rotation/tilt in
vertical axis, either medial tilt or lateral tilt.
Investigations
Infraorbital nerve may get compressed or
branches of superior dental nerve may get • 30° occipitomental X-ray is used commonly
torn. but often obliquity of X-ray may be increased
• Unstable fracture with rotation around horizontal to 60°. In X-ray, findings observed are—
axis with medial tilt or lateral tilt. • Fracture line near infraorbital foramen,
• Comminuted fracture extending into the floor zygomatic arch and lateral wall of the
of the orbit. antrum.
• Orbital floor line for fracture.
• Fracture of the zygomatic arch causes a localized
• Opacity in the antrum due to blood.
depression of the arch which displaces
• CT scan is done to see orbital depression and
medially and tends to impinge on the
herniation of orbital fat.
coronoid process of the mandible.
• ‘Blow-out’ fracture of the orbit is due to direct
Treatment
blunt trauma on the eyeball causing
depressed comminuted fracture of the orbital • Every patient with zygoma fracture need not
floor with herniation of the orbital fat into require surgical correction.
the antrum. • Need for surgery is decided based on clinical
• En bloc dislocation of zygomatic bone medially/ features.
inferiorly/posterolaterally. Indications for surgery are
• Infraorbital anesthesia, trismus.
Clinical Features • Diplopia, enophthalmos.
• Swelling and bruising in the cheek with • Flattening of the cheek.
subconjunctival hemorrhage. • Undisplaced fracture with infraorbital
• Flattening of the cheek prominence. anesthesia.
..Arrogance is the obstruction of wisdom.

Figs 27.5A to G: Diagrams showing different types of zygomatic fractures: (A) Undisplaced fracture zygoma, (B) Medially
displaced fracture zygoma, (C) Laterally displaced fracture zygoma, (D) Comminuted zygoma fracture, (E) Arch fracture
zygoma, (F) Blow out fracture orbit, (G) Orbital floor fracture
Surgical Approaches
1. Closed reduction of the zygomatic arch
through Gillies temporal approach (Fig. 27.6)—
An oblique skin incision of 2 cm length temporal
is made between the two branches of the
superficial temporal artery. Care is taken to avoid
injury to artery. Whitish glistening temporal
fascia is identified and incised. Zygoma elevator
is introduced beneath the zygoma and fracture
fragments are manipulated and elevated into
proper position. An audible snap is heard when
fracture gets reduced into position. Reduced,
disimpacted fracture is always stable. Additional
corrections in other parts can be done by
different leverage actions of the elevator. Orbital
rim, zygomatic arch are palpated for completion
of correction. Skin wound is closed with sutures.
Elevators used are: Figs 27.7A and B: Disimpaction of maxilla using Rowe’s
disimpaction forceps by downward leverage action
- Bristow’s periosteal elevator.
- Rowe’s zygomatic elevator (Fig. 27.7). 2. Internal fixation by open reduction and
fixation is needed (Fig. 27.8)
• when fracture is unstable or
• comminuted or
• zygoma fracture with middle third fractures
By proper incisions infraorbital and zygoma-
ticofrontal fracture sites are exposed and after
open reduction they are fixed using wires/plates
and screws.
Fig. 27.8: Fracture zygoma showing open reduction and

Fig. 27.6: Technique showing method of temporal fixation using wires directly. Two types of incisions are shown
reduction using disimpaction forceps depending on the site of the fracture
..Hasty judgements are generally faulty ones.

3. Exploration of the orbital floor is necessary • Suppression wires to mandible—frontal/
whenever there is— circumzygomatic/zygomatic/intraorbital.
• Comminuted fracture in orbital floor • Antral pack/antral balloon support.
• Orbital fat herniation • Craniomandibular external fixation of maxilla
• Diplopia with entrapment of the inferior using box frame/halo frame (Fig. 27.9).
rectus muscle. • Craniomaxillary external fixation of maxilla
using halo frame/supraorbital pins/
MANAGEMENT OF FRACTURES IN zygomatic pins.
MIDDLE THIRD AREA • Internal suspension for stabilization of middle
Investigations and proper evaluation of the third fractures by circumzygomatic suspen-
sion/zygomatic suspension/infraorbital
patient by X-ray, CT scan is essential. Approa-
suspension/pyriform aperture suspension/
ches and timing of the surgery is decided. Often
frontal suspension (central or lateral)
it requires two or more staged procedures, which
(Fig. 27.10A).
should be informed to the patient clearly.
• Circumzygomatic suspension is used in sub-
zygomatic fractures with intact zygoma
Treatment of Middle Third Fracture
and wire is passed around zygomatic arch.
Fracture is reduced by manipulation of the • In zygomatic suspension through buccal
fragments into correct dental occlusion to their sulcus approach, inferior ridge of the
counterpart on the opposite alveolus. It is zygoma is used for suspension, using
maintained in that position until fracture wires (Fig. 27.10B).
becomes stable. If dental occlusion is correct it • In infraorbital suspension a drill hole in the
is presumed that fracture has been reduced lower border of the orbit is made to pass
accurately. Stabilization of the fractured bone to a wire which is used for suspension. Area
unfractured bone is called as intermaxillary is approached through an outer infra-
fixation. Indirect methods are effective in less orbital, lower orbital margin skin incision
severe injuries but are inadequate in injuries of or from intraorally through buccal sulcus
circumorbital elements, upper maxilla, glabellar
bone and medial orbital wall. Open craniofacial
technique like open surgical manipulation and
fixation using wires/screws and plates are more
ideal and standard way of approach.
‘Eyelet’ wires and ‘arch bars’ are used when
the teeth are used to fix the fracture segment in
reduced position. Gunning splintage is used in
old edentulous patients.
Surgical methods are—
• Direct internal fixation
• Transosseous wiring at fracture site.
• Stainless plates (steel/titanium).
• Dynamic/eccentric compression plates.
• Microplating.
• Polyglycolic resorbable plates.
• Transfixation with Kischner wire/ Fig. 27.9: Craniomandibular external fixation of maxilla
Steinman pin. using halo frame
Figs 27.10A to F: Different types of suspensions for middle third fracture internal fixation (A) Circumzygotic suspension,
(B) Zygomatic suspension, (C) Infraorbital suspension, (D) Pyriform aperture suspension, (E) Frontal lateral suspension, (F)
Frontal central suspension
above the canine fossa. Eyeball should be wires are used for suspension. In central
protected (Fig. 27.10C). type (Fig. 27.10F), wire is passed through
• In pyriform aperture suspension, pyriform a pin placed on the inner table of frontal
bony aperture is approached through a bone in the forehead through an incision
buccal mucosal incision above lateral in the skin above the frontal sinus and is
incisor, drill hole is made to pass passed across upper canine region, lateral
suspension wire (Fig. 27.10D). to pyriform margin of nose and lacrimal
• Frontal suspension could be lateral or gland. Procedure is repeated on the other
central. In lateral type (Fig. 27.10E), side. After reduction of the fracture
zygomatic process of the frontal bone just segments these wires are fixed to
above the frontozygomatic suture line maxillary/mandibular splints.
is approached through a lateral eyebrow
skin incision and drill holes one on each FRACTURE MANDIBLE
side are made to pass wires. Each wire Surgical Anatomy of the Mandible
on each side is directed towards the • Mandible is prominent, mobile horse shoe
buccal sulcus near the 1st molar tooth and shaped bone in the facial skeleton, which is
..A little may save a deal of friction.

pharynx. Inner surface has got groove for
lingual nerve, submandibular fossa, sublin-
gual fossa, genial tubercles for genioglossus
and geniohyoid muscles and mylohyoid
groove with mylohyoid vessels and nerve.
• Outer surface of the ramus of the mandible
gives insertion of the masseter muscle and
is related to parotid salivary gland.
• Inner surface of the ramus of the mandible
has got mandibular foramen which transmits
inferior dental/alveolar vessels and nerve.
Medial pterygoid muscle is attached to inner
surface of the ramus of the mandible.
• Coronoid process is flat triangular part with
pointed apex which curves and continuous
as condyloid process with mandibular notch
in between. Temporalis muscle is inserted to
this coronoid process.
• Condyloid process has got head which forms
temporomandibular joint with articulation
with temporal bone. Lateral pterygoid
muscle is inserted to pterygoid fovea in front
of the neck of the coronoid process.
• Mandibular notch transmits masseter vessels
Figs 27.11A and B: Anatomy of the mandible showing and nerves.
features of external and internal surfaces • It is thickest in the body in the region of the
mental prominence and third molar region.
• Ramus of the mandible has got central core
the largest and strongest bone of the face. It of cancellous bone with two thin layers of
has got U-shaped body and two rami one on cortical bone. Junction between body and
each side projecting upwards (Fig. 27.11). vertical ramus is weak line structurally.
• Body of the mandible has got outer surface • Neck of the condyle of the mandible is also
with symphysis menti, mental protuberance, weaker area.
mental tubercles, and mental foramen. • Teeth in the bone reduce the strength of the
External oblique line gives attachment to mandible and also a constant source of
depressor muscles, buccinator and platysma. infection.
Inner surface of the body of mandible has got • Medial pterygoid, masseter and temporalis
mylohyoid line for attachment of mylohyoid muscles influence the displacements in
muscle and superior constrictor muscle of the fracture angle of the mandible.
Classification of the fracture mandible (Fig. 27.12)
Depends on the type Depending on the anatomical site
• Simple. • Dentoalveolar fracture.
• Compound. • Condylar fracture.
• Comminuted. • Coronoid fracture.
• Pathological. • Fracture ramus of the mandible.
• Green stick fracture in children. • Fracture angle of the mandible.
• Fracture in the body of the mandible.
• Symphyseal region fracture.
b. Condylar Fracture (35%) (Fig. 27.13)
In condylar fracture condylar head is pulled
forward by the lateral pterygoid muscle. When
both condyles are fractured the displacements
of both heads causes the patient to gag on his
molars producing an open bite. It is the commonest
type of mandibular fracture.
Fig. 27.12: Different sites of fracture mandible
• Mandible is supplied by inferior dental artery

centrally and periosteal vessels peripherally.
In old people inferior dental arterial supply
is poor and blood supply mainly depends on
periosteal vessels, which often decides the
healing of fracture and results of open
reduction.
a. Dentoalveolar fracture
Features
• Horizontal fracture below the alveolar
margin.
• Dentoalveolar segment will be freely mobile.
• Tooth may get split vertically/horizontally.
• Derangement in occlusion and alignment.
• Gingival laceration.
• Bleeding.
• Infection and late osteomyelitis of mandible.
Management
• Look for other injuries in face.
• X-ray face to see injuries.
• Dentoalveolar segment reduction and
placing jaws in central occlusion position.
• Stabilization using interdental wires or arch
Figs 27.13A and B: Mandible gets shifted to same side (in
bars. figure left side) in unilateral condylar fracture. In bilateral
• Liquid diet for 3-4 weeks. condylar fracture anterior gagging with occlusion occurs
..Our senses don’t deceive us; our judgement does.

Classification Bilateral (Fig. 27.16)
• Fracture without displacement. • Condylar tenderness on both sides.
• Fracture with displacement with anterior • Absence of condylar movement.
• Bleeding from both ears.
overlap/with posterior overlap.
• Preauricular swelling on both sides.
• Fracture with dislocation. • Anterior open bite.
• Fracture with deviation.
• Extracapsular fracture condyle. Management
• Intracapsular fracture condyle (Fig. 27.14). • In children if it is intracapsular, active move-
ments without immobilization is the only
Clinical Features treatment. If it is extracapsular, intermaxillary
fixation for 10 days, later active movements
Unilateral (Fig. 27.15) is needed.
• Condylar tenderness of the side. • In adult if it is unilateral intracapsular and
• Decreased condylar movement on the side. painful, immobilization is advised for 2
• Jaw deviation towards fracture site. weeks and later active movements are
• Tear in external meatus and bleeding from encouraged. If it is intracapsular bilateral
ear of the side. condylar fracture intermaxillary fixation for
• Preauricular swelling of the side. two weeks and later fixation with night
Fig. 27.14: Intracapsular fracture mandible. (A) Shows fracture condyle with hematoma
whereas (B) shows comminuted fracture of the condyle
Fig. 27.15: Bilateral condylar fractures can cause an ‘open bite’ Fig. 27.16: Unilateral condylar fracture
elastics for another 4 weeks is done. In
extracapsular unilateral condylar fracture
intermaxillary fixation for 4 weeks is the
choice. Bilateral extracapsular fracture
condyles are most problematic. It needs
intermaxillary fixation for 6 weeks until
occlusion is stable. Often it needs proper open
reduction.
c. Fracture of the Ramus or Angle of the
Mandible
• If fracture is upwards and inwards, it is
impacted and undisplaced. It is favorable
fracture (Fig. 27.17). Fig. 27.17: Undisplaced fracture mandible
• If fracture is downwards and outwards, it
gets displaced and it is unfavorable fracture
(Fig. 27.18).
Clinical Features
• Pain and tenderness in the lower jaw with
bruising over the surface.
• Hematoma in the floor of the mouth is called
as Coleman’s sign.
• Difficulty in opening the mouth, speech and
swallowing.
• Anesthesia of the lower lip due to compres-
sion of inferior dental nerve.
• Deranged dental occlusion (Fig. 27.19).
• Step deformity.
Management
• X-ray of the mandible reveals the fracture site
• Antibiotics to prevent formation of osteo-
myelitis of the mandible.
• Open reduction of the fracture and fixation
of the fracture segments using titanium/
stainless steel plates or wires for 4–6 weeks.
Either intraoral buccal sulcus approach or
extraoral approach is used.
• Closed reduction of the fracture segments
and fixation by—
• Interdental wiring (Fig. 27.20).
• Using arch bars. Fig. 27.18: Muscle actions in mandible fracture causing
• Silver alloy or plastic caps. different displacements
..He who is angry is seldom at ease.

Fig. 27.19: Unreduced and reduced fracture mandible
Fig. 27.20: Upper and lower border wiring. It is used to fix

the mandibular fractures and is often done together with other Figs 27.21A to C: Different types of symphyseal
fracture fixations in the face fracture—(A) midline, (B) oblique and (C) bilateral
• Only fluid diet for 6 weeks. • Difficulty in closing the mouth.

• Irrigation washes to the oral cavity to • Occlusion discrepancy.
maintain the hygiene. • Mobile mandible with drooling of saliva.
d. Fracture of Symphysis of the Mandible Types
(Fig. 27.21) • Symphysis fracture,central without displace-
It causes— ment.
• Sublingual ecchymosis. • Symphysis fracture, oblique with displace-
• Step deformity of lower margin of the ment.
mandible. • Bilateral symphysis fracture.
Treatment
• Closed reduction with intermaxillary fixation
for 4 weeks.
• Open reduction and fixation using plates or
wires.
Complications of fracture mandible

• Obstruction of the airway.
• Osteomyelitis of the mandible.
• Trismus.
• Speech disturbances.
Management of the Mandibular Fracture
Closed reduction and indirect skeletal fixation
using— Fig. 27.24: Multiple loop wiring used in mandibular fracture
Dental wiring • Multiple loop wiring (Fig. 27.24).

• Direct interdental wiring (Fig. 27.22). • Continuous wiring.
• Clove hitch wiring. • Risdon wiring is used instead of arch bars
• Interdental eyelet wiring (Fig. 27.23) is in midline/paramedian fractures wherein
commonly used method for intermaxillary two wires are tied on the posterior teeth.
fixation. Five eyelets are used in upper and Arch bars are used in—
lower jaw. • When there are inadequate teeth for wiring
• Dentoalveolar fractures.
• When there is associated middle third area
fractures.
• Combination of body and condylar fracture.
Arch bar is done using a malleable metal bar
made of flattened soft German silver wire
(Fig. 27.25). It is moulded around the alveolar
Fig. 27.22: Interdental direct wiring. It is commonly used arch on its outer aspect at the level of the necks
and accepted method of wiring
of teeth to which it is then wired. Erich arch bar
is modified simple arch bar with cleats along its
length. Bar is wired to alveolus and using cleats
it is wired to the bar attached to the opposite
alveolus.
Gunning splints are used in edentulous
patients. Dental impressions are taken and
dentures without teeth called as ‘gunning
splints’ are made. They are wired circumferen-
tially to upper and lower jaws and to each other
to produce needed fixation (Fig. 27.26). It cannot
be used in severe fractured unfavorable
Fig. 27.23: Diagram showing steps in eyelet wiring fractures.
..You may be disappointed if you fail, but you are doomed if you don’t try.
Fig. 27.25: Arch bar wiring. Figure shows both simple and Erich arch bar wiring with cleats to pass wire
Fig. 27.26: Circum mandibular wiring used in gunning splints
Fig. 27.27: Noncompression bone plating used in

Cap splints are done when only few teeth are mandibular fracture
present. It is very lengthy procedure and
difficult. Cast silver cap splints or acrylic cap
splints are used.
• Unilateral dislocation after trauma is
Open Reduction and Direct Skeletal Fixation common.
• Transosseous wiring/osteosynthesis along • Bilateral dislocation occurs during yawning
lower border or upper border. and it is recurrent.
• Plating across fracture segments using either Clinical features are difficulty in opening the
noncompression plates or compression plates mouth with pain and tenderness over the joint.
(dynamic/eccentric) (Figs 27.27 and 27.28A
and B).
Treatment
• Fixation using screw (Fig. 27.29).
• Titanium or stainless steel mesh fixation. • Reduction of dislocation under general
anesthesia.
e. Dislocation of the Mandible
• If there is associated fracture mandible it
• It occurs at temporomandibular joint. should be dealt accordingly.
COMPLICATIONS OF MAXILLOFACIAL
INJURIES
• Infraorbital nerve anesthesia due to
compression/injury of infraorbital nerve in
zygoma or middle third area fractures.
• Lower lip anesthesia in fracture mandible
due to injury of mandibular nerve.
• Malunion and deformities of face.
• Infection and osteomyelitis.
• Airway block due to posterior pharyngeal
edema/backward fall of tongue in mandi-
bular fracture.
• Superior orbital fissure syndrome is seen in
zygomatic complex injury due to hematoma
in the fissure causing compression of 3rd, 4th
and 6th cranial nerves in the fissure. It causes
ophthalmoplegia, ptosis, proptosis and
dilated pupil.
Figs 27.28A and B: Compression plating of a mandibular • Deranged occlusion.
fracture. Note the different methods • Nonunion is not as common as malunion. It
is due to infection, improper immobilization,
systemic diseases and deficiencies, Ankylosis
of the temporomandibular joint is common
in children, in intracapsular fracture of the
condyle and in prolonged immobilization.
• Diplopia/enophthalmos/orbital complica-
tions/strabismus.
• Nasal deformity.
• Epiphora due to damage of nasolacrimal
duct.
• In comminuted fracture of nasoethmoid
complex, cribriform plate is injured causing
injury to olfactory nerve leading into loss of
smell.
Fig. 27.29: Fixation of the splint to skull. It is often used • Alteration in speech is usually temporary.
with gunning splints to fix it to skull • Cosmetic disability.
..A virtuous woman is a splendid prize; a bad...the greatest curse beneath the skies.
28 Neurosurgery
 Head injuries brain shrinks, as a result of which ‘mobility’

 Extradural hematoma of brain increases favoring rupture of veins
which cross the subdural space.
 Subdural hematoma
3. Configuration of interior of skull: Damage is less
 Depressed skull fracture
severe over the smooth area but is more
 Subarachnoid hemorrhage
severe over the rough and sharp areas. So the
 Intracranial abscess
damage is severe over the anterior cranial
 Intracranial aneurysm fossa, over the falx, and over the tentorium.
 Hydrocephalus 4. Deceleration and acceleration injuries: Decele-
 Intracranial tumors ration injuries occur when moving head strikes
 Pituitary tumors an immovable object. (Like in road traffic
 Spina bifida accidents). Acceleration injuries occur when
stationary skull is struck by a moving object
HEAD INJURIES (like in assault).
5. Cerebral concussion is slight distortion causing
Mechanism temporary physiological changes leading to
1. Distortion of the brain: Brain is a soft structure, transient loss of consciousness with complete
therefore has‘mobility’ and readily distorts. recovery.
This distortion and mobility is accentuated by 6. Cerebral contusion is more severe degree of
CSF and vascular components. Any impact damage with bruising and cerebral edema
creates shearing forces in the brain causing leading to diffuse or localized changes.
damage to neurons, supporting tissues and 7. Cerebral laceration is tearing of brain surface
with collection of blood in different spaces
blood vessels. This leads to loss of conscious-
and with displacement of dural parts.
ness, focal neurological deficits. Such distor-
tive damage may be temporary or permanent. Effects of Brain injuries
2. Mobility of the brain in relation to the skull and 1. Brain edema is accumulation of fluid both
membranes causes cerebral damage and intracellular and extracellular. It is due to
bleeding in dural spaces from torn vessels in congestion and dilatation of blood vessels.
the dura, commonly the veins. In old age, the It may be diffuse or localized.
Neurosurgery 359
Clinical types Causative types Primary lesions
• Open injury. • Blunt injury. • Diffuse axonal injury.
• Closed injury. • Sharp injury. • Shearing lesions.
• Missile injury. • Contusion.
Cerebral concussion • Laceration.
• It is temporary physiological Injuries
paralysis. • Cerebral concussion. Secondary lesions
• Transient loss of • Contusion, laceration. • Brain swelling due to edema,
consciousness. • Hemorrhages. hypoxia, congestion.
• Transient amnesia. • Midline shift, coning. • Hemorrhages like extradural,
• Usually shows complete • Brain edema. subdural, intracerebral.
recovery. • Diffuse neuronal injury. • Infections like meningitis,
• Should be observed for • Intraventricular injury/ subdural empyema with
any possible complications hemorrhage. pus collection as localized,
like extradural or subdural • Brainstem injury. encephalitis.
hematoma. • Coup and contre-coup • Features due to increased
injury. intracranial pressure.
• Electrolyte changes.
2. Brain necrosis is of severe variety with des- the ischemia and this forms a vicious cycle,
truction and is due to hemorrhagic causing progressive diffuse ischemia of
infarction. brain.
3. Extradural hematomas occurs usually in 8. Coup injury occurs on the side of the blow
temporoparietal region. It is commonly due to the head. Contre–coup injury occurs on
to tear in middle meningeal veins and often the side opposite to the blow on the head.
middle meningeal artery. It causes intra- 9. Coning
cranial hypertension, displacement, It is due to rise in intracranial pressure
Kernohan’s effect and often death. causing either—
4. Subdural hematoma is due to tear of veins 1. Herniation of contents of supratentorial
between cerebrum and dura due to shearing compartment through the tentorial hiatus
forces. It is diffuse and commonly asso- or
ciated with cerebral injury. 2. Herniation of the contents of infraten-
5. Intracerebral hematoma can occur in different torial compartment through the foramen
parts of cerebrum may be in frontal lobe, magnum.
temporal lobe, etc. In supratentorial herniation, there is
6. Intraventricular hemorrhage is very severe compression of ipsilateral third cranial
type of hemorrhage. nerve and midbrain.
7. Brain ischemia is due to increased pressure. Midbrain is displaced away from the
This in turn leads to alteration in the mass (hematoma) and midbrain is pressed
perfusion of brain which itself aggravates by the sharp edge of tentorium cerebelli of
..Do whatever your enemies don’t want you to do.

opposite side leading to dysfunction of Clinical Approach of a Patient with
corticospinal fibers (which after decussation Head Injury
supplies on the opposite side in the body. 1. Detail history of injury has to be taken and
i.e. same side of the injury). also the process of deterioration—rapid or
This leads to: gradual.
a. Deterioration in the level of conscious- 2. History of alcohol intake: Alcohol intake
ness. mimics head injury and alcoholism itself may
b. Dilatation of pupil on the side of com- mask the features of head injury.
pressing mass (hematoma). 3. Neurological assessment:
c. Hemiparesis on the same side of the By—
mass lesion (hematoma) due to com- • Level of consciousness.
pression of the contralateral cortico- • Glasgow Coma Scale.
spinal tract. This effect is called as • Pupillary reaction to light and size.
Kernohan’s notch effect (Fig. 28.1). • Pulse.
Herniation of infratentorial contents • Temperature.
through the foramen magnum causes • Blood pressure.
obstruction of cerebral aqueduct which • Respiratory rate.
further damages the brain function. • Reflexes.
10. Respiratory failure altering PO2 and PCO2 • Limb movements—normal\mild weak-
ness\severe weakness\spastic flexion\
levels.
extension\no response.
11. Raised intracranial pressure causing brady-
4. Status and protection of airway.
cardia, hypertension, vomiting. Raised 5. General assessment and other injuries like
intra-cranial pressure may precipitate fractures, abdominal organ injuries, and
coning and thus aggravates brain ischemia. thoracic injuries are looked for.
12. Fluid and electrolyte imbalance. 6. Presence of any scalp hematoma, fractures
13. Hyperpyrexia. of skull bone which may be depressed has
14. Convulsions due to irritation of gray matter. to be looked for Figure 28.2 shows a head
15. CSF rhinorrhea or CSF otorrhea. injury patient having a black eye.
Fig. 28.1: Coning with Kernohan’s notch Fig. 28.2: Head injury patient having black eye
Neurosurgery 361
7. Any blood from nose or ear, CSF rhinorrhea • Serum electrolyte measurement.
or CSF otorrhea has to be looked for. • Blood grouping and cross matching.
ADELAID COMA SCALE: It is used in children. • CT scan—Plain (not contrast) to look for
Scores for eye opening and motor responses are cerebral edema, hematomas (Figs 28.3 and
same as Glasgow Coma Scale. 28.4), midline shift, fractures, ventricles,
But verbal response score differs—Oriented-5. brainstem injury.
Words-4. Vocal sounds-3. Cries-2. Nil-1. • Carotid arteriography.
Orientation cannot be evaluated below 5 • Investigations for other injuries like ultra-
years. For first 6 months, the best verbal response sound of abdomen.
is cry.
• Monitoring of intracranial pressure.
Indications for hospitalization
• Any altered level of consciousness. Treatment
• Skull fracture.
General
• Focal neurological features.
• Persistent headache, vomiting, systolic • Protection of airway using mouth gag,
hypertension, bradycardia. endotracheal intubation or tracheostomy
• Alcohol intoxication. whenever required.
• Bleeding from ear or nose. • Throat suction, bladder and bowel care, good
• Associated injuries. nursing are very essential.
Investigations • Nasal oxygen or often ventilator support.
• X-ray skull: To look for fracture, relative • IV fluids initially, later Ryle’s tube feeding
position of the calcified pineal gland, has to be done.
presence of intracranial air. • Electrolyte maintenance.
Glasgow coma scale

Eye opening Verbal response Motor response
Spontaneous. 4 Oriented. 5 Obeys commands. 6.
To speech. 3 Confused. 4 Localizes pain. 5.
To pain. 2 Inappropriate words. 3 Flexion to pain. 4.
None. 1 Incomprehensible words. 2 Abnormal flexion. 3.
None. 1 Extension to pain. 2.
None. 1.
Total score—15.
Mild head injury: score 13-15.
Moderate head injury: 9-12.
Severe head injury: less than 8. (3-8).
Score 1—dead or dying. Score 2—vegetative state. Score3—severe disability.
Score 4—moderate disability. Score 5—good recovery.
..Friends come and go,but enemies accumulate.

hourly or Frusemide 40 mg IV 8th hourly.

It should not be given in conditions like
intracranial hematomas.
• Antibiotics like penicillins, ampicillins are
given to prevent the onset of meningitis.
• Corticosteroids either dexamethasone or
betamethasone is used commonly but its
beneficial effect is not confirmed.
Indications for Surgery

1. Acute extradural hematoma.
2. Acute subdural hematoma.
3. Depressed skull fracture.
Procedure: Craniotomy is done and cranial flap
is raised. After evacuating the clot hitch stitches
are applied between dural layer and scalp.
Fig. 28.3: CT scan head showing scalp hematoma Postoperative antibiotics, analgesics, anticonvul-
both sides. There is no internal injury sants are given.
Complications of Head Injuries

A. Early
1. Brainstem injury—due to coning.
2. Compression over cerebellum and medulla.
3. CSF rhinorrhea.
4. Meningitis—common.
5. Pituitary damage and endocrine failure—
requires high dose of hydrocortisone 200 mg
6th hourly.
6. Aerocele.
7. CSF otorrhea.
8. Depressed fractures often causes injury to
dural venous sinuses and may lead to
torrential hemorrhage which may be life-
threatening. So such depressed fractures
should never be elevated.
Fig. 28.4: CT scan head showing intracerebral hematoma B. Late

1. Chronic subdural hematoma.
2. Early post traumatic epilepsy—they need
Drugs anticonvulsants for 3 years.
• No sedation is given. 3. Late posttraumatic epilepsy is due to scarring
• Analgesics and anticonvulsants like and gliosis of cerebrum.
Phenytoin or Phenobarbitone is started. 4. Posttraumatic amnesia.
• Diuretics are given to reduce cerebral 5. Posttraumatic hydrocephalus.
edema—either mannitol 20%, 200 ml IV 8th 6. Posttraumatic headache.
Neurosurgery 363
CSF RHINORRHEA Pathology
It is due to communication between intracranial
cavity and the nose. There is a tear in the dura
following the fracture involving the sinuses—
frontal, ethmoid, sphenoidal sinuses. Meningitis
is the common complication of CSF rhinorrhea.
Treatment: Initial management is only conserva-
tive for 10 days—by antibiotics and observation.
Indications for surgical intervention:
a. Fracture middle third face.
b. CSF rhinorrhea persisting for more than 10
days.
c. Fracture of sinuses.
d. An aerocele.
e. An attack of meningitis.
Surgeries:
1. Reduction of middle third of face.
2. Exploration of anterior cranial fossa.
EXTRADURAL HEMATOMA
It is collection of blood in the extradural space
between the dura and skull. Commonest site is
temporoparietal region. It can be unilateral or
bilateral.
Vessels commonly involved:
• Middle meningeal veins.
• Anterior branch of middle meningeal artery.
• Posterior branch of middle meningeal artery.
Usually is associated with fracture of Clinical Features
temporoparietal region. History of transient loss of consciousness
Immediately after injury, there will be tran- following a history of blow or fall. Patient soon
sient loss of consciousness and the patient soon regains consciousness and again after 6–12hrs
becomes normal. Later after 6–12 hours, he again starts deteriorating (Lucid interval).
falls ill and the condition deteriorates. This is the Later the patient presents with confusion,
time taken to develop raised intracranial irritability, drowsiness, and hemiparesis on same
pressure, coning and its effects. This crucial time side of the injury. Initially pupillary constriction
gap which is unnoticed and often missed is called and later pupillary dilatation occurs on the same
as ‘lucid interval’. side, finally becomes totally unconscious.
..The greatest truths are the simplest; and so are the greatest men.
Death can occur if immediate surgical inter- Treatment
vention is not done. Immediate surgical intervention is essential to
Features of raised intracranial pressure like high save the life of patient.
blood pressure, bradycardia, vomiting is also Craniotomy is done and cranial flaps are
seen. Occasionally convulsions may be present. raised. The dura is opened and the clot is
Wound and hematoma in the temporal region of evacuated. The dura is fixed to galea using
scalp may be seen. interrupted sutures—Hitch stitches. Antibiotics
Investigations and anticonvulsants are given postoperatively.
• X-ray skull may show fracture of temporal Recovery is good after surgery.
bone. Complications
• Electrolyte estimation.
1. Posttraumatic epilepsy.
• CT scan—head is diagnostic. Extradural
2. Meningitis.
hematoma shows biconvex lesion (Figs 28.5
3. Posttraumatic amnesia.
and 28.6).
SUBDURAL HEMATOMA
Types
Acute or Chronic.
a. Acute subdural hematoma:
It is a collection of blood between the brain and
dura. It is due to injury to the cortical veins and
often due to laceration of cortex of brain which
bleeds and blood gets collected in the subdural
space forming a hematoma..
Here hematoma is extensive and diffuse.
There is no lucid interval. There is a severe
primary brain damage.
Fig. 28.5: Extradural hematoma. Note the biconvex
configuration of the hemtoma
Hematoma may be coup and contre-coup
type.
Loss of consciousness occurs immediately
after trauma and is progressive.
Convulsion is common.
Features of raised intracranial pressure are
obviously seen—High BP, bradycardia,
vomiting.
Focal neurological deficits or hemiparesis can
occur.
CT scan shows concavo-convex lesion.
Treatment: Antibiotics, anticonvulsants, etc.
Surgical decompression has to be done by craniotomy.
b. Chronic subdural hematoma:
It is due to the rupture of veins between dura
Fig. 28.6: CT scan head showing extradural hematoma and brain (cerebral hemispheres), causing
with biconvex lesion gradual collection of blood in subdural space.
Neurosurgery 365
It is commonly seen in elderly people following
any minor trauma like fall, slipping, etc. (which
might have gone unnoticed). In elderly people,
brain atrophies and even minor injuries can
cause shearing and bleeding from these veins.
Blood collects gradually over 2– 6 weeks. Plasma
and cellular components get separated.
Eventually cellular part gets absorbed leaving
only fluid component. It is called as subdural
hygroma.
Usual hematoma collection is 60–120 ml.
Often it is bilateral in 50% of cases.
This chronic hematoma may get infected, gets
filled with localized pus and is called as chronic Fig. 28.7: Subdural hematoma. Note the Concavo-convex
subdural empyema. configuration of the lesion (C/W EDH)
Clinical Features
• Common in old age, with history of minor
trauma.
• Patient presents with confusion, disorienta-
tion, gradually with altered level of cons-
ciousness and drowsiness.
• Later convulsions, features of intracranial
hypertension, features of coning develop.
• Extensor plantar response and pupillary
changes develop eventually.
Investigations (Figs 28.7 and 28.8)

• CT scan (shows concavo-convex lesion).
• Serum electrolytes. Fig. 28.8: CT scan head showing subdural hematoma with
• Blood grouping and cross matching. concavo-convex lesion
Differential Diagnosis Complications

• Electrolyte imbalance. 1. Epilepsy.
• Intracranial space occupying lesion. 2. Meningitis.
3. Coning.
Treatment 4. Neurological deficits.
• Craniotomy and evacuation of clot has to be
done when required on both sides. DEPRESSED SKULL FRACTURE
• Antibiotics. It is a common neurosurgical problem among
• Anticonvulsants for 3 years. the head injuries.
..It does not matter if you fall down as long as you pick up something while you get up.
—Allen Smith
It means fracture depression is more than the • Neck stiffness.
depth of the inner table of skull. • Focal neurological deficits: hemiplegia,
dysphasia.
Problems in depressed fracture • Eye changes: ptosis, dilated pupil, changes
• Tear in the dura beneath. in the eyeball movements.
• Hematoma in the deeper plane. • Sudden loss of consciousness.
• Injury to the cerebrum. • Features of brain edema and cerebral
• Injury to the venous sinuses—may cause life ischemia.
threatening hemorrhage. Fracture should not In 40% of recovered patients, rebleeding
be elevated in such occasion as it itself can occurs in 6–8 weeks which is commonly fatal.
precipitate bleeding.
• Convulsions. Differential Diagnosis
• Meningitis. • Meningitis.
• Coning due to any cause.
Investigations
CT scan. Investigations
a. Lumbar puncture should be done to differen-
Treatment tiate from meningitis.
Antibiotics, anticonvulsants. • It has to be done carefully as it may
Elevation of the depressed fracture: Burr holes are precipitate coning.
made in the adjacent normal skull. Fracture is • In subarachnoid hemorrhage blood
elevated. Bony fragments and necrotic materials stained CSF is collected.
are removed. Dural tear is closed with inter- b. CT scan.
rupted sutures. c. Carotid and vertebral angiogram.
SUBARACHNOID HEMORRHAGE Treatment

It is a type of intracranial hemorrhage into the • Clipping, or wrapping the aneurysm.
subarachnoid space usually from basal cisterns. • Craniotomy and proceed.
It is usually spontaneous. • Ligation of common carotid artery—there is
risk of hemiplegia.
Causes • Therapeutic embolization.
• Excision of vascular malformations.
• Intracranial aneurysms. Commonest cause
(50%).
• Hypertension. INTRACRANIAL ABSCESS
• A-V malformations. Types
• Blood dyscrasias. 1. Extradural abscess: Caused by:
• Anticoagulant drugs. — Osteomyelitis of skull.
• Brain tumors (malignant). — Middle ear infection.
— Frontal sinusitis.
Clinical Features Pott’s puffy tumor is infection and inflam-
• Sudden onset of severe headache with mation of the scalp. There is acute localized
vomiting. headache and tenderness in the skull,
• Features of raised intracranial pressure. localized pitting edema of the scalp usually
• Photophobia. in the frontal region.
Neurosurgery 367
2. Subdural abscess is caused by septic 3. Carotid angiogram.
thrombophlebitis from the frontal sinusitis or 4. Ventriculography.
other infections. It is often very severe with 5. EEG.
extension into the venous sinuses. 6. Isotope brain scan.
3. Intracerebral abscess is caused by 7. Total count, ESR.
1. Extension from middle ear or sinuses. 8. Investigation specific for focus of infection.
2. Blood born infection. Lumbar puncture should be avoided in acute
3. After intracranial injuries. abscess as coning can occur.
Common sites: Temporal lobe, cerebellum, frontal Treatment
lobe.
1. Antibiotics—high dose Penicillins, Benzyl
It can be:
penicillins are given.
a. Acute—There is acute septic encephalitis
2. Burr hole exploration is done and Dandy’s
without pus formation. It may cause
brain cannula is placed. Pus is aspirated and
ventriculitis or localized abscess formation.
sent for culture and cytology.
b. Subacute—Commences in 3 weeks, by the
3. In case of chronic abscess, exploration of
formation of a glial wall, i.e. thickness is more
cranial cavity and excision of brain abscess
near the cortex and less towards ventricle.
has to be done.
c. Chronic—Occurs in 6 weeks with thick wall
which may persist or may get enlarged Complications
behaving like a space occupying lesion. 1. Intracranial hypertension.
d. Metastatic—Abscess in brain occurs either in 2. Coning.
cerebrum (parietal or temporal lobes) or in 3. Neurological deficits.
ventricles (Ventriculitis is more dangerous
and often fatal). INTRACRANIAL ANEURYSM
• Evidence of focus of infections are seen, i.e. 1. Subclinoid type occurs in the internal carotid
middle ear (CSOM), sinusitis. artery within the cavernous sinus. It causes
• Focal neurological features are seen, ptosis, defective external ocular movements,
depending on the location of abscess. In 5th nerve palsy. It can cause carotid
temporal lobe abscess they have dysphasia, cavernous fistula.
contralateral hemiparesis; all cerebellar 2. Supraclinoid type is common type.
symptoms are seen in cerebellar abscess. 1. Berry’s aneurysms: A congenital type occurs
• Epilepsy. in circle of Willis in relation to internal
• Features of raised intracranial pressure: a) carotid artery (40% (most commonly at
slow pulse, b) rising BP, c) headache and the origin of posterior communicating
vomiting, d) papilledema, e) deterioration in artery)), anterior communicating artery,
level of consciousness, f) visual disturbances. middle cerebral artery, vertebrobasilar
artery. It occurs due to weakness in the
Investigations media of major arteries.
1. CT scan. 2. Acquired aneurysms due to atheromas,
2. MRI. hypertension.
..Experience is a comb that nature gives man after he has gone bald.
—Thai Saying
3. Mycotic aneurysms occur due to infection Acquired
in the wall of cerebral vessels as a result • May be unilateral or bilateral (midline
of any bacteremia. Common sites are obstruction).
peripheral branches of middle cerebral • Chronic meningitis.
artery. • Trauma.
• Brain tumors.
Presentations • Colloid cyst of 3rd ventricle.
• Arachnoid cysts.
• Subarachnoid hemorrhage.
• Pressure effects.
• Convulsions.
• Eye and pupillary signs.
Investigations
• CT scan.
• Carotid and vertebral angiogram.
Treatment
• Clipping or wrapping of aneurysms.
• Therapeutic embolization.
• Open neurosurgical approaches.
HYDROCEPHALUS
Dilatation of ventricles due to blockage of
cerebrospinal flow (CSF).
Classification I
a. Communicating type: Ventricles communi-
cate freely into the subarachnoid space.
Here there is defective absorption of CSF
following any inflammation, subarachnoid
hemorrhage or trauma.
b. Noncommunicating type: Obstruction is in
the ventricle or its exit due to any tumors or
any inflammatory process.
Classification II
Congenital
• Associated with spina bifida and myelo-
meningocele.
• Failure of formation of CSF pathways.
• Arnold-Chiari malformation. Figs 28.9A and B: Hydrocephalus child. CT scan
• Congenital stenosis of aqueduct of Sylvius. head picture in hydrocephalus
Neurosurgery 369
Features chiasma, third ventricle, hypothalamus,
• Presents with widening of sutures, tense etc. They are irremovable but are radio-
fontanelles and decreased cortical thickness. sensitive.
• Enlargement of head occurs, either prenatal d. Medulloblastoma occurs in children,
(can cause obstructed labor) or postnatal. affecting vermis of the cerebellum which
grows rapidly with seedling elsewhere in
Clinical Features the brain.
e. Ependymomas: Cells here resemble
Bulging of anterior fontanel (Fig. 28.9A), ependymal cells. It can occur throughout
engorged scalp veins, separation of suture lines,
the cerebral hemispheres.
’sun-setting’ sign.
Investigations
CT scan (Fig. 28.9B), Ventriculography, air
encephalography, MRI.
Treatment
• Tapping of lateral ventricles.
• Ventriculocysternostomy using polythene
catheters—Torkildsen operation.
• Ventriculoatrial (VA) shunt.
• Ventriculoperitoneal (VP) shunt.
INTRACRANIAL TUMORS
Secondaries are the commonest malignant
tumor in the brain. Metastasis occurs usually
from lung(commonest), nasopharynx or from
any other organ in the body. Fig. 28.10: MRI brain showing glioma brain
Primary Brain Tumors 2. Meningiomas(18%): They are usually

1. Gliomas (43%) (Fig. 28.10). globular, arising from the arachnoids. Tumor
a. Astrocytomas are the commonest type. gets attached to the dura. It gets blood supply
They are usually malignant. They can from dural arteries and veins, from emissary
occur anywhere in the cerebral hemi- veins and veins of diploe and scalp. Along
spheres, medulla, and brainstem. They these veins tumor cells invade the bone,
can be diffuse, solid, or cystic. They contain causing bone destruction and reactive
star shaped cells resembling adult hyperostosis. Meningiomas can be calcified,
neuroglial cells. Astrocytic gliomas are fibroblastic, endothelial and angioblastic.
graded as Grade I, II, III, IV as per the Sites: 1) Parasagittal, 2) Frontobasal, 3)
quantity of adult and primitive cells. Posterior fossa, 4) Choroid plexus (Fig. 28.11).
b. Oligodendrogliomas. Microscopic: It contains whorls of spindle
c. Spongioblastoma polare arises from the cells, with central hyaline material, with
primitive spongioblasts affects optic Psammoma bodies.
..Anything good is either illegal, immoral, or fattening.

Specific Features
1. Frontal lobe tumors: Personality and emo-
tional changes, epilepsy of generalized type,
contralateral facial weakness.
2. Parietal lobe tumors: Jacksonian epilepsy,
progressive hemiparesis, astereognosis,
acalculia.
3. Occipital lobe tumors: Aura of flashing of
light in contralateral field, homonymous
hemianopia.
4. Temporal lobe tumors: Progressive aphasia,
visual, auditory, smell and taste hallucina-
tions, hemiparesis, superior quadrantic
hemianopia.
5. Midline tumors: Produces bilateral hydro-
cephalus.
6. Tumors of the third ventricle (colloid cyst is
common): Causes bilateral hydrocephalus,
progressive cerebral atrophy, dementia,
sexual precocity, endocrine disturbances.
7. Pineal tumors: Causes precocious puberty.
Fig. 28.11: CT scan head showing large meningioma
8. Cerebellar vermis tumors: Usually medullo-
frontal region blastomas, occur in young children, presents
with progressive hydrocephalus and features
of herniation of cerebellar tonsils through
3. Schwannoma (8%): Common in auditory
foramen magnum.
nerve also called as acoustic neuroma.
9. Cerebellar hemisphere tumors: commonly
Occurs in the internal auditory meatus
are astrocytomas, produce cerebellar syndro-
which projects into the cerebellopontine mes, nystagmus.
angle (C- P angle), compressing 5, 6, 7, 8th
nerves. It presents with compressive features Investigations
like unilateral deafness, trigeminal neuralgia, • X-ray skull
squint, cerebellar compression syndrome. a. Calcifications like in meningiomas,
4. Pituitary tumors (12%). craniopharyngiomas.
5. Craniopharyngiomas (5%). b. Separation of sutures.
6. Blood vessel tumors (2%). c. A beaten silver appearance.
d. Lateral displacement of pineal body.
Clinical Features e. Hyperostosis, expansion, destruction in
• Initial period of silent growth. skull bones.
• Focal syndromes with epilepsy. • Isotope scan.
• Raised intracranial pessure with headache, • CT scan.
vomiting, deterioration of level of conscious- • MRI.
ness, altered vision slow pulse, high BP, • Positron Emission Tomography (PET).
papilledema. • Carotid angiogram (Introduced by Egas
• Brain displacement and stage of coning. Moniz).
Neurosurgery 371
• Ventriculography. Initially it is intrasellar and after sometime
• EEG. becomes suprasellar. Later it extends intra-
cranially often massively, causing features of
Treatment intracranial space occupying lesion. It
1. Relief of raised intracranial pressure: presents with myxedema, amenorrhea,
a. Ventricular tap and drainage through a infertility, headache, visual disturbances,
posterior parietal burr hole. bitemporal hemianopia, blindness, intra-
b. Tapping of cystic tumors and abscesses. cranial hypertension, epilepsy.
c. Administration of mannitol. Differential diagnosis: Meningiomas, aneu-
d. Emergency decompression by partial rysms.
removal of tumor. CT scan, angiogram, X-ray skull are diag-
e. Steroid therapy—dexamethasone. nostic.
2. Establishment of pathological diagnosis: Treatment is surgical decompression by
a. Burr hole and biopsy. craniotomy through subfrontal approach or
b. Craniotomy and biopsy using brain transsphenoidal approach. Deep external
cannula. radiotherapy and steroids are also used.
c. Frozen section biopsy. 3. Basophil adenomas: are usually small. They
d. CT guided stereotactic biopsy. secrete ACTH and presents as Cushing’s
3. Removal of benign tumors—by different disease with all its features.
craniotomy approaches. 4. Prolactin secreting adenomas: Causes
4. Decompressive surgeries for malignant infertility, amenorrhea and galactorrhea.
tumors. It could be hypersecreting or hyposecreting
5. Shunt surgeries to drain CSF ventriculo- by compression and atrophy.
peritoneal shunt or ventriculoatrial shunt. It could be micronodular if tumor size is less
6. Radiotherapy—External radiotherapy is than 10mm.
used as primary treatment or as an adjuvant It could be macronodular if tumor size is
therapy after surgery. more than 10 mm.
7. Chemotherapy is occasionally used.
Investigations
Prognosis
• X-ray skull: shows calcifications, destruction
If tumor is benign and surgically accessible then of sella turcica, mass lesion, and enlarged
has got better prognosis. pituitary fossa.
• CT scan.
PITUITARY TUMORS • MRI.
Classification • Hormone assay—like prolactin, growth
hormone, ACTH, steroids, sex hormones, etc.
1. Eosinophil (Acidophil) adenomas: Tumor is
usually small. Rarely it causes compressive
features. Treatment
It secretes excess growth hormone • Surgery: By subfrontal craniotomy approach
causing acromegaly in adults and gigantism or transsphenoidal approach. Care should be
in children. taken not to injure optic chiasma, arteries,
2. Chromophobe adenomas: Are common in cavernous sinus.
females and in the age group (20-50 years). • External radiotherapy.
..Future comes one day at a time.

SPINA BIFIDA
• It is failure of enfolding of nerve elements
within the spinal canal during developmental
period.
• It is usually seen in lumbosacral region. There
is failure of fusion of the one or more
posterior vertebral arches.
• It is often associated with other anomalies.
Sites
• Lumbosacral.
• Thoracolumbar.
Types
Spina bifida occulta:

• There is dimpling of skin with dermoids, Fig. 28.12: Spina bifida with protruding dermoid
through the defect
lipomas in the site. Impulse on coughing can
be seen.
• Initially there is no neurological deficit but
later due to tethering, traction on dura, and
infection can lead to neurological deficits.
Spina bifida aperta:
• There neurological deficit is present. It may
be myelomeningocele wherein spinal cord and
nerve roots are in the sac. It may be menin-
gocele wherein sac consists of meninges and
fluid only.
• Meningocele is brilliantly transilluminant.
Myelomeningocele is not transilluminant. Fig. 28.13: Meningoencephalocele
Clinical Features (Figs 28.12 and 28.13) Investigations

• Motor paralysis. • Plain X-ray of the spine.
• Sensory paralysis. • CT scan/MRI of spine and head.
• Visceral paralysis with incontinence of urine
and feces. Treatment
• Swelling in the spine at the site of the lesion, • Correction of deformity.
may be lipoma or dermoid with impulse on • Maintaining the visceral function.
coughing. • Development of limb function.
• Bony defect at the site. • Ventriculoperitoneal shunt or ventriculo-
• Hydrocephalus. atrial shunt surgery for hydrocephalus.
Adjuvant Therapy 373
29 Adjuvant Therapy
 Radiotherapy Common malignancies which are Radio-

 Chemotherapy sensitive are:
 Immunosuppression • Squamous cell carcinoma.
 Hormonal therapy • Basal cell carcinoma.
 Immunotherapy • Bladder tumors.
 Hybridoma • Carcinoma cervix.
 Gene therapy • Seminoma testis.
• Hodgkin‘s lymphoma.
RADIOTHERAPY • In carcinoma breast with secondaries in bone
It is use of high energy ionizing radiation in the during postoperative period. Sometimes as
management of malignant tumors. It may be preoperative radiotherapy, as part of QUART
electromagnetic waves, X-rays, gamma rays, Regime.
electrons, protons, neutrons, or alpha particles. • In follicular carcinoma of thyroid: For secon-
It may be— daries, radioactive I131 5 m curies is given
• External radiotherapy/brachytherapy/ orally. External radiotherapy is also given for
combined. bone secondaries along with internal fixation
• Curative/palliative radiotherapy. if there is pathological fracture.
• Preoperative/postoperative/both pre- and • Malignant brain tumors like astrocytomas.
postoperative radiotherapy. • Many sarcomas.
• Carcinoma prostate.
Principle • Carcinoma esophagus.
• Carcinoma lung.
Radiation is used to kill actively proliferating
• Fixed secondaries in neck as palliation to
malignant cells at their mitotic level.
reduce pain, fungation and erosion into major
Other areas where radiotherapy is commonly vessels.
used are: • Multiple myelomas.
Sources of radiotherapy Classification Efficacy depends on

• X-rays, electrons-from high • Low LET (Low Energy Trans- • Cell cycle phase.
energy X-ray machine, i.e. fer) radiation- X-rays, gamma • Oxygen content of cells.
Linear accelerator. rays, electrons. Methods of delivery
• Gamma and beta rays from • High LET radiation – Neu- • External beam radiation
radioactive isotopes like trons, protons, alpha particles (Teletherapy).
cobalt-60, cesium 137, and negative ions. It has • Brachytherapy.
iridium 197. heavier mass with dense • Systemic irradiation using
• Protons, neutrons and heavy localization and hence radioisotopes like I131.
ion nuclei from cyclotrons. biologically more effective.
Radioresistant tumors include— Measurement of ionizing radiation

• All GI malignancies. Roentgen unit is a measure of ionizations
• Melanoma. produced per unit volume of air by X-rays and
• Medullary carcinoma of the thyroid. gamma rays but it is not used for photon energies
above 3Mev. SI unit for exposure is coulomb per
Sources of radiotherapy kg.
• Cobalt 60 machine—most commonly used.
• Kilovoltage machines. Radiation absorbed dose (RAD)
• Linear accelerator. Absorbed dose is De/dm. It is mean energy
• Betatron/microton. imparted by the ionizing radiation to material
• Radioactive materials like Cesium 137 of mass dm.
(pellets), Iridium 192 (wire), Gold 198 (seeds), Old unit is rad which is equivalent to 100 ergs
iodine 125 (seeds). of energy per gram.
Preoperative radiotherapy Postoperative radiotherapy Radiotherapy and

Advantages • More effective and extent of chemotherapy combined
• Down-stage the tumor and RT is well-defined. • Commonly used before or
reduces the tumor bulk. • Flap necrosis, fistula comp- during RT.
• No change in oxygenation lications are less. • Chemotherapy after RT is
of tissues. Indications not commonly followed.
• Blockage of lymphatics by • When resected margin is • Chemotherapy before RT is
RT prevents tumor spread positive for tumor. called as induction chemo-
during surgical dissection. • When bone/cartilage are therapy which reduces the
• Reduces the chances of involved. bulk of tumor without
microscopic spread. • Extracapsular nodal spread. altering the vascularity.
Disadvantages • Multiple neck nodes/node • Chemotherapy with RT is
• Delayed healing due to more than 3 cm in size in case called as concomitant RT
reduced vascularity. of neck disease. which improves the effect
• Flap necrosis, fistula forma- • Poorly differentiated tumor. of RT. Methotrexate and
tion. Bleomycin are radio-
• Carotid blow-out. sensitizers.
Brachytherapy
Types Advantages Disadvantages

• Intracavitary like in uterus, urinary • High, localized, single • Technically difficult.
bladder, maxillary antrum, continuous dose of RT. • Availability of the
bronchial or esophageal tree. • Deeper and adjacent tissues facility.
• Interstitial wherein radioactive are spared. • Local complications
needles/wires/ribbons/seeds are • High dose rate with short like displacement/
inserted into the tumor area like time. erosion.
in bladder or oral cavity. • Less side effects.
• Surface brachytherapy using • Curative and effective in
moulds like in tumors of skin/ early cancers.
eye/breast. • After loading devices are
available which reduces
Radionuclides used are Caesium 137
personal exposure.
(Cs137), Iridium 192 (Ir192), Gold 198
• Surgery is avoided and part
(Au198) and Iodine 125 (I125).
is retained.
Brachytherapy is often combined
with external beam radiotherapy.
Newer international unit is presently used. Problems in Radiotherapy

One Gray (Gy) is one joule of energy deposited • Loss of taste and sensations, loss of appetite.
per kilogram of material. One Gy = 100 rads = • Infection, trismus, fibrosis, mucositis, dryness
100 cGy. 1 cGy = 1 rad. of mouth.
• Skin necrosis, sloughing, infection.
Radiotherapy Plan • Laryngeal edema, candida infection.
Type and doses of radiotherapy is decided by • Radiation induced osteomyelitis commonly
following factors: in mandible.
• Site of tumor. • Radiation induced retinopathy and cataract.
• Lymphatic field. • Endocrinal deficit like of thyroid/pituitary.
• Tumor size and extent. • Radiation induced nephritis and renal failure.
• Histological type and grading. • Radiation induced thimble bladder.
• Radiation oophoritis and infertility.
BRACHYTHERAPY (REFER TABLE ABOVE) • Radiation induced frozen pelvis.
• Radiation induced malignancy.
It is radiation given with source close to the
• Hemopoietic suppression.
tumor.
• Transverse myelitis.
• It is given using Iridium needles or moulds.
Usual dose required depends on site, type
• It is curative radiotherapy.
of tumor, size of tumor and response of tumor.
• It is used in carcinoma oral cavity, penis,
Usually 20–25 doses required. It is given 5 days
breast, cervix and bladder.
a week. Two days gap is given so as to allow
Palliative Radiotherapy is always external dormant cells to get activated because only active
teletherapy using Cobalt 60. cells will be killed by radiotherapy.
..A fashion is nothing, but an induced epidemic.

—Bernard Shaw
Care of patients on radiotherapy • They also affect hemopoiesis, cellular

• Diet rich in proteins, vitamins and iron. activity, epithelial tissues and gonads.
• They also suppress the immune system.
• All infected/problematic teeth should be
extracted before RT. Side effects in general:
• Care of skin by keeping area dry. Avoid • Bone marrow suppression.
washing with soap and water. • Alopecia.
• Avoid exposure to sunlight and wet shaving. • Hepatotoxicity.
• Adhesive plaster/dressings should be • Nephrotoxicity.
avoided. MUSTINE HYDROCHLORIDE: Used in
• Soft silk cloth should be used to cover the RT Hodgkin’s lymphoma. It is Mechlo-rethamine.
area.
• Avoid alcohol, tobacco, spicy food. CYCLOPHOSPHAMIDE: It is used in ovarian
• Milk of magnesia is used for mucositis. carcinoma, lymphomas, colonic carcinoma,
Xylocaine gel 10% is used to relieve pain. bronchogenic carcinoma.
• Prevention of infection especially candida by Side effects: Alopecia, bone marrow suppression,
topical Nystatin/Clotrimazole. cystitis(hemorrhagic).
Dose: 3 mg/Kg IV daily for 5 days in dextrose,
CHEMOTHERAPY as monthly cycle for 6 months. Orally as 50 mg
tablets.
• Today chemotherapy is an important moda-
lity of treatment in management of cancer. MELPHALAN (Phenylalanine mustard): Used
• It is the main modality of treatment in most in multiple myeloma and melanoma.
of the advanced malignancies. Dose: 10 mg daily for 3 weeks. Available as 2 mg
• It is used preoperatively to downstage the tablets.
tumor so as to increase the possibilities of BUSULFAN: 2 mg tablet. 10 mg for 3 weeks.
surgical resection. Used in chronic myeloid leukemia.
• When used postoperatively it reduces the Side effect: Pulmonary fibrosis.
rate of recurrence.
• It is the primary treatment for NHL, CHLORAMBUCIL: 10 mg for 3 weeks. Used in
leukemia. chronic lymphatic leukemia.
• These drugs mainly act by blocking the METHOTREXATE: 10 mg orally. It competes
mitotic activity in the nucleus in different with folic acid.
phases of the cell cycle.
Side effects: Megaloblastic anemia, hepatic
• It is given either orally, intravenously
damage and dermatitis.
(systemic), intraarterial, intrathecal and
intravesical (regional) or as isolated limb 6-MERCAPTOPURINE: It alters the purine
perfusion. metabolism. 50 mg tablets.
• Intraarterial chemotherapy is used in head It is used in leukemias and choriocarcinoma.
and neck cancers and hepatic cancers. Dose: 150 mg for 5 days monthly for 6 months.
• Isolated limb perfusion is used in melanoma. It causes hyperuricemia
5-FLUOROURACIL: 15 mg/Kg. It is given daily
ANTIMALIGNANCY DRUGS for 5 days in dextrose bottle for 6 months cycle.
Mode of action: Uses: Adenocarcinomas of GIT, breast
• Damage the active cells. cancers and cancer cervix.
Side effects: Neurotoxicity, stomatitis, bone IMMUNOSUPPRESSION
marrow suppression.
• It is mainly used in transplantation to prevent
VINCA ALKALOIDS: It inhibits mitosis. graft rejection.
Vincristine: Dose: 1.4 mg/sq.m. It is neurotoxic. • In transplantation of kidney, liver, heart,
Vinblastine: Dose: 0.1 Kg body weight. It causes small bowel, pancreas.
bone marrow toxicity. Drugs used are:
RUBIDOMYCIN: 40 mg/m/day IV. Myocardial • Azathioprine: (Imuran, Purine analogue).
depressant. • Cyclosporine: It is a very good immunosup-
Used in acute myeloblastic leukemia. pressant, derived from fungus. It causes
inhibition of lymphocytic activity, delayed
ADRIAMYCIN: It is commonly used in NHL, hypersensitivity, interleukins, memory cells,
hepatoma, medullary carcinoma of thyroid, etc. It is initially given intravenously and later
osteosarcoma and soft-tissue sarcomas. It is given orally. It is given usually for long
cardiotoxic. So should be infused with cardiac duration for 12–24 months. It is nephrotoxic
monitoring. Dose: 30 mg/day for 3 days. as well as bone marrow suppressant. So
constant monitoring by blood urea, serum
0‘-p DDD(MITOTANE): It destroys selectively
creatinine, blood count, Hb% at regular
adrenal cortex. It is used in carcinoma adrenal
intervals is required. Dose should be adjusted
cortex.
depending on these parameters. Cyclos-
Dose: 10 gm orally for 8 weeks.
porine is very effective immunosuppressant
BLEOMYCIN: 20 units IV or IM twice a week. in transplantation.
It causes pulmonary fibrosis. • Antilymphocytic globulin.
It is used in squamous cell carcinoma of skin • Steroids.
and other regions and in lymphomas. • Cytosine arabinoside.
CYTOSINE ARABINOSIDE: 4 mg/Kg IV for 2 HORMONE THERAPY
days. Used in leukemias and lymphomas. Ablative procedures—Hormone therapy is
LOMUSTINE (CCNU) and CARMUSTINE often used as adjuvant therapy in certain
(BCNU): It is used in brain tumors and malignancies. Examples are oophorectomy and
lymphomas. adrenalectomy in carcinoma breast and orchi-
dectomy in carcinoma prostate.
PROCARBAZINE: 300 mg 3 times a day. Used
in Hodgkin’s lymphoma and oat cell carcinoma Added hormones in few malignancies like
lung. prednisolone, progestogens, estrogens and
androgens.
CISPLATIN: 30 mg daily. Used in testicular and
ovarian tumors. Hormone Antagonists
• Tamoxifen is used as estrogen receptor
ETOPOSIDE: Dose: 100 mg/sq.m.
antagonist in carcinoma breast.
Uses: Testicular tumor, bladder tumor, lympho-
• Cyproterone acetate competes for binding
mas.
receptors.
HYDROXYUREAS: 80 mg/Kg. • LHRH analogue like goserelin in carcinoma
Uses: Myeloma, leukemias. breast.
..Never explain—your friends do not need it and your enemies will not believe it.
—Elbert Hubbard.
• Phosphorylated diethyl stilbestrol in carci- • Nonavailability.
noma prostate. • Effect is not 100%.
Drugs that Interfere with HYBRIDOMA

Hormone Synthesis
• It is a biotechnological process wherein
• Aminoglutethimide as adrenal inhibitor.
multiplication property of Myeloma cells is
• L-thyroxine 0.3 mg daily as suppressor of
combined with synthetic property of some
TSH in papillary carcinoma of thyroid.
other required cells to achieve rapid and
large quantity manufacturing of required
IMMUNOTHERAPY chemical.
It is enhancing the host response of patient • Myeloma cells with only retained multipli-
whenever required commonly against malignant cation activity is fused with human cells or
cells. Often it is also used in conditions where lymphocytes or other cells (of nature to
there is severe immunosuppression due to any produce the required product) by hybridi-
reason like bone marrow suppression, or in zation. The resulting cell has got the capacity
specific conditions like severe hepatitis. to multiply rapidly and to produce required
Immunotherapy can be: product in large quantity. It is called as
• Active. hybridoma.
• Passive. • It is used to generate monoclonal antibodies,
• Restorative. insulin and many other antibodies, immuno–
• Adoptive. globulins, etc.
MONOCLONAL ANTIBODIES are used for—
Immunotherapy Agents
• Immunodiagnosis—For radioimmunoassay,
• Monoclonal antibodies. radionuclide scan.
• Bone marrow transplantation. • Antibody for detection of tumor antigen
• Cell transfer. • for cancer therapy,
• Lymphokines. • for serotherapy,
• Thymic hormones.
• as conjugates (with drugs, toxins,
• Levamisole and BCG (as immunomodu-
isotopes).
lators).
• For production of other chemicals and as a
• Prostaglandins.
• Interferons, Interleukins. research tool.
• Immunoglobulins.
• Antibody derived specific to certain tumor GENE THERAPY
like melanoma. The ability to alter specific genes of interest is
nowadays, an exciting and powerful tool in the
Tumors where immunotherapy is used
potential management of a wide range of
• Melanoma.
diseases. Instead of giving a patient a drug to
• Bladder tumor.
• Ca colon. treat or control the symptoms of the genetic
• Renal cell carcinoma. disorder, physicians may be capable of treating
• In many tumors it is under trial. the basic problem by altering the genetic makeup
of the patient’s cell.
Disadvantages Typically two methods have been consi-
• Very costly. dered: Germ line and somatic cell gene therapy.
• Germ Cell Therapy involves insertion of a gene • To protect vulnerable cell populations against
into fertilized egg for the correction of a treatments such as chemotherapy.
genetic disease. Because these genes are • To kill tumor cells directly.
dispersed throughout the tissues of the egg, Several single gene disorders are candidates
they end up in the germ cells of the fetus, for gene therapy. Current thinking has expanded
and hence are passed on to the future to include treatment of AIDS and atherosclerosis
generations. using gene therapy techniques.
• Somatic Cell Therapy involves the insertion of Vectors used for gene therapy fall into two
genes or otherwise manipulating the gene main classes—viral and nonviral.
machinery of a cell to treat a disease. In this • Viral:
case the cells are restricted to the population Initially retroviruses were used as vectors.
that has been treated and any genetic change Other potential vectors include adenovirus,
remains restricted to these cells and is not herpes virus and vaccinia virus.
passed to the germ cell line. • Nonviral systems:
The goals of Human somatic therapy are usually • Liposome mediated DNA transfer.
one of the following: • DNA protein conjugates.
• To repair or compensate for a defective gene However exciting and appealing the
• To enhance the immune response directed at prospects of gene therapy may appear, this
a tumor or pathogen. technique is still in the experimental stages.
..I shall pass through this world but once, any good thing I can do, or any kindness that I can
show to any human being, let me do it now and not defer it, for I will not pass this way again.
30 Instruments and
Suture Materials
 Instruments the cavities, to mop the oozing area, to hold gall-

 Suture materials bladder and cervix during surgeries, for blunt
dissections, and as ovum forceps.
INSTRUMENTS
CHEATLE’S FORCEPS (FIG. 30.1)
It is used to pick sterilized articles like
instruments and drapes so that touching of the
instruments can be avoided while transferring
them. It is kept dipped in antiseptic solutions.
It does not have lock.
Fig. 30.2: Sponge holding forceps

Fig. 30.1: Cheatle’s forceps MAYO’S TOWEL CLIP (FIG. 30.3)
SPONGE HOLDING FORCEPS • It is used to fix drapes in operative field.
(RAMPLEY’S) (FIG. 30.2) • It is used to fix suction tubes, diathermy
wires, and laparoscopic cables in operative
It has got fenestrated, serrated, flat distal end. table.
It is used to clean the operative field, to swab • It is used to fix ribs in flail chest.
Instruments and Suture Materials 381
Based on shape—
• Straight artery forceps.
• Curved artery forceps.
Features of artery forceps:
• Distal blades are having transverse serrations
which are well apposed.
• Lock in the proximal part.
Uses
• To catch bleeding points.
• To open the facial planes in different
surgeries.
• To pass a ligature.
• To hold fascia, peritoneum, aponeurosis.
Fig. 30.3: Mayo’s towel clip • To hold sutures.
• To drain an abscess like a sinus forceps.
ARTERY FORCEPS: (HEMOSTAT) • To hold gauze as pea nut.
(FIG. 30.4A TO C)
RIGHT ANGLE FORCEPS (FIG. 30.5)
It is used to dissect pedicles and to pass ligatures.
It is used in depth dissection. It is used in
thyroidectomy, neck dissections, laparotomy
procedures.
Fig. 30.5: Right angle forceps
KOCHER’S FORCEPS (FIG. 30.6)

It has got serrations in the distal blades and
apposing tooth in the tip.
Figs 30.4A to C: Artery forceps (A) Straight (B) Curved

(C) Mosquito
Types
Based on size—
• Small or mosquito artery forceps.
• Medium sized artery forceps.
• Large artery forceps. Fig. 30.6: Kocher’s forceps
..Many receive advice, only the wise profit by it.

It is used to hold pedicles, tough structures, It is used to hold bulky and tough structures,
cut ends of the muscles. to hold lymph nodes. It is also used as towel clip,
It is used to hold gauze for blunt dissection, as sponge holding forceps.
to hold resected bowel, to hold ribs during rib
resection.
ALLIS TISSUE HOLDING FORCEPS (FIG. 30.7)
Here distal blades are not apposing each other.
Tip has got teeth in each blade which are
apposing.
It has got lock.
It is used to hold skin flaps, fascias,
aponeurosis, and bladder wall. Fig. 30.9: Lane’s tissue holding forceps
SINGLE HOOK RETRACTOR (FIG. 30.10)

It is used to retract skin.
Fig. 30.10: Single hook retractor

Fig. 30.7: Allis tissue holding forceps
BABCOCK’S FORCEPS (FIG. 30.8) VOLKMANN’S RETRACTOR (FIG. 30.11)

Its distal part of blades is curved with triangular It is used to retract fascias in soles and palms.
fenestra in it which allows soft tissues to bulge
out. Tip is nontraumatic with transverse
serrations on it. It has got a lock.
It is used to hold any part of the bowel,
fallopian tubes, appendix, ureter, cord, etc.
Fig. 30.8: Babcock’s forceps
LANE’S TISSUE HOLDING FORCEPS (FIG. 30.9)

It has got thick, stout distal blades with oval
fenestra in each blade. It has got apposing tooth
in the tip. It has got lock. Fig. 30.11: Volkmann’s retractor
LANGENBECK’S RETRACTOR (FIG. 30.12) DEAVER’S RETRACTOR (FIG. 30.15)
It has got a long handle and a small solid blade. It • It is used to retract the abdominal wall.
is used in hernia surgery or any superficial • It is a retractor with a broad, gently curved
surgeries to retract skin, fascia and aponeurosis, blade.
etc. • It is used to retract liver, spleen and other
abdominal viscera.
• It is atraumatic and gives adequate exposure
of the surgical field.
Fig. 30.12: Langenbeck’s retractor
CZERNEY’S RETRACTOR (FIG. 30.13) Fig. 30.15: Deaver’s retractor

(HERNIA RETRACTOR)
This retractor has got thick, small blade on one DOYEN’S RETRACTOR (FIG. 30.16)
side and biflanged hook on the other side in It is used in pelvic surgeries.
opposite directions. It is used in surgeries like
hernia, laparotomy especially during closure.
Fig. 30.16: Doyen’s retractor
SELF-RETAINING RETRACTOR (FIG. 30.17)

Fig. 30.13: Czerney’s retractor It has got different adjustable blades so as to
MORRIS’ RETRACTOR (FIG. 30.14) retract abdominal wall and tissues during
surgery.
• It may be single blade type or double blade
type.
• It is used to retract abdominal wall incisions.
Fig. 30.14: Morris’ retractor Fig. 30.17: Self-retaining retractor
..Anger is short madness, so control your passion, or it will control you.

—Horace
DISSECTING FORCEPS (FIGS 30.18A AND B) Round body needles are used in soft
structures like peritoneum, muscle, vessel,
nerves, tendons, bowel, and soft tissues.
Cutting needles are used to suture skin,
aponeurosis and tough structures.
Reverse cutting needle is used to suture
mucoperiosteum.
Figs 30.18A and B: Dissecting forceps (A) Nontoothed

(B) Toothed
PLAIN NONTOOTHED DISSECTING

FORCEPS
It is used to hold delicate structures like
peritoneum, vessels, bowel, nerves, and tendons.
TOOTHED DISSECTING FORCEPS
It is used to hold skin and tough structures.
SURGICAL NEEDLES (FIG. 30.19)
Types
Based on the edge:
• Round body needle.
• Cutting needle.
• Reverse cutting needle.
• Taper cut needle.
Based on curvature:
• Straight needle.
• Curved needle. Half circle; 5/8th circle, etc.
Based on existence of the eye:
• Atraumatic needle is eyeless. Here suture
material is attached to the needle by swaging.
Size of the suture material and that of needle Fig. 30.19: Different types of needles
is same and so tissue trauma is less. Needle
once used is disposed. (Not reusable). NEEDLE HOLDER (FIG. 30.20)
• Traumatic needle is eyed needle. Needle in
the eye area is wider than the body of the Smaller distal blades with criss-cross serrations
needle and so tissue trauma is more. These often with a groove in the middle are the features
needles are reusable. of needle holder.
• It also occludes the vessels in the wall of the
bowel and so prevents bleeding during
surgery.
• It is used during anastomosis of the stomach
and other parts of the bowel.
Fig. 30.20: Needle holder
It may be straight or curved. It may be

available with different sizes. While holding a
needle in a needle holder one should get a good
control and good grip. This is achieved by Fig. 30.22: Moynihan’s occlusion clamp
placing the needle at proximal 2/3rd and distal
1/3rd. Needle holder should be held between PAYR’S CRUSHING CLAMP (GASTRIC)
thumb and ring finger. (FIG. 30.23)
It is stout and heavy instrument with double
JOLL’S THYROID RETRACTOR (FIG. 30.21) lever in the handle.
It is a self-retaining retractor specifically used for It crushes the bowel once applied. So before
thyroid surgeries. applying it, line of resection of stomach/bowel
should be assessed properly. It is applied to the
part which is removed. Viability of the bowel
is lost once it is applied.
It is used in gastrectomy and resection and
anastomosis of the bowel.
Fig. 30.23: Payr’s crushing clamp

Fig. 30.21: Joll’s thyroid retractor
DESJARDIN’S CHOLEDOCHOLITHOTOMY
MOYNIHAN’S OCCLUSION CLAMP (FIG. 30.22) FORCEPS (FIG. 30.24)
• It has got long distal blades with longitudinal It has got long distal blades with smooth
serrations. serrations and fenestra in the tip. It does not have
• It may be straight or curved. lock and so accidental damage of CBD mucosa
• It is nontraumatic, noncrushing type. or crushing of the CBD stone are avoided.
• It occludes lumen of the bowel/ stomach and so It is used for choledocholithotomy (removal
prevents spillage of the content of the bowel. of CBD stones).
..Progress is impossible without change; and those who cannot change their minds cannot
change anything.
—George Bernard Shaw
Fig. 30.24: Desjardin’s choledocholithotomy forceps
BAKE’S DILATOR (FIG. 30.25)

It is long malleable metallic instrument with club
at the terminal end.
It is used to assess the CBD, duodenal papilla
for patency or block.
Fig. 30.27: Tracheostomy tube (A) Fuller’s

(B) Jackson’s tracheostomy tube
Fig. 30.25: Bake’s dilator
SINUS FORCEPS (LISTER’S) (FIG. 30.26) 3. Red-rubber tracheostomy tube.

4. PVC tracheostomy tube.
It has got straight, long blades with serrations
Modern tracheostomy tubes are made of
in the tip. It does not have lock.
plastic. They are soft, least irritant and dispo-
It is used to drain pus from abscess cavity
sable. They have inflatable cuff which makes it
(Hilton’s method). It is called as sinus forceps
easier to give assisted ventilation. Cuff should
because it is initially originated to pack the sinus
be deflated at regular intervals to prevent
cavities. It is less traumatic.
pressure necrosis of trachea (For assisted
ventilation endotracheal tube can be kept for 7
days. Beyond that period patient needs
tracheostomy for further ventilation).
Indications for tracheostomy:
• In head, neck and facial injuries.
• Tetanus.
• Tracheomalacia after thyroidectomy.
• Laryngeal edema/spasm.
Fig. 30.26: Lister’s sinus forceps
• Major head and neck surgeries like
commando’s operation, block dissection, etc.
TRACHEOSTOMY TUBE (FIG. 30.27)
1. Fuller’s bivalved tracheostomy tube: It has DRAINS
got outer tube and inner tube. Outer tube is A drain is a created channel which allows any
biflanged and so insertion is easier. Inner tube fluid collected to come out after closure of the
is longer with an opening on its posterior main wound.
aspect. Inner tube can be removed and re-
inserted easily whenever required. Types
2. Jackson’s tracheostomy tube: It has got outer 1. Corrugated rubber drain (Fig. 30.28A): It
tube, inner tube and an obturator. drains by capillary action and gravity. It is
4. Sump suction drain: Here negative suction
with a parallel air-vent is used to prevent the
adjacent soft tissues being sucked into the
lumen of the drain.
5. Under water seal drain to drain pleural space.
Indications for Drains
• In drainage of an abscess.
• In bleeding surgical conditions like trauma,
peroperative bleed.
Figs 30.28A to C: Drains (A) Corrugated rubber drains
(B) Tube drain (C) Multiple perforated drains
• In hemo, pyo or pneumothorax.
• In acute abdominal conditions like peri-
cheaper and technically easier. But it allows tonitis, hemoperitoneum.
soakage of dressings and causes discomfort • In major abdominal surgeries like of
to the patient. pancreas, biliary tree, stomach, etc.
2. Tube drains (Fig. 30.28B): • In thyroid surgery.
• Malecot catheter can be used as tube • In hydrocele surgery.
drain.
Problems in Drains
• Penrose soft latex rubber tube.
• Multiple perforated tubes(Fig. 30.28C). • Infection through the drain.
3. Closed suction tube drain system. • Displacement.
4. Glove drain. • It may not drain adequately and can give a
5. Wick drain is a gauze drain to drain pus, false information.
discharge, etc. • It may interfere with healing process inside.
Presently keeping a drain itself a questioned debate
Advantages of Tube Drains and controversy all over.
• Quantity of fluid like bile, pus can be mea- Older dictum was ‘when in doubt keep a
sured. drain and the surgeon can sleep happily’—is
• It can be kept for longer time. questioned at present.
• Skin excoriation will not occur. DRAINS IF NOT USED PROPERLY MAY
• Patient will be more comfortable. BE COUNTER-PRODUCTIVE.
• Infection rate is less.
• Removal is easier. FOLEY’S CATHETER (FIG. 30.29)
Dye can be injected and cavity or communi-
cation can be assessed using ‘C-ARM’.
Classification of Drain Systems
1. Open (static) drains: e.g. corrugated drain,
Penrose drain. Infection rate is higher.
2. Closed siphon drains: Here drain is connec-
ted to a sterile bag with or without one-way
valve. It reduces the infection.
3. Closed suction drain: Here negative pressure
of –100 to –500 mm Hg is used to create
vacuum to drain the secretions. Fig. 30.29: Foley’s catheter
..A child is God’s opinion that the world should go on.

—Carl Sandburg
MALECOT’S CATHETER (FIG. 30.30) RYLE’S TUBE (FIG. 30.33)
It is one meter long which is made up of red
rubber or plastic.
It has got three lead shots in the tip which
makes it radiopaque. It also facilitates easy
passage of the tube through the esophagus.
It has got markings at different levels:
1. At 40 cm distance signifies the level of gastro-
esophageal junction.
2. At 50 cm distance signifies the level of body
of the stomach.
3. At 60 cm distance, the level of the pylorus.
Fig. 30.30: Malecot’s catheter 4. At 65 cm distance, the level of the duodenum.
SIMPLE RED RUBBER TUBE (FIG. 30.31)

Indications
Diagnostic:
• For gastric function tests. To assess free acid
and total acid.
• Hollander’s test for completion of vagotomy.
• To diagnose tracheoesophageal fistula.
• Baid test for pseudocyst of the pancreas.
Therapeutic:
• In acute abdominal conditions like peri-
tonitis/intestinal obstruction, etc.
Fig. 30.31: Red rubber catheter
LISTER’S URETHRAL DILATOR (FIG. 30.32)

It has got olive tip and it is used dilate stricture
urethra.
Other dilators are Clutton’s dilator and fili-
form bougies.
Fig. 30.32: Lister’s urethral dilator Fig. 30.33: Ryle’s tube

• In abdominal trauma.
• After abdominal surgeries.
• In pyloric stenosis.
• In upper GIT bleeding conditions.
• In paralytic ileus.
• For feeding purpose in cases like comatose
patients, faciomaxillary injuries, major head
and neck surgeries.
INFANT FEEDING TUBE (FIG. 30.34)

Infant feeding tube is used in newborn babies
and infants and children. Lead shots in the tip Fig. 30.35: Kehr’s ‘T’ Tube
are not present in this tube unlike in nasogastric
tube. Before removal of ‘T’ tube, CBD patency
should be confirmed.
It is done by following methods:
• Clamp the vertical limb (done in 12–14 days)
and observe for development of pain, fever
and jaundice in 24 hours. If normal then one
can presume that there is no obstruction in
the CBD.
• Water-soluble iodine dye is injected through
the tube to visualize biliary tree and free flow
of dye into the duodenum. (Postoperative ‘T’
tube cholangiogram). It is done in 14 days
which is the time required to develop fibrous
track. Once there is free flow, tube is removed
and track gets closed on its own.
Fig. 30.34: Infant feeding tube. Lead shots are not SCISSORS (FIG. 30.36)
present in the tip of infant feeding tube Scissors do not have ratchets. Scissors can be
Mayo’s tissue scissors, straight cutting scissors,
long scissors, fine scissors, stitch removal
KEHR’S ‘T’ TUBE (FIG. 30.35)
scissors. Scissors should not be sterilized in
• It is used after opening of CBD (choledo- autoclave as its sharpness will alter. It is sterilized
chotomy). CBD is closed with ‘T’ tube in the
by immersing it in glutaraldehyde solution.
CBD.
• It is made up of latex or red rubber.
• ‘T’ tube has got horizontal part which is kept GIGGLI’S WIRE/SAW (FIG. 30.37)
in the CBD and vertical part which is allowed Giggli’s wire is used to cut the bone like mandi-
to come out to drain bile. Amount of bile ble. Pubis, ilium, ischium, etc. It has got fine
draining daily is measured out. sharp projections which makes it to cut the bone.
..One thorn of experience is worth a whole wilderness of warning.

— Lowell
Fig. 30.38: Myer’s varicose vein stripper
Fig. 30.39: Volkmann’s scoop
Fig. 30.36: Different types of scissors

SCALPEL WITH BLADES (FIG. 30.40)
Scalpel handle (KNIFE) is used to make incisions.
Different types of handles are available. Different
types of blades are available. No. 11 blade (sharp)
is used for incision and drainage. No. 22 blade
is used for making incision.
Fig. 30.37: Giggli’s wire/saw
MYER’S VEIN STRIPPER (FIG. 30.38)

It is a long metallic stripper used in stripping
varicose veins. It has got a T shaped handle with Fig. 30.40: Scalpel handle (knife) with
blunt tip which is advancing. After passing different sized blades
through the vein tip is detached and specific
required sized round knob is attached to the tip HUDSON BRACE WITH PERFORATOR
with screwing action. Vein is stripped by jerky AND BURR (FIG. 30.41)
movements over the T handle. Hudson’s brace is used to do burr holes in skull
bone. Using brace initially, perforator is used to
VOLKMANN’S SCOOP (FIG. 30.39) reach and open the inner table. Perforator should
Volkmann’s scoop is used to scoop the be carefully used to avoid injury to deeper
granulation tissue, ulcer bed, sinus cavity. It has structures. Later burr is used to widen the hole
got a stiff handle. made by perforator.
of the proctoscope contains illuminating light.
Proctoscope is used to see piles, to do procedures
like banding, cryosurgery or to take biopsy.
SUTURE MATERIALS (FIG. 30.44)

Features of ideal suture material:
1. Adequate tensile strength.
2. Good knot holding property.
3. Should be least reactive.
4. Easy handling property.
Fig. 30.41: Hudson’s brace perforator and burr
5. Should have less memory.
6. Should be easily available and cost effective.
ANEURYSM NEEDLE
Aneurysm needle is stout instrument with a CLASSIFICATION I
deep hook in one end with an eye opening in
ABSORBABLE SUTURE MATERIALS
the tip. This facilitates the passage of the ligatures
across the deeper plane. 1. Plain catgut is derived from submucosa of
jejunum of sheep.
• It is yellowish white in color.
• It is absorbed by inflammatory reaction
and phagocytosis
• Absorption time is 7 days.
• It is used for subcutaneous tissue, muscle,
Fig. 30.42: Aneurysm needle
circumcision in children.
PROCTOSCOPE (FIG. 30.43) 2. Chromic catgut is catgut with chromic acid
salt.
Proctoscope is used to visualize anal canal and • It is brown in color.
only lower part of the rectum. It can be non- • Its absorption time is 21 days.
illuminating wherein torch from outside is used • It is used in suturing muscle, fascia,
during proctoscopy or illuminating wherein tip external oblique aponeurosis, ligating
pedicles, etc.
3. Vicryl (Polyglactic acid):
• It is synthetic absorbable suture material.
• It gets absorbed in 90 days.
• Absorption is by hydrolysis.
• It is violet in color (braided).
• It is multifilament and braided.
• It is very good suture material for bowel
anastomosis, suturing muscles-closure of
peritoneum.
4. Dexon (Polyglycolic acid) is synthetic
absorbable suture material like vicryl. It is
Fig. 30.43: Proctoscope creamy yellow in color (braided).
..Nature never deceives us. It is always we who deceive ourselves.

5. Maxon (Polyglyconate) monofilament. 4. Cotton is twisted multifilament natural
6. PDS (Poly Dioxanone Suture material) is nonabsorbable suture material. It is white in
absorbable suture material. It is cream in color.
color with properties like vicryl. It is costly 5. Linen is derived from bark of cotton tree.
but better suture material than vicryl. 6. Steel, polyester, polyamide (sutupack), nylon are
7. Monocryl (Polyglecaprone) monofilament. other nonabsorbable suture materials.
8. Biosyn (Glycomer) monofilament.
Uses of nonabsorbable suture materials
Uses of absorbable suture materials 1. In herniorrhaphy for repair.
1. In bowel anastomosis like gastrojejuno- 2. For closure of abdomen after laparotomy.
stomy, resection and anastomosis vicryl is 3. For vascular anastomosis (6–zero), nerve
used. suturing, tendon suturing.
2. In cholecystojejunostomy (CCJ), choledo- 4. For tension suturing in the abdomen.
chojejunostomy (CDJ), pancreatico- 5. For suturing the skin.
jejunostomy vicryl is used.
3. In suturing muscle, fascia, peritoneum, CLASSIFICATION II
subcutaneous tissue, mucosa, etc. Natural
4. In ligating pedicles. 1–zero chromic catgut or
vicryl are used, e.g. Ligation of pedicles 1. Catgut.
during hysterectomy. 2. Silk.
5. In circumcision usually 3-zero plain or 3. Cotton.
chromic catgut are used. 4. Linen.
6. In suturing tongue, inner aspect of lip, oral
mucosa, etc. Synthetic
1. Vicryl, dexon, PDS, maxon.
Absorbable suture materials should not be 2. Polypropelene, polyethylene, polyester,
used in suturing tendon, nerves, vessels (vas- polyamide.
cular anastomosis).
CLASSIFICATION III
NONABSORBABLE SUTURE MATERIALS
1. Silk is natural multifilament braided non- 1. Braided: Polyester, polyamide, vicryl, dexon,
absorbable suture material derived from and silk.
cocoon of silkworm larva. It is black in color. 2. Twisted: Cotton, Linen.
It is coated suture material to reduce capillary
action. CLASSIFICATION IV
2. Polypropelene (Prolene) is synthetic mono- 1. Monofilament: Polypropylene, polyethy-
filament suture material. It is blue in color.
lene, PDS, catgut, steel.
It has got high memory. (Memory of suture
2. Multifilament: Polyester, polyamide, vicryl,
material is recoiling tendency after removal
dexon, silk, cotton.
from the packet. Ideally suture material
should have low memory). (Prolene mesh
used for hernioplasty is white in color). CLASSIFICATION V
3. Polyethylene (Ethylene) is synthetic mono- 1. Coated: Polyamide, polypropylene, catgut,
filament nonabsorbable suture material. It is PDS.
black in color. 2. Uncoated: Cotton, polyester.
Numbering of Suture Material: TYPES OF SUTURING (FIG. 30.45)
2— Thick. For pedicle ligation. 1. Continuous suturing.
1— 2. Interrupted simple suturing.
0—zero. 3. Interrupted mattress suturing.
1—zero 4. Subcuticular suturing.
2—zero. For bowel suturing. 5. Horizontal tension suturing (Fig. 30.46).
3—zero. 6. Vertical tension suturing.
4—zero.
5—zero. For vascular anastomosis. TYPES OF KNOTS (FIG. 30.47)
6—zero. 1. Reef knot.
7—zero. 2. Granny knot.
8—zero. 3. Surgeon’s knot.
9—zero. For ophthalmic surgery. Requires
operating microscopy.
Fig. 30.44: Photo showing different types of suture

materials (with pack)
Fig. 30.46: Horizontal tension sutures
Fig. 30.45: Types of suturing Fig. 30.47: Types of knots
..Good, to forgive; Best, to forget.

—Browning
31 Sterilization and
Disinfection
Bearing in mind that it is from the vitality of ASEPSIS

the atmospheric particles that all the mischief Asepsis means—organisms are prevented to
arises, it appears that all that is requisite is to access the patient or individual.
dress the wound with some material capable of
killing these septic germs, provided that any DIFFERENT METHODS OF DISINFECTION
substance can be found reliable for this purpose, Physical Agents
yet not too potent as a caustic.
—Joseph Lister, 1867 Burning or incineration is used to disinfect
contaminated articles like dressings.
Joseph Lister is called as father of modern Hot-air oven: Here temperature used is 160°C
surgery and father of antisepsis. He introduced for one hour or 180°C for 20 minutes. Glassware,
carbolic acid as an antiseptic agent. He presumed scissors, scalpel, forceps and oil, powders are
that infection can be prevented by proper asepsis sterilized by this method.
and antisepsis.
Boiling: It kills bacteria but not spores and
viruses. Temperature is between 90° to 99°C. It
STERILIZATION is used to disinfect syringes, utensils. It is not
It is freeing an article by removing or killing all useful for gloves, rubber materials.
bacteria, spores, fungi and viruses. Autoclave (Fig. 31.1): It is steam under pressure.
Temperature attained is between 120 to 135°C.
DISINFECTION It is sterilized for 20 minutes with 15 pounds /
sq.inch pressure. It kills all organisms including
It is killing of all bacteria, fungi and viruses but
spores. Completeness of sterilization is
not spores.
confirmed by using specific gelatin protein
which precipitates only in steam under pressure
ANTISEPSIS for 20 minutes. Green colored strip turns to black
It is inhibition of growth of microorganisms. if autoclave is complete (signaloc). Surgical
Sterilization and Disinfection 395
gloves, linen, cotton, dressings, surgical Lysol is emulsified cresol with soap. 2 % solution
instruments are sterilized by this method. Sharp is effective.
and plastic instruments cannot be sterilized by Chlorhexidine (hibitane) is useful antiseptic.
this method. Bacillus thermophillus spores are
used to assess the completeness of the Hexachlorophane is not used in infants and
sterilization in mass scale. Double autoclaving children because it can get absorbed through
is done for instruments of orthopedic or intact skin in this age group causing severe
ophthalmic surgeries. neurotoxicity.
Dettol (chloroxylenol) 5% solution is used.
Cetrimide is cationic surfactant Cetavlon 2%
solution is used.
Savlon is combination of cetrimide and hibitane.
It is very commonly used antiseptic in operation
theaters, and wards.
HALOGENS
Bleaching powder.
Sodium hypochlorite.
EUSOL: Edinburg University Solution contains
sodium hypochlorite, boric acid and calcium
hydroxide.
Fig. 31.1: Autoclave machine EUSOL bath is dipping the ulcer bearing part
in dilute EUSOL for 30 minutes 2–3 times a day
Radiation: Ionizing type of radiation: Atomic (Fig. 31.2).
gamma radiation is used as commercial method
to sterilize suture materials, disposable materials
in packets. It is viable, safe and cheaper.
Nonionizing radiation either infra-red radia-
tion or ultraviolet radiation is used to reduce the
bacteria in air and water. Bacteria and virus are
vulnerable to ultraviolet rays below 3000 Å.
Exposure to eyes and skin can cause burn injury.
Chemical Agents
Phenol is used as standard to compare the
efficacy of other agents. It is also called as carbolic
acid. It is bactericidal at 1%. It is obtained by
distillation of coal in 170°C.
Cresol is more powerful and nontoxic. 5% Fig. 31.2: EUSOL bath is dipping the ulcer part in non-irritant
solution is used. It is obtained by distillation of EUSOL in a clean bucket for 20–30 minutes. It removes the
coal in 270°C. slough
..Look well to this day for yesterday is but a dream and tomorrow is but a vision. But today, well
lived, makes every yesterday a dream of happiness and every tomorrow a vision of hope.
—Kalidasa
All theater appliances Autoclave

Sharp instruments (scissors, needles, blades) Glutaraldehyde 2%, Lysol.
plastic materials.
Endoscopes Glutaraldehyde.
Rubber equipments Glutaraldehyde.
Syringes Autoclave, hot-air oven, gamma radiation.
Heart-lung machine Ethylene oxide.
Disposable articles Gamma radiation.
Operation theater and rooms Ideally by U-V radiation or by formaldehyde.
Sera and biological materials Filtration.
Lab glassware Hot-air oven.
Ward, sick room, furniture Formaldehyde, iodophor spray, glutaraldehyde.
Clothes, bed sheets especially for burns patients Autoclaving.
Soiled dressings, materials, animal carcasses Incineration, Lysol, iodophors.
Excreta Lysol, iodophors.
Cleaning of skin before surgery Iodophors 2%, Savlon, spirit.
For cleaning infected wounds Iodophors, acriflavine, Savlon, H2O2.
To remove slough from the wounds EUSOL, H2O2.
Before injection Spirit is used to clean the skin.
Cleaning the ward Phenol, cresol, Lysol.
Hand wash Chloroxylenol, Savlon, spirit, iodophors.
Bladder wash 0.1 % potassium permanganate solution (Condy’s
lotion), solution of acetic acid and silver nitrate.
Water Chlorination, potassium permanganate.
Fruits, vegetables Potassium permanganate.
Physical agents Chemical agents

• Sunlight. • Phenol.
• Drying. • Cresol.
• Dry heat is most reliable and rapid without • Lysol.
any residue. Incineration, flaming using • Hibitane.
Bunsen burner, hot-air oven are the different • Hexachlorophene.
methods. • Dettol.
• Moist heat like pasteurization (63°C for 30 • Savlon.
minutes–Holder method or 72°C for 20 • Halogens like EUSOL, iodophors.
seconds-flash method), boiling, autoclaving. • Alcohols.
• Filtration. • Formaldehyde.
• Radiation-ionizing or nonionizing. • Glutaraldehyde.
• Hydrogen peroxide.
• Gases like ethylene oxide.
• Dyes like acriflavine.
Sterilization and Disinfection 397
Iodine. Glutaraldehyde (cidex 2%) is used to sterilize
Iodophors: These are antiseptics and also sharp instruments. Instrument should be dipped
sporicidals. They are nonirritant and do not stain for 10 hours to achieve complete sterilization. It
skin. Povidone-iodine is a good example which is potent bactericide, sporicide, fungicide and
is commonly used. viricide. Scissors, needles, scopes like cystoscope,
bronchoscope, endoscopes, endotracheal tubes
Alcohols: Ethyl or isopropyl alcohols are used.
It is not effective against spores/viruses. It is are sterilized using this agent.
effective against bacteria and Mycobacterium Hydrogen peroxide (H2O2) is used as topical
tuberculosis. Isopropyl is better than ethyl alcohol.
oxygen therapy. Because of its effervescence and
Formaldehyde: It is useful to disinfect the rooms release of nascent oxygen it removes the tissue
like operation theater. It is effective at a high debris. It is used to clean wounds, cavities, ulcers,
temperature and humidity of 80–90%. It is as mouthwash and as eardrops to clear ear wax.
commonly used to fumigate the room. 500 ml
of formalin with one liter of water is boiled to Acriflavine and proflavine are orange-red
get formaldehyde vapor. Formaldehyde vapor colored dyes used as antiseptics. It is effective
can be created by adding potassium permanga- against gram-positive and few gram-negative
nate to the same solution. Room is kept closed organisms. It retains its activity in pus and body
for 12 hours. fluids.
..If we are to grow good corn, we must help our neighbours grow good corn.
—Steve Goodier
32 Cautery, Laser,
Cryosurgery and
Day Care Surgery
 Diathermy (Electrocautery)
 Laser in surgery
 Cryosurgery
 Day care surgery
DIATHERMY (ELECTROCAUTERY)
It is the method to control bleeding or to cut the
tissues during surgery.
TYPES
Based on type of current.
1. Unipolar cautery.
2. Bipolar cautery. It is safer because its effect
is seen only in between electrode points.
Adjacent tissues will never get damaged.
Based on type of action:
1. Coagulation cautery which causes hemo-
stasis by tissue coagulation. Here tempera-
Fig. 32.1: Diathermy machine with plate, foot switch for use
ture is 100°C.
2. Cutting cautery: Here temperature is 1000°C
which disintegrate the tissues. It is not Uses
hemostatic. • For coagulation of bleeders during surgery
3. Blended current is combination of both to achieve hemostasis.
coagulation and cutting. • To cut muscles, fascia, etc.
Cautery, Laser, Cryosurgery and Day Care Surgery 399
• It is essential for laparoscopic surgical • In ENT to treat vocal cord lesions, laryngeal
procedures. Bipolar is commonly used. lesions.
• It is used to remove small cutaneous lesions, • In ophthalmology it is very useful in retinal
to control bleeding duodenal ulcer. surgery like for detachment—
• Iridotomy.
Disadvantages • Dacrocystitis.
• Infection. • Capsulotomy.
• Cauterization of normal tissues. • To liquefy human lens.
• Explosive problems. • In glaucomas, etc.
• Diathermy burn to the patient where dia- In General surgery: In bleeding duodenal ulcer
thermy plate is kept. • For palliative decoring of tumors in
• Burn injury or electrical shock to surgeon and carcinoma esophagus.
assisting personnel. • In carcinoma rectum,
• In hemorrhoidal treatment (1st and 2nd
Precautions degree),
• Proper earthing. • In bladder tumor resection.
• Avoid loose contact of electrodes. • In cervical cancer.
• It should be kept off when not in use during • To achieve bloodless field.
procedure. • Often in making incisions in abdomen and
other places.
LASERS IN SURGERY
Advantages of laser
(Light Amplification Stimulated Emission of • Blood less field.
Radiation). • Faster.
Molecules are placed in a compact area and • Small lesions can be removed easily and
power is passed through this so as to activate completely.
the molecules. Molecules get activated at
different periods and move in different Precautions
directions, which they hit to each other releasing
All reflecting instruments should be avoided
energy. This energy is allowed to act through
otherwise laser will reflect and can injure normal
optical system to the area wherever required.
tissues or the working team in the OT itself.
Depending on the molecules used it is named. All should wear protective spectacles to
• Argon Laser. protect their eyes.
• Yttrium-Aluminium Garnet Laser (YAG
Laser). Disadvantage
• CO2 Laser. Availability and cost factors.
• Neon Laser.
• Holmium Laser. CRYOSURGERY
• Erbium Laser. It is the destruction of tissues by controlled
cooling.
Uses of Laser System contains an automatic defrosting
• In cranial surgery in children. device with a cryoprobe (Fig. 32.2).
..Your life is not a coincidence but it’s a reflection of you.

Procedures done in day care surgery

• Excision of cysts, lipomas, bursae,
neurofibromas.
• Lymph node biopsy, hemorrhoid surgery,
endoscopies, circumcision, hydrocele.
• Wound suturing, toe amputation.
Disadvantages
• Infection.
• Discharge from the site.
DAY CARE SURGERY

Fig. 32.2: Cryosurgery instrument kept
ready for procedure
Day care surgery is an upcoming field in surgical
practice. It is an unique method wherein general
practitioner, nurse at day care ward and theater,
Gases used are surgeon, anesthetist work in hand so that
1. Nitrous oxide – 98°C temperature. hospital stay and the cost is reduced. Patient
2. CO2 – 60°C. comes to hospital in morning for surgery and
3. Liquid N2 – 180°C. leaves the hospital on same day evening.
4. Freon – 190°C.
• Commonly used is nitrous oxide as it is easily Advantages
available, cheaper and achieves optimum
• Minimal hospital stay.
temperature required for different proce-
• Becomes cheaper.
dures.
• Patient’s acceptance.
Mode of Action
Precautions
1. It produces intracellular crystallization,
• Patient should be assessed properly before
dehydration and denaturation of proteins
sending to day care surgery.
and cell death.
• The nurse should give proper instruction to
2. It causes the obliteration of microcirculation
the patient as patient stays in the hospital for
and so cell death.
a short period.
• Patient should be warned about possible
Indications
problems like bleeding, vomiting, pain,
• To remove warts and lesions in the skin. discomfort, and sedation.
• Cryotherapy for piles. • Before discharging, patient should be seen by
• For chronic cervicitis. the doctor for the fitness.
• All records should be carefully documented.
Advantages • Patient should be advised to rush to hospital
• Relatively bloodless and painless. if any problems arise or to communicate
• Adequate control of extent and depth in immediately.
freezing. Nurses hold an important role in day care
• Equally effective. surgery.
Advanced Imaging Methods 401
33 Advanced Imaging
Methods
 Ultrasound 3. M-mode: Images are recorded as dots. It is

 Doppler mainly used in moving parts like Echocardio-
 CT scan graphy. M-mode is also called as TM Mode
 Magnetic Resonance Imaging (MRI) i.e. Time Motion Mode.
Uses
ULTRASOUND 1. All abdominal and pelvic conditions, often
in thoracic conditions.
Ultrasound contains waves with a frequency of 2. Ultrasound of thyroid is very useful method
more than 20,000 cycles/second which the to differentiate between solid and cystic
human ears cannot hear. lesions (Fig. 33.1).
In medical sonography frequencies used are 3. Ultrasound is used in testicular tumors,
commonly 2–10 MHz. The transducer or the epididymoorchitis, trauma to testis, erectile
probe works as both transmitter of sound waves dysfunction, etc.
and receiver of echoes. The piezoelectric crystal 4. Ultrasound breast to differentiate solid from
is the producer of ultrasound waves. Received cystic tumors.
signals from the patient are fed into the computer
which forms the image. Advantages
There are three types of ultrasound image 1. No radiation.
display. 2. Non invasive.
1. A-mode: Only one dimensional static display 3. Effective with efficiency.
as spikes obtained. It is used only in eye scan. 4. Painless.
2. B-mode: Two dimensional real time images 5. Low cost.
in the form of grains. It is most widely used 6. Availability even as portable machines.
type. Using this mode Transverse, Longitudinal 7. Stones are well-visualized with acoustic
or Oblique sections can be taken. shadow.
..Start by doing what’s necessary, then do what’s possible and

suddenly you are doing the impossible.
—Saint Francis of Assiss
Fig. 33.1: US thyroid showing thyroid both lobes Fig. 33.2: Cranial sonography is done to see intracranial
problems through suture lines—usually done in infants and
children
5. Soft tissue and musculoskeletal system
ultrasound.
6. Ocular ultrasound is ideal method to image
eye and intraocular structures. So it measures blood flow. Spectral Doppler
wave form and ultrasound image are combined
Disadvantages in Duplex scanning.
• Interpretation can be inadequate.
• Bowel shadow may prevent proper visualization. Types
• In obese patient image will be inadequate. 1. Continuous waves.
• Interpretation is based on echogenicity 2. Pulsed waves.
either hyperechogenic or hypoechogenic. Doppler will provide both audio and video
signals.
Advanced Ultrasound Techniques (Fig. 33.2) Color Doppler imaging displays flowing
blood as red when direction of flow is towards
1. Endosonography (EUS) used in visualization the transducer. Image will be blue if flow is away
of walls of esophagus or stomach through from transducer.
gastroscopy.
2. Transvaginal ultrasound. Uses
3. Transrectal ultrasound to see prostate.
4. Doppler ultrasound to study arterial and 1. To study cardiovascular system.
venous diseases. 2. To study vascularity of tumors.
3. To study blood flow and velocity in arterial
Ultrasound as Therapeutic Use diseases so as to assess stenosis(its extent,
1. To guide aspiration of amebic liver abscess, cause, etc.) like in Atherosclerosis, TAO,
pericardial tap. Cervical rib, Aneurysm, A-V fistulas.
2. On table ultrasound to assess the operability 4. To find out Deep Venous Thrombosis (DVT),
of tumor. (During laparoscopy to assess the Varicose veins, perforator incompetence.
extent of tumor, lymph node status, etc.). 5. To study grade of Varicocele in males.
Advantages
DOPPLER 1. It has replaced Venogram and Angiogram in
Doppler Effect is a change in the perceived many places as a diagnostic tool.
frequency of sound emitted by a moving source. 2. It is reliable and noninvasive.
CT SCAN • Neoplasms: To see the exact location, size,
vascularity, extent and operability (Fig. 33.3).
Computerized tomography scan was invented by
For example: Brain, abdominal, retroperi-
GODFREY HOUNSFIELD in 1963. He was a
toneal, thoracic and spinal tumors (Fig. 33.4).
Physicist. He received Nobel Prize (1972) for the
• Inflammatory conditions in various places
same. The first CAT scan is in the London museum.
also, e.g. Psoas abscess, pseudocyst of
Narrow X-ray beams are passed from
pancreas (Fig. 33.5).
rotating X-ray generator through the gantry
where patient is placed. When X-rays pass
through the tissues, some of the X-rays get
absorbed and some pass through, depending on
the tissue density. The different grades of
absorption in different tissues are detected
through sensitive detectors which are translated
to a Gray scale image by a computer.
Density of tissues is numbered as Hounsfield

Number (HN)
• Water—Zero HN.
• Air— –1000.
• Bone— +1000. Fig. 33.3: CT scan picture showing liver secondaries
Other tissues come in between air and bone
with different HNs.
Presently spiral CT scan has become

popular. They are faster and in a single breath-
holding time, whole CT scan can be taken.
Both Plain and Contrast CTs are done
whenever required.
Contrast Agents
• Ionic—Water-soluble iodide dyes like
Sodium diatrizoate, Meglumine iothalamate
(Conray, Urograffin, Angiograffin). They are
cheaper but often toxic and cause
anaphylaxis.
• Nonionic are safer but expensive, like Fig. 33.4: CT picture showing astrocytoma
IOHEXOL (Omnipaque), Iopamiro.
In abdominal CT, Contrast agents can be Advantages of CT scan
given orally to delineate bowel properly. • One to two mm sized sections are possible.
• Amount of X-ray exposure is less.
Indications • More accurate, sensitive, and specific.
• Trauma like Head injury, Chest injury, • Small lesions are also detected.
Abdomen trauma. In trauma only plain CT • CT guided biopsies are done at present
Scan is taken. safely.
..The worth of your lives comes neither in what we do nor whom we know but by whom we are.
MAGNETIC RESONANCE IMAGING (MRI)

Earlier named as nuclear magnetic imaging (NMR),
the term is not used now.
Principle
When patient is placed in an external high
magnetic field, protons of hydrogen atoms rotate
in phase with each other and gradually return
to their original position releasing small amounts
of energy which is detected by sensitive coils.
Proton density and relaxation time are assessed
by radiofrequency pulse and the computer
Fig. 33.5: CT scan showing ascites (gross) generates a Gray scale image from this data.
T1 relaxation time is the time taken to return
Disadvantages to original axis. T1 images are used to find out
• Interpretation by an experienced radiologist normal anatomical detail. It has got high soft
is important. tissue discrimination. Here fluid (CSF) looks
• Artefacts can be present. black.
• Cost factor and availability.
T2 relaxation time is the time taken by the proton
Findings to diphase. It is used to assess pathological
• Extradural hematoma—Biconvex lesion. processes. In T2 images fluid looks white.
• Subdural hematoma—Concavo-Convex
In Proton density images fluid looks in between
lesion.
black and white.
• Smooth margin in benign condition.
• Irregular margin in malignant condition. It can be Plain MRI or Contrast MRI. Contrast
agent is Gadolinium given intravenously.
Advantages of spiral CT scan
• Reduced scan time. Useful in children and
Uses of MRI (Figs 33.6 and 33.7)
critically ill patients.
• Imaging in both arterial and venous phases • It is very useful in intracranial, spinal and
is possible. musculoskeletal lesions including joint
• Improved lesion detection. Missing a lesion pathologies.
is uncommon. • It gives direct anatomical sections of the area
• Multiplanar and 3-Dimensional analysis like
with lesions at a high resolution.
CT angiography, Complex joint imaging,
• MR angiogram is done without injecting IV
Facial bone imaging is possible.
contrast agents.
High Resolution CT (HRCT) is a CT technique • Cardiac MRI is very useful.
used in chest scan where thin sections are taken • Breast MRI is used in multifocal recurrent
to have better quality images. cancers.
Fig. 33.6: MRI showing AV malformation Fig. 33.7: MRI picture, which shows extradural
schwannoma
• Magnetic resonance cholangiopancrea-

tography (MRCP) is a very useful non- Precaution
contrast diagnostic tool which may replace Before entering the MRI room, the patient and
other personnel should remove all magne-
diagnostic ERCP.
tically attractive materials.
• MR spectroscopy is chemical analysis of
elements in a tissue to differentiate between
tumor, inflammation, and degeneration. Disadvantage
Advantages • Availability and cost factor.
• Artefacts are not common. • It is time consuming.
• More sensitive and specific than CT scan. • Patient compliance is poor.
• In is not feasible in patients suffering from
Contraindications Claustrophobia.
Patients with Prosthesis in the body, metallic • It is not ideal in emergencies and critically
foreign bodies, pacemakers, Cochlear ill patients.
implants, cranial aneurysm clips should never • It is not useful in lung pathology and
undergo MRI. subarachnoid hemorrhage.
..Count your blessing not your problems.

34 Anesthesia
 Preoperative assessment Respiratory system: To look for asthma,

 General anesthesia tuberculosis, emphysema, COPD.
 Muscle relaxants Airway: Mouth opening, Malampatti scoring,
 Reversal agents tyromental distance, temporomandibular joint
 Instruments in anesthesia assessment.
 Complications in general anesthesia
 Postoperative care Cardiovascular system: Hypertension, ischemic
 Regional anesthesia heart disease, arrhythmias, cardiac failure,
 Spinal anesthesia valvular diseases.
 Epidural anesthesia Spine: Curvature, intervertebral space, skin over
 Caudal anesthesia the area for any infection.
Other systems: Abdomen, skeletal system.
PREOPERATIVE ASSESSMENT
History Preoperative Investigations
1. Chronic cough, smoking, alcohol, drug Hematocrit, blood sugar, blood urea, serum
intake, drug allergy. creatinine, electrolytes, chest-X ray, ECG, blood
2. Any previous diseases like hypertension, grouping, blood-gas analysis, cardiac assessment.
diabetes mellitus, epilepsy, bronchial asthma
tuberculosis, hepatitis, cardiac diseases. Preoperative Treatment
3. Drug therapy: Steroids, antihypertensives, • Control of respiratory and cardiac diseases.
sedatives, antibiotics, antiepileptics. • Improvement of Hb% status, if anemia is
present.
Examination • Preoperative antibiotics is given.
General: Posture, teeth, mouth opening, dilated • Blood should be kept ready for major cases.
veins, neck movements, tremor, airway. • Starvation for 4 hours for liquids and six hours
Anemia, edema, jaundice, cyanosis. for solids.
Anesthesia 407
• Bladder and bowel should be emptied to INTRAVENOUS ANESTHETICS
prevent soiling on the operation table. Thiopentone: It is ultrashort acting barbiturate
Urinary catheter may be passed and enema which causes hypnosis during induction of
may be given. anesthesia. It does not have analgesic effect. It
• Dentures, contact lenses, jewellery must be causes hypotension, respiratory depression,
removed. laryngeal and bronchospasm. Recovery is rapid.
• Surgical area should be cleaned and properly Extravasation of drug can cause skin ulceration.
prepared. Intraarterial injection causes vasospasm and
gangrene. Dose: 4–7 mg/Kg.
Premedication Methohexitone sodium.
It is given one hour before surgery:
• For sedation and relief of anxiety. Pethidine 50 Propanidid. 4–7 mg/Kg. It can cause anaphy-
mg/Morphine 10 mg/Diazepam 10 mg. laxis.
Midazolam 1-2.5 mg. Ketamine: 2 mg/Kg IV. It is a good analgesic. It
• To suppress vagal activity. Atropine 0.6 mg. IM. causes dissociative anesthesia. It can lead to
• To reduce vomiting. Promethazine (Phener- hypertension, apnea, laryngospasm. In children
gan) 12.5 mg. it can be given IM—5 mg/Kg. It does not require
intubation for small procedures.
GENERAL ANESTHESIA Propofol: It is widely used induction agent which
has got predictable onset and recovery. It has
It means abolition of all sensations, i.e. touch,
got least side effects on CVS and respiratory
pain, posture and temperature with a state of
system. It is also used for total IV anesthesia.
reversible loss of consciousness.
Dose: 1-2.5 mg/Kg.
It has got three components:
Fentanyl is neuroleptanalgesic. It causes
1) Analgesia, 2) Hypnosis and 3) Muscle
sedation, catatonia, dissociation, hypotension
relaxation.
and preferred in asthmatics.
VOLATILE ANESTHETICS: They vaporize in OXYGEN
room in air. • Oxygen is given through Boyle’s apparatus
Agents used are: Ether, Trichloroethylene, (33.3%).
Halothane, Enflurane, Isoflurane, Sevoflurane. • Oxygen in high concentration is respiratory
Ether which is irritant, unpleasant, flam- depressant and also affects eyes.
mable, is commonly used agent in developing • A 5% CO2 mixture in oxygen is called as
countries. carbogen.
Enflurane and isoflurane are noninflam- • Oxygen is available in black and white
mable, nonexplosive, nonirritant, stable. Here colored cylinder.
anesthesia is rapid with faster recovery.
GASEOUS ANESTHETICS MUSCLE RELAXANTS
Nitrous oxide: It is noninflammable, nonirritant, Depolarizing muscle relaxants
good analgesics but weak anesthetic agent. It is They act on the acetylcholine receptors which
given along with 30–50% oxygen for balanced widens the refractory period after depolarization
anesthesia (blue colored cylinder in India). causing paralysis. It is short-acting muscle
Cyclopropane is highly flammable. relaxant.
..No good deed goes unpunished!

—CB Luce
a. Suxamethonium chloride (scoline):
It lasts for 2–4 minutes.
It causes muscle twitching—fasciculations —
paralysis.
It is metabolized by plasma pseudocholi-
nesterase. Atypical or deficiency of this
enzyme prolongs the action of the scoline.
Side effects are hyperkalemia, myotonia,
apnea and cardiac arrest.
b. Suxthonium bromide.
Nondepolarizing Muscle Relaxants
They block the channels of entry of acetyl
choline. They are long-acting relaxants.
1. Tubocurarine: It lasts for 45 minutes. 30 mg
is the dose.
2. Gallamine (Flaxedil): Dose is 1-2 mg/Kg. It is
cheaper. It is contraindicated in renal
diseases.
3. Pancuronium bromide (Pavulon): It is synthetic
steroid muscle relaxant. It lasts for 45
minutes. Dose is 0.08–0.1 mg/Kg.
4. Vecuronium bromide: It is a steroid muscle Fig. 34.1: Boyle’s apparatus
relaxant, given at a dose of 0.05–0.1 mg/Kg.
5. Rocuronium is short-acting steroid muscle
d. Rotameter—to know the flow of gas.
relaxant. It starts its action in one minute.
e. Vaporizer.
6. Atracurium: It lasts for 20–30 minutes. Dose
is 0.6 mg/Kg. b. Endotracheal tube: These are tubes inserted
7. Mivacurium: Dose is 0.15–0.25 mg/Kg. into the trachea and is used to conduct gases
and vapors to and from the lungs. Depending
REVERSAL AGENTS on the diameter, it is available in various
They are anticholinesterase drugs which increase sizes. It has a cuff at one end which when
the acetylcholine and thus act as antagonizing inflated stabilizes the tube in position and
agents for nondepolarizing muscle relaxants. also prevents aspiration. Noncuffed tubes are
They cause bradycardia. also available. The other end near the mouth
Neostigmine (2.5 mg) is used commonly is connected to the breathing circuit through
along with atropine (1.2 mg). which anesthetic gases are delivered. The
Endrophonium (short-acting) and pyridosti- tube is inserted using a direct laryngoscope.
gmine (long-acting) are other drugs. The proper placement in the airway is
INSTRUMENTS IN ANESTHESIA confirmed by auscultating for the breath
sounds over the chest when the gases are
a. Boyle’s apparatus (Fig. 34.1)
It consists of: delivered.
a. Cylinders for N2O and O2.
Complication
b. Pressure guage—to know the amount of
1. Postoperative sore throat.
gas remaining.
2. Hoarseness after intubation.
c. Pressure regulator—to regulate the
3. Upper airway edema.
pressure of gas used.
Anesthesia 409
c. Magill’s forceps (Fig. 34.2). • Hypertension.
d. Mouth gag. • Laryngeal and bronchial spasm.
e. Laryngoscope. • Cardiac arrhythmias.
f. Connectors. • Respiratory failure.
g. Laryngeal mask airway (LMA). • ARDS.
• Mendelson’s syndrome: It is due to regurgi-
tation of the acid from the stomach causing
aspiration of acid leading into bronchospasm,
pulmonary edema and circulatory failure.
This is treated with oxygen, suction, hydro-
cortisone, aminophylline, antibiotics, Ryle’s
tube aspiration and ventilator support.
• Hypoxia.
• Pneumothorax.
Fig. 34.2: Magill’s forceps
• Anaphylaxis.
• Malignant hyperthermia: It is an inherited
Components of general anesthesia myopathic disorder occurs under anesthesia
• Premedication. due to drugs like halothane, scoline. There
• Induction. is marked increase in metabolic rate with rise
• Maintenance. of temperature. There is high levels of CPK
• Recovery. enzyme. Condition will cause metabolic
Premedication is given one hour before acidosis and hyperkalemia. It has got high
surgery with Pethidine 50 mg/Diazepam 10 mg, mortality. Treatment is IV Dantrolene,
Atropine 0.6 mg IM and Promethazine cooling, oxygen and cold IV fluids.
(phenergan) 12.5 mg. • Hypothermia.
Induction: Patient is preoxygenated with 100%
oxygen for 3 minutes then induced with IV POSTOPERATIVE CARE
Thiopentone given 4–5 mg/Kg. Patient loses Immediate postoperative period is important
consciousness. Induction is maintained by 67% and critical because patient may not be fully
nitrous oxide and 33% oxygen. conscious. Patient should be kept in recovery
Scoline is given IV to relax muscles so as to room until he/she recovers from anesthesia.
facilitate endotracheal intubation. 1. Care of respiratory system: Adequate breat-
Once intubated ventilation can be either hing is important otherwise hypoxia sets in
controlled using muscle relaxants or spontaneous which gradually lead to cardiac arrest.
using a volatile anesthetic agent. Respiratory problems may be:
Reversal is done using Neostigmine and
• Laryngeal spasm.
Atropine or Glycopyrrolate.
• Falling of tongue backwards blocking the
airway.
COMPLICATIONS IN GENERAL • Aspiration.
ANESTHESIA • Bronchospasm.
• Intraarterial injection of the drug. • ARDS.
• Myocardial depression and cardiac arrest. • Respiratory failure.
..Our friends show us what we can do. Our enemies teach us what we must do.
— Goethe.
Oxygen supplement through mask, obser- REGIONAL ANESTHESIA
vation, proper positioning are the treatment.
Carl Koller, an ophthalmologist introduced
2. Hypercarbia.
cocaine as local anesthetic in ophthalmic practice.
3. Circulatory problems:
• Hypotension. Mode of action: It causes temporary conduction
• Arrhythmias. block of the nerve, thus preventing the
• Hypertension. propagation of nerve impulse.
• Cardiac arrest.
4. GIT: Advantages of local anesthetic agent:
• Vomiting. • Technically simpler.
• Regurgitation. • General anesthesia is avoided.
• Mendelson’s syndrome. • Consciousness is retained.
5. Renal problems: • Patient can have food earlier after surgery.
Oliguria, i.e urine output is less than 30 ml/
Drugs used:
hour. It may be due hypovolemia, hypotension,
Cocaine, Procaine, Cinchocaine—amino esters.
acidosis, sepsis, transfusion reaction, toxins.
Lignocaine, Prilocaine, Bupivacaine, Ropiva-
The ratio of urine/plasma osmolality of 2: 1
caine amino amides.
signifies prerenal failure. Ratio of 1.7: 1 indicates
renal failure. Lignocaine/Lidocaine/Xylocaine: It is the
Blood urea and serum creatinine is done at commonest local anesthetic agent used. It is
regular intervals. available as 0.25–5% concentrations.
Fluid and electrolyte imbalance if any is It is metabolized in the liver and excreted in
corrected. the kidney as xylidines. It is also an antiarrhy-
100 ml 20% mannitol or frusemide 40–80 mg thmic drug and so commonly used in cardiology
are often required. and cardiac surgery.
Other problems:
Side effects: Giddiness, headache, postural
Restlessness, shivering, pain.
hypotension, tinnitus, circumoral anesthesia.
MONITORING THE POSTOPERATIVE Dose: 4 mg/Kg. Effect lasts for 90 minutes.
PATIENT
Uses:
• Pulse, temperature BP chart. Topical—4%.
• Breathing type.
Infiltration block—0.25%.
• Level of consciousness.
Field block—0.5%.
• Urine output.
Nerve block—1.0%.
• Oxygen saturation and heart rate using pulse
Epidural—1.5–2.0%.
oximeter.
• Checking and encouraging limb movements. Spinal—5%.
• Skin color, tongue color for adequacy of It can be used with or without Adrenaline.
oxygenation. Xylocaine with Adrenaline has got longer
• Tongue for hydration. duration of action. It creates relatively bloodless
• Cardiac monitor. field.
• Blood gas analysis in case of patient on But it should not be used in places where end
ventilator. arteries are present like glans penis, ear lobule,
• Serum electrolyte assessment. tip of the nose, lip, fingers and toes.
Anesthesia 411
Bupivacaine (Marcaine): It has got prolonged Complications are pneumothorax and injury to
action. It is a vasodilator also. the great vessels.
Dose: 3 mg/Kg. Other blocks:
Epidural block: 0.5% Cervical plexus block.
Spinal 0.5% 3 ml. Sciatic nerve block.
Femoral nerve block.
TOPICAL ANESTHESIA
It is used for minor surgeries of eye, INTRAVENOUS REGIONAL ANESTHESIA
laryngoscopy, bronchoscopy, cystoscopy, (BIER’S BLOCK)
gastroscopy, submucus injection. Limb is exsanguinated and occluded with
It is available as instillation, spray, viscous, tourniquet. Pressure in the tourniquet must be
ointment, gel, EMLA (Eutectic mixture of local 30 mm Hg more than the systolic pressure of the
anaesthetic). patient. Needle is placed in the selected vein. 40
ml of 0.5% xylocaine for upper limb and 80 ml
INFILTRATION BLOCK of 0.25% of xylocaine for lower limb is injected
Direct injection of local anaesthetic under the into the vein. Xylocaine with Adrenaline should not
skin for small procedures. be used. It gives very good analgesia for 2 hours.
Side effects: Sudden release of drug into the
FIELD BLOCK circulation can cause hypotension, convulsions
It is achieved by blocking the entire field of and often death.
excision where lesion is located. Bupivacaine should not be used.
Indications:
NERVE BLOCK
For upper and lower limb surgeries it can be used
• Block of inferior dental nerve and lingual without G/A or S/A.
nerves in the region of the mental foramen
for extraction of teeth.
• Finger block of digital nerves. Here plain
SPINAL ANESTHESIA
xylocaine is used. (without adrenaline). It is the injection of local anesthetic into the
• Intercostal block. subarachnoid space causing loss of sympathetic
• Ankle block. tone, sensation and motor function. The
• Median and ulnar nerve block. sympathetic block is 3 segments higher than
• Brachial plexus block:(Winnie’s block) sensory block, motor block is 3 segments lower
It can be given through than sensory block.
- Interscalene, Position: Lateral decubitus position with head,
- Axillary, hips and knees being fully flexed so as to open
- Supraclavicular approaches. the interlaminar spaces. Highest point of iliac
Supraclavicular approach is commonly used. crest corresponds to 4th lumbar vertebra.
1 cm above the mid-point of the clavicle, needle
is passed downwards, backwards and medially Drugs used:
towards first rib. Once needle hits the first rib, Lignocaine 5% in 6% dextrose 2 ml.
15-20 ml of 1.5% xylocaine is injected (with Bupivacaine 0.5% in 5% dextrose 3 ml.
walking or stepping over the first rib). Cinchocaine 0.5% in 6% dextrose 2 ml.
..Hope puts a smile on our face when the heart cannot manage.
Technique • It is spinal anesthesia using Xylocaine or
24-26 gauge needle with stilette is used. Needle bupivacaine given in sitting position.
is passed through the interspinous space and
ligamentum flavum to reach the subarachnoid EPIDURAL ANESTHESIA
space to get clear fluid(0.5 ml/sec). Needle is It is a potential space between dura anteriorly
rotated 360° and drug is injected slowly. Patient
and ligamentum flavum posteriorly which has
is repositioned to supine. Drug takes 15 minutes
got negative pressure inside. It extends from
to act.
foramen magnum to sacral hiatus.
Touhy needle is used for epidural anesthesia.
Types
Once the needle is in the space there will be
1. Caudal (upto L5). sudden indrawing of air or saline drop. An
2. Low spinal (upto L1). epidural catheter is placed in the space and fixed.
3. Midspinal (upto T10). 2% xylocaine with Adrenaline or 0.5% Bupi-
4. High spinal (upto T6). vacaine is injected into the space to achieve
5. Unilateral spinal. anesthesia upto the desired level.
Advantages
Advantages
• Economical.
• It can be used for continuous repeated
• Hypotension reduces the bleeding.
prolonged anesthesia.
• Adequate relaxation is achieved.
• It can be used for postoperative analgesia.
• Respiratory complications are less.
• It can be kept for several days.
Disadvantages and Complications
• CSF leak and aseptic inflammation of
CAUDAL ANESTHESIA
meninges causing headache. Caudal space is the sacral component of epidural
• Meningism. space and access is through the sacral hiatus.
• Infection.
• Paraplegia. It is very rare. Indications
• Occasionally it can become total spinal which • Hemorrhoidal surgery.
requires intubation and ventilator support. • Circumcision.
• Small procedures in the perineum like
Contraindications cystoscopy.
• Allergy.
• Increased intracranial pressure. It may Procedure
precipitate coning. It is given in lateral position. Needle is inserted
• Sepsis. through the sacral hiatus to enter the caudal
• Spinal tumors. epidural space. Drug is then injected into the
• Back pain and spinal diseases. space.
• Neurological conditions like syringomyelia.
Complications
SADDLE BLOCK • Trauma to anal canal.
• It is used for surgeries in perineal and • Intravascular injection.
anorectal region. • Failure of caudal block.
Miscellaneous 413
35 Miscellaneous
A. History of Surgery
The word ‘surgery’ is derived from French term Louis Pasteur (1895) brought the germ theory of
‘CHIRURGIEN’ a Latin word which in turn was diseases and infectious diseases; and operation
derived from Greek words—CHEIR means hand theater infections later came into picture widely.
and ERGON means work. Surgery has got a long
history to begin with. Rudolph Matas was a pioneer in vascular
surgery.
Edwin Smith Papyrus is one of the oldest scripts
about surgery written in 1600 BC. William S Halsted (1922) an American surgeon
contributed to surgeries of thyroid, breast, hernia
Susruta of ancient India described more than 100 and blood vessels. He introduced usage of
surgical instruments and is best known for rubber gloves during surgery.
plastic surgery of nose and ear.
Bernard von Langenbeck a German surgeon is
Hippocrates has written books on fractures, considered as father of modern residency system in
dislocations and surgical disorders. surgery (1887).
Celsus described inflammation and wrote ‘De Thodor Billroth, a pioneer in abdominal surgery
medicina’. brought different types of gastrectomies into
Ambroise Pare was French Surgeon popular in practice.
sixteenth century. Theodor Kocher did extensive work in thyroid
John Hunter was superb anatomist and teacher surgery and got Nobel Prize in 1909 for the same.
and is called as father of experimental surgery. He John H Gibbon (1973) cardiothoracic surgeon
described many surgeries for many surgical developed extracorporeal circulation.
conditions.
Alfred Blalock gave a detailed pathogenesis of
Sir Astley Cooper was the most popular surgeon shock and also was a pioneer innovator in the
from London in nineteenth century. field of cardiac surgery.
William TG Morton a Boston Dentist successfully Owen H Wangensteen did extensive work in
demonstrated ether anesthesia on October 16th surgical field and also a very good teacher at
1846. university of Minnesota.
Joseph Lister was the originator of antisepsis Francis D Moore described metabolism in
in surgery and is called as father of modern surgery. surgical patients.
Jonathan Rhoads introduced proper total Alexis Carrel in 1912, got Nobel Prize for his
parenteral hyperalimentation (1960). work on blood vessel anastomosis, organ
transplantation.
Charles B Huggins received Nobel Prize in 1966
Michael E DeBakey an American surgeon did
for his work on the effects of hormones on tumor
extensive work on cardiothoracic surgery. He
growth.
introduced occlusive roller pumps in extracorpo-
Wilhelm K Rontgen discovered X-rays in 1895. real circulation. He did first carotid endarterec-
tomy. He reported first the successful use of a
Alexander Fleming invented Penicillins as an saphenous vein bypass graft for coronary artery
antibiotic. occlusion in 1964.
In sixteenth century an Italian Surgeon Gasparo Christian Bernard from Capetown South Africa
Tagliacozzi was doing rhinoplasty. did first successful heart transplantation.
Miscellaneous 415
B. Laboratory Values
URINE
Specific gravity:
Normal: 1.010 to 1.025. Low: less than 1.000. High: more than 1.025
Fixed: 1.010 to 1.014
Reaction: Acidic with a pH of 6.0
Color: Clear and amber colored
Parameter Values
Aldosterone 2-10 μg/day
Nitrogen 0.4-1.0 gm/day
Amylase 30-250 somogyi units/hour
Calcium < 3.8 mmol/day
Catecholamines < 100 unit/day
Copper < 25 μg/day
Creatinine 1.0-1.6 g/day
Creatinine clearance 140-150 ml/min in males
105-130 ml/min in females
Estrogens 4-25 μg/day (in males)
5-100 μg/day (in females). Very high in pregnancy
17-hydroxy corticosteroids 2-10 mg/day
5-HIAA 2-9 mg/day
17-ketosteroids 7-25 mg/day in men
4-15 mg/day in women
Magnesium 6.0-8.5 mEq/24 hours
Metanephrines 1.3 mg/day
Urine osmolarity 38-1400 mOsm/Kg water
Phosphorus 0.9-1.3/day
Porphyrins
Coproporphyrin 50-250 μg/day
Uroporphyrin 10-30 μg/day
Potassium 25-100 mmols/day
Protein < 150 mg/day
Sodium 100-250 mEq/day
Urobilinogen 1-3.5 mg/day
VMA < 8 mg/day
BLOOD
Acetoacetic acid < 0.3 mmol/liter
Acid phosphatase 1.0-5.0 King-Armstrong units
Alkaline phosphatase 20-90 IU/liter
Amino nitrogen 3.5-5.5 mg/dl
Amylase 60-180 somogyi units
Ascorbic acid 0.4-1.0 mg/dl
Bicarbonate 23-29 mmol/liter
Bilirubin Total 0.3-1.0 mg/dl. Direct 0.1-0.3 mg/dl
Indirect 0.2-0.7 mg/dl
Calcium 9-11 mg/dl
Ionized—4.5-5.6 mg/dl
CO2 in plasma 20-30 mmol/l (50-70 volume %)
CO2 tension in artery 35-45 Hg
Ceruloplasmin 27-37 mg/dl
Chlorides 98-106 mmol/l
Cholesterol-total 150-250 mg%
Copper 115 + or –15 μg/dl
Cortisol 5-20 μg/dl
Creatine phosphokinase (CPK). 25-90 units/ml, in males. 10-70 units/ml in females
Creatinine < 1.5 mg/dl
Free fatty acids 0.7 mmol/liter
Gastrin 40-200 mg/dl
Glucose 70-110 mg/dl
17-OH corticosteroids 2-10 mg/day
IgG 800-1500 mg/dl
IgM 40-150 mg/dl
IgA 90-320 mg/dl
Insulin 6-26 uU/ml
17-ketosteroids 7-25 mg/day in males. 4 –15 mg/day in females
Lipase 1.5 units
Magnesium 0.8-1.3 mmol/liter
5‘ nucleotidase 0.3-2.6 Bodansky units/dl
Osmolality 280-300 mOsm/Kg of water
Oxygen 17-21 volume % in arterial blood
10-16 volume % in venous blood
Oxygen saturation 97% in arterial blood. 60-85% in venous blood
pH of blood 7.36-7.44
Phosphorus, inorganic 1-1.4 mmol/liter
Potassium 3.5-5.0 mmol/liter
Protein-total. 5.5-8.0 gm/dl
Albumin 3.5-5.5 gm/dl
Globulin 2.0-3.5 gm/dl
Sodium 136-145 mmol/liter
Sulfate inorganic 0.8-1.2 mg/liter
Testosterone < 100 ng/dl in females. 300–1000 ng/dl in males
TSH 0-5 IU/ml plasma
Thyroxine (T4) 5-12 μg/dl
Triiodothyronine (T3) 80-200 ng/dl
SGOT/AST 6-18 units/liter
SGPT/ALT 3-26 units/liter
Miscellaneous 417
Uric acid 2.5-8.0 mg/dl—males
1.5-6.9 mg/dl—females
Urea nitrogen (BUN) 10-20 mg/dl
RBC count 4.6-6.2 millions/mm3 in males
4.2-5.4 millions/mm3 in females
4.5-5.1 millions/mm3 in children
Reticulocyte count 25,000-75,000/mm3
WBC count 4,300-10,000/mm3
Platelet count 1,50,000-4,40,000/cu mm
Bleeding time 1-4 minutes
Hematocrit 40-54 ml/100 ml
Clotting time 2-15 minutes
Clot retraction time Apparent in 60 minutes, complete in 24 hours
Usually < 6 hours
Plasma fibrinogen 160-400 mg/dl
Partial thromboplastin time 68-82 seconds
Activated is 32-46 seconds
Prothrombin time 11-15 seconds
Hemoglobin 14-18 mg/dl—males
12-16 mg/dl—females
11-16 mg/dl—children
16-19 mg/dl—newborn
Fetal hemoglobin < 2%
Hemoglobin A2 1.5-3.5%
Osmotic fragility Begins in 0.45-0.39% NaCl and completes in 0.33-0.30%
Sedimentation rate(ESR) < 10 mm in one hour in males
< 20 mm in one hour in females
STOOL EXAMINATION
Bulk 100-200 gm
Water 75%
Osmolarity 250 mOsm/l
Color Brown
-pH 7.0-7.5
Fat < 7 gm/day
Stercobilinogen 50-280 mg/day
Urobilinogen 30-200 mg/100 gm
Nitrogen < 2.5 gm/day
Calcium 0.6 gm/24 hours
Trypsin 20-90 unit/gram
C. Clinical Methods for Dental Students

Basic clinical skill similar to a MBBS student is Whether painful or not
essential for a dental graduate. This is essential
even for their clinical examination in ‘surgery’. Pain
Hence clinical methods of different conditions When pain started? Location of pain/type of
which are kept as cases for dental students are pain/severity/whether it interferes with work
discussed here precisely. or not. Inflammatory conditions are painful
Common conditions, students have to learn whereas malignant conditions are painless to
for clinical examinations are: begin with but later it becomes painful.
• Examination of swelling
• Examination of ulcer-Please refer Chapter Presence of Fever
one.
In inflammatory conditions fever may be
• Arterial diseases- TAO, atherosclerosis
present. Certain malignancies also can present
• Varicose veins
with fever at later stage like in Hodgkin’s
• Examination of Thyroid
lymphoma or renal cell carcinoma.
• Oral carcinoma—refer chapter 20
• Neck swellings- secondaries/tuberculosis in
Presence of Other Lumps
lymph node/lymphoma- refer chapter 16
• Parotid swelling- refer chapter 19 Presence of other lumps/secondary changes in
• Hernia and hydrocele the swelling like ulceration/fungation
EXAMINATION OF A SWELLING/LUMP HISTORY OF PREVIOUS SURGERY

Swelling/lump denotes enlargement or protu- Loss of Function
berance in any part of the body due to con-
Loss of function of a part or as a whole
genital/inflammatory/traumatic or neoplastic
causes. Loss of Weight and Decreased Appetite
HISTORY Loss of weight and decreased appetite may
signify that swelling is related to malignant
Duration condition and also probably advanced.
Duration of swelling is important in all swellings.
Personal History
Swelling which is present since birth could be
congenital like meningocele. Swelling of short Personal history of alcohol consumption/
duration with pain may be inflammatory. Benign smoking/tobacco chewing/history of sexual
tumors are usually painless of long duration. contact/dietary habits are also important
Malignant tumors are of short duration, rapidly
Family History
enlarging, initially painless (but can be painful
later). Family history suggestive of similar swellings
is important. Neurofibromatosis is often familial.
Mode of Onset
Swelling whether started after trauma or GENERAL EXAMINATION
spontaneously. Detailed general examination is a must. Anemia/
Rapid or slow in progress—malignancy edema/jaundice/clubbing/lymphadenopathy/
progresses rapidly whereas benign swellings radial pulse/blood pressure/raise in tempera-
progress slowly. ture/attitude of the patient/nutritional assess-
Miscellaneous 419
ment by skin texture, subcutaneous fat, weight, Color of the Swelling
body mass index/any other relevant findings Blue color of hemangioma/black color of nevus
should be mentioned. or melanoma/blue color of ranula are often
LOCAL EXAMINATION diagnostic. Redness over the swelling suggests
inflammation.
Location of the Swelling
Exact anatomical location of the swelling/its size/ Surface Over Swelling
shape—globular or hemispherical or oval or pear-
Smooth/irregular/nodular/cauliflower like
shaped or irregular or kidney shaped/diffuse or
well localized. Vertical and horizontal dimension
Number of the Swellings
should be measured using a measuring tape.
Dermoid cysts occur in midline/outer canthus of Neurofibromas and sebaceous cysts can be
eye/or any line of fusion. Lipoma can occur multiple. Dermoid cyst is usually single.
anywhere in the body.
Figure 35.1 shows sebaceous cyst on the face Edge of the Swelling
whereas Figure 35.2 shows sebaceous cyst over Edge of the swelling whether well-defined or ill-
the scalp. defined/whether pedunculated or sessile should
be looked for.
Pulsation
Pulsation over the swelling
Arterial swelling has got expansile pulsation.
It is checked by keeping two fingers over the
swelling. Swelling which is very close to artery
or adherent to it also can show pulsation but it
is transmitted pulsation.
Reducibility
Whether swelling gets reduced while pressing
and disappears. Hernia is reducible.
Fig. 35.1: Sebaceous cyst face
Presence of Expansile Impulse
Presence of expansile impulse in coughing
signifies hernia or communication into the
deeper cavity like abdomen or thorax or
cranium.
Skin
Skin over the swelling should be inspected.
Skin over the swelling may be tense, glossy
with prominent veins in sarcoma and malig-
nancy. It is red edematous in inflammatory
swellings. Pigmentation, ulceration/fungation/
Fig. 35.2: Sebaceous cyst scalp. Note the loss of hair discharge from ulcer/bleeding from the
over the swelling fungation should be inspected. Scar its size,
features whether healed by primary intention or Surface of the Swelling
secondary intention should be mentioned. Linear Surface is palpated using palmar surface of the
and regular/broad, puckered and irregular. fingers. It may be smooth like in a cyst/nodular
in lymph nodes/lobular in lipoma/matted in
Inspect the Area and Distally tuberculous nodes/irregular in carcinoma. It
Inspect the area and also distally, specifically may be variable and if so should be mentioned
when swelling is in the limbs for any pressure as which part is smooth and which part is
effects and wasting. Wasting should be nodular.
confirmed by proper measurement of the part
keeping equal distance from a bony point. Consistency
It may be soft (like consistency of lip)/may be
PALPATION firm (like consistency of nose)/may be hard (like
consistency of forehead). Lipoma, cystic
Local Raise of Temperature
swellings, abscess are soft. Fibromas, neuro-
Local raise of temperature is checked using back fibromas, certain nodal enlargements are firm.
of fingers. It may be due to inflammation Chondroma, osteomas are bony hard. Malignant
(infection) or due to tumors. swellings are stony hard. Variable consistency
in one swelling may be observed. In such
Tenderness occasion which area is soft, which area is firm
Tenderness is checked while palpating the or hard should be confirmed properly. Varia-
swelling by observing the face of the patient. bility may be due to tumor necrosis/infla-
Patient expresses the tenderness. Inflammatory mmation. Swelling like sebaceous cyst or der-
conditions are tender. Neoplastic conditions are moid cyst which contains pultaceous material or
initially non-tender but later can become tender. putty like material gets moulded.
Size Fluctuation
Size is measured using tape; shape is confirmed Swelling is fixed usually by holding it with both
and extent of the entire swelling and its thumb and middle finger. With the index finger
anatomical location should be mentioned of one hand one side of the swelling is pressed
properly. and index finger of other hand placed on the
diagonally opposite side feels fluid movement
Edge or Margin and also a raise. Procedure should be done in
Edge or margin of the swelling can be well- perpendicular directions to confirm fluctuation
defined (distinct) or ill-defined (indistinct). In (two right angle planes). This is standard
acute conditions and deep swellings it is ill- fluctuation. Positive fluctuation signifies presence
defined. In superficial swellings it is well- of fluid. Examples are hydrocele, cysts etc. (Note:
defined. Margin may be irregular in malignancy Often muscle gives fluctuation like feeling when
and may be regular in benign swellings. elicited in one direction but not in two perpendi-
Edge of the swelling is examined using pulp cular directions).
of the index finger. Erosion of the margin into In swelling which cannot accommodate two
the deeper plane like bone should be checked. fingers to do standard fluctuation test, margin
Dermoid cyst commonly shows erosion into the of the swelling is fixed using two fingers (index
bone. In lipoma margin slips away from the and ring) and middle finger is used to press or
finger (slip sign). In sebaceous cyst margin gets indent the summit/center of the swelling to feel
yielded by the finger. displacement of the fluid/yielding sensation.
Miscellaneous 421
This test is called as Paget‘s test of fluctuation Compressibility
(Fig. 35.3). Swelling on pressure reduces in size only partially
Fluctuation may be present in a cystic and will not disappear completely and on releasing
swelling which contains fluid with two the pressure swelling again comes back to its original
components on either sides of an anatomical size and shape immediately. Usually vascular and
barrier (across an anatomical barrier). It is called lymphatic swellings are compressible.
as cross fluctuation. Ranula (across mylohyoid Example—hemangioma, lymphangioma.
muscle), psoas abscess (across inguinal
Pulsatility
ligament), compound palmar ganglion (across
flexor retinaculum), bilocular hydrocele (across Two fingers are placed over the swelling with
a band or superficial inguinal ring) are cross- adequate gap between two fingers. If fingers
fluctuant. over the swelling are raised and separated with
False fluctuation may be elicited in lipoma, each beat of the artery it means pulsation is
expansile. If fingers are only raised but not
myxoma and vascular swellings.
separated then pulsation of the swelling is
transmitted. Pure arterial swelling like aneurysm
shows expansile pulsation. Swellings that lie
close an artery shows only transmitted pulsation
due to its close proximity.
Fixity to the Skin
Mobility of the skin over the swelling is checked
or skin over the swelling is pinched to confirm
skin is free or attached to swelling underneath
(Fig. 35.4). Sebaceous cyst is having skin adhered
over the summit and a punctum (70%) often may
be present. In dermoid cyst skin is always free.
In lipoma skin is usually free. In neurofibromas
skin may be adherent and depends on from
Fig. 35.3: Paget‘s test is done for a small swelling to
which nerve neurofibroma arises whether from
elicit fluctuation
deeper plane or from cutaneous nerves.
Transillumination Test
When light is illuminated over the swelling it
transmits light through it. It is called as trans-
illumination/translucency. It is positive means
swelling illuminates to light and it suggests that
it contains clear fluid. It is negative when it
contains blood, pus, pultaceous material. Torch
light is placed on one side of the swelling and
illumination is observed on the diagonally
opposite side using a rolled paper or rolled
X-ray.
Lymph cyst, cystic hygroma, ranula, menin-
gocele, hydrocele are all transilluminant.
Reducibility
Swelling is pressed to get reduced completely Fig. 35.4: Skin over the swelling should be pinched/held to
and disappear. Hernia is reducible. check swelling is adherent to skin or not
Fixity to Deeper Structures Joints above and below the Swelling
If swelling is freely mobile it could be in subcu- Joints above and below the swelling should be
taneous plane (Fig. 35.5). Lipoma, sebaceous cyst, examined both for active and passive
often neurofibroma are subcutaneous. movements.
If swelling is adherent to muscle underneath,
then when muscle is contracted against Regional Lymph Nodes
resistance mobility of the swelling is restricted
but it becomes more prominent. While muscle Regional lymph nodes should be examined for
is relaxed swelling will be mobile. significant enlargement.
If swelling is arising from the muscle or deep
to muscle then size of the swelling decreases in Relevant Systemic Examination
size (less prominent) when muscle is contracted. Relevant systemic examination is a must like
Again mobility which was present initially respiratory, cardiac, skeletal and abdomen.
disappears completely during contraction of the
muscle. Disappearance occurs much more
Proper Diagnosis
significantly in swelling which is deeper to the
muscle. Proper diagnosis of the swelling should be given.
Swellings arising from vessels or nerves will
move only in horizontal/perpendicular direction Relevant Investigations
to the line of nerve but will not show any mobi- FNAC, U/S of part, CT scan, MRI for bony and
lity in longitudinal direction. Example- neuro- joint swellings, angiography and Doppler in
fibroma, aneurysm.
vascular swellings, biopsy in soft tissue
Swelling arising from the bone is hard and
sarcomas.
absolutely fixed and can not be moved separately
from the bone. Swelling may be congenital/traumatic/
inflammatory/neoplastic. It may be benign or
malignant. In malignancy it may be early or
advanced.
EXAMINATION IN ARTERIAL DISEASE

(ARTERIAL SYSTEM)
Arterial diseases occur in lower limb commonly
and also occasionally in upper limb. Often both
lower and upper limbs may get involved.
It is often classified as lower limb ischemia
and upper limb ischemia. But wherever the
disease is present detailed examination of both
Fig. 35.5: Mobility of swelling should be checked to find lower limb and upper limb vessels is required
out the plane of the swelling
in all patients.
Name: Age: Sex: Occupation:
Percussion over the swelling in relevant area
like hernia should be done. Address:
Atherosclerosis occurs in old age usually.
Auscultation Thromboangiitis obliterans (Buerger’s disease)
It is done to look for bruit over the swelling like in occurs in young males. Raynaud’s disease is
A-V malformation, arterial stenosis, aneurysms. common in young/middle aged females.
Miscellaneous 423
Chief Complaints • History of chest pain/cough or cardiac related
• Pain in the limb right/left/both—its duration symptoms
• Intermittent claudication—its duration • History of abdominal pain/bloody diarrhea/
• Blackish discoloration/ulceration. abdominal angina
• History of paresthesia over the skin
History of Present Illness • History suggestive of superficial thrombophlebitis
• Pain like swelling/redness/pain along the line of
Site of pain, type of pain—severe burning/ superficial vein.
aching/deep persisting.
Whether pain radiates or not. Past History and Treatment History
Intermittent claudication—duration, grade/how • Similar history earlier

much distance patient can walk/whether pain • History of drug intake earlier for similar
subsides after stopping walk or after continuous conditions like vasodilators/drugs to
walk/whether patient is able to walk in spite of increase the perfusion
pain/change in the claudication distance • History of earlier surgery like/sympa-
eventually/site of claudication- foot/leg/thigh/ thectomy/omentoplasty/their results or
buttock. effects.
Presence of rest pain—its location/severity/
whether patient has to hold the limb/foot/leg/
toes to relieve pain little bit (probably by
transmission of temperature from holding hand
into the part) or to hang the leg down to relieve
the pain or by apply warmth.
Pain, discomfort, color changes when
exposed to cold.
• Ulceration
Whether precipitated by trauma/sponta-
neous onset
Pain in the ulcer/type/duration/aggra-
vating or relieving factors Fig. 35.6: Ischemia of all four limbs. Note the ischemic
Discharge—type- serous-purulent-bloody ulcers in fingers and toes
Progression
• In gangrene Personal History
Site of gangrene/its onset/progression/pain.
History of smoking-beedi or cigarettes/
• History of difficulty in walking/altered gait.
duration/number per day/stopped now or
• Mode of onset—in atherosclerosis/Buerger’s
disease process is spontaneous and gradual. continuing/since when stopped smoking.
In gangrene due to embolism it is sudden in
Family History
onset, and rapidly progressive
• History of fever Any family history suggestive of atherosclerosis
• History of impotence—its duration or vascular diseases.
• History of tingling/numbness/weakness in the
limbs General Examination
• History of syncope/blackouts/loss of cons- • Pulse—rate/rhythm/character/condition of
ciousness/blurred vision vessel wall.
• Blood pressure of both arms and if possible 30°. If foot does not become pale or doubtful,
of both lower limbs then repeated ankle flexion and extension is
• Attitude of limbs done until it becomes pale with empty-
guttered veins on the dorsum of foot. After
Local Examination lowering the foot cyanotic congestion appears
in the foot.
Inspection
• Edema in the foot/feet/legs
• Inspect both lower limbs keeping side by side
• Status of the superficial veins—normally filled
as comparison is needed during clinical
veins or pale/discolored/guttered veins as
examination seen in ischemic limb.
• Change in color is very important sign of • Capillary filling time—initially elevated limbs
ischemia (Fig. 35.6) are made to hang down the bed. Normal limb
Color proximal to gangrene area/ischemic will remains pink in elevated as well as
area (usually ischemic area is pallor). depressed position because of rapid capillary
Limb deformity filling time. In ischemia, limb becomes pale
• Gangrene of toe/toes/foot/leg—its extent, on elevation and gradually becomes purple-
any discharge, type of gangrene—dry or wet, red and then pink in more than 20 seconds.
line of demarcation- type/level/depth, color Purple pink color is due to deoxygenated
of gangrenous area—black/purple/greenish blood. Prolonged capillary time signifies
black (in gas gangrene) severe ischemia.
• Ulceration if any—its extent/discharge/size/ • Venous refilling time—In elevated limb when
shape/floor/surrounding area laid horizontal on the bed normal venous
Patchy ulcers proximal to gangrenous area— refilling occurs within 5 seconds. It is delayed
skip lesions are usually black patchy lesions. in ischemic limb.
• Muscle wasting in the foot/leg/thigh should
be observed. It should be compared and also PALPATION
should be measured using a tape from a fixed
bony point keeping equal distance in both • Temperature of the skin is a important factor
limbs. in ischemic limb. Extent of skin color and
• Features of ischemia—shiny thin skin/loss of proximally where exactly limb/part become
subcutaneous fat/hair loss—its extent/nail warmer should be assessed.
changes—brittle nail/transverse ridges in the • Tenderness—Site/extent/severity should be
nail. assessed.
• Plantar aspect of the foot for infective focus/ • Gangrenous area to be palpated for extent/
abscess/callosities/skin changes/superficial whether it is dry and shriveled or whether
ulcers in heel/malleoli/toes it is wet and edematous. Presence or absence
• Buerger’s postural test—patient in supine of Crepitus in gangrenous part should be
position is asked to raise his legs one after checked.
other with knee kept straight. Normal limb • Limb above the gangrenous area should be
remains pink even after 90° elevation without palpated.
any pallor. Diseased limb after elevation • Capillary filling
shows marked pallor (over foot) with empty- Tip of the nail or pulp of the finger or toe
guttered veins. The angle with which pallor is pressed to blanch it and pressure is released
develops (between limb and ground) is called to make it pink. Time taken for blanched area
as Buerger’s vascular angle of insufficiency. to turn into pink is capillary filling time. It is
In severe ischemia this angle will be less than prolonged in ischemic limb.
Miscellaneous 425
• Harvey’s venous refilling test • Adson’s test
Two fingers are placed over the vein. While feeling the radial pulse of the affected
Pressure is applied over the vein. Proximal side of the patient, patient is asked to take
finger is moved proximally for about 5 cm deep breath and to turn his neck/head
without releasing the pressure. Vein between towards the same side so as to compress the
the fingers gets emptied completely and thoraco-axillary channel. Pulse becomes
becomes flat. Distal finger is released now to feeble or absent in positive Adson’s test in
see the flow of the blood and its refilling is thoracic outlet syndrome/scalenus anticus
observed whether it is good or poor. It is poor syndrome. While taking deep breath thoracic
in ischemic limb. cage moves upwards and narrows the space
• Elevated arm stress test (EAST) causing aggravation of compression of
Both shoulders are abducted 90 degrees with subclavian artery by scalenus anterior
arms fully externally rotated. Patient will muscle. Contraction of scalenus anterior
open and close the hands rapidly for 5 further aggravates the feature (by turning
minutes. Normal individual can do this neck towards same side).
without any discomfort and pain. Patient • Branham’s/Nicoladoni’s sign
with thoracic outlet syndrome develops pain, In arteriovenous fistula—pressure over the
fatigue, paresthesia of forearm with tingling artery proximal to fistula causes reduction in
and numbness of fingers. Patient will not be pulse rate and size of the swelling with pulse
able to continue the test for 5 minutes. This pressure becoming normal and disappea-
test can also differentiate thoracic outlet rance of bruit.
syndrome from cervical disc prolapse • Allen’s test
disease. It is used in hand to find out the patency of
• Roos test radial and ulnar arteries. Both radial and
Patient is asked to elevate and abduct the ulnar arteries of the patient is felt and pressed
shoulders for 90 degrees along with external firmly at the wrist. Patient clinches his hand
rotation of arms and keep it for 5 minutes. firmly (often repeated clinching) and holds
Patient feels fatigue in the diseased side. it tightly. After 1 minute clinch is released
• Costoclavicular compression maneuver to open the palm of the hand which looks
While feeling radial pulse of the patient he pale. Pressure on the radial artery in wrist
is asked to place his shoulder backwards and is released to see area of distribution of the
downwards (exaggerated military position) radial artery. Normally it becomes flushed
causing absence/feeble radial pulse and with pink color. If there is radial artery block
while auscultating the supraclavicular region area will remain white. Test is repeated again.
a bruit may be heard. This is due to This time pressure on the ulnar artery is
compression of subclavian artery between released to check the patency of ulnar artery.
clavicle and first rib. Area will be pale and blanched after releasing
• Hyper abduction maneuver (Halsted test) in case of ulnar artery block. Otherwise in
While palpating the radial pulse, arm on the normal individual it turns pink after release.
diseased side is passively hyper abducted • Cold and warm water test
causing feeble or absence of radial pulse. This It is commonly done to confirm Raynaud’s
is due to compression of artery by pectoralis phenomena. Patient is asked to dip hands in
minor tendon (pectoralis minor syndrome). An cold water to precipitate the vasospasm and
axillary bruit may be heard on auscultation. Raynaud’s syndrome.
• Crossed leg test (Fuchsig’s test) (Fig. 35.7) space, against the navicular and middle
Patient is asked to sit with the legs crossed cuneiform bones. It is absent in 10% cases.
one above the other so that the popliteal fossa 2. Posterior tibial artery is felt against the
of one leg will lie against the knee of other calcaneus just behind the medial malleolus
leg. Oscillatory movements of foot can be midway between it and tendo Achilles.
observed synchronous with the popliteal 3. Anterior tibial artery is felt in the midway
artery pulsation. If the popliteal artery is anteriorly between the two malleoli
blocked oscillatory movements will be against the lower end of tibia just above
absent. the ankle joint lateral to extensor hallucis
longus tendon.
4. Popliteal artery (Fig. 35.9) is difficult to feel.
It is palpated better in prone position with
knee flexed about 40–90 degrees to relax
popliteal fascia. It is felt in the lower part
of the fossa over the flat posterior surface
of upper end of tibia. In upper end of the
fossa, artery is not felt as there is no bony
surface in the intercondylar region. It can
also be felt in supine position with knee
flexed 45 degrees to relax the popliteal
fossa so as to feel the pulsation over the
upper part against tibial condyles.
5. Femoral artery (Fig. 35.10) in the groin is
felt just below the inguinal ligament mid-
way between anterior superior iliac spine
and pubic symphysis (mid-inguinal
point). Often hip has to be flexed for about
10–15 degree to feel it properly.
6. Radial artery is felt at the wrist on the lateral
aspect against lower end of the front of
Fig. 35.7: Cross leg (Fuchsig’s test) test to see oscillations
radius.
• Disappearing pulse syndrome 7. Ulnar artery is felt at the wrist on the medial
Exercise the limb after feeling the pulse. Pulse end against lower end of the front of ulna.
will disappear once patient develops 8. Brachial artery is felt in front of the elbow
claudication. It is because of vasodilatation just medial to biceps brachii tendon.
and increased vascular space occurring due 9. Axillary artery is felt in lateral aspect of the
to exercise wherein arterial tension can not axilla against upper end of the shaft of the
be kept adequately and so pulse will humerus with raised and elevated arm.
disappear (unmasking the arterial obstruc- 10. Subclavian artery is felt against first rib just
tion). above the middle of the clavicle in
• Palpation of blood vessels supraclavicular fossa while patient is
1. Dorsalis pedis artery (Fig. 35.8) is felt just lifting the shoulder to relax deep fascia.
lateral to the extensor hallucis longus 11. Facial artery is felt against body of mandi-
tendon at the proximal end of first web ble at the insertion of masseter.
Miscellaneous 427
12. Common carotid artery (Fig. 35.11) is felt
medial to sternomastoid muscle at the
level of thyroid cartilage against carotid
tubercle (chaissagne tubercle) of
transverse process of 6th cervical vertebra
(in carotid triangle).
13. Superficial temporal artery is felt just in front
of the tragus of the ear against zygomatic
bone.
All pulsations should be written in a table form right
and left side
Pulse Right Left Fig. 35.9
Dorsalis pedis Should be Should be
Posterior tibial mentioned as mentioned
Anterior tibial present/absent as present/
Popliteal /feeble absent/feeble
Femoral
Radial
Ulnar
Brachial
Axillary
Subclavian
Carotid
Superficial temporal
Fig. 35.10
Condition of the vessel wall, thrill and any
tenderness on the artery should be mentioned.
Fig. 35.8 Fig. 35.11

Figs 35.8 to 11: Methods of palpation of dorsalis pedis, popliteal, femoral and carotid artery pulsations
Ulcer if present should be examined for presents as pulsatile mass above the
different features like tenderness/mobility/ umbilicus, vertically placed, smooth, soft,
fixity/base/induration. nonmobile, not moving with respiration,
resonant on percussion. Expansile pulsation
AUSCULTATION is confirmed by placing the patient in knee-
Auscultation over the artery for bruit is done elbow position.
using bell of the stethoscope placing gently over • Cardiovascular system
the artery (Fig. 35.12). It signifies localized stenosis CVS is essential part to be examined for any
causing turbulence flow. Machinery bruit/mur- associated or causative causes. There may be
mur also heard in AV malformations/fistulas. embolic focus in heart like fibrillation/
endocarditis etc.
• Other systems like skeletal and respiratory
systems should be examined in detail.
EXAMINATION OF VARICOSE VEINS

CHIEF COMPLAINTS
• Pain in the leg/thigh/foot with the side and
duration of pain.
• Swelling/dilated veins in the leg and its
duration.
• Pigmentation/ulceration in the leg with
duration.
HISTORY OF PRESENT ILLNESS

Pain
• Pain in the leg/foot/or thigh with duration.
Origin of pain, its severity, mode of onset
whether acute or insidious has to be asked.
• Character of pain dull aching or cramping.
Whether pain gets aggravated by walking/
Fig. 35.12: Auscultation of carotid artery for bruit standing. Dull aching pain along the line of
the vein is typical and is usually more
NEUROLOGICAL EXAMINATION towards evening and gets relieved on lying
Muscle tone/power at ankle, knee and hip, down. Pain in calf of short duration may be
sensory examination for touch, pain and due to associated deep vein thrombosis
temperature, reflexes at ankle and knee and (DVT).
plantar response should be checked when • Pain also can be due to ulcer/periostitis/
associated neurological conditions are suspected infection.
(like tabes dorsalis, syringomyelia, hemiplegia,
transverse myelitis). Pigmentation
• It is due to stasis and release of chemicals;
SYSTEMIC EXAMINATION usually occurs around ankle region.
• Abdomen should be examined for the • It is associated with itching and often
presence of abdominal aortic aneurysms. It ulceration.
Miscellaneous 429
Ulcer LOCAL EXAMINATION
• Ulcer history regarding mode of onset, Examination of lower limbs. First symptomatic
duration, site of onset should be asked. Ulcer limb should be examined first.
on the medial side of the ankle occurs in long
saphenous vein varicosity. On the lateral INSPECTION
aspect it is due to short saphenous vein Examination of veins in standing position is the first
varicosity. method in varicose veins (Figs 35.13 and 35.14).
• Discharge from ulcer its type, smell, quantity
signifies the severity of the infection
• Itching and bleeding in the ulcer bed are also
important
History of trauma. Often minor trauma precipi-
tates ulcer formation in patients with varicose
vein.
History of swelling around the ankle
History of pain/lump in the abdomen
History of urinary/bowel symptoms
Figs 35.13 and 35.14: Inspection of varicose veins should
History of similar complaints on the other leg. be done on standing. Long saphenous veins should be
inspected on both sides from medial aspect in standing
Varicose veins is often bilateral. position. Short saphenous vein should also be inspected from
behind
Past History
• Limb is looked for dilated veins on the medial
• History suggestive of deep vein thrombosis
side for long saphenous vein; and from
earlier like pain, calf swelling and fever.
behind and lateral side for short saphenous
• History of immobilization, hospitalization
vein. Other communicating veins are also
• History of surgery earlier.
looked for.
• Beginning of the varicosity in the foot, later
Treatment History
its extent above also should be looked. Great
• History of varicose vein surgery in the past, saphenous vein tortuosity often extends into
drug like warfarin intake for DVT, injection- the thigh whereas short saphenous vein
sclerotherapy, wearing stockings/crepe varicosity ends at popliteal region.
bandages. • Always limb is looked for skin changes,
pigmentation, edema, ankle flare, and ulcer.
Personal History Cough impulse at saphenous opening
• In females history of pregnancy, delivery and (Morrisey’s) may be significant.
postpartum, oral contraceptive intake. • Extent, size, shape, margin, edge and dis-
• Smoking/alcohol/working pattern. charge in an ulcer should be noted.
Family History Palpation
Family history relevant to varicose veins. • Ulcer if present should be described with
• Often familial varicose veins are bilateral tenderness, induration, warmness, mobility,
severe and observed in young individuals. fixity etc.
Valves are absent/defective in these patients. • Brodie-Trendelenburg test.
Fig. 35.15: Note the site of applying the tourniquet at

sapheno-femoral junction. It is 3.5 cm below and lateral to
pubic tubercle
Vein is emptied by elevating the limb and

milking the vein in lying down position and
a tourniquet is tied just below the sapheno-
femoral junction [or using thumb, sapheno-
femoral junction is occluded]. Saphenous
opening is located 3.5 cm below and lateral
to the pubic tubercle (Fig. 35.15). Pubic tuber-
cle is palpated along the adductor longus Fig. 35.16
tendon which is identified by adducting the
thigh against resistance. Patient is asked to
stand quickly. When tourniquet or thumb is
released, rapid filling from above signifies
sapheno-femoral incompetence. This is
Trendelenburg test I.
In Trendelenburg test II, vein is emptied again
in lying down position and tourniquet is
applied at sapheno-femoral junction. After
standing without releasing the tourniquet
limb is observed. Filling of blood from below
upwards rapidly within 30–60 seconds
signifies perforator incompetence.
• Three/multiple (Oschner’s Mahoner’s test)
Fig. 35.17
tourniquet test: To find out the site of
incompetent perforator, three tourniquets are
tied after emptying the vein (Figs 35.16 to
35.19).
1. At sapheno-femoral junction
2. Above knee level
3. Another below knee level
4. Additional tourniquets often may be
applied at below knee and above ankle
Fig. 35.18
level.
Patient is asked to stand and looked for filling Figs 35.16 to 35.18: Emptying of the superficial varicose
of veins and site of filling. Then tourniquets are vein is important in all tourniquet tests for varicose veins. It
is done by making the patient lie down, and elevating and
released from below upwards to again see for milking the vein. Emptying is not done in modified Perthe’s
incompetent perforators. Individual perforators test. Note the marking of the sapheno-femoral junction before
may be tested by repeating the procedure. applying the tourniquet
Miscellaneous 431
is asked to walk around and exercise.
Development of severe cramp like pain in the
calf signifies DVT.
• Modified Perthe‘s test: Tourniquet is tied just
below the sapheno-femoral junction without
emptying the vein. Patient is allowed to have
a brisk walk which precipitates bursting pain
in the calf and also makes superficial veins
more prominent. It signifies DVT.
DVT is contraindicated for any surgical
intervention of superficial varicose veins. It is also
Fig. 35.19: Note the placement of tourniquets in contraindicated for sclerosant therapy.
multiple tourniquet tests • Homan’s test is dorsiflexion of the foot to elicit
pain in the calf and Mose’s sign is squeezing
• Schwartz test: In standing position, when the relaxed calf muscles sidewards to elicit
lower part of the vein in leg is tapped, pain. Both tests signify Deep Vein Throm-
impulse is felt at the saphenous junction or bosis (DVT)
at the upper end of the visible part of the vein. • Point to be remembered is that in case of acute
DVT, Homan’s/Mose’s tests should not be
It signifies continuous column of blood and
done as it will precipitate the dislodgement
also signifies valves between two fingers are
of the clot and embolism.
incompetent. Positive test is usually found
• Bone thickening in the shin (tibia and in ankle
in gross venous varicosity. is important which signifies periostitis.
• Pratt‘s test: Esmarch bandage is applied to the • Limb length and girth measurement is
leg from below upwards with a tourniquet needed especially in arterio-venous malfor-
at sapheno-femoral junction. After that the mation with varicose veins and also to find
bandage is released to see the ‘blow outs’ as out deformities.
perforators.
Auscultation of the vein for bruit/venous hum.
• Fegan‘s test: Line of varicose vein is marked
out. On standing, the site where the perfo- Examination of peripheral pulses are important
rators enter the deep fascia bulges and this (dorsalis pedis/anterior tibial/posterior tibial/
is marked. Then on lying down, button like popliteal/femoral).
depressions (crescentric gaps) in the deep Regional lymph nodes (vertical inguinal nodes and
fascia are felt at the marked out points which external iliac nodes {above and medial aspect of
confirms the perforator site. the inguinal ligament}), ankle joint movements
• Ian—Aird test: On standing, proximal (plantar and dorsiflexion) are important.
segment of long saphenous vein is emptied Examination of the other limb both in standing and
with two fingers. Pressure from proximal lying down position should not be forgotten.
finger is released to see the rapid filling from
Abdomen should be examined for any mass which
above which confirms sapheno-femoral
might be compressing the inferior vena cava
incompetence.
(IVC) or iliac veins causing varicose veins.
• Perthe’s test: The affected lower limb is
wrapped with elastic bandage and the patient Examination of other systems also should be done.
EXAMINATION OF THYROID GLAND Past history: History of irradiation for carcinoma

thyroid. Irradiation to head and neck region for
CHIEF COMPLAINTS benign lesions like adenoids, tonsillitis, thymus,
• Swelling in front of the neck and its duration. acne vulgaris or hemangiomas or malignancy
• Pain in the swelling and its duration. like lymphomas in younger age group.
• Hoarseness of voice due to recurrent laryn- Chernobyl nuclear disaster in Ukraine in 1986
geal nerve palsy. caused increased incidence of papillary carci-
• Difficulty in swallowing or breathing. noma of thyroid in children.
• Tremor in the hands.
• Generalized weakness. Personal history: History of smoking, alcohol
• Palpitation. intake or any drugs which may cause alteration
• Loss of significant weight. in thyroid function. Patient may be on thyroxine
or on antithyroid drugs or beta blockers or other
HISTORY OF PRESENT ILLNESS drugs like lithium, PAS or sulphonylureas which
alter the thyroid function. Dietary habits should
• Swelling: Its duration, mode of onset sudden
be asked. Vegetables of Brassica family like
or insidious. Origin of the swelling, its
cabbage, kale and rape are goitrogens. Type of
progress whether gradual (benign), rapidly
progressive (malignancy) or rapid increase salt used in the family, iodized/home rock salt
in an existing swelling (benign turning into is also important.
malignancy) or sudden rapid increase may Family history: Dyshormonogenesis, medullary
be seen after hemorrhage. carcinoma of thyroid can be familial (MEN
• Pain: Its duration, character like dull aching/ syndrome). Endemic goiter and Grave’s disease
pricking, site of pain, radiation, factors which can occur in families. Altered thyroid function
alters the pain. may be cause for infertility.
• Pressure symptoms: Dysphagia, dyspnea,
hoarseness of voice. Menstrual history
– Their duration, onset and progression. Treatment history: History of undergoing investi-
• Features of toxicity: Increased appetite/loss of gations or treatment relevant to thyroid disease.
weight/diarrhea/chest pain that is
aggravated by exercise/palpitation/ GENERAL EXAMINATION
amenorrhea/irritability/nervousness/
• Like any other long case.
sleeplessness (insomnia)/hand tremors/
• Exophthalmos should be seen.
increased sweating/heat intolerance/
weakness in proximal muscles of thigh or • Myxedema face is typical.
arm like in getting down steps or lifting • Pulse-its character, whether tachycardia
weight using arms (myopathy)—due to (Fig. 35.20), collapsing or pulsus paradoxus
difficulty in isometric contraction and or ectopic or fibrillation has to be looked for.
increased muscle metabolism/wasting of • Blood pressure may be high in toxic thyroid.
muscles/visual disturbances with bulging of • Sleeping pulse rate is checked at late night
the eyes. or early morning for three consecutive nights
• Features of myxedema: Weakness/lethargy / and average is taken. Giving sedation like
weight gain/facial swelling/cold intole- diazepam or phenobarbitone to check
rance/menorrhagia/constipation/super- sleeping pulse rate prior to sleep is a
ciliary madarosis in lateral half of the eye controversial. Sleeping pulse rate is graded
brows (loss of hairs)/change in voice. as per Crile’s grading.
Miscellaneous 433
Crile’s grading Sleeping pulse rate/minute
I 90-100
II 100–110
III > 110
Fig. 35.21: Method of looking for tremor of

hands in thyrotoxicosis
isthmus or if it is one mass dimensions as a

Fig. 35.20: Checking radial pulse is single swelling)/shape (butterfly shape if
essential in thyroid enlargement both lobes are involved)/extent (from
posterior border of sternomastoid laterally to
• Patient with toxic thyroid will be thin and
underweight. In hypothyroidism, patient will midline in one sided gland enlargement or
be obese and overweight. In metastatic from one side to opposite sternomastoid if
thyroid cancer patient is cachexic. both lobes are enlarged)/upper extent is
• Agitated stressful facial expression is usually up to thyroid cartilage/lower margin
observed in toxic thyroid. Puffy, expression- is clearly visible or not or visible only during
less, dull and mask-like face is seen in deglutition/upward movement with degluti-
myxedema.
• Gait is rapid and aggressive in toxicity but tion (thyroid moves upwards during degluti-
lethargic and slow in hypothyroidism. tion due to attachment of the condensed
• Skin is wet and warm in hyperthyroidism vascular pretracheal fascia (Berry’s ligament),
(moist palm while shaking hands). which is attached above, medially and behind
• Ankle (Achilles tendon) reflex is prolonged to cricoid cartilage and also pretracheal fascia
with delayed relaxation in hypothyroidism is attached to larynx, trachea and inferior
and it is shortened and brisk in hyper-
constrictor muscle which moves upwards)/scar
thyroidism.
• Tremor of the hands and tongue (Fig. 35.21). or dilated veins (in toxic goiter, carcinoma
thyroid, venous compression, retrosternal
LOCAL EXAMINATION goiter) or pigmentation on the skin over the
Inspection swelling/pulsation over the swelling
• Swelling- its location/size ( both vertical and (toxicity, malignancy)/surface on inspection
horizontal dimensions of each lobe and (smooth or nodular).
Swellings which move upwards with • Thrill is checked in the upper pole of the
deglutition gland as superior thyroid artery is superficial
• Thyroid swelling and enters the gland in front upper pole.
• Sub hyoid bursa Thrill signifies toxicity or increased vascu-
• Thyroglossal cyst larity.
• Pretracheal/prelaryngeal lymph nodes • Method of palpation of thyroid gland-
• Swelling from larynx/trachea Thyroid gland is palpated from behind
(Fig. 35.22) with patient is sitting on a stool
• In some occasions whether swelling moves with neck partially flexed (Fig. 35.22). Both
with protrusion of the tongue or not should thumbs of the examiner are kept over the
be looked for. Thyroglossal cyst moves cervical spine and fingers in front to feel the
upwards with protrusion of tongue. Patient gland- both lateral lobes and isthmus are
is asked to open the mouth and the swelling/ palpated for all features.
cyst is held firmly. Now patient is asked to • Crile’s method of palpation of gland: It is the
protrude the tongue to feel the upward palpation of nodule/swelling in front using
movement of the swelling and also the the pulp of the thumb.
typical ‘tug’ in the swelling. • Pizzillo’s method of palpation (Fig. 35.23): It
• Any other swelling in the neck like lymph is the method of palpation of thyroid gland
nodes should be looked for. Lymph nodes in short neck and obese individuals. Patient
can be involved commonly in papillary carci- is asked keep her/his both hands over the
noma of thyroid and occasionally in follicular occiput so that the gland becomes prominent
carcinoma of thyroid. which is palpated from front or behind.
• Lahey’s method of examination: It is the
PALPATION method used to palpate any nodules in
• Swelling: Temperature over swelling posterior part of the gland (Fig. 35.24). It is
(swelling may be warm in toxic thyroid, malig- mainly useful in solitary nodule of thyroid.
nancy, thyroiditis)/tenderness (hemorrhage, Examiner should stand in front of the patient.
thyroiditis, tumor necrosis can cause If right lobe is needed to be palpated, left
tenderness)/extent/position shape/size lateral lobe is pushed towards right to make
(should be measured in centimeter both
vertically and horizontally)/movement of the
swelling upwards with deglutition/surface
(smooth or nodular)/consistency (soft or firm
or hard or variable and if so different
consistencies at different location should be
mentioned)/margin (well defined or diffuse,
lower margin which is most important)/
independent mobility of the swelling/plane
of the swelling (it is checked by contracting
the sternomastoid muscles after placing
examiner’s hand under the patient’s chin and
patient is asked to flex the neck against
resisting hand) (single side gland relation to
sternomastoid muscle is checked by
contracting the muscle by turning the chin
against resistance of the examiner’s hand)/
skin is free or not. Fig. 35.22: Method of palpation of thyroid gland from behind
Miscellaneous 435
get weakened which get narrowed/collapsed
due to compression. Because of forward
traction keeps goiter itself trachea patent. But
after thyroidectomy lack of support to trachea
causes tracheomalacia—weakening of the
tracheal rings. Such patients need temporary
tracheostomy for 2-3 weeks after thyroi-
dectomy. By then tracheal rings regain their
strength to maintain the patency of the
trachea.
Fig. 35.23: Caption: Pizzillo’s method of
examination of thyroid gland CONFIRMATION OF
RETROSTERNAL EXTENSION
• Lower margin of the swelling/goiter is not
visible-even on deglutition
• Lower margin is not palpable on deglutition
• Dilated veins over neck or chest wall may be
visible
• Normal resonant note becomes dull over the
sternum on percussion
• Pemberton’s sign—patient is asked to raise
both the arms above the shoulder so that it
touches the ears and keeps like that for 3
minutes. Patient will develop dilated veins
and cyanosis in the neck and upper chest
wall, puffiness in face and respiratory distress
and rarely dysphagia. It means sign is
Fig. 35.24: Lahey’s method of palpating thyroid gland positive signifying retrosternal extension of
goiter.
posterior aspect of the right gland more • Position of trachea is checked by palpation
prominent as gland gets pushed and rotated using three fingers from below. Middle finger
towards right side. Posterior surface becomes is kept just above the suprasternal space and
posterolateral or lateral which is felt for any index and ring fingers are placed over sternal
nodules. Posterior aspect of left lobe is heads of the sternomastoid muscles on each
palpated by pushing the right lobe towards side. Middle finger is run upwards along the
left side. trachea to feel the position-central or
• Kocher’s test: It is the test to check for tracheal deviated. In solitary nodule or disease of only
compression. Patient is asked to see straight. one lateral lobe trachea will be usually
With fingers and thumb both lateral lobes of
deviated towards opposite side. In enlarge-
the thyroid gland are gently compressed,
pressure directing postero-medially. If ment of both lobes trachea will be usually
patient develops stridor-Kocher’s test is central. Other features are absence of
positive. No stridor means it is negative. In hollowness on the side of the deviation (trail
a long standing goiter and large goiter, sign), on auscultation hearing of breath
because of constant pressure tracheal rings sounds on the side of the deviation.
Carotid pulsation should be checked. It is normally rectus muscles in case of primary
felt at the level of the upper border of thyroid thyrotoxicosis. There will be diplopia. It may
cartilage over medial aspect of the sternomastoid be an early sign of eventual ophthalmoplegia.
muscle on the Chaissagne tubercle (carotid
tubercle) on the transverse process of C6 Order of appearance of signs
vertebra. It may be deviated posteriorly/laterally 1. Stellwag’s sign—Mild. First sign to appear
in large goiter. It may be absent in advanced 2. von Graefés Sign—Mild.
carcinoma thyroid due to infiltration of the 3. Joffroy’s sign—Moderate.
carotid sheath by the tumor (Berry’s sign). 4. Moebius sign—Severe.
In thyroid swelling, it is very important to look
for eye signs (Fig. 35.25). In primary Important signs to be remembered
thyrotoxicosis, exophthalmos and all other eye • Visible lower sclera- sign of exophthalmos
signs are looked for: • Naffziger’s sign
• Both the eyelids partially cover the bulbar • von Graefés sign-upper lid lag-spasm of
sclera in normal individual. levator muscle
• Upper sclera is visible only in lid retraction— • Joffroy’s sign
due to spasm of involuntary levator pal- • Moebius sign- most important-early sign of
pebrae superioris muscle. Here lower eyelid ophthalmoplegia
is in normal position. It does not indicate
exophthalmos.
• In exophthalmos lower bulbar sclera is
clearly visible and lower eyelid is low and
does not cover the bulbar sclera. In severe
exopthalmos, sclera is visible all over both
above and below.
• Exophthalmos is measured using exophthal-
mometer.
Other eye signs
Eye signs are common in primary thyrotoxicosis.
Lid lag, lid spasm can occur in secondary
thyrotoxicosis also.
1. von Graefe‘s sign: Lid lag sign—white sclera is
visible above the corneal margin during lid lag
2. Naffziger’s sign: Standing behind patient’s
neck is extended and examiner looks from
behind along the superior orbital margin of Fig. 35.25: Looking for eye signs is very important in
the patient. Eyeball is seen beyond the thyroid swelling
superior orbital margin in exophthalmos. Examination of neck lymph nodes for secondaries. It
3. Dalrymple‘s sign: Upper eye lid retraction, so
is common in papillary carcinoma of thyroid. It
upper sclera is visible.
4. Stellwag‘s sign: Absence of normal blinking— is usually level III and IV nodes. It could be firm,
so starring look. First sign to appear. hard or cystic. It is usually brownish black in
5. Joffroy‘s sign: Absence of wrinkling on color often with papillary projections. Lymph
forehead when patient looks up [frowns]. nodes often can get enlarged in follicular
6. Moebius sign: Lack of convergence of eye ball. carcinoma thyroid and lymphoma. Lateral
Defective convergence is due to lymphocytic aberrant thyroid is earlier thought as aberrant
infiltration of inferior oblique and inferior thyroid in lateral part of the neck but actually
Miscellaneous 437
it is not so but it is secondary in lymph node with Cardiovascular System Examination
primary being papillary carcinoma of thyroid. Cardiovascular system examination is important
Percussion over the manubrium sterni is important. in thyrotoxicosis (Fig. 35.27) commonly secon-
Dullness signifies retrosternal extension. dary type. Tachycardia, ectopic beats, pulsus
Tenderness may signify the secondaries in paradoxus, extrasystoles, atrial fibrillation are
sternum from follicular carcinoma of thyroid. the cardiac presentations.
Auscultation over the upper pole of the gland for
Respiratory System
bruit- in toxic thyroid severe cases and very
vascular tumors (Fig. 35.26). Respiratory system examination to look for
secondaries and pleural effusion that occur in
follicular carcinoma of thyroid.
Examination of Abdomen
Secondaries in liver is known to occur in
follicular carcinoma of thyroid presenting as
hepatomegaly. Hepatosplenomegaly can occur
as part of Grave’s disease or Hashimoto’s
disease.
Examination of Skull and Spine

Localized, warm, vascular, pulsatile secondaries
can occur in skull commonly, rib and other bones
occasionally due to spread from follicular
carcinoma of thyroid.
Fig. 35.26
Thyroid swelling which does not move with
respiration
• Carcinoma thyroid with infiltration
• Riedel’s thyroiditis
• Anaplastic carcinoma thyroid
Causes of dyspnea/stridor in thyroid

diseases
• Carcinoma thyroid causing infiltration of
recurrent laryngeal nerve/trachea
• Large, long standing goiter causing
tracheomalacia
• Retrosternal goiter
• Congestive cardiac failure in thyrotoxicosis.
Recent rapid increase in thyroid swelling is

due to
• Previous multinodular goiter undergoing
Fig. 35.27
malignant transformation
Figs 35.26 and 35.27: Auscultation over superior pole of • Hemorrhage into a nodule
thyroid for bruit in toxic thyroid and over cardiac region for
any cardiac changes • Anaplastic carcinoma of thyroid
In a case of thyroid disease following things • Progress and extent of the swelling whether
should be made very clear only limits to the groin or extends to the
• Functional status—hyperthyroid/euthyroid scrotum.
/hypothyroid • Any changes in the size and extent of the
• Compression to trachea/recurrent nerve swelling on standing/walking/straining/
• Status of neck lymph node lying down.
• Tracheal deviation • Whether swelling is reducible on lying
• Carotid infiltration down/partially reducible or irreducible on
• Retrosternal extension lying down or needs any maneuver to reduce
• Systemic features like toxicity or malignant it. History of gurgling sound in the scrotum
spread to different organs like bone/liver/ signifies enterocele.
lungs. • If swelling is irreducible then history of
painful or abdominal distension/vomiting –
INVESTIGATIONS FOR THYROID should be asked.
DISEASES
Pain
• T3, T4, TSH, Free T3, Free T4
• Site of pain- whether it is in the groin or in
• U/S neck for thyroid and neck nodes
the scrotum.
• FNAC thyroid and lymph node
• Duration of pain
• Radioisotope study
• Severity of the pain, type of pain- dull aching
• CT neck in malignancies or large goiter.
or severe pricking type
• Trucut biopsy if two trials of FNAC are
• Aggravating or relieving factors. Aggravated
inconclusive. It can injure deeper structures
by straining/walking/weight lifting;
and also can cause hemorrhage.
relieved by lying down.
• On table Frozen section biopsy and proceed
may be needed. History relevant to Precipitating Factors
• Serum calcitonin, serum thyroglobulin • Chronic cough, tuberculosis, bronchial
estimation in neoplasms of thyroid. asthma or other respiratory diseases.
• Constipation, altered bowel habits, tenesmus,
EXAMINATION OF INGUINAL HERNIA bloody stool- in relation to anorectal
stricture/carcinoma
CHIEF COMPLAINTS • Dysuria/urgency/hesitancy/altered
• Swelling in the groin right or left or both stream/night frequency/retention of urine/
sided for — durations; or swelling in right/ burning urine/hematuria- in relation to
left/both inguinoscrotal region for— benign prostatic hyperplasia/urethral
durations. stricture.
• Pain over the swelling for—durations.
Past History
HISTORY OF PRESENT ILLNESS • Past history of hernia surgery- same side/
opposite side. Type of surgery whether mesh
Swelling used or repair done.
• Duration of the swelling • History of appendicectomy in the past and
• Mode of onset of the swelling –spontaneously if so detail about the surgery
or on straining. • Past history suggestive of irreducibility/
• Site of the first appearance of the swelling— obstruction and treatment given whether
in the groin or in the scrotum. conservative/surgical.
Miscellaneous 439
Personal History
• Smoking- duration, number of cigarettes per
day, whether beedi or cigarette. History of
pan chewing/alcohol intake.
• Appetite and altered weight.
Treatment History
GENERAL EXAMINATION
General built and nutritional status, pallor,
clubbing, cyanosis, jaundice, lymphadenopathy,
edema feet, pulse and blood pressure.
LOCAL EXAMINATION
Inguinoscrotal region should be examined in
standing position as swelling commonly gets
reduced and disappears in lying down position.
INSPECTION
Inspection in standing position:
• Mention the side of the swelling
• Extent of the swelling is important.
Incomplete indirect inguinal hernia and Fig. 35.28: Expansile impulse on coughing is better seen
usually direct inguinal hernias are in inguinal than felt. It should be inspected with patient standing and
region. Complete indirect inguinal hernia examiner sitting beside the patient
(rarely complete direct inguinal hernia) is
inguinoscrotal-extending down up the PALPATION
bottom of the scrotum. Swelling extends from • Temperature and tenderness over the
the proximal part of the inguinal canal
swelling
towards the scrotum below.
• Whether it is possible or not to get above the
• Both transverse and vertical dimensions of
swelling. One can get above the swelling in
the size should be mentioned
purely scrotal swelling but in inguino-scrotal
• Shape of the swelling is pyriform in indirect
inguinal hernia and globular in direct swelling one can not get above the swelling.
inguinal hernia • Position and extent of the swelling
• Expansile impulse on coughing over the swelling • Size in vertical and transverse directions
is diagnostic (Fig. 35.28). It is better seen than • Margin well-defined or ill-defined
felt • Surface smooth/lobular/tense
• Surface, smooth/uneven • Consistency is soft and elastic in enterocele;
• Margin—well-defined/ill-defined doughy in omentocele.
• Visible peristalsis over the swelling should • Location of the swelling- swelling is above
be noted if present. It means it could be and medial to pubic tubercle in inguinal
enterocele hernia and below and lateral to pubic tubercle
• Scar/dilated veins/discoloration/redness in femoral hernia.
over the swelling • Reducibility of the swelling is checked by
• On inspection, whether testis is seen different methods
separately from the swelling or covered by • Whether it is reducible spontaneously while
the swelling all over. lying down and gets reduced completely or
partially. In enterocele first part is difficult • Opposite inguinal region, opposite testis,
to reduce but last part reduces easily. In epididymis and spermatic cord should be
omentocele last part is difficult to reduce but examined. Presence or absence of cough
first part reduces easily. impulse on opposite side should be
• Whether swelling needs any manipulation to mentioned.
get reduced like taxis. Taxis is by flexion and
rotation of hip joint, contents of the scrotum Percussion
is reduced gradually by gentle manipulation. • Without reducing contents of the swelling,
Zieman’s test is done to find out over which finger percussion is done over the surface. If it is
impulse is felt and so which type of hernia it resonant, it is enterocele. If it is dull on
could be whether femoral/direct inguinal or percussion then it is omentocele.
indirect inguinal.
Auscultation
Deep ring occlusion test (Fig. 35.29)
Bowel sounds may be heard over the swelling
• Once deep ring is occluded if impulse on
if it is enterocele.
coughing is not present then it is indirect
inguinal hernia. If impulse on coughing still
Per Abdomen Examination
present then it is direct inguinal hernia.
• Abdomen muscle tone should be checked by
head raising test, leg raising test and valsalva
maneuver. It should be inspected for
Malgaigne bulging and should be palpated
for whether tone is adequate (firm) or
inadequate (supple).
• Any scar over the abdomen (appendicectomy
scar may cause right sided direct inguinal
hernia), ascites or mass per abdomen should
be mentioned.
Digital Examination of the Rectum (P/R)

Digital examination of the rectum (P/R) must
Fig. 35.29: Ring occlusion test is done to find out whether
hernia is direct or indirect. If after occluding the ring swelling
be done in all hernia cases to look for prostate
appears on the medial side, it is direct hernia. If swelling enlargement in elderly and rectal/anorectal
does not appear on occlusion and coughing it is indirect strictures.
hernia
Finger invagination test Size of the superficial ring Examination of Respiratory System
and site of the impulse felt whether on the tip
of the finger or pulp is noted. Examination of respiratory system for altered
• Palpation of testis, epididymis and spermatic breath sounds (rhonchi, bronchial breathing),
cord is done. Relation of swelling to testis also effusion etc. to find out any precipitating causes.
should be noted.
• Bulbar urethra is palpated by lifting the Other Systems
scrotum and feeling in the midline (To look Cardiovascular system, nervous system, spine
for thickening and button like depression-a and cranium should be examined before
feature of stricture urethra). management of hernia.
Miscellaneous 441
anatomy in the inguinal region is weak and also
due to the presence of natural weakness like deep
ring and cord structures.
Femoral is 17%; Umbilical is 8.5%.; Others are
1.5%.
ETIOLOGY
• Straining.
• Lifting of heavy weight.
• Chronic cough (Tuberculosis, chronic
bronchitis, bronchial asthma, emphysema).
• Chronic constipation (Habitual, rectal
stricture)
• Urinary causes
– Old age: BPH, carcinoma
prostate
– Young age: Stricture urethra
– Very young age: Phimosis, meatal
stenosis.
Fig. 35.30: Bilateral complete inguinal hernia. Here hernia • Obesity.
descends into scrotum. Usually indirect inguinal hernia
• Pregnancy and pelvic anatomy (especially in
becomes complete
femoral hernia in females).
• Smoking.
• Ascites.
• Appendicectomy through McBurney’s
incision may injure the ilioinguinal nerve
causing right sided direct inguinal hernia.
• An indirect inguinal hernia occurs in a
congenital, preformed sac, i.e.the remains of
processus vaginalis. Chances of presence of
bilateral preformed sac is 60%.
• Familial—collagen disorder -Prune Belly
syndrome.
PATHOLOGY OF HERNIA
Fig. 35.31: Bilateral direct inguinal hernia. Note medial
location of the hernia. It is always acquired Hernia comprises of:
• Covering
• Sac
DEFINITION OF HERNIA • Content.
Hernia means—‘To bud’ or ‘to protrude’. ‘off shoot’ Sac is a diverticulum of peritoneum with mouth,
[Greek]. ‘rupture’ [Latin]. neck , body and fundus. Neck is narrow in indirect
Hernia is defined as an abnormal protrusion sac but wide in direct sac. Body of the sac is thin
of a viscous or a part of a viscous through an in infants, children and in indirect sac but is thick
opening, artificial or natural with a sac covering in direct and long standing sac.
it. Hernia without neck: Those hernias with larger
Inguinal hernia (Figs 35.30 and 35.31) is the mouth lacks neck e.g. direct hernia, incisional
commonest hernia [73%] because the muscular hernia.
Hernia without sac: Epigastric hernia—it is into gangrene of the content. It is a surgical
protrusion of extra peritoneal pad of fat. emergency. Patient will be toxic, with
irreducibility and pain and tenderness.
Coverings of the sac are the layers of the
Emergency surgery, resection of the bowel
abdominal wall through which the sac passes.
and anastomosis should be done.
Contents of Sac
Classification II
• Omentum—Omentocele [Epiplocele]. Difficult
to reduce the sac at the end. Anatomical classification [in inguinal hernia]
• Intestine—Enterocele— commonly small
bowel, but sometimes even large bowel. Indirect hernia (Fig. 35.32) It arises through
Difficult to reduce the sac initially. internal ring along with the cord. It is lateral to
• Richter‘s hernia—a portion of circumference the inferior epigastric artery.
of bowel is the content.
• Urinary bladder may be the content or part Direct hernia (Fig. 35.33) It occurs through the
of the posterial wall of the sac. posterior wall of the inguinal canal. Sac is medial
• Ovary, often with fallopian tube. to the inferior epigastric artery.
• Meckel’s diverticulum—Littre‘s hernia.
• Fluid: Fluid secreted from congested bowel Classification III
or omentum. It may be a infected fluid or
ascitic fluid or blood from the strangulated According to the extent.
sac. Incomplete:
Bubonocele: Here sac is confined to the
GENERAL CLASSIFICATION OF HERNIA inguinal canal.
Classification I: (clinical) Funicular: Here sac crosses the superficial
inguinal ring but does not reach the bottom
1. Reducible hernia: Hernia get reduced on its
of the scrotum.
own or by the patient or by the surgeon.
Intestine reduces with gurgling and first Complete: Here sac descends to the bottom
portion is difficult to reduce. Omentum is of the scrotum (See Fig. 35.30).
doughy and last portion is difficult to reduce.
Expansile impulse on coughing present. Classification IV
2. Irreducible hernia: Here contents cannot be
Congenital.
returned to the abdomen due to narrow neck,
Acquired.
adhesions, overcrowding etc. Irreducibility
predisposes to strangulation.
3. Obstructed hernia: It is an irreducible hernia Classification V
with obstruction but blood supply to the According to the contents.
bowel is not interfered. It eventually leads Omentocele—omentum.
to strangulation.
Enterocele—intestine.
4. Inflamed hernia: It is due to inflammation of
the contents of the sac e.g. appendicitis, Cystocele—urinary bladder.
salpingitis. Here hernia is tender but not Litter’s hernia—Meckel’s diverticulum.
tense; overlying skin is red and edematous. Maydl’s hernia
5. Strangulated hernia: It is due to obstruction Sliding hernia
causing blockage of blood supply leading Richter’s hernia—part of the bowel wall.
Miscellaneous 443
inguinal ligament midway between the
symphysis pubis and the anterior superior iliac
spine.
Inguinal canal In infants both superficial and deep
rings are superimposed without any obliquity
of the inguinal canal. In adults it is 3.75 cm long,
directed downwards and medially from the deep
to superficial ring.
In males inguinal canal transmits the
spermatic cord, ilio-inguinal nerve and genital
branch of the genito-femoral nerve. In females,
its content is the round ligament.
Inguinal canal in female is called as canal of Nuck.
Fig. 35.34: Surgical anatomy of inguinal canal
Figs 35.32 and 35.33: Diagrammatic representation of BOUNDARIES

anatomical location of direct and indirect inguinal hernia
In front: External oblique aponeurosis and
conjoined muscle laterally.
SURGICAL ANATOMY OF Behind: Inferior epigastric artery, fascia
INGUINAL CANAL (FIG. 35.34) transversalis and conjoined tendon medially.
Superficial inguinal ring is a triangular opening Above: Conjoined muscle [arched fibres of
in the external oblique aponeurosis and is 1.25 internal oblique]
cm above the pubic tubercle. The ring is bounded
Below: Inguinal ligament.
by a superomedial and inferolateral crus.
An indirect inguinal hernia travels down the
Normally the ring does not admit the tip of little
canal on the lateral and anterior aspect of the
finger.
spermatic cord, whereas the direct hernia pops
Deep inguinal ring is a U-shaped condensation out directly forward through the posterior wall
of the transversalis fascia, lies 1.25 cm above the of the inguinal canal.
Neck of the indirect sac is lateral to inferior
epigastric vessels but direct sac emerges medial
to the inferior epigastric vessels with a wide
neck.
Saddle-bag or pantaloon hernial sac has got
both medial and lateral component.
Inguinal hernia is above and medial to the
pubic tubercle. Femoral hernia is below and
lateral to pubic tubercle.
HERNIOPLASTY
It is strengthening of posterior inguinal wall in
case of indirect hernia or in any large hernia with
weak abdominal wall using a supportive
material. This allows and supports good Fig. 35.35: Amber colored hydrocele fluid on table
fibroblast proliferation which in turn strengthens
the weak posterior wall of inguinal canal or
abdominal wall.
MATERIAL USED
• Synthetic: Prolene mesh [white in color]—
Dacron mesh,
• Biological: Tensor fascia lata, temporal fascia
and skin [Presently biological materials are
not well accepted as infection is common and
its efficacy is not proved].
Prolene mesh is commonly used at present
Hernioplasty is ideal procedure for inguinal
hernia. Fig. 35.36: Hydrocele is usually transilluminant. Thickened
dartos, thick sac, infected fluid makes it non-transilluminant
EXAMINATION OF HYDROCELE
• Hydrocele is collection of fluid in the scrotum nothing else. There is no impulse on
between two layers of the tunica vaginalis coughing. It is by this method hydrocele is
testis. It can be primary idiopathic, secondary differentiated from inguinal hernia. In hernia
due to filarial infection, trauma, tuberculosis, one cannot get above the swelling and there
syphilis or malignancy. is impulse on coughing (Fig. 35.37).
• Hydrocele fluid is amber colored which
contains water, salt, albumin and fibrinogen TYPES
(Fig. 35.35). Fluid per se does not clot but if • Vaginal hydrocele limits to only scrotum.
comes in contact with the blood it gets clotted. • Congenital hydrocele communicates to
• Primary vaginal hydrocele occurs in middle peritoneal cavity
age. • Infantile hydrocele-Here tunica and processus
• Hydrocele is smooth, soft, fluctuant and often vaginalis [hydrocele] are distended up to
transilluminant (Fig. 35.36). On holding root internal ring, but sac has no connection with
of the scrotum only cord structures are felt, the general peritoneal cavity.
Miscellaneous 445
• Fluid contains fat , rich in cholesterol, derived
from ruptured lymph varix into the tunica.
• It is often difficult to differentiate from
primary hydrocele.
Complications of Hydrocele
• Infection
• Pyocele
• Hematocele
• Atrophy of testis
• Infertility.
TREATMENT FOR HYDROCELE:

SURGERY
Fig. 35.37: Hydrocele is scrotal swelling. Get above the 1. Sub total excision. Radical cure—Hydro-
swelling is the clinical method used to differentiate it from
hernia celectomy.
2. Partial excision and eversion.
• Encysted hydrocele of the cord It is a smooth, 3. Evacuation and eversion.
oval, swelling associated with the spermatic 4. Lord‘s plication.
cord. On gentle traction to the testis, the
swelling becomes less mobile [traction test]. PROCEDURE
• Hydrocele en bisac: [Bilocular hydrocele]:
• Hydrocele has got two intercommunicating • Under G/A or spinal or L/A, after cleaning
sacs, one above and one below the neck of and draping, vertical incision of about 6-8 cm
the scrotum. in length is made over the scrotum, anteriorly
1cm lateral to the median raphe.
SECONDARY HYDROCELE • Skin, dartos, external spermatic fascia,
Causes: Infection : Filariasis internal spermatic fascia are incised.
Tuberculosis of epididymis Bluish hydrocele sac is identified [i.e. parietal
Syphilis layer of the tunica vaginalis of the testis].
Injury : Trauma,
Fluid is evacuated using trocar and cannula.
Postherniorrhaphy
Sac is opened.
hydrocele
• If the sac is small, thin and contains clear fluid,
Tumor : Malignancy
either Lords plication [ i.e. tunica is bunched
into a ‘ruff’ by placing series of multiple
It is usually small, lax and testis is usually
palpable [unlike primary hydrocele]. Exception interrupted chromic catgut sutures so as to
is secondary hydrocele due to filariasis. make the sac to form fibrous tissue] [it is
relatively avascular and so hematoma will
FILARIAL HYDROCELE AND CHYLOCELE not occur].
• Occurs commonly in coastal region and in • Or evacuation and eversion of the sac behind
and around the Equator. the testis [after eversion, everted sac is
• Usually occurs after repeated attacks of sutured with chromic catgut by continuous
filarial epididymitis. sutures] is done.
• Hydrocele is usually of large size and the sac • If the sac is thick, in large hydrocele and chylocele,
is thickened. subtotal excision of the sac is done [as tunica
vaginalis is reflected on to the cord structures EXAMINATION

and epididymis posteriorly, total excision Inspection
leads to orchidectomy with division of cord.].
• Site of lesion/type/extent/edge/margin/
• Aspiration must be avoided as much as possible
floor/mouth opening (trismus) is adequate
as it is only a temporary measure [recurrence or not/gums/dentition/floor of mouth/
occurs very early] and chances of hematocele tongue/palate/tonsils/lips/leukoplakia
and infection are higher. present or not
• A drain is placed near the root of the scrotum • Skin over the check also should be inspected
on the lateral aspect because it becomes the for swelling/edema/ulceration/discolo-
most dependent portion once scrotal support ration
is given. Scrotal support is given to reduce • Tongue depressor is needed for proper
the scrotal edema for 10 days. inspection of the oral cavity
• Wound is closed in layers.
• Drain is removed in 48 hours. Palpation
• Lesion is palpated after wearing a glove- for
Complications of surgery tenderness/extent/induration/mobility/
• Reactionary hemorrhage fixity/bleeding on touch/palpation of
• Hematocele different parts of the oral cavity
• Infection • Bone thickening is checked using two fingers
• Pyocele – thickening/tenderness/irregularity/
• Sinus formation evidence of fracture site (pathological)
• Recurrent hydrocele. • All parts of the oral cavity should be palpated
properly.
EXAMINATION OF ORAL CAVITY Neck is examined for significant lymph nodes of

different groups and levels. Submandibular
HISTORY nodes are checked with neck flexed and tilted
• Swelling-in detail towards same side. It should be differentiated
• Ulcer-detail from submandibular salivary gland by bidigital
• Pain palpation. Lymph gland is not bidigitally
• Type of pain, radiation to ear (through lingual palpable whereas salivary gland is bidigitally
and auriculotemporal nerves) or other places, palpable.
severity Relevant systemic examinations should be done.
• Fever
• Excessive salivation is common in carcino-
EXAMINATION OF SALIVARY GLAND
mas.
• Difficulty in speech HISTORY
• Voice change
• Swelling- duration- progress
• Halitosis- foul smelling breath
• Pain- duration/type/severity/radiation
• Fever
PERSONAL HISTORY
• Difficulty in opening mouth
Smoking history, chewing pan and keeping pan/ • Excess salivation during meals/more pain
quid in the cheek, alcohol intake, spicy diet, during meals/swelling become more
trauma by teeth. prominent during meals.
Miscellaneous 447
EXAMINATION • Palpation of oral cavity/bidigital examina-
Inspection tion for deep lobe
• Swelling in detail. • All features of facial nerve palsy- inability to
• Deep lobe of parotid enlargement is checked close eye/difficulty in blowing/altered
by inspecting the oral cavity for any bulge nasolabial groove/clinching of teeth
in the tonsil and lateral wall of pharynx • Neck nodes should be examined
• Stenson’s parotid duct should be inspected
• Examination of other neck nodes should be
• Skin over the swelling should be inspected
done
Palpation • Relevant findings should be elicited in case
• Tenderness/temperature/extent/size/
of submandibular salivary gland enlarge-
surface/consistency/mobility/fixity/plane
of the swelling/masseter involvement/facial ment
nerve involvement/skin over the swelling Proper diagnosis and investigations should
• Parotid duct palpation be mentioned.
Index
A Aneurysm cirsoid 84 Bisgaard method 97

Abdominal trauma 177 Aneurysm needle 391 Blair’s incision 250
Abscess 19 Aneurysm, dissecting 78 Block dissection, neck 217
Abscess drainage, Hilton’s Aneurysms 75 Block dissection,
method 21 Aneurysms, abdominal 77 supraomohyoid 217
Abscess, alveolar 300 Aneurysms, Berry’s 76 Block, Bier’s 411
Abscess, Brodie’s 329 Aneurysms, intracranial 367 Block, field 411
Abscess, cold 111 Aneurysms, peripheral 78 Block, infiltration 411
Abscess, dental 300 Angelchik prosthesis 312 Block, nerve 411
Abscess, intracranial 366 Angiography 67 Block, saddle 412
Abscess, parapharyngeal 210 Angiomyoneuroma 50 Blood coagulation,
Abscess, peritonsillar 288 Angioplasty, transluminal mechanism 122
Abscess, retropharyngeal 210 balloon 69 Blood fractions 126
Achalasia cardia 309 Anion gap 149 Blood loss, measurement 125
Achondroplasia 331 Ankylosing spondylitis 334 Blood substitutes 128
Acid-base balance 148 Ann-Arbor staging 107 Blood transfusion 126
Acidosis metabolic 148 Anthrax 35 Blood transfusion, massive 127
Acidosis respiratory 149 Anticoagulants 98 Boil 22
Acriflavine 397 Antisepsis 394 Bone disease of
Acrocyanosis 62 Antithyroid drugs 230 hyperparathyroidism 331
Actinomycosis 31 Apoplectic cyst 46 Bone tumors 336
Acute arterial occlusion 72 Arch bars 355 Bone, anatomy 320
Acute osteomyelitis 328 Arterial diseases, examination 422 Bone, infections 328
Acute pyomyositis 37 Arterial diseases, treatment 69 Boyd’s classification 64
Acute suppurative Arthritis 332 Boyle’s apparatus 408
tenosynovitis 167 Arthritis, acute pyogenic 332 Brachytherapy 375
Adamantinoma 298 Arthritis, chronic pyogenic 333 Brain injuries, effects 358
Adenolymphoma 254 Arthritis, rheumatoid 333 Branchial cyst 205
AIDS 38 Arthrodesis 326 Branchial fistula 206
Ainhum 82 Arthroplasty 326 Broder’s grading 184
Alcohols 397 Asepsis 394 Brodie’s abscess 329
Alkalosis, respiratory 148 Astrocytomas 369 Buerger’s disease 68
Ameloblastoma 298 Atherectomy 69 Burns 130
Amputations 80 Autoclave 394 Burns contracture 135
Anesthesia, caudal 411 Burns, chemical 136
Anesthesia, epidural 412 B Burns, classification 130
Anesthesia, general 407 Bacteremia 24 Burns, degrees 130
Anesthesia, intravenous Barium swallow X-ray 308 Burns, effects 133
regional 411 Barrett’s esophagus 312 Burns, electric 135
Anesthesia, regional 410 Basal cell carcinoma 197 Burns, management 133
Anesthesia, spinal 411 Bazin’s ulcer 101 Burns, pathophysiology 132
Anesthesia, topical 411 Bedsore 13 Burns, treatment 133
Anesthetics, gaseous 407 Berry’s aneurysms 367 Bursa anserina 54
Anesthetics, intravenous 407 Berry’s ligament 220 Bursa olecranon 54
Anesthetics, volatile 407 Biopsy 184 Bursa, adventitious 54
Bursa, psoas 54 Clark’s levels 200 Cyst, dental 300
Bursa, semimembranosus 55 Classification LAHS 292 Cyst, dentigerous 299
Bursae 53 Classification, Breslow’s 200 Cyst, epidermal 48
Bursitis, subhyoid 213 Classification, cleft diseases Cyst, lymph 50
291, 292 Cyst, Morran Baker 55
C Classification, Debakey’s 79 Cyst, periapical 300
Classification, diabetic foot 81 Cyst, radicular 300
Calcinosis cutis 55
Classification, goiter 223 Cyst, sebaceous 48
Callosity 170
Classification, hernia 442 Cystic hygroma 208
Cancrum oris 262
Classification, Kinmoth 102 Cysts 46
Carbimazole 230
Classification, Le Fort 342
Carbuncle 22
Classification, Lederman’s 278 D
Carcinoma cheek 263
Classification, Ohngren’s 277
Carcinoma cheek, verrucous 263 Day care surgery 400
Classification, Rappaport 109
Carcinoma esophagus 316 Deep vein thrombosis 89
Classification, Rye’s 106
Carcinoma esophagus treatment Defibrillation technique 121
Classification, Seddon’s 153
317 Delayed primary suturing 4
Classification, Shamblin 212
Carcinoma lip 269 Delphian nodes 220
Classification, Stanford 78
Carcinoma tongue 272 Dental wiring 355
Classification, Sunderland’s 154
Carcinoma, adenoid cystic 255 Depressed skull fracture 365
Claustrophobia 405
Carcinoma, hard palate 280 Dercum’s disease 43
Claw hand 158
Carcinoma, mucoepidermoid 255 Dermatofibroma 194
Cleft lip 291
Carcinoma, nasopharyngeal 276 Dermatofibrosarcoma
Cleft lip, Millard repair 293
Carcinoma, oral cavity, protuberans 194
Cleft lip, treatment 293
prognostic factors 279 Dermoid, external angular 47
Cleft palate 291
Cardiac arrest 120 Dermoid, implantation 48
Cleft palate, treatment 295
Cardiac massage, external 120 Dermoid, internal angular 47
Clinical methods for dental
Cardiac massage, internal 121 Dermoid, sequestration 46
students 418
Carotid blow out 218 Dermoid, teratomatous 48
Closed reduction of zygomatic
Cartilage 320 Dermoids 46
arch 347
Catheter, Foley’s 387 Dermoids, sublingual 261
Clostridium tetani 25
Catheter, Malecot’s 388 Dettol 395
Catheter, simple red rubber 388 Cock’s peculiar tumor 49
Diabetic foot 81
Causalgia 155 Collis vertical gastroplasty 312 Diagnostic peritoneal lavage 178
Cellulitis 17 Compartment syndrome 4 Diaphyseal achalasia 332
Central venous pressure 117 Compound palmar ganglion 168 Diathermy 398
Cervical rib 59 Congenital syphilis 30 Digital substraction angiography 67
Cetrimide 395 Coning 359 Dilator, Bake’s 386
Chemical agents 395 Contre–coup injury 359 Dilator, Lister’s urethral 388
Chemodectoma 211 Corn 171 Disease Mikulicz 252
Chemotherapy 376 Cortisol ulcers 11 Disease, Basedow’s 226
Cherubism 301 Coup injury 359 Disease, Bowen’s 195
Chimney sweep cancer 195 Cresol 395 Disease, Caisson’s 75
Chlorhexidine 395 Critical limb ischemia 64 Disease, decompression 75
Chondroma 336 Crush injury 2 Disease, Eve’s 298
Chondrosarcoma 191 Cryoprecipitate 126 Disease, Grave’s 226
Chronic osteomyelitis 329 Cryosurgery 399 Disease, Meige’s 102
Chylocele 445 CSF rhinorrhea 363 Disease, Milroy’s 102
Cimino fistula 86, 144 CT scan 403 Disease, Ollier’s 332
Clamp, Moynihan’s occlusion 385 CVP 117 Disease, Sipple’s 245
Clamp, Payr’s crushing 385 Cyclosporin-A 143 Disease, von Willebrand’s 122, 123
Index 451
Disinfection 394 Esophagitis, reflux 313 Forceps, sinus 386
Doppler 402 Esophagoscopy, 308 Formaldehyde 397
Doppler, venous 94 Esophagoscopy, negus 309 Fracture 320
Double barreled aorta 78 Esophagoscopy, rigid, 309 Fracture healing, factors affecting 322
DPL 178 Esophagus, anatomy 306 Fracture mandible 349
Drains 386 Esophagus, corrosive stricture 313 Fracture mandible classification 350
Drains, classification 387 EUSOL 395 Fracture middle third area 342
DSA 67 Ewing’s sarcoma 338 Fracture, clinical features 322
Dupuytren’s contracture 169 Exophthalmos 228 Fracture, Condylar 351
DVT, prevention 91 Exophthalmos, malignant 229 Fracture, Dentoalveolar 351
Dyshormonogenesis 223 Exotoxins 27 Fracture, Greenstick 320
Dysphagia 308 Extradural hematoma 363 Fracture, Guerin 343
Dysphagia, causes 308 Exuberant granulation tissue 11 Fracture, March 320
Fracture, maxillary 342
E F Fracture, maxillofacial 340
Fracture, pyramidal 343
EAST 66 Facial nerve 246
Fracture, stages of healing 321
Ecchondroma 336 Facial nerve palsy 259
Fracture, stellate 320
ECF excess 146 False cyst 46
Fracture, stress 320
ECF loss 146 Fat embolism 323
French disease 30
Elbow, miner’s 54 Felon 165
Fresh frozen plasma 126
Elbow, student’s 54 Fibrin cuff theory 91
Frog hand 166
Embolectomy 73 Fibrinolysins 74
Furuncle 22
Embolism 73 Fibrinolysins 90
Embolism, air 75 Fibromas 52
Embolism, fat 74 Fibrosarcoma 190 G
Embolus, saddle 74 Finger, base ball 170 Ganglion 53
Emil Theodor Kocher 240 Finger, Mallet 170 Ganglioneuroma 50
Enchondroma 336 Fistula 6 Gangrene 64, 79
Enchondromatosis 332 Fistula parotid 251 Gangrene, dry 64, 80
Endarterectomy 70 Fistula, arteriovenous 85 Gangrene, line of demarcation 64
Endotracheal tube 408 Fistula, tracheooesophageal 315 Gangrene, wet 64, 80
Epignathus 56 Flap, Estlander’s rotating 270 Gas gangrene 27
Epineurorrhaphy 154 Flap, Fries’ modified Bernard Gastroesophageal reflux disease 311
Epiperineurorrhaphy 154 facial 270 Gastrostomy 150
Epithelioma 195 Flaps 140 Gene therapy 378
Epstein’s pearls 296 Flaps, saltatory 141 GERD 311
Epulis 297 Fluids, electrolyte and nutrition 145 Gigli’s saw 389
Epulis, carcinomatous 298 FNAC 185 Gillies temporal approach 347
Epulis, congenital 297 Foaming liver 27 Glasgow coma scale 361
Epulis, fibrous 297 Follicular odontome 299 Gliomas 369
Epulis, giant cell 298 Forceps Allis tissue holding 382 Glutaraldehyde 397
Epulis, granulomatous 298 Forceps Babcock’s 382 Goiter, diffuse hyperplastic 224
Epulis, myelomatous 297 Forceps Cheatle’s 380 Goiter, nodular 224
Epulis, pregnant 297 Forceps sponge holding 380 Goiter, retrosternal 226
Erysipelas 18 Forceps, artery 381 Gonorrhea 41
Erythrocyanosis frigida 11 Forceps, Desjardin’s Grading, Brunner’s 104
Erythroplakia 262 choledocholithotomy 385 Grading, Crile’s 229
Eschar 134 Forceps, dissecting 384 Graft intake, stages 139
Escharotomy 134 Forceps, Kocher’s 381 Graft rejection 143
Esophageal endosonography 309 Forceps, right angle 381 Graft types 138
Graft, arterial 70 Hutchinson’s triad 30 Injury, axillary nerve 160
Graft, full thickness 140 Hybridoma 378 Injury, brachial plexus 155
Graft, in situ saphenous vein 70 Hydrocele 444 Injury, common
Graft, Mesher 139 Hydrocele, examination 444 peroneal nerve 159
Graft, partial thickness 138 Hydrocephalus 368 Injury, duodenal 179
Graft, reverse saphenous vein 70 Hydrogen peroxide 397 Injury, liver 179
Graft, skin 138 Hydrophobia 32 Injury, long thoracic nerve 160
Graft, split skin, 138 Hyperbaric oxygen 119 Injury, median nerve 156
Granulation tissue 11 Hyperkalemia 147 Injury, pancreatic 179
Great pox 30 Hypernatremia 147 Injury, penetrating 177
Gustatory sweating 258 Hyperparathyroidism 243 Injury, renal 180
Hyperparathyroidism, acute 243 Injury, small bowel 179
H Hyperparathyroidism, primary 243 Injury, spinal 176
Hyperparathyroidism, Injury, splenic 180
Haemaccel 128
secondary 243 Injury, ulnar nerve 157
Halogens 395
Hyperthyroidism 226 Injury, urinary bladder 180
Hamartomata 82
Hypertrophic scar 5 Inner Waldeyer’s ring 204
Hand, surgical anatomy 162
Hypokalemia 147 Instruments 380
Hansen’s disease 29
Hyponatremia 146 Intermittent claudication 63
Hashimoto’s thyroiditis 237
Hypoparathyroidism 240 Intervertebral disc prolapse 335
Haversian canal 320
Hypothyroidism 241 Iodophors 397
Head injuries 358
Hypovolemia 115 Isotope lymphoscintigraphy 102
Head injuries, complications 362
Heberden’s nodes 170
Hemangioma, capillary 82 I J
Hemangioma, cavernous 83 Immobilization 324 Jejunostomy 151
Hemangioma, strawberry 83 Immunohistochemistry 185
Hemangiosarcoma 191 Immunosuppression 377 K
Hemophilia 122, 123 Immunotherapy 378
Kang cancer 195
Hemorrhage 123 Induction 409
Kaposi’s sarcoma 191
Hemorrhage, classification 123 Infant feeding tube 389
Kehr’s T tube 389
Hemorrhage, effects 125 Infection, deep palmar space 166
Keloid 4
Hemorrhage, pathophysiology 124 Infection, HIV 38
Keratoacanthoma 194
Hemorrhage, reactionary 123 Infection, hospital acquired 35
Kernohan’s notch effect 360
Heparin 98 Infection, mid palmar space 166
Khangri cancer 195
Heparin antagonist 99 Infection, nosocomial 35
Knee, Clergyman’s 54
Hernia 441 Infection, opportunistic 36
Knee, housemaid’s 54
Hernia hiatus 312 Infection, terminal pulp space 165
Knots, types 393
Hernia, definition 441 Infections hand 163
Kyphosis 334
Hernia, etiology 441 Infections, webspaces 165
Hernia, pathology 441 Ingrowing toe nail 171
Hernia, rolling 313 Inguinal canal surgical L
Hernioplasty 444 anatomy 443 Laboratory values 415
Hexachlorophane 395 Inguinal hernia, examination 438 Laryngectomy 284
Hibernoma 43 Inhalation burns 136 Laryngocele 207
Hormone therapy 377 Injection sclerotherapy 95 Larynx, benign tumors 282
Hot-air oven 394 Injuries, blast 177 Larynx, malignant tumors 281
Hudson brace with perforator and Injuries, bullet 176 Larynx, papilloma 281
burr 390 Injuries, hand 168 Lasers in surgery 399
Humby’s knife 139 Injuries, neck 176 Leiomyosarcoma 190
Hunter’s ligation 87 Injuries, peripheral nerve 153 Leprosy 29
Index 453
Leucoplakia 261 Mayo’s towel clip 380 Noma 262
Lipodermatosclerosis 97, 98 Median mental sinus 8 Non-chromaffin paraganglioma
Lipoma 43 Medulloblastoma 369 211
Liposarcoma 190 Meggitt’s classification 81 Nutrition 149
Lower esophageal sphincter 308 Melanoma 200 Nutrition, enteral 150
Lucid interval 363 Melanoma, acral lentiginous 201 Nutrition, home parenteral 152
Ludwig’s angina 18, 209 Melanoma, amelanotic 201 Nutrition, total parenteral 151
Lugol’s iodine 231 Melanoma, lentigo maligna 200
Lupus vulgaris 15 Melanoma, nodular 200 O
Lymph nodes in neck, secondaries Melanoma, superficial
Obesity 152
213 spreading 200
Odontogenic tumors 298
Lymph nodes in neck, Melanoma, treatment 202
Odontomes 297
secondaries, with an occult Melon seed bodies 168
Oligodendrogliomas 369
primary 216 Meningiomas 369
Omentoplasty 72
Lymph nodes neck, levels 213 Methimazole 231
Onychocryptosis 171
Lymphadenitis, tuberculous 110 Microsclerotherapy 95
Open reduction 324
Lymphedema, classification Minor salivary gland tumors 257
Operation Kondolean’s 105
101, 102 Mixed salivary tumor 252
Operation sistrunk 105
Lymphangioma, cavernous 208 MODS 115, 119
Operation Thompson’s 105
Lymphatics of head and neck, MODS 24
Operation, Belsey–Mark 4 312
anatomy 204 Molluscum sebaceum 194
Operation, Charle’s 105
Lymphoma Hodgkin’s 106 Monoclonal antibodies 378
Operation, Cockett and Dodd 96
Lymphoma Non-Hodgkin’s 109 MRI 404
Operation, commando 218
Lymphoma, Burkitt’s 110 Muir and Burclay regime 134
Operation, Fowler’s 172
Lymphoma, REAL Multiple chondroma 337
Operation, Heller’s 310
classification 106 Multiple exostoses 332
Operation, Homan’s 105
Lymphomas 106 Multiple myeloma 339
Operation, Patterson 266
Lysol 395 Muscle relaxants 407
Operation, Trendelenburg 95
Myer’s stripper 95
Operation, Wardill-Kilner push
M Myer’s vein stripper 390
back 295
Myositis ossificans 323
Macroglossia 272 Operation, Zadik’s 172
Madura foot 31 Oral anticoagulant 99
Magill’s forceps 409 N Oral cavity, examination 446
Magnetic resonance imaging 404 Nasoethmoid complex Oral cavity, premalignant
Malignant edema 27 fracture 342, 344 conditions 262
Malignant hyperthermia 409 Neck dissection, bilateral 217 Oral submucosal fibrosis 262
Malignant lymphoma of Neck dissection, modified Orphan Annie eye nuclei 234
Africa 110 radical 217 Orrhinger’s transhiatal
Malignant neurilemmoma 191 Necrosis 64 esophagectomy 317
Malignant salivary tumors, Necrotizing faciitis 36 Orthopentomogram 296
management 256 Needle holder 384 Osteitis fibrosa cystica 243
Mandible, dislocation 356 Neoplasm 181 Osteoarthrosis 333
Mandible, fracture of Neoplasm of lip 268 Osteochondroma 337
the ramus 353 Nerve suturing 154 Osteoclastoma 337
Mandible, fracture of the Neurilemmoma 52 Osteogenesis imperfecta 331
symphysis 354 Neurofibroma 51 Osteoma 336
Maxillofacial injuries, Neuroma 50 Osteomalacia 331
complications 357 Nevi 199 Osteomyelitis, acute 328
Maxillofacial injuries, Nissen’s fundoplication 310, 312 Osteomyelitis, chronic 329
primary care 341 Nodule, dominant 225 Osteoporosis 331
Osteosarcoma 338 Problems in radiotherapy 375 Rhinophyma 195
Osteotomy 328 Proctoscope 391 Rickets 330
Oxygen 407 Profundaplasty 70 Roentgen unit 374
Oxygen therapy 119 Propranolol 231 Rule of nine 130
Propylthiouracil 231 Ryle’s tube 388
P Psammoma bodies 369
Pulmonary capillary wedge S
Paget’s disease, bone 330
pressure 118
Paget’s, recurrent fibroid of 53 SAG-M blood 127
Punctum 49
Palate, diseases 296 Salivary calculus 248
Pyemia 24
Palatoplasty 295 Salivary gland, examination 446
Pyogenic abscess 19
Palsy, saturday night 159 Salivary gland,
Pyogenic granuloma 11, 24
Palsy, tourniquet 159 submandibular 246
Pyrosis 311
Papillary carcinoma 234 Salivary neoplasms 252
Papilloma 44 Salmon patch 82
Paralysis, Erb-Duchenne 155 Q Saphenous neuralgia 96
Paralysis, Klumpke’s 155 Quinsy 288 Sarcoma, TNM staging 188
Parathyroid, anatomy 242 Sarcomas 186
Parathyroidectomy 244 R Savlon 395
Parkland regime 133 Schwannoma 370
Rabies 32
Paronychia, acute 164 Scissors 389
RAD 374
Paronychia, chronic 164 Scoliosis 334
Radial nerve lesions 158
Parotid gland, anatomy 246 Scurvy 331
Radiation absorbed dose 374
Parotidectomy 259 Secondaries in bone 338
Radioactive iodine 233
Parotidectomy, complications 259 Secondary lymphedema 102
Radioiodine therapy 232
PCWP 118 Secondary suturing 4
Radiotherapy 374
Perforator veins 89 Seldinger technique 67
Radiotherapy sources 374
Pharyngeal pouch 206 Septicemia 24
Rains factor 125
Pharyngitis, acute 290 Sequestrum 64, 329
Ram’s horn penis 104
Phenol 395 Shock 113
Ranula 260
Phlegmasia alba dolens 90 Shock, anaphylactic 116
Raynaud’s disease 61
Phlegmasia cerulea dolens 90 Shock, causes 113
Raynaud’s phenomenon 61
Plantar fasciitis 171 Shock, effects 115
Raynaud’s syndrome 61
Plaster of Paris 324 Shock, pathophysiology 114
Reconstruction and
Pleomorphic adenoma 252 Shock, septic 116
transplantation 138
Policeman’s heel 171 Sialadenitis 248
Reduction of fracture 324
POP 324 Sialectasis 250
Rest pain 64
Port-wine stain 83 Sialography 248
Retractor, Czerny’s 383
Postoperative care 409 Sialosis 250
Retractor, Deaver’s 383
Postoperative patient, Sign Coleman’s 353
Retractor, Doyen’s 383
monitoring 410 Sign Panda 345
Retractor, Joll’s thyroid 385
Potato nose 194 Sign, Branhan’s 86
Pott’s puffy tumor 23 Retractor, Langenbeck’s 383 Sign, Cowen’s 228
Preauricular sinus 296 Retractor, Morris 383 Sign, Dalrymple’s 227
Pregangrene 64 Retractor, self retaining 383 Sign, Enroth 228
Premedication 409 Retractor, single hook 382 Sign, Froment’s 157
Preoperative assessment 406 Retractor, Volkmann’s 382 Sign, Gifford’s 228
Pressure sore 13 Reversal 409 Sign, Homan’s 90
Pretibial myxedema 229 Reversal agents 408 Sign, Jellinek’s 228
Primary suturing 4 Rhabdomyosarcoma 190 Sign, Joffroy’s 228
Pringle maneuver 180 Rheumatoid arthritis 333 Sign, Kanavel 167
Index 455
Sign, Knie’s 228 Syndrome, auriculotemporal 258 Test, Perthe’s 93
Sign, Kocher’s 228 Syndrome, Boerhaave’s 315 Test, Pratt’s 93
Sign, Loewi’s 228 Syndrome, carpal tunnel 156 Test, Schwartz 93
Sign, Moebius 228 Syndrome, central cord 176 Test, three tourniquet 93
Sign, Mose’s 90 Syndrome, compartment 73 Tetanus 25
Sign, Nafziger’s 228 Syndrome, DiGeorge’s 242 Tetany 245
Sign, Nicoladoni’s 86 Syndrome, disappearing pulse 65 Thoracic outlet syndrome 58
Sign, Rosenbach’s 228 Syndrome, Frey’s 258 Thoracic outlet, anatomy 57
Sign, Stellwag’s 227 Syndrome, Horner’s 214 Thrombectomy 70
Sign, Stemmer’s 104 Syndrome, hungry bone 245 Thrombophlebitis 98
Sign, Tinel’s 154 Syndrome, Kasabach-Merritt 83 Thrombus, fixed 90
Sign, von Graefe’s 227 Syndrome, Klippel-Trenauny- Thrombus, free 90
Sinus 6 Weber 83 Thyrocardiac 233
SIRS 115, 118 Syndrome, Mallory-Weiss 314 Thyroglossal cyst 221
Skin adnexal tumors 193 Syndrome, MEA 245 Thyroglossal fistula 222
Skin tumors, classification 193 Syndrome, MEN 245 Thyroid acropachy 229
Skin, premalignant conditions 195 Syndrome, Mendelson’s 409 Thyroid function tests 230, 233
Slough 64 Syndrome, paraneoplastic 183 Thyroid gland, examination 432
Soft tissue sarcoma, clinical Syndrome, Patterson-Kelly 314 Thyroid neoplasm 234
features 187 Syndrome, Pierre-Robin 301 Thyroid steal 239
Soft tissue tumors 186 Syndrome, Plummer-Vinson 314 Thyroid storm 240
Sources of radiotherapy 374 Syndrome, Sturge-Weber 83 Thyroid, agenesis 223
Spina bifida 372 Syndrome, subclavian steal 62 Thyroid, anaplastic carcinoma 236
Spina ventosa 170 Syndrome, Treacher-Collins 296 Thyroid, anatomy 219
Spondylolisthesis 335 Syndrome, Wermer’s 245 Thyroid, congenital
Spongioblastoma polare 369 Synovial sarcoma 191 anomalies 221
Spread of malignant tumors 183 Syphilis 30 Thyroid, development 219
Squamous cell carcinoma 195 Thyroid, ectopic 221
Staging laparotomy 108 T Thyroid, follicular carcinoma 235
Stensen’s duct 246 Thyroid, lateral aberrant 223
TAO 68
Sterilization 394 Thyroid, lingual 221
Tear cancer 197
Subarachnoid hemorrhage 366 Thyroid, malignant
Tendon 160
Subdural hematoma 364 lymphoma 237
Tendon graft 161
Subdural hematoma, chronic 364 Thyroid, medullary
Tendon healing 161
Subfascial ligation 96 carcinoma 236
Tendon repair 161
Surgery, history 413 Tendon suturing, Goldner Thyroid, solitary nodule 225
Surgical needles 384 method 161 Thyroidectomy 238
Surgical wounds, classification 2 Tendon suturing, Thyroidectomy,
Suture materials 391 Kessler method 161 complications 239
Suturing, types 393 Tendon transfer 161 Thyroiditis Dequervain’s 238
Swelling, examination 418 Tendonitis 332 Thyroiditis Riedel’s 238
Swellings 43 Test, Adson’s 60, 65 Thyrotoxic crisis 240
Sympathectomy, cervical 62 Test, Allen’s 66 Thyrotoxicosis 226
Sympathectomy, chemical 71 Test, Brodie-Trendelenburg 93 Tongue, benign tumors 272
Sympathectomy, lumbar 71 Test, Buerger’s postural 65 Tongue, carcinoma 272
Syndactyly 170 Test, elevated arm stress 66 Tongue, lymphatic drainage 271
Syndrome Brown-Séquard 176 Test, Fegan’s 94 Tongue, spread of carcinoma 273
Syndrome Maffucci 83 Test, Halsted 66 Tongue, treatment of
Syndrome Sjögren’s 251 Test, modified Perthe’s 93 carcinoma 274
Syndrome, abdominal Test, Morrissey’s cough Tonsilitis, acute 287
compartment 180 impulse 93 Tonsillectomy 288
Tonsillectomy, hemorrhage 289 Tumor, glomus 49 Varicose veins, examination 428
Tonsillitis, chronic 287 Tumor, potato 211 Varicose veins, familial 92
Tonsils, anatomy 286 Tumor, Pott’s puffy 366 Varicosities, primary 92
Torticollis 212 Tumor, sternomastoid 212 Varicosities, secondary 92
Touhy needle 412 Tumor, Warthin’s 254 Veins of lower limb, anatomy 88
Tourniquets 128 Tumors pituitary 371 Venography 94
Toxic nodule 229 Tumors, intracranial 369 Venous blood flow in lower limb,
Toxic thyroid, children 232 Tumors, jaw 296 physiology of 89
Toxic thyroid, pregnancy 232 Tumors, maxillary 277
Tracheooesophageal fistula 315 Venous ulcers, complications 98
Tumors, submandibular salivary
Tracheostomy 302 Verrucous carcinoma 196
gland 256
Tracheostomy care 304 Virchow’s triad 89
Tracheostomy tube, U Volkmann’s scoop 390
Fuller’s bivalved 302 Von Recklinghausen’s disease 52
Ulcer classification 9
Tracheostomy tube, Ulcer decubitus 13
Jackson’s 302 W
Ulcer diabetic 14
Tracheostomy tubes 302, 386
Ulcer edges 9 Wallace’s rule 130
Tracheostomy, complications 304
Ulcer Meleney’s 14 Warfarin sodium 100
Tracheostomy, functions 304
Ulcer, Barrett’s 312 Water intoxication 146
Tracheostomy, technique 303
Ulcer, chilblains 15
Transplantation 141 Water loss 145
Ulcer, clinical examination 15
Transplantation, bone marrow 143 Wen 48
Ulcer, cryopathic 10
Transplantation, liver 143 Wharton’s duct 246
Transplantation, renal 142 Ulcer, definition, parts 8
Ulcer, frostbite 15 White cell trapping theory 91
Treatment of middle third Wound debridement 3
area 348 Ulcer, hypertensive 10
Ulcer, investigation, treatment 11 Wound healing 3
Triage 173
Ulcer, management 12 Wound healing types 3
Triage algorithm 173
Trigeminal neuralgia 160 Ulcer, Marjolin’s 196, 197 Wound healing, factors
Trotter’s triad 277 Ulcer, Martorell’s 10 affecting 2
True cysts 46 Ulcer, Rodent 197 Wounds, classification 1
Tuberculosis 28 Ulcer, trophic 12 Wounds, definition 1
Tuberculous lymphadenitis, Ulcer, venous 97 Wounds, management 3
staging 110 Ulnar paradox 158 Wry neck 212
Tubulodermoids 47 Ultrasound 401
Tumor markers 185 Z
Tumor, acinic cell 255 V
Tumor, carotid body 211 Varicose veins 91 Zygomatic complex
Tumor, desmoid 53 Varicose veins, complications 97 fracture 342, 345

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SRB’s Surgery for

Sriram Bhat M MS (General Surgery)

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

SRB’s Surgery for Dental Students

© 2008, Jaypee Brothers Medical Publishers

First Edition: 2008

Dr. V Surendra Shetty

1. Wounds, Sinus Fistula and Ulcer ................................................................................................ 1

Factors Affecting Wound Healing

Primary suturing means suturing the wound CRUSH SYNDROME

Sites: Common over sternum (Figs 1.2 and 1.3A).

Differential diagnosis: Hypertrophic scar.

Differences between keloid and hypertrophic scar (Fig. 1.4)

surrounding tissues. Sinus sprouts outside and

FISTULA (FIG. 1.6)

Fig. 1.5: Sinus Fig. 1.6: Fistula

• Raised indurated edge, indurated base, non- TREATMENT

INVESTIGATIONS (FIG. 1.7)

Commitment is what transforms a promise into reality.

Different discharges in a sinus/fistula

Fig. 1.9: Median mental sinus. Note the origin of the

teeth forming root abscess, which eventually

PARTS OF AN ULCER (FIG. 1.10)

Margin: It may be regular or irregular. It may be

Different edges are (Fig. 1.11)—

Base: Base is the one where ulcer rests. It may

Let our advance worrying become advance thinking and planning.

Every exit is an entry somewhere else.

DIABETIC ULCER (FIG. 1.18)

Fig. 2.2: Incision for draining—Ludwig’s angina

Fig. 2.3: Lymphangitis of the leg.

Sites Modes of Infection

Differences between cellulitis and pyogenic abscess

..Success is the ability to go from failure to failure without losing enthusiasm.

Differential Diagnosis for an Abscess

POTT’S PUFFY TUMOR

..Learning patience takes a lot of patience!

PYOGENIC GRANULOMA SEPTICEMIA

Differential Diagnosis Treatment

Perfection is the best excuse.

..Positive attitudes create a chain of positive thoughts.

Thorax: Lungs and pleura get infected by direct Treatment

..Positive attitudes create positive people.

Fig. 2.13: Madura foot. Note the multiple sinuses Investigations

..Praise loudly and blame softly.

..Not in time, place and circumstance, but in man lies success...

HIV INFECTION AND AIDS • Blood transfusions, organ transplantations.

HIV completely suppresses immune res- • CNS lymphomas.

Tumors in HIV Infection

..Problems are only opportunities in work clothes.

..Prosperity begins with the state of mind.

 Lipoma • It can be diffuse or localized.

..Pursue one great decisive aim with force and determination.

Fig. 3.2: Pedunculated lipoma

Fig. 3.4: Pedunculated papilloma

Fig. 3.6: Papilloma tongue. Note: papilloma can also occur

..Real leaders are ordinary people with extraordinary determination.

CYSTS • Distention cyst: Lymph cyst, ovarian cyst,

..Money is like manure, if you spread it around it does a lot of good.