Navaidot Internal Medicine
Navaidot Internal Medicine
Navaidot Internal Medicine
• Diseases
• Medication
• Laboratory
Ngam Punlork
2. Emergency problems…………………………………….
5. Hematology ………………………………………………..
6. Immunology …………………………………………........
7. Cardiology …………………………………………………
12. Dermatology………………………………………….........
14. Rheumatology………………………………………….......
23. Toxicology…………………………………………………..
25. Laboratory……………………………………………………
Preface
I am NGAM PUNLORK. I studied and finished successful at University of Health
Science, Diploma in Nurse 2003 and Diploma in Medical Doctor 2010, other Diploma
in Child Health 2011, Diploma in Economy 2012, Diploma in Development
Management and Diploma in English Language 2012. I have worked in health
system more than ten years as national hospital, international organizations, and
companies.
NAVAIDOT INTERNAL MEDICINE-my personal book was not audited, it only edited
throughout my experiences and information update from the other books. First edition
in 2007 described pediatric, geriatric, surgery, and gynecology obstetric. As new
research and clinical experience broaden knowledge, changes in treatment and drug
therapy are required.
I hope that NAVAIDOT INTERNAL MEDICINE will be a useful resource for medical
students and junior residents in medicine.
NGAM PUNLORK, MD
The Intergumentary System/Skin
________________________________________
Hair
Sweat pore
Stratum corneum
Epidermis
Sebaceous gland
Dermis
Receptor for
touch(Corpuscule) Sweat gland
Hypodermis
(Subcutaneous)
Hair follicle
Adipose tissue
Nucleus
Dendrites
Axon
Cell body
Schwann cell
nucleus
Axon
Receptor
The neuron
PNS CNS
Mix nerve
V Trigeminal
V1 Ophalmic Sensory from cornea, skin General sensation from
of upper 1/3 of face, skin of face
superior nasal mucosa.
V2 Maxillary Sensory from middle 1/3 of General sensation from
face, teeth and gums, skin of face
jaw, lateral-inferior nasal.
V3 Mandibular Sensory from lower 1/3 of General sensation from
face, teeth, mouth and skin of face
tongue.
Motor to mastication Chewing of food
VII Facial nerve Sensory from taste buds. Test
Motor to facial muscle, Movement of face,
lacrimal gland, salivary secretion of saliva and
gland tears
IX Glossopharyngeal Sensory from pharyngeal Taste, muscle sense
muscle and taste buds.
Motor to pharyngeal Swallowing
muscles and salivary Secretion of saliva
glands
X Vagus Sensory from viscera, Taste , vomiting ,
taste peristalsis
Motor to viscera Visceral muscles and
glands
• None
Corpus callosum
Cerebrum
Lateral ventricle
Third ventricle
Cerebellum
Pons varolii
Fourth ventricle
Medulla
oblongata
Thalamus Spinal cord
Parotid gland
Teeth
Pharynx
Tongue
Esophagus
Sublingual gland
Submandibular gland
Liver Stomach
Spleen
Gallblade
r Pancreas
Duodenum
Transverse colon Small intestine
Ascending colon
Descending colon
Cecum and appendix Rectum
The organs of the digestive system
Serosa
(Peritoneum)
Cardiac orifice
Muscularis
Longitudinal
Circular
Lesser curvature
Oblique
Submucosa
Pyloric sphincter (Submucous layer)
Greater curvature
Duodenum Pyloric
antrum
Divisions of intestine
Small intestine Large intestine
Duodenum : C-shaped, 4-segments, Colon : 1-1.5m-long, 400-800mL-water
25cm-long, from pyloric to jejunum, absorption.
there are common bile duct and Cecum : First portion, a dilated pouch,
pancreatic duct. appendix 13-15cm-long and 5cm-
Jejunum : Middle section of small diameter.
intestine, 3-3.5m-long. Ascending colon : Right colon
Ileum : Joins the cecum of the large Transverse colon : Upper peritoneal
intestine at the ileocecal valve. 3m- cavity.
longe. Descending colon : Left colon
Sigmoid colon : S-shaped
Rectum : Terminal portion
Intestinal Enzymes
Enzyme Function
Peptidase Converts protein in amino acids
Sucrase ( Maltase and lactase) Converts disaccharides in to
monosaccharides
Lipase Converts fats into fatty acids and glycerol
Amylase Converts starch and glycogen into
disaccharides
Nuclease Converts nucleic acid into nucleotides
Enterokinase Activates trypsin secreted from the
pancreas
Oral Cavity
Teeth
• First teeth are primary teeth about 20 and it will fall out during 4-5 years of age
• Permanent teeth 32, four types : 8 incisors, 4 canines, 8 premolars, 12 molars.
Tongue : Moves food around mouth during mastication, assists in swallowing, speech
sound, location of taste buds.
Salivary glands : 3 glands
• Parotid gland : Over the master muscle
• Submandibular gland : Inferior to the base of the tongue
• Sublingual gland : Under the tongue
Palate : Hard palate anterior and soft palate posterior, the uvular is suspended from
the soft
Accessory Organs
Liver Gall bladder Pancreas
Anatomy : 8 segments Anatomy : Pouchlike Anatomy : Inferior to the
- Right and left, separated organ attached to inferior stomach, Pancreatic islets
by the falciform ligament surface of the liver. (islets of Langerhans)
- Caudate lobe is near - Gall bladder : 10cm-long Function
inferior vena cava and 5cm-wide. - Exocrine secretions
- Quadrate lobe : - Common bile duct : (Alkaline pH 8)
Gallbladder 7.5cm-long, 6mm-diameter . Peptidase : Convert
- Crosses by portal vein Function protein into amino acids
- Weigh : 1200g (2% of - Stores and concentrates . Lipase : Convert fats
body) - Store bile about 60 mL into fatty acid and
Function and excreted about 500- glycerol
- Synthesis, storage and 1000 mL per day. . Amylase : Convert
release of vitamin A, D, - Bile product by liver, glycogen into
E, and K, glycogen, when the small disaccharides
iron. intestine is empty, - Endocrine secretions
- Phagocyte, removal bile is forced up the . Glugagon : Secreted
toxic and production of cystic duct to the by alpha cells,
bile salt. gallbladder for storage increased blood
- Breaks down the by hepatic duct glucose.
nucleoprotein of worn- - When eating, bile to the . Insulin : Secreted by
out cells of the body duodenum by bile duct. beta cells, decreased
from uric acid which is blood glucose.
excreted in the urine. . Somatostatin :
Secreted by delta cells,
cartilage and collage
formation.
Hepatic duct
Body and tail
Cystic duct of pancreas
Superior mesenteric
Theiliary and pancreatic tract artery and vein
11
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Blood component
Whole blood (Total blood)
• Plasma 50-60%
- Water 90%
- Solutes10% (Protein7% and electrolyte, urea, glucose 3%)
• Formed elements
- Erythrocyte : 3.8-5.5 million / mm3
- Platelets : 150-400 000 / mm3
- Leukocytes 4 000-10 000 / mm3 (Netrophils, Monocytes, Eosinophils,
Basophils, Lymphocyts )
HEMOCYTOBLAST
(Stem cell)
Proerythrocyte Myeloblast
Megakaryocyte
Normoblast
Granulocytes
Erythrocytes
Neutrophil
Reticulocyte
s
Basophil
Normoblasts
Bands cell
Eosinophil
Thrombocytes Stem Cell
(Platelets)
Natural killer cell
Monocyte
B cell
T cell
Lymphoblast
Lymphatic system
Lymphatic vessels : Lymph flows into right and left subclavian vein, the right
lymphatic duct which drains lymph from the upper right quadrant of the body, and the
large thorax duct .
Lymph nodes : Produce lymphocytes and macrophages, some principal groups are
popliteal, inguinal, lumbar, cubital, axillary, cervical, and mesenteric nodes
Lymphoid organs : Tonsils, palatine, lingual, spleen, thymus
Cell-Mediated Immunity
T lymphocytes : Produce cell-mediated immunity by thymus, there are 3 types
• T-cells Memory : Remain inactive until future exposure to same antigen.
• T-cells Killer : Release cytokines and lysis antigen, tumor or foreign cells.
• T-cells Helper : Help to activate other T or B cells.
B lymphocytes : Produce antibody-mediated immunity, and specific antibodies from
clones of daughter cells
• B-cells Memory : Turn in plasma cell upon a later exposure to same antigen.
• Plasma cells : Produce specific antibodies (Immunoglobulins)
Immunoglobulin (Ig)
Name Location Functions
IgG Blood • Crosses the placenta to provide passive
Extracellular fluid immunity for newborns
• Provides long-term immunity following
recovery or a vaccine
IgA External secretions • Present in breast milk to provide passive
(tears, saliva, etc.) immunity for breast-fed infants
• Found in secretions of all mucous
membranes
IgM Blood • Produced first by the maturing immune
system of infants
• Produced first during an infection (IgG
production follows)
• Part of the ABO blood group
IgD B lymphocytes • Receptors on B lymphocytes
IgE Mast cel ls or basophils • Important in allergic reactions (Mast cells
release histamine)
Antibody-Mediated Immunity
• Active-mediated immunity : Post-immunization
• Passive immunity : Result of the of antibodies from one person to another,
post infection or transfer across the placenta
Immunization
Heart Valves
Atrioventricular valves (AV valves)
• Tricuspid valve : Between the right atrium and the right ventricle
• Bicuspid valve : Between the left atrium and left ventricle
Semilunar valves
• Pulmonary semilunar valve : Between the right ventricle and pulmonary truct
• Aortic semilunar valve : Between the left ventricle and ascending aorta
Function of vessels
Vessel Structure Function
Artery • Strong elastic • Distributive channel to
take blood from the heart vessel, contain all body tissues, blood
three tunics, lumen carried under high
diameter large pressure.
relative to wall
thickness.
Vein • Thin, distensible • Serves as fluid
take blood into the heart vessel consisting of reservoir, constricts in
three tunics, lumen response to
diameter very large. sympathetic
• Valves present stimulation.
• Valves ensure unidi-
rectional blood flow.
Capillary • Wall composed of • Allow exchange of
exchange area of the system single layer of endo- fluid, nutrients, and
• Arteriole : Small artery thelium (Tunica gases between the
• Venules : Small veins interna), smooth blood and the
mus-cle cuff at its interstitial fluid.
origin regulates flow.
Cardiac Cycle
• Cardiac Output (CO) : Stroke volume (SV) x Heart rate (HR)
• Increased cardiac output
- Sympathetic stimulation of heart (Increased heart rate)
- Increased end-diastolic volume (Increased blood volume)
- Various forms of anemia that result in decreased total peripheral resistant
• Diastolic : The atria and ventricle relaxation, AV valves are open and
semilunar valves are closed. Blood flows from atria into ventricle.
• Systolic : Ventricle contraction, AV valves are close and semilunar valves are
opened. Volume of blood ejected from either ventricle into aorta and
pulmonary artery.
- Stroke volume ejected from either ventricle about 70-90 mL
- Right ventricle exceeds the diastolic pressure in the pulmonary artery 10
mmHg
- Left ventricle exceeds the diastolic pressure in the aorta 80 mmHg
- Under normal resting conditions, the pressure reaches 25 mmHg on the right
side and 120 mmHg on the left side.
Cardiac Circulation
The two pathway of circulation
• Systemic circulation (Major circulation)
• Pulmonary circulation (Minor circulation)
Pulmonary circulation
• The right ventricle pumps blood into the pulmonary artery (or trunk), which
divides into the right and left pulmonary arteries, one going to each lung.
Within the lungs each artery branches extensively into smaller arteries and
arterioles, then to capillaries. The pulmonary artery with blood carbon dioxide
carries.
• The pulmonary capillaries surround the alveoli of the lungs; it is here that
exchanges of oxygen and carbon dioxide take place. The capillaries unite to
form venules, which merge into veins, and finally into the two pulmonary veins
from each lung that return blood to the left atrium. The pulmonary vein return
with oxygen carries.
Systemic circulation
• The left ventricle pump blood in the aorta, the large artery of the body with
oxygen carries. We will return to the aorta and its branches in a moment, but
first we will summarize the rest of systemic circulation. The branches of the
aorta take blood into arterioles and capillary networks throughout the body.
Capillaries merge to form venules and veins.
• The veins from the lower body take blood to the inferior vena cava veins from
the upper body take blood to the superior vena cava. These two caval veins
return blood to the right atrium with carbon dioxide carries.
Aorta
The aorta is a continuous vessel, but for the sake of precise description it is divided
into sections that are named anatomically: ascending aorta, aortic arch, thoracic
aorta, and abdominal aorta.
• The ascending aorta is the first inch that emerges from the top of the left
ventricle. The two branches : the right and left coronary arteries, which supply
blood to the myocardium.
• The aortic arch curves posteriorly over the heart and turns down ward. The
three branches into carotid and subclavian arteries (Brachiocephalic).
• The thoracic aorta continues down through the chest cavity and through the
diaphragm.
• Below the level of the diaphragm, the abdominal aorta continues to the level of
the 4th lumbar vertebra, where it divides into the two common iliac arteries.
Along its course, the aorta has many branches through which blood travels to
specific organs and parts of the body.
The body circulation
The Muscular System
______________________________________
Deltoid
Rhomboideus major
Teres major
Latissimus dorsi
External oblique
Gluteus maximus
Deltoid Deltoid
Pectoralis
major Teres
Corachobrachialis Triceps
Biceps
Brachioradialis
Gluteal
Sartorius muscles
Rectus femeris
Hamstring
muscles
Vastus
lateralis
medialis
Pathology
Neuromuscular disorder
Some bacteria cause disease by producing toxins. A neurotoxin is a chemical
that in some way disrupts the normal functioning of the nervous system. Because
skeletal muscle contraction depends on nerve impulses, the serious
consequences for the individual may be seen in the muscular system.
Tetanus
• Tetanus is characterized by the inability of muscles to relax. The toxin
produced by the tetanus bacteria (Clostridium tetani) affects the nervous
system in such a way that muscle fibers receive too many impulses, and
muscles go into spasms.
• Symptom : Lockjaw (Trismus), dysphagia, neck stiffness, opisthotonos,
central contraction but peripheral flaccid, photophobia, phonophobia.
• Treatment requires the antitoxin (SAT or TIG) to neutralize the toxin. In
untreated tetanus the cause of death is spasm of the respiratory muscles.
Botulism
• Botulism is usually a type of food poisoning, but it is not characterized by
typical food poisoning symptoms such as diarrhea or vomiting. The
neurotoxin produced by the botulism bacteria (Clostridium botulinum)
prevents the release of acetylcholine at neuromuscular junctions. Without
acetylcholine, muscle fibers cannot contract, and muscles become
paralyzed.
• Symptoms of botulism include : Diplopia, dry mouth, dysphagia, dilated
pupils, digestive symptoms.
• Treatment with the antitoxin (The specific antibody to this toxin), botulism
is fatal because of paralysis of the respiratory muscles.
Myasthenia gravis
Myasthenia gravis
• Myasthenia gravis is an autoimmune disorder characterized by extreme
muscle fatigue even after minimal exertion. Women are affected more
often than are men. Cause by acetylcholine receptor antibody and block of
neuromuscular
• Symptom : Ptosis, diplosia, dysphagia, facial weakness and arthralgia
• Treatment of myasthenia gravis may involve anticholinesterase (Neo-
stigmin) and corticoid or azathioprim. If severe form should be
thymectomy.
The Skeletal System
________________________________________
Structure and function of bone
The skeletal system consist of bones, cartilage, and joints. The functions of the
skeletal system fall into five categories.
1. Support
2. Protection
3. Movement
4. Hemopoiesis
5. Mineral and energy storage
Bone formation
• Osteogenic cells are progenitor cells that give rise to all bones cells
• Osteoblasts are the principle bone building cells, they synthesize the
collagenous fibers and bone matrix and promote mineralization during
ossification.
• Osteoclasts are bone dystroying cells that contain lysosomes and phagocytic
vacuoles thal demineralize bone tissue.
Classification of bones
• Long bones : The bones of the arms, legs, hands, and feet (but not the wrists
and ankles). The shaft of a long bone is the diaphysis, and the ends are called
epiphyses. Although red bone marrow is present in the epiphyses of children’s
bones, it is largely replaced by yellow bone marrow in adult bones.
• Short bones : The bones of the wrists and ankles.
• Flat bones : The ribs, shoulder blades, hip bones, and cranial bones.
• Irregular bones : The vertebrae and facial bones.
The bones of skeleton are divided into two groups
• The axial skeleton : Skull, vertebral column, ribs and sternum.
• The appendicular skeleton : Shoulder girdle, upper and low limbs, pelvic girdle
Proximal epiphysis
Diaphysis
Bone marrow
Marrow (Medullary) cavity
Compact bone
Spongy bone
Parietal bone
Frontal bone
Temperal bone
Lacrimal bone
Sphenoid bone
Lambdoidal suture Zygomatic bone
Squamous suture
Maxilla bone
Mastoid process
Coronal suture Condyloid process
Styloid process
Mandibula nocth
Mandible
Coronoid process
Sinuses
• Sinuses are lighten the bones of the face and cranium. They are all in
communication with upper air passages and are lined with ciliated mucous
membrane. There are maxillary, ethmoid, sphenoid and frontal sinuses.
• Function
- Air warmed
- Secretion drainage
- To give resonance to the voice
Face bone
The are 13 bones which from the skeleton of the face but for completeness, the
frontal bone which has already been described should be added
• 2 zygomatic or cheek bones
• 1 maxilla (Originated as 2)
• 2 nasal bones
• 2 lacrimal bones
• 1 vomer
• 2 palatine bones (L-shaped)
• 2 inferior conchae or turbinated bones
• 1 mandible
Hyoid bone
This is an isolated horse-shoe-shaped bone lying in the soft tissue of the neck just
about the larynx and below the mandible. it doesn’t articulate with any other bone but
is attached to the styloid process of the temporal bone by ligaments. It gives
attachment to the base of tongue.
Frontal bone
Sphenoid
Temporal bone
Ethmoid
Nasal bone
Zygomatic bone Vomer
Mandible bone
Vertebral column
The vertebral column supports and permits movement of the head and trunk and
provides a site for muscle attachment. The vertebrae also support and protect the
spinal cord and permit the passage of spinal nerves. There are
• 7 cervical vertebrae
• 12 thoracic
• 5 lumbar
• 4 to 5 sacral fused into 1 sacrum
• 4 to 5 small coccygeal vertebrae fused into 1 coccyx
• The seven cervical vertebrae are those within the neck. The first vertebra is
called the atlas, which articulates with the occipital bone to support the skull
and forms a pivot joint with the odontoid process of the axis, the second
cervical vertebra. This pivot joint allows us to turn our heads from side to side.
The remaining five cervical vertebrae do not have individual names.
• The thoracic vertebrae articulate (Form joints) with the ribs on the posterior
side of the trunk. The lumbar vertebrae, the largest and strongest bones of
the spine, are found in the small of the back. The sacrum permits the
articulation of the two hip bones : the sacroiliac joints. The coccyx is the
remnant of tail vertebrae, and some muscles of the perineum (Pelvic floor) are
anchored to it.
• The lumbar vertebrae are the largest and the vertebral foramina are the
smallest. The spinous processes are the short, flat-sided and project back.
• The sacrum, There are five vertebrae fused to form a wedge-shaped bone
with a concave anterior surface. The upper part attached with the fifth lumbar
vertebra. On each side it articulates with the ilium to form a sacroiliac joint,
The first sacrum into the pelvic cavity is called the promontory.
• The coccyx , The are 4 to 5 terminal vertebrae fused and very small
triangular bone the broad base of which articulates with the tip of the sacrum.
7 Cervical
vertebrae Odontoid process
of axia
Atlas
12 Thoracic
vertebrae Axis
Spine of axis
Body of
7th thoracic Pedicle
5 Lumbar
vertebrae Transver
process
Spinous
Sacrum Faces for ribs process
articulation
Coccyx
1st lumbar
7th cervical
vertebral
Ribs Manubrium
of sternum
Costal Body of
cartilages sternum
Xiphoid process
of sternum
Appendicular skeleton
Shoulder girdle, Each shoulder girdle consists of the following bones
• 1 clavicle or collar bone is a long bone which attached sternum to acromial
process
• 1 scapula or shoulder blade is a flat triangular-shaped bone which lies on the
posterior chest wall . It is described as having : 3 borders, 3 angles, 3 fossae
Upper limb, Each shoulder girdle consists of the following bones
• 1 humerus
• 1 radius
• 1 ulna
• 8 carpal bones
• 5 metacarpal bones
• 14 phalanges
Acromial end
Acromial process
Sternum end
Coracoid process
Clavicle
Humerus
Scapula
Radius Ulna
8 carpal bones
- Lunate
- Triquetrum
- Pisiform 5 metacarpal bones
- Hamate
- Scapoid 14 phalange bones
- Trapezum
- Trapezoid
- Capitate
The right shoulder girdle and upper limb
Pelvic girdle
The pelvic girdle is formed by two ossa coxae united anteriorly by the symphysis
pubic. It is attached posteriorly to the sacrum of the vertebral column at the
sacroiliac joint. Each os coxae (Hipbone) :
• Ilium
• Ischium
• Pubis
Sacroiliac joint
Pubic symphysis The bones of the pelvis
Iliac crest
Ilium
Pelvis
Sacrum
Coccy Acetabulum
x Pubis
Ischium Obturator
foramen
Lower limb
The lower extremity is divided into the thigh and the leg. The femur is the only bone
of the thigh. The kneecap (Patella) is the sesamoid bone (Tendon) of the anterior
knee region. The tibia and fibula are the bone of the leg. The distal end of the tibia
articulates with the talus in the ankle.
Tarsal or angle bones
There are seven tarsal bones which from the posterior part of the foot. They are :
• 1 talus
• 1 calcaneus
• 1 navicular
• 3 cuneiform
• 1 cuboid
Pelvis
Head of femur
Obturator Greater trochanter
foramen Lesser trochanter
Surgical
Neck
Femur
Patella
Tibia Fibula
Navicular
3 cuneiform
Talus
Calcaneus
Cuboid
14 phalanges
5 metatarsal
Articulation
Articulations or joints, may be classified according to structure or function. In the
structural classification, a joint is fibrous, cartilaginous, or synovial. The function
classification distinguishes synarthroses (Immovable joints), amphiarthroses (Slightly
movable joints), and diarthroses (Freely movable joints)
Fracture of bone
A fracture means that a bone has been broken. Pathologic (Spontaneous) a bone
breaks without apparent trauma, may accompany bone disorders such as
osteoporosis. There are different types of fractures classified as to extent of damage.
• Simple (Closed fracture), the broken parts are still in normal anatomic
position; surrounding tissue damage is minimal (skin is not pierced).
• Compound (Open fracture), the broken end of a bone has been moved, and
it pierces the skin; there may be extensive damage to surrounding blood
vessels, nerves, and muscles.
• Greenstick, the bone splits longitudinally. The bones of children contain more
collagen than do adult bones and tend to splinter rather than break
completely.
• Comminuted, two or more intersecting breaks create several bone fragments.
• Impacted, the broken ends of a bone are forced into one another; many bone
fragments may be created.
The Repair Process
• Fragments of dead or damaged bone must first be removed.
• The repair process is usually relatively rapid, and a simple fracture often heals
within 6 weeks. Some parts of bones, however, have a poor blood supply, and
repair of fractures takes longer.
• Other factors that influence repair include the age of the person, general state
of health and nutrition.
Herniated Disc
• The terms herniated disc or ruptured disc more accurately describe what
happens. The nucleus pulposus is forced out, often posteriorly, where it puts
pressure on a spinal nerve. For this reason a herniated disc may be very
painful or impair function in the muscles supplied by the nerve.
• Healing of a herniated disc may occur naturally if the damage is not severe
and the person rests and avoids activities that would further compress the
disc.
• Surgery may be required, however, to remove the portion of the nucleus
pulposus that is out of place and disrupting nerve functioning.
34
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Aorta
Rib
Inferior vena cava
Right adrenal gland
Left kidney
Distal tubule
Collecting tubule
Artery
Nephron
Adrenal glands
Adrenal cortex
• Glucocorticoids (Corticosterone and cortisol) :
- Regulation of carbohydrate and lipid metabolism, breakdown of proteins
- Inhibited inflammatory responses
- Help the body resistance with stress
- Vasoconstriction
• Mineralocorticoids (Deoxycorticosterone and aldosterone) : Regulate
concentration of extracellular electrolytes, especially sodium and potassium.
Aldosterone secretion controlled by the renin-angiotesin system, plasma
potassium concentration, and ACTH.
Adrenal medulla
• Amine hormones (Epinephrine and norepinephrine) : Release stimulated
by sympathetic stimulation. Increases release of ACTH and TSH from the
adenohypophysis.
Decreased blood pressure Stimulates juxtaglomerular Angiotensin
or dehydration of kidney to secrete renin (Plasma protein)
Erythroporietin
Anemia is one of the most debilitating consequences of renal failure, one that
hemodialysis can not reverse. Diseased kidneys stop producing erythropoietin, a
natural stimulus for RBC production. Erythropoietin can be produced by genetic
engineering and is available for hemodialysis patients. In the past, their anemia could
only be treated with transfusions, which exposed these patients to possible
immunologic complications of repeated exposure to donated blood or to viral
diseases. The synthetic erythropoietin eliminates such risks. Others who benefit from
this medication are cancer patients and AIDS patients with severe anemia.
Contents of urine
Blood Daily filtration Actual excretion
Salts 700 g 15 g
Glucose 170 g 0
Urea 50 g 30 g
Urine
• Daily output 1200 to 1500 mL
• 95 % water, 5 % salts & organic matter
• Urea, uric acid, salts of potassium, magnesium and calcium
Endocrinology
________________________________________
Pituitary gland
Anatomy and physiology
• On the inferior side of the brain
• 2 divided lobes
- Anterior lobe : Adenohypophysis
- Posterior lobe : Neurohypophysis
Anterior lobe (Antero-hypophysis) secreted by the adenohypophysis
• Human growth hormone (HGH) : Targets the bones and soft tissue.
Action : Stimulating amino acid, synthesis of tRNA, increased the number of
ribosomes.
• Thyroid stimulating hormone (TSH) : Targets the thyroid gland. Stimulates
synthesis and release of thyroid hormones.
• Adrenocorticotropic hormone (ACTH) : Targets the adrenal cortex.
Stimulates and secretion of glucocorticoids.
• Prolactin (PRL) : Targets the mammary glands. Promotes development of
mammary glands , production of milk.
• Follicle stimulating hormone (FSH) : Targets the ovaries and testes.
Stimulates growth of ovarian follicles and spermatogenesis.
• Luteinizing hormone (ADH) : Targets the ovaries and testes. Stimulates
maturation of follicles, estrogen and progesterone in females. Secreted
testosterone in males.
Posterior lobe (Post-hypophysis) secreted by the neurohypophysis
• Antidiuretic hormone (ADH) : Targets the kidney collecting duct. Release
stimulated when dehydration or increased plasma osmolarity.
• Oxytocin : Targets the uterus and mammary glands. Secretion of milk and
uterus contraction during delivery.
Adrenal glands
Adrenal cortex
• Glucocorticoids (Corticosterone and cortisol) :
- Regulation of carbohydrate and lipid metabolism, breakdown of proteins
- Inhibited inflammatory responses
- Help the body resistance with stress
- Vasoconstriction
• Mineralocorticoids (Deoxycorticosterone and aldosterone) : Regulate
concentration of extracellular electrolytes, especially sodium and potassium.
Aldosterone secretion controlled by the renin-angiotesin system, plasma
potassium concentration, and ACTH.
Adrenal medulla
• Amine hormones (Epinephrine and norepinephrine) : Release stimulated
by sympathetic stimulation. Increases release of ACTH and TSH from the
adenohypophysis.
Decreased blood pressure Stimulates juxtaglomerular Angiotensin
or dehydration of kidney to secrete renin (Plasma protein)
Thyroid gland
Anatomy : Located in the neck on either side of the thyroid cartilage at the top of the
trachea
Physiology : Secreted of triodothyronine (T3) and tetraiodotyrosine (T4 or
Thyroxine) are secreted under the stimulation of TSH from the pituitary.
• The hormone accelerate metabolic rate
• Oxygen consumption
• Glucose absorption
• Increased body temperature
• Body growth and development
Parathyroid glands
Anatomy : Small glands and posterior surface of the thyroid gland, 4-glands.
Physiology : Secreted of Parathyroid hormone (PTH) : Increased plasma calcium l
• Osteoclasts : Break down bone tissue, release calcium from the bones into the
blood
• Increased calcium reabsorption by kidney
• Absorption calcium from GI tyract
• Increased synthesis of 1/25-dihydroxycholecalferol
Pancreatic hormone
• Glugagon : Secreted by alpha cells, increased blood glucose.
• Insulin : Secreted by beta cells, decreased blood glucose.
• Somatostatin : Secreted by delta cells, cartilage and collage formation.
Respiration
• Respiratory means ventilation or breast, all cells require a continuous supply
of oxygen and must continuously eliminate a metabolic waste product, carbon
dioxide.
• The organs of the respiratory systems are
- The nose
- The pharynx
- The larynx
- The trachea
- Two bronchi (Bronchus)
- The bronchioles
- Alveoli
Sinus frontal
Sphenoid bone
Nasal bone
Nasopharynx
Nasal cavity Soft palate and
Maxilla uvula
Palatine tonsil
Hard palate
Epiglottis
Tongue
Laryngopharynx
Mandible
bone Esophagus
Hyoid bone
Epiglottis
Thyroid
Epiglottis
gland
Thyroid
cartilage
Vocal cords
Trachea
Cricoid
cartilage
cartilage
Pulmonary
capillaries
Nose Alveolar duct
Pharynx
Alveolar
Epiglottis
Larynx
Venous
Trachea
R-bronchus
L-bronchus
Middle lobe
Mediastinum
space
Lower lobe
Heart space
Diaphragm
Sternum
Lung
Diaphragm
Inhalation Exhalation
The Reproductive System
________________________________________
Sex determination
XX = Female, all ova produced contain a single X chromosome
XY = Male, equal number of X and Y spermatozoa are produced
Sex of offspring determined by whether the fertilizing spermatozoa is X-bearing or Y-
bearing.
Peritoneum
Urinary
bladder
Sacrum
Deferent
ducts Rectum
Testicular artery
Spermatic cord
Vein
Nerve
Deferent duct
Head of epididymis
Rete testis
Septum of testis
Epididyme
Convoluted
seminiferous
tubular
Tunica vasculosa
Tunica albuginea
Tunica vaginalis
Muscle
Midsagittal section of portion of a testis
46
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Uterine
tube Ovary
Peritoneum
Uterus
Ureter
Symphysis pubic Cervix
Urinary
bladder Rectum
Clitoris
Vagina
Urethra
Body of uterus
Ovary Endometrium
Myometrium
Broad
ligament Cervix of uterus
Skin
Areola
Pectoralis major
muscle
Nipple
Lactiferous
duct Intercostal muscles
Lactiferous
glands
Menstrual Cycle
The menstrual cycle includes the activity of the hormones of the ovaries and
anterior pituitary gland and the resultant changes in the ovaries (Ovarian cycle) and
uterus (Uterine cycle). These are all incorporated into, which may look complicated at
first, but refer to it as you read the following. Notice first the four hormones involved:
FSH and LH from the anterior pituitary gland, estrogen from the ovarian follicle, and
progesterone from the corpus luteum. The fluctuations of these hormones are shown
as they would occur in an average 28-day cycle. A cycle may be described in terms
of three phases: menstrual phase, follicular phase, and luteal phase
• Menstrual phase, may last 2 to 8 days (Menstrual flow 4 days), secretion of
FSH is increasing, and several begin to develop. The loss of the functional
layer of the endometrium is called menstruation or the menses.
• Follicular phase (Proliferative phase 10 days)
LRH stimulates secretion of follicle-stimulating hormone (FSH) and Luteinizing
hormone (LH), which stimulates follicle development in the ovaries. The
secretion of LH is also increasing, but more slowly. FSH and estrogen
promote the growth and maturation of the ovum, and estrogen stimulates the
growth of blood vessels in the endometrium to regenerate the functional layer.
• Luteal phase (Secretory phase 14 days)
- After ovulation, the corpus luteum secretes progesterone and estrogen,
which act to level off the endometrium and ready it for implantation.
- As progesterone secretion increases, LH secretion decreases, and if the
ovum is not fertilized, the secretion of progesterone also begins to
decrease. Without progesterone, the endometrium cannot be maintained
and begins to slough off in menstruation. FSH secretion begins to increase
(as estrogen and progesterone decrease), and the cycle begins again
(Ischemic phase of the menstrual cycle)
Embryo-Fetus Growth
Month of Organs development Size in inches
Gestation
(end)
1 • Heart begins to beat; limb buds, backbone 0.25
forms, facial features, not distinct
2 • Calcification of bones begins, fingers and 1.25–1.5
toes are apparent on limbs; facial features
more distinct; body systems are
established
3 • Facial features distinct but eyes are still 3
closed, nails develop on fingers and toes,
ossification of skeleton continues, fetus is
distinguishable as male or female
4 • Head still quite large in proportion to body, 5–7
but the arms and legs lengthen, hair
appears on head, body systems continue
to develop
5 • Skeletal muscles become active 10–12
(“Quickening” may be felt by the mother),
body grows more rapidly than head, body
is covered with fine hair (lanugo)
6 • Eyelashes and eyebrows form, eyelids 11–14
open, skin is quite wrinkled, pulmonary
surfactant is first produced
7 • Head and body approach normal infant 13–17
proportions, deposition of subcutaneous
fat makes skin less wrinkled
8 • Testes of male fetus descend into 16–18
scrotum; more subcutaneous fat is
deposited, production of pulmonary
surfactant is sufficient to permit breathing
if birth is premature
9 • Lanugo is shed, nails are fully developed, 19–21
cranial bones are ossified with fontanels
present; lungs are more mature
Apgas Score
The Apgar score is an overall assessment of an infant and is usually made 1 minute
after birth (may be repeated at 5 minutes if the first score is low). The highest
possible score is 10. Infants who score less than 5 require immediate medical
attention.
Score 0 1 2
Respiratory No respiratory Weak cry Strong cry
effort
Heart rate No < 100 > 100
Muscle tone No response Some motoin Spontaneous action
Stimulation of No response Grimace in Cry in response
sole the foot response
Color Central cyanosis Peripheral cyanosis Pink color
Grunting No Minimal Obvious
Air entry Good Decreased Very poor
LH
FSH FSH
1 4 14 28
Antidote
ANTIDOTE INDICATION DOSE
______________________________________
ADVANTAGE
• Rehydration
• Resuscitation of shock
- Hypovolemic shock
- Septic shock
- Anaphylactic shock
• Drug-intravenously route
• Child sickness
DISADVANTAGE
• Fluid overload
• Acute pulmonary edema
• Cerebral edema
• Heart failure risk of edema
SURVEILLANCE
• Urine (Normal : 0.5-1mL /kg/h)
• Lung sound auscultation
• Cardiac function (JVD, increased central vein pressure)
• Apparent : Face or lower extremity edema
Clinical signs of fluid overload
• Lung : Dyspnea and crackle sound
• Edema : Face or lower extremity
• Cause : Heart failure or anuria
DOSAGE
• Oral route
• IV route (IV Fluid : Infusion : PIV)
• 1 mL = 1 cc = 20 drops = 60 droplets
VOLUME EXPANDERS
Cristalloids Duration Volume Indications Advantag Disadvantage
Lactate 1 to 2 hs 3 times the -Hypovolemia -Isotonic -Rapidly
NSS 0.9% estimated -Dehydration -Fluid overload
Colloids 2 to 3 hs 1-1.5 times -Hypovolemia -Good -Allergy
Polygeline Estimate expansion -Expensive
Gelufexil fluid loss
Dextran 40 3 to 4 hs Expansion -Hypovolemia -Good -Anaphylactic
of volume expansion -Renal failure
Emergency Problems 61
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Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Increase body temperature that upper normal limit (N : 36.5-37.5 ˚C)
• Febrile or pyrexia or hyperthermia
• Characteristic
- Moderate fever 38.3 ˚C
- Elevate fever > 39 ˚C
- Severe hyperthermia > 40.5 ˚C
ETIOLOGY
• Hyperthermia : Viral or bacterial infection, other infectious diseases
• Metabolic trouble : Hyperthyroidism
• Dehydration : Severe dehydration, hypovolemia
• Drugs allergy : Penicillin, sulfonamide, anticholinergic
• Systemic inflammation : Rheumatic fever, SLE, IBD
• Hematology : Hemolytic anemia, leukemia, sickle cell disease
• Neoplasm : Lymphomas, leukemia, hepatoma, metastatic carcinomas
PATHOPHYSIOLOGY
• Fever is caused by increased prostaglandin E2 (PGE2) synthesis in the
hypothalamus.
• Autonomic discharge from hypothalamus raises core temperature
through shivering and dermal vasoconstriction.
• Both exogenous and endogenous factors can raise the body's set
thermoregulatory point :
- Endogenous factors include IL-1 and IL-6, tumor necrosis factor,
and IFN.
- Exogenous factors include endotoxin (lipopolysaccharide) and
other toxins and metabolites produced by infectious organisms.
PARACLINIC
• Complex blood count, CRP, ESR
• Electrolyte, glycemia, calcemia ,TSH, T3, T4 test
• Hemoculture, urinalysis, uroculture, puncture lumbar
CLASSIFICATION OF FEVER
• Acute fever < 7 days
• Persistent fever 7-14 days
• Chronic fever > 14 days
DIFFERENTIAL DIAGNOSIS
• Fever of unknown origin ( FUO ): Defined as fever > 38.3 °C for at
least 3 weeks as an outpatient and 3 days of inpatient evaluation or
three outpatient visits without determining etiology.
62 Emergency Problems
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•Fever with infections
- Bacterial infections ( Media otitis, urinary tract infections, respiratory
infections, meningitis, septicemia )
- Infectious diseases (Malaria, typhoid fever, shigella, clostridium
difficile, dengue infection)
- Viral infections (Rotavirus, Herpes simplex, Dengue, HIV)
• Fever with localizing signs
- Fever with change position (Septic arthritis, osteomyelitis,
appendicitis)
- Fever with neurological (Meningitis, convulsion, brain abscess)
- Fever with digestives (Diarrhea, abdominal pain, constipation,
appendicitis, pancreatitis, gall stone, bowel obstruction)
• Fever with hematology
- Leukemia, aplastic anemia, thalassemia
- Immune response : Post transfusion hemolytic, anemia hemolytic
auto-immune,HUS, ITP.
• Fever with chronic diseases : TB, neoplasm, HIV, rheumatology
COMPLICATION
• Convulsion with fever ( Convulsion febrile or convulsion hyperthermic )
- Convulsion febrile physiologic : Durant < 15mn, in children 1-
years, most common ENT infection, but without sign of neurologic.
- Convulsion febrile pathologic : Durant > 20mn, in children < 9
months, with sing of neurologic.
• Dehydration
• Neurological disorder
MANAGEMENT
1. Admission Criteria Infants
• All toxic patients
• Infants 0-28days of age with temperature >38 °C
• Nontoxic infants 28-90days of age with temperature >38°C
• Poor compliance or follow-up
2. Treatment in children and adult
• High fever ( T > 39 ˚C or > 102.2 F )
- Paracetamol® 15mg/kg/dose PO, IM or Intra-rectal
or NSAIDs : Aspirin®, Ibuprofen®
• Fever with convulsion ( Convulsion febrile )
- Diazepam 0.5-1mg/kg/dose intra-rectal, may be repeted for 2 doses
- Paracetamol® 15mg/kg/dose IM, repeated 15mg/kg/dose every 6 h
• Supportive care
- For children put out of clothes
- Coolness compress
- Increased fluid by oral or intravenous if necessary
• Treat underlying disorders
References
Hospital care for children (WHO)
Rosen and Barkin’s 5 minute medicine
Emergency problem 63
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Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Seizure is collection of cerebral neurons excessive active abnormality
• Convulsion due febrile seizure or afebrile seizure
• Febrile seizures less 15mn in development mentally normal but more
than 15mn risk consequent of epilepsy or meningitis or other
neurological disease.
ETIOLOGY
• Hyperthermia : Acute pharyngitis, acute tonsillitis
• Infections : Meningitis, encephalitis, brain abscess, septicemia
• Intoxications
- Lead poisoning
- Drugs : Opiates, cocaine, aspirin, theophylline, metoclopramide
- Drug withdrawal : Diazepam®
• Metabolic disorder
- Hypoglycemia < 45mg/dL ( < 2.2mmoL/L )
- Hyponatremia < 135 mmoL/L, hypernatremia > 145mmoL/L
- Hypocalcemia < 2.2mmoL/L, hypomagnesemia < 0.8mmoL/L
• Neurological disorder
- Epilepsy ( Recurrent seizure )
- Cerebral tumor, hypertension intracranial, Stoke
• Head trauma ( Hematoma )
CLINICAL SIGNS
• History of seizure
- Benign or recurrent seizure
- Onset, frequency, time of seizure
• Any factors
- Family history of seizure
- Congenital malformation
- Head trauma or CNS infection
• Any evidence of progressive intracranial lesion
- Headache, vomiting, leathagy, somnolent, visual disorder, mental
status change
• Physical examination and vital signs : Neurologic signs finding
• Common childhood infections :
- Upper respiratory illnesses
- Otitis media
- Roseola
- Gastrointestinal infections
- Shigella gastroenteritis
64 Emergency problem
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CHARACTERISTIC
Generalized tonic-clonic seizure most common :
• Tonic phase:
- Muscular rigidity
- Apnea and incontinence
- Self-limited and last only a few minutes
• Other seizure types:
- Staring with stiffness
- Limpness
- Jerking movements without prior stiffening
PARACLINIC
• CBC, CRP, electrolyte , glycemia
• Lumbar puncture CSF gram stein or culture
• CT scan and EEG
MANGEMENT
1. Admission Criteria in children
• Intensive care unit : Active status epilepticus, intubated, or persistent
mental status changes.
• Inpatient unit:
- Status epilepticus resolved in the ED
- Underlying cause of seizure not resolved or controlled
- Intracranial hemorrhage
- Meningitis/Encephalitis
- Mass lesion, drug, toxin ingestions
2. Admission Criteria in adult
• Patients with status epilepticus should be admitted to the intensive
care unit.
• Patients with seizures secondary to underlying disease (e.g.,
meningitis, intracranial lesion) must be admitted for appropriate
treatment and monitoring.
• Patients with poorly controlled repetitive seizures should be admitted
for monitoring.
• Delirium tremens
3. Treatment
• Basic assessment of resuscitation : ABCDE
• Control of seizure : Diazepam 0.5mg/kg intrarectal , may be
repeated after10mn for 2doses
• Control hyperthermia : Paracetamole 10-15mg/kg IM, compress cold
• Monitoring to follow up vital signs and oxygen
• Treat underlying disorders
4. Drugs
• Lorazepam : 0.1mg/kg IV per dose (Max. 10 mg)
• Paraldehyde : 0.3-0.5mL/kg (Peds: 0.3mL/kg PR 1:2 in mineral oil)
• Phenobarbital : 15-20mg/kg IV at rate of 1mg/kg/min
• Phenytoin: 15-20mg/kg IV (Peds : use rate of 0.5-1.0 mg/kg/min)
References
Handbook of pediatric
Rosen and Barkin’s 5-minute medicine
Emergency problem 65
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Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
_____________________________________
DEFINITION
• Shock is hypoperfusion and circulatory collapse
• Shock is delayed progression due compensate of multiple organs
reversible.
• Shock may be hemodynamic measurements depend upon causes
• Shock may be damage any all tissue and organ systems in body
ETIOLOGY
• Hypovolemic : Dehydration, hemorrhage, burn
• Ischemic heart disese, sepsis
• Distributive of brain, cardiac, CNS
• Miscellaneous : Denal failure , hepatic failure
CLASSIFICATION
• Hypovolemic shock
• Distributive shock ( Vascular shock )
- Anaphylactic shock
- Neurologic shock
- Painful shock
- Septic shock
• Cardiogenic shock : Obstructive shock
DIAGNOSTRIC
• Depend upon history
- Dehydration, hemorrhage, sepsis, trauma, drug-anaphylaxis,
heart disease, renal or hepatic failure
• Clinical signs
- Oliguria, sweaty skin with pallor, altered mental status, cyanosis,
somnolence, capillary time refill retarded
• Physical exam
- Hypothermia, tachycardia, hypotension, tachypnea
• Vital signs : Temperature, RR, Pulse, BP, Saturation evaluation
CLINICAL SIGNS
• Generalized shock : Hypotension, decreased peripheral pulses,
tachycardia, tachypnea, decreased urine output, diaphoresis,
obtundation, lethargy.
• Hypovolemic shock : Cold and clammy extremities, pallor, flattened
neck veins, decreased capillary refill, narrowed pulse pressure
• Cardiogenic shock : Chest pain/pressure, dyspnea, orthopnea, JVD,
cool, clammy, sweaty extremities, pales, wheezes, dullness at lung.
66 Emergency problem
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• Septic shock : Warm flushed extremities, strong pulses, hyperthermia,
hypothermia, purpura or petechial rash
• Anaphylactic shock : Warm flushed extremities, urticaria, stridor,
throat tightness, hoarseness, wheezing
• Neurogenic shock : Flaccid paralysis, loss of rectal tone, hypotension
with bradycardia.
PARACLINIC
• CBC, CRP, electrolyte, glycemia, calcemia
• Creatinine, BUN, transaminase
• ABG : Acid-base status
• Urinalysis, urine culture, blood culture
• Imagery : Chest radiography, ECG
MANAGEMENT
1. Admission Criteria
• All patients in shock need to be admitte
• All patients with persisting shock need ICU monitoring.
• Patients with shock definitively reversed may be admitted to non-ICU
setting (e.g., tension pneumothorax that has been decompressed and
chest tube placed).
2. Treatment
• Resuscitation ABCDE
• Correct cause of shock
- Hypovolemic with NSS 20mL/kg body weight Bolus
- Sepsis with broad spectrum antibiotic
- Correct of hemorrhage
• Correct of cardiovascular
- Dopamine or epinephrine
- Corticotherapy
• Correct of electrolyte and metabolic acidosis : Sodium bicarbonate
• Dextrose 10 % : 5mL/kg for hypoglycemia, intravenous
• Treat underlying disorder
3. Drugs
• Albuterol : 2.5mg/2.5 cc nebulizer PRN
• Bicarbonate sodium 8.4% : 1mL/kg/dose infusion
• Calcium gluconate 10% : 1mL/kg/dose IVL
• Cimetidine : 300mg IV
• Dopaminergic : 1-3µg/kg/min IV
• Epinephrine :
- Infusion 1-4µg/min IV
- SQ/IM (1 :1000) : 0.1-0.3mg repeat q5min-20min to 3 PRN
- IV (1 :10,000) : 10mL (1mg) over 10min IV
• Glucagon : 1-5 mg IV bolus initial, then 1-20mg/h infusion
• Hydrocortisone : 5-10mg/kg IV
• Naloxone : 0.05-0.1mg/kg IV initial, titrate to effect
References
Pediatric emergency medicine (McGraw-Hill)
Urgences Reanimation Transfusion (Masson)
Rosen and Barkin’s 5-minute medicine
Emergency problem 67
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______________________________________
DEFINITION
• Dysfunction of the reticular activating system in the brainstem or
bilateral cerebral dysfunction.
•Coma is defined as a state of lost consciousness not respond to
- Ordinary verbal
- Sensory
- Physical stimuli
ETIOLOGY
• Traumatism
• Intoxication
- Salicylic : Hyperventilation, seizure, dehydration, ↑serum salicylate
- Hypoglycemia : Sweating, headache, seizure, BS < 45mg/dL
- Barbiturates : Hypoventilation, hypotension, myosis
- Hyperglycemia in diabetes mellitus ( Ketoacidosis )
- Opiots
• Electrolyte disorder : Hypernatremia, hyponatremia, hypocalcemia
•CNS infections : Meningitis, encephalitis, encephalopathy, epilepsy .
•Reye syndrome : Hypercapnia, pupils dilated, seizure, increased
serum ammoniac.
• Hypertension (Renal, coartation of aorta) : Increased brachial BP and
decreased femoral BP.
• Lead poisoning : Vomiting, abdominal pain, seizure
• Hemolytic uremic syndrome : Anemia, bruising, oliguria or anuria,
elevated BUN .
• Coma post seizure : Pupils dilated, Barbinski +, rapid return of
consciousness .
STAGES OF COMA
• Light coma : Responds to noxious stimuli
• Deep coma : Does not respond to pain
• Unresponsiveness
- Loss of either arousability or cognition
- Stupor : Deep sleep, although not unconsciousness
- Obtundation : Mental blunting with moderate reduction in alertness
- Delirium : Floridly abnormal mental status and motor restlessness
- Clouding of consciousness : Disturbance of consciousness
68 Emergency problem
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EVALUATION
1. Primary assessment for coma
• Urgent medication
- A : alert
- V : verbal response
- P : pain response
- U : unresponsive to pain
• Access adequate breathing ( Retraction, nasal flaring, grunting ,
cyaosis, tachpnea )
• Access adequate cardiovascular (Pulse volume, hypotension, pale,
cyanosis, capillary time refill, tachycardia, or bradycardia)
2. Secondary assessment for coma
• Glasgow coma scale (No urgent)
- Eye opening 4
- Verbal response 5
- Motor response 6
• EVALUATION
- GCS : 13-15 normal
- GCS : 9-12 pre-coma
- GCS < 8 coma
- GCS : 6-4 profound coma
- GCS : 3 dead
3. General physical examination and Vital signs
• Cerebral hemorrhage
• Cerebrovascular accident (Stroke)
• Head trauma
• Hepatic encephalopathy
• Meningitis
• Metabolic disorders : DKA, HHNC, myxedema, hyperglycemia
MANAGEMENT
1. Basic assessment of resuscitation : ABCDE
2. Coma Cocktail : DON’T in adolescent
• Dextrose 10% : 5mL/kg IV
• Oxygen
• Naloxone 0.05-0.1mg/kg/dose IV
• Thiamine 100 mg IVL
3. Treat underlying disorder
References
Rosen and Barkin’s 5-minute medicine
Emergency Problem 69
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______________________________________
DEFINITION
• Poisoning may be intentional or unintentional
• Intoxication
- Toxic ingestion : Clostridium botulism type A, B or E, food smoked
eating, fish poisoning (Ciguatera, Scombrotoxin, Paralytic
shellfish poisoning)
- Drug overdose or intravenous drug caused by black tar heroin
ETIOLOGY
1. Intentional :
• Depression
• Suicide
• Homicide
• Recreational drug abuse
2. Unintentional (accidental) :
• Common cause in children
• Therapeutic error (Double dose, overdose)
• Recreational drug experimentation
DIAGNOSIS
• Neurologic :
- Lethargy
- Agitation
- Coma
- Hallucinations
- Seizures
• Respiratory :
- Tachypnea/bradypnea/apnea
- Inability to protect airway
• Cardiovascular :
- Dysrhythmias
- Conduction blocks
• Vital signs :
- Varies depending on toxic substance
- Hyperthermia/hypothermia
- Tachycardia/bradycardia
- Hypertension/hypotension
70 Emergency Problem
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CLINICAL SIGNS
1. Food poisoning
• History food-smoked eating
• Onset 12-36 hours after ingestion of the toxins
• Sudden symptoms : Diplopia, Dry mouth, Dysphagia, Digestive trouble
(Vomiting, nausea, abdominal pain) and Dilated pupils fixed 50 %
• Sudden onset of cranial nerve paralysis and muscle weakness
• Muscle weakness progressing to respiratory paralysis
2. Selected Toxidromes
• Anticholinergic : Altered mental status, dry skin and mucous
membranes, fixed dilated pupils, tachycardia, hyperthermia, flushing,
urinary retention
• Cholinergic : Salivation, lacrimation, urination, diaphoresis, miosis,
bronchospasm and wheezing
• Opiate : CNS and respiratory depression, pinpoint pupils
• Sympathomimetic : CNS excitation, seizures, tachycardia,
hypertension, diaphoresis
PARACLINIC
• Complex blood count
• Stool test / culture
• Demonstration of toxin in blood or food
DIFFERENTIAL DIAGNOSIS
• Poliomyelitis
• Mayasthenia gravis
• Tick paralysis
• Guillain-Barré syndrome
MANAGEMENT
• Removal of unabsorbed toxin from gut (Gastric decontamination < 1h)
• Active charcoal per oral
- Adult : 30-100mg/day
- Enfant : 1-2g/day
• Specific antitoxin
• Rehydration and electrolyte
• Vigilant support, including attention to respiratory function
• Treatment by symptomatic (Atropine, cimetidine)
• Heroin poison or coma
- Dextrose 50% : 1mL/kg IVL
- Oxygen therapy
- Naloxone 0.05-0.1mg/kd/dose IV
- Thiamin 100 mg IV
References
Maladies infectieuses (E. PILLY)
Pediatric emergency medicine (McGraw-Hill)
Rosen and Barkin’s 5-minute medicine
Fluid and electrolyte 73
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Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Metabolic acidosis
- Decreased serum pH < 7.35
- Decreased serum HCO3
ETIOLOGY
• Most common in shock : Hypovolecmic shock, septic shock
• Diabetes ketoacidosis
• Other : Diarrhea with severe dehydration, diuretic, lactic acidosis, uremia,
renal tubular disease, pulmonary or liver diseases.
• Cause
- Gap acidosis (SLUMPED) : Salicylate, lactic, uremic, methanol,
paraldehyde, ethylene glycol, diabetes .
- Non-gap acidosis (2-RGD) :
2Renal : Renal tubular acidosis, renal failure
2GI : Enterocutaneous fistula, urine diversion to gastrointestinal tract
2Drugs : Ammonium chloride, acetazolamide
CLINICAL SIGNS
• History of severe disease
• Early hyperventilation , late hypoventilation
• Tachypnea or Kussmaul respirations with metabolic acidosis
• Tachycardia
• CO2 narcosis
• Conscious : Somnolence, confusion, lethargy, coma
PARACLINIC
• Hyperkalemia and hypercalcemia with severe metabolic acidosis
• Arterial blood gas (ABG) measurement
• pH < 7.35
• Calculate anion gap : Na – (Cl + HCO3)
- Anion gap < 15 : HCO3 loss : Diarrhea, renal tubular disease,
acetazolamide.
- Anion gap < 15 : H excess : Lactic acidosis , DKA , methanol ingestion
ethyleneglycol ingestion , salicylate intoxication.
- Anion gap >25 mEq/L is seen only with : Lactic acidosis, ketoacidosis
,toxin-associated acidosis.
MANAGEMENT
• Rehydrate with 0.9% normal saline if patient hypovolemic
• Sodium bicarbonate (NaHCO3 8.4%) : 1mL/kg intravenous
• Coma Cocktail : DON’T in adolescent :
Dextrose, oxygen, naloxone, and thiamine.
• Treat underlying disorder : Diabetic ketoacidosis, Lactic acidosis,
Alcohol ketoacidosis, Ingestion.
Reference
Current essentials of fluid and electrolyte (LANGE)
Rosen and Barkin’s 5-minute medicine
74 Fluid and electrolyte
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Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Defined as PaCO2 >45 mm Hg or higher than expected for calculated
respiratory compensation for metabolic acidosis
- Inadequate ventilation
- Carbon dioxide accumulation
ETIOLOGY
• Acute airway obstruct, aspiration, respiratory arrest, chronic respiratory
disease, pulmonary edema, respiratory failure
• Reduced pH owing to alveolar hypoventilation with elevated PaCO2
• Divided into three broad categories :
- Primary failure in central nervous system drive to ventilate : Sleep
apnea, anesthesia, sedative overdose
- Primary failure in transport of CO2 from alveolar space : Chronic
obstructive pulmonary disease, myasthenic crisis, severe hypokalemia,
Guillain-Barré syndrome
- Primary failure in transport of CO2 from tissue to alveoli : Severe heart
failure
CLINICAL SIGNS
• Respiratory distress
- Hypoventilation
- Cyanosis
• Neurologic signs : Headache, confusion, convulsion, somnolence, coma
PARACLINIC
• Respiratory acidosis :
- Acute: expected HCO3- increased by 1mEq/L for every 10mmHg
increase in PaCO2
- Chronic: expected HCO3- increased by 4mEq/L for every 10mmHg
increase in PaCO2
• Increased pCO2 > 45mmHg
• Decreased serum pH < 7.35
• HCO3 > 25 mmoL / L
MANAGEMENT
• Rehydrate with 0.9% normal saline if patient hypovolemic
• Intubation if necessary
• Chronic or rapid correction may lead to severe metabolic alkalosis
• Coma Cocktail : DON’T in adolescent :
Dextrose, oxygen, naloxone, and thiamine.
• Respiratory acidosis :
- Treat underlying disorder.
- Provide ventilatory support for worsening hypercapnia.
- Identify and correct aggravating factors (pneumonia) in chronic
hypercapnia.
References
Current essentials of fluid and electrolyte ( LANGE )
Rosen and Barkin’s 5-minute medicine
Fluid and electrolyte 75
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Increased serum pH > 7.45
• Increased serum HCO3
ETIOLOGY
• Most common acid-base distrucbance in surgery patients
• Pathogenesis involves of loss of H via nasogastric suction, volume
depletion, and hypokalemia.
• Mixed metabolic alkalosis with respiratory acidosis
• Loss of H+ :
- Gastrointestinal, vomiting, nasogastric suctioning, bulimia
- Antacid therapy
• Renal loss :
- Diuretics (loop and thiazide)
- Post-chronic hypercapnia
- Mineralocorticoid excess
- Hyperaldosteronism
• Bicabonate sodium infusion
• Milk-alkali syndrome
• Blood transfusions
CLINICAL SIGNS
• Bradypnea
• Sign of hypokalemia
- Decreased muscle contractility
- Decreased peristalsis
- Muscle clamp
- Paralysis
• Signs of hypocalcemia
- Paresthesia, carpopedal spam, positive Chvostek sign
- Numbness, tingling
PARACLINIC
• Elevated HCO3- with metabolic alkalosis
• Evaluate for hypokalemia and hypocalcemia.
• Diagnostic depend on ABG pH measurement
- pH > 7.45
- HCO3 > 25mmoL/L
- Urine chloride > 40mEq/L
MANAGEMENT
• Antiemetics for vomiting
• Proton pump inhibitors for patients with nasogastric (NG) suction
• Rehydrate with 0.9% saline for chloride-responsive alkalosis .
• Potassium chloride for chloride-responsive alkalosis in edematous states.
KCL : 20-120mEq PO daily
Reference
Current essentials of fluid and electrolyte (LANGE)
Rosen and Barkin’s 5-minute medicine
76 Fluid and electrolyte
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Acute hyperventilation lower Pco2
ETIOLOGY
• Septic shock
• Hyperchloremia acidosis
• Chronic respiratory disease, pulmonary embolus, liver disease
• Hyperthyroidism
• Drugs : Progesterone, Methylxanthines, Salicylates, Catecholamines
CLINICAL SIGNS
• Signs of hypocalcemia
- Paresthesia, carpopedal spam, positive Chvostek sign
- Numbness, tingling
- Tetany, seizure
- Arrhythmias
- Altered mental status
PARACLINIC
• Evaluate for hypocalcemia.
• Diagnostic depend on ABG pH measurement
- Decreased Pco2
- Increased plasma bicarbonate
- Increased serum pH > 7.35
1. Acute Respiratory Alkalosis
• HCO3- decreases secondary to intracellular shift and buffering within 20mn
• Expected HCO3- decreased by 2mEq/dL for each 10mmHg decrease
in PCO2
2. Chronic Respiratory Alkalosis
• HCO3- decreased secondary to renal secretion of HCO3- (48-72 hours)
• Expected HCO3- decreased by 5mEq/dL for each 10mmHg decrease
in PCO2
- If HCO3- greater than predicted, concomitant metabolic alkalosis
- If HCO3- less than predicted, concomitant metabolic acidosis
MANAGEMENT
• Respiratory alkalosis does not generally require treatment
• Treatment of chronic respiratory alkalosis may lead to metabolic acidosis
and hyperchloremia
• Dextrose 50% 1mL/kg/dose IVL
• Naloxone: 2mg (Peds : 0.1mg/kg) IV or IM initial dose
• Thiamine (vitamin B1) : 100mg (Peds: 50mg) IV or IM
• Calcium gluconate 10% : 1mL/kg/dose IVL
References
Current essentials of fluid and electrolyte (LANGE)
Rosen and Barkin’s 5-minute medicine
78 Fluid and electrolyte
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Elevated serum calcium > 11mg/dL (N : 8.8-10.2 mg/dL)
• Hypercalcemic crisis, usually >14mg/dL, associated with serious signs
• Calcium in bloodstream in three forms :
- Ionized : 45%
- Bound to protein (Primarily albumin) : 40%
- Bound to other anions : 15%
ETIOLOGY
• Primary hyperparathyroidism
• Malignancy : Cancer bone with metastases
• Miscellaneous
- Most common in patients with hyperparathyroidism
- Excess parathyroid hormone (PTH)
- Other : Vitamin D or calcium intake, prolonged thiazide diuretics,
addison disease, Milk-alkali syndrome.
CLINICAL SIGNS
• Neurologic
- Headache, fatigue, muscle weakness
- Depression, altered mental status, coma
• Renal
- Polydipsia, polyuria but anorexia
- Chronically : Nephrocalcinosis, interstitial nephritis
• Cardiovascular : Tachycardia, hypertension or hyotension
• Digestive : Anorexia, nausea, constipation and peptic ulcer, pancreatitis
• Dermatologic : Pruritus, ectopic calcification
• Pediatric Considerations
- Characteristic facies : Pug nose, fat nasal bridge
- Failure to thrive, slow development, hypotonia
- Mental retardation may ensue
PARACLINIC
• Diagnostic hypercalcemia with PTH >15% above normal
• Electrolyte, BUN, creatinine, glycemia for oliguric renal failure
• ECG :
- Shortening of QT interval
- Prolongation of PR interval
- QRS widening
- Sinus bradycardia, bundle branch block, AV block, cardiac arrest with
severe hypercalcemia (rare)
MANAGEMENT
• If severe ( Ca > 14mg/dL ), intravenous isotonic saline with furosemide
• Corticotherapy for sarcoidosis, vitamin D intoxication and Addison’s
• Plicamycine with metastases cancer
• Calcitonin for patient with renal failure or cardiopathy
Reference
Rosen and Barkin’s 5-minute medicine
Fluid and electrolyte 79
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• High serum potassium > 5.5mmoL/L (3.5 and 5.0 mmoL/L)
ETIOLOGY
1. Increased Potassium Distribution
• Extracellular space 2% (Speudohyperkalcemia)
- Severe hemolytic, thrombocytosis > 1 000 000/µL
- Severe trauma, burn
• Intracellular space : 98%
2. Decreased Potassium Excretion
• Renal 90% : Renal excretion of potassium affected by
- Distal renal tubular function, acute renal failure
- Acid-base balance
- Mineralocorticoids, addison’s disease, hypoaldosteronism
- Drugs : Drugs : Antialdosteron, NSAIDs, insulin
• GI 10% : Dietary intake, oral KCL
CLINICAL SIGNS
• History of acute renal failure
• Neuromuscular : Weakness which can progress to paralysis
• Respiration : Dyspnea owing to respiratory muscle weakness
• Cardiovascular : Palpitation, chest pain, dysrhythmia, syncope
PARACLINIC
• Electrolytes, BUN, creatinine, glucose :
- Elevated BUN, creatinine in renal failure
- Hyponatremia with mineralocorticoid deficiency
- Mild metabolic acidosis with type IV renal tubular acidosis
• Arterial blood gases : Assess acid-base status
• Hypocalcemia
• ECG : Heightened T waves or loss of P wave
MANAGEMENT
1. Mild hyperkalemia > 5.5mmoL/L
• Furosemide : 0.5mg/kg/day PO
• Calcium or sodium polystyrene sulfonate orally or by enema (PR)
• Avoid in patient bowel obstruction
2. Modered and severe hyperkalemia > 7mmoL/L
• Insulin 20 ui in dextrose 50% (100mL) IVL
• NaHCO3 : 1mEq/kg IVL or infusion
• Beta-Agonist : Inhaled albuterol
3. Hyperkalemia with ECG change
• Pulse weakness : Calcium gluconate 10% : 1mL/kg infusion
• Hydrocortisone : 2mg/kg IVL
• Dialysis for renal failure
Reference
Rosen and Barkin’s 5-minute medicine
80 Fluid and electrolyte
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• High serum magnesium > 2.5mEq/L (N : 1.5-2.5mEq /L)
ETIOLOGY
• Most common in patients with renal failure
• Hypokalemia
• Post-operation is rare
CLINICAL SIGNS
• History of chronic renal failure
• Neuromusular
- Weakness
- Decreased deep tendon reflex
- Lethargy
- Somnolence
• Severe hypermagnesemia
- Confusion
- Coma
- Death
PARACLINIC
• When serum magnesium reaches 6 mEq/L, risk deep tendon reflex lost
• Magnesium > 10mEq/L, risk somnolence, coma and death
• ECG :
- Widened QRS complex
- Depressed ST segment
- Peaked T waves
MANAGEMENT
• Intravenous isotonic saline to increase renal excretion
• Infusion of calcium chloride
• Dialysis my be necessary
• Monitoring electrocardiogram and serum magnesium
References
Current essentials of fluid and electrolyte (LANGE)
Rosen and Barkin’s 5-minute medicine
Fluid and electrolyte 81
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• High serum sodium > 145mEq/L
- Mild hypernatremia: serum sodium 146-155mEq/L
- Severe hypernatremia: serum sodium >155mEq/L
ETIOLOGY
• Pure water loss (Hypovolemic hypernatremia)
- Acute diarrhea (Loss of water > sodium)
- Dehydration of extravascular
- Diabetes insipidus
• Hypertonic sodium gain (Hypervolemic hypernatremia)
- Hypertonic sodium infusion or feeding solution
- Sodium bicarbonate therapy
- Sea water ingestion or drowning
- ACTH disorders : Primary hyperaldosteronism, Cushing syndrome
CLINICAL SIGNS
• History of
- Acute diarrhea
- Repeated vomiting
- Oliguria
• Severe hypernatremic dehydration
- Mental status : Seizure, lethargy to coma
- Cerebral edema, or hemorrhagic
• Hypervolemic hypernatremia
- Respiratory distress
- Peripheral edema
- Pulmonary edema
PARACLINIC
• Electrolytes, BUN/creatinine, glucose
• CBC
• Urinalysis :
- Urine/serum osmolality
- Urine Na
• Chest radiography :
- For infection/aspiration
- Pulmonary edema with hypervolemic hypernatremia
MANAGEMENT
• Water replacement with sodium restriction
• Hypervolemic hypernatrenia : Remove excess water with diuretics or
dialysis.
• Hypovolemic hypernatremia
- Replace volume contraction with 0.9% NS IV bolus
• For children with Diabetes Insipidus : Hormonal replacement therapy
- The drug of choice is desmopressin (DDAVP)
- Intranasal vaspressin
Reference
Rosen and Barkin’s 5-minute medicine
82 Fluid and electrolyte
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Depressed serum calcium < 8mg/dL (2mmoL/L)
ETIOLOGY
• Post thyroidectomy / parathyroidectomy
• In newborn : Premature, neonatal infection
• Vitamin D deficiency, prolonged administration of total parenteral nutrition
• Malabsorption, poor dietary intake (Severe malnutrition : MPC/MPE)
PATHOPHYSIOLOGY
• Calcium in bloodstream in three forms
- Ionized : 45%
- Bound to protein (Primarily albumin) : 40%
- Bound to complexing ions (Citrate, phosphate, carbonate) : 15%
• Serum levels of calcium are primarily controlled by three hormones
- Parathyroid hormone (PTH) : Decrease in calcium levels leads to an
increase in PTH secretion (Increasing bone resorption, renal
absorption, intestinal absorption, and urinary phosphate excretion).
- Vitamin D (1,25-dihydroxyvitamin D) : Decrease in calcium level
activates vitamin D (Increasing bone resorption and GI absorption).
- Calcitonin : Direct inhibition of bone resorption with increased Ca.
• Hypoalbuminemia is most common cause of hypocalcemia
PARACLINIC
• Diagnostic hypercalcemia with PTH > 15% above normal
• ECG : Prolonged QT interval
CLINICAL SIGNS
• Neuromuscular : Increased muscle contractility
- Hyperactive deep tendon reflexes
- Muscle-abdominal cramps
- Peripheral spasm (Carpopedal spam) and positive Chvostek sign
- Mental status : Headache, convulsions
• Cardiovascular
- Hypothermia , bradycardia , bradypnea
- Hypotension, dysrhythmia
• Pediatric Considerations
- Children have higher values of normal calcium (9.2-11mg/dL).
- Neonatal hypocalcemia: total serum calcium concentrations < 7mg/dL
or serum-ionized calcium levels < 4.4mg/dL
- Symptoms of hypocalcemia in infancy: Hyperactivity, tachypnea, apneic
MANAGEMENT
• Correct alkalosis respiratory if present
• Acute hypocalcemia with convulsion, give calcium gluconate 10% :
1mL/kg slow intravenously or in 500mL of D5% infusion
• Long-term treatment : Oral vitamin D, calcium, or sterogyl®
Reference
Rosen and Barkin’s 5-minute medicine
Fluid and electrolyte 83
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Depressed serum potassium < 3.5mEq /L (< 3.5mmoL/L)
- Mild to moderate 2.5-3.5mEq/L
- Moderate to severe < 2.5mEq/L
ETIOLOGY
• GI losses
- Severe dehydration (Acute diarrhea , repeated vomiting)
- Laxative abuse
- Alcoholism
- Prolonged NPO status
• Congenital disorders :
- Bartter and Gitelman syndromes with hypotension
- Liddle syndrome is the same but with hypertension
• Miscellaneous
- Post-operation potassium < 2.8mEq/L
- Hyperaldosteronism
- Drugs : Loop diuretic, insulin
CLINICAL SIGNS
• Neuromuscular : Decreased muscle contractility
- Decreased peristalsis (Potassium < 2.8mEq/L)
- Muscle clamp
- Decreased reflexes
- Paralysis
• Cardiovascular : Dysrhythmia, cardiac arrest
• Polyuria, fatigue, malaise
PARACLINIC
• Decreased magnesium, decreased urine potassium < 30mEq/L
• Electrolytes, BUN, creatinine, glucose :
- High HCO3 suggests diuretic abuse, vomiting, mineralocorticoid
- Low HCO3 suggests renal tubular disease.
• Urine K (Spot sample) :
- < 20mEq/L suggests GI loss, potassium shift into cells, poor intake.
- > 40mEq/L suggests renal loss.
• Urine Na < 20mEq/L with elevated urine K suggests secondary
hyperaldosteronism.
• Plasma renin if hypertensive :
- High renin : Secondary hyperaldosteronism, renal artery stenosis
- Low renin : Primary hyperaldosteronism
• ECG findings : Low-voltage T waves and Sagging of the ST segments
MANAGEMENT
• Replace magnesium if necessary (MgSO4) : 2g infusion
• Correct alkalosis if present
• Potassium chloride (KCL) oral or 0.1-0.2mEq/kg infusion
• Do not give IV potassium until urine production is assured
Reference
Rosen and Barkin’s 5-minute medicine
84 Fluid and electrolyte
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Depressed serum magnesium < 1.5 mEq / L
ETIOLOGY
• GI losses
- Chronic diarrhea
- Malabsorption
- Poor dietary intake (Severe malnutrition : MPC/MPE)
- Prolonged NPO status (Prolonged administration of total parenteral
nutriction)
• Miscellaneous
- Hyperaldosteronism
- Hypercalcemia
- Acute pancreatitis
- DKA
- Burn
CLINICAL SIGNS
• Increased muscle contractility
- Tremors
- Hyperactive deep tendon reflexes
• Mental status
- Headache
- Delirium
- Convulsions
• Positive Chvostek sign
PARACLINIC
• Diagnostic depends on clinical suspicion and serum magnesium levels
MANAGEMENT
• Correct underlying problem
• Replace magnesium for mild to moderate hypomagnesium
- Oral magnesium sulfate
- Magné-B6 orally
• Severe hypomagnesemia
- Magnesium sulfate 2g IVL or infusion
References
Handbook of pediatric
Current essentials of fluid and electrolyte (LANGE)
Fluid and electrolyte 85
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DIFINITION
• Low serum sodium < 130mEq/L
ETIOLOGY
• Severe dehydration (Acute diarrhea , repeated vomiting, burn, diuretics)
• Syndrome of inappropriate antidiuretic hormone ( SIADH )
• Occurs in post-operation
• Hypothyroidism
• Drugs : Chlorpropamide, NSAIDs, barbiturates, amitriptyline, clofibrate
CLINICAL SIGNS
• Mild hyponatremia >120mEq/L
- Headache
- Nausea, vomiting, anorexia
- Weakness
- Muscle cramps
- Rhabdomyolysis
• Moderate hyponatremia 110-120mEq/L
- Impaired response to verbal stimuli and painful stimuli
- Visual/Auditory hallucinations
- Bizarre behavior
- Hyperventilation
• Severe hyponatremia <110mEq/L
- Bradycardia, hypertension
- Altered temperature regulation
- Dilated pupils, seizure activity
- Respiratory arrest
- Coma/Unresponsive
PARACLINIC
• Electrolytes, blood urea nitrogen, creatinine
• Glucose : Correct sodium value accordingly if severe hyperglycemia.
• Urine sodium
MANAGEMENT
• Replace sodium
• Mild to moderated hyponatremia
- Initiate IV fluid with 0.9% NS
• Give hypertonic sodium when condition is severe
- DON’T : Dextrose 50%, Oxygen, Naloxone, Thiamine
- Raise serum sodium no more than 1-2 mEq/L/h
• Calculate sodium deficit = 0.6 (Weight in kg) x (140 –Na deficit)
- Half-dose give slow intravenously
- Half-dose infusion over 4hours
• Hypervolemic hyponatremia
- Water restriction to less than 1 L per day with high dietary salt intake
- Furosemide 20-40mg intravenously
Reference
Rosen and barkin’s 5-minute medicine
Neonatal disorders 89
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Souffrance foetal aiguë
• Anoxia encephalopathy
• Post delivery asphyxia depend upon
- Apgar Score < 7 at 5mn
- Respiratory failure
• Effect asphyxia : ischemia and hypoxia affective to brain, liver, kidney
, heart.
ETIOLOGY
• Ante-partum 90 %
- Meconium staining of liquor, abnormal lung
- Hypertonia or hypotonia of uterus
- Prolonged menbraneous rupture
- Metabolic acidosis
• Post partum 10 %
- Hypoxic ischemic encephalopathy
- Multiorgans systemic dysfunction (Lung, liver, kidney, heart, brain)
CLINICAL SIGNS
• Early
- Apgar Scare < 7 at 5mn
- Respiratory failure
- Cyanosis
• Late
- No feeding
- Seizure, loss muscle tone and Reflex (Moro’s)
CLASSIFICATION
• Stage I (Mild) : Hyper excitability, extremities contraction
• Stage II (Moderate) : Loss reflex, lethargy
• Stage III (Severe) : Repeated convulsion, coma
PARACLINIC
• CBC, CRP
• Peripheral Blood Gaz (pH)
• Electrolyte, glycemia, calcemia, blood culture
• Radiography, ultrasound, transfontanel ultrasound, MRI
• Presence : Hypoglycemia, hypocalcemia and prolong PT
90 Neonatal disorder
D-ork-L
MANAGEMENT
• Prophylaxis
- Regular antenatal check (In pregnancy > 2 times) and fetal’s
arrhythmia, scal pH < 7. 2
- Abnormal ultrasound : Cesarean
• Assessment of resuscitation ABCDE
• Monitoring
- Maintain of saturationSaO2 90-95%, pulse, urine
- If apgar score < 3 at 5mn transfer to neonate ICU
- Avoid ventilation : Diaphramatic hernia, meconium aspiration
- Nasogastric milk : 5-10mL/kg/day
• Medication
- Vitamin K : 2mg IM or IV
- Dextrose10% : 5mL/kg IVL or infusion
- Calcium gluconate10% : 1mL/kg infusion
- For seizure give Phenobarbital 20mg/kg and 5mg/kg/day after 24h
- Antibiotherapy if necessary
References
Handbook of pediatric
Hospital care for children (WHO)
Pulmonary disorder 91
Pediatric-Medicine disorder D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Episodic and chronic symptom of airway obstruction
- Chronic inflammation disease
- Recurrent dyspnea type bradyspnea expiration
- Periodic wheezing > 3 times
ETIOLOGY
• Most common trigger inhaled allergen
• Multifactor : SRV infection in nourrisson, psychologic, medication
- Viral infections, particularly respiratory syncytial virus (RSV),
during infancy may play a role in the development of asthma or
may modify the severity of asthma.
- Exposure to cigarette smoke and other airway irritants influences
the development and severity of asthma.
- Atopy and asthma are related : Eosinophilia and the ability to
make excess IgE in response to antigen is associated with
increased airway reactivity. Asthma is more common in children
who have allergic rhinitis and eczema.
PATHOPHYSIOLOGY Immune and inflammatory responses in the airways are
triggered by an array of environmental antigens, irritants, or infectious organisms.
• Increase immune response : Inflammatory cells respond to and
produce various mediators (Cytokines, leukotrienes, lymphokines),
augmenting the inflammatory response.
• Bronchial edema : Airway epithelium is inflamed and becomes
disrupted, and basal membrane is thickened. Bronchospasm : Airway
smooth muscle is hyperresponsive, and bronchoconstriction ensues.
• Hypersecretion : Airway epithelium is inflamed and Goblet cell
secrete mucous.
CLINICAL SIGNS
• A family history of asthma
• History of periodic wheezing > 3 times
• Recurrent dyspnea
- Nocturnal dyspnea
- Bradypnea expiration
• Cough or running nose
• Not able to drink
• Physical exam
- Chest in drawing
- Central cyanosis
- Wheezing expiration
128 Pulmonary disorder
D-ork-L Pediatric-Medicine disorder
PARACLINIC
• CBC (Increase eosinophil)
• ABG (pH)
• Spirometry test
• Chest x-ray : Chest distension, increased intracostal space,
hyperinflation.
COMPLICATION AND EVOLUTION
• Complication : Pneumothorax, pneumomediatin
• Asthma in nourrisson (Wheeze> 3times / year) : Persistent to 2-3
years-age.
• Asthma in children (Bradypnea , nocturnal dyspnea and prolong ENT
infection) : Persistent to adolescence.
FORMS OF ASTHMA
• Exercise asthma
• Occupation asthma
• Cardiac asthma
• Triad asthma
CLASSIFICATION
• Benign asthma : No daily, sometime dyspnea a month
• Moderated asthma : A few times a week, but not nocturnal dyspnea.
• Severe asthma : Everyday or nocturnal dyspnea, associated with
cough or infection ENT.
DIFFERENTIAL DIAGNONIS
• Congestive heart failure (Nocturnal dyspnea, JVD, Edema)
• COPD (No reversible, hyper inflation)
• Foreign body aspiration (Stridor)
• Pneumonia
MANAGEMENT
• Bronchodilater test, response with ventolin inhaled after 15mn
• Asthma Attack
- Inhalation Ventolin or Adrenaline : 5drops + 5ml NSS
for 4 times per day
- Dexamethasone : 0.5mg/kg/day IV
- Subcutaneous epinephrine if respiratory distress
0.01mg/kg SC, maybe repeat the dose once
- Oxygenotherapy with cyanosis
• Asthma manifestation
- Ventoline® : 0.1-0.3mg/kg/day in 3 divided oral
or Montigat® 1cp everyday
- Prednisolone 1-2mg/kg/day PO
• Treat at home
- Seretide® 1-2 bouffée with Babyhaler per day
- Or Montelukast (Montigat®) : 1cp PO
• Other drugs : Terbutaline, aminophylline, magnesium sulfate,
cyclosporine, methotrexate.
References
Hospital care for children (WHO)
The 5-Minute Pediatric
Pulmonary disease 93
Pediatric disorder D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Obstruction inflammatory of bronchioles by viral
• Children 2months -2years
ETIOLOGY
• Respiratory Syncytial Virus 70%
• Other virus 30%
- Adenovirus
- Rhinovirus
- Myxovirus
- Para-influenza virus
PATHOPHYSIOLOGY
• Virus proliferates in coryza of the nasal epithelium with profuse rhinorrhea.
• Infected secretions are aspirated into the lower respiratory tract.
• There is goblet cell proliferation and mucus hypersecretion. The airway lumen
becomes filled with debris consisting of dead cells and mucus resulting in
plugging, which causes partial or complete airway obstruction, increased
airways resistance, hypoxemia, and decreased lung compliance.
CLINICAL SIGNS
• Onset rhinorrhea
• Initially hoarse cough for 3-5days
• Fever persisted
• Dyspnea persisted
• Physical exam
- Dyspnea persisted
- Respiratory rate < 50b/mn
- Cyanosis
- Ronchi, or ronflant, or wheezing
PARACLINIC
• CBC (Supra infection)
• CRP (N < 6mg/mm³)
• Chest x-ray : Distension thorax, hyperinflation
DIFFERENTIAL DIAGNOSIS
• Rhinopharyngitis
• Bronchitis (Most common in children > 2years)
• Bronchopneumonia
• Gastroesophageal reflux disease (GERD)
• Foreign body aspiration
• CHF
94 Pulmonary disease
D-ork-L Pediatric disorder
•Cystic fibrosis
•Bronchiolitis Obliterans with Organizing Pneumonia (BOOP)
- Obstruction of bronchi and bronchioles by fibrous tissue
- Causes : Inhalation of toxic gases, chronic pulmonary infection, AIDS,
Stevens-Johnson syndrome, idiopathic.
- Clinic signs : Persistent cough, wheezing, sputum, digital clubbing-rare
- Investigation : Chest x-ray nonspecific, confirmed by lung biopsy
- Treatment : Antibiotic, bronchodilator, corticoids
COMPLICATIONS
• Common complications
- Otitis media
- Broncho-alveolitis
- Pneumonia
• Respiratory Distress Syndrome (Acidosis)
• Aspiration Syndrome (Aspiration pneumonia)
• Hypersecretion of ADH Syndrome (Fluid overload)
• Sepsislike Syndrome (Septicemia)
MANAGEMENT
• Admission Criteria
- Need for supplemental oxygen
- Inability to self-hydrate
- Apnea
- Severe underlying chronic lung disease or cardiac disease
- Persistent severe respiratory distress after several doses of β2-agonists
therapy or 4 hours after corticosteroids
- In the patient premature, immunodeficiency or immunosuppressive therapy
- Strongly consider in infants younger than 8 weeks
• Treat by symptomatic
- Paracetamole 40-60mg/kg/day PO
- Desobstruction : Nasal lavage with NSS for 3 times/day
• Nebulizer Berodual (3drops + 4mL of NSS) : 3times/day
• Respiratory kinesitherapy
• Antibiotherapy
- Not usually indicated
- Other than otitis media, the incidence of concurrent serious bacterial
Infection (Pneumonia, meningitis, sepsis) is < 2% in healthy infants with no
underlying disease who have RSV bronchiolitis.
• Antiviral agents (Ribavirin) : Respiratory Syncytial Virus
References
Acute respiratory infection ( WHO )
Handbook’s pediatric
The 5-Minute Pediatric
Pulmonary disease 95
Pediatric-Medicine disorder D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Inflammation of bronchiolar, alveolar and parenchyma
• 5 criteries
- Age < 24 months
- Polypnea > 50/mn
- Chest retraction
- Fever
- Breast sound : Crackle and wheezing
ETIOLOGY
- Respiratory syncytial virus 70%
- Adenovirus , influenza , rhinovirus
- Super infections : Pneumococcal, staphylococcal, streptococcal
PATHOPHYSIOLOGY
• Infected secretions are aspirated into the lower respiratory tract.
• The airway lumen becomes filled with debris consisting of dead cells and
mucus resulting in plugging, and bacterial super infection into parenchyma,
increased airways resistance, hypoxemia, and decreased lung compliance.
CLINICAL SIGNS
• History of upper respiration infection
- Fever > 38° C
- Rhinorrhea or congestion nasal
- Productive cough
• Polypnea expiration (RR > 50b/mn)
• Chest retraction
• Crackle inspiration and wheezing expiration
• Cyanosis
• Physical examination
- Chest in drawing intercostals
- Tachycardia > 140b/mn
- Crackle and wheezing
Gravity signs
- Chest retraction
- Nasal flaring
Air hungry - Balancement thoraco-abdo
- Geignement expiration
Hypoxia - Cyanosis
Respiratory distress - SaO2 < 95%
96 Pulmonary disease
D-ork-L Pediatric-Medicine disorder
PARACLINIC
• CBC (Increase WBC : Bacterial infection)
• CRP positive : Bacterial infection
• Chest x-ray :
- Opacity macro-micro nodular with infiltration
- Thorax distension
DIFFERENTIAL DIAGNOSIS
• Asthma (Recurrent dyspnea)
• Pneumonia
• Pertussis (Severe isolated cough : toux quinteux)
• Myocarditis
COMPLICATIONS
• Common complications
- Pleural effusion
- Pneumothorax
- Atalectasia
- Empyema
- Pericarditis
• Respiratory Distress Syndrome (Acidosis)
• Aspiration Syndrome (Aspiration pneumonia)
• Hypersecretion of ADH Syndrome (Fluid overload)
• Sepsislike Syndrome (Septicemia)
MANAGEMENT
• Admission Criteria
- Need for supplemental oxygen
- Apnea
- Severe underlying chronic lung disease or cardiac disease
- Persistent severe respiratory distress after several doses of β2-agonists
therapy or 4 hours after corticosteroids
- In the patient premature, immunodeficiency or immunosuppressive therapy
- Strongly consider in infants younger than 8 weeks
• Treat by symptomatic
- Paracetamole 40-60mg/kg/day PO
- Desobstruction : Nasal lavage with NSS for 3 times/day
- Nebulizer Berodual (3drops + 4mL of NSS) : 3times/day
• Respiratory kinesitherapy
• Antibiotherapy if necessary
• Oxygenotherapy (Child < 2months : 0.5L/mn and child > 2months : 1L/mn)
• Corticotherapy : Dexamethasone 0.3mg/kg/day IV or IM
References
Acute respiratory infection ( WHO )
Handbook’s pediatric
Most Common Pediatric 97
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Infectious disease by dengue virus
- Primary infection : Dengue Fever
- Secondary infection : Dengue Hemorrhagic Fever
ETIOLOGY
• Transmission by female Aedes mosquito
- Aedes aegypti (Indoor)
- Aedes albopitus (Around the house)
• Dengue virus-RNA (D1, D2, D3, D4), Flavivirus family
• 3 structural proteins
- Capsid : C
- Membrane protein : M
- Envelope glycoprotein : E
PATHOPHYSIOLOGY
• Extrinsic incubation period about 8-10days
• Intrinsic incubation period about 4-8days
• Primary infection is a dengue fever, which neutralizing, antigen-the
same serotype dengue virus.
• Secondary infection is dengue hemorrhagic fever, causing non-
neutralize other serotype dengue viruses (Ag-Ab complex), that
inflammatory response (Histamine, prostaglanding, IL1, IL6, C3a, C5a)
- Leukopenia : Viral invade to bone marrow, and suppression
- Increased vascular permeability : Ag-Ab complex
- Plasma leakage : Hyperpermeability
- Thrombocytopenia : Bone marrow suppression, platelet
aggregation and immune complex on platelet.
World Health Organization required criteria for diagnosis of DF
• Fever unresponsible to antipyretic
• Flushed face
• Headache
• Myalgia
• Retro-orbital pain
• Cutaneous rash
• Abdominal pain
• Vomiting
• Hemorrhagic manifestation
• Leucopenia
• Platelet count normal
98 Common Pediatric Disotder
D-ork-L Infectious disease
World Health Organization required criteria for diagnosis of DHF
• Fever
• Positive tourniquet test or bleeding phenomenon
• Hepatomegaly
• Shock
• Thrombocytopenia (<100,000/mm3)
• Increased vascular permeability with elevated hematocrit (>20%)
World Health Organization required criteria for diagnosis of DSS
• Rapid or weak pulse
• Narrow blood pressure (< 20 mmHg)
• Hypotension
• Cold skin or extremities
• Restlessness
• Capillary refill time > 3 seconds
Clinical signs Paraclinic
- Fever 39-40°C - Leukopenia
- Flushing - Atypical lymphocyte
DF - Periorbital pain - Platelet normal
- Rash - Hematocrit normal
- Abdominal pain
- The same signs - Platelet <100,000/mm3
I - Tourniquet test (+) - Ht > 20% of normal
DHF --------------- ---------------------------------- ----------------------------------
II - The same signs - The same
- Spontaneous bleeding
- Hypotension - The same test
- Pulse weaknss - Severe bleeding
III - GI bleeding - Ht decreased
- Agitation
DSS …………… ---------------------------------
IV - Profound shock
- Pulselessness
PARACLINIC
• Complex blood count
- Leukopenia
- Atypical lymphocyte
- Thrombocytopenia
- Increased hematocrit > 20% of normal range : DHF
• Positive IgM anti-dengue serology test
• PCR serotype finding
• Transaminase, PT, aPTT, glycemia
• Chest x-ray and ultrasound
Infectious disease 99
Pediatric disorder D-ork-L
MANAGEMENT
1. IV fluid for DHF grade I and II
Improvement No improvement
3mL/kg/h 6mL/kg/h
(1-3h) (1-3h)
Improvement No improvement
6mL/kg/h 10mL/kg/h
(3h) (1h)
Improvement
No improvement Improvement
10mL/kg/h
Improvement No improvement
5% AC or 5%NSS AC or NSS
10mL/kg/h 10mL/kg bolus
Improvement
No improvement No improvement
Reduce dose
6-3-1.5mL/kg/h Improvement
• Hematocrite, ABG
• Electrolyte, calcemia
• Glycemia, BUN, creatinin
• Transaminase
• SaO2
Reference
Hospital care for children (WH)
102 Pediatric disorder
D-ork-L Infectious disease
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Acute infectious disease caused by Corynebacterium diphtheriae,
affects primarily the membranes of the upper respiratory tract with the
formation of a gray-white pseudomembrane or skin wound.
ETIOLOGY
• Corynebacterium diphtheriae, a Gram-positive pleomorphic bacillus
• Transmitted by air droplets of nose or mouth
PATHOPHYSIOLOGY
• Corynebacterium enter mucus membrane of pharynx and epiglottis,
and 2-4 days of incubation at one of these sites, the bacterium
elaborates toxin.
• Locally, the exotoxin induces formation of a necrotic coagulation of the
mucous membranes (Pseudomembrane) with underlying tissue
edema, respiratory compromise may ensue.
• Elaborated exotoxin may also have profound effects on the heart,
nerves, and kidneys in the form of myocarditis, demyelination, and
tubular necrosis, respectively.
CLINICAL SIGNS
• History of immunization : DTP-absence
• Onset rhinorrhea
• Fever (T : 38° C)
• Sore throat
• Hoarseness
• Other : Anorexia, dysphagia, cervical lymphadenitis
Physical exam
• Nasal diphtheria : Rhinorrhea become serosanguineous
• Tonsil and pharynx diphtheria : Pseudomembrane, cervical lymph
node, low grade fever, anoxia, sore throat.
• Larynx and epiglottis diphtheria : Gray membrane, inspiration
stridor, airway obstruction.
• Cutaneous and mucosa diphtheria : Nonhealing ulcer with gray
membrane, conjunctivitis and vulvovaginitis.
Consequent : Exotoxin
• Myocarditis : Arrhythmia, heart block, heart failure
• Neuropathy : First cranial nerve (Diplopia, slurred speech, swallowing)
Pediatric disorder 103
Infectious disease D-ork-L
PARACLINIC
• Smear and culture from throat
• Fluorescent antibody test
• Examination of a methylene blue-stained lesion : Metachromatic granules
may be helpful if performed by an experienced technician.
DIFFERENTIAL DIAGNOSIS
• Streptococcal pharyngitis
• Infection mononucleosis EBV)
• Candidasis
• Herpes simplex infection
• Adenovirus infection
• Croup
• Acute epiglottitis
MANAGEMENT
• Prophylaxis with DPT vaccination
- Age 6 weeks : DTP1 : 0.5 mL IM
- Age 10 weeks : DTP2 : 0.5 mL IM
- Age 14 weeks : DTP3 : 0.5 mL IM
- Over age 4 months : DTP 2 doses given IM at least 4 weeks apart
and a booster dose 1 year later.
• Diphtheria antitoxin (DAT) antiserum, produced in horses
- Pharyngeal or laryngeal disease of < 48 hours duration :
20 000-40 000 units IV (Mild)
- Nasopharyngeal lesions : 40 000-60 000 units IV (Moderate)
- Extensive disease of 3 days' duration or diffuse neck swelling :
80 000-120 000 units IV (Severe)
• Removal gray membrane
• Severe form : Laryngoscopy
• Oral antibiotherapy for 14days
- PNC V : 250 mg x 4 times a day PO or
- Erythromycin : 40-60mg/kg/day
References
Handbook of pediatric
The 5-Minute Pediatric
104 Infectious disease
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Inflammatory reaction occurs within brain parenchyma with destruction of
neurons (CSF), parenchymal edema, and petechial hemorrhages.
• Meningoencephalitis is inflammation of the brain and the meninges.
ETIOLOGY
• Mode infections
- Direct invasive
- Infections (Airborne, droplet, and contact precautions)
- Post-traumatism or surgery
- Blood stream
• Causes
- Viral infections : Japanese encephalitis, rhabdovirus/lyssavirus,
enteroviruses, varicella, flaviridae, adenovirus.
- Bacterial infections : Chlamydia, TB, listeria monocytogene, HIB
- Protozoan infections : Cryptococcal, toxoplasmose, cat-scratch
PATHOPHYSIOLOGY
• Acute infections : Direct infection by viral or bacterial risk neural cell
• Chronic infections (Fungal , syphilis) : Obstruct of CSF flow, resulting
hydrocephalus, cranial nerve palsies.
CLINICAL SIGNS
• Prodrome of upper respiratory infection : Cough, coryza, malaise, fever,
anorexia, and digestive symptoms.
• Encephalitis is often heralded by fever, headache, hypersalivary, seizure
but hypotonia, motor weakness and Babinski reflex-positive.
- Meningoencephalitis : Headache, fever, neck stiffness, confusion
- Varicella-zoster encephalitis : Hallucination, ataxia, clonus
- Japanese encephalitis : Parkinsonism, delirium, confusion, coma
- Flavivirus (West Nile virus) encephalitis : Febrile illness, often with
rash, headache, lymphadenitis, polyarthropathy, poliolike syndrome.
- Rabies encephalitis : History of animal bite, fever, hypersalivary,
hydrophobia, paralysis.
- Noviral encephalitis : High fever, headache, vomiting, neck stiffness
• Physical exam
- Hypertension, bradycardia, cranial nerves-facial palsy, papilledema,
apnea maybe brain swelling.
- Neck : Stiffness, Kernig or Brudzinski signs (Meningoencephalitis)
- Adenopathy (Mycobacterium, cat scratch, Bartonella)
- Chest : Signs of pneumonia, rales, rhonchi ( Mycobacterium and
Mycoplasma infections, HIB)
- Abdomen : Hepatosplenomegaly (Epstein–Barr virus, Ehrlichia)
- Skin : Purpura (Rickettsial, meningococcemia) to erythematous or
papular (Lyme disease, Enterovirus)
- Neurologic exam : Confusion to delirium with hallucinations to stupor
and aphasia (Herpes virus), poliolike syndrome (West Nile virus),
hydrophobia (Lyssavirus-Rabies), parkisonian syndrome (JEV).
Infectious disease 105
D-ork-L
PARACLINIC
• Complex blood count
- WBC usually elevated and CRP positive : Bacterial Infection
- Electrolytes, glucose, BUN, creatinine
- Bacterial and viral blood cultures
- Liver function tests, ammonia level if hepatic failure suspected
• Carboxyhemoglobin level if CO poisoning suspected
• Toxicology screen if ingestion suspected in differential
• Increased intracranial pressure : Cryptococcal suspected
• CSF examination : Cell count and chemistry
- Elevated WBC, predominantly neutrophils (Bacterial infection)
- Normal or elevated WBC, predominantly lymphocytes (Viral infection)
- Elevated protein
- Glucose (Normal in viral infection)
- Gram stain with or without India ink for suspected/confirmed HIV
• Viral and bacterial cultures (Fungi if indicated by history)
• Serum antibody : ELISA
• CSF-PCR
• CT scan
- To rule out trauma, hemorrhagic conditions, and mass lesions
- Cerebral edema may be the only finding consistent with encephalitis.
- HSV may show parenchymal hemorrhagic areas of the frontal and
temporal lobes, along with edema.
• MRI : Hypodense temporal lobes in HSV.
DIFFERENTIAL DIAGNOSIS
• Meningitis
• Meningo-encephalitis
• Brain abscess
• Stroke (Hemorrhagic or ischemic)
• Head injury
• Subarachnoid hemorrhage
• Encephalopathy (Hepatic, uremic)
MANAGEMENT
• Admit to ICU
- ABCDE resuscitation
- Supporting care
- DON’T : Dextrose, Oxygen, Nalaxone, Thiamine
- Stop seizure with Diazepam, or Phenobarbital
• Treat underlying disorder
- Viral encephalitis : Ganciclovir® or foscanet® and antiretroviral for HIV
- Bacterial encephalitis : Antibiotherapy with antibiogram specific
- Fungal encephalitis : Cryptococcal with amphothericine B and continue
fluconazole or Toxoplasmosis with cotrimoxazole long life.
• Prevention by vaccination : HIB vaccination, JE vaccination.
References
Pediatric emergency medicine (McGraw-Hill)
The 5-Minute Pediatric
Rosen and Barkin’s 5-minute medicine
106 Common pediatric disorder
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
•
Diarrhea : Watery stool or semi liquid stool more than 3times or
increased fluid content of the stool >10 mL/kg/day.
ETIOLOGY
• Viral infections 70%(Rotavirus, in children < 18months)
• Bacterial infections (Enterobactery or entero-invasif)
• Protozoan (Amoeba, parasites)
• Other causes : Yeast, lactose intolerant, oil, milk allergy
PATHOPHYSIOLOGY
• Hypersecretions : Submucosa of colon inflammation or damage
• Hyperperistasis : Incomplete bowel obstruction
• Malabsorption : Poorly absorbed or nonabsorbable solute is present
in the intestinal lumen. This can occur with the ingestion sugars,
carbohydrate malabsorption. Usually cause by prolonged antibiotic or
fungal infection.
• Hyperosmolarity : In general, the solute composition of intestinal fluid
is similar to that of plasma. Osmotic diarrhea occurs when poorly
absorbed risk of increased osmolar in the intestinal lumen. Water into
intestinal lumen that cause of acute diarrhea.
CHARACTERISTIC
• Acute diarrhea : < 14 days
• Persistance diarrhea : 14-28 days
• Chronic diarrhea : > 28 days
CLINICAL SIGNS
Evaluation Without Moderate Severe
dehydration dehydration dehydration
Conscious Anxious Agitation, somnolent Lethargy , coma
Drink & thirsty Drink well Thirsty, vomiting No able drinking
Eye Tear No tear, dry eye Sunken eye
Skin pinch Anxious Retardation > 3sec Severe retardation
PARACLINIC
• Completed blood count (CBC)
- Elevated WBC, predominant neutrophils : Bacterial infection
- Normal WBC, CRP negative : No bacterial infection
• Stool test, yearst, oil, lactose
• Stool culture (Coproculture)
• Ultrasound : Intussusception, bowel obstruction finding
Gastrointestinal diseases 107
D-ork-L
COMPLICATION
• Dehydration (Hypovolemic shock)
• Electrolyte inbalance (Hypokalemia)
• Hypoglycemia
• Pseudomembranous colitis
• Necrotizing colitis
• Septicemia
• Hemolytic uremic syndrome
• Renal complications : Kidney or adrenal necrosis, failure
• Pneumonia
• Severe malnutrition
DIFFERENTIAL DIAGNOSIS
• Diarrhea by vibrio cholerae (Cholera)
• Dysentery (Shigella or entamoeba histolytica)
• Food poisoning (Clostridum botulism)
• Helminthic infections
• Bacterial gastroenteritis
- Temperature >39 °C
- Toxic clinical appearance
- Crampy abdominal pain
- Bloody mucoid stools
• Viral gastroenteritis
- Seasonal epidemics
- Guaiac-negative stool
• Noninfectious
- Milk allergy : Heme-positive stool, vomiting
- Malrotation with midgut volvulus
- Inflammatory bowel disease
- Intussusception: Currant jelly stool, abdominal mass
MANAGEMENT
1. Prevent of diarrhea
• Exclusive breast feeding
• Improvement wearing practice
• Use of plenty of clean water
• Hygiene
• Use of latrine
• Proper disposal of stool young children
• Immunization again measles
2. Treat of dehydration
• Dehydration < 5% (Table A : Without or mild)
- Oral rehydration
- SRO : 15-20mL/kg/h
- Enfant < 2 years : 50-100mL after a diarrhea or vomiting
- Enfant > 2 years : 100-200mL after a diarrhea or vomiting
108 Gastrointestinal diseases
D-ork-L
• Dehydration 5-10% (Table B : Moderate)
- Follow up 4hours : SRO 75mL/kg/4h
- If vomiting or no drinking give IV fluid
• Dehydration > 10% (Table C : Severe)
- First time give lactate ringer : 30mL/kg/h bolus
- Second time give lactate ringer : 70mL/kg/5h
3. Treat underlying of enterobacterial
• Cause : E-coli, salmonella, shigella, helicobacter pyloric, yersinia
• Clinical signs : Fever, abdominal pain, mucus or bloody stool
• Treatment : Ciprofloxacin 30mg/kg/day PO
4. Treat underlying disorder
• Ameba : Metronidazole 30mg/kg/day PO
• Fungal (Leuvur or yeast) : Stop antibiotic and give bioflor®,
nystatin® and vita- B1 per oral.
• Parasite
- Ascariasis : Pyrentel® 12mg/kg/dose PO
- Ankylosis : Albendazole® 400mg/day PO for 3 days
- Taenia solium or saginata : Niclosamide
- Schistosoma : Praziquentel® 40-60mg/kg/day PO
• Lactose intolerance : Free lactose milk
5. Treat by symptomatic
• Antipyretic : Paracetamole 40-60mg/kg/day PO
• Anti-diarrhea : Smecta®, Biolactyl®, Polysilane®, Bioflor®
• Antiemetic : Domperidone®, Promethazine®
• Antispamodic : Dispan®, Buscopan®, Spasfon®
• Absorbant : Carbophos®, Acticarbin®
• Bloating with rhinorrhea : Colicaid®
References
Handbook of pediatric
Hospital care for children (WHO)
The 5-Minute Pediatric
Neonatal disorder 109
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Jaundice in newborn is the clinical manifestation of hyperbilirubinemia
• Yellow pigmentation of tissues due to elevated serum bilirubin
PATHOPHYSIOLOGY
• Bilirubin is formed by destruction of red blood cells and heme protein (
Fe + biliverdin), into circulation (Unconjugate bilirubin) indirect ,
transported to liver (Conjugate bilirubin-water soluble), bilirubin is
excreted in blood 80% and enterohepatic cycle 20% (Converse by
bacterial to urobilin and stercobilin)
• Prehepatic : Hemolysis (G6PD deficiency, AIHA, Malaria), increased
indirect bilirubinemia (Unconjugated bilirubinemia)
• Intrahepatic : Liver disease, liver abscess, malaria (Increased total ,
conjugated bilirubinemia)
• Posthepatic : Gallbladder stone, biliary atresia/obstruct, Budd-chari
syndrome (Conjugated bilirubinemia)
ETIOLOGY
• Most common in premature 80%
• Hyperbilirubinemia in neonate
• Materno-fetal blood incompatibility
• Miscellaneous
- Hemolysis
- Anoxia, hypoxia, acidosis
- Infectious causes
- Hypoglycemia, hypoalbuminemia, polyglobulia
- Gestation Diabetes Mellitus
- Drugs-used : Paracetamole, indometacine, furosemid, diazepam,
tetracycline, chloramphenicole, caffeine, aminoglycosides.
DIAGNOSIS
1. Physiologic jaundice
• Present 24-48h after birth and continue until 7days
• Durant 2-7days
• Bilirubin 6-12mg/dL or total bilirulin < 200 µmoL/L
• No signs of neurologic : No seizure, feeding normal
2. Pathologic jaundice
• Prolonged jaundice > 7days
• Pathology jaundice (Soon after birth)
• Hepatomegalia
• Anemia
• Seizure and neurologic signs
110 Neonatal disorder
D-ork-L
3. Bio-chemic
• Physiologic : Total bilirubin (TB) < 200µmoL/L
• Pathologic : TB > 200µmoL/L for premature, TB > 350µmoL/L neonate
4. Pediatric Considerations
• Intrahepatic cholestasis
• Cardiovascular (Congenital heart disease, congestive heart failure,
shock, asphyxia)
• Metabolic or genetic (Trisomy 18 and 21, cystic fibrosis, Gaucher's
disease, Niemann-Pick disease, glycogen storage disease type IV)
• Infectious (Bacterial sepsis, cytomegalovirus, enterovirus, herpes
simplex virus, rubella, syphilis, tuberculosis, varicella, viral hepatitis)
• Hematologic (Severe isoimmune hemolytic disease)
PARACLINIC
• CBC, blood group, Rhesus
• Total bilirubin, direct and indirect bilirubin
• Liver function, PT and PTT
• Glycemia, calcemia
• Blood film morphology
• Coombs test, G6PD test
• Hypoalbuminemia : Decreased with severe liver disease
• Prothrombin time : Prolonged level is an important prognostic
indicator in patients with acute hepatitis or vitamin K deficiency
• Increased transaminases
- Alanine aminotransferase (ALT, SGPT): primarily in the liver
- Aspartate aminotransferase (AST, SGOT): liver, heart, kidney,
skeletal muscle, and brain.
• Alkaline phosphatas / glutamyltranspeptidase: Biliary tree
obstruction/cholestasis
• Stool color : Acholic (White) stools suggest biliary atresia.
• Imagery : Ultrasound, CT scan
DIFFERENTIAL DIAGNOSIS
1. Unconjugated hyperbilirubinemia 80%
• Physiologic jaundice : After 24 hours, in premature, 6-12 mg/dL
• Breat milk jaundice : In general jaundice, breat-fed infant can develop
elevations, starting first week of life 15-27mg/dL by the second or third.
• Increased hemolysis : Materno-fetal incompatibility (ABO) , G6PD
deficiency, autoimmune hemolytic anemia (AIHA), newborn hemolytic
syndrome (NBHD)
• Miscellaneous : Hypothyroid, Down’s syndrome, pyloric stenosis,
urinary infection, hemoglobinopathy, Wilson disease, Gilbert disease,
Crigler-Najjar syndrome.
2. Conjugated hyperbilirubinemia 20%
• Etiology
- Intra hepatic : Cholestasis due viral infections (HBV, CMV, herpes
, rubella), E-coli infection, malaria include increased hemolysis
Neonatal disorder 111
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- Extrahepatic diseases : Biliary atresia, cholangitis, Budd-chiari’s
- Metabolic causes : Metabolic abnormalities include in alpha1-
antitrypsin deficiency, cystic fibrosis, and galactosemia
• Clinical signs
- Prolonged jaundice
- White stool
- Hepatomegalia
• Investigation
- CBC, Bilirubin, Transaminase, Coombs test, G6PD test, hepatitis
- Abdominal ultrasound (Hepatic)
MANAGEMENT
• Isotonic IV fluid therapy if dehydrated
• Toxic-appearing patients :
- Supplemental oxygen, cardiac monitoring
- Nasogastric suction and bladder catheterization
• Phenobarbital : Seizure in sepsis and drug-induced causes,
decreases conjugated bilirubin.
• For NBHD give vitamin K and infectious causes give antibiotic
• Phototherapy and transfusion
Therapeutic in jaundice-newborn Phototherapy Transfusion
Healthy full-term Bilirubinemia level > 15mg/dL > 25mg/dL
Sickness full-term Bilirubinemia level 10-15mg/dL 20mg/dL
Premature Bilirubinemia level 5-14mg/dL 14-20mg/dL
References
Handbook of pediatric
The 5-Minute Pediatric
Rosen and Barkin’s 5-minute medicine
112 Infectious disease
D-ork-L Pediatric-Medicine disorder
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Malaria is a protozoan disease caused by the genus Plasmodium and
transmitted by female Anopheles mosquitoes.
ETIOLOGY
• It is characterized by hectic fever and often presents with classic
malarial paroxysm. Four species of genus plasmodium usually infect
humans.
- Plasmodium Vivax
- Plasmodium Falciparum
- Plasmodium Malariae
- Plasmodium Ovale
• Mode transmission
- Female Anopheles
- Blood transfusion, congenital
PATHOPHYSIOLOGY
• Sexual cycle
- Develops in the female Anopheles mosquito providing the
sporozoites to the host.
- Male and female gametocytes are taken up by a female anopheline
mosquito with a blood meal where they fertilize in the mosquito gut
to produce a diploid zygote that matures to an ookinete, haploid
sporozoites are generated that migrate to the salivary gland of the
mosquito to infect another human.
• Asexual cycle
- After bite in the human (Sporozoites in blood steam), first in the
liver producing merozoites and then in the erythrocytes.
- In the hepatocytes, the sporozoites mature to tissue schizont or
become dormant hypnozoites.
- The tissue schizont amplify the infection by producing large number
of merozoites (10,000 to 30,000).
- When merozoites affected to RBC are called trophozoites
- Each merozoite does not replication in RBC, developed to
gametocytes.
Infectious disease 113
Pediatric-Medicine disorder D-ork-L
CLINICAL SIGNS
• Incubation 1-2weeks
• History of living malaria zone
• Fever frequent evening
- Tertian : Every 3days
- Quatian : Every 4days
- Subtertian : Disease is lethal
• Classic malarial paroxysm characterized by
- Cold stage : Frisson (30-60mn)
- Hot stage : Fever > 41° C (3-4hs)
- Sweating stage : Sweat
1. Plasmodium Falciparum
• Simple malaria (Benign Malaria)
- Frisson, fever, sweating, headaches, myalgia, fatigue
• Severe malaria (Malign Malaria)
- Hypoglycemia
- Hemoglobinuria 4H
- Hepatomegaly
- Hypoxia
- Convulsion
- Colapsus vascular 4C
- Cerebral malaria
- Coma
- Renal failure 2R
- Respiratory distress
- Jaundice
- Anemia 2Pallors
2. Plasmodium Vivax
• Tertian malaria : Fever occurs every 3days
• Incubation period after exposure is 14days (Range: 8 to 27days)
• Hypnozoites may cause relapse of infection after years
• Infects mainly reticulocytes
• Irregularly shaped large rings and trophozoites, enlarged RBC, and
Schüffner's dot are seen in peripheral blood smear
• Pigment color is yellow-brown
• P. vivax from Papua New Guinea have reduced sensible-chloroquine
• Primaquine needed to eradicate the hypnozoites
3. Plasmodium Ovale
• Also known as tertian malaria, fever occurs every other day
• Incubation period after exposure is 14days (Range: 8 to 27days)
• Hypnozoites may cause relapse of infection
• Infects mainly reticulocytes
• Infected RBC seen as enlarged, oval shape containing large ring or
trophozoites with Schüffner's dot. Pigment color is dark brown
• Primaquine needed to eradicate the hypnozoites
• No chloroquine resistance encountered
114 Infectious disease
D-ork-L Pediatric-Medicine disorder
4. Plasmodium Malariae
• Quartan malaria : Fever occurs every 3 days
• Chronic malarial infection, persist 20 to 30 years
• May cause soluble immune-complex, resulting in nephritic syndrome
• May persist in blood for many years if treated inadequately
• Incubation period after exposure is 30 days (Range: 16 to 60 days)
• Lacks hypnozoites (Intrahepatic stage)
• Infects mainly mature RBC
• Band or rectangular forms of trophozoites are commonly seen in
peripheral blood smear. Pigment color is brown-black
• Chloroquine can be used cautiously for falciparum malaria acquired in
chloroquine-sensitive areas (Chloroquine is more rapidly than quinine)
• Treatment is oral quinine sulfate 10mg (salt)/kg (Usually 650 mg) q8h
for 3 to 7days, followed by pyrimethamine with sulfadoxine (Fansider)
3tablets (Each tablets contains 500mg sulfadoxine and 25mg
pyrimethamine) or doxycycline 200mg loading dose, then 100mg bid
for 7days to eradicate asexual forms of the parasite.
5. Congenital malaria : In the pregnant patient, increased perinatal mortality
has not been reported with malaria in stable, endemic regions. However,
for semi-immune or non immune mothers, transplacental antibodies may
be lacking, and the risk of congenital infection may be higher in this
subgroup.
• Early symptom after birth, jaundice, hepatomegaly, fever, trouble
hemostasis. Cause by occlusion of microvasculature of placenta
(Transplacental antibodies)
• Late symptom after 14-21days, transmitted during at birth.
6. Cerebral malaria are caused by occlusion of the cerebral
microvasculature from infected red cells. It is the most serious
consequence of malaria infection. Prognosis depends on the management
of other complications (Acidosis, renal failure). Cerebral malaria will
manifest with signs of increased intracranial pressure, encephalopathy,
and seizures.
7. Black water fever is due to acute renal failure caused by accumulation of
hemoglobin in the renal tubules resulting in hemoglobinuria with dark
urine. This often occurs after repeated attacks of P. falciparum.
8. Hemolytic anemia, the most common disease finding, can be severe,
especially in P. falciparum, the predominant mechanism is due to
intravascular hemolysis from fragile erythrocytes (G6PD deficiency, Sickle
cell disease, thalassemia) rather than solely rupture from infected cells.
9. Hypoxia : Sequestation, cytoadherance, rosetting, reduce RBC
deformability.
10. Mechanism of hepatomegaly and sphenomegaly
Tropical splenomegaly syndrome seen in chronic infections caused by P.
malariae produces splenomegaly, hepatomegaly, portal hypertension, and
pancytopenia. In P. vivax malaria, acute splenomegaly can induce rupture.
Infectious disease 115
Pediatric-Medicine disorder D-ork-L
PARACLINIC
• CBC (Hb decrease)
• Blood smear of malaria
• Hypoglycemia
• G6PD test
• Electrolyte
• Liver and renal function
• PCR of malaria
DIFFERENTIAL DIAGNOSIS
• Dengue Fever, DHF
• Enteric Fever
• Urinary tract infection
• Yellow fever
• Influenza
• Viral hepatitis
• Trypanosomiasis
MANAGEMENT
1. Prophylaxis
• Personal protective measures against Anopheles mosquito bites
• Chemoprophylaxis is strongly advised for travelers in endemic zoon
• Chloroquine is the drug of choice in resistant areas (500 mg once a
week or 5 mg/kg once a week) and 4 weeks after leaving the endemic.
• Mefloquine is recommended in chloroquine-resistant areas (250 mg
once a week.
2. Treat underlying cause
• Severe Plasmodium Falciparum
- Artesunat (Artemather®)
D1 : 3.2mg/kg IM
D2 : 1.6mg/kg/day
---------------------
---------------------
D5 : 1.6mg/kg/day IM
D6 : Mefloquine : 25mg/kg/day PO
- Check malaria test before exit hospital
• Mild Plasmodium Falciparum : Malarine® , or A+M5®
3. Resistant
• Quinine : 20mg/kg infusion follow up every 4h, quinine : 10mg/kg
repeated every 8h oral, associated with tertracycline 250mg x 3 times
for 7days.
4. Severe malaria infectious
• If Hb < 4g/dL : Transfusion packed cell 10-15mL/kg
• Coma and renal failure : Dialysis
5. Hypoglycemia : D10% : 5mL/kg infusion
References
Hospital care for children (WHO)
Vademecum clinique (MASSON)
Ferri’s Clinical Advisor
116 Pediatric disease
D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Acute systemic viral illness
• Rubeola, First disease
ETIOLOGY
• Measles virus is a single-stranded RNA paramyxovirus
• Transmission by droplet and highly contagious
• Measles is a highly contagious disease in nonimmune persons
PATHOPHYSIOLOGY
• The virus enters the body through the respiratory tract, incubation 10-
14 days between exposure and onset of symptomatic , multinucleated
giant cell can be recovered from urine, and nasal secretions.
CLINICAL SIGNS
• History of the patient’s nonimmune
• Onset prodrome : Fever, coryza, cough, conjunctivitis, photophobia
• Exanthems after 3 days of prodrome
- Irregular marculopapular rash
- Brick-red on face to trunk extremities
• Koplik’s spots on the bucal mucosa
• Associated : Diarrhea, anorexia, fatigue, sore throat, lymphadenitis
PARACLINIC
• CBC : Leukopenia
• Nasopharyngeal secretions culture
• Smear (Frottis nasal : Warthin-Finekeldey)
• Serologic testing (Measles-specific IgM < 72hours from onset of rash)
• Monoclonal antibody immunofluorescence
DIFFERENTIAL DIAGNOSIS
• Other acute exanthems fever
- Rubella
- Herpes simplex (HSV1, HSV2)
- Varicella (Herpes zoster : HHV3)
- Epstein-Barr virus infection (HHV 4)
- Cytomegalovirus (HHV 5)
- Roseola (Exanthem subitum : Human herpes virus 6)
- Enterovirus (Coxsackivirus)
• Drug allergy
• Scarlet fever
• Kawasaki disease
Pediatric disease 117
D-ork-L
COMPLICATIONS
• Diarrhea
• Otitis media
• Laryngitis
• Pneumonia
• Encephalitis
MANAGEMENT
• Primary immunization preventive : At age 9 months or after
15months.
• Treatment of patient
- Bed rest and analgesic
- Isolating for 1 week following onset of rash
- For children with ophthalmologic evidence of vitamin A deficiency, a
3rd dose at 4 weeks is indicated.
• Specific treatment
- Passive immunoglobulin : 0.25 mL/kg IM (Max 15 mL)
- Double the dose for immunocompromised persons
- Ribavirin for severe measles pneumonitis
- Secondary bacterial complications by antibiotic
References
Pediatric emergency & medicine (McGrow-Hill)
Current essentials of medicine (LANGE)
The 5-Minute Pediatric
118 Pediatric disorder
D-ork-L Medicine disorder
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Inflammation of meninges and CFS infection
ETIOLOGY
• Micro organism (Bacterial, viral, fungi) direct or extension from
- The ear (Chronic otitis)
- Nasopharyngeal infection
- Cranial injury
- Congenital meninges
- Blood stream spread
• Non infections : Drug , malignant cell (Subarachnoid hemorrhage)
PATHOPHYSIOLOGY
• Bacterial meningitis is an inflammation of meninges with increased
intracranial pressure, and pleocytosis or increased WBCs in CSF
secondary to bacteria in the pia-subarachnoid space and ventricles,
leading to neurologic sequelae and abnormalities(Hydrocephalus,
cerebral edema)
- Neonate : Streptococcus B, E-coli, Listeria monocytogene
- Enfant : Haemophilus influenzae B, meningococcal, pneumococcal
- Chronic illness : Mycobacterium TB
• Viral meningitis is acute aseptic meningitis usually with lymphocytic
pleocytosis and negative CSF stains and cultures.
- Lynphocytosis > PMN
- CSF without pus
- Not cerebral edema exception encephalitis
- Gems: Enterovirus (Echovirus, coxakivirus), Mump virus, Herpes
• Fungal meningitis
- Immuno-compromised patient (HIV, Cytotoxic)
- Cryptococcal meningitis
- Gems : Cryptococcus neoformans, Candida, Histoplasma
capsulatum Blastomyces dermatidis (USA)
CLINICAL SIGNS
1. Meningitis Syndrome (Triad)
- Headache
- Neck rigidity
- High fever or vomiting
2. Children and adult
• Vomiting are often present
• Seizure
• Photophobia
Pediatric disorder 119
Medicine disorder D-ork-L
References
Handbook of pediatric
The 5-Minute Pediatric
Rosen and Barkin’s 5-minute medicine
122 Genitourinary Diseases
D-ork-L Pediatric Disorders
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
Acute glomerulonephritis
DEFINITION
• Post streptococcal glomerulonephritis
• Acute glomerulonephritis (AGN) is acute inflammatory damage to
glomerulus, associated with :
- Edema
- Hypertension : Increase afferent artery pressure
- Hematuria : Active urine sediment (RBC casts)
- Proteinuria : Nonselective
ETIOLOGY
• Most common in children between 3-7 years and under 2 years of age
are rarely affected
• Post-streptococcal infection
- 5-10% in pharyngitis : 1-3weeks after infection
- 25% in skin infections : 2-4weeks after infection
• IgA Nephropathy : Most common cause of AGN (>25%)
- Ab-Ag causes immune complex deposition of IgA and C3.
- Complement levels are usually normal
• Noninfectious Causes of glomerulonephritis
- Systematic lupus erythematosus
- Henoch-Schönlein purpura, vasculitis
- Wegener granulomatosis
- Goodpasture syndrome
PATHOPHYSIOLOGY
• Glomerulonephritis probably results from the deposition of circulating
immune complexes in the kidney, theses immune complexes are
deposited on the basement membrane, reducing glomerular filtration.
• Inflammatory complex depend upon :
- Infection by grope A beta-hemolytic streptococci
- Complex Ag-Ab attack of basement membrane of glomerula
- Toxin effect of streptococcal to basement membranous glomerula
• Exact mechanism of AGN unclear :
- Combination of autoimmune reactivity to specific antigens at renal
glomeruli
- Glomerulonephritis comprises 25-30% of end-stage renal disease
CLINICAL SIGNS
• Post streptococcal infection of pharynx (Exposure 1-2weeks)
- Fever
- Sore throat
Genitourinary Diseases 123
D-ork-L
- Malaise
- Abdominal pain
• Acute glomerular inflammation
- Sudden onset 1-7days
- Edema and hematuria (90%)
- Oliguria 80% ( Urine < 400mL/day )
anuria prognosis to acute renal failure in 2% of children
- Hypertension (60-70%)
- Proteinuria non selective (2g/m2/24h)
PARACLINIC
• CBC
• BUN ( Blood Urea-Nitrogen ) and creatinine-elevated
- Creatinine clearance > 200mg/24h
- Ratio protein / creatinine (< 0.2 normal)
• Azotemia
• ASLO positive
• Urinalysis
- Proteinuria non selective
- Erythrocyte cast
- Leukocyturia
- Hyaline, glanular
• Renal ultrasonography, IVP and renal biopsy
• 3 Serologic markers
- Serum C3 level is reduced in 90-100% of children during the first 2
weeks of illness, returning to normal with 3-4 weeks.
- Anti glomerula basement membrane antibody (AGBM antibody)
- Anti nucleo cytoplasmic antibody (ANC antibody)
• Streptococcal antibodies :
- Antistreptolysin (ASO) more reactive in pharyngeal infections
- Antistreptokinase (ASK) elevated in recent hemolytic streptococcus
- Antideoxyribonuclease B (ADNase B), anti-nicotinyl adenine
dinucleotidase (ANADase), and antihyaluronidase (AH) : Skin
COMPLICATION
• Anemia
• Hyperkalemia
• Acute renal failure
• Chronic renal failure evolution to ESRD
DIFFERENTIAL DIAGNOSIS
1. Nephrotic syndrome
• Proteinuria > 50mg/kg/24 h
• Hypoprotidemioa < 60g/L
• Hypoalbuminemia < 25g/L
• Hypercholesterolemia
2. Henoch Schönlein Purpura (Rheumatoid purpura)
• Purpura rash, arthralgia
124 Genitourinary Diseases
D-ork-L
• GI bleeding
• Glomerular syndrome
3. Wegener’s Granulomatosis : Vasculitis associated with
• Glomerulonephritis
• Respiratory symptoms : Cough, dyspnea, chronic sinusitis, otitis
media, hemoptysis
• Neuropathy, purpura, arthritis, scleritis
• Conformed diagnosis : C-ANCA, large nodular by chest x-ray, biopsy
• Treat by corticoids or cyclosporine and cotrimoxazole
4. IgA Nephropathy
• Most common cause of AGN (>25%), worldwide
• Antibody-Antigen causes immune complex deposition of IgA and C3.
• Complement levels are usually normal.
• IgA-Nephropathy has different presentations :
- Gross hematuria following upper respiratory infection (URI)
- Microscopic hematuria with proteinuria
- Hematuria occurs either during viral illness or after exercise.
- Prognosis is related to serum creatinine, blood pressure, and
proteinuria.
- 50% of patients with proteinuria may develop progressive renal
disease.
• Angiotensin converting enzyme inhibitor or angiotensin receptor
blocker RBS may help.
5. Proteinuria (> 100mg/24h)
• Proteinuria + leukocyturia : Urinary tract infection
• Proteinuria + hematuria : Glomerulonephritis, Alport syndrome,
Berger ’s disease (Ig A nephropathy), HUS, Lupus nephritis
• Proteinuria + edema : Lipoid nephrosis
6. Hematuria (≥ 100 000/mL)
• Nephroblastoma
• Lithiasis
• Urinary tract infection
• Kidney traumatism
• Glomerular syndromes : Glomerulonephritis, Berger’s, Alport’s, HUS
MANAGEMENT
• Fluid and salt restriction
• Supporting diet and vitamin B
• Edema and hyperkalemia are often required to diuretics
Furosemide 0.5-1mg/kg/dose
• Hypertension (Calcium channel blocker)
• Antibiotherapy : Benzathine penicillin or ceftriaxone
• Follow up every months, ASLO test
and Extrancilline® 2.4 millions/month
References
The 5-Minute Pediatric
Rosen and Barkin’s 5 minute medicine
Pediatric Disorder 125
Genito-urinary Disease D-ork-L
Internal Medicine 2010, 4th ed.
Ngam Punlork, MD.
______________________________________
DEFINITION
• Endocrinology
• Idiopathic nephrotic syndrome
• Diseases causing defect in glomerular filtration barrier, producing
- Proteinuria >3.5g/day(Protein selective)
- Hypoalbuminemia (Serum albumin < 3 g/dL)
- Peripheral edema due to hypoalbuminemia
- Hyperlipidemia (Fasting cholesterol >200mg/dL)
PATHOPHYSIOLOGY
1. Immunologic factor
• A number of immunologic abnormalities are seen with nephrotic syndrome
that predispose to infection.
• Risk decreased serum levels of complement factors D and B, abnormal
humoral immunity, decreased delayed hypersensitivity and proliferative
responses, and increased suppressor-cell activity and suppressor
lymphokine levels .
2. Mechanic of proteinuria
• Electron microscopy reveals widening and effacement of the visceral
epithelial foot processes, which are reversible, occur in association with
proteinuria, and are not specific for MCNS.
• Plasma protein : Albumins, globulins, and fibrinogens
3. Mechanic of hyperlipidemia
• Hyperlipidenia due to hepatic lipoprotein synthesis stimulated by
decreased plasma oncotic pressure.
• Decreased lipoprotein lipase risk of elevated cholesterolemia
4. Mechanic of edema
• Abnormal glomerular infiltration barrier, producing of large amount of
proteinemia risk of hypoalbuminemia
- Decreased plasma oncotic and increased plasma hydrostatic pressure
- Fluid and plasma move down interstitial space
- Fluid accumulation in body spaces (ascites, pleural effusions, scrotal
swelling)
CLINICAL SIGNS
• Fatigue and general malaise
• Weight gain and facial swelling
• Puffy eyes
• Abdominal swelling or pain
• Pitting-dependent edema
• Fluid accumulation in body spaces (Ascites, pleural effusions, scrotal)
• Hepatomegaly