A Kham
A Kham
A Kham
Clinical Medicine
Essentials of
Clinical Medicine
Samir Kathale
MBBS Intern. Std.
Mahatma Gandhi Memorial Medical College
and
Maharaja Yashwant Rao Holkar Hospital
Indore (MP)
JAYPEE BROTHERS
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This book has been published in good faith that the material provided by author is original. Every
effort is made to ensure accuracy of material, but the publisher, printer and author will not be held
responsible for any inadvertent error(s). In case of any dispute, all legal matters are to be settled
under Delhi jurisdiction only.
ISBN 81-8061-615-0
MY GRANDPARENTS
PARENTS
Shri ANANT KATHALE
Smt. SAVITA KATHALE
BROTHER
SAGAR KATHALE
&
ALL MY WELL WISHERS
whose blessings have only made this venture possible...
Preface
Medicine can be compared to an endless ocean. The farther we step into it, the more unboundable it seems to become. It
is an ever-growing science. The expanding clinical experiences, advancements in technologies, newer inventions and
better drugs in the field of pharmacology, all together have contributed to the enormous growth of literature in medicine.
While I was an undergraduate student, I felt dearth of a single comprehensive book in clinical medicine which could
provide most of the information that an undergraduate student should know to get a firm grip over clinical practices in
medicine, so as to become a full-fledged doctor. My friends also shared the same idea. Most textbooks of clinical
medicine originate from the West and many a times are difficult to be appreciated in the Indian setup. These authors
sometimes, unnecessarily, deal in great depth, with certain topics that does not suit to our setup, while leaving other
topics (though of similar importance) to the students. So, being constantly insisted and hard pressed by my beloved
friends and colleagues, I ultimately ventured to write a textbook on clinical medicine, which should be comprehensive as
well as oriented to improving the hands of our budding doctors in the field of clinical practices. This book also finds itself
to be examination oriented. My sole intention has been to write in a clear, concise and easily understandable way, in my
own style, keeping always a vigilant watch to the student’s interest.
An earnest attempt has been made to merge the clinical methods and principles of internal medicine and to present it
in a condensed form. To keep the size and volume compact, and small, only certain important clinical topics are included
in this manual, even references are not included since high-tech reference system is available in all good libraries.
This book is primarily intended for the undergraduate medical students and practicing physicians with special emphasis
on clinical methods and clinical features. The book does not provide much information about the investigations and
management part of various clinical disorders, because, the author is of the opinion that these can be read by the students
from any standard textbook of medicine.
The core skills of communications, clinical examination, objective assessment and planning are as important clinical
practices as ever. These skills can only be gained by learning and practice. Medicine is a noble profession, there is a
relationship of trust between patients and doctors, and the doctor is recognized to have acquired knowledge and skills
relevant to the practice of medicine. In addition, a code of ethics binds the doctors to certain modes of conduct in the
clinical relationship with a patient and in relation with colleagues. All these matters are a part of clinical method in the
modern world. Essentials of Clinical Medicine seems to teach an integrated approach to clinical practice, so that new
methods and techniques of examining a patient are merged into established patterns.
All of us find new things to learn everyday, and the more alert we are, more we find there is to learn. Knowledge and
understanding are the keys to good practice. With the advent of Internet, and easy availability of information, people are
generally better informed than in the past. The modern doctors need to be aware of this and to develop particular skills in
dealing with the informed patient and their family. A firm foundation in clinical methods is essential to this process.
This book is divided into six sections: The General History Taking, The Common Symptoms Presented by the Patients
and Questions to be Asked for Them, Symptomatology and its Causes; The General Examination; The Systemic Examination
and Common Cases Encountered in Clinical Medicine. It also includes X-rays, CT-scans, MRI, photographs, ECGs and
procedures routinely followed in medical wards. The whole text is organized into both body system-related and problem-
oriented chapters. The basic method of cardiology, neurology and other specialities are described in chapters devoted to
these topics. The special skills required in dealing with unconscious patients are also discussed. There are many illustrations
and diagrams to help the students to understand the topic well.
In preparing a textbook like this, I have freely utilized the knowledge and experience of the stalwarts in this profession
and I have consulted many books on clinical medicine and various established global journals.
I would sincerely like to acknowledge the supporting hands of MY TEACHERS; Dr (Mrs) SHWETA PAWAR; my
colleagues Dr KUMAR SAURABH GAUR, Dr (Ms) MEGHNA MAHESHWARI, and Dr SAURABH ARGAL and my
viii Essentials of Clinical Medicine
friends ABHISHEK SAXENA and ASHISH SAXENA (SOFTWARE ENGINEERS) for their full co-operation and
support. They all stayed besides me when I needed their help.
I sincerely thank my patients who allowed me to picture themselves in this textbook. I am deeply indebted to GOD
AND MY PARENTS for supporting and encouraging me during the complete period from writing to the printing of the
text.
Last but not the least, I wish to acknowledge the help and encouraging attitude of Editorial Board and the entire
staff of Jaypee Brothers Medical Publishers (P) Ltd. for their generous cooperation and coordination in bringing out
this first edition. I am definitely confident that this manual will help the students to look into the subject of clinical
medicine in much simpler, better and broader way.
Once again, my heartful thanks to Dr KUMAR SAURABH GAUR, Dr SAURABH ARGAL, Dr (Ms) MEGHNA
MAHESHWARI, ABHISHEK SAXENA and ASHISH SAXENA (Software Engineers) for encouraging me and providing
their invaluable help.
Samir Kathale
All that a man achieves and all that he fails to achieve is the direct result of his own thoughts.
James Allen
Love cures people, both, the ones who give it and the ones who receive it.
Dr Karl Menninger
Lack of will power has caused more failure than lack of intelligence or ability.
Flower A Newhouse
Some people see things and ask, why? Some people dream of things
that never were and ask, why not?
George Carlin
Nothing great was ever achieved without enthusiasm.
RW Emmerson
2. Common Symptoms Presented by the Patients and Questions to be Asked for Them ................................ 9
Through this book, the author has tried to make a sincere effort to look into the field of Clinical Medicine through the
eyes of a student. Keeping in mind the difficulties which the author used to face, as a student, in various elements of
clinical medicine, such as eliciting the relevant history in a correct manner, the perfect general as well as the local
examination, reaching to the provisional diagnosis and differentiating it from other similar illnesses and clinical disorders
(what is known as the differential diagnosis of the clinical problem), he has tried to simplify the work of a medical student
to get a tight grip over clinical aspects of internal medicine.
The author considers himself to be a part of the student community and hence, best understands the lacunae of the
students and the areas where they are likely to commit mistakes. The clinical medicine forms the foundation of the
internal medicine. Realising this, every possible effort has been made to make the clinical medicine easier, interesting and
easily absorbable.
The author sincerely suggests the students not to feel the subject of medicine a havoc but to grasp it in an easier and
interesting manner. Remember “It’s all Possible”. Just as the scientists have their research laboratories; the lawyers work
in the court room; so also the medical students have hospitals and clinics as their workshops. Therefore, it is expected
from them to attend the clinics regularly and sincerely so as to turn themselves into the undefeatable and ever-progressing
clinicians.
Introduction
The word “patient” is derived from the Latin word patiens, meaning sufferance or forbearance. Although our health
experts have given a perfect definition of “health”, but they have not yet succeeded in defining the term “disease”. This is
because disease has many shades (called the spectrum of disease) ranging from inapparent (subclinical) cases to severe
manifestations of illness.The Oxford English Dictionary defines disease as “a condition of the body or some part or the
organ of the body in which its functions are disrupted”. The main aim of medical practice is to cure the patient or to
relieve the patient’s sufferings. In order to solve this purpose, it is of utmost importance to know how to approach to the
problems of the patient, to make a diagnosis and to design an appropriate scheme of management and treatment for each
patient.
To arrive at a correct diagnosis, a physician has to follow a certain path (or rules). This includes:
1. The interview or the history taking.
2. The physical examination which includes both the general as well as local examination.
3. Drawing a provisional diagnosis.
4. Performing the relevant investigations needed.
5. And at last, reaching to the final diagnosis of the illness.
The clinicians (and of course the students also) should always attempt to take a good history, as this practice will help
them to arrive at a correct diagnosis.
1
History Taking
PROPER HISTORY TAKING temperature is also solved). Pleasant surroundings are very
important. Both, the consultant and the patient, should feel
Proper history taking helps a clinician to come to 60-70
at ease with each other. Always try to make the patient to
percent of the diagnosis of a clinical illness/problem.
sit to your left. This makes your observation more accurate
History taking is an art, which forms an important part
and even better.
in approaching the patient’s problems and arriving at a
correct diagnosis. History taking helps to form a healthy Observing the Patient
doctor-patient relationship. It also helps a physician to win The process of observing the patient must begin right from
the confidence of the patient. the moment he walks into your chamber. While communi-
Certain points are to be given attention to while eliciting cating with him, try to make judgments about the patient’s
the history. The patient should be encouraged to tell about general demeanour. Does he present himself in a clean, well-
his/her problems in his/her own words as far as possible. spoken, intelligent manner? Do you find any signs of
Very few physicians are good interviewers and very few disability, whether mental or physical? What does the
patients are good narrators. Therefore, a careful elicitation gestural language of the patient says? Is the patient confident,
of the patient’s problems is needed. This needs an examiner knowledgeable or perhaps depressed and miserable? Does
to have a thorough knowledge regarding the disease. For he or she describe his/her problem in a relevant manner? Is
example, the doctor may sometimes need to ask about past there any embarrassment about something that is not spoken
history of fever, chronic cough and gradual weight loss if of ? Is the patient talking about the things that really bothers
he/she suspects tuberculosis in his/her patient. him? Have a look over the patient’s clothes and belong-
Raising the Set-up (The General Scene) ings. This tells a lot about your patient’s language, interests
and educational level. Try to explore the patient’s knowledge
Most of the medical introductions or consultations between about his own illness or disease.
the patients and the clinicians occur in the out-patient setting.
The achievement of confidence and the assessment of Persons Accompanying the Patient
personality and social skills of each patient can be done A good clinician always likes to spend some time during the
here. Either the doctor must himself go to fetch the patient initial exchange of greetings to know and identify who is
from the waiting room or the patient may be brought into present and to get some idea of the persons accompanying
the consultation room by the nurse or receptionist (which the patient. Identify the seniormost person present. Try to
is usually seen). This creates a friendly atmosphere and the know the expectations of this consultation. Inquire whether
patients too feel assured of being at the right place. Introduce the patient has taken medical care of any other physician.
yourself and greet the patient gently. Try to observe his Assure him that it is only to make his treatment better and
response. Does the patient smile or look frightened or successful. Make sure why the accompanying persons wish
anxious? Does he make good eye contact? Is he depressed to be present, and, certainly, whether this is also the patient’s
or normal? Do you find any signs of breathlessness? You wish. Sometimes the information obtained from a concerned
may try to feel his body temperature when you give him a and observant relatives may be of great importance to you.
handshake. Always handshake by using both the hands of But avoid unnecessary interpretation by them.
yours. By this, the patient gets a feeling of being at your In certain ethnic groups, including Asians and Muslims,
concern and care (and your main purpose of feeling the the patient is usually accompanied. A female patient may
2 Essentials of Clinical Medicine
come with several other family members. As far as possible, the patients, to observe them,and then finally report to a
always attend to and examine a female patient in the senior doctor about the findings in the patients and learning
presence of one of her family members (of course, an adult) more about the cases.
or a person with whom she is accompanied.
Taking the Notes
Communicating with the Patient
Try to keep eye contact with the patient while making notes.
Never try to start the interview immediately. It is better to Do not be in a hurry to make notes. First listen carefully to
engage in certain preliminary exchange of ideas. This way, the patient, make up your mind what is being said and record
the patient will be at ease and this will also lend you the way enough (in the form of the points) to help you remember
to go confidently. At times, you may try to create some humor the important points narrated by your patient. Later, you
(of course, after judging the mood and condition of the can make a detail out of these points. Always use the words
patient). narrated by the patient. Never try to use medical terminology
A word of caution—always check that you have the right for the complaints described by the patient until and unless
patient—there may be many patients of same name or same you are very much sure about that. For example, never use
surname (for example, there may be many Mr Sharma or the words like vertigo for “chakkar” or dyspnea for
Mrs Shrivastava waiting for you). Check the address, date “difficulty in breathing.” The same is to be applied while
of birth as well as name. Also, have a look at the patient’s talking to the patient.
papers and hear what the patient has to say. Let communi- Requirement of Direct Questions
cation be a two-way process.
You will always find time and place for direct questions in
Assuring the Patient history taking. Direct questions are indeed an essential
Always try to tell your patient that you expect him to talk component of relevant history taking. A good physician
freely. Assure the patient that you will be able to reach to always stores up the direct questions until the patient has
the correct diagnosis only if he narrates to you the complete finished talking. If you are not sure of something, ask for
and detailed facts. Assure him that his secrets will not be more details. If you have noticed an abnormality not
disclosed to anybody and he/she is in the safe hands. mentioned by the patient (for instance, a swelling, a rash,
an abnormal posture, a visible scar mark, etc.), ask about it
Explaining the Patient directly. Now if you think that you have a clear understanding
From the patient’s perspective, the most important compo- of the patient’s complaints, you should take each main
nent in the process of history taking and clinical examination symptom in turn and have a detailed examination. Some
is “the explanation.” The clinicians who are gentle, patient, examples of direct questions are:
interested and kind to the patient, those who encourage the Have you ever coughed blood?
patient and relatives to ask questions and who spend the • Do you feel better after vomiting?
time explaining the situation in a way it is understood are • Do you have fever with chills and rigors?
regarded as “good doctors”. A clinician, who readily accepts Non-Verbal Clues
his mistakes instead of trying to hide it, is more respectable
in the eyes of the patients and his relatives. He should assure A vigilant doctor will always try to look for non-verbal clues.
them that still many “good things” can be done for the Look at the facial expressions of the patient. Whether it
patient. He should well explain the patient and his relatives shows any signs of grief, tiredness, stress or anxiety. Does
about the illness of the patient. the patient catch his breath, appears confused, has abnormal
breathing pattern, looks pale or flushed, is restless or shows
Role of the Medical Students any abnormal body posture or body movements? Does he
Every medical student should try to make his best efforts at catch hold his head while speaking or takes along pause to
good history taking and thorough and complete clinical narrate the next point to you? Always behave peacefully
examination. If the students are asked by a patient to give a with such patients. Be sympathetic to them. Try to know
medical opinion, they should gently remind the patient of the causes of his worries; and if possible at your level, try to
their status and suggest them to undergo a more useful solve his problem. You should put your pen down and listen
consultation with the doctor. Always remember that an carefully to the patient and you should give an eye-contact
undergraduate medical student is not there to give opinions to the patient. Many a times, it may happen that the points
or medication to the patients. He is supposed to examine which the patient is narrating to you may not be useful for
History Taking 3
you or for your process of history taking. In such a case, television. You turned sweaty and started vomiting and were
you should be at your norm and should peacefully try to breathless also. Then you turned restless and could not sleep
explain him what you expect him to tell to you. Many the whole night. And this morning you are here. Am I right?”
patients have the habit of telling about their complaints in
an exaggerated manner in order to gain your attention. They Success of a Good Interview Depends Upon
may complain of “all the time” pain or headache or they Asking the relevant questions tactfully
may complain of having anorexia or abdominal discomfort ↓
for last few weeks. Indeed, in spite of his exaggeration, the Yields accurate history Good basis for physical
examination, investigations and interventions
complaint is real (no doubt, it may be of mild degree), but
you should definitely pay your full attention to it. ↓
Good doctor-patient relationship
Bearing the Insults ↓
Patient is satisfied and trusts on you
Many a times, the patient may be so frustrated and worried
↓
about his problems, or he may be waiting for his turn since
Good patient compliance
long, that he may burst open on you. In such a situation,
you should handle the patient very gently. After the day’s
tiring work, it may seem difficult for you, but remember it is Qualities that Every Clinician must
not impossible. Always try to have a soothing attitude. After Try to Develop
all, you are there for the same. If at all the patient is so
angry that he tries to dominate you, it is good for both of 1. Technical skill, scientific knowledge and human
you “to end up the consultation”, to have the consultation understanding.
on some other occasion or some other day/date, or you may 2. Courage, humility and wisdom.
even refer the patient to some other doctor also. 3. Edifice of character within himself.
4. A professional attitude, coupled with warmth and
Five “W”s and One “H” openness.
This stands for six utmost important questions to be asked 5. Respect and sincere concern for the patient.
while taking the history. They are as follows: 6. Alertness and consciousness.
• What are the chief presenting complaints? Or what has 7. Honesty and love for the job.
made the patient to approach to you? 8. To be empathic.
• When did the problem start? 9. To be an active listener and be vigilant.
• Where, i.e. the body part where the problem started first? 10. To be articulate—knowing when to speak, what to
• Which steps the patient has taken to cure himself before speak, how to speak.
reaching to you? (This also includes the consultation 11. To be best at his non-verbal communication.
with some other physician.) 12. To be caring, compassionate and friendly.
• Whether the patient has been taking medications for the 13. Show interest in other’s problems and be enthusiastic.
same illness earlier also and whether he has shown 14. Never show impatience, even if you are short of time.
himself to any other physician? 15. Never look tensed or worried. This is the worst
• How has the problem affected the daily activities of the impression you can give to your patient. Keep aside
patient? all your worries while attending the patient.
16. Be humble, modest and soft-spoken.
Summing Up 17. Be neat and tidy, well-dressed and up-to-date.
The summary is the main crux of the matter that you have
Elements in a Clinical History Taking
discussed with the patient. In this process the history narrated
(The Proforma)
by the patient is read in front of him within a very short
time (say, one or two minutes). For example, “Let’s have a • Name
quick look at what we have discussed so far and please • Father’s name
correct me wherever I go wrong. You were absolutely alright • Husband’s name (for female patients)
till last evening when you suddenly developed crushing pain • Age and sex of the patient
in the middle of your chest while you were watching the • Address
4 Essentials of Clinical Medicine
• Date and time of admission (if the patient is admitted) and dye industries; scrotal cancer—chimney sweeps; pneu-
• Marital status (single or married) moconiosis, silicosis and anthracosis—mining, sand blasting
• Socio-economic history and coal industries; lead poisoning—lead using industries
• Education (of both husband and wife) and plumbers; cirrhosis of liver—chemical industries;
• Religion, caste and race surgeons, traffic police and housewives—varicose veins.
• Occupation (of both husband and wife) Thus, the list goes on and on. Questions that you should
• Presenting complaints ask to the patient are:
• History of presenting complaints • Is your job dusty? What type of dust is it?
• History of any previous illness (past history) • Which tools make dust?
• Any medical history and treatment history (along with • How long have you been working there?
exposure to radiation) • Are the protective clothes provided ?
• Any surgical history • Are goggles and suits required and why ?
• History of any drug allergy or allergy due to some other • Any such illness affected any other fellow employee?
substances • Is the job sedentary type ?
• Personal history • Are the fumes, vapors and chemical substances invol-
• Family history. ved?
Occupational Diseases
DETAILS OF HISTORY TAKING
Occupational diseases are defined as the diseases arising
Name: Asking the name is an opening question in an
out of or in the course of employment. They are grouped
interview. It is good to use the patient’s name or the surname
as in Table 1.1.
(depending upon his age). This way the patient feels himself
to be at your concern; and no doubt, it helps to go on with Table 1.1: Occupational diseases
the discussion. For example, “Mr Paul, please come in,” Diseases due to physical agents:
Or, “Hello Ram, how are you?” 1. Heat Heat hyperpyrexia, heat exhaustion, heat
Age and sex: Certain diseases are more common at certain syncope, heat cramps, burns and local
effects such as prickly heat.
age groups. For example, atherosclerosis and certain degene- 2. Cold Trench foot, frost bite, chillblains
rative disorders occur at a later age, whereas certain 3. Light Occupational cataract, miner’s nystagmus
congenital anomalies manifest themselves at younger age 4. Pressure Cassion disease, air embolism, blast
except for a few disorders like valvular heart disease with a (explosion)
5. Noise Occupational deafness
mild degree of abnormality or syringomyelia that manifests 6. Radiation Cancer, leukemia, aplastic anemia, pancy-
at a later age. topenia
Certain diseases are more common in a particular sex. 7. Mechanical factors Injuries, accidents
For example, hemophilia manifests itself only in males, 8. Electricity Burns
whereas the carriers are the females. Atherosclerosis and Diseases due to chemical agents:
myocardial infarction are more common in males. But 1. Gases CO2, CO, HCN, CS2, NH3, N2 H2S, HCl,
SO2. These cause gas poisoning.
women too are not spared. Rheumatic mitral stenosis, breast 2. Dusts (pneumoconiosis)
cancer and thyrotoxicosis are commoner in females. i. Inorganic dusts:
Address: The place where the patient lives, i.e. the area, the a. Coal dust Anthracosis
b. Silica Silicosis
locality, the state or the country holds certain significance. c. Asbestos Asbestosis, cancer lung
For instance, endemic goiter is mostly seen in the foothills d. Iron Siderosis
of the Himalayas. Lathyrism caused by the long-term ii. Organic (vegetable)
consumption of khesri dal is commoner in the North Indian dusts:
a. Cane fiber Bagassosis
states. Skin diseases and respiratory disorders like b. Cotton dust Byssinosis
pulmonary tuberculosis is more common in people of lower c. Tobacco Tobacosis
socio-economic groups and those living in slums and d. Hay or grain dust Farmer’s lung
crowded, ill-ventilated environment. 3. Metals and their Toxic hazards from lead, mercury,
compounds: cadmium, manganese, beryllium, arsenic,
Occupation: The occupation and the working conditions of chromium, etc.
a patient can provide direct clues towards the etiological 4. Chemicals Acids, alkalies, pesticides
factors of the disease. For example, bladder cancer—paints Contd...
History Taking 5
Contd... • Occupation:
5. Solvents Carbon disulphide, benzene, trichlo- – Current and previous
roethylene, chloroform, etc. – Exposure to hazards, e.g. chemicals, accidents
Diseases due to biological Brucellosis, leptospirosis, anthrax, – Unemployment—duration and reason
agents: actinomycosis, hydatidosis, psittacosis,
tetanus, encephalitis, fungal infections,
– Attitude to job or unemployment.
etc. • Economic condition:
Occupational cancer: Cancer of skin, lungs, bladder – Financial circumstances including loss of income
Occupational dermatosis: Dermatitis, eczema and debts.
Diseases of psychological Industrial neurosis, hypertension, • Relationships/domestic circumstances:
origin: peptic ulcer, etc.
– Marital status:
Quality of relationship and any problems
Religion, caste and race: Although the patient may feel it
Spouse’s occupation and attitude to patient’s
awkward and may also find it useless when you ask him
about his caste or religion; but you should try to explain illness
him that in some cases, it may provide important clues in Sexual identity—any problems
Other occupants of the house—any problems,
the diagnosis of the disease. Some of the diseases are more
common in particular groups or communities. For example, e.g. violence, health and bereavement.
the largest concentration of thalassemia patients is seen in – House:
Type of home—size, owned or rented
South-East Asia, Sri Lanka, Bangladesh, North-West India,
Pakistan, Middle East countries, North Africa, Greece and Problems with the house and neighbors
Italy. Its prevalence in India is high among Gujaratis, Supporting friends or family.
Punjabis, Sindhis, Lohanas, etc. Over 30 million people are – Community support:
Social and health services involvement
carriers of thalassemia gene in our country. Ten thousand
Attitude to the help being provided.
thalassemic children are born every year in India. Sickle
– Leisure activities:
cell disease is common in Africa and in American Blacks
Habits
and in aboriginal tribes in Central India (Mahars, Kunbi
Tobacco
and Telis) inhabiting areas around Chhota Nagpur, in
Alcohol
Maharashtra, in MP and extending to Orissa. Nearly 20
Caffeine
million people are affected in India. Hemoglobin D disease Illicit drugs
(also called hemoglobin Punjab) is seen in 10 percent of Dietery restrictions/eating habits.
Punjabis and Gujaratis in India. Hemoglobin D thalassemia Presenting Complaints
is a very mild clinical syndrome like thalassemia minor. It • What are the complaints?
has been seen in Punjabis. Hemoglobin E thalassemia is • How long? (Duration)
common in West Bengal, Assam and in Bangladesh. • Note the complaints in non-medical terms (i.e. the way
Hemoglobin C thalassemia is seen in Italians (severe form) the patient describes them).
and in Blacks (relatively milder). • If there are more than one complaint, then they should
Social history: You should ask the patient about: be recorded in chronological order. For example:
• His upbringing (Whether it was at home or away from – Cough with expectoration = 1 month
his parents?) This question is especially important in – Breathlessness on exertion = 20 days
psychiatric cases. – Headache = 7 days
– Birth injury or complications – Vomiting = Since the previous night.
– Early parental attachments and disruptions • What is the mode of onset?
– Schooling, academic achievements and difficulties • Is there any progress in the symptoms? If yes, slow or
– Behavioral problems. fast?
• Insults: • Special time of occurrence?
– Emotional, physical or sexual abuse (this requires • Any kind of periodicity in the symptoms?
good training and skill) • Aggravating and relieving factors?
– Experiences of death and illness • Associated symptoms?
– Interest and attitude of parents. • Conclusion?
• Education/occupation: (When you have recorded the chief complaints, you should
– Higher education and training ask about each and every symptom in detail. This is because
6 Essentials of Clinical Medicine
a single (same) symptom may be due to the involvement of • Inquiry about sleep—duration and soundness of sleep
two or more systems. For example, dyspnea (breathlessness) • Sanitary habits
may be due to respiratory or cardiovascular system • Marital history, and if the patient is female, you should
involvement. As a medical person, you should be familiar take menstrual history and also inquire about the methods
with etiology of dyspnea. of contraception used by her.
Exertional dyspnea – cardiac origin • History of addiction is very important to be looked for.
Dyspnea occurring You should inquire about the substance for which the
paroxysmally, with – respiratory origin patient has addiction and also the form in which he
wheeze and associated consumes it. You should also ask about the duration of
with respiratory tract consumption. If the patient denies of any addiction
infection currently, then you should ask whether he had any such
• Any other special inquiry or questions? in the past and how long did he do it and how long had
History of any previous illness or past history: Try to make it been after giving up the consumption? Why did he
detailed inquiry about all the illnesses right from the patient’s gave up or whether there were any signs and symptoms
childhood, especially about those diseases/symptoms that of some illness fearing which he gave up the substance
are related to the presenting complaints and also their of abuse?
duration and severity. *Alchol intake:
• How long has the patient been taking it?
Medical history and treatment history: A detailed inquiry
• Quantity per day—Is there any change as compared to
should be made about significant illnesses which the patient
earlier?
had suffered in his life and whether he was ever admitted
• Type of alcohol consumed?
for that. What was the outcome of that illness? Is it still
• Money spent over it—Whether it is drunk alone or in
continuing? Did the patient took any medications to cure
group and place of drinking?
the disease? What were they? (If he still remembers the
• Whether consumed daily, weekly or on particular
names of those medicines?) How long did he do so? Was
occasions?
the complete treatment taken with proper dosages? And
• What is the the purpose of drinking?
few other questions which you find significant. Was there
• His attitudes towards drinking?
any recurrence of the illness? Were there any side effects
• Any withdrawal symptoms?
of the therapy and if yes, what were they?
(Similarly, the questions about tobacco chewing or smoking
Surgical history: Whether the patient was operated anytime can also be asked to the patient.)
for some illness? What was the case? What was the outcome
of the surgery? Was there any recurrence of the illness? Alcohol-Related Disorders
Were there any serious complications of the surgical 1. Alcohol dementia (cortical atrophy)
procedure? 2. Subdural hematoma
History of drug allergy (allergic reactions due to certain 3. Withdrawal symptoms
drugs): Has the patient ever shown allergic manifestations 4. Delirium tremens
due to any specific drug? What were they like? Also, inquire 5. Cardiomyopathy
about their severity and duration. What did the patient do to 6. Hypertension
get rid of these signs and symptoms? 7. Hepatic cirrhosis
Personal history 8. Portal hypertension
• Educational status of the patient? 9. Pancreatitis
– Any kind of addictions—smoking, alcohol or 10. Dupuytren’s contracture
tobacco? (see the details below)* 11. Proximal myopathy
• History of blood transfusion—the reason, the age, 12. Peripheral neuropathy.
number of times; and if the patient remembers, the Tobacco-related disorders: (You should inquire about the
amount of blood transfused. form in which the tobacco is consumed that is—smoking
• Immunization—received or not. If yes, complete or not? cigarettes or beedis, or chewing simply in betel leaf (paan)).
• Apetite, diet, thirst, frequency of micturition and bowel 1. Cardiovascular accidents
habits and constipation should be recorded. 2. Tobacco amblyopia
• History of weight change—gain, loss or the same? 3. Carcinoma mouth
History Taking 7
Contd... Contd...
• Any kind of pain or discomfort in the abdomen? Central Nervous System
• Change in bowel habits? • H/o of recurrent headache, its duration, frequency, severity, does the
• Stool color—dark, pale, black, fresh blood? patient point out any particular area or part of the head for the pain
Urogenital System and any kind of medication taken for that?
• Fits (any H/o epileptic attacks, any H/o head injury or any central
• Pain on urination? (dysuria) nervous disorder in the past?)
• Frequency of micturition, and any H/o nocturia? • H/o of blackouts and faints, their severity, frequency, duration, any
• Abnormal (altered) urine color kind of medication taken.
• Number of sexual partners • Tingling sensations (paresthesia) and numbness in any part of the
• Males: body.
– In old age, prostatic symptoms like hesitancy in micturition, • Any complaint of muscle weakness?
poor stream, terminal dribbling, frequency, urgency, etc. are to • Any history or complaint of hearing problem, visual disturbances,
be noted. altered sense of smell or taste (any H/o of ear, nose or throat operation)?
– If appropriate, mental attitude to sex (libido), morning erections, Locomotor and Joint System
frequency of intercourse, ability to maintain erections, ejacu- • H/o joint pain, stiffness, etc.?
lation, urethral discharge, etc. are to be asked. A word of caution • Muscle pain or weakness?
—These questions are to be asked in a very tricky manner. You Endocrine System
should not irritate the patient. • H/o heat or cold intolerance?
• Females: • Any alteration in sweating, weight loss or gain, etc?
– The detailed menstrual history as mentioned earlier. • Prominence of eyes as seen in thyroid disorders.
– If the patient is postmenopausal, ask her about any problem of • Any kind of swelling in the neck, its exact site, size (in centimeters),
bleeding. number, color, temperature over the swelling, duration, mode of onset,
– Any problem like stress or urge incontinence? other symptoms associated with it, pain, progress of the swelling,
– Ask about libido, dyspareunia (pain during intercourse). fever, presence of other swellings, secondary changes like ulceration,
Remember—Again, it is a tricky question and you need to be softening, inflammatory changes, any impairment of function,
tactful. recurrence of the swelling, any family H/o such complaints
• Excessive thirst, hunger or frequency of micturition.
Contd...
2
Common Symptoms Presented
by the Patients and Questions
to be Asked for Them
after belching. Whether the patient takes any kind of yellow color) or gastric contents (reddish-brown
medication for relieving pain should also be inquired. color).
• Associated symptoms: You should ask about: • Is the vomitus copious (copious means pure blood) and
– fever sour-smelling?
– vomiting • Whether it is associated with pain, colic, attacks of
– micturition myocardial infarctions or angina, after ingestion of
– weight and appetite certain drugs or due to any metabolic disorder (if the
– swelling patient knows about it beforehand).
– trauma Flatulence
– abdominal distention
Excessive gas in the stomach and intestines.
– menstrual history for ectopic pregnancy
• Whether the patient brings the wind up (i.e. belching) or
– vaginal discharge
passes it down (i.e. flatus)?
– rectal discharge
• Does the patient want to get rid off flatulence but cannot
– type of discharge. do so?
Appetite • Whether he gets relief on passing wind?
• Time of the day or the activities after which the
• Has the appetite of the patient changed in the recent few complaint/problem is maximum?
days or weeks or is it the same as before? • How long (duration) is the patient suffering from such
• Has it increased or decreased? a problem?
• It may be an indication of a serious disorder if the apetite • Try to know about the severity of the problem
has become perverted. • Does the patient complain of excessive fullness in the
• Any other associated symptoms? abdomen even after taking less amount of diet?
Vomiting Water Brash
Vomiting is a neurogenic response triggered by the • Does the patient complain of his mouth getting filled
chemorecepters in the brainstem or reflexly through the with tasteless saliva?
irritation of the stomach. Vomiting consists of a phase of • When does he complain of it? (Time or any special event
nausea, followed by hypersalivation, pallor, sweating and related to it.)
hyperventilation. Retching, an involuntary effort to vomit, • What is the duration and frequency of complaint?
then occurs followed by expulsion of gastric contents • Are there any associated symptoms and what are they?
through the mouth sometimes through the nose. A H/o • Water-brash may be associated with heartburn.
vomiting in itself is not very helpful because vomiting occurs
as a response to pain of any type. However, H/o vomiting Heartburn (Pyrosis)
provides us certain important hints. In most of the cases, • Does the patient complain of any bitter or sour fluid
nausea and vomiting are due to local pain in abdomen. coming in the mouth with burning?
Painless vomiting suggests any neurological disorder.You • Whether this hot burning sensation is associated with
should ask about: retrosternal discomfort?
• What is the frequency of vomiting that is how many times • Does it occur after meals,on bending or lying down?
does the patient vomit in 24 hours? • Problem of heartburn is very common in pregnancy and
• Try to inquire about the quantity, odor and taste of the also in obese people.
vomitus.
• Does the vomiting occur at any particular time of the Dysphagia
day that is after getting up in the morning, immediately Dysphagia is defined as the difficulty in swallowing.
after any meals or drinks, after receiving any particular • Does the patient complain of something sticking in the
kind of stimulus such as sudden loud noises, sudden throat or the chest?
strong flashes of light, etc. or does it occur after any • Whether the problem is more with solids or liquids or
attack of fever? both equally?
• What is the color of the vomitus? Does it indicate any • Whether the difficulty in swallowing was first with solids
traces of fresh blood (bright red color), bile (greenish- or liquids ?
Common Symptoms Presented by the Patients and Questions to be Asked for Them 11
• Does the patient reveal a H/o any significant and • General causes of abdominal distention are 6 “F”s—
prolonged drug therapy? What was the reason, duration fat, fluid, flatus, feces, fetus and full bladder.
and type of medication? • Is the distention localized or diffuse, symmetrical or
• Is there any family H/o jaundice? assymetrical?
• Any sexual contact history ? • Any movements of the swelling?
• Travel history and immunization status • Is the abdominothoracic respiration visible or is it not
• H/o alcohol intake for long duration. appreciable?
• Has the patient ever been indulged in the habit of skin • Is the onset sudden or gradual?
tattooing (Hepatitis B and C)? • What is the duration and how is the progress?
• Any associated pruritis or rigor? • Any H/o vomiting, loose motions, chronic hepatic
• Any alteration in bowel habit? disease, fever (especially low grade in the evening
• Gastrointestinal bleeding? hours), pulmonary tuberculosis?
• Any association with dyspnea or orthopnea?
Indigestion (Dyspepsia) • Edema over any body part or generalized edema
Indigestion is generally a vague term used by the patient to (anasarca)?
describe some other symptoms such as: • Any significant change in bowel habits?
1. nausea • Any loss of body weight—rapid or gradual?
2. heartburn • Is the swelling increasing in size or is stable?
3. epigastric discomfort • Does the swelling move from one area to another?
• Any association with fever or weakness?
4. abdominal pain
5. belching Weight Loss
6. postprandial bloating
• Inquire whether there is excessive loss of fluid in the
7. angina
recent few days or weeks?
8. functional dyspepsia which may be—reflux like, ulcer
• Take detailed notes on the nutritional habits of the
like or dysmolity like. patient.
Hiccups (Hiccough) • Increased energy expenditure recently due to certain
reasons along with inadequate dietary intake?
(Probably of imitative origin) A spamodic periodic closure • Any previous H/o significant weight loss?
of glottis following spasmodic lowering of diaphragm, • Associated symptoms/diseases?
causing a short, sharp, inspiratory cough. It may be caused • What is the rate and severity of weight loss?
by indigestion, irritation of diaphragm, alcoholism, new • What is the duration and extent of weight loss?
growths of the pleura, certain cerebral lesions, hysteria or a • H/o anorexia or anorexia nervosa?
disturbance of phrenic nerve. If prolonged, it has serious • H/o depression/tension?
significance. • Any significant physical, psychological and social
Treatment factors associated with weight loss?
• Associated amenorrhea whether present?
Hiccups may be treated by antiemetic drugs, rebreathing in • Changes in social well being and lifestyle?
a paperbag, briefly applying the ice-cubes to both sides of
the neck at the level of larynx, or inhalation of carbon dioxide. Weight Gain
Stimulation of nasopharynx with a soft rubber tube or • Inquiries are similar to that of weight loss.
placement of a thin coating of dry granulated sugar in the • In addition, inquire about hypertension, hyperlipidemia
hypopharynx may also be tried. If these are not effective, and diabetes mellitus.
anesthetization of the phrenic nerve may be helpful.
Rectal Bleeding (Hematochezia)
Abdominal Distention
• In most of the cases, it is associated with hemorrhoids
Can be examined in detail at the time of inspection only. (piles) or constipation.
You should look for: • You should try to search for the causes of raised intra-
• Normal contour and fullness of the abdomen. abdominal pressure—such as urethral stricture, enlarged
• The shape of the abdomen—scaphoid, oval, pot-like prostate, big pelvic tumor or pregnancy.
belly, etc. • Any past H/o or family H/o such complaints?
Common Symptoms Presented by the Patients and Questions to be Asked for Them 13
• Does the patient suffer from any bleeding disorders? 1. Oral hygiene
• H/o drug/alcohol abuse? 2. Oral infections
• Any H/o dyspeptic syndrome? 3. Atrophic rhinitis
• Complaint of recurrent vomiting or diarrhea? 4. Any tumor of nasal passage
• H/o anorexia or weight loss? 5. H/o of bronchiectasis
• Any complaint of dizziness or fainting? 6. H/o gastric outlet obstruction
7. Dietary/abuse habits
Blood in the Vomit (Hematemesis) and Blood
8. Drinking habits.
Loss in Stools (Melena)
• Onset: How many hours/days ago did the problem start? CARDIOVASCULAR SYSTEM
• Quantity: Roughly the quantity of blood lost (in terms
Dyspnea, Orthopnea, Paroxysmal Nocturnal
of cupfulls of blood).
Dyspnea (PND) and Dyspnea at Rest
• Color: Fresh or coffee colored.
• Any upper abdominal pain (relieved by food) a few • What is the onset, progress and duration of breath-
months or even years before the onset of hematemesis. lessness? Is the progress very rapid or it took a few days
• H/o chronic alcoholism or jaundice. or months to become severe?
• H/o of drug intake: Aspirin, other NSAIDs, corti- • Is it paroxysmal or is there any variability in the
costeroids or any anticoagulant drugs taken for a long symptoms?
time. • Does it trouble the patient continuously or worsens on
• Associated pain in abdomen. exertion only?
• If no H/o pain or drug intake, then ask for acute or • Is it precipitated by any allergen or change in weather?
chronic cough, respiratory tract infection or recent abdo- • Is it associated with chest pain or fever?
minal or thoracic surgery. • Any associated symptoms like cough (with or without
• H/o fever about a week preceding melena. sputum), hemoptysis, wheeze, etc.?
• H/o dyspepsia or upper gastrointestinal bleeding. • H/o cardiac or respiratory disorders?
• Is the bleeding preceded by intense retching? • Any H/o tobacco or alcohol addiction?
• H/o recent travel to abroad?
Xerostomia
• Aggravating and relieving factors, i.e. what makes the
(Stoma meaning mouth) Dryness of mouth caused by signs and symptoms more severe and what provides
abnormal reduction in the amount of salivary secretions. It relief to the patient?
may occur in diabetes, hysteria, paralysis of facial nerve • What is the severity of the disease—mild, moderate or
involving chorda tympani, acute infections, and some types severe?
of neuroses. It is induced by certain drugs such as nicotine
Chest Pain (Details in the Section of Pain)
and atropine.
Approach to the Patient
Dysgeusia
1. Could the chest discomfort be due to an acute, potentially
(Geusis—taste) Impairment or perversion of the gustatory
life-threatening condition that warrants immediate
sense so that normal tastes are interpreted as being unpleasant
hospitalization and aggressive evaluations?
or completely different from the characteristic taste of a
– Acute ischemic heart disease.
particular food or chemical compound. Other types of
– Aortic dissection.
abnormal taste sensations are—cacogeusia, heterogeusia,
– Pulmonary embolism.
hypogeusia, idiopathic and phantogeusia.
– Spontaneous pneumothorax.
Halitosis 2. If not, could the discomfort be due to a chronic condition
(Latin—Halitus meaning breath; Greek—osis meaning likely to lead to serious complications?
condition). Bad breath. – Stable angina.
You should inquire whether the patient is aware of his – Aortic stenosis.
bad breath, (i.e. either he himself might have realized it or – Pulmonary hypertension.
he might have been told by somebody else). You should 3. If not, could the discomfort be due to an acute condition
also inquire about his: that warrants specific treatment?
14 Essentials of Clinical Medicine
of even up to one week. The pattern repeats itself. For • Daily caffeine and alcohol consumption
example, the Pel-Ebstein fever in case of Hodgkin’s • Drug therapy prescribed or self-medication.
disease in which the fever lasts for about 3 to 10 days • Nonspecific symptom of recent ill health (to consider
followed by afebrile period of the same duration. unusual causes such as infective endocarditis or Lyme’s
5. Low fever: When the temperature does not rise above disease.)
38 degree Celsius and occurs at any time of the day. For • If attacks are paroxysmal?
example, tuberculosis, chronic infection of any part of
– Precipitating factors ( exercise, stress or anxiety)
the body.
– Nature of onset of attack and associated symptoms
6. Hectic or septic fever:
• Accompaniments of fever (presyncope or chest discomfort)
– Chills – Relieving factors (breath-holding exercise).
– Tachycardia Table 2.3: Symptoms and clues
– Sweating
– Respiratory rate Cardiovascular Diseases Presenting with Non-Cardiac Symptoms Like:
– Herpes labialis • Stroke
• Abdominal pain
– Delirium
• Oliguria.
– Febrile convulsion. Facial Clues to Heart Diseases
• Corneal arcus
Table 2.1: History of diseases which can lead to the
• Xanthelasma
diagnosis of a cardiovascular disorder
• Cyanosis
1. Classical H/o rheumatic fever: • Malar flush
– Pain in the joints which fleets from one major joint to other. • Venous pulsations
(Remember that rheumatic fever may be present without joint Clues other than the Facial Clues
pains.) • Carotid bruit
– H/o sore throat, upper respiratory tract infections (URTI), fever • Palmar or tendon xanthomata.
and systemic infections.
– H/o “gnawing pains” may lead to the diagnosis of rheumatic Some Points about Infective Endocarditis
valvular disease in adulthood.
2. H/o syphilis: 1. Typical patient:
– Males: Exposure to infection followed by local sore.
– Females: H/o repeated abortions • Elderly with mitral or aortic valve disease.
– H/o of syphylitic aortitis, aortic regurgitation. • Younger with coronary HD (usually VSD or PDA)
3. H/o hypertension and diabetes mellitus: • Patient with prosthetic heart valves or intravenous
– Record of previous blood pressures.
drug abuse
– Symptoms like headache and dizzy spells.
– H/o polyuria, nocturia, polydipsia and polyphagia. 2. Major symptoms:
4. H/o tobacco consumption: • Nonspecific feverish (flu-like) illness.
– Required in cases of atherosclerotic cardiac disease. 3. Major signs:
• Fever, heart murmur (aortic or mitral regurgitation)
Table 2.2: History of complications produced by
cardiovascular disorders • Splinter hemorrhages and vasculitis
• Clubbing, Osler’s node, rash and Roth’s spot.
1. H/o embolization:
– Record of monoplegia or hemiplegia
Table 2.4: Jones criteria for rheumatic fever
– Hematuria with renal colic
– Sudden shooting pain in a limb with local swelling and cyanosis 1. Major criteria:
– Left hypochondrial tenderness, spleenic infarction – Carditis
– Sudden blindness. – Polyarthritis
2. H/o pressure symptoms due to enlargement of heart chambers: – Erythema marginatum
– LAH (left atrial hypertrophy)—hoarseness, dysphagia – Chorea
– Aneurysm of arch of aorta—pressure on sternum – Subcutaneous nodules
– Erosion of spine with local pain and even paraplegia in patients
2. Minor criteria:
with aneurysm of descending aorta.
– Fever
Arrhythmias – Arthralgia
– Previous rheumatic fever
• Family H/o premature heart disease or sudden death. – Elevated ESR (eosinophillic sedimentation rate) or C-reactive
• Past history of RF, previous heart attacks or other heart protein
diseases Contd...
Common Symptoms Presented by the Patients and Questions to be Asked for Them 17
– now also occur in children and adults >50 years. 5. Attacks with sudden or subacute in repeated short
– Altered sensorium for 5 days and may have con- bursts with pain free intervals lasting weeks or months.
fusion like psychotic reactions. 6. Attacks are usually cyclical, weekly or monthly,
– Full recovery is rule. premenstrual
7. Condition is well between attacks
Carotidynia: lower half headache or facial migraine
8. Headache at times of stress relief (e.g. weekend and
Description of pain: holidays)
1. Most common among older 4th–6th decades 9. Relieved by analgesic or 5-HT agoinsts like sum-
2. Pain is usually located at jaw or neck although periorbital patriptan
or maxillary pain may occur. 10. In 15 to 20 percent of patient visual disturbances (tie-
3. May be continuous, deep, dull and aching, becomes chopsia and fortification spectra) and/or peripheral
pounding and throbbing episodically and circumoral paresthesiae occur before headache
4. Superimposed sharp, ice-pick like jaws phase (migraine aura)
5. One to several times a week, each lasting for several 11. Cessation of headache during pregnancy, especially
min. to hours. in 2nd or 3rd trimester is pathognomonic of migraine.
6. Tenderness and prominent pulsations of cervical carotid
a. and soft tissue swelling overlying carotid ipsilaterally. Cluster Headache or Raeder’s Syndrome or
7. Many patients complain throbbing, ipsilateral headache Histamine Cephalalgia or Sphenopalatine Neuralgia
with carotidynia as well as between attacks. Description of pain:
8. Dental trauma is a common precipitating factor for this Severe pain, waking the patient from sleep in early hours of
syndrome morning.
9. Carotid tenderness more common in hemicranial migraine All ages, above 10 years, mainly in men.
attacks. 1. Distinctive and treatable vascular headache.
Non-pharmacological approach to migraine: 2. Episodic type is most common.
1. Identify and avoid: 3. One to three short-lived attacks of periorbital pain per
– Alcohol (red wine) day over 4 to 8 weeks followed by pain-free interval
– Foods (chocolate, certain cheese, monosodium- that averages 1 year.
glutamate, nitrate containing food) 4. Chr. pain has sustained periods of remission.
– Hunger 5. Each form may transform into other.
– Irregular sleep pattern (both lack and excess) 6. Men >8 times of female.
– Odors (organic) 7. Usually 20 to 50 years, may be in 1st decade.
– Sustained exertions 8. Propanolol and amitryptyline—ineffective.
– Acute changes in stress level 9. Lithium unlike migraine is effective here.
– Miscellaneous (glare, flash) 10. The cluster headache is clinically, genetically and
2. Attempt to manage environmental shifts: therapeutically different from migraine.
– Time zone shifts 11. Periorbital or temporal pain without warning and
– High attitude reaches a crescendo within 5 minute.
– Barometric pressure 12. It is excruciating and deep, nonfluctuating and
– Weather changes explosive, rarely pulsatile.
3. Assessment of menstrual cycle relationship. 13. Strictly unilateral and affects same sides in subsequent
Migraine attacks build up usually over hours and months.
maintained for several hours to days and 14. Lasts for 30 minutes to 2 hours.
characteristically relieved by sleep. 15. With homolateral lacrimation, reddening of eye, nasal
stiffness, lid ptosis, nausea.
Few Other Features of Migrainous Headache 16. Alcohol provokes it
1. Sickening, dull ache or throbbing ache 17. On-off vulnerability to alcohol is pathognomonic to
2. Marked severity cluster headache.
3. Unilateral—different sides on different occasions 18. Unlike migraine, only rarely do foods or emotional
4. Attack usually lasts for 24 to 72 hours but occasionally factors precipitate pain
less than 6 hours. 19. Stricking periodicity of attacks in 85 percent.
40 Essentials of Clinical Medicine
20. At least one bout of daily attacks recurs at about same Petechiae are found on trunk and lower extremity, in
hour each day for duration of cluster bout. mucous memb. and conjunctiva and on palms and sole.
21. Reaches peak over 3 to 5 minutes, remain maximum • Increased ICP (intracranial pressure)
for about 45 minutes and taper off. – > 180 mm H2O in 90 percent cases.
– > 400 mm H2O in 20 percent cases.
Chronic Paroxysmal Hemicrania
• Signs of ICP include:
Similar to cluster headache – Decreased consciousness.
Tension-Type Headache – Papilloedema.
• Episodic tension type – Dilated poorly reactive pupil.
• Chronic tension type. – 6th n. palsy.
Description of pain: – Decerebrate posturing.
a. Used to describe chronic headache. – Cushing’s reflex—bradycardia.
b. Characterized by bilateral tight band-like discomfort. Hypertension
c. In cycles which repeat after several years. Irregular
d. Feels as if the patient is in vise and posterior neck muscles Respiration
are taut. – Cerebral herniation.
e. Pain typically builds slowly, fluctuates in severity and • Causes of neck stiffness:
may persist more or less continuously for many days. – Meningitis.
f. Exertion does not increase pain. – SAH (subarachnoid hemorrhage)
g. Episodic or chronic (> 15 days/ months). – Tetanus.
h. Common in all age groups and females tend to – Strychnine poisoning.
predominate. – Hysteria.
i. In some, anxiety or depression coexist with tension – Cervical spondylosis.
headache. – Meningism.
j. Relaxation always relieves headache; for example, – In meningitis, neck stiffness is absent in severe and
bedrest, massage, or formal biofeedback training. terminal cases or in very young infants.
k. For chronic type tension headache, prophylactic therapy
is recommended. Viral Meningitis
1. Syndrome includes:
Meningitis – Fever.
Bacterial Meningitis – Headache.
– Meningeal irritation coupled with inflammatory CSF
Description of pain:
profile.
• Acute severe headache.
2. Fever may be accompanied by:
• Stiffness of neck and fever.
• Striking accentuation of pain with eye movement – Malaise.
• May be confused with migraine because both have – Myalgia.
pounding headache, photophobia, nausea, vomiting. – Anorexia.
• Acute fulminant illness that progresses rapidly in a few – Nausea/vomiting.
hours or as a subacute infection that progressively – Abdominal pain .
worsens over several days. – Diarrhea.
• Classic triad is: – Lethargy/drowsiness.
– Fever. 3. Profound alteration in consciousness, such as stupor,
– Headache. coma and confusion.
– Nuchal rigidity (stiff neck). 4. Seizures, cranial nerve palsy, suggest parenchymal
• Alteration in mental state—lethargy to coma. involvement but are not typical of uncomplicated viral
• Kernick’s sign and Brudzinski’s sign are classical of meningitis.
meningeal irritation. 5. Headache is usually frontal or retro-orbital and often
• Seizures occur initially in 40 percent. associated with photophobia and pain on moving eyes.
• Rash of meningococcemia—diffuse erythematous 6. Nuchal rigidity is present in most cases but may be mild
maculopapular rash, skin lesion becomes petechial. and present only near limit of neck anteflexion.
Symptomatology and its Causes 41
6. Hemorrhage occurs always when the patient is awake Cerebellar hemorrhage—(may develop over several
and slightly stressed. hours)
7. Presents as abrupt onset of focal neurological deficit. – Characterized by occipital headache, repeated
8. Seizures are uncommon. vomiting and ataxia of gait.
9. Focal deficit typically worsens steadily over 30 to 90 – Dizziness or vertigo may be prominent.
minutes and is associated with decreased conscious- – Paresis of conjugate lateral gaze towards side of
ness and sign of increased ICP such as headache and hemorrhage, forced deviation of eyes to opposite
vomiting. sides or ipsilateral 6th n. palsy
10. Putamen is the most common site for hemorrhage – Ocular sign may include blepharospasm, involuntary
and adjacent internal capsule is invariably damaged. closure of one eye, ocular bobbing and skew devia-
11. Contralateral hemiparesis is sentinel sign. tion.
12. When mild—face sags on one side over 5 to 30 minutes – Dysarthria and dysphagia
speech becomes slurred, the arms and leg weaken – No Babinski’s sign until late.
and eyes deviate away from side of hemiparesis. – Later the patient becomes stuporous and comatose.
14. When severe—drowsiness appears, and also stupor Other Causes of Intraparenchymal Hemorrhage
and sign of upper brainstem compression.
1. Cerebral amyloid angiopathy.
15. Coma with deep, irregular or intermittent respiration,
2. Cocaine-induced stroke.
a dilated and fixed ipsilateral pupil, bilateral Babinski’s
3. Head injury.
signs and decerebrate rigidity.
4. Anticoagulant therapy.
16. In milder cases—edema in adjacent brain may cause
5. Hematological disorders.
progressive deterioration over 12 to 72 hours.
6. Hemorrhage into brain tumor.
17. Thalamic hemorrhage produces a contralateral
7. Hypertensive encephalopathy.
hemiplegia or hemiparesis from pressure into int. 8. Primary intraventricular hemorrhage.
capsule.
– Prominent sensory deficit in all modalities Subarachnoid Hemorrhage
– Aphasia with preserved verbal repetition • Sudden transient loss of consciousness in 1/2 of the
apractagnosia or mutism in nondominant hemorr- cases
hage • It may be preceded by brief moment of excruciating
– Homonymous visual field defect headache.
– Deviation of eyes downwards and inwards, • The patient often calls the headache “as the worst
unequal pupils with absence of light reflex, skew headache of my life”.
deviation with the eye opposite to the hemorrhage, • Usually generalized and vomiting is common.
displaced downwards and medially, ipsilateral • Although sudden headache in the absence of focal
Horner’s syndrome, absence of convergence, neurological symptoms is hallmark of aneurysmal
paralysis of vertical gaze and retraction nystag- rupture, focal neurological deficits may occur.
mus. Patients may later develop a chronic, • Hemiparesis, aphasia and abulia develops
contralateral pain syndrome.(Dejerine-Roussy • Third n. palsy associated with papillary dilatation, loss
syndrome) of light reflex and focal pain above or behind eye may
occur with an expanding aneurysm at the junction of
In pontine hemorrhage, deep coma with quadriplegia
posterior communicating artery and internal carotid
usually occurs over a few minutes.
artery.
– Prominent decerebrate rigidity and pinpoint (1 mm)
• Sixth n. palsy may indicate an aneurysm in cavernous
pupil that reacts to light.
sinus and visual field defect may occur with expanding
– Impairment of reflex, horizontal eye movement supraclinoid carotid or anterior inf. cerebellar artery
evoked by head turning (doll’s head, oculocephalic aneurysm.
maneuver) or by irrigation of ears with ice cold water. • Pain in or behind the eye and in low temple can occur
– Hyperpnea, severe hypertension and hyperhidrosis with an expanding MCA (middle cerebral artery)
are common. aneurysm.
– Death usually occurs within a few hours, but there • Growing aneurysm rarely cause headache in the absence
are occasional survivors. of neurological symptoms and signs.
Symptomatology and its Causes 43
• Aneurysm can undergo small rupture and leak of blood 4. Mostly in men and rarely familial.
into subarachnoid space. Therefore called “sentinel 5. Headache (without bleeding) may be hemicranial and
bleeds.” throbbing like migraine or diffuse.
6. Focal seizures with or without generalization in 30
DELAYED NEUROLOGICAL DEFICIT percent.
Re-Rupture 7. 1/2 of AVM cases present as IC hemorrhage.
8. Hemorrhage may be massive leading to death, or may
a. In first month following SAH is about 30 percent with
peak at 7 days be small as 1 cm leading to minor focal symptoms or
b. Sixty percent mortality, poor outcome no deficit.
9. Large AVM of ant. circulation may be associated with
Hydrocephalus a systolic and diastolic bruit (sometimes self-audible)
over eye, forehead, or neck and bounding carotid
a. Can cause stupor and coma.
pulse.
b. Develops over a few days or weeks.
10. Headache at onset of AVM rupture is not generally as
c. Progressive drowsiness or slowed mentation (abulia)
with incontinence. explosive as with aneurysmal rupture.
d. Chronic hydrocephalus may develop weeks to month Venous Anomalies
after SAH and manifest as gait, difficulty, incontinence
1. Development of anomalous cerebral, cerebellar or
or impaired mentation.
e. Lack of initiative in conversation or failure to recover brainstem drainage.
independence. Capillary Telangiectasia
1. Are true capillary malformations that often form extensive
Vasospasm
vascular networks through an otherwise normal brain
a. Signs of ischemia appear 4 to 14 days after hemorrhage, structure.
Mostly 7 days. 2. Pons and deep white matter are typical location and these
b. Spasm of MCA causes contralateral hemiparesis and capillary malformations can be seen in patients with
dysphagia. hereditary hemorrhagic telangiectasia (Osler-Rendu-
c. Proximal Ant. cerebral artery vasospasm causes abulia Weber syndrome)
and incontinence.
3. If bleeding does occur, it rarely produces mass effect
d. Severe vasospasm of postcerebral artery causes
hemianopia. or significant symptoms.
4. No treatment option exist.
Hyponatremia Acquired Vascular Lesions
a. Develops within first 2 weeks after SAH. a. Cavernous angiomas
b. Cerebral salt - wasting syndrome clears over the course 1. Familial cavernous angiomas have been mapped to
of 1 to 2 weeks. several different chromosomal loci, the gene
Vascular Anomalies responsible for 7q linked form encodes a protein
that interacts with a member of RAS family of
Congenital GTPases.
True arteriovenous malformations (AVM): 2. Seizures may occur if malformation is located near
Description of pain: the cerebral cortex.
1. Headache, focal seizures and IC hemorrhage. b. Dural AV fistula
2. AVM occurs in all parts of cerebral Hemisphere, brain- 1. Patients may complain of a pulse-synchronous
stem and spinal cord, the largest one, are most cephalic bruit (pulsatile tinnitus) and headache.
frequent. In posterior half of hemisphere—commonly
2. Increased ICP.
a wedge-shaped lesion extending from cortex to
• So vascular etiology of headache may be due to:
ventricle.
3. Although lesion is present from birth, bleeding or other – IC aneurysms
symptoms are most common between ages 10 and – Malignant hypertension
30 years and sometimes late 50. – SAH, etc.
44 Essentials of Clinical Medicine
Table 3.2: The clinical features of arterial, neurogenic and venous claudication
Arterial Neurogenic Venous
Pathology Stenosis or occlusion of major Lumbar nerve root or cauda Obstruction to the venous outflow of the
lower limb arteries equina compression (spinal stenosis) to iliofemoral venous occlusion
Site of pain Muscles, usually the calf but may III-defined. Whole leg. May be
involve thigh and buttock associated with numbness and tingling Whole leg. ‘Bursting’ in nature
Laterality Unilateral if femoropopliteal, and Often bilateral Nearly always unilateral
bilateral if aortoiliac disease
Onset Gradual after walking the Often immediate upon walking or Gradual, often from the moment walking
claudication distance even standing up commences
Relieving features On cessation of walking,
pain disappears completely Eased by bending forwards and Usually necessary to elevate leg to relieve
in 1–2 minutes stopping walking. May have to sit discomfort
down to obtain relief.
Color Normal or pale Normal Cyanosed. Often visible varicose veins.
Temperature Normal or cool Normal Normal or diseased
Edema Absent Absent Always present
Pulses Reduced or absent Normal Present but may be difficult to bellowing to
edema
Straight leg raising Normal May be limited Normal
Skeletal Anomalies 4. Pain is usually dull ache but may be throbbing, its location
a. Metastasis is occipitofrontal.
b. Paget’s disease: 5. Nausea and stiffness often accompany headache.
6. Some report blurred vision, photophobia, tinnitus and
Description of pain: vertigo.
1. Enlargement of skull is often unnoticed by patients except 7. May resolve over a few days but may persist for months
by awareness of increasing hat size. or weeks.
2. Facial pain and headache are initial complaints in some. 8. Often seen in patients over 10 years of age.
3. Backache is dull or shooting or knife like in lumbar region 9. Both sex.
and may radiate into buttocks or lower extremities.
4. More serious neurological complications can result from Extracranial Causes
overgrowth of bone at base of skull (platybasia) and
compression of brainstem. Temporal (Giant-Cell) Arteritis
5. Compression of spinal cord may cause paraplegia. Description of pain:
6. Pathological fracture of vertebrae may also produce 1. An inflammatory disorder of arteries that frequently
spinal cord lesions. involves the extracranial carotid circulation.
2. Usually over 55 years, either sex.
Tumors, Granulomas and Abscess 3. Average age of onset is 70 years and women account
Headache is dull aching, either hemicranial or generalized, for 65 percent of cases.
progressively becomes severe and refractory to therapy. 4. About 1/2 patients with untreated temporal arteritis
Fever occurs in 50 percent cases and is of low grade. develop blindness due to involving of ophthalmic artery
and its branches, indeed the ischemic optic neuropathy
Post Lumbar Puncture
induced by giant cell arteritis is a major cause of rapidly
Description of pain: developing bilateral blindness in patients over 60 years.
1. Usually begins with 48 hours, may be delayed up to 12 5. Typical presenting complaints are headache,
days. polymyalgia, rheumatica, jaw claudication, fever,
2. Incidence 10 to 30 percent. weight loss.
3. Positional (usually)—begins when the patient sits or 6. Headache is a dominant symptom and often appears
stands upright; relief upon reclining or with abdominal in association with malaise and muscle aches.
compression. 7. Headache may be unilateral or bilateral and is located
– Worsened by head shaking and jugular vein com- temporally in 50 percent but may involve any and all
pression. aspect of cranium.
Symptomatology and its Causes 45
Headache Associated with Nonvascular Table 3.5: Headache caused by systemic illness
Intracranial Disorder • Inf. mononucleosis.
1. Increased pressure of CSF • SLE.
• Chronic resp. failure (hypercapnia).
2. Decreased pressure of CSF • Hashimoto’s thyroiditis.
3. IC infection. • Drugs (glucocorticoids withdrawal, OCPs, ovulation promoting drugs).
4. Sarcoidosis and other noninflammatory diseases. • Inflammatory bowel disease.
5. Related to intrathecal drug administration. • HIV.
• Malignant hypertension, pheochromocytoma (diastolic pressure of
6. IC neoplasm. at least 120 mm Hg are required for headache).
7. Other IC disorders. • Orthostatic headache suggests subdural hematoma or benign IC
hemorrhage or a lumbar puncture done a few hours back.
Headache Associated with Substances • Headache due to ICT is more in early morning, causes sleep
or Their Withdrawal disturbances associated with projectile vomiting with or without focal
1. By acute substance use or exposures. neurological deficit.
2. By chronic substance use or exposures. Table 3.6: Pain sensitive and insensitive structures
3. By withdrawal (acute use).
Pain sensitive structures of CNS:
4. By withdrawal (chronic use). Scalp.
Headache with Noncephalic Infection Aponeurosis.
Middle meningeal a.
1. Viral postherpetic pain. Dural sinuses.
2. Bacterial. Flax cerebri.
3. Others. Proximal segments of large plial artery
Pain insensitive structures of CNS:
Headache with Metabolic Disorders Most of brain parenchyma.
1. Hypoxia (decreased O2 supply). Ventricular ependyma.
Choroid plexus.
2. Hypercapnia (increased CO2 accumulation). Plial veins.
3. Mixed hypoxia and hypercapnia.
4. Hypoglycemia. There is a midbrain locus for generation of headache.
5. Dialysis.
6. Others. JOINT PAIN
3. Cardiac – Hand-foot-mouth
– Acute infections – Vincent’s angina (ulcerative gingivitis)
– Valvular heart disease – Glandular fever
– LVF 3. Miscellaneous:
– Congenital acyanotic heart disease – Trauma from teeth/dentures
– Left vent systolic dysfunction – Leukoplakia
– Hypertension – Carcinoma
– Cardiomyopathies 4. Associated with systemic disorders
– Arrhythmias—AF – Drug allergies—sulfonamides, gold, cytotoxics
– Orthopnea indicates severe heart failure. – Iron, folate, vit-B12 def.
4. Metabolic – Leukoplakia
– Hypokalemia – Acute leukemia
– Uremia – Reiter’s syndrome
– Diabetes – Beçhet’s disease
5. Neurological – Crohn’s disease
Respiratory center depression as in – Ulcerative colitis
– Syringobulbia
– Coeliac disease
– Motor neuron disease
5. Associated with skin disorders
– Guillain-Barré syndrome
– Lichen planus
– Bulbar polio
– Erythema multiforme
– Myasthenia gravis
– Pemphigoid
6. Psychogenic
– Pemphigius vulgaris.
7. Pharmacological:
– Drug-induced respiratory disorders
– Drug-induced cardiac disorders. SORE TONGUE
(Small multiple ulcers centrally located)
SORE MOUTH • Vit-B complex (vit-B12) deficiency
i. Aphthous ulceration. • Iron deficiency
ii. Sharp edges of caries teeth (traumatic ulcers). (ulcers which are laterally located)
iii. Vincent’s angina. • Malignant ulcers
iv. Thrush (Candida albicans). • Leukoplakia
v. Spirochetal in origin.
vi. Ill-fitting dentures (traumatic ulcers). BAD BREATH
vii. Angular stomatitis (riboflavin). (Halitosis)
viii. Scurvy—recurrent gingivitis. • Chronic infection of upper respiratory tract
– Blood dyscrasia—recurrent gingivitis. • Caries tooth
– Persistent ulceration due to agranulocytosis. • Pyorrhea
– Local malignancy. • Stasis in pharyngeal pouch, esophagus or stomach
(pyloric stenosis or ca.)
Causes of Painful Mouth • Achalasia cardia
1. Idiopathic—recurrent aphthous mouth ulcers. • Bronchiectasis or lung abcess by E. coli and B.
2. Infections: pyocyaneus
– Candidiasis • Musty breath in hepatic coma (dead mouse)
– Dental sepsis • Uriniferous in uremia
– Herpes simplex virus (HSV-1) • Sweet—diabetic acidosis
– Coxsackie virus • Alcohol, paraldehyde and organophosphates give peculiar
– Herpangina smell.
50 Essentials of Clinical Medicine
v. Barrett’s ulcer. Of the various causes mentioned above, the common causes
vi. Polyps and carcinoma. are:
vii. Achalasia and foreign bodies. i. Chronic peptic ulcer.
ii. Acute ulcers and multiple erosions.
Stomach and Duodenum iii. Esophageal varices.
i. Chronic duodenal ulcer. iv. Mallory-Weiss syndrome.
ii. Chronic gastric ulcer.
Dealing with the Patient of Hematemesis
iii. Multiple erosions and acute peptic ulcer.
iv. Tumors, polyps and carcinoma. 1. If in shock:
– Measure BP, (i.e. manage shock), blood / plasma
Small Intestine expanders, then —
i. Very rarely, Meckel’s diverticulum may present with – Upper GI endoscopy, then —
hematemesis. – Seal that particular site of bleeding (varices are
ii. Peutz-Jeghers syndrome. present, as cherry red spots.)
• Inject at that site, sclerosing agent to obliterate
iii. Polyps.
the varices (e.g. absolute ethyl alcohol but now-
iv. Vascular malformation.
a-days 3 percent polido canal is used).
v. Various tumors. • If gastric varices – polido canal is not affectve.
We use Nectacryl (glue), when comes in contact
General Causes with tissue, it solidifies. But if this gets released
i. Hemorrhagic disorders—thrombocytopenia, purpura anywhere during the process, it will solidify and
may damage this endoscope, if fall in eyes,
hemophilia, pernicious, and other anemias, Ehlers-
corneal damage.
Danlos syndrome, DIC, liver disease, periarteritis
– Variced banding—tie the varices.
nodosa, amyloidosis, Turner’s syndrome, Kaposi’s – Thermal probe—we can seal that varices.
sarcoma, neurofibromatosis, etc. • In case of MW tear and Boerhaeves—we have to do
ii. Ingestion of drugs—steroids, NSAIDs, etc. surgical procedure.
iii. Salicylates and alcohol. – Upper GI bleeding, treatment is totally symptomatic.
54 Essentials of Clinical Medicine
Table 3.11: Differences between hemoptysis and hematemesis PRECIPITANCY AND HESITANCY OF URINE
Hematemesis Hemoptysis Definitions
1. With vomiting • With cough
Hesitancy: The patient notices that he must wait for urination
2. Not frothy • Frothy due to admixture of air.
3. Altered or coffee color • Frank red color
to start. If he strains, he has to wait more as the median
4. pH acidic • pH alkaline lobe bends down on straining to obstruct the internal urethral
5. Clots may be passed • Fresh frothy. orifice.
with frank blood Dysuria: The stream is often weak and tends to dribble
6. Mixed with food particles • Mixed with macrophage and towards the end of micturition because of increasd urethral
neutrophil resistance and derangement of internal urethral opening,
7. With food • Without food
more force is required for urination.
8. Gastrointestinal symptoms • Respiratory symptoms present.
present Frequency: This seems to be the earliest symptom in majority
9. Malena present • Malena absent of cases. In the beginning, frequency is mostly nocturnal.
10. Vomitus not stained for • Sputum is tinged pink for The patient gets up twice or more during night. Such
following days following 2–3 days frequency is mainly due to vesical introversion of the
11. Previous H/o peptic ulcer • Previous H/o. respiratory disease sensitive prostatic mucous membrane due to its enlargement
disease
upwards. Gradually, the frequency is experienced in both
12. Diagnosis made by • Diagnosis made by gastroscopy
by day and night. This is due to irritability of bladder and
bronchoscopy
amount of residual urine
Urgency: Intense desire to urination due to obstruction.
PALPITATIONS
Renal causes—bladder neck obstruction.
1. Physiological—exercise, emotional or sexual • Prostate—enlarge prostate (benign prostatic
excitements, etc. hypertrophy).
2. Excessive—tea, coffee, tobacco, alcohol consump- • Cerebral causes—cerebrovascular accidents (CVA)
tion. cerebral tumors, head injuries/trauma.
3. Anxiety state.
4. Extrasystoles—atrial, ventricular. FREQUENCY OF MICTURITION AND NOCTURIA
5. Tachyarrythmias—atrial and ventricular. 1. Renal causes—pyelitis, stone, TB, movable kidney.
6. Endocrinal causes—pheochromocytoma, thyro- 2. Urinary bladder—congenitally contracted bladder (small-
toxicosis, hypoglycemia. sized bladder), tumors, cystitis, vescicular calculus,
7. High output states—anemia, pyrexia, aortic regurgi- cystocele, benign prostatic hypertrophy causing incom-
tation, PDA, beri-beri, A-V fistula, Paget’s disease. plete evacuation.
8. Drugs—atapine, adrenaline, aminophylline, thyroxine. 3. Ureter—ectopic ureter partial stricture of ureters, stone.
9. Psychogenic – prolonged anxiety states (soldier’s heart, 4. Urethra—stricture of urethra, incompetent internal
neurocirculatory asthenia, Da Costa’s syndrome). urethral sphincter, urethritis, neoplasm, balanitis,
10. Non-cardiac conditions: Thyrotoxicosis, hypogly- phimosis.
cemia, pheochromocytoma fever. 5. Prostatic causes—prostatitis, senile enlargement and
malignant prostate.
POLYURIA 6. Other causes—all the causes of polyuria (as described
earlier)
• Excessive water drinking. — PSU psychogenic, pregnancy pressure due to
• Diuretic therapy. enlargement of surrounding structures.
• Cold weather.
• Stress/anxiety. RETENTION OF URINE
• Diabetes mellitus.
Causes
• Diabetes insipidus (pituitary and nephrogenic).
• Renal-chronic renal failure, recovery phase of acute Mechanical
tubular necrosis. i. Urinary bladder—stones, tumors, blood clots, and
• Psychogenic—psychogenic polydipsia. contracture of bladder neck.
Symptomatology and its Causes 55
– Diagnosis of obstr. lesions (seen luminal or extra- We spray Lugol’s iodine on area:
luminal) • Yellow color—normal
• 2nd Phase: • No stain—malignant
– Double constrast study Endoscopy: Then methylene blue is used—Blue color, i.e.
– To diagnose ulcers and muscle lesion. malignant will become blue.
• 3rd Phase:
• Then water—to remove extra strain
– Follow through study of esophagus
• Then biopsy and then lab.
– Image intensifier study
– Done for motility disorders Endosonography: (sensitivity = 60-70 percent)
2. 24 hrs. pH monitoring Small US (ultrasound) wave is sent through endoscope.
A narrow lumen fire catheter is used and end is kept 5 • To diagnose the carcinoma of submucosal region, i.e.
cm above LES and kept for 24 hr. These patients will very early stage-very sensitive
perform all normal activities. And pH is recorded with • To diagnose—mediastinal carcinoma
the help of small recorders. (up to duodenum upper endosonography)
To diagnose severity of reflex esophagitis. Gamma Scintigraphy: (Sensitivity = 90 percent)
3. Pressure monitoring • To diagnose reflex esophagitis.
To study pressure changes in esophagus Amount of regurgitation is studied with the help of gamma
– Balloon catheter camera.
– Pull the catheter gradually out
– As soon as we reach LES, we keep the catheter To Differentiate Between Angina and
here for 10-30 sec and pressure changes are studied. Due to Esophagus
(normal is 10-30 mm Hg during act of swallowing) 1. ECG – typical changes but not so effective in esophageal
– If pressure > 30, then hypertensive LES disorder (also similar changes may be seen).
– If pressure < 10, then GERD (Gastroeosphageal 2. Tread Meal Test (TMT)
Reflex Disease)
3. Thallium scan—film of heart is taken with gamma or
Then 10-30 sec at midesophagus (normal pr. = 30-70
(exercise thallium scan) scan.
mm Hg)
4. Endoscopy.
– If pressure > 70, motility disorder
– If pressure > 100, nutcracker esophagus
– If pressure < 30, achalasia cardia CONSTIPATION
Then catheter toward UES (Cricopharyngeus) (normal Table 3.12: Types of constipation and causes
60-80 mm Hg) Example
– If pressure > 80, then hypertensive UES • Recent onset
– If pressure < 60, then hypotensive UES • Colonic obstruction Neoplasma: Structure: Ischemic,
4. Upper GI endoscopy diverticular, inflammatory.
– Esophageal direct endoscopy • Anal sphincter spasm Anal fissure, painful haemorhoids
– Exclude other pathological disorders • Medications
– Motility disorder is not pathology but a functional • Chronic irritable bowel
syndrome Constipation–predocument, alter-
disorder.
nating.
– (Sensitivity of barium X-ray only 65 percent) • Medications Ca blockers, antidepressant.
– In endoscopy, one can mark out any signs of • Colonic pseudo-obstruction Slow transit constipation
inflammation and site of inflammation and distance Megacolon (rare, Hirschsprung’s,
from incisors. Chagas)
– Severity of lesions/obstruction. • Disorders of rectal evacuation Pelvic floor dysfunction, anismus,
• Grade I—Streak of blood vessels esophagitis descending perineum syndrome, rectal
mucosal prolapse, rectocele.
• Grade II—Streak + patchy esophagitis
• Endocrinopathies Hypothyroidism, hypercalcemia,
• Grade III—Streak + patches + ulcers pregnancy
– By endoscope, we can make out varices (portal • Psychiatric disorders Depression, eating disorders, drugs.
hypertension) • Neurologic disease Parkinsonism, multiple sclerosis,
– To differentiate between malignant and benign spinal cord injury
carcinoma, we use chromoendoscopy. • Generalized muscle disease Progressive systemic sclerosis.
58 Essentials of Clinical Medicine
This has been described in great detail in the section of “enterogenous” cyanosis, produced by abnormal hemo-
“Neurological Examination”. globins such as sulphemaglobin and methemoglobin may
b. Hints provided by gait about the locomotor abnorma- also be caused by drugs such as dapsone and some
lities. sulfonamide.
i. Any trauma to the lower limb—indicated by cast The pink color characteristic of carbon monoxide
(plaster) or wound dressing. poisoning from coal gas is due to excessive carboxy
ii. Painful gait: If the gait is moderately painful, the hemoglobin in the blood. Metabolites of same drugs cause
patient spends as short a time as possible with the striking abnormal coloration of skin; for example, mepacrine
affected foot on the ground. This gives rise to a dot (yellow), clofazamine (red) and phenothiazines (slate gray
darn pattern of rhythm, the dot represents the time on exposed areas), the artificial lightening may influence
spent on the painful limb. If the pain is very severe, the appearance of the normal skin color. Therefore, it is
the whole limb is held flexed and foot is placed always suggested that the physical examination of the patient
delicately on the ground for a very very short period. should be carried out in the normal daylight as far as possible.
The painful gait usually requires a support for
walking. PALLOR
iii. Painless gait: In a painless gait, the normal smooth
rhythm is disturbed either because of short limb, a Pallor is defined as lack of color or paleness.
deformed or because of stiff joint or weak muscles. Seen in conditions like:
The effect of muscle weakness will depend on the • Anemia or progressive anemia (if the pallor increases
site and degree of muscle pathology. For example, continuously in magnitude).
unilateral abductor muscle weakness at the hip • Vasoconstriction.
produces Trendelenburg’s gait. • When the person is faint or frightened.
Bilateral weakness of gluteal muscles causes a (Examination of the mucous membranes may help to
waddling gait. If the gait is bizarre or seems greatly distinguish the pallor of anemia from that of other causes)
exaggerated in comparison with other objectives,
finding psychological causes should be considered. Causes of Pallor without Anemia
However, in adolescents, disk problem may also
• Peripheral circulatory failure.
present with bizarre gait.
• MS/AS severe.
• Myxoedema.
Clothing
• Nephrotic syndrome
The clothing of a person may provide important clues like: • Sheehan’s syndrome
• The place to where the patient belongs? Its culture, • Vasovagal attack.
tradition, etc.
• The socioeconomic status may also be judged. PLETHORIC COMPLEXION
• Sometimes the clothings may provide hint about the
occupation of the patients. • Vasodilation causes deep pink complexion even in the
• The clothing may give as the idea about the patient’s absence of anemia.
personality, state of mind, social circumstance. • Polycythemia, some alcohol abuser’s with a pseudo-
• It may provide hints about the neurological disorders Cushing’s syndrome and Cushing’s syndrome.
like fecal soiling of clothes indicate towards learning
difficulties or dementia. Improper/inappropriately juvenile CYANOSIS
dress may suggest anorexia nervosa. The word cyanosis has been derived from a Greek word
“Kyanos” meaning dark blue and “osis” meaning condition.
COMPLEXION It is defined as the bluish, grayish, slate like or dark purple
The color of the face depends upon the variations in discoloration of the skin and mucous membrane caused by
oxyhemoglobins, reduced hemoglobin, melanin and to a the presence of abnormal amounts of reduced hemoglobin
lesser extent carotene. Unusual skin colors may help us to in the blood. At least a level of 5 gm percent of reduced
make a clear-cut diagnosis of the disease process; for hemoglobin should be present in the blood for cyanosis to
example, shallow brownish tinge. The bluish tinge of appear.
The General Examination 63
In case of deep and longstanding jaundice, a distinct • Wet ginger, chronic suppuration, necrotic tumors and
greenish color develops in the sclerae and in the skin owing certain skin disorders give out characteristic odors.
to the oxidation of bilirubin to biliverdin which is greenish • Halitosis (Latin-Lalitus, breath + Greek Osis condition).
in color. Bad breath or malodorous breath is often unrecognized
by the patient. Halitosis is often caused by the remains
INVOLUNTARY MOVEMENTS of food particles in the mouth, any pathologic conditions
They have been described in detail in the section of section like gingivitis, stomatitis, atrophic rhinitis, tumors of
of “Neurological Examination”. nasal passages, as well as pulmonary suppusation.
• Offensive breath is also seen in conditions like bron-
VOICE AND SPEECH chiectasis (with foul-smelling expectoration). Gastric
outlet obstruction (like scarring, pyloric stenosis, gastric
Each individual has his/her own characteristic (typical) voice carcinoma) may cause foul-smelling erructations.
and speech. Any disturbances in the functioning and • Addictive substances like alcohol, tobacco and marijuana
structure of tongue, palate, nose, integrity of mucosa, and can be identified by their smell.
nerve supply of larynx and capacity of lung causes
abnormality in the normal speech. Many of the causes of HEIGHT AND WEIGHT
abnormality may be recognized by inspection; for example,
Obesity
a cleft palate, nasal obstruction, loose dentures or a dry
mouth. Voice in myxoedema may be so characteristic that Obesity is defined as a condition when energy intake (in the
diagnosis can be made over the telephone without seeing form of diet) exceeds the energy expenditure. It is a
the patient. The normal infections or tone disappear, speech multifactorial condition. It is often associated with
is low pitched, slow and deliberate and seems to require hypertension, hyperlipidemia, and diabetes mellitus. Obesity
more effort than normal and also it sounds thick. These also has a familial (hereditary inheritance).
changes are due to myxoedema infiltration of the tissues Types of Obesity
concerned in voice production.
1. Generalized obesity: It is deposition of excess amount
The following points are to be considered in the
of fat uniformly all over the body. The most important
examination of speech and language:
cause seems to be overeating. It is characterized by the
• Spontaneous speech. presents of double chin.
• Articulation. 2. Android obesity: Excessive deposition of fat over the
• Fluency. region of waist.
• Paraphasios (it is a form of aphasia, the misuse of spoken 3. Gynoid obesity: Excessive fat deposition over hips and
words or word combinations). thighs.
• Grammar. 4. Superior (central) type of obesity: Excessive fat deposi-
• Syntax (a way that words and phrases are put together tion over face, neck and upper part of trunk. The arms
to form a sentence in a language). are thin, e.g. Cushing’s syndrome. Regional distribution
• Naming objects concepts. of fat holds greater prognostic significance than absolute
• Comprehension of spoken comments. degree of obesity. Simple and best assessment of this is
• Repetition of spoken phrases. done by calculating waist-hip ratio.
• Reading aloud. • Hip measurement: Done at a level of maximum
• Handwriting. measuring portion, i.e. over the buttocks.
• Waist measurement: Done at a level of minimum
ODORS (narrowest) measuring portion, i.e. between the bony
Sometimes “odors” can help the clinician to come to the cage of rib and iliac crest.
diagnosis of certain disease processes. If the waist-hip ratio is 0.8 or less and the con-
• Fetor hepaticus—liver failure. figuration (type of obesity) is pear shaped, then the
• Sweetness of breath—in diabetes and severe starvation, subjects have better prognosis over those who have
ketoacidosis. their waist-hip ratio of 0.9 or more and configuration
• Smell of certain wounds—Pseudomonas aeruginosa or of apple-shaped type because these people have a
ulcers. greater chance of developing cardiovascular disease.
66 Essentials of Clinical Medicine
(Causes of “weight gain” and weight loss have • Recording of JVP: It is another way to assess the state
been described in the section of symptomatology). of hydration.
Complication of Obesity • Dehydration: It occurs in conditions like vomiting,
diarrhea, sweating, polyuria. A detailed history about the
• Benign intracranial hypertension.
nature and quantity of fluid loss should be taken. Loss
• Sleep apnea.
of skin elasticity should be assessed carefully because it
• Exertional breathlessness. may be due to other causes like collagen damage also.
• Reflux symptoms. Elevation of hemoglobin concentration, packed cell
• Increased blood pressure. volume (PVC) and plasma osmolality provide of evidence
• Gallstones. of severity of dehydration.
• Abdominal striae.
• Impaired fertility. EDEMA
• Stress/urge incontinence.
The term edema has been derived from the Greek word
• Gynecological malignancy.
oedema meaning swelling. It is defined as a local or
• Osteoarthritis. generalized condition in which the body tissue contains an
• Varicose veins. excessive amount of tissue fluid. A generalized edema was
• Dependent edema. previously called dropsy; now it is called anasarca. Various
• Pes planus (flat foot). terminologies have been given depending upon the site of
accumulation of tissue fluid as follows:
Hydration
• Ascites – Abnormal collection of fluid in
About sixty to seventy percent of our total body weight is peritoneal cavity.
comprised by water. Two-thirds of it is intracellular, another • Hydrothorax – Abnormal accumulation of fluid
two-thirds is interstitial fluid and rest is in the form of in pleural cavity.
circulation blood. • Anasarca – Generalized edema.
Assessment of Hydration • Pericardial effusion – Abnormal collection of fluid in
• Skin elasticity test: Skin over different body parts, the pericardial cavity.
especially the extremities and the trunk, is pinched for 5 • Pleural effusion – Pathological collection of fluid in
seconds and then left to regain its normal position. If the pleural cavity.
the skin is well hydrated, it will immediately return to its Conditions Causing Anasarca
normal condition; whereas it will take comparatively
longer time to do to if it is dehydrated. Anasarca is generalized swelling all over the body.
• Other tests for assessing hydration are: Causes are:
– Recording of intraocular pressure (IOP). It falls as • Severe anemia with hypoproteinemia.
the dehydration continues. Normal IOP varies • Nephrotic syndrome.
between 10 and 25 mm Hg (with a mean of 16 ± • CCF (Rt.) pericardial effusion.
2.5). • Chronic malabsorption with hypoprotein.
– Recording the blood pressure. • Hepatic cirrhosis, protein losing enteropathy.
– Looking for a postural drop in blood pressure. • Allergic—angioneurotic edema.
• Presence of edema: It is checked by applying firm
Causes of Pedal Edema
pressure (for at least 3-10 seconds) over the angle behind
the medial malleolus. And, if it is present, then its extent • CCF.
elsewhere is assessed by pressing over the shin of tibia, • Cirrhosis of liver.
in medial thigh region and in sacral area also. It may • Anemia with hypoproteinemia.
also be assessed by pressing over the dorsum of the (Pitting on pressure is noticed when the circumference of
foot with the thumb. the limb increases by 10% of the original).
The General Examination 67
Table 4.5: Differences between venous edema and lymphatic edema Blood Pressure
Venous edema Lymphatic edema • Record the BP in all the four limbs.
1. Pitting Non-pitting Jugular Venous Pressure (JVP)
2. Venous collaterals present No venous collaterals present
3. Homan’s sign present Not present • Raised or normal?
4. Peu de orange skin not present May be present
5. Reversible after treatment Usually not reversible
HAIR
Areas of Special Attention in You should look for:
Case of Edema • Presence (normal or sparse) and color of sparse hair.
Assessment • Presence (normal, sparse or excessive) and distribution
• Fundal hemorrhage. hair over the body parts.
• Periorbital edema. According to the age, 3 different types of hair are seen
• Tonsils. over the body:
• JVP (Jugular venous pressure). – Lanugo/fine long hair covering the body of fetus but
• Cardiac size. normally shed about a month before birth.
• Gynecomostia and other signs of hepatic disease. – Lanugo hair are replaced by vellous hair (which cover
• Blood pressure. much of the body surface).
• Pleural effusion signs. – They are replaced by terminal hair on the scalp.
• Signs of liver and spleen disorders. • Inspection of scalp hair for its lusture, calibre, structure,
• Ascites, bowel sounds. tensile strength and density.
• Clubbing leukonychia. • If defect is alopecia, then determine whether the
• Abdominal veins. pathology is of hair or scalp itself.
• Edema of genital parts.
• Fungal infection, lice, or nits.
• Petechial hemorrhage.
• Pedal edema. • Examine secondary sexual hair for its nature and
distribution.
PHYSICAL EXAMINATION • Presence of dandruff over the scalp.
Vitals The amount and distribution of hair varies in normal
individuals and is characterized by their familial and racial
Pulse factors; for example, Asians—long, straight hair; Mongoloids
• Pulse rate. —sparse facial and body hairs, Negroes—curly hair,
• Regular or irregular (rhythmic or non-rhythmic). Europeans—wavy hair.
• Normovolemic, hypervolemic, or hypovolemic.
• What is the tension in the pulse? Related to Scalp Hair
• Conditions of vessel wall. • Alopecia—loss of hair
• Any special characteristic. – Alopecia areato—hair fall in patches.
• Radiofemoral delay. – Alopecia universalism—loss of all body hair.
• Peripheral pulsations present or absent. Fungal infection (affected areas contain hair broken off
Temperature close to the skin).
• Whether the patient is febrile or afebrile? You should look for posterior cervical lymphadenopathy
• If febrile, how much is the temperature in oF? (infection by nits and lice).
68 Essentials of Clinical Medicine
Contd... 3. Hypoxic:
Features Condition – Persistent hypoxia causes opening of deep A-V
Pitting Psoriasis.
fistulae of the terminal phalanx.
Onycholysis. Trauma, psoriasis 4. Ferritin:
Straie leukonychia Minor trauma, may be a normal finding – Decreased ferritin in systemic circulation – dilatation
Severe leukonychia (white Hypoalbuminemia, chronic liver disease of AV anastomosis and hypertrophy of terminal
nails or Terry’s nails) and other wasting disease. phalanx.
Transverse ridging (Bean’s Recent acute illness. 5. Platelet-derived growth factor (PDGF):
lines) due to temporary
– Released secondary to infection anywhere in the body
arrest of nail growth
Fungal infection Thickening, crumbling and discolor- also causes vasodilation and this is latest and “most
ation. acceptable” theory of clubbing.
Red half moons Congestive cardiac failure.
Causes of Clubbing
Blue half moons Hepatolenticular degeneration, Wilson’s
disease. • Respiratory causes
Half and half nails Chronic renal failure. – Bronchial carcinoma.
Black nails Silver poisoning, Addison’s disease (rarely) – Intrathoracic suppuration.
Nailbed infarcts Vasculitis, especially in SLE
– Bronchiectasis.
(systemic lupus erythematosus) and in
polyarteritis. – Empyema.
– Lung abscess.
Clubbing – Fibrosing alveolitis.
– Pulmonary tuberculosis.
Clubbing is a condition that affects the fingers and toes in • Cardiovascular causes
many diseases of varying etiologies. The most outstanding – Cyanotic congenital heart disease.
feature of clubbing is the lateral and longitudinal curvatures – Bacterial endocarditis and subacute bacterial endo-
of the nails accompanied by soft tissue enlargement, carditis.
presenting a bulbous shiny appearance (Fig. 4.1) • Chronic abdominal disorders:
Theories of Clubbing – Hepatic cirrhosis.
– Ulcerative colitis.
1. Related to nervous system: – Crohn’s disease.
– Vagal stimulation causes vasodilation and clubbing. – Coeliac disease.
2. Endocrinal: d. Congenital:
– GH, PTH, estrogen, PG, and bradykinin cause vaso- – Familial clubbing.
dilation and clubbing. – Cervical rib is a common cause of unilateral clubbing.
Grades of Clubbing
• Grade I — Slight hollowing between the finger pulp
and nail.
This angle becomes full (obliterated) in
early stages of clubbing.
• Grade II — Abnormal motility of nails in the nailbeds
due to spongy thickness of the hyper-
trophied nailbeds (parrot beak appea-
rance).
• Grade III — Thickening of nailbed, producing bulbous
enlargements of ends of fingers (drum-
stick appearance).
• Grade IV — Fingers are markedly enlarged and the
nails and bones are also hypertrophied.
These changes may be associated with
thickening of ends of long bones
(hypertrophied osteoarthropathy).
Fig. 4.1: Clubbing of nails
70 Essentials of Clinical Medicine
The normal angle between the nail and nailbed is 160° For example
and is known as lovibond angle. The minimum duration – Sitting with back straight?
required for clubbing to manifest is 2 to 3 weeks. And index – Leaning forwards?
finger is the first to be involved. • Hands over the abdomen chest, head or any other body
parts?
Schammroth’s Maneuver or Schammroth’s Sign
Appearance
As shown in Figure 4.2, when the dorsum of the distal
phalanges of the fingers of both hands (especially the index • Whether the patient looks restless, anxious, agitated,
fingers) are brought in close contact with each other, a gap angry, emotional, depressed, or in agony of severe pain?
is visible through it and this gap is of diamond shaped (due • Whether the bedside has certain items like oxygen
to the presence of lovibond angle). The clubbing is diagnosed cylinder, drip bottle, container for collecting urine, stool
by the disappearance of this gap (due to the obliteration of or vomitus, etc? Sometimes the appearance may provide
angle of lovibond) (Fig. 4.3, Plate 2). clues for spot diagnosis of cases. For example, blue
If the normally visible space formed between the nails sclera in case of osteogenic imperfecta, scleroderma
of two approximating index fingers is obliterated, then facies with beaking of nose and taut skin around mouth,
Schammroth’s sign is said to be positive and clubbing is acromegaly facies or leg of elderly male with scurvy
said to be confirmed (Fig. 4.4, Plate 2 and Fig. 4.2). showing large ecchymosis in thigh (woody leg) with
perifollicular hemorrhages in calf muscles.
EXAMINATION IN THE HOSPITAL WARDS
Posture (or Attitude)
If the patient is examined in the hospital wards (patient lying
on the bed), then the examination pattern should be as • Posture/attitude of the patient should be observed both
follows. in lying down (decubitus) as well as sitting and standing
position, if possible.
Decubitus • Posture of the patient sometimes provides a very strong
clue about the system involved and nature of the disease
Decubitus means the position of the patient in the bed. This process. This has been explained as follows.
term is generally used for the lying down position:
• Whether the patient is lying supine, prone or in lateral Posture Related to Nervous System Involvement
position? Photophobic attitude
• Whether the patient is sitting over the bed and in what • The patient turning away from the source of light?
position? • Keeping clothes or hands over the face?
• Lying curled up with legs flexed over the trunk and
bending interiorly?
It signifies inflammation or irritation of meninger.
Pleurosthotonus: Body arched to one side or lateral curling
of the body.
Opisthotonus: Arching of the back (extreme spasm of the
back muscles) and body weight supported by head and feet
only, rest of the body being above the bed.
It signifies tetanus, strychnine poisoning, meningitis
preparalytic poliomyelitis. It is also seen in a case of major
burn. In severest cases of meningitis, the neck may be bent
backwards so that the head appears to bore into the pillow.
This is called neck retraction.
Hemiplegic
Acute Stage: In early stage, the patient lies supine with his
eyes, head and neck turned to one side. The direction of
eyes and head is in the direction (side) of the brain, head or
eyes affected limbs of the affected side are flaccid without
any movement and lower limbs are externally rotated with
Fig. 4.2: Testing for fluctuation of the nailbed a foot drop.
The General Examination 71
In Late Stage: No rotation (movements) of eyes, head and distance between the top of the head and symphysis pubis
neck. Assymetry of face with loss of nasolabial furrow on to that between symphysis pubis and sole of the feet) is
the affected side. The upper limbs show flexion at elbow 1 : 1].
joint and slight pronation with flexion of fingers at Conditions in which the height is greater than arm span:
metacarpophalangeal joints. The shoulder joint shows • Hyperpituitarism.
adduction and internal rotation. The lower limbs show • Adrenal cortex tumor.
extension at hip joint and knee joints along with plantar • Precocious puberty.
flexion of the foot. • This occurs before puberty when epiphysis of bones
are not united.
Posture Related to Cardiovascular and
Conditions in which arm span is greater than height:
Respiratory System Involvement
• Marfan’s syndrome.
Orthopnea/Dyspnea: The patient with heart failure or with • Klinefelter’s syndrome.
any respiratory system disorder is usually found sitting • Eunuchoidism.
upright over the bed. He becomes uncomfortable as he lies • Hypogonadism.
down (orthopnea). Two or more pillows, kept over the bed, • Homocystinuria.
on one another, may provide an important clue about the Conditions in which the upper segment is greater than the
dyspnea. It is also seen in cases of gastroesophageal reflux lower segment of the body.
disorders (GERD) where the patient is advised to sleep with • Adrenal cortex tumor.
his head held above the level of abdomen (to prevent reflux • Precocious puberty.
from the stomach). Orthopneic posture is seen in cardiac Conditions in which lower segment is greater than the
causes like left ventricular failure, pericardial effusion, cor upper segment of the body
pulmonale; respiratory causes like emphysema, bronchial • Klinefelter’s syndrome.
asthma, massive pleural effusion, pneumothora, etc. • Marfan’s syndrome.
Forward bending position (with kneeling or without • Homocystinuria.
kneeling): It is seen in cases of severe dyspnea. The patient • Eunuchs.
sits up in the bed, bends forwards with a support on his lap • Hypogonadism.
on which he kneels. The hands usually support the sides so
DWARFISM: (SHORT STATURE)
as to make better and efficient use of normal and accessory
muscles of respiration by providing a fixed point at their The causes are:
point of insertion. • Familial trait (hereditary)—constitutionally small.
It signifies massive pleural effusion, severe degree of • Racial—certain tribes of African continent.
congestive cardiac failure, aortic aneurysm. It is also • Constitutional growth delay.
sometimes (but rarely) seen in cases of pancreatic carcino- • Causes before the birth like intrauterine growth
mas and abdominal aortic aneurysms so as to relieve pain retardation; infections like TORCH, AIDS, syphilis, etc.;
caused by the pressure over the spine. excessive consumption of tobacco, alcohol by the
pregnant mother; certain genetic disorders like Down’s
Build syndrome, Turner’s syndrome; metabolic disorders like
• Normosthenic: Persons with normal body built. glycogen storage disease; skeletal abnormalities like
• Asthenic: Slender, thin, long body with flat chest. They achondroplasia; osteogenic imperfecta, chondro-
are prone to neurasthesia and visceroptosis. dystrophies:
• Sthenic: Short-heighted persons with muscular body, • Causes after birth like malnutrition (protein energy
muscular chest, short neck and extremities and stumpy malnutrition, anorexia nervosa); endocrinal disorders
and short fingers. such as pituitary-hypothalamic axis defects, (Frohlisch’s
• Height: Height mostly depends upon the hereditary and syndrome), pituitary defects (pituitary dwarfs), thyroid
racial factors. hypofunction since birth (cretinism) and gonadal
[Normally, the height of a person is equal to his arm abnormalities; chronic diseases like tuberculosis;
span that is distance between the fingertips when hands are cardiovascular disorders like cyanotic and acyanotic
stretched parallel to the ground and normal upper segment heart disease, early onset rheumatic heart disease;
—to lower segment ratio of the body (e.g. the ratio of respiratory disorders like Kartagener’s syndrome, cystic
72 Essentials of Clinical Medicine
lung disease, childhood asthma; renal disorders like renal Hydrocephalus: (Kephale = head). The condition is associated
tubular necrosis, renal rickets, nephrotic syndrome, with increased accumulation of cerebrospinal fluid (CSF)
chronic anemia, like thalassemia, sickle cell anemia, within the ventricles of the brain, resulting from the
leukemia; psychosocial disorders like maternal interferences with normal circulation and with absorption
deprivation syndrome, paternal deprivation syndrome; of the fluid and especially from destruction or blockage of
gastrointestinal disorders such as coeliac disease, foramina of Magendie and Luschka. It may be caused by
malabsorption syndrome, gluten enteropathy, Crohn’s developemental anomalies, infection, injury or brain tumors.
disease, cystic fibrosis, etc. In severe cases in children, the head is usually globular or
pyramidal in shape. The condition is seen in children before
STATE OF NUTRITION the sutures have united. The face is disproportionately small
The state of nutrition indicates a correlation between height and eyeballs are pushed downwards with the sclera being
and weight. It nutrition depends upon the distribution of visible above the corners (sunset sign). There occurs bulging
adipose tissue in the body. The condition of the skin, muscle of fontanelles and poor hair growth. After the skull has
mass and distribution of subcutaneous fat should be looked formed in older individuals, there are headache, vomiting,
for when assessing the state of nutrition of the patient. choked disks, atrophy of optic nerve, mental disturbances.
• Body mass index (BMI) = weight in kg/height in m2 Hydrocephalus is also called hydrencephalus.
• Normal BMI = 19-25 males = 20–25 Abnormal enlargements of head due to hypertrophy of
females = 18–23 bones as seen in Paget’s disease.
• If BMI < 18—underweight.
Microcephaly: The head is abnormally small in size and
• If BMI 25-30—overweight.
• If BMI 30-40—obese. brain growth is poor. The condition is usually associated
• If BMI > 40—very obese. with mental retardation.
Note: Causes of weight loss and weight have been Craniostenosis: Skull shape is abnormal and is usually due
enumerated in the section of symptomatology. to early closure of the sutures.
In case of obesity, you should inquire about: Tower skull (oxycephaly, or turricephaly): The condition of
• Family history. having a malformed cranial vault with a high or peaked
• Obstetric history. appearance (a vertical index above 77). It is caused by
• Psychological stress. premature closure of the coronal, sagittal and lambdoid
• Anxiety and depression. suture. It is also called acrocephaly.
• Binge eating. Dolichocephaly: The term has been derived from the Greek
• Alcohol and other fluid intake. word Dolichos meaning long and kephale meaning head. It
• Symptoms of diabetes. is defined as a condition having a skull with a long
anteroposterior diameter with prominent eyebrows and
HEAD
occiput.
The examination of head includes the examination of hair, Brachycephaly: It is a condition caused by early closure of
cranium, face, forehead, eyes, ears, nose and mouth. The coronal sutures, the head is wider. The skull may show
examination of mouth further includes—inspection of unilateral flattening on occipital side with a corresponding
(outside in) lips, teeth, gums, tongue floor of the mouth,
flattening of opposite forehead which results in plagio-
mucosa of cheeks, palate tonsils, oropharynx:
cephaly (appearance of twisted or lopsided head). The
Hair cephalic index is 81.0 to 85.4. This is considered a short
head but not necessarily abnormal, as this index falls within
Discussed earlier. the standard range of variation among humans.
It is usually due to disease in infancy which forces the
Skull patient to lie down with his head turned to one side for a
Shape and Size of the Skull long time.
Macrocephaly: Abnormal enlargement of head along with Platybasia (Basillar invagination): Head is extended, and
proportionately larger size of brain. The ventricles are rests over a short neck with the hair line at a low land
normal in size. usually seen in condition of craniovertebral anomalies.
The General Examination 73
causes wondering red patches across the surface of the chronic smokers. A bulge on the surface of PPW is seen in
tongue. retropharyngeal abscess. Ulceration of PPW is seen in
• Bald tongue—absence of papillae, seen in pernicious agranulocytosis.
anemia, iron deficiency anemia, pellagra, syphilis.
• Leukoplakia—a precancerous condition characterized Salivary Glands
by gray opaque areas interspersed with a few red
While carrying out the examination of mouth, the opening
inflamed patches.
of parotid duct may be seen on the buccal mucosa as small
• Fasciculation of the tongue at rest—motor neuron
papillae opposite the second upper molar tooth. Purulent
disease.
infections of the salivary glands may be investigated by
• Wasting of tongue muscles—lesion of hypoglossal n.
which causes the tongue to deviate to affected pide. culturing the pus expressed through the opening of ducts
• Enlarged tongue—Down’s syndrome, acromegaly, of these glands.
myxoedema, in somes cases of amyloidosis. Causes of Enlargement of Parotid Glands
• Mumps.
Palate
• Sarcoidosis.
• Look for cleft palate. • Tumor.
• High-arched palate is congenital. It may not have clinical • Suppurative parotitis.
significance but may be present in condition of Marfan’s • Obstruction of the duct causes intermittent swelling with
syndrome or mongolism (Down’s syndrome). High pain while eating.
arching of palate may also be seen in those with mouth • Obstruction due to salivary calculi is very commonly
breather’s such as in patients with recurrent attacks of seen in submandibular ducts.
cold, cough, URIC and adenoids.
• Perforation of palate may be seen in syphylitic gumma- Lymph Glands
tous involvement.
• Uvula varies greatly in shape and size. It seldom presents Causes of Lymphadenopathy
clinical problem except to some patients, with obsessional Inflammation
anxiety. • Acute—acute lymphadenitis
• Chronic—chronic lymphadenitis due to TB
Tonsils
• Syphilis
Tonsils are massive of subepithelial lymphoid tissues • Septic causes.
scattered in the pharynx. • Filariases
• Streptococcal tonsillitis causes the tonsils to be swollen • Lymphogranuloma inguinal (Fig. 4.5, Plate 2).
and inflamed, often with pus exudating from the tonsillar
crypts. Follicular tonsillitis may cause yellowish spots Neoplasm
on the surface of the tonsils. Diphtheria causes grayish • Primary—lymphosarcoma
white membrane on the surface of tonsils and, therefore, • Secondary—carcinoma, sarcoma, malignant melanoma.
has to be very carefully differentiated from follicular
tonsillitis. Quinsy (peritonsillar abscess) causes bulging Blood Related
of ant pillar of fauces and palate on the affected side. • Chronic lymphatic leukemia (CLL)
Enlargement of the tonsils may occur in systemic • Hodgkin’s lymphoma
condition like lymphoma. Tumors of the tonsils may • Non-Hodgkin’s lymphoma.
occur either in isolation or as a part of lymphatic leukemia • HIV and AIDS.
or lymphomas.
Immunity Related
Posterior Pharyngeal Wall (PPW) • SLE
The posterior pharyngeal wall becomes red and inflamed in • Drug reaction
pharyngitis, chronic granular pharyngitis, causes multiple • Rheumatoid arthritis (RA)
granular enlargements in the PPW and is mostly seen in • Serum sickness.
5
Respiratory System
Like all the other “System Examinations” (except the • Severe grade dyspnea for prolonged duration
“Nervous System”), the “Respiratory System” examination (chronic)
is also carried out in four steps (Fig. 5.1, Plate 2): • Type-1 respiratory failure.
1. Inspection. 3. Bronchitis obliterans with organizing pneumonia
2. Palpation. (BOOP):
3. Percussion. • Clinical features of pneumonia
4. Auscultation. • Associated features of connective tissue disorders
But before moving to systemic examination, we must • Occupational history, constant exposure to pollution.
have an approach to patients of respiratory system. 4. Lung abscess:
• H/o of pneumonia.
APPROACH TO PATIENTS OF • H/o of hospital-acquired infection / pneumonia within
RESPIRATORY SYSTEM 72 hours of admission.
• Immunocompromised state.
Approach to a Case of Respiratory Tract • Recurrent infection by Staph aureus, Klebsiella.
Infection with Weight Loss • H/o recurrent aspiration pneumonia.
• Chronic bronchitis • H/o of chronic smoking/alcoholism (chronic alco-
• Bronchitis obliterans (BO) holism causes recurrent aspiration).
• Bronchitis obiliterans with organizing pneumonia (BOOP) • H/o of dyspepsia (similar to gastroesophageal reflex
disorder).
• Chronic pyogenic infection
• H/o of diabetes mellitus.
• Lung abscess
• H/o of pyorrhea (gum infection).
• HIV/AIDS
• Pediatric age group.
• Malignancy
5. Malignancy:
• CHSP (Chronic hypersensitivity pneumonitis)
• H/o of hemoptysis.
• CHSP with eosinophilic pneumonia.
• History of paraneoplastic syndromes (ADH,
Ruling Out the Causes One by One Erythropoietin – hyperviscosity syndrome, Eaton-
1. Chronic bronchitis: Lambert syndrome, Cushing’s-like features, etc.).
• H/o of chronic smoking. 6. Tuberculosis
• H/o of constant exposure to pollution—for this you • Evening rise of temperature.
need to take occupational history. • H/o of contact.
• H/o of chronic respiratory illness. • H/o of weight loss.
• Investigation for alpha antitrypsin—for emphysema. 7. HIV/AIDS:
2. Bronchitis obliterans (BO): • H/o of chronic respiratory illness
(Inflammation of distal airways and surrounding areas) • H/o of sexual contact (sexual history) with an infected
• H/o chronic smoking person.
• H/o of recurrent viral infections • H/o of blood transfusion, drug abuse, etc.
• Clinical features of autoimmune disorders 8. Chronic hypersensitivity pneumonitis (CHP):
• H/o of hospital-acquired infections. (Farmer’s lung actinomycetes, Chlamydia, moldy hair)
80 Essentials of Clinical Medicine
• H/o chronic exposure to allergens 4. The trachea bifurcates into 2 principal bronchi at this
• H/o progressive dyspnea. level.
9. CHSP with eosinophillic pneumonia: 5. It marks the upper unit of the base of the heart.
• It is an allergic phenomenon. 6. The pulmonary trunk divides into two pulmonary arteries
• Seen in tropical eosinophilic syndrome, ascariasis, just below this level.
Loeffler’s pneumonia. 7. The cardiac plexuses are situated at this level.
• H/o of chronic mild/moderate grade fever.
• Progressive weight loss. Before starting the inspection of respiratory system
proper, the examiner should make some important
Progressive Dyspnea assessments about the upper and lower respiratory tracts.
The examination of upper respiratory tract includes
Before carrying out the inspection, it should be well known (a) the inspection of oral cavity—oral hygiene, dental status/
and understood that the chest (thoracic portion of the body)
hygiene, signs and symptoms of any oral pathology,
is divided into certain quadrants by some imaginary lines. It
helps us to perform the examination process in a more condition of tonsils, etc., (b) inspection of nose/nasal cavity
accurate manner. It also gives an idea about the boundaries for—deviated nasal septum, nasal polyps (as seen in allergic
of the thoracic contents. This is explained as follows: asthma, cystic fibrosis, Wegener’s granulomatosis, etc.),
epistaxis, recurrent attacks of cold and cough, and (c)
Significance of Angle of Louis (Sternal Angle) inspection of pharynx for—granulation, postnasal drip,
It is felt as a transverse ridge about 5 cm below the supra- lymphoma deposits, etc.
sternal notch. It marks the manubriosternal joint, and lies at
the level of second costal cartilage interiorly and the disk
INSPECTION (Figs 5.2 and 5.3)
between the fourth and fifth thoracic vertebrae posteriorly.
This is an important landmark for the following reasons: Inspection is a very significant part of examination of
1. The ribs are counted from this level downwards. There respiratory system because it may provide important clues
is no other reliable point (anteriorly) from which the about the nature and site of the disease process.
ribs may be counted. The second costal cartilage and For inspection to be accurate, the chest should be
rib lie at the level of sternal angle. The ribs are counted inspected from (a) the front (it is best to examine the patient
from here by tracing the finger downwards and laterally
from the foot end of the patient as it may highlight any
(because the lower costal cartilages are crowded and
bulging present on any side of the chest as well as the position
the anterior parts of intercostal spaces are very narrow).
2. It marks the plane which separates the superior media of apex beat if they are visible properly), (b) the back with
stinum from the interior mediastinum. the patient in the sitting position, (c) from the sides—it
3. The ascending aorta ends at this level. The arch of aorta solves the purpose of examination more meaningfully, and
begins and ends at this level. The descending aorta begins (d) from above downwards over the shoulders of the patients,
at this level only. examine the apical areas.
SIZE AND SHAPE OF THE CHEST Deformities which are Symmetrical in Nature
The size and shape of the chest vary with the individual. 1. Rachitic chest (also called keel breast, or pigeon chest
• Chest in sthenic individual—broad, short and deep set or pectus carnitum).
chest. There occurs protrusion of the anterior chest wall,
• Chest in asthenic individuals—long, narrow, and flat. with sternum and costal cartilages protruding anteriorly.
Normally, the chest is bilaterally symmetrical and Along with anterior protrusion of the sternum and costal
ellipsoidal in cross section (Figs 5.4 and 5.5). The transverse cartilages, there may be a sort of depression on either
diameter of the chest is more than the anteroposterior side of sternum in association with bead-like enlargement
diameter (the ratio being 7.5). The intercostal spaces are at costochondral junction (defined as rickety rosary)
broader in the front than posteriorly. There is a depression and a transverse sulcus (groove) passing outwards from
(normal) in the sternum which is most prominent at its the lower end of sternum (xiphisternum) to mid-axillary
lower end. The subcostal angle is acute and varies from line (known as Harrison’s sulcus). Rickety rosary (seen
70°-11° (average 90°). It is more in females as compared especially in the lower ribs) is due to enlargement of
to males. metaphyseal end of the ribs. A similar cases of scurvy,
in which case, it is known as scorbutic rosary or
ABNORMALITIES IN THE SHAPE OF CHEST scorbutic beads. The Harrison’s sulcus are horizontal
This is a very important of the examination process because depression on the chest wall corresponding to the
there are certain disease which produce significant changes attachment of diaphragm. Their extent is from 6th and
in the shape (contour) of the chest. Missing these changes 7th costal cartilage downwards from the xiphoid process
may lead the examination on the path of incorrect diagnosis. producing transverse construction of the thoracic wall
Fig. 5.4: The normal rib cage Fig. 5.5: Cross sectional view showing shape of the chest
82 Essentials of Clinical Medicine
(sometimes instead of horizontal grooves, longitudinal 1. Scoliosis: It denotes the lateral curvature of the spine
grooves may be seen on the outer chest wall. They are and is the most common thoracic of the spine deformity.
produced by the softened ribs being pulled inwards due The condition may be associated with some degree of
to negative pressure in the thoracic cavity. Harrison’s rotation of vertebral column. Due to convexity on one
sulcus are also seen in children with chronic respiratory side, the ribs are separated widely on that side and show
disease, childhood asthma, rickets, adenoids causing angulation at their posterior side indicating the rotation
blocked nasopharynx, pigeon chest is also seen in of vertebral column. There occurs crowding of the ribs
Marfan’s syndrome). on the concave side. The crowding of ribs causes
2. Funnel chest (also called cobbler’s chest or pectus compression of the lungs on that side.
excavatum). In this type, the body of sternum is curved 2. Kyphosis: In this condition, there occurs angular
backwards producing a deep depression in the lower curvature of thoracic spine. The convexity appears on
part of outer chest wall. The center of this depression the posterior side. The condition is characterized by the
being the xiphisternal junction. The etiology may be appearance of a lump at the back. The outer chest wall
congenital, due to rickets in childhood or as an
and sternum show forward bulging resembling the
occupational deformity seen in cobblers. The thoracic
pigeon chest.
cage appears to be narrow and longer. Mild deformity is
(A condition called kyphoscoliosis is also sometimes
usually symptomless. Severe degrees of deformity may
seen which is a combination of kyhosis and scoliosis. It
produce symptoms like breathlessness (dyspnea),
may result in severe displacement of thoracic viscera.)
palpitation (indicating shift in the position of heart or
lungs), dysphagia (due to pressure over esophagus)
Bulging of Chest Wall
chest radiography shows enlarged cardiac shadow of
the term pomfrets heart has been given to this type of a. Unilateral bulging is seen in pleural effusion, pneumo-
cardiac shadow. Funnel-shaped chest is also seen in thorax, tumors, aneurysm, empyema, cardiomegaly,
Marfan’s syndrome. scoliosis may also give rise to unilateral bulging.
3. Barrel chest: The shape of the chest is like a barrel is the b. Localized bulging is seen in aortic aneurysm, pericardial
anteroposterior diameter of the chest is equal to effusion liver abscess, tumor of chest walls.
transverse diameter (1:1), widening of subcostal angle
occurs, there is prominence of sternal angle, sternum Retraction
shows arching, concavity of spine is in the forward
direction (kyphotic changes) and obliquity of ribs is a. Unilateral retraction of chest wall may occur in conditions
decreased and they become more horizontal and appear like fibrosis, collapse, pleural adhesion, unilateral muscle
fixed in position of deep or mid-inspiration. The wasting seen in poliomyelitis, the condition may also
respiratory movements of the chest are decreased and arise as a congenital abnormality like absence of pectoralis
are mainly of abdominal type. There also occurs the muscles.
hypertrophy of accessory muscles of respiration. b. Localized retraction is seen in pulmonary tuberculosis
This condition is most commonly seen in emphy- and pleural fibrosis (retraction especially in the lower
sema (COPD) which is an overinflation of the lungs part of chest).
and their fixation in a position of overinflation.
4. Flat chest: (AP diameter : Transverse diameter = 1:2) Respiratory Rate
It is also called phthinoid chest. In this type of deformity
of chest wall, the AP diameter of chest is reduced and • Normal rate – 16-20 / min (in adults)
the thoracic cage becomes narrow and long. In severe – 40 / min (in children)
cases, the sternum may reach near to the vertebral • Resp. Rate : Pulse rate = 1.4 (normal).
column and scapula shows winging (alar chest). The Causes of Increased Respiratory Rate (Tachypnea)
condition usually results from chronic nasal obstruction,
due to various reasons like adenoid hypertrophy, or from • Exertion and excitement exercise.
tuberculosis or rickets in childhood. • Fever (pyrexia) due to any reason.
• Anoxemia and acidosis.
Deformities which are Asymmetrical in Nature • Anemia.
These are usually associated with the deformities of the • Poisoning.
vertebral column. • Pain while breathing (e.g. pleurisy).
Respiratory System 83
Causes of Decreased Respiratory Rate Excessive use of accessory muscles of respiration (alae
(Bradypnea) nasi, trepezius sternocleidomastoid) by the patient indicate
• Narcotic poisoning—morphine, codeine, etc. respiratory distress:
• Brain tumor or other space-occupying lesions of brain
Table 5.2: Causes of tracheal/mediastinal shifts
(SOLS) like hemorrhages.
Causes of hyperpnea—increase in the depth of Central position Deviation towards Deviation towards
respiration are 1. Acidosis, 2. Hysteria, and 3. Brainstem same side opposite side
lesion. • Bronchial asthma
• Bronchitis Fibrosis Pneumothorax
Movements of Respiration • Bronchiectasis Collapse Hydropneumothorax
• Emphysema Thickening of pleura Pleural effusion
Usually, the chest walls shows bilateral and uniform • Lung abscesses
movements with no bulge or depression over it. Some • Interstitial fibrosis
pathological conditions cause diminution of chest wall • Pneumonia
[Remember- 3
movements.
Beautiful and Exquisite
a. Diminution of movements or one side of the chest: (pair of) LIPS].
• Pleural effusion.
• Hydropneumothorax. Rhythm of Respiration
• Massive collapse.
• Consolidation. Normal individuals have regular respiration in which the
• Fibrosis of lungs. duration of inspiration is greater than that of expiration.
• Pleural adhesion. Sometimes the respiratory process becomes irregular. Some
• Obstruction in the main bronchus. of the conditions causing irregular breathing are discussed
b. Diminution on both sides: below.
• Emphysema. The skin over the chest wall should be examined
• Bronchial asthma. for:
• Fibrosis affecting both lungs. 1. Engorged veins and collateral veins – over the out chest
• Bilateral collapse, consolidation or hydropneumo- wall indicates superior vena cava (SVC) obstruction.
thorax. The cause is generally a mass in mediastinum (may be
Table 5.1: Types of breathing
Type of breathing Description Causes
1. Cheyne-Stokes respiration (Fig. 5.6A) Period of apnea is followed by gradual Central respiration failure.
increase in the rate and amplitude of resp. Left ventricular failure.
movements which reach a peak and again Increased intracranial pressure with damage
gradually subside to apneic phase to both cerebral hemisphere and diencephalons.
Narcotic poisoning–opium, etc.
Uremia.
2. Bitot’s breathing (chaotic breathing) Respiration is of irregularly-irregular type Advanced central respiratory failure meningitis.
(Fig. 5.6B) Two or three inspiratory movements are Meningitis
superimposed upon are another before the Raised intracranial pressure.
expiratory movement. There are periods
of apnea in between several periods of
shallow or deep inspiration
3. Kussumaul’s breathing (Fig. 5.6C) Characterized by deep and rapid respiration Diabetes ketoacidosis.
(air hunger). The resp. has a sighing Alcoholics.
character Starvation ketoacidosis.
Uremia.
4. Stridor Prolonged inspiration through an obstructed Growth in mediastinum.
upper airway Laryngeal diphtheria.
Trached or laryngeal obstruction.
5. Wheeze Prolonged expiration through an obstructed Bronchial asthma.
lower airway Cardiac asthma.
Renal asthma.
6. Stertorous breathing Rattling sound in the throat Coma Deep sleep
Dying patient (Death rattle)
84 Essentials of Clinical Medicine
Positions of the Patient 2. The middle finger (or sometimes the index finger) of
the examiner’s right hand that is used with the middle
In percussion of outer chest walls, the hands of patient
phalanx of pleximeter is called the plexor.
hang by the side of his body and he sits with his back in the
3. The movement of the percussing hand (the hand that is
erect posture. In percussion of post-thoracic wall, the patient
used to strike) should be allowed only at the wrist joint.
is made to cross his arm over the outer chest wall and he
The elbow joint should remain fixed while percussing.
keeps his hands on the opposite shoulders. The patient also
4. The percussum should proceed from the area of normal
bends his head forwards while percussing the lateral thoracic
resonance to the area of abnormal note. This helps clear
wall, the patient sits with his hands held over his head.
appreciation of the difference in notes produced.
Aims of Percussion 5. The pleximeter should be kept parallel (in the direction
of) to the border of the organ which is being percussed.
Percussion is carried out to assess the amount (degree) of
resonance over the various areas of chest and to find out Sites over the Outer Chest Wall (Figs 5.8 and 5.9)
those areas which have abnormal note. 1. Medial 1/3rd of clavicle.
2. Kronig’s isthmus (supraclavicular region).
Basic Mechanism It is a band of resonance of 5 to 7 cm. In width it is
used to assess the resonance of lung apices. The
In a normal individual, the percussion note is due to the
boundaries of this area are:
normal amount of air present in the air vesicles, air sacs
Medially: Scalenus muscle of neck, laterally the
and passages. Normally, the percussion note has a low pitch.
acromion process of scapula, anteriorly the clavicle and
The percussion note on the outer chest wall is usually more
posteriorly – trapezius. Emphysema leads to hyper-
resonant than that on the posterior thoracic wall because
resonance and pul TB or malignancy of lung often causes
the front of the chest has less musculature as compound to
impaired resonance over this area.
the back.
3. Region just below the clavicle.
Basic Principles of Percussion 4. Intercostal spaces—especially second to sixth.
1. The middle finger of the examiner’s left hand that is Sites over the Lateral Wall of Chest
placed tightly over the chest wall (over the intercostal Intercostal space, especially fourth to seventh.
spaces) is called the pleximeter. The term pleximeter is Sites over the Back
derived from a Greek words—plexis = stroke and metron
Usually involves the complete back, i.e. in the suprascapular,
= measure. The other finger should be kept free (away
interscapular and infrascapular regions.
from) from touching the chest wall.
Fig. 5.8: A. Sites for percussion—anterior and lateral chest wall, B. Sites for percussion—posterior chest wall
Respiratory System 87
Table 5.5: Abnormal percussion notes The lower border of the lung can be percussed up to the
6th intercostal space in midclavicular line, up to the 8th
Percussion note Description Condition intercostal space in the midaxillary line and up to 10th
1. Hyper resonant The percussion note Emphysema (generalized intercostal space in the midscapular line. The tidal percussion
note is greater in inten- or compensatory)
sity than the normal Pneumothorax
helps to differentiate upward enlargement of liver or
one [resonare (Latin) Large cavity subdiaphragmatic abscess from the right-sided parenchymal
means to resound] Congenital lung cyst or pleural disorders.
Emphysemotous bullae
Eventration of diameter Interpretation
2. Skodiac (sub- It is a peculiar quality Above the level of pleural After full range of inspiration (deep inspiration), if the
tympanic) note and is produced due effusion
to relaxation of lung previous dull note in the fifth right intercostal space on the
tissues (above the midclavicular line becomes resonant, it is an indication that
level of perfusion). dullness was due to liver (which has now been pushed down
3. Tympanic note Drum like resonance Over the hallow viscous, by the downward movement of diaphragm on deep
or tympanitic over the tension pneumo-
note thorax or over the large inspiration). In contrast, if the dullness persists even after
cavity or emphysematous deep inspiration, then it is an indication of underlying right-
bullae of lung sided prolonged or pleural pathological involvement.
4. Impaired note Due to decrease in Consolidation
the amount of air in Fibrosis
the alveoli, the lung Infiltration Traube’s Semilunar Space
fails to vibrate enough Collapse of lung
on percussion
It is present in the midclavicular line around the left 7th
5. Dull note More decrease in Consolidation space. Its relations are—on its right left lobe of liver; on its
resonance as com- Fibrosis left spleen; superiorly—heart, inferiorly—left costal margin.
pared to impaired Infiltration The presence of air in the fundus gives rise to tympanic
note. Collapse of lung
Thickening of pleura. note.
6. Amphoric Note is low pitch and Pneumothorax
resonance is characteristic in Large cavity
Interpretation
nature. It is a type of The lateral extension of Traube’s space to outer axillary line
tympanic resonance. indicates massive collapse of left lung (or left lower lobes).
Has a peculiar hollow
quality. Obliteration of Traube’s space indicates pleural effusion on
7. Cracked pot The note produced Large cavity communi- the left side. Obliteration also occurs in cases of enlarged
resonance resembles to that cating with the bronchus. left lobes of liver, fully filled stomach, fundal growth and
produced while
massive pericardial effusion.
percussing over a
broken earthenware Upward shifting of Traube’s space is seen in:
vessels. • Fibrosis of left lung.
88 Essentials of Clinical Medicine
• Collapse of left lower lobe. occurs an alteration in the percussion on deep inspiration
• Left diaphragmatic paralysis. and expiration. This can be better elicited when the patient
is made to breath through open mouth (Wintrich’s sign). A
Percussion in Pleural Effusion change in the note appears when the patient breaths while
1. Ellis “S” shaped curve: the mouth is closed. Another situation is seen when the
It denotes the upper level of fluid in a patient suffering cavity has both air and fluid (partially filled cavity) this time
from pleurisy with effusion. In moderate degree of pleural the percussion note over the affected area changes with
effusion, the uppermost level of dullness due to fluid is change in posture of the patient (Gerhardt’s sign).
highest in the axilla (as compared to anterior or posterior
Table 5.6: Stony dullness and impaired note
surfaces) – giving an “S” shape to the upper level of
fluid in this presentation is thought to be due to capillary Stony dullness Impaired note
suction mechanism. As the two layers of pleura are very Pleural effusion Pneumonia
close to each other in the axillae, and we know that fluid Massive collapse-consolidation Collapse
rises to the highest level in the capillary, which is the Solid tumors Thickened pleura
Fibrosis
thinnest, therefore the fluid level reaches the highest
Sequestration of lung
level in axillae. However, some believers are of the opinion Abscess
that it may be only a false radiological appearance. Infarct
2. Grocco’s triangle:
It is a triangular shaped area of dullness elicited in some AUSCULTATION
patients with pleural effusion. It can be appreciated on
opposite side of pleural effusion close to the vertebrae. Aims
The thoracic spine forms the medial border of the 1. To find out the type and amplitude of breath sounds.
triangle. At the base of the triangle, lies the 10th intercostal 2. To know the quality and amplitude of conducted voice
space for about 5 to 7 cm. And by joining these two sounds.
sides with each other, we get a complete triangle. The 3. Additional sounds—their number, position; and type.
posterior mediasternum is thought to be the reason for
this dullness. General Principles
Percussion in Hydropneumothorax 1. Most of the sounds coming to the chest wall from the
(Shifting Dullness) underlying lung tissues and air passages lie in the low-
frequency range (low pitch). Therefore, the bell (bell of
Just as we elicit the shifting dullness in case of ascites, so
the stethoscope) with a rubber rim over it should be
we do in case of pleural effusion also. Firstly, the patient is
preferred over diaphragm (the diaphragm of the
made to sit with his back straight, and the upper level of
stethoscope). There is another significant reason why
fluid is marked by percussing. Now the patient is made to
the bell is preferred. The skin and hair under the
lie down and the same area is percussed again. Resonant
diaphragm during deep breathing produces some sounds,
note this time indicates shifting of pleural fluid.
which may be confused with pleural rub or crepitations.
Percussion in Pneumothorax (Coin Test) The third important reason for selecting the bell is the
difficulty in making full contact between the diaphragm
The examiner keeps a metallic coin over the anterior chest and chest wall in case of debilitated and thin individuals.
wall of the patient and strikes it with another similar coin. 2. Sounds produced by the partial closure of nose (due to
On simultaneous auscultation over the back of the patient, discharges present in the nasal cavity) can be avoided
a clear metallic sound can be heard. This is because the by making the patient to breath through his mouth (fully
sound travels through the air easily without getting open) while performing auscultation.
deteriorated indicating a cavity in side.
3. Avoid auscultation within 2 to 3 cm. From the midline,
it generally has bronchial character.
Percussion in Case of Cavity in the Lungs
The auscultation should be carried out in a very
When there is a communication pathway between the cavity systematic manner. The sequence of auscultation should
and the air passages (especially the main bronchi), there be—the outer wall of chest, the axillae and the back.
Respiratory System 89
• When the alveoli contain a mixture of air and fluid, • Hollow character.
bronchovesicular sounds are produced. • Best heard in the early phase of inspiration.
• Inspiratory phase is similar to that of vesicular breathing. b. Sibiliant rhonchi: The features are:
• The expiratory phase is prolonged and harsher. • Produced due to spasm of smaller bronchi.
• Duration of inspiration is equal to expiration (1:1). • High pitched.
• No pause between expiration and inspiration. • Shrill in quality.
• They are heard in pneumonitis, tuberculosis, congestive • Best heard at the end of expiratory phase.
cardiac failure, bronchial asthma, chronic bronchitis, c. Intermediate rhonchi: The features are:
and emphysema. • Produced due to spasm of intermediate sized bronchi.
Conditions in which the breath sounds are absent: • Medium pitched (between sonorous and sibilant).
• Pneumothorax. d. Polyphonic rhonchi: The features are:
• Pleural effusion (severe). • They are complex musical sounds produced during
• Thickening of pleura. expiration.
• Collapse of lung. • The sound contains various notes of different pitch.
• Severe attack of asthma. • Usually, all the components of musical notes start at
• Congenital conditions like agenesis of lung tissues. the same time, continue and also end together in
• Surgical procedures like pneumonectomy. expiration.
• They are usually produced by the osillation of various
Adventitious Sounds large bronchi simultaneously, e.g. emphysema.
The adventitious sounds are those vibrations which are e. Monophonic rhonchi: The features are:
produced by pathological process in the respiratory tract in • They are single musical sounds resulting from
lungs, tracheobronchial tree or pleura. Whenever an localized narrowing of airway.
adventitious sound is heard, it always indicates underlying • Monophonic rhonchis can be further divided into
pathology. (i) Fixed monophonic and (ii) Random monophonic
rhonchis.
RHONCHI (also called Wheeze)
Rhonchi is a continuous musical sound caused by narrowing RALES/CRACKLES/CREPITATIONS
of the lumen of a respiratory passage. They may be low Rales are a type of adventitious lung sounds heard on
pitched (sonorous), arising from large airways or high auscultation of the chest produced by air passing out retained
pitched (sibilant) arising from small airways. airway secretion or the sudden opening of collapsed airways.
Rhonchi are produced whenever a portion of tracheo- It may be heard on inspiration or expiration. A crackle is a
bronchial tree is narrowed, either by the spasm or discontinuous, non-musical adventitious lung sound as
sometimes due to presence obstructing neoplasm or due to opposed to a wheeze which is continuous. Crackles are
inflammatory swelling (such as bronchitis or allergy).
described as fine or coarse or medium rales. The classi-
Narrowing of bronchi during expiration makes the rhonchi
fication is made on the basis of their pitch and also on the
better audible during expiration.
predominant phase of inspiration in which they occur.
Causes of Rhonchi a. Coarse rales: Louder, rather long, low pitched, lung
sounds, arise from bronchus and bronchioles. The coarse
i. Bronchial asthma. inspiratory and expiratory crackles indicate excessive
ii. Chronic obstructive pulmonary diseases (COPD) airway secretions.
iii. Bronchitis. b. Fine crackles: Soft, very short, high pitched lung
iv. Tumors. sounds. Fine late inspiratory crackles are often heard in
v. Cardiac failure (congestive heart failure). pulmonary fibrosis and acute pulmonary edema. Fine
vi. Allergic conditions like tropical eosinophilia. rales are also called crepitations. They arise from alveoli
and are due to the presence of fluid in the alveoli and
Classification of Rhonchi
hence heard only at the end of deep inspiration. The
a. Sonorous rhonchi: The features are: sound of crepitation is usually compared to that produced
• Produced due to spasm of larger bronchi. by rubbing a lock of hair between the fingers.
• Low pitched. Crepitations are present in conditions which produce
Respiratory System 91
close to the chest wall of the patient suddenly shaking the • Syllable are not clearly distinguishable.
patient. to and fro. • Spoken pectoriloque – When lung parenchyma becomes
It is heard in conditions like hydropneumothorax and completely dense, the sound is heard more clearly and
diaphragmatic hernia. hence called spoken pectoriloque.
Gurgling sound: Heard in case of bronchopleural fistula. Conditions: Consolidation, collapse of lung with the patient
Mechanism of production may be the air entering the pleural (normal), bronchi, a large tumor, massive pleural effusion.
fluid through the fistula.
Whispering pectoriloque: The patient is asked to whisper
Auscultatory Vocal Resonance (AVF) “one-two-three” or “nine-nine-nine” and the sound is
auscultated.
Vibration of vocal cords in the larynx gives rise to certain
Interpretation: In normal lungs only rustling sound can be
audible sound (audible through stephoscope). This sound
is called vocal resonance (VR). heard. But if the sound is clear and audible, it is called
whispering pectoriloque.
Procedure Conditions:
The patient is made to repeat certain words like “nine-nine- • Massive consolidation of lung near to the bronchis.
nine or “one-one-one” or “one-two-three” and the different • Cavity communicating with the bronchus.
corresponding areas of chest wall on both sides are Egophony: When AVR is auscultated as a nasal sound over
auscultated one by one. The common mistakes which the chest wall, usually heard above the level of pleural
students do is to completely auscultate one side of the chest effusion.
first and then shifting to other side. This is wrong. You Mechanism: Mechanism of production has been thought to
should alternately auscultate the corresponding areas of chest be the relaxation of alveolar membranes just above the level
wall. of pleural effusion. Therefore, there occurs an alteration in
Interpretation normal transmission of sound to the chest wall.
Conditions:
Normally, the sound is not heard clearly with the
• Above the level of pleural effusion.
stethoscope. In fact, it is heard as a weak, rumbling sound
• Pneumothorax.
where words appear to mix with each other. The sound
• Sometimes over the area of consolidation and lung
appears as if coming from the area near to chest piece of
cavities partially filled with exudates (Fig. 5.11).
the stethoscope. In normal conditions, the AVF is heard
maximum at the right apex and interscapular area and louder CASE TAKING
in men than women.
Respiratory System
Causes of Decreased AVF
• Pleural effusion. 1. A patient with low-grade fever and weight loss has poor
• Pneumothorax. excursion on the right side of the chest, with decreased
• Thickened pleura fremitus, flatness to percussion, and clear cased breath
sounds on all the right. The trachea is deviated to the
• Emphysema.
left. The likely diagnosis is:
• Bronchial obstruction (partial or complete).
Pleural effusion
• Collapse of lung.
2. A 30-year-old male is admitted to the hospital after a
• Fibrosis of lung (?)
motorcycle accident that resulted in the fracture of right
femur. The fracture is managed with traction; three days
Conditions in which TVF is Increased
later, he becomes confused and tachypnoic. A petechial
or Altered
rash is noted over the chest. Lungs are clear to auscul-
The TVF is altered in conditions where the lungs become tation. Arterial blood gas shown PO2 of 50, PCO2 of 28,
more dense. pH of 7.49. The most likely diagnosis is:
Bronchophony: Fat embolism
• Sounds are louder and clear. 3. A patient is found to have an unperfectly high volume
• The sound appears to be coming from the ear piece of for diffusing capacity. This finding is consistent with:
the stethoscope (rather than the chest piece). Intrapulmonary hemorrhage
Respiratory System 93
Fig. 5.11: Clinical findings in: A. Right-sided effusion, B. Right-sided consolidation, C. Collapse, with bronchial obstruction
on the right-side and with patent bronchi on the left side, and D. Right pneumothorax
4. A 65-year-old man presents with progressive shortness headache, and poor sleep quality. He is quite tired during
of breath. Other than a history of heavy tobacco use, the day and frequently falls asleep while he reads or
the patient has a benign past medical history, breath watches television. Physical examination reveals a ruddy
sounds are absent, two-thirds of the way on the left complexion but is otherwise normal except for elevation
side of the chest. Percussion of the left chest reveals in hematocrit and plasma HCO3 concentration. Poly-
less resonance than normal while you place your hand sonography demonstrates a decreased ventilatory
on the left side of chest and have the patient say “ninety- response to hypercapnia and many episodes of central
nine”, no tingling is appreciated in the hand. The trachea apnea (no diaphragmatic activity) is noted. The maximum
appears to be deviated towards left. Which is the most respiratory pressure that he generates against an occluded
likely diagnosis? airway is general. Which is the most likely cause of the
Bronchial obstruction patient’s problem?
5. A 65-year-old man presents for an evaluation because
he is “feeling poorly”. Symptoms include morning Carotid body dysfunction
94 Essentials of Clinical Medicine
Fig. 5.12: Chest radiograph of carcinoma of lung. Fig. 5.14: Chest radiograph of carcinoma of lung. This
This patient has left hilar mass patient has a large mass in the right upper lobe
Fig. 5.13: Chest radiograph showing rising fluid level in left Fig. 5.15: Chest radiograph post-pneumonectomy
hemothorax rising fluid level in left hemothorax
102 Essentials of Clinical Medicine
Fig. 5.16: Pneumothorax showing mediastinal shift and Fig. 5.17: Retrosternal goiter causing deviation
compression of contralateral lung of trachea (arrows)
6
Alimentary System
The human alimentary system is the most complex system 28. Proteinuria, anuria, oliguria, polyuria, nocturia, dysuria
of the body next only to the nervous system. The gastro- 29. Urinary frequency, urgency, urinary incontinence
intestinal tract consists of various interconnected organs enuresis
and perhaps, the alimentary system is the only system in 30. Pyuria, hematuria, isolated hematuria without
our body that has such a variety of organs, each performing significant proteinuria, hemoglobinuria
different functions (control of passage, digestion, absorption 31. Pneumaturia—rare symptoms consist of passing air
and removal of ingested food materials). bubbles in urine, most often caused by a fistula bet-
The history taking plays a highly crucial role in the process ween bladder and color usually as a diverticular
of diagnosing a gastrointestinal tract (GIT) disorders. The abscess or a malignant tumor.
various important symptoms of GIT disorders are:
1. Pain in abdomen Examination of Alimentary System
2. Dysphagia/odynophagia (painful swelling) The examination of alimentary system includes:
3. Heart burn (Pyrosis) a. The general examination; b. The systemic examination.
4. Indigestion (dyspepsia)
5. Flatulence and belching The points to be noted in the general examination of alimen-
6. Hiccups tary system are as follows.
7. Vomiting General Appearance
8. Constipation and diarrhea Whether the patient appears to be in severe pain, agony, or
9. Abdominal distension (bloating) restlessness or anxiety? (as in case of colicky pain—renal,
10. Weight loss and anorexia intestinal or biliary colic)
11. Bleeding
12. Hematemesis Assessing the Nutritional Status of the Patient
13. Rectal bleeding (hematochezia) It forms a very important part of examination of the patient.
14. Malena Severe degree of malnutrition can be judged very easily, but
15. Dry mouth (xerostomia) it becomes too difficult for a clinician to recognize mild
16. Excess salivation (water brash) degrees of undernourishment (or malnutrition), especially
17. Painful lips, tongue, mouth in the presence of other associated illnesses and symptoms
18. Altered taste sensations (dysgeusia) like edema, hypoalbuminemia, etc. or if the malnourishment
19. Foul taste in mouth (cacageusia) is due to any underlying pathology like malabsorption
20. Bad breath (halitosis) syndrome, improper digestion, etc. Another most common
21. Feeling of lump in throat (globus) cause of malnutrition in the developing countries (including
22. Retrosternal chest pain India) is starvation.
23. Nausea and vomiting Thus, it becomes an important necessity for the physician
24. Jaundice, itching (pruritus) to recognize and understand the nutritional status of the
25. Aerophagia patient in order that he may take prompt actions to cure his
26. Fecal incontinence patient. The clinical history taking, the dietary history,
27. Maroon-colored stool the physical examination including anthropometrics
104 Essentials of Clinical Medicine
examiner should also inspect the groin and genitalia because Special Points
a patient presenting with intestinal obstruction may have a • Note if there is any movement of swelling, either with
strangulated femoral or inguinal hernia as the underlying or without independent respiration.
pathology. (Remember: You cannot force the patient to • Chronic urinary retention may cause palpable enlarge-
expose his private parts against his/her will. This is absolutely ment in the lower abdomen.
against the rules of conduct of medical profession.) • It is very important to note whether the bulging is more
In inspection, the following points should be given attention. laterally, i.e. in the flanks (as seen in accumulation of
fluid in the abdomen, and sometimes also due to obesity,
Shape or Contour of the Abdomen pregnancy or large ovarian cyst) or bulging is in antero-
The shape or contour of the abdomen varies in different posterior diameter which is produced by intestinal
individuals; but for the sake of convenience of examination, obstruction or gaseous distention. Visible bulges may
the abdomen has been roughly categorized into the following also be due to gross enlargement of liver, spleen, or
shapes: kidney or due to large tumors. Pyloric obstruction causes
a. Generalized fullness or distention bulging in the upper part of abdomen.
fat, fluid, flatus, feces fetus or full urinary bladder • Diverticulation of rectus is seen in—congenital defects,
(“6 Fs”) after pregnancy, in obesity, ascites.
b. Localized distention—may be symmetrical or • Generalized distention is seen in ascites, obesity,
assymetrical. excessive flatus. Localized distention is seen in
i. Symmetrical and centered around the umbili-cus, neoplasms, hepatomegaly (in right hypochondrium), full
small bowel obstruction. bladder (in hypogastrium).
ii. Asymmetrical—gross enlargement of spleen or liver • Differentiating the “6 Fs” as the cause of distention—
or ovary. (i) Fat—the abdomen is pendulous and cutaneous folds
c. Scaphoid abdomen (boat-shaped abdomen)—advanced are symmetrical, and enlarged, (ii) Fluid in the abdomen
stages of starvation and malignant disease, particularly may be noted by fluid thrill, shifting dullness and horse-
carcinoma of esophagus and stomach, and also in shoe-shaped dullness (this is a part of percussion),
muscle wasting disorders. (iii) Flatus (on percussion, tympanic note is obtained
106 Essentials of Clinical Medicine
abdominal organs in the epigastric region will also abdominal veins are dilated and provide a collateral
transmit pulsations from aorta in the same area. The circulation. The dilated veins that radiate from the umbilicus
distinguishing point between the visible pulsation due to are given the name caput medusae. They are typically seen
aneurysm and tumor is that (i) the pulsation of aortic in portal obstruction in which blood flow is upwards above
aneurysm is more obvious and secondly, and (ii) pulsation the umbilicus and downwards below the umbilicus. In
due to abdominal aortic white those due to transmission inferior vena caval obstruction, the thoracoepigastric vein
through falls away from the aorta in that position open up, connecting the great saphenous vein with the axillary
(However, this does not happen if the tumor is adherent vein. In superior vena caval obstruction, the blood in the
to the aorta. The distinction is best confirmed by the thoracoepigastric veins flows downwards.
abdominal ultrasonography). Procedure: The direction of blood flow should be tested by
c. Epigastric pulsations due to right ventricular hypertrophy: selecting a vein with no side branches and compressing it
They correspond with the apex beat. with one finger of either hand held near each other. The
d. Hepatic pulsations: They are seen in case of tricuspid fingers are then drawn apart so that the vein collapses
incompetence or due to hepatic hemangioma. (milking of vein) under them. The pressure of these fingers
Note: To aid the recognition of pulsations over the is released in turn and the side from which the vein fills up
abdominal wall as well the abnormal movements (absent is noted.
or restricted) of the abdominal wall, throw light across
(tangentially) the patient’s abdomen. Even small move- Causes of IVC Obstruction
ments may be detected by alterations in the pattern of 1. Hypercoagulable states like nephrotic syndrome.
shadow cast by the abdomen. 2. Compression by massive ascites.
3. Thrombosis of femoral iliac veins.
Prominent Superficial Veins
4. Secondary to infection and prolonged intake of oral
They are apparent in three situations: contraceptive pills (OCPs), trauma/injuries, etc.
a. Thin veins over the costal margin. 5. Idiopathic retroperitoneal fibrosis.
b. Occlusion of inferior vena cava (IVC). 6. Congenital anomalies or tumors of the walls of the veins.
c. Venous anastomosis in portal hypertension. These veins 7. Thromboembolism.
are usually tortuous and dilated.
Visible Peristalsis of Stomach or Small Intestine
Thin veins over costal margins/subcostal margins: They are
common and usually of no significance. They are more It may be observed in the following situations:
clearly visible in thin and lean individuals. a. Obstruction at the pylorus: This occurs due to fibrosis
following chronic duodenal ulceration or less commonly
Occlusion of inferior vena cava: It causes edema of limbs,
by carcinoma of the stomach in pyloric antrum.
buttocks and groin and also leads to distended veins on the
Peristalsis will be seen as a slow wave either passing
abdominal wall and chest wall. They signify dilated
across the upper abdomen from left to right hypo-
anastomotic channels between the superficial epigastric and
chondria or if gross gastric dilatation is present, passing
circumflex iliac veins below, and the lateral thoracic veins
down to the suprapubic region and ascending to
above, conveying the diverted blood from long saphenous
vein to axillary vein; the direction of flow is, therefore, terminate in the right epigastrium. In pyloric obstruction,
upwards. In sufficiently prominent and dilated veins, try to a diffuse swelling may be seen in the left upper abdomen,
detect the direction of blood flow. but where obstruction is long standing with severe gastric
distention, this swelling may occupy the left mid and
Venous anastomosis in portal hypertension: Distended vein lower quadrants. Such a stomach may contain up to
around the umbilicus (caput medusae) are uncommon; but, two liters of fluid; and on shaking the abdomen, splashing
if present, indicates portal hypertension, other signs of which noise is usually heard (succussion splash). This is
include splenomegaly and ascites. The distended vein frequently heard in healthy individuals for up to 3 hours
represents the opening up of anastomoses between the portal after a meal, so inquire when the patient last ate or drunk.
and systemic veins and are also seen in other sites like b. Congenital pyloric stenosis of infancy: Not only may
esophageal varices and hemorrhoids. (Fig. 6.2, Plate 2)
visible peristalsis be apparent but also the grossly
Interpretation: (Direction of Blood Flow) hypertrophied circular muscles of the antrum and pylorus
When the portal vein, the superior vena cava (SVC) or may be felt as a “tumor” to the right of midline in the
inferior vena cava (IVC) is obstructed, the superficial epigastrium. Both these signs may be elicited more easily
108 Essentials of Clinical Medicine
after the infant has been given a feed. Standing behind and medial to pubic tubercle. It is often difficult to accurately
the mother with the child in her lap may allow the child’s differentiate between direct and indirect inguinal hernias.
abdominal musculature to relax sufficiently to feel the An indirect inguinal hernia occurs into a persistent remnant
walnut-sized swelling. of the processus vaginalis. It occurs in young men and
c. Obstruction in the distal small bowel: Peristalsis may may extend to testes. Following reduction, control can be
be seen when there is instestinal obstruction in the distal achieved by pressure over the internal inguinal ring, just
small bowel or co-existing large and small bowel hold- above the midpoint of the inguinal ligament. A direct inguinal
up produced by distal colonic obstruction, with an hernia occurs directly through the weakened posterior wall
incompetent ileocecal valve allowing the reflux of gas of the inguinal canal medial to the inferior epigastric artery
and liquid into the ileum. Not only is the abdomen and lateral to the rectus muscle. It is more common in older
distended and tympanitic (hyper-resonant) but also the men and does not reach the testes. It will be controlled by
distended coils of small bowel may be visible in a thin pressure over the external inguinal ring.
patient and tend to stand out in the center of the abdomen
in a “ladder” pattern (writhing movements in the center SKIN AND SURFACE OVER THE ABDOMEN
of the abdomen). The skin and surface of the abdominal wall should be
d. Visible peristalsis: It may be a normal finding in very observed for the presence of scar marks of injuries or marks
thin, elderly patients with lax abdominal muscles or large, of any previous surgical intervention. Note their number,
wide-necked incisional hernia seen through an abdominal site and whether they are old (white) or fresh (red or pink)
scar. Striae atrophic or gravidarum are white or pink wrinkled
e. Large intestinal obstruction: It can also produce linear marks on the abdominal skin. They are produced by
peristaltic wave in the epigastrium and here the wave is gross stretching of the skin with rupture of elastic fibers
seen passing from right to left. and indicate a recent change in size of the abdomen, such
All the peristaltic movements are observed more clearly marks are found in pregnancy, ascites, wasting disease and
when the abdomen is viewed transversely, gastric peristalsis severe dieting. Wide purple striae are characteristic of
in pyloric obstruction can be made more prominent if the Cushing’s syndrome and excessive steroid treatment.
patient drinks a glass of water. Any cold stimulus like a Prominent superficial veins are seen as distended veins
spray of ethyl chloride over the abdominal wall also around umbilicus (caput medusae) and they signify portal
stimulates the underlying peristalsis. The peristaltic waves hypertension but are rarely seen. Pigmentation of the
may also be made more clear by applying a sharp tap with abdominal wall may be seen in the midline below the
the fingers over the abdominal wall. umbilicus, where it forms the linea nigra and is a sign of
pregnancy. Erythema ab igne is a brown mottled
Hernial Sites
pigmentation produced by constant application of heat,
The hernia is a common cause of localized swelling and usually with hot water bottle or heat pad, on the skin of the
should be distinguished from divarication of rectus abdominal wall. It is a sign that the patient is experiencing
abdominis. Divarication of the recti, common in multiparous, severe pain and is most commonly associated with chronic
becomes more obvious as the supine patient attempts to sit pancreatitis. In elderly patients seborrhoeic warts, ranging
upright, the intra-abdominal pressure rises and the region from pink to brown or black, and hemangiomas (Campbell
of line alba bulges between the rectus. An umbilical hernia de Morgan spots) are so common that they could be
bulges through the navel. It is very common in babies and considered normal changes. Lineae albicantes (linea alba)
usually disappears spontaneously. An epigastric hernia is are produced by stretching of the abdomen and are evidence
visible as a small swelling usually not more than 1 cm in of previous pregnancies, abdominal tumors or ascites. Linea
diameter. It is due to the herniation of extraperitoneal fat nigra is the term used to describe the black line produced
through defect in the linea alba. By gentle massage with the by deposition of melanin in midline and is also seen in
fingertip, it is often possible to reduce such hernia and then females who have had multiple pregnancies. The abdominal
the small defect can be felt. An incisional hernia may form skin may show presence of multiple small modules which
at the site of an operation in the abdomen, especially if the are evidence of widespread hematogenous metastasis.
wound has been complicated by the sepsis. A femoral hernia However, these are rarely the result of an abdominal
is palpable below the inguinal ligament and lateral to the malignancy. The abdominal skin appears to be smooth,
pubic tubercle. An inguinal hernia emerges from abdominal shining and stretched when there is abdominal distention
wall through the external inguinal ring and is palpable above due to pathological cause.
Alimentary System 109
The examiner keeps his one hand over the loin sudden movements of a deeply placed, inflamed organ,
(posteriorly) and other hand over the anterior abdominal resulting in pain.
wall. With the help of posterior hand, the examiner pushes
Other Abnormal Findings
the kidney (or any mass) upwards, i.e. towards the ant.
abdominal wall and palpates it with the hand placed anteriorly. • Generalized “board-like rigidity” implies peritonitis, the
Normally, the kidney is not palpable, but the lower pole of abdomen does not move and respiration (respiration is
right kidney may be palpable in thin and lean individuals. completely thoracic) and bowel sounds are
characteristically absent.
Abnormal Findings • Feces may be palpable in any part of colon in severe
constipation. Indentation of a lump by finger pressure
Muscle Guarding is evidence that it is fecal. Sometimes, however, a hard,
It is done voluntarily by the patient, as a protective procedure craggy lump of feces can only be distinguished from
(self-defense mechanism) when the examiner palpates over malignancy by re-examination following defecation.
a tender region. It occurs due to muscle contraction. The
patient should be made relaxed and comfortable and must Liver
be assured that there will be no harm to him/her by palpation. Procedure
Guarding is usually seen in conditions like localized The examiner places his hand flat on the abdomen so that
peritonitis and can be elicited over the area of actual his fingertips point upward towards the ribs. The fingers
anatomical locations of the organ, for example: that mainly sense the liver (middle and index fingers) are
• In appendicitis—over right iliac fossa.
positioned lateral to rectus muscle so that the fingertips lie
• In perforated peptic ulcer—over epigastric area.
to parallel to expected liver edge. Now the examiner presses
Rigidity his hand firmly inwards and upwards and keeps it steady
It is also due to muscular contraction and again self-defense while the patient takes a deep breath through the mouth.
mechanism. It is also seen (elicited) over the inflamed When the inspiration reaches to its peak, the pressure
organs, the only difference between the guarding and rigidity towards the upward direction is still maintained but the
is that the guarding occurs only when the abdomen is pressure towards inward direction is released. By the tip of
palpated, whereas rigidity is present all the time in order to the fingers slip over the edge of a palpable liver is palpated
prevent (or minimize) the movements of abdominal organs using the fingertip keeping them steady in a new position
with respiration. Hence, the type of respiration that is seen each time the patient takes a deep breath. The examiner
in case of rigidity is usually thoracic type (in males, the feels the irregularities as the liver slides under the fingertips
respiration is generally of the abdominal type). Rigidity with each inspiration.
occurs in the conditions like peritonitis, perforation of a
Alternate Method
hollow organ, acute pancreatitis, cholecystitis, ectopic
pregnancy, twisted ovarian cyst or torsion of fibroid, Though this method is less accurate; in this method, the
thrombosis of superior mesenteric artery, etc. right hand is placed below and parallel to right subcostal
margin. The liver edge is then felt against the radial border
Tenderness of the index finger. The liver is often palpable in normal
It suggests an underlying inflammatory process of abdominal patients without being enlarged. If the edge is indefinitely
viscera and the surrounding peritoneal structure. Tenderness felt, percuss in the right hypochondrium, keeping the hands
over a particular area gives a clue about the organ involved. still as the patient breathes. Movement of lower border
For instance:
• Over right iliac fossa—may be appendicitis.
• Over epigastrium—may be peptic ulcer.
• Over light hypochondrium—may be hepatitis or
cholecystitis.
Rebound tenderness: Deep seated inflammation not causing
localized guarding may be revealed by rebound tenderness.
Although initial pressure of palpation may fail to elicit a
painful response, the abrupt withdrawal may cause the Fig. 6.3: Palpation of viscera
Alimentary System 111
together with dullness on respiration is further supporting the costal margin more towards left side. Then the patient
evidence of liver enlargement. is made to breathe deeply. The examiner presses in deeply
with fingers of right hand beneath the costal margin, at the
Points to be Noted in Palpation of Liver same time exerting considerable pressure medially and
Size downwards with the left hand. The procedure is repeated
It can be measured and expressed either in terms of with the right hand being moved more medially beneath the
centimeters, below the costal margin (in midline, midclavi- costal margin on each occasion.
cular line and in mid-axillary line) or in terms of finger breadth If the patient presents with the history and clinical
below costal margins. features of splenic enlargement and still the spleen is not
palpable, the examiner turns the patient half on to right side
Interpretation and asks him to relax back on to his left hand (which now
• Severly enlarged liver – Congestive cardiac failure, supports the lower ribs). The procedure mentioned above
(gross enlargement) malignancy, blood dyscrasias, is repeated.
amebic abscess.
Second method: The examiner stands on the left side of the
• Moderate enlargement – Alcoholic hepatitis, fatty
degeneration, obstructive patient. He curls his fingers of the left hand beneath the
hepatitis in cirrhosis. costal margin, while the patient is made to breathe deeply.
• Mild enlargement – Infective hepatitis, anemia. Third method: It is used to detect massive splenomegaly. In
this method, the examiner stands on ‘right’ side of patient
Conditions in which Hard Nodular Liver is Seen
facing towards the footend of bed. He starts palpating the
It is seen in secondary carcinoma of liver—commonest spleen from the right iliac region. The radial border of index
tumor of liver, primary arising from portal territory stomach,
finger of right hand (sensing finger) is placed parallel to left
pancreas, large bowel. Through hematogenous—breast,
costal margin (with fingertips pointing towards the pubic
bronchus, kidney, thyroid.
symphysis of the patient) and he moves his hand more
Causes of Firm Liver, Hard Liver and Soft Liver towards left hypochondrium. The enlarged spleen will be
Causes of firm liver: felt by the index finger.
• Cirrhosis of liver Fourth method: Dipping method as mentioned above.
• Amyloid
• Hodgkin’s or chronic myeloid leukemia. Interpretation
Causes of hard liver: • Mild enlargement—just palpable below the left costal
• Primary and secondary carcinoma margin.
• Hydatid cyst. • Moderate enlargement—palpable but not reaching
Causes of soft liver: umbilicus.
• CCF • Severe enlargement—up to umbilicus or beyond that.
• Infective hepatitis
Table 6.1: Differentiation between splenic lump and
• Amebic hepatitis lump due to splenic flexure carcinoma
• Fatty liver.
Splenic lump Carcinoma lump (splenic)
Spleen Moves (Not fixed) Does not move (fixed)
Not hard. Firm to hard.
Procedure No history of bowel Bowel disturbances like malena,
disturbances or malena altered bowel movements.
Normal spleen is not palpable. To become palpable, the spleen
has to be enlarged to 2-3 times of its normal size. Enlarged Differences between pancreatic lump and spleen:
spleen is felt below the left subcostal margin. Prior to its • Pancreatic lump is situated in midline, umbilicus,
becoming palpable, the spleen enlargement takes place in epigastric region.
superior and posterior direction, spleen enlarges downwards • Pancreatic pain is deep into back towards L-1 vertebra.
and towards right iliac fossa. • It is fixed and does not move.
While standing on ‘right’ side of the patient, the examiner • Cystic in nature.
places the flat of his left hand over the patient’s lowermost • Percussion is dull.
rib cage posterolaterally, and the right hand is placed beneath • No notch is felt.
112 Essentials of Clinical Medicine
Table 6.2: Differences between carcinoma fundus of be pushed from one hand to the other in an action which is
stomach from splenic mass called “balloting”.
Carcinoma fundus of stomach Spleen
Right Kidney
Fixed Not fixed
Hard Not hard The right kidney is palpated in a way similar to the left. The
UGI symptoms, like nausea No GI symptoms examiner stands on the “right” side of the patient and places
vomiting, weight loss. Fundus gas shadow his right hand horizontally in the right lumbar region
Fundus gas shadow lost in X-ray
anteriorly with the left hand placed posteriorly in right loin.
Causes of Tender Spleen The patient is asked to take a deep breath and the left
hand is pushed forwards and right hand inwards and
• Splenic abscess. upwards.
• Subacute bacterial endocarditis with splenic infarct.
Normally (unlike the left kidney), the lower pole of the
• Sickle cell anemia with splenic infarct.
right kidney is commonly palpable in lean and thin individual
• Mitral stenosis with splenic infarct.
and is felt as a smooth, rounded swelling which descends
• Subcapsular hematoma.
• Splenic rupture. on the inspiration and is bimanually palpable and may be
• Splenic vein thrombosis. “balloted”.
The kidney should be examined (palpated) for size,
Table 6.3: Differences between left kidney and spleen surface, consistency, and tenderness.
Features Left kidney Spleen Differential Diagnosis of Kidney Mass
1. Site Posteriorly L1 region Anteriorly 9th, 10th,
and 11th ribs
1. Spleen—notch, moves with respiration, interiorly
2. Notch Absent Present enlarged, renal angle free.
3. Edge Smooth and rounded Sharp edge 2. Left lobe of liver—no notch, irregular surface, moves
4. Finger insinu- Possible Not Possible with respiration.
ation between
organ and
3. Ca. fundus of stomach—fixed, hard, no notch.
costal margins 4. Omental mass—edge not clear, no notch, gap between
5. Band of colonic Present Absent costal margin and lump (due to TB/malignancy)
resonance 5. Ca. splenic flexure—hard and fixed.
6. Movement No Moves freely on inspi-
ration with respiration
6. Malignancy of tail of pancreas.
7. When organ It grows towards It grows towards right 7. Suprarenal tumor—deeply placed, can reach the sub-
enlarges lumbar region iliac fossa. costal angle.
8. Bimanual Possible (palpable) Not palpable. 8. Pancreatic tumor—no notch.
palpation
9. Ballotable Ballotability possible Not possible
9. Ca. of colon.
10. Fullness and Present Absent 10. Ovarian tumor.
dullness in loin
Gallbladder
Kidneys
The normal gallbladder is not palpable. Enlarged gallbladder
Normal kidney is not palpable. The kidneys being is palpated in the same way on the enlarged liver. When
retroperitoneal organ are palpated by bimanual technique. enlarged it is palpated as a firm, smooth, rough or globular
pear-shaped swelling with distinct borders just lateral to the
Left Kidney
edge of rectum abdomens near the tip of ninth costal
The examiner stands on the “right” side of the patient and cartilage. It moves up and down with respiration. When
places his right hand anteriorly in the left lumbar region severe enlargement, it may not be felt in the right
while the left hand is placed in the left loin. hypochordrium, but in the right lumps or region or even
The patient is asked to take a deep breath in, and the left low down as the right illiac region.
hand is pressed forwards and right hand backwards, The palpation of gallbladder is possible in the following
upwards and inwards. The left kidney is not usually palpable situations (painless swelling):
unless either low in position or enlarged. Its lower pole, • Carcinoma of head of pancreas as well as the other
when palpable, is felt as a rounded firm swelling between malignancies—obstruction of common bile duct. The
both right and left hands (i.e. bimanual palpation) and it can patient presents with clinical features of severe jaundice.
Alimentary System 113
Urinary Bladder Percussing over the liver: Normally, the upper and lower
borders of the right lobe of liver can be assessed accurately
Normally, the urinary bladder is not palpable. In cases of by percussion. The examiner begins anteriorly, at the 4th
retention of urine, a smooth, firm, regular oval-shaped intercostal space where the note is resonant over the lungs
swelling is palpated in the suprapubic region and its upper and then he goes vertically downwards under normal
border (also called the dome) may even reach the umbilicus. conditions, the upper border of liver is at about the 5th
It is dull on percussion and on applying pressure over the intercostal space, where the note is dull. This dullness is
swelling, the patient develops a desire to micturate. present up to the right subcostal margin. In certain
The differential diagnosis of distended urinary bladder conditions, the dullness over the upper part of liver is reduced
in case of women: or absent. These conditions are severe emphysema, presence
• Gravid uterus—firm, mobile from side to side, with of large right pneumothorax and presence of gas or air in
certain specific vaginal signs. the peritoneal cavity (indicating perforation of a viscus).
• Ovarian cyst—eccentric swelling on the right or left In case of hepatomegaly, percussing below the right
side. costal margin is useful. The patient is asked to take deep
• Uterine fibroid—firm, bosselated and vaginal signs breath which the examiner percusses lightly. The fingers
different. are kept parallel to the rib margin. During inspiration, the
Note: Abdomen gives doughy feeling in tuberculous liver descends down and change in the note from resonance
peritonitis. to dull signals the edge of the liver. The percussion of upper
Percussion: Percussion of the abdomen is done with light border (margin) is also done. This gives the measure of
hands. Normally, resonant (tympanic) note is heard liver size.
throughout except over the liver, where dull note is heard. Spleen: Percussion over the enlarged spleen adds confir-
Percussion is generally helpful in making the diagnosis of matory findings to the palpation. Dullness of spleen can be
hepatomegaly or splenomegaly. elicited from left lower ribs to left hypochondrium and left
Normal liver span: Normal liver extends, from 5th rib (or lumbar region. Dullness of spleen gives way to the resonance
just below the right nipple in men) to the palpable margin or of surrounding bowel.
right costal margin. It is about 12 to 15 cm in height. The Urinary bladder: The percussion over the urinary bladder
hepatomegaly can also be measured in terms of centimeters differentiates it from swelling due to gases (the urinary
below the right costal margin at the midclavicular line or in bladder gives a feel of cystic or solid swelling). Its superior
terms of finger breadth (again below the same right costal and lateral borders can be readily defined from the adjacent
margin). bowel, which is resonant.
114 Essentials of Clinical Medicine
Right iliac fossa masses Middle masses Left iliac fossa masses
• Hard or impacted feces (scybala) Lymphoma (lymphadenopathy) • Carcinoma colon, left ovary
• Psoas abscess Carcinoma—gastric, pancreatic, colonic • Transplanted
• Appendix abscess • Kidney (note any overlyng scar)
• Carcinoma—colon, right ovary Aortic aneurysm
Pancreatic pseudocyst • Diverticular abscess
• Transplanted kidney (note any overlying scar) Ovarian cyst or tumors (benign or malignant) • Psoas abscess
Horseshoe-shaped kidney • Hard or impacted feces (scybala)
• Crohn’s disease (often adherent bowel loops) Uterine masses, pregnancy, fibroid, tumors,
• Tuberculosis of illeocecal region Bladder enlargement retention of urine
• Auscultate for peristaltic sounds for at least 3 minutes • Few hours after meals.
before deciding that they are absent. • Delayed gastric emptying as in diabetic autonomic
• The stethoscope should be placed on one site on the neuropathy.
abdominal wall (just to the right of the umbilicus is the
best) and kept there until sounds are heard. It should Arterial Bruits
not be moved from site to site. Normal bowel sounds
are heard as intermittent, low or medium pitched gurgles They are harsh systolic murmurs heard due to turbulence
interspersed with an occasional high-pitched noise or of blood flow. Care should be taken not to press the chest
tinkle. piece too firmly in the epigastrium as otherwise an artificial
systolic murmurs may be produced by compressing the
Peristaltic Sounds abdominal aorta.
Peristaltic sounds are produced by the contractions of Table 6.6: The sites of bruits and their causes
muscular walls of the gut and the resultant vibration of the
Site of bruit Cause
gut wall produced by movements of a gas-fluid mixture
through the gut. • Over liver • Vascular tumor like
hepatoma or hemangioma
Causes of increased bowel sounds (hyperperistalsis): • Hepatocellular carcinoma
• Subacute intestinal obstruction (high-pitched tinkling • Acute alcoholic hepatitis
quality) • Over spleen • Vascular tumor
• Diarrhoea/Dysentery. • Over aorta • Aortic aneurysm, atheroscle-
• Severe gastrointestinal bleeding rosis, extreme tortuosity of
• Small bowel malabsorption. aorta
• Over kidneys • Renal artery stenosis
• Carcinoid syndrome (marked borborygmi) • Mid-abdomen • Hypertension due to stenosis
Causes of diminished or absent bowel sound: of renal artery stenosis
• Perforation • Over common illiac artery or • Aneurysm or stenosis
• Immediately after abdominal surgery. femoral artery
• Paralytic ileus follwing intestinal obstruction or • Over pancreas • Coeliac artery stenosis
• Carcinoma pancreas.
necrotizing enterocolitis.
• Hypokalemia.
Causes of Splenic Bruit
• Bowel atony
• Peritonitis. • Intrahepatic portal obstruction.
• Vascular tumors as angioma of spleen, angiosarcoma.
Succussion Splash
Venous Hum
It is somewhat similar to that heard in case of
hydrothoraxes. It is produced by shaking the patient and • It is a continous, softer and low-pitch sound.
auscultating over the epigastrium. It is heard in cases of: • Heard between xiphisternum and umbilicus due to
• Pyloric obstruction turbulence of blood flow in well-developed collaterals
• Severe intestinal obstruction as a result of portal hypertension. (Cruveilhier-
• Paralytic ileus accompanied with bowel distention. Baumgarten syndrome)
116 Essentials of Clinical Medicine
• Signifies portal systemic shunting of venous flow when sus (SLE), chronic alcoholism, rheumatoid arthritis,
portal flow is obstructed. thyrotoxicosis.
• Heard over liver and umbilicus.
Causes of Bilateral Parotid Enlargement
Friction Rub • Mumps
Heard in cases of perihepatitis or perisplenitis. • Portal cirrhosis.
• Fibrocalculus pancreatitis.
Common Cases in GIT Cirrhosis • Sarcoidosis.
History in a Case of Cirrhosis of Liver • Mikulicz syndrome.
• Sjögren’s syndrome.
• Ask for fatigue, weight loss, flatulent dyspepsia, anorexia
and low-grade fever Complication of Portal Cirrhosis
• History of hematemesis, malena, leg swelling, • Hematemesis
progressive abdominal swelling, drowsiness and • Anemia.
inversion of sleep rhythm in prehepatic coma cases • Hepatic encephalopathy.
• Past history of viral hepatitis • Spontaneous bacterial peritonitis (SBP)
• History of drug intake, INH, rifampicin, anabolic steroid, • Hypersplenism.
oral contraceptive pills, NSAIDs for malena • Hepatorenal syndrome.
• Past history of blood transfusion—viral hepatitis B, C • Peptic ulcer.
and D or transfusion of any blood products, recent • Infection—TB, etc.
tattooing, acupuncture, drug abuse. • Chronic cholecystitis.
• Alcohol consumption. • Pigment stone.
• Hematochezia, lower GI malignancy and hemorrhoids.
Clinical Features of Hepatic Encephalopathy
Clinical Features of Cirrhosis of Liver • Early—confusion, inversion of sleep rhythm, flaps (Aste-
a. Features of portal hypertension: rixis), constitutional apraxia, micrographia, slurred and
• Ascites monotonous speech.
• Splenomegaly. • Late—coma
• Opening of portosystemic collaterals. • Deep jaundice
b. Features of liver cell failure: • Fetor hepaticas
• Jaundice—terminal. • Liver dullness obliterated bleeding, decerebrate rigidity.
• General weakness, weight loss, muscle wasting, • Cerebellar sign
anorexia, flatulence.
• Fever low grade Causes of Enlarged Liver in Cirrhosis
– Gram-negative bacteremia • Hepatoma.
– Hepatic cell necrosis. • Fatty liver.
• Endocrine manifestation—loss of libido, spider nevi, • Postnecrotic cirrhosis.
spare hairs, palmer erythema gonadal atrophy. • Primary biliary cirrhosis.
• Bleeding diasthesis—PT increased, purpura.
• Cardiac cirrhosis.
• Anemia—microcytic, iron loss due to upper GI
• Budd-Chiari syndrome.
hemorrhage, normocytic due to hypersplenism.
• Ascites—transudate type. • Constructive pericarditis.
• Spider dilated capillaries—face, dorsum of hand, Table 6.7: Causes of anemia, fever, and exudative ascites in cirrhosis
forearm, chest.
Anemia in cirrhosis Fever in cirrhosis Exudative ascites in
Mechanism of Portal Hypertension cirrhosis
• Decreased vascular bed due to fibrosis. Upper GI bleeding Liver cell necrosis Tuberculosis peritonitis
• Distortion of vascular tree. Hypersplenism Portal bacteremia Hepatoma
• Transmission of hepatic arterial pressure to the portal Folate deficiency reaching systemic Subacute bacterial
B12 and iron deficiency blood Peritonitis
system. Melena Associated After diuretic therapy
• Compression of portal tributaries by regenerating nodule. Zieve’s syndrome malignancy Splenic vein thrombosis
Hemolyses
Causes of Palmar Erythema
Anorexia—malnutrition
• Portal cirrhosis, pregnancy, systemic lupus erythemato-
Alimentary System 117
Table 6.25: Diarrhea due to small bowel and large bowel dysfunction Table 6.27: Amebic and bacillary dysentery
Table 6.28: Hemolytic, hepatocellular and cholestatic jaundice Deep jaundice: When jaundice takes greenish hue due to
oxidation of bilirubin to biliverdin seen in obstructive
Haemolytic Hepatocellular Cholestatic
jaundice.
Primaquine Isoniazid Chlorpromazine
Mepacrine Halothane Anabolic steroids
Chloramphenicol Rifampicin Oral contraceptive
Conditions under which the Tissues
Nitrofurantoin Carbon tetrachloride Erythromycin estolate
are not Stained in Jaundice
Staining of tissues depends on blood flow and protein content
• Intermittent (recurrent) jaundice—gallstone, Dubin of fluid. In edematous limb, scar tissue and hemiplegic limbs
Johnson, Gilbert’s syndrome, hemolytic, recurrent staining are absent.
familial cholestasis
Table 6.29: Differences between conjugated and unconjugated bilirubin
• Jaundice with ascites—gland at porta hepatis, late stage
of cirrhosis, primary cirrhosis Properties / Features Conjugated Unconjugated
bilirubin bilirubin
• Palpable gallbladder with jaundice—carcinoma pancreas,
gallbladder • Affinity to lipids No Yes
• Water solubility Yes No
• Enlarged liver with jaundice • Renal excretion Yes No
– Soft tender—infective hepatitis, fatty liver • Vender Berg’s reaction Direct Indirect
– Firm—cirrhosis amyloid • Bound to protein Mildly Strongly
– Hard—secondary carcinoma Table 6.30: Jaundice and hepatocellular jaundice
• Hepatorenal syndrome—viral hepatitis, Weil’s diseases,
halothane Bile acids Very high Moderate increases
• Left supraclavicular gland enlargement and jaundice- Cholesterol Increased Decreased
SGOT/SGPT Slight increase Marked increase
carcinoma stomach Alkaline phosphatase more than 3 times less than 3 times normal
• Lymphadenopathy and jaundice—infectious mono- normal
nucleosis, type B hepatitis, Hodgkin’s disease Prothrombin time Yes No
response to vit K
• Anemia with jaundice—hemolytic, carcimona pancreas,
Steatorrhea Common Uncommon
secondary carcinoma liver. Splenomegaly with jaundice-
hemolytic, cirrhosis of liver, 1/3rd cases of viral hepatitis Table 6.31: Differences among hemolytic, hepatocellular
• Extrahepatic manifestations—arthralgia, rash, lympha- and obstructive jaundice
denopathy Hemolytic Hepatocellular Obstructive
• Short stature, arthritis, mild jaundice, leg ulcer—hemo- jaundice jaundice jaundice
lytic anemia • History • H/o blood • H/o contact with • H/o marked
• Parotid swelling, Dupuytren’s contracture, gyne- transfusion in patient with pruritus and
comastia, testicular atrophy family/siblings/ jaundice (hepa- abdominal pain
patient himself titis)
• Coma and jaundice—hepatic coma, hepatorenal syn- • H/o drug intake • H/o drugs (AKT) • H/o surgery/
drome. • H/o abdominal • H/o vomiting, weight loss
pain during right hypocho-
Where do You See for Jaundice? acute episode. ndriac pain
• Exami- • Pallor may be • Tenderness over • Pallor may be
• Bulbar conjunctiva, buccal mucosa, frenulum of tongue, nation present the liver may be present
nails and skin. findings present
• Ascites may be • Scratch marks
• Bulbar conjunction first gets stained yellow because it
present due to itching
is rich in elastin and elastin has high affinity for bile may be present
pigments. • Ascites may be
present
Differential Diagnosis of Yellow • Investi- • S Bilirubin–Mild • S Bilirubin-Mode- • Bilirubin-mode-
Discoloration of Skin gation increase rate-to-severe rate increase
increase
• Carotenemia—Skin • SGOT/SGPT- • SGOT/SGPT
• Mepacrine—All over except bulbar conjunctiva usually normal markedely
• Drugs—B Complex, Nitrofurantoin, Pyridium and many increased
more. Contd...
Alimentary System 127
Contd... Alcohol
Hemolytic Hepatocellular Obstructive
jaundice jaundice jaundice Drug Toxicity
• S Alkaline Phos- • S Alkaline phos- • S Alkaline phos- • Predictable, dose dependent, e.g. acetaminophen, unpre-
phatase usually phatase phatase marked- dictable, idiosyncratic, e.g. isoniazid.
normal increased ly increased
• Urine Absent Present Present
Environmental Toxins
exami- • Vinyl chloride
nation: • Jamaica bush tea – pyrolizidine alkaloids.
• Bilirubin Present Present Absent • Wild mushrooms – Amanita phalloides or verna.
Urobilinogen
• Wilson’s disease
• Stool Present Present Absent
exami- • Autoimmine hepatitis.
nation:
sterco- Cholestatic Conditions that may
bilinogen Produce Jaundice
• Retic count Increased Normal Normal
Intrahepatic
Causes of Jaundice • Viral hepatitis:
i. Fibrosing cholestatic hepatitis—hepatitis B and C.
Causes of Isolated Hyperbilirubinemia ii. Hepatitis A, Ebstein—Barr virus, cytomegalovirus.
Indirect Hyperbilirubinemia • Alcoholic hepatitis
• Hemolytic disorders • Drug toxicity
i. Inherited: i. Pure cholestasis—anabolic and contraceptive
a. Spherocytosis, elliptocytosis G-6-PD and pyru- steroids.
vate kinase deficiency. ii. Cholestatic hepatitis—chlorpromazine, erythromycin
b. Sickle cell anemia. estolate.
ii. Acquired: iii. Chronic cholestasis—chlorpromazine and prochlor-
perazine.
a. Microangiopathic hemolytic anemias.
• Primary biliary cirrhosis.
b. Paroxysmal noctural hemaglobinuria.
• Primary sclerosing cholangitis.
c. Immune hemolysis.
• Vanishing bile duct syndrome:
• Ineffective erythropoiesis i. Chronic rejection of liver transplants.
i. Cobalamin, folate, and iron deficiencies. ii. Sarcoidosis.
• Drugs iii. Drugs.
i. Rifampicin, probenecid, ribavarin. • Inherited
• Inherited condition i. Benign recurrent cholestasis
i. Crigler-Najjar type I and II • Cholestasis of pregnancy.
ii. Gilbert’s syndrome. • Total parenteral nutrition.
Direct Hyperbilirubinemia • Non-hepatobiliary sepsis.
• Inherited condition. • Benign postoperative cholestasis.
• Paraneoplastic syndrome.
i. Dubin-Johnson syndrome
• Veno-occlusive disease.
ii. Rotor’s syndrome.
• Graft versus host disease.
Hepatocellular Conditions that may Extrahepatic
Produce Jaundice • Malignant
Viral Hepatitis i. Cholangio carcinoma.
ii. Pancreatic cancer.
• Hepatitis A, B, C, D and E. iii. Gallbladder cancer.
• Ebstein-Barr virus. iv. Ampullary cancer.
• Cytomegalovirus. v. Malignant involvement of porta hepatitis, lymph
• Herpes simplex. nodes.
128 Essentials of Clinical Medicine
• Benign Contd...
i. Choledocholithiasis. Intrinsic G-6-PD deficiency Extrinsic
ii. Primary sclerosing cholangitis. • March hemoglobin
iii. Chronic pancreatitis. uria
iv. AIDS cholangiopathy. 3. Miscellaneous
Chemical drugs,
infection, burn, lead
Causes of Ascites with Jaundice and
poisoning.
Hard Liver
• Budd-Chiari syndrome. Causes of Hepatocellular Jaundice
• Gland at porta hepatis.
• Secondary seedling peritoneum. • Active liver disease, viral hepatitis, infectious mono-
• Cardiac cirrhosis. nucleosis, yellow fever.
• Constrictive pericarditis. • Non-viral relapsing fever, septicemia.
• Drugs, anti-TB drugs, halothane, etc.
Causes of Intermittent Jaundice • Fatty liver of pregnancy.
• Chronic liver disease—primary biliary cirrhosis, primary/
• Hemolytic anemia.
secondary tumor of liver.
• Congenital hyperbilirubinemia.
• Gallstone impaction and disimpaction. Table 6.33: Causes of obstructive jaundice
• Carcinoma of ampula of Vater. Intrahepatitic cholestasis Extrahepatic jaundice
• Viral hepatitis • Porta hepatitis – ampula of
Causes of Unconjugated Hyperbilirubinemia
• Drugs –Methyl testosterone, Vater
• Overproduction—hemolysis, ineffective erythro-poiesis. chlorpromomide, anabolic, • Causes in lumen – stone,
• Decreased hepatic uptake—septicemia, starvation, drug. steroid, chlorpromiazine, parasite, stricture
PAS, oral contraceptive pills. • Causes in wall of lumen –
• Defect in bilirubin conjugation (decreased glucuronyl
• Alcoholism carcinoma bile duct, trauma,
transferase) • Jaundice in pregnancy. acute pancreatitis chronic
• Gilbert’s syndrome, Criggler-Najjar syndrome, neonatal • Dubin-Johnson and Rotor’s pancreatitis
jaundice, drug induced) (chloramphnicol, novobiocin, syndrome • Causes outside the wall –
pregnanediol). • Postoperative jaundice carcinoma head of pancreas,
• Sclerosing cholangitis pseudocyst
Table 6.32: Causes of hemolytic jaundice • Biliary atresia
(unconjugated hyperbilirubinemia)
Intrinsic G-6-PD deficiency Extrinsic Sequelae of Viral Hepatitis
• Spherocytosis • Antimalarial drugs 1. Immune mechanism • Acute fulminant hepatitis.
• Elliptocytosis • Sulfonamides • Autoimmine,
• Chronic persistent hepatitis.
• Hemoglobino- • Chloromphenicol Warm and cold
pathies. antibodies • Chronic active hepatitis.
• Sickle cell disease • Nitrofurantoin • Cold hemoglobin- • Posthepatitis syndrome.
• Hbs • Quinine uria • Cirrhosis of liver.
• Thalassemia • Drugs and chemicals
• Carcinoma of liver (hepatoma)
• Hemoglubinuria • Viral pneumonia
• Malaria • Cerebral edema, GI bleeding.
• Hypersplenism • Hepatorenal failure.
• Incompatible blood • HBs Ag carrier.
transfusion
2. Non-immune
• Rarely pancreatitis, myocarditis, atypical pneumonia,
mechanism: aplastic anemia, peripheral neuropathy, glomerulo-
• Mechanical hemo- nephritis.
lysis due to cardiac
valve Sequelae of Fulminant Hepatic Failure
• Microangiopathic
hemolytic anemia • Hepatic encephalopathy.
Contd... • Cerebral edema.
Alimentary System 129
• Respiratory failure. Table 6.34: Distinctive features of Crohn’s disease and ulcerative colitis
• Hypothermia. Feature Crohn’s disease Ulcerative colitis
• Infection.
Macroscopic
• Bleeding, pancreatitis. Bowel region Ileum ± colon Colon ± ileum Colon only
• Renal failure. Distribution Skip lesions Skip lesions Diffuse
• Metabolic Stricture Early Variable Late/rate
Wall
– Hypoglycemic, hypokalemia, hypomagnesemia, acid- appearance Thickened Thin Thin
base disturbance. Dilation No Yes Yes
Microscopic
MAJOR CAUSES OF NEONATAL Psuedopolyps No to slight Marked Marked
CHOLESTASIS Ulcers Deep, linear Deep, linear Superficial
Lymphoid Marked Marked Mild
• Bile duct obstruction reaction
Serositis Marked Moderate Mild
• Extrahepatic biliary atresia Granulomas Yes (50%) Yes (50%) No
• Neonatal infection Fistulas/sinus Yes Yes Yes
• Cytomegalovirus Clinical
• Bacterial sepsis Fat/vitamin Yes Yes If ileum
Malabsorption No No
• Urinary tract infection Malignant Yes Yes Yes
• Syphilis potential
• Toxic drugs Response to Poor Fair Good
surgery
• Parenteral nutrition
• Metabolic disease RUPTURE SPLEEN
• Tyrosinemia
As the shock passes off, there are signs which point to
• Niemann-pick disease intra-abdominal bleeding.
• Galactosemia
• Defective bile acid synthetic pathways General Signs
• Antitrypsin deficiency
Increasing pallor, rising pulse rate, sighing respiration and
• Cystic fibrosis restlessness.
• Miscellaneous
• Shock/hypoperfusion Local signs
• Indian childhood cirrhosis
• Abdominal rigidity more in left upper quadrant.
• Alagille syndrome (paucity of bile ducts) • Local bruising and tenderness in left upper quadrant.
• Abdominal distention 3 hours after the rupture due to
INFLAMMATORY BOWEL DISEASE irritative effect of intraperitoneal blood which produces
Diagnosis in favour of irritable bowel syndrome: peritonitis and ileus.
Continuous or recurrent abdominal pain or discomfort • Kehr’s sign—pain referred to left shoulder due to blood
– relieved by defecation, or associated with altered stool in contact with undersurface of diaphragm, pain
frequency or consistency together with either or both of mediated via phrenic nerve.
• Shifting dullness in flanks.
the following features:
• Ballance’s sign—dull note in both flanks, but on right
a. Altered pattern of defecation—for at least 25 percent of
side it can be made to shift; whereas on left, it is
the time is two or more of the following:
constant. Reasons for this is that blood near the lacerated
– Altered stool frequency (> 3 / day or < 3 / week). spleen has coagulated though there is blood in peritoneal
– Altered stool form (lumpy, hard, loose, watery). cavity.
– Altered stool passage (straining, fecal urgency, feeling • Rectal examination—tenderness, soft swelling due to
of incomplete emptying). blood or clot in rectovesical pouch.
– Passage of mucus.
b. Abdominal distention or a feeling of abdominal Radiological Signs
bloating. • Obliteration of splenic outline and psoas shadow.
130 Essentials of Clinical Medicine
• Identification of left side of gastric air bubble. 3. A 60-year-old male is noted to have mild jaundice and
• Fracture of one or more lower ribs on left side. weight loss. Alkaline phosphates is very elevated. He
• Elevation of left side of diaphragm. had very pale stools. The most probable diagnosis is:
• Free fluid between gas-filled intestinal coils. Pancreatic carcinoma
GIT Nephrology
1. A 40-year-old male with longstanding alcohol abuse 1. A 70-year-old male with a history of urinary tract infection
complains of abdominal swelling which has been pro- and congestive heart failure was admitted to the hospital
gressive over several months. He has a history of gastro- for sepsis and pulmonary edema. He was treated with
intestinal bleeding. On physical examination, there are clindamycin and tobramycin and also received intra-
spider angiomata and palmar erythema. Abdominal venous furosemide. After several days, the signs of sepsis
collateral vessels are seen around umbilicus. There is improved, but the BUN rose to 60 mg/dl and creatinine
shifting dullness, and bulging flanks are noted. A to 5.0 mg/dl. The blood pressure changed. Weight was
paracentesis is performed in this patient. The serum unchanged throughout the hospital course. The most
albumin minus ascitic fluid albumin equals 1.2 gm/dl. likely diagnosis is:
The most likely diagnosis is: Acute tubular necrosis
Portal hypertension 2. A young man presents to the emergency room with
2. While hospitalized, the patient’s mental status cyanosis and disorientations. Blood gases show a pH of
deteriorates. He has been having guaiac-positive stools 7.2, PCO2 of 68 mm Hg., HCO3 of 35 mg/dl. There are
and low-grade fever. He also has received sedation for multiple needle tracks in the antecubital fossa. The rest
agitation. On physical examination, the patient is of the examination is normal. The most likely acid-base
confused. He has no meningeal irritation signs and no problem is:
focal, neurological and no rhythmic flapping tremor of Acute respiratory acidosis
the wrist. The most likely explanation for mental status
change is:
Hepatic encephalopathy
Alimentary System 131
Fig. 6.7: Duodenal ulcer shown by barium meal Fig. 6.8: Renal artery stenosis
Fig. 6.9: Almost achalasia, but note the irregularity of Fig. 6.10: Plain radiograph showing radiopaque
the taper, which indicates carcinoma of cardia stones in gallbladder
132 Essentials of Clinical Medicine
Fig. 6.11: Retrograde ureterogram showing double ureter on the left Fig. 6.12: Radiograph showing a vescicle calculus
(no contrast has been used)
Fig. 6.13: Retrosternal goiter causing deviation of Fig. 6.14: Plain radiograph of a perforated ulcer,
a) trachea b) esophagus (barium swallow) showing air under diaphragm
Cardiovascular System
Fig. 7.4
The pulses which come under this category are: of systole. And as the mild aortic stenosis also
a. Pulsus alternans accompanies, it causes an extra high velocity jet to be
b. Pulsus bisferience thrown out, giving rise to secondary rise.
c. Dicrotic pulse iii. Conditions:
d. Anacrotic pulse. – Combined aortic stenosis and aortic regurgitation.
– Severe aortic regurgitation (without aortic
Pulsus Alternans stenosis)
Definition: A pulse with alternating strong and weak – HOCM (hypertrophic obstructive cardiomyo-
pulsations. The rhythm of the pulse is normal. This differs pathy)
from pulsus begeminus where there is a distinct pause after c. Dicrotic pulse: See above
two beats. d. Anacrotic pulse: See above
Procedure: Pulsus alternans can be easily detected by
measurement of blood pressure of the patient. By using Tension of the Pulse
auditory method when the SBP is measured at the highest Definition
level, then only auditory sounds are audible. But all the
sounds become audible as soon as the pressure is lowered. An opposite to the force of the pulse, the tension of the
This is because the pulse wave produced by the weaker pulse indirectly indicates diastolic blood pressure (DBP).
beat is not sufficient to get recorded as the highest systolic Procedure
pressure (highest SBP). This type of pulse is best appreciated The examiner palpates the arterial pulse of the patient (usually
by palpating radial or femoral pulses, rather than the carotids. radial pulse). A very heavy pressure is required to feel the
Mechanism/genesis: It is produced most probably due to high tension pulse which indicates high DBP. Accordingly,
alternate rather than regular contraction of the muscle fibers medium or normal DBP requires moderate pressure and
of the left ventricle. It usually indicates grave prognosis. low DBP requires light pressure.
Conditions:
• Severe left ventricular failure Volume of the Pulse: (Amplitude of the pulse)
• Tonic myocarditis
• Paroxysmal tachycardia Definition
• Several beats following a premature beat in an otherwise It indirectly indicates stroke output of the heart (i.e. left
normal heart. ventricular output per beat.)
• Coupled ventricular premature beats may also resemble Procedure: The examiner palpates the arterial pulse of the
pulses alternans; but in this case, the rhythm is irregular. patient. When pulse waves pass through the artery, an uplift
Pulsus Bisferience is felt by the palpating finger, the extent for this uplift
(amplitude) is a rough estimate of the volume of the pulse.
Definition: A pulse marked by two systolic peaks on the
– Pulse pressure between = 30-60 mm Hg – Volume normal
pulse waveform. It has 2 systolic peaks separated by mid-
– Pulse pressure between < 30 mm Hg – Small (low)
diastolic dip. In this type of pulse, every pulse beat is
distinctly felt to have a double impulse. volume pulse
– Pulse pressure between > 60 mm Hg – Large (high)
Mechanism/genesis: volume pulse
i. Idiopathic hypertrophic subaortic stenosis: In the early – Pulse volume depends on stroke volume and arterial
phase, there is no obstruction to outflow of the blood compliance.
and nearly more than 3/4th (i.e. about 80%) of the
stroke volume is ejected in the early part of systole. Character of the Pulse: (Form)
As the systole proceeds, the obstruction occurs in
midsystole when aortic value comes close to Definition
hypertrophied septum. Therefore, there occurs a dip, Sometimes a very confusing term is used called character
due to sudden cessation of the blood flow followed of the pulse. What does the character of pulse actually mean?
by a secondary rise as the left ventricle gets over the The character of the pulse is a congregate description of its
obstruction. “volume, force and tension”. Pulse is not only an expansion
ii. Severe aortic incompetence and mild aortic stenosis: (dilatation) and contraction (returning to original size) of
Due to severe aortic incompetence, the volume of the vessels; but the whole vessel is made taut and let loose
flowing blood initially increases during the early part thus undergoing a physical sinuous movement because of
Cardiovascular System 137
INSPECTION
Inspection forms a very important part of cardiovascular
system examination. The points to be examined in inspection
Fig. 7.6: The normal JVP and its component waves of cardiovascular system are:
140 Essentials of Clinical Medicine
Apex Beat
• In extreme shift to the right side when the apex beat lies Mobility of the beat: It is defined as the change in position
behind the sternum. of apex beat with the change of body position. Normally, a
• Diffuse apex beat. change (mobility of apex beat occurs with the change in
Exact site: (Exact site has been mentioned earlier) body position).
Apex beat visible but shifted or displaced: a. Mobility absent:
a. Cardiac causes: • Adhesive pericarditis.
Outward and horizontal shift (which may later on also b. Excessive mobility
go upwards) – Right ventricular hyper trophy. • Cor mobilale.
• Downwards and outwards—left ventricular hyper- • Tear drop heart
trophy. • Congenital heart disease.
• Apex impulse on right side in the 5th intercostal space
– Dextrocardia. Retraction of Chest Wall over the Precordium
b. Extra cardiac causes: • Retraction of apex along with parasternal:
There are mostly due to respiratory disorders, where – Pulsation—massive right ventricular hypertrophy
the heart (mediastinum) is pulled or pushed to one side. (right ventricular rock).
Push Pull • Prominent apex beat with retraction of parasternal.
• Pleural effusion Pulmonary fibrosis – Area (left side)—massive left ventricular hypertrophy
• Pneumothorax Pulmonary collapse (left ventricular rock).
• Hydropneumothorax • Prominent apical and left parasternal impulses with
• Massive hemothorax retraction in between—biventricular hypertrophy
– Intrathoracic tumor. (biventricular rock).
– A massive ascites may cause the shift of the
impulse upwards. Visible Pulsations
c. Deformities of thoracic cage:
• Kyphosis a. Pulsations over the precordium:
• Scoliosis Left parasternal – Right ventricular hypertrophy
• Kyphoscoliosis – Left atrial enlargement
• Pectus excavation (shifts the apex laterally by – Aneurysm of aorta.
compressing and flattening the heart). (Aortic aneurysm may be seen as a pulsating mass either
at base of heart on the right side in 2nd ICS or rarely when
Type of apex beat: it erodes through the sternum).
a. Hearing apex beat • Pulmonary area – Pulmonary hypetension
b. Hyperdynamic apex beat (rarely).
c. Tapping apex beat. • High output – Pulmonary artery dilatation,
(The above three are more a part of palpation and have states pulmonary hypercirculation
been explained there). (ASD).
d. Retraction at the site of apex beat. is seen in adhesive • Second right – Dilated pulmonary artery
pericarditis. intercostal – Aneurysm of aorta.
e. Dome-shaped apex beat—severe left ventricular space – Hyperkinetic space.
hypertrophy, which is of the following types— – Enlarged left atrium.
hypertrophy in parallel (concentric hypertrophy), b. Pulsation outside precordium:
hypertrophy in series, work hypertrophy, anoxic • Suprasternal – Hyperdynamic circulatory
hypertrophy. states like anemia, thyrotoxi-
f. Bifid apex beat—[double heart beat – due to left bundle cosis, beri-beri
branch block (LBBB)]. – Aortic aneurysm.
Extent of apex beat: Normal apex beat extends to a distance – Coarctation of aorta.
of about 2.5 cm (1 inch). If the apex beat extends > 2.5 – Abnormal thyroidea ima artery.
cm, it is called diffused apex beat. – Pulsating thyroid gland.
In hyperdynamic circulatory states, we get diffuse heart – Syphilitic aortitis.
beats. – High arch aorta.
142 Essentials of Clinical Medicine
Fig. 7.9: Diagram showing the projections of heart valves and the
auscultatory areas 1- pulmonary artery valve; P – pulmonary area; 2
Fig. 7.8: Percussion of borders of heart – aortic valve; A – aortic area; 3 – tricuspid valve; T – tricuspid area;
4 – mitral valve; M – Mitral area
• Pericardial effusion (increased dullness).
• Emphysema—where there occurs enlargement of Some Interesting Facts Related to Auscultation
cardiac borders (decreased cardiac dullness).
• Detecting the aortic dilatation as in aneurysm of aorta • Stethoscope was invented by Lennaec
and pulmonary artery dilation as in pulmonary • Total ideal length of stethoscope—12 inch (the
hypertension or idiopathic pulmonary artery dilation. stethoscope that we generally use is 18 inch long).
• Dextrocardia (which may or may not be associated • Diameter of lumen—1/8 inch (minimum)
with situs invertus). • Thickness of diaphragm—0.003 inch.
• Dilated cardiomyopathy. • Diameter of diaphragm—4 cm
• Diameter of bell—2.5 cm.
Principles of Percussion
Sounds Best Heard by the
1. Always start percussing from resonant to dull area. Diaphragm of Stethoscope
2. Finger should be parallel to the border being percussed. High-pitched sounds (including murmurs also)
3. No space (gap) should be left between the finger and • First and second heart sounds
chest wall. • Systolic murmurs (especially early diastolic)
4. Scratching and stethoscope method: That is when the • Pericardial rubs
stethoscope is placed over the chest wall and the chest
• Opening snaps
wall is scratched, then over the area which is dull, there
• Clicks
will be change in the intensity of the sounds which can
be very well detected by the stethoscope. Sounds Best Heard by Bell of the Stethoscope
• Pericardial effusion—increases cardiac dullness Low-pitched sounds (including murmurs also)
• Emphysema—encroachment of cardiac dullness. • Mild diastolic murmurs
AUSCULTATION (Figs 7.9 and 7.10) • Third heart sound
• Fourth heart sound.
Table 7.5: Conduction speed in cardiac tissue
Sites to keep the stethoscope (areas of auscultation) auscultating beyond the point of appearance (as explained
a. Over precordium: above) we may sometimes come across another sound
(or murmur), the intensity of which (the intensity of
Table 7.6: Mitral area and cardiac apex sound) is maximum.
Mitral area Cardiac apex Significance: If an examiner does not ausculdate
• Tricuspid area Lower left parasternal area carefully, he may assume the second sound as the
• Aortic area 2nd right intercostals space close “radiation of first murmur and involvement of another
to sternum valve may be missed”. Therefore, all the students are
• Secondary aurtic area (erbs area) 3rd left intercostals space close to advised to auscultate every centimeter (or every inch)
sternum between two murmur sounds.
• Pulmonary area 2nd left intercostals space close
to sternum Principles of Auscultation
• Gibson’s murmur or murmur 1st left intercostals space close to
1. Low-pitched sounds/murmurs are best heard by the bell
of PDA sternum
of the stethoscope and high intensity sounds/murmur
by the diaphragm.
b. Other ausculatory areas: 2. Always start auscultating the chest from the aortic area.
The significance of this is that, over the aortic area only
Table 7.7: Other auscultatory areas
A2 (i.e. aortic component of second heart sound) is
Axilla (anterior mid and posterior Murmurs of mitral stenosis audible and you have no chance of getting confused by
axillary lines) the other type of murmur.
Epigastrium Abdominal cortic murmurs
3. Then you should auscultate the pulmonary area where
Carotids Carotid shudder
Inter-and infrascapular areas you auscultate only P2 (pulmonary component of second
Supra-and infraclavicular areas heart sound). Again no chance of confusion.
4. Then, go to the tricuspid area when you auscultate 1st
Auscultation can be performed at any other site of the heart sound.
body where you suspect pulsations/bruits. 5. And at last, auscultating, the mitral area. The mitral
area is auscultated at last because here you have 1st
Scratching and the Stethoscope Method heart sound as well as A2 (aortic component of second
The examiner keeps his stethoscope over the chest wall of heart sound), as the aorta originates from the left
the patient and he scratches the chest wall (either with ventricle and vibration of aortic valve closure may be
fingernails or with other solid objects). Increased intensity transmitted via blood to the area of mitral valve.
of sound will be heard over the area of dullness as compared Thus, the sequence for auscultation → aortic area
to other areas, which are normal. ↓
Triangular and hour glass auscultation: Pulmonary area
a. Triangular auscultation:
↓
Every murmur has its peculiar area of origin (exact site
of origin). It forms the base of the triangle. We all know Tricuspid area
that every murmur is heard over some extent (it may be ↓
a few millimeters or a few centimeter from the exact Mitral area
site of origin). As we go on auscultating away of murmur
(This sequence is for the beginners so that they can
sound goes on decreasing and ultimately it disappears .
differentiate various murmurs clearly. Experienced ears, of
Now, if we join, the base with this point (beyond which
the sound of murmur disappears), we get a triangular course, require no rules).
area. Purpose of Auscultation
Significance: It gives us the idea about:
1. Heart sounds (1st and 2nd)
1. Which valve is involved/affected?
2. Murmurs
2. Radiation of murmur
3. Added sounds (third heart sound, fourth heart sound,
3. The point where maximum intensity is heard.
b. Hour glass auscultation: opening snap ejection clicks, pericardial rub, plop sounds
This method is used to differentiate between two similar due to prosthetic valves, gallop, which is in fact
types of murmurs. This method is similar to the pathological HS3)
triangular method, but the difference is, if we go on • First heart sound is auscultated for:
Cardiovascular System 147
Although events of the two sides of the hearts are similar, apex, the split is usually due to mitral valve closure,
they are somewhat asynchronous. Right atrial systole pulse on atrial sound (S4) or mitral valve closure plus an
proceeds left arterial systole, and contraction of right ejection sound, and not true splitting of S1.
ventricle starts after that of the left. However, since a. Wide splitting of S1 occurs with delayed closure of
pulmonary arterial pressure is lower than the aortic pressure, the tricuspid valve in the right bundle branch block
right ventricular ejection begins before left ventricular (RBBB).
ejection. During expiration, the pulmonary and aortic valves 4. The intensity of S1 depends on the rate of pressure
close at the same time. But during inspiration, the aortic development in the ventricular, the structure of the valve
valve closes slightly before the pulmonary. The slower leaflets, and the position of the AV valves at the beginning
closure of pulmonary valve is due to lower impedance of of the ventricular contraction.
the pulmonary vascular tree. When measured over a period 5. The examiner can recognize S1 of increased intensity
of minutes, the outputs of the 2 ventricles are, of course, by noting that S1 is louder than S2 at the base of the
equal, but transient differences in output during the heart. S1 increased in intensity occurs:
respiratory cycle occurs in normal individuals. a. In hyperkinetic states exhibiting increased contra-
The first event in a cardiac cycle is atrial depolarization ctility and myocardial tension development. Such
(p wave on the surface ECG). Followed by right atrial and conditions include anemia, pregnancy, anxiety,
then left atrial contraction. hyperthyroidism and fever.
Ventricular activation (the QRS complex on the ECG) b. In the presence of mitral valve leaflet thickening and
follows after a short interval (the PR interval). Left scarring as long as the leaflets maintain some motility.
ventricular contraction starts and shortly thereafter right This is characteristic of mitral.
ventricular contraction begins. The increased ventricular c. When the mitral valve is wide open at the onset of
pressures exceed the artrial pressure, and close first the the ventricular contraction. This occurs when there
mitral and then the tricuspid valves. Until the aortic and is a short P-R interval (0.11-0.13 seconds) on the
pulmonary valves open, the ventricles contract with no ECG and the onset of ventricular contraction
change in volume (isovolumetric contraction). When following atrial contraction occurs earlier than normal.
ventricular pressures rise above the aortic and pulmonary The mitral valve also occurs earlier than minimal.
artery pressures, the pulmonary valve and then the aortic The mitral valve is also wide open at the onset of
valve open and ventricular ejection occurs. As the ventricles ventricular contraction in mitral stenosis because of
begin to relax, their pressures fall below the aortic valve the high left atrial pressure seen in this disease.
closure. Isovolumetric relaxation then occurs. After the 6. The examiner will recognize S1 of decreased intensity
ventricular pressures have fallen below the right atrial and when S2 is louder than S1 at the cardiac apex. S1 is
left arterial pressures, the tricuspid and mitral valves open. decreased in intensity:
a. In states of impaired ventricular contractility and
BASIC SOUNDS decreased myocardial tension development. Such a
situation occurs in congestive heart failure.
The First Heart Sound (S1)
b. When the mitral valve is completely immobile. This
The first heart sound (S 1) is produced by the events occurs in severe cases of mitral stenosis.
associated with closure of mitral and tricuspid valves, in c. When the mitral valve is already nearly closed at the
that order. onset of ventricular contraction. This situation occurs
1. Normally, in (S1) is louder than (S2) at the cardiac apex. when there is a prolonged P-R interval (>0.2 seconds)
(S1) is heard well with the diaphragm and the bell of the on the ECG where the onset of ventricular
stethoscope. contraction following atrial contraction is delayed.
2. Because the sound produced by tricuspid valve closure As a result, the mitral and tricuspid valves to have
is much fainter than the sound produced by mitral valve already floated particularly shut at the onset of
closure, audible splitting of S1 into its mitral and tricuspid ventricular contraction.
components is uncommon in normal patients. 7. S1 varies in intensity from beat to beat when the position
3. Splitting of S1 into two components, about 0.03 seconds of the AV valves at the onset of the ventricular contraction
apart, can sometimes be heard normally at the lower is variable. This occurs in atrial fibrillation, third degree
left sternal border where the tricuspid valve component, heart block and in patients with ventricular demand
is the louder when splitting of S1 is heard at the cardiac pacemakers. In each of these conditions, there is no
150 Essentials of Clinical Medicine
fixed relationship between atrial excitation and ventricular a. The mechanism responsible for widening of the split
contraction. Thus, the position of the AV valves at the is somewhat complicated, but related primarily to a
beginning of ventricular systole is variable, sometimes delay in the closure of the pulmonic valve with
being particularly shut, and at other times being inspiration.
completely open. b. During inspiration, the capacitance (volume) of the
pulmonary vascular bed increases when intra-
Causes of Loud S1
thoracic pressure decreases. As the smallest
• Mitral stenosis, tricuspid stenosis. pulmonary vessels pop open during inspiration, the
• AV block, short P-R interval. pulmonary vascular impedance falls.
• Tachycardia. c. The decrease in the pulmonary vascular impedance
• Hypodynamic circulation. allows forward flow from right. Ventricular ejection
• Increased AV flow from left to right. persists for a longer period of time, and in effect
• Shunt—ASD, VSD. delays the closure of the pulmonic valve until forward
flow. Thus, P2 occurs first.
The Second Heart Sound (S2) d. The S2 split widens to 0.04-0.05 seconds and is heard
The second heart sound (S2) is produced by the events as two discrete sounds (A2–P2) in the second left
associated with closure of aortic and pulmonary valve. ICS.
1. S2 is normally higher pitched and shorter in duration e. During expiration, the pulmonary vessels close off
than S1. due to a rise in intrathoracic pressure. As a result,
2. S2 is normally louder than S1 at the cardiac base (second the pulmonary vascular impedance increases, thereby
intercostal spaces), and is heard well with both the shortening forward flow from right ventricular
diaphragm and bell. ejection. P2 occurs earlier, and the S2 split narrows
3. Two components of S2 are normally heard in many to 0.1-0.2 seconds, and it is heard as a single sound.
patients. Although right ventricular ejection, right 6. Wide physiologic splitting of S2 is due to a delay in the
ventricular ejection has a longer duration, and finishes closure of the pulmonic valve (P2), or early closure of
after left ventricular ejection. As a result, P2 occurs after aortic valve (A2). On inspiration, the split widens to 0.06
A2. seconds; and on expiration, it narrows to 0.03 –0.04
a. The first component (A2) is associated with closure seconds. Wide splitting is easily detected by nating both
of aortic valve, and is readily heard in the second components of the second heart sound during expiration.
right. ICS, the second and 3rd left ICS, and lower a. Wide physiologic splittings occur in conditions that
left sternal border and at the cardiac apex. prolong right ventricular ejection (pulmonary
b. The second component (P 2) is associated with stenosis), delay the onset of right ventricular ejection
closure of the pulmonic valve. Because P2 is softer (RBBB), or shorten left ventricular ejection (mitral
than A2, P2 is normally heard only at the second or regurgitation, VSD).
third left intercostal spaces. P2 may increase in 7. Wide fixed splitting of S2 describes the situation where
intensity as a result of pulmonary hypertension, and splitting is detectable during both inspiration and
then may be heard along the lower left sternal border expiration and does not vary with breathing. It is
and at the cardiac apex. characteristic of arterial ventricular septal defects.
c. When S2 is increased in intensity, it will be louder a. The left to right shunting of blood that occurs in the
than S1 at the cardiac apex. If S2 is louder than S1 at septal defects causes the right ventricular forward
the apex, and if splitting of S2 is heard at the apex, cardiac output to exceed the left ventricular forward
then pulmonary hypertension is likely. cardiac output. As a result, the pulmonary vascular
4. Separation of S2 into its two components is termed S2 capacitance is always high and relatively independent
splitting which is more commonly heard in individuals of breathing.
less than 50 years of age than in older patients. Splitting b. Because the pulmonary vascular capacitance is high,
of S2 should be assessed with the patient sitting upright. the pulmonary vascular impedance tends to be lower
5. Physiologic splitting of S2 characterizes the normal than normal, and is relatively unaffected by breathing.
occurrence of the aortic component (A 2) and the The low pulmonary vascular impedance assures that
pulmonic component (P2) widening during inspiration. forward flow from right ventricular ejection is
Cardiovascular System 151
prolonged, and this situation gives rise to a wide apex. Turning the patient into the left lateral decubitus
split. position may augment detection of an S3 which is heard at
c. The splitting of S2 in fixed impedance is lower than the 4th intercostal space adjacent to the sternum.
normal, and because it is subject to little change with 1. S3 occurs at the end of early ventricular filling when the
respiration, breathing has only a small effect on the ventricle reaches its elastic limit. There is some evidence
duration of forward flow from right ventricular that the sound heard during auscultation is due to the
ejection. impact of the heart against the chest wall.
d. There are two pathways for blood return to the right 2. S3 occurs when the ventricle reaches its elastic limit
heart in the septal defects. One path comes from the during early diastolic filling. S3 may be produced when
great veins, and the other from the left-sided cardiac normal or subnormal amounts of fluid enter an already
chamber through the hole in the septum. During the overfilled ventricle (congestive heart failure), or when
inspiration, the systemic venous return increases and very rapid filling occurs in a more normal ventricle
column of blood shunted through the septal defect (valvular regurgitation and high output states).
decreases. As a result, the final amounts to eight 3. Maneuvers that increase venous return (leg elevation)
ventricular ejections. tend to increase the intensity of S3 and move it closer to
8. Reversed (paradoxic) splitting describes the condition S3 while things that decrease cardiac filling cause the S3
where the audible split of S2 narrows with inspiration to decrease in intensity move farther away from S2.
and widens with expiration. Reversed splitting results The Fourth Heart Sound (S4)
from a prolongation of left ventricular ejection to the
extent that A2 occurs after P2. The fourth heart sound (S4) or atrial sound, is alone pitched
a. The most common causes for reversed splitting is sound, heard almost exclusively with the bell of stethoscope.
left bundle branch block (LBBB). An S4 occurs in late diastole approximately 0.04-0.12
b. Reversed splitting may also be observed in aortic seconds prior to S1. For this reason, S4 is sometimes referred
stenosis, IHSS, severe systemic hypertension, and to as a presystolic gallop. When originating from the left
in patients having a right ventricular demand heart, S4 is best heard at the cardiac apex.
pacemaker. Turning the patient into the left lateral decubitus position
9. Narrow physiologic splitting is characteristic of severe may augment detection of a left-sided S4. When originating
pulmonary hypertension, where the P2 component is from the right heart, S4 is best heard at the 4th left intercostal
increased in intensity, and where right ventricular ejection space adjacent to the sternum or at the xiphoid.
1. “An audible S4, is rare in normal subjects”. This is a
is shortened due to high pulmonary vascular resistance.
controversial statement that has been the source of much
When the right ventricular begins to fail in pulmonary
debate. Studies from the 1970s indicate that apparently
hypertension, wide splitting of S2 will result.
normal men over age 50 may have audible S4 gallops.
S1 Split 2. An S4, when pathologic, is produced by atrial contraction
Points 2: and 3(a) of the heading “The first heart sound against a stiff, non-compliant ventricle. Stiff ventricles
(S1) are characteristic of ventricular hypertrophy, as such
are commonly seen in pulmonary or systemic hyper-
S2 Split tension, pulmonic or aortic stenosis, and scarring
Points 4; 5 (a), (b), (c), (e), 6 (a), 7(a) (b) (c-1) (c-2); 8 secondary to previous myocardial infarction.
(a), (b); 9 of the heading “The second heart sound S2. 3. S4 increases in intensity and moves farther from S1 with
maneuvers that increase venous return or with the
The Third Heart Sound (S3) sympathetic stimulation.
4. S4 often decreases to the point of inaudibility with
The third heart sound (S3) is a low-pitched sound that is standing.
heard almost exclusively with the bell of the stethoscope 5. S4 is dependent on atrial contraction and is always absent
while S3 may occur normally in younger age groups; it is in patients with atrial fibrillation.
nearly always pathologic when heard in people older than 6. A left-sided S4 can be distinguished from split S1 by
forty. S3 occurs in early diastole, about 0.12-0.20 seconds location (S1 is loudest at the LSB, while S4 is loudest at
after S2. S3 is sometimes referred to as a protodiastolic the apex) and the fact that the S4 should disappear with
gallop. When originating from the LV, S3 is best heard at the firm pressure on the diaphragm.
152 Essentials of Clinical Medicine
Effect of respiration posture, exercise and drugs: 2. Due to regurgitation: (pan. or holosystolic)
a. Respiration: a. AV valve incompetence—mitral incompetence
– Inspiration: increases blood flow through tricuspid (pathological or functional)
and pul. valves. – Tricuspid incompetence (pathological or
– Hence murmur produced by defects on right side of functional).
heart are heard louder during inspiration. b. Left to right shunt
– During inspiration, a large part of heart may be – VSD.
covered by pul. tissue and hence mechanical – Early cases of PDA.
muffling of murmurs. Diastolic:
– Murmurs on left side of heart may become softer 1. Early Diastolic
during inspiration. a. Aortic:
– Murmurs caused by right to left shunts may be softer i. Valvular incompetence
during inspiration. ii. Dissecting aneurysm
b. Posture:
iii. Bicuspid aortic valve (congenital).
Certain murmurs are heard when the patient is lying
b. Pulmonary:
down in particular pain.
i. 1° or 2° pul. hypertension (Graham-Steel murmur)
– Left lat. position—MS
ii. Pul. incompetence.
– Sitting and bending forward—AI.
iii. Aneurysm of pul. a.
c. Exercise:
2. Mid-diastolic
– Faint murmurs are better heard after exercise.
a. AV stenosis mitral or tricuspid
– May also augment a thrill which was previously
b. AV valve obstruction
doubtfully palpable.
– ball-valve thrombus
d. Drugs:
– atrial myxoma.
– Amylnitrite lowers peripheral vasculature resistance
c. Increased flow across AV valves:
and hence it makes ejection, aortic murmur
i. Across mitral valve:
prominent, and regurgitant left side murmur fainter.
1. Mitral incompetence.
– Phenylephrine and nor epinephrine increases the
2. VSD.
peripheral vascular resistance and have an opposite
3. PDA (flow murmur)
effect.
ii. Across tricuspid valve:
Non-Pathogenic Murmurs 1. ASD
1. Innocent murmurs—usually midsystolic. 2. Anomalous pul. venous drainage.
2. Flow murmurs—seen in hyperdynamic circulation. d. AV valve inflammation:
– rare in AV fistula. Carey-Coombs murmur occurs in RHD to be
different from MS murmur by the fact that in RHD,
Pathogenic heart sounds are muffled, the murmur changes its
Systolic: character from time to time. In MS, HS, at mitral
1. Due to forward flow (ejection or midsystolic) area is loud and sharp and murmur does not have
a. Aortic area: changing character.
i. Increased flow—aortic incompetence or rarely 3. Presystolic or Late Diastolic
in heart block. a. AV valve stenosis
ii. Obstruction—Aortic stenosis. 1. mitral stenosis.
– Supra-aortic stenosis. 2. tricuspid stenosis.
– Coarctation of the aorta. b. AV valve obstruction
b. Pulmonary area 1. due to ball valve thrombus or atrial myxoma.
i. Increased flow—left to right shunt. 2. due to regurgitant blood flow from aortic incom-
– VSD petence implying upon mitral valve cusp (Austin-
– ASD. Flint murmur).
ii. Obstructive: PS
iii. Dilation of distal chamber pul. artery. Holosystolic Regurgitant Murmur
Primary or secondary hypertension. Holosystolic murmurs (pansystolic) are generated by
156 Essentials of Clinical Medicine
retrograde flow from a high pressure chamber to a low intercostal spaces to the left of the sternum) and is
pressure chamber. often associated with a palpable thrill.
i. > Start with S1 and continue through and beyond A2 1. Unlike the murmur of MR, the murmur of VSD
ii. > Have a blowing quality to them. does not radiate into axilla.
iii. > Do not exhibit post extrasystolic potentiation 2. Unlike the murmur of TR, the murmur of VSD
following a long diastole. does not increase with inspiration.
3. The murmur of VSD is associated with fixed
Table 7.9: Causes and sometimes wide splitting of S2.
4. Like MR, the apical in pulse is hyperdynamic
Patent ductus arteriosus Proximal coronary artery stenosis
Coronary AV fistula Mammary soufflé
and displaced down and to the left.
Ruptured aneurysm of sinus of Pulmonary artery branch stenosis Midsystolic Ejection Murmur: or
Valsalva
Midsystolic Murmur (MSM)
Aortic septal defect Bronchial collateral circulation
Cervical venous hum Small (restrictive) ASD with MS MSM (Systolic Ejection Murmur) are typically produced
Anomalous left coronary artery Intercostal AV fistula by the forward flow of blood across the ventricular flow
tract.
iv. > The murmur of mitral regurgitation is holosystolic MSM:
and plateau shaped. It is loudest at the cardiac apex a. Begin after S1 and end prior to S2.
where it may completely obscure S1. It radiates to b. Are diamond shaped (crescendo-decrescendo).
the axilla. If the murmur is secondary to a ruptured c. Tend to be harsh and saw like in quality.
anterior chordae, it may radiate to the top of the d. Exhibit postextrasystolic potentiation, increasing in
head/midthoracic spine. Anything that increases intensity after a long diastole when ventricular filling is
peripheral vascular resistance (hand grip exercise) increased.
will make the murmur louder. Anything that decreases e. MSM result from one of the following situations:
peripheral vascular resistance (amyl nitrate) will make 1. The rate or amount of blood flow across a normal
the murmur softer. The murmur increases with semilunar valve. The systolic murmurs of preg-
Valsalva’s and inspiration. nancy, thyroid excess states, exercise, anemia and
1. Associated findings in mitral regurgitation are: fever are caused by this mechanism.
a. A brisk pulse (small water hammer pulse).
2. Ejection of blood into the dilated aorta that results
b. A wide split and left ventricular ejection is
from arteriosclerosis or aneurysm formation.
shortened, causing A2 to come early.
3. Ejection of blood past thickened valve cusps and
c. A hyperdynamic apical impulse that is
calcified plaque lining the wall of the aorta up to 50
displaced down and to the left.
people older than 50 years of age will have a murmur
d. An S3 gallop at the apex.
related to this mechanism (aortic sclerosis). Aortic
v. The murmur of tricuspid regurgitation is also
sclerosis can be distinguished from aortic stenosis
holosystolic and plateau shaped. It can be distin-
by the fact that carotid artery pulse is normal in
guished from that of mitral insufficiency by:
1. The murmur of tricuspid regurgitation is best patients with aortic stenosis.
heard at the 4th and 5th intercostal spaces along 4. Ejection of a blood across a narrow semilunar valve
the left sternal border. or narrow outflow tract (semilunar valvular stenosis,
2. The murmur of tricuspid regurgitation does not subvalvular stenosis).
radiate into axilla. f. Valvular aortic stenosis produces the classic midsystolic
3. The murmur of tricuspid regurgitation becomes ejection murmur.
louder with inspiration (Carvallo’s sign). 1. The murmur is caused by turbulence across a
4. Tricuspid regurgitation causes prominent OcvO narrowed aortic valve orifice.
waves in the JVP. The ear lobe may pulsate with 2. The murmur is crescendo-decrescendo in shape and
each heart beat. may be heard in 2nd right intercostal space, 3rd left
vi. The murmur of VSD is holosystolic but tends to be intercostal space and at the apex. The murmur may
more harsh than that of mitral or tricuspid radiate into the carotid arteries bilaterally and is
regurgitation. The murmur of VSD is typically heard frequently proceeded by an ejection sound grade 3-
over the entire precordium (best at 4th, 5th and 6th 4/6 is common.
Cardiovascular System 157
3. Aortic stenosis is associated with a narrow pulse (Valsalva’s standing), by decreasing ventri-cular after
pressure and a slow, delayed carotid upstroke. load and by increasing contractility. These same
4. Chronic pressure overloading on the left ventricle alterations also move the click closer to S1.
results in a sustained apical impulse characteristic b. The murmurs of mitral and tricuspid valve prolapse may
of left ventricular hypertrophy. be transient, coming and going from day to day.
5. S2 may be narrowly split, singly or paradoxically
Early Diastolic Murmur
split as aortic ejection is increasingly prolonged.
6. The murmur decreases in intensity with sustained a. Diastolic murmurs are classified according to their
Valsalva’s and inspiration. mechanism of production. Diastolic filling murmurs
g. The murmur of hypertrophic obstructive cardio- (rumbles) are produced by forward flow across the AV
myopathy is midsystolic in timing and occurs as a result valves. Diastolic regurgitant murmurs are produced by
of hypertrophy of the interventricular septum. During retrograde flow across incompetent semilunar valves.
systole, the thickened interventricular septum makes b. The best example of diastolic regurgitant murmur
contact with the anterior leaflet of the mitral valve and originating in the left heart is that associated with aortic
obstructs left ventricular outflow. This transient regurgitation. The murmur begins with A 2 , is
obstruction results in a systolic pressure gradient, decrescendo and ends in late diastole. Mild forms or
turbulence and a midsystolic murmur. aortic regurgitation may produce murmurs that end in
1. The murmur is harsh, best heard along the left sternal mid-diastole. The murmur of aortic regurgitation is heard
border. best at the 2nd right intercostal space, 3rd left intercostal
2. The murmur of obstructive cardiomyopathy can be space and apex. It is accentuated by having the patient
distinguished from the murmur of aortic stenosis by forward and hold his breath in forced exhalation. The
the fact that the murmur of obstructive cardio- murmur has high-pitched blowing quality. The murmur
myopathy increases in intensity during any maneuver S in intensity with maneuvers that peripheral vascular
that makes the left ventricle smaller (sustained resistance (handgrip, squatting, exercise). Other
Valsalva’s standing). Maneuvers that make the left manifestations of aortic insufficiency may include:
ventricle larger, the intensity of the murmur in 1. A wide pulse pressure due to elevated systolic
obstructive cardiomyopathy. pressure and decreased diastolic pressure.
h. The MSM of pulmonic stenosis is due to narrowing of 2. Water hammer pulse.
the pulmonic valve orifice. This murmur can be 3. A to and fro pulsation of the blood in the proximal
distinguished from the murmur of aortic stenosis by the fingernail bed when pressure is applied to the distal
following features: nailbed (Quincke’s pulse). While this finding may
1. The murmur of pulmonic stenosis is best heard in occur normally in some, it is more common and
2nd and 3rd left intercostal spaces and is usually of often prominent in patients with aortic insufficiency.
lesser grades than that of aortic stenosis. 4. De-Musset’s sign—head bobbing with each heart-
2. The murmur of pulmonic stenosis does not radiate beat.
into the carotid arteries. 5. Duroziez’s sign—a bruit with systolic and diastolic
3. Pulmonic stenosis is associated with prominence of components auscultated over the femo-ral artery
the ‘a’ wave on the JVP. while manual pressure is applied proximal to femoral
4. Pulmonic stenosis produces a left parasternal artery.
sustained impulse from right ventricular hyper- 6. Dullness to percussion, the tactile fremitus, and
trophy. egophony at the lower tip of the left scapula
5. The murmur increases with increased venous return secondary to ring consolidation from the enlarged
to the right heart (inspiration). heart. This same constellation of findings occurs in
Late Systolic Murmur: (LSM) large pericardial effusions and is termed Ewart’s sign.
LSM occurs in mitral and tricuspid valve prolapse. The 7. S2 is single and snapping.
murmurs start in midsystolic and are often proceeded by a 8. The apical impulse is displaced down and to the left
midsystolic click. The murmur may crescendo into S2 and having a hyperdynamic quality typical of ventricular
is rarely as loud as grade 3. dilatation.
a. The murmur of atrial-ventricular (AV) valve prolapse is 9. An S 3 is common due to rapid, high volume,
made longer and louder by decreasing ventricular volume ventricular filling.
158 Essentials of Clinical Medicine
10. Two additional murmurs often occur in aortic 4th intercostal space at the left sternal border or
regurgitation. xiphoid. The murmur of tricuspid stenosis
• An aortic ejection (midsystolic) murmur occurs increases in intensity during inspi-ration and
due to the volume of blood that is ejected across when firm pressure is applied over the liver. The
the aortic valve in the forward direction. JVP shows giant ‘a’ waves and slow ‘y’ descent.
• A low pitched, mid-to-late diastolic rumbling
Mid-Diastolic Murmur
murmur (Austin-Flint) at the apex that due to the
regurgitant flow impinging upon the anterior The (D) point of previous (early diastolic murmur).
leaflet of the mitral valve and partially closing it. Functional Murmur or Innocent Murmur
This situation creates a “functional” mitral • Systolic
stenosis. The presence of this murmur suggests • Best heard in pulmonary area
severe aortic regurgitation. • Not radiating
• The murmur of pulmonary regurgitation can be • Changes the character with respiration and position
distinguished from the murmur of aortic • Not associated with thrill
regurgitation by the fact that pulmonary • Seen in anemia, thyrotoxicosis.
regurgitation murmur increases in intensity with Grade Murmur:
inspiration, and is not associated with any of the • Gr-I - Faint murmur picked up phonocardio-
peripheral manifestation of aortic regurgitations graphycally. Head in quiet room
(wide pulse pressure, bounding pulses, large left • Gr-II - Easily audible but not loud
ventricle, etc.). The murmur of pulmonary
• Gr-III - Loud but no thrill
regurgitation that results from pulmonary
• Gr-IV - Murmur with thrill audible with full chest
hypertension is termed the Graham-Steel
piece of stethoscope
murmur.
• Gr-V - Loud murmur with thrill can be heard even
• The murmur of mitral stenosis is the typical
with edge of chest piece
diastolic filling murmur:
• Gr-VI - Loud murmur with thrill audible with chest
1. The murmur is low pitched and rumbling and
piece lifted off the chest.
is only heard with the bell (2). It is localized
to the cardiac apex in an area no larger than Causes of Systolic Murmur
2.5 cm2. • Ejection
2. The murmur of mitral stenosis may only be – Aortic—systemic hypertension, atherosclerotic
audible while listening to the patient in the aortic disease
left lateral decubitus position. – Pulmonary—functional
3. The murmur which may begin with an – Pulmonary stenosis—increased flow in ASD with
opening snap following S 2 decreases in hyperdynamic circulation
intensity toward mid-diastolic and then again • Pansystolic or holosystolic
S in intensity into S1. This crescendo effect – MR
into S1 is termed presystolic accentuation, – TR.
and is augmented significantly by atrial – VSD
contraction. • Late systolic—mitral valve prolapse precipitated by
4. The murmur is commonly no louder than muscle dysfunction
grade 1 or 2 and may be amplified by elevating Causes of Diastolic Murmur
the legs above the level of heart. Other findings • Mid-diastolic
of mitral stenosis include: – Obstructive lesions
i. S1 is increased in intensity. - MS
ii. A left parasternal impulse secondary to - TS
right ventricular hypertrophy. - Atrial myxoma
iii. The apical impulse is normal with respect • Increased flow across mitral valve
to its quality and location. – VSD
• The murmur of tricuspid stenosis differs from – PDS
that of mitral stenosis by being localized to the – MR.
Cardiovascular System 159
Non-Rheumatic Causes of MS
• Congenital
• SLE, rheumatoid arthritis
• Mucopolysaccharoidoses
• Methysergide therapy
• Carcinoid heart disease.
Causes of Soft S1 in MS
• Calcified mitral valve
• Associate dominant MR
• Enlarged RV forming the apex.
Mitral Facies
Pinkish purple patches on cheek. Low cardiac output in
MS produces vasoconstriction, peripheral cyanosis often
on lips, lip of nose and cheeks. Seen due to vasodilatation
Fig. 7.14A: Chest radiograph of long standing mitral stenosis of molar area.
showing a massive left atrium
Causes of Muffled P1 in MS
– Bronchitis (in winter season) • Associated MR or AR
– SABE (Subacute bacterial endocarditis) • Mitral valve calcification
e. Others: • Acute rheumatic carditis (PR interval prolonged)
– CCF • Digitalis overdose (PR interval prolonged)
– LVF due to back pressure. • Acute M1
– Left atrial hypertrophy (LAH) • LAF
– Pulmonary edema • AF
– Right ventricular hypertrophy (RVH) Rotation of heart due to gross right ventricular
– TR-Rt. atrial enlargement.
hypertrophy. Right ventricle from the apex.
Pulmonary Hypertension in MS Table 7.15: Aortic stenosis, aortic regurgitation,
mitral regurgitation and septal defects
• Clinically, decreased mitral valve orifice leads to increased
left atrial pressure and left atrial enlargement and Aortic stenosis Aortic regurgitation
pulmonary congestion, thereby pulmonary hypertension. Pulse: Sinus rhythm, low volume, Pulse: Sinus rhythm, large
• Pulmonary anterior construction due to left atrial and slow rising volume, collapsing
pulmonary venous congestion leads to reactive Aortic area: Systolic thrill Blood pressure: Wide pulse pressure
Apex: Not displaced, sustained Apex: Displaced, diffuse, hyper-
pulmonary hypertension. Sounds: Ejection, click, soft A2, S4 dynamic
• Obliterative (organic) changes in pulmonary vascular Murmurs: Systolic, low pitched, Pulse: Sinus rhythm, large volume,
bed. Clinically, the signs are left parasternal heave, ejection, radiating to carotids collapsing
palpable P2, loud P2 component of second heart sound 1. High pitched, early diastolic at
and epigastric pulsations. Apex beat may be shifted up LSE
2. Ejection systolic at base and
and out due to Rt. ventricular hypertrophy symptoms into neck
are angina, syncope, hypoxia, and hypertension (due to 3. Mid-diastolic rumble at the
decreased cardiac output). apex
(Austin-Flint)
Embolic Manifestations of Mitral Stenosis Mitral regurgitation Mitral stenosis
Thrombus from the left atria may embolize to brain, kidney, Face: Mitral facies
spleen and extremities. A large pedunculated one may Pulse: Sinus rhythm, atrial fibrillation Pulse: Artrial fibrillation
RV: Hearing, substanced
suddenly obstruct the stenotic mitral orifice leading to ball Apex: Hyperdynamic, displaced, Apex: Localized, tapping
valve thrombus. systolic thrill
Contd...
162 Essentials of Clinical Medicine
AORTIC REGURGITATION
[(Figs 7.16A, (7.16B, PLATE 3)]
Causes of Aortic Regurgitation
• Congenital
• Bicuspid valve or disproportionate cusps.
• Acquired
• Rheumatic disease
Fig. 7.14B: Chest radiographic appearance of mitral regurgitation • Infective endocarditis
Cardiovascular System 163
EBSTEIN’S ANOMALY
Fig. 7.16A: Chest radiograph of patient with aortic regurgitation, • Tricuspid valve is dysplastic and displaced into RV, right
left ventricular enlargement and dilatation of ascending aorta ventricle “ atrialized”
164 Essentials of Clinical Medicine
Signs
(See Table 7.18)
HYPERTENSION
Symptoms and Signs of Hypertension
Symptoms
• Due to elevated pressure itself
– Headache—in occipital region when the patient
awakens in the morning and it subsides
spontaneously after several hours
– Dizziness
– Palpitations
– Easy fatiguability
– Impotency
• Due to hypertensive vascular disease
– Epistaxis
– Hematuria
– Blurring of vision owing to retinal changes
– Episodes of weakness due to transient cerebral Fig. 7.17: Coarctation of the aorta showing a prominent ascending
ischemia aorta, double aortic knuckle and rib notching
166 Essentials of Clinical Medicine
History Examination
1. Known renal disease 1. Femoral pulse delayed
2. Thirst, polyuria, nocturia 2. Palpable kidney
3. Dysuria 3. Enlarged bladder
Fig. 7.18: Renal artery stenosis 4. Hematuria 4. Uremic feature
5. Loin pain/renal colic 5. Edema
6. Stones 6. Abdominal bruits
– Angina pectoris, dyspnea due to cardiac failure 7. Abdominal trauma 7. Features of Cushing’s or
– Pain due to dissection of aorta or leaking aneurysm. acromegaly
• Due to underlying disease is secondary hypertension 8. Analgesic use 8. Cafe-au lait patches
– Polyuria, polydipsia, muscle weakness, secondary 9. Other drugs like oral contra- 9. Neurofibroma
to hypokalemia in patients with primary aldo- ceptive, steroids, liquorice, 10. Orthostatic hypotension
sympathomimetic, appetite
steronism suppressants, and carbenoxolone
– Weight gain and emotional liability in patients with sodium
Cushing’s syndrome
– Episodic headaches, palpitation, diaphoresis, postural Table 7.20: Renal causes of hypertension
dizziness, pheochromocytoma
Unilateral Bilateral
– Recurrent backache or UTI—chronic glomerulo-
nephritis and pyelonephritis Renal artery steroids Glomerulonephritis
Chronic pyelonephritis Interstitial nephritis
Signs Vesicoureteric reflux Pyelonephritis
TB kidney Polycystic kidneys
• General appearance—round face and truncal obesity of Obstructive uropathy Analgesic nephropathy
Cushing’s syndrome. Collagen disorder
• Muscular development in the upper extremities out of Obstructive uropathy
proportion to that of lower extremities suggesting Diabetic nephropathy
coarctation of the aorta TB kidney
Amyloidosis
• Rise in diastolic pressure when the patient goes from Irradiation to kidney
supine to standing position Chronic renal failure
– Essential hypertension. A fall in the absence of
antihypertensive medications suggests secondary Choice of Antihypertensive Agents
hypertension. • Angina with hypertension—beta blocker/diltiazem.
• Pulse feels forcible and more difficult to compress in • Tachycardia with hypertension—beta blocker / diltiazem.
diastole • Raised plasma rennin with hypertension—beta blocker/
• Hypertensive retinopathy changes in fundus diltiazem.
• Palpation and auscultation of carotid arteries for evidence • CCF with hypertension—diuretics as adjuvant, enalapril,
of stenosis amiloride.
• Cardiac examination—left ventricular hypotrophy, • LVF with hypertension—diuretics, adjuvants, enalapril,
accentuation of aortic component of second heart aniloride, spironolactone.
Cardiovascular System 167
• Renal involvement with hypertension—hydralazine or 4. Such patients are at high risk from vascular
prazosin. complications.
• Moderate-to-severe hypertension—methyldopa.
• SVT with hypertension—verapanil. Intermittent Claudication
• Asthma with hypertension—calcium channel blockers 1. Pain on walking a distance (claudication distance)
• Hypertension with diabetes—ACE inhibitors. 2. Starts and on continued walking pain is aggravated and
• Resistant hypertension—minoxidil. compels the patient to take rest
• Malignant hypertension—diazoxide IV, hydralazine, 3. Disappears when exercise stops
sublingual nifedipine. 4. Typically occurs in calf muscles but may be felt in thighs
• Pregnancy with hypertension—methyldopa, hydralazine. and/or buttocks if obstruction to flow is sufficiently
• Pheochromocytoma and hypertension—phenoxy- proximal
benzamine. 5. Described as tightness or cramp like
• Hypertension in postmenopausal women with meno- 6. Male patients with gluteal claudication due to internal
pausal symptoms—clonidine. iliac disease are almost invariably impotent
7. Term claudication is also used to denote pain in leg on
Causes of Hyper-reninemia walking due to neurological and musculo-skeletal
• Hemangioparicytoma. disorders of lumbar spine (neurologic claudition) and
• Wilm’s tumor. due to venous outflow obstruction from legs (venous
• Barter’s syndrome. claudication). However, these are much lesser than arterial
• Renin producing undifferentiated bronchial carcinoma. claudication.
Stepwise Approach to Treatment of Hypertension Rest/Night Pain
• Step 1 — Diuretics/beta blockers 1. The patient awakens 1 to 2 hours later after falling asleep
• Step 2 — Calcium channel inhibitors, due to pain in foot, usually in instep. This is due to loss
clonidine, methyldopa. on recumbency of beneficial effects of gravity on lower
• Step 3 — Vasodilators, calcium channel limb perfusion. Also, due to decrease in heart rate, BP,
blockers. and cardiac output in sleep.
• Step 4 — Prazosin, guanethedin. 2. Pain relieved by hanging their legs out of bed or by
getting up and walking around .
PERIPHERAL ARTERIAL DISEASE (PAD) 3. When the patient returns to bed, symptoms reccur.
4. The patient feels comfortable by sleeping in a chair. This
1. Mainly in elderly > 60 years. leads to dependent edema and increased interstitial tissue
2. Mostly due to atherosclerosis affecting large and medium pressure causes further reduction in tissue pressure and
sized vessels. more pain. Rest pain usually indicates the presence of
3. Family H/o of premature arterial disease and DM. multilevel disease.
a. Limb symptoms
b. Neurological symptoms Tissue Loss (ulceration and/or gangrene)
c. Abdominal symptoms 1. When in patients with rest pain there occurs trivial
d. Vasospastic symptoms injuries, they fail to heal and provide a portal of entry
for bacteria leading to gangrene and/or ulceration .
Lower Limb Symptoms 2. Without re-vascularization, the ischemia will rapidly
i. Asymptomatic progress.
ii. Intermittent claudication Table 7.21: Signs suggesting of vascular disease
iii. Rest pain
iv. Tissue loss (ulceration/gangrene) Signs Implication
Hands and arms
Asymptomatic Ischemia 1. Nicotine stains – Smoking
1. Defined by reduced ankle 2. Purple discoloration of – Atheroembolism from a
2. Brachial pressure index is very common in middle- aged fingertips proximal subclavian aneurysm.
3. Pits and healed scar in finger – Secondary Raynaud’s syn-
and elderly
pulps drome
3. Asymptomatic because they choose not to walk very 4. Calcinosis and visible nailfold – Scleroderma and CREST
far, or because their exercise tolerance is limited by other capillary loops syndrome
pathology. Contd...
168 Essentials of Clinical Medicine
• If dominant hemisphere is affected, there may be also 8. Atheroembolism may arise from AAA and cause the blue
dysphasia. toe syndrome characterised by purple discoloration of
• A bruit over neck may arise from stenosis in other toes/forefoot usually in association with a full set of
vessels such as ext. carotid artery pedal pulses.
• Or there may be so little blood flowing through a critical
int. carotid artery stenosis that no bruit is audible. Vasospastic Conditions
This consideration is equally applicable over other sites Raynaud’s phenomenon (RP) describes digital ischemia
(e.g. femoral and subclavian a.) induced by cold and emotion and comprises of three phases:
1. Pallor due to digital artery spasm and/or obstruction.
Vertebrobasilar Artery Territory 2. Cyanosis due to deoxygenation of static venous blood
1. Less common TIA and strokes (this phase may be absent).
3. Rubor due to reactive hyperemia.
2. Giddiness, collapse, with or without loss of conscious-
RP may be primary (Raynaud’s disease) owing to
ness, transient occipital blindness or complete loss of
idiopathic digital a. vasospasm or secondary (Raynaud’s
vision in both eyes.
syndrome) because of digital a. obstruction caused by:
1. Connective tissue diseases (most commonly systemic
Subclavian Artery Territory sclerosis).
1. Stenosis or occlusion proximal to origin of vertebral a. 2. Vibration injury (secondary to use of power tools).
may cause vertebrobasillar symptom as a part of 3. Atheroembolism from a proximal source such as
“subclavian steal syndrome”. subclavian a. aneurysm.
2. Signs of this include asymmetry of pulses and BP in
arms and sometimes a bruit over the subclavian a. in Venous Disorders
supraclavicular fossa. Pain
1. Patients with uncomplicated varicose veins may
Visceral Ischemia
complain of an aching discomfort in leg, itching and a
1. For signs and symptoms of chronic mesenteric vascular feeling of swelling.
insufficiency, there should be stenosis or occlusion of 2 2. Symptoms are aggravated by prolonged standing and
or 3 major visceral a, i.e. celiac axis superior and inferior are often worse towards the end of the day.
mesenteric a. 3. Pain of DVT deep seated and associated with swelling
2. Patients develop central abdomen pain (mesenteric below the level of obstruction.
angina) 10 to 15 minutes after eating. 4. SVT produces a red painful area overlying the vein
3. Diarrhea may also be a feature. This leads to fear of involved.
eating and weight loss. 5. Varicose ulceration may be painless; but if there is pain,
4. Acute mesenteric ischemia is surgical emergency. The it may be relieved by elevation of limb.
patient typically presents with severe abdominal pain,
Swelling
shock, bloody diarrhea and profound acidosis.
5. Renal angle pain from renal infarction or ischemia is 1. May be associated with varicose veins, deep venous
rare. It is associated with micro or macroscopic reflux and DVT.
hematuria. Discoloration
1. Chronic venous insufficiency is associated with
Abdominal Aortic Aneurysm (AAA)
deposition of hemosiderin in the skin leading to
1. Five percent men aged over 65 years. lipodermatosclerosis (LDS). This may vary from deep
2. Men 3 times > women. blue/black to purple or even bright red.
3. Present with abdominal and back pain or an awareness 2. Typically affects medial aspects of lower third of leg
of pulsation. but may be laterally placed if superficial reflux
4. Many are asymptomatic until aneurysms rupture. predominates in short saphenous veins.
5. As aortic bifurcation is at level of umbilical artery,
Ulceration
palpable AAA is felt in epigastrium.
6. A pulsatile mass below the umbilicus suggests the iliac Always associated with LDS.
aneurysms. • Question for deep venous thombosis:
7. Commonest misdiagnosis of ruptured AAA is renal colic. 1. Recent bedrest or operation (esp. to leg or pelvis)
170 Essentials of Clinical Medicine
interstitial infiltrates, ECG was unremarkable except for at 20/10 mm Hg (normal 12-28/3-13) and pulmonary
sinus tachycardia. Antibiotics were administered and the capillary wedge pressure is 8 mm Hg (normal range 3-
patient was transferred to ICU, where a right heart 10). What may be the possible abnormality?
catheterization was performed. Pulmonary capillary Right ventricular infarction
wedge pressure was 28 mm Hg. Cardiac output was 3. A 75-year-old man presents with recurrent episodes of
1.9 L/min. Right arterial mean pressure was 10 mm Hg. shortness of breath on minimal exertion. He has no prior
The most likely cause of this hypertension was: significant past medical history. Physical examination
Left ventricular dysfunction reveals blood pressure of 110/70 without pulses. Heart
2. A 53-year-old man presents to the emergency room after rate of 110, respiratory rate of 25, and temp. of 27°C
the acute onset of chest pain. The episodes occurred (98.6°F) orally. Jugular veins are distended and heart
8 hr prior to his arrival and lasted for a resolved. The sounds are distant, but there are third and fourth heart
patient has a long history of diabetes mellitus and sounds and pedal edema is present. The liver is enlarged.
hypocholesteremia and has smoked approximately 1 to The electrocardiogram shows non-specific ST-T wave
1½ packs per day of cigarettes for the past 30 years. changes and occasional premature ventricular
On physical examination, he has a BP of 84/52, and his contractions. The chest X-ray reveals clear lung fields
pulse is 54. He has jugular venous distention to the angle and a mildly dilated cardiac silhoucteke. Echo-
of mandible and clear lung fields. His rhythm strip reveals cardiography reveals normal systolic function and
a Wenkebach’s pattern, given his hypertension, a swan thickened ventricular walls with a speckled appearance.
ganz catheter is placed. Right arterial pressure is estimated Which condition is most consistence with the patient’s
at 16 mm Hg (normal 0-5), pulmonary artery pressure clinical presentation?
Amyloidosis
8
1. Type : What type of headache is described by the patient? Table 8.2: Characteristics of headache
2. Occurrence: When did it begin? It is cyclical or daily? Characteristics Disorder
3. What is the duration and progress of each attack of Feeling of tight band around head or Tension headache
headache? like a pressure over head
4. Is it unremitting? Sickening, dull aching or throbbing Migraine
5. Character of headaches: Lancinating, paroxysmal pain like Trigeminal neuralgias
– What is the intensity of headache? red-hot needles thrust through the
face
– What is the nature and quality of headache?
– Whether the patient is able to localize the exact site Table 8.3: Severity of headache
of headache?
Severity Disorder
– Does the headache radiate or does it have a spreading
Explosive and sudden onset of Subarachnoid hemorrhage
feature? severe headache associated with
– Is it associated with any other symptoms? neck stiffness
6. What are the precipitating, aggravating and relieving Slowly progressive headache Raised intracranial tension from
factors? increasing in duration and severity a cerebral tumor
7. Limitation: Are the daily activities of the patient limited Severe headache is also seen in Migraine, cluster headache and
trigeminal neuralgia
due to headache?
Sometimes the patient winces and Paroxysms of severe pain
8. Whether any medications and treatment are used and cries out momentarily due to pain
what was the response?
9. Health between the attacks: Inquire about the health of Table 8.4: Duration of headache
the patients between attacks. Whether the symptoms Long history of headache without Benign cause
persist or is the patient completely well between attacks? progression
Is there any sort of depression, fear or anxiety? Lasting 24-72 hours but occasionally Migraine
10. Does the patient tell you his idea about the causation of last < 6 hours
Cluster headache attacks Last > 1 hour
disease? Trigeminal neuralgia each paroxysm lasts only
11. Main site: What is the main site of headache? Whether it seconds recurring over several
affects the entire head, half the head or a smaller area of Tension type headache variable ranging from 15 minutes
the head, neck or face. For more details, see Table 8.1. to many weeks or even months.
Central Nervous System 175
Table 8.5: Frequency and periodicity of headache Causes of raised intracranial tension:
Migraine, trigeminal neuralgias and Attacks are sudden or subacute • Cerebral hemorrhage
cluster headache onset occurring in reported short • Intracranial tumor
bursts with pain-free intervals • Meningitis
lasting weeks or months.
Migraine Often cyclical, occurring weekly
• Encephalitis
or monthly and frequently • Benign intracranial hypertension
premenstrual in women. In • Hydrocephalus
between the attacks, migraine • Hypoxic encephalopathy.
sufferer is usually well.
Postherpetic neuralgia and Subacute onset but are Symptoms of raised intracranial tension:
cranial arthritis continuous • Headache
Meningitis and subarachnoid Acute onset with rapid • Projectile vomiting
hemorrhage progression
• Convulsions
Table 8.6: Special times of occurrence of headache
• Altered sensorium
Signs of raised intracranial tension:
Times Type of headache
• Bradycardia
Severe pain awakening the patient in Cluster headaches and raised
early hours of the morning intracranial pressure • BP may be higher
Pain precipitated by facial movement Trigeminal or glossopharyngeal • Respiration is slow and deep eventually Cheyne-Stokes
such as eating, drinking, shaving or neuralgias breathing
brushing the teeth
• Papilloedema
Jaw pain during chewing Cranial arthritis
Headache occurring at times of Migraine • False localizing signs—unilateral or bilateral 6th nerve
stress relief (weekends and holidays) palsy
• Bilateral Babinski’s sign
Table 8.7: Aggravating factors of headache • Bilateral grasp reflex.
• Increased by bending, straining, Raised intracranial tension X-ray with raised intracranial tension:
and coughing • Silver beaten appearance in children
• Precipitated by bright light, loud, Migraine
noise, strong odors, missed meals, • Sutural diastasis (children)
intake of chocolates, cheese, • Erosion of clinoid process
alcohol, and citrus fruits, changes • Deep sella tursica
in weather, travel and by
• Enlargement of internal auditory meatus
contraceptive pills
• Sensitivity to even small amounts Cluster headache Tension headache is usually not accompanied with
of alcohols and other vasodilators nausea and vomiting.
• Headaches associated with weight Headache due to benign • Intolerance to light (photophobia), or noise (phono-
gain and use of corticosteroids, intracranial hypertension
tetracycline or OCPs
phobia), irritability, food cravings and hunger are usually
typically seen in migraine. In some patients, visual
Relieving Factors disturbances (teichopsic and fortification spectra) and
sometimes peripheral and circumoral (around the mouth)
• Acute attacks of migraine usually respond well to 5- paresthesia occur before the headache phase. It is called
HT1 agonists such as sumatriptan and are usually less aura or migrainous aura.
frequent and less severe during pregnancy. • Watery discharge from the eye or nose or even ptosis
• Tension headache, especially when chronic and is of eyelid during attack may be seen in cluster headaches.
resistant to analgesics. • Whether the patient has syncopal attacks, seizures, ataxia
• A rapid and dramatic response in cranial arthritis to dizziness or any other associated features.
corticosteroids therapy is characteristic.
Headache Symptoms which Suggest Some
Associated Features Important Underlying Pathology
• Migraine is usually accompanied by nausea and vomiting • Worst headache ever
• Vomiting without nausea seen in headache due to raised • First severe headache
intracranial tension (ICT) • Subacute worsening over days or weeks
176 Essentials of Clinical Medicine
• Abnormal neurologic examination The motor output is of two types: (i) Reflective or
• Fever or unexplained systemic signs involuntary, and (ii) Voluntary.
• Vomiting preceding headache Lesions of motor system might result in total weakness
• Induced by bending, lifting or coughing (paralysis) or partial weakness (paresis) or involuntary
• Disturbs sleep or presents immediately upon awakening movements or ataxia due to fibers and their terminal
• Known systemic illness abnormal branches.
• Onset after 55 years of age.
Note: Headache has been described in detail in section of Area 4—Motor Cortex or Motor Area
“Symptomatology and its Causes”. The major portion of the motor cortex occupies almost the
entire length of the precentral gyrus. A small portion, called
BASIC COMPONENTS OF NERVOUS SYSTEM supplementary motor area, extends medially beyond the
The nervous system consists of central and peripheral motor margin of the central sulcus over on to the medial surface
and sensory pathways, the cerebellar system and cerebral of the cerebral hemorrhage which lies above the cingulated
hemisphere. gyrus. The motor cortex is the main region of origin of the
Another important part of nervous system is the spinal pyramidal tracts. In the motor cortex, the body is
cord in which motor and sensory pathways are in close represented upside down in the cortex.
association with each other. The size of representation of indivdual body part is
Various signs and symptoms are produced in our body proportional to the skill with which the part is used in fine,
due to abnormal functioning of these structures of nervous voluntary movements. Separate foci are present for each
system. It causes some negative symptoms and signs like of the fingers, the focus for thumb being the most inferior
weakness, loss of vision, sensory loss or difficulty in walking and that for little finger the most superior. The structure
or positive abnormalities such as seizures, pain or involving having bilateral representation are face, pharynx vocal cords,
movements. and muscles for the closure of jaw. Stimulation of this part
of brain causes discrete and isolated movements of opposite
MOTOR SYSTEM side of the body.
The neurons in the motor area also receive the input
The part of cerebral cortex or the frontal lobes which on signals from somatosensory area I (SSA-I) and II (SSA-
stimulation gives rise to skeletal muscle responses II). It plays a very important part in use of individual muscle
constitutes the motor areas (Figs 8.2 to 8.4, Plate 11). As groups for the accuracy of motor control. Supplementory
this region lies anterior to central sulcus, it is also called motor area is engaged primarily in the volunry movements
precentral motor cortex. Histologically, it is divided into: that involve complex planning.
• Area 4—motor cortex or motor area.
• Area 6—premotor cortex or premotor area Area 6—Premotor Cortex
• Area 8—frontal eye field
The somatic motor activity depends ultimately upon the The area 6 or premotor cortex lies anterior to the area 4
pattern and rate of discharge of spinal motor nerves and (the motor cortex) of cerebral cortex. It gives rise to three
homologous nerves in the motor nuclei of cranial nerves. subdivisions of fibers. (i) Descending fibers to pyramidal
The nerves are actually the final common pathway to skeletal tract, (ii) Horizontal fibers passing posteriorly to stimulate
muscle and are bombarded by impulses from an immense area 4, and (iii) Descending fibers not involved in the
array of pathways. The whole system of nerves functions pyramidal tract (therefore called extrapyramidal tract).
with the coordination between input and output signals. The The major function of area 6 is to involve in complicated
inputs converging on the motor neurons subserve three motor function such as an alteration in the force or velocity
distinct functions. They are: (i) Bring about voluntary activity, of a movement, action done in response to visual input as
(ii) Adjustment of body posture to provide a stable back- spoken command, two-handed coordination to perform
ground for movements, and (iii) They coordinate the action more complicated tasks and postural support so as to
of various muscles to make movements smooth and precise. perform a wide variety of movements.
In this, the main role is played by corticospinal and It also acts as an important channel for the relay of
corticobulbar systems. Other areas which also hold a major processed information to the primary motor cortex or
share are posture regulating systems, spinocerebellum, basal directly to the descending pathways from other areas of
ganglia and neocerebellum. brain. Stimulation of this area leads to excitatory response
Central Nervous System 177
such as gross rotation of eyes, head and trunk to opposite converge upon the alpha-motor nerves by three mechanisms
side of the body. The extrapyramidal pathways and namely:
intracortical spread of the stimuli to pyramidal tracts also • Synapsing directly upon the alpha-motor neurons (speed
help in such kind of movements. and specificity).
• Synapsing directly on the gamma-motor neurons (control
Area 8—Frontal Eye Field of stretch reflex)
The area 8 or frontal eye field lies anterior to area 6 (the • Synapsing on interneurons which act as switches that
premotor cortex) of the cerebral hemisphere. Its excitation enable a movement to be turned “on and off” under the
causes conjugate deviation of the eyes to opposite side giving demand of higher motor centers.
it the name of frontal eye field. Different areas of cerebral hemispheres give rise to two
The neurons from the specific sensory nuclei of the types of descending (or motor) pathways:
thalamus, project in a highly specific way to two somato- 1. Pyramidal tracts
sensory areas of the cortex—primary and secondary. 2. Extrapyramidal tracts.
Although these tracts are functionally different, but these
Primary Sensory Area
are usually considered together because lesion within the
The primary sensory area [also called somatosensory area cerebral cortex almost always involves both of them.
I (SSA-I)] is located in postcentral gyrus which involves
Broadman’s area 3,1, and 2. Each area (3, 1, and 2) performs Pyramidal Tracts: Corticospinal and
some specific functions. Area 3 responds to the ‘light touch’ Corticobulbar Tracts
and receives a dense input from the thalamus, whereas areas
1 and 2 respond to deep stimuli. The primary sensory area The longest tract extending from motor cortex up to last
(SSA-I) receives the afferents from opposite side of the segment of spinal cord. It is present only in higher animals
body but from both sides of face. The thalamic projection and humans where cerebrum is highly developed. Mostly,
represents itself in such a way that the body is represented the fibers (85–90%) in the pyramidal tract are of small
upside down with legs on the top and head at the foot of the diameter (≤ to lum diameter) making it a slowly conducting
gyrus. The fingers, thumb and lips occupy the largest areas pathway. Almost half of the fibers are without myelination
of somatosensory cortex. (unmyelinated).
Secondary Sensory Area Components of Pyramidal Tracts
The secondary sensory area [also called somatosensory area (Fig. 8.5, Plate 11)
II (SSA-II)] is located in the cerebral cortex and is mostly The pyramidal fibers run from motor area to spinal ventral
buried in the superior wall of the sylvian fissure (lateral horn cells and to all motor cranial nuclei with the exception
cerebral sulcus). Unlike from both sides of the body like of those supplying external eye muscles.
SSA-I, it shows a dermatomal (point to point) sequence of a. Corticospinal tracts—those pyramidal fibers which reach
representation. The posterior region receives afferents from to spinal ventral horn cells.
the legs, while the anterior parts receive afferents from the b. Corticobulbar or corticonuclear tracts—those pyramidal
face (the face area of SSA-II lying just adjacent to that of fibers which reach to motor cranial nuclei. It starts in
SSA-I); thus, the body has two times representation in the cerebral cortex and ends up in the brainstem (bulbar—
somatosensory cortex, in areas SSA-I and SSA-II. Neurons brainstem)
in anterior part respond to touch and those in posterior part
The pyramidal cells and tracts (corticobulbar and
respond to touch, auditory, visual and nociceptive stimuli.
corticospinal tracts) constitute the upper motor neurons
Note: Lesions of the cortex do not disturb/destroy the (UMNs), whereas the spinal and cranial motor neurons
somatic sensation. However, the proprioception and fine which directly innervate the muscles constitute the lower
touch are mostly affected. Thus, perception is possible even motor neurons (LMNs).
in the absence of cerebral cortex. The corticobulbar fibers end near the motor neurons
that innervate muscles of the face, eyes, tongue and throat.
DESCENDING TRACTS: MOTOR PATHWAYS
Therefore, they act as a remote control for the voluntary
The motor pathways play a very important role in altering movement of the muscles of head and neck and the
the balance between excitatory and inhibitory input that corticospinal fibers control the muscle of rest of body parts.
178 Essentials of Clinical Medicine
Origin of Pyramidal Tracts way which include—nuclei of cerebral cortex, basal ganglia,
• 30 percent from motor cortex—area 4 in precentral hypothalamus and nuclei of reticular formation in brainstem.
gyrus In spinal cord, these fibers form separate groups according
• 30 percent from area 6—premotor cortex to their site of origin. The extrapyramidal system plays an
• 40 percent from somatosensory areas I and II (SSA-I important role in postural mechanisms like sitting, standing,
and II) and adjacent parietal lobe—association cortex. turning over in lying position, walking and running. The
peripheral lobe. complex movements such as reaching for an object requires
both postural adjustments and fine distal movements, which
Table 8.8: Damage or injury and its consequences are under corticospinal control (Figs 8.6 and 8.7, Plate 12)
Structure/Area Result
Area 4 Monoplegia (one limb) Functions of Extrapyramidal Tracts
Level of internal capsule Hemiplegia (one side of the body) • Corticobulbar (corticonuclear) fibers control the
Brainstem level Paraplegia (60th lower limbs) movements of eyeballs.
or quadriplegia (all the 4 limbs).
• Control of tone, posture, and equilibrium (rubrospinal
tract for tone and posture, tectospinal for visuospinal
Functions of Descending Motorways
reflex, vestibulospinal for equilibrium.
Functions of corticospinal tracts: • Control of complex movements of body and limb such
1. Motor impulses to spinal cord → control of voluntary as coordinate movements of arms and legs during
movement (especially the fine) precise movements of walking.
fingers and hands → skilled work.
• They show tonic inhibitory control over the lower
2. Part of pathways for superficial reflex like cremasteric
centers. Their damage increases rigidity to muscles
abdominal and plantar reflexes.
called release phenomenon.
3. Excitatory effect (via alpha and gamma motor neurons
or inhibitory effect or excitatory effect via the • In case of damage to pyramidal tracts, the extra-
interneurons. pyramidal tracts carry out voluntary movements to some
4. Affect afferent system neurons by → extent.
• Ending either presynaptically an axon termenal of Note: Both pyramidal as well as extrapyramidal tracts cause
afferent neurons as these fibres enter the CNS or effects on motor neurons of the opposite side of the spinal
• Ending directly on dendrites or cell bodies of neurons cord. Some pyramidal fibers end an interneuron that play
in ascending pathways. important roles in posture, whereas the extrapyramidal tract
5. Those arising from SSA-I and II are concerned with fibers sometimes end directly on L-motor neurons to control
sensory motor coordination, e.g. aiming the hands discrete muscle movement. Due to this extra control
towards an object and manipulating it, hand-eye mechanism, loss of function resulting from damage of one
coordination, etc. Lesions of these areas cause defect system may be compensated for by the remaining system,
in motor performance characterized by inability to although not completely. A total separation of functions
perform learned sequences of movements such as eating between pyramidal and extrapyramidal tract is not clear-
with knife and fork. cut; therefore, all movements, whether voluntary, require
Functions of corticobulbar (corticonuclear) tracts: the continuous coordinated interaction of both the systems.
Responsible for voluntary control of muscles of larynx,
Table 8.9: Differences between pyramidal and extrapyramidal tract
pharynx, palate upper and lower face jaw, eyes, etc.
Pseudobulbar palsy is a condition resulting in paralysis or Pyramidal tract Extrapyramidal tract
weakness of muscles which control swallowing, talking, 1. Origin of these tracts is as follows Rubrospinal tract from the red
tongue, and lip movements due to bilateral lesion of these nucleus (magnocellularis, i.e.
tracts. large nucleus located in mid-
brain)
Thirty percent from motor cortex Tectospinal and tectobulbar
Extrapyramidal Tracts area 4 in precentral gyrus tract- from superior colliculus
The system consists of basal ganglia, subthalamic nuclei, Thirty percent from premotor (which is an optic center)
cortex, area 6
substantia nigra and other structures in brainstem. These Fourty percent from SSA-I and II Reticulospinal tract from
are those neurons which are concerned with muscular and adjacent parietal lobe neuron of reticular formation
movements and posture. Its fibers make many synapses in association cortex in pons and medulla
their descending path with cells of nuclear masses on the Contd...
Central Nervous System 179
Contd... Contd...
Pyramidal tract Extrapyramidal tract Lower motor neuron lesions Upper motor neoron lesions
Vestibulospinal tract from b. Superficial reflexes, only
lateral vestibular nucleus abdominal cremasteric and
located at the junction of pons anal reflexes are lost
and medulla 6. Babinski’s sign or Babinski’s 6. Babinski’s sign—positive
Medial longitudinal fasciculus plantar not elicited (abnomal)—stroking outer
(or bundle) from medial edge of the sole of foot with
vestibular nucleus reticular firm, tactile stimulus produces
formation, superior colliculus
first an upward movement
and interstitial nucleus of Cajal
2. Axons pass without relay to spinal They have many synapses in (dorsiflexion) of the great toe
segmental levels where they form their descending path descend- and fanning out (abduction) of
synapses with either interneurons ing path nuclei of the straitum small toes. This is due to con-
in the dorsal horn or directly (caudate and putamen), the traction of extensor hallucis
themselves globus pullidus, the hypothala- longus (Anatomists mislead-
mus and nuclei of the reticular ingly call it an “extensor
formation response”. It is physiologically
3. They have greater influence over They are more involved with a “flexor” (withdrawal)
motor neurons that control coordination of large muscle response. Note that all the
muscles involved in fine move- groups used in the maintenance
muscles which contract during
ments, particularly those of of upright posture, in loco-
fingers and hand. motion, and in head and body a flexor response are called
movements when turning physiological flexors)
towards a specific stimulus. Note: Note:
4. Lesions of this tract produce Its tract lesion produces
“spasticity in muscles involved “rigidity of the involved 1. The response is obtained by 1. Babinski’s sign once becomes
muscles stroking (to pass gently in positive, it remains positive
one direction) outer edge of for the rest of the life thereaf-
Table 8.10: Differences between upper and lower motor neuron lesions sole of foot with firm tactile ter. In some normal individuals,
stimuli; it produces a downward it is always positive
Lower motor neuron lesions Upper motor neoron lesions
movement (plantar flexion) of
1. Due to lesion of lower motor 1. Due to lesions of upper motor great toe and small toes
neurons (LMNs). The LMNs neurons (UMNs) in the brain (Babinski’s—negative)
include the spinal and cranial that forms the pyramidal 2. Babinski’s sign appears with the 2. Individuals with Babinski’s
motor neurons that directly tracts development of pyramidal positive can neither run fast
innervate muscles. tracts; therefore, its presence nor can travel long distances.
2. Usually single or individual 2. Usually a group of muscles is indicates the development of
muscle is affected. affected these tracts. Normally, it is a
3. Muscles become completely 3. Affected muscles become flexor response (withdrawal
paralysed (flaccid paralysis). hypertonic (spastic paralysis reflexes)
It is due to complete loss of a. Release phenomenon, i.e.
3. Causes of positive Babinski’s
muscle tone which depends loss of higher inhibitory cont-
sign:
on integrity of reflex arc. rol
a. Infants—pyramidal tracts
b. Denervation hypersensiti-
are not developed till child
vity of centers below the level
starts walking
of transaction.
b. During deep sleep
4. There occurs “disuse atrophy” 4. The muscle atrophy is not
c. Inhibition of pyramidal
of muscles (i.e. shrinkage of severe (if present-very mild)
tracts
muscle fibers which is finally because muscles though not
d. Chyene-Stokes respiration
(fibrous used in voluntary movements,
due to hypoxia
muscle) they are continuously in action
to maintain posture by “refle-
xes”. Levels of Motor Control System (Fig. 8.8)
5. All reflexes (superficial or 5. a. Deep reflexes are hyperacti-
deep) are absent as motor ve (accentuated) because of a. Highest level—the cerebral cortex
pathway is damaged. increased gamma motor b. The middle level—subcortical centers
discharge
c. The lowest level—brainstem and spinal cord
Contd...
180 Essentials of Clinical Medicine
Contd...
Spasticity Rigidity
a. Lead pipe rigidity: Passive
movements of an extre-
mity meets with a plastic
dead feeling resistance as if
bending a lead pipe
b. Cogwheel rigidity: The
resistance to passive move-
ment of an extremity is
regularly or irregularly
variable. This is described
as like a lever rubbing on
teeth of a cogwheel, i.e. a
series of catches passive
movements of the extre-
mity.
4. It is a form of spasticity which 4. No such phenomenon is seen
is stretch sensitive. The degree here.
of increased tone development
during any passive stretch is
proportional to the speed of
the applied stretch.
4. The extensors in upper limb and flexors of lower limb anterior horn cells). Early signs of paralysis are loss of tone
show more weakness (opposite to that of tone distri- and absent or reduced tendor reflexes. The classical sign of
bution). hypertonia and increased tender reflexes of a corticospinal
5. The muscle group which is affected first is the last to lesion appear after a few hours or days interval.
recover; for example, the distal movements of hands
are the last to recover. Signs of Extrapyramidal Lesion
6. Abdominal reflex is absent.
Lesions of extrapyramidal system cause difficulty in initiating
7. Babinski sign (as stated earlier in the text) is positive
the voluntary movements and certain other positive as well
(extensor plantar response).
as negative features.
8. Deep tendon reflexes are brisk or exaggerated and tone
is sustained. The positive or released features include:
• Alteration in muscles tone
Signs of Lower Motor Neuron • Involuntary movements.
Lesions (LMNLs)
The negative features include:
LMNLs cause weakness, with especially, absence of • Difficulty in initiating voluntary movement (as mentioned
appropriate tendon reflexes. The amount and distribution
above)
of abdominal features depend on the causative process.
• Impairment of orientating and balancing reflexes.
When the single nerve or nerve root lesion occurs, it causes
focal neurogenic weakness. Distal weakness of neurological The strength of the muscle mass is generally not affected.
origin occurs in peripheral neuropathy. Anterior horn cell Table 8.13: Signs and sites of extrapyramidal lesion
disease (amiyotrophic lateral sclerosis), includes generalized Sign Site of lesion
neurogenic weakness. Thus, generalized neurogenic weak-
Resting tremor Substantia nigra, red muscles
ness also occurs in spinal muscles atrophy. Muscles rigidity Substantia nigra, putamen
The typical signs of LMNLs are: Hypokinesia Substantia nigra, globus pallidus,
1. Weakness or paralysis of muscles supplied by the putamen
affected anterior horn cells or axons. Chorea Caudate nucleus
Hemiballismus Subthalamic nucleus
2. Hypotonia, that is decrease in muscle tone. Dystonia, athetosis Putamen
3. Absent or reduced deep tendon reflexes
4. Severe wasting of affected muscles.
HIGHER FUNCTIONS
5. Fasciculation in affected muscle groups (fasciculation
is a sign of degenerating anterior horn cells or irritative Introduction
lesions of the neuron roots or peripheral nerves).
Testing of higher functions forms a very important and
6. Flexor/absent plantar response.
unseparable part of nervous system examination. It should
The extensive lesions affecting the extrapyramidal or
be done early in the examination, because the examination
the subcortical structures, in addition to corticospinal fibers
of CNS requires full understanding and cooperation from
themselves, result in the clinical feature of severe paralysis
the patient.
of one side of the body (hemiplegia), with upper limb in
flexed position or of a single limb (monoplegia). Even in
Examination of Higher Functions
case of dense hemiplegia, movements of the head and trunk
(called axial movements of the body), are usually uninvol- 1. Consciousness
ved. The reason for this being that the pathways for such 2. Mental state, behavior, mood, thought, personality.
postural movements ate mostly under the control of 3. Attention and orientation in time, place and person.
subcortical area and have bilateral representation in the brain. 4. Alertness memory (immediate, short term and long
Virtually, most of lesions of corticospinal tract (system) term)
are not of isolate type. They usually involve neighboring 5. Intelligence.
extrapyramidal nuclei and pathways and group of 6. Calculation
corticospinal lesions. 7. Speech and language function
Sudden damage or destruction of the corticospinal 8. Abstract thought
system (due to hemorrhage or injury) is presented as 9. Spatial
neuronal shock (a temporary depressant effect on the 10. Visual and body perceptions.
182 Essentials of Clinical Medicine
There are many sophisticated tests of higher functions. If you consider the patient as depressed, ask:
They can be applied to test intelligence as well as in disease. • Are you ever able to cheer up?
However, much can be learned from simple bedside testing. • Do you see any hope in the future?
Patients with depression say they find it difficult to cheer
Mental State up and see little hope in the future.
The mental state relates to the mood and thoughts of a Patients with schizophrenia often have an apparent lack
patient. Abnormalities may reflect: of mood—blunted affect—or inappropriate mood, smiling
• Neurological illness, such as frontal lobe disorders or when you expect him to be sad—incongruous affect.
dementia (memory-related disorders) In mania, patients are euphoric.
• Psychiatric disorders which may be causing neurological
symptoms (e.g. anxiety leading to panic attacks) Vegetative Symptoms
• Psychiatric disorders secondary to neurological disease Ask the patient about vegetative symptoms:
(e.g. depression following stroke). • Weight loss or gain
Mental State Examination • Sleep disturbance (waking early or difficulty getting to
It attempts to distinguish: sleep)
• Focal neurological deficit • Appetite
• Diffuse neurological deficit • Constipation
• Primary psychiatric illness such as depression, anxiety • Libido
or hysteria presenting with somatic symptoms Find out symptoms of anxiety:
• Psychiatric illness secondary to, or associated with • Palpitation
neurological disease. • Sweating
• Hyperventilation (tingling in fingers, toes and around
Appearance and Behavior
the mouth, dry mouth, dizziness and often a feeling of
The clinician must watch the patient while taking the history. breathlessness).
Here are some questions you can ask yourself in assessing
the appearance and behavior. Minimental State Test
• Are there signs of self-neglect?
– Dirty or unkempt—consider depression, dementia, Orientation
alcoholism or drug abuse Score one point for correct answers to each of the following
• Are there any signs of depression? questions:
– Furrowed brow, immobile, downcast facies, slow • What is the time? Date? Day? Month? Year? (5 points)
monotonous speech. • What is the name of this: Ward? Hospital? District?
• Are there any signs of anxiety? Town? Country? (5 points)
– Fidgety, restless
• Are there any signs of inappropriate behavior? Registration
– Overfamiliar and disinhibited or aggressive— Name three objects. Score up to 3 points if, at the first
consider/frontalism attempt, the patient repeats, in order, the three objects you
– Unresponsive, with little emotional response-flat have randomly named. Score 2 or one if this is the number
affect. he repeats correctly. Endeavors, by further attempts and
• Does the patient show appropriate concern about his prompting, to have all three repeated, so as to test recall
symptoms and disability? later.
– Lack of concern in the face of significant disability
—consider hysterical disease. Attention and Calculation
• Are there any signs of rapid changes in mood? Ask the patient to subtract 7 from 100, and then 7 from the
– Crying or laughing easily—emotional lability. result—repeat this five times, scoring one for each time a
correct subtraction is performed (5 points).
Mood
Recall
Inquire about his mood:
• How are your spirits at the movement? Ask for the three objects repeated in the registration test,
• How would you describe your mood? scoring one for each correctly recalled (3 points).
Central Nervous System 183
Language until the patient makes several mistakes at one of the digits.
Score one point for two objects (a pencil and a watch) Then ask him to repeat the numbers backward; for example,
correctly named (2 points). when I say one, two, three, you say three, two, one.
Score one point if the following phrase is correctly Note the number of digits the patient is able to recall
repeated “No ifs, ands or buts”. forwards and backwards.
Score 3 if a three-stage command is correctly executed. • Normal : seven forward, five backwards
Score 1 for each stage; for example, ‘with the index finger • Hint: use parts of telephone numbers you know (not
of your right hand touch the tip of your nose and then your 111 or 777).
left ear’, or ‘take this piece of paper in your right hand, fold
it in half and place it on the floor’ (3 points). Memory
On a blank piece of paper write, ‘close your eyes’ and a. Immediate recall and attention
ask the patient to obey what is written. Score one point if • Name and address test:
he closes his eyes (1 point). Tell the patient that you want him to remember a
Ask the patient to write a sentence. Score one if the name and address, and give the patient a three-line
sentence is sensible and has a verb and a subject. name and address, e.g. Amit Gupta, Tilak Nagar,
Construct a pair of intersecting pentagons. Each side Indore. Ask immediately to repeat it back to you.
1 inch long. Score one if this is correctly copied (1 point). Note how many errors are made in repeating it
Conclusion and how many times you have to repeat it before it
Less than 23 = cognitively impaired. is repeated correctly.
NB: Does not distinguish focal from diffuse disease. Aphasic • Normal: Immediate registration.
patients do especially badly. • Hint: Give a name and address that you use regularly
so that you do not make mistake yourself.
Note b. Short-term memory
1. Apraxia is a term used to describe an inability to perform About 5 minutes after asking the patient to remember
a task when there is no weakness or incoordination or the name and address, ask him to repeat it.
movement disorder to prevent it. It will be described Note how many mistakes are made.
here though clearly requires examination of the motor Give the patient 5 minutes to do so.
system before it can be assessed. c. Long-term memory
2. Before starting, explain that you are going to ask a Test factual knowledge you would expect the patient to
number of questions. Apologise that some of these have. This varies greatly from patient to patient and you
questions may seen very simple. need to tailor it accordingly. For example, a retired soldier
Test attention, orientation, memory, and calculation should know the commander-in-chief in the Second
whenever you test higher function (often best done with World War; a football fan should know the year England
MMS test). won the World Cup, and a neurologist should know the
names of the cranial nerves. The following may be used
Attention and Orientation as examples of general knowledge: dates of the Second
Orientation: Test orientation in time, place and person World War, the American President, who was shot dead,
• Time: What day is it? What is the date? What is the the Chernobil disaster of Russia, the year when man
month, the year? What is the season? What is the time first landed on the moon.
of day?
• Place: What is the name of the place we are in? what is Calculation
the name of the ward/Hospital? What is the name of the
Serial Sevens
town/city?
• Person: What is your name? What is your job? Where • Ask the patient if he is good with numbers, explaining
do you live? that you are going to ask him to do some simple
Make a note for errors made. calculations.
Attention: digit span • Ask him to take seven from a hundred, then seven from
Ask the patient to repeat some numbers that you give what remains.
him. Start with three- or four-digit numbers and increase Note mistakes and the time taken to perform calculation.
184 Essentials of Clinical Medicine
Test for parietal lobe and premotor cortex of the frontal Lobe Alteration in higher Associations
function
lobe function; very useful in dementias
Frontal Apathy, disinhibition Contralateral hemiplegia, Broca’s
Ask the patient to perform an imaginary task: show me aphasia (dominant hemisphere),
how you would light a matchstick, how would you smoke, primitive reflexes.
swimming action and act of hitting a ball with a bat. Temporal Memory Wernicke’s aphasia (dominant
Observe the patient. If there is a difficulty, give the patient hemisphere), upper quardanta-
nopia
an appropriate object and see if he is able to do it with the
Parietal Calculation, perceptual Apraxia (dominant hemisphere),
appropriate prompt. If there is further difficulty, demonstrate and spatial orientation homonymous hemianopia
and ask him to copy what you are doing. (non-dominant hemi- hemisensory disturbance. Neglect
• The patient performs the act appropriately—normal sphere)
• The patient is unable to initiate the action though under- Occipital Perceptual and spatial Hemianopia
standing the command—ideational apraxia orientation
• The patient performs the task but makes errors; for
Table 8.15: Ultimate impression that you get
example, uses his hand as a cup rather than an imaginary
cup—ideomotor apraxia. 1. Impaired attention and Occurs with diffuse disturbances of
If inability is related to a specific task; for example, orientation cerebral function
dressing, this should be referred to as a dressing apraxia. If acute, often associated with
disturbance of consciousness.
This is often tested in a hospital by asking the patient to put
If chronic, limits ability for further
on a dressing gown with one sleeve pulled inside out. The testing—suggestive of dementia.
patient should normally by able to overcome this easily. N.B: also occurs with anxiety,
depression.
Three-Hand Test
2. Memory Loss of short-term memory in
Ask the patient to copy your hand movements and alert patient—usually bilateral—
demonstrate: 1. make a fist and tap it on the table with your limbic system (hippocampus,
thumb upwards, 2. then straighten out your fingers and tap maxillary bodies) disturbances—
on the table with your thumb upwards, 3. then place your seen in diffuse encephalopathies,
bilateral temporal lesions;
palm flat on the table. If the patient is unable to perform this
prominent in Korsakoff’s
after one demonstration, repeat the demonstration. psychosis (thiamine deficiency)
• Inability to perform this in the presence of normal motor loss of long-term memory with
function—limb apraxia. preserved short-term memory,
functional memory loss.
Interpretation 3. Calculation Impaired calculation usually
Three patterns can be recognized: indicates diffuse encephalopathy.
1. Inappropriate attention If associated with finger agnosia
Tests useful to document level of function, but are of (inability to name fingers), left-
right agnosia (inability to
limited use in distinguishing focal from diffuse disease.
distinguish left from right) and
2. Patients with deficits in many or all major areas of testing dysgraphia—Gerstmann’s
Indicates a diffuse or multifocal process. syndrome—indicates a dominant
• If of slow onset—dementia or chronic brain syndrome. parietal lobe syndrome.
• If of more rapid onset—confusional state or acute brain Perverse but consistent
syndrome calculation errors may suggest
Common mistakes: psychiatric disease.
4. Abstract thought If interpretations of proverbs are
Dementia has to be differentiated from:
concrete—suggests diffuse
• Low level of intelligence—usually indicated from a encephalopathy.
history of intellectual attainment. If interpretation includes
• Depression—may be difficult especially in the elderly. delusion—suggests psychiatric
Often suggested by the patient’s demeanour. illness, with particular frontal lobe
• Aphasia—usually found on critical testing. involvement.
Poor estimates suggest frontal or
3. Patients with deficits in one or only a few areas of testing
diffuse encephalopathy or
control focal process. Identify areas affected and seek psychiatric illness.
associated physical signs. Contd...
186 Essentials of Clinical Medicine
Contd... Delusion
5. Loss of spatial appreciation (copying, drawing, astero-genosis)
—parietal lobe lesions. Delusion is a false belief in something which is not a fact,
6. Visual and body perception Prosopagnosia—bilateral and which persists even after its falsity has been clearly
temporo-parietal lesions demonstrated.
Neglect
Sensory agnosia, astereognosis Types
and agraphesthesia are signs of 1. Grandeur or exaltation: A man imagines himself to be
parietal lobe lesions. very rich while in reality he is a pauper.
7. Apraxia Ideomotor apraxia—lesion
2. Persecution: The person imagines that attempts are being
either of the dominant parietal
lobe, premotor cortex or a diffuse
made to poison him by nearest relatives like wife, sons
brain lesion. or parents. Delusion of grandeur and persecution are
Ideational apraxia—suggests often present together in the same person.
bilateral parietal disease. 3. Reference: The person believes that people, things,
events, etc. refer to him in a special way. He believes
Table 8.16: Interpretation that even strangers in the street are looking at him and
a. Diffuse or multifocal abnormalities: are talking about him, or items in the radio or newspapers
1. Common are referring to him.
• Alzheimer’s disease 4. Influence: They occur in schizophrenia. The person
• Vascular disease (multi-infarct) complains that thoughts, feelings and actions are being
2. Rare degenerative conditions
influenced and controlled by some outside agency, like
• Pick’s disease
• Huntington’s disease
radio, hypnotism, telepathy, etc.
3. Nutritional 5. Infidelity: A man imagines his wife to be unfaithful while
• Thiamine deficiency (Korsakoff’s psychosis) in fact is chaste.
• Vitamin B12 deficiency 6. Self-reproach: The person scolds himself for the past
4. Infective failures and misdeeds which are often of no importance.
• Quaternary syphilis 7. Nihilistic: The person declares that he does not exist or
• Cruetzfeldt-Jacob disease that there is no world, etc.
• HIV encephalopathy
8. Hypochondriacal: The person believes that there is
5. Structural
• Normal pressure hydrocephalus something wrong with his body, though he is healthy.
• Demyelination 9. Other types: are of jealousy, of religion, etc.
• Multiple sclerosis
b. Focal deficits Hallucination
May indicate early state of a multifocal disease
1. Vascular Hallucination is a false sense of perception without any
• Thrombosis, emboli or hemorrhage external object or stimulus to produce it. They are purely
2. Neoplastic imaginary, and may affect any or all the special senses.
• Primary or secondary tumors
3. Infective Types
• Abscess 1. Visual: A person imagines of being attacked by a lion
4. Demyelination
when no lion exists.
• Multiple sclerosis
2. Auditory: A person hears voices and imagines that a
person is speaking to him when no one is present.
Delirium 3. Olfactory: A person smells pleasant or unpleasant odor
when none is present.
Delirium is a disturbance of consciousness in which
4. Gustatory: A person feels sweet, sour, bitter, good or
orientation is impaired, the critical faculty is blunted or lost
bad taste in the mouth, though no food is actually present.
and thought content is irrelevant or inconsistent. In the early 5. Tactile: A man imagines rats and mice crawling into his
stage, the patient is restless, uneasy and sleepless. He then bed, when there are none.
completely loses self-control, becomes excited and talks 6. Psychomotor: A man will have feeling of movement of
furiously. some part of the body in the absence of such movement.
Central Nervous System 187
Visual hallucinations are the commonest in organic wife may continuously believe her husband to be unfaithful
mental disorders, while the auditory hallucinations are the in spite of proof to the contrary. A person may go to bed at
commonest in functional disorders. Hallucinations occur in night after securely bolting the door of his room, but he
fevers, intoxications, and insanity. Visual and auditory soon gets up to see he has done so. A sane person may
hallucinations are the most common. They may be pleasant, repeat it once or twice, but an insane person does not sleep,
but more often they are unpleasant. A person suffering from and spends the whole night in frequently seeing whether
unpleasant hallucinations may be incited to commit suicide the door is bolted.
or homicide.
Phobia
Illusion
Phobia is excessive or irrational fear of a particular object
Illusion is a false interpretation by the senses of an external or situation.
object or stimulus which has a real existence, e.g. when a
person sees a dog and mistakes it for lion, or hears the Neuroses
notes of birds and imagines them to be human voices, or
imagines a string hanging in his room to be snake, or may The patient suffers from emotional or intellectual disorders,
mistake the stem of a tree for a ghost in the dark. A sane but he does not lose touch with reality. They occur mostly
person may experience illusion, but is capable of correcting in the form of anxiety, depression, or hysteria. The effects
the false impressions. An insane person continues to believe may be mild or may cause considerable distress to the patient,
in the illusions, even though the real facts are clearly pointed but they are not associated with severe affective change,
out. Illusions are a feature of psychoses, particularly of the nor with disturbances of thought.
organic type. Types
Field of Vision with your left hand. Extend your right arm full length and
hold your hand midway between yourself and the subject.
The part of the outside world which is visible to one eye, Keeping the fingers moving, bring your hand nearer until
when it is kept fixed on one object or point, is called field of you can yourself perceive the finger movements ‘with the
vision for that eye. It is restricted medially by the nose, tail of your eye.’ At this time, ask the subject if he can catch
above by the orbital margin, below by the cheek bones, but the movement. If he fails to see the fingers, continue bringing
it extends more than 90° on the lateral side. An approximate the hand nearer, until he can. Test the peripheral field of
idea of the peripheral field of vision can be obtained by the vision in this manner—upwards, downwards and from the
‘confrontation test’, but an accurate assessment and a left side. Test his field for a stationary object in a similar
permanent record can be obtained only by a perimeter. manner by asking the subject to indicate when he sees your
Confrontation test: Ask the subject to sit opposite to you at finger held at rest. Only gross changes in the field of vision
a distance of about 3 feet. When testing his left eye, he can be detected by this method. Scotomatas (blind areas
places his cupped right hand over his right eye; and with within the field of vision) are impossible to locate.
the left eye he fixes his gaze on your right eye. Instruct him
not to move his eye in any direction. Cover your left eye Color Vision
(i) Holmgren’s wools: Place small lengths of woolen threads
of different colors and hues in a heap on the surface of a
table (white or neutral background), in good light. Pick up
a test skin and ask the subject to pick up those wool threads
from the heap which are like the test skein, whether they
are of a darker or lighter shade (or hue). He is to match the
color only and not to name it. Test him first with a pure pale
green thread and then with a purple. Note if there is red-
green blindness (or weakness); blue-yellow blindness (or
weakness), or total color blindness;
(ii) Ishihara’s pseudoisochromatic plates: These are available
in the form of a book, and the instructions should be read
carefully before testing the color vision. The plates are so
constructed that a subject with normal color vision will
read one number, made up of dots of different colors and
size against a background of differently colored dots, while
Fig. 8.11: Pathway for light reflex. The input from the left eye decussates a person with defective color vision will read a different
at the chiasma and reaches both oculomotor nerve nuclei number on the same plate. For example, number 8 will be
Central Nervous System 193
Some Important Points upwards, and 50° downwards. Test the rotatory move-
• Papilloedema: Common causes—raised intracranial ments of the eyes also. Observe if there is any limitation
pressure (N.B: absence does not exclude this); rarer of movement in any direction
caused: malignant hypertension, hypercapnia Usually, the signs of involvement of one or more of
• Papillitis: Common causes—MS, idiopathic these nerves are: (i) Pupillary abnormalities, (ii) Presence
• Optic atrophy: Primary: common causes—MS, optic of diplopia, (iii) Defective movements of the eyeballs, and
nerve compression, optic nerve ischemia: rarely (iv) Presence of a squint.
nutritional deficiencies, B12, B1, hereditary Skew deviation of the eye, i.e. one eye is directed
• Secondary—following papilloedema upwards and the other downwards—is seen in diseases of
• Deep optic cup: Chronic glaucoma—commonly cerebellum, labyrinth, and 8th nerve.
idiopathic.
Abnormalities
Third, Fourth and Sixth Nerves Abnormalities can arise at any level.
(Fig. 8.13) Lesions can be:
The oculomotor (3rd nerve), trochlear (4th nerve) and the
abducent (6th nerve) are tested together as they innervate
1. Supranuclear
2. Internucler MLF
3. Nuclear
} Patients do not
perceive double vision
the external ocular muscles which move the eyes. The 6th
nerve supplies the lateral rectus, the 4th nerve innervates
the superior oblique, and the 3rd nerve supplies all the other
extraocular muscles, along with the sphincter pupillae, ciliary
muscle (the muscle of accommodation) and the levator
4. Nerve
5. Neuromuscular junction
6. Muscle
} Patients perceive
double vision
Intranuclear and supranuclear lesions rarely cause double
palpebrae superioris. vision.
1. Ask the patient to look at your finger held at a distance
of about 2 feet from his eyes. Notice if there is any Rules of Double Vision
squint (strabismus). Ask the patient if he has double 1. Double vision is maximal in the direction of gaze of the
vision (diplopia) or gets attacks of vertigo. affected muscle
2. Test for pupillary light reflexes and the convergence 2. False image is the outer image
accommodation reflex. Notice the size, shape and 4. False image arises in the affected eye
mobility of the pupil.
3. Fix the chin of the patient with left hand and ask him to The Cover Test
follow the movements of your right forefinger with his This test is useful in the detection of latent squint (Fig.
eyes. Move your finger in the cardinal directions. The 8.14).
eyes move normally 50° outwards, 50° inwards, 33° The patient is asked to look with both eyes at your right
eye. Then, the left eye is uncovered rapidly and cover his
right eye. Pay attention to see if the left eye has to correct
to look back at your eye. Repeat, covering the left eye and
watching the right eye.
Findings: If one eye has to correct as it is uncovered, this
indicates the patient has a latent strabismus (squint), which
is classified as divergent or convergent.
Interpretation:
Latent squint: Congenital squint usually in the weaker eye
(and myopia in childhood)—common.
Test the Eye Movements
The clinician holds a pen vertically about 50 cm away from
the patient in the center of his gaze. He asks him to follow
it with his eyes without moving his head and to tell the
Fig. 8.13: Extraocular eye muscles clinician if he sees double. Hold his chin tightly to prevent
The movements they produce and their cranial nerve (N) supply head movement.
196 Essentials of Clinical Medicine
called Bell’s phenomenon. In Bell’s palsy (see below) as and the semicircular canals, the upper part is affected and
the patient is asked to close his eyes, the upward is concerned with posture and equilibrium.
movement of the eyeball becomes obvious because
closure of the affected eye is not possible. Case: Facial Nerve Palsy
3. Ask the subject to smile or show his upper teeth, or to Sites of lesion in the following conditions:
whistle. When there is paralysis of the facial muscles • Acoustic neuroma—CP angle
on one side, the angle of the mouth is drawn towards • Ramsay-Hunt syndrome—geniculate ganglion
the healthy side. • Bell’s palsy—at the exit from stylomastoid for a men.
4. Ask him to inflate his mouth with air and below out his
Causes of Infranuclear 7th Nerve Palsy
cheeks; then tap each inflated cheek with a finger; air
escapes more easily on the affected side. • CP angle tumor
5. Taste sensation: Though the seventh nerve is almost • Acoustic neuroma
• Ramsay-Hunt syndrome—secondary to herpes zoster
entirely a motor nerve, the taste fibers from the anterior
of geniculate ganglion
two-thirds of the tongue pass from the lingual nerve
• While mastoidectomy 7th nerve may be damaged
into the chorda tympani and then througn the geniculate
• Infective polyneuritis
ganglion of the facial nerve and the nervus intermedius • Leprosy
of Wrisburg into the medulla to enter the tractus • Diabetes mellitus
solitarius. It has been suggested that these taste fibers • Parotid tumor
sometime run in the maxillary division of the trigeminal • Tetanus—cephalic tetanus
nerve; this, however, is rare. The sensation of taste • Hypertension
should always be tasted whenever a lesion of a cranial • Bell’s palsy
nerve is suspected. • TB—basal meningitis.
How to test the taste sensation: Use strong solutions of
Nuclear 7th Nerve Palsy
sugar and common salt and weak solutions of citric
acid and quinine in order to test the sensations of ‘sweet’, • Associated with 6th nerve palsy—7th and 6th lower
motor ipsilateral
‘salt’, ‘sour’ and ‘bitter’ respectively. Ask the subject
• Contralateral hemiplegia
to protrude his tongue and dry the surface with clean
• No taste involvement
cloth. Apply a small amount of sugar solution, on one
• Fovile syndrome—crossed hemiplegia plus ipsilateral
side of the midline, with a clean toothpick, and ask him: paresis of conjugate gaze
Is this ‘salt’? If the taste sensation is normal he will • Millard-Gubler syndrome—crossed hemiplegia with
shake his head. Try salt and then the others in the same internal strabismus, due to abducent nerve palsy.
manner, rinsing the mouth each time. The tongue should
be kept out during the test and not withdrawn. This is Causes of Bilateral 7th Nerve Palsy
to avoid the spreading of the test substance into the • Diabetes mellitus
posterior part of the tongue since taste from this region • Infective polyneuritis—Guillain-Barré syndrome
is carried by the 9th cranial nerve. Test the taste sensation • Sarcoidosis (parotid fever—Heerfordt’s syndrome)
on the posterior part in similar manner. If the subject • Leprosy
can write, then he should write down the taste • Bulbar lesion
• Mobius syndrome.
accordingly. The loss of sense of taste is called ageusia.
The patient should always be asked whether he Muscular Causes of Facial Palsy
experiences any abnormal test sensations. These, like • Myopathy
hallucinations of smell, may form the aura of an epileptic • Myasthenia gravis
fit, especially in cases of temporal lobe epilepsy. • Dystrophica myotonia.
Supranuclear and Infranuclear Seventh Nerve Taste Sensation will be Affected
Lesions of Facial Nerve • Lower motor facial proximal to point at which chorda
The chief difference between supranuclear and infranuclear tympani leaves the facial nerve.
lesions of the facial nerve is that in the former, the lower • In post-fossa-C.P. angle tumor where pars intermedia
part of the face is chiefly affected, while in the vestibule and 8th nerve will be damaged in addition to 7th nerve
Central Nervous System 201
palsy, e.g. fracture base of skull, spread of middle ear • Surgical decompression of facial nerve if there is no
infection, leukemic deposits and CP angle tumor. recovery after 2 months
Table 8.23: Differentiation between lower motor and • Usually recover spontaneously within 2 to 12 weeks.
upper motor facial palsy
Complication of Bell’s Palsy
Description Bell’s palsy Upper motor • Deformity
infranuclear facial palsy
• Contracture of facial muscle
• Involvement of face One half of face Lower half of face,
• Facial tics and spasms
forehead spared
• Taste sensory loss Can be No • Crocodile tear
• Bell’s phenomenon Yes No • Jaw winking.
• With emotion
paralysis increases Poor Prognostic Signs of Bell’s Palsy
• Usually associated No Yes • Extremes of age
with hemiplegia with
same side facial palsy • If delay in blinking reflex occurs in recovery stage
• Corneal-reflex Lost Preserved • EMG evidences of denervation after 10 days
• Plantar response Flexor Extensor with • Severe 7th nerve palsy with axonal degeneration there
hemiplegia is slow recovery.
• Facial muscle atrophy Yes No
Some Important Facts
Case: Bell’s Palsy (Fig. 8.16) • Unilateral LMN Weakness: Lesion of the facial nerve or
About Bell’s Palsy its nucleus in the pons—common cause—Bell’s palsy:
more rarely: pontine vascular accidents, lesions at the
Cause not known. It is due to non-suppurative inflammation
cerebellopontine angle, herpetic infections (Ramsay-Hunt
of 7th nerve. Site within stylomastoid foramen, always
syndrome—note vescicles in external auditory meatus),
unilateral, 80 percent recover in 3 weeks time. More seen
lesions in its course through the temporal bone, parotid
in males. In the differential diagnosis, polio and disseminated
tumors.
sclerosis are to be kept in mind.
• Bilateral LMN weakness: Common causes—sarcoidosis,
Treatment of Bell’s Palsy Guillain-Barré syndrome: rarer causes: myasthenia gravis
• Prednisolone one mg. per kg × 2 weeks. can produce bilateral fatiguable facial weakness
• Electrical stimulation (Galvanic) on every day after 2 (neuromuscular junction); myopathies can produce facial
weeks weakness (N.B. Dystrophia myotonica and fascio-
• Massage upwards of facial muscles 5 to 10 minutes/ scapulo-humeral dystrophy).
twice a day • Unilateral UMN—cerebrovascular accidents, demy-
• Infra-red therapy elination, tumors—may be associated with ipsilateral
• Tarsorrhaphy to prevent exposure keratitis hemiplegia (supratentorial lesions) or contralateral
• Vasodilator therapy. Nicotinic acid 100 mg three times a hemiplegia (brainstem lesions).
day • Bilateral UMN—pseudobulblar palsy, motor neuron
disease.
• Emotional paralysis—Parkinsonism.
Barany’s Caloric Test Cool water (30°C) is instilled into one ear over 40 seconds
Barany’s caloric test syringe the external auditory meatus (usually about 350 ml). The patient is asked to look straight
with water at 30°C or 44°C, while the head is tilted back ahead and the eyes are watched. This is repeated in the
60° and pointing to the opposite side, and up to the ceiling other ear, and then in each with warm water (44°C).
(the horizontal canal is placed vertical). The endolymph in Findings/Observation
the canal moves down by convection currents produced Normal responses:
by cold-water syringing. Note the following: 1. Cold water—nystagmus fast phase away from
1. Nystagmus. stimulated ear.
2. Past pointing. If the subject is asked to touch a given 2. Warm water—nystagmus fast phase towards stimulated
point on a tape held in front of him (when the eyes are ear.
closed), the arm deviates out towards the stimulated 3. Reduced response to cold and warm stimuli in one ear;
side. canal paresis.
3. If asked to stand, there is a tendency to fall towards the 4. Reduced nystagmus in one direction after warm stimuli
stimulated side. The subject complains of giddiness and from one ear and cold stimuli from the other—directional
nausea, and may even vomit. All these reactions indicate preponderance
normal functioning of vestibular apparatus. A patient N.B: In the unconscious patient, the normal responses are
suffering from vestibular disease complains of paroxys- as follows:
mal attacks of vertigo, tinnitus, nausea and vomiting. • Cold water—tonic movement of the eyes towards the
stimulus.
Interpretation: • Warm water—tonic movement of the eyes away from
a. Conductive deafness—common causes: middle ear the stimulus.
disease, external auditory meatus obstruction, e.g. wax. (The fast phase of nystagmus is produced by the
b. Sensorineural deafness: correction of this response which is absent in unconscious
i. Lesions of the cochlea—otosclerosis, Ménière’s patient).
disease, drug or noise-induced damage. Interpretation:
ii. Lesions in the nerve—meningitis, cerebellopontine • Canal paresis: Lesion of the semicircular canal (Ménière’s
angle tumors, trauma. disease) or nerve damage (causes as for sensorineural
iii. Lesions in the nucleus in the pons—vascular or deafness, plus vestibular neuronitis)
demyelinating lesions. • Directional preponderance: Vestibular nuclear lesions
Table 8.24: Tuning fork tests and their interpretation (brainstem)—common causes: vascular disease,
demyelination.
Tests Normal Conductive deafness SN deafness
Rinne AC>BC BC>AC AC>BC Additional Tests of Vestibular Function
(Rinne positive) (Rinne negative)
Weber Not lateralized Lateralized to poorer Lateralized to
Hallpike’s Test
ear better ear Procedure: Used in patients with positional vertigo.
ABC Same as Same as examiner’s Reduced • Sit the patient on a flat bed so that when he lies down
examiner’s his head will not be supported.
• Turn the head to one side and ask the patient to look to
Vestibular Gait that side.
Always test heel-toe walking. Gait is unsteady, veering to • The patient then lies back quickly till he is flat with his
the side to the lesion. neck extended with his head supported by the examiner.
• Watch for nystagmus in the direction of gaze. Note if
Nystagmus this is associated with a delay, whether it fatigues when
the test is repeated and if the patient feels vertigo. Repeat
Vestibular nystagmus is associated with vertigo, horizontal for the other side.
and unidirectional. It may be positional.
Table 8.25: Hallpike’s test: Interpretation
Caloric Test (Normally Performed in a 1. No nystagmus Normal
Test Laboratory) 2. Fatiguable rotatory Peripheral vestibular syndrome,
The patient is lying down with head on a pillow at 30° so nystagmus with delay usually benign positional vertigo.
3. Non-fatiguable nystagmus Central vestibular syndrome.
the lateral semicircular canal is vertical. without delay
Central Nervous System 203
Turning Test 2. Uvula does not move on saying ahh or gag : bilateral
• Ask the patient to stand facing you. palatal muscle paresis.
• Ask him to point both arms straight out in front of him 3. Uvula moves on saying ahh, but not on gag, with
towards you. reduced sensation of pharynx: IX palsy (rare).
• Ask him to walk on the spot and when he is doing this Larynx
to then close his eyes. Observation
• Watch his position. 1. Gradual onset cough: Bovine cough—suggests vocal
Interpretation and palsy.
• He gradually turns to one side, and may turn through 2. Bubbly voice and cough—suggests combined cord palsy
180°. This indicates a lesion on the side he turns towards. and pharyngeal pooling due to tenth nerve lesion.
3. Swallow followed by coughing indicates aspiration due
Ninth or Glossopharyngeal Nerve (Mixed) to poor airway protection—suggests tenth lesion.
4. Unilateral cord palsy—recurrent laryngeal palsy or vagal
This nerve is motor for the middle constrictor of the pharynx lesion.
and the stylopharyngeus muscle, and sensory for the Interpretation
posterior third of the tongue (taste fibers also) and the Tenth nerve palsy is caused by lesion in the medulla—
mucous membrane of the pharynx. Paralysis of 5th nerve observe for associated ipsilateral cerebellar signs, loss of
alone is rare. pain and temperature in the face on the same side and on
1. Test the pharyngeal reflex. the body on the opposite side and an ipsilateral Horner’s
2. Test the taste sensation of the posterior third of the (lateral medullary syndrome).
tongue. Extramedullary and intracranial observation to confirm
associated XI cranial, IX cranial nerves.
Table 8.26: Mouth: Interpretation
Left-sided recurrent laryngeal palsy may arise from
• Gum hypertrophy Phenytoin therapy mediastinal or intrathoracic pathology.
• Red, ‘beefy’ tongue Vitamin B12 deficiency. Bilateral lower motor neuron X occurs in progressive
• Large tongue amyloidosis, acromegaly,
congenital hypothyroidism. bulbar palsy (a variant of MND)—be observant for
• Small tongue With fasciculations—bilateral associated tongue fasciculations and mixed upper and lower
lower motor neuron lesion; motor motor neuron signs without sensory loss in the limbs.
neuron disease (progressive bulbar
palsy type), basal meningitis, Tenth or Vagus Nerve (Mixed)
syringobulbia.
• Small tongue With reduced range of movements It is motor for the soft palate except tensor palati, pharynx
—bilateral upper motor neuron and larynx. It is also motor and sensory for the respiratory
lesion—often associated with
labile emotions, increased jaw jerk: passages, the heart and most of the abdominal organs (motor
pseudobulbar palsy parasympathetic). Paralysis of this nerve is evident clinically
• Tongue deviates to one side Weakness on the side it moves only through its palatine and laryngeal branches.
towards. 1. Ask for the history of regurgitation of fluids through
– With unilateral wasting and Unilateral lower motor neurone the nose during swallowing. This is due to total paralysis
fasciculation (rare)—causes : syringomyelia,
basal meningitis, early motor of the soft palate. Use a tongue depressor to watch the
neurone disease, foramen magnum movements of palate when the patient is asked to say
tumour. ‘Ah.’ If one side is paralysed, the soft palate on that side
– With normal bulk Unilateral upper motor neuron will remain flat and immobile. In bilateral paralysis, the
weakness (common)-associated entire soft palate remains motionless. Conclusions drawn
with hemiparesis: strokes, tumors.
• Tongue moves in and out on Cerebellar disease, essential from the position of uvula are usually unreliable, since it
tremor, protrusion (‘trombon’ may normally be deviated to one side.
tremor) extrapyramidal syn- 2. Laryngoscopy is done to note the position of true vocal
dromes. cords.
Pharynx and Gag Reflex
Eleventh or Accessory Nerve (Motor)
Interpretation
1. Uvula moves to one side: upper or lower motor lesion This nerve is motor to sternomastoid and upper part of
of vagus on the other side. trapezius muscle.
204 Essentials of Clinical Medicine
1. Press on the shoulders from behind and ask the patient Contd...
to shrug his shoulders. Note any weakness or paralysis 3. Temporal bone—fracture 7th nerve lower —
of the upper part of the trapezius. base of skull infection motor paralysis
2. Ask the patient to turn his head first to one side and then of middle ear—mastoid
surgery
to the other, against resistance, by placing your hand on
4. Geniculate ganglion— Ramsay-Hunt Rash over palate
either side of the chin alternately. Herpes zoster syndrome Rash over external
Interpretation ear
5. Over face after exit Lower motor Lower motor 7th
1. Weakness of sternocleidomastoid and trapezius on the from facial canal 7th nerve palsy nerve palsy
same side indicates peripheral accessory palsy. Look a. Sarcoidosis
for associated ipsilateral IX and X lesions—suggests a b. Leprosy
jugular foramen lesion (glomus tumur or neurofibroma). c. Parotid tumor
d. Trauma to face
2. Weakness of ipsilateral sternocleidomastoid and e. Parotid surgery
contralateral trapezius—upper motor neuron weakness 6. At exit of facial canal 7th nerve lower Bell’s palsy
on ipsilateral side. within stylomastoid motor palsy
3. Unilateral delayed shoulder shrug—suggests contralateral foramen
upper motor neuron lesion.
Table 8.28: Syndromes of cranial nerve palsies
4. Bilateral wasting and weakness of sternocleidomastoid
indicates myopathy (such as dystrophia myotonica, Syndrome Cranial nerves Clinical features
involved
fascio-scapulo-humeral dystrophy or polyositis) or
motor neuron disease (look for associated bulbar Weber’s Nerve 3rd nerve palsy with contralateral
hemiplegia lesion at midbrain
abnormalities).
Benedict’s 3rd nerve 3rd nerve palsy with contralateral
5. Unilateral sternocleidomastoid abnormalities: indicate hemiplegia lesion at midbrain, and
unilateral trauma, unilateral XI nerve weakness or upper tumor with rigidity and cerebellar
motor neuron weakness (check opposite trapezius). ataxia due to red nucleus involve-
ment in addition.
Tolosa-Hunt, 3,4,5,6 nerves Lesion in cavernous sinus
Twelfth or Hypoglossal Nerve (Motor)
Milliard-Gubler- 6,7th nerves Nuclear type of facial palsy with
It is purely motor to the muscles of tongue, and depressors and Foville 6th nerve involvement and
contralateral hemiplegia. In foville
of the hyoid bone. gaze palsy is to the side of the
1. Ask the patient to push out his tongue as far as possible. lesion
If the 12th nerve is paralysed, the tongue is pushed over Vemet’s (jugular 9,10,11 Loss of taste in posterior 1/3 rd
to the side of the lesion by the contraction of the muscles foramen) tongue, vocal cord palsy, palate,
sternomastoid, paralysis.
on the healthy side. Ask him to move the tongues from Schemidt’s 10,11 nerve
side to side, over the lips and against the walls of the Tapia’s 10,12 nerve Paralysis of larynx, pharynx,
cheeks. A finger may be placed on a cheek while the tongue atrophy
Jackson’s 10,11,12 nerves
patient presses against it with tongue through the wall Collect Sicard 9,10,11,12 nerves
of the cheek. Villaret’s 9,10,11,12 nerves Homer’s syndrome along with
2. Note if there is any fasciculation wasting, or tremor. and cervical sym- 9,10,11,12th nerves involvement
Wasting and tremor indicate a nuclear of infranuclear pathetic nerves
lesion (lower motor neuron).
EXAMINATION OF MOTOR SYSTEM
Table 8.27: Site of lesion in the cranial nerve palsy (Fig. 8.17, PLATE 13)
1. Pons—neoplastic, 6th and 7th Lateral rectus palsy, The examination of the motor system is covered under the
syringobulbia, multiple nerve affected 7th nerve palsy, following subheadings:
sclerosis, poliomyelitis, conjugate deviation 1. Muscle strength and movements (power)
motor neuron disease affected
2. Posterior fossa— 7th nerve, Deafness, loss of taste,
2. Bulk of muscles (nutrition)
cerebellopontine 8th nerve and lower 7th nerve palsy 3. Muscle tone
angle tumor pars intermedia 4. Reflexes testing
5. Gait pattern
Contd...
6. Involuntary movements.
Central Nervous System 205
Interossei C8 – T1 Ulnar n Patient made to flex the metacarpophalangeal • When these muscles are paralyzed and
Lumbricals C8 – T1 Ulnar and joints and to extend the distal interphalangeal power is retained in long flexors and
median n joints extensors of two fingers, as in ulnar
palsy, a claw-hand deformity is prod-
uced
• The proximal phalanges are overexten-
ded and distal two are flexed. The fing-
ers are slightly separated
Flexors of the fingers:
• Flexor digitorium C8 – T1 Ulnar n Asking the patient to squeeze the examiner’s Examiner can feel the crushing of his fin-
profundus fingers can test all the flexors. gers between fingers of the patient
• Opponens digit C7 – T1 Ulnar n Allowing to squeeze only the index and middle
fingers is sufficient to assess the strength
• Flexor minimi C7 – T1 Ulnar n
• Flexor digitorium C7 – T1 Median n
sublimes
• Flexor pollicis longus C7 – C8 Median n
• Flexor digitorium C7 – T1 Median n
• Flexor pollicis brains C8 – T1 Median n
• Opponens pollicis C8 – T1 Median n
Extensor of the wrist:
• Extensor carpi radialis C6 – C8 Radial n Ask the patient to make a first (this causes It is very difficult to overcome the wrist
longus contraction of both flexors and extensors of extensor of a healthy man
wrist). Examiner should try to forcibly flex
the wrist against patient’s efforts to maintain
posture • Weakness of extensors may be tested
by asking the patient to grasp someth-
ing firmly in his hands. Weakness of
the extensors will cause the wrist to
Contd...
Contd...
Muscle Cord segment Nerve supply Procedure Inference
flex because flexors are stronger than the
extensors (in case of extensor weakness)
• Weakness or paralysis of extensors of
wrist as in radial palsy
Flexors of the wrist:
Flexor carpi radialis C6 – C7 Median n First allow the patient to squeeze the fingers With normal muscle strength, it is almost
of the examiner. Ask the patient to make a impossible
fist and try to overcome his wrist flexion
Brachioradialis C5 – C6 Radial n Patient is made to place the arm midway Healthy muscle (normal) will be seen and
between the prone and supine positions. The felt to stand out prominently at its upper
patient is then made to bend up the forearm, part
while the examiner opposes the movement
by grasping the hand
Biceps brachi C5 – T1 Musculo- Patient is asked to bend up the forearm against The muscle will stand out clearly.
cutaneous n resistance with the forearm in full supination
Triceps C6 – C8 Radial n Patient is asked to straighten the forearm
against the resistance offered by the examiner
Supraspinatus C5 – C6 Suprascap- Patient is asked to lift the arm straight out at
ular n right angle to the side. The first 30° (one-third)
of the movement is carried out by the supra-
spinatus and remaining 60° (two-thirds) is
produced by deltoid
Deltoid C5 – C6 Axillary n Deltoid helps in abduction of arm, therefore, In case of paralyses of deltoid, abduction,
patient is asked to abduct the arm against flexion, medial rotation, extension and
resistance. Acrominal fibers are powerful lateral rotation all are affected at shoulder
abductors of arm. Anterior fibers are flexors joint (intramuscular injections are given in
and medial rotators of arm. And the posterior the lower half of deltoid to avoid injury to
fibers are extensors and lateral rotators of arm axillary nerve)
Intraspinatus C5 – C6 Supracap- Patient is asked to move (tuck) the elbow into The muscle can be seen and felt to contr-
ular n the side with the forearm flexed at right angle. act. In case of paralyses or weakness,
Then ask the patient to rotate the thumb out- there movements are severely affected
wards against your resistance the elbow being
at the side throughout the procedure
Pectorals pectoralis C5 – T1 Pectoral n Patient is asked to stretch the arms out in Paralysis of pectoralis major:
(major and minor) front and then to clasp out in front and then • Adduction and medial rotation of shou-
to clasp the hands together while the examiner lder, flexion of the arm, extension of
efforts to hold them apart flexed arm against resistance and clim-
bing all become impossible
Contd...
Central Nervous System 207
Contd...
Contd...
Contd...
Muscle Cord segment Nerve supply Procedure Inference
• Plantar flexion of feet S1 S 2 Tibial n
and toes by gastroc- (both)
nemius and soleus
Extensors of the knee
a. Quadriceps femoris L2,3,4 Femoral n Patient is asked to bend up the knee then he Look for the atrophy of quadriceps musc-
is made to straighten the knee against the ulature
resistance offered by the examiner (over the
skin)
Flexors of the knee
a. Biceps femoris L5, S1, S2 a. Long head Patient is asked to raise one of the legs from Normally the muscle is stronger so that
by tibial part the bed, while the examiner supports the thigh examiner is unable to overcome its stre-
of sciatic with his left hand and holding the ankle with ngth
nerve his right. Then patient is made to bend the
b. Short knee against the resistance
head by per-
oneal part of
sciatic nerve
b. Semitendinosus L5, S1, S2 Tibial part
of sciatic
nerve
c. Semimembranosus L5, S1, S2 Tibial part
of sciatic
nerve
Extensors of the hip
a. Gluteus maximus L5, S1, S2 Inferior gl- Patient is made to extend his knee and to lift Normally the examiner is unable to over-
uteal n his foot off the bed, then he is made to push come this movement
it down against the examiner’s resistance
Flexors of the hip
a. Psoas major L2, L3 and Branches The patient is made to extend his legs raise
sometimes L4 from (roots) off his leg off the bed against resistance
of spinal n
L2 L3 and L4
b. Iliacus L2, L3 Branches Alternatively, the related movements of flexion
from femo- of the thigh, with the thigh already flexed to a
ral n right angle, can be tested
Contd...
Central Nervous System 209
Contd...
Muscle Cord segment Nerve supply Procedure Inference
Adductors of thigh
Adductor longus, L2, L3, L4 Obturator Patient is asked to abduct the limb first and then
brevis and magnus nerve made to bring it back towards midline against
resistance
Abductors of thigh
Gluteus medius L5, S1 Superior After placing the patient’s legs together. The
and minimus L5, S1 gluteal n (to patient is asked to separate them against
both) resistance
210 Essentials of Clinical Medicine
Rotators of thigh
a. Medial rotation
• Tensor fascia L4, L5 Sup. gluteal After extending the limb of the patient, he is
latae n asked to roll it outwards or inwards against
• Ant. fibers of L5, S1 Sup. gluteal resistance
gluteus medius n
and minimus
b. Lateral rotation
• Obturator L5, S1 Nerve to
obturator
internus
• Quadratus femoris L5, S1 Nerve to
quadratus
femoris
• Gemelli L5, S1 Nerve to
obturator
internus and
quadratus femoris
Central Nervous System 211
– It is always due to corticospinal pathway lesion. and radiculopathy and lumbar radiculopathy (with sensory
Therefore, it is an upper motor neuron lesion. abnormalities).
(UMNL)
2. Crossed paralysis FUNCTIONAL WEAKNESS
– Weakness in an ipsilateral cranial muscle group with This should be considered when:
a contralateral hemiparesis. 1. The weakness is not in a distribution that can be
– It is branistem disease sign. understood on an anatomical basis.
3. Paraplegia 2. When there are no changes in reflex or tone.
– Paralysis of both the lower limbs. 3. The movements are very variable and power erratic.
– Almost always due to spinal cord lesion. Therefore, 4. There is a difference between the apparent power of
it is upper motor neuron lesion (UMNL) moving a limb voluntarily and when power is being tested.
4. Monoplegia Power when tested is graded conventionally using the
– Paralysis of one limb. It may affect arm (brachial Medical Research Council (MRC) scale. This is usually
monoplegia) or the leg (crural monoplegia). amended to divide grade 4 into 4 + and 4–, as below:
– It is due to root or plexus disease. • 5 = Normal power
5. Quadriplegia • 4+ = Submaximal movement against resistance
– Paralysis of all the four limbs. • 4 = Moderate movement against resistance
– A feature of cervical cord disease. • 4– = Slight movement against resistance
Other Patterns of Muscular Weakness • 3 = Moves against gravity but not resistance
• Myasthenic weakness • 2 = Moves with gravity eliminated
• Neurogenic weakness • 1 = Flicker
• Peripheral neuropathy • 0 = No movement.
• Myopathic weakness Power should be graded according to the maximum
• Myotonia. power attained, no matter how briefly this is maintained.
2. According to types of nerve fibers involved Along with JPS, and two point discrimination the
a. Motor disorders of touch, pain and temperature perception
b. Sensory (hypoesthesia, dysesthesia and hyperesthesia) are also
c. Autonomic common in peripheral neuropathies and nerve injuries,
d. Mixed discogenic radiculopathies and spinal injuries.
3. According to size of nerve fibers In case of individual peripheral nerves or sensory nerve
a. Large (posterior column) root lesion, the subjective feeling of membrane and
b. Small (pressure and temperature) diminution of all sensory modalities develop in their areas
c. Mixed of distribution. An incomplete or partial lesion of peripheral
4. According to distribution nerve causes pain of a burning, unpleasant quality, as in
a. Proximal
causalgia, a condition occurring infrequently after injury to
b. Distal
either the median or the sciatic nerve. In polyneuropathies
c. Diffuse
the numbness or paresthesia and objective sensory features
5. According to clinical pattern of involvement
a. Mononeuropathy affect the distal parts of the limbs and often involve the legs
b. Mononeuritis multiplex before the arms.
c. Radiculopathy
d. Symmetrical sensory motor neuropathy General Assessment in Case of
e. Symmetrical sensory neuropathy Peripheral Neuropathy
f. Autonomic neuropathy (DM) (or inquiries made into a case of peripheral
g. Secondary to systemic disorders neuropathy)
6. According to pathology You should inquire about:
a. Axonal • Diabetes
b. Demyelination • Alcohol intake (addition)
c. Mixed.
• Drug consumption like amiodarone, vincristine
Usually, the vibration sense over the bony prominences
• Renal symptoms
gets impaired as the age advances and is often lost at the
• Travel
ankles over the age of 70. However, in certain cases, the
loss of vibration sense is seen in some patients at a stage • Weight loss
earlier than impairment of JPS. A very good example of it is • Dietary inquiry like folate deficiency.
diabetic peripheral neuropathy. Joint position sense (JPS) is You should examine for:
most commonly impaired in patients with large fiber • Diabetic retinopathy.
peripheral neuropathies and spinal and disorders • Butterfly rash over the face.
(myelopathies) affecting the dorsal columns. JPS disturbance • Smooth tongue.
may occur without paresis also. • Goiter
In such patients, the following findings may be noted: • Carcinoma of bronchus.
• Impairment of fine-finger function and alterations of • Liver and spleen pathology.
gait as a result of loss of feedback concerning muscle • Nerve thickening (leprosy—Hansen’s disease)
activity and joint position. • Small kidneys
• When finger nose test is carried out with the eyes closed, • Bone marrow dysfunctions
the sensory ataxia is noted. • Clubbing of fingers.
• Rhomberg’s test is positive. • Burns/ulcers/scars/injuries
• The patient may fall when he is required to perform • Vascular bruits
movements that require complex postural adjustments • Ulcer over the foot
such as walking in the dark room. • Distal muscle wasting in any of the four limbs.
• When the patient is made to close his eyes with his
hands outstretched, his fingers may make small slow Ruling out Myasthenia Gravis
movements (pseudoathetosis)
In certain peripheral neuropathies, especially those Diagnosis of Myasthenia Gravis
involving large sensory fibers, and in cervical mylo- History of:
radiculopathies, the two-point discrimination test in the • Diplopia, ptosis, weakness
fingers is impaired. • Weakness in characteristic distribution
214 Essentials of Clinical Medicine
in hand and fingers, it occurs more at night and is extension of metacarpophalangeal joint along with flexion
relieved by shaking hand at interphalangeal joint.)
– Sensory loss—occurs over tips of median innervated Froment’s sign: Consist of thumbs flexion excessively at
fingers (Fig. 8.19). interphalangeal joint when the patient attempts to pinch.
Sensory loss: Dorsal and palmar aspects of medial side of
CAUSES AND CLINICAL MANIFESTATIONS OF hand and half fingers.
ULNAR NERVE INJURY (MUSICIAN’S NERVE)
Lesion at the Wrist or Hand
Lesion at Elbow
Cause
Causes • Compression by ganglion.
• Entrapment of nerve in cubital fossa in heavy manual • Repeated occupational trauma.
workers.
Clinical Features
• Tordy—ulnar palsy occurs due to excessive carrying
Motor:
angle at elbow following previous malunited supra-
• Damage to nerve at wrist spares the dorsal branch so
condylar fracture of humerus.
that cutaneous sensations over dorsum of hand and
• Osteoarthritis elbow. fingers are spared.
Clinical Features • But lesion just proximal to wrist gives rise to sensory
1. Ulnar flexion of wrist aspect of hand and fingers alone along with weakness
2. Paralysis of flowers of terminal phalanges of the ring of all ulcer innervated intrinsic hand muscles (Fig. 8.20).
and ulnar finger (flexor digitorum profundus). • Right upper brachial plexus birth injury leading to right-
3. Muscles of hypothenar eminence (is abductor flexor sided Erb’s palsy. There is a paralysis of shoulder
and opponens minimi digiti) are paralyzed. abduction, external rotation of the arm, and paralysis of
4. Abductor pollicis muscle it also affected. forearm supination leading to a characteristic “porter’s
5. Palmaris brevis is also involved. tip” (or policeman’s tip) position of the right hand.
6. Involvement of all interosseous and inner two lumbricals Difficult delivery is a common cause of acute injury to
involvement results in claw hand deformity (i.e. peripheral nerves.
Table 8.34: Differences among myelopathy, neuropathy and myopathy
Myelopathy Neuropathy Myopathy
Age Any age Any Age Childhood
Tingling and Rare Present Never seen
numbness
Bladder and Occurs Usually absent Never occurs
bowel affect
Atrophy and Only atrophy Only atrophy Both present
pseudoatrophy
Bilaterally May be Usually Yes
symmetrical
Cranial nerve None GBS, Diphtheria Yes, 7th n affec-
involvement ted in some
Girdle-like Present Absent Absent
sensation
Sensory Upper level seen Stock and glove No sensory
involvement change seen
Motor According to Distal Proximal
involvement level of
involvement
occur
Tone Spastic Hypotonia Hypotonia
Deep reflexes Exaggerated Lost Normal
Plantar Extensor Flexor or no Flexor
response
Confirmation Myelography N.conduction EMG
Fig. 8.19: Branches of median nerve studies
Central Nervous System 219
Hypertrophy of Muscles
sign is the occurrence of regular, rhythmic contractions of in Table 8.39. Spasticity in the upper limb is frequently
a muscle subjected to sudden, maintained stretch. Ankle more obvious in attempted extension; whereas in
clonus is a typical example. This is initiated by brisk. the lower limb, it is more obvious with attempted
maintained dorsiflexion of the foot, and the response is flexion.
rhythmic plantar flexion at the ankle. The stretch reflex b. Rigidity: Refers to sustained resistance to passive
inverse stretch reflex sequence described above may movements. It is more frequently encountered in
contribute to this response. However, it can occur on the patients with Parkinson’s disease (who have other
basis of synchronized motor neuron discharge without golgi manifestations of this disorder such as bradykinesia,
tendon organ discharge. The spindles of the tested muscle tremor, gait and postural abnormal). The rigidity may
are hyperactive and burst of impulses from them discharge be of lead type or the cogwheel type.
all the motor neurons supplying the muscle at once. The 2. Hypotonia: In the upper limb, the hypotonia is evident
consequent muscle contraction stops spindle discharge. from the posture of the outstretched hands, with slow
However, the stretch has been maintained, and as soon as flexion at wrist and extension of the fingers (dinner fork
the muscles relaxes, it is again stretched and the spindle deformity). It is a feature of LMNL, cerebellar disorders
stimulated. and in chorea. The causes of hypotonia are described in
Although a few beats of clonus are present in some Table 8.39. It is associated with hyporeflexia, muscle
normal people, sustained clonus indicates damage to the wasting and paresis. Hypotonia is also seen transiently
upper motor neurons and is a sure-shot neurological sign. in the initial phase following capsular cerebrovascular
accident in which the plegic (weak) limb is atonic prior
Examination of Tone to becoming spastic and hyper-reflexes.
Clonus: Described earlier.
The patient is asked to relax the muscles. Then the examiner
Dystonia: The patients maintain posture at extreme of
passively flexes and extends each joint in turn, slowly at
movement with contraction of agonists and antagonists.
first and then more rapidly to get a feel of muscle tension.
Percussion myotonia: It is demonstrated when a muscle
In the upper extremities the muscle tone is tested at shoulder,
dimples following percussion with patellar hammer. Most
elbow joint and wrist joint and in the lower limbs, by
commonly seen in abductor pollicis brevis.
internally and externally rotating the resting leg and by briskly
raising the patient’s knee off the bed and observing whether Table 8.38: Tests
the ankle is also raised off the bed. Tests Normal Hypotonia Hypertonia
Palpation of muscles Normal Flabby Rigid
Examination of Knee Clonus Posture of limb Normal Limp Stiff
Resistance to passice Normal Decreased Increased
The examiner sharply pushes the patella towards the foot
movements
while the patient lies supine and relaxed with knee extended Range of passive Normal Increased Decreased
following the initial jerk, exert sustained pressure with the movements
thumb and index finger in a downwards direction on the
patella. Table 8.39: Causes of hypertonia and hypotonia
Hypotonia Hypertonia
Examination of Ankle Clonus
Lower motor lesion Upper motor lesion
The examiner supports the flexed knee with one hand in the Cerebellar lesion Extrapyramidal lesion
popliteal fossa so that the ankle rests gently on the bed. Rheumatic chorea Hysterical
Using the other hand briskly dorsiflex the foot and sustain Hysterical Tetanus
Posterior column lesions tabes dorsalis Strychnine poisoning
the pressure. Deep sleep
Abnormal Findings Drugs—anesthetic, sedatives, hypnotics
Hypokalemia
1. Hypertonia: Manifests itself as rigidity or spasticity. Hypercalcemia
a. Spasticity: Characterized by increased resistance
during the first few degree of passive movements; REFLEXES
and as the movement is continued, the resistance
suddenly decreases. It is a feature of UMNL and is Testing of Reflexes
usually associated with increases deep tendon The term reflex is derived from a Latin word “reflexus”
reflexes, clonus, an anterior plantar reflex and typical meaning “bend back”. Reflex is an involuntary response to
pattern of weakness. Causes of hypertonia are given stimulus (an involuntary action) (Fig 8.22). Reflexes are
222 Essentials of Clinical Medicine
Polysynaptic Reflexes
(Withdrawal Reflexes)
They are those reflexes in which there are many synaptic
connections between afferent and efferent neurons. Such
complex pathways (reflex pathways) including the rever-
berating circuits are common in the brain and spinal cord.
Fig. 8.26: Jandressik’s maneuver Other complex of polysynaptic reflexes are chelo-minal
and cremasteric reflexes.
knee jerk reflexes do not elicit without applying Definition
reinforcement (also called Jandressik’s maneuver).
It is a type of polysynaptic pathway that occurs in response
In this, the patient is asked to perform strong voluntary
to a various or painful stimuli.
muscular effort with the upper limb; for instance, he is
The withdrawal reflex is a protective reflex, as the “flexor
made to hook the fingers of the two hands together and
responses” can be produced either by non-damaging
then pull them against one another as hard as possible or he
stimulation of skin or by stretch of the muscle, but strong
may be asked to clench fist with the ipsilateral hand.
flexor response with withdrawal are produced only by
Mechanism of action of the reinforcement maneuver is to
nociceptive stimuli. Therefore, while the stimulated limb is
increase the excitability of alpha-motor neurons and to
withdrawn to get away from the source of stimulus, the
increase the sensitivity of the muscle spindle primary sensory
ending to stretch (by increased gamma-efferent drive). extension of other limb supports the body.
• Cremasteric
• Gluteal and
• Plantar reflexes
or on center in the medulla; for example:
• Conjuctival and corneal
• Pupillary
• Palatal reflexes.
Superficial reflex is induced by a very light stimulus, such
as stroking the skin gently with a soft cotton wad.
Deep Reflexes
The reflex caused by the stimulation of parts beneath skin,
such as tendon or bone.
For example:
• Elbow
• Wrist
• Triceps
• Biceps Fig. 8.27: The figure of “8” position (Patient in supine position on
• Knee bed). It is the best position of body in which all the reflexes (both
• Ankle jerk reflexes (Fig 8.28) superficial and deep) can be beautifully elicited
(courtesy: Dr Kumar Saurabh Gaur)
Some Special Points Contd...
1. May be extensor bilaterally. This is a normal response in tially flexing the quadriceps muscle
infants. However, unilateral extensor plantar response knees and supporting
is definitely pathological. them with the hands
in the supine position
2. The deep tendon reflexes are elicited in older children Ankle Sciatic nerve Tap the tendo-Achi- Plantar flexion of
by tapping at specific points/sites with the help of a (S1-2) lles after partially the ankle and visi-
hammer. In infants and younger children the reflexes flexing the knee and ble contraction of
are elicited with the finger or the edge of diaphragms of externally rotating the gastroenemius
stethoscope instead of hammer. the leg. muscle
Table 8.40: Deep tendon reflexes and their Table 8.41: Superficial reflexes and their methods of elicitation
mode of elicitation
Superficial Method of Response
Reflex Nerve and Elicitation Response reflexes elicitation
spinal level Plantar reflex*(S1) Stroke the lateral Normal response is
Biceps Musculocutaneous Tap the biceps ten- Further flexion of border of the sole of plantar flexion of all the
(C5-6) don after partial the elbow and the foot from the toes. In pyramidal lesions
flexion and prona- visible contraction heel to the toes there is dorsiflexion of the
tion of the elbow of the biceps muscle big toe with fanning of
Triceps Radial (C7-8) Tap the triceps ten- Extension of the the others toes.
don just above the elbow and visible Abdominal reflexes Stroke the skin of the Contraction of the abdo-
elbow after flexing contraction of the (D6-12) abdomen from the minal muscles of the same
the elbow above the triceps muscle lateral end towards side of stimulation.
chest the midline
Supinator Radial (C7-8) Tap the brachio- Further of the knees Cremasteric reflex Stroke the skin of the Contraction of cremas-
radialis tendon at and visible contra- (L1,2) medial side of the teric and elevation of the
the lower end of the ction of the quad- thigh from above testicle on the stimulated
radius after partial riceps muscle downwards side.
flexion and pro- Anal reflex (S4-5) Stroke the skin in the Contraction of the anal
nation of the elbow perianal region sphincter
Knee jerk Femoral (L3-4) Tap the quadriceps Extension of the
tendon just below knees and visible * In infants less than 2 years of age, the plantars may be extensors
the knee after par- contraction of the bilaterally. This is a normal response in infants. However, unilateral
extensor plantar response is definitely pathological.
Contd...
Central Nervous System 227
Contd...
228 Essentials of Clinical Medicine
Contd...
Reflexes How elicited Response Afferent path Center Efferent path
Visceral reflexes
a. Pupillary reflexes:
1. Light (direct) Shining of light Constriction of pupil Cranial II Midbrain Cranial III
on retina in one eye on that side
2. Light (indirect Shining of light on Constriction of pupil Cranial II Midbrain Cranial III
or consensual) retina in one eye on other side
3. Accommodation Subject looks on finger Constriction of pupil Cranial II Occipital Cranial III
held in front of one eye in that eye cortex
4. Ciliospinal Pinching of skin on back Dilatation of pupil Sensory Th-1,2 Cervical
of neck nerve sympathetic
b. Oculocardiac Pressure over eyeball Slowing of heart and fall Cranial V Medulla Cranial X
with thumb in blood pressure
c. Carotid sinus Pressure over carotid Slowing of heart and fall in Cranial IX Medulla Cranial X
reflex sinus on one side blood pressure
d. Bulbocavernosus Pinching dorsum of glans Contraction of bulboca- Pudendal S-2,3,4 Pelvic
penis vernosus autonomic
e. Sphincter Distension of bladder Emptying of bladder or Pudendal S-2,3,4 Pudendal and
reflexes or rectum rectum autonomic
7. When there is a loss of reflex alone without any other • Gordon’s reflex, press tendon Achilles.
pathology, it indicates radioculopathy of that segment. • Chaddock’s on lateral border of feet.
8. Symmetrical (bilateral) loss of reflexes may show in
isolated or generalized peripheral neuropathy. Absent Abdominal Reflex
9. While eliciting Hofmon’s sign, the thumb will flex
Obesity, previous abdominal operations or frequent
excessively if there is hyper-reflexia.
pregnancy, age, a pyramidal tract involvement above of that
10. Inverse stretch reflex may be seen with combined
spinal cord and root pathology (myeloradiculopathy) level or a peripheral nerve abnormality.
11. Crossed extensor reflex may be seen in spinal cord
lesion; for example, the elicitation of knee jerk on one Conclusions Drawn from the Babinski’s Sign
side may produce reflex response on the contralateral • Flexion of all toes—flexor plantar response—Babinski’s
side. sign negative—normal.
12. If the abdominal reflexes easily get fatigued in a young • Extension of hallux and spreading of other toes—
person, then it may be a sign of early pyramidal extensor plantar response—Babinski’s sign positive.
disease. The reflexes may not be elicited in patients • Extension of hallux, extension of other toes and flexion
who are very fat (obese), after multiple pregnancies, of ankle—withdrawal response, repeat more gently or
after repeated or major abdominal surgery or in very
try alternative stimuli.
tense patients who cannot relax their abdominal
• No movement—indicating no response
muscles.
• Babinski’s sign positive—upper motor neuron lesion
13. In case of corneal reflex, elication, if there is VIIth n
lesion, then there is no response from paralysed side • Babinski’s sign negative—normal
but there is blink reflex from the normal side. • No response—may occur with profound upper motor
neuron weakness (toe unable to extend), may occur if
Wartenberg’s Sign there is a sensory abnormality interfering with the
afferent part of reflex.
The patients hand is held by the examiner in supinated • Common mistake —the examiner should not place too
position and the fingers of the patient and examiner are much weight on the plantar response in isolation. A
interlocked. Both of them are then made to flex the fingers
negative Babinski’s sign may be found in upper motor
against each other’s resistance. Normally, the thumb and
neuron lesion (UMNL). A positive Babinki’s which
terminal phalanges may bend slightly. In pyramidal tract
surprises an examiner needs to be interpreted with
lesion, the thumb adducts and flexes strongly. It may be
taken as an equivalent of Babinski’s sign in case of caution, could it be a withdrawal response?
amputation of both the lower limbs.
Alternative Stimuli
Supinator Reflex • Stimulion lateral aspects of foot—Chaddock’s reflex
A misnomer for this reflex because the muscle involved is • Thumbs and index finger run down the medial aspect
brachioradialis. of the tibia—Oppenheim’s reflex
fingers involuntarily reflex slowly and group the object/ N.B. Reflexes can be absent in the early stages of severe
finger. It is seen in contralateral frontal lobe lesion. upper motor neuron lesion—‘spinal shock’.
2. Groping reflex: When an examiner shows an object to • An inverted reflex—the reflex tested is absent, but there
the patient (or touches the object on the hands of the is spread to a lower level. The level of the absent reflex
patient) and then takes the object away from the patient indicates the level of the lesion. For example, a biceps
on seeing or feeling the object, tries to catch (or grope) reflex is absent but produces a triceps response. This
it is seen in contralateral frontal lobe lesion. indicates a lower motor neuron lesion at the level of the
3. Palmomental reflex: On stroking the skin of flexor absent reflex (in this case C5) with upper motor neuron
examiner of the hand, of the patient, with a blunt object lesion below indicating spinal cord involvement at the
(such as back of the hammer), a sort of puckering of level of the absent reflex.
the skin over the chin on the same side is produced by • Pendular reflex—this is usually best seen in the knee
the contraction of the ipsilateral mentalis muscle. jerk where the reflex continues to swing for several
4. Sucking reflex: When the angle of the mouth or borders beats. This is associated with cerebellar disease.
of lips of the patient is touched with the examiner’s • Slow relaxing reflex—this is especially seen at the ankle
index finger, an involuntary opening of mouth occurs, reflex and may be difficult to note. It is associated with
as if the patient is trying to suck the finger. hypothyroidism.
5. Snout reflex: On keeping a finger on the upper lip and
tapping lightly over it causes puckering and protrusion COORDINATION
of the lips.
Introduction
6. Glabella tap reflex: When the examiner gives a tap over
the glabella (root of the nose) of the patient repeatedly A coordinated combination of a series of motor actions is
with his index finger, (from above and behind the patient’s needed to produce a smooth and accurate movement. This
head), the patient is seen to blink his eyes with each tap. requires integration of sensory feedback with motor output.
Normal individuals respond by blinking to the first 2 to This integration occurs in cerebellum.
3 taps and then there is no response. It is seen in The coordination of groups of muscles is a function of
parkinsonism and diffuse degenerative disease of the various factors, such as efferent impulses coming from the
brain. muscles and joint receptors, cerebellar function and
corticospinal tract function.
MOTOR SYSTEM REFLEXES In the pressure of weakness, tests for coordination must
be interpreted with caution and are unlikely to be informative
Further Maneuvers if there is significant weakness.
Demonstration of Clonus Loss of joint position sense can produce some incoordi-
At the ankle: Dorsiflex the ankle briskly, maintain the foot nation (sensory ataxia). This is made more worse when the
in that position, a rhythmic contraction may be found. More eyes are closed. Joint position sense should be tested before
than three beats is abnormal. coordination. Sensory ataxia occurs typically in sensory
neuropathies posterior column lesions, when position sense
At the knee: With the leg straight, take the patella and bring is impaired in the legs. Proximal weakness of muscle may
it briskly downwards; a rhythmic contraction may be noted. be seen in cerebellar ataxia, but this can usually be recognized
Always abnormal. easily by testing of muscular strength.
INTERPRETATION Testing the Coordination
Increased reflex or clonus—this indicates upper motor 1. Testing the gait: (See section for “GAIT”) Expect the
neuron lesion above the root at that level. right hand to be slightly better (in a right-handed person.)
• Absent reflexes: 2. a. Testing the coordination in the arms: The patient is
– generalized—indicates peripheral neuropathy. asked to hold his arms outstretched and to close his
– isolated—indicates either a peripheral nerve or, more eyes. Ask the patient to maintain this position. Then
commonly, a root lesion. push his arm up or down suddenly. In normal person,
• Reduced reflexes (more difficult to judge)—occurs in a the arm will again regain the original position; whereas
peripheral neuropathy, muscle disease and cerebellar in case of abnormalities of coordination, this may
syndrome. not be so.
Central Nervous System 231
Interpretation: The arm oscillates several times before (which requires greater coordination). There complex
coming to rest which indicates cerebellar disease. If and practiced everyday movements offer very
they return rapidly to normal position—normal sensitive way of assessing the coordination.
b. Finger-nose test: Hold your finger out about an arm’s 3. Testing the coordination in the legs:
length in front of the patient. Ask him to touch your a. Heel-shin-ankle test: The patient is made to lie down
finger with his index finger and to touch his nose supine ask him to lift his leg and place the point of
with the sense finger. When he has done this his heel on his knee and then run it down the sharp
correctly, ask him to repeat this faster. part of his shin (Fig. 8.29).
Interpretation: The patient is able to complete the Common mistake: Allow the patient to run his instep
task quickly, accurately—normal along his shin.
• The patient develops a tremor as his finger Interpretation:
approaches its target—intention tremors; finger • Disorganization of movement with the heel falling
overshoots the targets—past pointing or off the anterior part of the skin, knee falling from
dysmetria. side to side.
• Coordination of fingers in rapid movements (e.g. • In cerebellar ataxia, a characteristic, irregular,
rapidly touching each finger in turn with the side to side series of errors in the speed and
thumb, or the thumb and index) are specially direction of movement occurs. The test should
useful tests. In cerebellar ataxia, the error of also be performed with the eyes open.
movements tend to occur at light angles to the b. Making circle in air: The patient is asked to draw a
intended direction of movement. In anxious large circle smoothly and accurately, with the help
subjects, errors tend to occur in direction of of leg.
movement itself. Interpretation: In cerebellar ataxia, the movements
c. Repeated movements: The patient is asked to pat one are generally “squared off” irregularly.
hand on the back of the other quickly and regularly. Note: The finger-nose test and heel-shin test can be
(The examiner should first demonstrate this to the used as an indication of loss of joint position sense.
patient.) The movements are accurate but when repeated with
• The patient is asked to twist the hand as if opening the eyes closed, are substantially worse. This
a door or unscrewing a light bulb (demonstrate). indicates impairment of joint position sense (JPS).
• The patient may be asked to tap the back of his c. Rhomberg’s sign: This test is used to diagnose the
right hand alternately with the palm, and then loss of position sense (sensory ataxia) in the legs,
back of his left hand. Repeat with right hand not of cerebellar function.
(demonstrate).
Interpretation:
• Disorganization of the movements of the hands
and elbows taking wide excursions than expected,
irregularity of the movements which are
performed without rhythm. Compare the two
sides—these changes indicate cerebellar
incoordinations often the abnormal is heard as a
slapping sound rather than normal tapping noise.
• Mild upper motor neuron weakness would impair
fluency of the fast repeated movement, but the
movements will not be of wide excursion or
irregularly.
• When there is disorgainsation of tapping the hand
and then turning it over, this is referred to
dysdiadochokinesia.
d. Watch the patient while he is dressing or undressing,
handling an object or doing some fine type of work. Fig. 8.29: The heel-shin test
232 Essentials of Clinical Medicine
In this test, the patient is asked to stand with his hand and may hit his own face; whereas in normal
feet close together, and to maintain this posture with individuals, it does not happen so.
his eyes closed. c. Dysmetria: The patient is asked to close his eyes and
If the patient begins to sway (or may fall) then hold his one upper lower limb in particular position.
Rhomberg’s sign is said to be positive. In case of Then he should put other limb in the some position.
defective position sense in the legs (as seen in sensory The patient is unable to do so because of the inability
of judgment of the range of movements.
neuropathy or tabes dorsalis), the patient is unable
(The term dysmetria has been derived from the
to stand without visual fixation. The same is the case Greek words, dye meaning bad and metron meaning
with labyrinthine lesion with cerebellar ataxia. If a measure. Thus, dysmetria is the inability to fix the
person has labyrinthine lesion, he suffers from range of movement in a muscular activity. Rapid
positional nystagmus and in cerebellar ataxia there is and brusque movements are made with more force
ataxia (defective muscular coordination), especially than necessary. Dysmetria is due to cerebellar lesion).
that manifested when voluntary muscular move- d. Pointing and past pointing test: The patient is first
ments are attempted) of limbs. Another confirmative asked to touch the examiner’s finger (held at a
test that whether Rhomberg’s sign is due to distance from the patient) by his own finger. He is
labyrinthine disease is to ask the patient to jump then made to repeat this action twice or thrice. The
quickly up and down on both feet with his legs kept patient is made to close his eyes and made to perform
together, hands outstretched and eyes closed the same action keeping the examiner’s finger at the
(Unterberger’s test) if the patient has any labyranthine fixed position.
In case of cerebellar lesion, the finger of the
lesion (or disease), he will gradually progress across
patient past points the examiner’s fingers (on the
the floor, or fall to one side, the side of labyrinthine
affected side).
leision. e. Barony’s pointing test: The patient is made to fully
d. Tendem walking test: In this test, the patient is made outstretch his both upper limbs and set parallel to
to walk along a straight line by placing the heel of each other. In cerebellar lesion/disease the patient is
one foot immediately adjacent to the toe of the one unable to keep his hands (arm) parallel to each other,
behind. A patient with ataxia (in coordination) is rather the ipsilateral limb will deviate outwards. He
unable to do so and will or deviate towards the is then made to close his eyes and asked to bring his
affected side (in case of unilateral cerebellar arm to the same original position again. It is found
diseases). In case of bilateral or midline cerebellar that he is unable to do so on the affected side.
diseases his gait will be drunken and patient will sway f. Merry-go-round test: In this the patient is made to
to either side. go round a chair are for some time. In case of
e. Toe finger test: The patient is made lie in the supine unilateral cerebellar disease, the patient will come
position, he is then asked to lift his toe and touch it nearer and nearer to the chair if the affected side is
towards the chair. This is called centripetal type.
to the examiner’s finger held at some distance.
And if the affected side is on the opposite side, the
Interpretation: In case of cerebellar lesions there will
patient will move in circles of increasing diameter
be overshooting of leg with incoordination. The (wide and wide). It is called centrifugal type of merry
patient will not be able to perform the test in posterior - go-round test.
column lesions with his eyes closed. g. Pointing in a circle test: In this test, the examiner
4. Special tests for in coordination: (showing cerebellor draws a circle on paper (usually of 1 cm in diameter)
involvement) and the patient is made to mark dots within the circle.
a. Dysdiadochokinesis of adiadochokinesis: In case of In any ataxia, the patient will spread the dots
cerebellar involvement, the patient will either show irregularly over a wide area, outside as well or inside
dysdiadochokinesis or adiadochoikinesis (i.e. inability the circle.
to perform repetitive alternative movements quickly). h. Coordination testing of the trunk: Ask the patient to
b. Rebound phenomenon: The patient is asked to flex sit up from the lying position without using hands.
his forearm at the elbow and to pull his forearm Observe whether he falls on one side.
against the resistance affixed by the examiner. The Interpretation: The patient is unable to sit from lying
examiner then, suddenly releases the forearm. In case position without falling to one side—truncal ataxia.
of cerebellar lesion, the patient is unable to stop his It is usually associated with gait ataxia.
Central Nervous System 233
GAIT
Gait is defined as the manner of walking. The examination of the patient’s gait is of great importance in the diagnosis of
the neurological disease process. Gait is a coordinated action requiring integrations of sensory and motor function.
Various types of gait disorders are: hemiplegias, parkinsonism, marche a petits pas, ataxic unsteady gait. In order to test
the gait, the patient is made to walk and while doing so his lower limbs should be adequately exposed. The examiner
should also make the patient to walk on a straight line while the patient has a walk, the examiner should look out for
certain things like “Is the patient able to walk? Does he need any assistance from somebody? Is he able to walk on a
straight line? Whether the patient feels that he may fall while walking and on which side (this may provide hint for the side
affected)?
While investigating the underlying causes of an abnormal gait, the examiner should try to rule out the local causes like
osteoarthritis, pain in the leg or pelvis.
Table 8.46: Causes of unilateral gait defects and bilateral gait defects
Unilateral Bilateral
Hemiplegic Spastic
High stepping Scissor
Limping Ataxic
Hysterical Toppling
Festinant Waddling
Jaunting Stamping
Contd...
Gait How the patient walks? Interpretation
2. Marche a petit pas (Russian The gait resembles to the rapid steps of Bilateral diffuse cortical dysfunction.
Ballet Master) ballet dance on points. Common causes are: Diffuse cerebrovascular
disease “Lacunar State”.
3. Scissoring spastic gait The gait is such that the legs of the patient UMNL accompanied by spasticity. Common
Bipyramidal gait (involving cross in walking. It is due to bilateral adductor causes are: Cerebral palsy, multiple sclerosis,
both the lower limbs) spasm and weakness of dorsiflexors of legs. cord compression.
4. Sensory ataxic gait or Patient usually walks looking down to the Indicates loss of joint position sense (JPS)—
stamping gait ground or to his feet all the time, as if he has Rhomberg’s positive. Common causes are:
fear of falling down. He may show slight Peripheral neuropathy, posterior column loss
swaying movements. He shows stamping gait (tabes dorsalis)
or legs are raised too high and thrown
outwards waved about before bringing them
down in a stamping fashion. The heel come
in contact with the ground first.
5. Cerebellar ataxia or Patient walks on a broad base, the feet planted Common causes—drugs (e.g. phenytoin)
drunken or reeling gait or widely apart, and placed irregularly. Ataxia is alcohol, multiple sclerosis, cerebrovascular
ataxic gait equally severe whether the eyes are open disease.
or closed. Other signs of cerebellar disease
are usually present.
The patient walks in a zig-zag manner, and
sways on any side in reeling or staggering
fashion. This gait is also seen in patient with
Friedreich’s ataxia and multiple sclerosis.
6. Waddling gait The body is often lifted backwards (walking A feature of proximal pelvic girdle muscular
like a duck) with an increased lumbar lordosis, weakness especially of myopthies and
the feet are placed rather widely apart and the muscular dystrophies. Common causes are:
body sways from side to side. As each step is Lordosis, congenital bilateral dislocation
taken weakness of glutes, especially gluteus of hip (CDH)
medius, causes the hip to drop when the
affected leg is held off the ground in erect
posture accept Trendelenburg’s position.
7. Apraxic gait Loss of concept of walking, often associated Indicates that cortical integration of the
with tiny rapid steps. movement is abnormal, usually with frontal
lobe pathology. Common causes are normal
pressure, hydrocephalus, cerebrovascular
disease
8. Hemiplegic gait While walking, the patient drags his foot Unilateral UMNL. Common causes are stroke,
on the affected side. The resultant multiple sclerosis, hemiparesis.
obstruction to walking is avoided by
throwing the whole leg outwards from the
hip with bending forwards the opposite
side circumduction of leg to clear the
ground. Arm is flexed across the body and
does not take part in normal walking
movements. The affected arm is adducted
at the shoulder and flexed at the elbow,
wrist and fingers.
9. Foot drop or high The patient raises the foot high in order to Common causes are:
stepping gait overcome the foot drop and on keeping the a. Unilateral: Common peroneal palsy. Pyramidal
Contd...
Central Nervous System 235
Contd...
Gait How the patient walks? Interpretation
foot down the toe hits the ground first. lesion L5 radiculopathy. b. Bilateral: Peripheral
There is not ataxia. neuropathy.
10. Functional gait It is variable, may be inconsistent with rest —
of the examination worse when watched.
May be mistaken for gait in chorea (esp.
Huntington’s disease), which is shuffling,
twitching and spasmodic and has associated
findings on examination. It is usually asso-
ciated with hysteria. The patient does not fall.
11. Gait in chorea dystonia In chorea of any etiology the patient has a In disorders of chorea.
wide based, lordotic gait in which he lurches
from side to side on his heels and has
tendency to fall. In chorea and hysteria the
involuntary movements are usually exag-
gerated during walking, and unusual foot
placement responses may occur so that the
toes may extend away from the floor (avoiding
response) or the feet may appear glued to the
floor (grasping response).
Extrapyramidal Syndromes
• Parkinson’s disease
• Dystonia
Fig. 8.30: Figure showing various types of abnormal gaits • Involuntary movements
236 Essentials of Clinical Medicine
syncope or drop attack. They walk pushing one foot forward Pin prick
while leaning right back on other. The arms are held at 90° Temperature } Spinothalamic tract Small fiber
Central Nervous System 239
Figs 8.34A to D: Sensory loss in the leg: A. Lateral cutaneous nerve of the thigh;
B. Common peroneal nerve; C. Femoral nerve; D. Sciatic nerve
Sense of Joint Position gradually reduce the angle moved until errors are made.
Test distal joints first and move more proximally.
With the patient’s eyes open, show him what you are going
to do. Hold the distal phalanx between your two fingers Joints to be tested in the arm: Distal proximal interphalangeal
Ensuring that your fingers are at 90º to the intended direction joint, middle proximal interphalangeal joint, metacarpal
of movement, move the digit, illustrating which is up and phalangeal joint, wrist, elbow, shoulder.
which is down. Joints to be tested in the leg: Distal interphalangeal joint,
Procedure: Ask the patient to close his eyes; move the toe metacarpal phalangeal joint, ankle, knee and hip. N.B.
up and down. Start with large movements in either direction; Romberg’s test is a test for joint position sense (Fig. 8.35).
Central Nervous System 241
Light Touch
A piece of cotton wool is generally used. Some people prefer
to use a fingertip. Try to ensure a repeatable stimulus. Avoid
dragging it across the skin or tickling the patient.
Explanation: With the patient’s eyes open show him that
you will be touching an area of skin. Ask him to say ‘yes’
every time he is touched.
Procedure: Ask the patient to close his eyes, test the areas
as for pinprick, apply the stimulus at random intervals.
Caution: This is done by noting the timing of the response
to the irregular stimuli. Frequently, a pause of 10 to 20
seconds may be useful.
Temperature Sensation
It is usually adequate to ask a patient if the tuning fork feels
cold when applied to the feet and hands.
Bed Side Easy Testing
Fill a tube with warm water and cold water. Ideally, these
Fig. 8.35: Testing the joint position sense (JPS) are controlled temperatures though normally the warm and
cold tap is adequate. Dry both bottles.
Pin Prick Test Explanation
Use a pin, a disposable neurological pin, dressmakers or ‘I want you to tell me if I touch you with the hot tube’
safety pin, not a hypodermic needle or a broken orange (touch unaffected area of skin with the cold tube). Apply
stick. If a hypodermic needle is used (to be discouraged), it hot or cold at random to hands, feet or an affected area of
must be blunted before use. Dispose of the pin after use. interest.
Stimulus should be of equal intensity every time. The random order allows assessment of concentration.
Explanation: Show the patient what you are going to do.
Other Modalities
Explain that you want him to tell you if the pin is sharp or
blunt. Touch an unaffected area with the pin and then touch The other modalities to be tested in sensory system
an unaffected area with the opposite blunt end of the pin. examination are as follows.
Procedure: Ask the patient to close his eyes then apply Two-Point Discrimination
randomly sharp and blunt stimuli and note the patient’s This requires a two-point discriminator—a device like a
response. blunted pair of compasses.
segmental innervation of S4 and S5 for sensory and motor • Normal > 90°, less in older patients
components. • Limitation with pain in back—nerve root entrapment.
Tests for Meningeal Irritation
Palpation of Nerves
i. Neck Stiffness
Causes of Thickening of Nerves
(Not to be performed if there could be cervical instability,
e.g. following trauma or in patients with rheumatoid • Leprosy
arthiritis). • Amyloidosis
• The patient should be lying flat. • Some hereditary neuropathies
• Place your hands behind the patient’s head. • Neuropathies
• Gently rotate the head—moving the head as if the • Recurrent variety of CIDP (chronic inflammatory
patient was indicating no. Feel the stiffness. demyelinating polyneuropathy)
• Gently lift the head off the bed—feel the tone in the • Refsum’s disease.
neck. Nerves Palpable in Leprosy
• Watch the legs for hip and knee flexion.
Interpretation 1. Ulnar nerve
• Neck moves easily in both planes, with the chin easily 2. Dorsal cutaneous branch of radial and ulnar n.
reaching the chest on neck flexion—normal. 3. Several n (behind lateral malleolus)
• Neck rigid on movement—neck stiffness 4. Greater auricular n
• Indicates: meningeal irritation—common causes: viral 5. Lateral popliteal n.
and bacterial meningitis, subarachnoid hemorrhage—
rarer causes: carcinomatous, granulomatous, fungal HEMIPLEGIA
meningitis. Past History in Hemiplegia
• May also occur in : severe cervical spondylosis,
parkinsonism, with tonsillar herniation • Similar attacks with full recovery indicate TIA.
N.B. proceed to test for Kernig’s sign. • Head injury with waxing and wanning neurologic deficit
• Hip and knee flexion in response to neck flexion— indicate subdural hematoma.
Brudzinski’s sign. This indicates meningeal irritation. • History of exposure to STD during young age and
Hint: Cervical lymphadenopathy and severe adulthood hemiplegia after a few decades suggest
pharyngitis may simulate neck stiffness—but neurosyphilis.
stiffness is usually only on flexion and appropriate • Hypertensive history suggests cerebral thrombosis and
physical signs of these pathologies are easily found. hemorrhage.
• Diabetes history suggests accelerated atherosclerosis and
ii. Testing for Kernig’s sign
hypertension.
• The patient is lying flat on the bed.
• Past history of rheumatic fever with valvular heart
• Flex the leg at the hip with the knee flexed.
disease suggests cerebral emboli.
• Then try to extend the knee
• With epilepsy and migraine in past history, think of Todd’s
• Repeat on the other side
palsy, which recovers in 24 hours.
Interpretation • With past history of TB arteritis, TB meningitis and
• Knee straightens without difficulty—normal tuberculoma.
• Resistance to knee straightening—Kernig’s sign : • History of oral contraceptive pill use for more than
indicates meningeal irritation or, if unilateral, may 5 years may predispose to stroke in females.
occur with radiculopathy (cf straight leg raising). • Anticoagulant therapy and stroke occurring simul-
N.B. Kernig’s sign is absent with other causes of taneously think of cerebral hemorrhage.
neck stiffness. • Fever in hemiplegia suggests meningitis, cerebral abscess,
iii. Straight leg raising test encephalitis, leukemia, lymphoma.
Test for radicular entrapment: • Pain in chest with recent or past myocardial infarction
• With the patient lying flat on the bed, lift the leg, can get embolic stroke from mural thrombosis.
holding the heel. • Intermittent claudication suggests atherosclerosis.
• Note angle attained and any difference between the • History of severe headache in subarachnoid and cerebral
two sides hemorrhage.
246 Essentials of Clinical Medicine
– Myelodysplasia of lumbosacral cord flexion is said to occur with the damage to reticulospinal
– Friedriech’s ataxia tract and vestibulospinal tract. Reflux evacuation of bladder
– Birth injuries and bowel occurs. Mass reflex may be present.
– Primary muscle atrophy
– Marasmic child Table 8.54: Causes of lower motor type of paralysis
– Thrombosis of superior sagittal sinus Ant. horn Polio/Motor neuron disease
• Old age –MND Ant. root, post root, and post Radiculitis—cervical / lumbar
– Neoplasm ganglions spondylosis
• Middle age—Pott’s disease Peripheral nerve, myoneural Herper zoster
junction, muscle.
Diabetic, alcoholic, beri-beri,
Table 8.53: Causes of paraplegia leprosy
Gradual onset Acute onset Myasthenia gravis, myopathy.
With longer duration of paraplegia, there is flexor spasms Three Main Components of
occurring spontaneously. It is called paraplegia in flexion. Parkinson’s Disease
This carries poor prognosis. Even a surgical intervention to • Tremor
remove a spinal cord tumor is attempted, paraplegia will • Muscular
not improve. Neurological defect persists. Paraplegia in • Hypokinesia (Bradykinesia).
250 Essentials of Clinical Medicine
Parkinsonism Plus Syndrome Table 8.58: Myasthenia gravis and myasthenic syndrome
When the symptoms of parkinsonism are present along with Myasthenia gravis Myasthenic syndrome
the following disorders, it is called parkinsonism plus Sex Female Male
Age Young and middle age Old age
syndrome. These disorders are: Muscle affected Ocular, facial, bulbar, Pelvic girdle, proximal
• Shy-Drager syndrome proximal muscles muscle of neck, middle
• Wilson’s disease (late) trunk
• Huntington’s chorea Etiology Antibodies against Defective release of acety-
muscle endplate lcholine from terminals
• Steele-Richardson-Olzewik syndrome Muscle power on Deteriorates Increases
• Progressive supranuclear palsy exercise
• Normal pressure hydrocephalous Treatment Anticholinergic drugs Removal of tumors,
• Striato niagral degeneration. quinidine hydrochloride
20-30 mg/kg/day in divided
Table 8.56: Differention between classical and doses
arteriosclerotic parkinsonism
Table 8.59: Distinguish between cerebellar and sensory ataxia
Classical parkinsonism Arteriosclerotic parkinsonism
Feature Cerebellar Sensory
1. No UMNL sign UMNL sign present
Lesion Cerebellum or its connec- Mainly of local reflexes
2. Onset is gradual Onset is acute, condition worsens
tion including vetibule
in between attackes
Muscle atrophy Absent May be present
3. Upper limbs affected first Gait and lower limbs affected first.
Tone Decreased Markedly diminished
4. Levo dopa improves the Effect of levo dopa is doubtful
Power Normal Usually decreased
condition
Contd...
Central Nervous System 251
Proximal muscle wasting and weakness are signs of 6. Peripheral nerve lesion
primary muscle disease except myotonic dystrophy, a. Hansen’s disease (especially hypothenar)
mitochondrial myopathy, inclusion body myositis and distal b. Carpal tunnel syndrome (especially thenar)
muscular dystrophy of Gower. c. Lead poisoning (wrist drop)
Predominantly Distal Muscle Wasting 7. Muscle diseases
a. Distal muscular dystrophy
a. Motor neuron disease b. Polymyositis
b. Syringomelia
c. Myotonia
c. Cervical cord tumors (affecting segmental levels C8-
d. Distal myopathy of Gower.
T1)
8. Disuse atrophy
d. Lesion of lower brachial plexus (Klumple’s paralysis)
a. Therapeutic immobilization (fracture)
e. Cervical ribs
b. Arthritic (RA)
f. Cervical glandular enlargement
c. Postparalytic (hemiplegia)
g. Pancoast syndrome (superior pulmonary sulcus
e. Volkmann’s ischemic contracture (tight improper,
tumors)
plaster application).
h. Traumatic lesions of radial, median and ulnar nerves.
i. Peroneal muscular atrophy (Charcot-Marie-Tooth
Muscle Wasting in Lower Limbs
syndrome or hereditary sensory motor neuropathy
types I and II) Isolated wasting of muscles in lower limb is less common
j. Peripheral neuropathies. than in upper limb. The wasting usually occurs in
Distal muscle wasting and weakness are signs of the combination with that of upper limb.
peripheral neuropathy except porphyric neuropathy,
Conditions Producing Wasting in Lower Limb
diabetic amyotrophy and Guillain-Barré syndrome.
a. Cauda equina lesion
Both Proximal and Distal Muscle Wasting b. Peripheral neuropathy
a. Motor neuron disease c. Peroneal muscular atrophy (Charcot-Marie-Tooth
b. Syringomyelia. syndrome or hereditary motor-sensory neuropathy types
Small Muscle Wasting of Hand (C8-T1) I and II)
d. Poliomyelitis
1. Vertebral lesions e. Peripheral nerve trauma (lateral popliteal nerve)
a. Craniovertebral anomalies f. Tarsal tunnel syndrome.
b. Vertebral metastasis
2. Spinal cord lesion Conditions Causing Wasting in
a. Syringomyelia Both Upper and Lower Limbs
b. Cord compression by tumor
3. Anterior horn cell lesion a. Peroneal muscular atrophy (Charcot-Marie-Tooth
a. Motor neuron disease syndrome or heriditary motor-sensory neuropathy types
b. Poliomyelitis I and II)
c. Spiral muscular atrophy b. Chronic polyneuropathy.
4. Root lesion c. Spinal muscular atrophy (Werdnig-Hoffman’s disease
a. Cervical spondylitis in childhood later stages of Kugelberg-Welander
b. Cervical cord tumor syndrome)
c. Cervical hypertrophic pachymeningitis d. Distal myopathy of Gower
d. Pancoast tumor e. Hansen’s disesase.
e. Peroneal muscular atrophy
f. Cervical disc prolapse HYPERTONIA
5. Brachial plexsus lesion
Definition
a. Cervical rib
b. Klumpke’s paralysis (avulsion of lower brachial Increased resistance to passive movements, a heightened
plexsus) salience of muscles and increased firmness on palpation.
256 Essentials of Clinical Medicine
Herniation or Coning
Coning is what occurs when part of the brain is forced
through a rigid hole—either:
1. The uncus and the temporal lobe through the cerebellar
tentorium (which separates the cerebrum from the
cerebellum)—uncal herniation row
2. The cerebrum is pushed centrally through the tentorium
—central herniation.
There is a characteristic progression of signs in both
types of herniation.
N.B. The signs of herniation are superimposed on top of
signs due to the supratentorial mass causing the coning and
are progressive.
Uncal Herniation
Fig. 8.44A to C: CT – TB in a patient with advanced AIDS. A woman
A unilateral mass forces the ipsilateral temporal lobe through with status positive for HIV was shown at autopsy to have bilateral
the tentorium compressing the ipsilateral third nerve and pulmonary infiltrates. (A) Extensive lymphadenopathy, (B arrows)
later the contralateral upper brainstem, and eventually and multiple lytic bone lesion, (B-C) (arrowheads)
260 Essentials of Clinical Medicine
the whole brainstem. Once CSF flow is interrupted, Table 8.62: Glasgow coma scale
the process is accelerated by an increase in intracranial Score
pressure. Eyes open
Never 1
Physical signs: To pain 2
• Early - Ipsilateral dilated pupil and signs of supra- To verbal stimuli 3
tentorial mass lesion Spontaneously 4
• Later - Ipsilateral hemiplegia Best verbal response
- Progressive ptosis and third nerve palsy No response 1
Incomprehensible sounds 2
- Cheyne-Stokes respiration
Inappropriate words 3
• Later - Tetraparesis Disorientated and converses 4
- Bilateral fixed dilated pupils Orientated and converses 5
- Erratic respiration Best motor response
- Death No response 1
Extension (decerebrate rigidity) 2
Progression is usually rapid
Abnormal flexion (decorticate rigidity) 3
Flexion—withdrawal to pain 4
Central Herniation Localizes pain 5
A supratentorial lesion forces the diencephalon (the thalamus Obeys commands 5
and related structures between the upper brainstem and 15
cerebral hemispheres) centrally through the tentorium. This
compresses first the upper midbrain, later the pons and The three categories of information required in the GCS
medulla. assessment require no special skills and are thus particularly
suited for special observations by relatively untrained staff.
Physical signs The GCS is much used in the manage-ment of head injury.
• Early - Erratic respirations This simple non-timers clinical rating scale enables relatively
- Small reactive pupils accurate assessment of improvement or deterioration in a
- Increased limb tone patient’s conscious state by physicians, nurses and ambu-
- Bilateral extensor plantars lance staff alike. The best score is 15, worst is 3, representing
• Later - Cheyne-Stokes respiration “none in” all the categories assessed. Abnormal extension
- Decorticate rigidity implies decerebrate posturing.
• Later - Fixed dilated pupils Look at the Patient
- Decerebrate posturing
This is best of ten done from the end of bed.
Progression usually slower. • Is the patient lying still or moving? If there is movement:
Terms used to Describe the Levels – Are all the four limbs moved equally?
of Unconsciousness – Is the patient lying symmetrically?
– Are there any abnormal movements?
Drowsiness, confusion, stupurous, coma lose, are in
everyday language and are used in different senses by Inference
different observers. It is, therefore, better to subscribe • Arms flexed at elbow and wrist and legs extended at
the level of consciousness individually in terms described knee and ankle
below: – Decorticate posturing
• Change in the level of consciousness and associated • Arms extended at elbow, promoted and flexed at wrist
physical signs are very important and need to be and legs extended at knee and ankle
monitored. Always record findings. – Decerebrate posturing
• The Glasgow coma scale (GCS) is a quick, simple, • Head falls to one side, with flexion of the arm
reliable method for monitoring level of consciousness. – Hemiparesis
It includes three measures—eye opening, best motor • Brief spasms, lasting less than a second, of arms or legs
response and best verbal response. – Myoclonus
Central Nervous System 261
Investigations to be Done in a Case of Coma Spinal reflex activity in response to peripheral stimulus
• Cervical spine X-ray (e.g. pressing the toe nailbed) is usually absent but may be
• CT head scan preserved in brain-death. EEG testing is not necessary to
• Chest X-ray diagnose brain death but usually shows a flat, isoelectric
• X-ray of suspected fractures/bruised limbs trace.
• Blood for cross-matching The brain death tests should be performed by two
• Check hemoglobin, hematocrit, WBC count experienced clinicians either together or separately. The tests
• Drug screen are then repeated, after an interval, prior to the declaration
• Electrolytes and liver function tests of brain death.
• Blood gases and pH.
THE AUTONOMIC NERVOUS SYSTEM (ANS)
Table 8.65: Important papillary signs The various components of autonomic nervous system
Abnormal features of pupil Suggestive of pupil includes—afferents, postganglionic sympathetic and para-
Bilaterally dilated and fixed pupil Bilateral 3rd nerve (owing to sympathetic neurons in the periphery, together with the
massive brain swelling and tentorial herniation or midbrain damage) central prepanglionic components of these systems in
and following ingestion of the intermediolateral cell columns in the spinal cord, and
anticholiner- gic drugs [e.g. magic rostal connections in the brainstem and cerebral hemispheres.
mushrooms, tricyclic antidepressants
The various important functions of ANS include—
(TCA)]
Unilateral fixed dilated pupil Ipsilateral intracranial mass lesion modulation of function in cardiovascular and gastro-
(e.g. spontaneous intracerebral intestinal systems, with temperature regulation, secured
hemorrhage, traumatic hematoma) reflexes, bladder and bowel control, detrusor and sphincter
causing a 3rd nerve palsy. control and pupillary and respiratory reflex control
Pinpoint pupil Pontine vascular lesions and
mechanisms.
after narcotic overdose.
Metabolic Pupils are normally reactive to light.
Clinical Features of Disorders of ANS
Unconscious patients are unable to fixate and will, • Postural hypotension
therefore, have roving “eye movements”. Not infrequently • Retention and incontinence of urine
the ocular access will not be conjugate. • Constipation, and fecal incontinence
Assessing the Brain Death • Importance and erective failure
Prior to testing for brain death, it is necessary that the cause • Poor urine stream (failure of detrusar muscles)
of irreversible brain damage has been established, (e.g. • Esphageal and gastrointestinal dysmotility
intracerebral hemorrhage, encephalitis), and that reversible • Immobility of pupils
conditions such as hypothermia, drug intoxication and • Snoring and sleep apnea
metabolic defects have been excluded. In patients who have • Impairment of sweating.
been previously neuromuscularly paralyzed, respiration of Rare syndromes like “program autonomic
normal neuromuscular function requires to be tested electri- failure” involves the degeneration of both pregonglionic and
cally by elicitation of deep tender jerks. Brain death post-ganglionic neurons which in turn results in various
can only be diagnosed in the absence of the following abnorma-lities of autonomic nervous system functioning
functions: such as:
• Pupil reflex to light • Incontinence of urine
• Corneal reflex • Constipation and other disorders of gastrointestinal
• Oculovestibular reflex using iced-water irrigation of the motility
external ear canal • Inability to maintain blood pressure in the erect posture
• Gag reflex (orthostatic hypotension)
• Cough reflex • Impotence
• Spontaneous respiration when Pa CO2 > 6.6 kPa or > • Pupillary areflexia
50 mm Hg • Loss of cardiovascular reflexes
• Response to painful stimuli, within the cranial nerve • Syncope due to orthostatic hypotension
territories. • Disturbances of sweating
Central Nervous System 265
Table 8.66: Evaluate autonomic functions the SBP falls > 30 mm Hg. The 30th : 15th pulse ratio >
Proceedure Normal response Inference 1.03 normal subjects and ≤ 1.0 in case of autonomic
Standing – Decrease in systolic Excessive response indi-
disturbances
BP less than 20 cates:
– Moderate tachy- – Adrenal dysfunction Loss of Cardiovascular Reflexes—Causes
cardia—Increase – Endorgan refractoriness
in plasma nordre- • Tachycardia at rest
naline level • Absence of normal slowing of pulse in response to
Deep breathing – Variation in pulse Impaired vagal function
Valsalva’s maneuver
rate of 10 beats or
more/min • Absence of normal slight increase in the pulse rate and
Hyperventilation – Reduction in sys- blood pressure on standing
tolic BP by • Absence of normal increase in blood pressure during
10-20 mm Hg. hand grip
Valsalva’s man- 4 phases or stage res- Disorder of sympathetic
euver ponse system • Absence of BP increase with stressful tasks such as
Cold pressor Tachycardia in res- Sympathetic lesion central mental arithmetic.
ponse to systemic or efferent
Test immersion arterial hypertension Sympathetic lesion either Bladder and Bowel Function
of an extremity central or efferent
in ice-cold water Patterns of Abnormality
for 1-3 minutes
Amynitrate Tachycardia in res- Sympathetic lesion either a. Frontal bladder: Urinary urgency, precipitant and
inhalation ponse to systemic central or efferent uncontrolled voiding of large volumes without residual urine.
arterial hypotension Periods of urinary control. Normal anal tone. Frontal release
Induction of Sweating –do–
hyperthermia
signs.
Occurs in dementia, normal pressure, hydrocephalus,
Assessing the Functions of ANS frontal tumors.
• The papillary response to light and accommodation b. Spinal bladder: Initially urinary retention + overflow
• Skin—normal or dry (due to absence of sweating) incontinence. Later bladder contracts and voids small
• Tachycardia at rest—present or absent volumes of urine automatically and precipitantly.
• Change in pulse rate with deep inspiration Constipation. Normal anal tone. May develop reflex
• Trophic changes in distal skin—absence of hair growth. penile erections—called priapism (after the Greek god
Priapus).
Standing Test for Orthostatic Hypotension (OH) Occurs in spinal cord lesions—common causes: trauma,
The patient is made to lie supine for about 15 minutes (with multiple sclerosis, spinal tumor.
sphygmomanometer, cardiac rate meter or lead 1 ECG c. Peripheral neurogenic bladder: Painless distention of
attached). Check the resting blood pressure. Then the patient flaccid bladder with overflow in continence and large
is made to stand. Then the pulse rate from RR interval at residual volumes. Fecal incontinence. Reduced anal tone.
the 15th and 30th beats after standing are noted and BP There may be saddle anesthesia. Impotence.
taken one and three minutes after standing. Occurs in cauda equina lesions—common causes:
central lumbar disc protrusion; rarer causes: spina bifida,
Interpretation ependymomas, cordomas, metastases—or peripheral nerve
In normal individuals, the SBP should not decreases by more lesions—common causes: diabetes mellitus, rarer causes:
than 10 mm Hg. In patients with autonomic dysfunction, pelvic surgery, malignancy.
9
A collection of nerve fibers that connects two masses of Class Sensations Pathway
gray matter within the central nervous system is called a Exteroceptive i. Pain and temperature Lateral spinothalamic
tract. Tracts may be ascending or descending. They are tract
(conscious) ii. Touch and pressure Ventral spinothalamic
usually named after the masses of gray matter connected tract
by them. Some tracts are called fasciculi or lemisci or Proprioceptive
funiculi. a. Conscious i. Position and movement
(muscle and joint sense)
Descending Tracts ii. Vibration sense Gracilis and cuneatus
iii. Light touch Fasciculi in the dorsal
1. The corticospinal tract descends from the cerebral cortex column
to the spinal cord. It consists of two parts (i) the lateral iv. Two-point discrimi-
corticospinal tract, which lies in the lateral funiculus, nation
b. Unconscious Proprioceptive impulses Anterior and posterior
and (ii) the anterior corticospinal tract which lies in the for coordination spinocerebellar tracts
anterior funiculus. The corticospinal tracts are also called function of cerebellum
the pyramidal tracts.
2. The rubrospinal tract.
3. The olivospinal tract.
4. The vestibulospinal tract.
5. The tectospinal tract.
6. The lateral and medial reticulospinal tracts.
7. The medial longitudinal bundle tract.
Ascending Tracts (Figs 9.1 and 9.2)
1. Tracts in the posterior funiculus
a. Fasciculus gracilis (medially).
b. Fasciculus cuneatus (laterally)
The fasciculus gracilis and cuneatus are also called
posterior column tracts.
2. Tracts in the lateral funiculus
a. Lateral spinothalamic tract.
b. Anterior and posterior spinocerebellar tract.
c. Spino-olivary tract.
d. Spinotectal tract.
3. Tracts in anterior funiculus
a. Anterior spinothalamic tract.
the detrusor muscle which shows slow recovery). The increases intravesicle pressure to threshold level,
favorable consequence of this is the urine. After some similarly reflex evacuation of rectum also occurs.
time, the evacuation of urinary bladder is gradually c. Profuse sweating below the level of lesion, the
established in a perfectly normal manner. The regain of sweat fibers to head and neck arises from T1 and
anal sphincter activity also occurs in the same way. T2 and those to arms from T5-9, therefore, a lesion
• Paralyzed blood vessels also regain their normal tone at T2 level causes sweating of whole of the body
(as the connector cells in the spinal cord begin to act when mass reflex is obtained as all the sympathetic
independently of VMC): fibers leave the cord below the level of the lesion.
– Sweating restarts from the skin (which was lost iii. Deep (tendon) reflex: The knee or ankle jerk returns
earlier) and also skin appears to be more healthy. about 1 to 5 weeks later than the flexor response
– Rapid healing of ulcers occurs. – The ankle jerk may return still later.
– As the circulation becomes better in the limbs, they – About 6 months after the transaction has
become warm and also gain good color. occurred, marked activity appears in the extensor.
• BP is normal at rest but may show wide fluctuations. This results in exaggerated extensor reflexes with
Muscle tone: the appearance of extensor spasms.
• Return of tone in the skeletal muscle occurs after Note: The mass reflex can also be used as a therapy (a sort
2 to 3 weeks. of exercise) for the patient. It can be used to give paraplegic
– Flexor muscles show early and better return of tone patients a degree of bladder or bowel control. They can be
as compared to extensor muscles. trained to initiate urination and defecation by stroking or
• All the muscles (including the flexors) are hypotonic pinching their thighs thus producing on intentional mass
because stretch reflexes which are responsible for reflex.
muscle tone are feebly mediated by the spinal cord alone Coitus (or Sexual) Reflex
and need reinforcement from brainstem centers.
The coordinated sexual activity depends upon a series of
• Limbs show paraplegia in flexion.
reflexes integrated at many neural levels and is absent after
• Wasting of muscle do not occurs because although they
spinal transaction. Human experiments have shown that
are paralyzed for voluntary movement they are in
genital manipulation in male with spinal cord transaction
constant reflex activity.
produces erection and even ejaculation. A similar type of
Reflex movements: The body takes a period of about 2 weeks response in (sexual excitation) also occurs in case of fender
from the time when transaction of spinal cord has occurred when their external genital parts are stimulated.
till the beginning of return of reflexes. Recovery of reflex
excitability occurs due to phenomenon of “denervation Failure of Reflex Activity
hypersensitivity” to the mediators released by the remaining There are conditions in which the reflex activities fail to
spinal excitatory endings, and development of collaterals appear, some of these conditions are infection, malnutrition
from the existing neurons with the formation of additional and toxemia. The important features are:
excitatory endings on interneurons and motor neurons. 1. The reflexes become increasingly difficult to obtain
i. Flexor reflex: (or withdrawal reflex): Spontaneous because the threshold of reflex activity is highly
involuntary reflex movements of the limbs is the first increased.
reflex response to appear. This can be best elicited by 2. The receptive field is narrowed down to the optimum
positive Babinski’s sign. areas from which reflexes can be obtained.
ii. Mass reflex: It appears several months after the original 3. The mass reflex disappears.
lesion. It is due to irradiation of afferent stimuli from 4. The threshold of all the reflexes is increased and a few
one reflex center to another. The mass reflex can be group of muscles are involved in the motor response.
elicited by scratching any point on the lower limb or 5. The muscles get wasted and become flaccid and bed
anterior abdominal wall below the level of lesion. The sores also develop, which further decrease the general
mass reflex consists of: state of well being of the patient.
a. Flexor response of both the lower extremities and
Incomplete Transaction of the Spinal Cord
contraction of anterior abdominal wall.
b. Evacuation of urinary bladder due to hyperactive In this type of lesion of the spinal cord, few tracts escape
reflex activity and abdominal compression which injury and are prevented from being cut.
272 Essentials of Clinical Medicine
i. Stage of spinal shock is similar to that of complete other functional changes which occur are listed into 3
transaction of spinal cord. categories.
ii. Stage of reflex activity:
Changes below the Level of Hemisection:
As the transaction of the spinal cord is not of complete On the Same Side
type, therefore, some of the descending tracts in the
Sensory changes:
ventrolateral columns of the spinal cord (especially vestibulo-
• Loss of fine touch, tactile localization and tactile
spinal and reticulospinal tracts) may escape injury and some
discrimination, vibration sense and kinesthetic sensation,
connections persist between the brain and spinal cord. These
i.e. sensation of movement and position, due to damage
tracts mainly reinforce the activity of the extensor motor
of dorsal column.
neurons producing extensor hypertonia, i.e. paraplegia in
• Unaffected pain temperature and crude touch as the
extension. As a result, the legs lie extended at hip and knee
spinothalamic tracts (anterior and lateral) carrying these
and knee with toe pointing slightly downwards.
sensations cross to the opposite side and escape injury.
Characteristic Features Motor changes:
• All features of UMNLs are seen (They have been • Extensive paralysis of UMNL due to damage of cross
described in section of “Neurological Examination”). pyramidal tracts. Since some fibers of direct pyramidal
• Involuntary movements are relatively infrequent, but tract of opposite side (which and in the same side) escape
when they occur, they involve an increase in the extensor injury, therefore, some muscles on the same side of
tone, producing downward movement of toes and feet. lesion may not be paralyzed.
• Temporary loss of vasomotor tone due to damage to
• Extensor thrust reflex:
the descending fibers from the vasomotor center (VMC)
This reflex can be elicited by passively flexing the lower
in the medulla to the lateral horn cells. This leads to the
limb and allowing it to rest on the bed, the patient’s foot
dilatation of blood vessels and fall in BP. Later, intact
is then pressed up with the palm of the hand. Active
lateral horn cells start acting as supplementary VMC
contraction of quadriceps and posterior calf muscles
and tone returns.
occurs, and the limb straightened out. Physiologically it
is an extensor response because all the muscles which On the Opposite Side
contract during an extensor response are called Sensory changes
physiological extensor. This reflex is absent in complete • Complete loss of pain, temperature and crude touch due
transaction of the spinal cord. to damage to spinothalamic fibers which come from
• Cross extensor reflex: the opposite side.
Stimulus to the sole of the foot produces withdrawal Motor changes
(flexor) reflex extending up to the knee only. It is usually • Complete LMNL type paralysis is seen due to damage
accompanied by active and forcible extension of opposite to anterior horn cells.
limb. • Complete and permanent vasomotor paralysis occurs
• Phillipson’s reflex: due to damage of the lateral horn cells.
Gentle flexion of one limb causes extension of opposite
Hemisection: On the Opposite Side
limb. The flexed limb then becomes extended and
opposite one flexed, the response alternate in each limb 1. Sensory changes: Some loss of pain sensation due to
producing a steppage movements in which the legs are injury of pain fibers of spinothalamic tract which cross
horizontally in the same segment and may be caught up
lifted abnormally high, occurring due to foot drop.
in the lesion.
Failure of Reflex Activity 2. Motor changes: Nil or very slight due to damage of some
pyramidal tract of the same side.
Similar to that of “stage of spinal shock”.
Changes the Same Side
Hemisection of Spinal Cord: A band of hyperesthesia present due to irritation of upper
(Brown-Sequard Syndrome) cut end of damaged fibers.
In this type of lesion, only one lateral half of spinal cord is On the Opposite Side
affected. The autonomic functions are usually normal. The Hyperesthesia may be referred.
Examination of the Spine 273
Hemisection in Cervical Region movement in the feet and loss of sensation in the buttocks
due to the involvement of anterior and posterior gray
• Constriction of pupil on same side because pupillary
dilator fibers coming from medulla and passing via T1,2,3 horns, paralysis of bladder and rectum due to involve-
anterior roots are damaged. ment of intermediolateral cell column. The syndrome is
• If L4,5,6 segments are involved, it results in loss of biceps, usually caused by injury to vertebra L1 or prolapse of
triceps, supinator and pronator jerks. intervertebral disc between L1 and L2 since the sacral
• Paralysis of diaphragm on the same side due to phrenic segments lie against these.
nerve (C4,5,6) involvement.
Lesions of Sensory Tracts
Hemisection in the Lumbar Region • Degeneration of dorsal column (fasciculus gracilis and
If it involves the L3,4 loss of knee jerk and disturbances in fasciculus cuneatus) is seen in tabes dorsalis. There is
the micturition occurs. loss of sense of position and vibration and two-point
discrimination in the extremities. Patients have a positive
Hemisection in Lumbosacral Region Rhomberg’s sign, i.e. when the patient stands with his
feet together and closes his eyes, he begins to sway and
This leads to control over the sphincters of urinary bladder
perhaps loses his balance and falls indicating loss of
and anus.
sense of position in the legs. By opening his eyes, he
Complications Arising due to can partially compensate by the visual knowledge of
Transaction of Spinal Cord uncrossed fibers of the posterior column. This selective
disturbance of sensation is known as ‘dissociated
• Immobilization in case of paraplegia and quadriplegia sensory loss’.
causes increased catabolism of large amounts of body If the cavitation round the central canal enlarges to
protein, ultimately leading to negative nitrogen balance. include the motor cells in the anterior horn, then there is
• Decubitus (postural) ulcers which heal poorly due to flaccid paralysis of the intrinsic muscles of the hand as
depletion of body proteins. the disease usually involves the lower cervical and upper
• Hypercalcemia, hypercalciuria and calcium stones in the thoracic regions of the cord.
urinary tract due to increased breakdown of protein from • Intractable pain can be treated by cutting the spino-
bone matrix. thalamic tract in the operation known as cordotomy. A
• Stones may lead to urinary retention, urinary tract needle is inserted into the lateral column of the cord.
infection, septicemia, uremia, coma, and ultimately When the needle is in the spinothalamic tract, the patient
patients demise may occur (Fig. 9.3). reports tingling on the opposite side of the body. The
tract is then destroyed electrolytically. The pain fibers
CLINICAL APPLICATIONS
are superficially placed in the tract, while the temperature
Lesions of Motor Neurons and fibers are deeply situated.
Corticospinal Tracts
Brown-Sequard Syndrome (Fig. 9.3)
• Upper motor neuron lesions are caused by transaction
of the corticospinal tract or destruction of the cells of It is characterized by the following signs:
origin in the cortex. Spastic paralysis results with • On ipsilateral side—spastic paralysis (lateral cortico-
pyramidal signs (Babinski’s sign). spinal tract interruption); loss of position sense, tactile
• Lower motor neuron lesions are caused by damage to discrimination and vibration sense (interruption of dorsal
motor neurons. Flaccid paralysis occurs with loss of column); Horner’s syndrome (interruption of hypo-
reflexes. Poliomyelitis results from damage to motor thalamospinal tract).
neurons in the anterior horn. • On contralateral side—there is loss of pain and
• Combined upper motor neuron and lower motor neuron temperature sensation one segment below the lesion
disease is caused by damage to the corticospinal tract (interruption of lateral spinothalamic tract).
and motor neurons in the anterior horn. An example is – Complete transaction of the cord results in total loss
afforded by amyotrophic lateral sclerosis. of sensations in the region below the level of injury
• Direct injury to conus medullaris destroys segmental (interruption of all sensory tracts), flaccid paralysis
neurons (conus syndrome). It results in weakness of (interruption of corticospinal tracts).
274 Essentials of Clinical Medicine
identical to those of substantia nigra, the dopaminergic position shifts upwards on making the patient to get up
neurons from this area enter the mesolimbic pathway against resistance from bed.
which supplies the limbic structures of the forebrain. • T12 to L1- Sensory-Groin. Motor T12-Abdominal reflexes
Excess activity in the mesolimbic pathway is thought to intact. L1-Muscles of lower limb involved including hip
be related to the onset of schizophrenia characterized flexion. Lower abdominal muscles may be weak, with
by thought disturbances and delusions. absent cremasteric reflex and exaggerated knee and ankle
reflex.
Localization of the Site of Lesion in • L1 to L3- Sensory-anterior aspect of thigh, motor L2
Spinal Cord Lesion same as L1 but knee reflex may be decreased. No
weakness of abdominal muscles. At T12 vertebra and
• Localization is made from: below as cord ends at L1 root involvement occurs, e.g
– Sensory level cauda equina is involved. Saddle anesthesia over gluteal
– Motor reflex level region with lower motor paraplegia.
– Vibration sensation level. • L4- Sensory level anterior lower aspect of thigh and
For sensory level determination: medial aspect of leg. Motor hip flexion, adduction, knee
• add 1 to cervical segment flexion, leg extension preserved. Knee jerks not elicitable.
• add 2 to upper dorsal segment Ankle jerks exaggerated.
• L5- Lateral aspect of leg and medial aspect of foot from
• add 3 to lower dorsal segment (9th to 12th).
the sensory level. Motor level is formed by normal knee
Sensory motor level landmarks correspond to spinal
jerk but exaggerated ankle jerk.
cord segments. • S1-Sensory little toes, most of sole of interior and lower
• What is the syndrome of foramen magnum? border of foot. Motor weak gastrocnemius with weak
Weakness of shoulder, arm followed by weakness of small muscles of foot with absent ankle reflex.
ipsilateral leg than contralateral leg, finally contralateral • S2-Sensory posterior aspect of thigh and leg. Motor
arm constitutes the foramen magnum syndrome. Mass paralysis of small muscles of foot.
in this region can produce suboccipital pain spreading • S3,4,5 Sensory –anal, scrotal, perineal anesthesia. Motor
to neck and shoulders. paralysis of rectum, bladder, sphincters with impaired
• High cervical compression C 1, C 2, C 3 sensory C2 erection.
interaural vertex meatal line. Motor C1-4 muscles of hand
and neck C1, C2 vasomotor and respiratory center in NECK PAIN AND SHOULDER PAIN
addition can have cranial nerve involvement: Trauma to Cervical Spine
– Papilloedema
• (Fractures, subluxation)
– Ophthalmic division of trigeminal is affected because
• Motor vehicle injury (87%)
spinal tract of trigeminal nerves are affected
• Violent crimes, and falls
– Spinal accessory affected by 11th cranial nerve.
• C4 diaphragmatic paralysis Whiplash Injury
• C5-6 sensory radial division of arm, forearm and hand. 1. Due to trauma (automobile accidents)
Motor paralysis of rhomboid supraspinatus, infra- 2. Causes cervical musculoligamental sprain or strain due
spinatus, teres major and minor, deltoid, biceps and to hyperflexion or hyperextension
brachioradialis. Arms adducted and internally rotated. 3. Objective data on pathology of neck soft tissue injuries
Inversion of supinator jerk, i.e. brachioradialis contrac- is lacking.
tion is absent but finger flexion seen. Cervical Disk Disease
• C7—paralysis of triceps with flexion, extension of wrist 1. Herniation of a lower cervical disk is common cause of
and fingers. Loss of tricep reflex or paradoxical response neck, shoulder, arm or hand pain.
leading to flexion of forearm instead of extension. 2. Neck pain (worse with movement), stiffness and limited
• C8 to T1—sensory ulnar side of forearm and hand. Motor range of neck motion are common.
atrophic paralysis of small muscles of hand. Finger 3. With nerve root compression, pain may radiate into
flexion reflex is decreased or lost. shoulder or arm.
• T4—sensory nipple level 4. Extension and lateral rotation of neck narrows the
• T 6—motor loss of all abdominal reflexes below intravertebral formation and may reproduce radicular
umbilicus. Beevor’s sign is present, i.e. umbilicus symptoms (Spurling’s sign).
276 Essentials of Clinical Medicine
Cervical n. Pain distribution • Neck pain may be referred from heart in setting of
Roots coronary artery ischemia (cervical angina syndrome).
C5 - lat. arm, medial scapula • The injury to thoracic outlet (first rib, subclavian a. and
C6 - lat. forearm, thumb, index finger v., branchial plexus, the clavicle and lung apex), may
C7 - post arm dorsal forearm, lat. hand result in posture or taste-related pain around shoulder
C8 - 4th and 5th finger, medial forearm and supraclavicular region.
T1 - medial arm, axilla
Lymphatic Gland and Salivary Glands
Cervical Spondylosis
• In inflammation of tonsils, the lymph glands at angle of
1. Osteoarthritis of cervical spine may produce neck pain jaw are enlarged. Those below the jaw are enlarged in
that radiates into back of head, shoulder, and arms patients with metastasis from cancer in mouth.
2. Arthritic or other pathological condition of the upper
• Enlarged TB glands may occur in groups or in long
cervical spine may be source of headache in posterior
chains behind sternocleidomastoid. Scar shows past
occipital region (supplied by C2-C4 n. root).
suppuration in untreated cases.
3. Cervical spon. with osteophyte formation in lateral recess
or hypertropic forced joints may produce a mono- • In HIV, Hodgkin’s, other reticuloses and secon-dary
radiculopathy. neoplasms, the glands are enlarged and discrete.
4. In some, a combination of radiculopathy and myelopathy • In lymphatic leukemia there may be great enlargement
occurs of gland on both sides.
5. An electrical sensation elicited by neck flexion and • In secondary syphilis, glands under upper parts of
radiating down the spine from neck (Lhermite’s trapezium are often palpable.
syndrome or symptoms) usually indicates cervical or • If glands are swollen and tender, their opening of ducts
upper, thoracic (T1-T2) spinal cord involvement into mouth should be inspected with the tip of patients
6. When little or no neck pain accompanies the cord tongue rolled upwards this may reveal a salivary calculus.
compression, the diagnosis may be confused with • In young babies the sternocleidomastoid muscle should
amyotrophic lateral sclerosis, multiple sclerosis, spinal be checked for thickened area known as SCM tumor.
cord tumors or syringomyelia. Lump in Neck
7. Lumbar radiculopathy or polyneuropathy may mask an
associated cervical myelopathy. 1. Less than 20 years of age
a. Inflammatory
Other Causes of Neck Pain b. Congenital—thyroglossal and brachial cyst, midline
dermoid, cystic hygroma
• Rheumatoid arthritis of cervical apophyseal joints result c. Lymphoma.
in neck pain, stiffness and limitation of motion. 2. Between 20 and 40 years
• In advanced RA, synovitis of atlantoaxial joints (C1-C2) a. Salivary gland pathology—calculus, inflam-mation
may damage the transverse ligament of atlas, producing and tumor
forward displacement of atlas on axis atlantoaxial b. Thyroid pathology—goiter, inflammatory thyroiditis
subluxation. lymophoma, tumor.
• When subluxation is present, careful neurological c. Chronic infection—HIV, TB, actinomycosis.
assessment is important to identify early sign of 3. More than 40 years
myelopathy.
a. Secondary malignancy.
• Occasional patients develop high spinal cord
b. Primary malignancy—lymphoma.
compression leading to quadriparesis, respiratory
insufficiency and death. Features that suggest malignancy are—progressive
• Ankylosing spondylitis can cause neck pain and on enlargement, hardness, lack of tenderness, fixation to deep
occasion atlantoaxial subluxation. When spinal cord structures and size (as node >2 cm is likely to be malignant.)
compression is present or threaten, surgical intervention • Neck pain may radiate through the occiput to the vertex
is indicated. or to shoulder and down to arms with paresthesiae if
• Herpes zoster produces neck and postoccipital pain in there is nerve root impingement
C2-C3 distribution prior to outbreak of vesicles. • The most common cause of local discomfort and
• Neoplasms metastatic to cervical spine, infection tenderness in neck is infammatory lymphadenopathy,
(osteomyelitis and epidural abscess) and metabolic bone severe tenderness of thyroid itself, especially when
disease may also cause neck pain. accompanied by fever and sign of thyrotoxic suggest a
Examination of the Spine 277
diagnosis of viral subacute thyroiditis (de Quervain’s 3. Spasmodic torticollis results in chronic jerking of head
thyroiditis) with rotation. This is also seen in cranio - cervical
• Occasionally, autoimume thyroiditis may give rise to pain spasms due to extrapyramidal lesions.
and tenderness, which mimics a viral thyroiditis but is
Acute Lymphadenitis
less severe.
• A sudden onset of localized pain and swelling in thyroid 1. The glands are swollen, painful and tender.
is indicative of bleeding into pre-existing thyroid nodule 2. Fixed and skin overlying them is red in color and warm
and is a recognized complication of multinodular goiter. to touch.
The symptoms are self-limiting. 3. As acute lymphadenitis is secondary to septic focus in
• In addition to meningeal irritation, neck rigidity is also mouth, head and neck or scalp, the examination of these
caused by disease of cervical spine and by increased areas should be carried out to find it. Common infection
ICT especially due to posterior fossa tumor with rostral in scalp is lice infestation.
-caudal displacement of vermis in foramen magnum Chronic Lymphadenitis
leading to local dural irritation It is seen in TB and syphilis is generally painless.
• Head retraction—now rare, represents an extreme degree
of neck rigidity. It was formally a feature of untreated Lymphosarcoma
TB meningitis. 1. Massive enlargement of affected glands.
2. Glands are tender and invade the surrounding structure
Meningitis and they can ulcerate through skin.
1. Meningitis may be recognized by rapid onset of 3. Mediastinal lymphadenopathy is usually associated with
drowsiness, lethargy or stupor with fever and signs of this cervical enlargement and precedes it.
meningeal irritation. Thyroid
2. The pulse may be unexpectedly low in relation to fever
1. Diffuse tenderness usually implies thyroiditis.
in pyogenic meningitis although the respiration is usually
2. Localized tenderness may occur following bleeding into
rapid.
a cyst.
3. Seizure and focal neurological sign may develop and
there is H/o of headache and neck stiffness perhaps Others
vomiting. 1. Degenerative arthrosis of cervical spine is common in
4. In meningococcal septicemia, there may be characteristic middle age and elderly such patients may develop neck
rash. pain, long tract features or radicular symptoms.
5. A primary site of infection such as otitis media or 2. Flexion of neck sometimes evokes electric shock-like
sinusitis may be apparent in other forms of purulent sensation which shoot into limbs, when the cervical spinal
meningitis or brain abscess. cord sensory tracts are diseased (Lhermitte’s sign). The
6. The ocular fundi is examined with ophthalmoscopy for phenomenon is particularly common in multiple sclerosis
papilloedema, retinal hemorrhages or exudates or intra- but is also seen in syringomyelia, cervical cord tumors
arterial emboli which appear as luminescent highly and spondylotic myelopathy.
3. Neck movements are restricted by meningeal irritation.
refractive yellow or white plaque-like material occluding
4. When a node is found, it should be assessed properly.
vessels.
Nodes which are >0.5 cm in diameter, firm in
7. Causes of neck stiffness with coma: consistency and round in shape, usually pathological, a
a. SAH common cause being metastases from a bronchial
b. Meningitis—bacterial and viral (aseptic) carcinoma.
c. Encephalitis 5. Large fixed masses are present in some cases. Hard,
d. Intracerebral hemorrhage craggy nodes may, however, be caused by healed and
e. Cerebral malaria calcified TB. Other pathological processes include
Torticollis lymphoma and sarcoidosis.
6. Nerve roots particularly in lower cervical spine may be
1. May be of a continues or of spasmodic variety compressed or irritated by lateral disk prolapse or
2. Acute torticollis causing deviation of head on one side, osteophytes causing from facet of neurocentral joints.
associated with pain is usually due to inflammation of 7. A central disk prolapse may produce pressure on cord
sternocleidomastoid or trapezius. itself.
278 Essentials of Clinical Medicine
Common Abnormal Findings 2. Disk lesions are rare but may be accompanied by girdle
1. Local cervical tenderness may help to identify the site pain radiating around chest, mimicking cardiac or pleural
of pathology. disease.
2. Regional and paraspinal muscle tenderness, is commonly 3. Pain arising from joints at thoracolumbar junctions may
associated with neck pathology. occur in ankylosing spondylosis and again may be
3. Widespread muscle tenderness may be a feature of confused with pulmonary, renal, or cardiac problems.
psychological disorders. 4. Patients with osteoporosis may complain of becoming
4. Loss of movement. progressively stooped (Dowager hump) with loss of
5. Torticollis associated with acute neck pain. height but without neurological features.
6. Loss of cervical lordosis associated with chronic neck 5. Acute osteoporosis and malignant vertebral collapse are
pain. common causes of acute thoracic pain and the latter is
7. Loss of sensation in upper limb, dermatomes, associated not infrequently associated with spinal cord com-
with n. root irritation. pression.
6. With acute pain, infection should be suspected.
Disorders (Causes of Abnormal Neck Postures) 7. When thoracic pain is poorly localized and no satisfactory
1. Loss of lordosis or flexion deformity—acute lesions, explanation could be found, intrathoracic causes such
RA. as aortic aneurysm should be thought of.
2. Increased lordosis—ankylosing spondylitis
Causes of Pain in Thoracic Spine
3. Torticollis (wryneck)—sternocleidomastoid contracture
4. Lateral flexion (Cock-Robin position)—erosion of lateral 1. Adolescent and young adults:
mass of atlas in RA. • Scheuermann’s disease.
• Ankylosing spondylosis
Cervical Spine • Disk protrusion (rare)
1. The patient may report paresthesia in arm due to nerve 2. Middle age and elderly:
root irritation, or less commonly when spinal cord is • Degenerative change.
involved, symptoms of lower limb weakness, difficulty – Osteoporotic, fracture.
in walking, loss of sensation and sphincter control. 3. Any age:
2. Disease of upper cervical spine affecting the atlantoaxial • Tumor
joints produce pain radiating into occiput in distribution • Infection.
of C2 nerve root.
3. Disease of middle and lower cervical spine tends to Lumbar Spine
cause pain radiating into upper border of trapezius,
interscapular region or into arms, often associated with Causes
local tenderness. 1. Acute disk protrusion
4. Irritation of C6 and C2 nerve root can give rise to widely 2. Spinal stenosis
referred pain in the interscapular region or into radial 3. Ankylosing spondylosis
fingers and thumbs. 4. Osteoporotic fracture
5. Irritation of C8 can produce pain on ulnar side of forearm 5. Infection
and into ring and little finger. 6. Tumors—weight loss and fever
6. Neck pathology should also be considered in any patient 7. Abdominal or retroperitoneal pathology
complaining of diffuse pain in arm, head, upper trunk 8. Age-related degenerative changes in disk or facet joints
or interscapular region if associated with sensory or (spondylosis)
other neurological disturbances. 9. Psychological distress
10. Low back pain due to standing too long, sitting in
BACKACHE poor posture.
11. Poor posture: pain worsens as day passes on and
Thoracic Spine relieved after rest or awakening.
Description of pain 12. Mood disturbances.
1. May present as pain radiating around chest wall or as 13. Inflammatory disease pain such as ankylosing
symptom of paresis, sensory loss, leg weakness and spondylosis worsens in morning or after inactivity
loss of bladder or bowel control. and ease with movement.
Examination of the Spine 279
14. Morning stiffness in osteoarthritis lasting 30-60 min. 5. Pain associated with muscle spasm:
15. Other clues—peri.joints, non-articular features such – Spine disorders
as iritis or family H/o spondylarthritis – With abnormal posture
16. Acute onset with bending or lifting is a feature of – Taut paraspinal muscles and dull pain
acute disk protrusion. Coughing exacerbates this pain.
17. Poor posture. Congenital Anomalies of Lumbar Spine
18. Loss of sensory sensation, loss of bowel, sphincter Spondylolysis
control and perianal sensation.
19. Long steroid therapy may cause osteoporosis. Pain Bony defects in pars interarticularis (a segment near the
of this type is eased by lying, exacerbated by spinal junction of pedicle with the lamina) of vertebra.
flexion and is not associated with neurological Spondylolisthesis
symptoms. • Anterior slippage of vertebral body pedicles and superior
20. Acute onset of progrssively Increasingly pain with articular facets
malaise, weight loss, night sweat—pyogenic or TB • Associated with spondylolysis and degeneration
of lumbar spine—may spread to psoas muscle causing • Occurs frequently in women
painful flexed hip or as a swelling in groin. • The slippage may be asymptomic but may cause low
21. Unremitting spinal pain of recent onset with sleep back pain, nerve root injury (L5 mainly) or symptomatic
disturbances, malignant disease involving a vertebral spinal stenosis
body should be considered. H/o carcinomas, sys-temic • The trunk may be shortened and abdominal protruberant
symptoms or weight loss is present. Tumors rarely as a result of extreme forward displacement of L4 on
affect intervertebral disk. L5 in severe degree
22. Diffuse pain in buttock or thighs brought on by • In these cases cauda equina syndrome may occur.
standing too long or walking is the presenting
complaint of lumbosacral spinal stenosis which can Trauma
be difficult to distinguish from intermittent clau-
dication. Relieved by rest or flexion of spine. • Back pain.
23. Narrowing of spinal canal or neural exit foraminae, is • Inability to move legs—may be due spinal fracture or
usually caused by degenerative changes in inter- dislocation.
vertebral disk and facet joint. There is long H/o • Fracture above L11—spinal cord compression.
discomfort typical of degenerative joint disease.
Sprains and Strains
TYPES OF BACK PAIN • Confined to lower back.
1. Local pain: Stretching of pain sensitive structures. • No radiation to buttocks or legs.
2. Pain referred to back: from abdominal viscera • Patients with low back pain and para spinal muscle spasm
– Pelvis viscera often assume unusual postures.
– Unaffected by posture.
3. Pain of spinal injury Vertebral Fractures
– May be localized • Pars interarticularis fractures of L5 vertebrae is common
– May be reffered to buttocks, posterior thighs, calves, • Neurological impairment is commonly associated with
feet these injuries.
– Sclerotomal pain. • Bones may be weakened by osteomalacia, hyper-
4. Radicular back pain parathyroidism, hyperthyroidism, multiple myeloma,
– Sharp and radiates from spine to legs within the metastatic carcinoma, glucocorticoid therapy.
territory of nerve root
– Coughing, sneezing, voluntary control of abdominal Lumbar Disk Disease
muscles (stool, lifting object) may elicit radiating
pain. • Most likely at L4-L5 and L5-S1 levels
a. Sitting stretches the sciatic nerve (L5-S1) • Risk in overweight persons
b. Femoral nerve (L2, L3, L4) passes anterior to hip • Sneeze, cough or trivial movement may cause nucleus
and not stretched on sitting palposus to prolapse, pushing the frayed and weakened
280 Essentials of Clinical Medicine
• Onset males >40 years. • Back pain exacerbated by motion and unrelieved by
• Associated with rest, spine tenderness over the involved spine
– Morning back stiffness segment and an elevated ESR.
– Nocturnal pain • Fever with elevated WBC count in some patients.
– Unrelieved by rest 2. Spinal epidural abscess
– Increased sedimentation rate • Back pain (aggravated by palpation or movement)
• HLA-B-27. and fever.
• The patient may exihibit nerve root injury or spinal
Differential Diagnosis (D/D) of cord compression with sensory level, inconti-nence,
Ankylosing Spondylolitis or paraplagia.
1. Tumor
2. Infection. Osteoporosis and Osteosclerosis
– Onset at young and back pain improving with exercise • Loss of bone with hyperparathyroidism, chronic
suggests ankylosing spondylolitis glucocorticoid use, or immobilization.
– Loss of normal lumbar lordosis and exaggeration of • Compression fractures occur in up to half of patients
thoracic kyphosis are seen as the disesase progresses. with severe osteoporosis.
– Bamboo spine • The sole manifestation of a compression fracture may
– Similar restricted movements may accompany be focal lumbar or thoracic aching (often after a trivial
Reiter’s syndrome, psoriatic arthritis, chronic bowel injury), i.e. exacerbated by movement.
disease. • Other patients experience thoracic upper lumbar radicular
– Stress fracture through spontaneously ankylosed pain.
posterior bony elements of the rigid, osteoporotic • Focal spine tenderness is common.
spine may result in focal spinal pain, spinal cord • Compression fractures above the midthoracic region
compression and cauda equina syndrome suggest malignancy.
– Sometimes atlantoaxial subluxation with compression • Osteosclerosis may or may not produce back pain.
occurs.
– Bilateral ankylosis of ribs to spine and a decrease in Referred Pain from Visceral Diseases
height of axial thoracic structures may cause marked • Occasionally, back pain may be the first and only sign
impairment of respiratory function. of a referred pain from diseases of pelvis, abdomen and
thorax.
Neoplasms • Local signs (pain with spinal palpation, paraspinal muscle
Description of pain spasm) are absent and minimal or no pain accompanies
1. Back pain is the most common neurologic symptom normal spine movements.
among patients with systemic cancer. Low Thoracic and Upper Lumbar Pain in
2. Metastatic ca. (breast, lung, prostrate, thyroid, kidney, Abdominal Diseases
GIT) multiple myeloma, non-Hodgkin’s and Hodgkin’s
• Paraspinal pain or midline back pain due to peptic ulcer
lymphoma frequently involve spine.
or tumor of post. stomach or duodenum. (if the
3. Pain is dull, constant, unrelieved by rest and worse by retroperitoneal extension is present).
night (in contrast mechanical low back pain is usually • Back pain due to peptic ulcer may be precipitated by
improved with rest). ingestion of an orange, alcohol, coffee, and relieved by
food and antacids.
Infection • Fatty foods are more likely to induce back pain
1. Verbal osteomyelitis associated with biliary disease.
• Caused by Staphylococcus. But other bacteria or • Disease of pancreas may produce back pain to right of
tubercle bacilli (Pott’s disease) may be the causative spine (head of pancreas involved) or to left (body or tail
microorganisms. involved).
• Primary source of infection most often is from • Pathology in retroperitoneal structures (hemorrhage,
urinary tract infection, skin or lungs in 40 percent. tumors, pyelonephritis) may produce paraspinal pain
Intravenous drug abuse is a well-recognized risk with radiation to lower abdomen, groin, or anterior
factor. thighs.
282 Essentials of Clinical Medicine
• Mass in iliopsoas region often produces unilateral lumbar • Low back pain with radiation into one or both thighs is
pain with radiation towards groin, labia, or testicles. common in last week of pregnancy.
• The sudden appearance of lumbar pain in a patient • Urologic sources of lumbosacral pain:
receiving anticoagulant therapy suggests retroperitoneal – chronic prostatitis
hemorr-hage. – prostatic carcinoma with spinal metastasis
• Isolated low back pain occurs in 15 to 20 percent of – diseases of kidney and ureter.
patients with rupture of an abdominal aortic aneurysm. • Lesions of bladder and testis usually do not cause back
• Classic triad of abdominal pain, shock, back pain in pain.
elderly men occurs in fewer than 20 percent of patients. • Infections, inflammatory, or neoplastic renal disease may
• Two of these features are present in 2/3rd of patients. result in ipsilateral lumbosacral pain as can renal artery
And hypotension is present in ½. Ruptured abdominal or vein thrombosis.
aortic aneurysm (AAA) is typically the elderly patient • Ureteral obstructions due to renal stone causes paraspinal
male with back pain. lumbar pain.
• Common misdiagnosis include nonspecific back pain,
diverticulitis, renal colic, sepsis, and myocardial Postural Back Pain
infarction. A careful abdominal examination revealing a
pulsatile mass (in 50-75 percent patients) is an important 1. Chronic non-specific low back pain with no anatomic
finding. or pathologic lesion can be found despite exhaustive
investigation.
Lumbar Pain with Lower Abdominal Disease 2. The patient complains of vague diffuse, backpain with
• Inflammatory bowel disease (colitis, diverticulitis) or prolonged sitting or standing that is relieved by rest
colonic neoplasms may produce lower abdominal pain, 3. Physical exam is unrevealing except for “poor posture”.
midlumbar back pain or both.
• Pain may have belt like distribution around the body. Psychiatric Diseases
• Lesions in transverse or initial descending colon may 1. Chronic low back pain (CLBP) may be encountered in
refer pain to upper sacral or midline suprapubic regions patients with compensation hysteria, maligering,
or left lower quadrant of the abdomen. substance abuse, chronic anxiety states or depression.
2. Many patients with CLBP have a history of psychiatric
Sacral Pain in Gynecological and illness (depression, anxiety and substance abuse) or
Urological Diseases childhood trauma (physical or sexual abuse).
• Endometriosis or uterine carcinoma may invade the Unidentified
uterosacral ligaments, malposition of uterus may cause 1. Cause is unclear.
uterosacral ligament traction. 2. No definite neurological sign or a minor disk bulge noted
• Pain associated with endometriosis begins during the
on CT or MRI.
premenstrual phase and often continues until it merges
3. Some patient have had multiple operation for disk disease
with menstrual pain.
but have persistent pain and disability.
• Malposition of uterus (retroversion, descensus, and
prolapse) may lead to sacral pain after standing for several Physiological
hours. 1. Faulty posture
• Other pelvic sources of low back pain include neoplastic 2. Asthenic individual.
invasion of pelvic nerve, radiation, necrosis and 3. Pregnancy.
pregnancy.
• Menstrual pain may be felt in sacral region. The poorly Trauma
located cramping pain can radiate down to legs. 1. Prolapsed intervertebral disk.
• Pain due to neoplastic infiltration of nerves is typically 2. Lumbosacral strain.
continuous, progressive in severity and unrelieved by
Infection
rest at night.
• Radiation therapy of pelvic tumors may produce sacral 1. Osteomyelitis.
pain from late radiation necrosis of tissues or nerves. 2. TB of spine (Pott’s disease).
Examination of the Spine 283
Neoplastic 2. Osteoarthritis.
1. Primary tumor. 3. Ankylosing spondylolysis.
2. Secondaries. Referred
3. Multiple myeloma.
1. Pancreatitis.
Metabolic 2. Retroperitoneal tumor.
1. Osteoporosis. 3. Cholecystitis.
2. Osteomalacia. 4. Diverticulitis.
3. Hyperparathyroidism. 5. Retroverted uterus.
6. Uterine prolapse.
Congenital
Spinal Abnormalities
1. Spina bifida.
1. Kyphosis.
Arthiritis 2. Scoliosis.
1. RA (rheumatoid arthritis). 3. Lordosis.
10
Common Cases Encountered in
Clinical Medicine: Hypothyroidism,
Myxoedema and Thyrotoxicosis
2. Disturbances of hematological systems: (It should not be confused with corneal arcus senilis
• Lethargy and breathlessness associated with anemia this in a broader band at edge of cornea and merges
of impaired production of erythropoietin by kidneys. with sclera).
• Defective coagulation and excessive bruising – Arcus senilis — superior and inferior.
(advance renal failure) – Coneal calcification — medially and laterally
• Hemorrhage from GIT tract or lungs. • Retinal hemorrhages and exudates thrombosis of central
3. Disturbances of CVS: retinal artery or its branches and of central retinal vein
• Cardiac failure or angina associated with fluid and its branches
overload, hypertension, anemia and impaired ventri-
cular function (uremic cardiomyopathy) NEPHROTIC SYNDROME
• Pericardial chest pain due to pericarditis
Clinical Presentation of Nephrotic Syndrome
• Cardiac arrhythmias associated with hyperkalemia/
hypokalemia. • Pale, BP normal except in membranoproliferative
4. Disturbances of respiratory system: nephritis
• Breathlessness and hemoptysis from fluid overload. • Edema foot, sacral edema
• Chest pain due to pleurisy. • Ascites, pleural effusion, bilateral
5. Disturbances of musculoskeletal system: • Oliguria
• Muscular weakness and bone pain due to impairment • Ultrasound—enlarged kidneys.
of vit. D activation and to exclusive parathyroid gland
activity. Table 10.22: Common causes of nephrotic syndrome
• Acute pain due to gout. Causes Children Adults
6. Disturbances of nervous system: 1. Minimal leision 70% 15%
• Hypertensive stroke and encephalopathy. 2. Mesangio proliferative 15% 5%
• Clouding of consciousness, fits, coma in advanced 3. Focal glomerulosclerosis 10% 10%
renal failure. 4. Secondary 5% 30%
• Impaired sensations of parethesiae in the feet, due 5. Membranous 35%
6. Membranoproliferative Rare 5%
to peripheral neuropathy in longstanding uremia.
• Impaired higher/mental/intellectual functions.
7. Disturbances of eye: Complications of Nephrotic Syndrome
• Pain from conjunctivitis caused by local deposits of • Protein catabolism.
calcium. • Impaired resistance.
• Visual blurring from hypertensive retinal damage or • Thromboembolism due to loss of antithrombin III in
retinal vascular disease. urine.
• Hypovolemia.
Eye of Uremia
• Renal failure.
• Corneal calcification (limbus calcification): Hyper- • Accelerated sclerosis.
porathyroidism • Fluid retention, hydrothorax, pericardial effusion.
Skin Lesion
ENNUMERATE SKIN LESION Table 10.23: Various skin tests in the diagnosis of
lymphadenopathy and other diseases
• Skin nodules—rheumatic fever, rheumatoid arthritis,
gout, hyperlipidemia Name of the test From which disease When to read
• Rash—SLE, rheumatic fever, juvenile chronic arthritis, 1. Montoux test TB 48-72 hours
psoriasis, Reiter’s disease, dermatomyositis, cutaneous 2. Kveim’s test Sarcoidosis 6 weeks
vasculitis, drugs, Lyme arthritis, viral infection, Kaposi’s 3. Frie’s test Lymphogranuloma 48-72 hours
venerum
sarcoma 4. Casoni’s test Hydatid disease (40- 25 mm diameter at 20-
• Erythema nodosum—TB drugs, streptococcal sore (15% false) 90% positive) 30 minutes
throat, Behçet’s syndrome, sarcoidosis 5. Dick’s test Scarlet fever Tells susceptibility to
• Pancreaculitis—Crohn’s disease, SLE toxin
• Raynaud’s phenomenon—progressive systemic 6. Schick test Diphtheria Tells susceptibility to
sclerosis, polymyositis, dermatomyositis, SLE toxin
• Sclerodactyly—psoriasis, CREST
• Leg loss—SLE, polyarteritis nodosa Table 10.24: Campbell de Morgan spots and vascular stars
• Hair loss—SLE, cytotoxic drugs, hypothyroidism Campbell de Morgan spots Vascular stars
• Skin pustules—Behçet’s syndrome, gonococcal 1. Site—over anterior abdominal 1. Site
• Heberden’s node—osteoarthritis wall, chest on back
• Bouchard’s nodules—osteoarthritis 2. Seen in elderly, very commonly 2. Seen more clearly in fair skin
• Oral cavity in chronic venous congestion people
– Aphthous ulcer—Behçet’s syndrome 3. Size—usually large in size 3. They are also usually large in
– Superficial painless ulcer—reactive arthritis 4. Disappearance—do not size
– Palatal excoriation—SLE disappear on applying pressure 4. They also do not disappear on
– Dry mouth—Sjögren’s syndrome applying pressure.
5. Diagnosis—We rub ice-cubes
• Occular—conjuctivitis—reactive arthritis
over this area, and when the area
– Anterior uveitis—juvenile chronic arthritis becomes white (blenched), then
– Iritis—spondyloarthritis vascular stars are confirmed.
– Dry eye—Sjögren’s syndrome.
Case of Anemia
Pallor suggests anemia. But pallor can be there without • GIT signs—liver enlarged in hemolytic jaundice,
anemia also. retracted in cirrhosis, massive splenomegaly in chronic
So best way to confirm anemia is by hemoglobin CML, small spleen in sickle cell anemia, epigastric
estimation, which is reduced in anemia. renderness, glossitis, gastric atrophy.
• SVS signs—hemic murmur, venous hum over jugular
HISTORY IN ANEMIA vein, third heart sound present. Water hammer pulse,
a. History to find the effect of anemia on the body and to cardiomegaly.
find from history the cause of anemia. Effect of anemia • Respiratory signs—basal crepts if LVF is there.
are as follows: • CNS (a) peripheral neutritis- deep tendon reflexes poor,
Palpitation LVF,CCF, breathlessness, edema feet, stock and glove anesthesia present, (b) subacute
giddiness—due to reduced cerebral flow. Syncope— combined degeneration—deep tendon reflexes lost with
blackouts in front of eyes. GIT symptoms like epigastric stock and glove anesthesia present, plantar extensor.
burning due to duodenitis in hookworm infestation. • Skin changes—xerosis, perifollicular hyperkeratosis,
b. Iron deficiency—nutritional history, bleeding from any angular stomatitis, cheilosis (fissuring of angle of lips),
site, multiple pregnancy, chronic dysentery, worm scrotal dermatitis, niacin deficiency causes dermatitis
infestation, drug intake like aspirin, lactation, chronic of exposed surface of skin, glossitis.
blood loss, upper GI hemorrhage as seen in cirrhosis
of liver from esophageal varices, piles.
NEUROLOGICAL SIGNS OF ANEMIA
History of drugs: History of intake of primaquine,
nitrofurantion in hemolytic anemia, history of intake of • Peripheral neuritis—nutritional deficiency
DBITD-B 12 deficiency, 6 mecraptopurine- folate • Subacute combined degeneration—pyramidal, posterior
deficiency, pregnancy, hemolytic anemia, phenytoin column, and lateral column are affected.
therapy, chronic hemodialysis. In aplastic aneamia, ask • Korsakoff’s pshychosis
history of intake of heavy metals, e.g. gold, arsenic and • Dementia in pellagra.
use of chloramphenicol, and anticancer drugs.
History of nocturia, polyuria with hypertension and ABDOMINAL FINDINGS OF ANEMIA
anemia suggest chronic renal failure. Here erythropoietin
deficiency causes anemia. • Splenomegaly—chronic malaria, chronic myeloid
Chronic infections like PTB, rheumatoid arthritis are leukemia, lymphatic leukemia
associated with anemia. History of passing black urine- • Hepatomegaly—soft tender in CCF with anemia
black water fever, nocturnal paroxysmal hemoglobinuria. • Hard or firm—cirrhosis, malignancy of liver
History of recent jaundice-hemolytic anemia. History of • Ascites
malabsorption-chronic diarrhea. History of “PICA” that • Abdominal glands, lump in right illac fossa (ileocecal
is craving for: TB)
• Starch - Amylophagia • Epigastric veins prominent.
• Ice - Pagophaiga
• Clay - Geophagia
Causes of Anemia with Generalized
Children with iron defiency and PICA have risk of lead
Lymphadenopathy
poisoning.
• Acute leukemia
SIGNS OF ANEMIA • Chronic lymphatic leukemia
• Pallor, spoon-shaped nails—koilonychias, edema, • Lymphoma non-Hodgkin’s
glositis, angular stomatitis, breathlessness and tachy- • Hodgkin’s lymphoma
cardia • TB lymphadenitis with anemia.
Common Cases Encountered in Clinical Medicine 297
Pelvic Pain
Contd... Contd...
Appendix-II 303
Contd... Contd...
Reference value Reference value
Component Fluid Conventional SI Units Component Fluid Conventional SI Units
Glucose tolerance Whole troponin 1 (cTnl) Serum 0-0.1 mg/L 0-0.1 mg/L
test (GIT) blood/plasma Urea Blood 15-40 mg/dl
Immunoglobulins Serum Urea nitrogen
IgA 90-325 mg/dl (BUN) Blood 10-20 mg/dl
IgD 0.8 mg/dl Uric acid Serum 0.24-0.51
IgE <0.025 mg/dl Males 2.5-8.0 mg/dl mmol/L
IgG 800-1500 mg/dl Females 1.5-6.0 mg/dl 0.16-0.43
IgM 45-150 mg/dl mmol/L
Lactate Serum 80-120 units 38-62 U/L OTHER BODY FLUIDS
dehydrogenase Body volume,
(LDH) water
Lactate/pyruvate Total 50-70% (60%)
ratio 10/1 Intracellular 33%
Lipids Serum Extracellular 27%
Interstitial fluid 12%
Non-protein Serum <35 mg/dl including
nitrogen (NPN) lymph fluid
Oxygen Intravascular 5%
(% saturation) fluid or blood
Arterial blood Whole blood 94-100 % plasma
Venous blood Whole blood 60-85 % Fluid in mesenchymal tissues 9%
pH Blood 7.38-7.44 Transcellular fluid 1%
Phosphatases Serum Catecholamines 24 hr urinary excretion
Acid phosphatase 1.0-3.0 king- 2.2-10.5 U/L Epinephrine <10 ng/day
armstrong units Free
Alkaline 4.0-13.0 king- 20-130 U/L catecholamines <100 mg/day
Phosphates armstrong units alkaline Free
Phosphates, Serum 3-4.5 mg/dl 1.0-1.4 mmol/L catecholamines <100 mg/day
inorganic Metanephrine <13 mg/day
Potassium Serum 3.8-5.0 mEq/L 3.8-5.0 mmol/L Vanillyl mandelic
Proteins Serum acid (VMA) <8 mg/day
Total 5.5-8 g/dl Cerebrospinal
Albumin 3.5-5.5 g/dl (50-60%) fluid (CSF) CFC
Globulin 2.0-3.5 g/dl (40-50%) CFC volume 120-150 ml
αl globulin 0.2-0.4 g/dl CFC pressure 60-150 mm water
α2 globulin 0.2-0.4 g/dl Leukocytes 0-4 lymohocytes/ml
β globulin 0.5-0.9 g/dl pH 7.31-7.34
γ globulin 0.7-1.7 g/dl Glucose 50-80 mg/dl
A/G ratio 1.5-3:1 Proteins 15-45 mg/dl
Renal blood flow 1200 ml/min FIGLU 24-hr urine <3 mg/day <17.2 mmol/day
Sodium Serum 136-145 mEq/L 136-145 mmol/L Gastric analysis Gastric juice
pH 2-3 L
Thyroid function Basal acid
tests output (BAO) 1.6-1.8 1.6-1.8
Radioactive iodine Maximal acid
uptake output (MAO) 1-5 mEq/hr 1.5 mmol/hr
(RAIU) 24 hr 5-30% after injection
thyroxine (T4) Serum 4-12 mg/dl of stimulant
thyroidothyro- BAO/MAO ratio <0.6
nine (T3) Serum 80-100 ng/dl Glomerular
thyroid stimula- filtration rate Urine 180 L/day
ting hormone Serum 0.4-5 m /ml (GFR) (about 125 ml/min)
(TSH) 5-HIAA 24 hr urinary 2-8 mg/day
Troponins, erection
cardian (cTn) Females 4-15 mg/day
Troponin 1 (cTn) Seminal fluid Semen
troponin 1 (cTnl) Serum 0-0.6 mg/ml 0-0.6 mg/L Liquefaction within 20 min.
Contd... Contd...
304 Essentials of Clinical Medicine
Contd... Contd...
Reference value Reference value
Component Fluid Conventional SI Units Component Fluid Conventional SI Units
Contd... Contd...
Reference value Reference value
Component Fluid Conventional SI Units Component Fluid Conventional SI Units
Adults
Females 35 mg/kg
Infants
body weight
Transferrin Serum 200-900 pg/ml 200-900 pmol/L
Iron storage form
Vitamin B12 Serum
(ferritin and
Baby stores 10-12 mg
hemosiderin) 30% of body iron
Daily requirement 2-4 mg
Osmotic fragility Blood
Serum level 200-900 pg/ml 200-900 pmol/L
Slight hemolysis at 0.45 to 0.39 g/dl NaCl
Leukocytes in Blood
Complete at 0.33 to 0.36 g/dl NaCl
Health
hemolysis 0.4-0.45 g/dl NaCl
Total leukocyte 4000-11000/ml
Mean corpus-
count (TLC)
cular fragility
Adults 10000-25000/ml
Reticulocytes Blood
Infants (full term, at birth) 6000-16000/ml
Contd... Infants (1 year)
Index
Speech 188 pathophysiological basis 122 proptosis 286 carotid artery 168
aphasia 189 Spot diagnosis 61 secondary 286 subclavian artery 169
assessment 189 Stridor 91 signs 285 vasospastic conditions
dysarthria 189 classification 91 symptoms 285 169
dysphonia 189 Succussion splash 91 Tobacco-related disorders 6 venous disorders 169
Spinal cord 168 Symptomatology 24 Tonus 220 vertebrobasilar artery
clinical applications 273 Syncope 59 clonus 220 169
Brown-Sequard ankle 221 visceral ischemia 169
syndrome 273 T knee 221 Vertebral column 266
corticospinal tracts 273 Temperature 26 lengthening reaction 220 cervical spine 266
medulla oblongata 274 physiological variation 26 tone 221 inspection 266
midbrain 274 Tests 268 Tracheal signs 85 lumbar spine 267
motor neurons 273 bowstring sign 268 Tricuspid regurgitation 163 neck posture 267
pons 274 femoral nerve stretch test 268 causes 163 palpation 266
sensory tracts 273 flip test 268 sacroiliac joints 267
signs and symptoms 274 nerve root compression 268
U sacrum 267
complications 273 straight leg raising test 268 thoracic spine 267
functions 269 Thrills 143 Ulcer pain 32 Vertigo or giddiness 59
hemisection 272 golden rules 144 Urine 54 central 59
lesions 268 mechanism 143 retention 54 functional 59
site 275 murmurs 144 causes 54 non-pathological 59
pathways 269 pathology 144
peripheral 59
tracts 269 pericardial rub 144
ascending 269 tracheal tug 144
V Voice and speech 65
descending 269 Thyrotoxicosis 285 Valvular heart disease 159
transaction 270 complications 286 Vascular diseases 168 W
Spine 266 differential diagnosis 285 neurological presentation 168 Weight gain 12, 24
Splenomegaly 121 history taking 285 abdominal aortic Weight loss 12, 24
mechanism 121 primary 286 aneurysm 169 Wheeze 90