T C Ankrah

Clinical Examination of the Patient
T. C. Ankrah
Chapter 1
TAKING THE HISTORY
 Introduction
 Rapport
 Presenting Complaints
 Systemic Enquiry
 Drug History
 Past History
 Family History
 Social History Including Travel
 Psychological Assessment
 History from a Third Party
 Writing up the History
 Syntheses of the History
Typed and Edited by:

Efua Quansion Konadu
MBChB 1
Chapter 1 Taking the History
HISTORY TAKING
The term clinical examination comprises three essential processes:-
1. History taking
2. Physical examination
3. Side room investigation
HISTORY TAKING
Two doctors performing clinical examinations on the same patient may come out with the same
findings and yet come out with different histories. A good history constitutes 60-70% of the final
diagnosis.
The taking of an accurate and detailed history however comes with experience and repeated
practice.
Certain terms should be made clear from the onset. Symptoms are what the patient complains of
e.g. cough, chest pains, breathlessness and easy fatigability. Signs are what the examining doctor
finds on examining the patient e.g. swollen leg, rash, a shriveled limb or an irregular pulse.
In taking the history one must use language that is simple and easily understood by all.
Rapport
An accurate mutual introduction should be made at the start of the interview and the patient should
be set at ease. In developing countries most patients still regard doctors as powerful all knowing
beings and they are apprehensive when they come into contact with the doctor. It is one’s duty as a
doctor to allay his fears and get him relaxed. In this relaxed atmosphere one is likely to get all the
necessary information that one is seeking.
Presenting Complaints
Be sensitive to the patient and let him feel that one cares. Give him time to express himself and
explain what he feels is wrong himself. This is the ideal situation but in practice one will either have
to help the patient come out with what is wrong with him and sometimes one has to curb a patient
who is so very verbose and gives a lot of irrelevant and unnecessary details. Patients can be grouped
into three main groups.
a) The intelligent, business-like straight to the point patient who gives a correct and detailed
account of his illness without any emotion or hesitation and with little or no help from the
doctor.
b) The shy poor historian who needs a lot prompting and leading questions to get the
facts out of him.
c) The verbose, talkative patient who gives a lot of irrelevant information and who
needs sympathetic guidance from the doctor to retrieve the important facts from
long story.
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Only practice and experience will tell one which patient one is dealing with and how much one
should interfere to get the facts of the history.
Start with an open question such as “What do you feel is wrong with yourself?” or “How did your
illness begin?” followed by “What happened next?”
Then give him time to answer the questions and to express himself freely. Ask about the duration of
each complaint and let him expand each of the presenting complaints. Most patients will require
prompting to get all the facts one needs.
Systemic Enquiry
Now make a systematic enquiry about symptoms in other systems, which the patient has failed to
mention. One will be surprised at the number of symptoms the patient will admit that he has got
even though he did not volunteer them earlier.
Because patients may not remember everything that has happened to them or may consider that
what they do remember is irrelevant or too trivial to mention, it is permissible to jog their memory
with some structured questions on each of the systems.
 General Health
Ask about the weight, appetite, fever, sleep and mood.
 Respiratory System
Ask about cough, sputum production, chest pains, haemoptysis, breathlessness and wheeze.
 Cardiovascular System
Ask about palpitations, breathlessness on lying flat (orthopnoea), chest pains, ankle swelling,
paroxysmal nocturnal dyspnoea, and tiredness. Also ask about exercise tolerance for simple
everyday things like climbing up a flight of stairs or walking uphill or even shaving in the mornings
and leg pains on exertion.
 Alimentary System
Ask about condition of the mouth or bleeding gums, nausea, vomiting, bowel habits and nature of
the stools. Ask about abdominal pains, difficulty with swallowing, belching, haematemesis, epigastric
fullness and flatus. Ask about indigestion and weight loss, the colour of stools (pale, dark, black or
bloody stool).
 Urinary System
Ask about dysuria, polyuria, nocturia, oliguria, stress and/or urge incontinence, poor stream and
stress incontinence. Also ask about strangury which is a constant desire to urinate although there is
little or no urine to be voided. Ask about the frequency of micturition both during the day and during
the night.
 Nervous System
Ask about headache, numbness/tingling, muscle weakness, dizziness, vertigo, blackouts, fits, sleep
pattern, vision and double vision, syncope, hearing (e.g. deafness, tinnitus) and disturbed sensation.
These symptoms need considerable amplification to make sure that the patient and the doctor
mean the same thing.
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 Genital System
Ask about menarche, frequency and duration of periods, blood loss e.g. clots, flooding. Are periods
painful? Ask about sexual activity, libido, impotence, infertility, urethral or vaginal discharge and
post-menopausal bleeding.
 Locomotor System
Ask about muscle pain or weakness, stiffness and swelling of the joints.
If from the history, any system is found to be the prime suspect, then one will need to expand on the
sub-headings.
Also if mental illness is deemed to play a part then one will need to frame additional questions in
this area.
Drug History
One must then ask the patient if he is taking any drugs, either prescribed by a doctor or acquired by
the patient himself. Ask about allergies/hyper-sensitivities to drugs. Take the patient’s history of
allergy seriously as patients have been known to die after they have been given a drug they are
allergic to even though they told the doctor about their allergy but the doctor ignored the
information.
Past Medical History

Now proceed to ask the patient about any past illnesses. Some patients would have forgotten and
one has to jog their memory by asking if they have ever been admitted to hospital and with what
condition. Has he had any surgery in the past? If so does he know what operation he had?
Family History
Ask about a family history of tuberculosis, diabetes mellitus, systemic hypertension, gout, arthritis,
epilepsy, mental illness and coronary heart disease like myocardial infarction. The presence of any of
these illnesses in the family should increase one’s awareness of the possibility of the disease being
present in the patient information about the age and health or the cause of death of the patient’s
close relatives is often valuable.
Social History
Ask about the home conditions, housing, occupation, interests, and habits. Ask about food, tobacco
and alcohol consumption. Tactful exploration of income and commitments can follow, together with
details of the educational background. One must then enquire in all cases about the occupational
history, because some jobs can cause disease e.g. iron deficiency anaemia from hookworm
infestation in farmers, Weil’s disease in sewage workers, mesothelioma in exposure to asbestors and
dyestuffs and byssinosis in exposure in cotton dust.
Foreign Travel
History of foreign travel should be enquired. Certain tropical diseases e.g. amoebiasis and malaria is
acquired by living in endemic areas. Hence any travel within and outside an area should be enquired
about as it may give a clue to the present illness.
The importance of the history of travel is demonstrated by the fact that certain diseases are endemic
in certain areas and one acquires the disease when one travels to that area. For example, if one
wades through or swims in a river, which is known to be infected with schistosomiasis, one can get
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the disease. Also if one travels to an onchocerciasis endemic area one can be bitten by the
transmitting agent-simulium damnosum and one can acquire the disease.
One must also ask of history of foreign travel as a high percentage of people who have Acquired
Human Immune-Deficiency Virus (HIV) give a history of foreign travels.
Psychological Assessment
Psychological factors affect both the patients handling of the current illness as well as the outcome
in all patients. The account of the history and the manner it is delivered will reveal much about the
patients’ personality.
When the physical examination reveals negative findings then it becomes more important to get a
more detailed psychological assessment.
All diseases will influence the ability of the patient to return to work. Some disease-job combinations
will totally preclude a return to that occupation e.g. epilepsy in a pilot or a heart attack in a driver of
heavy goods vehicles.
History from a Third Party

In unconscious patients, people who have had epilepsy or people with mental impairment, one has
to depend on the history from a third person who can give an accurate account of what took place
and the progress of the illness.
Synthesis of the History

When the history has been taken to one’s satisfaction, the first step has been taken to the diagnosis.
The information must now be appraised taking into account the reliability of the patient. The
relevant facts must be separated from irrelevant facts and evaluated objectively.
At the end of the history one must be able to find which system is involved in the disease process
and one must at this stage have an idea of the provisional diagnosis of differential diagnosis or be
still undecided.
Following the history, the examiner should proceed to the physical examination to elicit the
evidence either to confirm or refute his provisional diagnosis based on the history. Sometimes the
findings may point to a different direction altogether.
It is important during the history taking the one looks at the patient all the time. This will help one to
get the added evidence from the facial expression as well as the non-verbal communications from
his face and gestures.
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Writing up the History

After one has completed taking the history, one must now write up. This is an example of the format
of writing up the history in a hypothetical case.
Name: Kwasi Mensah

Sex: Male
Religion: Methodist
Age: 32
Occupation: Labourer
Marital status: Married
Address: N.T.E.R. 54
Fanti New Town, Kumasi
Presenting Complaints: 1) Haemoptysis – 1 day

2) Chest pains – 5 days
3) Cough – 2 months
4) Loss of weight – 3 months
History of Present Illness

Patient was preparing to go to work when he coughed up about 10 ml. /table spoonful of blood. This
is the first time he has coughed up blood and he was so scared and frightened that he reported to
the hospital immediately.
For the past five days he has had pains in the right upper chest anteriorly. The pains radiate to the
back and it is sharp in character. The pains are sometimes severe and made worse by coughing,
sneezing or laughing. The chest pains are present all the time and there are no relieving factors.
The cough is low pitched and bovine in character. It is worse on waking up in the morning and it is
productive of grayish sputum which is mucoid.
He has lost one kilogram in weight over the past three months. He started weighting himself when
he noticed that his trousers were getting loose one him. There has been no change in his eating
habits.
Drug History
He is on cough mixture and paracetamol which he bought himself from a pharmacy shop. He has no
known allergies.
Past Medical History

He was knocked down by a car at the age of 10. He stayed in hospital for two weeks.
He had jaundice at the age of 22 and he was treated at the Outpatients Department.
Family History
His maternal uncle died of pulmonary tuberculosis and his sister is currently receiving treatment for
pulmonary tuberculosis.
There is no family history of diabetes, hypertension or arthritis. Neither is there any family history of
coronary heart disease, epilepsy or mental illness.
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Social History
He works as a labourer with a building firm. He is married with two children and the whole family
sleeps in one room. There are pipe borne water and toilet facilities in the house.
He drinks about half a bottle of local gin a week, mostly the weekends and he smokes ten cigarettes
a day.
Evaluation of the History

From the above history, the symptoms point to a disease of the respiratory system. Now from the
strong family history of tuberculosis and the symptoms, pulmonary tuberculosis is very likely.
However, you must have pneumonia or even bronchial carcinoma in mind, though they appear less
likely.
Summary
In summary I present the case of 32 year old labourer, Kwesi Mensah who presents with a day’s
history of Haemoptysis-5 days, history of chest pains-2 months duration and 3 month history of
weight loss.
In the physical examination, therefore, you must pay more attention to the respiratory system to
support or refute pulmonary tuberculosis, even though you are going to examine all the systems.
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T. C. Ankrah
Chapter 2
GENERAL AND SUPERFICIAL FEATURES
 First Impressions
 Facial Expression
 Characteristic Faces
 Pigmentation
 Abnormal Movements
 Abnormal Sounds
 Anthropometry
 Hydration
 The Hand
 The Mouth
 The Skin, Subcutaneous Tissues Lymphadenopathy
 The Endocrine Diseases
 The Reticulo-endothelial System
 Principles of Examination of the Systems

Agnes Amankwa Arthur
MBChB 1
Chapter 2 General and Superficial Features
GENERAL AND SUPERFICIAL FEATURES

General Examination
The physical examination begins with the examination of the patients as a whole. One’s faculties
should be alert from the onset. While taking the patient’s history, one must observe the patient’s
demeanour. The examination must be carried out as gently as possible without tiring the patient
unnecessarily. The greeting, handshake or dressing of the patient will give one early impression of
the patient’s condition. The gait may indicate neurological or locomotor disturbance. The posture of
the patient can be informative.
First Impression
On seeing the patient the first question one must answer is “Does this patient look ill?” Although this
appears to be a simple question to answer, experience is essential to make a fair judgment. It is not
always possible to define specifically why the patient looks ill. Relatives and friends may draw
attention to deteriorating health unnoticed by professional health workers.
Facial Expressions
Observe the patients facial expression. A look of pain, fear, excitement, anxiety or grief may be
noticed.
Characteristic Faces
Much can be learnt from the patient’s facial appearance and, this may allow a “spot diagnosis” to be
made. Once seen in real life and committed to memory, these are often easy to recognize.
Unfortunately, many of the so called “classical” appearance of disease portrayed in some textbooks
are so gross that the student or young doctor fails to recognize the early cases. Do not fall into the
sin of diagnostic greed in expecting every criterion to be fulfilled before daring to identify a
syndrome.
The immobile stare an d poverty of facial movements associated with the shuffling gait of
Parkinsonism; the startled appearance and gross exophthalmus in hyperthyroidism in a young
person; the coarse features with large jaws and hands of acromegaly; the big head of Paget’s
disease, the rash of ophthalmic herpes zoster; puckered mouth of scleroderma and stiff awkward
movements of ankylosing spondylitis can all be diagnosed at a glance, as can the pale puffy face of
nephritis or the eyes of a patient with Down’s syndrome.
In some diseases a new observer may have advantages. The slow and almost imperceptible changes
in appearance in myxoedema may be unrecognized by a conscientious doctor who sees the patient
regularly for a succession of seemingly unconnected trivial complaints; a new doctor immediately
recognizing the conditions may be astonished by the lack of clinical acumen of the earlier medical
attendant.
A common feature of illness is loss of weight and this needs careful assessment. The wasted patient
with gaping collar bone, baggy trousers and tightened belt does not have to confirm his weight loss
with documented serial recordings. The patient’s demeanour may give clues as to the cause of his
weight loss. The inexorable life-sapping progress of the patient with extensive tuberculosis or
disseminated cancer may be suspected at first sight. The perky, bird-like features of the school girl
with anorexia nervosa may provide early clues as may the restlessness of the thyrotoxic.
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Anaemia is another pointer to organic disease but may at times be surprisingly difficult to detect
clinically. A glance at the nail beds and fingers may be more helpful. Nevertheless the only
infallibility to anaemia is the measurement of the haemoglobin level.
The alcoholic presents with plethoric and suffused conjunctiva associated with a pervading aroma of
alcohol especially early in the morning and sweating palms and fine tremors.
The smoker smells of nicotine and a quick look at his nicotine-stained finger confirms this.
Also look for signs of self inflicted trauma in the young.
The patient’s face may betray psychiatric disease. Depression is probably the earliest to identify. The
withdrawn expressionless retarded patient with advanced disease is quickly identified but milder
depression may be difficult to distinguish from simple unhappiness. At the other extreme the
hypomanic patient may demonstrate few obvious facial stigmata but the constant flow of
conversation and disarmingly frank comments may all alert the doctor.
Finally local knowledge is important. Appearances familiar to doctors in the tropics may perplex
those working in the western world. Tuberculoid leprosy in an African visitor might confuse a Boston
Casualty officer yet would be quickly recognized in Kumasi. The medical registrar in Hong Kong
quickly looks for the nasopharyngeal tumour in his patient with cranial nerve lesions; his counterpart
in New York may not think of that diagnosis when examining the proprietor of a Chinese restaurant.
Pigmentation
The cause of increased skin pigmentation of chronic debilitating illness or neoplastic disease is
poorly understood but it is mainly due to increased deposition of melanin. In renal failure,
deposition of urochromes in the skin occurs. A diffuse telangiectatic mat over the cheeks may be
seen in patients with cirrhosis of the liver.
Some increased pigmentation of the cheeks and forehead (chloasma) occurs during and fades after
pregnancy. The most gross hypermelanotic pigmentation in disease is seen with Addison’s disease
and with Nelson’s syndrome in association with extremely high levels of adrenocorticotrophic
hormone. The pigmentation of haemochromatosis is characteristically slaty grey. The chronic
administration of some drugs such as Busulphan may darken the skin. Patchy loss of pigmentation of
the face may be due to vitiligo, a curious disorder linked with other auto-immune disorders such as
Addison’s disease, pernicious anaemia and thyrotoxicosis. However, the commonest cause of patchy
depigmentation of the skin is bleaching of the face for cosmetic reasons. Inflammatory skin
eruptions can also cause patchy depigmentation of the skin as seen in onchocerciasis infestation.
Complete depigmentation of skin hair and uveal tract is seen in oculo-cutaneous albinism.
Abnormal Movements
Observe any abnormal movement such as the coarse pill rolling tremor of Parkinsonism, the flapping
tremor of encephalopathy due to hepatic failure, uraemic twitching in renal failure and the fine
tremor thyrotoxicosis.
Abnormal Sounds
Pay attention to the patient’s voice and speech. Note the hoarseness of voice in laryngitis and a
lesion of recurrent laryngeal nerve. Note the presence of dysarthria and the pitched slow deliberate
‘thick’ speech in myxoedema. Note the presence of wheezing, rattling or stridor in respiratory
illness.
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Abnormal Odour
Note the smell of foetor hepaticus in liver failure, the sweet smell of acetone in the breath of the
patient with diabetic ketoacidosis.
Mal-odour from dirty clothes and general soiling occur in the elderly infirm patients who are unable
to look after themselves as in mentally defective patients.
Halitosis may be due to poor oral hygiene or pulmonary suppuration.
Anthropometry
Note obesity or thinness in the patient. Increase in height may indicate gigantism or Marfan’s
syndrome. Note dwarfism or the presence of achondroplasia.
Hydration
Assess the state of hydration in all cases of vomiting, diarrhoea, sweating and polyuria by looking at
the tongue and assessing the skin elasticity in the anterior chest wall.
THE HANDS
The hand provides an easily accessible area with which to start the physical examination by contact
with the patient.
Look at the colour of the hands. The palm is pale in anaemia. Palmar erythema-reddening on the
thenar and hypothenar areas, is seen in liver diseases. Observe for Dupuytren’s contracture –
thickening and contraction of the tendons in the middle of the hand, seen in patients with chronic
liver disease. Observe any wasting of the intrinsic muscles of the hand in nerve or muscle lesions.
Observe any deformity of the hand. Clawing of the fingers seen in ulnar nerve lesions (fig. 2:1). Look
for the presence of Heberden’s nodes – bony swelling of the distal inter-phalangeal joint – seen in
osteoarthrosis (Fig. 2:2) and Bouchard’s node – fusiform swelling or proximal inter-phalangeal joint –
seen in rheumatoid arthritis (Fig. 2:3).
Figure 2:1 Clawing of Hand.
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Figure 2:2 Heberden’s Nodes. Figure 2:3 Bourchard’s Nodes.
Look for arachnodactyly – long spidery fingers seen in Marfan’s syndrome, Achard syndrome, the
MASS syndrome and kindred hereditary disorders of connective tissue (Fig. 2:4).
Figure 2:4 Arachnodactyly.
Then observe for the presence of finger clubbing which occurs in respiratory, cardiovascular and
alimentary diseases.
Clubbing of fingers is staged according to its severity (Fig. 2:5):
STAGE I - increased sponginess of the nail fold.
STAGE II - obliteration of the angle between the nail and the nail fold.
STAGE III - increased convexity of the nail in both directions longitudinally

and transversely.
STAGE IV - Bulbous swelling of the distal end of the finger.
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STAGE I STAGE II
STAGE III STAGE IV
Figure 2:5. Stages of Clubbing.
Nail
Examination of nail may give diagnostic clues. Note koilonychia (concavity of the nail) in iron
deficiency anaemia (Fig. 2:6), pitting of the nail in psoriasis (Fig. 2:7); splinter haemorrhages in
infective endocarditis and whitening of the nail (leuconychia) in hypoalbuminaemia.
Figure 2:6 Koilonychia. Figure 2:7. Pitting of the nails in Psoriasis.
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THE MOUTH
Uvula
Hard Palate
Soft Palate
Fauces
Tonsil Pharynx
Figure 2:8 Mouth
Tongue
The Lip
Note any cracking of the lips more common in the Harmattan/Dry season. Red denuded epithelium
in the line of closure of the lips, known as cheilosis occurs in riboflavine deficiency. Angular
stomatitis, consisting of painful inflamed cracks at the corners of the mouth is due to deficiency of
iron or riboflavin deficiency. A torch and a tongue depressor are needed for examination of the
mouth.
The Teeth
Inspect the teeth for discolouration, caries and missing teeth. The teeth may be pitted, mottled and
yellow in colour in fluorosis and poorly developed (hypoplastic) in juvenile hypoparathyroidism.
The Gums
Gingivitis is common and may bleed. Hypertrophy of the gums occurs in epileptics who are on
Phenytoin. Painful ulcero-membranous gingivitis may be due to Vincent’s infection which is due to a
combination of a spirochaete and a fusiform bacillus. This leads to cancrum oris.
Note the soft spongy haemorrhagic gums of scurvy, the hypertrophied bleeding gums of acute
leukaemia and the blue line in chronic lead poisoning.
The Tongue
Fasciculation of the tongue is seen in lower motor neurone disease such as progressive bulbar palsy.
Wasting of the tongue occurs with lesions of the hypoglossal (XII cranial nerve) and when the tongue
is protruded forwards it deviates towards the affected side (Fig. 2:9). The tongue is enlarged in some
cases of primary amyloidosis, in acromegaly and myxoedema.
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Figure 2:9 Lower Motor Neurone Lesion of the Right Hypoglossal Nerve (XII)
Surface of the Tongue

This varies greatly both in regard to colour and appearance. Variation in colour may be due to foods,
particularly coloured sweets or they may be due to changes in the haemoglobin.
Central cyanosis is best assessed by inspecting the under surface of the tongue.
Fungiform papillae are small red flat elevations seen on the surface of the tongue especially at the
tip and edges. Filiform papillae are situated in parallel rows across the tongue and they give rise to
the fur. Transient denuded islands give rise to the term ‘geographical tongue’. This is usually a
symptomless change of no known significance but some patients can be worried a great deal about
this and they need reassurance about the harmless nature of this lesion.
Iron or Vitamin B deficiency cause a smooth, clean looking tongue from diffuse atrophy of the
filiform papillae.
Excessive furring is of little diagnostic significance. It occurs following a soft or milky diet or in the
presence of fever or dehydration. Leukoplakia is characterized by grey opaque areas interspersed
with few red inflamed patches. This lesion is precancerous.
The circumvallate papillae separate the anterior two thirds from the posterior one third of the
tongue. They are set in a wide V with its apex pointing backwards and originating at the foramen
caecum. Patients may discover these for themselves and are often alarmed in case they suffer from
cancer. They only need to be reassured. Congenital fissuring of the tongue occurs in varying degrees
but has no pathological significance whatsoever.
The Palate
The soft palate with the uvula comprise the posterior one third of the palate. In lesion of the vagus
(X cranial nerve) the soft palate on that side remains immobile while the normal size moves up,
moving the uvula towards the normal side when the patient is asked to say ‘ah’. Note any deformity
such as cleft palate.
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The Tonsils
Look for enlarged and inflamed tonsils. The tonsils, in common with lymphoid tissue elsewhere
enlarge to reach a maximum size between the ages 8-12 years after which it involutes.
Tumours of the tonsils may occur either in isolation or as part of lymphatic leukaemia or lymphoma.
Buccal Mucosa
Inspect the buccal mucosa for Koplik’s spots – whitish areas like sprinkled salt on a reddish
background, seen in measles and also look for pigmentation. Pathological pigmentation of the
mouth is seen in Addison’s disease. Other conditions giving pigmentation of the buccal mucosa are
chronic cachexia, malabsorption syndrome, haemochromatosis or the rare Peutz-Jeghen’s syndrome
of polyposis of the small intestine with pigmentation in and around the mouth and particularly on
the lips and fingers.
Any indolent ulcer in the mouth for which an adequate explanation is not forthcoming and which
persists should be suspicious of carcinoma.
Thrush
Thrush is seen as white deposits on the mucous membrane of part of the mouth. It is caused by the
fungus – candida albicans. Thrush occurs in the elderly in association with febrile or debilitating
diseases. Thrush is also common in patients being treated with antibiotics, prednisolone or immuno-
suppressive drugs.
THE SKIN
The most important abnormalities in the skin relevant to general examination are pallor, yellowness,
pigmentation, cyanosis and cutaneous eruptions.
The skin is not only an important organ with vital physiological functions but it is also the flag with
which we communicate with the outside would. Skin disease places a strain on sufferers out of
proportion to the disturbances in function which the pathology produces. A leper complex is
frequent and social and sexual contact may be shunned. It is therefore understandable that patients
with psoriasis, a persistent and often lifelong condition show an increased incidence of alcoholism
and psychiatric disease.
Certain skin conditions may indicate an internal disorder. For example pigmentation and thickening
of the skin in the axilla and flexures of the limbs a rare condition termed acanthosis nigricans may be
a marker of internal malignancy especially carcinoma of the stomach. Another example is
pyodenrma gangrenosum. This rare skin lesion is a classic example of a skin condition associated
with internal disease. The necrotic ulcers, most often on the legs are usually associated with
ulcerative colitis. Total proctocolectomy almost always results in rapid healing.
THE HISTORY
Skin problems which bring a patient to see his doctor can be grouped into:
1. Localised blemishes and abnormalities which although minor may loom
very large in the patients mind, together with skin tumours both
benign and malignant.
2. More generalised eruptions and also problems with skin appendages such as sweat glands,
hair or nail and sabeceous glands.
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Presenting Complaint
Find out the patient presenting complaint. Has he come to see the doctor because of the rash or he
has other symptoms as well. Is the condition spreading rapidly? Did he notice the skin lesion or
somebody pointed it out to him?
Duration
Try and get an accurate idea of the duration of the skin condition. Patients tend to under-estimate
the length of time such lesion have been present.
Nature of the Lesion

What exactly did the patient notice first? Was it something visible that was noted by chancee when
the patient undressed? Did symptoms such as itching or soreness develop before there was anything
visible? What did the original lesion look like?
Subsequent Change
What has happened to the lesions since they started? Have the original ones disappeared and been
replaced by others or has there been relentless spread. Do the lesions come in crops?
Is there a pattern to their spread? Has the lesion got a centripetal or a centrifugal distribution?
Associated Symptoms
The presence of pain, weeping, bleeding and above all, itching should be noted. If present the
periodicity of the itching and exacerbating and relieving factors must also be noted.
Topical Application
Ask what the patient has been applying to the skin. Patients often apply some topical preparations
on the skin rash before seeking medical attention. What one actually sees may be the result of self
medication or inappropriate therapy. The original condition may have long since undergone
spontaneous resolution.
General History
Ask about the patient’s previous skin diseases. Ask about other illness both past and present and any
medication that was given. Ask about the patient’s occupation and hobbies, as these may be the
source of the trouble. Also ask any travels both within and outside the country.
EXAMINATION
The whole skin including the hair, nails and assessable mucosae, should be fully exposed, preferably
in natural light. The main aspects of examination are inspection and palpation. Whilst inspection
must have the pride of place, palpation is also important not only to aid diagnosis but also to
reassure the patient that one does not fear their skin diseases.
INSPECTION
Distribution of Lesions
In order to carry out a proper examination of the sin the patient should be fully undressed within the
limits of decency. Note any hypopigmentation (seen in fungal infection) hyperpigmentation or
general redness (erythroderia). What is the pattern of the lesions on the skin surface? Are they for
example symmetrical or just affecting exposed areas? If so does the distribution suggest
photosensitivity or a reaction to external factors? Note the presence of contact dermatitis in the
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dorsum of the feet with wearing shoes/sandals made with allergic substance or ear rings or
necklaces to which the patient is allergic. The distribution of the rash gives the game away.
Examine the surface of the scalp for fungal infection, alopecia and scarring. Look behind the ears and
the external auditory meatus. Include an inspection of the mouth. Raise the arm and inspect the
axilla.
Look at the nails and nailfolds for clubbing, pitting of the nails and fungal infection of the nails. Look
in between the fingers for the burrows of scabies.
Look under the breasts for intertrigo and fungal infection and gaze into the depths of the umbilicus.
Look at the feet and in between the toes for fungal infection e.g. athletes foot.
Finally look at the genitalia and perianal area for any skin lesion.
Morphology
Look closely at the lesions and determine their morphology. A macule is a lesion which can be seen
easily but is impalpable e.g. a freckle. When a lesion can be felt a well as seen, it may be described as
a papule or if more extensive a plaque or if deeper a nodule. Dermal edema with no overlying
epidermal change produces a weal e.g. urticaria.
Fluid filled blisters on the skin are arbitrarily divided on the basis of size into smaller vesicles,
medium blisters and large bullae. Blistering is an important physical sign. A number of conditions
always blister such as pemphigus; others occasionally so as like erythema multiforme. Pustules
contain debris, leukocytes and micro-organisms as well fluid but do not automatically indicate
infection; the pustules of psoriasis for example are sterile.
Where the epidermis is lost an erosion is formed the consequent oozing of serous fluid when this
dries produces crusts. Erosion will heal without damage to the skin but ulcers produced by
penetration into the dermis will heal to give scarring.
Scaling is the accumulation of keratin, either normal or abnormal, on the skin surface. It may be the
only visible change, as in some ichtyoses or accompanied by inflammation as in psoriasis. Shedding
of the horny layer is termed desquamation and can follow an inflammatory disorder such as
exanthema, drug reaction or underlying cellulitis.
Outline
The margin of the individual lesion should be carefully examined. Some disorders give rise to lesions
with a clear-cut division between normal and abnormal skin whereas in others the abnormal blends
into the normal. Generally a convex border indicates the direction of spread. Where multiple small
lesions have coalesced to produce larger patches the margin will appear scalloped. Lichen planus is
characteristically limited by fine skin creases producing polygonal lesions. If the skin in the centre of
a lesion returns to normal as it spreads an annular lesion is formed. This is typical of ringworm but it
is not pathognomonic. Linearity may imply either an underlying structural defect or a response to
external factors applied to the skin in a linear fashion such as occurs in the Koebner phenomenon.
This occurs most commonly in psoriasis and lichen planus.
Colour
Colour changes in dark skins may be difficult as redness may not be so obvious. As a general rule
very bright red erythema indicates an active disorder and as activity begins to decline the lesions
become paler, sometimes with the redness being replaced by post inflammatory pigmentation.
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Texture
Is the surface of the lesion scaling or not? If it is difficult to determine the removal of surface grease,
using a little ether is helpful. If scaling is present and makes it difficult to see the base of the lesion a
little oil can be applied to the surface. White scales are seen typically in the discoid lesions of
psoriasis.
PALPATION
Palpation should never be omitted. It can be a great relief to the patient to know that one is not
afraid to tough their skin. Relatives and friends may keep a discrete and their sex lives may be
nonexistent so the last thing they want is a medical adviser who confirms their untouchability.
Palpation also conveys a lot of information. The skin may be thickened in which case it should be
possible to identify whether it is the epidermis which is thickened (lichenified) or the dermis. The
lesion might spread much further than is evident visually, as calcified or cystic, cooler or warmer
than the surrounding skin, as in erythema nodosum or atrophic with loss of dermal collagen. Note
any tenderness; in erythema nodosum the red nodules in the skin of the legs are painful. Causes of
erythema nodosum include infections like streptococcus, tuberculosis, leprosy, deep mycosis and
cattle ringworm. Other causes are sarcoidosis, Crohn’s disease, and ulcerative colitis. The rest are
drugs like sulphonamides and malignancies; especially after radiotherapy. Erythema nodosum may
be persistent and the cause is unknown.
Crusts when present should be removed from the sample area so the underlying surface can be
inspected. As crusts are not firmly adherent to the surface, the simplicity of removal will also help to
distinguish them from keratin, which is an integral part of the lesion and can rarely be removed with
ease. Any scale should be tested for silveriness which is pathognomonic of psoriasis.
ENDOCRINE DISEASES
THE THYROID GLAND

The gland may present abnormalities of function or of size; although there is no correlation between
the two. The grossly thyrotoxic patient may have a small gland and a large gland may be under-
active. The symptoms of an over or under active thyroid may be so insidious that the patient or the
close family fails to notice them.
The gland secretes thyroxine (T4) and tri-iodothyronine (T3) which circulate largely bound to
proteins e.g. thyroid-binding globulin and pre-albumin. T4 is converted in peripheral tissues to the
move active T3. Over-activity of the thyroid gland is confirmed by the finding of high levels of free
and bounds T4 and T3 with low levels of thyroid stimulating hormone (TSH). Primary hypothyroidism
is confirmed by high TSH levels since abnormally low T4 and T3 levels fail to suppress pituitary TSH
secretions.
SYMPTOMS
 Swelling In The Neck
The patient or the relatives may have noticed a swelling in the neck. Pain is common only in sub-
acute (De Quervain’s) thyroiditis or in the case of haemorrhage into a cyst. Constant discomfort
sometimes occurs in Hashimoto’s thyroiditis.
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 Appetite and Weight

Thyroid over-activity is classically associated with increased appetite and weight loss, although
occasionally the hyperphagia is such as to cause weight gain or appetite is actually diminished.
Conversely, hypothyroidism causes weight gain.
 Tolerance of Heat and Cold

Intolerance of heat and night sweats are common but not invariable features of thyrotoxicosis.
Cold intolerance is associated with hypothyroidism.
 Neuro-Psychiatric Symptoms
Thyroid over-activity may cause tremor, irritability, restlessness, over-activity and insomnia. It
may exacerbate underlying psychiatric disorder and in severe cases hallucinations and psychosis
are described.
Conversely the hypothyroid patients may be slowed and dull, and occasionally depressed but
sometimes quite cheerful with the so called “myxoedema wit”. In extreme cases psychosis may
occur.
 Cardiovascular and Respiration Symptoms

Atrial fibrillation, palpitations or shortness of breath are commonly associated with toxic nodular
goiter in the older patients but may be a feature of thyrotoxicosis at any age. Shortness of
breath may also occur in myxoedema in which pericardial effusion, myocardial degeneration and
coronary artery disease are not infrequent. A large retrosternal goiter may compress the trachea
and cause stridor and dsypnoea.
 Gastro-Intestinal Symptoms
In thyrotoxicosis intestinal hurry may be such as to cause diarrhoea and in extreme cases
steatorrhoea. In hypothyroidism there is usually constipation.
 Menstruation
Oligomenorrhoea is typical of thyrotoxicosis and menorrhagia of hypothyroidism.
 Muscles
Myopathy, particularly of the proximal and girdle muscles is a common feature of Grave’s
disease.
 Skin and Hair

With hypothyroidism, the patient complains of dry skin and thinning hair. Increased sweating is
characteristic of the thyrotoxic patient who may also complain of hair loss, particularly early
after treatment.
EXAMINATION
The Thyroid Gland
The normal gland consists of two lateral lobes extending from thyroid cartilage to the sixth tracheal
ring and connected by an isthmus. It relates posteriorly to the carotid artery and recurrent laryngeal
nerves. The four parathyroid glands lie within its fascia posteriorly.
Look for swelling or asymmetry from the front and side. Ask the patient to take a sip of water into
the mouth and then to swallow. Swellings of the thyroid usually move freely on swallowing and even
a retrosternal goiter may be detected in the suprasternal notch.
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Palpation is best carried out from behind the seated patient with the fingers over the anterior
triangle of the neck pointing downwards towards the suprasternal notch.
In Grave’s disease {exophthalmic goiter} the thyroid is diffusely and symmetrically enlarged with a
softish consistency and a systolic bruit on auscultation. The gland of Hashimoto’s disease is of similar
appearance but is often firmer and may be slightly tender.
In sub acute or De Quervain’s thyroiditis the gland is very tender.
Diffuse enlargement is seen with many non-toxic and iodine deficient goiters. The nodular goiter is
frequently asymmetrical and firm with one or more nodules. Palpation may be deceptive in that
what seems to be a single nodule often turns out on further investigation to be just part of a multi-
nodular goiter.
Single nodules may represent functional adenomas associated with thyroid over-activity. These
functioning single nodules should always be viewed with suspicion and investigated further to
exclude malignancy.
Undifferentiated carcinoma of the thyroid may present as diffuse enlargement of the thyroid which
is fixed and fails to move on swallowing. Palpate carefully for enlarged local lymph glands which may
be the site of secondary spread.
Very large goiters may embrace the whole neck or cause superior vena caval obstruction. When the
goiter is completely substernal the clinical diagnosis is often difficult.
Signs of Thyrotoxicosis
The patient is agitated and the face is flushed and shiny. The hands are warm and sweaty. The
patient is restless and hyperkinetic. There is fine tremor of the outstretched hands. Finger clubbing
occurs but is rare.
 Cardiovascular Signs
The systolic blood pressure is raised and the pulse pressure is increased with a collapsing quality.
The apex beat is forceful and a functional systolic bruit may be heard over the pericardium as
well as over the thyroid. In severe cases there may be high output heart failure.
 Eye Signs in Thyrotoxicosis

Upper lid retraction due o over-activity of the levator palpebrae superiors is the most common
eye sign in thyrotoxicosis. The white sclera is constantly exposed between the upper lid and the
iris and is most apparent when the patient’s gaze follows the examiner’s fingers upwards. As the
finger is lowered the upper lid lags behind the movement of the eye in a series of jerky
movements. Other eye signs are exophthalmos, chemosis, periorbital oedema and
ophthalmoplegia. An important sign in thyrotoxicosis is pretibial myxoedema which are raised
purplish/brown blotches over the shins. This is seen in severe Grave’s disease and it persists
despite cure of thyrotoxicosis.
 Myopathy
Myopathy may be present. Hence, look for wasting and weakness of muscles, particularly in the
scapular and shoulder regions. Some patients with myopathy of the buttocks and thighs may
have problems climbing stairs and rising from a squatting position.
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Signs of Hypothyroidism
The patient is usually overweight with dry scaly skin, thinning hair and eyebrows, translucent
puffiness of the features, low pitched slow voice, slow movements and bradycardia. The tongue is
enlarged and the hands puffy. The ankle jerk shows slow relaxation.
DISORDER OF BODY WEIGHT
Obesity
The vast majority of fat people have simple obesity and endocrine cause is found in less than 2%.
Cushings’ syndrome is rare whereas overweight associated with hirsutism, oligomenorrhea and
hypertension is common. Weight gain in most hypothyroid patients is modest. Rarely, as a result of
head injury or tumour damaging the hypothalamic region, a pathological appetite may develop.
Overweight is caused by an imbalance between energy intake and expenditure over years.
In the history try and find the weight of parents and siblings and try and establish if obesity dates
from childhood or is of recent origin. Make some estimate of daily energy intake and of exercise.
Oligomenorrhea is caused by overweight as well as underweight. In the examination compare the
weight and height of the patient with that of standard tables. Measure the circumference of the
upper arm with a tape measure midway between the acromion and the olecranon and the triceps
skin and fat fold at the same level with skin calipers. Use a special large cuff in measuring the blood
pressure to avoid falsely high readings when the standard cuff is used. Test the urine or preferably
the blood sugar to exclude diabetes mellitus as a consequence of obesity.
Anorexia Nervosa
Non-specific anorexia and cachexia may result from serious organic disease or from depressive
illness. The more specific condition of anorexia nervosa is usually seen in young women and
associated with disordered body image which leads them to exclude carbohydrate and to some
extent fat, although protein intake is normal. There may be a history of self-induced vomiting.
Secondary to weight loss, there is depression of hypothalamic function with amenorrhoea. Despite
evidence to the contrary, the patient persists with the delusion of being too heavy.
Growth and Development

When a patient complaints of short statue or delayed development, try and obtain the data on
birthweight and subsequent height and weight measurements. Enquire about maternal height and
intercurrent illness during pregnancy, and drug treatment during infancy and childhood. Bronchial
asthma, renal disease, heart disease, nutritional deficiency and steroid treatment may all impair
growth. The family history is critical, since the average of parents’ height is a guide to that expected
in the child. Is the short statue the result of heredity? Ask the age at which puberty took place in the
parents, since delay in puberty and the growth spurt associated with it is often inherited. Also plot
serial height data on a growth velocity chart. A growth rate of more than 4-5 cm per annum virtually
excludes any disease process.
Growth hormone, thyroxine and sex hormones all contribute to growth and specific deficiencies
should be sought. Look for chromosomal abnormalities e.g. Turner’s syndrome with its short stature,
neck webbing and increase carrying angle of the arm. The stages of puberty in girls are assessed
according to breast development, body hair and menarche (onset of period). Failure of any signs of
puberty to appear by the age of 14 years warrants concern. In boys onset of puberty is rarely
delayed beyond the age of 17 and it is staged by changes in penile and testicular size, voice changes
and body hair development. If the testes appear undescended, palpate again after the patient has
had a warm bath. Retraction should not be mistaken for maldescent.
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THE PITUITARY
The pituitary gland may cause disease either because of enlargement or changes in function or both.
Pituitary tumours can give rise to local effects of the tumours such as bitemporal hemianopia, raised
intracranial pressure; hormone production eg acromegaly and destruction of remaining functioning
pituitary resulting in hypopituitarism. Non functional tumours may arise within the pituitary or
outside it e.g. craniophyaryngioma and cause disease by pressure on surrounding parts, particularly
the optic-chiasma causing bitemporal hemianopia. Lateral extension may occur downwards into the
sphenoid bone. Pressure from functioning or non functioning tumours may hypothalamus causing
anterior pituitary damage with defect in secretion of gonadotropic, growth hormone, thyroid-
stimulating hormone or adreno-cortico-trophic hormone. Damage to the posterior pituitary gives
rise to diabetes insipidus.
History and Examination

Local Effects of an Enlarged Pituitary
The patient may complain of recent deterioration in vision, particularly of the lateral part of the
visual field. Such a patient demands formal examination of the optic and visual fields as well as a
detailed history and examination. Infraction and haemorrhage into a tumour is described as pituitary
apoplexy and presents with sudden onset of severe headache and visual failure, constituting a
neurosurgical emergency.
Hypopituitarism
An expanding tumour or other destructive process first damages gonadotropins and growth
hormone secretion with failure of growth and development in childhood and adolescence,
impotence in the make, amenorrhoea and infertility in the female and loss of body hair with
regression of secondary sexual characteristics in both sexes. Further destruction result in Thyroid
Stimulating Hormone and Adreno-Cortico-Trophic hormone failure with secondary hypothyroidism
and failure of glucocorticoid secretion. In contrast to Addison’s disease, some mineralocortiroid
secretion is maintained. Panhypopituitarism causes lethargy, tiredness and lack of energy with
anorexia, weight loss and general debility. Acute intercurrent illness may precipitate a hypopituitary
crises characterized by coma, hypothermia, hypoglycaemia and hypotension.
Examination shows the patient to be pale. The scalp hair is thin and eyebrows sparse and the body
hair absent. The skin is thin and often smooth. In the male, muscle mass is lost and the testes are
small and soft. Blood pressure may be low.
Sheehan’s syndrome refers to a form of hypopituitarism which is caused by pituitary infarct

associated with severe postpartum haemorrhage. The patient fails to lactate or re-established
menstruation.
Functioning Tumours
Prolactinma: This causes excess prolactin secretion. Prolactin causes galactorrhoea and inhibits the
pituitary gonadal axis causing amenorrhea and infertility in the female and diminished androgen
secretion n the male.
Acromegaly
Growth hormone secreting tumour may cause damage by space occupancy but also give rise to the
characteristic symptoms and signs of growth hormone excess. Before epiphyseal closure this results
in gigantism but once the epiphyses have closed the effect is to cause the thickening of tissue known
as acromegaly. The patient may notice an increase in the hands and feet. Many complain of
headache and sweating. There is coarsening and thickening of the skin and features with enlarges.
Overgrowth of bone results in osteoarthritis with joint pains, carpal tunnel syndrome, myelopathy
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and nerve root compression. Many patients have a tendency to hypertension and early
cardiovascular disease as well as diabetes mellitus.
Cushing’s Syndrome
This syndrome results from prolonged exposure to glucocorticoid excess and falls into four
categories:
1. Iatrogenic due to prolonged high dose of steroid treatment.

2. Ectopic adreno-cortico-trophic hormone (ACTH) production from secreting tumour eg oat-
cell carcinoma of lung or carcinoid. Both adrenals are enlarged and hypersecrete.
3. A benign or malignant tumour of the adrenals.
4. Cushing’s disease due to an adreno-cortico-trophic hormone (ACTH) secreting tumours of
the pituitary giving rise to bilateral adrenal hyperplasia.
Clinical features of Cushing’s syndrome are central obesity and moon face with wasting of limb
muscles. Purple striae are seen upon the obese trunk.
The skin is characteristically thin and fragile and large purpura may be present. There may be
oedema of legs and conjunctivae. Evidence of hypertension and hyperglycaemia should be sought.
Malignant causes of Cushing’s syndrome are associated with low serum potassium levels adding to
the muscles weakness associated with the wasting effect of cortisol.
Nelson’s Syndrome
When the adrenals have been removed for the treatment of Cushing disease the Adreno-cortico-
trophic hormone secreting tumours continues to enlarge and secrete Adreno-cortico-trophic
hormone and allied compounds such as melanocytes-stimulating hormone (MSH) resulting in skin
pigmentation as well as the space-occupying effect of the tumour.
THE ADRENALS
Addison’s Disease
This is caused by destruction of the adrenal cortex by tuberculosis or autoimmune endocrinopathy
which results in failure of both gluco-corticoid and mineralocorticoid secretion. Symptoms are of
weakness, anorexia and weight loss. On examination the patient is often thin and wasted. There is
pigmentation of the skin particularly striking in the palmar creases and in areas of pressure from
clothing straps. Pigmentation should also be sought in the buccal mucosa. The blood pressure should
be taken lying and standing. It is usually low with an excessive postural drop. In the face of
intercurrent illness an acute Addisonian crisis may be precipitated because of the inadequate
cortisol response to stress. This presents with abdominal pain, vomiting and collapse mimicking an
acute abdomen.
DIABETES MELLITUS
The three most common presenting symptoms are thirst, polyuria and weight loss. Other
presentations include pruritus vulva, balanitis and tiredness. Polyphagia (excessive appetite) is very
rare and suggests coincidental thyrotoxicosis. In the newly diagnosed middle age diabetic patient
loss of appetite is sinister and suggests carcinoma of the pancreas. Hyperglycaemia can be
asymptomatic and they are diagnosed at routine medical examination (e.g. for work or life
insurance). In others, the hyperglycaemia is undetected until the patient presents with a diabetic
complication.
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Examination
The purpose of the examination is to confirm the diagnosis, classify the type of diabetes and detect
any complications.
Confirmation
In health the blood sugar levels are remarkable constant and rarely outside the range of 3.5-8.0
mmol/L. In those who present with symptoms a single fasting blood sugar over 8 mmo1/L or a
random value over 11.1 mmo1/L clinches the diagnosis. Glucose tolerance tests are rarely necessary.
Classification
Diabetes is like anaemia and jaundice, a syndrome with many possible causes. An important part of
the history and examination is to look for these rare causes. The causes of diabetes include Cushing’s
syndrome, acromegaly, thyrotoxicosis, phaeochromocytoma, Conn’s syndrome
{hyperaldosteronism}. Others are haemochromatosis, chronic pancreatitis and carcinoma of the
pancreas. The rest are drugs e.g. steroids, diuretic (thiazides) and very rare genetic syndrome e.g.
DIDMOAD (diabetes inspidus, diabetes mellities, optic atrophy and deafness).
Beta-blockers do not cause diabetes per se but they suppress the therapeutic sympathetic induced
correction of hypoglycaemia.
Most cases of diabetes are idiopathic and are simply classified as:
1. Insulin dependent (IDDM) type I or juvenile onset diabetes.
2. Non-insulin dependent (NIDDM) type II or maturity onset diabetes)
Complication
Complications as the presenting feature of diabetes are usually present in middle aged and elderly
where the diabetes has been present for a long time. These complications include retinopathy,
nephropathy and neuropathy. Others are claudication, angina, heart attack and stroke. The rest are
necrobiosis lipoidica diabeticorum, cataracts, psychological problems and hyperlipidaemia.
The diagnosis of diabetes is easy and most newly diagnosed patients will have no physical sign.
However, when one finds the raised blood glucose, one is diagnosing an incurable (but controllable)
illness the treatment of which requires more patient participation than most other illness.
RETICULO- ENDOTHELIAL SYSTEM
SYMPTOMS
Anaemia, haemorrhagic disorders, haematological malignancies and lymphomas require a blood
count, bone marrow examination and / or lymph node biopsy for a definite diagnosis to be made.
Nevertheless, a basic clinical examination well help one arrive at a realistic diagnosis.
The common symptoms that patients present with are tiredness, bleeding and bruising, swollen
glands, pruritus, fever and sweating.
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Tiredness
Tiredness correlates poorly with anaemia and most tired patients have normal haemoglobin levels.
Undoubtedly patients with haemoglobin levels below 7.0 gm/1 are likely to be tired but they will
probably also complain of breathlessness, faintness and pounding headache. The rate of fall in the
haemoglobin levels is often the major factor in determining the severity of the symptoms. A 40 year
old farmer who is a mother of eight may be unaware of her anaemia of 6 gm/dl whereas her
previously healthy 18 year old son would fall grievously ill if he dropped his haemoglobin from 11 gm
to 6 gm after melaena stools.
With anaemic patients it is of critical importance to measure haemoglobin level rather than to rely
on symptoms. The blood examination will also give one the type of anaemia.
The young housewife with iron deficiency anaemia needs to be asked about her periods, previous
pregnancies and duration of breast feeding as well as dietary habits. A 52 year old teacher with
similar blood count should be asked about indigestion, abdominal pain and rectal bleeding as these
will lead to possible site of gastro-intestinal bleeding.
Bleeding and Bruising

Much depends on whether this is new or old. If haemophilia is suspected, then one needs to know
about family history and one must also ask about blood loss in previous operations like circumcision.
Someone who has undergone surgery of this kind without excessive blood loss is unlikely to have a
significant hereditary coagulation problem. A recent onset of unusual bleeding from the mouth and
gums with gross bruising after trivial trauma suggests a serious acquired defect. However, senile
purpura is common in the elderly appearing on the extensor surfaces of the forearms.
Swollen Glands
If one can exclude an acute infection as the cause of the swollen lymph glands then the swelling is
serious and one must find out the duration of the swelling and whether or not they are painful. Pain
in enlarged glands after drinking alcohol is suggestive of Hodgkin’s disease.
Pruritus
Pruritus (skin itching) may be a symptoms of lymphoma, polycythaemia, myeloproliferative disorders
eg myelosclerosis and simple anaemia. The skin irritation may become a torment after a hot bath.
Fever and Sweating

These are non-specific features of disease. However, recurrent and persisting fever in the absence of
other pointers may indicate occult lymphoma. The classical Pel-Ebstein fever associated with
Hodgkin’s disease is uncommon.
Drugs
All patients with unexplained anaemia must be questioned about drugs. These should include those
prescribed by the doctor as well as the drugs he bought himself from the Pharmacy shop. Some
mixtures may contain drugs which the patient may be unaware of e.g. chloramphenicol in cough
mixture.
EXAMINATION
Anaemia: The traditional sites for assessing anaemia are palpebral conjunctivae, nail bed, fingers,
palms, tongue and buccal mucosa. A lemon-yellow tinge of the sclera with intense pallor of the
conjunctivae should suggest a possibility of associated haemolysis. Clinical assessment of anaemia is
unreliable and only true measure is that of the haemoglobin concentration in the blood.
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Spoon-shaped, ridged nails (koilonychia) are associated with longstanding iron deficiency anaemia
with depletion of body iron stores. Retinal haemorrhages frequently co-exist with severe anaemia of
B12 deficiency. Leg ulcers are seen in chronic haemolytic anaemia like sickle cell disease. A smooth
delapillated tongue with angular cheilosis is seen in both chronic iron deficiency anaemia and the
macrocytic anaemia of B12 or folate deficiency. In hereditary haemorrhagic telangiectasia (Osler-
Weber-Rendu syndrome) one gets red spots around the mouth, lips and nose. Chronic blood loss
from these lesions may cause an iron-deficiency anaemia.
Excessive Bleeding
Spontaneous and excessive bleeding into the skin may be the result of thrombocytopenia, disorders
of the small blood vessels, coagulation defects and dysproteinaemia. In general the bleeding due to
thrombocytopaenia and small vessels defects is initially into the skin (purpura and ecchymosis),
whereas with the hereditary coagulation effects, it is into muscles and joints.
Purpura is the extravasation of blood from small vessels into the skin and mucus membranes. The
lesions are a few mm in diameter and do not blanche on pressure.
The bleeding of hereditary coagulation defects is episodic often unpredictable but frequently
provoked by trauma. The most common of these diseases is haemophilia which is a sex-linked
recessive disorder associated with deficiency of factor VIII. The less common Christmas disease in
inherited in precisely the same way but is associated with factor XI deficiency. Von Willebrand
disease is transmitted as an autosomal dominant trait and is characterized by a prolonged bleeding
time and an abnormality of the factor VIII. Recurrent joint bleeds result in chronic arthropathy.
Bleeding due to excess anticoagulant therapy such as Warfarin is frequently retroperitoneal.
Excessive and spontaneous bleeding may be seen in the dysproteinaemias, particularly in such high
viscosity states as macroglobulinaemia. The chronic periorbital haematomas occasionally seen in
amyloidosis constitute a rare but striking and diagnostic physical sign.
LYMPH NODE ENLARGEMEMT
Palpation for Cervical Lymph Nodes

The cervical lymph nodes are best examined from behind the patient. With the patient relaxed and
the neck held in a comfortable position, stand behind the patient and palpate for the cervical lymph
node. Roll the hand gently over the nodes and note the number, character, tenderness and whether
it is attached to the overlying skin or not. If multiple, note whether they are mated together or they
are discreet (Fig. 2:10).
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Palpate also for lymph node on the supra clavicular area and it is associated with abdominal
malignancies especially of the stomach.
Figure 2:10 Palpation for Cervical Lymph Nodes.
Palpation of Axillary Lymph Node

In palpating for the left axillary lymph node, rest the patient’s left upper limb on the left forearm and
using the right hand palpate for the apical, central, anterior and medical group of lymph nodes (Fig.
2:11). Change over and use the left hand to palpate for the lateral group of lymph node.
Figure 2:11 Palpating for the Left Axillary Lymph Nodes.
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In palpating for the right axillary lymph node, rest the patient’s right upper limb on the right forearm
and using the left hand palpate for the apical central anterior and medical groups of lymph nodes
(Fig. 2.12). Change over and use the right hand to palpate for the lateral group of lymph node. Note
the characteristics of the lymph nodes as described for the cervical lymph node.
Figure 2.12 Palpating for the Right Axillary Lymph Nodes.
Palpating For Supra-Trochlear Lymph Node

Flex the elbow to 90 degrees and palpate for the supra trochlear lymph nodes at the posterior
aspect of the lower end of the humerus just above the supra trochlear fossa (Fig. 2.13). Palpate for
lymph nodes in both upper limbs. These are enlarged in leprosy and Acquired Immuno-Deficiency
Syndrome (AIDS)
Figure 2.13 Palpating for Supra-Trochlear Lymph Node
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Palpating for Inguinal Lymph Node
Expose the inguinal region within the limits of decency then palpate for inguinal lymph nodes in both
right and left inguinal regions using the right hand. Note the characteristics of the enlarged lymph
nodes as described above.
In the tropics where most people walk bare footed in childhood, inguinal glands are usually palpable
in health persons. Hence make sure the lymph nodes present are pathological. Causes of generalised
lymphadenopathy include infections, leukaemia, lymphoma, tuberculosis, sarcoidosis and metastatic
disease. Enlarged epitrochlear nodes used to stigmatise worry about progressive generalised
lymphadenopathy (PGL) related to Human Immune Deficiency Virus (HIDV) infection. Tuberculosis is
one of the few causes of infective lymphadenopathy in which the nodes coalesce. Massive rubbery
firm lymphadenopathy is a feature of the lymphomas. Broadly speaking, in Hodgkin’s disease the
glands are initially restricted to the neck whereas in non-Hodgkin’s lymphomas the
lymphadenopathy is diffuse at an early state of the disease. Malignant lymphadenopathy is marked
by hard, irregular and fixed glands in the drainage area of the primary tumour.
Acute and Chronic Leukaemia.
Although the diagnosis of leukaemia is based on full haematological examination, certain physical
signs points strongly to a suspected diagnosis. Bleeding, swollen infected gums are common in acute
leukaemia. Gum hypertrophy may be very gross in acute monoblastic leukaemia. Hemorrhage and
exudates may be seen in the fundi. Skin manifestations include itchy indurated papules and
ulcerative nodules. Chronic granulocytic (myeloid) leukaemia often presents in middle age with
malaise, anaemia and massive splenomegaly. Chronic lymphatic leukaemia occurs in middle age or
elderly folks with lymphadenopathy and splenomegaly. Here the enlarged glands may be quite soft.
Splenomegaly is very gross in myelosclerosis and chronic granulocytic leukaemia.
Herpes simplex, herpes zoster and chicken pox are opportunistic infections, which may be, life
threatening in the immuno-suppressed patients.
Haemoglobinopathies
The two most important haemoglobinopathies are sickle cell disease and thalassaemia. In sickle cell
disease, the patients are usually small for their age, although occasionally, they may be giants with
arachnodactyly
Anaemia is associated with lemon coloured jaundice. There is bossing of the forehead with
gnathopathy. The spleen which is enlarged in childhood shows auto-infarction which leads to
hyposplenism in adult life. Chronic leg ulcers are found especially in the medial, lower one third of
the legs. They often developed painful infarctive crisis.
In thalassaemia the patients are small the faces is mongoloid in type and spleen is grossly enlarged
and there is hepatomegaly. They do not often survive after early adult life.
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Principles of Examination of the Systems

After the general examination of the patient, one is now ready to examine the patient system by
system. Irrespective of the system one is examining one must go through four basic processes in the
correct sequence. If one does this all the time one is unlikely to miss any important findings.
The processes are:-

1) INSPECTION
2) PALPATION
3) PERCUSSION
4) AUSCULTATION
Hence in the examination of the cardiovascular system one must NOT immediately dash for one’s
stethoscope but inspect, palpate and percuss before one makes use of one’s stethoscope.
The recommended position for examination is to stand on the RIGHT side of the patient. This must
be made a habit so that it is done automatically each time one examines a patient.
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T. C. Ankrah
Chapter 3
CLINICAL EXAMINATION OF THE
CARDIOVASCULAR SYSTEM
 Symptoms of the Cardio-Vascular System
 Peripheral Signs of Cardio-Vascular Disease
 Pulsations in the Neck
 Jugular Venous Pressure
 The Pulse
 Location of the Apex Beat
 Auscultation of the Heart Sounds
 Measurement of the Blood Pressure
 Heart Failure

Eunice Mintah
MBChB 1
Chapter 3 The Cardio-Vascular System
CLINCICAL EXAMINATION OF THE

CARDIO-VASCULAR SYSTEM
INTRODUCTION
The history should record details of presenting symptoms, of which the most common are chest
pain, fatigue and dyspnoea, palpitations, and presyncope or syncope, cough. Previous illness should
also be recorded, as it may provide important clues about the cardiac diagnosis - thyroid, connective
tissue and neoplastic disorders, for example, can all affect the heart. Rheumatic fever in childhood is
important because of its association with valvular heart disease and hypertension; and diabetes and
dyslipidaemias because of their association with coronary artery disease.
Smoking is a major risk factor for coronary artery disease. Alcohol abuse may predispose to cardiac
arrhythmias and cardiomyopathy. The cardiac history should quantify both habits in terms of pack-
years smoked and units of alcohol consumed.
The family history should always be documented because coronary artery disease and hypertension
often run in families, as do some of the less common cardiovascular disorders, such as hypertrophic
cardiomyopathy. Indeed, in patients with hypertrophic cardiomyopathy a family history of sudden
death is probably the single most important indicator of risk.
Finally, the drug history should be recorded, as many commonly prescribed drugs are potentially
cardiotoxic. β-Blockers and some calcium channel blockers (diltiazem, verapamil), for example, can
cause symptomatic bradycardias, and tricyclic antidepressants and β-agonists can cause
tachyarrhythmia. Vasodilators cause variable reductions in blood pressure which can lead to
syncopal attacks, particularly in patients with aortic stenosis. The myocardial toxicity of certain
cytotoxic drugs (notably doxorubicin and related compounds) is an important cause of
cardiomyopathy.
SYMPTOMS
Disease of the cardio-vascular system causes six main symptoms. These are chest pains,
breathlessness, cough, palpitation, ankle swelling, and dizziness or blackout. (syncope and
presyncope)
All these symptoms can occur with disease of other systems and they also occur in healthy people. A
careful history is the best way of deciding whether the symptoms are significant and whether they
are due to non-cardiovascular disease.
Chest Pain
The important cardiovascular causes of chest pain are cardiac ischemia, pericarditis and dissecting
aneurysm. Cardiac ischemia may be related to exercise when it causes the pain called angina; it may
be reversible but only closely related to exercise when it is sometimes called unstable angina; and it
may be persistent when blockage of a coronary artery causes myocardial infarction.
Ischemic pain is felt in the front and the centre of the chest. It is usually described as “tight”,
“pressing” or “crushing”. It frequently radiates to the left arm and less frequently to the right arm
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and to the back, sometimes it radiates to the neck, jaw and teeth. It is virtually diagnostic of cardiac
ischaemia.
Ischemia of the heart results from an imbalance between myocardial oxygen supply and demand,
producing pain called angina. Angina is usually a symptom of atherosclerotic coronary artery
disease, which impedes myocardial oxygen supply. Other causes of coronary artery disease are rare.
The history is diagnostic if the location of the pain, its character, its relation to exertion and its
duration are typical. The patient describes retrosternal pain which may radiate into the arms, the
throat or the jaw. It has a constricting character, is provoked by exertion and relieved rapidly by rest.
Box 3.1 Myocardial Ischaemia

Typical patient
 Middle-aged or elderly man or woman often with a family history of

coronary heart disease and one or more of the major reversible risk
factors (smoking, hypertension, hypercholesterolemia)
Major symptoms
 Exertional chest pain and shortness of breath. Pain often described as

'heaviness' or 'tightness', and may radiate into arms, neck or jaw
Major signs
 None, although hypertension and signs of hyperlipidaemia`

(xanthelasmata, xanthomas) may be present
 Peripheral vascular disease, evidenced by absent pulses or arterial
bruits, is commonly associated with coronary heart disease
Diagnosis
 Typical history is most important diagnostic tool

 ECG: often normal; may show Q waves in patients with previous
myocardial infarction
 Stress test: exertion ST depression
 Isotope perfusion scan: exertion perfusion defects
 Coronary arteriogram: confirms coronary artery disease
Additional investigations
 Blood sugar and lipids to rule out diabetes and dyslipidaemia
Comments
 A careful history is the single most important means of diagnosing

angina
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Pericarditis
Pericarditis causes pain with distribution similar to ischeamia but it is often made worse by breathing
and it is markedly affected by posture. It is usually worst lying flat and it is relieved by sitting up and
leaning forward.
Box 3.2 Pericarditis

Typical patient
 Middle-aged (male) or elderly (either sex), often with a family history of

coronary heart disease and one or more of the major reversible risk factors
(smoking, hypertension, hypercholesterolaemia)
 In many patients there is no preceding history of angina
Major symptoms
 Chest pain and shortness of breath. Pain usually prolonged and often described
as 'heaviness' or 'tightness', with radiation into arms, neck or jaw. Alternative
descriptions include 'congestion' or 'burning', which may be confused with
indigestion
Major signs
 Ischaemic myocardial damage, fourth heart sound, dyskinetic precordial

impulse
 Autonomic disturbance, tachycardia (anterior MI), bradycardia (inferior MI),
sweating, vomiting, syncope
Diagnosis
 Markers of injury: raised CKMB and troponins

 ECG: may be normal or show ST depression or T-wave change (non-ST elevation
myocardial infarction). ST elevation myocardial infarction denotes higher risk
 Biochemistry: blood sugar and lipids to rule out diabetes and dyslipidaemia
 Risk stratification: echocardiogram (LV function) and stress testing (reversible
ischemia)
Comments
 History and troponin testing most useful diagnostic tools
Aortic Dissection
Dissection of the aorta causes severe central chest pain that is often described by the patient as
“tearing”. It typically radiates through to the back. It is of sudden onset and it is frequently
accompanied by dizziness or transient loss of consciousness.
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Box 3.3 Aortic Dissection
Typical patient
 Middle-aged or elderly patient with a history of hypertension or arteriosclerotic

disease
 Occasionally younger patient with aortic root disease (e.g. Marfan's syndrome)
Major symptoms
 Chest pain
Major signs
 Often none
 Sometimes regional arterial insufficiency (e.g. occlusions of coronary artery
causing myocardial infarction, carotid or vertebral artery causing stroke, spinal
artery causing hemi- or quadriplegia); subclavian artery occlusion may cause
differential blood pressure in either arm; aortic regurgitation; cardiac
tamponade; sudden death
Diagnosis
 CXR: widened mediastinum, occasionally with left pleural effusion

 Transoesophageal echocardiogram: confirms dissection
 CT scan: confirms dissection
 MRI scan: confirms dissection
 None
Comments
 Having established the diagnosis, emergency surgery is usually necessary,

particularly if the dissection involves the ascending thoracic aorta
Breathlessness
Breathlessness may result from cardiac or respiratory disease. Whatever the cause it is usually first
noticed on exertion though with increasing disease it may occur at rest. The identification of the
system responsible for breathlessness depends on associated symptoms and on the physical
examination.
Cough
When left ventricular failure occurs, pressure in the left atrium rises. This increases pressure in the
pulmonary veins and capillaries and the lung becomes stiff. When pulmonary capillary pressure
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exceeds the oncotic pressure of the plasma, fluid leaks into the alveoli and pulmonary oedema
occurs. The patient then begins to cough up frothy sputum which may be pink or sometimes stained
with blood. With the rise in the left atrial pressure and increasing stiffness of the lung, the patient
becomes breathless on lying flat. This is called orthopnoea.
Sometimes in patients with left ventricular failure, the patient gets recurrent attacks of being woken
up in the night with shortness of breath. He rushes to the window, opens the window for fresh air
and he paints for breath. These attacks are known as paroxysmal nocturnal dyspnoea.
Dyspnoea
Dyspnoea is an abnormal awareness of breathing occurring either at rest or at an unexpectedly low

level of exertion. It is a major symptom of many cardiac disorders, particularly left heart failure but
its mechanisms are complex. In acute pulmonary oedema and orthopnoea, dyspnoea is due mainly
to the elevated left atrial pressure that characterizes left heart failure. This produces a
corresponding elevation of the pulmonary capillary pressure and increases transudation into the
lungs, which become oedematous and stiff. The extra effort required to ventilate the stiff lungs
causes’ dyspnoea. In exertion dyspnoea, however, other mechanisms apart from changes in left
atrial pressure are also important.
Exertional Dyspnoea
This is the most troublesome symptom in heart failure Exercise causes a sharp increase in left atrial
pressure and this contributes to the pathogenesis of dyspnoea by causing pulmonary congestion
(see above). However, the severity of dyspnoea does not correlate closely with exertion left atrial
pressure, and other factors must therefore be important. These include respiratory muscle fatigue
and the effects of exertion acidosis on peripheral chemoreceptors. As left heart failure worsens,
exercise tolerance deteriorates. In advanced disease the patient is dyspnoeic at rest.
Orthopnoea
In patients with heart failure lying flat causes a steep rise in left atrial pressure, resulting in
pulmonary congestion and severe dyspnoea. To obtain uninterrupted sleep extra pillows are
required, and in advanced disease the patient may choose to sleep sitting in a chair.
Paroxysmal Nocturnal Dyspnoea
Frank pulmonary oedema on lying flat wakes the patient from sleep with distressing dyspnoea and
fear of imminent death. The symptoms are corrected by standing upright, which allows gravitational
pooling of blood to lower the left atrial pressure, the patient often feeling the need to obtain air at
an open window.
Fatigue
Exertion fatigue is an important symptom of heart failure and is particularly troublesome towards
the end of the day. It is caused partly by deconditioning and muscular atrophy but also by
inadequate oxygen delivery to exercising muscle, reflecting impaired cardiac output
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Palpitations
Palpitation is an awareness of the sensation of the heart beat. When the patient complains of
palpitation, it is helpful to ask him to tap the rhythm on the table so that one can assess the rate,
severity and regularity of the palpitations.
Ankle Swelling
Ankle swelling may be due to cardiac disease, to venous or lymphatic obstruction in the legs or low
plasma albumin which may be the result of liver, kidney or
Gut disease. If the patient is lying in bed, the oedema collects over the sacrum rather than the ankle.
Ankle oedema due to heart failure unlike that resulting from unilateral venous obstruction is
symmetrical. The patient may complain of aching legs but the feet are not actually painful.
Blackouts
Palpitations may result in syncope. Syncope means sudden loss of consciousness with a fairly quick
recovery. The most common cause is simple fainting but cardiac arrhythmias both tachycardia and
bradycardia may be responsible. The ultimate cause of loss of consciousness is a lack of oxygen
supply to the brain and this may cause epileptic seizure. Seizures or fits may have a cardiac or
neurological cause.
In complete heart block, the ventricle beats at their own inherent rhythm of 20 – 40 beats per
minute. This extreme bradycardia and poor cardiac output may become so slow that the patient
loses consciousness. This may last for only a few seconds but such episodes may be recurrent and
they are called Stokes-Adams attack after the Irish physician who first described them.
EXAMINATION
Before examining the cardio-vascular system proper, look for peripheral signs that can aid one’s
diagnosis. These are clubbing of the fingers, pallor and cyanosis.
Look for signs of clubbing and note the degree of clubbing. Stage 1 clubbing is tested by resting the
middle finger on one’s thumbs and testing for increased sponginess by pressing the nail fold with
one’s index fingers {Fig. 3:1}. Look for the presence of other stage of clubbing as described in chapter
2.
Figure 3.1 Testing For Early Clubbing
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Cardio-vascular causes of clubbing includes cyanotic congenital heart disease like Fallot’s tetralogy
and transposition of the great vessels – aorta and pulmonary arteries. Other causes are infective
endocarditis and mitral stenosis.
Pallor is examined by looking at the sub-conjunctiva of the eyes, the tongue, buccal mucosa and
inner aspect of the lower lip. One then looks at the palms and nails for their colour. The colour will
be pale if the patient is anaemic and reddish if he or she is normal.
In Blacks, the pigmentation of the skin and mucous membrane makes the sign less reliable.
Central cyanosis is detected by the examination of the under surface of the tongue for bluish
discolouration. Peripheral cyanosis is detected by looking for bluish discolouration of the finger nails.
Once there is a central cyanosis one is bound to have peripheral cyanosis. But one can have
peripheral cyanosis without central cyanosis when the circulation is sluggish in the periphery.
For central cyanosis to be present one must have at least 5gm of haemoglobin in the reduced state.
Hence people who are very anaemic (Hb less 5gm) will not show cyanosis even though they may be
severely hypoxic.
One can start the examination of the cardio-vascular system by examining the pulse. However, from
experience students after examining the pulse move straight to examine the precordium without
examining the pulsations in the neck. Hence I would recommend that one starts examination of the
cardio-vascular system with the pulsations in the neck.
Pulsations in the Neck
Observe the neck for any pulsations. Decide whether the pulsations in the neck are arterial or
venous. Arterial pulsations have a strong outward thrust while a venous pulsation has gentle double
peaks on its outward thrust.
Differentiating arterial and venous pulsations in the neck
1. An arterial pulsation can be felt; a venous pulsation is usually impalpable.
2. Gentle pressure just above the clavicle will obliterate a venous pulsation and the vein will fill
above the point of pressure. An arterial pulsation will not be affected.
3. The pulsation in the jugular vein is best seen at the limit of venous distension, so its position
in the neck will change when the patient sits up or lies down.
4. Deep inspiration reduces intra-thoracic and therefore right atrial and jugular venous
pressures. The position of the venous pulsation therefore moves downwards in the neck on
inspiration and upwards on expiration. The position of an arterial pulse is unaffected.
However, the venous pulsations are paradoxical in pericardial effusion or constricture
pericarditis.
5. There are valves between the superior vena cava, the right atrium, the inferior vena cava
and the hepatic veins. Thus if pressure is applied over the liver just below the ribs, blood will
be expressed from the liver and the right atrial pressure will rise with a consequent rise of
the jugular venous pressure and pulsation. This is called hepato jugular reflex.
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6. The pulse waveform in the carotid artery is a simple “up and down” but that of the jugular
venous pulse is more complex usually seen as rapid oscillation at the top of the venous
column.
JUGULAR VENOUS PULSATIONS

The jugular venous pulsation essentially reflects the sequence of pressure changes within the right
atrium but the waveform of the venous pulse is complicated by transmission of a pulse from the
carotid artery that runs adjacent to the internal jugular veins. The venous pulse therefore has three
components which are called “a”, “c” and “v”.
The “a” wave is due to atrial contraction. It is accentuated when right atrial pressure is high as in
pulmonary hypertension and it is lost when atrial activity is disorganized by artrial fibrillation. The
“c” wave is transmited from the carotid artery. The “v” wave occurs while the tricuspid valve is shut
and is therefore associated with atrial filling. The fall in venous pressure after the “a” wave is called
“x” descent and that after the “v” wave is called the “y” descent (Fig. 3:2).
c v
x y
Diastole Ventricular Systole Diastole
Figure 3.2 Diagram of Jugular Venous Pulsations.

a = atrial systole
c = transmitted pulsation of carotid artery
v = peak pressure in right atrium
a-x = x descent due to atrial relaxation
v-y = y descent at commencement of ventricular filling
JUGULAR VENOUS PRESSURE

Determination of the jugular venous pressure enables one to assess the pressure in the right atrium
and the waveform of the pulsation helps one in the diagnosis of a variety of quite different
conditions.
The jugular veins act as a manometer, the height of the column of blood above the heart measures
the right atrial pressure. The pulsations in the jugular veins reflect pressure changes in the right
atrium.
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To assess the jugular venous pressure, the patient must be inclined at 45 degrees in the bed. The
reason for inclining him at 45 degrees is that at this degree of inclination, the sterno-manubrial
junction also called the angle of Louis from where one is going to measure the height of the jugular
venous pressure is at the same horizontal level as the root of the neck or the top of the right atrium.
The patient must be relaxed and the head turned slightly to the left so that the sterno cleido muscles
on the right side of the neck are very relaxed. Then look for the point if collapse of the column of
blood in the right internal jugular veins.
Even though the external jugular vein is superficial and it is easily seen, the internal jugular vein
which is deep and not easily seen is used to measure the jugular venous pressure for these three
reasons:
1. The internal jugular vein is in direct continuity with the right atrium and hence pressure
in the internal jugular veins gives a true reflection of the pressure in the right atrium.
2. The external jugular vein is very tortuous in its course as it passes through the fascial
planes and hence subject to kinking and giving false readings.
3. There are valves in the external jugular veins which may give false readings; but there
are no valves in the internal jugular veins and hence reflects the actual pressure in the
right atrium.
To measure the height of the jugular venous pressure, place a ruler vertically at the angle of Louis.
Then place another ruler horizontally at the point of collapse of the column of blood in the internal
jugular vein to meet the vertical ruler placed at the angle of Louis. The jugular venous pressure is the
height from the angle of Louis to where the horizontally placed ruler meets the vertically placed
ruler (Fig. 33).
a Point of collapse of Internal Jugular vein
b Angle of Louis
45o
Figure 3:3 Measurement Of The Jugular Venous Pressure (JVP).
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Conditions that can be diagnosed from the jugular venous pressure are:
1. Heart failure. The jugular venous pressure is more than 2-3 cm above the angle of Louis.
Ensure that the jugular venous pressure is pulsating and the height is affected by position and
expiration to differentiate it from mediasternal tumour e.g. lung cancer where the jugular
venous pressure is distended but non-pulsatile.
2. Tricuspid regurgitation. A prominent “v” wave which collapse due to a deep “y” descent.
3. Heart block: In complete heart block the atria contract independently of the ventricles so the
“a” waves in the jugular venous pulse are not regularly followed by “c” or “v” waves. At times
the right atrium will by change contract against a closed tricuspid valve and when this happens
the whole of the right atrial volume will be expelled up the superior vena cava. This will cause a
sudden and marked single pulsation in the neck which is called cannon wave.
4. Pulmonary hypertension: High pressure in pulmonary artery causes a rise in right ventricular
pressure and so a rise in right atrial pressure. The “a” wave is then prominent and can be seen as
a regular “flick” in the jugular pulse.
5. Constrictive pericarditis and Pericardial Effusion: In some chronic disease like tuberculosis or
collagen diseases, the pericardium becomes thickened and stiff. On inspiration the pericardium
is pulled down by the diaphragm and the heart is compressed. Instead of the usual fall in venous
pressure on inspiration the jugular venous pressure rises and at the same time the reduced
inflow to the heart reduces the left ventricular output and the systemic pressure falls. These
abnormal responses to inspiration are called venous arterial paradox.
PULSE
Examination of the pulse is usually done by examining the radial pulse. The radial pulse is felt on the
lateral side of the wrist or its anterior aspect, just above the flexor retinaculum. In examining the
pulse one is looking for five attributes of the pulse. These are the rate, rhythm, volume, character
and the state of the arterial wall.
Rate
Count the pulse rate for one minute. With experience you may count for half a minute and multiply
by two and later for only fifteen seconds and multiply by four. It the heart rate is slow e.g. less than
60 beats per minute this is described as bradycardia. if the heart rate is fast e.g. more than 100 beat
per minute it is described as tachycardia. When either bradycardia or tachycardia is found try and
find the cause.
Rhythm
In health the rate is regular. If the rhythm is irregular one should determine the type of irregularity.
Regularly irregular heart rate may be due to ectopic focus. Irregularly irregular may be due to atrial
fibrillation or multiple ectopic beats or flutter with varying block. One can differentiate these
clinically by demonstrating the presence of pulse deficit in atrial fibrillation. When the patient is
made to exercise, the irregularity due to multiple ectopic beats disappears while that due to atrial
fibrillation persists and may even become worse.
10 | P a g e
Volume
The pulse volume indicates the movement imparted to the finger applied gently to the pulse. This is
the strength of the pulse wave. Tension reflects the pressure needed to abolish the pulse. The pulse
volume may be normal or strong in hyperdynamic circulation. It is weak and thready in hypovolemic
shock.
Pulse Character
If the pulse is recorded with a device that measures the rise and fall that can be felt with the finger
and the rise and fall is displayed on a moving paper or an oscilloscope, a waveform will be produced.
The shape of this waveform is what is meant by pulse character.
Expiration Inspiration Expiration Inspiration
Normal Pulse Normal

Plateau Pulse
Stage 1
Stage 2
Collapsing Pulse
Pulsus Paradoxus
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Figure 3.4 Pulse Characters.
Pulsus Alternans Pulsus Bisferens
Figure 3.4 Pulse Characters.
The waveform of the normal pulse is made up by a rapid upstroke, a very brief plateau and a less
steep downstroke. The downstroke is interrupted by a dicrotic notch, which coincides with closure
of the aortic valve, but the notch seldom be appreciated clinically.
In aortic valve stenosis the upstroke of the pulse is slow an the plateau prolonged: The plateau pulse
is characteristic of significant stenosis. The normal blood pressure in an artery reaches a peak of
about 120 mm Hg and a minimum of about 80 mm Hg. The pulse pressure is therefore 120-80 = 40
mm Hg and it is this difference that can be felt in the pulse. It is not possible to judge any absolute
figure with narrow pulse pressure say 110-90 = 20 mm Hg which is typical of a plateau pulse.
If the pulse pressure is wide a downstroke of the waveform is steep and the pulse seems to drop
rapidly. This is described as a “collapsing” pulse. In aortic valve incompetence, the diastolic arterial
pressure begins to approach the diastolic pressure in the left ventricle, which is usually only 5 – 0
mm Hg. A typical blood pressure in a patient with a collapsing pulse of aortic incompetence might
therefore be 150/50, the pulse pressure thus being 100 mm Hg. (Fig. 3:4).
To test for the character of a pulse, one raises the whole of the patient’s right upper limb up and
places one’s palm on the middle of the right forearm. Then one feels how the pulse wave hits one’s
palm and runs away (Fig. 3:5). In collapsing pulse, the pulse hits one’s palm and rapidly runs away.
There are several causes of collapsing pulse and this includes atrial septal defects, ventricular septal
defects arterio-venous malformations, aneurysms, fever, hyperdynamic circulation, exercise,
pregnancy, aortic incompetence and thyrotoxicosis.
45o
12 | P a g e
Figure 3.5 Testing for collapsing pulse.
State of the Arterial Wall

Roll the radial artery against the patient’s distal end of the radius at the wrist. Normally one should
not feel anything but in people with arteriosclerosis, one feels a rubber-like tube due to thickening
of the arterial wall.
Other aspects of the Pulse

One must also detect other findings like pulsus alternans – here one feels alternating strong and
weak pulses. It is seen in left ventricular failure.
Pulsus bisferens here one feels a double element in the waveform of the pulse. This occurs in
patients with both aortic stenosis and aortic regurgitation.
Pulsus Paradoxus
Normally the pulse volume increases on inspiration. In pulsus paradoxus the opposite occurs. It is
see n in the bronchial asthma and left ventricular failure. Pulsus paradoxus is also a feature of
constrictive pericarditis and massive pericardial effusion.
PERIPHERAL PULSES
Having elicited all the information from the radial pulse, now feel for the presence or absence of the
pulse in other arteries.
Superficial temporal pulse – this is in front of the upper border of the ear lobe, running upwards and
medially over the forehead.
Carotid pulse – this is felt for in the neck between the larynx and the sternomastoid muscle.
Brachial pulse – this is felt in the medial side of the upper arm at the lower end of the elbow on the
medial side of the anti-cubital fossa preferable with the elbow slightly flexed.
Femoral pulse – this is felt in the mid-inguinal point half way between the anterior superior iliac
spine and the centre of the symphysis pubis.
Popliteal pulse – this is felt by firm pressure in the upper part of the popliteal fossa. Here one has to
flex the knee a bit in order to feel the pulse.
Posterior tibialis pulse – this is felt midway between the medial malleolus and the prominence of the
heel.
Dorsalis pedis or anterior tibial pulse – this is felt along a line about midway between the medial
malleolus to the proximal part of the first metatarsal space. Remember the artery dips down at
about the middle of the foot to form the palmar arch. So do not go too near the toes and miss the
pulse.
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Delayed Femoral Pulses

In young people with coarctation of the aorta, the femoral pulse is delayed and weak or absent;
there are also collateral pulses over the scapulae from an anastomotic communication.
LOCATION OF THE APEX BEAT
Now move to the pericardium and have a very good look. Look for any pulsations in the pericardium
and look for a visible apex beat. Place the right hand over the pericardium feeling for a thrill. A thrill
is a palpable murmur. Then locate the apex beat. This is the most inferior and the most lateral point
of the pericardium where the palpating finger is lifted at right angles to the chest wall. After locating
the apex beat with the right middle finger, leaves the finger there and count level of the intercostals
space by first feeling for the angle of Louis or sternal angle, then move to the next lower intercostals
space which is the send intercostals space and place the left little finger there. Then move down
counting the intercostals spaces using the left fingers. When the left fingers are exhausted, use the
left thumb. One still has the right thumb and the right index finger free to count any remaining
intercostals spaces. Leave the left fingers on the pericardium with the right middle finger still located
on the apex beat so that one can re-check the position of the apex beat (Fig. 3:6).
Sterno-manubrial Junction Intercostal spaces Apex beat
Figure 3:6 Locating the Apex Beat.
The apex beat may be displaced from its normal position in the fifth left intercostals space in the mid
clavicular line by three mechanisms.
a) Mediasternal shift
b) Left ventricular hypertrophy
c) Right ventricular hypertrophy
14 | P a g e
Mediasternal shift may occur when it is pulled towards the side of a collapsed or fibrotic lung or
when it is pushed away from the side of a large pleural effusion or tension pneumothorax. For each
case the trachea will deviate from the midline in the suprasternal notch and it is important to check
this in any patient whose apex beat is displaced.
Rarely the heart may be on the right side of the chest (dextrocardia) and the apex will then be in the
right fifth intercostal space in the mid clavicular line but the trachea will be central.
When the apex beat is displaced by left ventricular hypertrophy, it shifts downwards and outwards
and its position should be described either as being a certain number of centimeters beyond the mid
clavicular line or it may be release to the anterior axillary line (a line below the anterior border of the
axilla formed by the pectoralis major).
Right ventricular hypertrophy is associated with left parasternal heave. This is the lifting or heaving
motion that can be felt if the flat of the hand is placed just to the left of the sternum.
PERCUSSION OF THE HEART

Percussion of the heart is not done routinely as the information gained is limited. Moreover with the
wide spread use of x-rays any enlargement of the heart is readily evident of the chest x-rays.
AUSCULTATION OF THE HEART

The heart sounds are associated with the opening and closure of the heart valves.
Use the bell of the stethoscope for low pitched sounds at the apex of the heart and the diaphragm of
the stethoscope for high pitched sounds at the base of the heart.
Diaphragm
Bell
Figure 3.7 Stethoscope showing the diaphragm and the bell
First listen at the mitral area with the bell of the stethoscope and listen for the first and second heart
sounds. The mitral area in the normal is the fifth left intercostals area in the mid clavicular line.
One can determine which is the first heart sound by timing the heart sounds with the carotid pulse.
Place the left thumb on the right side of the neck. The pulse one feels is the carotid pulse; the first
heart sound coincides with the carotid pulse and the second heart sound follows.
15 | P a g e
The first heart sound is due to closure of the mitral and tricuspid valves at the beginning of systole.
The second heart sound is due to closure of the aortic and pulmonary valves (Fig. 3:8).
SYSTOLE DIASTOLE
I II I II I II
Figure 3:8 Normal Heart Sounds
In young people the second heart sound is usually single on expiration but inspiration delays
pulmonary closure as blood is sucked into the chest the right ventricular output is increased. The
doubling of the second heart sound on inspiration is lost with increasing age (Fig. 3:9)
SYSTOLE DIASTOLE
I II I II I II
Figure 3.9 The Splitting of Second Heart Sounds in Young People.
After satisfying oneself with the presence and character of he first and second heart sounds, one
must listen for the third and fourth heart sounds, if present. The third heart sound follows the
second heart sound and the fourth heart sound precedes the first heart sound.
The third heart sound is associated with ventricular filling and is heard soon after the second heart
sound. It is dull and low pitched and is nearly always localised to the cardiac apex. A soft third heart
sound may be normal especially in young people but in order patient is usually an indication of
constrictive pericarditis or pericardial effusion.
The fourth heart sound is associated with atrial contraction and therefore occurs at the end of
diastolic just before the first sound. When audible it is always pathological and indicates heart
failure. Like the third heart sound it is low pitched and is localized to the cardiac apex (Fig 3:10).
SYSTOLE DIASTOLE
I II III IV I II III IV I II
III and IV Heart Sound
Figure 3:10 The Third and Fourth Heart Sounds
16 | P a g e
HEART MURMURS
A murmur is essentially the same thing as a bruit and is due to turbulent blood flow. Murmurs arise
when a valve is thickened and fails to open properly (stenosis) or when it fails to shut properly and
leaks (incompetence or regurgitation). Murmurs also occur when an abnormally large amount of
blood flows past a normal valve. Murmurs can occur in systole or diastole and identifying which part
of the cardiac cycle the murmur occurs in an essential prelude to determining the cause of the
murmur.
Listen for murmurs in the four classical areas. Although modern echocardiography has shown that
the classical areas do not exactly correspond to the position of the valves, the murmurs produced by
lesions of the various valves are best heard in these classical areas. The mitral area is in the 5th left
intercostals space in the midclavicular line. The tricuspid area is the left sternal border adjacent to
the xiphisternum at the level of the 4th left intercostals space. The aortic area is the second right
intercostals space just lateral to the sternum and the pulmonary area is the second left intercostals
space lateral to sternum (Fig. 3:11).
First Rib
Lungs at full expiration

A P
Right Margin Left Margin of heart
of heart
T
Nipple
Costal Margin
M
Liver
Lungs at full
inspiration
Mitral area: 5th left intercostal space

M
in midclavicular line
Tricuspid area: 4th left intercostal

T
space in the para sternal line
A Aortic area: 2nd right intercostal

space in the para vertebral line
Pulmonary area: 2nd left intercostal

P
space in the para vertebral line
Figure 3.11 Classical Auscultatory Areas.
After listening to these four classical areas, listen all over the pericardium for murmurs. When a
murmur is heard, locate its maximum intensity, its character and its radiation.
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The intensity or loudness of murmur is graded over a scale of 4.
Grade 1 The murmur is heard quietly in an ordinary room.
Grade 2 The murmur is moderately loud.
Grade 3 The murmur is loud and it is also accompanied by a thrill.
Grade 4 The murmur is audible even without a stethoscope.
Murmur of Mitral Regurgitation

The murmur is usually loud at grade ¾. It is a pan systolic murmur which starts immediately after the
1st heart sound and it is heard in the whole of systole. The murmur is radiated to the axilla (Fig 3:12).
SYSTOLE DIASTOLE
Murmur of mitral regurgitation.
Heard best at apex; radiates to the axilla.
Figure 3.11 Murmur of mitral regurgitation
I II I
SYSTOLE DIASTOLE
Murmur of Ventricular septal defect.
Heard best at apex; No radiation.
Figure 3.12 Murmur of ventricular septal defect
I II I
SYSTOLE DIASTOLE
OS – Openning Snap
Low pitch rumbling mid-diastolic murmur
Figure 3.13 Murmur of Mitral Stenosis
OS
I II I
Listen at the mitral area with the bell of the stethoscope. Note the intensity and character of the
murmur then follow the murmur into the axilla as it radiates there. Even though we listen to the low
pitched murmur with the bell of the stethoscope, convention behoves us to listen to the murmur of
mitral regurgitation with the diaphragm as well.
Murmur of Ventricular Septal Defect

A ventricular septal defect may also produce a pan systolic murmur best heard to the left of the
sternum. It has a rough quality and it is accompanied by a thrill. Sometimes the murmur is best
heard with the diaphragm of the stethoscope at the 3rd or 4th left intercostal space (Fig. 3:13).
18 | P a g e
Murmur of Mitral Stenosis

In mitral stenosis, the 1st heart sound is loud, the second heart sound is normal, then there is an
opening snap followed by a low pitched rumbling mid-diastolic murmur which is located at the apex
without any radiation.
There may be pre-systolic accentuation when patient is in sinus rhythm (Fig. 3:14).
Listen wit the bell of the stethoscope at the mitral area. Note the character of the mitral stenosis
murmur. If the murmur cannot be heard easily, turn the patient to his left side so that the heart is
pushed to the chest wall and then listen for the murmur. Note the absence of radiation of the
murmur. Note any pre-systolic accentuation of murmur, when the patient is in sinus rhythm.
Murmur of Aortic Regurgitation

The murmur of aortic regurgitation is best heard along the left parasternal area. It is a high pitched
early diastolic murmur. It immediately follows the 2nd heart sound and it is decrescendo in type and
best heard at the end of expiration (Fig. 3:15)
Listen to the left sternal border with the diaphragm of the stethoscope. Get the patient to sit up and
take deep breath in and expire deeply out and hold the breath in expiration. Then listen along the
left para sternal area for the early high pitched decrescendo murmur of aortic regurgitation.
SYSTOLE DIASTOLE
I II I
Figure 3.15 Murmur of Aortic Regurgitation
Murmur of Aortic Stenosis

The murmur of aortic stenosis is an ejection, diamond shaped systolic murmur which is best heard at
the aortic area and radiates up into right side of the neck.
Listen at the aortic with the diaphragm and follow the murmur up into the right side of the neck (Fig.
3:16).
SYSTOLE DIASTOLE
I II I
Figure 3.16 Murmur of Aortic Stenosis
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Other Murmurs
Tricuspid murmurs are similar to mitral murmurs and pulmonary murmurs are similar to aortic
murmurs but the intensity is usually less and the location also varies. Tricuspid regurgitation murmur
is best heard to the left of the sternum in the 4th intercostals space and pulmonary stenosis murmur
is loudest in the second left intercostals space and the murmur radiates to the left shoulder. Atrial
septal defect may produce a pulmonary ejection murmur.
Pericardial Friction Rub
Use the bell of the stethoscope and listen over the whole of the precordium. Pericardial friction rub
varies from soft shuffling sounds to scratchy noises in time with the cardiac cycle and is often
influenced by respiration. It is due to pericarditis and the common causes are tuberculosis, viral
infections, myocardial infarction, rheumatic fever, connective tissue disease, trauma, uraemia and
infiltration of the pericardium with tumours.
Now proceed to measure the blood pressure and then examine the fundus if the patient is found to
be hypertensive.
Measurement of the Blood Pressure

The pressure of the blood within an artery cannot be assessed simply by feeling the pulse. Blood
pressure is measured with sphygmomanometer with which a variable pressure is applied to the
upper arm to find out how much pressure is needed to impair blood flow.
Fat arms take more compressing than thin ones so a record made in a fat arm may give a spuriously
high value for the blood pressure. Therefore the size of the cuff should be appropriate to the patient
and the cuff width should be about 40% of the arm circumference. In practice standard cuffs are
used in adults but the possibility of falsely high results in fat people must be kept in mind.
To measure the blood pressure:

1. Place the cuff fairly tightly around the upper arm.
2. Ensure that the brachial artery is at the same level as the heart.
3. Find the brachial pulse by palpation at elbow.
4. Inflate the cuff until the brachial pulse can no longer be felt.
5. Place the diaphragm of the stethoscope over the position of the brachial pulse.
6. Reduce the pressure in the cuff slowly by not more that 2 mm per heart beat. The pressure
of which the pulse can first be heard is the systolic pressure, the highest pressure generated
by the heart.
7. Continue to reduce the pressure slowly. The intensity of the pulse sound will increase and
then change character becoming muffled. Reducing the pressure by a few more millimeters
of mercury will lead to the pulse sound becoming inaudible.
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KOROTKOFF
Phase I and V
In 1905, Korotkoff suggested the method which is still being used clinically even till today. He
described the sounds discernible over the brachial artery just distal to the sphygmomanometer cuff.
There are five phase of these sounds described by Korotkoff as following:
Phase I - Sounds of clear tapping quality which appear when the cuff pressure falls to the arterial
peak systolic pressure.
Phase II - Sounds become drawn into a murmur.
Phase III - Sounds become clear and increased in intensity.
Phase IV - Abrupt muffling of sounds.
Phase V - Complete disappearance of sounds.
There has been in the past a disagreement as to whether the point of muffling or disappearance of
the sound should be taken as the diastolic pressure. (The minimum pressure in the artery when the
aortic valve is closed and the left ventricle is relaxing). It is now generally accepted that the point of
disappearance is closer to the true diastolic pressure and furthermore it is the more reproducible of
the two measurements. The point of disappearance should therefore be recorded as the diastolic
pressure.
Phase I is taken as the systolic blood pressure and Phase V is taken as the diastolic blood pressure.
Elevated blood pressure reduces life expectancy.
HEART FAILURE
The signs of right ventricular heart failure are:
1. Raised pulsatile jugular venous pressure.
2. Hepatomegaly which is soft and tender.
3. Sacral and ankle oedema.
The signs of left ventricular failure are:
1. Cardiomegaly; apex best is displaced outwards and downwards.
2. Bilateral basal crackles which persist after coughing.
21 | P a g e
If a patient’s symptoms and signs suggest the presence of heart failure it is important to remember
that this is a description and not a full diagnosis. Congestive cardiac failure (right heart failure
secondary to left heart failure) must be distinguished from cor-pulmonale (right heart failure,
secondary to lung disease).
Additional signs in congestive heart failure are basal lung crackles due to pulmonary oedema and
pink frothy sputum as well as symptoms and signs suggesting left ventricular disease.
Additional signs of cor-pulmonale are coarse lung crackles as in bronchiestasis or fibrosing alveolitis,
sputum which is sticky, white, grey, yellow or green.
There may also be symptoms and signs of chronic lung disease as well as right ventricular
hypertrophy.
Box 3.4 Congestive Heart Failure

Typical patient
 Patient with acute myocardial infarction or known left ventricular disease
Major symptoms
 Severe dyspnoea and variable circulatory collapse
Major signs
 Low-output state (hypotension, oliguria, cold periphery); tachycardia; S3; sweating;

crackles at lung bases
Diagnosis
 CXR: bilateral air space consolidation with typical perihilar distribution

 Echocardiogram: usually confirms left ventricular disease
 ECG: may show evidence of acute or previous myocardial infarction

 Blood gas analysis: shows variable hypoxaemia
Comments
 Although most cases are caused by acute myocardial infarction or advanced left
ventricular disease, it is vital to exclude valvular disease or myxoma, which are
potentially correctable by surgery
22 | P a g e
T. C. Ankrah
Chapter 4
RESPIRATORY SYSTEM
 Symptoms of the Respiratory System
 Inspection of the Sputum
 Peripheral Signs of Disease in the Respiratory System
 Shape and Movements of the Thorax
 Locating Position of the Trachea
 Palpation for Lymph Nodes in the Neck, Supraclavicular
 Region and Axilla
 Percussion of the Chest
 Auscultation for Breath Sounds

William Frank Hill Koomson
MBChB 1
Harriette Dufie Adu

MBChB 1
Chapter 4 The Respiratory System
CLINICIAL EXAMINATION OF THE

RESPIRATORY SYSTEM
There are six cardinal symptoms in the respiratory system. These are cough, sputum production,
breathlessness, wheeze, chest pain and haemoptysis.
COUGH
Cough is a manoeuvre involving three phases. First there is a deep inspiration; this is followed by
expiration against a closed glottis. Then the glottis suddenly opens with an explosive blast of air carrying
with it respiratory secretions.
The cough reflex is initiated by irritant receptors in the larynx and major airways which are stimulated
both by materials within the airway lumen such as sputum, foreign bodies or inhaled irritants and events
in the airway wall such as infection.
One must enquire about the duration of the cough: long standing cough may be due to tuberculosis,
while a cough of one or two weeks duration may be due to common cold.
Variability: Nocturnal cough may occur. Likewise daytime cough is variable in asthma while a persistent
cough of few weeks or months in a smoker should make you think of bronchial carcinoma.
If the cough is episodic, ask about precipitating factors such as inhalation of pollen, dust or cold air.
Cough related to meals or lying down may be due to aspiration of oesophageal contents.
With unilateral vocal cord paralysis as in recurrent laryngeal nerve palsy e.g. due to malignant
mediasternal invasion, the cough may be rather prolonged and has likened to the lowing of cattle hence
bovine cough.
Laryngitis leads to a harsh “croupy” cough.
A weak cough occurs in bilateral vocal cord palsy, respiratory muscle weakness, severe illness of any
cause and when the cough causes pain.
SPUTUM
If the patient’s cough is productive, then one must know how much is being produced. About 100 ml of
sputum per day is produced by the normal respiratory tree and this is usually swallowed. Patients can
often give a useful guide to sputum volume in terms of small cupful, a small chamber pot full or a small
bucket. Such large volumes are found in bronchiectasis sometimes larger with a lung abscess. Smaller
volumes of sputum may be found in chronic bronchitis.
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Ask about the sputum colour and consistency. Clear or white sputum (mucoid) is typical of bronchial
mucus gland hypersecretion as in chronic bronchitis. When the sputum is yellow or green (purulent)
often thick, it contains white cell indicating infection, except that in asthma green sputum may
represent sputum eosinophilia due to asthma, not to bacterial infection. Asthmatics often have very
viscid stringy sputum and less commonly may cough up small bronchial casts (Curschmann’s spirals)
which may be brown in broncho-pulmonary aspergillosis; frothy, sometimes pink sputum is seen in
severe acute pulmonary oedema but very copious watery secretion of alveolus cell carcinoma is
extremely rare.
Sputum with an offensive smell suggests anaerobic infection, often in a lung abscess or an empyema
with bronco-pleural fistula.
BREATHLESSNESS
This is the uncomfortable awareness of the need to breathe. Three basic mechanisms can lead to
breathlessness and they act singly or even jointed. These are increased work of breathing as in airway
obstruction e.g. asthma, stiff lungs e.g. pulmonary fibrosis and stiff chest wall e.g. scoliosis. The others
are decreased neuromuscular power eg muscular dystrophies and increased drive to breathe such as
chemical drive e.g. hypoxia, acidosis and neurological drive e.g. stimulation of lung receptors such as
pulmonary oedema.
To diagnose the cause of breathlessness one must make sure that one understands exactly what the
patient is complaining about. One must be able to differentiate between shortness of breath, chest
tightness and pain such as angina.
The time scale of the onset of breathlessness is an important diagnostic feature though there is a lot of
overlap. If the breathlessness has been present for seconds or minutes one must think of left ventricular
failure, pulmonary embolism and pneumothorax. If the breathlessness has been present for days or
weeks, think of asthma, pneumonia, allergic alveolitis and pleural effusion if breathlessness has been
present for months or years, then consider chronic airway obstruction, asthma, anaemia and pulmonary
fibrosis.
One must determine the severity of the breathlessness in order to understand how the patient’s life has
been affected by it and in order to be able to assess whether any treatment would be beneficial. One
can assess the severity by asking the patient how far he can walk on the flat without stopping or how he
can get on with his daily chores of living at home.
Variability
In chronic airway obstruction, the breathlessness is slowly progressive and in asthma the breathlessness
is also episodic with day to day variation.
Nocturnal
Breathlessness that wakes the patient at night usually in the early hours occurs in pulmonary oedema
and bronchial asthma. Pulmonary oedema due to left ventricular failure or mitral stenosis causes
paroxysmal nocturnal dyspnoea. The patient will give history of being woken up by breathlessness,
relieved by sitting up or getting out of bed. Both manoeuvres reduce the capillary hydrostatic pressure
and this tends to relieve pulmonary oedema. Poorly controlled asthmatics frequently wake up at about
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2.00am or 3.00am with breathlessness which is usually associated with cough or wheeze of variable
severity. This reflects an exaggeration of the normal circadian variation in airway calibre.
Postural
Increased breathlessness on lying flat – orthopnoea-occurs in cardiac failure and bilateral diaphragmatic
paralysis.
Precipitating Factors
Some asthmatics may become breathlessness when exposed to cats or certain perfume. Some allergens
cause breathlessness due to an alveolitis rather than asthma as in farmers’ lung or pigeon breeders who
develop symptoms four to six hours after exposure.
One must ask all patients with persistent breathlessness how their symptoms relate to their work. Is the
breathlessness better during weekends or when he had travelled away from the work place?
In exercise induced asthma the attack often occurs after a period of exercises.
Response to Treatment
Response to treatment may be an important clue. Breathlessness relieved by diuretics is usually due to
pulmonary oedema while marked improvement over a few days with topical systemic steroids strongly
suggests asthma or less commonly parenchymal disease such as an allergic alveolitis. Rapid relief with a
broncho-dilator inhaler supports a diagnosis of asthma.
Associated Symptoms
The relationship of a symptom to others may be crucial. Breathlessness in a smoker with haemoptysis
and weight loss may well be due to pulmonary collapse or pleural effusion due to cancer while its
occurrence with wheeze in a young person is almost always due to asthma.
Breathlessness is a common symptom of anxiety, often unrelated to exertion and occurring with a wide
spectrum of symptoms such as palpitations, tingling in the arms, dizziness and chest pains.
WHEEZE
Wheeze is noisy breathing. Wheeze is the sound heard when one blows over a narrowed tube. The
sound heard with the naked ears is called wheeze and the same sound heard with stethoscope is called
rhonchi.
Wheeze is a cardinal symptom of airflow obstruction. Many of the important features of wheeze are
similar to those described for breathlessness. Thus wheeze that is variable, either spontaneously or
following precipitating factors such as exercise, allergens, occupation, drugs e.g. aspirin, beta blockers
which wakes the patient at night is likely to be due to asthma. Causes of persisting wheeze include
asthma, chronic bronchitis, emphysema and major airway obstruction e.g. due to tumour.
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CHEST PAIN
The lung itself is not supplied with pain fibres, so fibrosing lung disease, multiple secondaries and other
parenchymal conditions do not cause chest pains. Pleuritic chest pains can however be very severe.
Typically this is sharp stabling pain worsened by movement such as breathing in, or coughing. Pleuritic
pain can occur due to inflammation of the pleura (pleurisy) since the parietal pleura is very sensitive, or
to musculo – skeletal causes since chest wall pain can closely mimic the pain of pleurisy. Fever and
purulent sputum indicate infection; breathlessness and haemoptysis support infarction and a history of
trauma and pain reproduced by palpation at the site of the pain favour a musculo-skeletal cause.
Central diaphragmatic pleurisy often causes pain referred to the shoulder since the pain fibres from this
part of the diaphragm run with the phrenic nerve (cervical 3,4 & 5) while pleurisy involving the outer
part of the diaphragm causes pain referred to the lower chest and upper abdomen.
Large pleural effusions often cause a dull heaviness and pleural malignancy (especially mesothelioma)
may characteristically cause a constant, often severe pain. Pneumothorax may cause a pleuritic type of
pain but patients often describe it as a dragging or draining sensation. Pain and swelling over the sterno-
costal junction is called Tietze’s syndrome.
Tracheitis may cause an uncomfortable central chest pain often described as a “raw feeling” and
occasionally mediasternal or hilar lymphadenopathy as in sarcoidosis can cause similar problems.
Persistent coughing due to any cause may lead to soreness in the central chest as well as possibility of
causing rib fracture.
HAEMOPTYSIS
Haemoptysis is one of a few symptoms that will make a patient rush to see his doctor immediately.
Patients are usually alarmed when they see blood in their sputum. When the patient complains of
coughing up blood (haemoptysis) one must ensure that he has actually coughing up the blood from the
chest. This must not be confused with haematemesis – vomiting of blood. In haemoptysis the blood is
usually mixed with food particles and the blood tends to be darker due to the action of the hydrochloric
acid in the stomach. Bleeding from the nasopharynx may be difficult to distinguish from haemoptysis. If
there is nose bleeding or the blood just appears in the mouth, then a nasopharyngeal source is more
likely; whereas if the blood definitely comes up with a cough or is mixed with or streaked in the sputum
then the chest is the likely sourced. Blood from the chest is usually bright red and frothy.
One must estimate the amount of blood coughed up. The volume of blood loss being coughed up is a
guide to the immediately seriousness of the problem and is therefore important in management. There
is no cut off point but haemoptysis of more than 200ml in 24 hours has a high mortality. Tuberculosis
patients have known to die suddenly from severe haemoptysis. The cause of haemoptysis is only found
is about half of the patients presenting with the symptoms. Some clues may come from the history and
examination. Frank haemoptysis with pleuritic pain, breathlessness and sometimes a pleural rub is seen
in pulmonary infarction or with fever, purulent sputum and signs of consolidation in pneumonia.
Recurrent haemoptysis over several years is common in bronchiectasis. In a smoker aged 40 years or
more, bronchial carcinoma must always be considered.
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Causes of Haemoptysis
Traumatic Infective Neoplastic Vascular Parenchymal

Wounds Bronchiectasis Bronchial Pulmonary Cystic fibrosis
carcinoma infarction
Post-intubation Acute bronchitis Bronchial Osler-Weber- Sarcoidosis
adenoma Rendu
Foreign body Pneumonia Wegener’s Idiopathic
granulomatosis haemosiderosis
Lung abscess Rheumatoid Idiopathic
arthritis interstitial fibrosis
Parasites(hydatid Systemic lupus Goodpasture’s
disease, flukes) erythematosus syndrome
Tuberculosis Atrioventricular
malformation
Chronic
obstructive
pulmonary
disease
Fungi
Paragonimiasis
EXAMINATION
During the examination, the patient should be resting comfortably on a bed or couch, propped up
comfortably at an angle of 45°.
Inspection of the Sputum

Examination of the respiratory system begins with the examination of the sputum. Ask the patient if he
has a sputum mug, which may be on top of the locker or kept away in a bag or pocket or under the bed.
Inspect the sputum for amount, colour, viscosity, odour and presence or absence of blood.
The normal sputum is whitish and sero-mucous. When the sputum is yellowish or green, suspect chest
infection.
The presence of blood should alert one to the possibility of neoplasm, bronchiectasis or infection.
In pneumonia, the sputum is described as rusty due to the brownish red colour imparted to the sputum
by the iron in the blood.
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With the examination of the sputum over, look, for signs that can aid your diagnosis. These are may
include:
 Clubbing of the finger

 Pallor
 Cyanosis
 Tar stains in the finger nail
 CO2 retention flap
 Cachexia
 Intercostal recession
 Use of accessory respiratory muscles
Clubbing
This was discussed on the chapter on general and superficial features: Clubbing is the bulbous swelling
of the distal ends of fingers and toes this has also been discussed in chapter Two.
Look at the fingers for clubbing and stage the severity of the clubbing. Early clubbing is tested by resting
the distal phalanx of the middle finger on the pulp of the examiner’s two thumbs and palpating for
increased sponginess at the base of the nail fold with your index fingers (see Fig. 3:1). Clubbing also
affects the toes.
The pathogenesis of clubbing remains unknown. Certainly there is increased blood flow through the
fingers and a neurogenic component seems likely as vagotomy can abolish clubbing.
Hypertrophic pulmonary osteoarthropathy results in pain and sometimes swelling over the ends of the
long bones above the wrists and ankles symmetrically. It almost always occurs with clubbing and most
cases are associated with a squamous cell carcinoma of the lung.
Respiratory causes of clubbing include suppurative lung diseases like empyema, lung abscess,
bronchiectasis and cystic fibrosis. Others are bronchial carcinoma, fibrosing alveolitis, asbestosis and
pleural fibrosis. Clubbing may also be congenital.
Pallor
To evaluate pallor, take a good look at the palms of the hands, the nails, the inner aspects of the lower
conjunctiva, the tongue and the inner aspect of buccal mucosa. Evert the lower lips in order to see the
buccal mucosa properly.
In Negroes there may be pigmentation of the mucous membranes of the mouth, gums and even of the
palms, making clinical assessment of pallor more difficult than in the Caucasian.
Cyanosis
Central cyanosis is examined by looking at the tongue for bluish discolouration. For central cyanosis to
be present at least 5 gm of reduced haemoglobin must be present. Hence in severely anaemic patients it
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is difficult to demonstrate central cyanosis while it is very easy to detect cyanosis in patients with
polycythaemia.
Methaemoglobinaemia can be confused with central cyanosis as its presence gives a bluish tinge to the
tongue.
Peripheral cyanosis gives a bluish discolouration of the distal parts of body like fingers, toes and lips.
Peripheral cyanosis is usually due to increased oxygen extraction with a slow moving circulation. It is
seen in cold weather or in Raynaud’s phenomenon or peripheral vascular disease. Central cyanosis gives
rise to peripheral cyanosis but not vice versa.
FACE AND NECK

The lips and tongue should be inspected for central cyanosis, which almost always indicates poor
oxygenation of the blood by the lungs, whereas peripheral cyanosis alone is usually due to poor
peripheral perfusion. A breathless patient may be using the accessory muscles of respiration (e.g.
sternomastoid), and in the presence of severe COPD many patients find it easier to breathe out through
pursed lips.
Inspect the neck for tracheal tagging (descent of trachea with inspiration) often seen in patients with
COPD.
THORACIC CAGE
Now proceed to examine the thorax. Look for any deformities or abnormalities (Fig. 4:1). A barrel
shaped chest is seen in emphysema (Fig. 4:2). The sternum may be depressed in its lower half – a
condition called pectus excavatum (Fig. 4:3) or it may be prominent in the lower half like a pigeon
shaped chest – a condition called pectus carinatum (Fig 4:4)
Figure 4.1 Normal Shaped Chest
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Y
X
X=Y
Figure 4.2 Barrel Shaped Chest
Observe the thoracic spine for kyphosis, scoliosis or kyphoscoliosis of the thoracic vertebrae. See the
spine in Chapter 6 for the definition of these terms.
Pursed lip breathing is a sign of severe airway obstruction.
If on lying flat the patient becomes breathless or pre-existing breathlessness worsens, a condition called
orthopnoea, then one should think of pulmonary oedema or bilateral diaphragmatic paralysis.
Note any scars indicating previous chest operation or signs of trauma. Look at the skin of the chest wall
and assess any lumps present. Observe any dilated veins on the chest wall. Superior vena caval
obstruction is betrayed by dilated veins on the anterior chest wall. There are also engorged, fixed, non
pulsatile jugular veins, swollen face and neck as well as conjunctival oedema. Superior vena caval
obstruction is most often due to pressure from a bronchial carcinoma or its associated mediasternal
glands. Patients may complain of headache and sometimes worsening breathlessness as well as a puffy
face or that their collar feels tight.
Observation of Respiration
Rate: Count the rate of respiration. The normal respiratory rate is about 16 breaths per minute. The
range is 12-20 breaths per minute. A rate above 20 per minute is fast and it is known as tachypnoea.
Tachypnoea is an important sign and can sometimes be the only apparent clue to the presence of
respiratory disease. An increase in rate of respiration is sometimes found with fever due to non
respiratory causes.
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Patterns of Respiration (Fig. 4:5).

Observe the pattern of respiration carefully as it may give important diagnosis clues. Shallow breathing
is seen when breathing is restricted either by certain type of pulmonary disease (eg fibrosis) or chest
wall disease or by pain. A large increase in the depth of respiration (Kussmaul’s breathing) is often due
to metabolic acidosis such as in renal failure or diabetic keto-acidosis. Cheyne-stoke or period breathing
is a cyclical variation in depth and rate of breathing. Each cycle can last up to two minutes and involves a
period of apnoea followed by a gradual return of respiration before this declines again to another period
of apnoea. Cheyne-Stokes breathing usually indicates serious brain stem dysfunction. It is normal to sign
from time to time but when the patient sighs frequently while you are examining him, there is likely to
be a psychogenic component to his symptoms.
(a) Normal Breathing (b) Swallow Breathing (c) Kussmaul’s Breathing
(d) Cheyne-Stokes Breathing
Figure 4.5 Pattern of Respiration
Chest Wall Movements

Observe and compare the movements on both sides of chest. If one suspects pneumothorax or chest
trauma, feel for the cracking sensation of sub-cutaneous emphysema. Detect any local tenderness
present. Then confirm the chest movement by placing one’s hands on the chest. In the upper chest,
place both hands vertically parallel to the c hest with fingers pointing to the apices of the chest and
one’s two thumbs meeting in the midline. Ask the patient to breathe deeply in and out and observe the
movements of the hands especially the gap between the two thumbs (Fig 4:6). The normal chest
expansion measured with a tape measure at the level of the nipple is about 5cm or more. In routine
clinical practice exact measurements of chest expansion is unnecessary. It is sufficient merely to note on
inspection whether expansion appears normal or is obviously reduced. It is much more important to
look for unilaterally reduced expansion which will point to local pathology whether this is consolidation,
fibrosis, effusion or pneumothorax. Paradoxical inward movement of part of the rib cage during
inspiration indicates a flail chest.
9|Page
Figure 4.6 Movement of Upper Chest Wall
In severe airway obstruction, the accessory muscles of respiration such as the alae nasi, intercostals
muscles, sub-costal muscles as well as scalenus anterior and sternomastoid muscles are used to help the
work of breathing. Such patients may also fix the shoulder girdle with their arms to increase the
effectiveness of the accessory muscles further.
In the lower half of the chest, grasp the chest with the fingers and let the thumbs be equi-distant from
the midline then observe the movements of the thumbs from the midline (Fig. 4:7).
Figure 4.7 Movement in Lower Chest
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Palpation of the Trachea

Now palpate for the position of the trachea with the middle finger as well as the index and ring fingers.
Feel for the trachea in the supra-sternal notch with the middle finger of the right hand. The ring and
index fingers help to confirm if the trachea is deviated to one or the other side (Fig. 4:8)
Figure 4.8 Palpation of Trachea
Palpation for Lymph Glands

Palpate for lymph glands in the neck and axilla. The cervical lymph nodes are best examined from
behind the patient. With the patient relaxed and the neck held in a comfortable position, palpate for the
cervical lymph nodes. These are enlarged in bronchial carcinoma, lymphoma, tuberculosis and
sarcoidosis (See Fig 2:10).
Palpation of Axillary Lymph Nodes

In palpating for the left axillary lymph nodes, rest the patient’s left upper limb on the left forearm and
using the right hand palpate for the apical, central and medical group of lymph nodes. Change over and
use the left hand to palpate for the lateral group of lymph nodes (See Fig. 2:11).
To palpate for the right axillary lymph node, rest the patient’s right upper limb on the right forearm and
using the left hand palpate for the apical central and medial group of lymph nodes with the left hand.
Change over and use the right hand to palpate for the lateral group of lymph nodes (See Fig. 2:12)
Tactile Fremitus
To test for tactile fremitus, place the right hand on the chest and ask the patient to repeat the words
“Ko Ko” or “Ninety nine”. Repeat the procedure on the other side of the chest. Compare the feel of the
vocal sounds on one side with that on the other side. Move down the chest wall comparing the two
sides all the time.
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Tactile fremitus is palpable over normal lung and remains palpable or increased over consolidated lung
but is reduced over an effusion. When one finds reduced percussion note for which the reason is not
clear then a reduction in tactile fremitus favours a pleural effusion or thickening.
PERCUSSION OF THE CHEST
The technique of percussion is acquired with practice. Start by percussing directly on the clavicle then
place the middle finger of the left hand flat on the chest wall and strike the middle phalanx smartly with
the tip of the terminal phalanx of the right middle finger. The hammer action of the right hand should all
come from the right wrist.
Percuss down the mid-clavicular line moving about one inch each time and comparing the left and right
sides. Then percuss along the anterior auxillary line on the two sides using the same technique as before
(Fig. 4:9).
Figure 4.9 Percussion of the Chest Anteriorly
To percuss the axillary region let the patient rest his hands on head in order to expose the axilla and
percuss as before.
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Percuss the back using the same procedure. First percuss along the medial border of the scapular and
then along the posterior axillary line (Fig. 4:10).
Figure 4.10 Percussion of the Chest Posteriorly
One must constantly compare percussion note in the corresponding sites on the opposite sides of the
chest. If one’s attention is drawn to a particular area of the chest by an altered percussion note or by
other signs or local symptoms then one will need to examine the area in greater detail one should assess
each percussion note as being normal, hyper-resonant, dull or stony dull.
If the percussion note on one side is different to the other side there is likely to be an abnormality.
If however, one finds the same apparent abnormality on both sides then it is much less likely that one is
dealing with a significant problem. Thus while bilateral basal dullness may be due to bilateral pleural
effusion, it may simple be due to obesity.
Percussion Note Type of Lesion
Resonant Normal.
Hyper-resonant Pneumothorax
Impaired Pulmonary consolidation,

Fibrosis and collapse.
Dull Pulmonary consolidation and

Collapse.
Stony dull Pleural effusion and empyema.
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THE BREATH SOUNDS
Sounds at the Mouth

With a healthy person breathing at rest, one should not be able to hear the breath sounds at the mouth.
By contrast, in airway obstruction e.g. chronic bronchitis and asthma, the breath sounds will often be
easily heard. In general the worse the airway narrowing, the noisier is the breathing. These sounds arise
from increased turbulence of the gas flow in the main airway and the noisy breathing should be
considered separately from wheeze though the two may co-exist. Stridor is a harsh, often musical note
heard at the mouth marked on inspiration and denoting major airway obstruction.
Auscultation
Auscultate the chest for breath sounds. Avoid using the diaphragm of the stethoscope as in a hairy
patient the friction between the hair and the stethoscope will produce crackling sounds and one may
confuse this with adventitious sounds in the chest. Also in very thin patients it may be difficult to get the
diaphragm flat on the chest wall. Hence always use the bell of the diaphragm in auscultating the chest
for breath sounds.
Instruct one patient to “take deep breaths in and out with your mouth open”. Note the pattern of
breathing. Be very gentle with patients with pleuritic pain who will be unable to take deep breaths.
It is vitally important to compare the two sides. At each position that one listens, one must compare
with the corresponding position on the opposite side (Fig. 4:11).
First Rib
Lungs at full expiration
Right Margin Left Margin of heart

of heart
Nipple
Costal Margin
Liver Lungs at full

inspiration
Figure 4.11 Surface Marking of the Lung
14 | P a g e
Figure 4.12 Anterior and posterior aspects of the lungs showing the divisions of the lungs
One must listen more that 2 – 3cm away from the midline so that one listens over the lungs rather than
the airways.
The normal sounds may be reduced or absent if there is a barrier to their transmission as in pleural
effusion or pneumothorax or when airflow is reduced locally to a part of the lung in collapse. The breath
sounds will be quiet bilaterally in obesity, hyperinflation and when ventilation is depressed as in an
unconscious patient.
The sound one hears over the normal lung is described as vesicular. This is like the sound one hears
when the wind blows through the leaves on a tree. When the lung between the large airway and the
chest wall is relatively solid the breath sounds are transmitted with mush less loss than the normal and
are called bronchial. This is like blowing a sound through a narrowed tube. Bronchial breathing is
therefore heard over consolidation, collapse and sometimes fibrosis. Bronchial breath sounds are
normally heard by listening directly over the larynx or trachea. In bronchial breathing, the sounds are:
1. Harsher with high frequency
2. Have a definite pause between inspiration and expiration
3. Can be heard throughout expiration
Other terms used to describe variations in breath sounds are tubular which is the same as bronchial,
broncho-vesicular which is a combination of normal and bronchial breath sounds and cavernous or
amphoteric when the sounds appear to originate from a cavity beneath.
Added Sounds
There are three added sounds. These are wheeze, crackles and rubs.
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WHEEZE/RHONCHI
Wheeze are the sounds heard with the naked ear and the same sounds heard with a stethoscope are
called rhonchi. Wheeze is musical sounds produced by airway walls oscillating between the open and
nearly closed position. Wheeze indicate narrowing of an airway and usually occurs mainly on expiration
but also an inspiration in severe airway narrowing. However, in severe airway obstruction wheeze may
be absent. If one localizes a wheeze which is unaltered by coughing one should strongly suspect a local
airway obstruction most commonly due to a tumour or a tuberculosis induced stenosis.
Stridor is a loud mainly inspiratory noise usually heard at the mouth. It is produced by the potentially
serious situation of laryngeal, tracheal or major airway obstruction and must therefore be recognized.
Always suspect stridor if the inspiratory noise of wheeze is louder than the expiratory sound.
CRACKLE/RALES/CREPTATIONS
Crackles are produced by sudden opening of lightly occluded airways. Secretions in the terminal bronchi
and alveoli give rise to coarse crackles. Pulmonary oedema gives rise to fine crackles.
Note if the crackles are located to certain areas of the lung. Ensure that the crackles are not being
produced by hair moving under the stethoscope but rather emanating from the chest. Crackles are
heard in consolidation of the lungs as in pneumonia and also in fibrosing alveolitis.
Pleural Rub
This is a coarse creaking sound said to be produced by the irregular movements of the visceral and
parietal pleura on each other when the surfaces are inflamed. Pleural rub is heard in both inspiration
and expiration and it disappears when fluid collects between the two surfaces of the pleura. Pleural rub
is heard in acute infection, chronic inflammation pulmonary infarction or pleural trauma.
In auscultating the lungs therefore one is looking for three things.

1. Air entry. Is this reduced / absent or increased.
2. Type of breath sounds. Is this vesicular or bronchial
3. Presence or absence of adventitious sounds – crackles, rhonchi / wheeze and rub.
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PHYSICAL SIGNS OF RESPIRATORY DISEASE
Pathological Chest wall Mediastinal Percussion Breath Vocal Added

process movement displacement note sounds resonance sounds
(reduced)
Consolidation (i.e. Affected None Dull Bronchial Increased Fine crackles
lobar pneumonia) side
Collapse
Major bronchus Affected Towards lesion Dull Diminished Reduced None
side or absent or absent
Peripheral Affected Towards lesion Dull Bronchial Increased Fine crackles
bronchus side
Fibrosis
Localized Affected Towards lesion Dull Bronchial Increased Coarse
side crackles
Generalized (e.g. Both sides None Normal Vesicular Increased Fine crackles
cryptogenic
fibrosing
alveolitis)
Pleural effusion (> Affected Away from Stony dull Vesicular Reduced None
500 mL) side lesion (in reduced or or absent
massive absent
effusion)
Large Affected Away from Normal or Reduced or Reduced None
pneumothorax side lesion hyper absent or absent
resonant
Asthma Both sides None Normal Vesicular Normal Expiratory
Prolonged polyphonic
expiration wheeze
Chronic Both sides None Normal Vesicular Normal Expiratory
obstructive Prolonged polyphonic
pulmonary disease expiration wheeze and
coarse
crackles
17 | P a g e
T. C. Ankrah
Chapter 5
ALIMENTARY SYSTEM
 Symptoms of the Alimentary System
 Positioning of the Patient for the Examination of the
 Alimentary System
 Examination of the Mouth
 Inspection of the Abdomen
 Palpation for the Liver
 Palpation for the Spleen
 Palpation for the Kidney
 Distension of the Abdomen
 Examination Of The Groin And External Genitalia
 Rectal Examination

Adeline Obuo Ofori
MBChB 1
Paul Boateng
MBChB 1
ALIMENTARY SYSTEM
SYMPTOMS
The main symptoms of gastrointestinal tract disorders include pain, anorexia, nausea and vomiting;
problems with swallowing, changes in bowel habit (constipation and diarrhoea), wind, heartburn and
weight loss.
The diagnosis of diseases of the alimentary system depends more on analysis of the history than
physical examination.
Symptoms of gastro-intestinal disorders appear vague and imprecise. For example, heartburn to one
patient may be due to reflux of acid fluid into the lower oesophagus and to another patient it may be
due to retrosternal burning after food. Hence, the doctor should find out what exactly the patient
means.
Other patients may attribute their symptoms to “stomach upset” but yet have serious diseases
elsewhere. For instance, the retired school master with nausea and vomiting may have uraemia due to
enlarged prostate whereas the young nurse may have similar problems because of hypercalcaemia due
to her parathyroid tumour. Hence, gastrointestinal symptoms are not necessarily due to disease of the
alimentary system.
Abdominal Pain
Here, a few minutes of careful history taking may yield more dividends than hours of expensive
investigations. Intense constant generalized abdominal pain of sudden onset often implies perforation
of a peptic ulcer, acute pancreatitis or a ruptured aortic aneurysm. Remember that the pain of
myocardial infarction may be felt in the epigastrium. Waxing and waning pain felt diffusely over the
abdomen suggests gut colic as with intestinal obstruction. When colicky pain starts in the flank and
radiates to the lower abdomen or genitalia, ureteric colic must be considered. Severe upper abdominal
colicky pain radiating to the right upper quadrant and through to the back at the angle of the right
scapular suggests biliary colic and gall bladder disease. Acute central abdominal pains shifting after a
few hours to the right iliac fossa are likely to be due to appendicitis. Some metabolic disorder such as
sickle cell anaemia may present with severe abdominal pain.
Patients with duodenal ulcer may have relapsing/remitting pattern of disease extending over many
years. The pain in peptic ulceration is usually epigastric but may radiate through to the back, but often
the patient is unable to locate its site. Worsening of the pain before meals, nocturnal wakening and
relief with food may characterize duodenal ulcer. In gastric ulcer the pain is worse after meals. Colicky
abdominal pains related to disturbances of bowel habit and abdominal distension point to obstructive
lesions of the gut such as colonic cancer or Crohn’s disease. Concurrent weight loss, anaemia and
anorexia with abdominal pain should always alert you to the possibility of underlying malignancy.
ANOREXIA
Anorexia is loss of appetite. It is an expected symptom of many conditions such as fever, hepatitis,
anaemia, alcoholism and hypercalcaemia. It may be an early symptom of a gastro-intestinal disorder.
Loss of appetite with fastidiousness about food is often part of a makeup of the neurotic patient. This
loss of appetite in extreme form is anorexia nervosa. This is a serious disorder in young women
characterized by a refusal to eat sufficient food, resulting in severe weight loss and amenorrhoea.
Nausea and Vomiting
Nausea as an isolated symptom without vomiting is much more likely to be due to depression or
neurosis than primary gastrointestinal disease. When nausea is associated with vomiting, careful
enquiry must be made about associated symptoms such as weight loss and abdominal pain which may
lead on to the diagnosis of peptic ulceration or carcinoma. The vomiting of gastric outlet obstruction is
profuse and the vomitus may contain undigested food taken many hours previously. Substernal burning
or heartburn after meals characterizes gastro-oesophageal reflux. This may be aggravated by lying down
or bending over. Vomiting of fresh or altered blood (haematemesis) is usually a serious symptom
indicative of an ulcerative lesion of the upper gastrointestinal tract as far as the second part of the
duodenum. However, severe retching, as with an alcoholic binge, may tear the mucosa at the
gastroesophageal junction to cause fresh bleeding; this is known as the Mallory-Weiss syndrome.
Recurrent periodic vomiting is a feature of migraine in young adults. So enquire about associated
headache with the bouts of vomiting.
The effortless and unexpected vomiting of raised intracranial pressure is relatively uncommon and is
usually accompanied by other more prominent features of the primary disease. Other non
gastrointestinal causes of nausea and vomiting include uraemia, hypercalcaemia and Digoxin toxicity.
Remember the possibility of pregnancy as a cause of vomiting in women in the reproductive years.
Problems with Swallowing
The complaint of food sticking in the throat or gullet must always be taken seriously, particularly when it
is of recent onset and of increasing severity. In middle aged people it is often caused by a carcinoma of
the pharynx, oesophagus or gastroesophageal junction; sometimes an adjacent invading tumour such as
a bronchial carcinoma may announce its presence by dysphagia – difficultly or pain on swallowing.
Chronic and / or intermittent dysphagia may be due to benign oesophageal stricture or achalasia of the
cardia. Most patients with swallowing problems have more difficulty with solids than liquids but
sometimes in achalasia the reverse is true.
Discomfort or pain on swallowing is usually due to oesophagitis. It is usually associated with gastro-
oesophageal reflux or heartburn. In globus hystericus, the patient, usually a female of a nervous
disposition, feels she must swallow frequently to overcome the obstruction. Physical examination
reveals no abnormality.
Choking on swallowing is another serious symptom implying a neurological lesion of the larynx or a
fistula between the upper gastrointestinal tract and bronchi or lungs.
CHANGE IN BOWEL HABIT
Any changes in bowel habit must be critically assessed. For some patients, especially people living in the
rural areas, defecating three to four times a day is normal. In others, defecating once a week is
compatible with normal health. Remember to ask about medication causing altered bowel habit.
Constipation
If the stools are hard and difficult to pass, the patient should be regarded as constipated irrespective of
the frequency of bowel movements.
Diarrhoea
Enquire about the consistency of the diarrhoea. Is it watery, and very frequent as in colitis; are the
motions porridgy, bulky, pale and offensive as in steatorrhoea? Is nocturnal diarrhoea a problem?
Diarrhoea that wakes the patient from sleep is nearly always of an organic basis whereas a flurry of two
or three bowel actions on waking up in the morning is often of nervous origin. If the diarrhoea has lasted
for more than a month, one should think of Human Immuno- Deficiency Virus Infection and test for this
on the patient’s blood.
Bloody Stools
Enquire about the passage of blood or mucus with the stools. Fresh blood passed with the stools which
splatters the lavatory pan and is present on the toilet paper is likely to be due to bleeding piles
(haemorrhoids). However, the diagnosis must be confirmed after careful examination including
sigmoidoscopy. Blood and mucus with diarrhoea and a sensation of incomplete emptying of the rectum
is almost pathognomonic of rectal tumours.
Melaena Stools
In melaena, the stools are black, tarry and sticky. It indicates bleeding from the upper gastro-intestinal
tract. The stools are black because of the action of the hydrochloric acid in the stomach on the blood.
Parasites or infections of the gut may be causing the diarrhoea so remember to send stools for
laboratory examination after the physical examination.
Wind
This dyspeptic symptom is often of no significance but some patients are very worried about it and they
need to be assured. Mostly flatulence means bringing wind up (belching) and flatus means passing wind
down below (farting).
Excessive belching usually means that the patient is an air swallower. Excessive flatus may be due to
alactasia. Some patients complain of excessive flatus but for those who work alone in the open and who
can ease themselves without any embarrassment, this is rarely a symptom they complain about.
Borborygmi is a lovely onomatopoeic word that doctors often use to describe the gurgling and rumbling
abdominal noises that arise from peristaltic bowels. It is usually of no significance but in patients with
obstructive gut lesions, borborygmi may be heard in excess.
Heartburn
This is retrosternal or epigastric discomfort felt by the patient as a result of gastro-oesophageal reflux of
acid secretions. Make sure that one does not misdiagnose angina for heartburn.
EXAMINATION
Positioning of the Patient
Physical signs are easily missed with the patient in a bad position, often hunched up with too many
pillows. The patient should lie supine and flat with the arms by the sides, preferably with no pillows but
if he is breathless, then one pillow may be needed. The examiner must put the patient at ease and the
abdomen should be exposed properly from the xiphoid to the pubis making sure that the genitalia is
well covered in order not to embarrass the patient.
GENERAL SIGNS
Look for the presence of clubbing. Alimentary causes of clubbing include malabsorption syndrome, liver
diseases like cirrhosis of the liver and hepatoma, ulcerative colitis and Crohn’s disease, abdominal
Tuberculosis, GI lymphomas and celiac sprue.
Look for stigmata of chronic liver disease. Look at the hands for palmar erythema at the thenar and
hypothenar eminences. Look at the nails for whiteness {leuconychia, which indicates
hypoalbuminaemia} and there may also be a brownish crescent at the distal part of the nail. Look for
Dupuytren’s contracture in the palm. Observe the face for facial telangiectasia and spider naevi. Look at
the skin around the eyes including the eyelids for xanthelasma which is seen in chronic cholestasis, in
primary biliary cirrhosis and in other hyperlipidaemias. Also observe any exanthemata on extensor
surfaces.
Male patients with chronic liver disease of varied aetiology become feminised whereas some female
patients tend to become masculinised. Significant endocrinological features may be seen in the male
cirrhotic of which gynaecomastia is the most obvious occurring in 40% of cirrhotic men. Other changes
include loss of body and facial hair.
Look for asterixis (flapping tremors) by asking the patient to extend his arms with hands cocked up and
observe the brief downward ‘flapping’ motion of his hands. Asterixis also occurs with renal and
respiratory failures.
Box 5.1 Peripheral stigmata (signs) of chronic liver disease

Skin, nails and hands
 Spider naevi - small telangiectatic superficial blood vessels with a central feeding vessel
 Clubbing
 Leukonychia - expansion of the paler half-moon at the base of the nail
 Palmar erythema - seen on the thenar and hypothenar eminences, often with a blotchy
appearance
 Bruising
 Dupuytren's contracture - can occur in the absence of liver disease
 Scratch marks - particularly in cholestatic liver disease
Endocrine - due to excess oestrogens
 Gynaecomastia
 Testicular atrophy
 Loss of axillary and pubic hair
Other
 Parotid swelling - particularly in alcohol-related liver disease

 Hepatic fetor - characteristic sweet-smelling breath
 Hepatic flap - a sign of encephalopathy and advanced disease
Jaundice (Icterus)
Observe the sclera for jaundice. Jaundice is obvious clinically when the total serum bilirubin rises above
three times the normal level {ie above 50umol/L or 3.0 mg/100 m1}. It is best detected in the sclera
where the bilirubin stains the elastic tissues.
As jaundice deepens the sclera colours may change from a lemon tinge to deep yellow and eventually to
a greenish brown colour. In haemolysis, the accompanying anaemia gives the patient a characteristic
pale lemon-yellow tinge.
Box 5.2 Types of jaundice and causes

Pre-hepatic
Haemolysis, ineffective erythropoiesis,
Ineffective glucuronidation (Gilbert’s syndrome, Crigler Najjar syndrome)
Hepatocellular
Viral: Hepatitis A, B, C; (other infections: CMV, EBV, toxoplasmosis, leptospirosis, Q fever)
Drugs (paracetamol, anti-TB drugs, statins, sodium valproate, halothane), toxins, herbal
medications
Alcoholic hepatitis
Autoimmune hepatitis
Cirrhosis, hepatic metastases, hepatic abscess
Wilson’s disease, haemochromatosis, 1-antitrypsin deficiency, Budd-Chiari syndrome
Septicaemia
Dubin-Johnson syndrome, Rotor syndrome
Obstructive
Gallstones (in the common bile duct)
Carcinoma of head of pancreas/ampulla of Vater/bile duct
Lymphadenopathy at the porta hepatis
Benign stricture (following invasive procedures)
Drugs: (antibiotics, OCPs, chlorpromazine, sulphonylureas, gold)
Primary sclerosing cholangitis, primary biliary cirrhosis
Parasities (e.g. schistosomiasis/fasciola), pancreatitis, AIDS cholangiopathy
Observe the cornea for Kayser-Fleischer rings. These are light brown rings of copper chelates at the
periphery of the cornea. These rings may be visible only on slit lamp examination.
Pallor
Look for pallor as discussed in earlier chapters. Presence of pallor may indicate gastro-intestinal
bleeding.
THE MOUTH {see Fig. 2:8}.
Now proceed to examine the mouth. The examination of the mouth allows the doctor to:
1. Assess the degree of dehydration from the state of the tongue and mucous membranes.
2. Look out for specific lesions of the mouth like ulcers, sore patches and lumps.
3. Search for local additional clues that may help in the diagnosis of systemic diseases. E.g. in
measles, a spotty enanthema in the oral cavity often precedes the rash; ulcerations on the
buccal mucosa about Stensen duct produce Koplik spots. In infectious mononucleosis, an acute
pharyngitis and tonsillitis that may be coated with a gray-white exudative membrane may be
present with enlargement of lymph nodes in the neck.
Physical damage of the lips may produce painful fissuring with scaling and crust formation called
cheilitis. Cracks at the corners of lips, called angular stomatitis or cheilosis, are common. They may be
due to anaemia and malabsorptive states. They can also be caused by overlapping of the lips in
edentulous patients or those with ill fitting dentures.
Herpes simplex is a common infection that affects the lips. This results in clusters of vesicles on the lips
and surrounding skin.
Localized chronic ulceration of the lips can be due to a carcinoma which may appear as a thickened
plaque or warty growth. The lower lip is a common site for carcinoma, particularly in men. Pipe smoking
is a predisposing factor. If one suspects carcinoma, one must not forget to feel for possibly enlarged
submental nodes.
Hereditary haemorrhagic telangiectasias are bluish spots on the lips, tongue, buccal and nasal mucosa.
Endoscopists have identified similar lesions in the upper gastrointestinal tract as far as the stomach. The
great importance of these lesions is that they bleed intermittently and produce a chronic iron deficiency
anaemia.
In Peutz-Jegher’s syndrome, there are brownish flecks of pigmentation at the mucocutaneous junction
of the lips or around the mouth. Their importance is in their association with small intestinal polyps that
may cause intestinal obstruction, intussusception or undergo neoplastic change.
Gums and Teeth
Gingivitis produces swelling and redness of the margins of the gums which bleed easily. Gingivitis may
progress to periodontitis, which is inflammation of deeper tissues around the teeth and is a very
common cause of tooth loss in adults.
Swelling of the gums occurs physiologically in puberty and pregnancy but also develops with long term
anti-convulsant therapy with Phenytoin. Gross hypertrophy, infection, bleeding and necrosis of the
gums are features of acute leukaemia. Rarely vitamin C deficiency (scurvy) will result in bleeding gums.
Acute necrotizing ulcerative gingivitis is a painful infection characterized by sloughy ulceration at the
gum margins and unpleasant halitosis.
In Addison’s disease, a brownish pigmentation of the gums and buccal cavity is seen. In Lead or Bismuth
poisoning, a dark line 1mm from the gum margin is seen.
The domed, notched and widely spaced teeth of congenital syphilis (Hutchison’s teeth) are rarely seen
today.
Enlargement of the mandible with underbite and increasing spacing of the lower teeth may be seen in
acromegaly. Tetracycline is deposited in growing bone and may stain the teeth and cause dental
hypoplasia if given to young children or pregnant women.
The Tongue
Both “scrotal tongue” (ie. The tongue is deeply furrowed and resembles the surface of the scrotum) and
“geographical tongue” should be regarded as normal variants. A geographic tongue is an inflammatory
disorder on the dorsal surface of the tongue characterized by numerous and continually changing areas
of loss and regrowth of the filiform papillae. Black hairy tongue is also a normal variant though it may
follow antibiotic therapy.
Inspect the tongue for hydration. Dry tongue is seen in severe diabetic ketoacidosis, mouth breathing,
absence of salivary secretions and drugs e.g. atropine, tricyclics, inhalers and anti-depressants.
Raw red beefy tongue should suggest possible deficiency syndrome like iron deficiency anaemia;
pernicious anaemia, malabsorption or pellagra. Similar changes occur in radiotherapy and
chemotherapy.
Leukoplakia is a premalignant condition characterized by white streaks and patches with sharply defined
edges like streaks of white paint.
The creamy-white curdy patches of candidiasis (thrush) are usually easily recognized in the
immunosupressed, debilitated elderly patient and people on antibiotic therapy. The presence of thrush
in a healthy young man should raise suspicions of Acquired Immuno-Deficiency Syndrome (AIDS) related
complex.
Lichen planus affects the tongue in 50% of cases with the lesion elsewhere. It may present as a white
plaque on the side of the tongue or as chronic ulcer of the tongue.
Carcinoma of the tongue is important. It is commonly sited along the edges or base of the tongue where
it is less readily detected. Most carcinomas of the tongue present with the characteristic features of a
malignant ulcer with indurated everted edges and a sloughy ulcerated base. Carcinoma of the tongue
initially metastasises to the submental nodes and then to the cervical nodes. It is important to look for
leukoplakia, which may be associated with the cancer. Lymphomatous ulcers of the tongue are rare
usually being high grade non Hodgkin lymphomas that develop as bulky tumour masses which quickly
ulcerate. Tuberculous ulcers of the tongue may be associated with gross submental and cervical
lymphadenopathy.
Macroglossia is seen in myxoedema, acromegaly, amyloidosis and massive infiltration with tumours.
Stomatosis
This term covers ulceration, infection, necrosis and desquamation of the mucous membranes. It ranges
from trivial conditions like aphthous ulcers to serious conditions like cancrum oris. Causes include
infection, drugs and haematological malignancies. The most extreme form of oral ulceration is cancrum
oris where there is complete necrosis around the mouth.
Oral Foetor
The stench of an anaerobic infection of lung abscess is as characteristic as that of a Vincent’s infection.
The breath in hepatic coma often has a sickly sweet aroma and some claim that the breath in uraemia
has a fishy uriniferous smell.
The sickly sweet smell of ketones on the breath of a patient with diabetic coma may give an early
warning of the severity of the metabolic crisis.
ABDOMEN
The examiner must put the patient at ease. A sagging mattress makes examination, particularly
palpation, difficult. Make sure there is good light, that the room is warm and that the hands are warm. A
shivering patient cannot relax and vital signs may be missed, especially on palpation.
Now inspect the abdomen noting the general contour, distension, local prominence and abnormal
masses, abnormal pulsation, scars, hair distribution, visible peristaltic waves, pigmentation, the
umbilicus and engorged superficial veins.
Is the abdomen of normal contour and fullness, or distended? Is it scaphoid (sunken)?
Generalized fullness or distension may be due to fat, fluid, flatus, faeces or a fetus. Localized distension
may be symmetrical and centred around the umbilicus, as in the case of small bowel obstruction, or
asymmetrical as in gross enlargement of the spleen, liver or ovary. Note if there is any movement of the
swelling, either with or independent of respiration. A scaphoid abdomen is seen in advanced stages of
starvation and malignant disease, particularly carcinoma of the oesophagus and stomach.
Normally there is a gentle rise in the abdominal wall during inspiration and a fall during expiration; the
movement should be free and equal on both sides. In generalized peritonitis this movement is absent or
markedly diminished (the 'still, silent abdomen').
Visible peristalsis in the upper abdomen from left to right is seen with gastric outlet obstruction as with
a stenosing duodenal ulcer or pyloric carcinoma. Visible peristalsis may also be seen in obstruction of
the distal small bowel and as a normal finding in the very thin patient; in elderly patients with lax
abdominal muscles or in large wide-necked incisional herniae.
If the superficial veins are engorged, demonstrate the direction of blood flow by emptying the blood in
the veins with the index fingers and then observing which direction the veins are filled from by releasing
one finger and repeating the procedure with the other finger. Prominent superficial veins may be
apparent in three situations: thin veins over the costal margin, usually of no significance; occlusion of
the inferior vena cava; and venous anastomoses in portal hypertension. In inferior vena caval
obstruction, the direction of flow is upwards. Distended veins around the umbilicus (caput medusae) are
uncommon but signify portal hypertension, other signs of which may include splenomegaly and ascities.
Pigmentation of the abdominal wall may be seen in the midline below the umbilicus, where it forms the
linea nigra and is a sign of pregnancy.
Note any stretch marks or striae. This is seen in women who have borne children. It is also seen in rapid
gain or loss of weight or in patients on high dosage steroids and those with Cushing’s syndrome.
Note any hernia or enlarged lymph nodes in each groin. Observe the umbilicus for the site of hernia and
note if the umbilicus is everted, inverted or flat. Normally the umbilicus is slightly retracted and
inverted. A common finding in the umbilicus of elderly obese people is a concentration of inspissated
desquamated epithelium and other debris (omphalolith).
Note the hair distribution. In liver disease, the hair distribution tends to be feminine with the hair
limited to the supra public line. Normally in males, the hair on the abdomen stretches to the umbilicus
and other parts of the abdomen.
Division of the Abdomen
Traditionally the abdomen is divided into nine segments by two imaginary vertical lines joining the
midclavicular and mid inguinal points and two imaginary horizontal lines, the upper one passing through
the transpyloric or sub-costal margin and the lower one joining the anterior superior iliac spines. (Fig.
5:1)
These imaginary lines divide the abdomen into nine regions as follows.
 Epigastrium, (E)
 Right Hypochondrium, (RH)
 Left Hypochondrium, (LH)
 Umbilicus/ Umbilical Region, (UR)
 Right Lumbar, (RL)
 Left Lumbar, (LL)
 Supra-pubic/ Hypogastrium, (H)
 Right Iliac, (RI)
 Left Iliac, (LI)
REGIONS OF THE ABDOMEN.
1 and 3: right and left hypochondrium;
2: epigastrium;
4 and 6: right and left lumbar;
5: umbilical;
7 and 9: right and left iliac;
8: hypogastrium or suprapubic.
Figure 5.1 Division of Abdomen
PALPATION
The examiner should enquire about sites of pain or tenderness and monitor the progress of the
examination by the patient’s facial response. This ensures that one does not hurt the patient. A small
proportion of patients find it impossible to relax their abdominal muscles when being examined. In such
cases it may help to ask them to breathe deeply, to bend their knees up, or to distract their attention in
other ways.
Palpation of the abdomen involves both superficial and deep palpation.
Palpation of the abdomen is performed predominantly using the right hand, with the examiner on the
right side of the patient. Avoid digging into the patient’s abdomen with the finger tips and palpate with
the pads of the finger tips with the forearm and hand horizontal. This may mean raising the bed if it is
low; alternatively do not hesitate to kneel down alongside the patient’s bed to palpate. Start by talking
to the patient to gain his or her confidence and taking his/her mind off the examination.
Do a gentle superficial palpation of the whole abdomen. The purpose of the superficial palpation is to
elicit any area of tenderness. So keep watching the patient’s face all the time as you are doing superficial
palpation to elicit tenderness in any area. . The purpose of superficial palpation is also to note the
presence of any mass and guarding. Having demonstrated an area of tenderness, palpate that area last
in your deep palpation, starting your palpation well away from the site of tenderness.
In deep palpation, one is palpating for characteristics of any mass noted on superficial palpation and
also the various abdominal organs – liver, spleen and kidneys. When a mass is present, one must know
the location, size, consistency, tenderness, surface and whether the edge is smooth or rough.
Remember to listen over any mass present for a bruit.
The Liver
To palpate for the liver, use the pads of the finger tips of the right hand and start palpating from the
right iliac fossa and work your way upwards (Fig. 5:2). After feeling the mass, look for the characteristics
of the liver mass as mentioned above.
Figure 5.2 Palpation for Liver
Sometimes one might like to know the upper border of a liver mass by percussing on the right
hemithorax where the upper border of the liver is the point of dullness from the tympanitic areas of the
lungs. The upper border of the liver is usually located 1cm above the upper border of the right 5th rib in
the midclavicular line.
Liver enlargement should be recorded accurately in centimeters below the costal margin in the right mid
clavicular line and below the xiphoid in the midline. Assessment of liver enlargement in finger breadths
is to be discouraged.
Palpation of the liver edge below the right costal margin does not necessarily mean that the liver itself is
enlarged. Hyperinflation of the lung as in asthma and emphysema may depress the liver. In end stage
cirrhosis the liver is usually shrunken but the left lobe may be palpable as a firm and often irregular edge
in the epigastrium just below the xiphoid.
Percussion of the liver may help to define the position of a shrunken cirrhotic liver or in acute yellow
atrophy (hepatocellular necrosis due to fulminant viral hepatitis).
In right heart failure, the liver is enlarged, soft and tender. Pressure over the liver may distend the
jugular veins. This is called the hepato-jugular reflex. Gross enlargement of the liver due to metastases
often causes elevation of the right diaphragm simulating a right pleural effusion. When the liver is
diffusely enlarged by infiltrative disease such as lymphoma, amyloidosis or sarcoidosis, a careful search
for associated splenomegaly or lymphadenopathy should be made.
Then listen over the hepatic mass for a bruit. An enlarged, firm, tender liver with a bruit is suggestive of
primary hepatocellular carcinoma.
The gall bladder
This is not palpable unless enlarged and it may then be felt (often with difficulty) in the midclavicular
line.
Corvoisier’s law states that ‘if in the presence of jaundice the gall bladder is palpable, then the cause of
the jaundice is unlikely to be a stone impacted in the common bile duct’. This is because gall stones will
probably have caused previous cholecystitis leading to a small fibrotic gall bladder.
Cholecystitis may be detected by pressing the fingers gently into the right hypochondrium as the patient
takes a deep breath in. a sudden catch of breath when the gallbladder touches your fingers indicates
inflammation (Murphy’s sign).
Hyperaesthesia over thoracic segments 9, 10 and 11 posteriorly on the right side (Boas’ sign) is also a
feature of cholecystitis.
The Spleen
In the young healthy adult, the spleen is 10cm in its long axis lying parallel to the left 10th rib, 7cm broad
and 4cm in thickness. The spleen atrophies from a maximum of 200g in the twenties to 60-70g in
extreme old age. It is not palpable in health and so when it is palpable this implies enlargement.
When the spleen enlarges, it enlarges towards the right iliac fossa. So start the palpation of the spleen in
the right iliac fossa with the pulps of the right fingers and work your way diagonally upwards to the left
costal margin. In gross splenomegaly, try to feel for the notch on the medial border of the splenic mass.
To detect mild to moderate degrees of splenomegaly, the examiner’s left hand should be placed in the
patient’s left loin to lift the spleen anteriorly. The right hand then palpates the spleen as it emerges from
below the left costal margin (Fig. 5:3).
Measure the length of the enlarged spleen below the costal margin along its line of enlargement
towards the right iliac fossa. NB. 1-2cm indicates tip enlargement, 3-7cm indicates moderate
enlargement while 7cm and more indicates marked enlargement.
Figure 5.3 Palpation of Spleen
Causes of splenomegaly
Massive splenomegaly, ( >7 cm)
CML, Myelofibrosis, HMS (hyperreactive malarial splenomegaly), Leishmaniasis,

Gaucher’s syndrome
Moderate splenomegaly, (3-7 cm)
infection (TB, malaria, endocarditis, schistosomiasis, EBV),Portal Hypertension (liver

cirrhosis), Haematological (haemolytic anaemia, leukaemia, lymphoma), Connective
tissue disease (rheumatoid arthritis, SLE), other causes include sarcoidosis and primary
antibody deficiency
Now listen with the stethoscope over the enlarged spleen and occasionally a splenic friction rub may be
heard over the site of splenic infarct.
The Kidneys
The kidneys are palpated bimanually. To palpate for the right kidney, put the left hand on the posterior
aspect of the trunk in the right renal angle and place the right hand over the right flank. The hands
should be parallel with the fingers pointing to the umbilicus. Then feel for and roll the kidney between
the two hands, noting the characteristics of the mass (Fig. 5:4).
Figure 5.4 Palpation for Right Kidney
To palpate for the left kidney place the left hand on the posterior aspect of the trunk in the left renal
angle then place the right hand over the left flank. Again the hands should be parallel but this time they
will be opposite, the left hand will be pointing to the spinal column while the right hand is pointing to
the lateral border of the abdomen. Feel for the left kidney and note its characteristics (Fig. 5:5)
Figure 5.5 Palpation for Left Kidney

Normally the kidneys are not palpable but in thin individuals the normal kidneys can be palpable. Both
kidneys are palpable in polycystic disease of the kidney.
A mass felt in the left hypochondrium could be an enlarged spleen or an enlarged left kidney. To
differentiate between the two, the following points should be noted.
1. One can get above the renal mass but cannot get above the splenic mass which ducks
under the left lower ribs.
2. One can feel a notch on the medial border of a splenic mass but not on a renal mass.
3. A renal mass is bimanually palpable but a splenic mass is not.
4. As a renal mass is a retro-peritoneal mass, percussion over it is tympanitic because of
the overlying descending colon while percussion over a splenic mass is dull.
Other Abdominal Masses
After feeling for the liver, spleen and kidney, palpate the abdomen for other abdominal masses that may
be present. Do not forget that a full bladder may present with a mass arising from the pelvis. If one
suspects a distended bladder, get the patient to void urine and the mass should disappear. In women,
remember that an enlarged uterus and ovarian cysts present as abdominal masses.
The fixed hard irregular epigastric mass in a middle aged or older patient is most likely due to advanced
carcinoma of the stomach. As the disease advances, the patient becomes wasted and anaemic. When
the tumour obstructs the outflow of the stomach, the patient may have the features of pyloric stenosis
with recurrent vomiting of large volumes of stale undigested food and distension of the proximal
stomach with visible peristalsis from left to right. Metastases may spread to the liver to cause associated
hepatomegaly and jaundice. Frequently, nodes in the supraclavicular fossa are involved. A palpable left
supraclavicular node constitutes Troisier’s sign. Occasionally, a carcinoma of the pancreas may be
palpable in the epigastrium. Primary and secondary tumours in the left lobe of the liver may cause
confusion in the identification of masses in the epigastrium.
The diagnosis of aortic aneurysm depends on the finding of a midline pulsating swelling usually, though
not necessarily, in an arteriopathic patient. The lateral expansion on pulsation in addition to the forward
pulsation is the initial diagnostic factor. Tumours or masses anterior to the aorta show transmitted
pulsations only. Vascular bruits may be audible over an aortic aneurysm or over adjacent diseased
vessels.
Masses of enlarged para-aortic or mesenteric glands may give rise to a lumpy central abdominal
swelling. These are usually due to lymphoma or chronic lymphatic leukaemia but may be secondary to a
primary tumour elsewhere such as a seminoma. Iliac or inguinal nodes with an enlarged spleen may also
be detected.
A Cystic swelling in the abdomen is characterized by a tense fluctuant feel. If large enough, a fluid thrill
may be elicited. Pancreatic pseudocysts in the lesser sac are usually fixed and situated in the
epigastrium. Mesenteric cysts usually move at right angles to the axis of the mesentery and may be
confused with hydatid cysts when they arise in this region (Epigastrium). Cysts arising from the pelvis are
mostly likely to be ovarian and if malignant, are often associated with ascites.
Masses in the Right Iliac Fossa
The diagnosis of a mass in the right iliac fossa is dependent upon age, circumstances and social
background. These conditions include tuberculosis, amoeboma, appendicular mass/abscess, Crohn’s
disease and carcinoma of the caecum.
A young adult with a recent history of central abdominal pain followed by pain in right iliac fossa is likely
to have an appendicular mass.
A sub-acute or chronic pain in the right iliac fossa, often of colicky type with diarrhoea, anaemia and
weight loss in a young or middle aged patient indicates tuberculosis of the ileum or caecum with
enlarged or inflamed lymph nodes. With a more acute illness, fever and diarrhoea, the mass might be
due to an amoeboma. In the Western world, the mass may indicate Crohn’s disease of the terminal
ileum. Often, the mass is composed of the diseased ileum with surrounding inflammation.
Carcinoma of the caecum in middle aged or old patients is often without local symptoms presenting
with diarrhoea and iron deficiency anaemia. A few patients may notice the mass themselves whereas
others may get intestinal obstruction.
The first sign of lymphoma may be a mass of nodes in the right iliac fossa. Here the lump may be
relatively painless and may be associated with enlarged para-aortic or inguinal glands and an enlarged
spleen. Such a mass of nodes is statistically more likely to be non-Hodgkin’s lymphoma rather than
Hodgkin’s disease. Less common causes of a mass in the right iliac fossa are psoas abscess, mobile
ovarian cyst and retroperitoneal tumour.
Masses in the Left Iliac Fossa
As with masses in the right iliac fossa, the diagnosis of a left sided mass depends on factors such as race
and age. The causes include diverticular mass or disease, faeces in the loaded colon and carcinoma of
the colon. Less common ones are Crohn’s disease, lymphoma, psoas abscess, mobile ovarian cysts and
retroperitoneal tumour.
PERCUSSION
DISTENSION OF THE ABDOMEN
When the patient complains of abdominal distension, one must go through the check list of the 7 “Fs” to
determine the possible cause of the swelling. These are fat, fluid, faeces, flatus, foetus, fibroid and full
bladder.
Fat
Obesity is easy to diagnose but it is sometimes surprisingly localized to the abdomen. The dullness does
not shift. Some patients, particularly women, accumulate enormous deposits of fat subcutaneously in
the abdominal wall producing an apron which hangs over the pubis, groin and the upper thighs. Truncal
obesity with wasted limbs is a feature of Cushing’s syndrome or of long term high dosage steroid
therapy.
Flatus
Excess gas in the alimentary tract produces a tympanitic distension of the abdomen. It may be due to air
swallowed, high fibre diet or alactasia. Gaseous distension due to more serious disorders such as large
bowel obstruction is usually generalized but may be localized; as with a sigmoid volvulus. When
mechanical obstruction of the gut is present, loud borborygmi are audible and persistalsis is visible.
Faeces
When the abdomen is distended by impacted faeces, one may be able to indent the faeces in the
descending colon by firm pressure. Acquired mega colon is most often seen in demented or
psychiatrically disturbed patients with hard faeces in rectum. The patient may complain of diarrhoea
which is in fact spurious, caused by seepage of mucus and soft faeces around the rectal mass.
Fluid (Ascites)
When there is less than 500ml of ascitic fluid present, there is a curious floppy, splashy feel to the
examining hand and there may be vague tenderness in the flanks.
With 500 -5000ml of ascitic fluid present, there is a V-shaped dullness in the lower abdomen together
with shifting dullness.
With more than 5000ml of ascitic fluid present, there is tense abdomen and fluid thrill present.
There are two methods to demonstrate the presence of fluid in the abdomen.
These are:
1. Demonstration of fluid thrill.

2. Demonstration of shifting dullness.
The demonstration of shifting dullness is preferred as one needs an assistant to block the fat thrill in
order to demonstrate fluid thrill while one does not need any assistance to demonstrate shifting
dullness.
To demonstrate the presence of shifting dullness, start the percussion of the abdomen from the midline
and move laterally. Fluid finds its own level and if there is ascites, the fluid will gravitate towards the
flanks. So as one percusses from the midline towards the flanks, the percussion note will become dull.
Now leave the hand on the flanks of the abdomen where the note is dull and ask the patient to roll to
the other side. Fluid will now gravitate towards that side and the side where the hand is, which was
previously dull, will now be tympanitic. Hence the dullness has shifted. This demonstrates the presence
of fluid in the abdomen.
Feotus
The history of amenorrhoea in a woman in the child bearing age group together with the palpation of
foetal parts will make the diagnosis of foetus easy.
Fibroid
Here, the history of heavy menses and the presence of anaemia with the palpation of a firm tumour
arising from the pelvis should make the diagnosis easy.
Full Bladder
The mass arises from the pelvis in both male and female patients. Percussion over the mass is stony dull.
The mass tends to be tender in acute retention of urine. It may or may not be tender in chronic
retention of urine.
AUSCULTATION OF THE ABDOMEN
Auscultation of the abdomen is for detecting bowel sounds and vascular bruits.
With the completion of the palpation and percussion of the abdomen, now proceed to listen to the
abdomen with the bell of the stethoscope in the right iliac fossa for the character of the bowel sounds.
Note whether the bowel sounds are present or absent. If they are present note whether they are
reduced or increased. In intestinal obstruction, the bowel sounds are increased while in paralytic ileus,
the bowel sounds are either reduced or they may be absent altogether.
Auscultation of the abdomen is particularly useful in acute surgical emergencies where the silent
abdomen indicates paralytic ileus due to perforation and / or peritonitis. Bowel sounds are normally
heard every few seconds with prolonged gurgles or borborygmi less frequently. These are excessively
loud in intestinal obstruction.
Vascular bruits: listen above the umbilicus over the aorta for bruit which occurs in the presence of an
atheroma or an aneurysm. Then also, place the stethoscope 2-3cm above and lateral to the umbilicus to
listen for renal artery bruits as in renal artery stenosis.
EXAMINATION OF THE GROIN AND EXTERNAL GENITALIA
Inspect the groins and the external genitalia for any abnormalities.
Note any hernia or enlarged lymph nodes in each groin. The patient should then stand for careful
inspection once more as some hernias reduce spontaneously when the patient lies supine. Ask the
patient to cough while standing and look for a visible expansile cough impulse over the femoral or
inguinal canals. If an expansile impulse is present on inspection, it is likely to be a hernia, so move to
whichever side of the patient the lump is on. Place one hand over the buttock to support the patient,
the fingers of the other hand being placed obliquely over the inguinal canal. Now ask the patient to
cough again. If an expansile impulse is felt then the lump must be a hernia. Next, decide whether the
hernia is inguinal or femoral. This is done by determining the relationship of the sac to the pubic
tubercle. The tubercle will be felt as a small bony prominence 2cm from the midline on the pubic crest.
If the hernial sac passes medial to and above the index finger placed perpendicularly on the pubic
tubercle, then the hernia must be inguinal; if it is lateral to and below, then the hernia must be femoral.
If it has been decided that the hernia is inguinal, then one needs to know these further points:
 What are the contents of the sac? Bowel tends to gurgle, is soft and compressible, whereas
omentum feels firmer and is doughy in consistency.
 Is the hernia fully reducible or not? Ask the patient whether the hernia is reducible, and if so get
them to reduce it. It is more painful if the examiner reduces it while lying down.
 Is the hernia direct or indirect? Determine this while the patient still lays down. Place one finger
just above the midinguinal point over the deep inguinal ring. If the hernia is fully controlled by
this finger then it must be an indirect inguinal hernia.
In examining the external genitalia of the male, note any obvious abnormalities of the penis( small size
of penis, phimosis, paraphimosis). Examine the scrotum and testis(size and consistency). The normal
adult testes are about 5cm in length and are firm and not tender. Small, soft testes indicate cirrhosis or
hypogonadism(eg.Klinefelter syndrome). Examine for swellings such as spermatocele, hydrocele and
varicocele.
In examining the external genitalia of the female, note the distribution of pubic hair, obvious
abnormalities of the introitus and enlargement of the clitoris. Extensive distribution of pubic hair over
the abdomen (hirsutism) is associated with alteration in oestrogen or androgen balance (eg. Polycystic
ovary syndrome, adrenogenital syndrome). Enlargement of the clitoris suggest androgen excess.
RECTAL EXAMINATION
Inspection of the perineum and anus and digital examination of the rectum completes the clinical
examination of the gastrointestinal tract.
Rectal examination is essential in middle aged and elderly adults of both sexes. Without it the
asymptomatic rectal carcinoma or polyp will be missed. The old adage “if you don’t put your finger in
you’ll put your foot in” taught by generations of surgeons still holds good! Indeed the only contra-
indications for doing a rectal examination are in a patient with a colostomy and hence has no rectum,
the examiner has no fingers and lastly if the rectal examination has already been done by someone else
and hence the findings of the rectal examination are already known.
The patient is placed in the left lateral position with hips and knees flexed and the buttocks at the edge
of the couch. The anus and perineum are inspected in good light by lifting the right buttock and noting
the presence of any fissures, skin tags, dermatological conditions, infestations or external haemorrhoids.
Gloves are worn and the right finger is lubricated with a water-based jelly and the pulp of the finger
placed flat on the anus. Gentle pressure is exerted and the patient is asked to bear down as though
having his bowels opened. The finger tip then slips into the anal canal and is inserted as far as possible
into the rectum (Fig 5:6).
Figure 5.6 Rectal Examination
The examining finger then sweeps round the rectum to palpate surrounding structures to assess the
state of the mucosa and to search for specific lesions. Pelvic structures may be palpable bimanually by
placing the left hand on the anterior abdominal wall suprapubically and in both iliac fossae.
In the male, the primary landmark is the prostate gland which is normally of a firm consistency but with
a shallow central groove. The nodular seminal vesicle may be palpable at the full extent of the finger on
each side. With advancing age, the prostate hypertrophies with enlargement and progressive protrusion
into the rectum. The enlargement may be asymmetrical. Carcinoma of the prostate starts as a hard
nodule in the gland which may be impossible to differentiate clinically from an area of calcification. As
the carcinoma enlarges, it produces a hard bumpy, irregular tumour with obliteration of the median
groove. With lateral extension, the tumour produces “winging” of the prostate as it extends beyond the
confines of the gland. An acutely tender prostate suggests an acute prostatitis.
Lateral to the rectum on both sides is the ischio-rectal fossa which may be the site of ischio-rectal
abscesses. Blumer’s shelf (metastasis of gastric carcinoma to the rectum) is palpable on rectal
examination. Posteriorly, it is usually possible to palpate the concavity of the coccyx.
In the female, the corresponding landmark to the prostate is the cervix, which, depending on its size and
maturity feels like a firm nodule, like the end of a nose, anteriorly. The uterus, depending on its size,
may be palpated bimanually. Pelvic tumours such as ovarian masses may be palpated on either side of
the rectum.
In both sexes, the characteristics of the rectal wall must be assessed. When inflamed as with ulcerative
proctitis, or amoebic colitis, it may have a velvety feel. Careful search must be made for polyps and
rectal carcinomas. In fact, about 90% of rectal carcinomas can be felt digitally. Small lesions may be
papilliferous or nodular but often only the edge of large ulcerating rectal carcinomas can be felt.
As the tip of the examining finger crosses the edge of the tumour, there may be a sensation as though it
is then entering a cavity; in fact this is the necrotic floor of the ulcer.
On withdrawing the finger, examine the glove for mucus and blood and note the characteristics of the
faeces especially the presence of melaena stools. Melaena stool would indicate an upper
gastrointestinal bleeding. The faeces can be sent for faecal occult blood tests if it is not obviously stained
with blood.
Bloody mucus suggests either an ulcerating tumour of the large gut or chronic inflammatory bowel
disease such as ulcerative colitis. Copious mucoid watery discharge may suggest a colonic villous
adenoma. In the debilitated or senile patient, a spurious diarrhoea may be the result of impacted faeces;
a mass of hard faeces filling and distending the rectum yet not capable of being evacuated by the
patient. Softer faeces seep round the impacted mass producing incontinence. Smelly pale sticky faeces
may indicate malabsorption as in celiac disease whereas putty-coloured stools are a feature of
obstructive jaundice.
T. C. Ankrah
Chapter 6
LOCOMOTOR SYSTEM
 Symptoms of the Locomotor Systems
 The Hand
 The Elbow Joint
 The Shoulder Joint
 The Hip Joint
 The Knee Joint
 The Ankle and the Foot
 The Spine

Joseph Bonney
MBChB 1
Sheila Adamu
MBChB 1
Chapter 6 Locomotor System

LOCOMOTOR SYSTEM
The locomotor system involves muscles, joints and bones – tissues that are inextricably linked with
support, protection and locomotion.
SYMPTOMS
The main symptoms patients complain of in the joint are pain, stiffness, swelling, instability, clicking and
loss of function.
Pain
Pain is the most common symptom especially in the lower lumbar spine. The important questions are
“where and when”?
 Where? We need to ask the patient to point as accurately as he or she can to the place where the pain is
worst. Determine whether the source of the pain is the joint, muscle or other soft tissue structures.
Bone pain is described as deep and characteristically worse at night. Muscle pain is poorly localized and
is aggravated by contraction of affected muscle.
 When? Ask the patient whether the pain is constant (in which case it is probably inflammatory) or
intermittent (in which case it is probably inflammatory) or intermittent (in which case it is probably
mechanical). If mechanical, what activity or position makes it worse and what gives relief? Many chronic
joint disorders (and also healed fractures) are worse in cold and wet conditions, although the reason for
this is not clear.
Stiffness
Usually this means a restriction in the range of movement of a joint. This may be due to an actual
physical limitation of movement or because the movement is painful and therefore, in practice it is not
made.
Morning stiffness lasting up to 15 minutes is common in many joint diseases, but if it lasts for an hour or
more than suggests an inflammatory arthropathy intermittent restriction of movement which comes
and goes suddenly indicates a mechanical disorder, usually in the joint, but occasionally in a tendon
which works the joint (e.g. trigger thumb). Stiffness after prolonged immobility is likely to be due to
osteoarthritis.
Swelling
This is common to any joint problems. If it follows an injury then the speed with which the swelling
appears is important. Injury to vascular structures such as bone and ligament leads to rapid swelling due
to bleeding. Reactive effusion from injured avascular structures takes longer (hours or days) to produce
swelling. Its site obviously matters but so may its shape. If it defines a synovial cavity as in the knee, then
the swelling is likely to be due to fluid within the joint.
Instability
This applies particularly to the weight bearing joints of the lower limbs. It conveys a sense of insecurity.
The patient feels that if he puts his weight on the leg something bad will happen or finds from bitter
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experience that it does so. This may be due to weakness of the muscles which support the limbs in the
upright position or it may be an abnormal movement take place at a joint.
Clicking and Clunking

Noises coming from joints are not necessarily pathological; some people produce harmless vacuum
clicks and in others noises are produced by tendons slipping over bony prominence. However, some
noises particularly those accompanied by pain are very significant.
Loss of Function
One must find out what function is lost and why. What exactly can the patient not do that he wishes to
do? The examination should reveal whether the problem is paralysis or stiffness.
EXAMINATION
The examination of the joints follow the same principles are the examination of the other systems. Here
you look, feel and then move.
Look
The whole limb should be exposed and also the other arm or leg should be exposed for comparison.
Look for deformity (mal-alignment of the bone above and below the joints) swelling, wasting of muscles
near the joint and scars.
Swelling which conforms to the outline is of a synovial cavity and should be distinguished from that
which is either more localized or more diffuse. It is further elucidated by palpation.
Scars may be very important as indicating a previous infection or operation which the patient has
forgotten to tell one about. Every scar around a painful joint must be explained.
Feel
While palpating the joint, watch the patient’s face. Localization of tenderness is the single most
important physical sign in joint disorders. Be gentle and feel systematically all around the joints, starting
where it is least likely to be tender. Palpation will determine the limits of swelling more accurately.
Move
The joint must now be put through a full range of movement. The quickest way is to show the patient by
making the movement yourself and then ask the patient to do the same i.e. testing active movements. If
the patient cannot do this take over and examine for passive movement. Limitation of passive
movement indicates something wrong in or around the joint. Full passive movements without pain
means that the joint is all right but there is something wrong with the mechanism which moves it.
Movements should be measured in degrees with a goniometer, using the neutral zero method. In this,
the anatomical position is zero and the degrees of flexion are measured from that point. While a joint is
being moved it is useful to keep one hand on it to feel crepitus or clicks. It is also necessary to test for
abnormal movements.
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Function
This is perhaps the most important part of the examination. The legs are meant for standing and
walking. It is not enough to examine them with the patient lying on a couch. One must get the patient to
stand up and watch him walking. If the patient uses a stick, watch him walking both with and without
the stick.
Similarly if the complaint concerns the upper limb, get the patient to do or mimic the thing which he
finds difficult.
THE HAND
Man’s dominant position is due to the development of is brain, but the way in which the brain
implements the required action involves the hand, which has been called the “cutting edge of the
mind”. The importance of the hand is shown by its very large representation in the cerebral cortex
where the thumb alone has more grey matters controlling it than all the thoracic and abdominal viscera.
The most obvious function of the hand is its motor activity which ranges from the power grip of the
labourer to the delicate manipulation of the musician, but the hand is also a sensory organ used to
explore the surface of objects.
SYMPTOMS
The symptoms associated with the hand are pain, sensory disturbance, deformity, clumsiness, stiffness
and loss of function.
Pain
Constant pain occurs in inflammatory conditions, acute infection or the synovitis of inflammatory
arthropathies. Intermittent pain occurs with constriction of tendon and nerves with arthritis of joint
surfaces.
Symptomatic osteoarthritis is uncommon in the hand except on the carpometacarpal joint of the thumb.
Patients with end stage rheumatoid deformities of the hands often no longer have severe pain but those
with active disease suffer aching pain worse with movement and associated with early morning
stiffness.
Sensory Disturbances
This may be a local manifestation of generalized neurological disorder.
The carpal tunnel syndrome causes painful aches and needles which wake the patient at night and are
relieved by movement or a change in position. The paraesthesia is mainly in the median nerve
distribution though it is hard to localize it exactly, especially in retrospect. The patient usually feels the
symptoms more on the palmar surface of the hand. There may be retrograde radiation to the elbow.
Cervical spondylosis causes a feeling of ordinary pain or just numbness in the appropriate root
distribution. The patient usually points to the back of the hand but may have little or no pain in the neck.
Ulnar nerve lesion also causes numbness or loss of feeling.
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Clumsiness
“Dropping things” is usually a sensory symptom. However, deformities and stiffness also contribute to
clumsiness. Patients with Dupuytren’s contracture often complain that when they wash their faces, the
bent fingers stick in their eyes.
Stiffness
Intermittent obstruction to movement occurs in trigger fingers or thumb. Permanent restriction of
extension develops in Dupuytren’s and other contractures after injury to the interphalangeal joint
disease or rupture of extensor tendons. In rheumatoid arthritis, the severe stiffness or walking eases
after an hour or so.
Loss of function
This embraces a huge range of problems such as being unable to unscrew bottle tops because of
rheumatoid arthritis, having difficulty in winding a watch because of peripheral neuropathy and being
incapable of buttoning a coat because of Parkinson’s disease.
EXAMINATION
To examine the hand, expose both hands and forearms up to the elbows. Get the patient relaxed and
lying or sitting comfortably in bed with both hands pronated on the abdomen. Compare the two hands
for any asymmetry.
INSPECTION - Then inspect the nails, skin muscles and finally the joints.
 In the nails, look for vasculitis and psoriatic

change. The nail fold capillaries are dilated and
prominent in connective tissue disease.
 In the skin look for scars. Erythema suggests

acute inflammation. Also look out for cutaneous
psoriasis, sclerodematous skin changes and
blotchy erythema seen in dermatomyositis and
systemic lupus erythematosus. Also note
vascular lesions in extensor surfaces of small
joints in dermatomyositis. One the palmar
aspect of the hand, observe cutaneous lesions
like palmar erythema which is seen in
rheumatoid arthritis.
 Look for wasting of thenar and hypothenar

muscles.
Figure 6.1 The Hand
 Observe the presence and distribution of any swelling. It is the characteristic distribution of the
swelling that leads to the diagnosis. Note any deformity such as Boutonniere’s deformity,
Heberden’s node, Bouchards node, mallet finger, swan neck deformity, z-deformity of the
thumb, ulnar deviation and sub-luxation of the metacarpal heads.
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PALPATION - Next bimanually palpate the joint by alternate movements for the nature of the swelling
(hard swelling suggests bony outgrowth and soft swelling suggests synovitis), effusion, synovial
thickening, bony enlargement and the joint itself for active inflammation.
 Using the mid forearm as the reference point, compare the temperature here with the
temperature of the hands. Then gently compress the fingers to see if they are tender. When
compression of the joint leads to pain, this indicates active synovitis.
 Get the patient to make a fist and notice the gutter in between the heads of the metacarpals. In
chronic arthritides the gutter are filled with soft tissue.
 Palpate the wrists for firm rubbery swelling of synovial thickening.
Next, test for the range of MOVEMENT. Get the patient to fully extend the fingers. If there is a rupture
of the extensor tendon, the patient will unable to extend the fingers – a condition known as finger drop.
If the patient is unable to fully flex the fingers, this may be due to:
1. Joint disease or
2. Flexor tendon sheath swelling, thickening or inflammation.
Movement at wrist assessed. Ask the patient to fully extend his wrists in a “prayer sign’ with hand at 90°
to the forearm to test extension. Flexing the wrist in a ‘reverse prayer sign’ with fingers pointing
downwards in a plane 90° to the forearm tests for flexion.
Test range of movements of all joints. If the individual joint move within their normal range of
movement then inability to make a full fist is due to involvement of the tendon sheaths.
Next test the FUNCTION of the hand. Test gripping large objects like holding one’s hand and test small
objects like holding one finger only inserted from the thumb side of the patient’s palm.
Test for pinch function:

a) Pulp pinch – hold the thumb against the hand tightly.
b) Finger tip pinch – hold thumb against fingers tightly.
c) Yale key pinch – like using a Yale key to open a door.
c) Tripod pinch – opposition of thumb and fingers.
After completion of examination of the hand, if no pathology is detected, then in patients with chronic
inflammatory arthritis the pain may be due to:
a) Compression or
b) Peripheral central neuropathy
Test for carpal tunnel syndrome and peripheral central neuropathy.
To test for peripheral central neuropathy compare light touch on the median nerve distribution –
thumb; with the ulnar nerve distribution – little finger.
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To test for carpal tunnel syndrome extend the wrist joint and tap down the carpal tunnel with a hammer
or the fingers. This leads to pain in the distribution of the median nerve. Alternatively, push the dorsum
of the wrist against each other for 30 seconds. This results in parasthesea in the area of distribution of
median nerve. These two tests are very reliable.
Assess the range of muscles supplied by the median nerve especially Abductor polices brevis, if one
suspects nerve involvement.
Lastly, examine the forearm and elbow for rheumatoid nodule, bursitis, tophi and psoriasis which may
give important clues as to the cause of the arthropathy.
THE ELBOW JOINT
The elbow is a hinge joint which on its postero-lateral and postero-medial aspects is quite close to the
surface of the skin. One is actually dealing with two joints, the elbow joint itself and the superior radio
ulnar joint (Fig. 6:2).
Rheumatoid arthritis may affect one or both joints.
SYMPTOMS
The commonest cause of elbow pain is not in
the joint but in the common origin of the
extension of the wrist and fingers – tennis
elbow. It is, therefore important to find out
precisely where the pain is felt. Slight loss of
extension is common after injuries and in early
rheumatoid arthritis of osteoarthritis but causes
little functional problem; lack of flexion is what
interferes with the patient’s life. Longstanding
elbow disorders may cause a tardy ulnar palsy
and this presents as weakness and loss of
feeling in the hand.
Figure 6.2 The Right Elbow Joint.
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EXAMINATION
Look at the alignment of the extended elbow. There is normally a carrying angle which is a valgus of 11°
– 13° when fully extended. Look for swelling on either side of the olecranon. This may be due to fluid in
the joint.
Feel for tenderness in the elbow. In tennis elbow the tenderness is on the lateral side of the elbow,
though it may be above, at or below the level of the joint. Golfer’s elbow is the corresponding condition
on the medial side at the origin of the flexors of the wrist and digits. Palpate for synovitis (spongy) and
bursae (soft bur firm if acutely infected). Also for rheumatoid nodules on the proximal extensor surface
of the forearm.
Move the elbow joint to measure the range of active flexion and extension with a goniometer held over
the lateral side of the arm. The normal range is 0 - 145°. In severe rheumatoid involvement, the
movement is so painful that it may be made very slowly and in a jerky manner. Assess the range of
pronation and supination. The neutral position for this purpose is in mid-rotation. Feel for crepitus
during movement of the elbow.
Function
Flexion of the elbow is needed to bring the hand to the mouth or face; thus limitations of flexion is an
enormous disability.
THE SHOULDER JOINT

The outstanding characteristic of the shoulder joint is that is able to have a very large range of
movements in all directions by a ball-and-socket joint. To permit this the socket is shallow and the joint
is held together by a musculotendinous cuff called the rotator cuff (Fig 6:3). Most patients with pain in
the shoulder have pathology affecting the rotator cuff, not the articular surfaces. The two common
examples are degenerative tears in the rotator cuff, causing a painful arc and ‘frozen shoulder’ in which
all movements are restricted. A third possibility which must be borne in mind is referred pain from the
neck, heart, diaphragm or an apical carcinoma of the lungs (Pancoast tumour).
SYMPTOMS
The symptoms patients complain of at the shoulder are
pain stiffness and instability.
Pain
Pain originating in the shoulder region is felt around the
glenohumeral joint or the insertion of the deltoid. Pain
felt across the top of the shoulder or around or
between the scapulae is more likely to be referred from
the cervical spine. Constant pain indicates an
inflammatory arthritis or a frozen shoulder.
In these conditions attempted movement will make the

pain worse, but in rotator cuff tears and osteoarthritis
(which is very rare in the shoulders) pain is only on
movement or if the patient lies on the shoulders at
night.
Figure 6.3 The Shoulder Joint.
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Stiffness
Here one must distinguish between a joint which will not move or a joint which is not moved because
the movement causes pain.
Instability
A patient who feels that his shoulder “goes out of joint” may be describing recurrent dislocation.
EXAMINATION
To examine the shoulder joint fully expose the upper part of the body to ensure adequate comparison
with the opposite side.
Note any swelling, deformity or bony enlargement. Note muscle wasting especially of the deltoid and
posterior shoulder muscles. Note the size and position of the scapula. ‘Winging’ of the scapula occurs
with paralysis of the nerve to the serratus anterior.
Palpate for tenderness, synovial swelling and fluctuancy for effusion. Tenderness around the shoulder is
common in normal people. Hence if an area of tenderness is detected compare it with the same site on
the opposite shoulder before you attach any significance to it.
Next text for the range of movement and compare the two sides. Rotate the shoulder with the elbow
flexed and hand supinated. Internal rotation is rarely limited.
Externally rotate the shoulder. Limitation of external rotation of the shoulder joint means pathology of
the gleno-humeral joint.
Get the patient to perform adduction and abduction movements at the shoulder. Notice any tenderness
as the patient performs this arc. Tenderness will lead to restriction of movement. Global restriction of
movement indicates disease of gleno-humeral joint e.g. synovitis, rheumatoid arthritis or septic arthritis.
Restriction of adduction is due to pathology from acromio-clavicular joint or acromio-humeral joint

space.
Pain with full range of movement means one of these:

1) Lesion of Sub-acromial bursa
2) Lesion of supra spinatus
3) Lesion of infra-spinatus
4) Lesion of sub-scapularis
To determine which of these lesions is involved, test for their specific movements at the shoulder joint.
Movement results in pain in shoulder joints and hence movement is restricted.
Combination of painful arc, restricted movements and possibly localized bony tenderness indicates
which lesion is present.
 Resistance to abduction means supra-spinatus tendonitis.

 Resistance to external rotation means infra spinatus tendonitis.
 Resistance to internal rotation means sub-scapularis tendinitus.
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This knowledge helps to determine where to place corticosteroid injection on the treatment of these
common inflammatory conditions.
A rare cause of painful shoulder movement is neuralgia amyotrophica. This results in painful restriction
of movement plus wasting and decreased sensation of the medial side of deltoid muscles.
Assess the function of the shoulder joint. Place the hand on top of the head as if one is combing the hair.
Then place the hand on the opposite shoulder then let the patient perform the complex movement of
the abduction extension and internal rotation of the shoulder and get him to place the hand on the
muscles of the back. The above movements are necessary for dressing and undressing.
If despite careful examination no pathology is detected then pain in the shoulder is referred from
cervical spine. Then it would be necessary to examine the neck for loss of movements and tenderness
and feel the shoulder and girdle muscles for spasm.
Referred pain does not only go the shoulder but is also referred down the arm in the distribution of the
dermatome.
THE HIP JOINT
The hip resembles the shoulder in that it is a ball-and-socket joint allowing movement in all directions. In
the hip the socket is deeper allowing a smaller range of movement but providing great inherent stability
(Fig. 6:4). Movements of the lumbar spine allow a fair range of movement of the leg even if the hip joint
has been arthrodesed.
SYMPTOMS
The symptoms of the hip joint are pain, limp,
stiffness ad clicking.
Pain
Pain arising in the hip joint is usually felt in or
around the groin although it may go down the
thigh. Pain felt mainly in the buttock is more
likely to be a limited form of sciatica, referred
from the lumbar spine. Pain arising from the hip
is usually worse when it is bearing the greatest
load i.e. when the patient is standing or
walking, though it may also disturb sleep when
the patient turns over. Referred pain is common
in the hip joint. Pathology in the hip may
present with pain in the knee and vice versa.
Figure 6.4 The Right Hip Joint
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Limp
The commonest cause of a limp is pain causing the patient to move his weight quickly off that leg onto
the other one. This is called an arthralgic gait and produces an altered rhythm of gait: a type of limp
which can be heard as well as seen. Mechanical causes of limp are a short leg, inefficient abduction of
the hip, stiffness, weakness and instability of the hip, knee and ankle joints as well as an artificial leg or
fracture.
Stiffness
Loss of movement at the hip can to some extent be overcome by movements of the lumbar spine so
that the whole pelvis tilts in the required direction and carries the leg with it. The most common
deformity to cause symptoms is an adduction contracture which makes access to the perineum difficult
and may interfere with sexual intercourse. Severe contracture may make one leg cross over the other.
Clicking
This is usually due to the tensor fascia lata slipping over the greater trochanter which, though it may be
uncomfortable, is of no great importance.
EXAMINATION
Examination of the hip joint is performed when the patient is lying and standing. The anatomy of the hip
joint does not allow direct inspection and palpation as in other joints. Movements are more important in
assessing hip pathology. The affected hip should be adequately expose (undress to their underwear and
pull down underwear to see the iliac crest) and compared with the opposite hip. With the patient
standing, observe from the front and note the stance (straight or not), shoulders (are they parallel to the
ground), pelvic tilt and deformities. From the side, look out for a stoop or lumbar lordosis. These may
result from a flexion contracture. From behind, look out for gluteal atrophy.
Note the muscle bulk and position of the hip joint. Inspect the nail and skin for evidence of psoriasis.
Inspect the sole of the feet for evidence of keratoderma blenorrhagica.
Inspect the skin for erythema nodosum. Inspect the joints for osteoarthritis. Also inspect the feet, ankle
and knees for important clues to the underlying pathology in the affected hip joint.
Compare the muscle bulk in the thighs and pelvic girdles. Wasting of the muscles is common in arthritis
of the hip joint. In fracture of the hip there is severe swelling in affected hip with or without bruising.
Note any shortening or deformity; shortening, adduction and external rotation of a deformed hip is seen
in fracture of neck of femur and severe arthritis of the hip joint.
Measure the leg length and assess any fixed flexion deformity. Using a tape, measure the distance from
the anterior superior iliac spine to the medial malleolus on the same leg. Locating the anterior superior
iliac spine is not easy in obese subjects. Apparent shortening of a limb but with normal measurement,
when compared to the other limb, is seen in adductor muscle spasms associated with weakness in
adduction of the hip leading to tilting of the pelvis and scoliosis of the spine (Fig. 6:5).
True shortening is seen in severe disease of hip or knee joint resulting in collapse and loss of bone.
Congenital shortening can also occur.
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Now palpate the hip joint and anterior triangle of the thigh for
any tenderness or fluctuation denoting an effusion.
Now test the range of movement – actively and passively. With

the hip and knee at 90 degrees test for rotation, adduction and
abduction of the hip. The range of passive flexion is slightly
higher than active movement.
In testing rotation of the hip we use the heel as the point of

reference. External rotation of the heel will result in internal
rotation of the hip and internal rotation of the heel will result in
external rotation of the hip.
Now assess the pelvis for the range of movement. Place the
hand on the anterior superior iliac spine and feel for tilting of
the pelvis as one test for adduction and abduction of the hip
joint.
In normal subjects the pelvis does not tilt. In disease of the hip
joint the pelvis tilts downwards on abduction and tilts upwards
on adduction.
Normally active examination of the hip joint is painless.
A – B - The True Length of the leg.
Figure 6.5 The Measurement of

True Leg Length.
Limitation of rotation and extension of the hip joint with the patient prone will detect early signs of hip
arthritis or synovitis. Be aware of crepitus of the hip joint felt by the examining hand which indicates
mechanical damage or osteoarthritis.
If no pathology is detected after examining the hip joint, then the cause may be referred pain from
spine, or soft tissue swelling or bursitis of trochanteric region. Greater trochanter has a small anterior
bursa and a large inferior bursa and inflammation of these can lead to pain. Enthesopthy at the insertion
of the gluteal muscles can cause pain. Enthesopathy is disorder of the muscular or tendinous
attachment to bone. Ischial bursitis and adductor tendonitis are other causes of pain arising from the
soft tissue.
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Examine the hernia orifices in the absence of hip pathology and also look for entrapment of the lateral
cutaneous nerve of the thigh leading to pain in the lateral side of the thigh. Examine for sensation in the
distribution of the nerve.
Examine the abdomen especially the renal angles which may give rise to referred pain in the groin on
weight bearing.
Then let the patient stand and observe the gait while he is bearing weight on the affected hip. Examine
the patient from the posterior aspect and observe the horizontal creases on the lower side of the trunk
for assessment of the position of the pelvis.
In the normal subject when weight is borne on the right hip, the pelvis tilts upwards to the left to allow
the left leg to swing through the arc.
In diseased hip with adductor spasm and weakness of the adductors, the pelvis is tilted downwards on
the disease side when the patient bears weight on the diseased hp. This is the Trendelenberg sign which
leads to waddling gait which demonstrate failure of the pelvis to tilt upwards on the opposite side when
the patient bears weight on one hip. The pelvis remains the same and tilts down on the affected side
whichever leg he bears weight on.
THE KNEE JOINT
The knee is also essentially a hinge biomechanically a very complicated one, with a moving axis and
allowing some rotation in the longitudinal plain when flexed. There are actually three joints one
between each femoral and tibial condyle and one patellofemoral (Fig. 6:6). In addition, the presence of
menisci introduces a whole new range of pathology. Injuries to the knee are common and it is
particularly important to ask about any possible trauma. Remember also that the symptoms may be
referred from the hip.
SYMPTOMS
The symptoms referred to the knee joint are
pain, stiffness, instability and giving way.
PAIN
Distinguish between constant pain (as in
synovitis) and pain on weight bearing (as in
damage to the joint surface). Localization of
pain is important: patello-femoral arthritis
needs quite different treatment to that arising
from the femoro-tibial joints. Injuries to
structures with a blood supply cause a
haemathrosis which appears within minutes;
this includes ligamentous tears and fractures.
Injuries to the avascular menisci produce a
synovial effusion which takes an hour or two to
develop.
Figure 6.6 The Right Knee Joint
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Bruising similarly indicates damage to a vascular structure but may be simple due to contusion of the
skin and subcutaneous tissues.
Stiffness
Limitation of both flexion and extension are common in the arthritic knee. Loose bodies and torn
menisci cause “locking” – a sudden block to full extension followed by sudden unlocking usually after
some manipulation or twisting movement by the patient.
Instability (Giving Way)
The knee joint has no inherent stability. The two surfaces are only held in their normal relationship by
the cruciate and collateral ligaments, injuries to which cause various complex types of instability.
Even if the ligaments are intact the quadriceps must contract powerfully to keep the knee straight
during the stance phase of gait. This muscle waste within a few weeks of the onset of knee problems so
that the knee may give way i.e. flex when it should not have flexed. This may cause the patient to fall
down suddenly. Patients with longstanding paralysis of the quadriceps due to poliomyelitis develop
hyper-extension of the knee and are able to stabilize it in that position, the strain being taken by the
posterior capsule.
EXAMINATION
In the examination of the knee joint we are looking for inflammatory, mechanical or traumatic
pathology.
Expose both knees for adequate visualization and comparison. Observe the knee for swelling,
discolouration, erythema, cyanosis or bruise.
Figure 6.7 Fixed Flexion Deformity of the Knee.
Look for wasting of the quadriceps muscles and compare with the opposite side. Look for evidence of
fixed flexion deformity (Fig. 6:7) and genu valgus (knock-knee) (Fig 6:8) or genu varus (Fig. 6:8) or genu
varus (bow leg) (Fig. 6:9). Sometimes angulation of the knee is the same on both sides, the so called
windswept knee (Fig. 6:10)
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Figure 6.8 Genu Valgus. Figure 6.9 Genu Varus. Figure 6.10 Windswept knee.
Thomas test is used in fixed flexion deformities. This is done by flexion both knees straight up to the
chest. Then holding the other knee to the chest try to bring down the back i.e. the popliteal fossa of the
affected knee on to the couch. In fixed flexion deformity the patient is unable to let the knee be f lat on
the couch. Measure the angle of fixed flexion deformity using a goniometer (Fig. 6:7).
Observe cutaneous lesions in sole of feet such as keratoderma blenorrhagica. Observe the nails and skin
for evidence of psoriasis. Observe the fore foot for deformity such as broadening in rheumatoid arthritis.
All these will give valuable information as to the possible cause of the pathology in the affected knee.
Palpate for the nature of any swelling present e.g. fluctuancy in effusion, synovial thickening,
osteophyte bony enlargement, then palpate the joint itself to detect any active inflammation.
Compare the temperature of the joint using the middle of the lateral thigh as reference point. Palpate
the soft tissues for any tenderness. The presence of warmth and tenderness indicates active synovitis.
Perform the patella tap sign to determine moderate effusion. If osteo-arthritis is present, the patella tap
sign is negative in the presence of small effusion. Small effusions are detected by trapping fluid in supra
patella pouch and gently stroking the fluid into infra medial compartment of the knee. A small wave
form is seen.
Synovial thickening is palpated by firm pressure of fingers and thumb upwards in the infra patella region
and feeling for the firm rubbery structure.
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Feel for any bony thickening and assess the distance between the two condyles.
Palpate over superior and anterior aspect of knee for evidence of pre-patella bursitis. Apply firm
pressure on medial and lateral aspects of knee for tenderness. Pain in young patients may indicate
chondromalacia patella. Palpate for cystic swelling behind the knee in Baker’s cystic. In rheumatoid
disease, this may extend down into the calf; this can then rupture causing pain and tenderness which
mimics a deep vein thrombosis.
If there is no swelling in a painful knee the pathology may be in the soft tissue or capsule. Firm pressure
in superior and inferior aspects of patella may lead to tenderness due to enthesopathy, which is disorder
of the muscular or tendinous attachment to the bone.
Point of insertion of ligament in tibia may also be tender.
Another cause of tenderness is infra patella bursitis. The collateral ligaments are also a potential source
of pain and enthesopathy.
Test for range of movements. Get the patient to actively bend the knee to assess the comfortable range
of movement for the patient. Place the hand on the knee as he bends the knee for crepitus. If crepitus is
detected this indicates osteoarthritis or in young adults it may indicate chondromalacia patella. Any
limitation of movement is measured with a goniometer and accurately recorded.
To test for the ligaments rest your elbows on this inner leg then firmly grip the upper end of the tibia,
lean forwards and try and induce anterior and posterior movements of the tibia on the femur. This is felt
as well as seen.
To test for instability of the collateral ligaments, slightly flex the knee and grip the lower end of tibia and
move it laterally. Assess mobility at the knee.
Attempt valgus and varus movements of tibia and assess the stability of the knee joint.
Rotate the tibia on the femoral condyle by firmly gripping the calcaneum with the right hand and
applying tension. This produces pain on the medial and lateral compartment. Now get the patient to lie
down in the prone position. Try and rotate the tibia on the femur.
To test for disease of the meniscus exert pressure downwards on the tibia to compress for the meniscus.
Pain in meniscus will increase if there is pathology in the meniscus. Distractions i.e. lifting the heel away
from the knee, reduces the pain in the meniscus.
In no pathology of the knee is detected after careful examination the cause may be pathology of the hip
on the same side giving referred pain to the knee. It may also be referred pain from the lumbar spine at
L3 and L4. In that case one needs a neurological examination to detect nerve root compression.
Function
Lastly, get the patient to stand and bear his weight. Get him to walk and observe the gait. Also observe
the knee for valgus or varus deformity which is more obvious when he is walking and also observe for
stiff knee joint.
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THE ANKLE JOINT AND THE FOOT
The ankle joint is a synovial joint, properly called

the tibio-latal joint although the fibula also takes
part in it (Fig. 6:11). It is usually described as being
of the hinge variety, but its movements are not
quite those of a simple hinge, for the axis of
rotation is not fixed but changes between the
extremes of plantar flexion and dorsiflexion. The
articular surfaces are covered with hyaline
cartilage.
Figure 6.11 The Right Ankle and the Foot.
The weight bearing surfaces are the upper facet of the latus and the inferior facet of the tibia. Stabilizing
surfaces are those of the medial and lateral malleoli which grip the sides of the latus. The joint is
enclosed in a capsule lined with synovial membrane.
SYMPTOMS
Symptoms from the ankle joint are pain, and swelling usually from trauma. The pain at the ankle is
mostly from sprain caused by torsion of the ligaments holding the ankle joint.
EXAMINATION
The ankle joint and foot are examined both in the lying and standing position. Both limbs should be fully
exposed to allow comparison.
Observe the nails and skin for cutaneous lesions like psoriasis or vasculitis. Examine the soles for the
rash of keratoderma blenorrhagica. Examine the shin for erythema nodosum. Examine the muscles for
wasting and the knee and hip joints for degenerative inflammatory arthritis.
Observe for evidence of deformity and swelling. Observe the foot for valgus or varus deformity, previous
trauma and degenerative or chronic inflammatory arthritis.
Look for Equinus deformity – foot held on mid foot in plantar flexion; pes planus deformity or flat foot
deformity due to collapse of the longitudinal arch. Observe also for pes cavus and calcaneus (Fig. 6:12)
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a. Normal foot –medial Normal foot –front view b. Calcaneus
c. Cavus d. Equinus e. Flat foot/ Pes Planus
Figure 6.12 Deformities of the Foot.
Examine the fore foot for hallux valgus (Fig. 6:13) which is common in normal people due to wearing of
non-fitting shoes. Observe also for hallux varus (Fig. 6:14). Observe for broadening of fore foot in
rheumatoid arthritis due to dorsal sub-luxation of toes at the metatarso-phalangeal joint with increased
flexion of inter-phalangeal joints associated with underlying callosities.
Figure 6.13 Hallux Valgus. Figure 6.14 Hallux Varus.
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Observe for swelling; the symmetry and distribution of the swelling which give a clue as to the exact
type of arthritis. Symmetrical swelling is seen in rheumatoid arthritis, asymmetrical swelling in one ankle
or foot is seen in sero-negative arthritis.
Swelling of all the three joints in one digit giving a sausage like appearance is seen in psoriatic arthritis.
Isolated swelling of the first metatarso-phalangeal joint is seen in osteo-arthritis.
Observe the soft tissues; Achilles tendon and dorsum of the foot for swelling bursitis. Observe the
underneath of the metatarsal heads for adventitious bursitis which may produce swelling.
Palpate the ankle and foot to confirm active inflammation and classify the cause of the swelling
observed. Using the midway between the knee and ankles as the reference point, palpate and compare
the temperature with that overlying ankle, mid foot and small joints of toes. Gently squeeze the ankle
joint, mid tarsal and inter-phalangeal for tenderness. Warmth and tenderness signify active
inflammation and synovitis.
Bimanually palpate the inter-phalangeal joints to determine the type of lesion causing swelling. Firm
rubbery swelling suggests synovial thickening. Fluctuancy suggests effusion. Bony swelling suggests
osteophyte or degenerative arthritis. Observe the separation of the toes in early synovitis, the so called
Daylight sign (Fig. 6:15), this is unusual in adults.
Now palpate the soft tissues. Palpate the

Achilles tendon for swelling and tenderness.
Note any nodularity or isolated hard painless
nodules as in rheumatoid arthritis. Palpate the
site of insertion of Achilles tendon on the
posterior aspect of Os calcaneum for Achilles
enthesopathy. This is painful.
Note any pre Achilles bursitis. Examine the

inferior part of heel for enthesopathy. Firm
deep palpation will lead to pain or one may
discover a rheumatoid nodule.
Figure 6.15 Daylight Sign-Spreading of Toes.
Palpate the tendon sheath for effusion, synovitis or rheumatoid nodules on the extensor tendons.
Isolated cause of pain in foot is compression of metatarsal heads. This produces localized pain in 2nd and
3rd and 4th metatarsal heads. Small bursa between metatarsal heads and inter-digital neuroma can also
produce pain.
Test for range of movements. First, test for active range of movements to determine the comfortable
range of movement for the patient. Dorsiflex and plantar flex the foot. Test for inversion and eversion of
the foot and then test for passive assessment of the range of movements.
Palpate for crepitus which is evidence of presence of osteoarthritis.
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Test for eversion and inversion of the foot by fixing the talus by holding the medial and lateral malleolus.
Then grabbing the Pes calcaneum evert and invert the foot.
Move the calcaneum medially and laterally while fixing the lower end of the leg.
Test movement at mid tarsal joint by fixing hind foot by gripping calcaneum. Then grip the foot and test
for inversion and eversion of the mid tarsal joint.
Test for range of movements of inter-phalangeal joint.
Lastly, perform a neurological examination, testing for sensation, proximally and distally. Establish
mono-neuritis multiplex in rheumatoid arthritis. Test for compression neuropathy in tarsal tunnel
syndrome by compression on the posterior tibial nerve which leads to shooting pain in the foot.
Finally get the patient to stand, bear weight and walk. Look for pes planus, valgus or deformity which is
more obvious when the patient is weight bearing.
As he is walking observe he gait and look for loss of mobility at ankle joint and first metatarsal
phalangeal joint which leads to stiff gait walk.
THE SPINE
This is a chain of joints or rather of joint complexes

because each vertebrae is joined to the next one by an
inter-vertebral disc (a syndesmosis which is very prone
to mechanical disorders) and by two posterior facet
Cervical Vertebrae(7) joints (which like any synovial joint are subject to
C1-C7 osteoarthritis) (Fig. 6:16).
Degenerative changes in the disc are known as

spondylosis. This must be distinguished from the two
Thoracic Vertebrae(12)
mechanical abnormalities. Spondylolysis, a defect in the
T1-T12 pars inter-articularis and spondylolisthesis when one
vertebrae has slipped forwards over the one below.
Spondylitis implies inflammation and in practice is only
used in ankylosing spondylitis, one of the inflammatory
arthropathies.
Lumbar Vertebrae(5)
L1-L5 SYMPTOMS
The symptoms referable to the spine are pain,
weakness and sensory changes, deformity and stiffness.
Sacrum (5 fused)
Coccyx (4 fused)
Figure 6.16 The Spine.
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Pain
This is mush the commonest symptom. Disc disorders are commonest in the lower cervical and lower
lumbar region and cause pain there but if the nerve root is compressed, there may be referred pain
down the arm or down the leg, the latter being called sciatica. The pain from lumba-sacral disc lesions is
often felt at the sacro-iliac joint. Sometimes the symptoms are virtually confined to the limb and the
patient does not complain of neck or back pain at all. Back pain may also arise from the facet joints or
even just from the muscles, but usually arises from disc strain or in more severe cases, disc prolapse.
Weakness and Sensory Changes

Collapse or damage e of vertebral or associated structures may cause cord damage e either by direct
compression or ischaemia.
Weakness or actual paralysis and/or sensory impairment in association with spinal disease demands
very urgent investigation and treatment. Of critical importance is involvement of the sacral nerve roots
causing difficulty in micturition and loss of sensation to pinprick in the perineum; if the compression is
not relieved by surgery within hours there may be permanent incontinence.
Deformity
The different types of deformity vary in themselves by the presenting complaint, especially in an
adolescent girl development scoliosis. Deformity of the feet may by an expression of muscle imbalance
caused by a spinal abnormality such as disastomatomyelia.
Severe scoliosis interferes with the function of the lungs and heart and in untreated cases this usually
causes premature death.
Stiffness
This can be due to many spinal diseases, but if it is dominant complaint, the diagnosis of ankylosing
spondylitis must be considered. For instance a lorry driver may be unable to turn his head to reverse his
lorry because of fixity of the whole spine.
EXAMINATION
Examination of the spine involves careful observation of cervical, dorsal and lumbo-sacral spine (Fig.
6:17).
Cervical
Lumbar
Figure 6:17 Normal Trunk Figure 6:18 Kyphosis.
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Figure 6:19 Scoliosis. Figure 6:20 Kypho-Scoliosis.
With the patient standing and looking away from the examiner, look for cutaneous lesions such as
psoriasis or neurofibromatosis giving a clue to the underlying pathology. Observe the patient from both
the posterior and lateral views, notice any kyphosis or scoliosis. Kyphosis is dorsal angulation of the
spine convexity on the posterior aspect of the spine (Fig. 6:18). Scoliosis is the lateral deviation of the
spine (Fig. 6:19). Sometimes there is combination of both deformities in the same patient giving one
kypho-scoliosis (Fig. 6:20).
Normally the spine assumes a curvature with cervical lordosis, dorsal kyphosis and lumbar lordosis (see
Fig. 6:16). This normal curvature is lost in pathology of the spine. The cervical lordosis is lost by muscle
spasm, severe degenerative disease and ankylosing spondylitis. The dorsal kyphosis is exaggerated with
severe degenerative disease, ankylosing spondylitis, elderly osteoporotic crush fracture or spinal sepsis.
In ankylosing spondylitis the earliest changes are seen in the lumbar spine where the normal lordosis is
lost and a straight back appearance becomes apparent. In patients with osteoporotic spine collapse with
loss of weight, a transverse crease over the abdomen is apparent with the lower rib cage overriding the
pelvic crest.
MOVEMENT OF THE VERTEBRAL COLUMN
In general the movements of the spine are simple enough. Flexion, extension and lateral flexion (or
abduction) are possible in cervical, thoracic and lumbar regions, though in varying degree in the three
parts. Rotation occurs strangely enough, mainly in the thoracic region. Movements of the head occur at
the specialized atlanto-occipital and atlanto-axial joints. For the vertebral column as a whole the
movements are best understood by considering each of the three regions separately. In each region
movement occur around the nucleus pulposus as around a ball – bearing joint and the direction of the
movement is determined by the direction of the articular facets on the neural arches.
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Cervical Region
The atlanto-occipital and atlanto axial joints are specialized for head holding and head rotation.
The articular facets of the other joints slope similarly to those in the thoracic region, but they do not lie
on the circumference of a circle. Looking along them will confirm that both lie in the same plane. While
flexion and extension are free, pure rotation is obviously impossible. Abduction is not a simple
movement. The reural arch of the abducted vertebra is slides downwards (and therefore backwards) on
the concave side and upwards (and therefore forwards) on the convex side thus inevitably producing a
concomitant rotation greater than that produced in abduction of the thoracic spine.
Thoracic Region
The special joint between thoracic 12 and lumbar 1, are lumbar in type; elsewhere the direction of the
articular facets on the neural arches is quite different. On any one neural arch the upper facets face
backwards and laterally; they lie on the circumference of a circle whose centre lies in the vertebral body.
The lower facet are reciprocal. Thus rotation of the bodies on each other is possible in spite of the
splinting effect of the ribs.
Flexion and extension occur as well as abduction (lateral flexion). The thoracic spine is thus the most
versatile region of all though the range of movement is limited by the ribs. Flexion of the thoracic spine
crowds the ribs together (expiration) extension spreads the ribs (inspiration), while abduction crowds
them on the concave side and spreads them on the convex side. Abduction involves sliding of the neural
arches downwards and backwards on the concave side and upwards and forwards on the convex side,
thus producing passively a certain amount of simultaneous rotation. This is well seen in the condition of
scoliosis where the lateral rotation of the spinous processes towards the convex side exaggerates the
apparent deformity.
Lumbar Region
The articular facets lie in an anteroposterior plane; they lock and greatly limit rotation of the bodies on
each other. Flexion and extension are free and a good deal of abduction is possible; combination of
these movements produces circumduction but practically no rotation is possible.
Now test for the range of spinal movements. In the cervical spine test for flexion and extension
movements. Get the patient to touch his chest wall with his chin as far as possible (Fig. 6:21). Then let
the patient extend the neck backwards as far as possible (Fig. 6:22). Test rotation by turning the head to
the right and then to the left.
Test lateral flexion by letting the patient touch the shoulder with the ear as far as possible (Fig. 6:23).
Test for lateral flexion to the right and then to the left.
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Figure 6:21 Figure 6:22 Figure 6:23

Flexion of the Cervical Vertebrae Extension Cervical Vertebrae Lateral Flexion of Cervical Vertebrae.
Dorsal spine movements are tested for by chest

expansion. In men use the nipple as the
reference point. In women use the position just
beneath the breast. With the patient’s hands
above the head, measure the circumference of
the chest with the tape. Let the patient take
deep breaths in and out and measure the chest
circumference at the end of inspiration and
expiration. Make three (3) runs and take the
best of the readings. The chest expansion
should be more than six (6) centimeters in
normal subject. Again sequential measurements
are more significant than single measurements.
Figure 6.24 Dorsal Spine Movement
All the range of movements of the spine originate from the lumbar spine section. Test for flexion of
lumbar spine by letting the patient touch the floor with his hands as far as he can. Let him lean
backwards as far as he can to test for extension. Test rotation to the right and then to the left. Test for
lateral flexion by letting the patient touch the outer part of the leg with his arm as far as possible on
both the right and left sides. However, be aware of certain pit falls as the patient can perform normal
flexion despite fixed lumbar spine as the pelvis moves to achieve that movement. To get full flexion in
the normal subject the lumbar lordosis becomes straight. To test for lumbo-spinal mobility spread the
fingers on the lumba r spine. One will find that one’s fingers spread out in lumbar flexion and they are
brought close together on extension of the lumbar spine.
Rotational movements of the spine is tested with the pelvis fixed and the spine rotated. Let the patient
sit on the couch. This fixes the pelvis. Now assess rotation of the spine with the pelvis fixed.
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To test for range of movements of the lumbar spine in conditions such as ankylosing spondylitis, identify
the Dimples of Venus at the junction of lumbar 5 and sacrum. Draw a horizontal line at this junction.
Then using a tape, measure vertically a length of fifteen (15) centimetres with the patient standing
upright and mark the point on the skin
(Fig. 6:25). Let him bend forward in maximal flexion. Re-measure this length. In the normal person this
length should increase about eight (8) centimeters (Fig. 6:26). Single measurements are not as
significant as sequential measurements as the sequential measurements give the progress of disease. In
ankylosing spondylitis the measurements should be carried out at the same time of the day as the
patients are stiffer in the morning than the afternoon.
15cm
Dimples of venues
Figure 6:5 Lumbar Spine Movements
15 + 8
A B Normal
In ankylosing spondylitis Distance A – B is less

Figure 6.26 Testing for range of Movement of the Lumbar Vertebrae.
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If the patient has scoliosis on standing, observe what happens on flexion. If the scoliosis disappears on
flexion, then it is a recently acquired deformity and the problems are due to muscle spasm. It the
scoliosis remains the same or deteriorates during flexion then it is a development abnormality.
To test the degree of kyphosis of the cervical spine, get the patient to stand against the wall with the
heel, sacrum and occiput against the wall. This is easy in healthy subjects but patients with ankylosing
spondylitis with cervical kyphosis it is not possible to put the occiput against the wall. Measure the
distance from the wall to occiput and this gives the degree of flexion kyphosis of the cervical spine (Fig.
6:27).
(a) Normal (b) Cervical Kyphosis
a= Degree of fixed neck flexion
Figure 6:27 Flexion Kyphosis of Cervical Vertebrae.
Now palpate the neck for spinal processes, inter spinous ligaments of the cervical spine and muscles for
isolated localized tenderness or muscle spasm.
Cervical spine problems can lead to referred pain in trapezius muscles and shoulder girdle area and
inter-scapular area.
Palpate the dorsal spine with firm pressure over the spinal processes for localized tenderness. Palpate
the inter-spinal spaces and laterally for para-spinal muscles. Palpate the lumbar spine in a similar
manner to palpation of the dorsal spine and also palpate the para-spinal muscles.
In the sacrum, exert firm pressure over the sacrum and coccyx for local tenderness. In sacral ileitis pain
is referred to the buttock and posterior thigh. Induce movements across the sacral joints and this
produces pain in buttocks and posterior aspects of thighs.
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Femoral stretch test is performed by the patient lying prone and extending the thigh. In the positive test
there is pain in the back muscles and muscle spasm in the anterior muscle. If the pain radiates to the
anterior thigh as far as the knee, think of root lesion of L3 and L4 in the distribution of the femoral
nerve.
Further assessment of sacro-iliac joint is performed by firm downward pressure on iliac crest to induce
movements across the sacro-iliac joint. The pressure produces pain. Flex the hip and knee, rotate the hip
joint laterally and exert firm pressure on the hip along the axis of the femur. This induces movement
across the sacra-iliac joint resulting in pain in the buttock. If the patient has back pain radiating to the
leg, especially in the posterior – lateral side and it is also associated with loss of sensation, this suggests
L5, SI root compression.
Straight Leg Raising Sign

With the patient relaxed, lift the lower limb as a whole to an angle of 90 degrees. This produces no pain
in normal subjects. In people with spinal pathology elevation of lower limb to 20-80 degrees produces
severe back pain and muscles spasm. This is positive straight leg raising test. Lower the limb until the
pain disappears, then forcibly dorsiflex the foot. This increases tension on tissues and pressure on the
dura and pain is produced.
Lasague’s Sign
Flex the thigh 90 degree to the pelvis. Then try to straighten the leg. This produces pain. This is positive
Lasague’s sign.
If cervical spinal pain is referred to the upper limb and lumbo-sacral spinal pain is referred to the lower
limb, then a neurological examination is necessary to confirm or refute root lesion.
Before concluding examination of the spine, examine the regional lymph node, breast, chest and
abdomen for evidence of malignancy.
When no pathology is found on the spine, it is vital to examine the nails, skins, eyes and peripheral joints
for sero-negative spondylo-arthritides such as psoriases, iridocyclitis or inflammatory bowel disease.
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T. C. Ankrah
Chapter 7
NERVOUS SYSTEM
 Symptoms of the Nervous System
 Higher Cerebral Function
 Cranial Nerves
 The Motor System
 The Sensory System
 Gait
 Testing for Cerebellar Function
 Examination of The Unconscious Patient
 The Diagnosis of Brain Death

Akosua Asiedu-Asante
MBChB 1
Kwasi Adjeipong Twum

MBChB 1
Manolo Abenorku
MBChB 1
Chapter 7 The Nervous System

NERVOUS SYSTEM
Generations of medical students have always regarded patients with neurological symptoms as being
‘difficult to diagnose’. This is because there are a large number of physical signs that can be elicited on
the examination of the nervous system. Putting the symptoms and signs together and locating the site
of the lesion appear like solving the mystery in a detective story. Yet paying attention to basic principles
will result in the diagnosis in most cases. However, I must admit that some neurological cases are
difficult to diagnose even at centres of excellence.
Symptoms
The main symptoms in neurological disorders are headache, dizziness, weakness and difficulty in
walking, blackouts, problems of vision and confusion. The rest are numbness/tingling sensation, vertigo,
fits, deafness, drowsiness, loss of memory, vomiting and involuntary movements.
Headaches
The patient complaining of headaches seldom shows any abnormality on physical examination and the
diagnosis is normally reached on the history. The differential diagnosis of headache is very large and
include migraine, tension headache, hypertension (after the patients have been told they are
hypertensive), as well as extra-cranial causes such as cervical spondylosis, raised intra-cranial pressure
and cranial arteritis.
Patients with brain tumour presenting with headache usually have associated symptoms or signs on
examination to indicate the cause.
In the elderly cranial arteritis is an important cause of headache, the patient may localize the headache
over the temporal arteries. Hypertension is often blamed but it is seldom the cause of headaches. The
typical headache is worse on waking, occipital in site and pounding in character. Mild hypertension
rarely causes headaches and severe hypertension is not necessarily associated with them.
Dizziness and Vertigo

When the patient complaints of dizziness, probe further to understand what exactly he means. Does he
mean true vertigo (hallucination of movement) or something else like impairment of consciousness or a
feeling of depersonalization? True rotational vertigo can usually be identified by careful interrogation in
many patients but symptoms such as giddiness, floating on air, ‘mazy heads’, light-headedness may not
infrequently deny their origins to the most astute diagnostician. Nevertheless disagreeable feelings of
dizziness may be due to a multiplicity of causes as disparate as anaemia, postural hypotension and
phenytoin toxicity, hence a careful history is essential.
Weakness and Difficulty in Walking

Here it is essential to establish the time course of the symptoms. Slowly progressive weakness of the
limbs over a period of many years in a young person may point to a muscular dystrophy, whereas recent
weakness of the legs may indicate cord compression or a demyalinating disorder. Where a cord lesion is
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suspected, further questions must be directed towards associated sensory disturbances and bladder
function. Patients with Parkinsonism by contrast complain of weakness when in fact their limbs are stiff.
In the very old, the leg weakness may be just part of the feebleness of senile cachexia.
Owing to the variable and fluctuating course of the disease, patients with multiple sclerosis must be
quizzed about apparently unrelated symptoms, almost forgotten in the distant past.
Blackout and Fits

When the patient complains about blackout, make sure if he actually means loss of consciousness or
something else. If there was loss of consciousness then much information has to be obtained from eye
witnesses. Did they observe convulsion or incontinence? Was the patient actually unconscious (that is
unaware or not recording continuous memory)? Was he standing or lying down at the time? Did he fall?
What happened next?
Causes of blackout include syncope, Stokes-Adams attack, hyperventilation and sleep-apnoea syndrome.
Epilepsy presents in many guises. Most eye witnesses will recognize immediately the generalized tonic-
clonic seizures. Was there a preceding aura? A combination of both the patient’s and the witnesses’
accounts is essential to arrive at the correct diagnosis.
Sudden collapses in the elderly may commonly be associated with serious heart arrhythmias but when
collapses occur on getting up from a lying or sitting position, then postural hypotension must be
considered.
Do not forget that fluid depletion after severe gastro-enteritis is a common cause of fainting in young
and previously healthy folk.
Problems with Vision

Acute and catastrophic loss of vision quickly brings the patient to his or her doctor for advice and
demands urgent attention and diagnosis. Primary ocular events such as vitreous hemorrhage or retinal
detachment may be associated with floaters, zig-zag lines and flashing lights as well as field loss. Attacks
of migraine often start with visual loss or with zig-zag lines (fortification spectra) that persist for 15-30
minutes and followed by headache, often hemi-cranial in site.
The symptoms of double vision (diplopia) rarely presents difficulties in interpretation but older people
often misinterpret a homonymous hemianopia as blurred vision complaining that they just cannot see
properly. Apparent movement of the visual image (oscillopsia) or central visual acuity impairment may
also be described as blurring.
Confusion
The history becomes unreliable or impossible when the patient is demented or has impairment of
consciousness or speech or memory defect. In these cases an independent history is obviously essential.
But in many other cases when the patient is capable of providing the history, the account of a close
member of the family or a friend may also be very valuable.
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Numbness or Tingling Sensation

The patient complains of altered or diminished sensation, usually in the feet and hands. The causes are
varied and include stroke, neuropathy, vitamin B12 deficiency and alcoholism. It may also occur in non-
neurological conditions like myocardial infarction. Determine the area of numbness and see if they
correspond to any dermatome.
Deafness
This is a common complaint in the elderly. It interferes with their communication and it gives a wrong
impression that they are demented. Physical examination will determine whether this is conductive
deafness or sensory-neuronal deafness.
Drowsiness
When the patient complains of drowsiness enquire about the duration of the symptom. What time of
the day is it most severe? Any history of trauma? Is it progressive or improving? If the patient sleeps all
day, one must suspect sleeping sickness and do the appropriate blood tests to exclude it.
Loss of Memory
Loss of memory occurs normally with age. This is a gradual process. However some people lose their
memory at rather at early age and these people may have pre-senile dementia. They may then show
other signs of inability to look after themselves and they may need constant care; other people retain
their memory even in every advanced old age.
Vomiting
Repeated vomiting when associated with headaches and papillodema should alert one to raised intra-
cranial pressure, usually due to brain tumours.
Involuntary Movements
Fine tremor of the hands occurs with anxiety, alcoholic withdrawal and thyrotoxicosis.
Intention tremor and past pointing signs occurs in cerebellar disorders. Pill rolling action of the hands
occurs in Parkinson’s disease.
Involuntary movement also occurs in Sydenham chorea which is associated with rheumatic fever and
occurs in children and occasionally during pregnancy in young women (chorea gravidarum). Choreiform
movements occur in Huntingon’s chorea which is inherited as Mendelian autosomal dominant. It is
associated with dementia in later life.
Athetosis is characterized by unilateral or bilateral involuntary movements. It is due to a lesion in the

putamen of the brain.
EXAMINATION
Whilst taking the history from the patient, one might have observed certain obvious neurological lesions
e.g. ptosis, squint, Bell’s palsy. Observe the patient’s gait, posture and mood. Abnormal involuntary
movements may be obvious.
When one starts the formal examination of the patient one should note whether he can undo his
buttons or remove his shoes and assess his general mobility (especially where pain in the back or neck is
the chief complaint). Any tendency to favour the use of one side more than the other should be noted.
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HIGHER CEREBRAL FUNCTION
Some assessment of general intelligence, memory and mood will have already been made while taking
the history with the patient still seated, test of higher mental function, memory, reading and writing
should be investigation.
When the history has suggested dementia or a confusional state, test of minor hemisphere function are
indicated.
Patients and their relatives often confuse memory defects (amnesia or dysmnesia) with disturbance of
language (dysphasia). Thus a patient with dysphasia may be thought to be unable to remember the
name of a person or place. But amnesic syndromes generally develop in isolation from language defects
so first test for speech deficits and then investigate the patient’s memory.
Dysphasia
This is usually a combination of receptive defect i.e. difficulty in understanding the spoken word; and an
expressive defect i.e. difficulty in putting thoughts into words.
Dysphasia indicates damage to or disturbance of function in the dominant temporal lobe (angular or
supra marginal gyrus) or the dominant premotor cortex (third frontal convolution). The dominant
hemisphere is almost always the left in right-handed individuals and is also the left in about 60 percent
of left handers.
In spontaneous speech the patient may use inappropriately restricted vocabulary, para-phrasing when
they cannot remember words. Occasionally mis-pronunciations or neologisms (words that do not exist)
may be noted and some patients with dysphasia develop a slight stammer.
The receptive component of dysphasia can be tested by asking the patient to do something simple like
‘hold out your hand’ or more complicated ‘touch you left ear with your little finger’. Problems with
expressive speech can be tested by asking the patient to name objects. Begin with simple objects like
nose and eyes. Then graduate to more difficult ones like mango, window and table.
Memory Impairment
When memory defect is suspected it is usually easy but nevertheless important to exclude disturbance
of consciousness as the cause. Thus a short loss of memory may be due to concussion or epilepsy. A
continuing memory defect may be isolated or part of a diffuse cerebral disorder. In the latter case,
dysphasia, perceptual defects and general cognitive defects will contaminate the memory disturbance
making testing more difficult and indeed unnecessary when the deficit is severe and causing dementia.
When testing memory, distinguish between immediate recall, recent memory and remote memory.
Immediate recall is tested by asking the patient to repeat back a series of numbers in the order given;
and then another series in reverse order. Patients can normally recall at least six digits forwards and four
backwards. Four repetitions should achieve a correct response. Failure of immediate recall usually
indicates either some impairment of consciousness (and is therefore very useful in assessing patients
with recent concussion for degree of recovery) or it may indicate a failure of attention either through
emotional pre-occupation with other symptoms or for other reasons.
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Recent memory is tested firstly by orientation in time, place and person. Then give the patient a name
and address and ask him to recall these after five minutes. An alternative is to tell a short story and to
question the patient after five minutes. Patients with the specific amnesic syndrome with damage to the
hypothalamus, mammillary bodies and temporal lobes (hippocampus) will characteristically show a
severe defect of recent memory.
Remote memory forms part of a permanent store of information in the brain. Defects of remote
memory imply a failure of retrieval. It is difficult to test remote memory although a difficulty recalling
general information such as the name of the President, or the party in power may indicate a general
decline in memory. Failure in these tests with relative preservation of recent memory implies the early
stages of a diffuse cerebral disturbance such as a dementia.
Personality Changes
This may characterize frontal lesions. The patient may become apathetic and disinhibited. He may give
his history with an inappropriate lack of concern or anxiety. He may be dirty or untidily dressed and
occasionally childish.
Parietal Lobe Lesion

Complex disorders of higher mental function may characterize parietal lobe lesion especially in the non-
dominant hemisphere. Thus while the left hemisphere is mainly concerned with symbolic thought such
as speech, writing, reading, calculation, musical notation etc. the right hemisphere is concerned with
spatial topographical and constructional skills. Damage to the right parietal lobe by stroke or tumours
may lead to difficulties in dressing and finding the way about the house.
Articulation and Voice Production

Dysarthria is disorder of the articulation of speech and there are three main varieties. Firstly the patient
with bilateral pyramidal deficit above the tenth nerve nucleus (as in motor neurone disease or after
bilateral strokes) may exhibit a spastic dysarthria, where speech seems to require some effort and is
squeezed out with little modulation of speech or pitch and lacking the gaps between words. The voice is
flat and slow.
Secondly, cerebellar dysarthria is drunken speech with slurring of the words and uncontrolled changes in
pitch, speed and volume.
Thirdly, in extra-pyramidal disorder such as Parkinson’s disease speech becomes soft and monotonous
often with a slight stammer.
Dysphonia is a disturbance of sound production which leads to a hoarse or soft voice. This is mainly due
to vocal abnormalities of the larynx but sometimes due to problems with the recurrent laryngeal nerve.
CRANIAL NERVES EXAMINATION

Before examining the cranial nerves one must know their anatomical relationship (both within and
outside the brain) and their function. Of particular importance are the anatomy of the visual pathway,
the function of the IIIrd, IVth and VIth cranial nerves; the cutaneous and buccal distribution of the main
divisions of the Vth cranial nerve and the muscles supplied by the Vth, VIIth, Xth and XIIth cranial nerves.
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CRANIAL NERVE I
The first cranial nerve is the olfactory nerve and it subserves the function of smell. To test the sense of
smell, close one nostril with the finger and with the patient’s eyes closed bring a familiar object such as
scented soap or perfume to the opened nostril and let the patient identify it. Test the other nostril using
the same procedure. Avoid using pungent substance like ammonia.
Patients with loss of sense of smell (anosmia) will frequently report an associated loss of taste.
This is because the appreciation of flavour of food depends on olfaction. Testing of primary taste with
sweet/sour/salt/bitter substances will be normal where the apparent loss of taste is due to the first
cranial nerve damage. The olfactory nerve is sometimes damaged in head injury (especially frontal or
occipital injuries) or in frontal tumours where the nerve on one or both sides may be directly
compressed.
CRANIAL NERVE II
The second cranial nerve is the optic nerve. In testing the optic nerve, one must test for:
a) Visual acuity
b) Colour vision
c) Visual fields
d) And examine the fundi.
Visual Acuity
In the clinic, if the patient is able to read the print in a newspaper or a book, his vision is satisfactory. If
the vision is impaired then show him different numbers of your fingers and see if he can count them.
One can test both eyes initially and then test the eyes individually.
For more accurate information, visual acuity is tested using Snellen Chart to measure the distant vision
and using Jaeger or Rayner Test Types for measuring near vision. In either case the patient should be
tested using his appropriate spectacles if he normally wears spectacles.
From left to right:

 Snellen letter chart,
 Arabic number chart,
 E game,
 Landolt broken rings,
 Children’s pictograph
Fig 7.1 Eye charts for testing visual acuity at a distance of 6 meters
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Colour Vision
To test for colour vision, bring different coloured objects to the patient and let him identify the colour of
the objects. Test both eyes together initially and then test each eye individually. For detailed assessment
use Ishihare or Stillin pseudo-chromatic plates for testing colour vision.
Visual Fields
To test for visual fields sit two feet away from the patient. Then move the hand in a plane one foot from
both of you. One is testing the patient’s visual field against one’s own visual field which is assumed to be
normal.
The patient is first asked to fix his eyes on the bridge of the examiner’s nose, then the examiner fixes his
eyes on the bridge of the patients nose. With the patient’s right eye closed and the examiner left eye
closed, test his left visual field against the examiner right visual field. This is done by moving the hand in
the plane a foot from both of you. Start with the finger far away out of vision of both of you and the
patient should indicate the first time he sees the finger out of the corner of his field of vision. One
should move the finger from each of the four peripheral quadrants of the visual fields as well as
diagonally. One can aid the patient by moving the finger which then becomes easy to see, asking the
patient if he can detect the movement of the finger. In this way a homonymous field detect can be
excluded (Fig 7:2).
Now using the same method, compare the patient’s right field of vision against the examiner’s left field
of vision.
This confrontation method has the advantage that the patient’s attention and visual fixation can be
assessed throughout the procedure.
With both eyes opened, simultaneous movement of the finger in the periphery of right and left fields
will exclude visual attention defect. Then use the same method on one eye separately with the other
eye closed to exclude the monocular peripheral visual field defect.
The central visual field and the blind spot has to be tested using coloured hat pin; and traditionally red
pin head 4mm in diameter is used. With one eye covered and the patient fixating on the examiner’s eye,
the pin head is moved in such a way that the patient can report the area affected by the blind spot.
Compare the size and shape of the blind spot with that of the patient and in the normal the two should
precisely coincide.
Using the red pin head, abnormal defects in the central visual field of each eye can be separately slotted.
Remember that the patient’s field of vision is a lateral inversion of the examiner’s field of vision.
(A) Testing the visual field in each eye separately.
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(B) Testing both eyes simultaneously for inattention hemianopia
Figure 7:2 Testing Visual Fields.
VISUAL FIELD DEFECTS
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(1) Total loss of vision in one eye due to a lesion of the optic nerve. (2) (3) Bitemporal hemianopia due
to compression of the optic chiasma. The quadrants are usually first affected. (4) Left homonymous
hemianopia from a lesion of the optic tract. (5) Upper left quadrantic hemianopia from a lesion of the
lower fibres of the optic radiation in the temporal lobe. (6) Less commonly a lower quadrantic
hemianopia occurs from a lesion of the upper fibres of the optic radiation in the anterior part of the
parietal lobe. (7) Right homonymous hemianopia with sparing of the macula from a lesion of the optic
radiation in the posterior part of the parietal lobe. (8)
FIGURE 7:3 The Visual Pathway and Effect of Lesions at Various Sites.
If any serious abnormality is found, then the patient must be referred to the Eye Department for
detailed examination of the visual fields using tangent Bjerrum screen and a perimeter for testing the
visual fields. Fig. 7:3 shows the visual pathways and the effects of lesions at various sites.
CRANIAL NERVES III IV VI
III. The third cranial nerve is the oculomotor nerve. This supplies the superior rectus, medial rectus,
inferior rectus, and inferior oblique muscles of the eye.
IV. The fourth cranial nerve is the trochlear and it supplies the superior oblique muscle.
VI. The sixth cranial nerve is the abducent and it supplies the lateral rectus muscle.
To help you remember: LR6 (SO4)3

Lateral Rectus CN VI, Superior Oblique- CN IV, all other muscles of eye movement are supplied by CN III
Superior Inferior
Rectus RIGHT Oblique LEFT
Lateral Medial
Rectus Rectus
Inferior Superior
Rectus Oblique
Figure 7.4 The extra ocular muscles with the patient facing the examiner
These nerves individually and collectively are responsible for:

a) Pupillary response.
b) Eye movements.
c) Elevation of the upper eye-lid
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Under [a] and [c] one is not only testing for a lesion of these cranial nerves but may also be testing for a
defect of sympathetic or para-sympathetic nervous system. Under [b] one may elicit nystagmus.
Nystagmus is the rhythmic movement of the eye ball. It may be horizontal, vertical or rotatory. One may
also elicit a disorder of conjugate eye movements (failure of the eyes to deviate together so that both
eyes are fixed on the same object). This indicates a disturbance of the cerebellum or the pathway in the
cerebral hemispheres.
Pupils
The pupil (P) should be equal (E) and react (R) directly and consensually to light (L) and convergence (C).
This may be abbreviated in the notes to ‘PERLC’.
The consensual light response is the papillary constriction that occurs when a light is shown in the
opposite eye. Observation in each of these characteristics should be carried out in order, ending with
direct stimulation of each pupil with a bright torch shone obliquely at the eye.
If the pupils are unequal and irregular, this may indicate damage or disease of the iris (eg due to surgery
or iritis). Neurosyphilis may cause small irregular unequal pupils (Argyll-Robertson pupil).
A unilateral small pupil may indicate Horner’s syndrome which is a combination of a small pupil (miosis)
drooping of the eyelids (partial ptosis), loss of sweating on the face (anhydrosis) and slight retraction of
the eye (enopthalmos). The syndrome results from dysfunction of the sympathetic nervous system on
that side. The sympathetic supply to the head leaves the spinal cord at Thoracic 1 and ascends to the
bifurcation of the carotid artery where the fibres to the pupil and upper eyelids separate from those
concerned with sweating. A lesion below this point will therefore give the syndrome, whereas a lesion
above this point will only affect the pupil and the eyelid.
A unilateral large pupil may indicate a lesion of para-sympathetic nerve supply (Holmes-Adie syndrome)
or a lesion of the oculomotor (IIIrd) cranial nerve which carries the pupillo-constrictor fibres to the eye
from the brain stem. In the Holmes Adie Syndrome, the large pupil reacts sluggishly to direct and
indirect stimulation whereas in the IIIrd cranial nerve lesion the dilated pupil will associated the disorder
of eye movements due to weakness of the muscles supplied by the IIIrd cranial nerve.
Eye movements
Instruct the patient to keep his head steady but to move his eyes to follow the fingers. With the hand
about a foot them the patient, move the finger laterally to both directions and let him follow the fingers
with his eyes to the limits of binocular gaze. Look for conjugate movements of the eye ball and also for
the presence of nystagmus and diplopia. Next, move the fingers superiorly and inferiorly. Then move the
fingers diagonally in all directions. Ask the patient if he develops double vision at any point of lateral or
vertical deviation of the eyes. If the eyeball is unable to move properly in any direction, it should be easy
to determine which muscle is affected and hence which cranial nerve lesion is present. In this way it
would be possible to identify the following abnormalities of eye movements:
a) Weakness in one eye of elevation and adduction indicating a IIIrd nerve lesion. This is
usually associated with drooping of the eyelid (ptosis and a large unreacting pupil) and
results in the eye looking downwards and outwards.
b) Weakness of abduction of one eye indicative of VIth nerve palsy.
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c) Double vision and torsion of the globe of the eye on downward gaze indicating a IVth nerve
lesion.
d) Loss or impairment of conjugate vertical or horizontal gaze-indicating a lesion above the

level of the brain stem oculomotor nuclei.
e) Weakness of adduction in one eye with nystagmus (jerky unsustained eye movement in the
abducting eye on lateral gaze) – indicating a lesion of the median longitudinal bundle in the
brain-stem between the IIIrd and Vth nerve nuclei. This is usually due to multiple sclerosis
but may occur with vascular or structural lesions.
f) Vertical nystagmus indicating an intrinsic lesion either high in the brain stem (vertical
nystagmus on upward gaze) or low in the brain stem (vertical nystagmus on downward
gaze).
(a), (b) and (c) usually indicate lesion of these nerves outside the brain stem due to
compression or stretching of the nerve or disturbance of its blood supply. (d, e and f)
indicate disturbance of brain stem or mechanical distortion of its structure.
Elevation of the eyelid may be weak resulting in ptosis. This occurs in IIIrd nerve palsy and Horner’s
syndrome on the same side. It may occur bilaterally although not always symmetrically in disorders of
muscle such as myasthenia gravis or the ocular myopathies where it is generally associated with some
weakness of the upper facial muscle (frontalis and orbicularis oculi).
CRANIAL NERVES V
The fifth cranial nerve is the trigeminal nerve. This has both a motor and sensory component. It is
trigeminal because the sensory component has three divisions which supply sensation to the face.
These are:
a) Ophthalmic
b) Maxillary
c) Mandibular
The ophthalmic supplies the forehead up to the angle of the eye. The maxillary supplies the face from
the angle of the eye to the angle of the mouth. The mandibular supplies the cheek from the angle of the
mouth downwards into the neck (Fig. 7:5)
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Figure 7:5The Face Showing Sensory Distribution Of V Cranial Nerve.
To test for sensation of the face, let the patient close his eyes and gently touch his face with the cotton
wool for touch and pin prick for pain and ask him if he can feel it or not, comparing the two sides.
Helpful patients will often report parts of the face where the pin feels ‘less sharp’. This is usually not
significant. Loss of the perception of pain (especially when associated with loss or impairment of cotton
wool, or light touch in the same area) is usually significant especially when it fills an anatomical territory
recognizably that of a branch or branches of the trigeminal nerve.
The corneal reflex tests sensation of the corneal conjunctiva supplied by the ophthalmic division. It is
elicited by touching the cornea with a wisp of cotton wool, having first warned the patient and asked
him to look up. Loss of the reflex blink is abnormal. In this case the patient should be asked whether
pain is felt (the corneal sensory receptors are only sensitive to pain.
The terminal parts of the mandibular division in its lingual branch carry taste sensation from the tongue
but loss of taste due to damage to this branch will be associated with loss of pain and touch over that
part of the front of the tongue.
Damage to the maxillary nerve in the sinuses or facial bones may affect the superior dental nerves giving
anesthesia in the upper teeth and hard palate on one side. Sensory loss in the areas is tested with a pin
or stick.
The motor component supplies the muscles of mastication and these are:
1) The masseter muscles

2) The temporalis muscles
3) Medial pterygoid muscles
4) Lateral pterygoid muscles
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To test for the motor component of the trigeminal nerve, ask the patient to clench his teeth strongly
and feel for the strength of the masseter muscles at the angles of the jaw then let the patient move the
lower jaw laterally to both sides against slight resistance.
Occasionally weakness of the muscles of mastication may occur when hollowing of the temporal fossa
may be seen; and the masseter muscle on the surface of the mandible may feel thinner than the other
side. When the patient is asked to open his mouth against resistance unilateral pterygoid weakness will
cause the jaw to deviate to the same side.
The jaw jerk is obtained by tapping with the patella hammer on the point of the chin with the patient
being asked to hold his mouth slightly open (Fig. 7:6). In the normal reflex closure of the mouth is just
detectable. Where the jaw jerk is increased, it implies a bilateral pyramidal lesion above the Vth nerve
nucleus in the brain stem. Conversely brisk jerks in the limbs with a normal jaw jerk suggest a pyramidal
lesion in the cervical region.
Figure 7:6 Demonstrating the Jaw Jerk.
CRANIAL NERVES VII
The seventh cranial nerve is the facial nerve and this supplies the muscles of facial expression. It runs a
complicated anatomical course accompanied initially by the sensory fibres subserving taste.
Weakness of half the face may occur as the result of a lesion of the facial nerve but may also result from
a motor neurone (pyramidal) lesion above the VIIth cranial nerve nucleus.
Course of the facial nerve

The facial nerve arises from its nucleus lateral to the nucleus of the sixth nerve winds round the sixth-
nerve nucleus and emerges from the front of the pons medial to the vestibulocochlear nerve. It passes
laterally through the petrous bone in the internal auditory meatus. In the middle ear it turns sharply
posteriorly at the geniculate ganglion to run back along the medial wall of the middle ear and then
vertically downward through the facial canal. In its bony course the facial nerve is vulnerable to basal
skull fracture and oedema. It emerges from the facial canal at the stylomastoid foramen anterior to the
mastoid process and spreads out within the parotid gland to supply all the superficial muscles of the
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face, neck and scalp, apart from the levator palpebrae superioris. The terminal branches of the facial
nerve are:
 Temporal
 Zygomatic
 Buccal
 Mandibular
 Cervical
Pneumonic: Tell -- Temporal

Ziggy -- Zygomatic
Bob -- Buccal
Marley -- Mandibular
Called —Cervical
Fig 7.7 Terminal Branches of The Facial Nerve
To test for the facial nerve ask the patient to frown his forehead and observe any asymmetry. Note the
contraction of the frontalis muscle.
In a , he will be able to frown the normal side but will not be able to frown the affected side as the
weakness affects both the upper and lower segments of the face. In upper motor neurone lesion of the
facial nerve, however, the patient will be able to frown both sides of the forehead.
This is because each nucleus of the facial nerve innervates the muscles on both sides of the forehead. So
that if one nucleus is affected the other can still function and frown the forehead. Hence emotional
movements such as smiling and yawning may be spared with cortical lesion (Fig. 7:5).
upper motor lower motor

normal neurone lesion neurone lesion
Figure 7.8 The Motor neuron Lesion of Cranial Nerve VII
Next, let the patient close his eyes very tightly and try to open his eyes with the two thumbs noting the
strength of orbicularis muscles. Note also if the eyelashes are buried symmetrically.
Then let the patient bare his teeth (or gums) in a big grin and to puff out his cheeks and feel for the
strength of the buccinator muscles. Alternatively, you can ask him to whistle and observe him.
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Bell’s palsy
The commonest cause of a lower motor neurone facial weakness is the idiopathic Bell’s palsy. This is a
benign condition where pain in the region of the ear is followed by the development of a unilateral facial
weakness. It is often associated with unilateral impairment of taste on testing. The symptoms of
hyperacusis are due to damage to the branch of the facial nerve to the stapedius muscles. With the
attempted closure of the eye-lids, the eye ball on the paralysed side rolls upwards. This is known as Bells
phenomenon.
Ramsay Hunt syndrome

This is herpes zoster (shingles) of the geniculate ganglion. There is a facial palsy (identical in appearance
to Bell's) with herpetic vesicles in the external auditory meatus (this receives a sensory twig from the
facial nerve) and/or on the soft palate. Deafness, or a fifth nerve lesion may occur. Complete recovery is
less likely than in Bell's palsy.
Muscles of facial expression:

Epicranius Buccinator
Frontalis Mentalis
Occipitalis Platysma
Orbicularis Oris Risorius
Zygomaticus major Orbicularis oculi
Levator labii superioris Corrugator supercilii
Depressor labii superioris Levator palpebrae
superioris
CRANIAL NERVES VII
The eight cranial nerve is the auditory and vestibular nerves. They subserve the functions of:-
a) Hearing
b) Balancing
To test hearing, the opposite ear is occluded by sticking a finger in the external auditory meatus and
then softly whispering a few words or sentences in a progressively louder voice at a distance of about
three feet and then asking the patient to repeat them after you. It is important to cover one’s mouth
with one’s hand so that the patient cannot lip read. Occlude the other ear and repeat the procedure.
Alternatively, one can bring a ticking watch from far away and move it towards one ear while the other
is occluded and note the distance from the ear at which the patient hears the ticking. Compare this with
the distance of one’s own hearing of the ticking watch, assuming one’s hearing to be normal.
Weber Test
Conductive deafness due to damage to the conductive mechanism in the external ear, ear-drum or
middle ear must be distinguished from perceptive or nerve deafness where the lesion affects the
cochlea or the auditory nerve itself. The distinction is made by performing Weber’s Test. A high pitched
tuning fork (>512 Hz) when placed on the middle of the forehead is heard louder in the deaf ear when
deafness is conductive or mixed, and louder in the opposite ear when the deafness is perceptive.
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Rinne’s Test
Rinne’s test of bone conduction is only necessary when a mild bilateral deafness is suspected. In this
case the patient is asked where the tuning fork seems louder- in front of the ear (air conduction) or
when placed on the mastoid process (bone conduction). In perceptive deafness the hearing is better in
the opposite ear while in conductive deafness the hearing is better in deaf ear (bone conduction).
In any case of conductive deafness, examine the external auditory meatus and tympanic membrane with
the auroscope. In any case of perceptive deafness, unless the cause can be readily identified on clinical
grounds, the patient should be referred for detailed testing of caloric responses and cochlea function.
Vestibular Nerve and Otolith Apparatus

The vestibular nerve and otolith apparatus of the inner ear may be tested at the bed side by examining
for nystagmus and by position tests. Thus horizontal nystagmus on lateral gaze with a rotatory
component usually indicates a recent disturbance of the vestibular nerve; its central nuclei or
connection or occasionally the semi-circular canals. Long-standing peripheral lesions are not associated
with nystagmus.
Positional tests may allow the symptoms of positional vertigo (vertigo induced by sudden head
movements) to be distinguished into central and benign peripheral types.
The patient is moved quickly from the sitting position to lying with his head back and turned to one side.
This change of position may either give rise to immediate vertigo and nystagmus indicative of a central
cause or lead to vertigo and nystagmus after a latent interval of about 15 seconds. This latter response is
indicative of a disturbance of otolith apparatus in the inner ear and is usually a benign self limiting
condition attributable to a viral infection or a head injury.
It is noteworthy that structural lesions affecting the auditory nerve in the posterior fossa such as an
acoustic neuroma give rise to a perceptive deafness usually associated with some degree of trigeminal
sensory loss and facial weakness. Where a unilateral perceptive deafness is therefore found very careful
testing of the corneal reflex and facial movement is mandatory.
CRANIAL NERVES IX
The ninth cranial nerve is the glossopharyngeal nerve and it supplies sensation to the pharynx. It is the
afferent limb of the gag reflex. Since the gag reflex is uncomfortable to the patient, it is not normally
elicited unless it is elicited accidentally as one tries to look at the pharynx with a tongue depressor and
the patient gags indicating an intact IXth cranial nerve.
Hence tests of sensation and movement of the pharynx are only relevant where there are symptoms of
dysphagia, dysphonia or dysarthria or where there are other signs of lower brain stem involvement.
Sensation in the pharynx (IXth nerve) is tested by getting the patient to open his mouth, depressing the
tongue with a spatula and then touching each side of the posterior wall of the pharynx with a spatula.
The patient is then asked whether the sensation was similar on the two sides.
CRANIAL NERVES X
The tenth cranial nerve is the vagus. This is tested by looking at the soft palpate. Note the position of
the uvula which should normally be central. Instruct the patient to say Aaaa! Both sides of the soft
palpate should rise like a curtain with the uvula in the middle. In a lesion of the vagus, the side of the
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soft palate supplied by the diseased nerve is unable to rise. The normal side rises and pulls the uvula
towards its side. Hence the uvula is drawn towards the normal side of the soft palate.
Bilateral Xth cranial nerve weakness gives rise to nasal speech and where the recurrent laryngeal nerve
is involved to dysphonia. Early degrees of weakness of the larynx are best tested by asking the patient to
cough. The vocal cords must be examined in any patient suspected of unilateral or bilateral vocal cord
paralysis.
CRANIAL NERVES XI
The eleventh cranial nerve is the accessory nerve. This supplies the sternomastoid and trapezius
muscles.
The sternomastoids are tested by asking the patient to turn his head to one side while the movement is
opposed by pressing on the side of the chin. The opposite sternomastoid can be seen to contract and
unilateral weakness can be confirmed by asking the patient to push his head forwards against
resistance, placing the examiner’s hand on the forehead and observing both muscles on the front of the
neck.
The upper fibres of trapezius are tested by asking the patient to shrug his shoulders ‘up to the ear’
against resistence. In the course of it the strength of the trapezius is assessed. The muscles can be seen
and felt running the upper part of the neck and the spine of the scapula.
A unilateral lesion of the accessory nerve implies compression or damage to the nerve in or near the
jugular foramen or in the neck.
CRANIAL NERVES XII

The twelfth cranial nerve is the hypoglossal nerve which is a pure motor nerve and it supplies the
muscles of the tongue.
Let the patient open his mouth and examine the tongue inside the mouth. Look for any sign of unilateral
wasting or generalized fasciculation. In lower motor neurone lesion the affected side of tongue will be
wasted and will show fasciculation.
Fasciculation is a continuous random, irregular contraction of groups of muscle fibres (comprising a

motor unit) and gives the appearance of tiny twitches and momentary dimpling of the tongue surface.
Now let the patient protrude his tongue out. Fasciculation and wasting is again looked for. Normally the
whole tongue moves out with the tip of the tongue in the middle. In a lesion of the XIIth cranial nerve,
the affected side is not able to move out. The normal side therefore moves out alone and it deviates
towards the affected side. Hence the tongue moves towards the side of the lesion (See Fig. 2:9).
The patient is then asked to flick the tongue rapidly from side and a slowness or poverty of movement
suggests either an upper motor neurone lesion or an extra-pyramidal deficit as in Parkinson’s disease.
Unilateral lower motor neurone weakness of the tongue is rare and suggests damage to the nerve in the
base of the skull. Fasciculation and atrophy of the tongue indicates a lesion of the anterior horn cells
usually motor neurone disease.
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Causes of cranial nerve lesions
Any cranial nerve may be affected by: Diabetes mellitus, stroke, multiple sclerosis, tumors, sarcoidosis,
vasculitis, polyarthritis nodosa, systemic lupus erythematosus and syphilis.
I trauma, respiratory tract infection, frontal lobe tumour, meningitis
II mononuclear blindness: multiple sclerosis, giant cell arteritis

Bilateral blindness: methanol, tobacco ambylobia, neurosyphilis
Field defects- bitemporal hemianopia: optic chiasm compression eg. Pituitary adenoma,
craniopharyngioma, internal carotid artery aneurysm.
Homonymous hemianopia: stroke, abscess, tumour.
III diabetes, giant cell arteritis. Syphilis, glaucoma, Leber’s optic atrophy, optic nerve
compression, idiopathic, increased intracranial pressure.
IV rare, usually due to trauma to the orbit
VI Multiple sclerosis, Wernicke’s encephalopathy, pontine stroke
V Sensory: herpes zoster, trigeminal neuralgia, nasopharyngeal cancer, acoustic neuroma,

Motor: rare
VII LMN: Bell’s palsy, polio, otitis media, skull fracture, cerebello-pontine angle tumours eg.
Acoustic neuroma, malignant parotid tumours, herpes zoster (Ramsay Hunt syndrome).
UMN: stroke, tumour
VIII Noise, Paget’s disease, Meniere’s disease, herpes zoster, acoustic neuroma, brainstem CVA,
drugs(aminoglycosides).
IX, X, XII Trauma, brainstem lesions, neck tumours.
XI Rare, polio, syringomyelia, tumour, stroke, bulbar palsy, trauma, TB
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THE MOTOR SYSTEM
The examination of the motor system aims to establish whether there is weakness, whether there is an
abnormality of cerebellar function or whether there is an extra-pyramid disturbance. If there is
weakness, examination of the patient must establish whether the weakness is due to an upper motor
neurone lesion or a lower motor neurone lesion or whether it is primarily due to disease of the muscle
itself (myopathy).
Follow the same traditional processes of clinical examination by inspection palpation percussion and
auscultation.
A useful check list for the testing various aspects of motor function are:
INSPECTION for Posture

Wasting
Fasciculation
Movements
PALPATION for Tone

Power
Co-ordination
PERCUSSION for Reflexes
AUSCULTATION for Carotid bruit.

Subclavian bruit
Posture
First note the posture of the patient. For instance note that flexion and adduction of the affected arm
across the hemiplegic patient with the legs on the same side stiffly extended. This is the posture of
decorticate rigidity (see Fig. 7:41b).
One may notice the opisthotonos posture with the extension of the neck, back and legs; the arms are
internally rotated, adducted and extended except at the wrist where they are flexed. This is the
decerebrate rigidity (Fig. 7:9). Such a posture suggests the presence of a lesion in the motor pathway in
the mid brain.
Figure 7:9 Opisthotonos
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A patient with Parkinsonism lies in the bed with his head held above the pillow because of flexion at the
neck (Fig. 7:10).
Figure 7:10 Cervical Kyphosis in a Patient with Parkinsonism.
Wasting
Then observe the muscle bulk for wasting of the muscles. Compare one side with the other. Careful
scrutiny of the small hand muscles is necessary if there is a possibility of median or ulnar nerve damage
i.e. Thoracic 1 root lesion.
Fasciculation
Observe for fasciculation especially if motor neurone disease is possible. This is seen as small irregular
twitches in the muscle flitting from place to place in a random way. Irregular worse twitches recurring in
the same place usually indicates myokinia which is a normal phenomenon.
If fasciculation is not obvious one can stimulate it by giving the muscles a gentle flicker with the finger.
When fasciculation is present it suggests a lower motor neurone lesion.
Movements
Observe for any involuntary movement such as tremors, choreiform movements or athetoid spasms.
Examination of the Tone

There are several ways of testing for the tone. One must learn and be conversant with one method and
try and test the tone in all patients so that one is familiar with normal, reduced and increased tone.
Different Ways of Testing for Tone (Fig. 7:11)

With the patient lying supine and well relaxed:-
(1) Flex and extend the elbow joint and note the resistance offered to the movements. One can use
the wrist joint or any convenient joint for that matter instead of elbow joint.
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(2) Raise the whole limb and allow it to fall on the bed. Note the speed and manner in which it falls.
One may have to catch the limb, especially the leg to prevent the limb landing on a hard surface and
injuring the patient.
(3) Holding the hand in the greeting position, pronate and supinate the forearm and note the
resistance imparted to the hands.
(4) Hold the proximal end of the wrist or foot and shake it up and down, noting the resistance to
the movements.
Figure 7:11 Testing for Tone
The tone may be decreased-hypotonia or increased-hypertonia. Hypertonia may be spastic (pyramidal)

or rigid (extra-pyramidal).
a) Spasticity
In spasticity, the resistance to passive movement increases initially and as the movement is continued
the resistance falls away – the clasp-knife phenomenon – referring to the resistance experienced when
the blade of a penknife is opened.
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b) Rigidity
The resistance to movement is sustained throughout the movement. This is described as lead pipe
rigidity. When the tremor is superimposed on the rigidity this becomes jerky and it is described as cog-
wheel rigidity as seen in Parkinson’s disease.
A brisk movement is more likely to initiate the clasp-knife phenomenon and the patient must remain
with the muscles relaxed throughout. Nervousness, cold, actual or expected pain will cause the patient
voluntarily to resist the movement imposed by the examiner and make testing for tone impossible. If
the patient is unable to relax, distract his attention with conversation while continuing the examination.
Occasionally in a patient with suspected Parkinsonism, tone in the neck muscles may be increased and
may be examined by rolling the head from side to side on the pillow. Power in the neck is tested by
opposing voluntary flexion of the neck by pressing on the forehead and the trunk muscles are tested by
asking the patient to sit up from lying flat with his arms folded. Deviation of the umbilicus during this
movement implies weakness of the anterior abdominal muscles on one side.
Clonus
When the tone is increased one may get clonus. This is the term applied to a rhythmic series of
involuntary muscular contraction evoked by a sudden stretch of muscle.
Patella Clonus
To test for patella clonus, let the patient relax in a supine position, then stabilise the leg with the left
hand and push it downwards towards the foot. This sudden downwards movement to the patella
stretches quadriceps and provokes involuntary repetitive jerking contractions (Fig. 7:12).
Figure 7:12 Testing for Patella Clonus.
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Ankle Clonus
With knee slightly flexed and the heel resting on the bed,
place the right palm against the sole of the foot. Then give a
brisk dorsiflexion of the foot with the hand maintaining the
pressure. Quick dorsiflexion of the ankle may cause a few
beats of clonus or involuntary jerks of plantar flexion at the
ankle usually indicating a pyramidal deficit but occasionally
seen in a very tense individual.
Figure 7:13 Testing for Ankle Clonus.
Testing for Power

First ask the patient to lift the whole limb and then let him lift the limb against resistance and note the
grade of power. One must then test the power compartment by compartment.
Testing for Power in Upper Limbs

Put the right hand on the anterior aspect of humerus and let the patient push the hand against
resistance. This is testing for flexion of the shoulder joint (Fig. 7:14). To test for extension of the
shoulder joint, put the right hand on the posterior aspect of the humerus and let the patient push
against it (Fig. 7:15).
Figure 7:14Flexion of the Shoulder.
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Figure 7:15 Extension of the Shoulder.
To test adduction of the shoulder joint, place the hand on the medial aspect of the humerus and let the
patient push against resistance (Fig. 7:16). To test for abduction of the shoulder joint, place the hand on
the lateral aspect of the humerus and let the patient push the hand against resistance (Fig. 7:17).
Figure 7:16 Figure 7:17

Testing for Adduction of the Shoulder. Testing for Abduction of the shoulder
To test for flexion of the elbow slightly flex the elbow joint and with the right hand on the anterior
aspect of the forearm, try to straighten the elbow joint while the patient flexes the elbow against
resistance (Fig. 7:18).
Figure 7:18 Flexion of the Elbow
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Figure 7:19 Extension of the Elbow.
To test for extension of the elbow joint, flex the elbow joint and with the right hand on the posterior
aspect of the forearm, let the patient push the hand against resistance (Fig. 7:19).
Flexion and extension of the wrist is done with the patient’s hand in a fisted position. To test for flexion
of the wrist joint, place the right hand on the palmar aspect of the fisted hand and let the patient push
against the hand (Fig. 7:20). To test for extension of the wrist joint, place the right hand on the dorsal
aspect of the fisted hand and let the patient push the hand against resistance (Fig. 7:21).
Figure 7:20 Flexion of the Wrist. Figure 7:21 Extension of the Wrist
Now test the power of the intrinsic muscles of the hand. The middle finger is taken as the midline and
movements of the fingers towards it are adduction and movements of the fingers away from it are
abduction. One can place a piece of paper between the fingers and try to pull the paper out while the
patient resists it. The strength with which the patient prevents the paper from being pulled away from
the fingers gives one an idea about the strength of the intrinsic muscles of the hand.
Movement of the thumb to the various fingers is described as oponens. One can test for adduction and
abduction of the thumb against resistance. Note that movements of the thumb is at right ankles to
movements of the fingers.
Finally, test for flexion and extension of the phalanges of the hand by letting the patient perform this
movement against resistance.
Always compare the power in the two upper limbs.
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Testing for Power in the Lower Limbs

The same order of examination is adopted in the lower limbs as for the upper-limbs – inspection for
wasting and fasciculation, then muscle tone, power, co-ordination and finally reflexes.
Fasciculation in the leg muscles may be of no significance but asymmetry of muscle bulk may indicate a
lower motor neurone lesion. Arthritis of the knee may also cause wasting of the quadriceps but the
reflexes are normal and muscle power if testable is also well preserved.
Muscle tone is tested at the knee and ankle by holding the leg at the knee and front of the foot and
feeling for resistance to flexion at the knee and ankle joints. As in the arm rigid (extra-pyramidal) or
spastic (pyramidal) hypertonia may be found
First, test for the power in the lower limb as a whole and then test for power compartment by
compartment.
To test for extension of the hip joint, place the right hands on the anterior aspect of the thigh and let the
patient push against the resistance of the hand (Fig. 7:22).
To test for flexion of the hip joint, place the right hands on the posterior aspect of the thigh and let the
patient push against the resistance of the hand (Fig. 7:23).
Figure 7:22 Extension of the Hip.
Figure 7:23 Flexion of the Hip.
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Now place the hand on the medial aspect of the thigh and get the patient to push against resistance.
This tests for adduction of the hip (Fig. 7:24). To test for abduction of the hip, place the hand on the
lateral aspect of the thigh and let the patient push against the resistance of the hand (Fig. 7:25).
Figure 7:24Testing for Adduction of the Hip Figure 7:25 Testing for Abduction of the hip.
To test for extension of the knee joint, flex the knee joint a little, place the right hand on the middle of
the anterior aspect of the leg and let the patient push against the resistance of the hand (Fig. 7:26).
Figure 7:26 Extension of the Knee
To test for flexion of the knee, flex the knee joint a little, and with the right hand on the posterior aspect
of the leg, try to straighten the lower limb while the patient resists the action by flexion the knee (Fig.
7:27).
Figure 7:27 Flexion of the Knee.
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To test for dorsiflexion of the foot, place the right hand over the dorsum of the foot while the patient
pushes his foot against the resistance (Fig 7:28).
Figure 7:28 Dorsiflexion of the Foot. Figure 7:29 plantar Flexion of the Foot.
To test for plantar flexion of the foot, place the right hand on the sole of the foot and let the patient
push against the resistance (Fig. 7:29).
Again compare both limbs when testing for wasting, fasciculation, tone and power as well as reflexes.
Assessment of what is normal in terms of muscle strength is largely acquired by experience but
comparison of the normal side with the abnormal is useful in detecting slight weakness.
The evaluation of the muscle power should be recorded quantitatively using the grading recommended
by the Medical Research Council Viz:
Grade Activity
0 Total paralysis with no active contractions.
1 Visible palpable contraction without active movement
2 Movement which is possible with gravity eliminated.
3 Very weak but power just able to overcome gravity
4 Weak but power sufficient to overcome gravity and slight resistance.
5 Normal power
It is often helpful to also assess upper neurone lesions (especially in the lower limb) in terms of
disturbance of function. How far can the patient walk on the flat? Can he manage stairs or getting out of
bed? What appliance (stick, crutch, frame) is necessary for walking?
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Tenderness to palpation of a weak muscle may occur in some neuropathies (e.g. alcoholic) and
inflammatory diseases of muscles (myositis).
Co-ordination
Co-ordination tests in the upper limb seek to identify either impairment of cerebellar function or extra-
pyramidal deficits as in Parkinson’s disease. Test of cerebellar function cannot be done when there is
severe weakness. Occasionally severe joint position sense loss will give inco-ordination indistinguishable
from cerebellar ataxia.
First ask the patient to touch the tip of his nose with the forefinger and then to touch the examiner’s
finger held about two feet from his face and then to go backwards and forwards a few times. Normally
the alternating movements should be smooth but in cerebellar ataxia, the movements become jerky and
the patient may ‘overshoot’ the target (past pointing).
‘Terminal intention tremor’ describes a tremor of the hand as it approaches the target and is
characteristic of cerebellar disease. Alternating movements such as tapping one hand on the back of the
other or alternating pronation-supination movements of the forearm becomes jerky and irregular
(dysdiadokinesia) (Fig.7:30).
Figure 7:30Dysdiadochokinesia
Fine controlled manipulative movements of the upper limb are characteristically impaired in extra-
pyramidal disorders but pyramidal deficit may also lead to slowness and awkwardness in these
movements. In the absence if signs of spastic weakness therefore an inability to perform nimbly discrete
finger movements is suggestive of Parkinson’s disease. Ask the patient to touch each finger tip to the
thumb in turn and then repeat the movement or to tap rapidly with the forefingers with the hand
resting on the desk. Writing is probably the best test of fine movement in the right hands.
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Co-ordination tests in the lower limb must include tests of balance, gait and
stance off the examination couch.
In Romberg’s test, the patient is asked to stand with feet together and eyes
closed. Impaired position sense in the feet or severe vertigo or cerebellar
ataxia will cause the patient to sway. ‘Tandem walking i.e. heel to toe
walking will reveal minor degrees of ataxia of gait (Fig. 7:31).
Figure 7:31 Heel to Toe.
On the couch the patient is asked to place the heel of one foot on the knee of the other leg and then
slowly and neatly slide it down and up on the front of the shin (Fig. 7:32). In cerebellar disturbance the
heel will wobble off the front of the shin. Repetitive tapping movements of the foot may be impaired in
patients with Parkinson’s disease when no other deficit is noticeable in the legs.
Figure 7:32 Heel to Knee.
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REFLEXES
Upper Limb
With the patient lying supine and very relaxed, place his two upper limbs on the abdomen with the
hands lying over the supra-pubic region. Place the left index finger in the ante-cubical fossa and holding
the tip of the patella hammer strike the finger which is overlying the biceps tendon. The biceps muscle
will be seen to contract and sometimes it even moves the forearm. This is the Biceps reflex and the root
valves are cervical 5 and 6. Compare the reflexes on the right and left sides (Fig. 7:33).
(a) Right side.
(b) Left side.
Figure 7:33 Testing for Biceps Reflex (Root Value C5,C6)
In testing for the Triceps reflex on the right side, rest the patient’s elbow joint on the left hand and hit
the tendon of the triceps muscle at the elbow just above the ulna. On the left side rest the patient’s left
forearm on your left forearm and hit the tendon of the triceps muscle which will be seen to contract.
The root value of the triceps reflex is cervical 7 and 8 (Fig. 7:34).
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(a) Right Side.
(b) Left Side
Figure 7:34 Testing for the Triceps Reflex. (Root value C7,C8)
With the forearm lying relaxed on the abdomen and the wrist slightly extended, hit the tendon of the
supinator (or brachio-radialis) muscle by tapping the region of the head of radius at the wrist a patella
hammer. A contraction of brachio-radialis can be seen. This is the supinator reflex and the root value is
cervical 5 and 6 (Fig. 7:35).
(a) Right Side (b) Left Side
Figure 7:35 Testing for the Supinator Reflex (Root value C5, C6)
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The Finger Reflex

This may be difficult to obtain and needs practice. With the patient’s arm pronated the hand is held with
the fingers semi-flexed and the wrist slightly extended. An upward tap on the tip will lead to a reflex jerk
on the forearm finger flexions. The root value of the finger jerk is cervical 8.
While one is looking for contraction of brachio-radius muscle in the supinator reflex, one must also look
for simultaneous finger flexion which may imply an increased finger jerk.
Lower Limb
To elicit the knee reflex, expose the quadriceps muscles and flex the knee. Then support the semi-flexed
knee with the left forearm then gently hit the tendon of the quadriceps muscles which is inserted just
below the knee joint with a patella hammer. As the tendon is hit, look over the anterior aspect of the
thigh for the contraction of quadriceps muscles. The root value of the knee reflex is Lumbar 3 and 4 (Fig.
7:36).
(a) Right Side.
(a) Left Side.

Figure 7:36 Knee Jerk. (Root value L3, L4)
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To test for the medial hamstring reflex place the fingers on the medial aspect of the knee over the
tendon of the medial hamstring muscle. Hit the hand and observe the adduction of the knee. The root
value of the medial hamstring reflex is Lumbar 4.
Figure 7:37 (a) Right Ankle Reflex. (Root value L5, S1)
Figure 7:37 (b) Left Ankle Reflex. (Root value L5, S1)
To elicit the ankle reflex, slightly flex the legs at the hip and knee with the hip externally rotated, then
hold the foot loosely at right angles to the leg. Then gently tap directly on the Achilles tendon with the
toes of the foot supported by the left hand. The foot should plantar flex (Fig. 7:37a & 7.37b). an easier
way of eliciting the ankle jerk is to let the patient kneel on a chair if he is able and then with the foot
hanging loosely from the edge of the chair, gently tap the Achilles tendon and the foot will plantar flex
(Fig. 7:37c). The root value of the ankle jerks is Lumbar 5 and Sacral 1.
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Figure 7:37 (c) Elicitation Ankle Reflex with Patient Kneeling on a Chair. (Root value L5, S1)
In all situations the force of the tap to elicit a jerk should begin quite gently and be reduced or increased
according to whether a reflex is obtained or not.
If the reflexes appear to be absent, then one must re-enforce and repeat the procedure. Re-enforcement
of the reflexes in the upper limb can be obtained by asking the patient to clench his jaws or push his
knees hard together. To re-enforce the knee and ankle reflexes ask the patient to clench his hands.
Sometimes by conversing with the patient his mind is taken off the procedure and one can then elicit
the reflexes very easily.
The Plantar (Babinski) Response

With the patient lying supine and holding the foot in a neutral position at the ankle, use a moderately
sharp object to scratch the outer lateral part of the sole of the foot. While doing this, watch for the first
movement of the big toe. This is the plantar reflex and the root value is Sacral 1 (Fig. 7:38).
Figure 7:38 Eliciting Plantar Reflex.
The normal reflex to stimulation of the sole of the foot is flexion of the big toe. In pyramidal lesions the
big toe extends and this is reliable indicating of cortico-spinal tract disturbance when the test is correctly
performed.
Abdominal Reflexes
The abdominal reflexes should be tested by stimulating the skin in each quadrant of the abdomen with a
stick. Observe for contraction of the underlying muscles. The abdominal reflexes are abolished in
pyramidal deficits as in lower motor neurone weakness. They may also be difficult to elicit in patients
who are obese or during pregnancy and shortly after childbirth.
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SENSATION
Testing for sensation is very subjective and tiring for both the examiner and the patient. In practice,
therefore, we depend on the information from the history rather than formal testing.
The aim of sensory examination is to establish the distribution of any sensory loss in such a way that
conclusions can be drawn about the anatomical site of the lesion producing the loss. Where the lesion
affects the peripheral nerves, the sensory loss is usually of an ‘associated type’ i.e. all the modalities
tend to be affected in the relevant territory. Pain sense, position sense, light touch and temperature will
therefore all be affected where for example damage to the brachial plexus leads to sensory loss in the
hand. But where the lesion affects central nervous system, the sensory loss is characteristically
‘dissociated’ i.e. one sensory pathway in the central nervous system will be more affected than the
other by virtue of their anatomical separation. The Brown-Sequard syndrome perhaps best exemplifies
this dissociation where hemi-transection of the spinal cord gives rise to loss of pain and temperature on
one side of the body below the level of the lesion and loss of position and vibration sense on the other
side.
Start the sensory examination with the lower limbs working upwards over the trunk and upper limbs to
the neck. This way the highest level of sensory disturbance can most easily be established. The lesion
cannot be below this level.
Examine first for loss or impairment of light touch, position and vibration, then for pain and temperature
so that any dissociation of sensory of loss can be immediately identified.
Light Touch
Touch the skin of the patient with a clean piece of cotton wool. Ask the patient if he can feel the touch.
Then with the patient’s eyes closed touch various parts of the body and get his response each time he
feels the cotton wool touching him. Two grades of abnormality are recognized – loss or impairment.
Where light touch is ‘lost’ the patient fails altogether to report the stimulus; where light touch is
‘impaired’ the patient recognizes that the perception is less than it should be or when compared with
the other side. The over-helpful patient may mislead you by reporting spurious impairments of light
touch but when such impairment is accompanied by paraesthesia, such as tingling it is usually
significant.
Position and Proprioception

Position sense should be tested in the big toe and index finger, extending the examination to other limb
joints when appropriate.
First instruct the patient on what one is going to do and what response one wants from him. Holding the
big toe on its lateral side, move the distal phalanx up and down. Explain to the patient that he should
say ‘up’ or ‘down’ according to the position of the phalanx. The initial displacement of the toe should be
fairly gross in order to train the patient as to what is required.
Now with his eyes closed, repeat the procedure several times to assess if he can get the position of the
big toe. The same procedure can be done with the index finger. In the big toe, a movement of 5 mm at
the tip should be easily detected and a movement of 2 mm in the index finger should also be easily
detectable.
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Avoid holding the big toe on the dorsal and plantar aspect as the patient may detect the difference in
pressure applied to these areas of the toe and give an answer according to the pressure applied rather
than the position of the toe. The same applies to the index finger (Fig.7:39).
Figure 7.39 Testing for Position Sense.
Note that loss of position sense may not be accompanied by any symptoms.
Vibration Sense
Vibration sense is tested using a 128 Hz tuning fork applied to the malleoli, ascending to the knee, hip
or costal margin if necessary. If the patient cannot feel vibration at the ankle then go on to test for
vibration sense at the knee, hip or costal margin as necessary.
Explain to the patient the buzzing sensation of the vibrating tuning fork which one is going to place on
his bony prominence. Then with the turning fork vibrating, place it on the malleolus and ask if he can
feel the buzzing vibrating. Then stop the vibrating of the tuning fork and ask him if he can feel the
vibration. The patient should not feel the vibration now. Having satisfied one’s self that the patient
understands what one is looking for repeat the procedure with the patient’s eyes closed and elicit his
response to the vibration or non-vibration of the tuning fork.
Pain
Pain sense is tested on the same principle as light touch. Pain sensibility is tested using a pin which
should be sharp enough to penetrate the skin. The distinction the patient is asked to make is whether
with his eyes closed he can perceive the pricking sensation of the pinpoint or whether it feels blunt like a
matchstick. Again pain sensation can be lost or impaired, thus implying different severity of sensory
disturbance.
Temperature
Temperature sensation should be tested using warm and cold test tubes. A rapid check of temperature
sensation can be made using the cold tuning fork and asking the patient whether he can feel the cold
temperature of the metal.
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Figure 7.40 Segmental Innervations of the Skin
Two Point Discrimination

In some patients the sensory examination may need extending to additional modalities. Two points
discrimination should be tested with blunt dividers specially made for that purpose. The patient is asked
to say whether with his eyes closed, he perceives one or two points of pressure on the skin. The normal
threshold of two-point discrimination over the instep is about 2.5 cm whereas on the finger tip less than
5 mm should be detected. This is a useful test in patients with peripheral or mononeuropathy. It is
essential in cases where parietal sensory loss is suspected.
Lesions of the parietal lobe may give rise to an unusual form of sensory dissociation where the patient
has preservation of light touch, pain and temperature but loses two point discrimination, and becomes
unable to identify objects by feel e.g. coin or key and cannot identify numbers written by pressure on
the palms of the hand (graphaesthesia). Sensory inattention may also be present in such a case. This id
demonstrated by touching or pin pricking both arms or (leg) simultaneously and symmetrically. In these
circumstances the patient reports the stimulus on the normal side but fails to perceive it on the affected
side. Careful instructions have to be given e.g. ‘please tell me if prick your right hand or your left hand or
both hands’.
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Rombergism
To demonstrate this, make the patient stand upright with his feet together and his eyes open. Now let
him close eyes with his feet still together. If there is loss of postural sensations, the patient will be
unstable on his feet and he begins to rock and sway.
One can further test his postural sensation by letting him stretch both upper limbs in front of him. Then
depress one limb down and let him position it at the same level as the other limb. The patient should
keep his eyes closed all the time. A normal person he should be able to position the depressed limbs at
the same level as the other limb but in postural sensation defect he is unable to do this.
GAIT
If the patient is able to stand, get him to stand and take a few steps and observe the gait. Note the
presence of scissors gait in spastic paralysis. Observe hemiplegic gait where the upper limb is flexed and
adducted across the chest and the lower limb makes a semi-circular sweep (circumduction) when
walking. Note the shuffling gait of Parkinsonism with failure to swing the arms when walking. Look for
arthragic gait of a patient with hip pain. Observe the high stepping gait in patients with foot drop (Fig.
7:41).
The abnormal gait can either be painful or painless.
In painful gait, the body takes weight off the painful limb as much as possible. So it is the rhythm which
is disturbed. Less time is spent bearing weight on the affected limb and more time is spent bearing
weight on the normal limb.
In painless gait the contour is abnormal. This may be due to:

1) Osteogenic - due to shortening and deformity of bone.
2) Arthrogenic - due to deformity, laxity or stiffness of gait.
3) Myogenic - due to weakness of muscle.
4) Neurogenic - due to organic disorders of the nervous system
5) Psychogenic - bizarre gait resulting from psychiatric causes.
6) Prosthetic - due to wearing an artificial limb.
In hemiparesis, the affected limb is usually held flexed at the elbow and adducted across the chest while
the leg on the same side is stiff and swings forward in a semi-circular fashion rather than being lifted
from the ground.
In paraparetic patients i.e. patients with upper motor neurone lesions of both legs, there is a slow stiff
movement of each leg in turn with the feet remaining in contact with the ground. In severe cases the
patient assumes a scissors gait.
In foot drop, the patient tends to lift the foot high to clear the toes from the ground and as it is returned
there is often a loud slapping noise. The lesion is readily detected by the ear as well as the eye.
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Unilateral foot drop may be due to compression of the common perineal nerve or to a prolapsed
intervertebral disc.
A high stepping gait affects both legs and is found in bilateral foot drop. It is caused by a generalized
polyneuropathy. Loss of postural sensation in the feet in tabes dorsalis also produce a high stepping gait.
Instability of the knee joint or wasting and weakness of the muscles of the knee joint leading to
hypotonia makes the patient fling the leg forward in a flail like manner as he walks. This is seen in
poliomyelitis.
A waddling gait is seen in congenital dislocation of the hip, wasting of gluteal muscles in primary disease
of muscle – myopathies and occasionally in lesions of the anterior horn cells.
In cerebellar lesion the patient walks unsteadily with a wide base or in drunken reeling manner.
In lesions confined to only one posterior lobe of the cerebellum, the patient staggers or drift to affected
side on walking. This becomes more obvious as he turns.
Lesion of the nerves causes a jerky rocking of the trunk from side to side similar to a man walking on a
tight rope.
In Parkinsonism, the gait is slow and shuffling, each step being smaller than normal with an absence of
arm swinging during walking. Some take increasingly rapid small steps forward in an attempt to
maintain an upright posture. This is known as festinant gait.
In arthragic gait the patient is unable to bear weight on the affected limb. The patient spends less time
on the affected limb and more time on the normal limb.
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(a) Scissors Gait. (b) Hemiplegic Gait.
(c) Festinant Gait in Parkinsonism (d) Arthragic Gait (e)High-Stepping Gait

(Foot Drop)
Figure 7.41 Different Types of Gait
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TESTING FOR CEREBELLAR LESION
The function of the cerebellum is to control and co-ordinate muscle movements. The signs of cerebella
disease have been described with the pneumonic PINDDAH.
P - Pendular jerks
I - Intention tremors
N - Nystagmus
D - Dysarthria
D - Dysdiadokinesia
A - Ataxia
H - Hypotonia
In testing for cerebellar signs start from the head and proceed down to the legs.
First look for and examine the eyes for nystagmus. Nystagmus is best observed with the eyes looking in
the lateral gaze. With the patient looking in the lateral gaze observe the eyeball for nystagmus which is
the jerky rhythmic movements of the eyeball.
Perform the finger/nose test by letting the patient touch his nose with his index finger and quickly touch
the examiner’s index finger. Observe for intention tremor, clumsiness and past pointing. One can make
the test more sensitive by moving one’s finger from place to place. Repeat the test with the patient
using the other hand.
Note any dysarthria – difficulty in articulation of the words as one converses with him.
Now instruct the patient to rapidly tap the dorsum of one hand with the palm of the other hand. Note
any clumsiness. Change over and let him tap the dorsum of the other hand with the palm of other hand.
An alternative method is to let the patient rapidly do alternating pronation and supination of the hand.
Repeat the procedure using the other hand. Inability to perform the action accurately id
Dysdiadokinesia.
Heel-Knee Test
Instruct the patient to place the heel of one leg on the opposite knee and roll the heel along the shin. In
cerebellar disases the movement is very clumsy. Repeat the test using the other shin with the other
heel.
Test for tone of the muscles in the limbs. In cerebellar disease there is hypotonia.
Let the patient sit on the edge of the bed with his legs hanging. Hit the quadriceps tendon at the knee
and observe the movement of the leg. In the presence of cerebellar disease, the leg swings to and fro
several times from one single tap. This is known as Pendular jerk.
Perform the Romberg’s test with the patient. Then get the patient to walk and note an ataxia. Make the
test more sensitive by letting him walk in a straight line and then walking heel to toe to bring up any
slight ataxia that may be present.
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SIGNS OF MENINGEAL IRRITATION
Neck Rigidity
In meningeal irritation flexing the neck is painful. The neck, therefore, becomes rigid and any attempt at
passive flexion of the neck is resisted by the patient.
Kernig’s Sign
The patient lies supine with both legs extended on the couch. The leg to be tested is flexed at the hip
and knee. While the hip joint remains flexed, the knee joint is extended. This produces meningeal
irritation causing spasm and pain in the lumbar region. This is known as Kernig’s sign.
Presence of neck rigidity and Kernig’s sign indicate meningeal irritation which may be due to infection as
in meningitis or blood as in sub-arachnoid haemorrhage.
Spinal Segmental Level

Spinal segmental level is tested on the trunk. Starting from an area just below the clavicle, test for pain
sensation on the trunk using a sharp pin. Then move downwards on the trunk and continue testing for
pain sensation until the patient cannot feel the pain prick any more. The point at which he can no longer
feel the pin prick demarcates the spinal level of loss of sensation. Note the dermatome at that level
which should correspond with the spinal level of the lesion.
Do not always expect a sharp demarcation of the loss of sensation; when the patient indicates a
‘change’ of sensation, that is enough to indicate the spinal level of lesion.
Sensory examination is exhausting and tiring for both the patient and the doctor. From the history and
motor examination one should have a fairly clear idea what one is looking for, so concentrate on the
sensory signs that will confirm or refute your suspicions. Thus when an ulnar nerve is suspected,
concentrate on the precise distribution of the sensory loss over the ring finger and at the wrist whereas
in a suspected cord lesion, the highest dermatome affected will point to the likely spinal segmental
level.
THE UNCONSCIOUS OR POORLY RESPONSIVE PATIENT
The examination of the unconscious patient presents an emergency and a clear plan of action is
essential. From the outset establish that the airway is clear and that ventilatory and circulatory support
have been provided where necessary.
Even when the diagnosis seems obvious as in severe alcoholic intoxication, possible alternative or
contributory causes of coma should always be considered. The history must be obtained from
eyewitnesses, family members and friends.
The examination of the unconscious patient should always start with a general physical examination and
venepuncture so that blood samples are sent for laboratory tests early. The neurological examination
should follow these preliminaries. The management of the patient depends on the circumstances. In the
tropics the association of coma with fever will lead one to consider conditions like meningitis,
encephalitis and cerebral malaria. In the western world one should consider drug poisoning, alcoholic
intoxication, head trauma and stroke.
43 | P a g e
An assessment of the level of consciousness should be made using the Glasgow coma scale as shown
below. Points are given for each of the three activities of eye movements, verbal response and best
motor response:
EYE MOVEMENTS: Spontaneous eye opening 4

Eye opening in response to speech 3
Eye opening in response to pain 2
Nil 1
VERBAL RESPONSE: Oriented 5

Confused Conversation 4
Inappropriate Words 3
Incomprehensible Sounds 2
Nil 1
BEST MOTOR RESPONSE: Obeys commands 6

Localises response to pain 5
Withdraws from pain 4
Abnormal flexion to pain 3
Extensor response to pain 2
Nil 1
The total Glasgow score is 15-Scores

 Scores 10 – 15 have good prognosis
 Scores 5 - 10 have a guarded prognosis
 Scores below 4 have very poor prognosis.
Determination of the Glasgow scale can be repeated as often as possible to assess the progress of the
coma.
The fundi should be examined for papilloedema and for haemorrhages which when subyaloid in type
indicate sudden recent rise of intracranial pressure.
Disturbance of function in the upper brain stem may lead to coma and such disturbance may result from
either displacement of the brain stem by a mass lesion above or below the tentorium cerebelli or by a
focal lesion in or adjacent to the brain stem. Signs of brain stem dysfunction are:-
1) Asymmetry of the pupils or poor light reaction or dilatation. In drug overdose the pupils
typically remain responsive to light although narcotic overdose may lead to pinpoint pupils.
2) Tonic deviation of the eyes, or loss of eye movements. Eye movements may be induced by
the ‘dolls head’ maneuver where the patient is turned quickly to one side with the eye. The
eye lags behind the head movements normally but follows passively with head movements
if fixation and oculocephalic reflexes are absent.
3) Unilateral ptosis
4) Corneal reflexes absent or asymmetrical.
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Physical evidence of hemiplegia should be sought. Unilateral facial weakness may be evident by one
cheek blowing out in expiration or one side of the face failing to grimace as strongly as the other to
painful stimuli. The posture of the limbs on one side may suggest hemiparesis and lack of reflex
withdrawn to pain, increased (or sometimes absent) reflexes and rarely a unilateral extensor planter
reflex may confirm this. Test pharyngeal sensation and gag reflex by stimulating he posterior wall of the
nasopharynx and test sensation in the limbs by observing the reactions of painful stimuli to the sternum,
nasions, hands and feet.
Status epilepticus (continuous epileptic discharges in the brain) may give rise to clonic movements that
are focal or generalized. The suspicion for status epilepticus is an indication for urgent
electroencephalography.
Decerebrate extensor spasms of the trunk and limb muscles suggest severe disturbance of function in
the upper brain stem or deep cerebral structures. Thus large cerebral haemorrhages compressing
thalamus and mid-brain but sparing the pons may present in this way.
It is important to realize that signs of brain stem dysfunction leading to coma may conceal signs of brain
disturbance in the hemisphere. Hence where facilities are available urgent computerized tomography
scan is necessary to establish the pathological anatomy of the brain.
The Diagnosis of Brain Death

Modern life support techniques and the use of organs for transplantation make it essential that rigid
criteria exist for the diagnosis of brain death.
To consider brain death, the following conditions should be fulfilled and should exist concurrently:
1) The patient should be deeply comatose
a) Inherent in this condition is the absence of any depressant drugs in the circulation such
as narcotics tranquilizers and hypnotics.
b) Primary hypothermia should be excluded.
c) Metabolic and endocrine causes for coma should have been excluded.
2) The patient should be, of necessity maintained on a ventilator because of previous inadequacy
or cessation of respiration.
3) A firm diagnosis of irremedial brain damage should have been established.
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Consequent upon these conditions being fulfilled the following tests which required
confirmation after an appropriate interval which might be as long as 24 hours are required
for definitive diagnosis of brain death. All brain stem reflexes should be absent. This is
accepted if:
1) The pupils are dilated and do not respond to light.
2) Vestibular ocular (caloric) reflexes are absent. These may be tested by irrigating, each
external auditory meatus in turn will 20 mls of ice cold water, care having been taken to
establish that tympanitic membranes are intact and the external auditory canals are
unobstructed. The reflexes are absent when no eye movement occurs.
3) Corneal reflexes are absent.
4) There are no motor responses within the cranial nerve distribution after adequate
stimulation of any somatic area.
5) There is loss of gag and bronchial stimulation reflexes.
6) There is no respiratory movement after disconnection from the respiratory for a sufficiently
long period to allow Pa CO 2 to reach 6.7 KPa (50 mmHg)
It is important to remember that spinal reflexes may persist after brain death and that
electroencephalography is not necessary to diagnosis brain death.
GENERAL MEDICAL EXAMINATION
Following the neurological examination general physical examination of the patient including blood
pressure measurements and urine testing is essential.
Certain aspects of the general examination are particularly relevant to the nervous system and may give
clues to the aetiology of the neurological lesion. Skin lesions may indicate neurofibromatosis, Sturge
Weber syndrome or tuberous sclerosis all of which has important neurological associations. The contour
of the skull may be a vital sign in a patient with Paget’s disease, meningioma or development anomaly in
the region of foramen magnum as in Arnold – Chiari malformation. The patient with signs suggestive of
a spinal cord lesion must always have his vertebral column carefully examined for deformity or
tenderness on percussion and to look for any focal skeletal abnormality. When the patient is unable to
raise the leg to 90 degrees above the couch, this may indicate nerve root irritation in the lumbar spinal
canal. A patient with suspected meningitis or sub-arachnoid haemorrhage should be examined for neck
stiffness on passive flexion. Auscultation of the skull or orbits may reveal a bruit denoting arterovenous
malformation, fistula or aneurym of the carotid and sub-clavian arteries.
In the patient with acute hemiplegia, possible aetiological factors in the cardiovascular system must be
identified including hypertension carotid bruit and rhythm disturbances.
Hypertension may result in cerebral haemorrhage. Presence of carotid bruit may indicate stenosis or
occlusion of the internal carotid artery. Rhythm disturbance which leads to cerebral arterial thrombosis
46 | P a g e
may result in cerebral embolism and a common cause of this is atrial fibrillation especially when it is
intermittent.
One must also examine all the peripheral pulses by both palpation and auscultation to detect any
abnormality.
Eye signs may denote thyroid disease associated with clinical features indicating thyrotoxicosis.
Metabolic disorders may be the cause of epilepsy or abnormal involuntary movements including tremor.
Any patient with signs of raised intra-cranial pressure such as headache, papilloedema and vomiting
must be examined for signs of a primary neoplasm such as bronchus, breast or kidney.
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T. C. Ankrah
Chapter 8
THE USE OF THE OPHTHALMOSCOPE

IN CLINICAL EXAMINATION
Chapter 8 Ophthalmoscope In Clinical Examination
THE USE OF THE OPHTHALMOSCOPE IN

CLINICAL EXAMINATION
The ophthalmoscope, like the stethoscope, should be accepted as a necessity at the start of the
student’s career. The inspection of the fundus should be included as part of the routine clinical
examination. Fundoscopic examination may show evidence of malignant hypertension, military
tuberculosis, raised intra-cranial pressure or malignant melanoma. Other important clues to the
diagnosis of systemic disorders may be found in examining the optic fundus.
Technique in the Use of the Ophthalmoscope

It is much better to have one’s own ophthalmoscope so that one is familiar and conversant with using it.
For routine clinical work, examine he fundus through the untreated pupil. Or thorough examination of
the fundus the patient’s pupil should be dilated with mydriate solution like tropicamide (mydracyl) or
cyclopentolate hydrochloride (mydrilate).
The environment should be darkened whenever possible.
The instrument should be held in the right hand with the forefinger on the lens adjustment wheel and
right eye used to look at the patient’s right eye and the left eye for the patients left eye.
The patient should look naturally at a distant object.
The examiner’s face should be kept parallel to the patient’s face. Avoid
blocking the patient’s view with your forehead.
The examiner’s eye should be very close to the small hole in the
ophthalmoscope and as near as possible to the patient’s pupil.
Try and look past the light reflected from the cornea at the fundus
beyond.
Rotate the ophthalmoscope with your head in order to examine the

peripheral parts of the fundus. Keep the instrument steady by resting the
middle and ring fingers of the holding hand on the patient’s cheek.
Figure 8.1 Picture of an ophthalmoscope
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Routine Inspection of the Fundus Oculi (Fig. 8:2)

1) Inspect the optic disc first. If it is not seen at first, it can be located by following the course of the
artery or vein. Note the sharpness of the edge of the optic disc, its colour and the optic cup.
2) Next inspect the arteries and veins. Note any tortuosity, width and colour. Note the appearance
of the arterio – venous crossing. Pulsation of the retinal veins is normal.
3) Examine the whole of the fundus especially the periphery.

4) Finally examine the macula and its surroundings. The macula is a dull red patch lying two disc
widths on the temporal side of the lower pole of the optic disc. The centre of the fundus is called fovea.
Lesions here cause serious loss of vision.
Figure 8:2 Normal Fundus.
FUNDUS IN SYSTEMIC DISEASE
Examination of the fundus may reveal the presence of a number of local well as systemic diseases.
In hypertension the state of the fundus is a better prognostic factor than the height of the blood
pressure. The fundus in hypertension has been graded depending on the severity.
Hypertensive Retinopathy
Stage I - Narrowing of arterioles which give a silver wiring appearance.
Stage II - Narrowing of the veins where they are crossed by arteries.

Arterio - venous nipping (Fig. 8:3)
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Stage III - Presence of exudates and flame-shaped haemorrhages.
Stage IV- Presence of papilloedema in addition to I-III
Figure 8:3 Arterio – Venous Nipping
Diabetic Retinopathy (Fig. 8:4)

In diabetes mellitus the fundus may show soft and hard exudates. Hard exudates are lipid deposits on
the retina. They disappear with time or treatment.
Soft exudates are ends of dead nerves. They are fluffy and ill-defined. They are caused by arteriolar
occlusion and they are permanent.
There are also dot and blot haemorrhages and micro-aneurysms which are hard, red, small, dense and
well circumscribed and neovascularisation which are now vessel formations.
Stage I Stage II
Thickening of retinal capillary wall. Punctate haemmorrhages
Leakage of fluid Capillary aneurysm
Yellow deposits (hard exudates)
Retinal vein engorgement
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Stage III Stage IV

Microinfarcts of the nerve fibres New vessel formation growing from
(cotton wool exudates) the retinal or optic nerve head
Figure 8:4 Diabetic Retinopathy
Other causes of haemorrhage on the retina include retinal vascular occlusion, severe anaemia, systemic
lupus erythematosus, bleeding disorders, infective endocarditis and advanced malignant disease.
Miliary Tuberculosis
In military tuberculosis in addition to phlenetulular conjunctivitis one may see choroidal tubercles on the
retina which will betray the presence of military tuberculoses and hence enable the doctor to give the
necessary anti-tuberclous therapy. Choroidal tubercles consists of yellowish white nodes varying in size
from very small to half disc diameter with indistinct borders.
Proliferating Sickle Retinopathy

Although the most severe form of retinopathy are associated with SC and S. Thal disease the milder
haemoglobinopathies may occasionally also cause retinopathy. Proliferative sickle retinopathy can be
divided into five stages.
Stage 1 is characterized by peripheral arterilor occlusion.
Stage 2 shows peripheral arteriovenous anastomoses which appear to be dilated pre-existent capillary
channels.
Stage 3 is characterized by the sprouting of new vessels from the anastomoses. Initially the new vessels
lie flat on the retina and have a fan-shaped configuration (sea-fan neovascularization).
Stage 4 is characterized by varying amounts of vitreous haemorrhages.
Stage 5 is characterized by vitreous traction and retinal detachment.
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OPTIC ATROPHY
Optic Atrophy (Fig. 8:5)
This is the term applied to the condition of the disc when
the optic nerve is degenerated. Loss of vision is the only
symptom. Pallor of the optic disc and loss of papillary
reaction are usually proportional to visual loss. The causes
are varied and includes occlusion for the central retinal
vein or artery, cerebromacular degeneration, optic
neuritis, pressure against optic nerve from aneurysm,
diabetes mellitus, direct injury to the nerve and glaucoma.
Fig. 8:5 Optic Atrophy
PAPILLOEDENA
Papilloedena (Fig. 8:6)

Papilloedema (choked disc) is a non inflammatory
congestion of the optic disc associated with increased
inter cranial pressure. The common causes are
cerebral tumours, abscess, subdural haemmorrhage,
hydrocephalus and systemic hypertension.
Fig. 8:6 Papillodena.
SUB-HYALOID HAEMORRHAGE
Sub-hyaloid haemorrhage (Fig 8:7)

This may be detected as haemorrhage around the optic disc associated
with subarachnoid haemorrhage.
Figure 8:7 Sub-hyaloid Haemorrhage.
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Tuberous Sclerosis (Bourneville’s Disease) (Fig. 8:8)

The rare intra ocular tumours (glea hamartoma) associated with tuberous sclerosis in about half the
cases varies in size and colour but is most often a yellow or white nodular smelling, frequently mulberry
in appearance located in any portion of the posterior fundus but with a predilection for the area near
the optic nerve. Other manifestation of tuberous sclerosis include skin changes (adenoma sebaceum)
intra cranial changes causing epilepsy and mental retardation and other neuralgic symptom. There is no
treatment. The prognosis is very poor with 75% of patients are dead by age 20.
Figure 8:8 Tuberous Sclerosis (Bourneville’s Disease).
CENTRAL ARTERY OCCLUSION
Central Artery Occlusion (Fig. 8:9)

Here the macular area shows a cherry-red spot. With lack of
blood supply providing the necessary nutrition to the eye,
the organ fails and vision becomes very poor.
Figure 8:9 Central retinal artery occlusion.
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ARTERIOVENOUS MALFORMATION
Arteriovenous malformation (8.10)

This may be evident on the fundi when the vessels appear
abnormal from the usual vasculature as in Fig. 8:9.
Figure 8:10 Arteriovenous Malformation.
MACULAR DEGENERATION
Macular Degeneration (Fig. 8:11)
Degeneration of the fundi especially when it affects the
macular areas greatly impairs visions.
Figure 8:11 Macular Degeneration
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T. C. Ankrah
Chapter 9
EXAMINATION OF EAR, NOSE AND
THROAT FOR THE NON-SPECIALIST
 Examination of the Ear

 Examination of the Nose
 Pharyngeal and Laryngeal Disease
 Examination of the Neck
Chapter 9 Examination Of Ear, Nose And Throat
EXAMINATION OF EAR, NOSE AND

THROAT FOR THE NON-SPECIALIST
All medical students and doctors must be aware of the basic physical signs of otorhinolaryngology.
While the non-specialist may be unable to visualize the nasopharynx or larynx expertly, he should be
able to carry out a reasonably thorough examination of ears, nose pharynx and neck. Although for many
parts of the examination an otolaryngologist will use a head mirror and bull’s eye lamp, much of the
examination can be carried out with a suitable auroscope.
EXAMINATION OF THE EAR
The patient’s hearing is assessed during the course of the history taking.
More formal examination of the patient’s ears is then carried out starting with the outer ear (Fig. 9:1).
Note major abnormalities of the pinna such as total absence or marked aplasia. Then assess the position
of the pinnae, heir symmetry, preauricular skin tags, pits and sinuses. The pinnae should then be
deflected forward to examine the postaural region for scars, bony depression and other abnormalities
including innocent swellings such as sebaceous cysts or more sinister lesions such as carcinoma. Look for
enlargement of the preauricular and postauricular lymph nodes.
Swellings of the pinna exquisite tenderness may present with cellulitis or following trauma where
subperichondral haematomata may cause the so-called cauliflower ear. Discharge from the meatus may
cause a secondary eczematous reaction which may extend on the skin of the neck.
Many abnormalities of size and shape of the pinna may be associated with various syndromes. One of
these is Treacher Collin syndrome in which there may be severe dysplasia of the pinna and canal as well
as other facial features. These include hypoplastic malae, antimongoloid slant of the eyelids. This
syndrome may be associated with severe degrees of conductive deafness. The canal should then be
examined using a suitable auroscope light. Examine the opening of the ear for discharge and note its
nature. It may be thin and watery as seen in some cases of otitis externa. Thicker mucopurulent
discharge may indicate tubotympanic or mucosal chronic suppurative otitis media. Scanty offensive
discharge is frequently the only symptoms of attico antral disease, a more serious type of chronic
suppurative otitis media in which the main pathological finding is the presence of a cholesteatoma.
The correct way of holding the auroscope will help considerably not only enabling a better view to be
obtained of the deep ear canal and ear drum but also reducing the risk of hurting and frightening the
patient. To examine the left ear the instrument should be held in the left hand, the right hand then
being free to retract the pinna, straightening the ear canal improving visualization of the ear drum. The
ulna border of the left hand may be rested upon the patient’s cheek so that should the patient move the
examiner’s hand holding the auroscope, the auroscope will also move and prevent the speculum
impacting in the ear.
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While introducing the speculum, abnormalities of the ear canal may be seen such as otitis externa, a
furuncle (which is extremely tender), a meatal exostosis (bony swelling of the canal) and rarely tumours.
If wax is present it may need to be carefully syringed away before further examination can take place.
Always enquire of a history of discharge and known perforation before syringing an air. The ear drum
may then be examined. A healthy tympanic membrane has a shallow concavity with an antro-inferior
reflection of the examining light, the core of light narrowing towards the umbo or middle part of the
membrane. The colour is typically a pale grey/pink and the incus/stapes assembly may just be visible
posteriorly through the drum.
Posterior
Helix maleolar folds
Chorda tympanic
nerve
Crura anthelix Pars flaccida
Anthelix
Crus of helix
Pars tensa
Tragus Pars tensa Umbo
Antiragus
Antiragus
External
Auditory Lobule
Meatus
Figure 9:1 Normal Ear Figure 9:2 Normal Ear Drum
A central perforation in pars tensa will indicate the tubotympanic or relatively safe type of chronic
suppurative otitis media; an attic defect is indicative of atticoantral disease, typically associated with
cholesteatoma. There is a higher incidence of intra cranial and other complications such as facial palsy in
attico antral chronic suppurative otitis media. Hyaline and chalky patches in the tympanic membrane are
relatively common finding and are evidence of previous inflammatory ear disease.
Deafness
In most patients there is nothing to find on aural examination.
In the Rinne test the patient’s ability to discriminate between air conduction and bone conduction is
tested. The tines of a 512 HZ tuning fork are held parallel to the ear canal and about one-inch away to
test air conduction. For bone conduction testing, the base of the fork is held firmly against the skull
adjacent to the ear; typically against the mastoid process. The patient is asked to compare the loudness
of bone-conducted and air-conducted sound. A positive Rinne is recorded when air-conducted sound is
heard better than that by bone-conduction.
In the Weber test the tuning fork is held on the forehead in the midline and the patient is asked whether
he can hear the sound and if so whether it lateralizes.
Simple voice testing may then be carried out using a quietly spoken voice or a whisper, the examiner
covering his mouth to prevent the patient lip-reading.
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Vertigo
In examining a patient with a history of vertigo, it is essential to examine the ears for abnormalities
including especially an attic perforation, which may be associated with a chronic serous labyrinthitis or a
labyrinthine fistula. With the latter the patient may volunteer a history of vertigo on pressing the ear to
occlude the ear canal. If occlusion of the ear canal with variation in the canal pressure produces vertigo
then the fistula sign is said to be positive. This is supported by assessing nystagmus which is in the
horizontal plane. In the case of a fistula with an infective labyrinthitis, persistent horizontal nystagmus
may be seen, the rapid phase being variable in its direction. Examination of a patient with vertigo is not
complete without assessment of the central nervous system and the cardiovascular system.
Nystagums is defined as rapid involuntary eye movements. They may be physiological or pathological.
The pathological cases may originate from ocular, vestibular or central nervous system diseases.
Other tests often helpful in the assessment of the patient with vertigo include Romberg and the
Unterberger test. In the Romberg’s test the patient is asked to stand with eyes closed and feet together
and his ability to maintain balance is noted. The test is said to be positive if the patient sways unduly or
is unable to maintain balance at all. A positive Romberg’s test usually indicates defective joint position
sense but vestibular impairment may also cause Romberg’s when position sense is normal.
In the Unterberger’s test the patient is asked to walk on the spot with eyes closed and arms stretched in
front; in patients with unilateral labyrinthine lesions there will be a tendency to rotate towards the side
of the lesion.
EXAMINATION OF THE NOSE
Is there obvious rhinorrhoea and if so what is its nature? Does the patient have a blocked nose, the
typical hypo-nasal speech or rhinolalia clausa or does the patient present with a nasal air leak on talking,
rhinolalia apenta as noted for example in patients with cleft palate. Is the patient obviously gasping for
breath when talking or does he have dry lips and sit open mouthed?
More formal examination of the nose starts with observation of the external nose and facial structures,
looking for displacement of the nose or abnormalities of the skin overlying it such as rhinophyma.
Rhinophyma is due to thickening of the skin of the nose and hypertrophy of the sebaceous glands.
Although seen with alcoholism, it is not always due to it! The nature of the nasal discharge should be
noted. Anterior rhinoscopy may then be carried out. In most instances, and adequate examination may
be carried out simple by lifting the tip of the nose with the thumb whilst inspecting inside the nose using
a good light. The hand-held auroscope may often be adequate. After examination of the tip and the
anterior part of the nose has been carried out a more detailed intranasal inspection may be performed
by using either a thudicum speculum or by utilizing the hand-held auroscope with a suitably large aural
speculum which may be introduced into the nostril.
Among points to note on anterior rhinoscopy are the position of the septum, any bleeding points, the
nature of the nasal mucosa and the appearance of the turbinates.
Examination of the or pharynx may yield important clues to nasal disease for example a mucopurulent
postnasal discharge from infected nasal sinuses perhaps even with a secondary pharyngitis.
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Finally the nose may be palpate noting nay structural abnormalities and testing also tenderness over the
maxillary sinuses and medially below the supraorbital ridges for frontal tenderness. Gentle percussion
similarly may elicit pain.
Nasal Obstruction
Nasal obstruction is one of the commonest nasal symptoms. The commonest cause of this is the
common cold, producing short-lived symptoms. In adults a common cause of chronic nasal airway
obstruction is a deviated nasal septum.
Vasomotor rhinitis and allergic rhinitis produce a similar clinical appearance, the distinction being made
o the history and on testing for appropriate allergies. The nasal mucosa, especially over the turbinates is
usually pale, almost a lilac colour and there is often considerable clear mucus present. Polyp may also be
seen.
Most patients with nasal obstruction resort to self medication with typical decongestant drugs, bought
from pharmacy shops. While useful for short term use, chronic usage produces a chemical rhinitis
(vasomotor rhinitis medicomentosa) with its characteristic appearance of a florid red mucosa and
engorged turbinates.
Nasal Discharges
Nasal discharge is similarly a frequent symptom and the appearance of the discharge may give a clue to
the underlying pathology; a clear, often profuse watery discharge is most commonly seen in allergic and
vasomotor rhinitis. Clear rhinorrhoea point to a CSF leak, usually from a fracture through the cribriform
plate. Purulent discharge typically is associated with sinusitis, although if the discharge is unilateral the
most likely cause particularly in the very young and the mentally infirm is a foreign body in the nose. In
an older patient a unilateral blood-stained discharge may be the first sign of a malignant tumour in the
nose or paranasal sinuses.
Cheek Swelling and Proptosis

Maxillary sinus tumours may present with cheek swelling and frontoethmoid tumours may be
associated with proptosis of the eye. Not all such swellings are neoplastic and mucoceles of the frontal
sinus typically may present with proptosis. The presence of orbital cellulitis should prompt full
investigation to exclude an underlying sinusitis, typically of the frontal sinuses in adults and of the
ethmoid sinuses in younger children.
Nose Bleeds
Nose bleeds (epitasis) are common especially in children, the majority arising from Little’s area, the
anterior part of the nasal septum, an area most easily touched by the patient’s probing finger. Although
nose bleeds can occur in adults with hypertension a torrential nose bleed in an adult is more likely to be
due to fright than to pre-existing hypertension. Exclude a bleeding disorder in a patient with recurrent
epitasis. Hereditary haemorrhagic telangiectasia can also lead to nose bleeds.
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PHARYNGEAL AND LARYNGEAL DISEASE
The Voice
The quality and timbre of the patient’s voice may give a clue to underlying disease both in the larynx and
pharynx and also more general disease such as hoarseness in patients with myxoedema. The weak,
“breathy” voice of a patient with a paralysed vocal cord indicates the possibility of an underlying
bronchial neoplasm affecting the left recurrent laryngeal nerve. Noisy breathing on inspiration,
inspiratory stridor, usually indicates glottic or supraglottic airway obstruction and if the stridor is
biphasic, both inspiratory and expiration, the possibility arises of tracheal airway narrowing.
The Mouth
The mouth must be examined thoroughly to discover any lesions as discussed earlier (see Fig. 2:8).
Sore Throat
Sore throat may be due to primary pharyngeal disease or as part of a systemic illness. Patients may
present with an acute sore throat and malaise and it is often extremely difficult to differentiate on
clinical grounds alone between a patient with an acute parenchymal tonsillitis and a patient with
glandular fever. In the latter disease the lymphadenopathy is much more generalized but the final
diagnosis rests on the peripheral blood film and the positive Paul-Bunnell test.
The tonsils drain to the upper deep cervical nodes, which quickly enlarge in acute tonsillar infections.
The node below the angle of the mandible and deep to the upper portion of the sternomastoid muscle is
termed the tonsillar node; this often the first to become tender and enlarged with a sore throat.
Recurrent throat infections may cause chronic firm enlargement of the node up to 2cm in diameter.
Larger glands than this should be regarded with suspicion and tuberculosis should be considered.
Cricoid Cartilage
Sternocleidomastoid Larynx
Muscle
Esophagus
Figure 9:2 The Throat and Tonsillitis.
The presence of thrush produces a very typical appearance. Its significance depends on the age and
clinical status of the patient. It is common at the two extremes of life, in babies and in debilitated old
people. In middle age it commonly complicates antibiotic and immunosuppressive therapy. It may also
suggest the possibility of Human Immuno Deficiency Virus (HIV) infection.
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Sometimes the tonsillar crypts may be seen to contain debris which in some instances may accumulate
and produce a large mass – a tonsillolith.
Finally one must be alert to the possibility of a tonsillar neoplasm and irregularity in appearance or
marked asymmetry in size of the tonsils needs further investigation to exclude either a carcinoma or a
lymphoma (Fig. 9:2).
EXAMINATION OF THE NECK
Examination of the ear, nose and throat is completed by examining the neck for any lesions such as
enlarged lymph nodes, enlarged salivary glands, a brachial cyst or a thyroglossal cyst or even a
metastatic disease.
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T. C. Ankrah
Chapter 10
Psychiatric Examination
Chapter 10 Psychiatric Examination
THE PSYCHIATRIC EXAMINATION

The presentation of any illness is affected by the way the patient reacts to his illness and the state of
mind can also affect the physical illness. Hence a short psychiatric examination is necessary in all cases.
Even though psychiatric examination is essentially history taking, a general physical examination should
be done in addition in order to discover any organic cause for the psychiatric presentation.
In practice a series of interviews may be needed to understand both the genesis and course of the
psychiatric illness. In addition, history form a third person may be necessary to come to a diagnosis.
In the first interview an overall history and prominent abnormalities of the mental state will be detected
as well as the patient’s personality is assessed. In a psychiatric case, the initial interview with an
experienced practitioner may take half an hour and subsequent interviews are briefer. It is advisable
that the patient and the clinician sit at right angles to each other in order to avoid fixed stares, but
throughout the interview the clinician must be observing the patients’ demeanour and the way the one
answers questions. A question and answer technique is not appropriate.
After taking particulars of the patient it is advisable to start with neutral questions, like her occupation,
marital status and religion. This gives the patient time to settle down.
Then find out the reason for referral. Did the patient come by himself? Was he accompany by relatives
or the police brought him for examination? The clinician must have time to expand the complaints.
Sometimes the presenting complaint may only be a forefront for the real complaints worrying one. After
gaining the patient’s confidence, a person who initially complained of intractable urethral pains
unresponsive to any medication has actually come because of importance.
The present illness, family history and personal history are then explored. Previous illness and
personality is explored.
Examination of Mental State

Assess the general appearance and behavior of the patient. Note his thought process and his mood. The
presence or absence of any delusion and hallucination and any obsessions are noted. Note any evidence
of intellectual defect.
Most of the signs will have revealed themselves during the history taking time but you do not
record them under history.
E.g. Patient may have told you he hears voices instructing him. This is auditory hallucination but you do
not explore or record it there. This is the time and place for it in Mental State Examination
Page | 1
MENTAL STATE EXAMINATION
Mental State examination follows a logical sequence and is goal directed, focused so you know what you
are looking for.
Order of examination
1. Appearance
2. Behavior
3. Mood
4. Speech
5. Perception
6. Thinking
7. cognition
1. Appearance
 This is what you immediately observe about patient;
o Facial appearance, facial palsy,
o Body build, weight loss, cachexia so possibly physical illness, HIV/AIDS
o Tidy or untidy, kempt or unkempt, hairdo, dreadlocked (rasta), cut low, ruggedly or
hurriedly cut,
o Finger nails, overgrown, neat
o Dressing, headgear (white, coming from a prayer camp?) neat, over-elaborately dressed,
appropriately dressed, colorful or mournful
2. Behavior
 Rapport and co-operation
 Motor activity
o Restless
o Disturbed
o Screaming and shouting
o Aggressive
o Fidgety
o Ambivatendence
o Negativistic
o Posturing
o Waxy flexibility
o Movements, tics, mannerisms, gesticulations, stereotypies,
3. Mood and Affect

Mood is the patient’s perception of the problem and Affect is how you see the patient
 From observation of his facial looks (will give the affect) and by asking (will give the mood)
 Anxious, depressed, elated, euthymic, cheerful, excited, blunted, flattened, expressionless,
labile, incontinent, incongruous, etc
4. Speech
Here concentrate on the rate of speech, the quality and the flow. Look at the physical attribute,
tone (Low tone, high tone), whether the speech is slurred, presence of Stammering, stuttering,
Page | 2
staccato. Examine for influence of drugs, like sedation, alcohol, ENT lesion, dementia, organic
problem?
Is the speech spontaneous or hesitant, garrulous, pressured?
In Disorders of flow look for sudden interruptions, pauses, (may indicate thought block but record it
under thinking).
Find out if the information the patient is providing is relevant or irrelevant, if irrelevant, give
examples, glossolalia. Is the speech coherent or incoherent?
5. Perception
hallucinations: the apparent, often strong subjective perception of an object or event when no such
stimulus or situation is present; may be visual, auditory, olfactory, gustatory, or tactile; if they are
present, what types?
6. Thinking (or thought process)

This you will judge from examining the speech and from the history taking, you certainly cannot ask
him ‘how is your thinking?’
Measure the stream of thinking if there is poverty of thought or the thinking is ‘rich’
Look at the various forms of thinking: flight of ideas, loosening of associations, knight’s move
thinking, tangential, circumstantial, neologisms, word salad, etc,
Assess the content of the thoughts.

Look out for
 delusions: a false belief or wrong judgment held with conviction despite
incontrovertible evidence to the contrary
Does the patient have obsessional thoughts and ruminations e.g. suicidal obsessions
Control – passivity phenomenon

o Possession- does the patient fell like the ideas in his/her head are from external
sources or that his thoughts are heard by others; thought alienation e.g. broadcast,
echo, withdrawal, insertion, etc
7. Cognition
Test for the orientation – time, space, person, situation. Ask the patient to tell you the estimated
time, his/her name and where you are present.
 Attention and Concentration

Throughout you’re history you might be able to find the level of attention and concentration.
Examine the level of concentration by asking the patient to subtract 7 from 100, keep subtracting till
there is none left, or ask them patient to repeat the days of the week backwards.
 Memory
You will have to assess short term and long term memories. For short term give the patient an
address and ask the patient to repeat it after ten minutes. For long term ask the patient an old
event e.g. the former president of Ghana.
Page | 3
 Insight
Is the patient aware of condition, does he recognize it as a mental illness, is he willing to be

treated for the condition and does he think treatment will be helpful ?
 Level of Intelligence and Judgment

General information and abstract thinking
Ask the patient general information about himself and the country. For abstract thinking, give
the patient a proverb and ask the patient to interpret.
PHYSICAL EXAMINATION
Do your full physical examination and systemic examination.
FORMULATION
Summary of history, physical and mental state examination

From the information gathered make a diagnosis and then have a plan of treatment – admitting or not,
what laboratory tests you want to do, what further follow up plan for more history you want to put in
place.
Page | 4
T. C. Ankrah
Chapter 11
Side Room Test

Chapter 11 Side Ward Test
SIDE WARD TESTS

Certain basic investigation can be carried out in the side room. These should give one the result
immediately which should guide one in prescribing the appropriate treatment instead of relying on the
hospital laboratory which takes a long time for the result to arrive. These days there are commercial kits
using dipsticks and tablets which will quickly give the results of side room tests.
The student or clinician himself can carry out the following tests in the side room.
BASIC SIDE ROOM TESTS
A. CHEMICAL PATHOLOGY TEST REAGENT/INSTRUMENT

1. Blood Glucose Glucometer
2. Australian Antigen Kit
(Hepatitis B-Virus)
3. Urine Pregnancy Test Kit
PRINCIPAL METHODOLOGY
1. Glucose Oxidase catalyzes Take a drop of blood onto the end of
oxidation of Glucose to plastic stick embedded with oxidase.
peroxide which reacts Allow to stand for time stipulated by
with 4-aminophenone to machine. Read results by inserting
produce is an imine dye into slot provided.
whose absorbance measured
in the Glucometer.
2. Hepatitis B antigen coated with latex Put a drop of Reagent on slide provided
reacts with Antibodies present by kit. Add one drop of serum to the
in Serum to produce reagent. Mix and rock gently for 2 minutes.
visible agglutination on the side. Observe for agglutination as Positive and
Negative for no agglutination.
3. Human Chorionic Gonadotropins Place a drop reagent on slide provided.
(HCG) antibodies coated with Add one drop of an early morning urine
latex particles react with urine (EMU) and mix. Rock gently for
containing HCG to produce 2mins. Examine for agglutination and
visible agglutination on a slide. negative or vice versa.
REMARKS: (1) Test performed earlier
than 4 weeks after LMP may show as
NEGATIVE.
(2) Molar pregnancy show high positivity
of even dilutions greater than 1 in 50.
(3) Cloudy or Turbid Urine must be
spun before examination as
precipitate might mimic agglutination.
Page | 1
B. HAEMATOLOGY AND TRANSFUSION
a) Haemoglobin (Hb) b) Packed Cell Dragbkins Solution COLORIMETER

Volume (PCV) Capillary Tube Coated with Anticoagulant
Haematocrit
c) BLOOD GROUP Anti-B, Anti-A, Rh (D) Antisera
d) SICKLING TEST 2% SODIUM METABISCULPHITE
Take 0.02ml of whole blood and add to
a) Whole blood mixed with cyanide 5.0ml of Drabkins solution. Mix well and
solution and allowed to stand for 5min. let stand for at Least 5min. blank
the Hb is converted to cyanment colorimeter with Drabkins Solution at 540nm.
Haemoglobin which is read at 540nm Read the test and standard.
and compared with a standard.
b) Blood drawn into capillary Tube through

capillary action. Spin in a Haematocrit
for 5min. the cells settle leaving plasma
on top. The level of plasma at red cell
interface is read off.
c) Whole blood mixed with Anti-A, Anti-B and

Anti Rh (D) separately And the
Agglutination Results read.
d) A drop of whole blood mixed with a

drop of metabisulplhite solution
on a microscope slide and covered
with a coverslip. The slides placed
under a microscope and examined
for sickle shaped rbcs.
e) Peripheral Blood Film.

Examine the thick and thin film for malaria
parasite. Examine the film for type of cells in
leukaemias
Page | 2
C) URINALYSIS
URINE:
Routine Urine examinations are performed at 3 levels.
(1) Physical Characteristics
(2) Chemical Examination and
(3) Microscopic Examination
STANDARD PROCEDURE:
Most testing on Random specimen of urine freshly voided by patient. The specimen is
collected in a clean, dry container and examined within one hour to avoid changes
or deterioration in the urine.
1) PHYSICAL CHARACTERISTICS:
NORMAL
(a) Colour Amber
(b) Appearance Clear
2) CHEMICAL
pH Specific Gravity
Protein Ketones
Glucose Blood
Bilirubin Urobilinogendone
Nitrite Lencoyte Esterase
The Chemical Analysis Multistix which have various assays embedded on a plastic stick.
METHODOLOGY:
The stick with the embedded ends are wholly immersed in the Urine for at least 5 seconds and removed.
Allow to stand for the time specified for each Analyte.
RESULTS:
Results for the analytes are qualitative varying from negative through to positive +++ except for the pH
and S.G which are quantitative.
Page | 3
3) MICROSCOPIC EXAMINATION
Using the light microscope.
Examine deposits of spun down urine for cells. - Red Blood Cells {RBC} and White Blood Cells {WBC}.
Examine for casts, Ova of Schistsoma haematobium etc.
STOOL Examine for ova of parasite like hookworm, Schistsoma Mansoni Enterobium vermicularis
{thread worm} Asacris lumbricoides {round worm}. Toxocara/canis and Trichurits trichiria {whipworm}.
Examine for ova of Taenia saginate, Taenia solium and Teania echinococcus.
Examine the fresh stool for pseudo-podia of amoeba.
Lastly examine the stool for flagellates
Page | 4
T. C. Ankrah
Chapter 12
Conclusion and Diagnosis

Chapter 12 Conclusion and Diagnosis
CONCLUSION AND DIAGNOSIS

At the end of the history taking and physical examination as well as side room investigation one may
come to a diagnosis or a differential diagnosis or no diagnosis at all. The diagnosis is a hypothesis about
the nature of the illness and its main etiological factors.
An attempt to come to one diagnosis is always attempted however, in practice one may be faced with
more than one diagnosis in a single patient, especially in the elderly.
Further investigations are now carried out to confirm or reject the working diagnosis and the
appropriate treatment is instituted.
WRITING UP OF THE PHYSICAL EXAMINATION

Here is an example of the format for writing up the physical examination of a hypothetical.
On examination:
The patient is emaciated middle aged man.
He looks ill. There is moderate jaundice but no pallor or cyanosis.
There are spider naevi on the forehead and upper chest.
There is clubbing of the fingers.
No cervical, axillary or inguinal lymph nodes palpable.
Cardio-Vascular System:
Jugular venous pulse is normal.
Pulse is 70/min, regular, good volume and not collapsing.
The arterial wall is not palpable.
No pulsations are visible over the precordium.
Apex beat is not displaced.
There are no thrills.
Heart sounds are normal with no murmurs.
BP 120/80.
Respiratory System:
The shape of the chest is normal.
There is no dysnoea.
Chest movements are equal and symmetrical.
Trachea is central.
Tactile fremitus is normal.
Percussion note is tympanitic.
Respiratory System (continued):
Breath sounds: Good air entry
Vesicular
No adventitious sounds.
1|Pa g e
Chapter 12 Conclusion and Diagnosis
Alimentary System:
The tongue is clean and healthy.
The teeth are healthy; there is no loss of teeth.
There is distension of the abdomen.
He has femine hair distribution.
There are no scars on the abdomen.
The liver is enlarged 5cm below the right costal margin.
It is firm and non-tender.
Both kidneys are not palpable.
There is shifting dullness.
Bowel sounds are present and normal.
No bruit is heard over the liver and the spleen.
Nervous System:
He is well orientated in time and space.
He appears intelligent.
The pupils are equal and react normally to light and accommodation.
Cranial nerves are intact.
There is wasting of the muscles but no fasciculation.
Tone is normal in all the limbs.
Power is grade five in all the limbs.
Reflexes are normal.
Sensation is intact.
Locomotor System:
There is bilateral pitting oedema of the ankles.
Movements and articulation of the limbs are normal.
EVALUATION OF THE PHYSICAL EXAMINATION

From the above examination the main findings are in the alimentary system. The presence of jaundice,
the spider naevi and the clubbing of the fingers should direct one to a pathology of the liver. The
feminine hair distribution should also alert one to the possibility of a liver pathology. The liver itself is
enlarged and firm but not tender and bruit is heard over it. The above findings should make one suspect
a chronic liver disease like cirrhosis.
However, the spleen is also enlarged and one must also consider other diagnosis like portal
hypertension of lymphoma.
The shifting dullness indicates the presence of ascites and this supports the diagnosis of a chronic liver
disease. The presence of ankle oedema also supports a liver pathology resulting in oedema from
hypoalbunaemia. So they must likely cause of the liver pathology in this man is cirrhosis of the liver.
Hence investigations must be carried out to confirm or refute the working diagnosis.
Note that NO investigation (specific of otherwise) is complete without a written report which should of
course be dated.
2|Pa g e

T C Ankrah

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Clinical Examination of the Patient

Typed and Edited by:

The term clinical examination comprises three essential processes:-

Past Medical History

History from a Third Party

Synthesis of the History

Writing up the History

Name: Kwasi Mensah

Presenting Complaints: 1) Haemoptysis – 1 day

History of Present Illness

Past Medical History

Evaluation of the History

Typed and Edited by:

GENERAL AND SUPERFICIAL FEATURES

Also look for signs of self inflicted trauma in the young.

Halitosis may be due to poor oral hygiene or pulmonary suppuration.

Figure 2:1 Clawing of Hand.

Figure 2:2 Heberden’s Nodes. Figure 2:3 Bourchard’s Nodes.

Figure 2:4 Arachnodactyly.

Clubbing of fingers is staged according to its severity (Fig. 2:5):

STAGE I - increased sponginess of the nail fold.

STAGE III - increased convexity of the nail in both directions longitudinally

STAGE III STAGE IV

Figure 2:5. Stages of Clubbing.

Figure 2:6 Koilonychia. Figure 2:7. Pitting of the nails in Psoriasis.

Figure 2:8 Mouth

Surface of the Tongue

Nature of the Lesion

THE THYROID GLAND

 Appetite and Weight

 Tolerance of Heat and Cold

 Cardiovascular and Respiration Symptoms

 Skin and Hair

In sub acute or De Quervain’s thyroiditis the gland is very tender.

 Eye Signs in Thyrotoxicosis

DISORDER OF BODY WEIGHT

Growth and Development

History and Examination

Sheehan’s syndrome refers to a form of hypopituitarism which is caused by pituitary infarct

1. Iatrogenic due to prolonged high dose of steroid treatment.

RETICULO- ENDOTHELIAL SYSTEM

Bleeding and Bruising

Fever and Sweating

LYMPH NODE ENLARGEMEMT

Palpation for Cervical Lymph Nodes

Figure 2:10 Palpation for Cervical Lymph Nodes.

Palpation of Axillary Lymph Node

Figure 2:11 Palpating for the Left Axillary Lymph Nodes.

Figure 2.12 Palpating for the Right Axillary Lymph Nodes.

Palpating For Supra-Trochlear Lymph Node

Figure 2.13 Palpating for Supra-Trochlear Lymph Node

Palpating for Inguinal Lymph Node

Acute and Chronic Leukaemia.

Splenomegaly is very gross in myelosclerosis and chronic granulocytic leukaemia.

Principles of Examination of the Systems

The processes are:-

Typed and Edited by:

CLINCICAL EXAMINATION OF THE

Box 3.1 Myocardial Ischaemia

 Middle-aged or elderly man or woman often with a family history of

 Exertional chest pain and shortness of breath. Pain often described as

 None, although hypertension and signs of hyperlipidaemia`