Pearls in PACES- Introduction

Adel Hasanin

INTRODUCTION TO PACES

AIMS OF PACES
MRCP Part 2 Clinical Examination or the Practical Assessment Clinical Examination Skills (PACES) will
test ability to:
• demonstrate the clinical skills of history taking
• examine a patient appropriately to detect the presence of absence of physical signs
• interpret physical signs
• make appropriate diagnoses
• develop and discuss emergency, immediate and long-term management plans
• communicate clinical information to colleagues, patients or their relatives
• appreciate the ethical issues that relate to day-to-day clinical practice

EXAM CONTENTS
PACES consist of five stations, each assessed by two independent examiners. Candidates will start at any
one of the five stations, and then move around the carousel of stations at 20 minute intervals, until they
have completed the cycle.
• Station 1 (respiratory 10 min, abdominal 10 min) → 5 min interval →
• Station 2 (history taking 20 min) → 5 min interval →
• Station 3 (cardiovascular 10 min, neurological 10 min) → 5 min interval →
• Station 4 (communication skills and ethics 20 min) → 5 min interval →
• Station 5 (skin 5 min, locomotor 5 min, eyes 5 min, endocrine 5 min)

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Pearls in PACES- Introduction
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PACES STATIONS
Number
Number of Distribution of Total
Station Case Time of mark
examiners time score
sheets
Station Same 2 examiners Respiratory 10
5 minutes for 2 mark 8
1 for both respiratory minutes examination sheets points
case and abdomen
5 minutes for
case discussion
Abdomen 10
5 minutes for 2 mark 8
minutes examination sheets points

5 minutes for
discussion
Station 2 examiners History taking 20
14 minutes for 2 mark 8
2 minutes history taking sheets points

1 minute for
“gathering
thoughts”

5 minutes for
discussion
Station Same 2 examiners CVS 10
5 minutes for 2 mark 8
3 for both CVS case minutes examination sheets points
and CNS case
5 minutes for
discussion
CNS 10
5 minutes for 2 mark 8
minutes examination sheets points

5 minutes for
discussion
Station 2 examiners Ethics, legal and 20
14 minutes for 2 mark 8
4 Communication minutes history taking sheets points
skills
1 minute for
“gathering
thoughts”

5 minutes for
discussion
Station Same 2 examiners Endocrine 5 Examination and 2 mark 8
5 for endocrine, minutes discussion sheets points
rheumatology, skin simultaneously in
and eye cases the 5 minutes
Rheumatology 5 Examination and
minutes discussion
simultaneously in
the 5 minutes
Skin 5 Examination and
minutes discussion
simultaneously in
the 5 minutes
Eye 5 Examination and
minutes discussion
simultaneously in
the 5 minutes
Total 10 examiners 100 14 mark 56
minutes sheets points

PASSING SCORE: A candidate will pass if they score a total mark of 41 or greater out of 56

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PACES MARKING SCHEME

Clear Pass Pass Fail Clear Fail
(Scores 4) (Scores 3) (Scores 2) (Scores 1)
System of Examines Examines Examines inadequately, Examines badly
Examination thoroughly and systematically either by omission or by and
systematically lack of system unsystematically
Language and Talks to patient in Talks to patient Uses unstructured Talks to the
Communication a structured but in a mainly language and is unaware patient in a
Skills flexible manner, structured of communication completely
using intelligible manner problems with the unstructured way
language and patient and uses technical
avoiding jargon. jargon.
Confidence and Displays Demonstrates May appear Causes the patient
Rapport confidence, rapport correct inappropriately visible physical or
and empathy approach to the confident, or mental distress
patient unconfident/hesitant. and is oblivious to
Poor rapport with the it.
patient.
Clinical Method Demonstrates Demonstrates Misses important or Misses or invents
correct and majority of obvious physical signs, the majority of
comprehensive clinical skills resulting in poor or physical signs and
clinical method and correctly and incorrect formulation of is unable to
skills, eliciting the elicits the differential diagnosis. appreciate their
correct physical majority of significance in
signs. physical signs solving clinical
correctly. problems.
Discussion and Discusses clinical Majority of Inadequate appreciation Demonstrates an
Appreciation of issues sensibly, discussion of patient’s problems inability to
Patient’s spontaneously and sensible and and concerns. Large discuss, or most of
Concerns with confidence, correct, with no part of discussion the discussion is
whilst able to important incorrect through incorrect, despite
negotiate and errors of fact or inadequate clinical examiner’s
acknowledge areas interpretation. skills or underlying attempts at
of doubt/ignorance. ignorance. Is unaware assistance. Lacks
Shows awareness of patient’s concerns or insight
of patient’s deals wit them
concerns inappropriately
Clinical Clear, appropriate Reasonable Examiner has to work Poor grasp of
Thinking and professional. clinical hard to give assistance. clinical concepts
Able to solve the thinking. and may be
problem posed by Muddled argumentative.
the patient. clinical
thinking.

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Pearls in PACES- Introduction
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GENERAL HINTS

PREPARATION FOR THE EXAM:

• There are eight clinical examination stations. For each system, be sure to have your own well-
rehearsed technique of examination, so that during the examination you do not have to think about
what to do but to concentrate on the abnormal physical signs.
• Frequently practice examining normal subjects just to master your technique of examination. Be sure
to have single method of examination for each system (do not hesitate between two methods of
examination)
• Physical findings that appear in the PACES examination are so clear that it is difficult to miss it. Most
of candidates have enough clinical experience to identify the abnormal clinical findings in the PACES
without further practice, however, it is strongly advised to attend at least one preparatory clinical
course for PACES (preferably one that is held in the same territory in which you plan to take the
examination so that you get into contact with the medical conditions common in that place)
• Try to formulate a modifiable scheme for presentation of each system and practice it frequently in
front of your colleagues.

AT THE EXAM:
• Always read the instructions carefully for clues, and recall it during the examination (sometimes the
first question is related to the complaint mentioned in the instructions)
• When examining or discussing the patient (or the surrogate), do so in an interested and kind manner
• Keep asking the patient if he (she) has any pain or tenderness before you put hands on
• Do your thinking and summarizes your findings in your head while you are examining the patient,
in order to be ready for the discussion once you finish examination.
• Do not forget to thank the patient and cover him after finishing your examination
• Approach the examiner in friendly and confident but polite manner.
• Eye contact should be appropriately maintained with the examiner. Do not look back to your patient
during the discussion.
• A common advice is to keep your hands by your sides or behind your back. This may make you feel
under pressure. It is better to keep your hands in the position that make you feel comfortable as far as it
does not make you look arrogant.
• Think for a while before you answer
• Say headings whenever possible, e.g. autoimmune profile, thyroid profile…
• If your examiner challenges, do not assume it means you are wrong. However, if there is uncertainty,
state it, and proceed to say how you would resolve the uncertainty (be certain in both your certainty
and uncertainty)
• The common question “how do you mange this patient?” may be answered in the following sequence:

I would first review the history, in particular…

A full examination might provide other clues such as …

Simple investigations may be helpful such as …

The crucial investigation is …

Management might be divided into:
1. Management of the underlying disease process
2. Symptomatic treatment
3. Rehabilitation including physiotherapy and occupational therapy
4. Social support
5. Patient and family education

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 Pearls in PACES- Respiratory
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STATION 1: RESPIRATORY

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Physical examination

General inspection

Confirms position of trachea, assesses chest wall movement
Clear Pass Fail Clear

Correctly percusses over both sides of the chest
Pass Fail

Assesses tactile vocal fremitus when applicable
□ □ □ □

Auscultates over both sides of chest

Auscultates vocal fremitus/whispering pectoraliquy and added
sound when applicable
2. Identification and interpretation of physical signs
Clear Pass Fail Clear

Identifies abnormal physical signs correctly
Pass Fail

Interprets signs correctly
□ □ □ □

Makes correct diagnosis
3. Discussion related to the case Clear Pass Fail Clear

Familiar with appropriate investigation and sequence Pass Fail

Familiar with appropriate further therapy and management □ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

1. Read the instructions carefully for clues
2. Approach the right hand side of the patient, shake hands, introduce yourself
3. Ask permission to examine him “I would like to examine your chest and lungs, if it is all right with
you”
4. Adjust the backrest so that the patient reclines at 45° to the mattress
5. Expose the chest completely

(2) GENERAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Scan the bedside locker.  Sputum pot (see theoretical notes for types of sputum),
inhaler, nebulizer , oxygen (what rate per minute),
temperature chart, peak flow chart, peak flow machine
2. Scan the patient.  Nutritional status: under/average built or overweight
 Abnormal facies: plethoric complexion (polycythaemia),
Cushingoid facies (steroid therapy)
 Dysponea (tachyponea + use of accessory muscles of
respiration; the scalene and the sternocleidomastoid)
3. Examine the eyes. Pull down  Anaemia (pallor) in the conjunctivae at the guttering between
the eyelid. the eyeball and the lower lid
 Polythycaemia → markedly engorged conjunctival vessels
 See theoretical notes for examples of eye conditions in
respiratory disease
4. Examine the mouth. Ask the  Lip pursing (indicates chronic small airways obstruction)
patient to protrude his tongue.  Central cyanosis in the under-surface of the tongue
5. Examine the hands: tell the  Clubbing (consider pulmonary fibrosis, malignancy, or
patient “outstretch your hands bronchiectasis)
like this (dorsum facing  Cyanosis in the nail bed (could be peripheral or central)
upwards)”… then “like this  Tobacco staining (consider airways disease or malignancy)
(palms facing upwards)”…  Rheumatoid arthritis (consider rheumatoid lung)
demonstrate.
6. Fine tremors: tell the patient  Fine tremors (fine trembling of the hand and fingers) may
“Hold your arms outstretched indicate β-antagonist therapy
in front of you, like this
(dorsum facing upwards and
fingers spread out), and
maintain this position”
(demonstrate)
7. Flapping tremors (asterixis):  Jerky flapping tremor (the hands are periodically dropped and
ask patient to maintain his then resume their position every 2-3 seconds) may indicate
hand in dorsiflexion and severe ventilatory failure and CO2 retention
fingers spread out
(demonstrate)
8. Feel the radial pulse (and  Warm hand and bounding pulse may indicate CO2 retention
count the respiratory rate if  See theoretical notes for causes of abnormal RR
patient looks dyspnoeic).
9. Examine the neck veins.  Raised venous pressure with prominent v waves indicates
RVF/corpulmonale
 Fixed distension of the neck veins indicates SVC obstruction

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 Pearls in PACES- Respiratory
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(3) TRACHEA
STEPS POSSIBLE FINDINGS
1. Ask patient to sit forward and look directly  Tracheal deviation: your middle finger should
forward and place the index and ring fingers rest equidistant from the index and ring fingers
over the prominent points on either side of the if the trachea is central. The trachea may be
manubrium sternae. Use the middle finger to slightly deviated to the right in normal people
feel the tracheal rings to detect tracheal due to the straightness of the right main
deviation and tracheal tug if any. bronchus. See theoretical notes for causes of
abnormal tracheal deviation
 Tracheal tug: the middle finger is pushed
upwards against the trachea by the upward
movement of the chest wall
2. Measure the notch-cricoid distance  A notch-cricoid distance < 3 fingers indicates
hyperinflation

(4) LOCAL INSPECTION:

STEPS POSSIBLE FINDINGS
1. Stand at end of bed and observe  Scars (thoracotomy, thoracoplasty, thoracoscopic biopsy,
chest. scar of phrenic nerve crush in the supraclavicular fossa)
 Radiotherapy stigmata: field markings (Indian ink marks),
radiation burns, telangiectasia
 Subcutaneous nodules (metastases)
 Engorged superficial veins (SVC obstruction)
 Deformities:

Hyperinflation/barrel chest (increased A-P diameter
compared with the lateral diameter) → emphysema

Localized apical flattening suggestive of underlying
fibrosis → old TB or pneumonectomy

Kyphoscoliosis (idiopathic or secondary to polio)

Pigeon chest (pectus carinatum – outward bowing of the
sternum) → chronic childhood respiratory illness or
rickets

Funnel chest (pectus excavatum – depression of the
sternum) → developmental defect
 Indrawing:

Generalized indrawing of the intercostal muscles and
supraclavicular fossae on inspiration → hyperinflation

Indrawing of the lower ribs on inspiration → low, flat
diaphragm in emphysema

Localized indrawing of the intercostal muscles →
bronchial obstruction
2. Assess the chest wall movement  Look carefully for asymmetry and the direction of
(expansion). Ask the patient to movement of chest wall and abdomen:
take a deep breath in and out.
Asymmetrical chest movement → unilateral pathology
on the side with reduced ventilation (fibrosis, collapse,
pneumonectomy, pleural effusion, or pneumothorax).

Symmetry is maintained → consider pulmonary fibrosis,
bronchiectasis, or airways disease.

Chest movement is mainly upwards → emphysema

Paradoxical movement of the abdomen → phrenic nerve
palsy

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(5) LOCALIZATION OF THE APEX BEAT:

STEPS POSSIBLE FINDINGS
1. Localize the apex beat first by inspection (the  A normal apical impulse is localized in the 5th
most inferior and most lateral point of cardiac ICS medial to the left MCL.
pulsation) then by laying your fingers on the  Apex may be displaced (indicates mediastinal
chest parallel to the intercostal spaces (If you displacement) if it is either pushed by pleural
cannot feel it, ask the patient to roll onto the effusion or pneumothorax; or pulled by collapse,
left side). fibrosis or pneumonectomy.
2. Then stand the index finger on it to localize  Impalpable apex may be due to hyperinflation
the point of maximum impulse. (other causes are obesity, pericardial effusion or
dextrocardia)

(6) PALPATION
STEPS POSSIBLE FINDINGS
1. Chest expansion:  On palpating for upper chest

Upper chest expansion: rest one hand lightly on either expansion, normally you should
side of the front of the chest just below the clavicle. feel your hands rise anteriorly and
Alternatively you may assess the expansion of the upper upwards symmetrically.
chest by observing the clavicles from behind during tidal  On palpating for lower chest
breathing expansion, normally the distance

Lower chest expansion: Grip the chest symmetrically between both thumbs should be at
with the fingertips in the rib spaces on either side and least 5 cm and the distance
approximate the thumbs to meet in the middle in a between your thumb and the
straight horizontal line in the inframammary regions. midline on each side should be
Keep your thumbs slightly lifted off the chest so they are symmetrical
free to move with respiration. Ask the patient to take a  Reduced expansion could be due
deep breath. Note the distance between both thumbs and to effusion, fibrosis,
compare the distance between your thumb and the pneumonectomy, collapse, or
midline on each side. pneumothorax.
2. Tactile vocal fremitus (TVF): ask the patient to say “one,  Normally, vibration produced by
one, one" whilst placing the ulnar aspect of your hand on the spoken sounds is transmitted to
chest wall. Use both hands simultaneously to compare right the chest wall and is felt as
with left, moving from above downwards (4 levels in the fremitus.
anterior chest wall and 3 levels in the axilla). You may wish  TVF becomes more palpable
to skip checking for TVF and tell the examiner that you whenever normal lung tissue is
would prefer to do vocal resonance, as an alternative, replaced by uniformly conducting
because it gives the same information and is more reliable. tissue (same causes of bronchial
breathing and increase vocal
resonance).

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 Pearls in PACES- Respiratory
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(7) PERCUSSION
STEPS POSSIBLE FINDINGS
1. The percussing finger should tap lightly,  Percussion note:
springing away after contact, to elicit signs
Resonant → normal lung
effectively.
Hyper-resonant→ pneumothorax
2. Consider starting your percussion by locating
Dull → pulmonary consolidation,
the upper border of the liver (see Ch 3. pulmonary collapse, or severe pulmonary
Abdomen) fibrosis
3. You may wish to proceed to percuss the
Stony dull → pleural effusion,
supraclavicular fossa or is preferably deferred haemothorax
to start with in percussion of the back of chest  Normally, on the right side, there is loss of
4. Proceed to percuss the clavicles within its resonance inferiorly as the liver is encountered
medial third (at the level of the 5th rib in the MCL), while on
5. Then percuss the chest anteriorly from above the left side, the lower border overlaps the
downwards in zigzag manner comparing right stomach so there is a transition from lung
with left and superior with inferior in 4 levels resonance to tympanitic stomach resonance
(left → right at same level → right inferiorly →  Avoid percussion of the clavicle laterally; as it
left at same level → left inferiorly → right at merely produces dullness from the muscles of
same level and so on) the shoulder
6. Then percuss the axillae from above  Axilla is the only place where the upper, middle
downwards in zigzag manner in 3 levels (lingual on the left) and lower lobes can be
examined together)

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(8) AUSCULTATION
STEPS POSSIBLE FINDINGS
1. Ask the patient to keep breathing regularly,  You should note the following:
deeply through the mouth, but not noisily
Type of breath sounds: see theoretical
(demonstrate). notes
2. Auscultate anteriorly from above downwards
Intensity of breath sounds: see theoretical
in zigzag manner comparing right with left and notes
superior with inferior in 4 levels from the lung
apex down to the 6th rib (avoiding the midline).

Added sounds: see theoretical notes
You may wish to start with auscultation of the  Avoid auscultation within 3 cm of the midline
supraclavicular fossa or is preferably deferred to anteriorly or posteriorly as these areas may
start with in auscultation of the back of chest transmit sounds directly from the trachea or
3. Then auscultate the axillae from above main bronchi
downwards in zigzag manner in 3 levels down
to the 8th rib.
4. If breath sounds appear reduced ask the patient
to cough, and repeat the auscultation (breath
sounds become more audible after coughing if it
is reduced due to bronchial obstruction by
secretions)
5. If you hear crackles, ask the patient to cough,
and repeat the auscultation, then ask the patient
to lean forward (in case of basal crackles), and
again repeat the auscultation.
6. Vocal resonance: ask the patient to say “one,  Normally, Vibration produced by spoken
one, one" whilst auscultating the chest wall sounds is transmitted to the chest wall and is
moving from above downwards in a zigzag just audible as resonant sound. Vocal resonance
manner as for conventional auscultation. becomes much louder (bronchophony)
whenever normal lung tissue is replaced by
uniformly conducting tissue (same causes of
bronchial breathing and increase TVF).
7. Whispering pectoraliquy: If you found an  In the normal lung, a whispered note will not be
area of bronchial breathing, ask the patient to heard, but over consolidated lung, the sound is
whisper “one, one, one”. transmitted producing "whispering
pectoraliquy".
8. Aegophony: You may check for aegophony  You should normally hear a muffled "ee"
above the level of a pleural effusion (and sound. Above the level of a pleural effusion or
possibly over an area of consolidation) by in some cases over an area of consolidation, the
asking the patient to say "ee" continuously. voice may sound nasal or bleating "ay" sound,
this is referred to as aegophony, but is an
unusual physical finding.

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(9) EXAMINATION OF THE BACK OF CHEST:

1. Ask patient to fold his arms in front of his chest (to move the scapulae laterally).
2. Look for asymmetry, scars or deformities
3. Assess expansion posteriorly: grip the chest symmetrically with the fingertips in the rib spaces on
either side (below the scapulae) and approximate the thumbs to meet in the middle in a straight
horizontal line.
4. Tactile vocal fremitus (preferably skipped)
5. Percuss posteriorly (include percussion of the supraclavicular area and axilla if not done during
examination of anterior chest):
 Start by percussing the upper posterior chest (above the scapulae) from medial to lateral in 1-3
lines on both sides (with the left middle finger applied to the chest parallel to the spine)
 Then Percuss from above downwards (medial to, and then below the scapulae) in 4 levels on both
sides (with the left middle finger applied to the chest parallel to the ribs)
 Avoid percussing near the midline as this produces a dull note from the solid structures of the
thoracic spine and paravertebral musculature
6. Auscultate posteriorly down to the level of the 11th rib (include auscultation of the supraclavicular area
and axilla if not done during examination of anterior chest)
7. Auscultate for vocal resonance, whispering pectoraliquy and aegophony

(10) LYMPHADENOPATHY
• Supraclavicular → cervical → axillary (see Ch 17. Endocrine - neck)

(11) ADDITIONAL SIGNS

1. Sacral or lower limb edema, and features suggestive of DVT
2. You may check for forced expiratory time (If your diagnosis is COAD) by asking the patient to exhale
forcefully after full inspiration while you are listening over the trachea. If exhalation takes more than 6
seconds, airway disease is indicated.
3. Tell the examiner that you would like to perform a Bedside respiratory function test (ward spirometry).

(12) THANK THE PATIENT AND COVER HIM (HER)

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Pearls in PACES- Respiratory
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THEORETICAL NOTES

TYPES OF SPUTUM
Type Appearance Cause
Serous Clear, watery Acute pulmonary oedema
Frothy, pink Alveolar cell cancer
Mucoid Clear, grey Chronic bronchitis / COPD
White, viscid Asthma
Purulent Yellow, green Bronchopulmonary infection:

pneumonia

bronchiectasis (copious mucopurulent sputum)

cystic fibrosis

lung abscess
Rusty Rusty, golden yellow Pneumococcal pneumonia

EXAMPLES OF EYE CONDITIONS IN RESPIRATORY DISEASE

Condition Respiratory disorder
Horner's syndrome Apical lung cancer
Iridocyclitis Tuberculosis
Sarcoidosis
Chemosis, conjunctival and retinal vein dilatation Carbon dioxide retention
SVC obstruction
Choroidal tubercles Miliary tuberculosis
Choroidal metastases Disseminated cancer

CAUSES OF ABNORMAL RESPIRATORY RATE

• Tachyponea is an RR > 15/min (caused by increased respiratory drive as in fever, asthma, and COPD,
or reduced ventilatory capacity as in pneumonia, pulmonary oedema, and interstitial lung disease. An
RR > 30/min is the most important prognostic sign associated with death in community-acquired
pneumonia.
• A slow RR can occur in association with opioid toxicity, hypothyroidism, raised ICP, hypothalamic
lesions, and hypercapnia

CAUSES OF ABNORMAL TRACHEAL DEVIATION

• Towards the side of the lung lesion

Upper lobe or lung collapse

Upper lobe fibrosis

Pneumonectomy
• Away from the side of the lung lesion

Tension pneumothorax

Massive pleural effusion

Upper mediastinal mass

Retrosternal goitre

Lymphoma

Lung cancer

PATTERNS OF BREATH SOUNDS

• Normal (vesicular) breath sounds:

Have a rustling quality and are described as "vesicular".

There is no gap between inspiration and expiration

During expiration, normal breath sounds rapidly fade because of decreasing airflow

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• Bronchial breathing (noise transmitted from a large airway directly to the chest wall, e.g. over an area
of consolidation, at the top of an effusion or over an area of dense fibrosis or collapse with the
underlying major bronchus is patent):

High pitched with hollow or blowing quality

Have equal inspiratory and expiratory component

The expiratory sound has a more sibilant (hissing) character than the inspiratory one and lasts for
most of the expiratory phase

INTENSITY OF BREATH SOUNDS

• Diminished vesicular breathing occurs either due to reduced conduction or reduced airflow:

Reduced conduction
1. Obesity/thick chest wall
2. Pleural effusion or marked pleural thickening
3. Pneumothorax

Reduced air flow
1. Generalized, e.g. hyperinflation due to COPD
2. Localized, e.g. over an area of collapse due to obstruction of a major bronchus (occluding
lung cancer).

ADDED SOUNDS
• Crackles are interrupted non-musical sounds. They are either fine or coarse, and either early, mid or
end inspiratory (and may be expiratory). Common patterns of crackles are:
Early inspiratory Small airways disease as in chronic bronchitis and asthma
Mid/late inspiratory
Restrictive lung disease, e.g. fibrosing alveolitis (fine crackles; reduced if
the patient is made to lean forward thereby the compressed dependent
alveoli, which crackle-open in late inspiration, are relieved of the pressure
of the lungs)

Pulmonary edema (fine/medium crackles)

Lung abscess, tubercular lung cavities and bronchial secretions in COPD,
pneumonia, etc. (coarse crackles)
Early and mid- Bronchiectasis (coarse crackles; altered by coughing)
inspiratory and
recurring on
expiration (biphasic)
• Wheezes are musical sounds associated with airway narrowing (always expiratory – mono or
polyphonic)
• Stridor: harsh, rasping or cracking noise, which may be aggravated by coughing (always inspiratory,
and indicate extrathoracic obstruction)
• Pleural rub is a creaking sound produced when inflamed parietal and visceral pleura move over one
another → pleurisy secondary to a pulmonary embolus or pneumonia
• Pneumothorax click is a rhythmical sound synchronous with cardiac systole, produced when there is
air between the two layers of pleura overlying the heart

SIGNS OF HYPERINFLATION:
• By inspection:
1. Increased A-P chest diameter
2. Flattening of the subcostal angle
3. Indrawing of the intercostal muscles and supraclavicular fossae
• By palpation:
1. Decreased chest expansion
2. Shortened cricoid-notch distance (normally greater than 3 finger breadths)
• By percussion:
1. Attenuation of heart and liver dullness (with liver descent)
2. Hyper-resonance

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SUMMARY OF CLINICAL FINDINGS IN COMMON RESPIRATORY CASES:

Trachea Expansion Percussion TVF / VR Breath sounds
Interstitial lung No change Reduced No change No change Fine end-
disease bilaterally inspiratory
crackles
COPD No change Reduced No change No change Variable; quiet
bilaterally (hyper- ± wheeze
(hyperinflated resonant in
case of
emphysema
Effusion Pushed away Reduced Stony dull Reduced Absent/reduced
if very large unilaterally (bronchophony, (bronchial at
effusion whispering the top)
(pulled in case pectoraliquy
of underlying and aegophony
collapse) at the top)
Consolidation No change Reduced Impaired Increased Bronchial
unilaterally note (bronchophony, breathing +
whispering crackles
pectoraliquy
and aegophony)
Collapse, local Pulled Reduced Impaired Reduced (zones Quiet (zones of
fibrosis, towards lesion unilaterally (nil note of increased bronchial
pneumonectomy in case of TVF/VR in breathing in
pneumonectomy) case of case of
fibrocavitary fibrocavitary
lesion) lesion)
Pneumothorax Pushed away Reduced Hyper- Reduced Absent/reduced
(large) if tension unilaterally resonant
pneumothorax

ANATOMICAL LANDMARKS OF LOBES AND FISSURES OF THE LUNG:

• Bifurcation of the trachea: anteriorly at the level of the sternal angle (junction of the body of the
sternum and the manubrium sterni), and posteriorly at the level of the disc between the 4th and 5th
thoracic vertebrae. (N.B. The large bump on the back of the lower part of the neck is the spinous
process of C7, called Vertebra prominens).
• Oblique fissure (major interlobar fissure): a line from the 2nd thoracic spine to the 6th rib in the
mammary line
• Horizontal fissure (minor interlobar fissure): a horizontal line from the sternum at the level of the 4th
costal cartilage, drawn to meet the line of the oblique fissure (on the right side only)

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 Pearls in PACES- Abdomen
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STATION 1 - ABDOMEN

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade
must be accompanied by clearly written explanatory comments)

1. Physical examination

Inspection, nutrition status
Clear Pass Fail Clear

Correctly palpates for organomegaly/masses
Pass Fail

Percusses and assesses for ascites if appropriate
□ □ □ □

Auscultates for bowel sounds/bruit

Comments on further features
2. Identification and interpretation of physical signs
Clear Pass Fail Clear

Identifies abnormal physical signs correctly
Pass Fail

Interprets signs correctly
□ □ □ □

Makes correct diagnosis
3. Discussion related to the case Clear Pass Fail Clear

Familiar with appropriate investigation and sequence Pass Fail

Familiar with appropriate further therapy and management □ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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Adel Hasanin

STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him “I am just going to feel your tummy, if it is all right with you”
• Position patient lying flat on the bed with one pillow supporting the head (but not the shoulder)
and arms rested alongside the body
• Expose the whole abdomen and chest including inguinal regions (breasts can remain covered in
ladies)

(2) GENERAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Scan the patient. Palpate for  Nutritional status: under/average built or overweight
glandular breast tissue in obese  Abnormal Facies: Cushingoid (steroid therapy in
subjects if gynaecomastia is suspected renal disease or post renal transplant),
bronzing/slate-grey skin (haemochromatosis)
 Skin marks: Spider naevi (see theoretical notes),
scratch marks, purpura, bruises, vitiligo
(autoimmune disease)
 Decreased body hair (in face and chest for males
and in axilla and pubic hair for both sexes)
 Gynaecomastia
 A-v fistula
2. Examine the eyes: pull down the  Xanthelasma (primary biliary cirrhosis).
eyelid.  Anaemia (pallor) in the conjunctivae at the guttering
between the eyeball and the lower lid
 Check the sclera for icterus
 Kayser-Fleischer rings (see theoretical notes)
3. Examine the mouth:  Central cyanosis (in the under-surface of the tongue)

look at the lips  Cheilosis/angular cheilitis (swollen cracked bright-

Ask the patient to evert his lips red lips in iron, folate, vitamin B12 or B6
(inspect the inner side of the lips) deficiency)

Then to open his mouth (shine  Abnormal odour of breath (see theoretical notes)
your pen torch into the opened  Mucous membrane ulcers
mouth),
 Mucosal telangiectasis (Osler-Weber-Rendu)…see

Then to protrude his tongue out
theoretical notes
and then to move it from side to
side (inspect the posterolateral  Gum hypertrophy (phenytoin, cyclosporine, AML)
edge of the tongue)  Abnormal pigmentation (Addison’s, drugs, Peutz-

Then to touch the roof of the Jeghers…see theoretical notes)
mouth with the tip of the tongue  Smooth and red tongue of B12 deficiency
(inspect the under surface of the  Smooth pale tongue of atrophic glossitis
tongue and the floor of the  Geographical tongue that may occur in
mouth). riboflavin/B2 deficiency
 Leucoplakia (see theoretical notes)
4. Examine the hands: tell the patient  Clubbing (cirrhosis, IBD, amyloidosis)
“outstretch your hands like this  Palmar erythema
(dorsum facing upwards)”… then  Cyanosis
“like this (palms facing upwards)”…  Leuconychia (hypoalbuminaemia)
demonstrate. Feel the palm with your
 Koilonychias (chronic iron deficiency)
thumb for Dupuytren’s contracture
5. Flapping tremors (asterixis): ask  In case of positive flapping tremors, this posture is
patient to maintain his hand in periodically dropped (usually every 2-3 seconds)
dorsiflexion and fingers spread out and then resumed resulting in a jerky flapping
(demonstrate) tremor. See theoretical notes for Pathophysiology
and causes.

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(3) LOCAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Stand at the end of bed (and if needed kneel at  Distension/swelling:
the patient’s side as well) and observe the
Generalized distension (see theoretical
abdomen carefully. notes for causes)
2. Ask the patient to take a deep breath in and look
Localized swelling (asymmetry), e.g.,
carefully for descending masses, e.g. liver, due to massive enlargement of liver or
spleen or kidney. spleen
 Scaphoid abdomen (see theoretical notes
for causes)
 Scars (see theoretical notes for types of
abdominal scars)
 Stretch marks (see theoretical notes)
 Intertrigo (see theoretical notes)
 Pubic hair distribution and thickness
 Corkscrew hairs with perifollicular
haemorrhage are frequently seen in
alcoholics with vitamin C deficiency
(along with gingivitis)
 Visible peristalsis: intestinal obstruction
3. Look for and palpate any visible pulsations  Visible pulsations of the abdominal aorta
may be noticed in the epigastrium. It must
be distinguished from an aneurysm of the
abdominal aorta, where pulsation is more
obvious and a widened aorta is felt on
palpation
4. Look for visible veins and detect the direction of  Prominent veins with direction of flow
blood flow: place 2 fingers side by side across away from the umbilicus → portal
the vein, move the lower finger away thus hypertension (e.g. caput medusa)
emptying part of the vein, then remove the  Prominent veins with direction of flow
lower finger: you may see the vein filling from upwards from the groin → IVC
down upward. If the vein remains empty, re- obstruction.
place the lower finger and remove the upper  Determining the flow in a vein below the
finger: the vein will be seen filling from above umbilicus will differentiate between portal
downward. hypertension and IVC obstruction.
 Rarely, obstruction to the SVC will give
rise to distended veins, which all flow
downwards
 Thin veins over the costal margin may be
seen in normal people

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(4) LIGHT AND DEEP PALPATION FOR MASSES

STEPS POSSIBLE FINDINGS
1. Kneel at the bedside. Ask the patient to show you • Describe the mass (while presenting
where he feels pain before you start and to report your findings) in the terms of:
any tenderness as you examine him. Look at the  Site: intra-abdominal or in the
patient’s face and not your hand whilst palpating to anterior abdominal wall, and in
ensure you are causing no discomfort which region (RIF, LIF, epigastric,
2. Palpate with your arm parallel to the patient's RIQ, LUQ, pelvic) …see
abdomen and the wrist and forearm in the same theoretical notes for types of
horizontal plane where possible. Palpate with the abdominal masses according to the
pulps of the fingers rather than the tips, with the site
relaxed hand is held flat and moulded to the  Shape, Size, consistency, surface
abdominal wall and the fingers slightly flexed at and edge
the MCP joints.  Tenderness, hotness, redness, and
3. Start away from the site of maximal pain and move skin overlying (normal, scar,
systematically through the nine regions (RIF → fistula)
hypogastrium → LIF → left flank → umbilical  Mobility in both the horizontal and
region → right flank → right hypochondrium → vertical axises, movement with
epigastrium → left hypochondrium). Initially respiration, and attachment to the
palpate the nine regions lightly then palpate again skin
more deeply for masses.  Whether you can get above it and
If you find a mass: whether it is bimanually ballotable
4. Ask the patient to tense the abdominal muscles  Pulsatility, thrill, percussion note
by lifting the head and shoulders off the pillow and bruit
while you press firmly against the forehead; a mass • See theoretical notes for examples of
in the anterior abdominal wall will still be palpable, abdominal masses according to
whereas a mass in the peritoneal cavity will not. characteristics
5. Estimate the size in two directions between your
thumb and index
6. Feel the surface and edges
7. Look at the patient face while palpating (for any
tenderness)
8. Feel the mass with the back of your hand (for
hotness)
9. Move the mass in both horizontal and vertical
axises (to check for mobility)
10. Ask the patient to take deep breath (to check for
movement with respiration)
11. Pinch the skin overlying (to check attachment to
the skin)
12. Try to get above it (i.e. to palpate its upper edge)
13. Try bimanual ballottement (for masses in the
flanks)
14. Place both your index fingers parallel to each other
over the mass to check for pulsatility
15. Feel over the mass with your palm (for thrill)
16. Percuss across the mass in two directions
17. Auscultate over the mass (for bruit)

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(5) PALPATION FOR THE LIVER

STEPS POSSIBLE FINDINGS
1. Palpate with the right hand, using the radial • Describe the liver (while presenting your
edge and the pulps of the index and middle findings) in the terms of:
fingers, while keeping your hand flat on the  Size by palpation (in cm below the costal
abdomen (Do not dig in with your fingertips as margin in the RMCL). The normal liver
you may get a false impression of the liver may be palpable 2 cm below the costal
edge). Start in the right iliac fossa, working margin)
upwards towards the right hypochondrium  Liver span by percussion (normally 12
2. Keep your hand stationary and ask the patient to cm in the right MCL) or at least the
breathe in deeply. Try to feel the edge of the location of the upper border by
enlarged liver as it descends on inspiration, at percussion (normally at the 5th left ICS).
which time you can gently press and move your This determines whether the palpable
hand inwards and upwards in an arc to meet it. liver is truly enlarged or just displaced
3. During expiration, advance your hand 1-2 cm inferiorly (see theoretical notes for causes
towards the costal margin of inferior displacement of upper border
4. Repeat the previous two steps until you reach of the liver)
the costal margin (or detect the edge).  Edge (smooth or irregular)
If the liver is palpable:  Surface: smooth or nodular (if nodular →
5. Estimate the size, e.g. In cm below the right micronodular or macronodular)
costal margin in RMCL (using your fingers or a  Consistency: soft (normal), firm
tape measure) (inflamed or infiltrated) or hard
6. Feel the edge, surface and consistency (advanced cirrhosis or metastasis)
 Tenderness → TR, Budd-Chiari
7. Look at the patient face while palpating (for any
syndrome, hepatitis, hepatocellular
tenderness)
cancer, abscess
8. Feel bimanually (for pulsatility)  Pulsatility → TR
9. Obtain direct measure of the hepatic size (liver  Bruits → hepatoma (increased blood flow
span) by percussion as follows: within the tumour)

Locate the lower palpable edge by light  Riedel’s lobe: a tongue-like projection
percussion proceeding from the resonant to from the inferior surface of the right lobe
dull areas. Percussion should follow a (it can extend to the right iliac fossa)
similar pattern to palpation, starting in the • See theoretical notes for causes of
right iliac fossa and moving vertically up. hepatomegaly

Locate the upper border by heavy
percussion from the 4th ICS in the right
MCL (right nipple in men) downwards. In
the normal liver, the upper border is found
at the 5th ICS, where the note will become
dull. Keep your finger on the site of
dullness and ask the patient to breathe in
deeply then percuss lightly again and if that
area is now resonant, this confirms that that
dullness was the upper border of the liver.

Estimate the liver span in cm (the distance
from the upper border to the lower edge)
using your fingers or a tape measure
10. Auscultate (for bruit)

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(6) PALPATION FOR THE SPLEEN

STEPS POSSIBLE FINDINGS
1. Palpate with the right hand, using the radial • Describe the spleen (while presenting your
edge and the pulps of the index and middle findings) in the terms of:
fingers, while keeping your hand flat on the  Size (e.g. in cm below the left costal
abdomen. Use your left hand to press forward margin). The spleen has to enlarge in size
on the patient's left lower ribs form behind threefold to be palpable, so a palpable
(the purpose of the left hand is more that of splenic edge always indicates
steadying the patient than feeling the spleen, splenomegaly. The lower border of a
which is protected largely by the ribs normal spleen is the 9th rib in the mid-
posterolaterally). Start in the right iliac fossa, axillary line. Dullness between this
working diagonally towards the left costal surface marking and the costal margin
margin may indicate mild splenomegaly even in
2. Keep your hand stationary and ask the patient absence of palpable spleen
to breathe in deeply. Try to feel the edge of  Edge and medial notch
the enlarged spleen as it descends on  Consistency and surface
inspiration, at which time you can press and  Tenderness
move your hand inwards and upwards in an  Bruit
arc towards the left costal margin to feel it. • See theoretical notes for causes of
3. During expiration, advance your hand 1-2 splenomegaly
cm towards the left costal margin
4. Repeat the previous two steps until you
reach the costal margin (or detect the edge).
Feel the costal margin along its length, as the
position of the spleen tip is variable.
5. If you cannot feel the splenic edge, ask the
patient to roll onto his right side facing
towards you (it may help to ask the patient to
place his left hand on your right shoulder).
Keep your left hand pressing forward on the
patient’s left lower ribs from behind. Place
the right hand beneath the left costal margin
and ask the patient to breathe in deeply, press
in deeply with the fingers of the right hand
beneath the costal margin, at the same time
exerting considerable pressure medially and
downwards with the left hand. The spleen
may be tipped in this position.
If you detect the splenic edge:
6. Estimate the size, e.g. In cm below the left
costal margin (using your fingers or a tape
measure)
7. Feel the edge and try to find its characteristic
medial notch midway along its leading edge
8. Feel the surface and consistency
9. Insinuate your hand between the enlarged
spleen and the costal margin to confirm that
you cannot feel its upper border.
10. Look at the patient face while palpating (for
any tenderness)
11. Locate the lower palpable edge by light
percussion proceeding from the resonant to
dull areas. Percussion should follow a similar
pattern to palpation, starting in the right iliac
fossa and moving diagonally up to the 9th rib
in the mid-axillary line (which is the surface
marking of the lower border of a normal
spleen)
12. Auscultate (splenic bruit)

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(7) PALPATION FOR THE KIDNEYS

STEPS POSSIBLE FINDINGS
1. Use the bimanual technique to feel the kidneys. • In very thin subjects, the lower pole of a
Place your left hand behind the patient's back normal right kidney may be palpable and
below the lower ribs, just lateral to the long strap is felt as a smooth, rounded, firm swelling
muscles of the spine. Place your right hand over which descends on inspiration and is
the upper quadrant anteriorly just lateral to the bimanually palpable and may be balloted.
rectus muscle.
• The left kidney is not usually palpable
2. Press the left hand forwards, and the right hand
unless either low in position or enlarged.
inwards and upwards as the patient breaths out.
Then ask the patient to breathe in deeply. You • Describe the kidney (while presenting
may feel the lower pole of enlarged kidney your findings) in terms of:
moving down between the hands (i.e. bimanually  Size, consistency and surface
palpable).  percussion note over it: percussion
3. Flex the posterior fingers quickly at maximal note over the enlarged kidney is
inspiration. You may feel the kidney floating usually resonant because of overlying
towards the anterior hand. If this happens, gently bowel
push the kidney from one hand to the other to • See theoretical notes for characteristic
demonstrate its mobility. This is known as features to differentiate kidney from
"balloting", and helps to confirm that the structure spleen
is the kidney.
If you feel the kidney
4. Get above it and separate it from the costal edge
to confirm that you can feel its upper border
5. Assess its size, consistency and surface
6. Percuss over it

(8) PALPATION BY DIPPING OR BALLOTING: palpation of the internal organs may be difficult
if there is ascites. In this case, the technique is to press quickly, flexing at the wrist joint, to displace
the fluid and palpate the enlarged organ.

(9) PERCUSSION
1. Use only light percussion in the abdomen (as the abdominal viscera can have thin leading edges
that are easily missed by heavy percussion). A resonant (tympanic) note is normally heard
throughout (due to gas content of the intestine) except over the liver, where the note is dull.
2. Always percuss from the area of resonance to the area of dullness to identify the position
accurately.
3. Assess each organ with both palpation and percussion before moving on to the next organ (liver,
spleen, bladder, any other localized swelling)
4. Shifting dullness: this test is to demonstrate the presence of ascites:

Percuss laterally from the midline, keeping your fingers in the longitudinal axis, until dullness
is detected (if no dullness detected, do not complete the test).

Keep your finger on the site of dullness and ask the patient to turn onto the opposite side.
Pause for at least 10 seconds to allow any ascites to gravitate; then percuss again and if that
area is now resonant, and the area of dullness has moved towards the umbilicus, then ascetic
fluid is probably present.
5. Fluid thrill: In patients with large volume ascites, a fluid thrill may be elicited as follows:

Place the palm of your left hand against the left side of the abdomen and ask the patient or
assistant to place the edge of a hand on the midline of the abdomen and press firmly down (to
prevent transmission of the impulse via the abdominal wall).

Flick a finger of your right hand against the right side of the abdomen. If you feel a ripple
against your left hand, this is a fluid thrill.

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(10) AUSCULTATION
1. Bowel sounds: listen to the right of the umbilicus (for up to 30 seconds) for bowel sounds: with
the diaphragm of the stethoscope. Bowel sounds are gurgling sounds caused by normal peristaltic
activity of the gut. They normally occur every 5-10 seconds, but the frequency varies widely. You
must listen for up to 2 minutes before concluding that they are absent (paralytic ileus or
peritonitis). In intestinal obstruction, bowel sounds occur at increased frequency and have a high-
pitched tinkling quality.
2. Aortic bruits: listen over the aorta (above the umbilicus) for aortic bruits (atheroma or
aneurysm)
3. Renal bruits: listen 2-3 cm above and lateral to the umbilicus, over the epigastrium, and in loins
(at the sides of the long strap muscles, below the 12th rib) for renal bruits (renal artery stenosis): It
is not possible to distinguish renal artery stenosis bruits from those arising in adjacent vessels,
such as the mesenteric arteries, but such bruits support a decision to investigate by renal
angiography.
4. Hepatic bruit: listen over enlarged liver for bruits (hepatocellular carcinoma, hepatoma, acute
alcoholic hepatitis, large AV malformation) or friction rub (perihepatitis)
5. Splenic bruit: listen over enlarged spleen for friction rub
6. Venous hum: listen in region of umbilicus or xiphoid for venous hum: due to collateral flow in
portal hypertension (rare, but almost pathognomonic)
7. Succussion splash (if one suspects pyloric obstruction):

Explain first what you are going to do. Place the stethoscope over the epigastrium. Shake the
abdomen by lifting the patient with both hands under the pelvis, then rolling the patient from
side to side to agitate in fluid and gas in the stomach.

If the stomach is distended with fluid a splashing sound, like shaking a half-filled water
bottle, will be heard.

An audible splash more than 4 hours after the patient has eaten or drunk anything, indicates
delayed gastric emptying, e.g. pyloric stenosis.

(11) LYMPHADENOPATHY
1. Cervical → supraclavicular → if you do find lymph nodes, proceed to examine the axillary and
inguinal lymph nodes (see Ch 17. Endocrine – neck)…N.B: enlargement of Virchow’s nodes in
the left supraclavicular fossa is Troissier’s sign, which is classically, but not exclusively seen in
advanced gastric carcinoma
2. Examination of the LN in the neck form behind is an opportunity to examine the patient’s back for
spider naevi, scars, tattoos, etc.

(12) HERNIAL ORIFICES

1. Ask the patient to cough and look for any expansile impulse over the inguinal or femoral canals
(the inguinal canal extends from the pubic tubercle to the ASIS; with an internal ring at the mid-
inguinal point and an external ring at the pubic tubercle- and the femoral canal lies below the
inguinal ligament).
2. If none is apparent, place both hands in the groins so that the fingers lie over and in line with the
inguinal canal, and ask the patient to give a loud cough and feel for any expansile impulse.
3. Identify the anatomical relationships between the bulge and the pubic tubercle to distinguish a
femoral from an inguinal hernia. To locate the pubic tubercle, push the index finger gently
upwards from beneath the neck of scrotum. The pubic tubercle will be felt as a small bony
prominence 2 cm from the midline on the pubic crest. If the hernial sac passes medial to and above
the index finger on the pubic tubercle, then the hernia is inguinal; if it is lateral to and below, then
the hernia is femoral.

(13) ADDITIONAL SIGNS

1. Examine for sacral or lower limb oedema
2. Tell the examiner that you would normally examine the genitalia and perform a rectal
examination, and test the patient urine with a dipstick

(14) THANK THE PATIENT AND COVER HIM (HER)

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THEORETICAL NOTES

IN PACES, THE MAJORITY OF PATIENTS WILL FALL INTO ONE OF THREE MAIN
PATTERNS OF PATHOLOGY:
1. Liver disease (primary or secondary) – cirrhosis, portal hypertension, encephalopathy; or
associated with heart failure, metastatic disease, infective agents, infiltration or inflammation
2. Splenomegaly or hepatosplenomegaly – myeloproliferative, lymphoproliferative or autoimmune
disease
3. Renal disease ± evidence of renal replacement therapy

SPIDER NAEVI: isolated telangiectatic lesions found in drainage site of SVC (the upper trunk, arms
and face). They are fed by a central arteriole; so, can be obliterated by pressure over the arteriole. Up
to five may be found in normal individuals (more in women on oestrogen therapy and pregnant
women). More than five are probably abnormal and signify chronic liver disease.

KAYSER-FLEISCHER RINGS: a brownish-yellow ring in the outer rim of the cornea of the eye. It
is a deposit of copper granules in Descemet’s membrane and is diagnostic of Wilson’s disease. When
well developed it can be seen by unaided observation, but faint Kayser-Fleischer rings may only be
detected by a slit lamp

ABNORMAL BREATH ODOURS:

• Fetor hepaticus: stale (mousy) smell of the volatile amine, methyl mercaptan, on the breath of
patients with liver failure
• Sweet odour in diabetic or starvation ketoacidosis due to acetone.
• Fishy odour of severe uraemia
• Halitosis (bad breath) caused by decomposing food wedged between the teeth, gingivitis,
stomatitis, atrophic rhinitis and tumours of the nasal passage.
• Alcohol

LEUCOPLAKIA: a thickened white patch on a mucous membrane, such as the mouth lining or uvula
that cannot be rubbed off. It is not a specific disease and is present in about 1% of the elderly.
Occasionally Leucoplakia can become malignant. Hairy Leucoplakia, with a shaggy or hairy
appearance, is a marker of AIDS

PEUTZ-JEGHERS’ SYNDROME: autosomal dominant condition with brown spots on the lips, oral
mucosa, around the mouth, face and occasionally elsewhere on the skin; associated with
hamartomatous polyps of the small and large bowel which only rarely become malignant

OSLER-WEBER-RENDU SYNDROME (HEREDITARY HAEMORRHAGIC

TELANGIECTASIA): autosomal dominant condition with mucosal telangiectasia; presents with GI
bleeding or epistaxis. The telangiectasia also occur in the retina and brain

PATHOPHYSIOLOGY OF FLAPPING TREMORS (ASTERIXIS): it is the result of intermittent

failure of the parietal mechanisms required to maintain posture

CAUSES OF FLAPPING TREMORS (ASTERIXIS):

Severe ventilatory failure and carbon dioxide retention
Liver failure and advanced renal failure
Acute focal parietal or thalamic lesions

CAUSES OF GENERALIZED DISTENSION:

1. Fat (obesity): the umbilicus is usually sunken in case of obesity, whereas in the other conditions it
is flat or even projecting
2. Fluid (ascites),
3. Flatus (obstruction/ileus),
4. Faeces (constipation), or
5. Fetus (pregnancy). In obesity,.

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SCAPHOID ABDOMEN is seen in advanced stages of starvation and malignant disease, particularly
carcinoma of the oesophagus and stomach.

TYPES OF ABDOMINAL SCARS:

Vertical scars: Midline, Right paramedian, or Left paramedian (each could be upper or lower
according to the position from the umbilicus):

Right subcostal scar = Kocher's (open cholecystectomy)

Mercedes Benz: liver surgery

Diagonal scar in the right iliac fossa: appendectomy

scar in either iliac fossa: nephrectomy or renal transplant (transplanted kidney would be palpable
as a smooth mass beneath the scar)

Diagonal scar in either inguinal region (hernia repair)

Small infra-umbilical incision (previous laparoscopy, previous chronic ambulatory peritoneal
dialysis scar)

Horizontal suprapubic scar = Pfannenstiel (gynaecological surgery)

Scars in the loins (renal tract surgery)

Puncture scars (laparoscopic surgery, e.g. in the right hypochondrium for lap-chole)

STRETCH MARKS: atrophic and silvery marks indicates previous distension (usually striae
gravidarum, occasionally drained ascites), or purple and livid marks (Cushing’s)

INTERTRIGO is a superficial inflammation of two skin surfaces that are in contact (such as between
the thighs or under the breasts) particularly in obese people. It is caused by friction and sweat and is
often aggravated by infection, especially with Candida.

ABDOMINAL MASSES ACCORDING TO THE SITE

Right iliac fossa masses:
 The caecum is often palpable in the right iliac fossa as a soft, rounded swelling with indistinct
borders
 ileocaecal TB (chest signs)
 Caecal cancer (elderly, non-tender hard mass, LN)
 Crohn's disease (look for mouth ulcers)
 Lymphoma (look for hepatosplenomegaly, lymph nodes elsewhere)
 Appendicular mass
 Ovarian tumour
 Transplanted kidney (smooth mass in either iliac fossa, an overlying scar, stigmata of renal
failure, artificial AV fistula)
 Amoebic abscess (history of amoebiasis or travel abroad)
 Ileal carcinoid
 Actinomycosis
 Ectopic kidney

Left iliac fossa masses:
 Pelvic colon loaded with faeces (constipation): pelvic colon is frequently palpable,
particularly when loaded with hard faeces. It is felt as a firm, tubular structure some 12 cm in
length, in the left iliac fossa, parallel to the inguinal ligament. Faeces in the bowel can be
indented by the examining finger, a unique feature
 Sigmoid colon cancer (non-tender, look for hepatomegaly)
 Diverticular abscess (tender, mobile)
 Ovarian tumour
 Transplanted kidney (smooth mass in either iliac fossa, an overlying scar, stigmata of renal
failure, artificial AV fistula)
 Amoebic abscess (history of amoebiasis or travel abroad)

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Epigastric masses:
 Aortic aneurysm: pulsatile (N.B. normal aortic pulsation may be palpable in thin people). The
aorta should be palpated for in the mid-line above the umbilicus. The normal diameter is up to
3 cm.
 Gastric or pancreatic tumour: may be pulsatile if transmitting underlying aortic pulsation.
Both gastric and pancreatic tumour may cause palpable scalene LN in the supraclavicular
fossa, most commonly on the left side (Troisier’s sign). Pancreatic cancer → enlarged GB
(Courvoisier’s sign) and jaundice.
 Lymphoma (look for hepatosplenomegaly, lymph nodes elsewhere)
 Pancreatic pseudocysts, if large, can be felt in the epigastric region; they feel fixed and do not
descend
 The transverse colon is sometimes palpable in the epigastrium. It is felt as a firm, tubular
structure (like the pelvic colon but rather larger and softer), with distinct upper and lower
borders and a convex anterior surface

Right upper quadrant masses:
 Liver: confirmed by classic palpation for the liver (see below)
 Right kidney: confirmed by classic palpation for the kidney (see below)
 Gallbladder: normal Gall bladder cannot be felt. However, when it is distended, it forms an
important sign and may be palpable in the right hypochondrium, just lateral to the edge of the
rectus abdominis near the tip of the ninth costal cartilage. It is felt as a firm, (smooth, rough,
or globular) swelling with distinct rounded borders, and, unlike the liver, you can palpate
above it. It is differentiated from the right kidney by its location just beneath the abdominal
wall and being not bimanually palpable. GB becomes swollen in case of obstruction either of
the cystic duct or the CBD. If the GB is palpable in jaundiced patient, the obstruction is likely
to be due to pancreatic cancer or distal cholangiocarcinoma but not due to gallstones
(Courvoisier's low)
 Carcinoma of the colon
 Retroperitoneal sarcoma
 Lymphoma (look for hepatosplenomegaly, lymph nodes elsewhere)
 Diverticular abscess (tender, mobile)

Left upper quadrant masses:
 Spleen: confirmed by classic palpation for the spleen (see below)
 Left kidney: confirmed by classic palpation for the kidney (see below)
 Carcinoma of the colon
 Retroperitoneal sarcoma
 Lymphoma (look for hepatosplenomegaly, lymph nodes elsewhere)
 Diverticular abscess (tender, mobile)

Pelvic masses:
 Distended bladder is palpable as a smooth firm regular oval-shaped swelling in the suprapubic
region and its dome may reach as far as the umbilicus. The lateral and upper borders can be
readily made out, but it is not possible to feel its lower border (i.e. the swelling is arising out
of the pelvis). On percussion, the upper and lateral borders can be readily defined from
adjacent bowel, which is resonant. Pressure on the distended bladder gives the patient a desire
to micturate. Palpable bladder will disappear after urethral catheterization.
 Gravid uterus: firmer, mobile side to side and vaginal signs different
 Fibroid uterus: may be bosselated, firmer and vaginal signs different
 Ovarian cyst or tumour: usually eccentrically placed to left or right side

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EXAMPLES OF PALPABLE ABDOMINAL MASSES ACCORDING TO

CHARACTERISTICS:

A pulsatile mass in the upper abdomen may be normal aortic pulsation in thin people, a gastric
or pancreatic tumour transmitting underlying aortic pulsation, or an aortic aneurysm.

The normal Gall bladder cannot be felt. When it is distended, however, it forms an important
sign and may be palpable in the right hypochondrium, just lateral to the edge of the rectus
abdominis near the tip of the ninth costal cartilage. It is felt as a firm, (smooth, rough, or globular)
swelling with distinct rounded borders, and, unlike the liver, you can palpate above it. Unlike the
right kidney, distended Gall bladder lies just beneath the abdominal wall and is not bimanually
palpable. GB becomes swollen in case of obstruction either of the cystic duct or the CBD. If the
GB is palpable in jaundiced patient, the obstruction is likely to be due to pancreatic cancer or
distal cholangiocarcinoma but not due to gallstones (Courvoisier's low)

A transplanted kidney is palpable as a smooth mass in either iliac fossa with an overlying scar

A distended bladder is palpable as a smooth firm regular oval-shaped swelling in the suprapubic
region and its dome may reach as far as the umbilicus. The lateral and upper borders can be
readily made out, but it is not possible to feel its lower border (i.e. the swelling is arising out of the
pelvis). On percussion, the upper and lateral borders can be readily defined from adjacent bowel,
which is resonant. Pressure on the distended bladder gives the patient a desire to micturate.
Palpable bladder will disappear after urethral catheterization. In women, the palpable bladder
should be differentiated from:

A gravid uterus (firmer, mobile side to side and vaginal signs different)

A fibroid uterus (may be bosselated, firmer and vaginal signs different)

Cystic masses are either pancreatic, mesenteric, or ovarian (an ovarian cyst is usually
eccentrically placed to left or right side)

The pelvic colon is frequently palpable, particularly when loaded with hard faeces. It is felt as a
firm, tubular structure some 12 cm in length, in the left iliac fossa, parallel to the inguinal
ligament.

The caecum is often palpable in the right iliac fossa as a soft, rounded swelling with indistinct
borders.

The transverse colon is sometimes palpable in the epigastrium. It feels like the pelvic colon but
rather larger and softer, with distinct upper and lower borders and a convex anterior surface.

CAUSES OF INFERIOR DISPLACEMENT OF THE UPPER BORDER OF THE LIVER: the

liver dullness normally extends from the 5th ICS down to the lower border (at or just below the right
subcostal margin). The upper border of the liver may be displaced inferiorly due to:

Severe emphysema

Large right pneumothorax

Shrunken liver

Gas or air in the peritoneal cavity

Interposition of the transverse colon between the liver and the diaphragm.
LIVER CIRRHOSIS is irreversible destruction and fibrosis of liver architecture on 4 stages: liver cell
necrosis, inflammatory infiltration, fibrosis, and nodular regeneration

CHRONIC LIVER DISEASE is chronic impairment of liver functions. Causes include all causes of
liver cirrhosis and causes of hepatomegaly or hepatosplenomegaly if associated with impairment of
liver function

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SIGNS OF CHRONIC LIVER DISEASE (Words in bold italic font are signs of decompensation)
Skin  Slate grey pigmentation (haemochromatosis)
 Purpura (bleeding)
 Scratch marks (itch)
 Tattoos (viral hepatitis)
 Needle track marks (viral hepatitis)
Hair  Paucity of body hair and inverted pubic hair distribution
Eye  Jaundice
 Pallor (anaemia)
 Xanthelasmas (PBC)
 Kayser-Fleischer ring (Wilson’s)
Tongue  Cyanosis (pulmonary venous shunts)
Nails  Clubbing
 Leuconychia
 Koilonychia (iron deficiency from blood loss)
Hands  Dupuytren’s contracture (alcohol)
 Palmar erythema
 Flapping tremors (encephalopathy)
Limbs  Muscle wasting
Neck  Parotid enlargement (alcohol)
 Hypothyroidism (autoimmune hepatitis)
Chest  Gynaecomastia
 Signs of obstructive airway disease (α-1 antitrypsin deficiency)
Abdomen  Hepatomegaly (alcohol, acute inflammation)
 Splenomegaly (portal hypertension)
 Ascites
 Caput medusa (portal hypertension)
Back  Spider naevi
Genital  Testicular atrophy

CAUSES OF LIVER CIRRHOSIS, HEPATOMEGALY, HEPATOSPLENOMEGALY

Liver cirrhosis Hepatomegaly Hepatosplenomegaly
Alcohol (most common in UK) Cirrhosis Cirrhosis with portal hypertension
Hepatitis B or C (most Cancer Budd-Chiari (hepatic vein thrombosis)
common worldwide) CCF Infection (malaria, schistosomiasis,
Immune hepatitis (Lupoid Infection (EBV,CMV, leishmaniasis, toxoplasmosis,
hepatitis, PBC) hepatitis A) brucellosis, TB)
Metabolic Infiltrative (sarcoidosis, Lymphoproliferative disorders
(Haemochromatosis, amyloidosis) (Hodgkin’s, non-Hodgkin’s, CLL,
Wilson’s, α-1 antitrypsin Lymphoproliferative ALL, myeloma, paraproteinaemia)
deficiency) disorders Myeloproliferative disorders (CML,
Drugs (methyldopa, Pyogenic liver abscess myelofibrosis, PRV,ET,
amiodarone, methotrexate) Amoebic liver abscess Infiltrative (sarcoidosis, amyloidosis)
Cryptogenic Hydatid cysts Storage diseases (Gaucher’s and other
Budd-Chiari syndrome sphingolipidosis, glycogen storage
Polycystic liver disease diseases)
Riedel’s lobe Pernicious anaemia and other
Emphysema (apparent megaloblastic anaemias
hepatomegaly) Haemolytic anaemias

CAUSES OF SPLENOMEGALY
• All causes of hepatosplenomegaly
• Infective endocarditis
• Felty’s syndrome

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CHARACTERISTIC FEATURES TO DIFFERENTIATE KIDNEY FROM SPLEEN

Kidney Spleen
Bimanually palpable Not bimanually palpable
You can get above the enlarged kidney and separate it from the Not possible to feel its upper
costal edge border
Percussion note over it is usually resonant because of overlying Has a medial notch
bowel

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CVS

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade
must be accompanied by clearly written explanatory comments)

1. Physical examination
• General inspection
Clear Pass Fail Clear
• Checks pulse, notes blood pressure, inspects JVP, palpates carotids
Pass Fail
• Inspects, palpates precordium, localises apex beat, auscultates valve □ □ □ □
areas with correct positioning
• Examines for peripheral pulses and ankle oedema when applicable
2. Identification and interpretation of physical signs
Clear Pass Fail Clear
• Identifies abnormal physical signs correctly
Pass Fail
• Interprets signs correctly
□ □ □ □
• Makes correct diagnosis
3. Discussion related to the case Clear Pass Fail Clear
• Familiar with appropriate investigation and sequence Pass Fail
• Familiar with appropriate further therapy and management □ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him “I am just going to feel your pulse and listen to your heart; is
that alright?”
• Adjust the backrest so that the patient reclines at 45° to the mattress
• Expose the top half completely

(2) GENERAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Scan the patient.
Nutritional status: under/average built or
overweight

Abnormal facies: Marfanoid (AA, AR, MR),
Down’s (VSD), Turner’s (coarctation,
bicuspid AV, AS), Noonan’s (PS), malar
flush (MS)

Dysponea (tachyponea + use of accessory
muscles of respiration; the scalene and the
sternocleidomastoid)

Earlobe creases → increased incidence of
coronary artery disease (see theoretical notes)
2. Examine the eyes. Pull down the eyelid.
Anaemia (pallor) in the conjunctivae at the
guttering between the eyeball and the lower
lid

Cornea (arcus senilis)

Pupil (Argyll-Robertson pupil) → consider
syphilitic aortitis
3. Examine the mouth. Ask the patient to
Central cyanosis in the under-surface of the
protrude his tongue. Teeth must be examined tongue (see theoretical notes for types of
in all cases (infective endocarditis) cyanosis)
4. Examine the hands: tell the patient
Clubbing (congenital heart disease, infective
“outstretch your hands like this (dorsum endocarditis, atrial myxoma)
facing upwards)”… then “like this (palms
Cyanosis (could be peripheral or central)
facing upwards)”… demonstrate.
Capillary pulsations (AR, PDA)

Splinter haemorrhage, Osler’s nodes and
Janeway lesions (infective endocarditis)…
see theoretical notes

Palmer erythema (consider CO2 retention)

Arachnodactyly (see theoretical notes)

Xanthomas (dyslipidaemia)

Cool peripheries (poor flow - hyperdynamic
circulation)

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(3) PULSE
STEPS POSSIBLE FINDINGS
1. Radial pulse:
Check for rhythm and rate.
 In patients with AF, re-measure the rate
by auscultation at cardiac apex, and
calculate the pulse deficit
 If you suspect complete heart block,
recount the pulse while standing (in
complete heart block, HR does not
increase on standing)
2. Feel the opposite radial simultaneously.
Check for any difference in pulse
volume…see theoretical notes for causes of
absent radial pulse
3. Radio-femoral delay: firmly apply the right
In coarctation of aorta, femoral pulses are of
thumb just below the mid-inguinal point low volume and delayed relative to radial
while feeling the radial with your left fingers. pulse
4. Check for collapsing pulse: left up the arm
If the pulse has a water-hammer character
and put the palmer aspect of the four fingers you will feel a flick (a sharp & tall up-stroke
of your left hand on the patient's wrist just and an abrupt down-stroke) which will run
below where you can easily feel the radial across all four fingers and at the same time
pulse. Press gently with your palm, lift the you may feel a flick of the axillary artery
patient's hand above his head and then place against your right palm
your right palm over the patient's axillary
If the pulse has a collapsing character but is
artery: not a frank water-hammer type then the flick
runs across only two or three fingers
5. Glance at the antecubital fossa for catheter
Check for abnormal pulse volume or
scars. Palpate the right brachial with your character
right thumb.
6. Glance at the carotid for Corrigan’s sign
Check for abnormal pulse volume or
(visible carotid pulsation in AR). Palpate the character (see theoretical notes for
right carotid pulse with the tip of your left components of carotid pulse and
thumb (between the larynx and the mid point abnormalities of the pulse volume and
of the anterior border of the character)
sternocleidomastoid) using gentle pressure
backwards.

(4) JVP: examine right JVP.

STEPS POSSIBLE FINDINGS
1. The patient should be lying at 45 degrees and
Recognize the JVP and differentiate it from
neck is fully supported by pillows so the arterial pulsation (see theoretical notes)
sternomastoids are fully relaxed. The head
Identify the height in centimetres vertically
should be turned slightly to the left side and a above the sternal angle (normal 3-5 cm).
light shone obliquely across the neck to
maximize the shadows of right venous
pulsations
2. While observing the right JVP, palpate the
Check for abnormal waveforms (see
left carotid with your right thumb to time the theoretical notes for normal JVP and
JVP waves in relation to the carotid pulse abnormalities of the JVP
3. If JVP is not visible, consider applying
manoeuvres to check for low or very high
levels (see theoretical notes)

(5) LOCAL INSPECTION:

 Scars: median sternotomy scar, left lateral/inframammary thoracotomy scar
 Devices: pacemaker/AICD implant

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(6) APEX BEAT

STEPS POSSIBLE FINDINGS
1. Localize the apex beat first by inspection
Apex beat is defined as the most inferior and
then by laying your fingers on the chest most lateral point of cardiac pulsation.
parallel to the intercostal spaces
A normal apical impulse briefly lifts the
2. If you cannot feel it, ask the patient to roll palpating fingers (just palpable) and is localized
onto the left side). Then stand the index (in the 5th ICS medial to the left MCL)…see
finger on it to localize the point of theoretical notes for abnormalities of the apex
maximum impulse and assess the extent of beat
its thrust

(7) PALPATION
STEPS POSSIBLE FINDINGS
1. Mitral area: place your hand from the lower
Palpable S1 (tapping impulse of MS)
left sternal edge to the apex
Palpable S3 (prominent early diastolic rapid-
filling wave), often accompanied by a third
heart sound in patients with left ventricular
failure or mitral valve regurgitation

Palpable S4 (marked presystolic distension of
the left ventricle), often accompanied by a
fourth heart sound in patients with an
excessive left ventricular pressure load or
myocardial ischemia/infarction

Systolic thrill of MR (acute MR is associated
with thrill in one-half of cases)

Diastolic thrill of MS (uncommon- best felt
with the patient in the left lateral position)
2. Left parasternal edge: place the flat of your
Left parasternal lift: starts in early systole and
right palm (or the heel of your hand) is synchronous with the LV apical impulse
parasternally over the left parasternal edge (See theoretical notes for causes of left
and apply sustained and gentle pressure. Ask parasternal lift).
the patient to hold his breathing in expiration.
Systolic thrill of VSD or HCM

Diastolic thrill of AR (uncommon- best felt
along the left sternal border with the patient
leaning forwards and holding his breath after
expiration)
3. Upper left sternal edge using the flat or
Palpable P2 in pulmonary hypertension
ulnar border of the hand. Check for:
Thrill of PS, PDA, or ruptured congenital
sinus of Valsalva aneurysm

Palpable pulmonary artery pulsations in
pulmonary hypertension, increased
pulmonary blood flow (ASD) or poststenotic
pulmonary artery dilation.
4. Upper right sternal edge using the flat or
Systolic thrill of AS (may also be palpable at
ulnar border of the hand. Check for the apex, the lower sternum, or in the neck-
best felt with the patient leaning forwards
and holding his breath after expiration). N.B.
thrill of subclavian artery stenosis may be
heard over the subclavicular area.

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(8) AUSCULTATION
STEPS POSSIBLE FINDINGS
1. Listen at the apex with the diaphragm (time During auscultation at any area, identify and
with the right carotid). If you hear systolic describe the following:
murmur (probably MR) → repeat on
S1 & S2 (see theoretical notes for
expiration, listen at the axilla and feel for recognition and abnormalities of S1 & S2)
thrill. S1 Just precedes the carotid pulsation, and
2. Listen at the apex with the bell (using light S2 follows it):
pressure). Repeat with patient in left lateral  Normally both are low pitched, best
position and his breath held after expiration heard with the bell of the stethoscope
(If unsure about the presence of mid-diastolic  See theoretical notes for
murmur → you may ask the patient to touch
Extra sound that may precede S1 (see
her toes and then reclines 10 times). If you theoretical notes for features and causes):
hear mid-diastolic murmur (probably MS) → 1. S4
time with the carotid and feel for thrill
Extra sounds that may follow S1 (see
3. Reposition the patient and listen with the theoretical notes for features and causes):
diaphragm over the lower left sternal edge. 1. Ejection click
If you hear systolic murmur (probably 2. Non-Ejection Click of MVP
TR/VSD) time with the carotid, repeat on 3. Opening click of prosthetic AV
inspiration and feel for thrill.
Extra sounds that may follow S2 (see
4. Listen with the diaphragm over the upper theoretical notes for features and causes):
left sternal edge, and the upper right 1. S3
sternal edge. If you hear systolic murmur 2. Opening Snap
(probably AS/PS) → time with the carotid 3. pericardial knock
and feel for thrill. 4. Split S2
5. Auscultate both carotids (for bruits and 5. Opening Click of prosthetic MV
radiated murmurs)
Pericardial rub (occupies both systole and
6. Ask the patient to sit up and lean forwards diastole; quality is noisy)
with his breath held after expiration. Listen
Murmurs: see the following theoretical
over the right 2nd interspace and the left 3rd notes:
interspace. If you hear diastolic murmur  Innocent murmur
(probably AR) → time with the carotid and  Pathological murmurs
feel for thrill.  The grades of murmurs
7. Listen over the lung bases (for basal crackles  Systolic murmurs
and radiating murmurs) and check for sacral  Diastolic murmurs
oedema  Continuous murmurs
 Differentiation between murmurs of TR
and MR
 Secondary murmurs in valvular lesions

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(9) ADDITIONAL SIGNS

• Lower limb:
 Feel for ankle edema
 Palpate a peripheral pulse (pedal or posterior tibial)
 Check for saphenous vein harvest used in bypass surgery
 Check for differential cyanosis (cyanosis in LL rather than the UL is seen in PDA with PH)
 Glance at the groins for angiography scar/bruising and consider auscultating the femoral
artery for Duroziez’s sign (audible femoral bruits) and Traube’s sign (pistol shots), if you
suspect AR (see theoretical notes for peripheral signs of AR)
• Examine (or ask to examine) the Blood pressure particularly in patients with AS/AR (if you
suspect AR ask for both the brachial and the popliteal BP):
 Check that the sphygmomanometer is set at zero, and ensure you have the correct cuff size
(standard cuff will give falsely elevated readings with obese subjects)
 Support the patient's arm comfortably at about heart level, and apply the cuff to the upper arm
with the centre of the bladder over the brachial artery
 Inflate whilst palpating the brachial artery until the pulse is impalpable (this is the systolic
pressure by palpation)
 Inflate the cuff another 10-20 mmHg, and apply the stethoscope (bell or diaphragm) to the
brachial artery
 Deflate the cuff slowly (2 mmHg/sec.) whilst listening through the stethoscope over the
brachial artery.
 The point at which you hear the first Korotkoff sound is the systolic pressure, and the point at
which sound disappears (fifth Korotkoff sound) is the diastolic pressure. The fourth Korotkoff
sound (the point of muffling) is acceptable in patients in whom muffled sounds persist and do
not disappear.
 Record measurements to the nearest 2 mmHg
 Tell the examiner that you would also check for a postural fall in blood pressure
 Be alert to a wide pulse pressure (AR) and a narrow pulse pressure (AS)
 Be aware of the significance of differences > 15-20 mmHg in BP between upper and lower
limbs (coarctation of aorta)
• Palpate (or ask to palpate) the liver particularly in TR/CHF:
 Check for Pulsatile liver in TR especially if you have seen a large v wave and heard a pan-
systolic murmur over the tricuspid area, in such cases you may be able to demonstrate a
pulsatile liver by placing your left palm posteriorly and the right palm anteriorly over the
enlarged liver
 Check for tender liver in CHF

(10) THANK THE PATIENT AND COVER HIM (HER)

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THEORETICAL NOTES

TYPE OF CYANOSIS
• Central cyanosis blue tongue, lips, and extremities with warm peripheries (CHD, lung disease as
emphysema, pneumonia, ARDS, chronic bronchitis, sometimes CHF)
• Peripheral cyanosis (result from sluggish circulation in the peripheries) reduction in oxygenated
Hb occur in capillaries (extremities are blue & cold) etiologies: low CO, hypovolemic shock)
• Differential cyanosis (lower limb cyanosed, upper limb pink) in CHD: PDA with revered shunt
due to PHTN
• Reversed differential cyanosis. The cyanosis of the fingers exceeds that of the toes; seen in
transposition of the great vessels (blood from RV ejected into the AO reaches the upper limbs and
head, blood from LV ejected into PA reaches the lower limb via PDA)

GRADES OF EARLOBES CREASES (associated statistically with CAD in most population

groups):
• Grade 3= a diagonal crease in the lobule of the auricle (Frank's sign)
• Grade 2A= crease more than halfway across the lobe
• Grade 2B= crease across the whole lobe, but superficial
• Grade 1= lesser degrees of wrinkling.

ARACHNODACTYLY: abnormally long and slender fingers; usually associated with excessive
height and congenital defects of the heart and eyes in Marfan’s syndrome

OSLER’S NODES: small, tender, purplish erythematous skin lesions due to infected micro-emboli
and occurring most frequently in the pads of the fingers or toes and in the palms of the hands or soles
of the feet.

JANEWAY LESIONS: slightly raised, non-tender haemorrhagic lesions in the palms of hands and
soles of the feet

SPLINTER HAEMORRHAGES: are Janeway lesions occurring under the nail-beds

CAUSES OF ABSENT RADIAL PULSE:

• Congenital
• Traumatic
• Surgery (Blalock shunt, cardiac catheter)
• Systemic embolization (e.g. AF with MS)

COMPONENTS OF CAROTID PULSE:

Percussion wave: the shock wave transmitted up the elastic wall of the artery
Tidal wave: the forward-moving column of blood follows the percussion wave
and is normally palpable separately
Dicrotic notch: occurs with aortic valve closure

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ABNORMALITIES OF THE PULSE VOLUME AND CHARACTER:

Abnormality Causes
Large volume (bounding or hyperkinetic Large stroke volume:
pulse)  AR, bradycardia (e.g.,
CHB)
High cardiac output state:
 Physiological: exercise,
emotion, heat, pregnancy
 Pathological: fever,
sepsis, thyrotoxicosis,
anaemia, peripheral A-V
shunts, and Paget's
disease of bone
Large volume collapsing pulse: a large  Severe AR, PDA
volume pulse characterized by a short duration
with a brisk rise and rapid fall (due to rapid
diastolic run-off from the aorta)
Small volume or hypokinetic pulse (pulsus  HF
parvus)  Obstructive valvular
(AS/MS) or vascular
(PAD) disease
 Hypovolaemia (thin
thready pulse),
 Restrictive pericardial
disease
 During tachyarrhythmias
Small volume , slow-rising, “plateau”, or  Severe AS
“anacrotic” pulse (pulsus parvus et tardus):
slow rising pulse with a delayed percussion
wave and sometimes a palpable judder
“anacrotic notch” on the upstroke
Small volume collapsing pulse: there is a  Ventricular run off states:
quickly rising percussion wave but it is small MR (pulse in MR is
sometimes described as
jerky), VSD
Bisferiens "biphasic" pulse: has two systolic  Mixed AVD,
peaks separated by a distinct midsystolic dip occasionally in HCM
Jerky pulse: sharp early percussion wave due  HCM (pulse in HCM is
to rapid ejection followed by jerky late systolic sometimes described as
phase as the dynamic obstruction supervenes. bifid or bisferiens)
This is followed by a smaller and more slowly
rising wave "tidal wave" due to continued
ventricular ejection and reflected waves from
the periphery
Dicrotic pulse has two palpable waves, one in  Very low stroke volume
systole and one in diastole (in most normal states: DCM
persons, a dicrotic wave is not palpable)
Pulsus alternans: alternating large and small  Advanced HF (poor
volume beats in the presence of a regular prognosis)
rhythm; often initially noted when taking the  During or following
BP paroxysmal tachycardia
 For several beats
following a premature
beat in patients without
heart disease
Paradoxical pulse: an exaggerated decrease in  pericardial tamponade
pulse volume on inspiration, corresponding to  constrictive pericarditis
inspiratory decline of SBP > 10-15 mmHg  severe asthma

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HOW TO DIFFERENTIATE JVP FROM ARTERIAL PULSATION

JVP Arterial pulsation
Two peaks with rapid inward movement One peak with rapid outward movement
Impalpable and diminished by pressure at the Palpable and unaffected by pressure at the root of the
root of the neck neck
Has a definite upper level, which falls during Independent of respiration, abdominal pressure, and
inspiration, rises with abdominal pressure, and position of patient
varies with position of patient

MANOEUVRES TO CHECK FOR INVISIBLE JVP (LOW OR VERY HIGH JVP LEVELS)
 If JVP is invisible, check for a low level by:

pressing firmly on the liver (or the centre of the abdomen) for a few seconds after explaining
to patient (this transiently increases the JVP by 2-3 cm)

Lying patient more horizontally
 If JVP is still invisible, check for a very high level by:

Looking at earlobe (this may be oscillating with cardiac cycle)

Sitting the patient vertical

If the pressure is very high, the hand veins may be used as a manometer as they collapse when
the hand is held at the appropriate height above the right atrium.

NORMAL JVP
a wave: atrial contraction
c wave: closure of TV
x descent: atrial relaxation
v wave: passive filling of RA against closed TV
y descent: emptying of RA into RV upon opening of TV

ABNORMALITIES OF THE JVP:

Abnormal JVP Causes
Elevation (> 4 cm)  Volume overload
commonly HF (sustained
abdomino-jugular reflux)
 Pericardial effusion
(prominent "Y" descent)
 Pericardial constriction
(Kussmaul’s sign)
 SVC obstruction (non-
pulsatile)
 Pulmonary embolism
Systolic V wave (cV wave): synchronous with the  TR (rapid y descent)
carotid pulse and sometimes oscillate the earlobe,
and usually associated with peripheral edema and
pulsatile liver
Prominent a wave (comes before the carotid  TS or PS
pulsation)  Pulmonary hypertension
(MVD, corpulmonale)
Cannon (giant a) wave (AV dissociation)  Irregular: CHB
 Regular: nodal rhythm,
VT, or ventricular paced
rhythm
absent a wave  AF

Steep x descent  Constrictive pericarditis

 Tamponade
 Restrictive CM
Inspiratory filling (Kussmaul’s sign)  Constrictive pericarditis
 Tamponade
 Severe asthma

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ABNORMALITIES OF THE APEX BEAT:

Abnormal apex beat Causes
Impalpable apex beat  Overweight or muscular subjects
 Asthma or emphysema
 Pericardial effusion or dextrocardia
Displaced apex  Chest deformity (scoliosis, pectus excavatum)
 Mediastinal shift: (in these situations trachea may also be deviated)

Large pleural effusion, tension pneumothorax (mediastinal shift
away from the affected side)

Pneumonectomy or lung collapse (mediastinal shift towards the
affected side)
 LV dilatation:

Volume overload (AR, MR, ASD)  apex beat diffusely
displaced inferiorly and laterally (hyperdynamic)

DCM
Hyperdynamic (lifting,  Volume overload: AR, MR, ASD (displaced inferiorly and laterally)
Thrusting): vigorous but not
sustained
Sustained (heaving):  Pressure overload: AS, hypertension (minimally displaced)
vigorous and sustained
Tapping impulse (Palpable  MS
S1)
Double impulse (two apical  HCM: due to palpable presystolic atrial impulse "palpable LA gallop"
pulsations with each heart (On occasion, a triple impulse may be palpable, due to a late systolic
beat) bulge that occurs when the dynamic obstruction is marked)
 Ventricular aneurysm: due to accentuated outward movement in late
systole "LV dyskinesia"

SUGGESTING VALVE ABNORMALITIES ACCORDING TO APEX DISPLACEMENT AND

PULSE VOLUME (BEFORE AUSCULTATION):
• Displaced apex + large volume pulse  AR
• Displaced apex + small volume pulse  MR
• Undisplaced apex + small volume pulse  AS
• Undisplaced apex + small volume pulse + AF  MS

CAUSES OF LEFT PARASTERNAL LIFT

1. RVH of any cause, e.g. PH (MVD, corpulmonale, ASD) or PS → RV sustained impulse (RV
heave), which starts in early systole and is synchronous with the left ventricular apical impulse. It
is frequently associated with prominent a wave (and giant v wave if there is secondary TR)
2. Anterior displacement of the right ventricle by an enlarged left atrium in severe mitral
regurgitation causes a left parasternal lift, which occurs distinctly later than the left ventricular
apical impulse

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RECOGNITION OF S1 & S2:

1) Normally both are low pitched, best heard with the bell of the stethoscope
2) The interval S2—S1 (diastole) is longer than S1—S2 (systole)
3) Timing: S1 with the upstroke of carotid pulse & S2 with its descent
4) Quality: S1 is lower in pitch & longer in duration than S2

ABNORMALITIES OF S1:
• Loud S1: mobile MS, hyperdynamic states, tachycardiac states, short PR interval, loud
tricuspid component (L-R shunt, Epstein’s anomaly)
• Soft S1: immobile MS, hypodynamic states, MR, poor ventricular function (HF), long PR
interval
• Wide splitting (normally single or narrowly split): RBBB, LBBB, VT, deep inspiration
• Variable S1: AF, CHB
• Metallic S1: metallic closing click of prosthetic MV

ABNORMALITIES OF S2:
• Loud S2: Hypertension, tachycardia states, loud P2 (PH, ASD)
• Soft S2: severe AS
• Persistent splitting: delayed P2 (RBBB, PS, deep inspiration), early A2 (MR)
• Fixed splitting: ASD
• Single S2: inaudible A2 (severe AS, large VSD), inaudible P2 (severe PS, F4, pulmonary atresia,
elderly, complete TGA), synchrony of A2 & P2 (Eisenmenger’s)
• Reversed splitting: delayed A2 (LBBB, AS, HCM), early P2 (RV pacing, PDA, WPW type B)
• Metallic S2: metallic closing click of prosthetic AV

EXTRA SOUND THAT MAY PRECEDE S1

Extra sound Features Causes
1. S4: produced in the  Precedes S1 (presystolic)  LV S4: HTN, AS, LVH,
ventricle during late  Low pitched (best heard amyloid, HCM, IHD,
ventricular filling, due with the bell of the acute MI, and acute MR.
to the atrial contraction stethoscope)  RV S4: RVH secondary
that fills a stiff  LV S4 is loudest at the to either PS or PH
ventricle apex
 RV S4 is loudest over the
left sternal border
 S4 is Absent in patients
with atrial fibrillation

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EXTRA SOUND THAT MAY FOLLOW S1

Extra sound Features Causes
1. Ejection click: occurs due to  Closely follows S1 (in  Aortic EC is heard in
semi-lunar valve stenosis or early systole) AS & some
dilation of the aorta or  Sharp (clicky), high- congenital heart
pulmonary artery pitched disease
 Aortic EC is heard best  Pulmonary EC is
at the apex and the heard in PS & PH
second right intercostal
space (first aortic area)
 Pulmonary EC is loudest
at the upper left sternal
border (pulmonary area).
 Usually followed by
ESM (lub-k-voo-dub)
2. Non-ejection (mid systolic)  May be single or  MVP
click: probably result from multiple, and may occur  Tricuspid valve
chordae tendineae that are at any time in systole but prolapse
functionally unequal in length on usually later than the EC
either or both AV valves  Heard best along the
lower left sternal border
and at the apex.
 Occurs with or without a
late systolic murmur
3. Opening click of prosthetic AV  Prosthetic AV

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EXTRA SOUNDS THAT MAY FOLLOW S2

Extra sound Features Causes
1. Split S2: splitting occurs  Heard best at the pulmonary area  Normal finding
normally during inspiration, & may be along the left sternal with inspiration
when the augmented inflow border  Persistent splitting
into the RV increases its SV that is wider during
and ejection time and thus inspiration than
delays closure of the during expiration
pulmonic valve. Splitting occurs due to either:
that persists with expiration
Delayed P2
is usually abnormal. (RBBB, PS, PE,
RVF, ASD)

Early A2 (MR)
 Wide fixed splitting
(ASD)
2. S3: produced in the  Low pitched (more muffled than  Normal finding
ventricle due to rapid S2 - best heard with the bell of in children
ventricular filling the stethoscope)  abnormal in
 S2—S3 interval is longer than adults &
A2—P2 interval (help in indicates either:
differentiating S3 from split S2)
HF
 LV S3 is best heard at the apex
The ventricle
 RV S4 is best heard at the left fills rapidly
sternal border or just beneath the with a large
xiphoid and is often accompanied volume (L-R
by the systolic murmur of shunt, MR,
functional TR. AR, TR)
3. Pericardial knock:  Earlier and higher-pitched than S3  Constrictive
occurs due to abrupt pericarditis
cessation of diastolic
filling that occurs when
further ventricular
relaxation is impeded by
the rigid pericardium
4. Opening snap  Brief, high-pitched (snappy)  MS
 Early diastolic  TS
 Best heard at the lower left
sternal border and radiates well to
the base of the heart. However, it
may be heard all over the
precordium (wide propagation)
 Nearly always followed by a
diastolic rumble (lub-ta-ta-roo)
 Distance from S2 is variable
according to severity of the MS,
but always longer than A2—P2
and shorter than S2—S3
 In the second intercostal space,
an OS is often confused with P2.
However, careful auscultation
will reveal both components of
S2, followed by the OS (lub-ta-
ta).
 The OS of TS occurs later in
diastole than the mitral OS and is
often overlooked in patients with
more prominent mitral valve
5. Opening click of   Prosthetic MV
prosthetic MV

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INNOCENT MURMUR:
 Ejection systolic
 Between LSE and pulmonary area, occasionally apical
 No thrill, added sounds, or cardiomegaly
 Normal ECG, CXR and echocardiography

PATHOLOGICAL MURMURS are either organic (valvular or subvalvular) or functional (dilated

valve ring or increased flow through the valve). Characteristics of pathologic murmurs include
 A sound level of grade 3 or louder
 A diastolic murmur
 An increase in intensity when the patient is standing

THE GRADES OF MURMURS: murmurs are graded on a scale from I to VI.

 A grade I is soft intermittent murmur that is usually heard only with special manoeuvres
 A grade IV is a palpable murmur (accompanied by a thrill)
 A grade VI is a murmur that can be appreciated without a stethoscope.

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SYSTOLIC MURMURS
Site of maximal Cause features
intensity
Systolic murmur with 1. MR  Timing: pan-systolic; starts at S1 (S1 may be
maximal intensity muffled by the murmur) and reaches up to S2
over the apex and (not a must)
propagated to the  Quality: blowing (high pitched & clear); of
axilla more than to the uniform intensity
sternum  MR caused by MVP  late systolic murmur,
usually preceded by mid systolic click
Systolic murmurs with 1. TR,  Timing: pan-systolic
maximal intensity  Quality: high pitched; blowing
over the lower left  increased with inspiration (due to negative
sternal border and intra-thoracic pressure that suck more blood
may propagate to the to the RA & RV)
axilla 2. VSD  Timing: pan-systolic but sometimes short
(early to mid-systolic) as in cases of VSD
associated with pulmonary hypertension or
small VSD in the muscular part of the septum
 Quality: harsher & usually associated with
thrill
3. Innocent murmur  Timing: short (early to mid-systolic)
of childhood  Quality: buzzing (musical vibratory), soft
(Still’s murmur) (grade 2) with uniform medium pitch
Systolic murmurs with 1. AS  Timing: mid-systolic of long duration
maximal intensity  Quality: Harsh diamond-shape (crescendo-
over the Aortic area decrescendo)
(2nd right ICS)  In early cases, cusps are mobile (although
thickened & fibrosed)  ejection click
precedes the ESM
 Increased severity of AS  increased
duration of the murmur with muffling of S2
(due to rigid calcified valve)
 Murmur is selectively propagated to the neck
& also to the apex
2. Functional ESM as  Timing: mid-systolic
in case of:  Quality: diamond-shape (crescendo-
 Hyperdynamic decrescendo)
circulation  In hypertension & aortic aneurysm, it’s
 Hypertension associated with accentuated, ringing S2
 Aortic aneurysm.
Systolic murmurs with 1. Congenital PS  Timing: mid-systolic of long duration
maximal intensity  Quality: Harsh diamond-shape (crescendo-
over the pulmonary decrescendo)
area (2nd left ICS)  Associated with split S2 and muffled P2
 When PS is a part of TOF, it’s associated
with single S2 (A2 only).
2. Functional ESM  Timing: med-systolic; very short murmur
as in case of:  Quality: diamond-shape (crescendo-
1. Hyperdynamic decrescendo)
circulation  Associated with normal S2
2. increased flow
across pulmonary
valve (e.g. ASD)
3. Pulmonary
hypertension

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DIASTOLIC MURMURS
Site of maximal intensity Cause features
Apical mid- 1. Organic MS (due to  Timing: mid-diastolic;
diastolic/pre-systolic narrowing of the valve) separated from S2
murmurs (heard with  Quality: Always of low
the bell of the pitch (rumbling)
stethoscope using light  Preceded by opening snap
pressure) and accentuated S1
 Tight lesion → increased
duration of the murmur,
till it reaches S1, with
presystolic accentuation
due to atrial contraction
 If associated with AF →
no effective atrial
contraction → no
presystolic accentuation &
the murmur is variable in
length from beat to beat
2. Relative (functional)  Timing: mid-diastolic;
MS (due to increased separated from S2
blood flow across the  Quality: Always of low
valve) as in case of: pitch (rumbling)
 MR  No opening snap and S1 in
 L-R shunt (VSD, normal (not accentuated)
PDA)
 AR (Austin Flint
murmur)
Diastolic murmurs with 1. Aortic regurgitation  Timing: early diastolic
maximal intensity over  Quality: very high pitched;
the aortic areas (2nd decrescendo murmur
right ICS & 3rd left  Associated with peripheral
ICS) signs of AR (see below)
 if AR is due to Syphilis, S2
will be ringing
Diastolic murmurs with 1. Pulmonary  Timing: early diastolic
maximal intensity over regurgitation (more  Quality: very high pitched;
the pulmonary area commonly caused by decrescendo murmur
(2nd left ICS) aortic regurgitation  Associated with signs of
murmur propagated pulmonary hypertension
from the aortic area) (see below)

CONTINUOUS MURMURS
Continuous murmurs should be differentiated from combined ESM & early diastolic murmur
associated with double aortic valve disease; especially if murmurs of AS & AR are prolonged &
fill the whole cardiac cycle (To & fro murmur)
1. PDA: gives continuous murmur differentiated from those of double AVD by being only one
murmur continuous all over the cardiac cycle with maximal intensity at S2 and minimal
intensity at S1. It sounds like a machine, so called machinery murmur
2. Venous hum: only heard over the neck and disappears on pressure over the root of the neck
3. Mammary soufflé: only heard over the lactating breast due to associated A-V shunting.

DIFFERENTIATION BETWEEN MURMURS OF TR AND MR: murmur of TR can mimic that

of MR (particularly in case of severe pulmonary hypertension, when a very large RV displaces the LV
posteriorly). However, the murmur of TR is differentiated by:
• Best heard at the lower left sternal border, and not heard at the axilla or over the spine.
• Increases with inspiration
• Giant v wave in the neck and pulsatile liver

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SECONDARY MURMURS IN VALVULAR LESIONS:

Valvular lesion Basic Murmur Secondary murmur
Aortic Incompetence basal early diastolic murmur apical mid diastolic murmur
(Austin flint) due to the aortic
regurgitant jet striking the
AML, restricting the mitral
inflow
MS apical mid diastolic murmur basal early diastolic murmur
(Graham Steel) due to
pulmonary artery dilatation in
pulmonary hypertension
complicating MS
sever mitral regurgitation mid-diastolic flow murmur
(without MS) (without OS) might be audible
at the apex
significant aortic regurgitation Systolic flow murmur (without
(without AS) EC) might be audible at the
heart base.

PERIPHERAL SIGNS OF AORTIC REGURGITATION: these signs are present only in severe
chronic aortic incompetence and are usually not clinically helpful.
Head 1. De Musset sign—head nodding in time with the heartbeat
2. Müller sign—pulsation of the uvula in time with the heartbeat
Neck 3. Corrigan sign—forceful carotid upstroke with rapid decline
UL 4. Collapsing radial pulse (water hammer pulse) (Corrigan’s pulse)
5. Quincke sign—marked capillary pulsation in the nail beds, with blanching during
diastole with mild nail pressure
LL 6. Duroziez sign—systolic and diastolic bruit over the femoral artery (to and fro
murmur) on gradual compression of the vessel by the stethoscope bell
7. Traube sign—a double sound heard over the femoral artery on compressing the
vessel distally; this is the “pistol-shot” sound that may be heard with very severe
aortic regurgitation
LL in 8. Hill sign—increased blood pressure in the legs compared with the arms (≥30 mm
relation to Hg discrepancy)
UL

AUSCULTATORY SIGNS OF PULMONARY HYPERTENSION

 Closely split S2 with accentuated P2
 Ejection click
 Functional ESM
 Early diastolic murmur at the LLSB due to dilatation of the pulmonary valve ring

MIXED MVD: WHICH IS DOMINANT?

Dominant MR Dominant MS
Apex beat displaced, and thrusting Apex beat is not displaced, and tapping
S1 muffled S1 Loud
S3 rather than OS OS rather than S3
ECG: LVH, LAD Loud dominant mid-diastolic murmur
Evidence of severe PH

MIXED AVD: WHICH IS DOMINANT?

Dominant AR Dominant AS
Pulse is Collapsing Pulse is slow rising
Apex is thrusting, displaced Apex is heaving, not displaced much
High systolic BP and wide pulse pressure Systolic thrill and loud, harsh systolic murmur
Low systolic BP and narrow pulse pressure

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CAUSES OF SPECIFIC VALVULAR LESIONS

Mitral Aortic
Stenosis  RHD, and rarely IE  RHD, and rarely IE
 Congenital (rare)  Congenital bicuspid valve (usually
 Carcinoid male; presents in sixth decade)
 Connective tissue disease  Degenerative calcification (elderly)
(SLE)  Sub-valvular: HCM, sub-aortic
 Mucopolysaccharidoses membrane stenosis
(glycogen deposits on cusps)  Supra-valvular: coarctation of aorta,
 Senile degeneration and conditions of accelerated
calcification, e.g. William’s syndrome,
Paget’s disease, ESRD.
Regurgitation  RHD, IE  RHD, IE
 MVP  Connective tissue disease: Marfan’s,
 IHD (papillary muscle rheumatoid, SLE, ankylosing
dysfunction) spondylitis, Reiter’s, Hurler’s,
 Dilated LV (functional MR) pseudoxanthoma elasticum
 Connective tissue diseases  Syphilitic aortitis
(Marfan’s)  Aortic dissection / trauma
 Infiltration (amyloid)  Hypertension
 Associated with ASD  Bicuspid AV
(primum) or HCM  Ruptured sinus of valsalva aneurysm
 VSD with prolapse of right coronary
cusp

SIGNS OF SEVERITY OF SPECIFIC VALVULAR LESIONS

Mitral Aortic
Stenosis  Early OS (< 60 msec from S2)  Slow rising pulse with
 Long diastolic murmur (extends narrow pulse pressure
throughout diastole)  Systolic thrill
 Signs of pulmonary hypertension (loud P2,  Soft single S2 or
RV heave, TR, PR) paradoxically split
 SPAP > 50 mmHg  Late peaking long
 Valve area < 1 cm murmur
 Pressure gradient > 10 mmHg  Signs of LVF
 Orifice area < 1 cm
 Pressure gradient > 40
mmHg
Regurgitation  Displaced apex  S3
 Systolic thrill  Lengthening diastolic
 S3 murmur
 Mid-diastolic flow murmur  Austin Flint murmur
 Signs of pulmonary hypertension (loud P2,  Diastolic blood pressure <
RV heave, TR, PR), or pulmonary 40
congestion  Pulse pressure > 100

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INDICATION OF SURGERY IN SPECIFIC VALVULAR LESIONS

Mitral Aortic
Stenosis 1) Severe MS (valve area < 1 cm) + any of 1) severe AS + any of the
the following: following:
 symptoms: dysponea NYHA III or IV  Symptoms
 Pulmonary hypertension (SPAP > 60  Patient undergoing CABG or
mmHg) surgery on the aorta or other
 MV repair may be considered in heart valves
patient with recurrent embolic events  EF < 50%
while receiving adequate  May be considered in
anticoagulation and who have valve asymptomatic patient if valve
morphology favorable for repair area < 0.6 cm, gradient > 60
2) Moderate MS (valve area < 1.5 mmHg or abnormal response
cm) + either symptoms or recurrent to exercise
embolic events 2) Moderate AS in patient
undergoing CABG or surgery
on the aorta or other heart
valve
Regurgitation 1) Severe MR + either: 1) Severe AR + either:
• Symptoms (NYHA II or greater) • Symptoms
• EF 30 - 60 % (implies marked LV • Patient undergoing CABG or
dysfunction as it should be above surgery on the aorta or other
normal in chronic MR) – less heart valve
favourable if EF < 30 % • EF 25-50 % (less favourable if
• LVESD ≥ 40 mm (less favourable if EF < 25%)
LVESD > 55) • LVESD > 50 - 55 mm
• Acute sever MR • LVEDD > 70 - 75 mm
• It is reasonable for asymptomatic • Acute severe AR
patient in experienced surgical centre 2) Moderate AR in patient
• SPAP > 50 mmHg undergoing CABG or surgery on
• New onset AF the ascending aorta

INDICATIONS OF AORTIC BALLOON VALVULOPLASTY

• Paediatric congenital AS
• Palliative for elderly with co-morbidities or before non cardiac surgery

TREATMENT OF MS WITH MITRAL BALLOON VALVULOPLASTY REQUIRES ALL

THE FOLLOWING:
• Leaflet tips and chordae are not heavily distorted, thickened or calcified
• Cusps are mobile at the base
• No or mild MR
• No LA thrombus on TEE

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CNS- General
CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Physical examination

Where appropriate, assesses higher cortical function, tests cranial
nerves in sequence including optic fundi and visual fields Clear Pass Fail Clear

Appropriately assesses motor function in limbs (tone, power, Pass Fail
pinprick, vibration sense, proprioception, temperature) and □ □ □ □
coordination/ cerebellar function

Assesses gait if appropriate
2. Identification and interpretation of physical signs
Clear Pass Fail Clear

Identifies abnormal physical signs correctly
Pass Fail

Interprets signs correctly
□ □ □ □

Makes correct diagnosis
3. Discussion related to the case Clear Pass Fail Clear

Familiar with appropriate investigation and sequence Pass Fail

Familiar with appropriate further therapy and management □ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

Instructions in the CNS case may request one of the following:

1. Examine the CNS (General)…see below

2. Examine the lower limb (neurologically)…see Ch 6. CNS-Lower Limb

3. Examine the upper limb (neurologically)… see Ch 7. CNS-Upper Limb

4. Examine the cranial nerves… see Ch 8. CNS-Cranial Nerves

5. Examine the gait… see Ch 9. CNS-Gait

6. Examine the speech and higher cerebral functions… see Ch 10. CNS-Speech & Higher Cerebral
Functions

7. Examine the cerebellar system… see Ch 11. CNS-Cerebellar

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CNS – GENERAL
STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him
• Expose the upper and lower limbs completely and keep the patient descent (genital area is covered)

(2) GENERAL INSPECTION: see “Ch 6. CNS – Lower Limb”

(3) EXAMINATION OF LOWER LIMBS (you may wish to start with the lower limb rather than the
upper limb as it takes shorter time and gives more information): see “Ch 6. CNS – Lower Limb”

(4) EXAMINATION OF UPPER LIMBS: see “Ch 7. CNS – Upper Limb”

(5) CRANIAL NERVES: see “Ch 8. CNS – Cranial Nerves”

(6) GAIT AND ROMBERG’S TEST: ask the examiner’s permission to examine the patient’s gait and
perform Romberg’s test: see “Ch 9. CNS – Gait”

(7) ADDITIONAL SIGNS: according to diagnosis, for example:

• Look for cataract and scar for pacemaker, palpate for local spinal tenderness and examine for sensory
level
• Tell the examiner that you would normally extend your examination to perform … (mention what is
missed in your examination because of lack of time) and woud ask about swallowing (Dystrophia
myotonica), bladder symptoms, test the anal tone (spinal cord syndrome), and to dipstick urine for
DM.

(8) THANK THE PATIENT AND COVER HIM (HER)

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CNS -1- LOWER LIMB

STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him
• Expose the lower limbs completely and keep the patient descent (genital area is covered)

(2) GENERAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Scan the bedside.
Walking stick, shoes-callipers, built-up heels
2. Scan the patient.
Nutritional status: under/average built or overweight

Abnormal facies: Sad, immobile, unblinking facies
(Parkinson’s disease), facial wasting (muscular dystrophy),
facial asymmetry (hemiplegia)

Abnormal movement or posture: rest or intention tremors,
dystonia, choreoathetosis, hemiballismus, myoclonic jerks,
tics, pyramidal posture…see theoretical notes for description,
types, features and causes of abnormal movements

Abnormal facial movements: hemifacial spasm, facial
myokymia, blepharospasm, oro-facial dyskinesia

Scar or deformity underlying an ulnar nerve palsy

Peroneal wasting (Charcot-Marie-Tooth disease)

Pes cavus (Friedreich’s ataxia, Charcot-Marie-Tooth disease)
3. Examine the eyes
Nystagmus (cerebellar syndrome)

Horner’s syndrome (syringomyelia, Pancoast’s syndrome)
4. Examine the hands: tell the
wasted hands (MND, Charcot-Marie-Tooth disease,
patient “outstretch your hands syringomyelia)
like this (dorsum facing
AF → consider thromboembolic complications
upwards)”… then “like this
(palms facing upwards)”…
demonstrate. Feel the radial
pulse for AF

(3) INSPECTION OF THE LOWER LIMB

Steps Possible findings
1. Scan the lower limb.
Muscle bulk: Look specifically for:
2. Note specifically the  Generalized disuse atrophy (e.g. severe spastic paraparesis)
quadriceps, the anterior  Unilateral loss of muscle bulk (old polio)
compartment of the shin,  Distal muscle wasting with preservation of the thigh muscle
the extensor digitorum bulk (inverted champagne bottle) → Charcot-Marie-Tooth
brevis, and the peroneal disease
muscles.  Isolated anterior thigh wasting (e.g. diabetic amyotrophy)
3. Compare right with left  Proximal muscle wasting (polyomyositis)
 Wasting confined to one peroneal region (lateral popliteal =
common peroneal nerve palsy)

Fasciculations: irregular twitches under the skin overlying muscle
at rest; represent contraction of a motor unit. They occur in LMNL;
usually in wasted muscles (nearly always indicate MND). Flicking
the skin over wasted muscle may elicit fasciculations. Non-
pathological fasciculations occasionally occurs after vigorous
exercise in healthy people.

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(4) TONE
Steps Possible findings
1. Tell the patient “Let your legs go loose and let me move
Normally there is light resistance
them for you” through whole range of
2. Roll the extended leg on the bed, rotating the hip externally movements.
and internally (compare right with left)
Normally the heel will lift
3. Put your hand behind the knee and lift it rapidly (feel for any minimally off the bed when the
catch; watch the heel) and let it drops (compare right with knee is lifted quickly
left)
See theoretical notes for
4. Hold the knee and ankle. Passively flex and extend the leg at abnormalities of the tone
the knee and hip joints repeatedly in an irregular and
unexpected rhythm (compare right with left)

(5) POWER
Steps Possible findings
Tell the patient “I am going to test the strength of Describe any weakness in terms of the medical
some of your muscles”. Fix the joint proximal to research council (MRC) scale from 5 (normal)
the group of muscles you are testing. Give the down to 0 (no visible muscle contraction)…see
patient a space to show his power before resisting theoretical notes for the MRC scale for power
him and look at the muscle contracts. Compare grading
right with left
1. Hip flexion: tell the patient “keep your leg Action by the iliopsoas (supplied by the femoral
straight and lift it up into the air. Now keep it nerve & direct branches from the lumbar sacral
up and don’t let me push it down” plexus; L1,2)
2. Hip extension: tell the patient “now push your Action by the glutei (supplied by the inferior gluteal
leg down into the bed and do not let me stop nerve; L4,5)
you”
3. Hip abduction: tell the patient “push out Action by the glutei (supplied by the superior
against my hands” gluteal nerve; L4,5)
4. Hip adduction: tell the patient “push in against Action by the adductor group (supplied by the
my hands” obturator nerve; L2,3,4)
5. Knee flexion: hold the patient’s ankle and tell Action by the hamstrings (supplied by the sciatic
him (her) “bend your knee and pull your heel nerve; L5,S1,2)
towards you; don’t let me stop you”
6. Knee extension: tell the patient “now Action by the quadriceps (supplied by the femoral
straighten your knee out and push my hand” nerve; L3,4)
7. Ankle dorsiflexion: tell the patient “pull your Action by the tibialis anterior and long extensors
foot up to you and push my hand” (supplied by the deep peroneal nerve; L4,5)
8. Ankle planter flexion: tell the patient “push Action by the gastrocnemius (supplied by the
your foot down against my hand” posterior tibial nerve; S1)
See theoretical notes for:
 Features & causes of the different patterns of weakness
 Clinical approach to weakness
 Motor root values in the lower limb
 Examples of mononeuropathies and radiculopathies in the lower limb

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(6) REFLEXES
Steps Possible findings
Explain to the patient. Use a long tendon hammer; flex your Grade the response from 0 (absent) up to
wrist and let the hammer fall with its own weight onto the 4+ (clonus)… see theoretical notes for
muscle. Compare right with left. If the reflex appears to be reflexes grading
absent, ask the patient to clench his teeth as you swing the
hammer (reinforcement).
1. Knee reflex: place the arm under the knee so that the Reflex arc through the femoral nerve;
knee is at 90 degrees. Strike the knee below the patella; L3,4
watch the quadriceps
2. Knee (patellar) clonus: with the knee extended, sharply A rhythmic contraction may be noted. It is
push the patella downwards with your thumb and always abnormal and indicates 4+ knee
forefinger, sustaining the pressure for a few seconds. Do reflex grading
not examine for knee clonus (as it is not expected to be
present) if knee reflex is diminished
3. Ankle reflex: hold foot at 90 degrees with a medial Reflex arc through the tibial nerve; S1,2
malleolus facing the ceiling. The knee should be flexed
and lying to the side. Strike the Achilles tendon directly.
Watch the muscles of the calf
4. Ankle clonus: support the patient’s leg with both the A rhythmic contraction may be noted.
knee and ankle resting in 90 degree flexion. Briskly More than three beats is abnormal and
dorsiflex and partially evert the foot and sustain the indicates 4+ ankle reflex grading.
pressure. Do not examine for ankle clonus (as it is not
expected to be present) if ankle reflex is diminished.
5. Plantar response (Babinski’s sign): Explain to the
Reflex arc through S1,2
patient: “I am going to scrape the bottom of your foot”.
always describe the response as either
Using a blunt object (orange stick, the end of the reflex downgoing, i.e. all the toes flex
hammer or car key), gently scrape the lateral portion of towards the plantar surface, or
the sole beginning near the heel and moving up towards upgoing where the big toe extends
the little toe then across the foot pad to the base of the dorsally (goes up), while the four
big toe. Watch the big toe and the remainder of the foot. small toes fan and turn towards the
N.B. Alternative stimuli to elicit the plantar response: sole

Chaddock’s manoeuver: scrape the lateral portion of the
See theoretical notes for patterns of
dorsum of the foot beginning near the lateral malleolus planter response
and moving up towards the little toe

Oppenheim’s sign: with your thumb and index finger,
press heavily from above downwards along the medial
aspect of the tibia

Gordon’s reflex: pinch the Achilles tendon
6. Abdominal reflexes: the patient should be supine and
Normal response is contraction of the
relaxed. Using an orange stick lightly scratch the recti with the umbilicus moving away
abdominal wall towards the umbilicus in the four from the direction of the scratch.
quadrants of the stomach.
Afferent: segmental sensory nerves

Efferent: segmental motor nerves

Roots: T8,9 above the umbilicus, and
T11,12 below the umbilicus

Abdominal reflexes are absent in
UMNL above their spinal level, and in
LMNL affecting T8-12.

It is often impossible to elicit
abdominal reflexes in anxious patients,
elderly, obese, multiparous women,
and those who have had abdominal
surgery
See theoretical notes for abnormal tendon reflexes, and the root values for reflexes

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(7) COORDINATION:
Steps Possible findings
1. Heel-shin test: the patient is lying supine. Tell the
In cerebellar lower limb ataxia, the
patient “Lift your leg and place the point of your heel on patient has difficulty placing or
your knee and then run it down the sharp part of your holding the heel on the opposite knee
shin; now up your shin, now down again…etc.” or cannot keep the heel firmly on the
(Demonstrate). Consider repeating the test while the tibia as the heel is moved downwards.
patient’s eyes are closed to test for sensory ataxia.
Sensory ataxia is similar to cerebellar
Compare right with left. Expect the right leg to be ataxia but is markedly worse when the
slightly better in right handed persons eyes are closed
2. Rapid repeated movements: Tell the patient “tap your
Bradykinesia: slowed movements or
foot quickly on my hand as if listening to fast music” break up easily – extrapyramidal sign
(demonstrate). Compare right with left. Expect the right
Dysrhythmia: inability to keep a
leg to be slightly better in right handed persons rhythm - cerebellar sign
3. Truncal ataxia: ask the patient to sit up with the arms
Truncal ataxia is caused by
folded or to rise from a chair with the feet together abnormalities of the midline
cerebellar vermis or the
flocculonodular lobe. It is usually
associated with gait ataxia and
symmetric nystagmus in absence of
limb incoordination
N.B. do not assess coordination if power < 3 (inability to move against gravity), and tell the examiner that
coordination cannot be assessed due to weakness
See theoretical notes for types of ataxia and causes of cerebellar ataxia

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(8) SENSATION
Steps Possible findings
1. Pin prick:
Reduced sensation over

Demonstrate the stimuli to the patient by testing on the sternum the lateral foot → tibial
(use each end of the hat pin): explain to the patient “this is nerve or S1 lesion
sharp…and this is blunt…now I’m going to test the sensation in
Reduced sensation over
your legs and I want you to close your eyes and say “Sharp” if it the medial foot →
feels sharp, and “blunt” if it feels blunt”. common peroneal nerve

Start distally and move proximally testing over each or L5 lesion
dermatome (and each main nerve): lateral foot → medial foot →
Reduced sensation over
outer calf → inner calf → inner thigh → outer thigh → inguinal the outer calf →
region. Repeat in the other leg then compare right with left common peroneal

Map out the boundaries of any area of reduced, absent or nerve or L5 lesion
increased sensation; starting from the area of altered sensation
Reduced sensation over
and moving towards normal to find the edges, noting any the inner calf → L4
difference between the two sides. lesion

If a stocking sensory loss is present, demonstrate that the
Reduced sensation over
sensory loss is present right round the limb. the inner thigh → L3

If compression of the cord is suspected, then demonstrate a lesion
sensory level.
Reduced sensation over
2. Light touch: the outer thigh → lateral

Demonstrate “I am going to touch you with this piece of cotton cutaneous nerve of the
wool and I want you to close your eyes and say (Yes) every time thigh or L2 lesion
you feel it”. Avoid dragging it across the skin or tickling the
Reduced sensation over
patient. Time the stimuli irregularly to check the patient the inguinal region →
reliability. L1lesion

Start distally and move proximally testing the lower limb in the
same sequence as for pin prick
3. Joint position sense:

Demonstrate: fix the proximal phalanx of the patient’s big toe
with one of your hands. Hold the lateral aspects of the distal
phalanx of the patient’s big toe between the thumb and index
finger of your other hand. Ensure that your thumb and index
finger are at 90 degrees to the intended direction of movement.
Tell the patient “I’m going to move your finger up and down; this
is up (move finger up)…, and this is down (move finger
down)…now close your eyes and tell me whether I am moving
your finger up or down”.

Start with the IP joint of big toe. If impaired, move to more
proximal joints progressively (IP → MTP → ankle → knee →
hip).
4. Vibration sense: N.B. vibration sense is

Demonstrate: use a 128 Hz tuning fork. Make the fork vibrate commonly reduced or absent
and place it on the sternum. Ask the patient “Do you feel it in elderly patients
vibrating (buzzing)?”

Tell the patient “Close your eyes”. Make the fork vibrate silently
and place it on the terminal phalanx of the big toe just below
the nail bed and ask the patient “Can you feel it now?” If patient
cannot feel the vibration, move progressively to more proximal
joints (terminal phalanx of the big toe → MTP joint → medial
malleolus → tibial tuberosity → ASIS).
See theoretical notes for:
 Modalities and tracts of sensation
 Patterns, causes and clinical approach to sensory loss

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(9) GAIT AND ROMBERG’S TEST: ask the examiner’s permission to examine the patient’s gait and
perform Romberg’s test (see Ch 9. CNS – Gait).

(10) ADDITIONAL SIGNS: according to diagnosis, e.g.

• Look for cataract and scar for pacemaker, palpate for local spinal tenderness and examine for sensory
level
• Tell the examiner that you would normally extend your examination to examine the upper limb and
cranial nerves and woud ask about swallowing (Dystrophia myotonica), bladder symptoms, test the
anal tone (spinal cord syndrome), and to dipstick urine for DM.

(11) THANK THE PATIENT AND COVER HIM (HER)

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THEORETICAL NOTES

HOW TO DESCRIBE AN ABNORMAL MOVEMENT: abnormal movements are described according

to the following fundamental characteristics:
• Is the movement present at rest (rest tremors), with holding of a posture (postural tremors), or during a
skilled movement (action or intention tremors)
• Is the movement disorder global (generalised dystonia), focal (focal dystonia), unilateral, or confined
to one limb
• Is the movement disorder predominantly distal (choreoathetosis) or proximal (hemiballismus) in the
limb
• Is the movement sinuous (choreoathetosis), twitchy (myokymia), or shock like (myoclonus)
• Does the limb hold abnormal postures for several seconds (dystonia)

TYPES OF ABNORMAL MOVEMENTS

1. Tremors (rest tremor, postural tremor, action tremor, intention tremor)
2. Asterixis
3. Dystonia
4. Chorea
5. Asthetosis
6. Choreoasthetosis
7. Hemiballismus
8. Myoclonic jerks
9. Tics (habit spasms)
10. Dyskinesia
11. Akathisia

TREMORS
Features Types Causes
Tremors are Rest tremor: present when limb is 1. Akinetic-rigid syndromes
oscillatory distal at rest and reduced by voluntary (parkinsonism)
movements resulting movement. It is usually rapid,
from alternating rhythmic, alternating tremor,
contraction and predominantly in flexion/extension
relaxation of but often with a prominent rotary
muscles. Tremors are component between finger and
described according thumb (pill-rolling tremor). It is
to their speed (fast almost always more severe in the
or slow), amplitude arm than in the leg, and is usually
(fine or coarse) and asymmetrical.
whether they are Postural tremor: present when 1. Benign essential tremor (50% familial):
maximal at rest, on limb is maintained in a position usually coarse tremor and often
maintaining a against gravity. exaggerated in awkward postures, as
posture or on when the outstretched fingers are held
carrying out an pointing at each other, in full inversion, in
active movement front of the patient’s nose.
(rest, postural, 2. Exaggerated physiological tremor (fine
action or intention) and rapid): seen with anxiety,
hyperthyroidism, excess alcohol or
caffeine, or β-agonists.
Action tremor: present during an 1. Lesions of the red nucleus and sub-
action thalamic nucleus (most often caused by
damage from vascular disease or MS)
Intention tremor: most prominent 1. Cerebellar disease
during voluntary movement
towards a target

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ASTERIXIS
Feature Causes
Asterixis (negative myoclonus): intermittent inhibition of 1. Metabolic encephalopathy (liver
muscle tone that leads, for example, to a momentary and failure, uraemia, poisoning with hypnotic
repetitive partial flexion of the wrists during attempted drugs)
sustained wrist extension (may superficially resemble a 2. respiratory failure
tremor).

DYSTONIA
Feature Types Causes
Dystonia literally means any abnormality of muscle Focal dystonia (affects 1. Idiopathic
tone, but most neurologists employ it to describe the only one part of the 2. Major
slow development of an abnormal posture (often of body): e.g. isolated tranquilisers,
the limb or the neck) which is maintained by co- torticollis or isolated 3. Treated
contraction of both agonists and antagonists. writer’s Parkinson’s
Positions maintained are usually at an extreme of disease on
extension or flexion. Common forms are torticollis excessive therapy
(the neck twisted to one side), anterocollis (the neck Segmental dystonia 1. As for focal
flexed forward), retrocollis (the neck extended (affecting two or more dystonia (see
backwards), lordosis (the arched back), and scoliosis adjacent parts of the above)
(twisted back). The arm is usually abducted at the body): for example
shoulder, extended at the elbow, pronated to an torticollis and dystonic
extreme position with the fingers extended. The leg posturing in the same arm
is usually extended at the hip and knee and inverted Generalised dystonia 1. As for chorea (see
at the ankle with the toes flexed. The term dystonia (affects parts of the body below).
frequently is qualified as torsion dystonia, to that are not adjacent): 2. Rare causes:
emphasize the twisted nature of the abnormal often associated with dystonia
postures chorea musculorum

CHOREA, ASTHETOSIS, CHOREOASTHETOSIS

Feature Causes
Chorea is a brief, fluid, involuntary movements which 1. Drug therapy of Parkinson’s disease
frequently appear pseudo-purposeful. In chorea, the (excess treatment)
ordinary voluntary movements, such as walking or 2. Wilson’s disease (look for associated liver
picking up a cup, may be embellished with rapid extra disease and Keyser-Fleischer rings on
little flourishes of movement. The outstretched upper cornea)
limbs may assume a hyperpronated posture and little 3. Huntington's disease (trace family history)
flicks of movement of the digits or wrist, or of the face 4. Post-pill or pregnancy chorea (chorea
and tongue may occur. gravidarum)
5. Sydenham's chorea
6. Stroke
Athetosis is a complex irregular slow, writhing 1. The term athetosis was introduced
movement; occurs nearly continuously in distal muscles. originally to describe the sinuous, writhing
It consists of an interaction between various postures of digital movements that may follow a
the hand or foot, especially grasping and avoiding. The stroke. Subsequently, athetosis became
fingers are alternately widely extended, the arm synonymous with one type of cerebral
following into an extended, abducted and externally palsy, resulting from brain damage due to
rotated posture, and then the fingers clench, often anoxia or kernicterus at birth.
trapping the thumb in the palm, and the limb flexes
slightly and rotates internally.
Choreoathetosis refers to something between the chorea and athetosis (or uncertainty on the part of the
observer!)

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HEMIBALLISMUS, MYOCLONIC JERKS, TICS, DYSKINESIA, AKATHISIA

Feature Causes
Hemiballismus (Ballism = to throw) is an irregular 1. Infarction of the contralateral sub-thalamic
sudden and often violent flinging movement of a nucleus or its connections
proximal limb, usually an arm. It most often involves
only one side of the body (i.e., hemiballism [us]).
There is no clear distinction from sever chorea.
Myoclonic jerks are sudden shock-like contractions 1. Healthy individuals may experience these
of one or more muscles which may be focal or diffuse. when falling asleep or surprised by a sudden
They may occur singly or repetitively. Myoclonus can noise
occur spontaneously at rest, in response to sensory 2. Metabolic encephalopathies
stimuli, or with voluntary movements. 3. Myoclonic epilepsies
4. Creutzfeldt-Jakob disease
5. Post-anoxic encephalopathy
Tics (habit spasms) are stereotyped, irresistible 1. Simple tics: isolated transient or chronic tics
movements, which are essentially purposeful in children that may persist to late adolescence
movements but recurring involuntarily in repetitive (good prognosis)
manner (may superficially resemble myoclonic jerks 2. Gilles de la Tourette syndrome: tics
but more stereotyped). Tics may be voluntarily associated with coprolalia (involuntary and
controlled at the expense of mounting inner tension. inappropriate obscene speech). The
pathophysiology is obscure. A dopaminergic
excess has been suggested by the clinical
observation that the tics may respond to
treatment with dopamine-blocking drugs.
3. Wilson's disease (associated with hepatic and
renal involvement, Kayser-Fleischer corneal
rings, low serum copper and ceruloplasmin
levels, and increased 24-h urinary copper
excretion)
4. Post-encephalitic syndromes
5. Stimulant or neuroleptic medication.
6. In association with obsessive compulsive
disorders.
Dyskinesia literally means any abnormal movement 1. Neuroleptic drugs (dopamine blocking
but the term has become synonymous with drug- agents): phenothiazines (chlorpromazine),
induced abnormal movements; particularly orofacial butyrophenones (haloperidol), substituted
dyskinesia. The term tardive (late) dyskinesia is used benzamides (metoclopramide), reserpine,
to distinguish movement disorders that occur as a late tetrabenazine
complication of treatment with neuroleptic drugs from 2. Antiparkinsonian agents (dopamine like
acute dystonia and extrapyramidal syndrome which effects): L-dopa, bromocriptine, lysuride,
develop early. pergolide
Akathisia: Motor restlessness where the patient 1. Late reaction to major tranquilisers (tardive
constantly shifts crossing and uncrossing his legs and akathisia)
walking on spot.

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ABNORMALITIES OF TONE:
Tone Features Causes
Normal  Slight resistance through whole range of movement. 1. Normal
 Heel will lift minimally off the bed when the knee 2. Myopathy → normal tone or
is lifted quickly hypotonia
3. Neuromuscular junction
diseases
4. Functional weakness
Hypotonia  Loss of resistance through movement. 1. LMN Lesion
 Heel does not lift off the bed when the knee is lifted 2. Cerebellar
quickly. 3. Myopathy (normal or
hypotonia)
4. Spinal shock
5. Chorea
Hypertonia Spasticity: 1. UMN Lesion
 Resistance is velocity-dependent, detected as a
“catch” at the beginning or end of passive
movement, has a sudden release after reaching a
maximum (the "clasp-knife" phenomenon)
 Heel easily leaves the bed when the knee is lifted
quickly
 Predominantly affects antigravity muscles (upper
limb flexors and lower limb extensors)
Rigidity 1. Extrapyramidal syndromes
 Lead pipe or plastic rigidity: Increased tone
through whole range, as if bending a lead pipe.
 Cogwheel rigidity: Increased tone through whole
range, with regular interruption to the movement
giving it a jerky feel (due to associated tremor)
Paratonia or Gegenhalten: 1. Bilateral frontal lobe
 Increased tone through whole range that varies damage (CVA, dementia)
irregularly in response to repetitive passive
movements, becoming worse when the patient
tries to relax (patient apparently opposes your
attempts to move his limb)

THE MEDICAL RESEARCH COUNCIL (MRC) SCALE FOR POWER GRADING:

0 = no muscle contraction visible
1 = flicker of muscle contraction but no movement
2 = movement when gravity eliminated (but not against gravity)
3 = movement against gravity but not against resistance
4- = slight movement against resistance
4 = moderate movement against resistance
4+ = submaximal movement against resistance
5 = normal power (full strength)
N.B. when testing power, allow patient to move the joint through the full range, and look at or feel the
muscle contract

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FEATURES OF THE DIFFERENT PATTERNS OF WEAKNESS

UMN Lesion LMN Lesion Muscle Neuromuscular Functional
disease junction (NMJ) weakness
(myopathy) disease
Muscle bulk No wasting Severe wasting Mild wasting No wasting No wasting
Fasciculations No fasciculations Fasciculations No No No
are common fasciculations fasciculations fasciculations
Tone Spasticity Hypotonia Normal tone / Normal tone / Normal tone
hypotonia hypotonia
Pattern of Pyramidal pattern Distal/ Proximal Fatiguable Erratic power
weakness of weakness segmental weakness weakness
(weak extensors in distribution of
the arm, weak weakness
flexors in the leg –
more distally and
more in the
abductors than
adductors)
Reflexes Hyperactive Hypoactive/ hypoactive/ Normal reflexes Normal
reflexes absent reflexes Normal reflexes
reflexes
Planter Extensor plantar Flexor plantar Flexor plantar Flexor plantar Flexor plantar
response response response response response response

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CAUSES OF THE DIFFERENT PATTERNS OF WEAKNESS

UMN 1. Spinal cord syndromes; differentiated by sensory signs
Lesion
Complete transverse lesion: trauma, spinal cord compression by tumour (usually
bony secondaries in vertebra), cervical spondylitis, transverse myelitis, MS,
intraspinal tumours (e.g. meningiomas), spinal abscess, post infectious (usually
viral)

Hemisection of the cord (Brown-Sequard syndrome): Causes as for transection

Central cord: syringomyelia and trauma leading to haematomyelia

Posterior column loss: any cause of complete transection, SCD (vitamin B 12
deficiency), tabes dorsalis

Anterior spinal syndrome: anterior spinal artery emboli or thrombosis.
2. Brainstem lesions: brainstem infarction or haemorrhage(elderly), MS(young patients),
tumours, trauma
3. Hemisphere lesions: infarction, haemorrhage, tumours, trauma, MS
LMN 1. Mononeuropathy:
Lesion
Compression (Saturday night palsy: compressing radial nerve in spiral groove by
leaning arm over chair- also reported to affect sciatic nerve after falling asleep
sitting on toilet)

Entrapment, e.g. median nerve in carpal tunnel, common peroneal nerve behind
head of the fibula at the knee; more common in DM, RA, hypothyroidism and
acromegaly
2. Radiculopathy:

Cervical or lumbar disc protrusion, e.g. L5/S1 disc protrusion compresses the S1
root.

At the level of a compressive spinal lesion (secondary tumours, neurofibroma)
3. Peripheral neuropathies:

Acute predominantly motor neuropathies: Guillan-Barre syndrome, diphtheria,
porphyria

Subacute sensorimotor neuropathy: vitamin B1, B12 deficiencies, heavy metal
poisoning (lead, arsenic, thallium), drugs (vincristine, isoniazid), uraemia

Chronic sensorimotor neuropathy: either acquired (DM, hypothyroidism,
paraproteinaemia, amyloidosis) or inherited (HSMN, e.g. Charcot-Marie-Tooth
disease)
4. Mononeuritis multiplex: inflammatory (PAN, RA, SLE, sarcoidosis)
5. Polyradiculopathy: indicates lesion of many roots. It is distinct from other peripheral
neuropathies because it produces a more proximal weakness. The term is commonly
applied to Guillan-Barre syndrome
Muscle 1. Inherited: muscular dystrophies (Duchene’s, Becker’s, fascio-scapular-humeral,
disease myotonic dystrophy)
(myopathy) 2. Inflammatory: polyomyositis, dermatomyositis, PMR
3. Endocrine: steroid-induced, hyperthyroid, hypothyroid
4. Metabolic (rare): glycogen storage disease (e.g. Pompe’s disease), McArdle’s disease
5. Toxic: alcohol, chloroquine, clofibrate
NMJ 1. myasthenia gravis: usually idiopathic; occasionally drug-induced (penicillamine,
hydralazine)
2. Lambert-Eaton syndrome: paraneoplastic syndrome (usually oat cell carcinoma)
Functional 1. may indicate hysterical illness
weakness

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CLINICAL APPROACH TO WEAKNESS

Features of weakness Possible diagnosis
Generalized weakness 1. Diffuse disease of nerve: poly-radiculopathy
(limbs and cranial nerves) 2. Diffuse disease of muscle: myopathy
3. Diffuse disease of NMJ: myasthenia gravis
Quadriparesis with 1. Cervical cord lesion
exaggerated reflexes and 2. Brainstem lesion
extensor plantar response 3. Bilateral cerebral lesions.
(i.e. UMN lesion pattern) Discriminate by sensory testing, cranial nerve signs, and hemisphere signs
Quadriparesis with 1. Poly-radiculopathy
hypoactive/absent reflexes 2. Peripheral neuropathy
(i.e. LMN lesion pattern) 3. Myopathy (normal/hypoactive reflexes): proximal weakness and normal sensations
4. Acute UMNL in the state of spinal shock
Quadriparesis with mixed 1. MND (normal sensations)
UMNL pattern (in the legs) 2. Combined cervical myelopathy and radiculopathy (with sensory loss)
& LMNL pattern (in the
arms)
Quadriparesis with 1. Myopathy: (normal/hypoactive reflexes): proximal weakness and normal
normal reflexes sensations
2. Myasthenia gravis: fatigable weakness with associated cranial nerve abnormalities
Hemiparesis (UMNL 1. Hemisection of cervical cord
pattern with contralateral
sensory findings
Hemiparesis (UMNL 1. Brainstem lesion
pattern with contralateral
III nerve palsy → midbrain lesion
cranial nerve lesion
VI and/or VII → pontine lesion

XII ± IX and XI → medullary lesion
Hemiparesis (UMNL 1. Internal capsule lesion
pattern with ipsilateral
UMNL VII palsy
Hemiparesis (UMNL 2. Cerebral lesion
pattern with hemisphere
Parietal lobe lesion → contralateral lower homonymous quadrantanopia
signs (aphasia, higher
Temporal lobe → contralateral upper homonymous quadrantanopia
function deficits,
Lesion in the anterior occipital cortex (posterior cerebral artery occlusion) →
contralateral visual field congruous homonymous hemianopia
defects, contralateral
Bilateral occipital lobe lesions → cortical blindness
inattention or neglect)
Paraparesis (UMNL 1. Spinal cord lesion above the root level of the highest motor abnormality. A level
pattern) may be ascertained with sensory signs (sphincter involvement)
Paraparesis (LMNL 1. Polyradiculopathy
pattern) 2. Cauda equinal lesion (sphincter involvement)
3. Peripheral neuropathy:

Acute (Guillan-Barre syndrome, porphyria, diphtheria)

Subacute (lead poisoning)

Chronic (HSMN, CIDP)
Monoparesis (UMNL 1. Lesion in spinal cord (above the highest involved level)
pattern) 2. Brainstem lesion
3. Cerebral lesion.
Discriminate by sensory testing, cranial nerve signs, and hemisphere signs.
Monoparesis (LMNL 1. Mononeuropathy
pattern) 2. Radiculopathy
See examples of mononeuropathies and radiculopathies below
Patchy weakness (UMNL 1. Multiple CNS lesions
pattern)
Patchy weakness (LMNL 1. Polyradiculopathy
pattern) 2. Multiple single nerves (mononeuritis multiplex)
Variable weakness (non 1. If progressively gets worse: consider myasthenia gravis
anatomical distribution) 2. If fluctuates; giving full power at times: consider functional weakness

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MOTOR ROOT VALUES IN THE LOWER LIMB

Root value Muscle action
L1,2,3 Hip flexion
L2,3 Hip adduction
L4,5,S1 Hip abduction
L5,S1 Hip extension
L3,4 Knee extension
L4,5 Ankle dorsiflexion and inversion
L5,S1 Ankle eversion
S1,2 Ankle plantar flexion
L5,S1,2 Knee flexion
L5,S1 Toes extension
S2,3 Toes flexion

EXAMPLES OF MONONEUROPATHIES AND RADICULOPATHIES IN THE LOWER LIMB

Common peroneal palsy L4 root L5 root S1 root
(compare to L5)
• Foot drop → high stepping gait • Weakness of • Weakness of foot • Weakness of
• Wasting of the muscles on the knee extension dorsiflexion, inversion plantar flexion
lateral aspect of the leg (tibialis and foot and eversion, extension and foot eversion
anterior and peronei) dorsiflexion of the big toe and hip • Loss of ankle
• Weakness of dorsiflexion • Loss of knee abduction reflex
(tibialis anterior; L5) and reflex • Sensory loss over the • Sensory loss over
eversion (peronei; S1). • Sensory loss lateral shin and dorsum the lateral border
• Sensory loss over the over the medial of foot of foot and sole
anterolateral aspect of the lower shin of foot
half of the leg (lateral shin) and
dorsum of the foot
• Characteristically: ankle reflex is
preserved (lost in tibial nerve
palsy, sciatic nerve palsy and S1
radiculopathy)
• Ankle inversion is intact (lost in
tibial nerve palsy, sciatic nerve
palsy and L4/5 radiculopathy)

CAUSES OF FOOT DROP

1. Common peroneal nerve palsy (ankle eversion is lost while ankle inversion and ankle reflex are
preserved)
2. Lumbosacral plexus lesion
3. Sciatic nerve palsy (ankle reflex and ankle inversion are lost)
4. Peripheral neuropathy, especially HSMN type 1
5. L4/5 radiculopathy most commonly due to prolapsed lumbar disc (ankle reflex and ankle inversion are
lost)
6. Motor neurone disease (MND)

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REFLEXES GRADING
0 = absent
± = present only with reinforcement
1+ = present but depressed (diminished)
2+ = normal
3+ = increased (hyperactive)
4+ = clonus

ABNORMAL TENDON REFLEXES

Reflex response Causes
Increased reflex or clonus 1. UMNL above the level of the increased reflex
Absent reflexes 1. Generalized peripheral neuropathy
2. Isolated root lesion or less commonly peripheral nerve lesion
3. Bilateral absent ankle reflexes peripheral neuropathy or -less
commonly- bilateral S1 root lesions or -very rarely- bilateral
sciatic nerve lesions
N.B. reflexes can be absent in the early stages of severe UMNL (spinal
shock)
Reduced reflexes 1. Peripheral neuropathy, muscle disease and cerebellar syndrome.
Inverted reflex: a combination 1. The level of the absent reflex indicates the level of the lesion. For
of loss of the reflex tested with example, in an inverted biceps reflex, when the biceps tendon is
spread of the reflex to muscle at a tapped there may be no biceps reflex but the triceps contracts; this
lower level. It is caused by indicates LMNL at the level of the absent reflex (in this case C5)
combined spinal cord and root with UMNL below; indicating spinal cord involvement at the
lesion level of the absent reflex. In an inverted supinator reflex, when the
supinator reflex is tested there is no response but finger flexion
occurs (C5/6 lesion)
Pendular reflex 1. Best seen in the knee jerk where the reflex continues to swing for
several beats. This is associated with cerebellar disease
Slow relaxing (myotonic) reflex 1. Especially seen at the ankle reflex and may be difficult to note. It
is associated with hypothyroidism.

THE ROOT VALUES FOR REFLEXES

Action Root values Reflexes
One two….…...buckle my shoe S 1,2 Ankle reflex
Three four... ….kick the door L 3,4 Knee reflex
C5 Biceps reflex
Five six….……pick up sticks
C6 Brachioradialis reflex
C7 Triceps reflex
Seven eight …..shut the gate
C8 Finger reflex

PATTERNS OF PLANTAR RESPONSE

Response What it means
Flexor plantar response (negative Babinski’s sign): all the toes  Normal
flex towards the plantar surface
Extensor plantar response (positive Babinski’s sign): The big  UMNL above the S1 level of the
toe extends dorsally (goes up), while the four small toes fan and spinal cord
turn towards the sole.  Normal in children below the age
of 1 year
Withdrawal response: The big toe extends (goes up), the other  Repeat more gently or try
toes extend and ankle dorsiflexes alternative stimuli
No response: no movement of the big toe (even if the other toes  profound UMN weakness (toe
flex) unable to extend)
 Sensory abnormality interfering
with the afferent part of the reflex.

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TYPES AND CAUSES OF ATAXIA

Features Causes Associated clinical signs
Cerebellar Abnormalities of the Unilateral limb ataxia  Dysmetria and intention
limb ataxia intermediate and lateral (ipsilateral cerebellar tremor (finger-nose and
portions of the syndrome): heel-shin tests)
cerebellum typically  Demyelination,  Dysdiadochokinesia
produce impaired limb  Vascular disease (rapid alternating
movements rather than  Less commonly trauma, movements)
truncal ataxia. If tumour or abscess  Muscle tone is often
involvement is Bilateral limb ataxia modestly reduced; this
asymmetric, lateralized (bilateral cerebellar contributes to the
imbalance is common syndrome): abnormal rebound due to
and usually associated  Drugs; e.g. decreased activation of
with asymmetric anticonvulsants segmental spinal cord
nystagmus (phenytoin) reflexes and also to
 Alcohol pendular reflexes, i.e., a
 Demyelination (MS) tendency for a tendon
 Vascular disease (stroke) reflex to produce
 Less commonly multiple swings to and
hereditary cerebellar fro after a single tap
degeneration
(Friedreich’s ataxia),
paraneoplastic disorders,
or hypothyroidism
Cerebellar Abnormalities of the Lesion of the cerebellar  Gait ataxia and
truncal midline cerebellar vermis vermis (Midline cerebellar symmetric nystagmus in
ataxia or the flocculonodular syndrome): cause as for absence of limb
lobe produce truncal bilateral cerebellar syndrome incoordination
ataxia which is usually
revealed during the
process of rising from a
chair, assuming the
upright stance with the
feet together, or
performing some other
activity while standing.
Sensory Porprioceptive Porprioceptive impairment: Depends on the site of the
limb ataxia impairment produced  Peripheral nerves lesions proprioceptive impairment:
sensory limb ataxia,  Posterior column lesion  The peripheral nerves →
which is similar to  Parietal lobe damage depressed or absent
cerebellar limb ataxia but reflexes
is markedly worse when  The posterior columns of
the eyes are closed. the spinal cord →
Examination also reveals spasticity with extensor
abnormal proprioception plantar response
and vibratory perception.  The parietal lobe (rare)
→ lateralized imbalance

MODALITIES AND TRACTS OF SENSATION

Vibration and joint position Pin prick and temperature Light touch
Ascend in the posterior column Ascend in the spinothalamic tract Ascends in both the posterior
(remains ipsilateral up to the (crosses within one to two column and spinothalamic tracts.
medulla, where it crosses over) segments of entry)

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PATTERNS AND CAUSES OF SENSORY LOSS

Sensory lesion Pattern Causes
Mononeuropathy Single nerve lesion most commonly
Entrapment neuropathy (e.g. median
median, ulnar, peroneal, lateral cutaneous nerve in carpal tunnel, common peroneal
nerve to the thigh nerve behind head of the fibula at the
knee, more common in DM, rheumatoid
arthritis, hypothyroidism)

May be presentation of more diffuse
neuropathy (see cause of peripheral
neuropathy below)
Mononeuritis Multiple single nerve lesions DM, connective tissue disease (SLE, RA),
multiplex vasculitis (PAN, Churg-Strauss), infection
(HIV), malignancy, or may be presentation of
more diffuse neuropathy (see above)
Radiculopathy Root or roots lesions most commonly C5, Compression by prolapsed intervertebral
C6 and C7, L4, L5 and S1 discs, tumours (e.g. neurofibromatosis)
Peripheral Peripheral nerves lesions: sensory loss DM, Vitamin B1, B12 deficiencies, Uraemic
neuropathy either in both legs or in both arms and legs - neuropathy, Alcohol, Drugs (vincristine,
without clear upper level → distal glove isoniazid), Carcinomatous neuropathy
and stocking deficit (especially CA bronchus), Amyloidosis, and
Leprosy
Spinal cord lesion → Complete transverse lesion → Trauma, spinal cord compression by tumour
sensory loss in both hyperaesthesia at the upper level with loss (usually bony secondaries in vertebra),
legs (or both arms and of all modalities a few segments below the cervical spondylitis, transverse myelitis, MS,
both legs) with clear lesion. intraspinal tumours (e.g. meningiomas),
upper level. spinal abscess, post infectious (usually viral)
Hemisection of the cord (Brown-Sequard As for transection
syndrome) → loss of joint position sense
and vibration sense on the same side as the
lesion and pain and temperature on the
opposite side a few levels below the lesion.
Central cord lesion → loss of pain and Syringomyelia and trauma leading to
temperature sensation at the level of the haematomyelia
lesion, where the spinothalamic fibres cross
in the cord, with other modalities preserved
(dissociated sensory loss).
Posterior column lesion → loss of joint Any cause of complete transection, SCD
position sense and vibration sense with (vitamin B 12 deficiency), tabes dorsalis
intact pain and temperature.

Anterior spinal syndrome → loss of pain Anterior spinal artery emboli or thrombosis
and temperature below the level with
preserved joint position sense and vibration
sense.
Brainstem lesion Hemisensory loss including face on the Demyelination (young patients), brain stem
contralateral side): loss of pain and stroke (lateral medullary syndrome), brain
temperature on the face and on the opposite stem tumours
side of the body
Thalamic sensory loss Hemisensory loss of all modalities Stroke, cerebral tumour, MS, trauma
including face on the same side)
Cortical loss Hemisensory loss including face on the As for thalamic sensory loss
same side): parietal lobe- the patient is able
to recognize all sensations but localizes
them poorly- loss of two point
discrimination, astereognosis, sensory
inattention
Functional loss This is suggested by a non-anatomical May indicate hysterical illness; however, this
distribution of sensory deficit frequently is a difficult diagnosis to make in the absence
with inconstant findings of appropriated psychopathology

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CLINICAL APPROACH TO SENSORY LOSS

Features of sensory loss Possible diagnosis
Sensory loss in the distribution of a single nerve Mononeuropathy; most commonly median, ulnar,
peroneal, or lateral cutaneous nerve to the thigh
Sensory loss in the distribution of a single root Radiculopathy; most commonly (C5, C6, C7) or
(L4, L5 and S1)
Sensory loss affecting both legs with clear upper Spinal cord lesion
level
Sensory loss affecting both legs (or both arms and Peripheral neuropathy
both legs) without clear upper level (glove and
stocking)
Sensory loss affecting both arms and both legs Cervical spinal cord lesion
with clear upper level
Hemisensory loss including the face on the same Thalamic lesion
side (all modalities)
Hemisensory loss including the face on the same Internal capsule lesion
side (not all modalities)
Hemisensory loss including the face on the Brain stem lesion
contralateral side

SCIATIC NERVE (L4,5,S1,2,3): most important branch of lumbosacral plexus and largest nerve in the
body. It terminates by dividing into medial popliteal (tibial) and lateral popliteal (common peroneal)
nerves

LATERAL POPLITEAL (COMMON PERONEAL) NERVE (L4,5,S1,2):

• Passes through the popliteal fossa, winding around the head of the fibula (more susceptible to injury
than the tibial nerve)
• Divides into terminal pressures: deep peroneal (anterior tibial) and superficial nerves
• Common peroneal nerve palsy (CPNP):
 Foot drop → high stepping gait
 Wasting of the muscles on the lateral aspect of the leg (tibialis anterior and peronei)
 Weakness of dorsiflexion (tibialis anterior; L5) and eversion (peronei; S1).
 Sensory loss over the anterolateral aspect of the lower half of the leg and dorsum of the foot
 Characteristically: ankle reflex is preserved (lost in tibial nerve palsy, sciatic nerve palsy and S1
radiculopathy)
 Ankle inversion is intact (lost in tibial nerve palsy, sciatic nerve palsy and L4/5 radiculopathy)

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CNS – UPPER LIMB

STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him
• Ask the patient to sit upright on the edge of the bed facing you with the upper limbs adequately
exposed

(2) GENERAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Scan the bedside.
Walking stick
2. Scan the patient.
Nutritional status: under/average built or overweight

Abnormal facies: Sad, immobile, unblinking facies
(Parkinson’s disease), facial wasting (muscular dystrophy),
facial asymmetry (hemiplegia), Horner’s syndrome
(syringomyelia, Pancoast’s syndrome)

Abnormal movement or posture: rest or intention tremors,
dystonia, choreoathetosis, hemiballismus, myoclonic jerks,
tics, pyramidal posture…see theoretical notes for description,
types, features and causes of abnormal movements

Abnormal facial movements: hemifacial spasm, facial
myokymia, blepharospasm, oro-facial dyskinesia

Nystagmus (cerebellar syndrome)

Scar or deformity underlying an ulnar nerve palsy

Peroneal wasting (Charcot-Marie-Tooth disease)

Pes cavus (Friedreich’s ataxia, Charcot-Marie-Tooth disease)
3. Examine the eyes
Nystagmus (cerebellar syndrome)

Horner’s syndrome (syringomyelia, Pancoast’s syndrome)
4. Examine the hands: tell the
wasted hands (MND, Charcot-Marie-Tooth disease,
patient “outstretch your hands syringomyelia)
like this (dorsum facing
AF → consider thromboembolic complications
upwards)”… then “like this
(palms facing upwards)”…
demonstrate. Feel the radial
pulse for AF

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(3) INSPECTION OF THE UPPER LIMB

Steps Possible findings
Scan the upper limb from the shoulder
Muscle bulk: wasting or hypertrophy
down to the upper arm, lower arm and
Fasciculations: irregular twitches under the skin
hands. Compare right with left overlying muscle at rest; represent contraction of a motor
unit. They occur in LMNL; usually in wasted muscles
(nearly always indicate MND). Flicking the skin over
wasted muscle may elicit fasciculations. Non-pathological
fasciculations occasionally occurs after vigorous exercise
in healthy people.
Pronator 1. Tell the patient “hold
Winging of scapula (lifts off the chest wall) → indicates
drift test your arms outstretched weakness of the serratus anterior muscle (long thoracic
in front of you, like this nerve; C5-C7).
(palms facing
Passive abduction of the little finger (myelopathy hand
upwards), and maintain sign) → indicates either a pyramidal lesion or ulnar nerve
this position”. palsy (sensory testing should distinguish). As the lesion
becomes more severe, adjacent fingers also passively
abduct. This sign is common in, but not specific for,
cervical pyramidal lesions.

Involuntary movements (e.g. intention tremor in
cerebellar disease → the arm oscillates several times
before coming to rest)
2. Tell the patient “keep
Overshoot (rebound phenomenon): in case of cerebellar
your arms up and do disease, the arm will fly past the starting point without
not let me push them reflex arrest.
down”. Press the
patient’s wrist
downward and then
suddenly release it.
3. Tell the patient “now
Arm pronates and fall downwards → indicates subtle
close your eyes”. UMN Weakness

Fingers continuously move up and down (sensory
wandering / pseudoathetosis) → indicates deficit of joint
position sense due to lesion of peripheral nerves, posterior
column, or parietal lobe (parietal drift).

Arm drifts upward → indicates cerebellar lesion

(4) TONE
Steps Possible findings
1. Tell the patient “Let your legs go loose and let me move them for
Normally there is light
you” resistance through whole
2. Hold the patient’s hand as if shaking hands, using your other hand range of movements.
to support the patient’s elbow. Flex and extend the wrist in rolling
See theoretical notes for
wave fashion (to elicit cog-wheel rigidity of Parkinson’s disease). abnormalities of the tone
3. Then pronate and supinate the patient’s forearm, and flex and
extend his elbow and shoulder in an irregular and unexpected
fashion (to elicit lead-pipe rigidity and clasp-knife spasticity).

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(5) POWER
Steps Possible findings
Tell the patient “I am going to test the strength of Describe any weakness in terms of the medical
some of your muscles”. Fix the joint proximal to the research council (MRC) scale from 5 (normal)
group of muscles you are testing. Give the patient a down to 0 (no visible muscle contraction)…see
space to show his power before resisting him and look theoretical notes for the MRC scale for power
at the muscle contracts. Compare right with left grading
1. Shoulder abduction: tell the patient “Hold your Action by the deltoids (supplied by the axillary
arms up, like this (chicken wings). Now keep nerve; C5). N.B: Lifting the arm from the side to
them up and don’t let me push them down”. 90 degrees tests the supraspinatus muscle
(supplied by the suprascapular nerve; C5)
2. Shoulder adduction: tell the patient “Now take Action by the pectoral muscles mainly pectoralis
them in towards you, like this and push my major and latissimus dorsi (supplied by multiple
hands” nerves mainly medial and lateral pectoral nerves;
C6,7,8)
3. Elbow flexion: tell the patient “Bend your arm, Action by the biceps (supplied by the
like this. Pull it towards you and don’t let me musculocutaneous nerve; C5,6)
straighten it”
4. Elbow extension: tell the patient “Now straighten Action by the triceps (supplied by the radial
your arm and push my hand” nerve; C6, C7,8)
5. Wrist flexion: tell the patient “Clench your fists Action by the flexor carpi radialis&ulnaris
and bend your hand up towards you, like this. (supplied by the median and the ulnar; C7)
Push my hand”
6. Wrist extension: tell the patient “Now push the Action by the extensor carpi radialis&ulnaris
other way” (supplied by the posterior interosseous nerve from
the radial nerve; C7).
7. Finger extension: tell the patient “Straighten Action by the extensor digitorum (supplied by the
your fingers, like this (palm down) and don’t let posterior interosseous from the radial nerve;
me bend them” (fix the patient’s wrist with your C7,8).
left hand and push against the fingers with the
ulnar surface of your right hand)
8. Finger flexion: tell the patient “Grip my fingers Action by the flexor digitorum profundus, flexor
tightly (offer two fingers)” digitorum superficialis, flexor policies longus,
flexor policies brevis and lumbricals (supplied by
the median and the ulnar nerves; C8, T1).
9. Finger abduction: tell the patient “Spread your Action by the dorsal interossei (supplied by the
fingers wide apart like this and don’t let me push ulnar nerve; T1).
them together”
10. Finger adduction: tell the patient “Hold this Action by the palmar interossei (supplied by the
piece of paper between your fingers and don’t let ulnar nerve; T1).
me pull it out”
11. Thumb abduction: tell the patient “Straighten Action by the abductor pollicis brevis (supplied
your hand, like this (palm upwards) and point by the median nerve: C8, T1).
your thumb towards the ceiling, like this. Now
keep it there and don’t let me push it down”
12. Thumb opposition: tell the patient “Touch the Action by the opponens pollicis (supplied by the
tip of your little finger with the tip of your thumb, median nerve; T1).
like this and don’t let me pull them apart”
N.B. you may wish to skip testing the power in fingers and thumb unless specific mononeuropathy or
radiculopathy is suspected or neurological examination of the hand is requested in the instructions.
See theoretical notes for:
 Features and causes of the different patterns of weakness
 Clinical approach to weakness
 Motor root values in the upper limb
 Examples of mononeuropathies and radiculopathies in the upper limb

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(6) REFLEXES
Steps Possible findings
Explain to the patient. place the patient supine on the bed in Grade the response from 0 (absent) up to
a comfortable relaxed position. Use a long tendon hammer; 4+ (clonus)… see theoretical notes for
flex your wrist and let the hammer fall with its own weight reflexes grading
onto the muscle. Compare right with left. If the reflex
appears to be absent, ask the patient to clench his teeth as
you swing the hammer (reinforcement).
1. Biceps reflex: place the patient’s hands on his abdomen Reflex arc through the musculocutaneous
(with the arms semiflexed and semipronated). Place your nerve; C5,6
index finger on the biceps tendon. Swing the hammer on
to your finger while watching the biceps muscle.
2. Supinator reflex: place your index finger on the radial Reflex arc through the radial nerve; C5,6
tuberosity. Swing the hammer on to your finger while
watching the brachioradialis muscle
3. Triceps reflex: draw the patient’s arm across the chest, Reflex arc through the radial nerve; C7
flexing the elbow to a right angle. Swing the hammer
directly on to the triceps tendon (just above the
olecranon) while watching the triceps muscle.
4. Finger reflex: rest the patient hand on the bed in partial Reflex arc through the median and ulnar
supination with the fingers slightly flexed. Place the nerves; C8
palmar surface of your middle and index fingers across
the palmar surface of the patient’s proximal phalanges.
Tap the back of your own fingers with the hammer.
Observe for flexion of the patient fingers (FDP and
FDS).
5. Hoffman’s reflex: Hold the patient’s wrist (with your Normally no reflex occurs unless the
left hand) in the horizontal pronated position with the patient is under emotional tension.
fingers and wrist relaxed. Place the ulnar surface of your In UMNL, the patient’s thumb undergoes a
right index finger under the palmar surface of the DIP quick flexion-adduction-opposition
joint of the patient’s middle finger. Using your right movement while the other fingers move in
thumb flick the patient’s finger downwards. flexion-adduction. This response is
labelled as a positive Hoffmann’s sign.
5. Abdominal reflexes: the patient should be supine and
Normal response is contraction of the
relaxed. Using an orange stick lightly scratch the recti with the umbilicus moving away
abdominal wall towards the umbilicus in the four from the direction of the scratch.
quadrants of the stomach.
Afferent: segmental sensory nerves

Efferent: segmental motor nerves

Roots: T8,9 above the umbilicus, and
T11,12 below the umbilicus

Abdominal reflexes are absent in
UMNL above their spinal level, and in
LMNL affecting T8-12.

It is often impossible to elicit
abdominal reflexes in anxious patients,
elderly, obese, multiparous women,
and those who have had abdominal
surgery
N.B. you may wish to skip testing the finger reflex and Hoffman’s reflex unless specific mononeuropathy
or radiculopathy is suspected or neurological examination of the hand is requested in the instructions.
See theoretical notes for abnormal tendon reflexes, and the root values for reflexes

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(7) COORDINATION
Steps Possible findings

1. Finger-nose test: hold your index finger out an arm’s
Dyssynergia or incoordination
length in front of the patient and tell the patient “Touch (cerebellar upper limb ataxia):
my finger with your index finger; now touch your nose; movements are imprecise in force and
repeat faster”. Consider repeating the test while the direction.
patient’s eyes are closed to test for sensory ataxia.
Dysmetria: movements are imprecise
Compare right with left. Expect the right side to be in distance. The finger overshoots its
slightly better in right handed persons target (past pointing) or it stops before
the target.

Intention tremor → the patient
develops a tremor as his finger
approaches its target

Sensory ataxia: in case of deficit of
joint position sense, the original
movements are accurate but when
repeated with the eyes closed are
substantially worse
2. Rapid alternate movements: tell the patient “repeatedly
Dysdiadochokinesia: disorganization
tap the palm of one hand alternately with the palm and of the movement – cerebellar sign
then the back of the other hand as quickly as possible”
Dysrhythmia: inability to keep a
(demonstrate). rhythm - cerebellar sign
Alternatively, tell the patient “Twist your hand as if
opening a door or unscrewing a light bulb” (demonstrate
by flexing your elbows at right angles and then pronating
and supinating your forearms as rapidly as possible).
Always compare right with left. Expect the right side to
be slightly better in right handed persons
3. Rapid repeated movements: tell the patient “rapidly
Bradykinesia (slowed movements or
bring thumb and index finger together” (demonstrate). break up easily – extrapyramidal sign)
Alternatively, tell the patient “rapidly touch the thumb
with each finger in turn” (demonstrate). Compare right
with left. Expect the right side to be slightly better in
right handed persons
N.B. do not assess coordination if power < 3 (inability to move against gravity), and tell the examiner that
coordination cannot be assessed due to weakness
See theoretical notes for types of ataxia and causes of ataxia

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(8) SENSATION
Steps Possible findings
1. Pin prick:
Reduced sensation over the

Demonstrate the stimuli to the patient by testing on the first dorsal interosseous →
sternum (use each end of the hat pin): explain to the patient radial nerve or C6 lesion
“this is sharp…and this is blunt…now I’m going to test the
Reduced sensation over
sensation in your legs and I want you to close your eyes and palmar surface of distal
say “Sharp” if it feels sharp, and “blunt” if it feels blunt”. phalanx of index finger →

Start distally and move proximally testing over each median nerve or C6 lesion
dermatome (and each main nerve): Skin over the first dorsal
Reduced sensation over
interosseous → Palmar surface of distal phalanx of index Palmar surface of distal
finger → Palmar surface of distal phalanx of middle finger phalanx of middle finger →
→ Palmar surface of distal phalanx of little finger → Inner median nerve or C7 lesion
aspect of forearm → Outer aspect of forearm → Outer aspect
Reduced sensation over
of proximal part of upper arm → Inner aspect of proximal palmar surface of distal
part of upper arm. Repeat in the other side then compare phalanx of little finger →
right with left. ulnar nerve or C8 lesion

Map out the boundaries of any area of reduced, absent or
Reduced sensation over inner
increased sensation; starting from the area of altered aspect of forearm → T1
sensation and moving towards normal to find the edges, lesion
noting any difference between the two sides.
Reduced sensation over outer

If a stocking sensory loss is present, demonstrate that the aspect of forearm → C6
sensory loss is present right round the limb. lesion

If compression of the cord is suspected, then demonstrate a
Reduced sensation over outer
sensory level. aspect of proximal part of
2. Light touch: upper arm → C5 lesion

Demonstrate “I am going to touch you with this piece of
Reduced sensation over inner
cotton wool and I want you to close your eyes and say (Yes) aspect of proximal part of
every time you feel it”. Avoid dragging it across the skin or upper arm → T2 lesion
tickling the patient. Time the stimuli irregularly to check the
See theoretical notes for
patient reliability. sensory root values

Start distally and move proximally testing the upper limb (dermatomes) in the upper
in the same sequence as for pin prick limb
3. Joint position sense:

Demonstrate: fix the proximal phalanx of the patient’s
index finger with one of your hands. Hold the lateral aspects
of the distal phalanx of the patient’s index finger between the
thumb and index finger of your other hand. Ensure that your
thumb and index finger are at 90 degrees to the intended
direction of movement. Tell the patient “I’m going to move
your finger up and down; this is up (move finger up)…, and
this is down (move finger down)…now close your eyes and
tell me whether I am moving your finger up or down”.

Start with the DIP joint of the index finger. If impaired,
move to more proximal joints (DIP → PIP → MCP → wrist
→ elbow → shoulder).
4. Vibration sense: N.B. vibration sense is commonly

Demonstrate: use a 128 Hz tuning fork. Make the fork reduced or absent in elderly
vibrate and place it on the sternum. Ask the patient “Do you patients
feel it vibrating (buzzing)?”

Tell the patient “Close your eyes”. Make the fork vibrate
silently and place it on the the DIP joint of the index finger
and ask the patient “Can you feel it now?” If patient cannot
feel the vibration, move to more proximal joints (DIP → PIP
→ MCP → radial styloid → olecranon → acromion).
See theoretical notes for modalities and tracts of sensation, patterns, causes and approach to sensory loss

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(9) Additional signs: according to diagnosis, e.g.

• Look for cataract and scar for pacemaker, palpate for local spinal tenderness, and examine for sensory
level
• Tell the examiner that you would normally extend your examination to examine the lower limb and
cranial nerves and woud ask about swallowing (Dystrophia myotonica), bladder symptoms, test the
anal tone (spinal cord syndrome), and to dipstick urine for DM.

(10) Thank the patient and cover him (her)

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THEORETICAL NOTES

DESCRIPTION, TYPES, FEATURES AND CAUSES OF ABNORMAL MOVEMENTS: See Ch. 6

CNS Lower Limb
ABNORMALITIES OF THE TONE: See Ch. 6 CNS Lower Limb
THE MEDICAL RESEARCH COUNCIL (MRC) SCALE FOR POWER GRADING: See Ch. 6 CNS
Lower Limb
FEATURES AND CAUSES OF THE DIFFERENT PATTERNS OF WEAKNESS: See Ch. 6 CNS
Lower Limb
CLINICAL APPROACH TO WEAKNESS: See Ch. 6 CNS Lower Limb

MOTOR ROOT VALUES IN THE UPPER LIMB

Root value Muscle action
C5 Shoulder abduction
C5,6,7 Shoulder adduction
C5,6 Elbow flexion
C7,8 Elbow extension
C6 Pronation, supination
C7 Wrist flexion and extension, finger flexion and extension
T1 Thumb opposition and splaying of fingers
N.B. all muscles on the back of upper limb (triceps, wrist and finger extensors) are innervated by C7

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EXAMPLES OF MONONEUROPATHIES AND RADICULOPATHIES IN THE UPPER LIMB

Lesion Features
Median nerve
Wasting of the thenar eminence
palsy
Weakness of opposition, abduction and flexion of the thumb

Sensory loss over the palmar aspect of the lateral 3½ fingers
Ulnar nerve palsy
Generalized muscle wasting and weakness sparing the LOAF (→ wasting of
the hypothenar eminence and first dorsal interosseous, and guttering of the
dorsum of the hand)

Ulnar claw hand (hyperextension at the MCP joints with flexion of the IP joints
in the fourth and fifth fingers)

Sensory loss over the medial 1½ fingers
T1 root lesion
Wasting of all small muscles of the hand.

Sensory changes are confined to the medial forearm
Radial nerve palsy
Weakness of fingers and wrist extension and probably brachioradialis &
supinator (if damage occurs at the middle third of humerus). Paralysis may
involve the triceps (if damage occurs at the axilla) → loss of elbow extension.

If the wrist is passively extended the patient is able to straighten his fingers at
the IP joints due to the action of interossei and lumbricals, but is unable to
extend the MCP joints

There appears to be a weakness in abduction and adduction of the fingers, but
this is not present when the hand is kept flat on a table and the fingers are
extended

Wrist-drop, and weak grip (due to missing synergistic effect of an extended
wrist)

Sensory loss over the first dorsal interosseous (at the anatomical snuff box)

Loss of supinator reflex (triceps reflex may also be lost if lesion above spiral
groove).

If there is no sensory loss whatsoever, in a patient with symptoms of
progressive radial nerve palsy, then a lesion of the posterior interosseous nerve
(the main, purely motor, branch of the radial nerve) may be suspected and
surgical exploration is considered.
Bilateral wasting of
With distal sensory loss → peripheral neuropathy
small muscles of
Without sensory loss → MND
the hand
C5 root lesion
Weakness of shoulder abduction and external rotation and elbow flexion

Loss of biceps reflex

Sensory loss over the outer aspect of upper arm
C6 root lesion
Weakness of elbow flexion, Pronation

Loss of supinator reflex

Sensory loss over the lateral aspect of forearm and thumb
C7 root lesion
Weakness of elbow and wrist extension
(compare to radial
Loss of triceps reflex
nerve)
Sensory loss over the middle finger
C8 root lesion
Weakness of finger flexion

Loss of finger reflex

Sensory loss over the medial aspect of forearm
Axillary nerve
Weakness of shoulder abduction (deltoid)
palsy
Sensory loss over small patch on lateral part of shoulder

REFLEXES GRADING: See Ch. 6 CNS Lower Limb

ABNORMAL TENDON REFLEXES: See Ch. 6 CNS Lower Limb
THE ROOT VALUES FOR REFLEXES: See Ch. 6 CNS Lower Limb
TYPES AND CAUSES OF ATAXIA: See Ch. 6 CNS Lower Limb
MODALITIES AND TRACTS OF SENSATION: See Ch. 6 CNS Lower Limb
PATTERNS AND CAUSES OF SENSORY LOSS: See Ch. 6 CNS Lower Limb

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CLINICAL APPROACH TO SENSORY LOSS: See Ch. 6 CNS Lower Limb

THE SENSORY ROOT VALUES (DERMATOMES) IN THE UPPER LIMB

Root value Dermatome
C3 The root of neck
C4 Tip of shoulder
C5 Lateral aspect of upper arm
C6 Lateral aspect of forearm and hand including the thumb
C7 Middle finger
C8 Medial aspect of the hand including the little finger
T1 Medial aspect of forearm
T2 Medial aspect of the upper arm
T3 Axilla

BRACHIAL PLEXUS (C5,6,7,8,T1): Gives rise to 3 cords (posterior, medial, and lateral), which give rise
to the 3 main nerves of the upper limb (radial, ulnar, and median)

RADIAL NERVE (C5,6,7,8):

 Radial nerve is the main continuation of the posterior cord → supplies the extensors in the back of
upper limb
 Motor to the “BEST” extensors of the upper limb (Brachioradialis, Extensors of wrist and fingers,
Supinator, Triceps)
 The axillary nerve (C5,6) is the smaller terminal branch, and supplies both the deltoid and teres major
muscle
 The radial nerve gives off two branches at the elbow:
 Superficial radial (entirely sensory)
 Posterior interosseous (entirely muscular)
 In contrast to median and ulnar nerves: the radial nerve has C5 root and has no Thoracic roots,
supplies no muscles in the hand, and no complete finger; whereas ulnar and median nerves supply no
muscles in the upper arm
 Radial nerve palsy:

Weakness of fingers and wrist extension and probably brachioradialis & supinator (if damage
occurs at the middle third of humerus). Paralysis may involve the triceps (if damage occurs at the
axilla) → loss of elbow extension.

If the wrist is passively extended the patient is able to straighten his fingers at the IP joints due to
the action of interossei and lumbricals, but is unable to extend the MCP joints

There appears to be a weakness in abduction and adduction of the fingers, but this is not present
when the hand is kept flat on a table and the fingers are extended

wrist-drop, and weak grip (due to missing synergistic effect of an extended wrist)

Sensory loss over the first dorsal interosseous (the anatomical snuff box)

Loss of supinator reflex (triceps reflex may also be lost if lesion above spiral groove).

If there is no sensory loss whatsoever, in a patient with symptoms of progressive radial nerve
palsy, then a lesion of the posterior interosseous nerve (the main, purely motor, branch of the
radial nerve) may be suspected and surgical exploration is considered.

MEDIAN NERVE (C6,7,8,T1):

 Median nerve arises from the lateral and medial cords → supplies lateral 2 lumbricals and lateral 3½
fingers
 Motor to “LOAF”: Lateral 2 lumbricals, Opponens pollicis, Abductor pollicis, Flexor pollicis brevis
& Forearm flexors except flexor carpi ulnaris & ulnar ½ of flexor digitorum profundus
 Median nerve palsy:

wasting of the thenar eminence

weakness of opposition, abduction and flexion of the thumb

sensory loss over the palmar aspect of the lateral 3½ fingers

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ULNAR NERVE (C7,8,T1):

 Ulnar nerve is the main continuation of the medial cord → supplies medial 2 lumbricals and
medial 1½ fingers
 Motor to “MAFIA”: Medial 2 lumbricals, Adductor pollicis, Flexor carpi ulnaris & ulnar ½ of
Flexor digitorum profundus, Interossei, Abductor & flexor digiti minimi
 Ulnar nerve palsy:

Generalized wasting and weakness of the muscle of the hand sparing the thenar eminence
(i.e. wasting of the hypothenar eminence and first dorsal interosseous, and guttering of the
dorsum of the hand)

Ulnar claw hand (hyperextension at the MCP joints with flexion of the IP joints in the fourth
and fifth fingers)

Sensory loss over the medial 1½ fingers

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CNS – CRANIAL NERVES

STEPS OF EXAMINATION

(1) APPROACH THE PATIENT

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him
• Ask the patient to sit upright on the edge of the bed facing you

(2) GENERAL INSPECTION

STEPS POSSIBLE FINDINGS
1. Scan the bedside.
Walking stick
1. Scan the patient.
Nutritional status: under/average built or overweight

Facial asymmetry (hemiplegia)

Abnormal facial movements: hemifacial spasm, facial
myokymia, blepharospasm, oro-facial dyskinesia…see
theoretical notes for movement disorders in cranial nerve
territory

Craniotomy scar

Neurofibromatosis

Naevi (consider Sturge-Weber syndrome…see theoretical
notes)
2. Examine the eyes
Ptosis

Proptosis

Strabismus (divergent or convergent)

(3) CRANIAL NERVE I (SENSORY): ask the patient "Has there been any change in your sense of smell
recently?"

(4) CRANIAL NERVES II, III, IV AND VI

• Visual Acuity (II): see Ch. 18 Eye- General
• Visual fields (II): see Ch. 18 Eye- General
• Eye movements (III, IV and VI): see Ch. 18 Eye- General
• Light reflex (II, III): see Ch. 18 Eye- General
• Swinging light test (II): see Ch. 18 Eye- General
• Accommodation-convergence reflex (III): see Ch. 18 Eye- General
• Optic disc (II): see Ch. 18 Eye- General

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(5) CRANIAL NERVE V

Cranial nerve V consists of 3 branches: the ophthalmic branch (sensory), the maxillary branch (sensory)
and the mandibular branch (mixed). The motor root runs with the mandibular branch.
Steps Possible findings
Motor 1. Look at the side of the face for wasting of the
Wasting of the masseters &
temporalis muscle temporalis.
2. Tell the patient "Clench your teeth"- feel the
masseters and temporalis simultaneously
3. Tell the patient "Open your mouth and don’t let me
Jaw will be pushed towards the
close it"- resist his jaw opening with your hand paralysed side due to
under his chin. Note if the jaw deviates to one side. unopposed action of the
contralateral pterygoid muscle
4. Jaw jerk: ask the patient to let his mouth hang
A mild or absent jaw jerk is
loosely open (but not too widely). Place your finger seen in normal individuals. In
on his chin. Percuss your finger with the hammer UMNL above the cervical cord
(or tap it suddenly with the other hand as in (e.g. pseudobulbar palsy), the
percussion). Feel and observe the jaw movement. jaw jerk is exaggerated
Sensory 1. Test light touch using a piece of cotton wool.
Forehead is supplied by V1:
Explain to the patient “I am going to touch you ophthalmic branch
with this piece of cotton wool and I want you to
Cheek is supplied by V2:
close your eyes and say (Yes) every time you feel maxillary branch
it” Test over each division comparing one side to
Lower lip is supplied by V3:
the other starting with the forehead, then cheek, mandibular branch
and then the lower lip. Apply the stimulus at
N.B: angle of Jew is not
random intervals. Avoid dragging it across the skin supplied by V nerve but the
or tickling the patient. greater auricular (C2)
2. Corneal reflex (V1 → VII): tell the patient “look
V1 lesion → failure of both
upwards to the ceiling”. Very lightly touch the side of face to contract, while
lateral edge of the cornea with a twisted wisp of VII lesion → failure of only one
cotton wool. Look for both direct and consensual side to contract), and then the
blinking lower lip (V3: mandibular

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(6) CRANIAL NERVE VII (MIXED + PARASYMPATHETIC)

Steps Possible findings
Motor Inspection 1. Look for facial asymmetry
Symmetry is retained in
(unilateral facial droop, bilateral disease
absent nasolabial fold and
forehead creases)
Lower part 2. Tell the patient “Smile.
The mouth is pulled towards
of the face Show me your teeth” the intact side
3. Tell the patient “Whistle”
Impossible in VII palsy
4. Tell the patient “Blow your
Air can be made to escape
cheeks out like this” Assess more easily on the affected
the strength by tapping with side
your finger on each inflated
cheek in turn
Upper part 5. Tell the patient “Close your
Bell’s phenomenon: the
of the face eyes tightly as if you have eyeball rolls upwards during
soap in them and don’t let attempted forced eye closure.
me open them” Observe for This is a normal phenomenon
Bell’s phenomenon. Look if that is particularly obvious
the eyelashes are equally when eye closure is
buried. Assess the strength impossible in a patient with
by trying to open his eyes LMN VII palsy
with your fingers.
The patient cannot bury the
eyelashes in LMN VII palsy
6. Tell the patient “Raise your
eyebrows like this, frown
like this”.
Stapedius 7. Ask the patient “Has you
Hyperacusis due to paralysis
muscle become intolerant to high- of stapedius muscle indicates
pitched or loud sounds?” a lesion proximal to the
stylomastoid foramen
Sensory 1. Ask the patient "Has there been any change
Altered taste due to
in your sense of taste recently?" Tell the involvement of chorda
examiner that you would like to test the tympani
taste sensation on the anterior 2/3 of the
Loss of taste indicates a
tongue. lesion proximal to the point
where the chorda tympani
joins the facial nerve and is
poor prognostic sign

Parasympathetic 1. Ask the patient “have you noticed reduced

(secretomotor) tear production and dry eyes?” Tell the
examiner that you would like to do
Schirmer’s tear test.
Look for causes 1. Palpate for parotid enlargement
VII nerve may be involved in
malignant tumour
2. Look at the external auditory meatus (the
Suggest HZ lesions in
cutaneous distribution of the VII nerve) and association with LMN VII
the fauces (the opening leading from the nerve palsy (Ramsay Hunt
mouth into the pharynx) for any vesicles syndrome).

3. Look at the tympanic membrane for
Rare cause of VII nerve palsy
evidence of otitis media) today
See theoretical notes for facial nerve palsy

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(7) CRANIAL NERVE VIII (SENSORY)

STEPS POSSIBLE FINDINGS
1. Ask the patient "Any problem with the hearing in either
ear? Can you hear that? Tell me when the sound
disappears"- rub finger and thumb together (or hold a
ticking watch) in front of each ear in turn and block the
opposite ear. Move your hand slowly away from the
patient’s ear and discover how far away from the ear the
sound is still heard. Compare both ears. If the hearing in
one ear is reduced proceed to the Rinné and Weber tests:
2. Rinné test: Hold a 512 Hz tuning fork on the mastoid
In normal subjects and in subjects
process (bone conduction) and then in the front of the ear with sensorineural deafness, air
(air conduction). Ask the patient which is louder conduction is louder than bone
conduction (positive test)

In subjects with conductive
deafness (e.g. wax or otitis media),
bone conduction is louder than air
conduction (negative test)

N.B. severe sensorineural deafness
in one ear → bone conduction is
louder than air conduction in the
other ear (false negative test)
3. Weber test: Hold a 512 Hz tuning fork on the vertex of
In normal subjects and in subjects
the head. Ask which ear it is louder in with sensorineural deafness, it is it
is louder in the good ear

in subjects with conductive deafness
(e.g. wax or otitis media), it is louder
in the deaf ear
4. Look in the ear if you suspect disease of the external ear
Perforated drum, wax, etc.

(8) CRANIAL NERVES IX, X (MIXED + PARASYMPATHETIC)

Steps Possible findings
Motor 1. Palatal movement (X): tell the patient "open
Normally both sides of the palate
your mouth; say aah". Look at the movement of elevate symmetrically. If one side
the soft palate using a torch. is paralysed (unilateral X nerve
palsy), it will remain flat and
immobile and the median raphe
will be pulled towards the intact
side. In bilateral paralysis the
whole palate remains motionless.
2. Swallowing (IX, X): give the patient a glass of
Two phases with a delay between
water to swallow. Watch for any difficulty with the aural phase and the pharyngeal
swallowing phase, coughing, spluttering or
nasal regurgitation
3. Speech: ask the patient to speak and cough. Nasal
Innervated by the recurrent
speech and bovine cough indicate vocal cord laryngeal from the vagus
palsy
Sensory 3. Pharyngeal sensation and gag reflex (IX→X):
An absence of gag reflex is
tell the examiner that you would like to test significant only if it is unilateral.
pharyngeal sensation (using an orange stick The most common cause of
gently), and elicit the gag reflex (sensory IX → reduced gag is old age. The gag is
motor limb X) by touching the posterior exaggerated in pseudobulbar palsy
pharyngeal wall or faucial pillars with a tongue (as it is an UMNL), whereas it is
depressor. Apply the stimulus to both sides in absent in bulbar palsy
turn.

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(9) CRANIAL NERVE XI (MOTOR)

• Sternocleidomastoids:
 Face the patient and inspect the sternocleidomastoids for wasting, fasciculations or hypertrophy
and palpate them simultaneously to assess their bulk.
 Test the power by asking the patient "Turn your head. Push your chin against my hand"- watch the
opposite sternocleidomastoid. Reverse the procedure to check the other sternocleidomastoid.
• Trapezii:
 Stand behind the patient to inspect the trapezii for wasting or asymmetry.
 Test the power by asking the patient "Shrug your shoulders; keep them shrugged" while you push
down on the shoulders with both your hands simultaneously. Watch for symmetry.

(10) CRANIAL NERVE XII (MOTOR)

Steps Possible findings
1. Tell the patient “Open your mouth "- look at
In unilateral LMN XII nerve palsy (bulbar
the tongue as it lies in the floor of the mouth for palsy) there is wasting and fasciculation on the
wasting or fasciculation. paralysed side.

In pseudobulbar palsy (bilateral internal
capsule or brain stem lesion), the tongue is stiff
and immobile (finding an exaggerated jaw jerk
[bilateral V lesion] in such cases can add
weight to the diagnosis).
2. Tell the patient "Push your tongue out straight.
In unilateral LMN XII nerve palsy, the tongue
Now move it from side to side"- note any is pushed towards the paralysed side.
deviation or weakness.
N.B: in unilateral facial paralysis, the protruded
tongue, though otherwise normal, may deviate
due to the mouth being twisted to one side
3. Test power by asking the patient “press your
tongue against the inside of your right then left
cheek, like this” while you press from outside
with your finger.

(11) THANK THE PATIENT AND COVER HIM (HER)

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THEORETICAL NOTES

MOVEMENT DISORDERS IN CRANIAL NERVE TERRITORY

Movement disorder Causes
Hemifacial spasm: intermittent spasm of Indicates compression of CN VII by ectopic vessels
muscles of one side of the face
Facial myokymia: persistent twitchy, Usually benign, possibly exacerbated by tiredness or caffeine.
often rhythmical movement usually Rarely indicative of brainstem lesion. may be caused by a
affecting the periorbital muscles. plaque of multiple sclerosis in the corticobulbar tracts or
brainstem course of CN VII
Blepharospasm: intermittent spasm of Idiopathic (elderly)
both eyelids
Oro-facial dyskinesia: lip-smacking and Usually a late reaction to major tranquiliser. May also occur
twisting of mouth as part of the syndromes listed under chorea (Wilson’s
disease, Huntington’s disease, post-pill or pregnancy chorea,
Sydenham’s chorea, stroke)

Sturge-Weber syndrome: port wine stain (purple birthmark on the face) associated with ipsilateral
vascular meningeal malformation and epilepsy

FACIAL NERVE PALSY

• The facial nerve consists of three roots that arise from the lower border of the pons. Leaving the
brainstem, it traverses the internal acoustic meatus into the facial canal to emerge from the skull at the
stylomastoid foramen. At the facial canal, it gives rise to the greater superficial petrosal nerve
(lacrimation) at the level of the geniculate ganglion, then the nerve to stapedius (lesion →
hyperacusis), and then it gives rise to the chorda tympani in the middle ear (taste from anterior 2/3 of
tongue and secretory to submandibular and sublingual glands)
• In unilateral UMN VII palsy, there is relative sparing of the upper face including eye closure
(orbicularis oculi) and forehead muscles (frontalis and corrugator superficialis) because there is
bilateral cortical innervation of the upper facial muscles. Also the Involuntary emotional movements of
the face, e.g. involuntary smiling and frowning, are subcortical, bilaterally represented and therefore
little, if at all, affected in UMN pyramidal lesions.
• In unilateral LMN VII palsy, there is paralysis of the upper and lower face, and the voluntary and
involuntary (emotional) facial movements on the affected side.
• If the intracranial part of the nerve is involved (lesion inside the facial canal or proximally), there
is:
 Decreased secretion from the lacrimal (greater superficial petrosal nerve) and submandibular and
sublingual glands (chorda tympani nerve)
 Hyperacusis (nerve to stapedius)
 Loss of taste over the anterior 2/3 of the tongue (chorda tympani nerve)
• Bell’s palsy: acute condition caused by swelling of the VII nerve in the facial canal, thought secondary
to viral infection, resulting in LMN paralysis of VII nerve. It may be associated with hypogeusia
(impairment of taste), hyperacusis (sounds appearing louder than normal) and decreased secretion from
lacrimal, submandibular and sublingual glands.
• Ramsay Hunt syndrome: HZ infection of the geniculate (facial) ganglion results in a severe LMN
facial palsy an a painful vesicular eruption within the external auditory meatus

CRANIAL NERVE PALSIES MAY ARISE FROM

• Specific lesions to the nerve
• Lesion in the nucleus
• Lesion in communicating pathway to and from the cortex, diencephalon (thalamus and associated
structures), cerebellum or other parts of the brainstem.
• As part of generalized problems of nerve or muscle

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MULTIPLE CRANIAL NERVE PALSIES ARE SEEN IN THE FOLLOWING CONDITIONS

• Lesion where several cranial nerves run together either in the brain stem (most commonly due to MS
in younger patients, and vascular disease in older patients) or within the skull (cavernous sinus,
cerebellopontine angle, or jugular foramen)
• Generalized disorder (e.g. myasthenia gravis → prominent involvement of eye muscles and facial
weakness)
• Multiple lesions (e.g. MS, CVA, basal meningitis)

CRANIAL NERVE PALSIES ARE USEFUL IN LOCALIZING A LESION WITHIN THE CNS
Clinical presentation Anatomical lesion
Hemiplegia When a cranial nerve is affected on The lesion must be at the level of the nucleus of
plus cranial the opposite side to a hemiparesis that nerve (III nerve palsy → midbrain lesion), (VI
nerve and/or VII → pontine lesion), (XII ± IX and XI →
affection medullary lesion)
Ipsilateral UMNL VII palsy Internal capsule lesion
Contralateral III palsy Weber’s – mid brain stroke
Contralateral VI and LMNL VII Millard-Gubler – stroke involving the
palsy pontomedullary junction
Pseudobulbar palsy Bilateral internal capsule or medullary lesion
When the tongue and face are affected on the same The lesion must be above the XII and VII nucleus
side as a hemiplegia respectively
Combined V, VII and VIII Cerebellopontine lesion (e.g. acoustic neuroma -
schwannomas involving the eighth cranial nerve)
Combined III, VI, V1 and VI Cavernous sinus lesion
Combined IX, X and XI Jugular foramen syndrome
Combined X, XI and XII LMNL Bulbar palsy
Combined X, XI and XII UMNL Pseudobulbar palsy
Prominent involvement of eye muscles and facial Suggests a myasthenic syndrome
weakness, particularly when variable

THE MOST COMMON CAUSE OF INTRINSIC BRAINSTEM LESIONS in younger patients is MS

and in older patients is vascular disease. Rarer causes include gliomas, lymphomas and brainstem
encephalitis.

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CNS - GAIT
STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask few questions “Could you tell me your name please? Are you right- or left-handed? Are you quite
comfortable? Do you feel pain anywhere?”
• Ask permission to examine him

Step 2: General inspection:

• Bedside: walking stick, shoes-callipers, built-up heels
• General appearance: scan the patient quickly looking for:

Nutritional status (under/average built or overweight)

Abnormal movement or posture (rest or intention tremors, dystonia, choreoathetosis,
hemiballismus, Myoclonic jerks, tics, pyramidal posture)

Abnormal facial movements (hemifacial spasm, facial myokymia, blepharospasm, oro-facial
dyskinesia)

Facial asymmetry (hemiplegia)

Nystagmus (cerebellar syndrome)

Facial wasting (muscular dystrophy)

Sad, immobile, unblinking facies (Parkinson’s disease)

Peroneal wasting (Charcot-Marie-Tooth disease)

Pes cavus (Friedreich’s ataxia, Charcot-Marie-Tooth disease)
• Hands: tell the patient “outstretch your hands like this (palms facing downwards)”… then “like this
(palms facing upwards)”

Check for wasted hands (MND, Charcot-Marie-Tooth disease, syringomyelia)

feel the radial pulse (AF → thromboembolism)

Step 3: Ask the patient “Can you walk without help? I will stay with you in case of any problems”.
Notice any cerebellar dysarthria during his reply.

Step 4: Ask him to walk to a defined point, turn and walk back. Look at the patient from behind, in
front, and the side. Go through the following questions in sequence to find out the diagnosis:
• Is the gait obviously asymmetrical:

Hemiplegic gait:
o One leg swing out to the side (abduction and circumduction at the hip)
o The leg is stiffly extended at the knee and ankle, the foot is inverted an the toes scrape the
floor (patient tries to avoid this by contralateral tilt of the trunk)
o The arm is stiffly flexed at the side (triple flexion posture of the arm) while in the mildest
form, the arm is held in a normal position but swings less than the normal arm

Unilateral foot drop:
o One knee lifts higher than the other to avoid catching the toe on the floor.
o The foot hangs down while elevated
o Patient is unable to walk on the affected heel

Antalgic or painful gait: The good limb hurries through and the painful limb buckles to cushion
the impact on each step

Orthopaedic gait: bony deformity (shortened limb, previous hip surgery, trauma)
• Is it short stepping gait:

Parkinsonian gait:
o Delayed initiation of walking. Short shuffling steps with modest flexion at hips and knees.
Turns are clumsy and freezing may occur
o Occasional festinant gait (indicates impairment of postural reflexes): the pace tends to
accelerate as the upper body gradually leans further ahead of the feet (propulsion). Similarly,
the patient takes several steps backward (retropulsion) when given a gentle pull from behind.

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o Stooped posture (flexion dystonia), arms adducted at shoulders and flexed at the elbow with
reduced arm swing,
o Additional signs: sad, expressionless, unblinking facies. The hands may show coarse (4- to 6-
Hz) pronation-supination rest tremor (pill-rolling)

Marche a petit pas:
o Upright posture, marked arm swing, short, quick tapping steps
o Additional signs: dementia, pseudobulbar palsy, emotional lability

Apraxic gait:
o When asked to walk while standing, a long pause often occurs before any attempt to walk, as
if the patient is glued to the ground (sticky feet/ magnetic gait). After few steps, walking is
stopped again for several seconds. The process is then repeated
o Disjointed movement (slow, shuffling, unsteady, short steps) as if forgotten how to walk,
neither turning or straight walking are fluent, and there is tendency to retropulsion
o Stooped posture
• Is the gait Broad based or scissoring:

Cerebellar ataxia:
o Broad-based, unsteady (ataxic), high-stepping gait that veers towards the side of lesion. Turns
are clumsy.
o Difficulty walking heel-to-toe
o Additional signs: scanning/staccato dysarthria and nystagmus

Sensory ataxia:
o Broad-based, unsteady (ataxic), high-stepping, slapping (stamping) gait, with clumsiness on
the turns (patient watch the floor intently and is more ataxic when eyes closed)
o Difficulty walking heel-to-toe
o Positive Romberg’s test

Scissoring (paraparetic) gait:
o Stiff legged gait: The patient has difficulty in bending the knees, so the foot is raised from the
ground by tilting the pelvis (abduction and circumduction at the hip). The stiff leg is then
swung forward, dragging the inverted foot along the floor, so that the foot tends to cross
(scissor)
o The arms are held in flexed and pronated position
o Additional signs: bedside wheelchair and/or walking sticks, diffuse atrophy and contractures
(if chronic), scars in the back or spinal deformity
• Is the gait high-stepping (but not broad based):

Bilateral foot drop:
o High stepping with the feet slapping the ground (knee lifted high to avoid catching the toe on
the floor)
o Unable to walk on heels
• Is the gait waddling:

Waddling (myopathic) gait:
o The body sways from side to side with each step, due to marked rotation of the pelvis and the
shoulder
o Additional signs: The body is often tilted backwards, with an increased lumbar lordosis
• Is the gait bizarre or chaotic:

Functional gait (Astasia-abasia): Bizarre, elaborated movement, worse when watched, however
they do not fall and hurt themselves (veer toward the examiner's arms or a nearby bed.
Inconsistent with rest of examination

Choreoathetotic gait:
o Chaotic walking (shuffling, twitching and spasmodic), due to Intermittent, irregular
movements that disrupts the flow of the gait and unpredictable flexion or extension
movements at the hip (pelvic lurch)
o Unusual foot placement responses may occur so that the toes may extend away from the floor
(avoiding response) or the feet may appear glued to the floor (grasping response)
o Involuntary movements are usually exaggerated during walking

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Step 5: If you suspect sensory ataxia, tell the patient “Close your eyes while walking”. In case of sensory
ataxia, he will become more ataxic with eyes closed

Step 6: Heel-to-toe (tandem) gait: tell the patient “can you walk as if on a tight rope like this”. This will
exacerbate ataxia (note the side to which the patient tends to fall).

Step 7: Walking on toes: tell the patient “Can you walk on your toes like this” (if unable → weakness of
gastrocnemius - S1 lesion).

Step 8: Walking on heels: tell the patient “Can you walk on your heels like this” (if unable → foot drop -
L5 lesion). N.B. if the patient has a spastic gait or a hemiparesis he may find both walking on toes and
walking on heels difficult to perform

Step 9: Romberg’s test: have the patient between you and a wall and tell him “stand with your feet
together like this; I am ready to catch you if you fall” allow him to stand like this for a few seconds. If he
doe not fall with his eyes open tell him “close your eyes”. Watch for unsteadiness with eyes opened and
with eyes closed:
• Severe unsteadiness with eyes open → cerebellar disorders, particularly those involving the vermis.
• Patient is able to stand with eyes open and tends to fall with eyes closed or patient is more unsteady
(tends to fall) with the eyes closed more than with them open → positive Romberg’s test (sensory
ataxia – posterior column lesion or peripheral neuropathy)
• False-positive Romberg’s test

In vestibular (labyrinthine) disorders, the patient has consistent unsteadiness which is worse with
eyes closed. It is different from sensory ataxia in that the imbalance appears after an interval and
consists of a slow swaying to one side (side of the lesion), while in sensory ataxia , the swaying
begins as soon as the eyes are closed, rapid, and occurs in all directions

Patients with hysteria tend to sway from the hips rather than the ankles. However they do not fall
and hurt themselves
Step 10: Additional signs according to suspected diagnosis:
• Parkinson’s disease: check for extrapyramidal signs (expressionless unblinking face, rest tremors,
cogwheel rigidity, glabellar tap sign)
• Cerebellar ataxia: check for cerebellar signs (nystagmus, staccato dysarthria, finger-nose
incoordination, dysdiadochokinesia)
• Sensory ataxia: check joint position sense and vibration sense , look for Argyll Robertson pupils and
clinical anaemia
• Paraparetic (scissoring) gait: look for scars in the back or spinal deformity, examine tone, reflexes,
plantar reflex and sensation
• Apraxic gait: frontal lobe signs (dementia, grasp and suck reflexes)

Step 11: Thank the patient and cover him (her)

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THEORETICAL NOTES

Phases of gait: for each leg, gait has two phases:

• Swing phase: from toe-off to heel-strike (foot clears the ground)
• Stance phase: form heel-strike to toe-off (foot on the ground and load bearing). When both feet are on
the ground this is double stance

Features and causes of abnormal gaits:

Abnormal gaits Causes
Hemiplegic gait Unilateral UMNL (stroke , MS)
Unilateral foot drop
Common peroneal nerve palsy (ankle eversion is lost while ankle inversion and
ankle reflex are preserved)

Lumbosacral plexus lesion

Sciatic nerve palsy (ankle reflex and ankle inversion are lost)

Peripheral neuropathy, especially HSMN type 1

L4/5 radiculopathy most commonly due to prolapsed lumbar disc (ankle reflex and
ankle inversion are lost)

MND
Antalgic or painful Arthritis, trauma
gait
Orthopaedic gait Shortened limb, previous hip surgery, trauma
Parkinsonian gait Extrapyramidal syndromes (basal ganglion dysfunction), e.g. Parkinson’s disease or
drug induced (major tranquilizers: phenothiazines)
Marche a petit pas Bilateral diffuse cortical dysfunction (multilacunar infarct)
(senile gait)
Apraxic gait Abnormal cortical integration of the movement, usually with frontal lobe pathology,
e.g. NPH or CVA
Cerebellar ataxia
Ipsilateral cerebellar syndrome: demyelination, vascular disease, trauma, tumour
or abscess

Bilateral cerebellar syndrome: drugs (phenytoin), alcohol, demyelination (MS),
vascular disease (stroke), hereditary cerebellar degeneration (Friedreich’s ataxia),
paraneoplastic disorders, hypothyroidism

Midline cerebellar syndrome (truncal ataxia and gait ataxia, in absence of limb
incoordination): lesion of the cerebellar vermis (causes as for bilateral cerebellar
syndrome)
Sensory ataxia
Posterior column lesion:
o Cord compression (e.g. cervical spondylosis, tumour)
o Tabes dorsalis
o Vitamin B12 deficiency (subacute combined degeneration of the cord)
o Degenerative spinal cord disease

Peripheral neuropathy (predominantly sensory): DM, Vitamin B1, B12
deficiencies, Uraemic neuropathy, Alcohol, Drugs (vincristine, isoniazid),
Carcinomatous neuropathy (especially CA bronchus), Amyloidosis, and Leprosy.
Scissoring Spastic paraparesis (corticospinal lesion):
(paraparetic) gait
Cerebral palsy

MS

Cord compression

Hereditary spastic paraplegia
Bilateral foot drop Peripheral neuropathy (predominantly motor): acute (Guillan-Barre syndrome,
porphyria, diphtheria), subacute (lead poisoning), chronic (HSMN, CIDP)
Waddling Weak proximal muscles (proximal myopathies, bilateral congenital dislocation of
(Myopathic) gait the hip)
Functional gait Hysteria
(Astasia-abasia)
Choreoathetotic gait Huntington’s disease

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• Patholophysiologic basis of Romberg’s test:

Central postural control (equilibrium) is dependent on input from three peripheral modalities:
1. Vision
2. Vestibular apparatus
3. Proprioception (joint sense and sense of position)

Disturbance in any one of these modalities can be compensated for (completely or incompletely) by
input from the other two systems.

Impaired proprioception can be overcome by visual and vestibular feedback. Asking the patient to
close his eyes during the Romberg’s test helps uncover any disordered proprioception that may have
been masked by vision.

• Causes of positive Romberg’s test (loss of joint position sense):

Posterior column lesion in the spinal cord
o Cord compression (e.g. cervical spondylosis, tumour)
o Tabes dorsalis
o Vitamin B12 deficiency (subacute combined degeneration of the cord)
o Degenerative spinal cord disease

Peripheral neuropathy (predominantly sensory): DM, Vitamin B1, B12 deficiencies, Uraemic
neuropathy, Alcohol, Drugs (vincristine, isoniazid), Carcinomatous neuropathy (especially CA
bronchus), Amyloidosis, and Leprosy.

N.B. causes of predominantly motor neuropathies are: acute (Guillan-Barre syndrome, porphyria,
diphtheria), subacute (lead poisoning), chronic (HSMN, CIDP)

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 Pearls in PACES (CNS- Speech & Higher Cortical Functions)
Adel Hasanin

CNS – SPEECH & HIGHER CORTICAL FUNCTIONS

STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask permission to examine him “I am just going to ask you some questions; is that alright?”

Step 2: General inspection:

• Bedside: walking stick, shoes-callipers, built-up heels
• General appearance: scan the patient quickly looking for:

Nutritional status (under/average built or overweight)

Abnormal movement or posture (rest or intention tremors, dystonia, choreoathetosis,
hemiballismus, Myoclonic jerks, tics, pyramidal posture)

Abnormal facial movements (hemifacial spasm, facial myokymia, blepharospasm, oro-facial
dyskinesia)

Facial asymmetry (hemiplegia)

Nystagmus (cerebellar syndrome)

Facial wasting (muscular dystrophy)

Sad, immobile, unblinking facies (Parkinson’s disease)

Ptosis, lack of facial expression, slack mouth (myasthenia gravis)

Myxoedematous facies (variegated dysarthria)

Horner’s syndrome (syringomyelia, Pancoast’s syndrome)

Peroneal wasting (Charcot-Marie-Tooth disease)

Pes cavus (Friedreich’s ataxia, Charcot-Marie-Tooth disease)
• Face (mouth):

Ask the patient to open his mouth: shine your pen torch into the opened mouth; look for poorly-
fitting or absent denture, painful ulcer

Look at the tongue as it lies in the floor of the mouth for wasting or fasciculation

Ask the patient to protrude his tongue out, then to move it from side to side (inspect the
posterolateral edge of the tongue)
• Hands: tell the patient and demonstrate “outstretch your hands like this (palms facing downwards)”…
then “like this (palms facing upwards)”

Check for wasted hands (MND, Charcot-Marie-Tooth disease, syringomyelia)

Feel the radial pulse (AF → thromboembolism)

Step 3: Speech assessment: ask the patient some general questions to get him talking: “Please could you
tell me your name? Your age? Are you right handed or left handed? What is your first language? Where do
you live?” If he does not appear to understand, repeat louder. Note the volume of sound, rhythm of speech
and clarity of enunciation. You should be able to quickly distinguish between dysphonia (disorders of
phonation), dysarthria (disorders of articulation), and dysphasia (disorders of Speech content)

Step 4: Dysphonia: the patient is able to give his name and address but is unable to produce normal
volume of sound, or speaks in a whisper (indicates impairment of voice production from the larynx). Ask
the patient to:
• “Cough”. Listen to the quality of the cough:

A bovine cough (cough lacks explosive start) → vocal cord palsy (innervated by the recurrent
laryngeal from the vagus)

Dysphonia with normal cough → local laryngeal cause e.g. laryngitis (most commonly due to
common cold) or hypothyroidism (thickening of the vocal cords from amyloid deposits), or
psychological disturbance (hysteria)
• “Say a sustained ‘eeeeee’”. If the note cannot be sustained and fatigues, consider myasthenia

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Step 5: Dysarthria: the patient is able to give his name and address but the words are not formed properly
(indicates inability to articulate properly because of local lesion in the mouth or disorder of speech muscles
or their connections).
• First ask about any poorly-fitting or absent denture, or painful mouth
• Then ask the patient to repeat difficult phrases (tongue twisters): e.g. “rhinoceros”, “British
constitution”, “Baby hippopotamus”, “egg”, “rub”, “yellow lorry”. Listen carefully for the rhythm of
the speech, clarity of enunciation (slurred words) and which sounds cause the greatest difficulty. You
must be able to recognize the various types of dysarthria and look for additional signs to support your
diagnosis (see theoretical notes)

Step 6: Dysphasia: If the patient has no dysarthria or dysphonia but the speech is meaningless (receptive
aphasia) or non fluent (expressive aphasia), assess the following:
• Comprehension (understanding): ask the patient (without gesturing) to perform a few simple
commands, e.g. “please put your tongue out, shut your eyes, touch your left ear with your right hand”.
• Speech fluency: test the patient’s ability to form sentence by asking the patient to describe something
in more detail, e.g. “what is your job? What you actually do when at work? How you would get home
from here?” Listen carefully for fluency of speech, word-finding pauses, jargon speech, paraphasias,
neologisms
• Naming: hold up your keys and ask the patient “what is this?” If no answer, then ask, “Is this a spoon?
Is it a pen? Is it keys?”
• Repetition: ask the patient to repeat simple sentence, e.g. “today is Tuesday”
• Orofacial dyspraxia: if there are expressive problem, check to see if the problem is true expressive
dysphasia or whether there is orofacial dyspraxia (difficulty in volitional movements of the lip and
tongue → hesitancy in word production). Ask the patient (without gestures) to perform various
orofacial movements (provided that there is no receptive dysphasia), e.g. “please show me you teeth.
Put out your tongue and move it from side to side” subsequently ask the patient to obey the same
commands but with gesture, i.e. so the patient can mimic. This should distinguish between ideational
dyspraxia and ideomotor dyspraxia, so that the type of speech therapy is tailored accordingly
• Ask if you may test reading (ask the patient to read a sentence and to obey a written command) and
writing (ask the patient to write a sentence): impaired reading (dyslexia) and impaired writing
(dysgraphia) indicate extension of damage to parieto-occipital region, and may be part of Gerstmann’s
syndrome. Now you must be able to recognize the various types of dysphasia and look for additional
signs to support your diagnosis (see theoretical notes)

Step 7: Higher mental functions: use the following “abbreviated mental test” (AMT) to test attention and
concentration, orientation, memory, general knowledge and intelligence. Each item scores 1 point (8-10 →
Normal, 4-7 → mild-moderate dementia, less than 4 → moderate-severe dementia)
• Age “How old are you?”
• Address “Where do you live (town or road)?”
• Address for recall at end of test “I’d like to test your memory. Please say this address ’42 west street’.
Now remember it and repeat it when asked”. Then at end of test ask ““Can you name the address I
named before?”
• Time (the nearest hour) “What time is it?”
• Year “What year is it?”
• Place “Where are we now?”
• Recognition of two persons” Who am I? Who is this (doctor, nurse, etc.)?”
• Name of national leader “Who is our president?”
• Year of World War 2 “When did the second world war start?”
• Count backwards from 20 to 1 “Begin with 20 and count backwards till one”

Step 8: Thank the patient and cover him (her)

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THEORETICAL NOTES

Process and abnormalities of speech

Process abnormality
Hearing Deafness
Understanding (comprehension) Dysphasia
Thought and word finding (expression) Dysphasia
Voice production Dysphonia
Articulation Dysarthria

Types of dysarthria:
1. Ataxic (cerebellar) dysarthria
Features: slurred, slow, jerky and explosive (lalling, staccato, Causes: cerebellar lesions
scanning) speech, with irregular breaks in articulation and Additional signs: other cerebellar signs, e.g.
equal emphasis on each syllable, thus “rhinoceros” is nystagmus, impaired finger-nose test with past
pronounced “rhi-noc-er-os”. There may be inspiratory whoops pointing and intention tremor, impaired heel-shin test,
indicating the lack of coordination between respiration and dysdiadochokinesia, ataxic gait with tendency to fall
phonation. to side of the lesion

2. Spastic (UMN) dysarthria

Features: laboured speech, patient hardly opens mouth Causes: bilateral UMNL of the corticobulbar tract
as if trying to speak from the back of the mouth, slurred, (pseudobulbar palsy) due to bilateral CVA of the internal
monotonus, high-pitched, ‘hot potato’, Donald Duck’ capsule and less commonly due to MS, MND, high
speech due to a tight, immobile tongue. The precision of brainstem tumours, head injury
consonant pronunciation is lost, thus “British Additional signs: other signs of pseudobulbar palsy, e.g.
constitution” becomes “Brizh conshishushon” as the emotional lability, cannot protrude his tongue which lies
crispness of the ‘ta’ sound depends on adequate power in on the floor of the mouth and is small and tight, dysphagia
the tip of the tongue. (particular to liquids, including saliva → dribbling from
the mouth), nasal regurgitation, absent palatal movement,
positive jaw jerk (bilateral V lesion), evidence of
associated bilateral corticospinal tract (pyramidal) lesions,
e.g. bilateral spasticity and extensor plantars

3. Flaccid (LMN) dysarthria

Bulbar palsy Causes: disease affecting bulbar cranial nerves, e.g. MND,
Features: nasal twang, indistinct, decreased syringobulbia, Guillan-Barre syndrome, poliomyelitis,
modulation, slurring of labial and lingual consonants. subacute meningitis, neurosyphilis
Additional signs: other signs of bulbar palsy:
• IX, X lesion, e.g. dysphagia (particular to liquids, including
saliva → dribbling from the mouth), nasal regurgitation,
absent palatal movement, palatal air escape may be audible
during phonation,
• XII lesions (tongue is wasted, wrinkled, flaccid and
fasciculating)
Paralysis of VII (facial palsy) Additional signs: VII lesion (unilateral facial droop, absent
Features: distorted speech especially labial consonants nasolabial fold and forehead creases)
(B, M, P) – test with phrase “baby hippopotamus”
Paralysis of IX, X (palatal dysarthria) Causes: vagal damage at or above the level of the pharyngeal
Features: nasal speech as with a bad cold. The patient branches.
is unable to pronounce words that require complete Additional signs: other signs of IX, X lesion, e.g. dysphagia
closure of the nasopharynx. Thus “egg” is sounded as (particular to liquids, including saliva → dribbling from the
“eng” and “rub” becomes “rum”. mouth), nasal regurgitation, absent palatal movement, palatal
air escape may be audible during phonation
Paralysis of XII (tongue palsy) Additional signs: signs of XII lesions (tongue is wasted,
Features: distorted speech especially lingual wrinkled, flaccid and fasciculating)
consonants (L, R) – test with phrase “yellow lorry”

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4. Hypokinetic (extrapyramidal) dysarthria

Features: monotonus Causes: Parkinson’s disease
without accents or Additional signs: other extrapyramidal signs, e.g. expressionless unblinking face, drooling
emphasis, low pitched (due to excessive salivation and some dysphagia), pill rolling tremor, blepharo-clonus
somewhat slurred (tremor of the eyelids when the eyes are gently closed), titubation, cogwheel rigidity at the
speech. wrist and lead-pipe rigidity at the elbow, bradykinesia (demonstrated by asking the patient
to touch his thumb successively with each finger), glabellar tap sign, Parkinsonian gait
(stooped posture, reduced arm swing, delayed initiation of walking, short shuffling steps,
occasional festinant gait)

5. Hyperkinetic (choreiform/dystonic) dysarthria

Features: Variable speaking rate (slower in dystonia), Causes: Choreiform disorders (Huntington’s
improper stress, inappropriate silences. This gives the speech a disease), myoclonic disorders, dystonia musculorum
bursting quality. deformans
Additional signs: other signs of Huntington’s in
choreiform dysarthria (chorea, dementia)

6. Myopathic/Myasthenic dysarthria
Features: weak hoarse voice with a nasal Causes: myopathy, myositis, myasthenia gravis
quality, soft accents. Muscle fatigability in Additional signs: other signs of myasthenia gravis in myasthenic
myasthenia gravis (demonstrated by making the dysarthria:
patient count). • Ptosis (accentuated by upward gaze)
• Variable strabismus (with diplopia)
• Facial and proximal muscle weakness all of which worsen with
repetition (lack of facial expression, mouth is slack, snarls when
tries to smile, cannot whistle, demonstrate proximal muscle
weakness and fatigability in the upper limbs)

7. Myotonic dysarthria
Features: slurred, Causes: myotonic dystrophy
suppressed speech due Additional signs: other sings of myotonic dystrophy, e.g. myopathic facies (long, thin and
to myotonia of tongue expressionless), wasting of facial muscles, sternocleidomastoid, shoulder girdle and
and pharynx. quadriceps, bilateral ptosis, frontal baldness, grip myotonia, percussion myotonia, difficulty
opening his eye after firm closure, dysphagia, wasting and weakness of the distal muscles
(forearm and legs) with areflexia

8. Variegated dysarthria
Hypothyroidism Additional signs: other signs of hypothyroidism, e.g. myxoedematous facies
Features: low pitched, catarrhal, (thickened and coarse facial features, periorbital puffiness and pallor), skin is
hoarse, croaking, guttural voice as if rough, dry , cold and inelastic, “peaches and cream” complexion (anaemia
the tongue is too large for the mouth and carotenaemia), hair is thin, dry and brittle with loss of outer third of
eyebrows, xanthelasma, goitre or thyroidectomy scar, generalized non pitting
swelling of subcutaneous tissue, bradycardia, slow relaxing ankle jerks
Amyloidosis
Features: rolling and hollow, hardly
modulated speech due to large tongue
Multiple ulcers or thrush in the
mouth
Features: some parts of the speech
indistinct

Parotitis or temporomandibular
arthritis
Features: monotonous, suppressed,
badly modulated

Generalized paresis of the insane Additional signs: other signs of GPI, e.g. dementia, vacant expression,
Features: slurred, hesitant or feeble tremor of the hands, lips and tongue (trombone tremor – the tongue darts in
voice and out of the mouth involuntarily), spastic paraparesis, brisk reflexes,
extensor plantars.

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Model of speech understanding and output

• Recognition of the sounds as language in Wernicke’s area
• Understanding of the meaning of the words in the concept area (temporo-parietal association areas)
• Generation of the speech output in Broca’s area
• Wernicke’s area is also connected directly to Broca’s area by the arcuate fasciculus
• All these areas are in the dominant hemisphere. The left hemisphere is dominant in all right-handed
patients and in 50% of left-handed patients

Types of dysphasia:
1. Wernicke’s (receptive) (sensory) (fluent) (Jargon) dysphasia
Features: Lesion of Wernicke’s area:
• Impaired comprehension posterior part of superior temporal
• Fluent (jargon) speech: the patient replies fluently (often rapidly), gyrus plus adjacent parts of
but often unintelligible. He puts words together in the wrong order parietal and occipital cortex of
and mixes them with paraphasias (syllabic substitution with some dominant hemisphere
phonemic relationship to the original word, e.g. “toothspooth” for Causes: embolus to the inferior
“toothbrush” or word substitution with a semantic relationship to the division of the middle cerebral
correct word, e.g. hand” for “foot”) and neologisms (syllabic or Additional signs: right
word substitution with no relationship to the original syllable/word) homonymous superior
• Impaired repetition, naming, reading, and writing. Attempts to quadrantanopia, right cortical
repeat result in paraphasic distortions and irrelevant insertions. sensory loss
• Loss of insight into his dysphasia
• The prognosis for recovery is poor

2. Transcortical receptive (sensory) (fluent) dysphasia

Features: similar to Wernicke’s Lesion: Disruption of the connection between Wernicke’s area
aphasia but with preserved and concept area (posterior parieto-occipital region)
repetition Causes: Infarctions in the posterior watershed zone or neoplasms
that involve the temporo-parietal cortex posterior to Wernicke’s
area

3. Broca’s (expressive) (motor) (non-fluent) (telegraphic) dysphasia

• Features: preserved comprehension Lesion of Broca’s area: inferior
• Non-fluent speech: the content is good but the patient says little. frontal gyrus of dominant
Speech is interrupted by many word-finding pauses and lacks the hemisphere
filler words (to, but, so, the…). For example, “phone daughter Causes: occlusion of the superior
evening” division of the middle cerebral
• Impaired repetition and naming and writing (reading is artery
comparatively preserved) Additional signs: right
• preserved Insight into his condition (so patient could be tearful and hemiparesis, right facial
depressed) weakness, orofacial ideomotor
• The prognosis for eventual adaptation of the patient to his dyspraxia
disability is good

4. Transcortical expressive (motor) dysphasia

Features: similar to Broca’s aphasia, but Lesion: disruption of the connection between the concept
with preserved repetition area and Broca’s area
Causes:
• Lesion of anterior watershed zone between anterior and
middle cerebral artery territories
• Lesion of supplementary motor cortex in the territory of
the anterior cerebral artery

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5. Global dysphasia
Features: Lesion: Combined dysfunction of Broca's and Wernicke's areas
• Impaired comprehension. Causes: strokes that involve the entire left middle cerebral artery.
• Non-fluent speech. additional signs: right hemiplegia, hemisensory loss,
• Impaired repetition, naming, homonymous hemianopia and general intellectual deterioration
reading, and writing.

6. Conductive dysphasia
Features: Lesion of the arcuate fasciculus in the
• Preserved comprehension dominant hemisphere
• Fluent speech output, but paraphasic Causes: occlusion of a portion of the
• Impaired repetition, naming and writing (reading loudly angular branch of the middle cerebral
may be similarly compromised; while reading silently for artery
comprehension is intact) Additional signs: vary according to
the primary lesion site.

7. Nominal (anomic) dysphasia

Features: Lesion:
• Preserved comprehension. • Nominal aphasia is found in both motor and receptive dysphasia
• Fluent speech output, but • Lesions of angular gyrus may produce a syndrome in which nominal
paraphasic dysphasia is associated with dyslexia plus Gerstmann’s syndrome
• preserved repetition (dysgraphia, right-left disorientation, acalculia, and finger agnosia)
• Impaired naming and word • Nominal aphasia is also seen in degenerative disorders such as
finding (excessive word- Alzheimer’s disease.
finding pauses)

N.B. Dyspraxia:

Inability to perform purposeful volitional familiar movements in the absence of motor weakness,
sensory deficit or severe incoordination.

The defect is often in the dominant parietal lobe, with disruption of connections to the motor cortex
(frontal lobe) and to the opposite hemisphere (corpus callosum).

It is classified into
o ideational dyspraxia: the patient is unable to perform movement though understanding the
command (due to loss of the concept of performing the movement)
o ideomotor apraxia: patient is unable to perform movement on command (or do it in odd or
bizarre fashion) , although he may do this automatically or when asked to mimic (as the
concept is present but the motor programme for the usage is not accessible)

Common types are dressing, gait, limb, truncal, constructional and orofacial dyspraxia

N.B. apraxia and agnosia are complex disorders and should not usually form part of the examination – RCP
UK statement

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CNS – CEREBELLAR

STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues (almost always there is problem with coordination or
equilibrium)
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask permission to examine him
• Expose the upper and lower limbs completely and keep the patient descent (genital area is covered)

Step 2: General inspection:

• Bedside: walking stick, shoes-callipers, built-up heels
• General appearance: scan the patient quickly looking for:

Nutritional status (under/average built or overweight)

Cachexia (paraneoplastic cerebellar syndrome, alcoholic cerebellar syndrome), unkempt
appearance and stigmata of liver disease (alcoholic cerebellar syndrome)

Kyphoscoliosis (Friedreich’s ataxia)

Intention tremors

Pyramidal posture (MS, Friedreich’s ataxia)

Myxoedematous facies

Abnormal facial movements (hemifacial spasm, facial myokymia, blepharospasm, oro-facial
dyskinesia)

Facial asymmetry (hemiplegia)

Nystagmus (towards the side of the lesion)

Skew deviation of the eyes

Radiotherapy burn (paraneoplastic cerebellar syndrome)

Pacemaker scar (Friedreich’s ataxia)

Pes cavus (Friedreich’s ataxia)
• Face (mouth): look for gingival hypertrophy (phenytoin), high arched palate (Friedreich’s ataxia)
• Hands: tell the patient and demonstrate “outstretch your hands like this (palms facing downwards)”…
then “like this (palms facing upwards)”

Check for clubbing and tar-stained fingers (paraneoplastic cerebellar syndrome)

Feel the radial pulse (hypothyroidism)
• Legs: pes cavus (Friedreich’s ataxia)

Step 3: Cerebellar dysarthria: Ask the patient some general questions to get him talking: “Please could
you tell me your name? Your age? Are you right handed or left handed? Where do you live?” In cerebellar
dysarthria, speech is slurred, slow, jerky and explosive (lalling, staccato, scanning), with irregular breaks in
articulation and equal emphasis on each syllable. There may be inspiratory whoops indicating the lack of
coordination between respiration and phonation.

Step 4: Nystagmus: see “Ch 18. Eye – General”

Step 5: Pronator drift test: see “Ch 7. CNS – Upper Limb”

Step 6: Coordination in UL: see “Ch 7. CNS – Upper Limb”

Step 7: Coordination in LL: see “Ch 6. CNS – Lower Limb”

Step 8: Gait and Romberg’s test: ask the examiner’s permission to examine the patient’s gait and
perform Romberg’s test (see Ch 9. CNS - Gait)

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Step 9: Examination of lower limbs: see “Ch 6. CNS – Lower Limb”

• Inspection
• Tone
• Power
• Reflexes
• Sensory

Step 10: Examination of upper limbs: see “Ch 7. CNS – Upper Limb”
• Inspection
• Tone
• Power
• Reflexes
• Sensory

Step 11: Cranial nerves: see “Ch 8. CNS – Cranial Nerves”

Step 12: Additional signs:

• Ipsilateral deafness and cranial nerves V and VII affection (cerebellopontine angle lesion, usually
acoustic neuroma)
• Fundal examination: optic atrophy (MS, Friedreich’s ataxia), papilloedema (posterior fossa space
occupying lesion)

Step 13: Thank the patient and cover him (her)

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SKIN

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Physical examination Clear Pass Fail Clear

Pass Fail
□ □ □ □
2. Identification and interpretation of physical signs Clear Pass Fail Clear
Pass Fail
□ □ □ □
3. Discussion related to the case Clear Pass Fail Clear
Pass Fail
□ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask permission to examine him

Step 2: General inspection: you may have been given a lead in the instructions such as look at the hands
or look at the face, however always start your visual survey systematically (scalp & hair → face → eyes
[eyebrows & eyelids] → mouth & lips → hands & nails → arms & elbows → neck, axilla & trunk → legs
& feet)
• Scalp & hair:

Psoriasis (redness and scaling at the hairline)

Alopecia:
o Diffuse non-scarring alopecia (age-related hair loss, hypothyroidism, hypopituitarism, iron
deficiency, cytotoxic agents)
o Localized non-scarring alopecia (alopecia areata, fungal infection, traction alopecia in
nervous children)
o Scarring alopecia (burns, lichen planus, discoid lupus, trigeminal zoster)
• Face:

Systemic sclerosis (tight, shiny skin, mask face, beaked nose)

Malar (butterfly) rash (SLE)

Linear scleroderma (en coup de saber)
• Eyes (eyebrows & eyelids):

Dermatomyositis (heliotrope discoloration of the eyelids with periorbital oedema)

Xanthelasma (familial hypercholesterolaemia – non specific)
• Mouth & lips: look at the lips, ask the patient to evert his lips (look at the inner side of the lips), then
to open his mouth (shine your pen torch into the opened mouth), then to protrude his tongue out, then
to move it from side to side (inspect the posterolateral edge of the tongue) then to touch the roof of the
mouth with the tip of the tongue (inspect the under surface of the tongue and the floor of the mouth).
Look for:

Hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

Lichen planus (white lace-like network on mucosal surface)

Addison’s (diffuse pigmentation next to the teeth)

Mouth ulcers (inflammatory bowel, Behcet’s, celiac disease, extragenital syphilis)
• Hands & nails:

Nail pitting (psoriasis or fungal infection)

Onycholysis (psoriasis, fungal infection or thyrotoxicosis)

Periungual telangiectasias (SLE, scleroderma, and dermatomyositis)

Sclerodactyly (systemic sclerosis, dermatomyositis)

Gottron’s papules (dermatomyositis)

Striate xanthomata (dysbetalipoproteinemia)

Tendon xanthomata (familial hypercholesterolaemia)

Skin crease pigmentation (Addison’s)

Thin skin with bruises and/or purpura (Cushing’s)
• Arms & elbows:

Psoriasis (extensor surfaces)

Eczema (dermatitis) (flexor areas)

Tendon xanthomata (familial hypercholesterolaemia)

Eruptive xanthomata (familial hypertriglyceridaemia, familial lipoprotein lipase deficiency,
familial apo CII deficiency)

Tuberous/tuberoeruptive xanthomata (familial hypercholesterolaemia, dysbetalipoproteinemia)

Rheumatoid nodules (around pressure points, especially the elbows)

Gouty tophi (in the skin around the joints, particularly the hands and feet, and on the helix of the
ear and the olecranon and prepatellar bursae)

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• Neck, axilla & trunk:

NF 1 (Von Recklinghausen's disease): 6 or more café-au-lait patches, cutaneous neurofibromas
(multiple, palpable, rubbery, cutaneous tumors), and freckling in non-sun exposed areas (axillary
or inguinal)

Morphoea: single or multiple plaques of skin induration (localized scleroderma)

Addison’s (areolar and scar pigmentation)
• Legs & feet:

Leg ulcer (venous, ischemic, neuropathic)

Pretibial myxoedema (Grave’s disease)

Psoriasis (knees, gluteal cleft)

Eczema (popliteal fossae)

Tendon xanthomata (Achilles)

Gouty tophi (feet and prepatellar bursae)

Step 3: Examine the lesion (or one typical lesion in pleomorphic rash) in terms of:
• Site: note the anatomical distribution of the lesion whether

Confined to a single area (morphoea, erythema nodosum, rodent ulcer, melanoma, alopecia areata)

Present in other areas (psoriasis, neurofibromatosis, acanthosis nigricans, dermatomyositis)

Widespread (drug eruption)

Predilection to extensor areas (psoriasis)

Flexor areas (lichen planus, eczema)

Mucous membranes (candidiasis), nails and face (tuberous sclerosis)

Both legs (necrobiosis lipoidica diabeticorum)

Joints of hands, elbows and on the ears (gouty tophi)

Sun exposed areas (drugs, SLE)

Dermatomal (HZ)
• Size & Shape, e.g. oval, circular, annular, etc.; measures (- x -)
• Colour, e.g. erythematous (red) or pigmented
• Consistency: palpate any lesion with your finger tips to find their consistency
• Character:

Erythema: redness due to increased skin perfusion

Purpura: discoloration of the skin or mucosa due to extravasation of red cells (does not blanch on pressure)

Petechiae: small purpuric lesions < 2 mm in diameter

Ecchymosis: large extravasation of blood

Telangiectasia: permanently dilated, visible small vessels

Macules: flat, circumscribed area of discoloration, not raised above the skin – size and shape varies

Papules: raised, circumscribed, firm lesions < 1 cm in diameter

Nodules: like papules but larger > 1 cm in diameter; usually lie deeper in skin

Plaques: raised, flat-topped, disc-shaped lesion

Weal: area of circumscribed elevation (dermal oedema), white with pink margins, compressible, associated
with itching and tingling; usually transient

Vesicles: circumscribed fluid containing elevation < 5 mm in diameter

Bullae: large vesicles > 5 mm in diameter

Pustules: circumscribed elevations containing purulent fluid which may, in some cases, be sterile (e.g.
Behcet’s)
• Surface

Scales: flakes of easily detached keratin (dead tissue from the horny layer) which may be dry (e.g. psoriasis)
or greasy (e.g. seborrhoeic dermatitis)

Crusts: an accumulation of dried exudates

Ulcers: excavations in the skin due to loss of tissue including the epidermal surface; remember that every
ulcer has a shape, an edge, a floor, a base and a secretion, and it forms a scar on healing

Excoriation: shallow linear abrasion due to scratching
• Secondary features, e.g.

Lichenification: areas of increased epidermal thickness and accentuated skin markings secondary to chronic
rubbing

Sclerosis: induration of the dermis or subcutaneous tissues
• Surrounding skin, e.g.

Scratch marks (itching)

Radiotherapy field markings on the skin in the vicinity of a radiation burn

Paper-thin skin with purpura (corticosteroid therapy)

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Step 4: Examine local lymph nodes if indicated (see Ch 17. Endocrine – Neck)

Step 5: Additional signs and associated features, e.g.

• Psoriasis: arthropathy and nail changes
• Eruptive xanthomas: scar from operative management of acute pancreatitis
• Hereditary haemorrhagic telangiectasis: GI bleeding

Step 6: Ask some questions to confirm the diagnosis (if mentioned in the instructions):
• Scleroderma: “Do you have any difficulty with swallowing? Diarrhoea? Bloating? Indigestion?
Do you have any shortness of breath (pulmonary or cardiac fibrosis)? Dry cough? Dry eyes? Do
your fingers change colour in the cold?”
• Raynaud’s: “Do your fingers change colour in the cold or with emotion? What colour do they
go? Is there a particular sequence of colours (White → Blue → Crimson red)? Is it painful?
Does it improve by heat? How long have you had the trouble? What is your job (Vibrating
tools)? Do you have any difficulty with swallowing (CREST)? Any Joint pains or dry eyes
(connective tissue disorders)?”

Step 7: Thank the patient and cover him (her)

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THEORETICAL NOTES

Skin layers:
• Inner dermis of collagen and elastic tissue lying on subcutaneous fat
• Outer continuously replenishing epidermis; extending from a basal layer of cells with scattered
melanocytes to a top layer of protective keratinocytes. These continuously degenerate and slough off to
be replaced by cells from beneath.
• The epidermo-dermal junction is demarcated by a basement membrane.

Onych-: prefix denoting nail(s)

Onycholysis: separation or loosening of part or all of a nail from its bed. The condition may occur in
psoriasis and in fungal infection of the skin and nail bed. It is commoner in women and may return to
normal spontaneously

Onychomycosis: fungus infection of the nails caused by dermatophytes or Candida. The nails become
yellow, opaque, and thickened.

Paronychia (whitlow): an inflamed swelling of the nail folds. Acute paronychia is usually caused by
infection with Staphylococcus aureus. Chronic paronychia occurs mainly in those who habitually engage in
wet work; it is associated with secondary infection with Candida albicans. It is vital to keep the hands dry
to control paronychia

Koilonychia: the development of thin (brittle) concave (spoon-shaped) nails, a common disorder that can
occur with anaemia due to iron deficiency, though the cause is not known. Any underlying disease should
be treated.

Xanthomatas and associated dyslipidaemia

Type of xanthomata Site Associated dyslipidaemia

Xanthelasmas (barely elevated
Eyelids
Familial hypercholesterolaemia (at
deposits of cholesterol) least 50% of the patients with
xanthelasma have normal lipid

Tendon xanthomata
Extensor tendons profiles)
of the knuckles
and Achilles
tendons

Striate xanthomata (yellow-
Palm creases
Remnant hypercholesterolaemia
orange lines) (dysbetalipoproteinemia)

Tuberous/tuberoeruptive
Elbows and
Familial hypercholesterolaemia
xanthomata (soft, painless buttocks
Remnant hypercholesterolaemia
nodules) (dysbetalipoproteinemia)

Eruptive xanthomata (small
Trunk and
Chylomicronaemia syndrome (familial
orange-red papules) extremities lipoprotein lipase deficiency &
familial apo CII deficiency)

Familial hypertriglyceridaemia

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Examples of lesion according to anatomical distribution:

Hair & Scalp:

Psoriasis: redness and scaling at the hair line

Alopecia: either diffuse non-scarring alopecia (age-related hair loss, hypothyroidism, hypopituitarism,
iron deficiency, cytotoxic agents), localized non-scarring alopecia (alopecia areata, fungal infection,
traction alopecia in nervous children), scarring alopecia (burns, lichen planus, discoid lupus, trigeminal
zoster)

Face:

Systemic sclerosis: tight, shiny skin, mask face, beaked nose

Malar (butterfly) rash: fixed erythematous rash (flat or raised) over the cheeks and bridge of the
nose, with fine scales and may be telangiectasis (SLE). A more diffuse maculopapular rash,
predominant in sun-exposed areas, is also common and usually indicates disease flare.

Linear scleroderma: involves an extremity or face. Linear scleroderma of one side of the forehead
and scalp produces a disfiguration referred to as “en coup de sabre” because it resembles a wound from
a sword. It may be associated with hemiatrophy of the same side of the face

Capillary haemangioma (port wine stain): purple birth mark on the face, may be associated with
ipsilateral vascular meningeal malformation and epilepsy (Sturge-Weber syndrome)

Rodent ulcer (Basal cell carcinoma): raised lesion with central ulceration and a pearly, rolled,
telangiectatic tumour border (usually below the eye or on the side of the nose)

Lupus pernio: dark-red discoloration of the nose (sarcoidosis)

Eyebrows & eyelids:

Dermatomyositis - heliotrope discoloration of the eyelids with periorbital oedema

Xanthelasma - barely elevated deposits of cholesterol on the eyelids (familial hypercholesterolaemia).
Non specific sign; at least 50% of the patients with xanthelasma have normal lipid profiles

Zoster ophthalmicus: HZ of ophthalmic branch of the trigeminal nerve

Lips & Mouth:

Hereditary haemorrhagic telangiectasia (Osler-Weber-Rendu syndrome): autosomal dominant
condition with mucosal telangiectasia; presents with GI bleeding or epistaxis. The telangiectasia also
occur in the retina and brain

Lichen planus: white lace-like network on mucosal surface

Addison’s: diffuse pigmentation next to the teeth

Mouth ulcers (inflammatory bowel, Behcet’s, celiac disease, extragenital syphilis)

Candidiasis (white exudates inside the mouth usually associated with a disease requiring multiple
antimicrobial therapy, or an immunosuppressive disorder, e.g. Leukaemia, AIDS, etc.)

Cheilosis: swollen cracked bright-red lips (iron, folate, vitamin B12 or B6 deficiency)

Pemphigus vulgaris: blistering of skin and mucus membrane. In half or more of patients, lesions
begin in the mouth

HSV: grouped and confluent vesicles with an erythematous rim on the lips. Persistent ulcerative HSV
are among the most common infections in AIDS.

Peutz-Jeghers’ syndrome: autosomal dominant condition with brown spots on the lips, oral mucosa,
around the mouth, face and occasionally elsewhere on the skin; associated with hamartomatous
polyps of the small and large bowel which only rarely become malignant

Leucoplakia: a thickened white patch on a mucous membrane, such as the mouth lining or uvula that
cannot be rubbed off. It is not a specific disease and is present in about 1% of the elderly. Occasionally
Leucoplakia can become malignant. Hairy Leucoplakia, with a shaggy or hairy appearance, is a marker
of AIDS

Gum hypertrophy (phenytoin, cyclosporine, AML)

Smooth and red tongue (B12 deficiency)

Geographical tongue (riboflavin/B2 deficiency)

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Nails & Hands:

Nail pitting (psoriasis or fungal infection)

Onycholysis: separation or loosening of part or all of a nail from its bed (psoriasis, fungal infection or
thyrotoxicosis)

Periungual telangiectasias: pathognomonic signs of the three major connective tissue diseases – SLE,
scleroderma, and dermatomyositis)

Sclerodactyly: thickening and tightening of the digital subcutaneous tissue (systemic sclerosis,
dermatomyositis)

Gottron’s papules: purplish discoloration seen over the knuckles (dermatomyositis)

Striate xanthomata: yellow-orange lines in the palm creases (dysbetalipoproteinemia)

Tendon xanthomata: extensor tendons of the knuckles (familial hypercholesterolaemia)

Skin crease pigmentation (Addison’s)

Thin skin with bruises and/or purpura (Cushing’s)

Lichen planus: thinning of the nail plate with longitudinal, linear depressions. Occasionally there is
destruction of the nail (pterygium)

Koilonychia: thin, brittle, concave, spoon-shaped nails (Iron deficiency)

Paronychia (whitlow): inflamed swelling of the lateral nail folds (acute paronychia is usually caused
by infection with Staphylococcus aureus. Chronic paronychia occurs mainly in those who habitually
engage in wet work; it is associated with secondary infection with Candida albicans)

Periungual fibromata: periungual fibrous hyperkeratotic outgrowths (tuberous sclerosis)

Dupuytren’s contractures: flexion deformity of the fingers, usually the ring and little fingers, caused
by thickening and shortening of the palmar facia (familial, alcoholism, chronic antiepileptic therapy ,
operators of vibrating machines)

Yellow nail syndrome: nails are yellow and excessively curved. Associations include recurrent
pleural effusions, chronic bronchitis, bronchiectasis, nephrotic syndrome, hypothyroidism,
lymphoedema and penicillamine therapy

Half and half nails: the proximal nail bed is white and distal half is pink or brown. They are
associated with CRF and RA

Arms and elbows:

Psoriasis: erythematous, sharply demarcated papules and rounded plaques, covered by silvery scale (extensor
surfaces). Traumatized areas often develop lesions of psoriasis (Koebner or isomorphic phenomenon). The most
common areas for plaque psoriasis to occur are the elbows, knees, gluteal cleft, and the scalp. Involvement tends
to be symmetric.

Eczema (dermatitis): ridging, redness, scaling and papulovesicular rash, commonly over flexural skin,
particularly the antecubital and popliteal fossae

Tendon xanthomata (familial hypercholesterolaemia)

Eruptive xanthomata: small orange-red papules on the trunk and extremities (familial hypertriglyceridaemia,
familial lipoprotein lipase deficiency, familial apo CII deficiency)

Tuberous/tuberoeruptive xanthomata: soft, painless nodules on the elbows and buttocks (familial
hypercholesterolaemia, dysbetalipoproteinemia)

Rheumatoid nodules: firm, 0.5- to 4-cm nodules that tend to localize around pressure points, especially the
elbows. They are seen in approximately 20% of patients with rheumatoid arthritis and 6% of patients with Still's
disease. Biopsies of the nodules show palisading granulomas. Similar lesions that are smaller and shorter-lived are
seen in rheumatic fever.

Gouty tophi: firm yellow papules or plaques (occasionally discharge a chalky material) due to deposition of
monosodium urate in the skin around the joints, particularly the hands and feet, and on the helix of the ear and the
olecranon and prepatellar bursae.

Lichen planus: small, purplish, discrete, flat-topped papules, most commonly on the wrist (flexor areas). The skin
lesions may occur anywhere but have a predilection for the wrists, shins, lower back, and genitalia

Pseudoxanthoma elasticum: abnormal deposition of calcium on the elastic fibres of the skin, eye, and blood
vessels. The primary sit of involvement in the skin is the flexural areas (neck, axillae, antecubital fossae, and
inguinal area). Yellow papules coalesce to form reticulated plaques, giving the plucked chicken skin appearance.
Hanging, redundant skin folds develop in severe cases.

Olecranon bursitis: bursitis is inflammation of a bursa, which is a thin-walled sac lined with synovial tissue.
Olecranon bursitis occurs over the posterior elbow, and when the area is acutely inflamed, infection should be
excluded by aspirating and culturing fluid from the bursa.

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Neck, Axilla & Trunk:

Neurofibromatosis type 1 (Von Recklinghausen's disease): autosomal dominant disease caused by
Mutation of the NF1 gene on chromosome 17. Major features include the presence of 6 or more café-
au-lait patches, cutaneous neurofibromas (multiple, palpable, rubbery, cutaneous tumors), freckling in
non-sun exposed areas (axillary or inguinal), hamartomas of the iris (Lisch nodules), and
pseudoarthrosis of the tibia. Neurofibromas are benign peripheral nerve tumors composed of
proliferating Schwann cells and fibroblasts. Patients with NF1 are at increased risk of developing
nervous system neoplasms, including plexiform neurofibromas, optic gliomas, ependymomas,
meningiomas, astrocytomas, and pheochromocytomas. NF2 is characterized by the development of
bilateral vestibular schwannomas in >90% of individuals who inherit the mutation of the NF2 gene on
chromosome 22. Multiple cafe au lait spots and peripheral neurofibromas occur rarely.

Morphoea: single or multiple plaques of skin induration (localized scleroderma)

Addison’s (areolar and scar pigmentation)

HZ (shingles): unilateral vesicular eruption along the intercostals nerves (dermatomes from T3 to L3
are most frequently involved)

Vitiligo: localized area of hypopigmentation as a result of loss of melanocytes, commonly associated
with other autoimmune disorders (hypothyroidism, Graves' disease, pernicious anemia, Addison's
disease, uveitis, alopecia areata, chronic mucocutaneous candidiasis, polyglandular autoimmune
syndromes types I and II)

Pemphigus: blisters over the trunk and limbs

Tinea (pityriasis) versicolor: asymptomatic, well-delineated, hyperpigmented or hypopigmented
macules centred on the upper trunk and upper arms. Confluent lesions may cover large areas, making
the border difficult to find. A fine "branny" scale or folliculitis is sometimes visible.

Pityriasis rosea: multiple, round to oval erythematous patches with fine central scale, distributed
along the skin tension lines on the trunk.

Dermatitis herpetiformis: itchy blisters over scapulae, buttocks, elbows, knees

Pseudoxanthoma elasticum: abnormal deposition of calcium on the elastic fibres of the skin, eye, and
blood vessels. The primary sit of involvement in the skin is the flexural areas (neck, axillae, antecubital
fossae, and inguinal area). Yellow papules coalesce to form reticulated plaques, giving the plucked
chicken skin appearance. Hanging, redundant skin folds develop in severe cases.

Acanthosis nigricans: pigmentation and velvety thickening of the major flexures particularly the
axilla, commonly associated with insulin resistance or malignancy

Abnormal pattern of secondary hair growth: axillary loss in hypogonadism, or hirsutism in
androgenisation, e.g. PCOS

Stretch marks (striae): atrophic and silvery indicates previous distension (usually striae gravidarum,
occasionally drained ascites), or purple and livid (Cushing’s)

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Legs & feet:

• Leg ulcer: venous - painless, over the gaiter area of lower leg (near the medial and lateral malleoli),
ischemic (arterial) - painful, over the distal extremities and pressure points, or neuropathic - painless,
over pressure areas, e.g. under the metatarsal heads or heals, commonly due to peripheral neuropathy.
In DM, ischemia and neuropathy both contribute to ulceration often wit superadded infection
• Pretibial myxoedema (Grave’s disease): noninflamed, indurated plaque with a deep pink or purple
color and an "orange-skin" waxy, appearance. Nodular involvement can occur, and the condition can
rarely extend over the whole lower leg and foot, mimicking elephantiasis. Non pitting pretibial oedema
is also seen in hypothyroidism, along with puffy face, oedematous eyelids and pallor (often with a
yellow tinge due to carotene accumulation).
• Psoriasis (knees, gluteal cleft)
• Eczema (popliteal fossae)
• Tendon xanthomata (Achilles)
• Gouty tophi (feet and prepatellar bursae)
• Lichen planus (shins)
• Pyoderma gangrenosum: irregular ulcer with necrotic base, overhanging purple edge, and a peripheral
erythematous halo. An estimated 30 to 50% of cases are idiopathic, and the most common associated
disorders are ulcerative colitis and Crohn's disease. Less commonly, it is associated with chronic active
hepatitis, seropositive rheumatoid arthritis, acute and chronic granulocytic leukemia, polycythaemia
vera, and myeloma.
• Necrobiosis lipoidica diabeticorum: painless yellowish plaques, usually bilateral, associated with DM
• Erythema nodosum: panniculitis characterized by tender deep-seated tender red nodules and plaques,
usually located on the lower extremities. Common causes are Streptococcal infection, other upper
respiratory tract infections, sarcoidosis, and inflammatory bowel disease.
• Henoch-Schonlein (anaphylactoid) purpura: systemic small vessel vasculitis characterized by
palpable purpura (most commonly distributed over the buttocks and lower extremities), arthralgias,
gastrointestinal signs and symptoms, and glomerulonephritis.
• Erythema ab igne: skin is dry, often with a yellow tinge due to carotene accumulation (due to sitting
too close to a fire)
• Pemphigoid: blisters over the legs and arms
• Keratoderma blenorrhagica (Reiter’s syndrome): consist of vesicles that become hyperkeratotic,
ultimately forming a crust before disappearing. They are most common on the palms and soles but may
occur elsewhere as well.

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LOCOMOTOR - HAND

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Physical examination Clear Pass Fail Clear

Pass Fail
□ □ □ □
2. Identification and interpretation of physical signs Clear Pass Fail Clear
Pass Fail
□ □ □ □
3. Discussion related to the case Clear Pass Fail Clear
Pass Fail
□ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Introduce yourself
• Ask the patient “Are you quite comfortable? Do you have any pain? Where do you feel the pain? Can
you point to it?”
• Ask permission to examine him “I would like to examine your hand, if it is all right with you”

Step 2: General inspection:

• Bedside: walking stick, shoes-callipers, built-up heels
• General appearance: scan the patient quickly looking for:

Nutritional status (under/average built or overweight)

Paget’s (enlargement of skull, bowing of tibia or femur, kyphosis)

Marfan’s (tall stature with disproportionately long limbs, arachnodactyly, dislocated lens)

Systemic sclerosis (expressionless facies, adherent shiny skin, sometimes with telangiectasis)

Ankylosing spondylitis (stooped posture and rigid spine)

Acromegalic facies (prominent supraorbital ridges and large lower jaw)

Cushingoid facies (steroid changes in a patient with rheumatoid arthritis), exophthalmos (thyroid
acropachy)

Horner’s syndrome (T1 lesion)

Muddy iris (iritis )

Gouty tophi or psoriasis (ears)

Peripheral arthropathy (knees, ankles)

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Step 3: Look at the hands: let the patient sit over the edge of the bed and place the hands over a pillow.
Expose the hands and forearm including the elbows. Study first the dorsal and then the palmar aspects of
the hands.
• Nails:

Nail pitting (psoriasis or fungal infection)

Onycholysis (psoriasis, fungal infection or thyrotoxicosis)

Clubbing (with painful swollen wrists in hypertrophic pulmonary Osteoarthropathy)

Nail-fold infarcts (vasculitis – usually rheumatoid)

Splinter haemorrhages (unlikely)
• Skin:

Colour:
o Erythema (suggests acute inflammation caused by soft tissue infection, septic arthritis, tendon
sheath infection or crystal-induced disease)
o Abnormal pigmentation (particularly skin crease pigmentation)

Consistency:
o Tight, shiny and adherent (sclerodactyly)
o Papery thin, ± purpuric patches (steroid therapy)
o Thick greasy (acromegaly)

Lesions: psoriasis, vasculitis, purpura, telangiectasis (systemic sclerosis), tophi, neurofibromata,
surgical scar (joint replacement)
• Muscles:

Isolated wasting of the thenar eminence (median nerve lesion)

Wasting of the hypothenar eminence and first dorsal interosseous, and guttering of the dorsum of
the hand but sparing the thenar eminence (ulnar nerve lesion)

Generalized wasting of the thenar and hypothenar eminences and the other small muscles of the
hand (T1 lesion, brachial plexus lesion, combined ulnar and median nerve lesions, arthritis leading
to disuse atrophy, cachexia)

Bilateral wasting of the small muscle with dorsal guttering (RA, syringomyelia, MND)
• Joints: observe the distribution of any abnormalities – symmetrical (RA) or asymmetrical (seronegative
arthritides); and proximal or distal

Swelling:
o Rheumatoid arthritis: soft swelling of the proximal joints (MCP & PIP)
o Osteoarthritis: bony swelling at the base of the DIP

Deformity:
o Rheumatoid arthritis: swan neck deformity at the DIP joint, boutonniere deformity at the PIP joint, Z
deformity of the thumb, ulnar deviation of the MCP joint, anterior subluxation of MCP joints, dorsal
subluxation of the ulna at the carpal joint
o Scleroderma: sclerodactyly with tapering of the fingers and may be flexion deformities (sometimes with
gangrene of the fingertips)
o Claw hand: hyperextension at the MCP joints with flexion of the IP joints in the fourth and fifth fingers
(ulnar nerve lesion)
o Arachnodactyly: The fingers are long and thin (Marfan’s syndrome)
o Dupuytren’s contracture: flexion deformity of the fingers, usually the ring and little fingers, caused by
thickening and shortening of the palmar facia (familial, alcoholism, chronic antiepileptic therapy ,
operators of vibrating machines)
o Mallet finger: flexion deformity at the DIP joint which is passively correctable. This is usually caused
by minor trauma disrupting the terminal extensor expansion at the base of the distal phalanx, either with
or without bony avulsion
o Rotational deformity: indicates phalangeal fracture, best detected by asking the patient to flex the fingers
together and then in turn (normally, the fingers should not cross and should all point to the scaphoid
tubercle in the wrist, while fractured finger crosses over its fellows and points away from the scaphoid
tubercle)

Nodules:
o Heberden’s nodes at the DIP or Bouchard’s nodes at the PIP (osteoarthritis)
o Rheumatoid nodules over the extensor tendons and in the palms
o Gouty tophi
o Calcified nodules in systemic sclerosis (usually localized to finger tips but may involve extensor aspects
of forearm or elbows)
o Vasculitic nodules in SLE and systemic vasculitis

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Step 4: Feel the hands (ask the patient if his hands are painful before touching them, and watch the patient
face during examination for any sign of tenderness):
• Hotness and tenderness are signs of activity
• Swelling, deformity, nodules: confirm the findings on inspection and palpate any swelling to detect
whether it is soft and boggy or hard and bony (To detect any soft swelling, press both sides of the joint
gently with your index and thumb and any swelling will bulge up. Now press on the swelling from top
to bottom with the index and thumb of your other hand to test for sponginess):

Soft swelling (synovitis): rheumatoid arthritis

Hard swellings (often at the base of the DIP) suggests bony outgrowth (osteophytes) characteristic
of osteoarthritis, mucous cysts or rarely tumours.

Painful swelling over flexor tendon sheaths in the hand and fingers (usually just proximal to the
MCP joints): volar flexor tenosynovitis

Painful swelling over tendon sheaths of abductor pollicies longus and extensor pollicis brevis
(along the radial aspect of the rest): De Quervain’s tenosynovitis
• Crepitus:

Crepitus over the joints are detected by placing your index finger over the joint, while it is moved
passively with your other hand. Crepitus over the joints may indicate osteoarthritis or loose bodies
(cartilaginous fragments) in the joint space, but should be differentiated from non-specific clicking
of joints.

Crepitus over the tendon sheaths may be appreciated during passive movement of the fingers in
tenosynovitis. It is usually associated with triggering phenomenon.

Step 5: Move the hand

• Hand grip: ask the patient to make a fist, then extends (stretch out) the fingers fully. Lack of full
extension of one or more fingers may indicate tendon rupture. To test the power of grip, ask the patient
“Grip my fingers tightly (insert two fingers from the thumb side into the palm of the patient’s hand)”.
• Pincer movement: tell the patient “Touch the tip of your index finger with the tip of your thumb, like
this and don’t let me pull them apart”
• Prayer sign: to assess extension, tell the patient “put the palms of the hands together and extend the
wrist full like this” (normal is 90 degrees of extension)
• Reverse prayer sign: to assess flexion, tell the patient “put the backs of the hands together and flex
the wrists fully like this” (normal 90 degrees of flexion) Have the patient hold this position for 30
seconds and then comment on how the hands feel. Pain, tingling, or other abnormal sensations in the
thumb, index, or middle fingers strongly suggest carpal tunnel syndrome (Phalen's Test). You may
wish to confirm median nerve compression at the wrist by doing the Tinel’s test (percussion of the
nerve at putative site of compression, usually using a tendon hammer, produces paraesthesiae in the
distribution of the nerve)
• Trigger phenomenon: normally, the tendon moves smoothly in and out of its surrounding sheath as
the finger straightens and bends. In trigger finger (flexor digital tenosynovitis), the inflamed tendon
can move out of the sheath as the finger bends. However, it cannot easily move back in as the finger
straightens and therefore the finger becomes locked in a bent position. Straightening the finger forces
the swollen area into the sheath—producing a popping sensation similar to that felt when pulling a
trigger. This could be elicited by passive extension of the previously flexed finger. Trigger finger can
result from repetitive use of the hands (as may occur from using heavy gardening shears) or from
inflammation (as occurs in rheumatoid arthritis).

Step 6: Assess function of the hand: undoing a button and writing

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Step 7: Neurological examination of the hand: perform brief neurological assessment focusing
particularly on the median and ulnar nerves. Always compare right with left.
• Power: Describe any weakness in terms of the medical research council (MRC) scale from 5 (normal)
down to 0 (no visible muscle contraction). Tell the patient: “I am going to test the strength of some of
your muscles”:

Finger abduction: tell the patient “Spread your fingers wide apart like this and don’t let me push
them together” → dorsal interossei (ulnar nerve; T1).

Finger adduction: tell the patient “Hold this piece of paper between your fingers and don’t let me
pull it out” → palmar interossei (ulnar nerve; T1).

Thumb abduction: tell the patient “Straighten your hand, like this (palm upwards) and point your
thumb towards the ceiling, like this. Now keep it there and don’t let me push it down” → abductor
pollicis brevis (median nerve: C8, T1).

Thumb opposition: tell the patient “Touch the tip of your little finger with the tip of your thumb,
like this and don’t let me pull them apart” → opponens pollicis (median nerve; T1).
• Sensory (pinprick):

Demonstrate the stimuli to the patient by testing on the sternum (use each end of the hat pin):
“this is sharp…and this is blunt…now I’m going to test the sensation in your hands and I want you
to close your eyes and say “Sharp” if it feels sharp, and “blunt” if it feels blunt”.

Screening test:
o Palmar surface of distal phalanx of index finger: median nerve; C6
o Palmar surface of distal phalanx of middle finger: median nerve; C7
o Palmar surface of distal phalanx of little finger: ulnar nerve; C8

Assessing a hypothesis: if you suspect a certain pattern of sensory loss (dermatomal or specific
nerve sensory loss), test within the area of interest with great care, particularly noting any
difference between the two sides

Step 8: Radial pulse: check for rate and rhythm

Step 9: Elbows: rheumatoid nodules, psoriatic plaques, scar or deformity underlying an ulnar nerve palsy

Step 10: Additional signs: e.g. evidence of carpal tunnel syndrome (if you diagnose rheumatoid arthritis or
acromegaly)

Step 11: Thank the patient and cover him (her)

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Pearls in PACES (Locomotor- Hand)
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THEORETICAL NOTES

Phases of clubbing: (cardiac causes include cyanotic heart diseases and infective endocarditis)
1. Swelling of the soft tissues of the terminal phalanx (→ increased nail bed fluctuation). To detect nail
bed fluctuation, place both thumbs under the pulp of the terminal phalanx and attempt to move the nail
within the nail bed using your index fingers. A “spongy feel” confirms nail bed fluctuation
2. Obliteration of the normal obtuse angle between the nail and nail bed (this defines clubbing). To
confirm obliteration of the angle between the nail and nail bed ask the patient to approximate the
dorsal aspects of the terminal phalanges (Shamroth's sign)
3. The nail loses its longitudinal ridges and becomes convex from above downwards (due to soft tissue
hypertrophy). In extreme cases the terminal segment of the finger is bulbous, like the end of a drum
stick.
4. Hypertrophic pulmonary osteoarthropathy (HPOA) representing the most extreme form, in which
beside the clubbing of fingers there is pain and swelling of the wrists and ankles due to periostitis
manifested by periosteal thickening and subperiosteal new bone formation (seen on X-rays of distal
forearm and lower legs). Isotope bone scanning demonstrates increased activity and often the serum
alkaline phosphatase is raised. This is almost always associated with lung cancer, usually squamous
cancer.

Causes of clubbing:
• Idiopathic
• Pulmonary causes:

Chronic fibrosing alveolitis

Chronic suppuration in the lungs (bronchiectasis, empyema, lung abscess, cystic fibrosis)

Bronchogenic carcinoma, mesothelioma

Severe chronic cyanosis

Pulmonary TB

Emphysema
• Cardiac causes:

Congenital heart disease, e.g. Fallot’s tetralogy

Infective endocarditis

Severe chronic cyanosis
• Chronic abdominal disorders:

Hepatic cirrhosis

Crohn’s disease

Polyposis of the colon

Ulcerative colitis

Coeliac disease
• Familial

Swelling and deformities of rheumatoid arthritis:

• Swelling of MCP joints produces loss of interdigital indentation, on the dorsum of the hand especially
when the MCP and IP are fully flexed → loss of normal “hill-vally-hill-vally” aspect.
• Swelling at the PIP joints produces a “spindling” appearance which is typically seen in rheumatoid
arthritis and collateral ligament injuries
• Swan neck deformity: flexion deformity at the DIP joint with hyperextension at the PIP joint
• Boutonniere (button-hole) deformity: flexion deformity at the PIP joint with hyperextension at the DIP
joint (imagine the tip of the finger pressed firmly onto a button)
• Z deformity of the thumb
• Ulnar deviation of the MCP joint is typical of rheumatoid arthritis
• Anterior subluxation of MCP joints
• Dorsal subluxation of the ulna at the carpal joint

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Sites of hand or wrist involvement and their potential disease associations

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 Pearls in PACES (Locomotor- Knee)
Adel Hasanin

LOCOMOTOR - KNEE

STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Approach the right hand side of the patient, shake hands, introduce yourself
• Ask the patient “Are you quite comfortable? Do you have any pain? Where do you feel the pain? Can
you point to it?”
• Ask permission to examine him “I would like to examine your knee, if it is all right with you”
• Position patient lying flat on the bed.
• Expose both legs from the upper thigh to the foot and ask the patient if he has any pain

Step 2: General inspection:

• Bedside: walking stick, shoes-callipers, built-up heels
• General appearance: scan the patient quickly looking for:

Nutritional status (under/average built or overweight)

Rheumatoid (symmetrical deforming polyarthritis in the hands)

Psoriatic arthritis (asymmetrical arthritis and skin plaques)

Gout (podagra of the first MTP joint)

Step 3: Look at the leg (comparing one side to the other):

• Skin: Scars, sinuses, redness, rash or wounds to suggest entry of infection
• Muscle: quadriceps wasting is almost invariable with inflammation or chronic pain and develops
within days to a fortnight. If wasting present, measure the thigh girth in both legs at 20 cm above the
tibial tuberosity
• Leg deformity:

Genu valgus (knock-knee)

Genu varus (bow-legs)

Flexion deformity (the patient lies with one knee flexed): hip, knee or combined problem)

Shorter leg: while both legs stretched out as far as possible and in equivalent positions, measure
with a tape from umbilicus to medial malleolus (the apparent length of leg) and from ASIS to
medial malleolus (the true length of leg)
• Swollen knee:

Enlarged prepatellar bursa (housemaid’s knee)

Effusion of the knee joint: Loss of medial and lateral dimples around the knee suggests the
presence of effusion. A large effusion is seen as horseshoe-shaped swelling above the knee.
Swelling extending beyond the joint margins suggests infection, major injury or rarely tumour.

Baker’s cyst: bursa enlargement in the popliteal fossa

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Step 4: Feel the knee

• Warmth and tenderness: place your whole hand gently over the patient’s knee and rest it there for a
few seconds. Compare the temperature of this knee with the mid calf and mid thigh on the same side as
well as the opposite knee. Watch the patient’s face for any sign of tenderness. Ask if the knee is tender
on palpation. By this stage you should have an idea of whether this is an inflammatory or non-
inflammatory problem and how active it is
• Examine for effusion:

Bulge sign (ripple test): with the knee extended, empty the suprapatellar pouch by sliding your
left hand down the thigh until you reach the upper edge of the patella. Keep this hand there. Now
empty the medial parapatellar fossa by sliding your right index from distal to proximal along the
medial aspect of the knee to force any fluid within the joint laterally. Now apply a similar firm
wiping motion from distal to proximal along the lateral aspect of the knee and watch the medial
side for a bulge or ripple as the fluid reaccumulates on that side (this is called the bulge sign and it
is positive with small effusions and absent with larger effusions)

Patellar tap (ballottement): with the knee extended, empty the suprapatellar pouch by sliding
your left hand down the thigh until you reach the upper edge of the patella. Keep this hand there.
With the right index or thumb press down briskly and firmly over the patella. Moderate-sized
effusion is indicated by a spongy feel followed by a tapping sensation as the patella strikes the
femur. You may also feel a fluid impulse in your left hand.
• Feel behind the knee for a Baker’s cyst

Step 5: Move the knee:

• Range of movement: ask the patient to flex the knee as far as possible then extend the leg back down
to lie on the couch. Observe the range of movement (and any discomfort). Normal range is 0 degree
(maximum extension) to 140 degrees (maximum flexion).
• Crepitus: place your hand over the knee joint, while it is moved passively with the other hand. Feel
for any crepitus between the patella and femoral condyles as, suggesting osteoarthritis, chondromalacia
patellae (especially in younger female patients) or loose bodies (cartilaginous fragments) in the joint
space, but should differentiated from non-specific clicking of joints
• Joint instability:

Cruciate instability (anterior and posterior draw test): flex the patient’s knee to 90 degrees and
maintain this position by sitting with your thigh trapping the patient’s foot. Check that the
hamstring muscles are relaxed and look for posterior sag (posterior subluxation of the tibia on the
femur). This is an important cause of a false-positive anterior drawer sign.
o The anterior drawer sign: with your hands behind the upper tibia and both thumbs over the
tibia and both thumbs over the tibial tuberosity, pull the tibia anteriorly. Significant movement
(compare with the opposite knee) the anterior cruciate ligament is lax. Movement of > 1.5 cm
suggests anterior collateral ligament rupture. There is often an associated medial ligament
injury.
o The posterior drawer sign: now push backwards on the tibia. Posterior movement of the tibia
suggests posterior cruciate ligament laxity.

Test for meniscal tears: meniscal provocation test (McMurray’s sign):
o Medial meniscus: passively flex the knee fully, externally rotate the foot and abduct the thigh
keeping the foot towards the midline (i.e. creating a varus stress at the knee). Then extend the
knee smoothly. In medial meniscus tears a click or clunk is felt or heard accompanied by
discomfort
o Lateral meniscus: passively flex the knee fully, internally rotate the foot and adduct the thigh
(i.e. creating a valgus stress at the knee). Then extend the knee smoothly. In tears of the lateral
meniscus a click or clunk is felt or heard accompanied by discomfort.

Step 6: Ask to examine the other joints, e.g. other knee and spine for associated inflammatory spondylitis

Step 7: Additional signs: features of psoriasis, inflammatory bowel disease, reactive arthritis (enthesitis, keratoderma
blenorrhagica, conjunctivitis, balanitis), gouty tophi

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Step 8: Thank the patient and cover him (her)

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 Pearls in PACES (Locomotor- Hip)
Adel Hasanin

LOCOMOTOR - HIP

STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask the patient “Are you quite comfortable? Do you have any pain? Where do you feel the pain? Can
you point to it?” (pain into the groin is more suggestive of hip disease)
• Ask permission to examine him “I would like to examine your hip joint, if it is all right with you”
• Position patient lying flat on the bed.
• Expose the patient legs up to his underwear and remove socks and shoes. You should be able to see the
iliac crests so you may need to pull down the top of his underpants.

Step 2: General inspection:

• Bedside: walking stick, shoes-callipers, built-up heels
• General appearance: scan the patient quickly looking for:

Nutritional status (under/average built or overweight)

Rheumatoid (symmetrical deforming polyarthritis in the hands)

Psoriatic arthritis (asymmetrical arthritis and skin plaques)

Step 3: Look at the leg (comparing one side to the other)

Abnormal postures (hip is held in flexed position or leg is externally rotated)

Shorter leg

Scars

Stigmata of rheumatic disease

Step 4: Feel the hip: tenderness over the greater trochanter (trocahnteric bursitis)

Step 5: Move the hip:

• Flexion: ask the patient to bend his knee then to flex his hip to the chest (the normal range of
movement is flexion 120 degrees).
• Internal and external rotation: With both the knee and hip flexed to 90 degrees rotate the hip joint
internally and externally using the foot as a pointer and the knee as pivot. Estimate the degree of
rotation (the normal range of movement is internal rotation 30 degrees and external rotation 45
degrees)
• abduction and adduction: place one hand on the opposite iliac crest (to keep the pelvis stationary)
then, place your other hand under the ankle of the leg being examined and abduct and adduct the hip
(the normal range of movement is abduction 60 degrees and adduction 30 degrees)
• Thomas test: if you suspect a hip flexion deformity that is masked by an increased spinal lordosis, flex
the opposite hip (with knee bent) to flatten out the lumbar lordosis (feel with your hand under the
patient’s spine). Any fixed flexion deformity of the opposite hip will be brought out by the flattening
of the lumbar spine
• Straight leg raise: slowly raise the patient’s leg by taking hold of his heel and lifting the leg slowly
(stop if pain occurs). Note the angle attained (normally > 90 degrees) and compare to the other side.
Pain in the leg to the foot indicates spinal origin (nerve root entrapment – lumbosacral radicular
entrapment). Consider testing for weakness (particularly of ankle plantar flexion) and abnormal
sensation or reflexes. Be prepared to differentiate a nerve root from a peripheral nerve lesion

Step 6: Measure (check for shorter leg): while both legs stretched out as far as possible and in equivalent
positions, measure with a tape from umbilicus to medial malleolus (the apparent length of leg) and from
ASIS to medial malleolus (the true length of leg)

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Step 7: Ask the patient to walk: see “Ch 9. CNS – Gait”

• Antalgic (painful) gait occurs when there is pain in one hip and the patient leans to the other side to
avoid putting weight on the affected side.
• Waddling (myopathic) gait indicates hip muscle weakness (e.g. osteomalacia, myositis)

Step 8: Ask to examine the other joints, e.g. knee and spine for associated inflammatory spondylitis

Step 9: Additional signs: features of psoriasis, inflammatory bowel disease, reactive arthritis (enthesitis,
keratoderma blenorrhagica, conjunctivitis, balanitis)

Step 10: Thank the patient and cover him (her)

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THEORETICAL NOTES

Causes of shorter leg:

• Protrusion of acetabulum: occurs mainly in rheumatoid arthritis when the femoral head migrates
through the acetabulum because of regional osteoporosis
• Undetected fracture at the neck of femur
• Occasionally following joint replacement (mainly hip, but may be with knee replacement also)
• Following a Girdlestone procedure in which no hip joint prosthesis is placed (or it is removed) because
of sepsis or patient’s general health does not allow a major operation (the neck of femur and femoral
head are excised and the femur is held in place by the joint capsule, but migrates upwards)
• Apparent leg shortening: due to pelvic tilt secondary to spinal disease

Origin of hip pain

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 Pearls in PACES (Endocrine- General)
Adel Hasanin

EXAMINATION OF ENDOCRINE SYSTEM

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Physical examination Clear Pass Fail Clear

Pass Fail
□ □ □ □
2. Identification and interpretation of physical signs Clear Pass Fail Clear
Pass Fail
□ □ □ □
3. Discussion related to the case Clear Pass Fail Clear
Pass Fail
□ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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Pearls in PACES (Endocrine- General)
Adel Hasanin

STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask permission to examine him

Step 2: General inspection: you may have been given a lead in the instructions such as look at the hands
or look at the face, however always start your visual survey systematically (Composure and complexion →
hands & arms → head & face → eyes → mouth → neck, axilla & trunk → legs & feet), asking yourself at
each stage, “is the hands normal?”, “is the face normal?”, etc. if it is abnormal describe the abnormality to
yourself in the mind trying to match it up with one of the common five diagnoses in endocrine station
(thyrotoxicosis, hypothyroidism, acromegaly, Cushing’s, Addison’s)

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Thyrotoxicosis Hypothyroidism Acromegaly Cushing’s Addison’s

(see Ch 17. (see Ch 17.
Endocrine – Endocrine –
Neck) Neck)
General Under/average Average built or Coarse features Centripetal Medica alert bracelet,
appearance built, anxious, overweight, obesity, bruised generalized
(uncover restless apathetic, thin skin, with hyperpigmentation
the hair) thinning hair, purple striae
“peaches and
cream”
complexion
Face (look – Lid retraction – Thickened and – Prominent – Moon face, Buccal mucosa
in the (staring eyes) coarse facial supra-orbital hirsute, with (hyperpigmentation)
mouth) – Grave’s features ridges acne
ophthalmopathy – Periorbital – Large nose and – Mouth
(exophthalmos, puffiness, loss of lips (superimposed
periorbital outer third of – Prognathism, thrush)
oedema, eyebrows widely spaced
conjunctival (unreliable), teeth and
injection, xanthelasma macroglossia
chemosis)
Hands – Thyroid – Dry and cold Large “spade Thin skin Hyperpigmentation
(dorsum – acropachy, – Pulse: like”, tight rings, (palmar creases)
check for warm and bradycardia coarse skin and
tremors, sweaty hands, sweaty
palm - feel palmar
for warmth erythema
and – Pulse:
sweating, tachycardia
and finally (note
feel the specifically the
pulse) presence or
absence of AF)
– Fine tremors
Neck & Obvious goitre Obvious goitre – Goitre – Increase pad – Hyperpigmentation
trunk (nodular or (nodular or – Skin tags fats above (nipples and scars)
(including symmetrical), symmetrical), (molluscum supraclavicular – Sparse axillary and
the breasts, scars scars (hemi/total fibrosum) fossae (more pubic hair
Pubic hair, (hemi/total thyroidectomy) – Acanthosis specific for – Abdominal scar
axillae and thyroidectomy) nigricans (black Cushing’s) (bilateral
the back) velvety – Excess adrenalectomy)
papillomas) interscapular
– Hirsutism fat (buffalo
– Gynaecomastia, hump)
galactorrhoea – Purple striae
– Kyphosis – Kyphosis
(osteoporosis)
Legs & feet Pretibial Non pitting Large feet Wasting (“lemon Hyperpigmentation
myxoedema pretibial oedema on sticks” body
(Grave’s) shape) and
oedema
N.B. Words in Bold Italic font indicates signs of disease activity

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Step 3: Once you have the diagnosis look for associated features:

Thyrotoxicosis (see Ch Hypothyroidism (see Acromegaly Cushing’s Addison’s

17. Endocrine – Neck) Ch 17. Endocrine –
Neck)
Lid lag: see “Ch 17. Examine the thyroid: Additional Additional Additional
Endocrine – Neck” see “Ch 17. Endocrine – findings: findings: findings:
Examine the thyroid: Neck”
Proximal
Proximal
BP
see “Ch 17. Endocrine – Lymphadenopathy: see myopathy myopathy (supine
Neck” “Ch 17. Endocrine –
Carpal tunnel (stand from and
Lymphadenopathy: see Neck” syndrome sitting or test standing)
“Ch 17. Endocrine – Check for tracheal
Visual field shoulder
Chest
Neck” displacement: see “Ch defect abduction) (TB)
Check for tracheal 17. Endocrine – Neck” (bitemporal
Visual field
Urine
displacement: see “Ch If there is a hemianopia) defect: dipstick
17. Endocrine – Neck” thyroidectomy scar,
BP (HTN) – 15% bitemporal
If there is a test for Chvostek’s sign
Urine dipstick for hemianopia
thyroidectomy scar, (hypoparathyroidism): sugar and
test for Chvostek’s sign “Ch 18. Endocrine –
Abdominal pigmentation
(hypoparathyroidism): Neck” examination: (pituitary
see “Ch 17. Endocrine – Additional findings: see enlarged organs tumour)
Neck” “Ch 17. Endocrine –
Cardiac
Fundus: optic
Additional findings: see Neck” examination: atrophy,
“Ch 17. Endocrine – (slow relaxing ankle cardiomegaly, papilloedema,
Neck” jerk, proximal CCF hypertensive
(brisk ankle jerk, myopathy, carpal tunnel,
Joint arthropathy or diabetic
proximal myopathy, ophthalmoplegia, visual (osteoarthrosis, retinopathy
carpal tunnel, field defects, fundus, chondrocalcinosi
Signs of RA or
ophthalmoplegia, visual HTN & urine dipstick) s) asthma
field defects, fundus, requiring
HTN & urine dipstick) steroids
(iatrogenic
Cushing’s)

BP and urine
dipstick
N.B. Words in Bold Italic font indicates signs of disease activity

Step 4: Thank the patient and cover him (her)

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 Pearls in Paces (Neck)
Adel Hasanin

ENDOCRINE - NECK

STEPS OF EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask permission to examine him

Step 2: General inspection:

Thyrotoxicosis Hypothyroidism
General
Under/average built, anxious, restless
Average built or overweight,
appearance apathetic, thinning hair,
“peaches and cream”
complexion
Face
Lid retraction (staring eyes): indicated by visible
Thickened and coarse facial
sclera above the cornea (normally covered by the features
upper eyelid). This result from sympathetic
Periorbital puffiness, loss of
stimulation of the levator palpebrae superioris in outer third of eyebrows
thyrotoxicosis of any aetiology (unreliable), xanthelasma

Lid lag: ask the patient to follow the slow
downward movement of your finger at a distance of
about 50 cm. In thyrotoxicosis, the upper lid lags
behind the descending eyeball

Grave’s ophthalmopathy (exophthalmos, periorbital
oedema, conjunctival injection, chemosis)
Hands
Thyroid acropachy, warm and sweaty hands, palmar
Dry and cold
erythema
Pulse: bradycardia

Pulse: tachycardia (note specifically the presence or
Carpal tunnel syndrome: Tinel’s
absence of AF) or Phalen’s test

Fine tremors: tell the patient “Hold your arms
outstretched in front of you, like this (with dorsum
facing upwards), and maintain this position” If the
tremor is not obvious, place your palm against his
outstretched fingers to feel for it. Alternatively, you
can place a piece of paper on the dorsum of his out-
stretched hands – it will oscillate if a fine tremor is
present.
Neck
Obvious goitre (nodular or symmetrical), scars
Obvious goitre (nodular or
(hemi/total thyroidectomy) symmetrical), scars (hemi/total
thyroidectomy)
Legs & feet
Pretibial myxoedema (Grave’s)
Non pitting pretibial oedema

Slow relaxing ankle jerk: best
demonstrated with the patient
kneeling on a chair or bed with
the feet hanging over the edge,
and the examiner standing
behind the patient.

N.B. Words in Bold Italic font indicates signs of disease activity

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Step 3: Examine the thyroid:

• Inspection: Arrange the patient comfortably in chair, give him a glass of water and tell him “take a sip
of water and hold it in your mouth” Look at the neck and tell the patient “now swallow” watch the
upward movement of the goitre, or the appearance of a nodule not visible before swallowing (behind
sternomastoid). The thyroid moves upwards on swallowing since it is enveloped in the pretracheal
fascia, which is attached to the cricoid cartilage. A thyroglossal cyst will move upwards on swallowing
and protrusion of the tongue, and can be transilluminated. If there is no evidence of a goitre so far you
may wish to check for lymphadenopathy before feeling for a goitre (particularly if there is visible
enlarged lymph nodes)
• Palpation: Ask the patient’s permission to feel the neck and apologize for any discomfort you may
cause. Approach him from behind and ask him to lightly flex the neck. Feel the isthmus of the gland
with your right index and middle fingers (lies over the trachea two finger widths below the thyroid
cartilage). Then palpate the two lobes of the thyroid gland (one lobe at a time) which extend laterally
behind the sternomastoid muscle. Ask the patient to swallow some water again while you continue to
palpate the thyroid. Extend palpation upwards along the medial edge of the sternomastoid muscle on
either side to look for a pyramidal lobe. If there is goitre, note its size, consistency (soft like the lips,
firm like the tip of the nose or hard like the forehead), texture (nodular or diffusely enlarged), mobility
(moves readily on swallowing?), tenderness, and test sternomastoid function (this muscle may be
infiltrated in thyroid malignancy)
• Percuss over the upper sternum to assess any retrosternal extension of goitre. You may wish to elicit
Pemberton’s sign (on raising the arms above the head, patients with retrosternal goitres may develop
signs of compression, i.e. suffusion of the face, syncope or giddiness)
• Auscultate over the thyroid gland for bruit (vascular murmur) – classically occurs in Grave’s disease.
You may need to occlude venous return to rule out a venous hum, and to listen over the aortic area to
ensure that the thyroid bruit you hear is not an outflow obstruction murmur conducted to the root of the
neck.

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Step 4: Lymphadenopathy: (supraclavicular/cervical lymphadenopathy may associate thyroid cancer or

acute thyroiditis)
• Technique: palpate one side at a time using the flat fingers of one hand and compare with the glands
on the contralateral side (assess site, size, consistency, mobility and tenderness).
• Sequence:

From behind with the patient sitting and the head slightly tilted to the side under palpation:
o Examine the (1) supraclavicular nodes by placing your fingertips in the supraclavicular
fossae then place your index finger between the clavicle and sternocleidomastoid muscle and
press down gently towards the first rib to feel the scalene node (felt as a soft mobile mass just
above the hard first rib).
o Then examine the (2) deep cervical lymph nodes behind the anterior border of the
sternomastoid.
o Then examine the (3) submental ,(4) submandibular and (5) preauricular nodes

From the front of the patient:
o Examine the (1) posterior triangles, up the back of the neck and
o Then examine the (2) postauricular and (3) suboccipital nodes

If you do find lymph nodes, proceed to examine the axillary and inguinal lymph nodes for
evidence of generalized lymphadenopathy (lymphoma, CLL)
o Axillary nodes: examine the right axilla from the right side of the patient and vice versa. Ask
the patient to relax his right arm on you examining hand (left hand) a little away from the
chest wall (use your left hand to examine the right axilla, and vice versa). Gently place your
fingertips into the vault of the axilla and then draw them downwards feeling the medial,
anterior, and posterior walls in turn
o Inguinal glands: palpate over the horizontal chain, just below the inguinal ligament, and then
over the vertical chain along the line of the saphenous vein.

Note whether the lymph nodes are:
o Separate (reactive hyperplasia, infectious mononucleosis, lymphoma, etc.) or matted together
(neoplastic, tuberculous)
o Mobile or fixed to the skin or deep tissues (neoplastic)
o Soft, fleshy, rubbery (Hodgkin’s disease) or hard (neoplastic)

Look for a scar from lymph node biopsy and radiotherapy markings and look in the mouth for
pharyngitis and palatal Petechiae (infectious mononucleosis), tonsillar infiltration (CLL) or
primary malignancies. Ask the examiners permission to feel for the liver and spleen and express
your wish to examine the chest clinically and radiologically (TB or CA)

Step 5: Check for tracheal displacement: place the index and ring fingers over the prominent points on
either side of the manubrium sternae. Use the middle finger to feel the tracheal rings to detect tracheal
deviation

Step 6: If there is a thyroidectomy scar, test for Chvostek’s sign (hypoparathyroidism): tap over the facial
nerve 3-5 cm in front of the tragus of the ear. The test if positive if this manoeuvre evokes involuntary
twitching of the lips and facial muscles

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Step 7: Additional findings (complications):

• Ankle jerk: brisk in thyrotoxicosis and slow relaxing in hypothyroidism (best demonstrated with the
patient kneeling on a chair or bed with the feet hanging over the edge, and the examiner standing
behind the patient)
• Proximal myopathy (thyrotoxicosis): test shoulder abduction by telling the patient “Hold your arms
up, like this (chicken wings). Now keep them up and don’t let me push them down”
• Carpal tunnel syndrome (hypothyroidism): Phalen’s test (reversed prayer sign) and/or Tinel’s tests
(tapping of the nerve at putative site of compression) will produce paraesthesiae in the distribution of
the nerve (see Ch 13. Locomotor - Hand)
• Ophthalmoplegia: test the pursuit eye movement (see Ch 18. Eye – General). Limitation of upward
gaze is the most common abnormality in Grave’s ophthalmopathy. However the combination of
enlarged ocular muscles ± subsequent fibrosis may lead to complex ophthalmoplegia that is not
explained by either single nerve or muscle disease.
• Bitemporal visual field defects (pituitary tumours)
• Fundus examination: optic nerve compression causing visual failure in Grave’s
• BP (hypertension due to hypercholesterolaemia with hypothyroidism)
• Urine dipstick for sugar (DM type 1 with autoimmune hypothyroidism)

Step 8: Thank the patient and cover him (her)

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THEORETICAL NOTES

Thyrotoxicosis: excess thyroid hormone

Hyperthyroidism: hyper-function of the thyroid gland

Causes of Thyrotoxicosis
• Primary hyperthyroidism

Graves' disease

Toxic multinodular goitre

Toxic adenoma

Functioning thyroid carcinoma metastases

Activating mutation of the TSH receptor (autosomal dominant)

Struma ovarii

Drugs: iodine excess (Jod-Basedow phenomenon)
• Thyrotoxicosis without hyperthyroidism

Subacute thyroiditis

Silent thyroiditis

Other causes of thyroid destruction: amiodarone, radiation, infarction of adenoma

Ingestion of excess thyroid hormone (thyrotoxicosis factitia) or thyroid tissue
• Secondary hyperthyroidism

TSH-secreting pituitary adenoma

Thyroid hormone resistance syndrome: occasional patients may have features of thyrotoxicosis

Chorionic gonadotropin-secreting tumours and gestational thyrotoxicosis (Circulating TSH levels
are low in these forms of secondary hyperthyroidism)

The hyperthyroidism of Graves' disease is caused by thyroid stimulating immunoglobulins (TSI) that are
directed to the TSH receptors (TSH-R)

Hands in thyroid disease:

• Thyroid acropachy: a form of clubbing found in <1% of thyrotoxic Graves' disease
• Palmar erythema (thyrotoxicosis of any cause)
• Tar staining (thyroid ophthalmopathy is worse in smokers)
• Feel the palm: warm and sweaty (thyrotoxicosis), or cool and dry (hypothyroidism). N.B. cold and
sweaty in anxiety
• Pulse: slow in hypothyroidism and fast in thyrotoxicosis - note specifically the presence or absence of
AF
• Fine tremors (thyrotoxicosis)

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Eyes in thyroid disease:

• Features of thyrotoxicosis from any cause:

Lid retraction (staring eyes)

Lid lag: ask the patient to follow the slow downward movement of your finger at a distance of
about 50 cm; the upper lid lags behind the descending eyeball.
• Thyroid ophthalmopathy of Grave’s disease - (also occurs in about 5% of patients with
autoimmune hypothyroidism):

Exophthalmos/proptosis: sclera visible below the cornea (normally covered by the lower eyelid)
with the patient sitting at the same level as you and looking straight ahead. This sign is not related
to thyroid status and occurs only in Grave’s disease. unilateral exophthalmos could be due to
Grave’s disease, however in such a case a retro-orbital tumour should always be considered

Soft tissue signs: periorbital oedema, conjunctival injection, chemosis

Ophthalmoplegia/diplopia: test the pursuit eye movement (see Ch 18. Eye - General). Limitation
of upward gaze is the most common abnormality in Grave’s ophthalmopathy. However the
combination of enlarged ocular muscles ± subsequent fibrosis may lead to complex
ophthalmoplegia that is not explained by either single nerve or muscle disease.

Optic nerve compression causing visual failure
• Ptosis is very rarely encountered in either Grave’s disease or hyperthyroidism. Its presence should
raise the possibility of coexistent myasthenia gravis.

Surface anatomy of the thyroid gland

OBSERVE:
• The hyoid bone (H) lies at the angle between the floor of the mouth and anterior aspect of the neck
• The laminae of the thyroid cartilage (T) project anteriorly from their point of union to form the
laryngeal prominence (P); the superior horn (G) is palpable
• The arch of the cricoid cartilage (C) projects further anteriorly than the rings of the trachea and lies
at the level of C6
• The first tracheal ring (I)
• The thyroid gland consists of right (RL) and left (LL) lobes and a connecting isthmus (S)

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Structures related to the thyroid gland

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EYE - GENERAL

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Physical examination Clear Pass Fail Clear

Pass Fail
□ □ □ □
2. Identification and interpretation of physical signs Clear Pass Fail Clear
Pass Fail
□ □ □ □
3. Discussion related to the case Clear Pass Fail Clear
Pass Fail
□ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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STEPS OF EYE EXAMINATION

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask few questions “could you tell me your name please? Are you right- or left-handed? Are you quite
comfortable”
• Ask permission to examine him “I am just going to test your eye; is that alright?”
• Ask the patient to sit upright on the edge of the bed facing you, while you position yourself one arm's
length from the patient at the same level.

Step 2: General inspection

• Bedside: walking stick, shoes-callipers, built-up heels
• Nutritional status (under/average built or overweight)
• Intention tremors (cerebellar syndrome – MS)
• Long, lean look of myotonic dystrophy
• Myasthenic facies
• Tabetic facies
• Facial asymmetry in hemiparesis
• Face and hands of acromegaly
• Foot ulcers in diabetes
• Pes cavus in Friedreich’s ataxia
• Foot ulcer or necrobiosis lipoidica in DM

Step 3: Look at the eyes:

• Ptosis
• Exophthalmos
• Strabismus (divergent or convergent)
• Skew deviation (vertical misalignment of the eyes)
• Nystagmus (consider cerebellar syndrome – MS)
• Xanthelasma, arcus senilis
• Kayser-Fleischer rings (brownish yellow ring in the outer rim of the cornea, diagnostic of Wilson’s
disease)
• Corneal calcifications
• Blue sclera
• False (glass) eye.

Step 4: Look at the pupils:

• Size (dilatation, constriction)
• Equality and regularity
• Iris abnormalities (e.g. Lisch nodules in neurofibromatosis)
• Foreign bodies in the anterior chamber (e.g. lens implants)

Step 5: Visual Acuity:

• Ask the patient “can you see from each eye? Do you use eye glasses? Put it on please. Cover your left
eye please”.
• Hold a pocket Snellen's chart 2 m from the patient's eyes and ask him to read sections of the print.
• Record the smallest print size read (e.g. No. 9 → visual acuity of 6/9).
• Repeat in the other eye.

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Step 6: Visual Fields:

• Visual attention:

Tell the patient "Keep looking at my eyes and point to the finger which moves" Place your index
fingers out on both sides approximately 50 cm apart and approximately 30 cm above eye level.
Your fingers should now be in the patient's upper temporal fields on both sides.

Move your fingers in turn, and then both at the same time.

Repeat with fingers approximately 30 cm below eye level.

If one finger is seen when moved by itself but is ignored when both fingers are moved together,
then there is visual inattention → sensory lesion above the thalamus
• Peripheral visual fields:

Tell the patient "Cover your right eye with your right palm and keep looking at my right eye" Now
you should shut your left eye and keep looking at the patient's left eye.

Hold up the index finger of your right hand (or white hat pin) midway between you and the
patient, at almost a full arm's length to the side.

Tell the patient "Tell me when you see my finger move" Move your wagging finger slowly from
the upper then the lower temporal periphery towards the center (to test his upper and lower
temporal quadrants against yours).

Then test the upper and lower nasal quadrants using the index finger of your left hand in a similar
manner.

Then test the visual fields of his right eye in a similar manner.

When there is a homonymous hemianopia, the macula needs to be tested. Bring your wagging
finger horizontally from the side with the defect towards the point of fixation. If your finger is
seen before it gets to the midline, there is macular sparing, while if your finger is only seen once it
crosses the midline, there is no macular sparing.

N.B. you may ask the patient to slightly raise his head up while testing the upper temporal fields to
remove his eyebrows from the field, and ask him to slightly tilt his head down while testing the
lower nasal fields to remove his nose from the field. This applies to you also.
• Central scotoma is tested for with a red hat pin (unless you have already found a field defect which
does not require further examination). It is useful to mount the pin on the rubber eraser of a pencil, in
order to be sure your hand is out of the patient's visual field:

Tell the patient "Cover your right eye with your right hand and keep looking at my right eye" Shut
your left eye and keep looking at the patient's left eye.

Hold up the pin at the eye level midway between you and the patient just inside the outer limits of
your temporal fields.

Tell the patient "Can you see the head of the pin? What color is it? Tell me if it disappears or
changes color" Move the pin slowly from the temporal periphery through the central field to the
nasal periphery. Patients with optic nerve neuropathy may report altered color vision even if there
is no absolute central loss of vision.

If there is no scotoma, examine the size of the blind spot: Tell the patient "Tell me if the head of
the pin disappears" Move the red hat pin from the point of fixation temporally and horizontally
slowly until you find your own blind spot. Now, compare the size of the patient's blind spot to
yours. The blind spot is situated 30 degrees to the temporal side of the point of visual fixation. Its
size should correspond exactly with your own blind spot when the red pin is held equidistant
between your eye and the patient's eye. The blind spot may be enlarged in chronic papilloedema or
consecutive optic atrophy.

Then test the right eye for central scotoma and size of the blind spot in a similar manner.

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Step 7: Eye movements:

• Pursuit eye movement:

Tell the patient "Look at my finger (or the white hat pin); follow it with your eyes without moving
your head and tell me if you see double".

Move your finger slowly, like a letter H: from side to side (lateral and medial recti), then up and
down at the extreme of lateral gaze (superior and inferior recti and superior and inferior oblique),
thus allowing the action of each muscle to be assessed.

If the patient reports he sees double; ask “Are the images side by side, up and down or at an angle?
Where the images are widest apart? ". Diplopia is maximal at the direction of action of the paretic
muscle. In this position cover one eye and ask “which image disappears: the inner or outer”.
Repeat this by covering the other eye. The outer (false) image disappears when covering the
affected eye. If diplopia persists with one eye covered it may be lens dislocation, astigmatism or
factitious. If the pattern of loss is complex and cannot be easily explained, always consider Grave’s
disease or myasthenia

If there is internuclear ophthalmoplegia, on attempted gaze to one side;
o the adducting eye (ipsilateral to the lesion) is slow or fails to adduct (unable to get closer),
and
o the abducting eye (contralateral to the lesion) shows ataxic nystagmus (in hurry saying “come
on come on”).
o Normal convergence differentiates INO from a medial rectus or III nerve lesion, and intact
abduction in the other eye differentiate INO from lateral gaze palsy (nuclear [VI nerve
nucleus] lesion, or supra nuclear [PPRF or frontal lobe] lesion)
• Nystagmus:

Ask the patient to follow your finger with both eyes. Move the finger in turn up, down and to each
side. Hold the finger at a point where the finger can be easily seen by both eyes (in the range of
binocular vision) and wait for at least 5 seconds in each position.

Describe the nystagmus in terms of the direction of fast phase and direction of gaze at which
nystagmus is most marked (right, left, up, down, or greater in the abducting > adducting eye), and
notice if it is central (sustained) or peripheral (fatigues, improves by fixation, aggravated by head
movement and associated with vertigo, deafness and tinnitus).

In cerebellar nystagmus, the fast-phase direction is towards the side of the lesion, and is maximal
on looking towards the lesion, whereas in vestibular nucleus/VIII nerve lesion, the fast-phase
direction is away from the side of the lesion, and is maximal on looking away from the lesion.

In ataxic (dissociated) nystagmus, there is nystagmus of abducting eye >> adducting eye, with
weakness of adduction, a characteristic sign of INO, commonly due to MS (associated with
cerebellar syndrome)
• Observe for fatigability on holding upwards gaze (myasthenia gravis).
• Saccadic eye movements: tell the patient “look to the right, to the left, up, down” Observe the eye
movements. Look particularly at the speed of adduction.
• Vestibulo-ocular reflex (doll’s eye manoeuver):

This test is used in patients with limited eye movement on command or pursuit to demonstrate
preserved eye movement on vestibulo-positional stimulation, indicating a supranculear eye
movement abnormality. Otherwise, the test is most commonly used in unconscious patients when
it provides a way of testing eye movements

Ask the patient to look into the distance at a fixed point, and then turn the patient’s head to the left,
then the right and flex and extend the neck. The eyes should move within the orbits, maintaining
forward gaze.
• Lid lag: Also while testing eye movement note any lid lag: the upper lid fails to cover the sclera above
the iris when the patient looks down. This is a cardinal feature of thyroid eye disease and its absence,
in the presence of proptosis, should make one suspicious of another orbital cause of proptosis (e.g.
orbital cellulites, caroticocavernous fistula, orbital metastasis, orbital haematoma, Wegener’s
granulomatosis, or pseudoproptosis)

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Step 8: Light reflex:

• Tell the patient “look into the distance”.
• Shine a bright light in the right eye. Look at the reaction of that eye (the direct reflex)
• Shine the light again in the right eye and look at the reaction in the left eye (the consensual reflex).
• Repeat the test for the left eye (shining the light twice, and looking at the reaction in the same eye in
the first time, and in the other eye in the second time)
• Afferent: II (sensory) → optic tract → LGG → efferent: parasympathetic EWN of III
(parasympathetic) → fibres to ciliary muscle

Step 9: Swinging light test:

• Shine a bright light into one eye and then the other at about 1 second-intervals.
• Swing the light repeatedly between the two eyes. Observe the pupillary response as the light is shone
into the eye.
• Shining the light in the healthy eye causes rapid constriction to both eyes.
• In relative pupillary afferent defect (RAPD), the pupil on the abnormal side dilates when the light is
shone into it (Marcus Gunn pupil), as the signal carried by II on the abnormal side is weaker than that
from the contralateral side. Lesion is always unilateral, anterior to the optic chiasm, commonly due to
optic neuritis, and rarely due to compression of the optic nerve or retinal degeneration.

Step 10: Accommodation-convergence reflex:

• Place your finger 10 cm in front of the patient's nose.
• Tell the patient "Look into the distance. Now look at my finger".
• Observe the eyes and pupils for their reaction to accommodation (the eyes should adduct, intort and the
pupils should constrict)
• Afferent: frontal cortex → efferent: parasympathetic EWN of III → fibres to ciliary muscle)

Step 11: Optic disc: Fundoscopy (see Ch 19. Eye - Fundus)

Step 12: Additional signs:

• Thyroidectomy scar, thyroid acropachy or pretibial myxoedema (in patient with exophthalmos)
• Acromegaly
• Cerebellar signs (in patient with nystagmus)
• Sympathectomy scar over the clavicle (in patient with Horner’s syndrome)
• Absent limb reflexes (in Holmes-Adie pupil)
• Hemiparesis

Step 13: Thank the patient and cover him (her)

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THEORETICAL NOTES

Visual acuity:
• The pocket Snellen's chart gives only an approximation because 6 m is the least distance at which the
effects of accommodation can be ignored; hence visual acuity is normally tested at 6 m with a Snellen's
chart three times as big as this.
• Remember that the commonest cause of diminished visual acuity is a refractive error so that to gain
information about other pathology in the eye (e.g. diabetic maculopathy), the corrected visual acuity
needs to be assessed (with glasses on or through a pinhole). In the UK you need a visual acuity of 6/10
or better to drive a car.

Abnormalities of the pupils:

Large pupil (mydriasis) Causes
Normally reacting Anisocoria: pupils are unequal but normally reacting (normal variant)
Doesn't react to light but Afferent pupillary defect: lesion anterior to the optic chiasma. Common
accommodation reflex cause: optic neuritis. Rarer causes: compression of the optic nerve, retinal
preserved degeneration
Doesn't react to light and Adie's (tonic) pupil: poor reaction to light and slow reaction to
reaction to accommodation. Causes: idiopathic degeneration of ciliary ganglion; may be
accommodation is slow associated with loss of tendon reflexes (Holmes- Adie pupil)
Doesn't react to light or 1) with ptosis → Surgical III palsy
accommodation 2) No ptosis → Mydriatic drugs

Small pupil (miosis) Causes

Normally reacting
Senile miosis: normal age-related change

Horner's syndrome: miosis, partial ptosis, enophthalmos, and hemi-
facial anhydrosis. Causes: lesion to sympathetic fibres either:
o Centrally in the hypothalamus, the medulla or the upper cervical
cord (exits at T1). Common causes: stroke (lateral medullary
syndrome) or demyelination. Rare causes: trauma or syringomyelia
o Peripherally in the sympathetic chain, the superior cervical ganglion
or along the carotid artery. Common causes: Pancoast's tumour
(apical bronchial carcinoma) or trauma. Rare causes: carotid
dissection. Sometimes no cause is found.
Doesn't react to light but Argyll-Robertson pupil: lesion in the rostral (upper) midbrain near the
accommodation reflex Sylvian aqueduct, in which the light reflex fibres are interfered with, but the
preserved more ventral accommodation reflex fibres are spared. Causes: syphilis, DM,
MS
Doesn't react to light or Miotic drugs
accommodation

Types of eye movement and site of control:

Type of eye movement Site of control
Pursuit: slow eye movement to maintain fixation on a moving object (looking at the Occipital lobe
person moving across the room)
Saccadic (command): rapid movement form one point of fixation to another (looking Frontal lobe
from the page to someone in the room)
Vestibular-positional (vestibule-ocular reflex): eye movement that compensate for Cerebellar
movement of the head to maintain fixation (looking at fixed point from moving car) vestibular nuclei
Convergence: movement that maintain fixation as an object is brought close to the Midbrain
face (rarely affected in clinical practice)

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Anatomical sites of abnormal eye movements:

Without Supranculear (above the nuclei) → conjugate disorder of eye movement (both eyes move
diplopia together and are equally impaired)
Internuclear (connections between nuclei; MLF) → disconjugate eye movement
Nuclear → disconjugate eye movement (except for lesion of VI nerve nucleus, which
produces ipsilateral conjugate horizontal gaze palsy; however can be overcome by doll’s
eye manoeuver)
With Nerve → disconjugate eye movement
diplopia Neuromuscular junction → disconjugate eye movement
Muscle → disconjugate eye movement

Concept of supranuclear gaze palsy:

• Supranuclear gaze centres control the individual cranial nerve nuclei to ensure that both eyes move
together in conjugate fashion.
• Lateral gaze is controlled by the PPRF in the pons, which controls the ipsilateral VI nerve nucleus
and, via the MLF, the contralateral III nerve nucleus.
• Vertical gaze is controlled by accessory oculomotor nuclei in the upper midbrain, which induce the
III nerve nuclei to turn the eyes upward or downward in coordinated fashion.

Examples of abnormalities of eye movements:

Lesion Features and Causes
III Features:
nerve – Ptosis
palsy – Eye deviated down and out (divergent squint) because of the unopposed action of the SO and LR
– Loss of upward, downward and medial movements (If the IV nerve is intact → intorsion of the
eyes upon attempted downward gaze due to unopposed action of SO muscle) (if VI nerve is
intact → lateral gaze is preserved)
– Angulated diplopia
– Dilated unreactive pupil → extrinsic compression, commonly by aneurysm of posterior
communicating or internal carotid artery (painful)
Syndromes:
– Nothnagel's syndrome: injury to the superior cerebellar peduncle causes ipsilateral oculomotor
palsy and contralateral cerebellar ataxia
– Benedikt's syndrome: injury to the red nucleus results in ipsilateral oculomotor palsy and
contralateral tremor, chorea, and athetosis
– Claude's syndrome incorporates features of both Nothnagel's syndrome and Benedikt's
syndrome, by injury to both the red nucleus and the superior cerebellar peduncle.
– Weber's syndrome: injury to the cerebral peduncle causes ipsilateral oculomotor palsy with
contralateral hemiparesis
IV Features:
nerve – Head is tilted away from the side of lesion
palsy – Adducted eye cannot look downwards
– Diplopia is maximal on looking downward and medially and images are at angle
VI Features:
nerve – Convergent squint at rest
palsy – Impaired lateral movement
– Diplopia is maximal on lateral gaze and images are side by side
Syndromes:
– Foville's syndrome: dorsal pontine injury results in lateral gaze palsy, ipsilateral facial palsy, and
contralateral hemiparesis
– Millard-Gubler syndrome: ventral pontine injury results in picture similar to Foville’s syndrome,
except for the eye findings. There is lateral rectus weakness only, instead of gaze palsy, because
the abducens fascicle is injured rather than the nucleus
– Gradenigo's syndrome: mastoiditis at the petrous apex produces deafness, pain, and ipsilateral
abducens palsy

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Internuclear Features:
ophthalmoplegia – Impaired adduction of the eye Ipsilateral to the lesion
– Ataxic nystagmus in the abducting eye contralateral to the lesion: adducting eye
is slow, and abducting eye is in hurry saying “come on come on”
– Normal convergence (differentiate INO from a medial rectus lesion)
Causes: Lesion in the MLF:
– Gradual onset of INO which is usually bilateral is highly suggestive of MS
(look for cerebellar signs, pyramidal signs, and pale discs).
– A sudden onset of INO with facial numbness is more in keeping with stroke
– INO with a contralateral hemiparesis and ipsilateral ataxia is indicative of
brainstem disease (medial pons – lesion of basilar artery or paramedian
branches)
Dysthyroid eye disease Features:
– Complex eye signs due to involvement of the eye muscles (exophthalmic
ophthalmoplegia)
– Exophthalmos, thyroid scar or goitre
Myasthenia gravis Features:
– Complex eye signs due to involvement of the eye muscles (diplopia worsen on
sustained gaze)
– Bilateral ptosis
Cavernous sinus and Features:
superior orbital fissure – Total or subtotal painful ophthalmoplegia
syndromes – Sensory loss over the first division of the V nerve
– Absent corneal reflex
Causes of cavernous sinus syndrome:
– Cavernous sinus thrombosis, is the most frequent cause; often secondary to
infection from orbital cellulitis (frequently S.aureus), a cutaneous source on the
face, or sinusitis (especially with mucormycosis in diabetic patients)
– Aneurysm of the carotid artery
– Carotid-cavernous fistula (orbital bruit may be present)
– Meningioma, nasopharyngeal carcinoma or other tumour
– Idiopathic granulomatous disorder (Tolosa-Hunt syndrome)
Ocular myopathy Oculopharyngeal muscular dystrophy
– Eye signs begin with ptosis (often complete), then ophthalmoplegia
– Dysphagia is usually the most prominent symptom
– Face and neck muscles are often mildly involved
Chronic progressive external ophthalmoplegia (CPEO)
– Absence of soft tissue in the lids and periorbital region
– Ophthalmoplegia and mild facial and neck weakness
Horizontal (lateral) Causes:
gaze palsy – Injury to one of the frontal lobes (acute stroke) may result in deviation of the
eyes toward the injured side due to the unopposed output from the intact frontal
lobe (since the voluntary movement towards one side is initiated in the frontal
eye fields on the other side). This sign is not always present; even when it is
present initially, it may resolve within a short time. Conversely, focal seizure
activity may induce deviation of the eyes to the contralateral side.
– Lesion of the PPRF (supranuclear lesion) → ipsilateral horizontal conjugate
gaze palsy (can be overcome by doll’s eye manoeuver)
– Lesion of the VI nerve nucleus (nuclear lesion) → ipsilateral horizontal
conjugate gaze palsy (cannot be overcome by doll’s eye manoeuver)
– One-and-a half syndrome is due to a combined lesion of the medial longitudinal
fasciculus and the VI nerve nucleus on the same side. The patient's only
horizontal eye movement is abduction of the eye on the other side.

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Vertical Features (that distinguish vertical gaze palsy from third, fourth or sixth nerve palsies):
gaze – Both eyes are affected
palsy – Pupils are often unequal but fixed
– Generally there is no diplopia
– Intact vestibule-ocular reflexes (e.g. On extending or flexing the neck)
Causes:
– Lesions of the rostral interstitial nucleus of the MLF and the interstitial nucleus of Cajal
(distal basilar artery ischemia is the most common aetiology) → supranuclear paresis of
upgaze, downgaze, or all vertical eye movements.
– Parinaud's Syndrome (Also known as dorsal midbrain syndrome) is a distinct supranuclear
vertical gaze disorder from damage to the posterior commissure.
o Features:
 Loss of upgaze (and sometimes downgaze)
 Convergence-retraction nystagmus on attempted upgaze
 Downwards ocular deviation ("setting sun" sign)
 Lid retraction (Collier's sign)
 Skew deviation
 Pseudoabducens palsy
 Light-near dissociation of the pupils (absent light reflex but intact convergence
reflex)
o Causes:
 Hydrocephalus from aqueductal stenosis
 Pineal region tumours (germinoma, pineoblastoma)
 Cysticercosis
 Stroke
– Steele-Richardson syndrome or progressive supra-nuclear palsy (PSP): akinetic-rigid
syndrome associated with progressive supra-nuclear palsy. It is characterized disorders of
vertical gaze, especially downwards saccades in early stage (can be overcome by vestibulo-
ocular reflex). Smooth pursuit is affected later in the course of the disease
– Parkinson's disease
– Huntington's chorea
– Olivopontocerebellar degeneration
o Myasthenia gravis
o Thyroid ophthalmopathy
o Miller-Fisher

Skew deviation refers to a vertical misalignment of the eyes, usually constant in all positions of gaze. It
has poor localizing value as it has been reported after lesions in widespread regions of the brainstem and
cerebellum (in cerebellar lesion, the ipsilateral eye deviates down and in, and the contralateral up and out).

Congenital squint (concomitant; non paralytic):

• Ocular misalignment equal in all directions of gaze (concomitant deviation)
• Eye movements are full
• Vision is suppressed from the nonfixating eye → No diplopia

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Causes of nystagmus:
• Physiological (end point nystagmus) (nystagmoid reaction) (Oculokinetic nystagmus): nystagmus
only at extremes of lateral gaze, as seen in people looking out of the windows of trains (usually
physiological)
• Ocular (retinal) (fixation nystagmus) (pendular nystagmus): due to inability to fixate, usually
congenital and may also occur when the vision is poor as in severe refractive error or macular disease.
• Vestibular nystagmus: the fast way is away from the side of the lesion

Peripheral: lesion in the vestibular apparatus or VIII nerve. Produces unidirectional nystagmus
away from the affected side irrespective of the direction of the gaze. It fatigues, improves by
fixation, aggravated by head movement and associated with vertigo, deafness and tinnitus.
Common causes: vestibular neuronitis, Meniere’s disease, vascular lesions

Central (central vestibular): lesion in the vestibular nuclei in the brain stem. Produces
bidirectional nystagmus and usually has vertical or rotatory component. It is sustained (not
adaptable).Common causes: MS (young patients), vascular disease (older patients)

Cerebellar nystagmus (central cerebellar): the fast way is towards the side of the lesion. Common
causes: cerebellar syndrome due to drugs, alcohol or MS. Rarer causes: cerebellar degeneration,
cerebellar tumour

Ataxic (dissociated) nystagmus: nystagmus of abducting eye >> adducting eye, with weakness of
adduction, associated with INO. Common causes: MS, CVA

Types of nystagmus:
• Oculokinetic (end point nystagmus) (nystagmoid reaction) (physiological nystagmus): nystagmus
only at extremes of lateral gaze, as seen in people looking out of the windows of trains (physiological)
• Pendular (fixation nystagmus) (ocular/retinal nystagmus): inability to fixate; the speed and
amplitude are equal in all directions, usually congenital and may also occur when the vision is poor as
in severe refractive error or macular disease.
• Jerk nystagmus: nystagmus with distinct fast and slow phases. The fast phase represents reflex
correction of a slower deviation in the opposite direction

Horizontal
 First degree: occurs only when looking to direction of fast phase, causes may be
central or peripheral
 Second degree: occurs in primary position of gaze, causes are usually central
 Third degree: occurs even when looking in opposite direction to fast phase, causes are
usually central
 Multidirectional (bidirectional) gaze evoked nystagmus: direction of nystagmus
changes with the direction of gaze (always in the direction of gaze); causes are always
central.
 Ataxic (dissociated) nystagmus: nystagmus of abducting eye >> adducting eye, with
weakness of adduction, a characteristic sign of INO, commonly due to MS and CVA

Vertical
 Upbeat: Indicates upper brainstem lesion. Common causes are demyelination, stroke,
Wernicke’s encephalopathy
 Downbeat: Indicates medullary-cervical junction lesion. Common causes are Arnold-
Chiari malformation, syringobulbia, demyelination

Rotatory (rotary): combination of vertical and horizontal nystagmus. Pure rotatory nystagmus is
always central; however peripheral horizontal nystagmus usually has a rotatory component

Causes of bilateral sudden blindness:

• Bilateral occipital lobe infarction or trauma
• Bilateral optic nerve damage, e.g. methyl alcohol damage,
• Hysteria

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Causes of unilateral sudden blindness:

• Retinal artery emboli
• Retinal vein thrombosis
• Retinal detachment
• Temporal arteritis
• Occasionally optic neuritis and migraine

Causes of unilateral/bilateral gradual blindness: cataract, glaucoma, macular degeneration, diabetic

retinopathy, optic nerve or chiasmal compression, nerve damage, e.g. tobacco amblyopia

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STEPS OF EYE EXAMINATION - FUNDUS

Step 1: Approach the patient

• Read the instructions carefully for clues
• Shake hands, introduce yourself
• Ask permission to examine him “I would like to examine your eyes, if it is all right with you”

Step 2: General inspection:

• General appearance (rarely helpful): foot ulcer or necrobiosis lipoidica in DM
• Look at the eyes:

Arcus lipidus at young age suggest DM.

Pupil is usually (but not always) dilated for the examination (in the absence of pupillary dilatation,
only the optic nerve can be reliably assessed)

Step 3: Check your ophthalmoscope: check that light works and is on the correct beam (standard), start
with short focal length (find ‘0’ and then rotate the focus ring clockwise until the number + 10 is obtained)

Step 4: Ask permission to turn off lights or draw the curtains

Step 5: Sit opposite the patient and tell him that you are going to shine the light into his eyes, and ask
him to keep looking at a distant point straight ahead at his eye level (e.g. a light switch, a spot on the wall).

Step 6: Hold the ophthalmoscope in your right hand to examine the patient’s right eye (and vice versa).
Place your other hand on the patient’s forehead, catch his upper eyelid with your thumb and gently retract it
against the orbital rim. Use your right eye to examine the patient’s right eye (and vice versa). Look at the
patient’s eye with the ophthalmoscope in the same horizontal plane as his eye, from a distance of about 30
cm and an angle about 15 degrees temporal to his line of fixation aiming at the centre of the back of the
patient’s head.

Step 7: Look through the pupil to check the red reflex (the pupil appears pink, as in bad flash
photographs): opacities in the media of the eye (cornea, anterior chamber, lens and vitreous) will appear as
black specks or lines against the red reflex of the fundus. The red reflex is attenuated or lost in any
condition affecting the transparency of structures in front of the retina (e.g. cataract, vitreous haemorrhage),
and in any condition affecting apposition of the normally transparent retina with the underlying red
vascular choroid (e.g. retinal detachment). Do not attempt fundal examination in an eye with absent red
reflex.

Step 8: Come closer to the patient’s head while progressively rotating the focus ring anticlockwise (to
increase the focal length) until the lens comes into focus. Look at the lens for early cataract in diabetics.
Cataracts usually have a fine web-like appearance structures in front of the fundus.

Step 9: Come further closer to the patient’s head while progressively rotating the focus ring
anticlockwise, to look through the vitreous for
• Opacity (e.g. asteroid hyalinosis)
• Haemorrhages
• Fibrous tissue or new vessel formation (proliferative diabetic retinopathy)

Step 10: Come further close to the patient’s head such that you are touching your hand resting on the
patient’s forehead while progressively rotating the focus ring anticlockwise until the retina comes into
focus. The retina is usually observed with a zero or a slightly negative lens if the patient is myopic. Tilting
your head sideways gives both the patient and yourself ‘breathing space’ and enables you to get close to the
patient’s eye. The closer you are, the easier it is to angle your ophthalmoscope into each quadrant and the
bigger your field of view of the fundus

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Step 11: Localize the disc and examine it and its margins: Staying in the same horizontal plane at an angle about 15
degrees temporal to the line of fixation aiming at the centre of the back of the patient’s head will bring the optic disc in
view. If it is not, focus on a blood vessel and follow it backwards against the angles of their branches, in the direction
of convergence of the blood vessels into the optic disc. If the optic disc is not sharply focused, the lenses of the
ophthalmoscope should be gradually adjusted until the disc becomes sharply focused. Note the optic disc margins,
colour and cup.
• Normal appearance of the disc:
1. Optic disc margins:

Normal disc is rounded or slightly oval with clear margins.

The nasal margin of the disc is normally blurred (less sharply demonstrated than the temporal margin).

A rim of dark pigment or white sclera is sometimes normally seen surrounding the optic disc
(particularly the temporal side) - common in highly myopic eyes
2. Optic disc colour:

Normal disc is pink in colour.

The temporal side of the disc is usually paler than the nasal side.

The colour of the optic disc varies (quite pale if only the four main vessels are seen on the disc; while
much pinker if the vessels have early branches on the disc itself).

In infancy and old age, optic disc is naturally pale due to thin vessels.
3. The optic cup is a depression in the central part of the optic disc. It is paler than the surrounding rim of the
disc, and from it the retinal vessels enter and leave the eye. Normal optic cup is slightly on the nasal side of
the centre of the optic disc and its diameter is less than 50% of the disc diameter
• Abnormalities of the optic disc:
1. Pinker disc with blurred disc margins (or with blurred cup) → swelling (oedema) of the optic nerve
head. The disc looks pinker than normal (hyperaemic) and may approach the colour of the surrounding retina
(often difficult to find, with the vessels disappearing without an obvious optic disc). Oedema of the optic
nerve head results form either raised ICP (papilloedema) or from inflammation (papillitis = optic neuritis):

Papilloedema usually produces more swelling, with humping of the disc margins and not usually
associated with visual loss (may enlarge the blind spot). If papilloedema develops rapidly, there will be
marked engorgement of the retinal veins with haemorrhages and exudates on and around the disc, but
with papilloedema of slow onset there may be little or no vascular change, even though the disc may
become very swollen.

In papillitis swelling of the optic disc is usually slight, distension of the retinal veins is less marked than
in papilloedema, haemorrhages and exudates are rarely present, and there may be signs of intraocular
inflammation, such as a hazy vitreous. There is often visual loss (central scotoma) and pain on moving
the eye.

Be aware of the following conditions which might be mistaken for papilloedema:
o The normally blurred nasal margin may be mistaken for papilloedema
o Hypermetropic fundus appears crowded due to small size of the eye, may be mistaken for
papilloedema
o Drusen: colloid bodies that may occur on disc, may be mistaken for papilloedema
o Myelinated nerve fibres: opaque white fibres or patches radiating (for a short distance) from the
disc, may be mistaken for papilloedema. The patch has a characteristic feathered edge and retinal
vessels may disappear for a short distance within it. It is harmless non progressive congenital
anomaly
2. Pale disc with normal cup → optic atrophy. Because there is wide variation in colour of the normal disc, a
useful sign of optic atrophy is reduction in the number of capillaries on the disc (the number of capillaries
that cross the disc margins is reduced from the normal 10 to 7 or less). Optic atrophy is either primary (due to
pressure, ataxia, Leber’s, dietary, ischemia, syphilis, cyanide, sclerosis) or secondary (following
papilloedema):

Primary optic atrophy: disc is flat and white with clear-cut edges

secondary optic atrophy(following papilloedema): the disc is greyish-white in colour and its edges are
indistinct

N.B. the following conditions may be mistaken for optic atrophy (pale disc):
o The normal temporal pallor may be mistaken for optic atrophy
o The normal pallor of the disc in infancy and old age (due to thin vessels) may be mistaken for optic
atrophy
o The normal rim of dark pigments or white sclera seen sometimes surrounding the optic disc may
make disc seem pale
o Myopic fundus (myopic eye is large, so disc appears paler)
3. Pale disc with deep cup → chronic glaucoma (commonly idiopathic)

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Step 12: Trace the arterioles and venules out from the disc noting particularly:
• Colour: arteries are light-coloured and veins are burgundy-coloured
• Calibre: the diameter of arteries is two-thirds the diameter of veins. Look for arteriolar narrowing and
vessel irregularity - seen in grade I hypertensive retinopathy
• Increased reflectiveness (silver wiring): seen in grade I hypertensive retinopathy
• AV crossing points: look for AV nipping (the vein narrows markedly as it is crossed by the artery) -
seen in grade II hypertensive retinopathy
• Microaneurysms: saccular pouch; appears as round dots separate from blood vessels (seen in
background retinopathy)
• Neovascularization: new vessels appear as fine frond-like vessels, often near the disc, frequently
coming off the plane of the retina and therefore may be out of focus (seen in proliferative diabetic
retinopathy)
• Bright yellow object within lumen of artery: cholesterol embolus, usually due to unilateral proximal
atherosclerotic lesion (often common or internal carotid stenosis)
• Look at the retinal veins as they turn into the optic disc and see if they pulsate, going from
convex to concave. This is best appreciated as you look along the length of a vein as it runs into the
optic disc. Retinal venous pulsation is normal finding and indicates normal intracranial pressure, while
its absence may reflect raised intracranial pressure or may be normal (absent in 15% of normal people)
• Common mistakes on examining the blood vessels:

Choroidal artery: a small vessel running from disc edge towards macula, mistaken for new vessels

Tortuous vessels (normal variant), may be mistaken as vessel irregularities of grade I hypertensive
retinopathy

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Step 13: Look at the retinal background: examine each quadrant of the fundus and especially the
macular area and its temporal aspect. The macula is an area of densely packed photoreceptors (the fovea
being its centre of excellence) and its corresponding visual axis is the area of central vision. So, the macula
will come in to view if you ask the patient to look at the ophthalmoscopic light. The macula is found two
disc diameters from the temporal margin of the disc and appears as a pale yellow spot on a slightly
darkened area of the retina. It can be difficult to see. Ideally, you should use the narrow beam (the dot light)
for this (if it is available in your ophthalmoscope). Look particularly for haemorrhages (dot, blot, flame-
shaped), microaneurysms, exudates both hard (well-defined edges; increased light reflex) and soft (fluffy
with ill-defined edges; cotton-wool spots). If hard exudates are present see if these form a ring (circinates in
DM).
• General background:

Pigmented background: normal especially in dark-skinned races. If striped, called tigroid

Pale background: either clear (normal in fair-skinned people, also seen in albino) or cloudy
(macula appears as “cherry-red” spot, vessels narrow – seen in retinal artery occlusion)
• Red lesions:

Dot haemorrhages: thin, vertical haemorrhages that may be difficult to differentiate from
microaneurysms - seen in background diabetic retinopathy

Blot haemorrhages: larger, full-thickness bipolar layer haemorrhages that represent larger areas
of capillary occlusion - seen in background diabetic retinopathy

Flame haemorrhages: superficial bleed shaped by nerve fibres into a fan with point towards the
disc - seen in grade III hypertensive retinopathy. Florid haemorrhages are seen in retinal venous
thrombosis – may be in only one quarter or half of the retina

Subhyaloid haemorrhages: irregular superficial haemorrhages usually with flat top - seen in
subarachnoid haemorrhages
• White/yellow lesions:

Hard exudates: yellowish sharp-edged lesions with increased light reflex. It may form a ring
around the macula (macular star) - seen in background diabetic retinopathy, grade III hypertensive
retinopathy

Soft exudates (cotton wool spots): white fluffy spots, caused by retinal infarcts - seen in
proliferative diabetic retinopathy, grade III hypertensive retinopathy, SLE, AIDS
• Black lesions:

Moles: flat, usually rounded lesions – normal

Laser burns: black-edged round lesions, usually in regular pattern; often mistaken for retinitis
pigmentosa

Retinitis pigmentosa: rare, black lesions like bone spicules in periphery of retina

Melanoma: raised irregular malignant tumour

Step 14: Stay examining until you have finished and are ready to present your findings. Stop at the disc,
the macula, and in each quadrant of each eye and ask yourself the question “are there any abnormalities?
What are they?” before moving on to the next area. Do not be put off by the impatient words of your
examiner

Step 15: Thank the patient

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THEORETICAL NOTES

Moving parts of the ophthalmoscope:

• On/off switch, usually with brightness control
• Focus rings (occasionally two):
a. -20/+20 for correction of the patient’s vision (usually set at zero): if the patient is myopic turn the
ring anticlockwise, and if hypermetropic, turn it clockwise. An oblique view of the patient with his
spectacles on tells you if he is long- or short-sighted; if his face is smaller through his eye glasses
he is myopic; if his face is larger he is hypermetropic. The severity is estimated according to how
much his face looks smaller or larger
b. -10/+10 for correction of your vision: if you are short- or near-sighted (myopic) and not using
glasses or contact lenses you will have to turn the focus dial anticlockwise to focus to look at a
normal eye. If you are long- or far-sighted (hypermetropic) turn the focus dial clockwise. Establish
what correction you need before approaching the patient
• Beam selector (sometimes): it gives you the following choices:
a. Standard: for general use
b. Narrow beam for looking at the macula
c. Target (like a rifle sight): to measure the optic cup
d. Green to look for haemorrhages (red appears as much darker)
• dust cover (sometimes)

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HISTORY TAKING

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Data gathering in the interview

• elicits presenting complaints, documents in logical and systematic
way and includes systems review
• Enquiries about past medical history/family/alcohol/smoking/ Clear Pass Fail Clear
treatment history Pass Fail
• follows leads about relevant psycho-social factors □ □ □ □
• Appropriate verbal and non-verbal (eye contact, posture etc.)
responsiveness, good balance of open and closed questions,
appropriate
2. Identification and use of information gathered
Clear Pass Fail Clear
• check information is correct with patient
Pass Fail
• Able to interpret history
□ □ □ □
• Able to create a problem list
3. Discussion related to the case Clear Pass Fail Clear
• Able to discuss the implications of the patient's problems Pass Fail
• Able to discuss strategy for solving the problem □ □ □ □
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

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STEPS IN HISTORY TAKING STATION

Step 1: In the 5 minutes before the interview

• Read the instructions carefully
• Write down the following information in the provided blank sheet:

Problems (from the instructions):

Differential diagnosis:

Risk factors/Associations/Complications:
This information would help you to recall certain questions related to the patient condition. You may
choose to proceed to these relevant questions immediately after analysis of complaint or to go through your
routine history taking in the usual order but to give more attention to these questions.

Step 2: Introduce yourself and approach the patient

• Good morning Mr/Mrs..., I have got the right person haven't I? I'm Dr… medical SHO in the
hospital
• We are here today to discuss your medical condition (may I ask you first what’s your job? are you
married? Have children?)
• I will need to make a few notes. So if I'm writing things down, I still will be listening to you
• I have a letter from GP, but first I would like you to tell me, in your own words, what is the trouble?
Allow the patient to talk freely (I see, nodding, till me more about …)

Step 3: Analysis of complaint

Use the following questions as a guide for analysis of any complaint mentioned in the instructions or
mentioned by the patient during the interview. Do not ask all the questions but only those belonging to the
system in concern.
• General:

Any recent change in your weight? How many kilograms? Over how many days?

Any change in your appetite?

Any undue fatigue?

Any rise in your temperature?

Any lumps or bumps in your body, in your abdomen, neck or armpit?

Any change in your sleeping hours?
• GIT:

Any mouth ulcers? Is it painful? Any problems with your teeth?

Any difficulty in swallowing? Sensation of food sticking in your throat? Where does it seem to
stick? Is it worse with drinks or solid foods? Any pain on swallowing?

Any nausea (feeling sick)? Retching? Regurgitation of clear tasteless fluid? Vomiting (getting
sick)? How frequent? Is it related to pain? Does it bring relief? What is the amount of vomitus (a
tea cup, bowl, bucket)? What colour is it? Does it taste sour? Does it contain foods? How long ago
were they eaten? Does it have any trace of blood in it? Any indigestion or dyspepsia? Describe
your indigestion to me. What is it like? When does it come on? Any heartburn? Describes the
burning sensation. Where is it? Does it go anywhere else? Is it related to food intake? Any pain in
your tummy? (Is it relieved by passing flatus, or defecation? Is it worse when you're hungry or
full? Is it associated with nausea, vomiting, belching, jaundice or fever?)

Any wind? Does it tend to be passed downwards (Passing of flatus) or upwards
(Belching/burping)? Do you feel better after burping or passing wind? What's your normal bowel
habit? How many times you go to the toilet to open your bowels in the normal days? Do you have
any change in your habit? Diarrhoea? Is it formed, unformed or watery? Does it smell, or float? Is
it difficult to flush away? Is there blood and/or mucus associated with the stool? Is it mixed in or
on top of the stool? Is there pain on defecation, or before? Is it relieved by defecation?
Constipation? Do they feel small and hard? Are they difficult to pass? Any change in color of
stool? Pale, dark, tarry, black, fresh blood?

Any yellowish discoloration of your eyes or skin

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• CVS:

Do you have any chest pain?
o Duration: How long has it been there? At what time of day does it affect you?
o Onset: What were you doing when it started? How did it start?
o Course: Is it there all the time or does it come and go? Is it improving or worsening with
time?
o Site: Where do you feel the pain? Can you point to it? Does it go anywhere else?
o Sort: Can you describe it?
o Severity: How bad is it? Does it stop you working or keep you awake at night? Can you scale
it out of ten?
o Aggravating/alleviating factors: Is there anything that brings on the pain or makes it worse or
better?
o Associated symptoms: Does it make you sweat? Is it associated with nausea, vomiting or
belching?
o Similar episodes: Have you had anything like this before?
o Investigations: Have you had any investigations (blood tests or images) for this?
o Treatments: Have you had any treatments for this? Did you feel better after this treatment?

Any shortness of breath? How long has it been there? Is it improving or worsening with time?
How bad is it? How far can you walk before feeling short of breath? Does it stop you working? Is
there anything that makes it better or worse? Have you had anything like this before? Have you
had any treatments for this? Did you feel better after this treatment? Can you lie flat? How many
pillows do you use? Do you ever wake at night with shortness of breath? If so: what do you do?

Any ankle swelling? How long has it been there? Is it improving or worsening with time? How
bad is it? Is there anything that makes it better or worse? Have you had anything like this before?
Have you had any treatments for this? Did you feel better after this treatment?

Any palpitations- a feeling of awareness of the heartbeat? Can you tap it out on the table top?
How long has it been there? Is it improving or worsening with time? How bad is it? Is there
anything that makes it better or worse? Have you had anything like this before? Have you had any
treatments for this? Did you feel better after this treatment?

Any blackouts? Tell me about them. How long has it been there? Is it improving or worsening
with time? How bad is it? Is there anything that makes it better or worse? Have you had anything
like this before? Have you had any treatments for this? Did you feel better after this treatment?

Any leg pain when you walk long distances? How far can you walk before you have to stop?
Where do you feel this pain exactly? How long it lasts? Can you continue walking after resting for
a few minutes? How long has it been there? Is it improving or worsening with time? How bad is
it? Is there anything that makes it better or worse? Have you had anything like this before? Have
you had any treatments for this? Did you feel better after this treatment?
• Chest:

Do you have any cough? Do you bring up sputum or phlegm- what color is it? How much phlegm
do you cough up each day- would it fill an eggcup or a teacup? What is it like- is it runny or thick?
What does it smell like? Have you ever noticed blood in your phlegm?

Any shortness of breath?

Any wheezes?

Any chest pain? (due to inspiration or cough)

Does your wife complain that you snore? Has she ever noticed that you stop breathing for a period
during the night?"

Did you notice any change in your voice?

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• CNS

Do you have any undue headaches? Any particular triggers, e.g. coughing, straining, exertion, stress,
particular foods, bright lights? Does it make your eyes water? Is it associated with nausea, vomiting,
photophobia, drowsiness, confusion, weakness, ataxia, neck stiffness, visual changes or fever?

Do you have any fits, faints, blackouts or funny turns? Do you remember anything about the attack? Did you
fall to the ground? Did you hurt yourself or wet yourself? Did anyone see you fall to the ground? How did
they describe it? Have you suffered from vertigo or dizziness (light-headed)?

Have you noticed any weakness in either the arms or legs?

Have you experienced any numbness or tingling (pins and needles) in the face, limbs, or trunk?

Have you noticed any change in your eyesight, hearing or sense of smell or taste? Have you noticed any
difficulty in talking or swallowing?

Have you noticed any unsteadiness or difficulty in walking? Have you noticed that you reel from side to
side?)

Do you have any trouble with your water works (problems in passing urine)? Have you had any problems in
opening your bowels? Have you unintentionally messed yourself?

Have you noticed any change in your mood, memory or powers of concentration? Have you suffered from
insomnia?
• Genitourinary:

Any problems with your water works (general question)

Pain:
o Dysuria: pain or discomfort felt during or immediately after passing urine. It is often described as a
burning sensation felt at the urethral meatus, or the suprapubic region.
o Strangury: suprapubic pain associated with repeated and urgent desire to urinate every few minutes,
often associated with severe dysuria or inability to pass urine. It is due to acute bladder neck obstruction
by a stone or blood clot.
o Renal pain: pain in the back or loin

Abnormal urine volume or frequency:
o Frequency: passing urine more often than usual without an increase in the total urine volume
o Polyuria: the passage of excessive volumes of urine (at least 2.5 litres per day for an adult) resulting in
profuse urination and urinary frequency (the need to urinate frequently and to rise at night to pass urine).
If there is polyuria, ask about polydipsia (intake of abnormally large amounts of water)
o Nocturia: passing urine during the night
o Oliguria: passing a smaller volume of urine than normal
o Anuria: total absence of urine output

Abnormal urine content:
o Haematuria: blood in the urine
o pneumaturia: passing air bubbles in the urine
o frothy urine

Abnormality of micturation process
o Urgency: a sudden need to pass urine
o Hesitancy: delay in initiating urine flow
o Poor urinary stream: reduced force of the urinary stream
o Postmicturition dribbling: dribbling of urine after micturation

Incontinence:
o Urge incontinence: involuntary passage of urine when an urgent need to urinate cannot be resisted
o Stress incontinence: leakage of urine in response to situations that increase intra-abdominal pressure,
such as coughing, sneezing or laughing
o Nocturnal enuresis: involuntary passage of urine while asleep (bed-wetting)

Sexual history: I need to ask you some rather personal questions, is that OK?
o Have you a regular sexual partner?
o Is your partner male or female? How many sexual partners there have been in the past year?
o Have you had any casual relationships recently?
o Are you practicing a safe sex?
o Are you worried that you might have picked anything up, I mean in asexual way?
o Have you noticed any change in your sexual desire or ability?
o Any urethral or vaginal discharge?

Obstetric history
o Menses: regularity, frequency, duration, heavy or light
o Number of pregnancies
o Post-menopausal bleeding

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• Endocrine:

Heat or cold intolerance

Distal largeness (acromegaly)

Proximal weakness

Muscle cramps

Breasts (gynaecomastia, galactorrhoea)
• Locomotor:

Pain: Show me the worst spot. Does it get better or worse during the day? Is it associated with
stiffness or swelling?

Stiffness: do you feel stiff? When? How long does it take you to get going when you get up in the
morning?

Swelling of joints: do your joints swell? Which joints are affected? Do they feel hot to the touch?
Do they go red? How long has it been there? How did it start? Is it there all the time or does it
come and go?

Deformity: how long has this been going on?
• Skin:

Any skin rash? Where is it? How long has it present? Is it painful? Does it itch? Does it blister?
Does it improve?

Any abnormal colouration of your skin?

Have you recently noticed that your skin is dry?

Any change in sweating?

Any loss of hair, or abnormal hair growth in your body? In which part of your body?
• Haematology:

Any bleeding from your gum when you brush your teeth? Any bleeding from your nose? Any
bloody spots under your skin?

Step 4: Review of Systems (ROS)

Use these general questions to cover all systems related or unrelated to the complaints (you may start with
those related to the complaint). Listen well to the answers and if you get a positive answer for any question
start analysis of complaint as before.
• General:

Any recent change in your weight or appetite?

Any undue fatigue or rise in your temperature?

Any lumps or bumps in your body, in your abdomen, neck or armpit?

Any change in your sleeping hours?
• GIT:

Any mouth ulcers or problems with your teeth?

Any difficulty or pain on swallowing?

Do you feel sick (nausea) or get sick (vomiting)?

Any repeated unavailing attempts to throw up (Retching)?

Any regurgitation of clear tasteless fluid (water brush)?

Any indigestion or dyspepsia?

Any heartburn or pain in your tummy?

Any wind? Any change in your bowel habit? Diarrhoea? Constipation? Pain on defecation, or
before? Any blood, mucus or change in color of stool?

Any yellowish discoloration of your eyes or skin
• CVS:

Do you have any chest pain?

Any shortness of breath?

Any ankle swelling?

Any palpitations- a feeling of awareness of the heartbeat?

Any blackouts?

Any leg pain when you walk long distances?

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• Chest:

Do you have any cough? Any wheezes?

Does your wife complain that you snore? Did you notice any change in your voice?
• CNS

Do you have any undue headaches? Blackouts (faints), or funny turns (Fits)?

Have you suffered from vertigo or light-headed (dizziness)?

Have you noticed any weakness in either the arms or legs?

Have you experienced any pins and needles (numbness or tingling) in the face, limbs, or trunk?

Have you noticed any change in your eyesight, hearing or sense of smell or taste?

Have you noticed any difficulty in talking or swallowing?

Have you noticed any unsteadiness or difficulty in walking?

Have you noticed any change in your mood, memory or powers of concentration? Have you
suffered from insomnia?
• Genitourinary:

Any problems with your water works?

I need to ask you some rather personal questions, is that OK? Have you a regular sexual
partner? Is your partner male or female? Have you had any casual relationships recently? Have
you noticed any change in your sexual desire or ability? Any urethral or vaginal discharge or
bleeding? Any problems with the menses? Number of pregnancies and any associated problems?
• Endocrine:

Heat or cold intolerance

Distal largeness (acromegaly)

Muscle cramps

Breasts (gynaecomastia, galactorrhoea)
• Locomotor:

Pain or swelling in joints or muscles?

Stiffness: do you feel stiff?

Deformity
• Skin:

Any skin rash or abnormal colouration of your skin??

Have you recently noticed that your skin is dry?

Any change in sweating?

Any loss of hair, or abnormal hair growth in your body?
• Haematology:

Any bleeding from your gum when you brush your teeth? Any bleeding from your nose? Any
bloody spots under your skin?

STEP 5: Past history, Family history, Allergies, Social & occupational history, Treatment and Travel
history
• PMH:

Surgical/dental procedures, hospital admissions, blood transfusions

Medical examination for insurance reasons and the outcome

Immunizations

Serious illness: do you receive regular treatment for this condition? Are you on regular follow-up
for this condition?
o Asthma
o Blood pressure (say: 'blood pressure problems')
o CVA (say: 'stroke')
o Diabetes mellitus (say: 'diabetes')
o Epilepsy
o Fever, rheumatic
o Gastrointestinal (jaundice)
o Heart attack
o Infection (TB)

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• Family history:

Are your father and mother alive? How are they? What did they die from?

Do you have sisters or brothers? How are they?

Do any close relatives have suffered the same symptoms?

Is there any illness that runs in the family? Is there a family history of heart attacks or sudden
death? What was the age of the relative when these events occurred?
• Allergy history: to medications or food. If positive ask about the form of drug that caused the allergy
and symptoms and signs of the allergy.
• Social & Occupational: (work → marriage → activities of daily living → depression → smoking,
alcohol, recreational drugs)

Occupation: so tell me what your job is? Yes- but what do you actually do? Can you manage it
without any difficulty? Is there much dust, fumes, vapours or chemical substances? Have not you
ever been exposed to chemical substances before?

Marital status /Home life: as part of your medical history, I need to ask you some rather personal
questions, is that Ok?
o Are you married? Who is at home with you? How is your spouse? Do you have household
pets?
o Do you live in house or flat? Do you own it? Are you up to date with the rent? How many
stairs are there? Can you get up and down them OK?
o Can you cope with the housework? Do you have help from other people?

Activities of daily living/exercise: what do you do during a normal day? Do you take any
exercise?

Psychological burden: Some of my patients with emphysema get quite depressed. I often ask
patients with emphysema if they have been feeling depressed.

Smoking, alcohol and recreational drugs: have you ever smoked? When did you start? How
many cigarettes were you smoking when you gave up? Do you ever drink any alcohol? How much
alcohol might you drink in a week? Any recreational drugs?
• Treatment history (including OTC and herbal remedies)
• Travel history

Step 6: Ask the patient for any further information and formulate management plan
• Ask the patient: Is there any thing else you feel I should know? Are you worried about anything in
particular?
• Formulate a management plan (examination, investigations, referrals and treatments), explain it to the
patient and take actions: from what we have discussed, it is possible that your symptoms could be due
to… after I examine you, we might consider doing…, then I will write a letter to your GP and give you
an appointment for follow up after having the investigations done
• Do you have any questions? Thank you

Step 7: Discussion
Discussion with the examiner almost always includes a question about your management plan. You may
consider the following outlines in answering this question:
• Full examination may provide other useful clues such as…
• Investigations:

Basic investigations:

Confirm the diagnosis:

Other investigations (search for aetiology, complications):
• Management plan can be divided into:

Management of the underlying disease process:

Specific symptom treatment:

General management including patient education, nursing, physiotherapy, and social, occupational
and psychological rehabilitation

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THEORETICAL NOTES

Irritable bowel syndrome

• Rome Criteria for the Diagnosis of IBS (Symptoms must have been present for > 3 months)
Abdominal Pain/Discomfort AND Two or more of the following symptoms for at
Least 25% of the time:
Relieved with defecation
Change in stool frequency
and/or
Change in consistency
With change in stool frequency
Difficult stool passage
and/or
Sense of incomplete evacuation
With change in stool consistency
Presence of mucus in stool
• Management of IBS:

Often, reassurance alone has a therapeutic effect.

Initial treatment for diarrhoea-predominant irritable bowel syndrome should include a trial of a
lactose-free diet.

A therapeutic trial of an anticholinergic agent, such as hyoscyamine or dicyclomine, and fibre
supplements is often very helpful.

Chronic life stress is an important factor for irritable bowel syndrome, and antidepressant
medications are often helpful.

Alarm symptoms, such as hematochezia and weight loss, may require a more extensive evaluation
with colonoscopy.

Malabsorption may be due to defective luminal digestion, mucosal disease or structural disorders.
• Causes:
Small bowel Pancreatic Hepatobiliary Miscellaneous

Coeliac disease
Chronic pancreatitis
Cirrhosis of the liver
Thyrotoxicosis

Dermatitis herpetiformis
Pancreatic
Biliary obstruction
Mesenteric ischemia

Bacterial overgrowth carcinoma of any type
Drugs (neomycin,

Giardiasis cholestyramine,

Whipples disease antacids)

Tropical sprue

Radiation enteritis

Crohn's disease

Hypogammaglobulinaemia

Zollinger Ellison
Syndrome

Intestinal
lymphangiectasia
• Clinical features of malabsorption:

Diarrhoea / steatorrhoea: steatorrhoea occurs as a result of defective fat absorption. It is most
commonly caused by pancreatic disorders. The stool is pale, bulky and malodorous.
Malabsorption occasionally occurs without diarrhoea. This is most common in intestinal causes.

Weight loss

General symptoms: Lassitude, abdominal discomfort/bloating.

Symptoms due to nutritional deficiency: e.g. oedema due to hypoalbuminaemia, bone
pain/proximal myopathy due to Vitamin D deficiency, aphthous ulcers due to Vitamin B or iron
deficiency.

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Chronic asthma
• Pathophysiology: chronic airway inflammation & hyper-responsiveness in atopic individual →
reversible, variable airflow obstruction.
• Investigations:

Assess the inflammation: Analysis of induced sputum: increased eosinophils & eosinophilic
cationic protein

Assess the hyper-responsiveness: Challenges tests with histamine or methacholine can be used to
assess airways responsiveness where the diagnosis is unclear. Responsiveness is expressed as the
concentration of provoking agent required to decrease the FEV1 by 20% (bronchial hyper-
responsiveness, defined as PC20 < 8 mg/ml for either agent, is characteristic for asthma, but may
be found in COPD, CF and allergic rhinitis)

Assess the atopy: Skin prick tests can be used to assess atopy, serum total IgE is commonly raised
in asthmatics, specific IgE may be measured by radio-allergo-sorbent testing (RAST)

Assess the reversibility: Significant (≥ 15%) improvement in PEFR & FEV1 post-bronchodilator

Assess the variability: Significant (> 25%) PEFR variability (usually in the form of morning
dipping)

Assess the obstruction: Reduced FEV1, increased lung volumes (due to gas trapping), reduced
FEV1/FVC ratio (<70%)

Horse voice with cough is probably due to laryngitis while Horse voice alone is probably due to recurrent
laryngeal nerve palsy due to carcinoma of the bronchus

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Chronic recurrent headaches

Tension headache Migraine Cluster headache
Age & gender: Common Over 80 % of migraineurs Although the onset is generally between
in all age groups. Females have their first attacks before ages 20 and 50, it may occur as early as the
tend to predominate the age of 30 years, and the first decade of life. Men are affected seven
diagnosis should be viewed to eight times more often than women
with suspicion in anyone over
40.
Duration & frequency: Multiple attacks, each lasting Attacks last from 30 min to 2 h. The
seldom lasts more than a 4 to 72 h. The frequency of episodic type is most common and is
few hours. May be attacks varies from 1 to 2 per characterized by one to three attacks per
episodic or chronic (i.e., week to a few sparsely day over a 4- to 8-week period, followed by
present more than 15 days scattered over a lifetime. Daily a pain- free interval that averages 1 year.
per month). headaches are never The chronic form is characterized by the
migrainous. absence of sustained periods of remission

Tension Migraine Cluster headache

headache
Features
Benign and recurring syndrome of headache, nausea,
Periorbital or, less

Bilateral vomiting, and/or other symptoms of neurologic dysfunction commonly, temporal pain
tight, band- in varying admixtures. begins without warning and
like
Can often be recognized by its activators (red wine, reaches a crescendo within
discomfort. menses, hunger, lack of sleep, glare, estrogen, worry, 5 min.

Typically perfumes, let-down periods) and its deactivators (sleep,
Often excruciating in
builds pregnancy, exhiliration, sumatriptan) intensity and is deep,
slowly,
Divided into two clinical categories: nonfluctuating, and
fluctuates in o Migraine without aura (common migraine): no focal explosive in quality; only
severity. neurologic disturbance precedes the recurrent headaches. rarely it is pulsatile.

Rarely moderate to severe head pain, pulsating quality,
Pain is strictly unilateral
significantly unilateral location, aggravation by walking stairs or and usually affects the same
disabling similar routine activity, attendant nausea and/or side in subsequent months.
vomiting, photophobia and phonophobia
There are often associated
o Migraine with aura (classic migraine): characteristic symptoms of homolateral
premonitory sensory, motor, or visual symptoms. Focal lacrimation, reddening of
neurologic disturbances are more common during the eye, nasal stuffiness, lid
headache attacks than as prodromal symptoms. The most ptosis, and nausea.
common premonitory symptoms are visual, arising from
dysfunction of occipital lobe neurons A spreading
scotoma may occur but "spots in front of the eyes" or
visual blurring is not diagnostic. There may be reversible
focal neurological disturbances such as hemianopia or
unilateral paraesthesia.
Treatment
Abortive: paracetamol, codeine ± antiemetic, ergotamine,
Abortive: Inhaled

Relaxation. sumatriptan oxygen (face mask),

Simple
Prophylactic: Very Volatile Pharmacotherapeutic Agents ergotamine, sumatriptan,
analgesics. For Migraine Prphylaxis ( Verapamil, Valproic acid, steroids.

Muscle Pizotifen, Amitriptyline, Flunarizine, Methysergide,
Prophylactic: lithium
relaxants. Propranolol)

N.B. Chronic paroxysmal hemicrania has the same features as cluster headache but with shorter and
more frequent attacks (each attack lasts 3-45 minutes and occurs 20-40 times per day). It almost invariably
responds to indomethacin

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 Pearls in PACES (History Taking)
Adel Hasanin

Serious causes of headache

Cause Symptoms
Meningitis Nuchal rigidity, headache, photophobia, and prostration; may not be febrile. Lumbar
puncture is diagnostic.
Intracranial Nuchal rigidity and headache; may not have clouded consciousness or seizures.
haemorrhage Haemorrhage may not be seen on CT scan. Lumbar puncture shows "bloody tap" that
does not clear by the last tube. A fresh haemorrhage may not be xanthochromic.
Brain tumour May present with prostrating pounding headaches that are associated with nausea and
vomiting. Should be suspected in progressively severe new "migraine" that is
invariably unilateral.
Temporal May present with a unilateral pounding headache. Onset generally in older patients (>50
arteritis years) and frequently associated with visual changes. The ESR is the best screening test
and is usually markedly elevated (i.e., >50). Definitive diagnosis can be made by arterial
biopsy.
Glaucoma Usually consists of severe eye pain. May have nausea and vomiting. The eye is usually
painful and red. The pupil may be partially dilated.

Diagnosis of Myasthenia Gravis (MG)

• History

Diplopia

Ptosis

Weakness in characteristic distribution (worse with repeated activity, improved by rest)
o "Snarling" expression when the patient attempts to smile (Facial weakness)
o Weakness in chewing.
o Speech may have a nasal timbre (weakness of the palate) or a dysarthric "mushy" quality
(tongue weakness).
o Difficulty in swallowing; nasal regurgitation or aspiration (weakness of the palate, tongue, or
pharynx).
o In approximately 85% of patients, the weakness becomes generalized, affecting the limb
muscles as well (often proximal and may be asymmetric).
o If weakness of respiration becomes as severe as to require respiratory assistance, the patient is
said to be in crisis.
• Physical examination

Ptosis, diplopia

Motor power survey: quantitative testing of muscle strength

Forward arm abduction time (5 min)

Vital capacity

Absence of other neurologic signs (deep tendon reflexes are preserved)
• Laboratory testing

Anti- acetylcholine receptor radioimmunoassay: ~90% positive in generalized MG; 50% in ocular
MG; definite diagnosis if positive; negative result does not exclude MG

Edrophonium chloride (Tensilon) 2 mg + 8 mg IV; highly probable diagnosis if unequivocally
positive

Repetitive nerve stimulation; decrement of >15% at 3 Hz: highly probable

Single-fiber electromyography: blocking and jitter, with normal fiber density; confirmatory, but
not specific

For ocular or cranial MG: exclude intracranial lesions by CT or MRI

Myopathic muscle weakness, affecting proximal muscles more than distal ones and sparing eye and facial
muscles, is characterized by a subacute onset (weeks to months) and rapid progression in patients who have
no family history of neuromuscular disease, no endocrinopathy, no exposure to myotoxic drugs or toxins,
and no biochemical muscle disease (excluded on the basis of muscle-biopsy findings).

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Criteria for Definite Diagnosis of Inflammatory Myopathies

Criterion Polymyositis Dermatomyositis Inclusion Body Myositis
Muscle strength Myopathic Myopathic muscle Myopathic muscle weakness with early
muscle weakness involvement of distal musclesa
weakness
Electromyographic Myopathic Myopathic Myopathic with mixed potentials
findings
Muscle enzymes Elevated (up to Elevated (up to 50- Elevated (up to 10-fold) or normal
50-fold) fold) or normal
Muscle biopsy Diagnostic Diagnostic or Diagnostic
findings nonspecific
Rash or calcinosis Absent Present and Absent
diagnostic

Cystitis: pain in the suprapubic region + dysuria, frequency or strangury (severe pain in the urethra referred
from the base of the bladder and associated with an intense desire to pass urine)

Haematuria from parenchymal renal disease is usually continuous, painless and microscopic
(occasionally macroscopic) while haematuria from renal tumour is likely to be intermittent, associated
with renal pain and macroscopic

Diagnostic criteria for Sjogren's syndrome: three items are present → Probable Sjogren's syndrome.
Four or more items are present →Definite Sjogren's syndrome.
Criteria Definitions
1. Ocular symptoms Dry eyes every day for more than 3 months, recurrent sensation of sand or gravel
in the eyes, or use of tear substitutes more than three times a day
2. Oral symptoms Daily feeling of dry mouth for more than 3 months, recurrent or persistently
swollen salivary glands, or use of liquids to aid in swallowing dry food
3. Ocular signs Positive Schirmer's I test (< 5 mm in 5 min), or a rose Bengal score of ≥ 4
according to van Bijsterveld's scoring system
4. Histopathology Focus score 1 in a minor salivary gland biopsy
5. Salivary gland Positive result in one of the following tests: salivary scintigraphy, parotid
involvement sialography, salivary flow (≤ 1.5 mL in 15 min)
6. Autoantibodies Antibodies to Ro (SS-A) or La (SS-B), antinuclear antibodies, or rheumatoid
factor

Diagnostic criteria for SLE: If four of these criteria are present at any time during the course of disease, a
diagnosis of systemic lupus can be made with 98% specificity and 97% sensitivity.
1. Malar rash Fixed erythema, flat or raised, over the malar eminences
2. Discoid rash Erythematous raised patches with adherent keratotic scaling and follicular
plugging; atrophic scarring may occur
3. Photosensitivity Exposure to UV light causes rash
4. Oral ulcers Includes oral and nasopharyngeal, observed by physician
5. Arthritis Non-erosive arthritis involving two or more peripheral joints, characterized
by tenderness, swelling, or effusion
6. Serositis Pleuritis or pericarditis documented by ECG or rub or evidence of pericardial
effusion
7. Renal disorder Proteinuria > 0.5 g/d or > 3+, or cellular casts
8. Neurologic disorder Seizures without other cause or psychosis without other cause
9. Haematological disorder Haemolytic anaemia or leucopoenia (< 4000/mL) or lymphopenia (<
1500/mL) or thrombocytopenia (< 100,000/mL) in the absence of offending
drugs
10. Immunologic disorder Anti-dsDNA, anti-Sm, and/or anti-phospholipid
11. Antinuclear antibodies An abnormal titer of ANAs by immunofluorescence or an equivalent assay at
any point in time in the absence of drugs known to induce ANAs

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Different types of joint swelling:

• Synovitis: boggy, symmetrical swelling which feel hot
• Osteoarthritis: hard, bony swelling which generally feels cool
• Fluid: soft, fluctuant swelling which feels hot
Joint pain that gets better with activity or as the day progresses is more likely to be due to inflammation
while pain that gets worse during the day is likely to be due to degenerative change.

Addison's disease (hypoadrenalism)

• Clinical features:

Weakness, weight loss

Anorexia, nausea, vomiting, abdominal pain, diarrhoea, constipation

Pigmentation of skin & mucous membranes, vitiligo, loss of pubic hair in women

Hypotension, syncope, salt craving, psychosis

Auricular cartilage calcification
• Biochemical:

hyponatraemia (& hypoglycaemia), hyperkalaemia (& hypercalcaemia)

Raised urea, raised ACTH &TSH.

Reduced Aldosterone → Na wasting → increased rennin, angiotensin II, and vasopressin.
• Haematological:

Lymphocytosis

Eosinophilia

normocytic anaemia.
• ECG: (Low & slow)

low voltage QRS & T waves (despite hyperkalaemia)

Prolonged PR & QT
N.B. Increased pigmentation and hyperkalemia are absent in 2ry hypoadrenalism since there are low levels
of circulating ACTH, and aldosterone continues to be secreted via the rennin- angiotensin- aldosterone
system.

Primary Aldosteronism (Conn's syndrome) – Clinical features

• Headache
• Muscle weakness and fatigue
• Polyuria
• Polydipsia.
• Diastolic hypertension
• Persistent hypokalaemia (in a non-oedematous patient who is not receiving potassium-wasting
diuretics)

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Idiopathic haemochromatosis:
• Clinical features: in the absence of alcohol abuse, the combination of a dilated cardiomyopathy with
normal coronary arteries, diabetes mellitus, arthropathy, and cirrhosis of the liver in a pigmented
individual can all be explained by idiopathic haemochromatosis.
• Conditions causing simultaneous cardiac and liver disease:

Alcohol abuse

Cardiomyopathy

Haemochromatosis

Pericardial constriction

Chronic tricuspid regurgitation

Carcinoid tumour with hepatic metastases

Pulmonary/tricuspid stenosis

Sarcoidosis

HIV

Acute hypercalcaemia
• Clinical features:

Dehydration, nausea and vomiting

Nocturia and polyuria

Drowsiness and altered consciousness
• Management: while investigation of the cause is under way, immediate treatment is mandatory if the
patient is seriously ill or if the Ca2+ > 3.5 mmol/L.

Adequate rehydration is essential - usually at least 4-6 L of saline on day 1, and 3-4 L for
several days thereafter. Central venous pressure (CVP) may need to be monitored to
control the hydration rate.

Intravenous bisphosphonates (pamidronate) are now the treatment of choice for
hypercalcaemia of malignancy or of undiagnosed cause.

Calcitonin has a short-lived action and is now little used.

Prednisolone (30-60 mg daily) is effective in some instances (e.g. in myeloma,
sarcoidosis and vitamin D excess) but in most cases is ineffective.

Oral phosphate produces diarrhoea. Intravenous phosphate rapidly lowers plasma Ca2+
but is dangerous and should not be used.

Thyrotoxicosis – Clinical features in descending order of frequency

• Hyperactivity, irritability, dysphoria
• Heat intolerance and sweating
• Palpitations
• Fatigue and weakness
• Weight loss with increased appetite
• Diarrhoea
• Polyuria
• Oligomenorrhoea
• Loss of libido

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 Pearls in PACES (Communication & Ethics)
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COMMUNICATION SKILLS AND ETHICS

CLINICAL MARK SHEET

Examiners are required to make a judgement of the candidate's performance in each of the following
sections by filling in the appropriate box then record the overall judgement (a fail or clear fail grade must
be accompanied by clearly written explanatory comments)

1. Conduct of Interview
• Introduces self to patient and explains role clearly
• Agrees the purpose of the interview with the patient Clear Pass Fail Clear
• Puts the patient at ease and establishes good rapport Pass Fail
• Explores the patient's concerns, feelings and expectations □ □ □ □
• Demonstrates empathy, respect and non judgemental attitude
• Prioritises problems and redirects interview sensitively
2. Exploration and problem negotiation
• Appropriate questioning style - generally open-ended to closed as
the interview progresses
Clear Pass Fail Clear
• Provides clear explanations (jargon-free) that the patient
Pass Fail
understands
□ □ □ □
• Agrees a clear course of action
• Summarises and checks the patient's understanding
• Concludes the interview appropriately
3. Ethics and Law
In relation to the clinical scenario the candidate demonstrates
knowledge of the relevant ethical and legal principles and appropriate Clear Pass Fail Clear
attitudes in making decisions Pass Fail
• Knowledge of ethical principles □ □ □ □
• Understanding legal constraints applicable to case
• Provides adequate reasoning as appropriate to case
Clear Pass Fail Clear
Overall judgement Pass Fail
□ □ □ □

Steps in preparation for communication skills and ethics station:

Step 1: Learn the ethical and legal issues in medicine
Step 2: Learn the general principles of communication with patient/family
Step 3: Practice an approach to the station (how to listen and respond to the patient’s concerns and impart
information in a clear and sensitive manner)

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Pearls in PACES (Communication & Ethics)
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STEP 1: ETHICAL AND LEGAL ISSUES IN MEDICINE

Principles of medical ethics

• Protect the patient’s life
• Respect the patient autonomy
• Fairness and justice
• Duty to do good (beneficence)
• Avoiding doing harm (non-maleficence)

Good medical practice principles (GMC)

• Show respect for human life
• Make the care of your patient your first concern
• Protect and promote the health of patients and the public
• Provide a good standard of practice and care
• Keep your professional knowledge and skills up to date
• Recognise and work within the limits of your competence
• Work with colleagues in the ways that best serve patients' interests
• Treat patients as individuals and respect their dignity
• Treat patients politely and considerately
• Respect patients' right to confidentiality
• Work in partnership with patients
• Listen to patients and respond to their concerns and preferences
• Give patients the information they want or need in a way they can understand
• Respect patients' right to reach decisions with you about their treatment and care
• Support patients in caring for themselves to improve and maintain their health
• Be honest and open and act with integrity
• Act without delay if you have good reason to believe that you or a colleague may be putting patients at
risk
• Never discriminate unfairly against patients or colleagues
• Never abuse your patients' trust in you or the public's trust in the profession.
• You are personally accountable for your professional practice and must always be prepared to justify
your decisions and actions
• In summary, good doctors make the care of their patients their first concern: they are competent, keep
their knowledge and skills up to date, establish and maintain good relationships with patients and
colleagues, are honest and trustworthy, and act with integrity

Hospital records
• Patients have the right to see their medical notes and computer records, which are subject to the Data
Protection Act 1998.
• If a patient asks to review their notes it should be done with a member of the medical team, to explain
medical terms.

Consent
• Patients have the right to self-determination and, after an informed two-way discussion, can refuse any
suggested treatment
• In order to obtain consent, an individual must be deemed competent to understand and retain the
information, using it to reach a reasonable decision
• It is not always deemed to be in the best interests of the patient to discuss extremely unlikely side-
effects, as it may lead to undue anxiety and poor decision-making.

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• Special situations in consent taking:

Unconscious patients: doctors can give emergency treatment for unconscious patients (who are
unable to give consent) if it is in the best interests of the patient (doctrine of necessity). If relatives
are available they should be informed rather than opinions canvassed

Patients with impairment of mental function: If mental impairment is suspected a psychiatrist
must be consulted to make the diagnosis “the patient is unable to give consent” - defined as any
disability or disorder of the mind or brain, whether permanent or temporary, which results in
impairment or disturbance of mental function. In these situations, medical staff may be required to
make decisions which are deemed to be in the best interests of the patient, without obtaining
informed consent. Guardians and relatives have no legal rights

Patients who are danger to themselves or to others: detainment of patients against their will
under the 1983 Mental Health Act is aimed at controlling patients who are a danger either to
themselves or to others due to temporary or permanent mental illness. They can be
detained/restrained for varying periods, depending on the clause of the Act, and can be given
treatment, but only for their mental illness, which is deemed in their best interests or the best
interests of the public.

Advance directives are recognized in law and must be respected, as long as they are completed by
a competent, witnessed, adult.

Relatives have a legal influence with regard to giving consent in only two situations: (1) In minor
who are not “Gillick competent” and (2) after death
o The Family Law Reform Act of 1969 defines a minor as below 18 years of age. However, for
the purpose of medical treatment a patient achieves adult status at 16.
o A competent child above 16 years of age can therefore give valid consent to any surgical,
medical or dental treatment, regardless of parental opinion. Where in case of mental
incompetence, a parent can act for the child until he (she) is of age 18.
o Children under the age of 16 years can give consent for medical intervention, or refuse it, if
they are deemed to be of sufficient maturity and intelligence to understand the implications of
the treatment. This is referred to as “Gillick competence”
o Parents must act in the best interests of their child in order to give valid consent. If it is
deemed by the medical staff this is not the case, the child can be made a ward of court and
treatment given without the parent’s consent.

Confidentiality
• In order to maintain a good patient relationship, consultations should be carried out in confidence. This
respect of confidentiality also applies after the patient has died (I will respect the secrets which are
confided in me even after the patient has died – Declaration of Geneva as amended in Sydney 1968)
• Situations where confidentiality must be broken (by law):

Notifiable diseases (e.g. TB, plague and food poisoning)

Under section 18 of the Prevention of Terrorism Act 1989

If a warrant from a circuit judge has been obtained

A doctor who suspects a patient has been involved in a road traffic accident is under a duty to give
information to the police, but only in order to identify the driver
• Situations where confidentiality can be broken:

Where one is acting in the best interests of the patient (only if unconscious or confused). For
example, if a patient is unconscious it may be in his (her) best interests to disclose information to
the relatives, not only to obtain more information, but also to relieve the anxiety of the relatives.

Acting in the best interests of society. For example, AIDS is not a notifiable disease and patient
has the right to confidentiality. However, patient should be strongly encouraged to inform others
at risk, and in exceptional circumstances, where it is considered to be of benefit to society,
disclosing information can be done without the express consent of the patient, i.e. to prevent
potential harm to other individuals. As a general rule, doctor must not ignore the risk to others
created by a patient, but weigh up one’s duty to society against one’s duty to an individual
• Situations where confidentiality should not be broken: in cases of sexually transmitted disease and
abortions confidentiality must be maintained.

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Negligence: a successful claim of a doctor’s negligence requires the presence of the following items:
• A duty of care between the doctor and patient must be established. For example, a doctor is not obliged
to help someone in distress on the street because no duty of care has been established
• A breach of this duty of care must be demonstrated. The patient must show that the treatment was not
in accordance with a reasonable body of medical opinion.
• This breach of duty of care caused harm.
• The claim should be brought within 3 years of the action occurring, unless under exceptional
circumstances

Gynaecological issues
• The 1976 Abortion Act states that a pregnancy can be terminated if the pregnancy has not exceeded 24
weeks, providing continuing the pregnancy poses a risk to the mental or physical health of the mother,
or existing children.
• Pregnancy can be carried out up to term if the baby is physically or mentally handicapped

Resuscitation
• Discussing resuscitation status with the patient is strongly encouraged, a view supported by the GMC.
However, common sense governs the timing of such a discussion.
• Resuscitation should be attempted if there is any uncertainty about the decision of the patient or nature
of the disease.
• If a competent patient does not wish to be resuscitated this should be respected
• Resuscitation should not be performed if it is deemed futile, or not in the best interests of the patient
• If a decision not to resuscitate has been made, it should be clearly documented in the medical notes
• If the patient is unconscious, discussion with the relatives may give an impression of what the patient
might have wanted. The opinion or wishes of relatives regarding resuscitation has no legal standing.

Death issues
• Diagnosing brain death requires the following

Deep coma with absent respiration

Absence of hypoxia, hypothermia, hypoglycaemia, acidosis, abnormal biochemistry and sedative
drugs

The following tests should be performed by a consultant or his deputy in the presence of another
doctor, and should be repeated after at least 24-hour interval:

Fixed dilated pupils, absent corneal response and vestibulo-ocular reflex

No gag reflex or motor response in the cranial nerves

No respiratory effort on stopping the ventilator and allowing the PaCO2 to rise to 6.7 kPa

In USA, an EEG is required to confirm brain death
• Persistent vegetative state (PVS): Patients, whose brainstem function persists despite loss of cortical
function, are described as having a “PVS”. Their quality of life is at best uncertain, and their life
depends on artificial feeding. However, it is only possible to withdraw this feeding via a court order
• Euthanasia – the process of accelerating death by active intervention artificially is illegal in the UK.
The only country to allow active euthanasia is Holland, but it is subject to strict guidelines.

In the UK, doctors performing an intervention to terminate life are guilty of manslaughter, despite
the wishes of the patient. However, competent patients have the right to refuse any active
treatment that may prolong their life.

Doctors can administer symptomatic treatment acting in the best interests of the patient (e.g.
increasing doses of opiates to control the pain of terminally ill patients), even if this treatment has
known adverse side-effects and may hasten the process of death. This is the principle of double
effect.

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Organ donation
• After death, the next of kin have lawful possession of the body. If someone dies and there are no next
of kin then the hospital has possession.
• If the patient expressed a wish to donate organs after death this should be respected. However, relatives
must give consent for donation; they can refuse donation even if the deceased wishes were well known
and even in the presence of organ donor card.
• Organ donation from a live donor must not be detrimental to the health of that individual
• The donor need not be an adult, e.g. matched related bone marrow donation
• Once donated, the organ is the possession of the recipient
• Organs cannot be legally bought or sold in the UK. If a donation is to take place between two unrelated
individuals it must be referred to the Unrelated Live Transplantation Authority

Research
• Research projects should be only commence after the approval of a research and ethics committee has
been given
• It is unlawful to carry our research on patients who are unable to give consent.
• Samples taken cannot be used for research retrospectively if consent was not given specifically when
the samples were taken, although these samples are not deemed the property of the patient

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Driving and epilepsy

• Candidates in PACES should review the “at a glance guide to the current medical standards of fitness
to drive” issued by the Driver and Vehicle Licensing Agency (DVLA) at its official website
• Diagnosing epilepsy

One seizure does not make the diagnosis of epilepsy

Epilepsy is by definition the continuing tendency to have such seizures, even if a long interval
separates such attacks

An EEG may support the diagnosis, but its main function is to ensure the seizures are correctly
classified to enable precise treatment.
• Current regulations regarding medical restrictions on driving (February 2007)
Group A (motor cars and motorcycles) Group B (Lorries and buses)
Simple faint (faints of benign nature with definite provocational factors, associated prodromal symptoms
and are unlikely to occur whilst sitting or lying): No driving restrictions
Unexplained syncope with low risk of re-occurrence Can drive 3 months after the event
(These have no relevant abnormality on CVS and
neurological examination and normal ECG): can drive 4
weeks after the event.
Unexplained syncope with high risk of re-occurrence Can drive 3 months after the event if the
(abnormal ECG, clinical evidence of structural heart cause has been identified and treated. If no
disease, syncope causing injury, occurring at the wheel or cause identified, then licence
whilst sitting or lying, or more than one episode in refused/revoked for one year.
previous six months) Can drive 4 weeks after the event if
the cause has been identified and treated. If no cause
identified, then require 6 months off.
Unprovoked seizure • Bus and lorry drivers who has suffered
• A person who has suffered an epileptic attack whilst unprovoked seizure, must demonstrate 10
awake must refrain from driving for one year from the years freedom from further seizures, without
date of the attack before a driving license may be issued anticonvulsant medications at that time
• A person who has suffered an epileptic attack whilst • Following a solitary seizure associated
asleep must also refrain from driving for one year from with either alcohol or substance misuse or
the attack. However, if they have had an attack whilst prescribed medication, a 5 year period free
asleep more than three years previously and have not had of further seizures, without anticonvulsant
any awake attacks since that original asleep attack then medication in that time, is required)
they may be licensed even though asleep attacks may
continue to occur.
• If the seizure is related to alcohol withdrawal, the
licence will be revoked for a minimum of one year from
the event
• Withdrawal of anti-epileptic medication is associated
with a risk of seizure recurrence. The current Epilepsy
Regulations require a period of 1 year free of any
manifestation of epileptic seizure or attacks occurring
whilst awake during this therapeutic procedure, before
resuming driving. Special consideration is given where
sleep only attacks have occurred
• Provoked or acute symptomatic seizures may be dealt with on an individual basis by DVLA if there is
no previous seizure history. Seizures associated with alcohol or drug misuse, sleep deprivation or a
structural abnormality are not considered provoked for licensing purposes. Similarly, reports of seizures as
a side-effect of prescribed medication do not automatically imply that such events will be considered as
provoked.
• The same DVLA rules apply to taxi drivers as to other motor vehicle users, although they are
additionally subject to restrictions from the Public Carriage Office or the local authority. Current best
practice advice is contained in the “Medical Aspects of Fitness to Drive” published by the Medical
Commission on Accident Prevention in 1995. This recommended that medical standards applied by DVLA
in relation to bus and lorry drivers, should also be applied by local authorities to taxi drivers

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• Notification to DVLA

It is the duty of the licence holder or licence applicant to notify DVLA of any medical condition,
which may affect safe driving. The DVLA is legally responsible for deciding if a person is
medically unfit to drive.

Therefore, where patients have such conditions, you should make sure that the patients understand
that the condition may impair their ability to drive. If a patient is incapable of understanding this
advice, for example because of dementia, you should inform the DVLA immediately.

Explain to patients that they have a legal duty to inform the DVLA about the condition. Before
discussing legal issues it is often beneficial to discuss the ethical context in which the law arises.
Individuals are more likely to comply with legislation if they understand the reasoning behind it.

If the patients refuse to accept the diagnosis or the effect of the condition on their ability to drive,
you can suggest that the patients seek a second opinion, and make appropriate arrangements for
the patients to do so.

You should advise patients not to drive until the second opinion has been obtained.

If patients continue to drive when they are not fit to do so, you should make every reasonable
effort to persuade them to stop. This may include telling their next of kin, if they agree you may
do so.

If you do not manage to persuade patients to stop driving, or you are given or find evidence that a
patient is continuing to drive contrary to advice, you should disclose relevant medical information
immediately, in confidence, to the medical adviser at DVLA.

Before giving information to the DVLA you should inform the patient of your decision to do so.
Once the

DVLA has been informed, you should also write to the patient, to confirm that a disclosure has
been made.

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STEP 2: GENERAL PRINCIPLES OF COMMUNICATION WITH PATIENT/FAMILY

General rules
• Always introduce yourself and explain your role
• keep eye contact and show interest and rapport
• Always ask before telling
• Establish the expectations and knowledge of the patient
• Allow the patient to speak openly and freely, but be prepared to direct the consultation
• Provide a frame work for your explanation
• Keep statements short and simple
• Repeat important information
• Check understanding
• Try to give the patient choices rather than instructions
• Allow pauses for the patient to digest information
• Encourage feedback
• Be honest and ready to admit uncertainty
• Be optimistic but realistic (always give hope and emphasis the positive points)
• Acting against the patient/family wishes should be the last course of action even if you have the legal
right to do so. This will usually result in a breakdown in the doctor-patient/family relationship, and
may ultimately compromise the healthcare of the individual.

Special situations
• Explaining procedure (investigation or treatment)

Explain the purpose of the procedure using short statements
o The purpose of this procedure is to …
o This will help us to … (mention all the expected benefits)
o Otherwise… (Mention all the sequels of not doing the procedure)

Explain the nature of the procedure (In this procedure the specialist doctor will…)

Explain the risks (A lot of patients undergo this procedure daily safely, however as any medical
procedure, it has its risks which may occur in small percentage of patients such as…eventually
weighing the great benefits against the low possibility of risks makes this procedure an advisable
option for you from the medical point of view).

Check understanding at each step (is it alright/clear up till now).

Seek consent (so far you are supposed to sign consent for this procedure. This will include the
main points that I have already explained to you. You should read it again and if you have any
further questions you may ask me, and even after signing this consent you have the right not to
undergo the procedure if you changed your mind for any reason before the scheduled time for the
procedure)
• Discussing prognosis

Establish facts about diagnosis and results of investigations

Discuss the prognosis with and without treatment

Discuss the complications of the disease and treatment (common and serious complications)
• Diagnostic uncertainty

Outline the possibilities including the most serious

Discuss the plan and when further consultation is required

Be honest and professional

Keep a safety net (exclude serious causes, arrange follow up...)
• Non-compliant patient

Explain the importance of treatment

Explore the patient concerns

Explain that the doctor and patient should work together as a team (we are one team and our goal
is to give you the best chance to go over this situation and you are the most important player in
this team)

Keep options clear and simple

Confirm understanding

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• Sharing bad news / discussing Do Not Attempt Resuscitation order

Having a relative or friend present may be helpful (If you want anyone else relevant to you to
attend this meeting, he or she is welcomed)

Establish what the patient knows (do you understand why we have been doing this test or suspect
what might be wrong?)

Disclose what the patient wants to know (Are you that kind of people who wants to know well
about their illnesses?)

Build up news layer by layer preferably starting from the beginning of the problem and giving
warning statement before telling the facts in short clear statements then giving realistic hope
o (You know your father had …..) → (The result of the test was not as we hoped, it showed…)
→ (however, this is now a manageable condition and we have a lot of things to do to help you
cope with this situation)
o (I know you have been suffering from this illness for long time now…) → (I know it is
difficult for you to give me an answer but let me ask you, if your heart stops do you want us
to resuscitate you) → (however, we are going to provide all other available treatments and
keep you free of pain and in a good shape)

Pause frequently to allow the patient time to think and ask questions

Be ready to answer questions related to life expectancy and chance for cure (No one knows what
will happen in the future, and so I do not like to give figures) (Everybody is different and some
people do much better than others, and I know a lot of people who had the same condition and
enjoyed a reasonable life for a relatively long time) (I do not think this disease will ever go away
completely, however we can do a lot of things to help you cope with it and make you free of pain
and in good shape)
• Request for autopsy or organ donation

acknowledge that it is a difficult time

explain the reason for autopsy or organ donation

Discuss arrangements about the body: confirm that there will be no delay in funeral arrangements,
standard invisible incisions will be used, and body can be viewed afterward.
• Dealing with angry patient / Admitting medical error

Acknowledge patient’s feeling (I understand your feeling and I am sorry for this)

Explore patient’s concerns (now let me ask you what does concern you most?)

Be honest and apologetic. However, stay away from areas of conflict and avoid confrontation, do
not incriminate colleague and take constructive actions (I will find out what went wrong and
actions will be taken to stop it happening again, but that now you must try to focus on the future
and the current medical problem)

Explain what the options are in the future (including seeking a second opinion)
• Patient resisting legal breach of confidentiality

Explore patient’s concerns

Explain importance of disclosure for the safety of the patient, family and society

Emphasise his (her) responsibility towards others

Inform the patient about your intentions
• Daughter knows her mother has serious illness but does not want you to tell her mother

Explain that you appreciate that she knows her mother much better than the doctors (I appreciate
that you know your mother much better than the doctors. However, having seen this situation
many times before, telling the mother the truth is usually what she wants and is best in the long
term)

Explain that telling the mother the truth is usually what she wants (most people know when there
is something seriously wrong, and finding out can be a relief)

Explain that you need to be sure that her mother does not want to know her diagnosis (How do
you know that your mother does not want to know?) (I would like to be sure that your mother does
not want to know her diagnosis) (I will talk to her and give her a small amount of information, and
if she does not want to know I will not tell her)

Ask for the daughter’s cooperation in the treatment plan (we are one team and our goal is to give
your mother the best chance to go over this situation)

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STEP 3: APPROACH TO THE STATION

Part 1: in the 5 minutes before the interview

• Establish your role and patient/relative name and location
• Establish the key issues, which must be conveyed (medical, social and medico-legal)

Part 2: The interview:

1. Introduce yourself and confirm the patient/relative identity

Good morning Mr. …, I have got the right person haven't I? I am Dr…

If he is the patient, ask how are you today?

If son/daughter, ask: does your father know that you’re coming to see me today?

If pregnant wife, ask: why your husband doesn’t attend this meeting? After we finish we may
arrange for second meeting and invite him. I think this would be useful for both of you
2. Listen

Assess the patient Knowledge and expectations of their condition (Now let me start by asking you
what do you know about your illness?)
3. Inform

Give simple information about the medical condition (let me give you a simple idea about this
condition)
4. Explore

Explore the patient’s worries (now let me ask you what does concern you most?)

Explore any social/psychosocial or ethical/legal problems (I need to ask you some rather personal
questions, is that OK?) (How does this problem affect you in your job?) (How does this problem
affect your marital status?) (Do you feel depressed because of this problem?)
5. Answer the patient’s questions/worries

If you do not know the answer (I will attempt to find the correct answer for the next consultation
or later today)

Ask about further questions (I hope you have found our discussion useful to you. do you have any
further questions?)
6. Management plan

Ask for patient’s cooperation in the treatment plan (we are one team and our goal is to give you
the best chance to go over this situation and you are the most important player in this team)

Seek consent if needed for the procedure/treatment (so far you are supposed to sign consent for
this procedure. This will include the main points that I have already explained to you. You should
read it again and if you have any further questions you may ask me, and even after signing this
consent you have the right not to undergo the procedure if you changed your mind for any reason
before the scheduled time for the procedure)

Provide written information, telephones and addresses (I will provide you with pamphlets for
further information and instructions regarding your condition, contact numbers of the hospital,
contact numbers and addresses of support groups which may be of great help, and also addresses
of respectable websites for further information)

Suggest additional help if needed (home visits, home nurse, occupational therapist, social worker)
7. Summarize
o Before finishing, summarize the consultation (now I want to emphasize the important points in our
discussion)
o Agree a management plan for the future (our plan…)
o ask if they want anything repeated or if they have any questions (do you want me to recover any
issue)
o arrange another appointment (I will arrange for the next appointment in couple of days to review
our plan and see what’s going on)

Part 3: discussion with the examiners

Question: How do you think it went?
Answer: I have explained…. The patient digested the information…I think he needs time to absorb the
situation…in follow-up consultations I would readdress the issue of…

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