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Clinical examination
• Sputum pot: note the contents.
• Nebulizer and medications.
• Pursed lip breathing and accessory muscle use: chronic
small airway obstruction.
• Voice: hoarse in bronchial carcinoma (recurrent
laryngeal nerve palsy).
• Note if a chest drain is present and look at the contents.
Position
Help the patient to adopt a comfortable position at 45 degrees with the chest exposed. In women, cover the chest until you are ready to examine it.
Hands
• Clubbing: see Table2.4
• Cyanosis: respiratory failure.
• Wasting of small muscles: infiltration of T1 by
bronchial neoplasm (Pancoast tumour).
• Tar-stained fingers: increased likelihood of malignancy
and obstructive airway disease.
• Asterixis (flap): carbon dioxide retention.
• Fine tremor: recent salbutamol use.
• Evidence of conditions which may involve the lungs
(e.g. systemic sclerosis, rheumatoid arthritis) (see
Chapter28).
Table2.7 Causes of tracheal deviation
Towards lesion Away from lesion
Collapse Tension pneumothorax
Apical fibrosis Massive pleural effusion
Pneumonectomy Large mass (e.g. thyroid)
Trachea
Warn the patient before you palpate the trachea! Note the
following:
• Tracheal deviation reflects disease in the upper
mediastinum (Table2.7).
• Feel for tracheal tug in acute respiratory distress.
• The distance from the cricoid cartilage to the
suprasternal notch should be 2–3 cm – this distance
reduces in hyperinflation.
COMMUNICATION
Always take care to explain what you are doing to
the patient when you are examining the trachea.
If done badly, it may be uncomfortable, and if you
hurt the patient, you are likely to fail.
Pulse
• Tachycardia: severe respiratory disease (e.g. pulmonary
embolism, acute asthma or pneumonia).
• Bounding: carbon dioxide retention.
• Atrial fibrillation: e.g. sepsis secondary to pneumonia.
Blood pressure
Pulsus paradoxus is seen in severe acute asthma.
Jugular venous pressure
• Right ventricular failure: chronic respiratory disease
with pulmonary hypertension.
• Superior vena caval obstruction: bronchial carcinoma.
Face and mouth
• Central cyanosis: respiratory failure.
• Anaemia: chronic respiratory disease, particularly
malignancy.
• Horner syndrome: apical carcinoma (Pancoast tumour)
involving cervical sympathetic nerves (see Chapter28).
• Fine tremor: β-agonists.
• Plethoric facies: secondary polycythaemia.
Thorax
Perform inspection, palpation, percussion and auscultation
on the front of the chest first. Then sit the patient forward,
palpate the front of chest for lymphadenopathy and then
repeat the examination on the back of the chest. Typical
patterns of respiratory abnormalities are shown in Table2.8.
Inspection
On inspecting the chest, assess:
• Respiration: use of accessory muscles (respiratory
distress).
• Recession: intercostal and subcostal (respiratory
distress).
• Scars: including previous surgery and chest drains.
• Deformity: barrel chest (seen in long-standing airways
obstruction as a result of hyperinflation), pectus
excavatum, pectus carinatum.
• Radiotherapy: tattoos or skin changes indicate previous
treatment for malignancy.
Expansion
• Ask the patient to take a deep breath in and note
symmetry and comfort.
18
Table2.8 Findings on clinical examination of common respiratory diseases
Pathology General signs Tracheal deviation Palpation Percussion note Breath sounds Causes
Pneumothorax Tachycardia and
Consolidation Pyrexia, tachycardia None Reduced expansion,
Pleural effusion Away from affected
Collapse Towards affected
Fibrosis Clubbing Towards affected
Bronchiectasis Clubbing, purulent
Bronchospasm Hyperexpanded
SLE, systemic lupus erythematosus; TVF, tactile vocal fremitus.
19
hypotension
in tension
pneumothorax
sputum
chest, tremor (if
taking a β-agonist),
Harrison sulci, pectus
carinatum
Away from affected
side if tension
side if large
side
side if apical
disease
Normal Normal or reduced
Normal Reduced expansion,
Reduced expansion,
reduced TVF
increased TVF
Reduced expansion,
reduced TVF
Reduced expansion,
reduced TVF
Reduced expansion,
increased TVF
expansion, normal or
increased TVF
normal TVF
Normal or
hyperresonant
Dull Increased vocal
Stony dull Absent Transudate (protein <30 g/L): cardiac
Dull Reduced or absent Foreign body or mucous plugs (asthma,
Normal or dull Fine inspiratory
Normal or dull Coarse inspiratory
Normal, hyperresonant over
bullae, reduced
liver dullness
Reduced or absent Spontaneous (particularly tall healthy males
resonance, whispering
pectoriloquy, bronchial
breath sounds
crepitations
crepitations, occasional
polyphonic wheeze
Polyphonic wheeze,
crepitations in chronic
obstructive airways
disease
and Marfan syndrome), trauma, airway
obstruction, cystic fibrosis, pulmonary
abscess
Pneumococcus, Haemophilus influenzae,
Staphylococcus aureus, Klebsiella,
Pseudomonas, Mycoplasma, Legionella,
influenza type A, Aspergillus
failure, liver failure, nephrotic syndrome,
Meigs syndrome, myxoedema
Exudate (protein >30 g/L): malignancy,
pneumonia, pulmonary embolus, rheumatoid
arthritis, SLE, subphrenic abscess,
pancreatitis, trauma, Dressler syndrome
aspergillosis) within the bronchial lumen,
bronchial carcinoma arising from the bronchus
itself, extrinsic compression by enlarged
lymph nodes (malignancy, tuberculosis)
Cryptogenic fibrosing alveolitis, sarcoidosis,
drugs (amiodarone, bleomycin), radiation,
inhalation of dusts (asbestos, coal),
extrinsic allergic alveolitis, ankylosing
spondylitis, rheumatoid arthritis, systemic
sclerosis, tuberculosis
Congenital (cystic fibrosis, Kartagener
syndrome, hypogammaglobulinaemia),
idiopathic, bronchial obstruction (foreign
body, carcinoma, lymphadenopathy), infection
(childhood measles or whooping cough,
tuberculosis, aspergillosis, postpneumonia)
Anaphylaxis
The respiratory system
22
Clinical examination
• The chest circumference should expand by at least 5 cm
on deep inspiration.
• Any significant pulmonary disease will reduce
expansion.
• In unilateral disease, the affected side will move less
than the other.
• Note any chest wall tenderness, which is usually caused
by musculoskeletal abnormalities.
Tactile fremitus and vocal fremitus
Ask the patient to say ‘99’ and palpate with the ulnar border
of the hand. Increased vocal fremitus indicates consolidation; decreased vocal fremitus indicates pleural effusion or
collapse.
Percussion
Compare one side with the other and remember the axillae.
The following signs are important:
• hyperresonance: pneumothorax;
• dull: solid organ (liver or heart), consolidation,
collapse, pleural thickening, peripheral tumours, severe
fibrosis, previous old pneumonectomy;
• stony dull: pleural effusion.
Auscultation
• Normal breath sounds are termed ‘vesicular’.
• Bronchial breathing, whispering pectoriloquy,
increased vocal resonance: consolidation (sometimes
fibrosis and above pleural effusion).
• Wheeze: small airway obstruction (polyphonic),
large airway obstruction (e.g. bronchial carcinoma
(monophonic or localized)) and cardiac failure.
• Fine crackles: pulmonary fibrosis, pulmonary oedema.
• Coarse crackles: infection.
• Absent breath sounds: pleural effusion.
• Pleural rub: pleural irritation due to pneumonia or
pulmonary embolus.
Summary
To conclude the examination, look for:
• Pitting oedema indicating right ventricular failure, or
low albumin level from chronic disease.
• Sputum inspection, peak flow, oxygen saturation,
temperature and chest X-ray: these can be remembered
by the mnemonic SPOT-X.
THE ABDOMEN
Visual survey
• Appearance: does the patient look well or ill?
• Is the patient in pain?
• Patient's position: think of peritonism if the patient
very still, appendicitis (psoas irritation) if the knees are
flexed and renal colic if the patient is rolling around in
ag ony.
• Cachexia: chronic disease, particularly malignancy.
• Drowsy: encephalopathy (hepatic or uraemia).
• Hydration status, you can assess this more carefully
with attention to mucous membranes, height of the
JVP, capillary refill time, patient weight and postural
blood pressure.
Position
The patient can initially be assessed sitting at 45 degrees.
For examination of the abdomen itself, the patient should
be as flat as can be tolerated comfortably (this relaxes the
abdominal muscles). Exposure should be from ‘nipples to
knees’, but bear in mind the patient's dignity.
Hands
• Clubbing: cirrhosis, inflammatory bowel disease.
• Leukonychia: clinical sign of hypoalbuminaemia.
Consider liver disease, nephrotic syndrome, proteinlosing enteropathy.
• Koilonychia: chronic iron deficiency. Consider occult
neoplasm, particularly in the stomach and caecum.
• Palmar erythema: cirrhosis.
• Hyperpigmented palmar creases: Addison disease.
• Asterixis: hepatic encephalopathy and uraemia.
• Dupuytren contracture: alcoholic liver disease.
Arms
• Scratch marks: obstructive jaundice (particularly
primary biliary cirrhosis), uraemia and lymphoma.
• Needle track marks, tattoos: viral hepatitis.
• Muscle wasting: proximal myopathy due to
alcohol, steroid excess or underlying malignancy
(paraneoplastic).
• Bruising: hepatic impairment.
HINTS AND TIPS
The upper border of the liver is normally at the sixth
intercostal space in the right midclavicular line. If
the percussion note remains resonant below this,
the lungs are hyperinflated.
20
Face and mouth
• Jaundice: prehepatic, hepatic or posthepatic (see
Chapter14).
• Pallor suggesting anaemia from any cause.
• Xanthelasmata: hypercholesterolaemia (primary biliary
cirrhosis or nephrotic syndrome).
• Kayser–Fleischer rings: Wilson disease (best seen by
slit-lamp examination).
The abdomen
22
• Glossitis and stomatitis: iron deficiency and
megaloblastic anaemia.
• Telangiectasia: associated with limited systemic
sclerosis (CREST syndrome), cirrhosis and hereditary
haemorrhagic telangiectasia (Osler–Weber–Rendu
disease).
• Crohn disease: mucosal ulceration.
Neck
Look for left supraclavicular lymphadenopathy—caused
by metastasis from underlying gastrointestinal carcinoma
(Virchow node or Troisier sign).
HINTS AND TIPS
Always palpate the neck from behind the
patient with the neck slightly flexed to relax the
sternocleidomastoid muscles.
Trunk and back
Spider naevi arise in the distribution of the superior vena
cava – five or more suggest underlying chronic liver disease, pregnancy or hyperthyroidism. Look for gynaecomastia, increased breast tissue in men. This is most
commonly associated with chronic liver disease or drugs
(e.g. spironolactone).
Abdomen
Inspection
Observe closely, looking for:
• Scars: previous surgery or trauma.
• Distension (Table2.9).
• Obvious mass: including movement with respiration.
• Bruising: Cullen (paraumbilical) and Grey Turner
(flanks) signs in acute pancreatitis (these are rare).
• Dilated veins and caput medusae: portal hypertension
or inferior vena cava obstruction (venous flow is
upwards).
• Striae: pregnancy or Cushing syndrome.
Table2.9 Causes of generalized abdominal swelling
Cause Example
Fluid Ascites
Faeces Constipation
Foetus Pregnancy
Flatus Bowel obstruction
Fat Obesity
Fibroids And any other tumour or
organomegaly
• Node: umbilical nodule (Sister Mary Joseph nodule) is
a metastasis from intraabdominal malignancy.
• Peristalsis: if visible, this indicates an obstruction,
although it may be normal in a thin or elderly
patient.
Palpation
Before you touch the patient, ask if the patient is tender anywhere and start palpation away from that area. Feel gently
in each of the four quadrants, noting tenderness or masses.
Then feel more deeply in each quadrant to determine the
characteristics of any mass found (Box2.8).
HINTS AND TIPS
Always look at the patient's face when palpating
the abdomen to ensure that you know immediately
if you are causing discomfort.
If a mass is present, consider what structures normally lie
at that site and what disease processes might affect that
structure (see Chapter9). Next, palpate for hepatomegaly
and splenomegaly, starting in the right iliac fossa. Examine
the patient for renal masses by bimanual palpation. If hepatomegaly or splenomegaly is present, comment on consistency (smooth or irregular), whether tender and size in
centimetres (not finger breadths) beneath the costal margin (the causes of hepatomegaly are shown in Table 2.10;
the causes of splenomegaly are discussed in detail in
Chapter21). The causes of a renal mass are summarized
in Table2.11.
Finally, palpate for abdominal aortic aneurysm and ex-
amine the groins for lymphadenopathy and hernias.
BOX2.8 FEATURES TO DETERMINE FOR ANY
MASS
Site
Shape
Size, including upper, lower and lateral limits
Consistency
Tenderness
Fluctuance
Fixation to underlying or overlying structures
Transillumination (where appropriate)
Local lymph node involvement
Bruit
21
Clinical examination
Table2.10 Causes of hepatomegaly
Cause Examples
Infection Viral hepatitis,a abscess, syphilis,
Tumour Benign, malignant, primary
Venous congestion Right ventricular failure, Budd–Chiari
Autoimmune Autoimmune liver disease, primary
Cysts Polycystic disease
Haematological Lymphoproliferative disease,a
Metabolic Nonalcoholic fatty liver, storage
Toxic/drug Alcoholic liver disease,a drug-
The liver may appear large in the absence of true hepatomegaly
when it is pushed down by a hyperinflated lung (as in acute
asthma or chronic obstructive airway disease) and when a Riedel
lobe is present (normal anatomical variation of the right hepatic
lobe).
a
Cause of hepatosplenomegaly.
Table2.11 Causes of unilateral and bilateral palpable
kidneys
Type Cause
Unilateral Tumour (hypernephroma,
Bilateral Polycystic kidneys (autosomal
Weil disease,a hydatid disease,
brucellosis
(hepatocellular carcinoma) and
metastases
syndrome, tricuspid disease
biliary cirrhosis and primary
sclerosing cholangitis
myeloproliferative disease
diseases,a amyloidosis,a
haemochromatosis, Wilson disease
induced hepatitis, e.g. statins
nephroblastoma)
Hydronephrosis, pyonephrosis
Hypertrophy of single functioning
kidney
Perinephric abscess or haematoma
Polycystic disease (only one kidney
palpable)
dominant in adults, autosomal
recessive in children)
Amyloidosis
Bilateral hydronephrosis
a
Percussion
Always percuss from resonance to dullness. Use percussion to determine the size of the liver and spleen, starting
at the chest, moving inferiorly. Percuss over any masses to
determine their consistency. Always assess for ascites by
looking for a fluid thrill and shifting dullness. Table 2.12
summarizes the causes of ascites. Look for tenderness on
percussion; this is a useful clinical sign that may indicate
peritoneal irritation.
Table2.12 Causes of ascites
Type Cause
High SAAG, >1.1 g/dL Cardiac failure
Liver failure
Hypoproteinaemia
Meigs syndrome
Myxoedema
Budd–Chiari syndrome
Constrictive pericarditis
(rare)
Cirrhosis with portal
hypertension
Low SAAG, <1.1 g/dL Intraabdominal malignancy
Infection (tuberculosis,
perforation, spontaneous)
Pancreatitis
Lymphatic obstruction
(chylous)
SAAG is a better discriminant than older measures of transudate
(high SAAG) and exudate (low SAAG).
SAAG, Serum ascites albumin gradient.
Auscultation
• Bowel sounds may be normal, increased or decreased:
increased in bowel obstruction (high-pitched and
tinkling) and absent with an ileus (functional motor
paralysis of the bowel) of any cause (Box2.9).
• Arterial bruits: may be heard over stenosed vessels such
as renal arteries.
• Succussion splash: any cause of gastric outlet
obstruction.
Concluding your examination
• If the patient has symptoms or signs rectal bleeding,
has iron deficiency or reports a change in bowel habit,
you should perform a digital rectal examination.
• You may have to examine the patient’s genitals in some
circumstances.
BOX2.9 CAUSES OF ILEUS
Handling of the gut during intraabdominal surgery
Peritonitis
Pancreatitis
Hypokalaemia
Uraemia
Diabetic ketoacidosis
Intraabdominal haemorrhage
Retroperitoneal haematoma
Retroperitoneal trauma, e.g. surgery for aortic
aneurysm
Anticholinergic drugs
22
The nervous system
22
Table2.13 Causes of lower limb oedema
Cause Examples
Pitting Unilateral:
Lymphatic
(nonpitting)
• deep vein thrombosis
• unilateral compression of veins
(tumour or lymph nodes)
• following hip/ knee replacement
• local infection or trauma
Bilateral:
• right ventricular failure
• constrictive pericarditis
• hepatic failure
• nephrotic syndrome
• protein-losing enteropathy
• immobility
• pregnancy
• kwashiorkor
Blocked lymph channels: surgical
damage, radiation, malignant
infiltration, infection (filariasis) or
congenital (Milroy disease)
• For both of these, in your clinical examinations you
should say that you would like to go on to examine
the genitalia and perform a rectal examination, but
generally you will not be asked to perform this.
• If there is hepatosplenomegaly, go on to examine all
lymph node sites, bearing in mind the multitude of
potential causes (see Chapter18).
• Examine the legs for pitting oedema (Table2.13).
• Do not forget to examine hernial orifices.
THE NERVOUS SYSTEM
Although it is true that neuroanatomy is complicated and many
different diseases can affect each part, the end result is a limited
repertoire of patterns of signs. The best approach is to identify
which signs are present using a well-rehearsed technique and
consider where the lesion is likely to be. You can then think of
which diseases affect that part of the nervous system and look
for additional evidence to support the diagnosis.
The clinical signs and common diseases associated with
different parts of the nervous system are discussed in detail
in Chapter22. This section covers a practical approach to
the examination technique itself. It is particularly important
to practice this routine over and over again.
Visual survey
• Appearance: does the patient look well or ill?
• Level of consciousness: is the patient alert, drowsy or
unresponsive?
• Age: for instance, a young patient is more likely to
have multiple sclerosis, motor neurone disease or an
inherited disease; an elderly patient is more likely to
have had a stroke.
• General clues: does the patient need a wheelchair or
walking stick?
• Posture: how is the patient sitting? Is the patient leaning
towards one side (hemiparesis)? Is there a tremor at
rest (parkinsonism)?
• Speech: when the patient speaks, does the speech
sound normal? (See Table1.3.)
Cranial nerves
Features and examinations of the cranial nerves include the
following.
Cranial nerve I (olfactory nerve)
• This is a sensory nerve only.
• Ask the patient if he or she has noticed anything
abnormal about the sense of smell.
• Sense of smell can be tested with bottles containing
essences, although this test is rarely performed. (Note
that ammonia should not be used as it also stimulates
the trigeminal nerve.)
• Anosmia can result from head injury (fracture of the
cribriform plate), upper respiratory tract infection or
tumour (olfactory groove meningioma or glioma),
or can be a feature of Parkinson disease or Kallmann
syndrome (anosmia with hypogonadotrophic
hypogonadism).
Cranial nerve II (optic nerve)
• This is a sensory nerve only.
• Visual acuity: ask the patient to read some print or a
Snellen chart (with spectacles if worn normally).
Test each eye separately. Any lesion from the
cornea, lens, retina, optic nerve, optic chiasm,
optic radiation or occipital cortex can result in
reduced acuity.
• Visual fields: test each eye individually. Make sure
your eyes are on the same level as the patient's. Move
your fingers from beyond your visual field inwards
and ask the patient to tell you when he or she can
see them. Check each quadrant. Use a red hatpin to
determine the blind spot. Typical field defects are
shown in Table2.14. Vision can be formally assessed
by perimetry. If the visual fields are intact, look for
inattention by simultaneously stimulating both the left
and the right.
• Pupillary reflexes: the pupillary reactions to light
and accommodation should be tested. Remember
sympathetic innervation causes mydriasis (dilated
pupil), and parasympathetic innervation causes miosis
(constricted pupil). Pupillary abnormalities in patients
who are in a coma are described in Chapter18. Other
clinical abnormalities include:
• Physiological anisocoria: slight difference in size.
• Senile miosis: small, irregular pupils in old age.
23
Clinical examination
Table2.14 Visual field defects
Defect Site of lesion Causes
Tunnel vision Retina Glaucoma, retinitis pigmentosa, laser therapy for
Enlarged blind spot Optic nerve Papilloedema (from any cause)
Central scotoma Macula, optic nerve Optic atrophy, optic neuritis, retinal disease
Monocular visual loss Eye, optic nerve Extrinsic compression, toxic optic neuropathy
Bitemporal hemianopia Optic chiasm Pituitary tumour, craniopharyngioma, sella
Quadrantic hemianopia Temporal lobe (superior),
parietal lobe (inferior)
Homonymous hemianopia Occipital cortex, optic tract Stroke, tumour
diabetic retinopathy
affecting macula
meningioma
Stroke, tumour
• Total afferent pupillary defect (complete lesion
of optic nerve): if, for instance, the left eye is
affected, shining a light in it fails to cause pupillary
constriction in either eye – absent direct and
consensual reflexes. However, if a light is shone in the
right eye, the left pupil constricts (i.e. the right eye
consensual reflex is intact).
• Relative afferent pupillary defect (RAPD), which occurs
if there is incomplete damage to the afferent pathway (e.g.
previous retrobulbar neuritis due to multiple sclerosis).
The swinging light test is performed (i.e. the light is moved
from one eye to the other alternately). If the left eye has a
RAPD, there will be reduced conduction along its afferent
pathway. Therefore if the light is initially shone in the left
eye, both pupils will constrict; when the light is moved to
the right eye, bilateral constriction occurs again; when the
light returns to the left eye, the pupil dilates because of its
reduced afferent conduction. This is diagnostic of a RAPD.
• Horner syndrome: a triad of a constricted pupil
(miosis), an eyelid droop (ptosis) and decreased
sweating (anhidrosis) caused by interruption of the
sympathetic chain at any level from the brainstem to
the ciliary ganglion (see Chapter32).
• Argyll Robertson pupil: a small, irregular pupil that
‘accommodates but does not react’ (i.e. fixed to light
but constricts on convergence). Almost diagnostic of
neurosyphilis (occasionally occurs in diabetes mellitus).
• Myotonic pupil (Holmes–Adie pupil): a dilated
pupil that reacts very slowly to light and constricts
incompletely to convergence. Most common in young
females, and if combined with absent tendon reflexes,
this is Holmes–Adie syndrome.
• Ophthalmoscopy: common abnormalities on
ophthalmoscopy are papilloedema (Table2.15), optic
atrophy (Table2.16), diabetic retinopathy (Table2.17)
and hypertensive retinopathy and in examinations,
retinitis pigmentosa. Pigmentary retinal degeneration
may also occur in other conditions, such as Refsum
disease and Laurence–Moon–Biedl syndrome.
Table2.15 Causes of papilloedema
Cause Examples
Raised intracranial
pressure
Venous occlusion Central retinal vein
Malignant hypertension Grade IV hypertensive
Acute optic neuritis Multiple sclerosis,
Metabolic Hypercapnia,
Haematological (rare) Severe anaemia, acute
Table2.16 Causes of optic atrophy
Cause Examples
Pressure on optic nerve Tumour, glaucoma,
Demyelination Multiple sclerosis
Vascular Central retinal artery
Metabolic Diabetes mellitus, vitamin
Toxins Methyl alcohol, tobacco,
Trauma Including surgery
Consecutive Extensive retinal disease
Hereditary prolonged
papilloedema
Tumour, abscess,
hydrocephalus, haematoma,
benign intracranial
hypertension, cerebral
oedema (trauma)
thrombosis, cavernous
sinus thrombosis
retinopathy
sarcoidosis
hypoparathyroidism
leukaemia
aneurysm, Paget disease
occlusion
B12 deficiency
lead, quinine
such as choroidoretinitis
Friedreich ataxia, Leber
optic atrophy
24
The nervous system
22
Table2.17 Stages of diabetic retinopathy
Stage Features
Background
nonproliferative
Moderate
nonproliferative
Severe
nonproliferative or
preproliferative
Proliferative All of the above, plus new vessel
Diabetic
maculopathy
The classification of diabetic retinopathy is based on which part
of the retina is affected and the degree of pathology, and does
not necessarily correlate with the patient’s degree of vision.
Note that cataracts are also more common in diabetes, and that
retinopathy may have been treated by laser photocoagulation
(burns around the periphery of the retina, destroying ischaemic
tissue and thus reducing the drive for new vessel formation).
At least one microaneurysm
Microaneurysms or intraretinal
haemorrhages with or without cotton
wool spots, venous beading and
intraretinal microvascular abnormality
Findings as for moderate
nonproliferative, but needs to be
present in a minimum number of
retinal quadrants
formation on the disc, retina
or iris (rubeosis iridis). Also,
retinal detachment, and vitreous
haemorrhage
Focal or diffuse macular oedema
Ischaemic maculopathy
Thickening of the retina and hard
exudates
COMMUNICATION
Prolonged gazing with an ophthalmoscope can be
uncomfortable for the patient. Be aware of this, and
consider giving the patient a short break every so
often.
and cranial nerve VI innervates the lateral rectus
muscle for abduction of the eye.
• Ask the patient to follow your finger with his or her
eyes while you slowly draw out the shape of two large
letter H’s joined in the middle. You should ensure that
the vertical movements are at extremes of lateral gaze
as well as in the midline.
• Ask the patient if he or she sees double (i.e. does the
patient have diplopia). Note when it occurs, and in
which direction. Diplopia in all directions of gaze may
result from myasthenia gravis, ocular myopathy or
disease in the surrounding tissue of the eye, such as
Graves disease, tumour or orbital cellulitis.
• Look for inability of the patient to move the eye (i.e.
ophthalmoplegia). If this is present, carefully note the
exact movement the patient was not able to make, and
whether it was at extreme gaze or in the midline.
• Look for nystagmus. This is involuntary rhythmic eye
oscillation. It occurs physiologically at the extremes of
lateral gaze, and more than two beats are required for it
to be significant.
CLINICAL NOTES
Nystagmus may be pendular, with equal
movement in all directions, or more commonly
'jerk nystagmus' with a slow drift away from the
point of fixation and a fast corrective phase. As a
general rule, peripheral lesions cause unidirectional
nystagmus that is horizontal or torsional, has a
fast phase away from the side of the lesion and is
relieved with fixation. In nystagmus due to central
lesions, the fast phase is towards the side of the
lesion, it may occur in more than one direction and
is not improved with fixation.
HINTS AND TIPS
A mnemonic to help you remember all the parts of
the second cranial nerve (optic nerve) examination
is AFRO; which stands for visual acuity, visual
fields, pupillary reflexes and ophthalmoscopy.
Cranial nerves III, IV and VI and eye movements
• It is best to assess the function of these cranial nerves
together as they are all involved in the movement of
the eye. Cranial nerve III (the oculomotor nerve) is
responsible for all eye movements except for those for
which cranial nerves IV and VI are responsible. Cranial
nerve IV innervates the superior oblique muscle to
cause downward movement of the eye in the midline,
Then assess conjugate gaze by asking the patient to look
at your hand and then at a finger on your other hand, and
then from one to the other as quickly as possible. If there
is an internuclear ophthalmoplegia (a lesion in the medial
longitudinal fasciculus), there will be slow movement in the
adducting eye and nystagmus in the abducting eye. If one
eye is covered, or if convergence is attempted, adduction is
normal, as this is a disorder of conjugate gaze. Internuclear
ophthalmoplegia is usually caused by multiple sclerosis but
may occasionally result from vascular lesions.
Cranial nerve III (oculomotor nerve)
You have already partly tested cranial nerve III (oculomotor nerve); however, you also need to test its innervation of
the levator palpebrae superioris (allowing elevation of the
upper eyelid), and its parasympathetic component, which
causes a miosis (constricted pupil).
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Clinical examination
CLINICAL NOTES
A complete oculomotor nerve palsy results in
ptosis, a dilated pupil with no reaction to light
or accommodation, and a down and out gaze.
This ‘down and out’ position is the result of
unopposed action of cranial nerve IV (trochlear
nerve) and cranial nerve VI (abducens nerve).
Cranial nerve III palsies are sometimes divided
into medical and mechanical (surgical) causes.
Medical causes, such as mononeuritis multiplex
or demyelination, tend to spare the pupil, and the
pupil can still constrict. Conversely, compressive
lesions, such as a posterior communicating
artery aneurysm or a tumour, are associated with
relatively less ophthalmoplegia. This is because
the parasympathetic fibres run on the surface
of the nerve and are first to be affected with a
compressive lesion.
Cranial nerve IV (trochlear nerve)
This supplies motor innervation to the superior oblique
muscle, allowing downward eye movement in the midline.
The patient is likely to report diplopia on downward gaze
and have difficulty with vision when walking downstairs or
reading a book.
CLINICAL NOTES
Lesions of cranial nerve IV are usually associated
with cranial nerve III lesions and have a similar
cause.
Cranial nerve V (trigeminal nerve)
This has both sensory and motor functions, providing sensation to the face with ophthalmic, maxillary and mandibular branches and motor supply to the muscles of mastication
(temporalis, masseter and pterygoid muscles).
When you are testing this nerve, test sensation in the
distribution of each division and compare one side with the
other. Remember the corneal reflex; this tests the sensory
function of the trigeminal nerve but also motor function of
cranial nerve VII, allowing them to blink in response to the
stimulus.
When you are testing the motor function:
• Ask the patient clench the teeth;
• Ask the patient keep the mouth open and resist you
trying to shut the jaw;
• Then test jaw jerk, which is increased in pseudobulbar
palsy (an upper motor neurone lesion) and reduced or
absent in bulbar palsy (a lower motor neurone lesion).
The causes of cranial nerve V lesions are shown in
Table2.18.
Cranial nerve VII (facial nerve)
This nerve has sensory and motor functions: supplying the
sensation of taste from the floor of the mouth, the soft palate and anterior two-thirds of the tongue and motor supply
to the muscles of facial expression and the stapedius muscle.
It also carries parasympathetic nerve fibres to the salivary
and lacrimal glands.
The sensory part of this nerve is not usually examined
formally, but ask the patient if he or she has noticed any
change in taste, or increased sensitivity to high-pitched
or loud sounds from impaired function of the stapedius
muscle.
To test the main motor functions of this nerve, ask the
patient to wrinkle the forehead, screw the eyes tightly shut,
show the teeth and blow the cheeks out. Table2.19 summa-
rizes the causes of facial nerve palsies.
Cranial nerve VI (abducens nerve)
This motor nerve innervates the lateral rectus. A cranial
nerve VI palsy results in an inability to abduct the orbit. The
patient will report diplopia (double vision) on abduction of
the affected eye.
CLINICAL NOTES
Examples of causes of a cranial nerve VI palsy
include mononeuritis multiplex, diabetes mellitus,
demyelination, tumour, infarction, thiamine
deficiency (Wernicke encephalopathy) and raised
intracranial pressure (referred to as a ‘false
localizing sign’).
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Table2.18 Causes of a trigeminal nerve lesion
Anatomical site Examples
Brainstem Tumour, infarction,
demyelination, syringobulbia
Cerebellopontine angle Acoustic neuroma,
meningioma
Petrous temporal bone Trauma, tumour, middle ear
disease, herpes zoster
Cavernous sinus Tumour, thrombosis,
aneurysm of internal carotid
artery
Peripheral Meningeal tuberculosis,
syphilis, lymphoma,
carcinoma, sarcoid
The nervous system
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Table2.19 Causes of facial nerve palsies
Anatomical site Examples
Upper motor neurone
central
Lower motor neurone pons
angle
Cerebellopontine angle Acoustic neuroma,
Petrous temporal bone Bell palsy, herpes zoster
Middle ear disease Infection, tumour
Peripheral Trauma, parotid disease,
Stroke, tumour
Stroke, tumour,
demyelination, motor
neurone disease
meningioma
(Ramsay Hunt syndrome)
mononeuritis multiplex,
sarcoid, Guillain–Barré
syndrome
HINTS AND TIPS
When you are assessing power for both cranial
nerves and with neurological examination of
the limbs, it is often best to test resistance. For
example, get the patient to screw the eyes shut
and say ‘screw your eyes tight shut and stop me
from opening them’ or ‘blow out your cheeks
and stop me from squashing them’ (you can
demonstrate the blowing out of cheeks). This is
a good way of assessing power and facilitating
communication of these actions, which the patient
may find hard to understand.
Cranial nerve VIII (vestibulocochlear nerve)
This nerve provides sensation to the utricle, saccule and
semicircular canals (vestibular), and to the organ of Corti
(cochlea).
To assess the function, ask the patient if he or she has noticed any difficulty with hearing. Assess the ability of the patient to hear whispered numbers with the other ear covered.
CLINICAL NOTES
There are two important tests you should perform:
a Rinne test and a Weber test. To perform a Rinne
test, place a vibrating tuning fork on the mastoid
process and then at the external auditory meatus.
The test result is positive if the sound is louder
when the fork is held at the external auditory
meatus (i.e. air conduction) than when placed on
the mastoid process (i.e. bone conduction). This
is normal. An abnormal test result (Rinne negative)
indicates conductive deafness.
If there are concerns about ability to hear, perform the
Weber test to differentiate between a sensorineural and
conductive deafness. This is done by the placing of a vibrating tuning fork at the centre of the forehead. The sound will
be heard towards the normal ear in sensorineural deafness
or towards the affected ear in conductive deafness.
• Vestibular disease is discussed further in Chapter20.
The causes of conductive and sensorineural deafness
are described in Table2.20.
CLINICAL NOTES
In lower motor neurone lesions affecting cranial
nerve VII, all the muscles are affected. In upper
motor neurone lesions, the forehead is spared (e.g.
there is normal eye closure and wrinkling of the
forehead).
HINTS AND TIPS
Crossed signs – cranial nerve abnormalities
contralateral to limb abnormalities – should alert
you to the possibility of a brainstem lesion.
Cranial nerve IX (glossopharyngeal nerve)
This supplies sensation to the pharynx and carotid sinus
and taste to the posterior third of the tongue. It has motor functions, supplying the stylopharyngeus muscle. It also
carries parasympathetic nerve fibres to the parotid gland.
Table2.20 Causes of deafness
Type Examples
Conductive Wax, foreign body, otitis externa,
injury to tympanic membrane, otitis
media, otosclerosis (e.g. Paget
disease), middle ear tumour (e.g.
cholesteatoma)
Sensorineural Presbycusis (due to old age), noise
induced, drugs (aminoglycosides,
aspirin overdose), infection
(meningitis, syphilis, measles),
congenital (maternal rubella,
cytomegalovirus, toxoplasmosis),
Ménière disease, acoustic neuroma,
trauma, Paget disease
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