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174 THE VISUAL SYSTEM
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8.1 Common causes of an acute change in vision
Cause Clinical features Cause Clinical features
Unilateral
Giant cell arteritis
Central retinal vein occlusion
Retinal detachment
Central retinal arterial occlusion
Corneal disease
Bilateral
Giant cell arteritis
Raised intracranial pressure
RAPD, Relative afferent pupillary defect (p. 182).
Painless loss of vision
Age >50 years
Weight loss
Loss of appetite, fatigue
Jaw or tongue claudication
Temporal headache
Pale or swollen optic disc
RAPD
Acute, painless loss of vision
May have RAPD if severe
Greater risk if hypertensive
Haemorrhages, exudates and tortuous retinal veins
(Fig. 8.7A)
Painless loss of vision
Association with ashing lights or oaters
History of a curtain coming across vision
Myopic patients at greater risk
RAPD if macula is involved
Pale raised retina usually with a retinal tear (Fig. 8.7B)
Acute, painless loss of vision
Carotid bruit may be heard
RAPD
Increased risk in vasculopaths
Examination: pale retina with a cherry red spot at the
fovea (Fig. 8.7C)
Usually painful
Foreign body sensation
Corneal opacity may be visible (e.g. Fig. 8.7D)
Painless loss of vision
Age >50 years
Weight loss
Loss of appetite, Fatigue
Jaw or tongue, claudication
Temporal headache
Pale or swollen optic disc
Headache
Often asymmetric
Pulsatile tinnitus
Swollen optic discs
Vitreous haemorrhage
Wet age-related macular degeneration
Anterior ischaemic optic neuropathy
Optic neuritis/ retrobulbar neuritis
Amaurosis fugax
Cerebral infarct
Migraine
Painless loss of vision
Risk in proliferative diabetic retinopathy
History of ashing lights or oaters may precede
haemorrhage in posterior vitreous detachment
Poor fundus view on examination
Reduction or loss of the red reex
Usually no RAPD if retina is intact
Sudden painless loss of central vision
Age >55 years
Increased risk in smokers
Haemorrhage at the macula (Fig. 8.7E)
Painless loss of upper or lower visual eld
Increased risk in vasculopaths
Examination may reveal optic disc swelling
Visual reduction over hours
Usually aged 20–50
Pain exacerbated by eye movement
RAPD
Reduced colour sensitivity
Swollen optic disc in optic neuritis (Fig. 8.7F)or
normal appearances in retrobulbar neuritis
Painless loss of vision for minutes
History of cardiovascular disease
May have associated atrial brillation or carotid
bruit
Normal ocular examination
May have associated headache and/or
neurological signs
Usually specic eld defects dependent on how
the visual pathway is affected (Fig. 8.5)
Normal fundus examination
If post chiasmal visual pathway affected, bilateral
visual eld abnormalities
Gradually evolving usually bilateral visual loss
Vision loss is usually preceded by visual aura
Normal ocular examination
Ocular examination: normal
Vision usually returns to normal after hours
Is pain exacerbated or relieved by anything?
Any other associated features (e.g. change in vision, red eye,
discharge, photophobia, watering eye)?
The most common cause of a painful eye is corneal irritation
from a foreign body or infection. The cornea is one of the most
highly innervated parts of the body. When the corneal nerves are activated, a patient experiences foreign body sensation, pain, reex watering and photophobia. There are, however, many other causes of a painful eye. Box 8.3 summarises the history and examination ndings associated with a painful eye.
A
Patient history 175
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C
B
8
D
Fig. 8.8 Common causes of a gradual loss of vision. A Cataract. B Altered red reex in cataract. C Dry age-related macular degeneration. D
Compressive optic neuropathy. Optic nerve sheath meningioma causing optic disc pallor and increased disc cupping with sparing of the outer optic nerve rim. Retinitis pigmentosa: a triad of optic atrophy, attenuated retinal vessels and pigmentary changes. The latter typically start peripherally with an associated ring scotoma and symptoms of night blindness.
8.2 Common causes of a gradual loss of vision
Cause Clinical features
Refractive error
Glaucoma
Cataract
Diabetic maculopathy
Compressive optic neuropathy
Retinitis pigmentosa
Dry age-related macular degeneration
No associated symptoms
Normal ocular examination
Vision can be improved by pinhole (Fig. 8.4D)
Usually bilateral but asymmetric loss of visual eld
Cupped optic discs on examination
Gradual clouding of vision
May be associated with glare
Usually seen in the elderly
Examination: clouding of the pupil and altered red
reex (Fig. 8.8A and B)
History of diabetes
Central vision reduced or distorted
Haemorrhages and exudates at the macula on
examination (Fig. 8.17A)
Gradual unilateral loss of vision
Pale optic disc on examination (Fig. 8.8D)
Gradual bilateral symmetric loss of peripheral
visual eld
Nyctalopia (poor vision in dim light)
Family history
Examination: bone spicule fundus, attenuated blood
vessels and waxy optic disc (Fig. 8.8E)
Gradual loss of central vision
Usually bilateral
Examination: drusen, atrophy and pigmentation at
the macula (Fig. 8.8C)
E
E
Red eye
The eye is covered in a network of vessels in the conjunctiva, episclera and sclera. Ciliary vessels are also found around the cornea. Dilatation or haemorrhage of any of these vessels can lead to a red eye. Additionally, in uveitis, acute angle­closure glaucoma and corneal irritation, the ciliary vessels around the cornea become more prominent (ciliary ush). The appearance is distinct from conjunctivitis, in which there is classically a relative blanching of vessels around the cornea.
Ask:
Is there any pain or photophobia?
Is vision affected? If so, how?
Has there has been any recent trauma or foreign body?
Is the eye itchy?
Is there any discharge? If so, what kind (e.g. watery, sticky,
clear, yellow)?
Has there been any recent contact lens use?
Box 8.4 summarises the features of the common causes of a
red eye on history and examination.
Double vision (diplopia)
Ask:
Does the double vision occur with one eye open or only with both eyes open? Binocular double vision is caused by an
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8.3 Causes and distinguishing features of a painful eye
Cause History Examination
Blocked gland on lid
Corneal foreign body
Corneal infection
Scleritis
Angle-closure glaucoma
Conjunctivitis
Uveitis
Optic neuritis
Orbital cellulitis
Thyroid eye disease
Pain on lid Tenderness to touch
Foreign body sensation
Watery eye
Photophobia
Foreign body sensation
Photophobia
Severe pain disturbing sleep
Association with recent infection, surgery or rheumatic
disease
Constant pain around eye
Acute reduction in vision
Haloes seen around lights
Associated nausea and vomiting
Clear or purulent discharge
Vision usually unaffected
Floaters
Blurry vision
Photophobia
Reduction in vision
Reduction in colour sensitivity
Constant pain, worsened by eye movement
Constant ache around eyes
Reduced vision
Double vision
Associated with recent infection/sinus blockage
Symptoms of hyperthyroidism (p. 222)
Sore, gritty eyes
Double vision
Redness and swelling of lid
Foreign body visible or found under the eyelid
Red eye
Corneal ulcer, (highlighted with uorescein stain (Fig. 8.7D)
White inltrates may be visible
Eye is sore to touch
Scleral injection
Fixed mid-dilated pupil, hazy cornea and usually a cataract
Red eye
Ciliary ush
Swollen disc in optic neuritis (Fig. 8.7F), normal disc in retrobulbar
neuritis
Conjunctival chemosis and injection
Restricted eye movements
Severe cases: visual reduction with RAPD
Lid retraction
Proptosis
Restricted eye movements
Conjunctival injection or chemosis (Fig. 10.2B)
RAPD, Relative afferent pupillary defect (p. 182).
imbalance in eye movement between the eyes. Monocular diplopia results from intraocular disease in one eye.
What is the character of the double vision (e.g. are images seen side by side, one above the other or at an angle)?
Has there been any recent trauma?
In binocular diplopia, test the eye movements (Fig. 8.9) and use your knowledge of the function of the extraocular muscles (see Fig. 8.2) to work out which cranial nerve is affected.
The causes of double vision are summarised in Box 8.5 and
Figs. 8.10 and 8.11.
Discharge
Ocular discharge results from either an increase in production or a decrease in drainage from the ocular surface. Irritation of
corneal nerves activates cranial nerve V(I), resulting in a reex tearing response.
Tears normally drain from the ocular surface through the puncta, small openings to the medial end of the upper and lower eyelid, into the nasolacrimal duct, which opens below the inferior turbinate in the nasal cavity. Consequently, blockage of tear drainage or an abnormal lid position can also result in excessive discharge.
Ask:
Is the discharge clear or opaque? If opaque, what colour?
Is the discharge watery or sticky?
Is the discharge associated with any other features (e.g. pain,
foreign body sensation, red eye or itchiness)?
The clinical features of different types of eye discharge are summarised in Box 8.6.
8.4 Common causes and distinguishing features of a red eye
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Causes History Examination
Allergic conjunctivitis
Viral conjunctivitis
Bacterial conjunctivitis
Trauma
Acute angle-closure glaucoma
Acute anterior uveitis
Episcleritis
Scleritis
Dry eyes
Subconjunctival haemorrhage
Corneal ulcer/abrasion
Orbital cellulitis
Thyroid eye disease
Itchy eyes
Clear discharge
May be seasonal
Watery discharge
Possible itch
Usually bilateral
Purulent discharge
Pain
History of trauma May reveal subconjunctival haemorrhage or
Acute reduction in vision
Pain
Blurring of vision
Haloes seen around lights
Nausea
Gradual onset of pain
Photophobia
Floaters
Red eye without pain
Vision not affected
Focal or diffuse injection
Vision may be affected
Association with recent infection, surgery or rheumatic disease
Severe pain disturbing sleep
Gritty or burning sensation
Watery eyes
No pain
Vision unaffected
Vision usually reduced
Foreign body sensation
Photophobia
Watering
Usually affects young children
Recent intercurrent viral illness
Vision may be affected
Possible double vision
Chronic red eyes
Sore, gritty sensation
Foreign body sensation
Double vision
Conjunctival injection
Swollen conjunctiva
Gland swelling and follicles under lid
Purulent discharge
injection
Fixed, mid-dilated pupil with a hazy cornea
Ciliary ush
Focal or diffuse injection
Possible association with a nodule
Eye painful to touch
Corneal uorescein staining
Mildly raised conjunctiva with a bleed
Ulcer seen on uorescein staining (Fig. 8.7D)
May be associated with a white corneal inltrate
Reduced vision and colour vision
Proptosis
Eye movement restriction
In severe cases, RAPD
Lid retraction
Proptosis
Conjunctival injection and chemosis (see Fig. 10.2B)
Patient history 177
8
RAPD, Relative afferent pupillary defect (p. 182).
Swollen eyes
The orbit is enclosed by bone on all sides, except anteriorly. As a result, orbital swelling can lead to the anterior displacement of the globe and proptosis.
Ask if the swelling is:
Unilateral or bilateral?
Acute or gradual in onset?
Associated with pain?
Associated with itch or irritation?
Associated with double vision?
Box 8.7 summarises the common causes of swollen
eyes.
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8.5 Causes of double vision
Monocular
High astigmatism
Corneal opacity
Abnormal lens
Iris defect
Binocular
Myasthenia gravis (p. 190)
VI nerve palsy (Fig. 8.10)
IV nerve palsy
III nerve palsy (Fig. 8.11)
Internuclear ophthalmoplegia
Thyroid eye disease (see Fig. 10.2A,B)
Complex or combined palsy
Severe orbital cellulitis or orbital inammation
Past ocular history
Ask the patient whether they have any known ophthalmic con­ditions. Enquire specically about amblyopia (a reduction in vision in one eye from childhood), as this may limit best-corrected visual acuity. Check whether the patient normally wears glasses or contact lenses, and ask about the last time they had their eyes checked for refractive correction. Also ask about any previous eye surgery, as this may also limit vision.
Past medical history
Focus on systemic diseases that can affect the eyes. In particular:
a history of diabetes or hypertension, especially in the context of visual loss
thyroid disease in the context of red, swollen eyes or double vision.
Drug and allergy history
8.6 Common causes of increased discharge from the eyes
Causes Clinical features
Bacterial conjunctivitis
Viral conjunctivitis
Blocked tear duct
Trichiasis/ foreign body
Allergic conjunctivitis
Blepharitis
Poor tear lm/ dry eyes
Mendelian inherited eye disease is retinitis pigmentosa (see
Fig. 8.8E).
Red eye
Yellow or green sticky discharge
Vision usually unaffected
Red eye
Clear, watery discharge
Occasionally itchy eyes
Vision usually unaffected
Ocular examination: conjunctival chemosis and
injection
White eye
Clear, colourless tearing
Possible occluded punctum
Possible malposition of the lid
Foreign body sensation
Clear discharge
Positive uorescein staining
Red eyes
Itchy eyes
Clear discharge
Possible history of hay fever or atopy, or recent
start of eye medication
Mild injection of lids
Deposits on lashes
Constant tearing
Watering increased in the wind
Improvement with tear supplements
Ocular examination: early break-up time (<3
seconds) with uorescein staining of tear lm
The eyes may, rarely, be affected by medication prescribed for other medical conditions. For example, oral glucocorticoids can cause glaucoma and cataract. Additionally, medication pre­scribed to treat eye conditions (such as beta-blocker eye drops) can aggravate systemic conditions like asthma.
Ask about a history of allergies, including hay fever, if the pa-
tient has itchy or red eyes.
Family history
Several eye diseases can be inherited. Ask specically about a history of glaucoma in rst-order relatives. The most common
Social history
Visual impairment can affect activities of daily living. If vision is reduced, ask about:
Daily activities requiring vision, such as reading, television, sport, hobbies and driving.
Effects on occupation. Certain professions are required to meet specic visual standards, including drivers of heavy goods vehicles and pilots.
Smoking and alcohol. These may affect retinal vascular dis­ease and optic nerve function.
8.7 Common causes of periorbital swelling and proptosis
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Category Causes Clinical features
Infective
Inammatory
Neoplastic
Systemic
Vascular
Pseudoproptosis
Orbital cellulitis Rapid onset unilateral swelling and erythema
Granulomatous polyangiitis
Idiopathic orbital inammatory disease
Vasculitis
Orbital tumours
Lymphoma
Metastases
Thyroid eye disease Bilateral asymmetric periocular swelling
Caroticocavernous stula Unilateral proptosis with conjunctival swelling
Orbital varices Intermittent unilateral swelling and proptosis associated with Valsalva manoeuvre
Ptosis Asymmetric palpebrae aperture
Severe viral conjunctivitis Bilateral conjunctival injection and oedema associated with serous discharge
Myopia Signicant difference in prescription between the two eyes
Lid retraction Difference in height of palpebral aperture between the two eyes
Pyrexia and signs of sepsis
Restricted ocular movements
Optic nerve compression in severe cases
Proptosis with conjunctival redness and swelling is seen.
Restricted eye movements
In severe cases optic nerve compression
Gradual onset unilateral periocular swelling.
Not inamed and rarely any erythema
Restricted eye movements
Associated proptosis and reduced ocular movements.
Most cases are not associated with inammation
Reduced ocular movements
Patient aware of a bruit
Occasional pain
The eye with the more minus prescription will look more prominent
The physical examination 179
8
The physical examination (Video 17)
General examination
Carefully and systematically examine:
posture and gait
head position
facial asymmetry and dysmorphic features
eyelid position and periocular skin
position and symmetry of gaze (any squint/strabismus?).
Visual acuity
The assessment of visual acuity is mandatory in all ophthalmic patients. Each eye must be tested separately. The most commonly used method of testing distance visual acuity uses a Snellen chart, which displays a random selection of letters in diminishing font sizes in successive lines. Ask patients to wear their distance spectacles if they usually require them. Near/ reading spectacles should be worn only when testing reading vision.
Examination sequence (Video 17A)
Use a backlit Snellen chart positioned at 6 metres and dim
the rooms lighting.
Cover one eye and ask the patient to read the chart from the
top down until they cannot read any further. Repeat for the other eye.
If the patient cannot see the largest font, reduce the test
distance to 3 metres, then to 1 metre if necessary.
If they still cannot see the largest font, document instead
whether they can count ngers, see hand movement or just perceive the difference between light and dark.
On the Snellen chart, lines of decreasing font size are
numbered according to the distance in metres that a person with normal vision could read them. Express visual acuity as the distance at which text is read (usually 6 metres) over the number of the smallest font line read correctly on the chart. For example, 6/60 means that the patient sees at 6 metres the font size that is seen at 60 metres by a person with normal vision.
If the patient cannot read down to line 6 (6/6), place a pinhole
directly in front of the eye (with the patient keeping their usual spectacles on, if used) to correct any residual refractive error (see Fig. 8.4D).
If visual acuity is not improved with a pinhole, this indicates the
presence of eye disease not related to the refractive apparatus alone, such as amblyopia, or retinal or optic nerve pathology.
180 THE VISUAL SYSTEM
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Assess near vision with a similar test using text of reducing
font size held at a comfortable reading distance. It is impor­tant to consider the need for reading spectacles in patients over the age of 40 years because of presbyopia (age-related deterioration in near vision).
Fig. 8.9 Testing the six positions of gaze. Sit facing the patient, 1 metre
away. Perform the test with both eyes open. Hold a pen torch or target in front of the patient and move it to the six positions of gaze (blue arrows). Ask if they see the target as double.
Fig. 8.10 L sided sixth nerve palsy causing weakness of the lateral
rectus. The patient is attempting to look left.
A
Orbit and periorbital examination
Examination sequence (Video 17B)
Observe the face and orbit for asymmetry and any obvious
abnormalities, including swelling or erythema.
Look for abnormalities in the position of the lids, such as
ptosis (Box 8.8).
Look for asymmetry in the position of the eyeballs. Eyeball
protrusion (proptosis) is best detected by examining the head from above.
Palpate around the orbital rim and orbit and look for any
masses.
Check eye movements (see Fig. 8.9).
Use an ophthalmoscope (Fig. 8.12) to look for optic disc
swelling from compression.
Pupils (Video 17C)
Inspect rst for squint and ptosis, which may reveal the cause of abnormal pupils. Examine pupil shape and symmetry. Physiological anisocoria (unequal pupil size) is seen in 20% of the population.
Anisocoria
Assess which is the abnormal pupil.
B
Fig. 8.11 Third nerve palsy. A Complete ptosis in R third nerve palsy. B
The same patient looking down and left. The affected R eye is unable to adduct or depress and remains slightly abducted due to unopposed action of the lateral rectus. From Forbes CD, Jackson WF. Color Atlas of Clinical
Medicine. 3rd ed, Edinburgh: Mosby; 2003.
Examination sequence
With the patient xating at a point in the distance, increase
and decrease the illumination and look for any change in the degree of anisocoria.
If the degree of anisocoria is greater in brighter lighting, then it is the larger pupil that is abnormal; if it is more pronounced in dim lighting, the smaller pupil is the abnormal one. An equal degree of anisocoria in all levels of lighting indicates physiological anisocoria.
Direct and consensual light reex
Examination sequence
With the patient xating on a point in the distance and in
ambient lighting, shine a bright light from the temporal side into one eye and look for constriction of the ipsilateral pupil.
The physical examination • 181
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8.8 Causes of eyelid ptosis
Associated distinguishing
Cause Diagnosis
Neurogenic Horners
Myogenic Myotonic
Neuromuscular junction
Mechanical Eyelid tumour Evident on inspection
Degenerative Levator
To test the consensual reex, assess the pupil response in
the contralateral pupil when light is directed towards the ipsilateral pupil. Repeat for the other pupil.
syndrome Cranial nerve III palsy
dystrophy Chronic progressive external ophthalmoplegia Oculopharyngeal dystrophy
Myasthenia gravis History of variable muscular
Eyelid inammation/ infection Trauma Scarring/history of trauma
aponeurosis degeneration Long-term contact lens wear
features
Ptosis, miosis, eye movement spared (Fig. 5.10, p. 96) Dilated pupil, eye movements affected ( Fig. 8.11)
Frontal balding, sustained handgrip Bilateral ptosis and impairment of eye movements, often without diplopia, sparing of pupil reexes History of swallowing abnormalities
fatigue
Evident on inspection
Often unilateral, eye movement normal
History of contact lens use
Relative afferent pupillary defect
Relative afferent pupillary defect (RAPD) is an important clinical sign that occurs when disease of the retina or optic nerve re­duces the response of the eye to a light stimulus. Testing for RAPD is an extension of the direct and consensual light responses.
8.9 Causes of anisocoria
Dilated pupil Clinical features
Physiological Normal pupillary reactions
Cranial nerve III palsy Pupil dilated and unresponsive to light
Trauma History of signicant ocular trauma
Adie’ s tonic pupil Slow to react to light
Pharmacological
treatment with a dilating agent (e.g. tropicamide or atropine)
Constricted pupil
Physiological Normal pupil reactions
Horner’ s syndrome Partial ptosis
Mechanical (e.g.
secondary to posterior synechiae in iritis or trauma)
Late-stage Adie’s tonic
pupil
Pharmacological
treatment with a constricting agent (e.g. pilocarpine)
Seen in 20% of population
Partial or complete ptosis
Eye deviated down and out
Rupture of pupillary sphincter muscle
sometimes seen on slit lamp examination
Vermiform movement of the iris seen on
slit lamp examination.
Constricts with dilute pilocarpine
(0.125%)
Unreactive dilated pupil, resolves with
time
History of pharmacological administration
Seen in 20% of population
Ipsilateral anhidrosis
Anisocoria more pronounced in dim light
History of trauma or iritis
Pupil margin may be irregular
Small slowly reactive pupil
History of the pupil being the larger one
in the past
Unreactive constricted pupil that will
dilate with time
History of pharmacological
administration
Accommodation
8
Examination sequence
Use a bright light source.
Maintain the light on each eye for a minimum of 3 seconds,
then move it between the eyes briskly.
In normal patients, the RAPD test results in symmetrical constriction of both pupils. If an RAPD is present, the pupil will dilate when the light is shone in the affected eye.
Examination sequence
Ask the patient to look at a distant target and then to quickly
focus on a close xation target (do not use a light source).
The pupils will constrict on near gaze.
Failure to constrict to light but constriction on near gaze is
referred to as light-near dissociation.
There are many causes of a dilated or constricted pupil
(Box 8.9).
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Horners syndrome
Horners syndrome results from a dysfunction of the sympathetic supply to the eye. The sympathetic innervation of the eye origi­nates in the hypothalamus and emerges in the root of the neck before innervating the pupil (see Fig. 8.6B). Damage at any point along this pathway will result in Horner’s syndrome. On examination, the pupil will be constricted (loss of sympathetic dilator tone) and have a partial ptosis resulting from denervation of Müllers muscle in the upper eyelid (see Fig. 5.10,p.96). There may also be anhidrosis (loss of sweating) on the affected side.
The diagnosis of Horners syndrome can be conrmed by administering drops of the alpha-2 adrenergic agonist apraclo­nidine to both eyes. This causes reversal of pupil constriction in the affected eye and no change in the unaffected eye. This re­sults in a reduction of anisocoria (difference in pupil size between the eyes). Causes of Horners syndrome include demyelination, neck trauma/surgery, apical lung tumour (Pancoast tumour) and carotid artery dissection.
Adies pupil
Adies pupil is a dilated pupil that responds poorly to both light and accommodation. With time, however, the affected pupil can become constricted. Adies pupil is thought to result from parasympathetic pathway dysfunction in the orbit leading to a lack of pupil constriction. It typically affects young women and is benign. When associated with diminished Achilles tendon re­exes, it is referred to as Holmes-Adie syndrome.
Examination sequence (Video 17D)
Check visual acuity and ensure that the patient has at least
enough vision to count ngers.
Sit about 1 metre away directly facing the patient and at the
same height.
With your eyes and the patient’s eyes open, ask the patient to
look at your face and comment on whether they have any difculty seeing parts of your face.
Ask the patient to keep looking straight at your face. Test
each eye separately. Ask the patient to close or cover one eye and look directly at your opposite eye; you should simi­larly close your contralateral eye.
Bring an extended nger in from the periphery towards the
centre of the visual eld. For an accurate assessment of the patient’s elds, it is vital that the testing nger is always kept in a plane exactly halfway between yourself and the patient. Wiggle your ngertip and ask the patient to say when they rst see it (Fig. 8.12). If the patient fails to notice your nger when it is clearly visible to you, their eld is reduced in that area.
Test all four quadrants separately, testing each eye separately.
More subtle visual eld defects can be elicited using a small
white hatpin or a white Neurotip. With the patient looking directly at your eye, bring the white target in from the pe­riphery to the centre (always in the plane halfway between you and the patient). Ask the patient to say when they rst see the target.
Argyll Robertson pupil
Argyll Robertson pupils are bilaterally small and irregular and react to near accommodation but not to light (light-near disso­ciation). These pupils are classically the result of neurosyphilis; however, they can also occur in diabetes mellitus, severe optic nerve disease and midbrain lesions.
Visual elds
The normal visual eld extends 160 degrees horizontally and 130 degrees vertically. The physiological blind spot is located approximately 15 degrees temporal to the point of visual xation and represents the entry of the optic nerve head into the eye.
Theaimofthevisualeld examination is to test the patientsvi­sual elds against your own (assuming that you have normal visual elds). The visual eld can be tested using the ngers for gross examination. Finer examination is performed using a hatpin.
Fig. 8.12 Confrontation visual eld testing. Sit facing the patient, 1 metre
away. To compare your visual eld (assumed normal) with the patients, present a white target or your ngers at a point equidistant between yourself and the patient in the periphery. Bring the target inwards in the direction of the blue arrows, asking the patient to alert you when they rst see it. Test each eye separately.
The physical examination 183
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open or latent (phoria) if revealed only by covering one eye. In addition, they can be conc om itan t (where the angle of squint remains the same in all positions of gaze) or incomitant (where the angle of squint deviation is greatest in a single position of gaze). The latter is comm on ly the result of extraocular muscle paralysis.
Detection of a squint
Examination sequence
Fig. 8.13 Testing the central visual eld. Sit facing the patient, 1 metre
away. Present a red target at a point equidistant between yourself and the patient in the periphery, starting when you can rst see the target as red. Bring the target inwards in the direction of the blue arrows, asking the patient to alert you when they rst see the target as red. Test each eye separately.
Check all four quadrants, testing each eye separately.
To assess very early visual eld loss, repeat the same test
using a red hatpin or a red Neurotip (Fig. 8.13).
It is important to sho w the patient the red target and ask
them to report what colour they see. A dull or pale red suggests colour desaturation, which may indicate optic nerve dysfunction.
When testing each quadrant with a red target, be sure to
explain to the patient that they should say when they rst see that the target is red and not when they rst see it. The target may be visualised before they appreciate the red colour.
To test the blind spot, place a red-tipped target equidistant
between the patient and yourself at the visual xation point.
Move the target temporally from central xation until it
disappears.
Once you have identied the blind spot, move the target
slowly up and down and side to side until it reappears. This allows you to compare the patients blind spot with yours.
Ocular alignment and eye movements
The eyes normally move in the same direction (conjugate motion) in all positions of gaze except during convergence. Any misalignment is referred to as a squint (strabismus). Squints are described as ma nif est (tropia) if present wit h both eyes
Sit directly facing the patient, approximately 1 metre away
and at a similar height.
Check visual acuity as part of the examination.
Look for any abnormal head posture, such as head tilts (seen
in cranial nerve IV palsy) or head turns (cranial nerve VI palsy). These signs may be subtle.
Hold a pen torch directly in front of the patient and instruct
them to look at the light. Observe the reection of the light on the cornea in relation to the pupil. The reections should be symmetrical between the two eyes. Ask the patient if they see a single or double light. If they see double, this may indicate the presence of a squint, but not seeing double does not exclude a squint. If the reection is on the nasal aspect of the pupil in one eye, this suggests that the eye is deviated out­wards and is described as an exotropia.
To conrm the presence of a squint, perform the cover/un-
cover test:
Ask the patient to look at the pen torch at all times and
then cover one eye.
Look at the uncovered eye for any movement. It may be
helpful to repeat this several times.
Inward movement of the uncovered eye suggests that it
was positioned abnormally outwards and is described as an exotropia (divergent manifest squint).
Conversely, if the eye moves outwards when the contra-
lateral eye is covered, this suggests that it was abnormally positioned inwards and is described as an esotropia (convergent manifest squint).
Repeat the cover/uncover test for the other eye.
Failure of an eye to move despite an obvious corneal light
reex may indicate that the eye has such poor vision that it cannot take up xation or else it is restricted from moving.
The alternating cover test involves covering the eyes alter-
nately and quickly while the patient is xated on the pen torch. Leave the cover on each eye for about 2 seconds but move between the eyes in less than 1 second. The move­ment is repeated multiple times. This test will help to elicit latent squint.
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