Chapter 11 http://t.

me/ErRoomData1 549

Ophthalmology
Approach to eye problems 550
Blunt eye injury 552
Penetrating eye injury 553
Corneal trauma 554
Contact lens problems 555
Sudden visual loss 556
The red eye 558
Pupillary abnormalities 560
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550 Chapter 11 Ophthalmology

Approach to eye problems

History
Always take a full ophthalmic history. Which eye is affected (are both)?
What is the disturbance? Are there flashing lights or floaters? How quickly
did the symptoms come on? How does it affect the patient’s lifestyle (job,
reading, watching TV)? Ask about prior ophthalmic/​optician treatment, and
take a full medical and drug history. Family history of glaucoma may also
be relevant.
Always measure visual acuity in anyone presenting with an eye problem.
Pointers to potentially serious pathology include those with:
• Sudden visual loss.
• Significantly d VA.
• Penetrating eye injuries.
• Chemical burns of the eye (these require immediate treatment and
specialist referral).
Have a low threshold for involving an ophthalmologist if a patient who is
already blind in one eye presents with a problem with the ‘good eye’.
Examination
Visual acuity This is the key to eye examination—​measure this first.
Failure to document VA may constitute negligence.
Use a Snellen chart, and read at 6m for each eye separately. Allow pa-
tients to use glasses, if available; if not, employ a pinhole (made using a
needle through a piece of card). Use of a pinhole eliminates refractive error.
VA is expressed as:
• Distance from the chart in metres/​number of lines on the chart (normal
vision is 6/​6), eg a patient whose VA is recorded as ‘Right eye 6/​5; left
eye 6/​60’ can read the bottom line with the right eye, but only the top
line with the left eye. If patients read additional letters of the line below,
record using + number of extra letters (eg 6/​12 + 2).
• Bring patients unable to read the chart at 6m forward until they can read
the chart (eg 3/​60 = top line read at 3m). Very poor vision: try counting
fingers or detecting hand movement at 1m, or light perception.
• A hand-​held chart at 30cm is an alternative if a full Snellen chart is
unavailable—​ability to read small print implies normal VA for that eye.
For patients who are illiterate, there is an alternative chart with various
different versions of the letter ‘E’—​ask the patient to state in which
directions the three limbs of the letter point.
Pupils Record pupil size, shape, and direct and consensual responses to light
and accommodation.
Eye movements Check full range and for diplopia. Look for nystagmus.
Visual fields Check carefully in patients with visual loss.
 Approach to eye problems 551

Fundoscopy In a darkened room, first check for the red reflex. A lost or
d red reflex is abnormal, typically caused by vitreous haemorrhage, cata-
racts, or major corneal abrasions. Assess the optic discs and look for retinal
haemorrhages and vessel abnormalities. Sometimes, there may be a poor
view—​leave the use of drops to dilate the pupil (eg tropicamide) to the
ophthalmologist.
Direct assessment Under a bright light, look for inflammation or FBs.
Subtarsal examination If there is a possibility of an FB, evert the upper eyelid
by pressing down lightly over the upper lid with a cotton bud or orange
stick and rotating the lid upwards over it. Ask the patient to look down
throughout.
Slit lamp examination Learn how to use a slit lamp. It allows a detailed view
of the conjunctiva, cornea, and anterior chamber. Fluorescein staining re-
veals corneal abnormalities, particularly when viewed under blue light when
abrasions appear yellow/​green. Fluorescein is available either in drop form
or dried onto a strip. Remember that fluorescein can permanently stain
clothes and contact lenses.
Intra-​ocular pressure Digital assessment is unreliable. Formal measurement
of intra-​ocular pressure is useful but requires training and is left to the eye
specialist in many departments.
Temporal arteries Palpate for tenderness if temporal arteritis is a possibility.
LA drops to aid examination
Sometimes, blepharospasm prevents satisfactory examination. Consider
LA drops (one or two drops of 1% amethocaine/​tetracaine or 0.4%
oxybuprocaine; 0.5% proxymetacaine causes less stinging and is useful in
children). Never discharge patients with a supply of LA drops.
Notes on ophthalmological treatments
Antibiotic ointment and drops Apply to the lower fornix (between the lower
eyelid and the sclera), then ask the patient to keep the eye shut for 1–​2min.
Ointment has the advantage over drops in that it lasts longer, eg chloram-
phenicol ointment needs to be given four times a day, whereas drops need
to be given every 2hr initially. Theoretical concerns about aplastic anaemia
are not well founded (see BNF).
Eye pads These were previously recommended following the administration
of LA drops and for patients with corneal abrasions; they tend not to be
useful.
Driving Advise patients not to drive until their vision has returned to normal
(this particularly applies after the use of mydriatic agents). In addition,
advise patients not to drive whilst wearing an eye pad. Document the advice
given in the notes.
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552 Chapter 11 Ophthalmology

Blunt eye injury

Blunt injury to the face may result in injury to the orbit or its bony margins.
Compression of the eye in an antero-​posterior direction (eg squash ball or
fist) can cause a ‘blow-​out’ fracture of the floor of the orbit.
Retrobulbar haematoma
This may lead to orbital compartment syndrome and blindness. Unless diag-
nosed and treated as an emergency, optic nerve ischaemia develops and
the patient can lose sight in the affected eye within a few hours. Proptosis,
reduced eye movements, reduced VA, and pain all point to a retrobulbar
haematoma. There may be an afferent pupillary defect.
Assessment
Swelling around the eye can make assessment difficult, and this situation may
worsen as swelling i, so try to examine the eye at the earliest opportunity.
• Look for proptosis.
• Check VA.
• Check pupillary reflexes.
• Check for enophthalmos and d infra-​orbital nerve sensation, both found
in a blow-​out fracture.
• Document the range of eye movements, looking, in particular, for
entrapment of the extra-​ocular muscles.
• Look for a hyphaema (a horizontal fluid level in the anterior chamber
when the patient is upright). It can cause pain, photophobia, and blurred
vision and can i the intra-​ocular pressure, causing nausea and vomiting.
• Stain the cornea and examine using the slit lamp for corneal abrasions.
• Ophthalmoscopic examination may reveal lens dislocation, hyphaema,
and vitreous, subhyaloid, or retinal haemorrhage. Sometimes retinal
oedema (‘commotio retinae’) may be seen as white patches with diffuse
margins on the posterior pole of the eye.
X-​ray if there is bony tenderness or clinical evidence of orbital or facial
bone fracture.
Treatment
Any patient suspected of a retrobulbar haematoma requires an emergency
lateral canthotomy and cantholysis. This should be performed by an oph-
thalmologist or a trained emergency physician, under LA in the ED, and it
reduces the retro-​orbital pressure.
Nurse patients with an obvious globe injury head up at 45°. Refer urgently.
Consider prophylactic oral antibiotics (eg co-​amoxiclav) for uncomplicated
facial or orbital fractures, according to local policy, and arrange for maxillo-
facial follow-​up, with advice to avoid nose-​blowing in the meantime.
 Penetrating eye injury 553

Penetrating eye injury

Suspect an intra-​ocular FB if there is a history of hammering or work involving
metal on metal. Establish if protective glasses were worn—​remember that
standard glasses (without a seal to the skin) do not provide full protection
against an FB. Ascertain whether a small FB travelling at speed may have
penetrated the orbit (eg during grinding, hammering, chiselling). Failure to
suspect and diagnose these injuries can have serious consequences.
Assessment
• Check VA.
• Look for pupil irregularity.
• Look for puncture/​entry wounds on both aspects of the eyelids,
the cornea, and the sclera. Corneoscleral wounds are often situated
inferiorly, due to upturning of the eyeball as the patient blinks.
• Examine the anterior chamber. There may be a shallow anterior
chamber, air bubbles, a flat cornea, a deflated globe, and a positive
Seidel’s test (dilution of fluorescein by aqueous humour leaking from the
anterior chamber).
• Look for a hyphaema.
• Look for vitreous haemorrhage on fundoscopy.
X-​ray all patients with possible globe penetration (consider also CT or USS).
Give analgesia, tetanus prophylaxis, and IV antibiotics (eg cefuroxime
1.5g), and refer all patients with penetrating eye injuries immediately to an
ophthalmologist, even if there are other major injuries needing attention at
the same time.
Do not manipulate or try to remove embedded objects (eg darts).
Eyelid wounds
Lacerations (and incised wounds) to the eyelids may be a pointer to the
presence of associated (more significant) globe damage. Most eyelid
wounds can be closed under LA using small (6/​0 or 7/​0) interrupted
nylon sutures—​in most instances, this is more appropriately undertaken
by a specialist.
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554 Chapter 11 Ophthalmology

Corneal trauma
Conjunctival FB
The typical history is of dust or grit blown into an eye by the wind. The FB
usually gravitates into the lower fornix—​remove it with a cotton bud, then
check for associated subtarsal/​corneal FBs.
Subtarsal FB
FBs may not gravitate into the lower fornix but may remain stuck under
the upper eyelid. The patient reports pain on blinking. Fluorescein staining
reveals characteristic vertical corneal abrasions (the cornea has been
likened to an ‘ice rink’). Evert the upper eyelid and remove the FB with a
cotton bud. Discharge with topical antibiotic (eg chloramphenicol ointment
qds or fusidic acid eye drops).
Corneal abrasions
These often result from a newspaper or fingernail in the eye. Irritation,
photophobia, and lacrimation occur. Use LA drops and fluorescein staining
to examine the cornea. Exclude FB or penetrating injury. Prescribe regular
antibiotic ointment (eg chloramphenicol) and oral analgesia. Only consider
an eye patch if the abrasion is very large (>1cm diameter). If the patient
is very uncomfortable, instilling a drop of 1% cyclopentolate to dilate the
pupil (this reduces iris spasm) or a drop of 0.1% diclofenac may help. Advise
the patient not to drive until vision has returned to normal. Advise also to
return for review if symptoms continue beyond 36hr.
Corneal FB
Instill LA and attempt removal with a cotton bud (moistening it and rolling
it over the FB to pick it up may help). If unsuccessful, remove with a blue
(23G) needle introduced from the side (ideally using a slit lamp). Ensure
that the patient’s head is firmly fixed and cannot move forward onto the
needle—​it can also help to attach the needle to a syringe and for the
operator’s hand to rest lightly on the patient’s cheek to help to keep it
steady. After complete removal of the FB, check that the anterior chamber
is intact; instill and prescribe antibiotic ointment, and advise the patient to
return if symptomatic at 36hr. Refer patients with large, deep, or incom-
pletely removed FB or if a rust ring remains afterwards.
Arc (welder’s) eye/​‘snow blindness’
Exposure to ultraviolet light can cause superficial keratitis. Climbers/​skiers,
welders, and sunbed users who have not used appropriate protective gog-
gles develop pain, watering, redness, and blepharospasm several hours later.
LA drops allow examination with fluorescein staining, revealing multiple
punctate corneal lesions. Consider instilling a drop of 1% cyclopentolate or
0.1% diclofenac into both eyes. Discharge with an eye pad, oral analgesia,
and advice not to drive until recovered. Anticipate resolution within 24hr.
Do not discharge with LA drops.
 Contact lens problems 555

Chemical eye burns

Chemical burns from alkali or acid are very serious. Triage urgently ahead;
check TOXBASE® (M https://​www.toxbase.org), and irrigate the eye im-
mediately with lukewarm normal saline for at least 20min or until the pH of
tears has returned to normal (77.4). A 1L bag of 0.9% saline with standard
IV tubing is ideal. LA may be needed to enable full irrigation. Consider the
need for protective clothing during irrigation. Try to identify the substance
involved, and contact the Poisons Unit. Refer alkali and acid burns immedi-
ately to the ophthalmologist.
Superglued eyelids
Wash with warm water. The eye will open within 4 days. If the patient re-
ports an FB sensation, this may represent a lump of glue, which may cause
an abrasion if untreated—​refer to the ophthalmologist.
Note that despite precautions, occasionally eyelids are glued together
during the application of tissue glue to close a forehead wound (see % Skin
tissue glue, p. 415). If the eyelids remain closed despite simple measures,
contact the ophthalmologist ± TOXBASE® (M https://​www.toxbase.org).

Contact lens problems

Contact lenses may be ‘soft’ (more comfortable) or ‘hard’. Avoid using
fluorescein with contact lenses, as permanent staining may occur.
‘Stuck lens’
Most contact lens users are adept at removing their lenses. New users,
however, can experience difficulty. Moisten soft lenses with saline, then re-
move by pinching between the finger and the thumb. Special suction devices
are available to help remove hard lenses.
‘Lost lens’
Patients may present concerned that they are unable to find their contact
lens and cannot remember it falling out. Check under both eyelids carefully
(evert the upper lid if the lens is not immediately apparent) and remove the
offending lens, if present.
Hypersensitivity and overuse
Preservatives in lens-​cleaning fluid cause itching and may evoke a reaction.
Advise to stop using the lenses; give antibiotic ointment, and arrange oph-
thalmological follow-​up.
Acanthamoeba keratitis
This protozoal infection of the cornea occurs in contact lens users, associ-
ated with poor lens hygiene or swimming whilst wearing contact lenses. The
eye becomes painful and red. Corneal oedema and ulceration develop. If
suspected, refer immediately for ophthalmological care.
Other problems related to contact lenses
Treat and refer conjunctivitis, corneal abrasions, or ulcers apparently
related to contact lenses, as outlined in % The red eye, pp. 558–9. Advise
avoidance of use of both contact lenses until the problem has resolved, and
arrange appropriate follow-​up with the GP or an ophthalmologist.
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Sudden visual loss

Sudden visual loss requires emergency assessment and treatment.
Amaurosis fugax
The patient describes temporary loss of vision in one eye, like a ‘curtain
coming down’, with complete recovery after a few seconds to minutes. The
cause is usually a thrombotic embolus in the retinal, ophthalmic, or ciliary
artery, originating from a carotid atheromatous plaque, but it can also be a
feature of giant cell arteritis (see % Giant cell (temporal) arteritis, p. 557).
Treat as for TIA (see % Transient ischaemic attacks, p. 155), and involve the
ophthalmology team (to exclude other ‘eye’ pathology).
Central retinal artery occlusion
The central retinal artery is an end artery. Occlusion causes an ischaemic
stroke of the retina. It is usually embolic (check for AF and listen for carotid
bruits), causing sudden painless d VA to counting fingers or no light per-
ception. The patient may have a history of amaurosis fugax. Direct pupil
reaction is sluggish or absent in the affected eye, but it reacts to consen-
sual stimulation (afferent pupillary defect). Fundoscopy reveals a pale retina,
with a swollen pale optic disc and a ‘cherry red macula spot’ (the retina is
thinnest here and the underlying choroidal circulation is normal). Retinal
blood vessels are attenuated and irregular—​there may be ‘cattle-​trucking’
in arteries.
Treat by digitally massaging the globe (with the eye closed) for 5–​15s, then
release and repeat to dislodge the embolus, whilst awaiting urgent arrival
of an ophthalmologist.
If there is any delay in the patient being seen by the ophthalmologist, dis-
cuss other options such as giving acetazolamide 500mg IV (to d intra-​ocular
pressure and i retinal blood flow). Note that current evidence does not
support the use of thrombolytic agents in this situation.
Do reconsider the diagnosis. In particular, consider whether or not giant
cell (temporal) arteritis (see % Giant cell (temporal) arteritis, p. 557) is a
possibility—​ask about jaw claudication, headaches, and scalp tenderness.
Central retinal vein occlusion
This is a more frequent cause of sudden painless visual loss than arterial
occlusion. Predisposing factors include: old age, chronic glaucoma,
arteriosclerosis, hypertension, and polycythaemia. Examination reveals
d VA, often with an afferent pupillary defect. Fundoscopy reveals a ‘stormy
sunset’ appearance—​hyperaemia with engorged veins and adjacent flame-​
shaped haemorrhages. The disc may be obscured by haemorrhages and
oedema. Cotton wool spots may be seen. Although the outcome is variable
and there is currently no specific treatment, refer urgently as the underlying
cause may be treatable, thus protecting the other eye.
 Sudden visual loss 557

Giant cell (temporal) arteritis

Inflammation of the posterior ciliary arteries causes ischaemic optic neur-
itis and visual loss. It is relatively common in those aged >50y and is as-
sociated with polymyalgia rheumatica. The other eye remains at risk until
treatment is commenced. Rapid and profound visual loss may be preceded
by headaches, jaw claudication, general malaise, and muscular pains—​often
these symptoms can worsen over several weeks or months. The temporal
arteries are characteristically tender to palpation. Retinal appearances
have been termed ‘pale papilloedema’—​the ischaemic disc is pale, waxy,
and elevated and has splinter haemorrhages on it. If suspected, give oral
prednisolone 60mg immediately; check ESR (typically >>40mm/​hr but can
be normal), and refer urgently.
Vitreous haemorrhage
This occurs in diabetics with new vessel formation and in bleeding disorders
and retinal detachment. Small bleeds may produce vitreous floaters with
little visual loss. Large bleeds result in painless dd VA, an absent red reflex,
and difficulty visualizing the retina. Refer urgently. Meanwhile, elevate the
head of the bed to allow blood to collect inferiorly.
Retinal detachment
This occurs in myopes, diabetics, and the elderly and following trauma. The
rate of onset is variable—​patients may report premonitory flashing lights
or a ‘snow storm’, before developing cloudy vision. There may be a visual
field defect. Macular involvement causes d VA. The affected retina is dark
and opalescent but may be difficult to visualize by standard ophthalmos-
copy. Refer urgently for surgery and surgical reattachment or retinal laser
photocoagulation.
Optic neuritis
This usually presents in a young woman. Optic nerve inflammation and
demyelination cause visual loss over a few days. Pain on eye movement
may occur. An afferent pupillary defect is associated with d VA, d colour
vision (the colour red looks faded), and a normal/​swollen optic disc. Most
recover untreated; later some develop MS. Refer to the ophthalmologist
(possibly to discuss steroid treatment—​currently controversial and not
proven).
Other causes
Patients with chronic visual loss due to a variety of conditions may present
acutely (senile macular degeneration, glaucoma, optic atrophy, cataract,
choroidoretinitis). Drugs which can cause painless visual loss include
methanol (see % Methanol poisoning, p. 211) and quinine (in overdose). Refer
immediately all patients in whom an acute visual loss cannot be excluded.
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The red eye

Refer all patients with new findings of d VA, abnormal pupil reactions, or
corneal abnormalities.
Orbital and preseptal cellulitis
(See % Cellulitis, p. 545.)
This is a major infection of the orbital tissues. The infection most fre-
quently spreads from the paranasal sinuses (ethmoid sinusitis), facial skin, or
lacrimal sac. Occasionally, the infection follows direct trauma to the orbit
or from haematogenous spread. Patients present with fever, eyelid swelling,
erythema, and proptosis. Assess for signs of severe sepsis (see % Sepsis,
pp. 62–3 and % Shock, pp. 64–5), and resuscitate as necessary. Obtain
venous access; take blood for cultures, and commence IV antibiotics (eg co-​
amoxiclav) and fluids. Refer urgently to the ophthalmologist. Some aggres-
sive infections may require surgical treatment. Cavernous sinus thrombosis
and meningitis are potential complications.
Acute iritis (acute uveitis)
A relapsing condition of the young/​middle-​aged, associated with ankylosing
spondylitis, ulcerative colitis, sarcoid, AIDS, and Behçet’s syndrome.
Symptoms Include acute-​onset pain, photophobia, ‘floaters’, blurred vision,
and watering.
Signs d VA, tender eye felt through the upper eyelid, circumcorneal ery-
thema, small pupil (may be irregular due to previous adhesions). Shining a
light into the ‘good’ eye causes pain in the other. Pain i as the eyes converge
and the pupils react to accommodation (Talbot’s test). Slit lamp examin-
ation may reveal hypopyon and white precipitates on the posterior cornea.
Refer Refer urgently to the ophthalmologist for steroid eye drops, pupil
dilatation, analgesia, investigation, and follow-​up.
Acute closed angle glaucoma
Long-​sighted middle-​aged or elderly individuals with shallow anterior cham-
bers are at risk. Sudden blocked drainage of aqueous humour into the canal
of Schlemm causes intra-​ocular pressure to i from 10–​20mmHg up to
70mmHg. This may be caused by anticholinergic drugs or pupil dilatation at
night (reading in dim light).
Symptoms Include preceding episodes of blurred vision or haloes around lights
due to corneal oedema. Acute blockage causes severe eye pain and nausea/​
vomiting.
Signs d VA, hazy and oedematous cornea with circumcorneal erythema,
and a fixed semi-​dilated, ovoid pupil. The eye feels tender and hard through
the upper eyelid. Measure the intra-​ocular pressure if this facility is available.
Treatment Instill a 4% pilocarpine drop every 15min to produce ciliary
muscle contraction and aqueous humour drainage. Apply prophylactic 1%
pilocarpine drops into the other eye also. Give analgesia (eg morphine IV
with antiemetic). Arrange an emergency ophthalmology opinion—​consider
giving acetazolamide 500mg IV (to d intra-​ocular pressure) in the meantime
and/​or mannitol 20% up to 500mL IVI over 1hr.
 The red eye 559

Conjunctivitis
This is caused by bacteria (Streptococcus pneumoniae or Haemophilus
influenzae), viruses (adenovirus), or allergy. The sensation of FB may in-
volve both eyes. The conjunctiva is red and inflamed, sometimes with eyelid
swelling. VA and pupils are normal. Bacterial infection classically produces
sticky mucopurulent tears, and viral infection copious watery tears (asso-
ciated with photophobia and pre-​auricular lymphadenopathy in the highly
contagious adenoviral ‘epidemic keratoconjunctivitis’). It is not possible to
clinically distinguish viral from bacterial cases.
Advise not to share towels or pillows. Most cases settle relatively quickly
with symptomatic measures—​advise patients to see the GP if not better
in 4 days or to return if significantly worse. Reserve a course of antibiotic
eye drops or ointment (eg fusidic acid, chloramphenicol, or gentamicin) for
patients whose symptoms last >5 days.
Ulcerative keratitis
Corneal ulceration causes pain with photophobia. It is apparent on
fluorescein staining under a slit lamp.
• Hypopyon (pus in the anterior chamber) implies bacterial infection.
• Vesicles in the ophthalmic division of the trigeminal nerve occur with
herpes zoster infection.
• Dendritic branching ulcers suggest herpes simplex. If misdiagnosed and
steroid eye drops are given, ulceration can be disastrous.
Whatever the infective agent, refer corneal ulceration cases immediately.
Episcleritis
Inflammation beneath one area of the conjunctiva is usually associated with
a nodule and a dull aching discomfort. VA, pupils, and the anterior chamber
are normal. Prescribe oral NSAIDs, and advise GP review ± outpatient
follow-​up to consider steroid eye drops if there is no resolution.
Blepharitis
This chronic problem is quite common. Eyelashes are matted together and
itchy. Ensure that there is no associated corneal ulceration; provide topical
antibiotics (eg chloramphenicol), and refer for GP follow-​up.
External hordeolum (stye)
Treat staphylococcal infections of eyelash roots with warm compresses.
Internal hordeolum (chalazion)
A chalazion is an inflammatory reaction in a blocked meibomian (tarsal)
gland, which may get secondarily infected. Treat infected tarsal glands
with topical antibiotics (eg chloramphenicol) plus oral antibiotics (eg co-​
amoxiclav). Refer patients who develop an abscess or nodule affecting vision.
Dacrocystitis (lacrimal sac infection)
This may follow nasolacrimal duct obstruction. Treat early infection with
oral antibiotics (co-​amoxiclav); later, refer for drainage.
Subconjunctival haemorrhage
This usually presents as a painless, well-​defined area of haemorrhage over
the sclera. It may result from vomiting or sneezing. Following trauma, con-
sider orbital or base of skull fracture, and treat accordingly. Reassure the
patient that subconjunctival haemorrhage will resolve in time.
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Pupillary abnormalities
Pupillary examination may yield valuable information (see Table 11.1).

Table 11.1 Syndromes relating to examination of pupils

Description Common causes
Abducens nerve palsy Diplopia, inability to Trauma, tumour,
look outwards Wernicke’s syndrome
Adie pupil Pupil is dilated and Commonly part of
responds abnormally Holmes-​Adie syndrome—​
slowly to light cause unclear
Anisocoria Unequal pupils May be physiological or
reflect disease process
(eg third nerve palsy or
Horner’s syndrome)
Argyll Robertson pupil Small pupils that Pathognomonic of tertiary
(usually bilateral) accommodate, but do not syphilis
constrict, to light
Horner’s syndrome Miosis, ptosis, and Lung cancer, trauma, lateral
(sympathetic nerve anhidrosis (usually medullary syndrome,
damage) unilateral) carotid artery dissection
Hutchinson’s pupil (Ipsilateral) pupil dilates Compression of the
and is unreactive to light oculomotor nerve can
follow trauma or tumour
often due to temporal lobe
herniation
Marcus Gunn pupil Light shone in affected Optic neuritis, giant cell
(relative afferent eye causes slow direct and arteritis, optic nerve
pupillary defect) consensual pupil reactions trauma, retinal detachment
(light in normal eye gives
brisk direct and consensual
reactions)
Miosis Excessive pupillary Drugs such as opioids
constriction (bilateral miosis), Horner’s
syndrome (unilateral
miosis)
Mydriasis Excessive pupillary Drugs, post-​cardiac arrest
dilatation
Oculomotor nerve palsy Ptosis, mydriasis, and Trauma, tumour,
movement of the eyeball aneurysm, demyelinating
downward and outward disorders, cavernous sinus
(unopposed action of thrombosis
fourth and sixth nerves)
Trochlear nerve palsy Vertical diplopia; Trauma, haemorrhage,
inability to look down infarction
and in