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298
CHAP TER10 The eye and eyelids
eTraumatic optic neuropathy
Traumatic optic neuropathy ( TON) occurs in approximately 0.5– 5 % of
closed head injuries. These can sometimes berelatively trivial in nature.
Visual loss is permanent inapproximately half. Injuring forces transferred
to the optic canal results in damage to the optic nerve. Stretching, contusion, or shearing forces can injure the nerve as it passes through the
relatively thick bony canal into the orbit. Deceleration injuries and blunt
trauma to the face and head are the common causes of TON. Motor
vehicle collisions, falls, and assault account for the major ity of cases.
Displaced fractures around the orbital apex together with bleeding and
oedema compress thener ve.
Diagnosis
• The diagnosis of TON is a clinicalone.
• Loss of consciousness is commonly associated.
• Visual loss is usually sudden and profound although it can be
moderate and delayed.
• There is decreased visual acuity and a relativeAPD.
• When the eye appears normal but there is reduced vision and an
APD, injury to the nerve near the optic canal should be suspected.
• Optic nerve avulsion, or nerve compression resulting in nerve head
swelling or central arter y and vein occlusion are readily recognizable
on fundoscopy.
Management
TON needs immediate refer ral. Treatment has long been controversial
and may be medical or surgical:
• Medical treatment aims to reduce oedema and inammation
however the role of high dose steroids is controversial with a growing
consensus againstthis.
• Surgical decompression is even more controversial. It may be
indicated for optic nerve haematoma or if a bony fragment is seen (on
CT) to be impinging on the opticnerve.
eCorneal abrasion
This is an area where part of the corneal epithelium is decient. The
patient complains of pain, water ing, and has a foreign body sensation.
They have diculty keeping the eye open. Usually there is a history of
trauma or contact lens wear. The eyelids may be in spasm and the conjunctiva is injected. With topical anaesthesia, the vision is normal. The
area of abrasion stains with uorescein.
Management
• Chloramphenicol drops or ointment should be prescribed four times
daily for 5days.
• Ensure that there is no opacity of the cornea (which indicates a
secondary infec tion of the underlying stroma) and that there are no
foreign bodies.
• Although an eye pad is not essential, it helps keep the eye closed and
patients tend to feel more comfor table. It can be kept on for1day.
EYELID LACERATIONS
• Repeated blinking and rubbing the eyes prevents epithelial healing.
• No contac t lens should be worn for 2 weeks and after the patient has
seen his/ her own optician.
• If the patient is very distressed, cycloplegic drops and or al analgesia
will provide some relief until abrasionheals.
Abrasions usually heal rapidly and the patient should be a lot more comfortable in 2days. Refer only if a secondary corneal ulcer or a recurrent
erosion syndrome develops. Long- term use of lubricating eye ointments,
bandage contact lens, and occasionally sur face treatment by needle
puncture or laser may then be required.
eArceye
This is a specic condition caused by ultr aviolet injury from welding, tanning lamps, and high- altitude snow (sometimes seen in inexperienced
skiers who don’t wear sunglasses). Ultraviolet light causes oedema and
sloughing of the corneal epithelium leading to punctate erosions or abrasions. Patients complain of pain, tearing, blepharospasm, photophobia,
and blurred vision sever al hours af ter exposure. Treatment is similar to
an abrasion.
Tense ‘proptosis’ in the elderly
Care is required when assessing the eyes in the elderly. AACG can be
precipitated by dim light , and some drugs. In some patient s the dilated
pupil may precipitate ocular problems. This should be considered in
any elderly patient who develops a painful, tense, ‘red eye’, even after
an injury. It may be misinterpreted as proptosis.
cEyelid lacerations
These require careful a ssessment and often referral to an appropriate
specialty (ophthalmology, oculoplastics, plastics, maxillofacial), depending on local protocols. The main concerns hereare:
• The possibility of an associated, yet hidden globeinjury
• Loss of function of the eyelids following treatment
• Injuries to the lacrimal drainage system.
Assess the eye carefully. A normal appearance does not rule out a serious
injury. The mechanism of injury may provide clues to possible globe prob-
lems. Small lid lacerations may conceal a large retained foreign body.
Always consider retained foreign bodies and image accordingly. Damage
to the canalicular system can occur with injuries to the medial a spect
of the lid margins. Suspected canalicular injuries should be referred.
Conjunctival, corneal, and scleral lacerations, hyphaema, lens dislocation, and globe rupture must all be excluded. Upper lid injuries may
aect the levator muscle and its function should be noted. Penetrating
globe, orbital, and cranial injur ies must be excluded in all penetrating lid
lacerations.
299
300
CHAP TER10 The eye and eyelids
eLacerations and loss ofeyelid integrity
Inability to eectively close the eyelids quickly results in drying of the
cornea, ulceration, and potentially loss of sight. Even relatively minor
eyelid lacerations may predispose to this andmay be easily overlooked.
Avulsion of the eyelids is a rare but devastating injury and extremely difcult to reconstruct.
Examination
• Visual acuity, visual elds, ocular movements, the pupil, and the
fundus should all be examined
• The position, length, and depth of the wound(s) should be
documented.
• Medially sited eyelid injuries can damage the lacrimal drainage system
and require special attention.
• Upper lid injuries may aect the levator muscle and its function
should benoted.
• Neurological examination is required if penetrating brain injury is
suspected. Even small lid lacerations may be the entry wound for a
signicant penetrating injury.
Plain orbital lms may reveal fractures and retained foreign bodies, but
CT scan is the investigation of choice.
Management
• Any associated injury must be treated accordingly.
• Refer urgently.
• Check tetanus status.
• Eyelid remnants should be pulled over to provide cornealcover.
• Apply plenty of chloramphenicol or ar ticialtears.
• Covered with a wet gauzeswab.
cLid lacerations not involving thelidmargin
Eyelids have an excellent blood supply and delayed primary closure is not
necessary. Simple lacerations can be explored and cleaned under local
anaesthesia and closed in layers as with any laceration. Eyelid function
(protecting the globe) is the primary consideration. Begin with irrigation,
antisepsis (non- irritant to the globe), and a check for retained foreign
bodies. Supercial lacerations of the eyelid, not involving the eyelid margin, may be closed with running or interrupted 6- 0 suture (Prolene®,
Ethilon®, Vicryl®,etc.).
Consider a penetrating eye injury if thereis:
• Loss ofvision
• Blood in the anterior chamber (hyphaema)
• Obvious corneal or scleral lacerations
• Dark uveal tissue presenting on the sur face of the eye (indicating an
openglobe)
• Pupil distortion
• Proptosis.
EYELID LACERATIONS
Deep lacerations should include the orbicular muscle and skin in the
repair. Care must be taken to ensure suture ends do not rub the cornea
and cause abr asions. Many shallow cuts can be apposed without sutures;
they scab over and heal extremely well. If skin is missing, seek advice on
possible reconstruction. Antibiotic ointments may be prescribed. Skin
sutures can be removed in 5days.
Complex lacerations (including any involving the lid margin, lateral and
medial canthal regions, medial third of the lids, and levator muscle) must
be referred for repair. These lacerations can disrupt the lacrimal drainage system and functional integrity of the lid. A s the lid is ver y vascular,
even necrotic- looking tissue can survive and thus no tissue should be
excised.
cLid lacerations involving thelidmargin
These usually require referral to a specialist. Primar y closure is of ten
possible if there is <25% tissue loss. Irregular edges may be excised
(minimally) by creating a pent agonal wedge, removing as little tissue as
possible. A4- 0 silk or nylon traction suture is placed in the eyelid margin 2 mm from the wound edges and 2 mm deep and is tied in a slipknot. Symmetric suture placement is critical to obtain good alignment.
Approximately 2 or 3 absorbable Vicryl® 5- 0 or 6- 0 sutures are placed
internally to approximate the tarsal plate. The skin and conjunctiva
should not be included in this internal closure. Ensure that the wound
edges are ever ted. Skin can be closed with 6- 0 nylon/ Prolene®/ Vicryl®
sutures. Skin sutures are removed in 5– 7days.
If there is tissue loss >25% this will require a ap or gr aft and is best
managed by a specialist. In the upper eyelid, if orbit al fat is seen, or if
ptosis is noted, damage to the orbital septum and levator aponeurosis
should be suspected.
If an eyelid is avulsed, the missing tissue can be sometimes reattached
if soaked in diluted antibiotic solution, wrapped in moistened sterile
gauze, and preser ved in ice. Refer urgently. If necrosis is present , minimal debridement should be undertaken to prevent further tissueloss.
Timing of repair of lid lacer ations depends on the general condition
of the patient and the presence of other injuries. Repair can be safely
deferred up to 48 hours (so long as the eye is protected), if other injuries t ake precedence. However, if unprotected, the cornea can dry
very quick ly. Under these circumstances, until the defect is repaired,
eyelid remnants should be pulled over the globe and suppor ted to provide corneal cover. If a delay in repair is expected, the wound should
be cleaned and irrigated with saline. Supercial foreign bodies should
be removed. Copious amounts of saline ir rigation under light pressure (using a 20 mL syringe and 18- gauge cannula) can be used to wash
out foreign bodies and reduce microbial load. IV antibiotic cover (e.g.
co- amoxiclav 500 mg three times daily) is needed for all bite injuries and
contaminated wounds.
301
302
CHAP TER10 The eye and eyelids
fChemical injuries
Chemicals that have a pH dierent to that of the eye (pH=7.4) can cause
a burn. Domestic and industrial accident s are the commonest causes of
chemical burns to the eye. Alkalis cause more damage than acids, as they
dissolve lipid membranes and penetrate deeper. Loss of vision results
from severe dr y eyes and scarring. Complications include cataract formation, glaucoma, and uveitis. Patients present with severe pain, blepharospasm, watering, and variable reduction in vision.
Management
• If the chemical is a dry powder, quickly brush as much of this o as
possible. Once you st art irrigating any residual powder will dissolve
producing more activeagent.
• Ir rigate with copious amounts of saline (litres) as soon as possible.
This must continue until the pH is normal before anything else is
done (it is not unusual to use over5L).
• It is important to irrigate the fornices as residual chemicals tend to
settlehere.
• Try to obtain the pH of the chemical and establish the baseline pH of
botheyes.
• Apply local anaesthetic drops if necessary.
• Note vision, epithelial defects, corneal clarity, cataract, and residual
particulate matter.
• Immediate referral to ophthalmology is then made, once the pH has
come back to normal.
• Further management with involves antibiotics, steroids, potassium
ascorbate, cycloplegia, and vitaminC.
• Patient s usually require admission especially if both eyes are involved
and vision is impaired.
The prognosis can be extremely poor. This depends on the pH of the
chemical and the ex tent damage. Hence rst- aid treatment received on
site and in casualt y is vitally important.
cThe redeye
This usually refers to injection and prominence of the super cial blood
vessels of the conjunctiva or sclera. This is dierent from the subconjunctival haemorrhage seen in trauma. There are many causes.
Examination
Causes of red eye (painful and painless)
• Acute glaucoma
• Injury
• Keratitis
• Iritis/ uveitis
• Scleritis
• Episcleritis
• Conjunctivitis
GLAU COMA
• Blepharitis
• Inamed pterygium
• Inamed pinguecula
• Dry eye syndrome
• Airborne contaminants or irritants
• Drug use (cannabis).
If an obvious cause is absent carefully examine the following.
• Visual acuity:any reduction indicates serious ocular disease, notably
keratitis, iridocyclitis, and glaucoma.
• Eyelids:blepharitis, entropion, ectropion, trichiasis.
• Conjunctiva:conjunctivitis, subconjunctival haemorrhage.
• Ciliar y ush:this is a ring of redness spreading out from around the
cornea of the eye. Seen in corneal inammation, iridocyclitis, or acute
glaucoma.
• Sclera:episcleritis (usually sectoral and relatively painless), scleritis
(usually painful and tender).
• Cornea:look for corneal foreign body, contact lens, and corneal
opacities. Stain with uorescein and look for corneal staining
(abrasion, ulcer, punctate staining). Corneal opacities are the fourth
leading cause of blindness.
• Anterior chamber:look for cells, hyphaema, hypopyon, and depth of
anterior chamber. Ashallow chamber may indicate a predisposition
to narrow- angle glaucoma. Any ‘red eye’ with a shallow anter ior
chamber sug gests acute glaucoma.
• Pupil:in iridocyclitis, the involved pupil will be smaller than the
uninvolved one, due to spasm of the sphinc ter muscle of the iris.
With A ACG, the pupil is generally xed in mid- position, oval, and
responds sluggishly to light, if atall.
• IOP should be measured. This is mostly normal or low in iritis. It is
elevated only in herpetic uveitis (which is not common). In traumatic
perforating ocular injuries, the IOP is usuallylow.
303
cGlaucoma
Glaucoma is a common condition with an estimated prevalence in the
over 40s of 1%. It is usually asymptomatic. It comprises a group of eye
disea ses in which there is damage to the optic nerve head and visual eld
loss, usually associated with abnormally elevated IOP (although a signicant number of patients can have normal eye pressures). If left untreated
this will ultimately lead to loss of vision.
IOP is normally maintained by a balance between for mation of aque-
ous within the eye and its subsequent drainage via a trabecular network
of tissues at the ‘dr ainage angle’. Increase in IOP usually occur s as a result
of obstruction to the outow of the aqueous. Obstruction can occur if
the periphery of the iris becomes displaced for wards so that it cover s the
drainage angle of the anterior chamber. This results in angle closure and
aects patients whose angle is very narrow. This will result in ‘closed’angle glaucoma. In open- angle glaucoma, pathological changes occur
304
CHAP TER10 The eye and eyelids
within the microstructure of the drainage system and so obstruct the
outow of aqueous. In these cases the angle is not closed but remains
‘open’.
cAcute angle- closure glaucoma
AACG occurs when sudden closure of the drainage angle leads to a rapid
rise in the IOP. Patients with narrow drainage angles are predisposed
to this when the pupil dilates. This bunches up the peripheral iris over
the angle and blocks it. The increasing size of the lens in the ageing eye
also pushes the iris forward, which further narrows the angle. Hence the
condition mainly aect s the elderly. Long- sighted patients are also at risk,
as they have smaller eyes and therefore narrower angles.
Diagnosis
Patients pr esent with a short history of incre asing eye pain. This become s
very severe. They also complain of nausea, vomiting, reduced vision, and
haloes seen around light s. Some patients may be mistakenly diagnosed
as having an abdomen problem, due to severe nausea and vomiting.
The cornea becomes cloudy and the pupil unreactive and mid- dilated.
The globe becomes hard to palpation. Both eyes have shallow anterior
chambers. There may have been previous milder att acks during the night
when the pupil naturally dilates. These may have resolved spontaneously.
Management
• Refer immediately to ophthalmology, as the pressure in the eye must
be reduced urgently.
• IV acetazolamide 50 0 mg stat, topical apraclonidine 1% three times
daily, timolol 0.25% twice daily may also be given to reduce the
pressure (if there are no systemic contraindications).
• Dexamethasone 0.1% four times daily is used to control
inammation.
• Pilocarpine 1% is given to the opposite eye to prevent acute closure.
• Laser peripheral iridotomies may be per formed to prevent an attack
of angle closure.
• In resistant cases, administration of IV mannitol or oral glycerine
can reduce the IOP by dr awing uid out of the eye. Caution must be
obser ved in patients with heart failure.
• If the pressures are controlled quickly, the prognosis isgood.
cOpen- angle glaucoma
Open- angle glaucoma is the commonest form of glaucoma. It is an insidious, slowly progressive disease, which occurs bilaterally and with no
symptoms until considerable visual impairment has occurred. Early diagnosis is therefore imper ative and may be achieved by regular screening
of the over 50s or those with a known family histor y.
Treatment can be both medical and surgical, the medical treatments
aim to increase the outow and/ or suppress the secretion of aqueous.
Surgical treatment aims to create an alter native out ow for the aqueous
or partially destroy ciliary body to reduce inow.
cSecondary glaucoma
In secondar y glaucoma, the raised IOP is secondary to a local cause such
as iritis, injur y, rubeosis (iris neovascularization due to diabetes or central retinal vein occlusion), and inappropriate use of steroid eye- drops.
Treatment involves controlling the underlying factors and then medical
or surgical treatment of glaucoma, as appropriate. Secondary glaucomas
generally have a poorer prognosis.
cCongenital glaucoma
Congenital glaucoma may present at bir th or in the ensuing months and
years. The condition is caused by the abnormal development of the
drainage angle, which result s in raised IOP. This in turn causes the immature eye to enlarge. This is referred to a s buphthalmos, which literally
means ‘ox eye’. Treatment is almost invariably surgical. Urgent ophthalmic referral is required.
eKeratitis
This is a condition in which the cornea becomes inamed. It is usually
painful and often associated with blurred vision. The patient may also
describe feelings of itchiness each time they blink. Two types are generally described:
• Supercial keratitis. This involves the supercial epithelium of the
cornea. After healing, there is usually no scarring.
• Deep ker atitis. This involves the deeper layers of the cornea and
therefore heals with scarring. This can permanently impair vision if it
is on visual axis. Treatment involves topical corticosteroid eyedrops.
Keratitis has multiple causes.
eViral keratitis
Herpes simplex keratitis (dendritic ker atitis) is a viral infection of the
cornea with herpes simplex virus. It frequently leaves a ‘dendritic ulcer’.
Herpes zoster keratitis is anothercause.
eBacterial keratitis
Bacterial infection of the cornea can follow from an injury or from wearing contact lenses. Common organisms are Staphylococcus aureus and
Pseudomonas aeruginosa, respectively.
eAmoebic keratitis
This is a protozoal infection of the cornea . It is a rare but severe complication of contact lens wear caused by washing and storing lenses in water
or swimming and bathing with contact lenses in the eye. The infection is
extremely dicult to diagnose and treat. Therefore the disease is usually
diagnosed late and r uns a long cour se with severe inammation.
eOnchocercal keratitis
This follows infection of a blacky bite. This is also k nown as ‘river
blindness’.
KERATITIS
305
306
CHAP TER10 The eye and eyelids
eFungal keratitis
Although not common, this can occur in injuries involving organic
material.
eExposure keratitis
This is due to dr yness of the cornea caused by incomplete or inadequate
eye- lid closure.
ePhotokeratitis
Keratitis due to intense ultraviolet radiation exposure (e.g. snow blindness or arceye.)
eUlcerative keratitis
This can be due to infective or inammatory causes.
cContact lens acute red eye (CLARE)
In CLARE, an infective cause must be r uled outrst.
cSevere allergic response
This may lead to corneal inammation and ulcer ation.
Management
This depends on the cause of the ker atitis:
• Infectious keratitis can progress rapidly, and generally requires urgent
antibacterial, antifungal, or antiviral therapy. Aciclovir is the mainstay
of treatment for herpes simplexvirus.
• Contact lens wearing should be prohibited.
• Steroids should not be used for infective keratitis.
Important warning symptoms
• Reduced visual acuity often indicates serious ocular disease.
If blurriness improves with blinking, it suggests ocular surface
discharge. Coloured halos occur with corneal oedema, and are a
warning that acute glaucoma may be present.
• Severe pain suggest s serious disease such as keratitis, corneal
ulceration, iridocyclitis, or acute glaucoma.
• Photophobia is often seen in iritis and injur y to the cornea, but may
also occur in acute glaucoma.
eIritis/ uveitis
This is inammation of the uveal tract of the eye (the pigmented layer —
the iris, ciliar y body, and choroid). If only the iris is involved, it is called
iritis or anterior uveitis. Uveitis can be associated with systemic inammatory diseases, such as sarcoidosis, SLE, and various arthritides.
Patients usually have a dull ache over the eye and may have blurred
vision and oaters. Photophobia can be severe. Conjunctival injection,
either ciliary (around the cornea) or generalized is often present . On slitlamp examination, inammatory cells can be seen in the anterior chamber, which can stick to the corneal endothelium (keratic precipitates) or
FOREIGNBODIES
form a hypopyon. The pupils may be irregular and immobile if the iris
adheres to the lens (due to posterior synechiae). Vitritis and yellow retinal inltrates may be present on fundoscopy in poster ior uveitis.
Refer as soon as possible to ophthalmology. Investigation is not
required initially if the patient is other wise well. Steroids (topical, local
injections, and systemically, depending on severity) and cycloplegics
must be started under ophthalmology supervision. Generally the prognosis is very good but uveitis can be chronic and recurrent.
eScleritis and episcleritis
This is an inammation of the scleral or episcleral layer of the eye. It
may be associated with systemic and connective tissue diseases, such as
rheumatoid arthritis and SLE. Onset is generally over a few days. Usually
there is unilateral aching in the eye associated with sectoral (localized)
injection of the eye. Scleritis is much more severe and can cause reduced
vision, chemosis, proptosis, and pain on eye movement. Episcleritis
should not aect any eye functions. Exudative retinal detachment, disc
oedema, and vascular occlusions can occur with scleritis. Secondary uveitis and keratitis may occur. Ultrasound B - scan may be required to show
scleral thickening in posterior scleritis.
Episcleritis is generally self- limiting over a period of around 4 weeks
and can be managed conservatively if mild. Episcleritis and mild scleritis
respond well to NSAIDs (e.g. ibuprofen 400 mg three times daily for
4 weeks). Moderate to severe scleritis usually requires systemic and
topical steroids under ophthalmology supervision. The prognosis is very
good for episcleritis and depends on system associations for scleritis.
Refer as soon as possible for scleritis. Although this is not required for
episcleritis, refer in severe or non- resolving cases and when diagnosis
is in doubt. Local irritation from lashes and foreign bodies need to be
excluded if there is sectoral injection of the eye with a gritty sensation.
307
cForeignbodies
Surface foreign bodies occur on the cornea, conjunctiva, or under the
lids (Figure 10.4). Slow velocity (grinding, welding, and wind- borne) foreign bodies do not have the force to penetrate the eye and only embed
themselves supercially in the epithelium. There is a foreign body sensation or grittiness in the eye, watering, and variable photophobia. Aclear
history of a foreign body may not always be present or it may precede
symptoms by hours. On examination the vision is normal, unless the for eign body is on the visual axis. The eye is injected and may be in spasm
until anaesthetic drops are instilled.
Foreign bodies in and around the eye can be dividedinto:
• Subtarsal foreignbodies
• Corneal foreignbodies
• Intraorbital foreignbodies
• Intraocular foreign bodies.