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CHAP TER10 The eye and eyelids
Management
• Instil local anaestheticdrops.
• Everting the lids is essential.
• Foreign bodies can sometimes be seen more readily if uorescein
drops are instilled.
• Surface foreign bodies should be directly visible and do not require
radiological investigation.
• Amoistened cotton bud is eective for removing most conjunctival
and subtarsal foreign bodies. However, a green needle used with a
slit- lamp is often needed for corneal foreign bodies.
• Prescribe chloramphenicol ointment four times a day for 5days and
padding for the rstday.
• Referral is not required unless a r ust r ing remains on the cornea or
an infected corneal ulcer has developed under the foreignbody.
IOFBs that have penetrated the eye as a result of high- velocity injuries
are discussed under penetrating injuries. IOFBs usually occur due to
high- velocit y injury like gunshot injury or industrial accident s. CT scan
is the investigation of choice for foreign body detection and localization.
Referral to ophthalmologist is necessary.
cRustrings
These can develop within hours from the iron in a metallic foreign body.
Removal may be deferred for a day or so, to allow the ring to become
more supercial. Antibiotic ointment may help to prevent infection. Rings
persisting for >72 hours should be removed or refer red. See Figure10.5.
Figure10.4 Eversion of upper lids showing fo reig n body. (See also P late3.)
Figure10.5 Cor neal ulcer w ith hy popyon . (See also Pla te4.)
CONTACT LENS-RELATED PROBLEMS
bContact lens- related problems
Contact lenses are widely used by many patients but are not looked
after, replaced, and cleaned properly. This can lead to sight- threatening
complications. Contact lenses can be hard, gas permeable, or soft. The
latter can be exed between ngers and generally speaking are more
comfor table than the others. Many soft lenses are disposable and are
therefore thrown away after each use. Hence they are less likely to get
infected or build- up lipoprotein deposits that can reduce oxygen permeability, comfort, and clarit y. Extended- wear lenses (worn for weeks) and
lenses designed for yearly disposal are more likely to cause problems.
Over- wear is by far the commonest cause of problems. This leads to
hypoxia and damage to the epithelium of the cornea. Epithelial microcyst
formation, abrasions, blood vessel growth, and increased risk of microbial keratitis canoccur.
Key questions
• What type of lens isworn?
• How old is thelens?
• How old is the lens case and solutions? (Look at how clean/ dirt y the
caseis.)
• What cleaning regimen isused?
• Does the patient ever clean the lens in water, or swim with the
lensesin?
• How many hours and continuous days are lensesworn?
• Pre- existing eye diseases. Dry eyes, blepharitis, and corneal scarring
increase infectionrisk.
eAbrasions
These are usually caused by over- wear and hypoxic damage to the epithelium, which swells and easily sloughs o when the lens is removed.
bContact lens intolerance
The patient complains of increased discomfor t and redness leading to
reduced wear time. The commonest reason is dr y eyes. Articial tear
drops (preservative free) may alleviate the problem. Other reasons for
intolerance are build- up of deposits on lens, lens solution allergy, and
giant papillary conjunctivitis (large papillae are seen under the upper
lids). This is an allergic response to lens deposits or mechanical ir rit ation.
cLost contactlens
Ever ting the eyelids will usually reveal any lostlens.
eInfections
Conjunctivitis and microbial keratitis need to be referred promptly as
serious complications canarise.
Management
• General advice on contact lens care, cleaning, and avoiding over-
wear must be emphasized.
• Dry eyes can be managed with articial tear s suit able for the t ype of
lens beingworn.
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CHAP TER10 The eye and eyelids
• Patient s must be told to stop lens wear when the eyes are inamed.
• Abrasions can be treated chloramphenicol four times daily for 5days.
• No lens should be worn for at least 2 week s after the eye has settled
and after the patient has seen their optician for a check- up to assess
suitability to continuewear.
• All infections should be referred to an ophthalmologist.
eLoss ofvision
Loss of vision can have many causes, some obvious, others less so. It can
occur instantly or over a brief period of time. Although all require urgent
referral to an ophthalmologist, some conditions are treatable and therefore need rapid diagnosis. The key elements in the histor yare:
• Speed of onset of symptoms.
• Whether it is binocular or monocular.
• Whether it is associated with pain or headache.
• Associated systemic risk factors (hyper tension, diabetes,
hypercholesterolaemia).
• Ocular history.
• Whether the patient is on anticoagulants.
To aid in diagnosis, loss of vision can be classied into painful and painless.
Painful loss ofvision
• AACG
• Arteritic anterior ischaemic optic neuropathy— temporal arteritis
• Optic neuritis
• Chemicalburns
• Cornealulcers
• Blunt and penetrating oculartr auma
• Uveitis— especially posterior and intermediate uveitis
• Scleritis— especially posterior scleritis
• Orbital cellulitis
• Herpes zoster ophthalmicus
• Retrobulbar haemorrhage
• Endophthalmitis— exogenous and endogenous.
In painful loss of vision, acute angle- closure glaucoma must be ruledout.
• Examine the cornea to rule out corneal pathology, e.g. corneal
ulcers. Consider chemical keratitis and blunt/ penetrating injury.
• Exclude uveitis.
• Consider arteritic anterior ischaemic optic neuropathy secondary
to temporal arteritis or giant cell arteritis in anyone over 50 — ask
about headaches, jaw claudication, malaise, weight loss, and appetite
loss. Palpate for tenderness and non- pulsating supercial temporal
arteries. Examine pupils for relative aerent pupil defect and look for
signs of swollen optic disc. Urgently check the ESR and CRP, which
are usually raised in this condition.
• Optic neuritis is commonly associated with demyelinating disease
(MS). It is usually associated with unilateral loss of vision deteriorating
over a few days, reduced colour and light perception, pain on eye
LOSS OFVISION
movements, and is typically seen in young (20 – 50years old) females.
Examine for reduced visual acuity, red colour desaturation, R APD,
centr al eld defects, and a swollen opticdisc.
• If the patient has undergone recent eye surger y (e.g. catarac t surgery,
trabeculectomy, vitrectomy, penetr ating trauma), or received a
recent injury consider exogenous endophthalmitis as a diagnosis.
In addition to pain and reduced vision, the eye is red, there is brin
in the anterior chamber, a hypopyon, and loss of red reex (red
reex may be present early)— urgent referral to ophthalmologists is
mandatory.
Painless loss ofvision
Suddenonset
• Amaurosis fugax— TIA involving the opticnerve
• Retinal artery occlusion— central orbranch
• Retinal vein occlusion— central orbranch
• Non- arteritic anterior ischaemic optic neuropathy
• Retinal detachment
• Vitreous haemorrhage
• Neurological diseases— occipital cortex strokes, lesions involving the
visual pathways.
Gradualonset
• Age- related macular degeneration— loss of centralvision
• Cataract
• Advanced glaucoma.
eRetinal detachment
Retinal detachment is the separation of the retina from the underlying
retinal pigmented epithelium as a result of uid gathering between the
two layers. The majorit y of cases follow vitreous degeneration and its
shrinkage, resulting in vitreous separation from the retina (posterior
vitreous detachment). If there are abnormal adhesions between the
two, the retina can tear as the vitreous shrinks, allowing uid to gather
beneath it. This is the commonest form of retinal detachment. Less commonly, ocular vascular abnormalities, cancers, or brosis in the vitreous
(advanced diabetic retinopathy) can cause detachment. Trauma, shortsightedness (myopia) and family history are risk fac tors.
The main clinical featuresare:
• Flashing lights (like lightning).
• Floaters (dots, lines, spider’s web or ies oating in front of vision)
occur because the collapsed strands of vitreous gel are moving
around within the eye and cast a shadow on the retina.
• Shadowing (dark curtain covering a part of vision).
There is usually a short history of hours to days. There may be reduced
vision if the macula is involved. Examine the visual acuity, visual elds, and
pupils (an APD may be detected if a signicant portion of the retina is
detached). Fundoscopy reveals an elevated retina with or withoutfolds.
If the patient presents at the retinal - tear stage, laser or cryother apy
can be utilized to ‘weld’ the retina down around the tear to stop uid
leaking underneath it. Surger y is of ten required to atten the retina if
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CHAP TER10 The eye and eyelids
a signicant detachment has occurred. The prognosis depends on the
cause and extent of detachment . If the macula is unaected, prognosis
for vision isgood.
Most patients with ashes and oater s only have a vitreous detachment.
It is, however, dicult to predict which ones go on to develop retinal
detachment from the history alone. Therefore all need urgent ophthalmology review.
eOptic neuritis
Optic neuritis is an inammatory optic neuropathy. It is commonly associated with demyelinating disease (MS). However viral infections, compressive lesions, or systemic disea ses such as sarcoidosis need to be
borne in mind. Usually there is unilateral loss of vision deteriorating over
a few days, reduced colour and light perception, typically in the young
(20– 50 years old) patients. Periocular pain, especially on eye movement, is often present. Examine for reduced visual acuity, red colour
desaturation, R APD, and central or para- central eld defects. Swelling
of the optic nerve and other focal neurological defects (e.g. weakness)
may be present . During the acute attack, vision deteriorates for 1 week
and then gradually resolves over the ensuing 3months to near normal.
Investigations should be directed towards this diagnosis if systemic or
other neurological associations are present, or if the clinical picture is
atypical.
In an acute att ack of demyelinating optic neuritis, a course of IV steroids followed by oral steroid has been shown to speed recover y and
reduce recurrence in the shor t term. However, the long- term prognosis is not altered. With other causes, the systemic associations dictate
prognosis. Prognosis is best for post- viral optic neur itis. Refer as soon a s
possible to a neuro- ophthalmologist or neurologist.
eRetinal artery occlusion
An occlusion of the central retinal ar ter y or any of its branches can result
from an embolus or thrombosis. Less common causes are temporal
arteritis and collagen vascular diseases. There is sudden unilateral painless loss of vision, which may be severe and total (central retinal artery
occlusion, CRAO) or partial with sectoral eld defect (branch retinal
artery occlusion, BRAO). The patient may have a history of ischaemic
hear t disease, diabetes, stroke, amaurosis fugax (sudden loss of vision
which resolved within 24 hours), and smoking. The following features are
noticed on examination:
• CR AO:visual acuity is at best counting ngers or light perception.
There is RAPD, narrow ar ter ies, and a white oedematous retina with
a cherry- red spot at the macula. If the patient ha s a cilioretinal ar tery
(separate ar ter y to the macula from the choroidal circulation, found
in 20% of the population), central vision is spared in CRAO. The
patient may have 6/ 6 vision with restricted elds.
• BRAO:vision is variably reduced (depending on how much the
macula is aected). The pupils usually react normally and there is
sectoral whitening of retina and arterial attenuation.
LOSS OFVISION
Refer immediately to ophthalmolog y. Get an ESR and CRP urgently to
exclude temporal arteritis. A full cardiovascular work- up can be done,
routinely including fasting glucose, cholesterol, triglycer ide, ECG, and
carotid Dopplers.
The aim of management is to tr y and dislodge the embolus by reducing the
eye pressure within 24 hours of occlusion. The simplest method is ocular
massage but IV aceta zolamide 500 mg stat or par acentesis (uid drainage
from the anterior chamber) is more eective, although the latter can
cause severe complications. The above measures generally have a poor
success rate. Usually the occlusion is not rever sible and the visual loss is
permanent.
Temporal arteritis must be excluded in all patients >50years.
eRetinal vein occlusion
Occlusion may involve the central retinal vein or any of its branches. The
retinal vein and ar ter y share a common sheath. The artery can therefore
compress the vein as they cross, leading to stasis and occlusion. The condition generally aects the elderly.
Patients present with unilateral, painless loss of vision developing over
a few hours. There may be a history of hypertension, diabetes, glaucoma, hormone replacement treatment, or hypercoagulable state. The
vision is variably reduced and there may be an R APD, visual eld defect,
and a raised IOP. On fundoscopy, a swollen disc, congested and dilated
veins, retinal haemorrhages, and cotton- wool spots are seen in the area
supplied by the occluded vein. FBC and coagulation prole should be
investigated. Auorescein angiogr am may be performedlater.
No treatment is shown to reverse acute vein occlusion. Control of
vascular risk factors, hypertension, IOP, and hypercoagulability states
aim to protect the second eye. Patients require long- term ophthalmic
follow- up to screen for treatable complications (such as neovascularization, macular oedema, and glaucoma). The prognosis depends on the
degree and extent of ischaemic damage and ensuing complications.
Poor initial vision and an R APD carry the worst prognosis. Up to 5% of
patients can have the second eye aected.
Vein occlusion should be suspected in asymmetrical diabetic retinopathy.
eVitreous haemorrhage
Sudden bleeding into the vitreous can occur for many reasons:
• Diabetes
• Retinal tear ± detachment
• Posterior vitreous detachment
• Retinal vein occlusion
• Trau m a
• Subarachnoid haemorrhage (Terson’s syndrome).
Patients present with sudden painless loss of vision. There is loss of the
red reex (without the presence of cataract), and fundoscopy is unable
to view the retina. Ultrasonography can conrm the diagnosis
Any unexplained vitreous haemorrhage is due to retinal tear(s) until proven
otherwise.
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CHAP TER10 The eye and eyelids
eAmaurosisfugax
Amaurosis fugax is painless and transient monocular visual loss. It can
be considered as a type of TIA, during which an embolus obstructs the
lume n of the reti nal or ophth almic ar tery, caus ing a decrea se in blood o w
to the retina. The most common source of these emboli is from an atherosclerotic carotid artery. Other pathophysiological mechanismsexist.
Patients present with monocular visual loss that usually lasts for seconds to minutes. The fundus usually appears normal. Check for atrial
brillation, carotid bruit , and examine for neurological defec t elsewhere.
FBC, fasting lipids, and blood sugar to rule out diabetes. Other investigations include carotid Dopplers, echocardiography as an outpatient.
Commence aspirin if no contraindications and refer to ophthalmology
or a TIA clinic.
cEyelid problems
The main function of the eyelids is to regularly spread the tears and other
secretions across the sur face of the eye to keep it moist. This keeps the
eyes from drying out. The blink reex protects the eye from foreign bodies. Any disorder of the eyelids aecting these func tions can result in
irritating symptoms and the risk of corneal injury.
Common eyelid disorders
• St ye (hordeolum) is an infection of the glands by Staphylococcus
aureus. The main symptoms are pain, redness of the eyelid margin,
and swelling. Styes usually disappear within a week without treatment
or with warm water compresses.
• Chalazion is caused by the obstruction of the oil glands. They can be
mistaken as styes but they are less painful and it tends to be chronic.
• Blepharitis is a common infective condition that causes inammation
of the eyelids. Treatment includes maintaining good hygiene
and warm compresses on the aected eyelid to remove crusts.
Antibiotics may be prescribed.
• Ectropion is the turning outwards of the lower lid from globe. It
usually results from ageing, but sometimes can be a complication of
surgery, injury, or disease. Entropion is where the lid tur ns inwards.
• Eyelid oedema can occur during an allergic reaction to food, drugs,
plants, or secondary to infections.
• Eyelid tumours (e.g. basal cell carcinoma).
• Blepharospasm (eyelid twitching) is involunt ary spasm of the eyelids.
• Ptosis is when the upper eyelid droops as a result of weakness of
the levator muscle or dysfunction of the ner ves to it. It can be par t
of the normal ageing process or secondar y to pathology elsewhere
(diabetes, stroke, Horner’s syndrome, myasthenia gravis).
WATERYEYES
bWateryeyes
The lacrimal apparatus
The lacrimal drainage system consists of the puncta, canaliculi, lacrimal
sac and nasolacrimal duct. Tears are produced by the lacrimal gland and
swept over the eye surface with each blink . Tears drain via the lower canaliculus predominantly (70%) and upper canaliculus (30%) by the lacr imal
pump mechanism (the action of the eyelids contracting and pumping the
tears into the lacr imalsac).
It is important to dierentiate between hypersecretion and epiphora as
both can present with wateryeye.
Acute
• Microbial keratitis
• Corneal foreignbody
• Corneal abrasion
• Allergic reaction
• Acute dacryocystitis.
Chronic
• Nasolacrimal obstruction— congenital or acquired
• Mucocoele
• Ectropion
• Punctal stenosis
• Functional, e.g. lacr imal pump failure, lower lidlaxity
• Entropion or trichiasis
• Dryeyes.
bEpiphora
Reduced tear drainage from lacrimal system obstruction at any point
from the punctum, canaliculus, sac, and nasolacrimal duct. Nasolacrimal
duct obstruction is the commonest.
bHypersecretion
Excess production of tears in response to stimulation from corneal irritation (e.g. corneal foreign body), dr y eye, or conjunctival irritation (e.g.
blepharitis, conjunctivitis).
bFunctional epiphora
Epiphora in the presence of patent nasolacrimal drainage pathway without hypersecretion. This can be due to eyelid malposition, e.g. lower
lid ectropion (lid turned out), lacrimal pump failure, (facial palsy) punctual, canalicular, and nasolacrimal duct stenosis (without complete
obstruction).
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CHAP TER10 The eye and eyelids
bMucocoele
This is a dilated lacrimal sac lled with mucous. It can present as a lump
around the medial canthus and is often confused with a skin cyst (dermoid, sebaceous). Patients also complain of epiphora. If these get large
they can cause considerable distor tion of the local anatomy, with canthal
drif ting. This can then appear like a tumour. Mucocoeles can also become
infected (dacryocystitis). Consider this in any patient presenting with an
abscess along the side of theirnose.
History taking inepiphora
• Is stickiness/ watering constant or intermittent? Is it worse outdoors?
• Any inammation or lump at the medial canthus?
• Histor y of nasal disease, sinusitis, polyps, or nasal trauma.
• Any photophobia, redeye?
• Previous conjunctivitis, eye drops anddrugs.
Examination
Look specically for periocular and medial canthus patholog y notably
eyelid malposition and a mucocoele.
• Fluorescein dye retention test. Adrop of uorescein 2% will rapidly
disappear from the conjunctiva if the system is patent. The dye will be
retained if blocked.
• Slit lamp examination to exclude corneal causes, blepharitis, punctual
stenosis, tear meniscus.
• Probe and syringe/ irrigate the lacrimal system (use topical
anaesthesia).
• Special clinical tests— Jones’ tests used to conrm and localize
functional epiphora are performed by ophthalmologists.
Aetiology ofthe water yeye
Management
Epiphora secondary to blockage of the nasolacrimal duct and functional
epiphora need a non- urgent referral to ophthalmology for surgical management. In cases of entropion (turning in of eyelid) steri- strips can be
used tempor arily to prevent the eyelid rolling in and causing damage to
the cor nea with the lashes. Trichiatic lashes (misdirected) can cause corneal abrasion and can be removed.
bAcute dacryocystitis
This is an acute infection of the lacrimal sac. There is usually a pre existing swelling close to the medial canthus. Patient s present with pain,
erythema, a water y eye, and oedema.
Management— oral or IV antibiotics depending on the severity. It is
important to remember that acute dacr yocystitis can cause orbital celluli tis and requires urgent ophthalmology assessment if not responding to oral
antibiotics.
Chapter11
317
The upper jaw and midface
Common presentations 318
Common problems and their causes 318
Useful questions and what to look for 320
Examination of the upper jaw (and midface) 322
Investigations 325
Fractures to the upper jaw and midface 326
Infections 332
Facial pain 336
Orofacial pain syndromes 337
Facial numbness 339
Facial palsy 340
Non- infective lumps and swellings 342