26 Ophthalmology

‘The eye is the window of the mind’

Richard II, William Shakespeare (1564–1616)

Community-based optometrists are a valuable resource available to GPs to help differentiate eye conditions and refine referral pathways. Getting an optometrist’s opinion can also assist in setting the appropriate priority level for referral or prevent unnecessary referrals.

Ask about pain, redness, watering, change in appearance of the eye, altered vision, and if the problem is unilateral or bilateral. Distinguish between blurred and double vision. Enquire about trauma, previous similar episodes, systemic illness, and eye disease in the family. If using medication, take a drug history (including eye drops).

Test and record the central (macular) vision of each eye separately for near and distance vision with glasses on. Cover the non-test eye carefully. On a full-size Snellen chart, line ‘6’ can be read by the normal eye at 6m (see Figure 26.3— p. 957). If unable to read the 6/9 line, use a pinhole to improve refraction. Near vision can be checked using a near-vision testing card (see Figure 26.2— p. 956) or newspaper.

Takes practice. Darken the room and ensure you have good batteries in your ophthalmoscope.

Dilating the pupils with a short-acting mydriatic (e.g. 0.5–1% tropicamide) makes examination much easier, but warn patients they may have temporarily blurred vision and should not drive home.

Test peripheral vision by sitting in front of the patient and comparing their visual field to your own (1 eye at a time)—the most basic test is to check the patient can see hand movement in each of the 4 quadrants. Refer for formal tests. Visual field defects— p. 971.

If the patient complains of double vision, move an object to the nine positions of gaze (see Figure 26.1). Ask the patient to tell you in which direction the double vision increases.

Should be round, central, of equal size, and respond equally to light and accommodation Pupil abnormalities:

See Table 26.1

Cause discomfort, a ‘foreign body sensation’, and watering. They can be difficult to see so examine very carefully (see Figure 26.5), including everting the eyelids. The foreign body sensation may come from an abrasion.

Due to corneal epithelial damage as a result of exposure to UV light. Seen in welders, sunbed users, skiers, mountaineers, and sailors who do not use adequate eye protection. Symptoms include severe eye pain, watering, and blepharospasm a few hours after exposure.

Pad the eye and give analgesics and cyclopentolate 1% eye drops bd (causes pupil dilation). Recovery should occur in <24h—if not refer. Advise on suitable protective wear for future exposure.

Caused by fists, squash balls, etc. The result may be anything from a ‘black eye’ to globe rupture. Globe rupture is usually obvious with a wound and severely ↓ vision. More minor injuries include subconjunctival haemorrhage ( p. 967) or corneal abrasion.

Uncommon fracture due to blunt trauma to the eye (e.g. squash ball injury). Can present with blurred or double vision and pain on moving the eye. Signs: enophthalmos (often masked by swelling), infraorbital nerve loss, and inability to look upwards due to trapping of inferior rectus muscle. Refer for X-ray and assessment of eye trauma via A&E.

Refer urgently to eye casualty if penetrating injury is a possibility, i.e. history of flying object or working with hammers, drills, lathes, or chisels where a metal fragment may fly off. X-ray/CT scan can confirm diagnosis and help locate the foreign body. Symptoms/signs:

Can cause great damage—particularly alkali injuries. Use topical anaesthetic (e.g. proxymetacaine 0.5%) before examining. Hold the lids open, brush out any powder, and irrigate with large amounts (1–2L) of clean saline or water immediately. Do not try to neutralize the acid or alkali. Refer urgently to eye casualty.

Consider:

(see Figure 26.6). Causes:

Oedema around the eyes gives the face a bloated appearance. Swollen eyelids may partially close the eyes. In severe cases the whole face becomes oedematous. Associated with nephrotic syndrome, allergic reactions (e.g. pollen, dust, or insect bites), angio-oedema, and periorbital cellulitis.

The eyes protrude from the orbit and thus have a staring appearance. Stand at the same level as the patient and look at the patient’s eyes. There should be no white of the sclera visible below the iris. If the eye is pushed forward, as in exophthalmos, white sclera is seen below the iris and the patient can look upwards without moving his/her eye-brows (distinguishes from lid retraction).

Infections of the upper lid may cause significant swelling and redness around the eye. Typically affects children following mild trauma. The eye is unaffected—infection is localized to skin and superficial tissues. Treat as localized cellulitis with oral antibiotics (e.g. flucloxacillin). Monitor carefully as can progress to orbital cellulitis.

Typically due to spread of infection from the paranasal sinuses. Usually presents with pain, double/blurred vision, and general malaise. Signs: fever, eyelid swelling, proptosis, and inability to move the eye. Severe cases can lead to septicaemia, meningitis, and cavernous sinus thromboses. If suspected, refer immediately to ophthalmology for IV antibiotics/surgical drainage.

The eye is in a confined space within the orbit. Any ↑ in mass pushes the eye forwards. Symptoms/signs:

Causes an irritable foreign body feeling in the eye ± recurrent infection. In severe cases, the ingrowing lashes may damage the cornea. Refer to ophthalmology.

Usually due to blepharitis ( p. 964), in which case the condition is bilateral and associated with other symptoms/signs of blepharitis. Other causes include plucking/rubbing (may be unilateral or bilateral), alopecia areata, and discoid lupus (scarring madarosis). Sometimes no cause is found. Treat the cause if possible.

Vitiligo can affect the eyelids. There is usually a family history. Associated with other autoimmune disease (e.g. thyroid disease) and Vogt–Koyanagi–Harada syndrome (a rare disorder of ocular depigmentation associated with chorioretinal disease, anterior uveitis ± tinnitus and meningism).

In-turning of the eyelids due to degenerative changes or secondary to scarring. Most commonly affects the lower lid. ↑ with age (rare <40y). The eyelashes rub on the cornea and irritate the eye. Taping the lower lid to the cheek can give temporary relief. If left untreated, can cause corneal vascularization, ulceration, and infection. Refer for rapid surgical correction.

Turning out of the lower eyelid. Causes eye irritation and watering. Most common in the elderly or those with facial nerve palsy ( p. 538). Refer for surgery.

From the Greek meaning ‘to fall’, ptosis describes drooping of the upper eyelid. When the normal eye is looking straight forwards, the margin of the upper lid is situated ~2mm above the pupil. Ask the patient to look downwards as far as possible and then upwards as far as possible. The lid margin should move >8mm. The lid margin moves <4mm in patients with severe ptosis. Treat the cause where possible. To determine the cause, look at the pupil:

Common eyelid infection. 2 forms:

Most common form of stye. Infection of a lash follicle or associated gland of Moll (sweat gland) or Zeis (sebum gland) usually by Staphylococcus aureus. Confined to the skin and always points outwards. Treat with hot compresses and oral or topical antibiotics (e.g. chloramphenicol ointment)

Abscess of a meibomian gland. Often causes less swelling than external stye. May point inwards onto the conjunctiva (seen as red patch with yellow centre before it bursts) or outwards through the skin. Treat in the same way as external stye with hot compresses and oral or topical antibiotics.

Non-infected swellings of the glands of Zeis/Moll. No treatment needed unless troublesome when refer.

Following an internal stye, the Meibomian gland may become blocked forming a cyst. Cysts may resolve spontaneously but often become infected (treat with topical antibiotics) and/or chronic. If recurrent infection or chronic cyst refer to ophthalmology for incision and curettage. Refer early if <7y as large cysts can affect refraction and generate amblyopia.

Benign skin tumour—which may form a horn-like lesion. Refer for excision/curettage.

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Chronic, low-grade, inflammation of meibomian glands and lid margins. Presents with long history of irritable, burning, dry, red eyes. Eyelids have red margins ± scales on the eyelashes (see Figure 26.7). On elevation of the upper lid, look for inflamed meibomian glands. Associated with dry eyes, internal stye ( p. 963), and ingrowing eyelashes.

Lid papilloma and warts can become inflamed and mimic blepharitis.

Prolonged treatment over 2–3mo with regular eye care 3x/wk is needed. Warn patients to persevere as there may be no improvement for up to 2wk:

After an initial treatment period, it is often necessary to continue to use warm compresses and lid scrubs from time to time to keep the lid scales under control. Treat dry eye symptoms with preservative-free tear supplements, e.g. Liquifilm Tears®.

Treat with topical antibiotics (place a 1cm strip of fucithalmic or chloramphenicol ointment onto a clean finger and rub it into the base of the eyelashes). Oral antibiotics (e.g. doxycycline 50mg od) for 3mo may be useful for patients not responding to lid care and topical antibiotics. Topical steroid drops or ointment may sometimes be useful but use only on specialist advice.

Tear secretion ↓ with age. Dry eyes cause eye irritation and redness which is often worse in centrally heated buildings. The eye feels gritty, vision is occasionally blurred, and there is reflex watering of the eye in severe cases. Commonly associated with blepharitis.

↓ tear production (e.g. age, Sjögren’s syndrome); ↑ evaporation of tears (e.g. exposure keratitis).

Longer acting drops, (e.g. Celluvisc®, Viscotears®) blur vision for a time. Short-acting drops (e.g. Liquifilm Tears®) only give relief for ~30min and may need very frequent application.

Due to overproduction of tears or outflow obstruction. Caused by corneal irritation (e.g. blepharitis, dry eyes, corneal abrasion, foreign body, conjunctivitis, entropion), iritis, acute glaucoma, ectropion, blocked tear duct.

Acute infection of the tear sac, can spread to surrounding tissues. Treat immediately with antibiotics, e.g. flucloxacillin. Abscess can form—if it does surgical drainage is required so refer.

Seen in the middle-aged and elderly. Presents with a watery eye which discharges mucus regularly. The eye does not look inflamed. Refer for syringing of the lacrimal system or surgery.

Think systematically about the structures within the eye to come to a differential diagnosis—see Table 26.2.

Inflammation of the conjunctiva is the most common eye problem seen in general practice (see Figure 26.8)—1 in 8 children have an episode of acute infective conjunctivitis every year. Presents with unlateral/bilateral red eye with surface irritation; eye discharge (clear, mucoid, or muco-purulent); sticking of the eyelids, especially on waking; no change in visual acuity. Examination may reveal enlarged papillae under the upper eyelid and/or pre-auricular lymph node enlargement.

Clinically difficult to distinguish—doctors get it right only ~50% of the time. Both present with acute red eye—usually starting in one eye and often spreading to involve both, together with watery/purulent discharge. The eyes are often crusted ± stuck together on waking. Visual acuity is not impaired. Both may occur in association with viral URTI.

Bilateral symptoms appear seasonally (e.g. hay fever) or on contact with an allergen (e.g. animal fur). Presents with red, watery, itchy eyes ± photophobia ± family/personal history of atopy. Signs: follicles in the lower tarsal conjunctiva and ‘cobblestones’ under the upper lid.

Treat with topical or systemic antihistamines (e.g. sodium cromoglicate, nedocromil, or olopatadine eye drops). Avoid topical steroids due to long-term complications (cataract, glaucoma, fungal infection). Consider cold compress and washout with cold water during acute exacerbations. Refer if symptoms are persistent despite treatment, or if vision is affected.

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Spontaneous painless localized haemorrhage under the conjunctiva (see Figure 26.9). Common in the elderly. Looks alarming but generally painless (may cause some aching of the eye). Clears spontaneously in 1–2wk but may recur. Associations: ↑ BP, clotting disorders, leukaemia, ↑ venous pressure. Check BP. If severe/recurrent, check FBC and clotting screen.

Consider referral if follows trauma—especially if the posterior edge of the haemorrhage cannot be seen (may be associated with orbital haematoma, penetrating injury, or orbital fracture).

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Common (see Figure 26.10). Found particularly in people who work outdoors in hot, dusty climates. Creamy coloured raised triangular plaque on the conjunctiva on either side of the cornea—nasal side > temporal side. No need to treat unless encroaching over the pupil and causing visual loss → refer for surgical excision—recurrence is possible. Differential diagnosis is carcinoma in situ—if any atypical features, refer for excision biopsy.

Growth of blood vessels onto the cornea. Occurs in patients with severe lid disease, rosacea, or due to excessive contact lens wear. If a contact lens wearer, advise to remove contact lenses for at least 2mo. Refer to ophthalmology for specialist management to prevent long-term damage.

Presents with a very painful eye, blurred vision, photophobia, and profuse watering. On examination there is ↓ visual acuity, circumcorneal injection (blood vessel dilatation concentrated around the limbus), conjunctivitis (particularly the quadrant most associated with the injury/infection) ± a creamy white, disc-shaped lesion on the central or inferior cornea. The pupil may be small due to reflex miosis. Corneal ulcers stain green with fluorescein—use a bright light with a blue filter to see them.

Bacterial—2° to trauma, foreign body, dry eyes, entropion, blepharitis; viral—herpes simplex, herpes zoster, or adenovirus; fungal; protozoal—history of foreign travel/contact lens wear; non-infective, e.g. 2° to autoimmune disease or trauma.

Treatment depends on cause. Delay in treatment may result in loss of sight so refer for same-day ophthalmology assessment.

HSV keratitis is common and can be recurrent in the same eye with the virus lying dormant within the trigeminal nerve between attacks. Presents with acute keratitis or keratoconjunctivitis. Occasionally may present as an irritable eye with little discomfort. Examination and fluorescein staining reveal a characteristic corneal ulcer with a delicate branching pattern (dendritic ulcer). Refer for urgent (same-day) ophthalmology opinion. Treatment is with 3% aciclovir ointment 5x/d continued for 3d after healing.

Zoster in the ophthalmic branch of the oculomotor (3rd) nerve. Pain, tingling, or numbness around the eye precedes a blistering rash and inflammation. In 50% the eye is affected with conjunctivitis, scleritis, episcleritis, keratitis, iritis, visual loss, and/or oculomotor nerve palsy. Nose tip involvement makes eye involvement likely (nerve supply is the same as the globe). Prescribe oral aciclovir (800mg 5x/d) and refer immediately. The cornea may become anaesthetic/scarred and require grafting.

The episclera is the thin layer of vascular tissue overlying the sclera. Episcleritis is unilateral in two-thirds of cases. It presents with diffuse inflammation of the eye with minimal tenderness and no discharge. Try treatment with an NSAID (e.g. ibuprofen 400mg tds or ketorolac 0.5% eye drops qds). If NSAID is ineffective, refer to ophthalmology for consideration of treatment with steroids.

Inflammation of the sclera. Can be unilateral or bilateral. ♀ > ♂. Peak age: 40–60y. Affects the anterior or posterior segment and may be diffuse, nodular, or necrotizing. Presents with painful, red eye. Vision may be blurred due to corneal, iris, or posterior segment involvement, and visual acuity ↓. The eye is tender to touch and may have a deep purple hue. Look for scleral nodules. There may be accompanying uveitis and keratitis.

In ~50%, associated with systemic illness, e.g. herpes zoster, rheumatoid arthritis, systemic lupus erythematosus, polyarteritis nodosa, Wegener’s granulomatosis, trauma, infection, or surgery.

Refer urgently to ophthalmology. Treated with steroids. Complications include cataract, glaucoma, and retinal detachment.

Most common in young/middle-aged adults. Acute onset of pain, photo-phobia, blurred vision and ↓ visual acuity, watering, circumcorneal redness, small or irregular pupil ± keratitic precipitates on the posterior surface of the cornea ± hypopyon (anterior chamber pus, causing a white ‘fluid level’ line). Pain ↑ as eyes converge and pupils constrict. May be secondary to corneal graft rejection or eye infections, e.g. toxoplasmosis, herpes virus keratitis. In 30% associated with seronegative arthropathies, e.g. ankylosing spondylitis.

Refer urgently to ophthalmology. Complications include posterior synechiae (irregular pupil shape), glaucoma, and cataract. Relapses are common.

Not all patients who have a visual field loss are aware of it. If you suspect visual field loss, refer to a community optometrist or ophthalmology for formal field testing. Causes: see Figure 26.11.

Is defined as inability to perform any work for which eyesight is essential (not the total absence of sight). In practice this means <3/60 vision (may be >3/60 if patient has severe visual field defect, e.g. glaucoma). 157,000 people are registered blind in England.

Does not have a standard definition but usually implies vision in the range 3/60—6/60; 155,000 people are registered partially sighted in England.

Worldwide, cataract, glaucoma, and chlamydial infection causing trachoma are common causes.

Voluntary in England. Refer patients for low vision assessment. Application is made by a consultant ophthalmologist to social services.

Many patients benefit from links with national support organizations that provide information, and active local organizations who support the blind and partially sighted with drivers and guides.

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Inherited as a sex-linked characteristic. ♂:♀ ≈20:1. The Ishihara test consists of series of cards with a number in coloured dots against a contrasting background of more coloured dots. Coloured dots are paired to detect different patterns of colour blindness. Lack of red/green discrimination is most common. Colour blindness prohibits certain types of employment (e.g. airline pilot).

Occurs later in life. Red is the most common colour affected. May be an early sign of an optic nerve disorder. Patients complain of colour looking ‘washed out’ (desaturated) in one eye compared to the other—refer.

Incidence ↑ with age. More common than arterial occlusion. Presents with:

Refer as an emergency to ophthalmology. Laser treatment may prevent neovascular glaucoma and vitreous haemorrhage due to retinal neovascularization. Macular oedema may be helped by intraocular steroids or intraocular anti-vascular endothelial growth factor medication (e.g. bevacizumab or ranibizumab).

Usually due to thromboembolism. Sudden visual loss in one eye (counting fingers or light perception) and afferent pupil defect. The retina appears white ± cherry red spot at the macula. A retinal embolus may be visible. Exclude temporal arteritis ( p. 524).

Refer as an emergency to ophthalmology. There is no reliable treatment. Optic atrophy and blindness is the usual outcome. Treat any risk factors for atherosclerosis or embolism, i.e. ↑ BP, hyperlipidaemia, smoking, DM, carotid/cardiac disease.

Presents with sudden ↓ in vision, loss of red reflex, and difficulty visualizing the retina. Risk factors: DM with new vessel formation, bleeding disorders, retinal tear/detachment, central retinal vein occlusion, trauma, head injury, tumour. Refer urgently to ophthalmology. Treatment is with vitrectomy and repair of retinal damage with laser- or cryotherapy.

Affects 1:7,000 people each year. Presents with:

Refer urgently for treatment to secure the retina.

Small dark spots in the visual field usually caused by opacities in the vitreous. Floaters continue to move when the eye comes to rest. Risk factors: myopia, cataract operation, trauma. Usually harmless and may settle with time but patients may benefit from vitrectomy if floaters are interfering with vision (e.g. preventing reading).

Disc swelling due to inflammation or demyelination. Presents with rapid visual loss (hours to days) and ↓ colour vision (red desaturation); discomfort on eye movements; temporary worsening of symptoms when hot; optic disc swelling. Refer urgently to ophthalmology for confirmation of diagnosis. Steroids may help in severe cases. Visual loss usually stabilizes after week 2 and recovers over 6wk.

Multiple sclerosis (1:4 patients with MS present with optic neuritis— p. 568); DM; viral infections, e.g. influenza, measles, chickenpox; familial, e.g. Leber’s disease.

Occurs when the short ciliary arteries are damaged. 2 forms:

Central vision drops suddenly and irreversibly. Examination reveals a complete or altitudinal visual field defect. The disc appears swollen and pale ± haemorrhages. May be accompanied by symptoms of the underlying condition (e.g. temporal arteritis— p. 524).

Refer as an ophthalmology emergency. Treatment depends on cause.

Most common cause of blindness in the UK—2% of people >65y old are blind in one or both eyes due to AMD. Always a bilateral disease but one eye is usually more severely affected than the other. Risk factors: ↑ age, +ve family history, smoking, ↑ BP.

Difficult to detect in primary care. Signs are often minimal. Symptoms:

All patients start with this form of AMD. Caused by atrophy of the neuroretina. The cells of the macula break down, resulting in drusen formation (yellowish lipid deposits). As number/size of drusen ↑, central vision ↓.

Accounts for 50% of blindness due to AMD. In some patients with dry AMD, drusen lifts the retinal pigment epithelium away from its blood supply. New blood vessels grow from the choroid and may bleed forming scars → irreversible loss of central vision.

If progressive loss of vision, refer to ophthalmology for confirmation of diagnosis—urgently if recent onset or rapid ↓ in vision. For those with dry AMD and loss of vision, treatment with AREDS2 food supplement (containing omega-3 fatty acids, antioxidants, and zinc) ↓ progression by 25%^R. Treatment of other coexisting conditions (e.g. cataract and glaucoma) can also help. Provision of visual aids, registration of blindness and social support are important.

Is a monoclonal antibody to the vascular growth factor that stimulates new vessel growth. It is approved as an effective treatment by NICE for the treatment of patients with active wet AMD and visual symptoms. It is only administered in secondary care settings. Injections are given into the eye 1x/mo for 3mo with further injections thereafter, titrated against disease activation. Ranibizumab and bevacizumab are alternatives.

Typically occurs in hypermetropic middle-aged patients. Vision is blurred and distorted particularly for reading. The cause is a serous leakage of fluid from abnormal choroidal vessels. The condition is generally self-limiting but can be bilateral and chronic. Refer to ophthalmology for photodynamic therapy.

Typically ♀ in mid-60s. Presents with gradual central visual loss/distortion and colour loss. If it occurs in the non-dominant eye, the patient may be relatively asymptomatic. Refer to ophthalmology. Vision takes 4–12mo to recover following treatment.

Several inherited retinal diseases (e.g. Best’s disease; Stargardt’s macular dystrophy; Bull’s eye maculopathy) present with progressive loss of central vision either in early adulthood or aged 40–60y. Ask if there is a history of visual loss in a family.

Familial disorder resulting in retinal degeneration. Usually first noticed in adolescence and progresses to blindness. 2 forms exist—the autosomal dominant form is more common than the autosomal recessive form and milder.

Presents with distortion and blurred central vision, particularly for near vision. Associated with previous peripheral vascular disease, retinal detachment/break, branch retinal vein occlusion, uveitis, trauma, or tumour. Refer to ophthalmology for vitrectomy and membrane peel.

Signs: gradual visual loss; pale optic disc. Causes: glaucoma, MS, ischaemia (e.g. retinal artery occlusion), retinal damage (choroiditis, retinitis pigmentosa), toxic (tobacco amblyopia, methanol, arsenic, quinine). Refer for confirmation of diagnosis to ophthalmology or neurology.

(e.g. meningioma, glioma, abscess, arteriovenous malformation). Can cause visual field defects—type depends on the site of the lesion— p. 971

Most common tumour affecting the eye. Usually detected during routine examination by an optometrist. Other presentations include gradual central visual loss and/or retinal detachment. Can affect the iris, ciliary body, or choroids. Refer for urgent ophthalmology opinion.

Metastasis to the eye can occur from tumours of the breast, lung, or kidney. Appear as pale elevations of the choroid. Symptoms are variable but include visual loss and retinal detachment. Refer urgently for confirmation of diagnosis.

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Common. Affects ~2% of all >40y olds. Accounts for ~1:4 ophthalmology outpatient appointments and 10% of new blindness registrations.

Steroid use (systemic or topical in or close to the eye) can cause ↑ intraocular pressure.

May be detected during routine optometrist examination or through routine screening for diabetics or patients with family history. Otherwise patients present late as glaucoma is asymptomatic and visual acuity is preserved until visual fields are severely impaired. Signs: optic nerve damage (glaucomatous disc cupping), visual field loss (sausage-shaped blind spots), and ↑ intraocular pressure.

Advise all patients >40y to have regular optometry check-ups. Those with a family history of glaucoma should have biannual checks of their intraocular pressures (tonometry) and annual visual field checks at an optician from 40y of age. Refer patients with ↑ pressures, or in whom you notice (or are doubtful about) disc cupping to ophthalmology for assessment. Patients with ↑ intraocular pressure must be followed up life-long. Aim is to ↓ intraocular pressure to slow disease progression (even with ‘normal’ pressures).

Trabeculectomy is considered when the ‘target’ intraocular pressure is not met with medical treatment (especially in patients <50y). Side effects: failure, worsening cataract.

Uncommon. Affects 0.1% of patients >40y—typically elderly, long-sighted women with early cataract. Closed-angle glaucoma may present in one of 3 ways:

Vision ↓; cornea looks hazy (due to oedema); pupil is fixed and dilated (often slightly oval in shape with long axis vertical); circumcorneal redness; eyeball feels hard (due to ↑ pressure); poor fundal view ± cataract.

Refer acute or subacute glaucoma as an emergency to ophthalmology. Specialist treatment is with miosis to open drainage channels (e.g. pilocarpine 4% drops) and acetazolamide ± apraclonidine and/or latanoprost drops to ↓ aqueous production. Surgery or laser treatment (peripheral iridotomy) to allow free aqueous circulation is undertaken once intraocular pressure has been ↓. Patient may need prophylactic surgery on the contralateral eye to prevent AACG in that eye too. AACG may damage the trabecular meshwork and patients are at risk of developing chronic glaucoma following an attack. Regular check-ups are necessary.

May occur in patients with diabetic retinopathy, central or branch retinal vein obstruction, or ocular ischaemia. Blood vessels grow across the iris and the iridiocorneal angle, preventing fluid drainage. Pressures can be very high (40–70mmHg) and the patient may suffer pain from corneal oedema. Treatment is surgical and, in severe cases, if the eye is blind, it is removed.

Lens opacity is found in 75% >65y olds. Most do not need treatment.

Unilateral cataract may not be noticed by the patient—but loss of binocular vision affects judgement of distance.

A shadow in the red reflex/absent red reflex; difficulty visualizing the fundus.

Check fasting blood glucose to exclude DM. Advise patients to have their visual acuity checked regularly. Refer to ophthalmology if ↓ sight (or any other symptom) interferes with social functioning, driving, or independence.

Removal of the natural lens ± posterior chamber lens implantation. Usually done as a day case procedure under LA. Healing takes 2–6wk depending on the technique used. 75–95% without other ocular pathology have 6/12 vision or better 3mo post-op. Patients require testing for new spectacles 6wk post-op to allow refractive changes to settle.

Look through the patient’s glasses:

Poor vision in the absence of ocular or visual pathway disorder. Squint, ptosis, cataract, unequal refractive errors, or astigmatism can cause the image from one eye to be disregarded. If this persists >7–8y of age, it becomes irreversible. Treatment is with glasses ± patching, and squint surgery if necessary.

Most common refractive error. Common in infants and lessens with age. Distant objects focus behind the retina. Ciliary muscle contraction (to make the lens more convex) is needed to focus the image. This can lead to convergent squint, eye tiredness, and headache. Convex lenses are used for correction.

Distant objects focus in front of the retina. There is often a +ve FH. Concave lenses are used to correct the defect. Contact lenses may be necessary in high myopia (>–8 diopters). Myopia is unusual <6y old and tends to worsen until the late teens. Regular (6-monthly) eye checks are needed to ensure correct lenses are prescribed. In adults increasing myopia can indicate developing cataracts. High myopia (8–20 diopters) predisposes to retinal detachment—these patients should have an annual eye examination (more frequent if floaters).

Curvature across the cornea or lens differs in the vertical/horizontal planes. Objects are distorted longitudinally or vertically. Lenses can be used to correct this defect.

Age-related loss of accommodation. The lens becomes less easy to deform from 45–65y. Focussing on close objects (accommodation) is more difficult and glasses may be needed for near-work (e.g. reading).

Increasingly being undertaken as an alternative to spectacles. LASIK (Laser Assisted In Situ Keratomileusis) is a combination of surgery and laser therapy. It can be used for higher degrees of refractive error and astigmatism. Complications are rare.

Abnormality of coordinated eye movement; 3% of children have a congenital squint. Due to an imbalance in the muscles of the eye; there is full range of eye movement in both eyes and no double vision. Note the light reflexes from different parts of the cornea—they should be symmetrical. If not, there is a squint. Squint may be convergent (esotropia) or divergent (exotropia). Esotropia (see Figure 26.13) is most common and often associated with long-sightedness.

Family history of squint, high refractive errors, neurological disease (e.g. cerebral palsy), cataract, Down’s syndrome, Turner’s syndrome, retinoblastoma, optic atrophy, craniofacial anomalies, retinal disease.

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Refer to ophthalmology. Without treatment, children with squint risk developing amblyopia, failure of binocular vision, and long-term visual problems. Visual maturity occurs at 7–8y. Eye patching, correction of refractive errors (spectacles), and realignment surgery can improve sight up to this age.

Caused by damage to the extraocular muscles or the nerves supplying them. Usually acquired and caused by cranial nerve palsy. Results in diplopia—maximal when looking in the direction requiring the action of the paralysed muscle. The image from the eye that is not moving correctly is peripheral to the image from the normal eye. Refer for urgent neurology/ophthalmology opinion^N. Once sinister causes have been excluded, management involves treatment of the underlying condition ± patching and/or prism spectacles ± surgery.

Inability to perform coordinated movements of the 2 eyes together in the same direction. In all cases, refer to neurology—treatment depends on cause (see Table 26.3).

20% are worn because they are more suitable for the eye condition than spectacles, 80% for cosmetic/convenience reasons. Some are worn just to change eye colour. Contact lenses are used in high myopia or hypermetropia, presbyopia, and after cataract removal because thick spectacle lenses cause visual field distortion. They are also useful when the cornea has been damaged, e.g. after ulceration or trauma and in keratoconus (a rare corneal degenerative disease).

Hard, gas-permeable (larger hard lenses are designed to allow air to reach the cornea), and soft lenses are available. Some soft lenses are ‘daily disposable’ or ‘monthly disposable’. Hard and gas-permeable lenses can correct for minor astigmatism; normal soft lenses cannot as the lens is too flexible. A high astigmatism requires spectacles or a special (toric) soft lens (delicate and needs careful cleaning). Patients with poor tear secretion do not tolerate contact lenses well.

Careful cleaning of the lenses and contact lens container is vital—particular solutions are used for each type of lens, and these should not be interchanged. Contact lenses can be stained by fluorescein or rifampicin—ask before prescribing.

Many eye complaints can be treated with topical medication.

(e.g. tropicamide, cyclopentolate) dilate the pupil and cause cycloplegia thus causing blurred vision. They are used to dilate the pupil for examination and to prevent adhesions to the lens in iritis. They can precipitate acute closed-angle glaucoma in susceptible patients.

(e.g. pilocarpine) constrict the pupil and ↑ aqueous drainage. They are used in glaucoma. They can cause systemic side effects, e.g. sweating, ↑ BP, pulmonary oedema.

(e.g. oxybuprocaine, proxymetacaine) can help examination of painful eyes and foreign body removal. Protect the eye with an eye pad until the anaesthetic has worn off to prevent corneal damage (corneal reflex is suppressed).

are used in scleritis, episcleritis, iritis. Prescribe only after slit lamp examination and on the advice of an ophthalmologist. Can cause severe eye damage if used when a dendritic ulcer is present. Long-term use may cause glaucoma, thinning of the cornea/sclera and may facilitate fungal infection.

(e.g. timolol, betaxolol) are used in glaucoma. Beware of systemic side effects—bronchospasm, bradycardia.

(e.g. brimonidine) are used in glaucoma. May cause dry mouth, headache, fatigue.

(e.g. latanoprost, bimatoprost) used in glaucoma. May cause lash growth and ocular inflammation.