Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Arrange panretinal photocoagulation for neovascularization. Consider macular grid laser for patients <50 years with macular oedema and no angiographic evidence of macular ischaemia. Hypertension predisposes to recurrence, so involve the patient’s general practitioner.

Alternative therapies Not proven but under review:

■Laser: chorioretinal anastomosis.

■Surgical : sheathotomy, radial optic neurotomy.

■Medical : haemodilution; tissue plasminogen activator; intravitreal steroids.

Follow–up Every 4 weeks for the first 3 months, then as clinically indicated. The Royal College of Ophthalmologists recommend follow-up for 2 years.

Recommended reading The Royal College of Ophthalmologists CRVO guidelines (contact details, p. 710).

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Branch retinal vein occlusion

Branch Retinal Vein Occlusion

Background Branch retinal vein occlusion (BRVO) occurs 2–3 times more commonly than central retinal vein occlusion (CRVO) but has similar risk factors. The main sequelae are macular oedema and vitreous haemorrhage from disc, and retinal new vessels. BRVO affecting the entire superior or inferior retina (hemicentral vein occlusion) has a higher risk of rubeosis and disc new vessels.

Symptoms Usually painless loss of vision in one eye but may be asymptomatic.

Signs Same as CRVO (see previous page) except for branch distribution (Fig. 10.37). Rubeosis is less common; macular oedema, disc and retinal new vessels, more so.

Classification

■Ischaemic : >5 disc areas of ischaemia on fluorescein angiography.

■Nonischaemic : <5 disc areas on angiography.

1.With macular oedema.

2.With macular ischaemia.

History and examination Similar to CRVO. Fully exclude systemic causes in patients with multiple BRVOs.

Investigations Same as for CRVO.

Treatment Arrange macular laser at 3 months (p. 434) if there is no macular ischaemia and VA remains <6/12 from oedema. Treat neovasculization with scatter retinal laser.

Follow–up The Royal College of Ophthalmologists’ (address, p. 710) recommend 3 monthly review for up to 2 years. Nonischaemic or treated BRVO may require less frequent review.

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Central retinal artery occlusion

Central Retinal Artery Occlusion

Background Most commonly caused by atheroma, but also heart and carotid emboli, severely raised IOP, arteritis, or rarely vasospasm (retinal migraine).

Symptoms Sudden, painless, unilateral, often severe visual loss.

Signs Acute changes include retinal opacification, whitening, and oedema; cherry-red spot at the macula; RAPD; intra-arteriolar blood column segmentation (box-carring); possible cilioretinal artery sparing. An example is shown on page 446. Disc pallor occurs later.

History and examination Ask about transient ischaemic attacks, cerebrovascular accidents, symptoms of giant cell arteritis, or amaurosis fugax (retinal emboli causing transient uniocular visual obscuration lasting a few minutes). Auscultate the carotids for bruits using the stethoscope bell, check heart

sounds for a valvular murmur, and radial pulse for atrial fibrillation. Look for intra-arteriolar calcific, cholesterol, or fibrinoplatelet emboli.

Differential diagnosis See the differential diagnosis of cherry-red spot at the macula (p. 446). Also consider giant cell arteritis, intraocular gentamicin toxicity, and acute ophthalmic artery occlusion.

Investigations Arrange BP; urgent ESR and CRP; blood sugar; FBC; lipids; ANA, rheumatoid factor, serum protein and haemoglobin electrophoresis; thrombophilia screen if suggested by history (p. 471); carotid artery Doppler; fluorescein angiogram and cardiac examination for embolic source. Investigations

other than basic blood tests may be best undertaken by a physician.

Treatment If symptoms suggest occlusion for <24 hours duration, attempt to dislodge an embolus by:

■Firm ocular massage through closed eyelids for 15 minutes.

■Stat crushed acetazolamide 500 mg p.o., G. iopidine, and G. beta blocker.

■Offer anterior chamber paracentesis but explain that results are variable. If performed, prescribe G. chloramphenicol q.d.s. one week.

Follow–up Review initially in 2–4 weeks. Examine for iris neovascularization. Perform or review investigations and liaise with relevant clinicians. Advise immediate ophthalmic review if visual obscuration occurs in either eye. Local policies for carotid endarterectomy vary and depend on the degree of carotid occlusion, so discuss with a vascular surgeon.

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Branch retinal artery occlusion

Branch Retinal Artery Occlusion

Symptoms Unilateral, painless, sudden, visual field loss.

Signs Retinal swelling similar to central retinal artery occlusion (CRAO, previous page), except for branch distribution (Fig. 10.38). Emboli may be present.

Classification

■Single episode.

■Multiple episodes: consider systemic disease and urgent medical review.

History, examination, investigations See CRAO, above. Cilioretinal occlusion may occur in the presence of central retinal vein occlusion and is commonly missed. Exclude giant cell arteritis.

Treatment No therapy is of proven value.

Follow–up Initiate medical follow-up as indicated by the investigations. Evaluate for recurrences or new disease in 3–6 months. About 80% of symptomatic cases achieve VA of 6/12 or better.

Hypertensive Retinopathy

Symptoms Usually asymptomatic, but may have visual loss if there is optic disc swelling or macular oedema.

Signs These include venous deflection and narrowing at arteriovenous crossings; arteriolar narrowing and sclerosis producing altered light reflex (so-called copper and silver wiring); cotton-wool spots; lipid exudates with a macular star if severe (Fig. 10.39); retinal haemorrhage; macular oedema; macroaneurysms; focal choroidal infarctions that can produce acute, yellow, RPE spots; vitreous haemorrhage; retinal vascular occlusions; neovascularization. Retinal detachment, and later hyperpigmentation (Elschnig’s spots) may occur in accelerated hypertension.

Classification

■Grade 0: normal.

■Grade 1: barely detectable arteriolar narrowing.

■Grade 2: obvious widespread plus focal arteriolar narrowing, ateriovenous crossing changes.

■Grade 3: retinal haemorrhages or exudates.

■Grade 4: disc swelling.

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Hypertensive retinopathy

History and examination Ask about known hypertension, diabetes, radiotherapy, or other systemic disease. Measure BP.

Differential diagnosis Consider diabetic retinopathy; collagen vascular disease; anaemia; retinal vein occlusion and radiation retinopathy.

Treatment Control of hypertension by a physician.

Follow–up Hypertensive retinopathy does not require regular ophthalmic review but concomitant disease may, e.g. retinal vein occlusion.

Macroaneurysm

Background An acquired dilation of the retinal arterioles, most common in late-middle-aged women. Associated with hypertension, embolic disease, and hyperlipidaemia.

Symptoms Blurred vision if the macula is involved.

Signs Arteriolar aneurysm, often with a large haemorrhage, exudation, and surrounding retinal oedema. Usually an isolated finding but bilateral in 10%.

Differential diagnosis Consider diabetic retinopathy; retinal telangiectasia; choroidal tumour; retinal capillary haemangioma; cavernous haemangioma; haemorrhagic agerelated macular degeneration.

Investigations Haemorrhage produces masking on fluorescein angiography but otherwise early arterial filling is often seen. Late staining of the aneurysm may occur. Dilated leaking capillaries sometimes surround the aneurysm (Fig. 10.40). ICG may show flow in cases with haemorrhagic masking on FFA. Check BP, lipids, and glucose.

Treatment Many macroaneurysms thrombose and spontaneously involute. Laser photocoagulation may help patients with severe or persistent macular leakage and flow confirmed on angiography, but the evidence is uncertain and there are risks. The laser technique is described on page 437.

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