Ординатура / Офтальмология / Английские материалы / Oxford American Handbook of Ophthalmology_Tsai, Denniston, Murray_2011

436 CHAPTER 13 Medical retina

Vigabatrin

This anticonvulsant is used in the treatment of complex partial seizures and certain other types of epilepsy. In around a third of cases, visual field defects may be noted.

Clinical features

•Usually asymptomatic with good central VA.

•May develop optic atrophy.

•Bilateral visual field defects: generalized constriction or binasal; generally static once established, with no improvement on withdrawal of treatment.

•Normal retinal appearance.

Prevention and screening

Table 13.12 Summary of recommendations

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TOXIC RETINOPATHIES (2) 437

Toxic retinopathies (2)

Thioridazine

This phenothiazine is used second line in the treatment of schizophrenia. Doses of >1 g/day for just a few weeks may result in retinopathy.

Clinical features

•Asymptomatic, scotomas (paracentral or ring), dVA, nyctalopia, brownish visual discoloration.

•Pigmentary disturbance at the posterior pole; geographic areas of chorioretinal atrophy.

Prevention

Current prescribing practice (maintenance <300 mg/day) should not lead to retinopathy.

Chlorpromazine

This phenothiazine is used in schizophrenia and other psychoses. Doses of >2 g/day for a year may result in retinopathy.

Clinical features

Prevention

Current prescribing practice (<300 mg/day) should not lead to retinopathy.

Tamoxifen

This estrogen antagonist is used in the treatment of breast cancer. Doses of >180 mg/day for a year may result in retinopathy.

Clinical features

•Asymptomatic or mild dVA.

•Crystalline maculopathy with fine white refractile deposits in the inner retina centered around the fovea.

•Associated features include vortex keratopathy and optic neuritis.

Prevention

Current prescribing practice (<40 mg/day) rarely leads to retinopathy.

Deferoxamine

This chelating agent is commonly used to treat overload of iron (e.g., after multiple transfusions in chronic anemias such as thalassemia) and aluminium (e.g., dialysis patients). There appears to be no “safe” dose; retinopathy occurred in one instance after a single administration.

438 CHAPTER 13 Medical retina

Clinical features

•dVA, nyctalopia, abnormal color vision, scotomas (usually central/ centrocecal).

•Central and peripheral pigmentary disturbance.

Didanosine

This nucleoside analog antiretroviral is used in the treatment of HIV infection. It is a reverse transcriptase inhibitor commonly used as a part of the ART regimen. In children it has occasionally been observed to cause a retinopathy.

Clinical features

•Asymptomatic or mild peripheral field loss.

•Peripheral well-defined areas of retinal/RPE atrophy.

Clofazimine

This antimycobacterial is used in the treatment of leprosy and AIDSrelated Mycobacterium avium infection.

Clinical features

•Unusually extensive bull’s-eye maculopathy with irregular pigment and atrophy extending beyond the arcades.

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RETINAL VEIN OCCLUSION (1) 439

Retinal vein occlusion (1)

Retinal vein occlusions are common, can occur at almost any age, and range in severity from asymptomatic to the painful, blind eye. They are divided into branch, hemior central retinal vein occlusions (equating to occlusion anterior or posterior to the cribriform plate), and ischemic or nonischemic types.

Most occlusions occur in those over age 65, but up to 15% may affect patients under 45. BRVO is three times more common than CRVO.

Central retinal vein occlusion (CRVO)

Although the division of nonischemic from ischemic CRVO is an arbitrary cutoff based on disc area of nonperfusion determined by FA findings, it is a useful predictor of visual outcome and risk of neovascularization. The clinical picture also differs.

Clinical features

Nonischemic

•Painless dVA (mild to moderate), metamorphopsia.

•Dilated, tortuous retinal veins with retinal hemorrhages in all four quadrants; occasional cotton-wool spots (CWS); mild optic disc edema.

•Complications: CME.

Investigations

For all patients

•BP, CBC, ESR, glucose, lipids, protein electrophoresis, TFT, and ECG. Further investigation is directed by clinical indication and may include CRP, serum ACE, anticardiolipin, lupus anticoagulant, autoantibodies (RF, ANA, anti-DNA, ANCA), fasting homocysteine, CXR, and thrombophilia screen (e.g., proteins C and S, antithrombin, factor V Leiden).

FA

•Nonischemic: vein wall staining, microaneurysms, dilated optic disc capillaries.

•Ischemic: as for nonischemic but capillary closure (5–10 disc areas is borderline; >10 is significantly ischemic), hypofluorescence (blockage due to extensive hemorrhage), leakage (CME, NV).

440 CHAPTER 13 Medical retina

Fig. 13.10 Central retinal vein occlusion with extensive nerve fiber layer and intraretinal hemorrhage with associated diffuse retinal and optic nerve edema. See insert for color version.

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Treatment

There is no proven treatment. The following are common practice (see also Table 13.13):

•dIOP: if elevated (in either eye).

•Panretinal photocoagulation for neovascularization or high risk.

•Intravitreal triamcinolone acetonide or intravitreal dexamethasone implant for treatment of CME.

•Intravitreal bevacizumab and ranibizumab for treatment of CME and neovascularization.

•Pars plana vitrectomy and endolaser for vitreous hemorrhage secondary to neovascularization.

•Treat underlying medical conditions (Table 13.14): coordinate care with a PCP.

Prognosis

•Nonischemic: recovery to normal VA is <10%.

•Nonischemic: progression to ischemic is 15% by 4 months, 34% by 3 years.

•Ischemic: progression to rubeosis is 37% by 4 months. Highest risk is with VA <20/200 or 30 disc areas of nonperfusion on FA.

•Risk of CRVO in contralateral eye is 7% by 2 years.

442 CHAPTER 13 Medical retina

Retinal vein occlusion (2)

Branch retinal vein occlusion (BRVO)

Clinical features

•May be asymptomatic; dVA, metamorphopsia, visual field defect (usually altitudinal).

•Acute: retinal hemorrhages (dot, blot, flame), CWS, edema in the distribution of a dilated, tortuous vein; superotemporal arcade most commonly affected; usually arise from an arteriovenous (AV) crossing.

•Chronic: venous sheathing, exudates, pigment disturbance, collateral vessels.

•Complications: CME, neovascularization (NVE > NVD > NVI), recurrent vitreous hemorrhage.

Investigations

Hypertension is the most common association with BRVO. BRVO may be investigated similarly to CRVO (see Treatment, p. 440).

Prognosis

•Recovery to 20/40: 50%.

•Risk of macular edema: 57% (for temporal BRVO).

•Risk of retinal neovascularization: 20%, usually within the first 6–12 months.

Hemispheric BVO

In around 20% eyes, the central retinal vein forms posterior to the lamina cribrosa from superior and inferior divisions. These are generally regarded as a variant of CRVO. Ischemic hemispheric vein occlusions have an intermediate risk of rubeosis (compared to ischemic BRVO and CRVO) but a greater risk of NVD than either ischemic BRVO or CRVO. Treatment (in particular the role of laser) is as for BRVO.

Table 13.15 Summary of recommendations for management of BRVO

RETINAL ARTERY OCCLUSION (1) 445

Treatment

Treat affected eye (if within 24 hours of presentation).

•dIOP with 500 mg IV acetazolamide, ocular massage ± AC paracentesis (all common practice, but no proven benefit); ocular massage. Selective ophthalmic artery catheterization with thrombolysis is performed in some centers.

Protect other eye, e.g., treat underlying GCA with systemic steroids immediately (p. 524).

Prognosis

Visual outcome: 94% of cases are CF or worse at presentation; about 1/3 show some improvement (with or without treatment).

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