Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Toxic Retinopathies

Chloroquine and hydroxychoroquine

Symptoms Blurred vision, abnormal colour vision and scotomas.

Signs

■Reversible : whorl-like corneal epithelial changes (verticillata) and abnormal foveal reflex.

■Irreversible : fine granular macula appearance (Fig. 10.55). ‘Bull’s-eye’ maculopathy is the only sign associated with impaired VA and central visual field disturbance.

History and examination Determine the dose and duration of treatment. Test near and distance acuity, macular function (Amsler grid), colour vision, and visual field. Use a red pin to detect central scotoma or colour desaturation. Examine the cornea on a slit lamp for verticillata and perform dilated fundoscopy.

Differential diagnosis

■Granular macular changes : age-related macular degeneration (AMD).

■‘Bull’s-eye’ maculopathy : retinal dystrophies such as cone dystrophy, Stargardt’s disease, and benign concentric annular macular dystrophy can usually by differentiated by drug and family history and electrodiagnostic testing. Consider also AMD, and lipofuscinosis (usually presents in childhood).

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Toxic retinopathies

Treatment Stop medication if toxicity develops.

Follow–up For routine screening in cases without macular damage, arrange the following follow up:

■Chloroquine : 6–12 months depending on local protocol.

■Hydroxychloroquine : toxicity is rare at normal doses not exceeding 6.5 mg/kg/day unless there is impaired renal/ hepatic function. Patients should be monitored yearly by a physician or optometrist who should enquire about visual symptoms, and recheck near and distance VA. Arrange ophthalmology review if a baseline assessment by the physician/optometrist is abnormal, or if the patient develops change in acuity or blurred vision (as assessed by reading chart) whilst on treatment.

Desferrioxamine (Deferoxamine)

Symptoms Decreased vision, scotomata, nyctalopia, photopsia, metamorphopsia, and hearing loss. Acute toxicity occurs typically 7–10 days post-i.v. infusion.

Signs May appear normal early in the course of the disease despite positive symptoms. Signs are usually bilateral, including irregular outer retina/RPE pigmentation, RPE hypopigmentation, and granularity (late phase). May involve just the macula or the entire retina. Disc swelling and optic atrophy are reported.

Investigations Arrange visual fields. Fluorescein angiography shows a variable mottled appearance with blocked fluorescence in the transit phase and late hyperfluorescence, even in the presence of a normal-appearing retina. Electroretinogram, electrooculogram, and visually evoked potential may all be affected.

Treatment Discontinue deferoxamine if possible.

Follow–up Visual recovery is possible over 3–4 months. Damage may be more common in the presence of an abnormal blood–retina barrier, e.g. diabetes.

Signs

■Thioridazine : the fundus may be normal initially, then develop fine to coarse pigmentary retinopathy, usually uniformly in the macula to midperipheral retina (Fig. 10.56). Late stages show nummular area of atrophy and severe diffuse outer retinal degeneration.

■Chlorpromazine : mild pigmentary retinal changes, cataract, and corneal deposits.

Differential diagnosis

■Late atrophy : gyrate atrophy, Bietti’s crystalline dystrophy, syphilis, and choroideremia.

■Pigmentary retinopathy : retinitis pigmentosa (p. 496).

Investigation Fluorescein angiography may be helpful in detecting mild RPE abnormalities. The electroretinogram is abnormal.

Treatment Discontinue medication but liaise with psychiatrists.

Follow–up If the thioridazine dosage exceeds 800 mg/day or chlorpromazine dosage exceeds 2400 mg/day, review 6 monthly, otherwise screening is not required.

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Optometry and general practice guidelines

Optometry and General

Practice Guidelines

General comments

The most urgent retinal referral is central retinal artery occlusion. It is sometimes possible to dislodge the embolus, but as the period of retinal ischaemia extends, the visual prognosis declines. Visual symptoms are often acute and severe, with patients classically describing a curtain coming over the vision. There may be a history of cardiovascular risk factors. Also consider retinal detachment (p. 556).

Any history of acutely blurred or distorted central vision is worrying. For example, the choroidal neovascularization (CNV) associated with ‘wet’ age-related macular degeneration (AMD) often produces distortion occurring over a few days, whereas atrophic ‘dry’ AMD typically has a more insidious onset. The former may require urgent treatment; the latter can be referred routinely.

Beware the absence of acute symptoms in those with good vision in the fellow eye; they may be unaware of monocular blurred vision. Conversely, many patients experience a chronic decline in monocular vision as an acute symptom, when for some reason the better eye is covered. A careful history may help.

are more likely to get sight-threatening AMD, and diabetics with poor glucose control are more likely to lose vision. Encourage near relatives to accompany patients referred to hospital with suspected inherited disease, e.g. retinitis pigmentosa.

The following guidelines for hospital referral urgency are not prescriptive, as clinical situation vary. In particular, macular disease with an uncertain diagnosis should be referred urgently.

Immediate

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Optometry and general practice guidelines

Indirect ophthalmoscopy

tears. It is sometimes necessary to gently indent directly on the ocular surface to view the retina at 3 and 9 o’clock.

8.Draw the findings. The image is inverted, so it is helpful to draw the disc and fovea then rotate the paper 180º, and draw as seen. Some surgeons use colour to show the attached (red) and detached (blue) retina (see Fig. 11.6).

Posterior Vitreous Detachment

Background Spontaneous posterior vitreous detachment (PVD) is extremely common, but PVD may also follow eye surgery, trauma, uveitis, or laser. In the majority of cases it causes no serious problem. In others it causes troublesome floaters or retinal tears that can lead to retinal detachment.

Symptoms Photopsia (flashes) commonly in the temporal field, and floaters. Vitreous haemorrhage may reduce VA.

Examination Maximally dilate both eyes. PVD can be difficult to detect but biomicroscopy may show a ‘Weiss ring’ of thickened vitreous cortex avulsed from the optic disc (Fig. 11.1). The space behind a PVD is usually optically clear, unlike the condensed vitreous. The detached vitreous face is sometimes visible without a lens, using a slit beam focused in the midvitreous cavity. This fine, crumpled membrane slopes away when viewed top to bottom, and swirls with eye movement. In eyes with no previous surgery check for Shafer’s sign. Using a bright, thin, slit beam focused into the anterior vitreous (no lens), ask the patient to look up-down-straight ahead. If fine, pigmented cells (tobacco dust) are visible the test is positive (Fig. 11.2).

Repeat looking left-right-straight ahead. The test may help exclude a break; only 8% of eyes with retinal breaks are Shafer negative. If positive, arrange urgent vitreoretinal review, even if no break is found.

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