Ординатура / Офтальмология / Английские материалы / Ophthalmology A Short Textbook_Lang_2000

12.2 Examination Methods 313

Electroretinogram (ERG).

Fig. 12.12

a Retinal potentials are recorded with a corneal contact lens electrode and skin electrode.

b Normal electroretinogram.

potential to dark-adapted potential (Arden ratio) is obtained to evaluate the eye; this ratio is normally greater than 1.8. The ratio will be decreased in the presence of abnormal changes.

The typical indication for an electro-oculogram is macular vitelliform dystrophy (Best’s vitelliform dystrophy) with a significantly decreased Arden ratio.

Visual evoked potential (VEP): This examination is used to diagnose damage along the visual pathway. The VEP is not a specific examination of the retina such as an electroretinogram or electro-oculogram. This method is briefly discussed in Chapter 13, Optic Nerve.

12.3 Vascular Disorders 315

(Table 12.1) is based on the classification of the Diabetic Retinopathy Study. A distinction is made between nonproliferative stages (1. mild, 2. moderate, 3. severe; Fig. 12.14) and proliferative stages (1. non-high-risk 2. high-risk; Fig. 12.15–12.17).

Table 12.1 Changes in diabetic retinopathy

Moderate nonproliferative diabetic retinopathy.

Fig. 12.14 Microaneurysms, intraretinal hemorrhages, hard exudates (arrow), and cot- ton-wool spots (arrowheads).

316 12 Retina

Proliferative diabetic retinopathy.

Fig. 12.15

a Preretinal neovascularization (arrows) is a typical sign.

b Corresponding angiographic image. Fluorescein dye leakage is seen in the neovascularized area (arrows).

Symptoms: Diabetic retinopathy remains asymptomatic for a long time. Only in the late stages with macular involvement or vitreous hemorrhage will the patient notice visual impairment or suddenly go blind.

Diagnostic considerations: Diabetic retinopathy and its various stages (see Table 12.1) are diagnosed by stereoscopic examination of the fundus with the pupil dilated. Ophthalmoscopy and evaluation of stereoscopic fundus photographs represent the gold standard. Fluorescein angiography is used to determine if laser treatment is indicated. The presence of rubeosis iridis is confirmed or excluded in slit-lamp examination with a mobile pupil, i.e., without the use of a mydriatic, and by gonioscopy of the angle of the anterior chamber.

12.3 Vascular Disorders 317

High-risk proliferative diabetic retinopathy.

Fig. 12.16 The clearly visible vitreous hemorrhage seen here (arrow) is a typical sign of this stage of diabetic retinopathy. The patient will only notice deterioration of vision in this later stage.

Differential diagnosis: A differential diagnosis must exclude other vascular retinal diseases, primarily hypertonic changes of the fundus (this is done by excluding the underlying disorder).

Treatment: Clinically significant macular edema, i.e., macular edema that threatens vision, is managed with focal laser treatment at the posterior pole. Proliferative diabetic retinopathy is treated with scatter photocoagulation performed in three to five sessions.

Prophylaxis: Failure to perform regular ophthalmologic screening examinations in patients with diabetes mellitus is a negligent omission that exposes patients to the risk of blindness. Therefore, all type II diabetics should undergo ophthalmologic examination upon diagnosis of the disorder, and type I diabetics should undergo ophthalmologic examination within five years of the diagnosis. Thereafter, diabetic patients should undergo ophthalmologic examination once a year, or more often if diabetic retinopathy is present. Pregnant patients should be examined once every trimester.

Clinical course and prognosis: Optimum control of blood glucose can prevent or delay retinopathy. However, diabetic retinopathy can occur despite optimum therapy. Rubeosis iridis (neovascularization in the iris) in proliferative diabetic retinopathy is tantamount to loss of the eye as rubeosis iridis is a relentless and irreversible process.

The risk of blindness due to diabetic retinopathy can be reduced by optimum control of blood glucose, regular ophthalmologic examination, and timely therapy, but it cannot be completely eliminated.

318 12 Retina

Proliferative diabetic retinopathy before and after laser treatment.

Fig. 12.17

a Proliferative diabetic retinopathy with clinically significant macular edema before laser therapy.

b Findings after successful laser treatment (laser burns appear whitish brown).

12.3.2Retinal Vein Occlusion

Definition

Vein occlusion occurs as a result of circulatory dysfunction in the central vein or one of its branches.

Epidemiology: Retinal vein occlusion is the second most frequent vascular retinal disorder after diabetic retinopathy. The most frequent underlying systemic disorders are arterial hypertension and diabetes mellitus; the most frequent underlying ocular disorder is glaucoma.

12.3 Vascular Disorders 319

Frequent underlying systemic disorders of retinal vein occlusion include arterial hypertension and diabetes mellitus. Frequent underlying ocular disorders include glaucoma and retinal vasculitis.

Etiology: Occlusion of the central vein of the retina or its branches is frequently due to local thrombosis at sites where sclerotic arteries compress the veins. In central retinal vein occlusion, the thrombus lies at the level of the lamina cribrosa; in branch retinal vein occlusion, it is frequently at an arteriovenous crossing.

Symptoms: Patients only notice a loss of visual acuity if the macula or optic disk are involved.

Diagnostic considerations and findings: Central retinal vein occlusion can be diagnosed where linear or punctiform hemorrhages are seen to occur in all four quadrants of the retina (Fig. 12.18a). Often one will find distended and increasingly meandering veins. In branch retinal vein occlusion, intraretinal hemorrhages will occur in the area of vascular supply; this bleeding may occur in only one quadrant (Fig. 12.18b) or in two quadrants (hemispheric vein occlusion). Cotton-wool spots and retinal or optic-disk edema may also be present (simultaneous retinal and optic-disk edema is also possible). Chronic occlusions may also be accompanied by lipid deposits. One differentiates between non-ischemic and ischemic occlusion depending on the extent of capillary occlusion. Ischemic occlusion is diagnosed with the aid of fluorescein angiography.

Differential diagnosis: Other forms of vascular retinal disease must be excluded, especially diabetic retinopathy. An internist should be consulted to verify or exclude the possible presence of an underlying disorder.

Treatment: In the acute stage of vein occlusion, hematocrit should be reduced to 35–38% by hemodilution. Laser treatment is performed in ischemic occlusion that progresses to neovascularization or rubeosis iridis. Focal laser treatment is performed in branch retinal vein occlusion with macular edema when visual acuity is reduced to 20/40 or less within three months of occlusion.

Prophylaxis: Early diagnosis and prompt treatment of underlying systemic and ocular disorders is important.

Clinical course and prognosis: Visual acuity improves in approximately onethird of all patients, remains unchanged in one-third, and worsens in onethird despite therapy. Complications include preretinal neovascularization, retinal detachment, and rubeosis iridis with angle closure glaucoma.

320 12 Retina

Retinal vein occlusion.

Fig. 12.18

a Central retinal vein occlusion: intraretinal hemorrhages are visible in every retinal quadrant.

b Occlusion of the two main inferior branches. Bleeding occurs only in the affected areas of the retina in branch retinal vein occlusion.

12.3.3Retinal Arterial Occlusion

Definition

Retinal infarction due to occlusion of an artery in the lamina cribrosa or a branch retinal artery occlusion.

Epidemiology: Retinal artery occlusions occur significantly less often than vein occlusions.

Etiology: Emboli (Table 12.2) are frequently the cause of retinal artery and branch retinal artery occlusions. Less frequent causes include inflammatory processes such as temporal arteritis (Horton’s arteritis).

Horton’s arteritis should be excluded where retinal artery occlusion is accompanied by headache.

Symptoms: In central retinal artery occlusion, the patient generally complains of sudden, painless unilateral blindness. In branch retinal artery occlusion, the patient will notice a loss of visual acuity or visual field defects.

Diagnostic considerations: The diagnosis is made by ophthalmoscopy. In the acute stage of central retinal artery occlusion, the retina appears grayish white due to edema of the layer of optic nerve fibers and is no longer transparent. Only the fovea centralis, which contains no nerve fibers, remains visible as a “cherry red spot” because the red of the choroid shows through at this site (Fig. 12.19a). The column of blood will be seen to be interrupted. Rarely one will observe an embolus. Patients with a cilioretinal artery (artery originating from the ciliary arteries instead of the central retinal artery) will exhibit normal perfusion in the area of vascular supply, and their loss of visual acuity will be less. Atrophy of the optic nerve will develop in the chronic stage of central retinal artery occlusion.

In the acute stage of central retinal artery occlusion, the fovea centralis appears as cherry red spot on ophthalmoscopy. There is not edema of the layer of optic nerve fibers in this area because the fovea contains no nerve fibers.

In branch retinal artery occlusion, a retinal edema will be found in the affected area of vascular supply (Fig. 12.19b). Perimetry (visual field testing) will reveal a total visual field defect in central retinal artery occlusion and a partial defect in branch occlusion.

Differential diagnosis: Lipid-storage diseases that can also create a cherry red spot such as Tay-Sachs disease, Niemann-Pick disease, or Gaucher’s disease should be excluded. These diseases can be clearly identified on the basis

322 12 Retina

Retinal artery occlusion.

Fig. 12.19

a Central retinal artery occlusion. The paper-thin vessels and extensive retinal edema in which the retina loses its transparency are typical signs. Only the fovea is spared, which appears as a cherry red spot.

b Branch retinal artery occlusion. Multiple emboli are visible in the affected arterial branches (arrows).

of their numerous additional symptoms and the fact that they afflict younger patients.

Treatment: Emergency treatment is often unsuccessful even when initiated immediately. Ocular massage, medications that reduce intraocular pressure, or paracentesis are applied in an attempt to drain the embolus in a peripheral retinal vessel. Calcium antagonists or hemodilution are applied in an attempt to improve vascular supply. Lysis therapy is no longer performed due to the poor prognosis (it is not able to prevent blindness) and the risk to vital tissue involved.

Prophylaxis: Excluding or initiating prompt therapy of predisposing underlying systemic disorders is crucial (see Table 12.2).