Chapter 029. Disorders of the Eye (Part 10)

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Central retinal artery occlusion combined with ischemic optic neuropathy in a 19-year-old woman with an elevated titer of anticardiolipin antibodies. Note the orange dot (rather than cherry red) corresponding to the fovea and the spared patch of retina just temporal to the optic disc. Figure 29-7 Hypertensive retinopathy with scattered flame (splinter) hemorrhages and cotton-wool spots (nerve fiber layer infarcts) in a patient with headache and a blood pressure of 234/120. Impending branch or central retinal vein occlusion can produce prolonged visual obscurations that resemble those described by patients with amaurosis fugax. The veins appear engorged and phlebitic, with numerous retinal hemorrhages...

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Chapter 029. Disorders of the Eye (Part 10) Central retinal artery occlusion combined with ischemic optic neuropathy in a 19-year-old woman with an elevated titer of anticardiolipin antibodies. Note the orange dot (rather than cherry red) corresponding to the fovea and the spared patch of retina just temporal to the optic disc. Figure 29-7
Hypertensive retinopathy with scattered flame (splinter) hemorrhages and cotton-wool spots (nerve fiber layer infarcts) in a patient with headache and a blood pressure of 234/120. Impending branch or central retinal vein occlusion can produce prolonged visual obscurations that resemble those described by patients with amaurosis fugax. The veins appear engorged and phlebitic, with numerous retinal hemorrhages (Fig. 29-8). In some patients, venous blood flow recovers spontaneously, while others evolve a frank obstruction with extensive retinal bleeding ("blood and thunder" appearance), infarction, and visual loss. Venous occlusion of the retina is often idiopathic, but hypertension, diabetes, and glaucoma are prominent risk factors. Polycythemia, thrombocythemia, or other factors leading to an underlying hypercoagulable state should be corrected; aspirin treatment may be beneficial. Figure 29-8
Central retinal vein occlusion can produce massive retinal hemorrhage ("blood and thunder"), ischemia, and vision loss Anterior Ischemic Optic Neuropathy (AION) This is caused by insufficient blood flow through the posterior ciliary arteries supplying the optic disc. It produces painless, monocular visual loss that is usually sudden, although some patients have progressive worsening. The optic disc appears swollen and surrounded by nerve fiber layer splinter hemorrhages (Fig. 29-9). AION is divided into two forms: arteritic and nonarteritic. The nonarteritic form of AION is most common. No specific cause can be identified, although diabetes and hypertension are frequent risk factors. No treatment is available. About 5% of patients, especially those over age 60, develop the arteritic form of AION in conjunction with giant cell (temporal) arteritis (Chap. 319). It is
urgent to recognize arteritic AION so that high doses of glucocorticoids can be instituted immediately to prevent blindness in the second eye. Symptoms of polymyalgia rheumatica may be present; the sedimentation rate and C-reactive protein level are usually elevated. In a patient with visual loss from suspected arteritic AION, temporal artery biopsy is mandatory to confirm the diagnosis. Glucocorticoids should be started immediately, without waiting for the biopsy to be completed. The diagnosis of arteritic AION is difficult to sustain in the face of a negative temporal artery biopsy, but such cases do occur rarely. Figure 29-9
Anterior ischemic optic neuropathy from temporal arteritis in a 78-year-old woman with pallid disc swelling, hemorrhage, visual loss, myalgia, and an erythrocyte sedimentation rate of 86 mm/h