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 29-7Hypertensive 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) Chapter 029. Disorders of the Eye (Part 10) Central retinal artery occlusion combined with ischemic opticneuropathy in a 19-year-old woman with an elevated titer of anticardiolipinantibodies. Note the orange dot (rather than cherry red) corresponding to the foveaand the spared patch of retina just temporal to the optic disc. Figure 29-7 Hypertensive retinopathy with scattered flame (splinter) hemorrhagesand cotton-wool spots (nerve fiber layer infarcts) in a patient with headache and ablood pressure of 234/120. Impending branch or central retinal vein occlusion can produce prolongedvisual obscurations that resemble those described by patients with amaurosisfugax. The veins appear engorged and phlebitic, with numerous retinalhemorrhages (Fig. 29-8). In some patients, venous blood flow recoversspontaneously, while others evolve a frank obstruction with extensive retinalbleeding (blood and thunder appearance), infarction, and visual loss. Venousocclusion of the retina is often idiopathic, but hypertension, diabetes, andglaucoma are prominent risk factors. Polycythemia, thrombocythemia, or otherfactors leading to an underlying hypercoagulable state should be corrected; aspirintreatment 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 ciliaryarteries supplying the optic disc. It produces painless, monocular visual loss that isusually sudden, although some patients have progressive worsening. The opticdisc appears swollen and surrounded by nerve fiber layer splinter hemorrhages(Fig. 29-9). AION is divided into two forms: arteritic and nonarteritic. Thenonarteritic form of AION is most common. No specific cause can be identified,although diabetes and hypertension are frequent risk factors. No treatment isavailable. About 5% of patients, especially those over age 60, develop the arteriticform of AION in conjunction with giant cell (temporal) arteritis (Chap. 319). It isurgent to recognize arteritic AION so that high doses of glucocorticoids can beinstituted immediately to prevent blindness in the second eye. Symptoms ofpolymyalgia rheumatica may be present; the sedimentation rate and C-reactiveprotein level are usually elevated. In a patient with visual loss from suspectedarteritic AION, temporal artery biopsy is mandatory to confirm the diagnosis.Glucocorticoids should be started immediately, without waiting for the biopsy tobe completed. The diagnosis of arteritic AION is difficult to sustain in the face ofa negative temporal artery biopsy, but such cases do occur rarely. Figure 29-9 Anterior ischemic optic neuropathy from temporal arteritis in a 78-year-oldwoman with pallid disc swelling, hemorrhage, visual loss, myalgia, and anerythrocyte sedimentation rate of 86 mm/h