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Occurs in young patients with abrupt elevations of blood pressure, which may occur in
Can be a surrogate marker for current and future nonocular end-organ damage
In chronic hypertension
Retinal arterioles become more tortuous and narrow and develop abnormal light reflexes ("silver-wiring" and "copper-wiring")
There is increased venous compression at the retinal arteriovenous crossings ("arteriovenous nicking"), an important factor predisposing to branch retinal vein occlusions
Flame-shaped hemorrhages occur in the nerve fiber layer of the retina
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Detected by nonmydriatic fundus photography
Acute elevations of blood pressure
Result in loss of autoregulation in the retinal circulation, leading to the breakdown of endothelial integrity and occlusion of precapillary arterioles and capillaries that manifest as cotton-wool spots, retinal hemorrhages, retinal edema, and retinal exudates, often in a stellate appearance at the macula
Vasoconstriction and ischemia in the choroid result in exudative retinal detachments and retinal pigment epithelial infarcts
These infarcts later develop into pigmented lesions that may be focal, linear, or wedge-shaped
The abnormalities in the choroidal circulation may also affect the optic nerve head, producing ischemic optic neuropathy with optic disk swelling
Fundal abnormalities
Are the hallmark of hypertensive crisis with retinopathy
Require emergency treatment
If marked, are likely to be associated with permanent retinal, choroidal, or optic nerve damage
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Control of blood pressure with antihypertensive medications (see Hypertension, Chronic) is key
However, precipitous reduction of blood pressure may exacerbate retinal, choroidal or optic nerve damage