Clinical Features of Acute Retinal Necrosis

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Although numerous clinical findings have been described, none is pathog-nomonic for ARN. Keratic precipitates that usually appear as white, mutton fat deposits often occur during the onset of HSV or VZV ARN. In the chronic phase, white mutton fat-like precipitates may be replaced by pigmented precipitates (fig. 1). Although anterior granulomatous uveitis is ameliorated within 2 weeks, resolution of the prominent vitritis tends to be delayed compared to the anterior uveitis. The prominent vitreal inflammatory reaction and vitreous opacity usually resolve within 3 weeks, but a vitritis may recur 3-4 weeks later. Fibrotic changes of the vitreous decrease the mobility of vitreous gel, leading to the development of a posterior vitreous detachment which in turn produces vitreous traction on the peripheral retina, resulting in retinal detachment [20].

Development Vitreous Retina

During the acute phase of ARN, disk edema is a common finding with occasional disk hemorrhage. Optic neuritis may develop early, and ARN should be suspected if there are optic nerve changes even though typical retinal lesions are not seen. Hemorrhage or distension of the optic nerve may be important signs of viral infiltration via the optic nerve (fig. 2).

White-yellow retinal lesions in the peripheral retina enlarge concentrically in the early phase of ARN. Patchy granular lesions in the retina may fuse to form geographic lesions. In the early phase, the granular lesions in the peripheral retina mimic signs of circulatory blockage (fig. 2). If treated by antiviral therapy, the retinal lesions may become confluent and necrotic due to the immune-mediated attempt to clear the virus. With further progression of the immune reaction, an inflammatory occlusive vasculopathy may develop with arteriolar involvement. The retinal vascular lesion of ARN is an occlusive vas-culopathy with arteriolar involvement, and may be divided into an acute phase and a chronic phase. During the acute phase, retinal arteritis and periphlebitis occur with retinal hemorrhage. Fluorescein angiography shows diffuse fluores-cein leakage along the retinal artery and areas of early hypofluorescence consistent with ischemic changes. During the chronic phase, venous occlusions develop with severe visual loss. On average, two main arterial occlusions are seen, and ghost vessels occur in severe cases. Visual prognosis is poor when there are two or more ghost vessels.

Peripheral Retinal Lesions
Fig. 2. White-yellow retinal lesions in the peripheral retina and hemorrhage of the optic nerve. Laser surgery was performed posterior to the necrotic peripheral lesions to prevent retinal detachment.

The acute ocular inflammatory changes observed during the acute phase resolve over a period of several months. Vitreal infiltration is composed of fibroblasts and retinal pigment epithelial cells, and these infiltrations form vitreous membranes leading to retinal detachment. In the chronic phase, retinal detachment often occurs because of a giant retinal tear in the area between healthy posterior retina and necrotic peripheral retina. The necrotic retina is very thin, and rhegmatogenous retinal detachments develop because of the strong adhesion between the vitreous and necrotic retina.

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