Acute retinal necrosis

Acute retinal necrosis: Description, Causes and Risk Factors: Abbreviation: ARN. The acute retinal necrosis first described in Japan in 1971, is characterized by panuveitis, vitritis, vaso-occlusive retinal arteritis, and necrotising retinitis. It is rapidly progressive and often has a devasting effect on vision due to retinal arteritis, retinal necrosis, and rhegmatogenous retinal detachment (RRD) and traction retinal detachment (TRD). According to researchers, the disease is bilateral in 36% of cases. The sexes are affected equally, and patients are usually well with no significant past medical or ocular history. In 50 to 75% of patients the retina becomes detached within three months of the onset of symptoms. In 76% the final visual acuity is less than 6/60 and visual prognosis may also be poor owing to macular edema and optic nerve damage secondary to vascular insufficiency. acute retinal necrosis Acute retinal necrosis may be a result of dormant herpes simplex virus 1 (HSV-1), herpes simplex virus 2 (HSV-2), or varicella-herpes zoster virus (VZV) viral reactivation in the retina. Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) have also been implicated as causative agents. The exact etiology of this reactivation is still elusive; however, an immunogenetic predisposition to the disease is likely. Since these early description about 60 cases have been reported in the literature, and as 65% have been unilateral acute retinal necrosis. The retinal necrosis that is characteristic of ARN can develop because of direct lytic viral infection, immune complex deposition producing inflammation with intraluminal obliteration, and a T-cell mediated attack on blood vessels. Inflammation and occlusion can similarly occur in choroidal blood vessels. Optic nerve dysfunction does not seem to occur secondary to the presence of virus particles or viral antigens; rather it appears that swollen vascular endothelial cells, thrombotic arteriolar occlusion, and infiltration by inflammatory cells may produce an optic neuropathy. The stages of the diseaes process have been defined as acute and late. The syndrome has an insidious onset with a mild anterior uveitis and slight reduction in visual acuity. There may be ocular pain and high intraocular pressure. A panuveitis follows. Rapid progression then ensues over a matter of days or weeks, during which time large areas of peripheral retina become white and necrotic, eventually coalescing to produce confluent peripheral retinal necrosis. A vaso-occlusive retinal vasculitis can be observed during this phase, which particularly affects the retinal arterioles. Vitreous turbidity is increased and retinal traction may begin at this stage. A swollen optic nerve head and arcuate neuroretinitis have been noted in the acute phase, but most reports describe a relative sparing of the posterior pole. The second eye, if affected, usually becomes involved within weeks or months. With evolution to the late phase the cloudy white, necrotic peripheral retinal areas regress, leaving sharply demarcated zones with mild pigmentary scarring and increased vitreous debris. Visual acuity may rapidly worsen at this stage because of occlusion of vessels supplying the optic nerve head and central retina. Fibrous organization of the vitreous may lead to tractional retinal detachment. Rhegmatogenous retinal detachment also occurs, the breaks usually being located at junctions between necrotic and normal retina. Surgery is technically difficult and even with good anatomical result. The final visual outcome may be poor because of optic atrophy, macular pucker, and macular edema. Symptoms: Early symptoms of ARN may be minimal and include redness, periorbital pain, photophobia, floaters, and blurred vision. Episcleritis or scleritis along with an anterior uveitis, which may be either granulomatous or stellate in appearance, occur early in the course of the disease. As the vitritis becomes worse, patients report increasing floaters and decreasing vision. Peripheral, full-thickness, multifocal patches of yellowish-white retinal infiltrates appear within 1 or 2 days following the onset of symptoms. The retinal lesions typically start in the mid-periphery, although occasionally they can be first seen in the posterior pole. Over the next several weeks, the yellow-white patches increase in number, enlarge, concentrically coalesce, and spread toward the posterior pole. The macula is usually spared, although its involvement does not preclude the diagnosis of ARN. Active vasculitis is another prime manifestation of ARN syndrome. The vasculitis is characterized by perivascular sheathing, limited hemorrhages, and obliteration of distal arterioles by thrombi. Occasionally, an obstruction can develop in more proximal vessels, even the central retinal artery; in this case, the visual prognosis for the patient is greatly reduced. There can be inflammatory-induced hypoperfusion in the choroidal vasculature that can be recognized by early hypofluorescence and late staining on fluorescein angiography. In contrast to other ocular vascular occlusive diseases, neovascularization of the retina or iris does not commonly occur. Disc edema is a common early finding; sometimes, it can be a nonspecific manifestation of ocular inflammation. The disc edema may also represent the development of an optic neuropathy and, if present, further lowers the potential for vision improvement. An optic neuropathy should be suspected in patients with an afferent pupillary defect and severe visual loss despite relatively little retinal pathology. Diagnosis: Acute retinal necrosis is a clinical diagnosis, and laboratory tests may not be conclusive.Viral titers may be helpful.For baseline, obtain the following: CBC (Complete blood count).
  • RFT (Renal function tests) or KFT (kidney function tests).
  • LFT (Liver function tests).
Imaging: Fluorescein angiography.
  • Ocular ultrasound.
  • CT scan may show optic nerve sheath enlargement.
  • MRI may demonstrate concurrent lesions of the optic tract and the lateral geniculate body, suggesting axonal spread.
Treatment: Acute retinal necrosis treatment consists of the following: Antiviral therapy, including intravenous acyclovir, oral valacyclovir, oral famciclovir, or intravitreal foscarnet, valacyclovir, or famciclovir.
  • Anti-inflammatory therapy.
  • Antithrombotic therapy.
  • Retinal detachment prophylaxis.
  • In severe ARN, early vitrectomy with laser demarcation of areas of retinal necrosis together with intravenous antiviral agents should be considered.
Current treatment trends vary widely, including single agents or combinations of oral, intravenous, and intravitreal agents. Differing strategies did not affect outcomes. The final visual acuity in ARN was generally poor. Retinal detachment was common and could neither be predicted nor prevented. Development of ARN in the unaffected fellow eye occurred rarely. Long-term oral antiviral treatment strategies varied with unclear relative efficacy. NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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