Skip to main content. Log in via OpenAthens. Log in using your username and password For personal accounts OR managers of institutional accounts. Forgot your log in details? Register a new account? Forgot your user name or password? Search for this keyword. Am J Ophthalmol ; —8. Article Google Scholar. Varicella-zoster virus retinitis in patients with the acquired immunodeficiency syndrome. Vitreous sampling and viral genome detection for the diagnosis of viral retinitis in patients with AIDS.
J Med Virol ; 43 — Use of the polymerase chain reaction to analyse sequence variation in major neutralising epetope of glycoprotein B gp58 in clinical isolates of human cytomegalovirus. J Gen Virol ; 72 —9. Latent varicella-zoster viral DNA in the human trigeminal and thoracic ganglia. N Engl J Med ; — Rapid diagnosis of herpes simplex encephalitis by nested polymerase chain reaction of cerebrospinal fluid.
Lancet ; — Acute retinal necrosis in an immunosuppressed patient [letter]. Am J Ophthalmol ; 98 —7. Presumed varicella zoster retinitis in immunocompromised patients. Retina ; 7 :9— Chess J, Marcus DM. Zoster-related bilateral acute retinal necrosis syndrome as presenting sign in AIDS. Ann Ophthalmol ; 20 —8. A proposed mild type of acute retinal necrosis syndrome.
Chickenpox-associated acute retinal necrosis syndrome. Ophthalmology ; 98 —6. Recurrence of presumed Varicella-zoster retino-pathy in patients with acquired immunodeficiency syndrome. In: Handbook of Antibiotics. Bostom Little, Brown, Gnann JW Jr. An acute reactive inflammatory granulomatous response within the retinal and choroidal vasculature also plays a role in retinal ischemia, however this occlusive vasculitis is a more prominent feature of ARN than PORN.
A hallmark feature of PORN is the lack of intraocular inflammation. If present, it was found to be predominantly mild. This is likely a reflection of the severely immunocompromised state of affected patients. Original descriptions of the disease emphasized posterior pole involvement, with initial multifocal lesions throughout the posterior pole that progressed later to confluence, and involved the peripheral retina at late stages.
However, more recent reports show that deep necrosis can be present in any or multiple parts of the outer retina. These lesions can rapidly progress to full thickness as well as confluence without consistent directionality of spread.
Serous retinal detachments can occur secondary to fluid leakage from full thickness necrosis, often resolving with treatment leading to disease inactivity. Rhegmatogenous retinal detachments are also theorized to occur secondary to multi-level holes in the setting of full thickness necrosis. Diagnosis is made based on history and clinical exam findings. Imaging studies may be helpful in identifying extent of retinal involvement but are not essential to the diagnosis.
Patients classically have vague clinical complaints that may initially be out of proportion to clinical findings. On exam, large patches of discrete yellow-white retinal opacification consistent with necrosis of the deep retinal layers are identified. These lesions can be found either in the peripheral retina, posterior pole, or both. Multifocal lesions can progress rapidly to confluence without consistent direction of disease spread. The majority of patients have a quiet anterior chamber and absence of vitreous cell; if present, reaction is classically minimal.
Other clinical features include a retinal vasculopathy with vascular sheathing and occlusion and optic nerve abnormalities including hyperemia or edema. While the diagnosis of Progressive Outer Retinal Necrosis is made primarily by clinical history and exam findings, certain testing modalities may aid in the diagnosis if necessary. Fluorescein angiography FA findings can be variable. Active areas of necrosis demonstrate late staining, while inactive, atrophic regions display window defects.
Focal vascular occlusions may be evident on FA as well. Optical coherence tomography OCT is significant for not only outer retinal disorganization, consistent with necrosis of the outer layers, but also hyper-reflectivity of the inner layers as well. Cystoid spaces and foveal thickening can also be observed.
Fundus autofluorescence classically shows stippled areas of mixed hyper- and hypo- autofluorescence, indicative of adjacent "sick" RPE cells, accumulating lipofuscin hyper-autofluorescent and RPE and adjacent photoreceptor death hypo-autofluorescent. Blood work indicating immunocompromised state with decreased CD-4 count or otherwise low white blood cell count in instances of hematologic disease or pharmacologic immunosuppression may aid in the diagnosis.
Vitreous tap with viral PCR analysis is typically performed to isolate the pathogen. In cases of a younger patient or otherwise dry vitreous tap, an anterior chamber tap may yield positive results with greater facility. Differential diagnosis can be broad, general categories which include infectious, inflammatory, neoplastic.
Inflammatory: Sarcoidosis, Behcet's, other retinal vasculitides Neoplastic: intraocular lymphoma, leukemia, metastasis.
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