Acute retinal necrosis overview: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
Acute [[retinal]] [[necrosis]] was first discovered in 1971 by Urayama A, Yamada N, Sasaki T. Acute [[retinal]] [[necrosis]] was first officially classified as bilateral acute [[retinal]] [[necrosis]] in 1978 by N.J. Young and A.C. Bird, applied to 4 cases of bilateral necrotizing [[retinitis]] that progressed to [[retinal detachment]] and [[phthisis]] despite [[corticosteroid]] and [[antibiotic]] therapy. In the 1980s, emergence of [[pathological]] and [[electron]] findings from analysis of [[vitrectomy]] and [[enucleation]] specimens led to the discovery of acute [[retinal]] [[necrosis]]' cause as members of the herpes virus family. The official diagnostic criteria for acute [[retinal]] [[necrosis]] was proposed by the American [[Uveitis]] Society in 1994. | |||
==Classification== | ==Classification== | ||
Acute retinal necrosis may be classified both by staging - Acute or Late - or by severity: Mild or Fulminant. | |||
==Pathophysiology== | ==Pathophysiology== | ||
The pathogenesis of Acute retinal necrosis is characterized by [[retinal]] [[inflammation]] due to ocular [[viral]] infection. Particles from [[Herpes simplex virus]] 1 (HSV-1), [[Herpes simplex virus]] 2 (HSV-2), and [[Varicella zoster]] virus (VZV) infiltrate the [[retina]] via various locations of [[epithelial]] penetration, including the skin, [[conjunctiva]], [[cornea]], and [[nasal cavity]]. Acute retinal necrosis develops from HSV-1, HSV-2, and VZV due to the viruses' unique ability to transmit and replicate in the [[Central Nervous System]] (CNS), as well as their ability to transport [[anterograde]] through the [[optic nerve]], establish [[virus latency|latency]], reactivate, and cause [[retinal]] [[inflammation]]. For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 [[antigens]] are correlated to genetic predisposition to ARN. For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 [[antigens]] are correlated to genetic predisposition to ARN. Acute retinal necrosis is associated with the following ocular conditions: [[Progressive outer retinal necrosis]], [[Uveitis]], [[Cytomegalovirus retinitis]], [[Toxoplasmic chorioretinitis]], and [[Endophthalmitis]]. | |||
==Causes== | ==Causes== | ||
Acute retinal necrosis is usually caused by reactivation of latent viruses: [[Herpes simplex virus]] 1 & 2, [[Varicella-zoster virus]], [[cytomegalovirus]], and [[Epstein-Barr virus]]. | |||
==Differentiating Acute retinal necrosis other Diseases== | ==Differentiating Acute retinal necrosis other Diseases== | ||
Acute retinal necrosis must be differentiated from other diseases that cause [[eye pain]], [[conjunctival infection]], [[photophobia]], and [[vision loss]]. | |||
==Epidemiology and Demographics== | ==Epidemiology and Demographics== | ||
Research in the United Kingdom resulted in an estimated incidence of approximately 6.3 per 100,000 individuals. Acute retinal necrosis (ARN) developed from [[Herpes simplex virus]] 1 and [[Varicella-zoster virus]] is most common among patients older than 50 years, while the incidence of HSV-2 caused ARN is highest in children and young adults between age 9 and 22 years. There is no racial or gender predisposition to Acute retinal necrosis. | |||
==Risk Factors== | ==Risk Factors== | ||
The primary risk factors for Acute retinal necrosis include [[Immunocompromise]] and immunosuppression from disease and prolonged corticosteroid use. Genetic predisposition for certain caucasian and Japanese populations heightens the possibility of developing Acute retinal necrosis. | |||
==Screening== | ==Screening== | ||
There is no established, diagnostic screening process for Acute retinal necrosis. | |||
==Natural History, Complications and Prognosis== | ==Natural History, Complications and Prognosis== | ||
Revision as of 14:01, 25 August 2016
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
Historical Perspective
Acute retinal necrosis was first discovered in 1971 by Urayama A, Yamada N, Sasaki T. Acute retinal necrosis was first officially classified as bilateral acute retinal necrosis in 1978 by N.J. Young and A.C. Bird, applied to 4 cases of bilateral necrotizing retinitis that progressed to retinal detachment and phthisis despite corticosteroid and antibiotic therapy. In the 1980s, emergence of pathological and electron findings from analysis of vitrectomy and enucleation specimens led to the discovery of acute retinal necrosis' cause as members of the herpes virus family. The official diagnostic criteria for acute retinal necrosis was proposed by the American Uveitis Society in 1994.
Classification
Acute retinal necrosis may be classified both by staging - Acute or Late - or by severity: Mild or Fulminant.
Pathophysiology
The pathogenesis of Acute retinal necrosis is characterized by retinal inflammation due to ocular viral infection. Particles from Herpes simplex virus 1 (HSV-1), Herpes simplex virus 2 (HSV-2), and Varicella zoster virus (VZV) infiltrate the retina via various locations of epithelial penetration, including the skin, conjunctiva, cornea, and nasal cavity. Acute retinal necrosis develops from HSV-1, HSV-2, and VZV due to the viruses' unique ability to transmit and replicate in the Central Nervous System (CNS), as well as their ability to transport anterograde through the optic nerve, establish latency, reactivate, and cause retinal inflammation. For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens are correlated to genetic predisposition to ARN. For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN. Acute retinal necrosis is associated with the following ocular conditions: Progressive outer retinal necrosis, Uveitis, Cytomegalovirus retinitis, Toxoplasmic chorioretinitis, and Endophthalmitis.
Causes
Acute retinal necrosis is usually caused by reactivation of latent viruses: Herpes simplex virus 1 & 2, Varicella-zoster virus, cytomegalovirus, and Epstein-Barr virus.
Differentiating Acute retinal necrosis other Diseases
Acute retinal necrosis must be differentiated from other diseases that cause eye pain, conjunctival infection, photophobia, and vision loss.
Epidemiology and Demographics
Research in the United Kingdom resulted in an estimated incidence of approximately 6.3 per 100,000 individuals. Acute retinal necrosis (ARN) developed from Herpes simplex virus 1 and Varicella-zoster virus is most common among patients older than 50 years, while the incidence of HSV-2 caused ARN is highest in children and young adults between age 9 and 22 years. There is no racial or gender predisposition to Acute retinal necrosis.
Risk Factors
The primary risk factors for Acute retinal necrosis include Immunocompromise and immunosuppression from disease and prolonged corticosteroid use. Genetic predisposition for certain caucasian and Japanese populations heightens the possibility of developing Acute retinal necrosis.
Screening
There is no established, diagnostic screening process for Acute retinal necrosis.