Sandbox:Acute retinal necrosis: Difference between revisions

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__NOTOC__
__NOTOC__
{{Acute retinal necrosis}}
{{SI}}
{{CMG}}; {{AE}} {{Faizan}}; {{LRO}}


'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''
==Overview==
'''Acute retinal necrosis''' is a type of [[retinitis]] which can be associated with viral infections.


{{CMG}}
It was first characterized in 1971.<ref name="titleeMedicine - Acute Retinal Necrosis : Article by Andrew A Dahl, MD">{{cite web |url=http://www.emedicine.com/oph/topic377.htm |title=eMedicine - Acute Retinal Necrosis : Article by Andrew A Dahl, MD |accessdate=2008-02-05 |work=| archiveurl= http://web.archive.org/web/20080216011141/http://www.emedicine.com/oph/topic377.htm| archivedate= 16 February 2008 <!--DASHBot-->| deadurl= no}}</ref><ref name ="Urayama">Urayama A, Yamada N, Sasaki T: Unilateral acute uveitis with retinal periarteritis and detachment. Jpn J Clin Ophthalmol 1971; 25: 607.</ref>


{{SK}}  
One study indicated an incidence of 1 per 1.6 to 2.0 million.<ref name="pmid17504853">{{cite journal |author=Muthiah MN, Michaelides M, Child CS, Mitchell SM |title=Acute retinal necrosis: a national population‐based study to assess the incidence, methods of diagnosis, treatment strategies and outcomes in the UK |journal=Br J Ophthalmol |volume=91 |issue=11 |pages=1452–5 |year=2007 |pmid=17504853 |doi=10.1136/bjo.2007.114884 |url=http://bjo.bmj.com/cgi/pmidlookup?view=long&pmid=17504853 |pmc=2095441}}</ref>


==[[Acute retinal necrosis overview|Overview]]==
==Historical Perspective==
*Acute [[retinal]] [[necrosis]] was first officially classified as bilateral acute [[retinal]] [[necrosis]] in 1978 by N.J. Young and A.C. Bird.<ref name="pmid708676">{{cite journal |vauthors=Young NJ, Bird AC |title=Bilateral acute retinal necrosis |journal=Br J Ophthalmol |volume=62 |issue=9 |pages=581–90 |year=1978 |pmid=708676 |pmc=1043304 |doi= |url=}}</ref>
**The classification was applied to 4 cases of bilateral necrotizing [[retinitis]], of which the patients developed bilateral confluent [[retinitis]] progressing to [[retinal detachment]] and [[phthisis]] despite [[corticosteroid]] and [[antibiotic]] therapy.<ref name="pmid24385671">{{cite journal |vauthors=Flaxel CJ, Yeh S, Lauer AK |title=Combination systemic and intravitreal antiviral therapy in the management of acute retinal necrosis syndrome (an American Ophthalmological Society thesis) |journal=Trans Am Ophthalmol Soc |volume=111 |issue= |pages=133–44 |year=2013 |pmid=24385671 |pmc=3868412 |doi= |url=}}</ref>
*The first extension of the classification of acute [[retinal]] [[necrosis]] to unilateral cases was given in 1983 by Hayasaka S. et al.<ref name="pmid6860612">{{cite journal |vauthors=Hayasaka S, Asano T, Yabata K, Ide A |title=Acute retinal necrosis |journal=Br J Ophthalmol |volume=67 |issue=7 |pages=455–60 |year=1983 |pmid=6860612 |pmc=1040094 |doi= |url=}}</ref>
**They identified that cases of bilateral acute [[retinal]] [[necrosis]] and cases of Kirisawa-type [[uveitis]] presented nearly identical characteristics:<ref name ="Urayama">Urayama A, Yamada N, Sasaki T: Unilateral acute uveitis with retinal periarteritis and detachment. Jpn J Clin Ophthalmol 1971; 25: 607.</ref><ref name="pmid708676">{{cite journal |vauthors=Young NJ, Bird AC |title=Bilateral acute retinal necrosis |journal=Br J Ophthalmol |volume=62 |issue=9 |pages=581–90 |year=1978 |pmid=708676 |pmc=1043304 |doi= |url=}}</ref>
***Periarteritis
***Opaque, dense [[vitreous]]
***Peripheral [[retinal]] [[exudates]]
***[[Retinal detachment]]
***[[Vision loss]]
***Resistance to [[antibiotic]] therapy
***Negative test results for [[bacterial]] infection
*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.


==[[Acute retinal necrosis historical perspective|Historical Perspective]]==
==Classification==
*Acute retinal necrosis (ARN) may be classified by staging and severity into the following:<ref name="pmid1645179">{{cite journal |vauthors=Gartry DS, Spalton DJ, Tilzey A, Hykin PG |title=Acute retinal necrosis syndrome |journal=Br J Ophthalmol |volume=75 |issue=5 |pages=292–7 |year=1991 |pmid=1645179 |pmc=1042358 |doi= |url=}}</ref>
**'''Acute stage''': Occurs at onset of disease and usually progresses past acute classification after a few weeks.
***Presents with coalescence of white, necrotic tissue in the peripheral retina.
***Vaso-[[occlusion|occlusive]] retinal [[vasculitis]] is usually present.
***The [[Optic nerve|optic nerve head]] of the affected eye will appear swollen, but the [[posterior pole]] will usually not be affected during the acute stage.
**'''Late stage''': Is the natural progression of the disease and will present differentiating characteristics after a few weeks up to a few months.
***Characterized by a regression of the coalesced [[necrosis]] in the peripheral [[retina]], presenting starkly contrasted [[necrotic]]/non-[[necrotic]] tissue and mild [[pigmentation]] [[scarring]] and increased [[vitreous]] debris
***[[Retinal detachment]], severe [[vision loss]], and potential [[blindness]] in the affected eye is indicative of late stage ARN.
***If the infection is bilateral, the second eye will usually present signs of ARN in the weeks and months following the initial symptom manifestation in the first eye.
*Acute retinal necrosis can also be classified by severity into the following:<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
**'''Mild''': Is used to characterize ARN that is stable and non-progressive.
***There is usually no sign of [[retinal detachment]].
**'''Fulminant''': ARN that is progressive and will usually lead to [[retinal detachment]] and further complications if untreated.


==[[Acute retinal necrosis classification|Classification]]==
==Pathophysiology==
===Pathogenesis===
*The pathogenesis of Acute retinal necrosis is characterized by [[retinal]] [[inflammation]] due to ocular [[viral]] infection:<ref name="pmid10682968">{{cite journal |vauthors=Ganatra JB, Chandler D, Santos C, Kuppermann B, Margolis TP |title=Viral causes of the acute retinal necrosis syndrome |journal=Am. J. Ophthalmol. |volume=129 |issue=2 |pages=166–72 |year=2000 |pmid=10682968 |doi= |url=}}</ref>
**Particles from [[Herpes simplex virus]] 1 (HSV-1), [[Herpes simplex virus]] 2 (HSV-2), and [[Varicella zoster]] virus (VZV) infiltrate the [[retina]] via various modes of transmission:<ref name="pmid22889540">{{cite journal |vauthors=Grose C |title=Acute retinal necrosis caused by herpes simplex virus type 2 in children: reactivation of an undiagnosed latent neonatal herpes infection |journal=Semin Pediatr Neurol |volume=19 |issue=3 |pages=115–8 |year=2012 |pmid=22889540 |pmc=3419358 |doi=10.1016/j.spen.2012.02.005 |url=}}</ref>
***[[Epithelial]] penetration of the skin: transmitted through the [[Ophthalmic nerve|ophthalmic]] branch of the [[Trigeminal nerve]].
***[[Epithelial]] penetration of the [[conjunctiva]]: transmitted directly through the [[optic nerve]].
***[[Epithelial]] penetration of the [[cornea]]: transmitted through the [[Maxillary|maxillary]] branch of the [[Trigeminal nerve]].
***[[Epithelial]] penetration of the [[nasal cavity]]: transmitted through the [[Olfactory nerve]] in the [[Subarachnoid space]].
**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]].<ref name ="HumanHerpes">{{cite book |last1=Whitley |first1=Richard |last2=Kimberlin |first2=David W. |last3=Prober |first3=Charles G. |date=2007 |title=Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis |url=http://www.ncbi.nlm.nih.gov/books/NBK47449/ |location=Cambridge, UK |publisher=Cambridge University Press |isbn=978-0511545313}}</ref>
***[[Retinal]] [[inflammation]] is caused by the up-regulated production of [[cytokines]].


==[[Acute retinal necrosis pathophysiology|Pathophysiology]]==
===Genetics===
*There is evidence of genetic predisposition to Acute retinal necrosis:
**For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 [[antigens]] are correlated to genetic predisposition to ARN.<ref name="pmid2801857">{{cite journal |vauthors=Holland GN, Cornell PJ, Park MS, Barbetti A, Yuge J, Kreiger AE, Kaplan HJ, Pepose JS, Heckenlively JR, Culbertson WW |title=An association between acute retinal necrosis syndrome and HLA-DQw7 and phenotype Bw62, DR4 |journal=Am. J. Ophthalmol. |volume=108 |issue=4 |pages=370–4 |year=1989 |pmid=2801857 |doi= |url=}}</ref>
**For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 [[antigens]] are correlated to genetic predisposition to ARN.<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
*Possession of the above [[antigens]] in their respective demographics are correlated to impaired immunity and increased predisposition to infection.


==[[Acute retinal necrosis causes|Causes]]==
===Associated Conditions===
*Acute retinal necrosis is associated with the following ocular conditions:
**[[Progressive outer retinal necrosis]]<ref name="pmid24926266">{{cite journal |vauthors=Coisy S, Ebran JM, Milea D |title=Progressive outer retinal necrosis and immunosuppressive therapy in myasthenia gravis |journal=Case Rep Ophthalmol |volume=5 |issue=1 |pages=132–7 |year=2014 |pmid=24926266 |pmc=4036147 |doi=10.1159/000362662 |url=}}</ref>
**[[Uveitis]]<ref name="urlFacts About Uveitis | National Eye Institute">{{cite web |url=https://nei.nih.gov/health/uveitis/uveitis |title=Facts About Uveitis &#124; National Eye Institute |format= |work= |accessdate=}}</ref>
**[[Cytomegalovirus retinitis]]<ref name="urlCMV retinitis: MedlinePlus Medical Encyclopedia">{{cite web |url=https://medlineplus.gov/ency/article/000665.htm |title=CMV retinitis: MedlinePlus Medical Encyclopedia |format= |work= |accessdate=}}</ref>
**[[Toxoplasmic chorioretinitis]]<ref name="pmid22116459">{{cite journal |vauthors=Davis JL |title=Diagnostic dilemmas in retinitis and endophthalmitis |journal=Eye (Lond) |volume=26 |issue=2 |pages=194–201 |year=2012 |pmid=22116459 |pmc=3272204 |doi=10.1038/eye.2011.299 |url=}}</ref>
**[[Endophthalmitis]]


==[[Differentiating Acute retinal necrosis from other diseases|Differentiating Acute retinal necrosis from other Diseases]]==
==Causes==
*Acute retinal necrosis (ARN) is usually caused by the reactivation of the following pathogenic [[viruses]] in the ''[[Herpesviridae]]'' family:<ref name="pmid24932179">{{cite journal |vauthors=Pikkel YY, Pikkel J |title=Acute retinal necrosis in childhood |journal=Case Rep Ophthalmol |volume=5 |issue=2 |pages=138–43 |year=2014 |pmid=24932179 |pmc=4049010 |doi=10.1159/000363130 |url=}}</ref>
**''[[Herpes simplex virus]]'' 1 (HSV-1)
**''[[Herpes simplex virus]]'' 2 (HSV-2)
**[[Varicella-zoster virus]] (VZV)
**Less commonly, ARN can be caused by [[Epstein-Barr virus]] and [[cytomegalovirus]].<ref name="pmid10682968">{{cite journal |vauthors=Ganatra JB, Chandler D, Santos C, Kuppermann B, Margolis TP |title=Viral causes of the acute retinal necrosis syndrome |journal=Am. J. Ophthalmol. |volume=129 |issue=2 |pages=166–72 |year=2000 |pmid=10682968 |doi= |url=}}</ref>
*[[Varicella-zoster virus|VZV]] and [[Herpes simplex virus|HSV-1]] are usually the causes of ARN in individuals older than 25 years.
**The majority of the ARN cases for individuals older than 50 years are caused by VZV and HSV-1.<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
*[[Herpes simplex virus|HSV-2]] is usually the cause of ARN in individuals younger than 25 years.


==[[Acute retinal necrosis epidemiology and demographics|Epidemiology and Demographics]]==
==Differentiating {{PAGENAME}} from Other Diseases==
*Acute retinal necrosis must be differentiated from other diseases that cause [[eye pain]], [[conjunctival infection]], [[photophobia]], and [[vision loss]]. Accurate and prompt diagnosis is critical to prevent [[blindness]] and complications.<ref name="pmid22116459">{{cite journal |vauthors=Davis JL |title=Diagnostic dilemmas in retinitis and endophthalmitis |journal=Eye (Lond) |volume=26 |issue=2 |pages=194–201 |year=2012 |pmid=22116459 |pmc=3272204 |doi=10.1038/eye.2011.299 |url=}}</ref><ref name="pmid3099921">{{cite journal| author=Dart JK| title=Eye disease at a community health centre. | journal=Br Med J (Clin Res Ed) | year= 1986 | volume= 293 | issue= 6560 | pages= 1477-80 | pmid=3099921 | doi= | pmc=1342247 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3099921  }} </ref><ref name="pmid10922425">{{cite journal| author=Leibowitz HM| title=The red eye. | journal=N Engl J Med | year= 2000 | volume= 343 | issue= 5 | pages= 345-51 | pmid=10922425 | doi=10.1056/NEJM200008033430507 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10922425  }} </ref><ref name=umichredeye>University of Michigan Eyes Have it (2009)http://kellogg.umich.edu/theeyeshaveit/red-eye/</ref>
**[[Progressive outer retinal necrosis]]<ref name="pmid24926266">{{cite journal |vauthors=Coisy S, Ebran JM, Milea D |title=Progressive outer retinal necrosis and immunosuppressive therapy in myasthenia gravis |journal=Case Rep Ophthalmol |volume=5 |issue=1 |pages=132–7 |year=2014 |pmid=24926266 |pmc=4036147 |doi=10.1159/000362662 |url=}}</ref>
**[[Uveitis]]<ref name="urlFacts About Uveitis | National Eye Institute">{{cite web |url=https://nei.nih.gov/health/uveitis/uveitis |title=Facts About Uveitis &#124; National Eye Institute |format= |work= |accessdate=}}</ref>
**[[Uveitis]]<ref name="urlFacts About Uveitis | National Eye Institute">{{cite web |url=https://nei.nih.gov/health/uveitis/uveitis |title=Facts About Uveitis &#124; National Eye Institute |format= |work= |accessdate=}}</ref>
**[[Endophthalmitis]]
**[[Toxoplasma chorioretinitis]]<ref name="pmid22116459">{{cite journal |vauthors=Davis JL |title=Diagnostic dilemmas in retinitis and endophthalmitis |journal=Eye (Lond) |volume=26 |issue=2 |pages=194–201 |year=2012 |pmid=22116459 |pmc=3272204 |doi=10.1038/eye.2011.299 |url=}}</ref>
**[[Cytomegalovirus retinitis]]<ref name="urlCMV retinitis: MedlinePlus Medical Encyclopedia">{{cite web |url=https://medlineplus.gov/ency/article/000665.htm |title=CMV retinitis: MedlinePlus Medical Encyclopedia |format= |work= |accessdate=}}</ref>
**[[Conjunctivitis]]
**[[Scleritis]]
**[[Corneal abrasion]]
**[[Glaucoma]]
**[[Corneal ulcer]]
**[[Retinal]] [[vasculitis]]<ref name="pmid20404987">{{cite journal |vauthors=Abu El-Asrar AM, Herbort CP, Tabbara KF |title=Differential diagnosis of retinal vasculitis |journal=Middle East Afr J Ophthalmol |volume=16 |issue=4 |pages=202–18 |year=2009 |pmid=20404987 |pmc=2855661 |doi=10.4103/0974-9233.58423 |url=}}</ref>
*Differentiating Acute retinal necrosis from other diseases is crucial due to varying etiologies of ocular diseases, particularly to ensure the best prognosis by applying the proper therapy.
**Acute [[papillitis]]<ref name="pmid20645925">{{cite journal |vauthors=Witmer MT, Pavan PR, Fouraker BD, Levy-Clarke GA |title=Acute retinal necrosis associated optic neuropathy |journal=Acta Ophthalmol |volume=89 |issue=7 |pages=599–607 |year=2011 |pmid=20645925 |doi=10.1111/j.1755-3768.2010.01911.x |url=}}</ref>


==[[Acute retinal necrosis risk factors|Risk Factors]]==
==Epidemiology and Demographics==
===Incidence===
*Research in the United Kingdom resulted in an estimated incidence of approximately 6.3 per 100,000 individuals.<ref name="pmid22281865">{{cite journal |vauthors=Cochrane TF, Silvestri G, McDowell C, Foot B, McAvoy CE |title=Acute retinal necrosis in the United Kingdom: results of a prospective surveillance study |journal=Eye (Lond) |volume=26 |issue=3 |pages=370–7; quiz 378 |year=2012 |pmid=22281865 |pmc=3298997 |doi=10.1038/eye.2011.338 |url=}}</ref>
**There is evidence that this incidence is underestimated due to biases in case adjudication and under-reporting of data.<ref name="pmid17504853">{{cite journal |vauthors=Muthiah MN, Michaelides M, Child CS, Mitchell SM |title=Acute retinal necrosis: a national population-based study to assess the incidence, methods of diagnosis, treatment strategies and outcomes in the UK |journal=Br J Ophthalmol |volume=91 |issue=11 |pages=1452–5 |year=2007 |pmid=17504853 |pmc=2095441 |doi=10.1136/bjo.2007.114884 |url=}}</ref>
*Worldwide, the increase of [[immunocompromised]] and aged populations in most countries evidences an increase in Acute retinal necrosis.


==[[Acute retinal necrosis screening|Screening]]==
===Age===
*Acute retinal necrosis (ARN) developed from [[Herpes simplex virus]] 1 and [[Varicella-zoster virus]] is most common among patients older than 50 years.<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
*[[Herpes simplex virus]] (HSV) 2 infection is more common among children and adolescents; the incidence of HSV-2 caused ARN is highest in children and young adults between age 9 and 22 years.


==[[Acute retinal necrosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==
===Gender===
*There is no gender predisposition to Acute retinal necrosis.
 
===Race===
*There is no racial predisposition to Acute retinal necrosis.
 
==Risk Factors==
*Risk factors for the development of Acute retinal necrosis (ARN) include the following:
**For caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens are correlated to genetic predisposition to ARN.<ref name="pmid2801857">{{cite journal |vauthors=Holland GN, Cornell PJ, Park MS, Barbetti A, Yuge J, Kreiger AE, Kaplan HJ, Pepose JS, Heckenlively JR, Culbertson WW |title=An association between acute retinal necrosis syndrome and HLA-DQw7 and phenotype Bw62, DR4 |journal=Am. J. Ophthalmol. |volume=108 |issue=4 |pages=370–4 |year=1989 |pmid=2801857 |doi= |url=}}</ref>
**For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
**Experiencing [[encephalitis]] from ''[[herpes simplex virus]]''<ref name="pmid18852442">{{cite journal |vauthors=Vandercam T, Hintzen RQ, de Boer JH, Van der Lelij A |title=Herpetic encephalitis is a risk factor for retinal necrosis |journal=Neurology |volume=71 |issue=16 |pages=1268–74 |year=2008 |pmid=18852442 |doi=10.1212/01.wnl.0000327615.99124.99 |url=}}</ref>
**[[Immunocompromise]] from prior or concurrent disease.<ref name="pmid1397473">{{cite journal |vauthors=Moutschen MP, Scheen AJ, Lefebvre PJ |title=Impaired immune responses in diabetes mellitus: analysis of the factors and mechanisms involved. Relevance to the increased susceptibility of diabetic patients to specific infections |journal=Diabete Metab |volume=18 |issue=3 |pages=187–201 |year=1992 |pmid=1397473 |doi= |url=}}</ref>
**Immunosuppresion from extended [[corticosteroid]] therapy.<ref name="pmid12714420">{{cite journal |vauthors=Yamamoto JH, Boletti DI, Nakashima Y, Hirata CE, Olivalves E, Shinzato MM, Okay TS, Santo RM, Duarte MI, Kalil J |title=Severe bilateral necrotising retinitis caused by Toxoplasma gondii in a patient with systemic lupus erythematosus and diabetes mellitus |journal=Br J Ophthalmol |volume=87 |issue=5 |pages=651–2 |year=2003 |pmid=12714420 |pmc=1771672 |doi= |url=}}</ref>
 
==Screening==
*There is no established, diagnostic screening process for Acute retinal necrosis.
 
==Natural History, Complications, and Prognosis==
===Natural History===
*Symptoms of Acute retinal necrosis (ARN) develop rapidly upon onset of pathogenic infection.<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
**Initial signs and symptoms include [[conjunctivitis]], [[vision loss]] and [[photophobia]], and [[eye pain]] and pressure.
*The natural progression of ARN depends on whether the case is mild or fulminant.
**Mild cases of ARN presents with white-yellow [[necrotic]] [[lesions]] that do not coalesce or lead to [[retinal detachment]]; the disease is [[self-limited]].<ref name="pmid2837090">{{cite journal |vauthors=Matsuo T, Nakayama T, Koyama T, Koyama M, Matsuo N |title=A proposed mild type of acute retinal necrosis syndrome |journal=Am. J. Ophthalmol. |volume=105 |issue=6 |pages=579–83 |year=1988 |pmid=2837090 |doi= |url=}}</ref>
**Fulminant cases of ARN will lead to progressive [[necrosis]] of [[retinal]] tissue, leading to pigmentation [[scarring]], [[vitreous]] debris, and [[retinal detachment]]
***There is a much greater chance of [[blindness]] in the affected eye.
*Without treatment, ARN will usually progress to Bilateral acute retinal necrosis (BARN) within weeks to a few months.<ref name="pmid1645179">{{cite journal |vauthors=Gartry DS, Spalton DJ, Tilzey A, Hykin PG |title=Acute retinal necrosis syndrome |journal=Br J Ophthalmol |volume=75 |issue=5 |pages=292–7 |year=1991 |pmid=1645179 |pmc=1042358 |doi= |url=}}</ref>
**There are exceptions in which the disease spread from the affected to the previously unaffected eye occurred up to 17 years later, due to reactivation of latent [[viral]] infection.<ref name="pmid21242577">{{cite journal |vauthors=Okunuki Y, Usui Y, Kezuka T, Takeuchi M, Goto H |title=Four cases of bilateral acute retinal necrosis with a long interval after the initial onset |journal=Br J Ophthalmol |volume=95 |issue=9 |pages=1251–4 |year=2011 |pmid=21242577 |doi=10.1136/bjo.2010.191288 |url=}}</ref>
 
===Complications===
*Complications resulting from Acute retinal necrosis occur due to [[retinal]] tissue damage and subsequent infection from the causative pathogen, including the following:<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref><ref name="pmid24385671">{{cite journal |vauthors=Flaxel CJ, Yeh S, Lauer AK |title=Combination systemic and intravitreal antiviral therapy in the management of acute retinal necrosis syndrome (an American Ophthalmological Society thesis) |journal=Trans Am Ophthalmol Soc |volume=111 |issue= |pages=133–44 |year=2013 |pmid=24385671 |pmc=3868412 |doi= |url=}}</ref>
**[[Retinal detachment]]
**[[Neurological]] conditions, such as [[encephalitis]]<ref name="pmid26622338">{{cite journal |vauthors=Liang ZG, Liu ZL, Sun XW, Tao ML, Yu GP |title=Viral encephalitis complicated by acute retinal necrosis syndrome: A case report |journal=Exp Ther Med |volume=10 |issue=2 |pages=465–467 |year=2015 |pmid=26622338 |pmc=4509005 |doi=10.3892/etm.2015.2557 |url=}}</ref> or [[meningitis]]
**[[Optic neuropathy]]
**Occlusive retinal vasculopathy
**Proliferative vitreoretinopathy<ref name="pmid16848208">{{cite journal |vauthors=Vukojević N, Popovic Suić S, Sikić J, Katusić D, Curković T, Sarić B, Jukić T |title=[Acute retinal necrosis] |journal=Acta Med Croatica |volume=60 |issue=2 |pages=145–8 |year=2006 |pmid=16848208 |doi= |url=}}</ref>
**[[Macular pucker]]<ref name="pmid1873262">{{cite journal |vauthors=McDonald HR, Lewis H, Kreiger AE, Sidikaro Y, Heckenlively J |title=Surgical management of retinal detachment associated with the acute retinal necrosis syndrome |journal=Br J Ophthalmol |volume=75 |issue=8 |pages=455–8 |year=1991 |pmid=1873262 |pmc=1042429 |doi= |url=}}</ref>
**[[Vitreous]] [[hemorrhage]]
**[[Neovascularization]]<ref name="pmid17184841">{{cite journal |vauthors=Lau CH, Missotten T, Salzmann J, Lightman SL |title=Acute retinal necrosis features, management, and outcomes |journal=Ophthalmology |volume=114 |issue=4 |pages=756–62 |year=2007 |pmid=17184841 |doi=10.1016/j.ophtha.2006.08.037 |url=}}</ref>
**[[Phthisis bulbi]]<ref name="pmid17184841">{{cite journal |vauthors=Lau CH, Missotten T, Salzmann J, Lightman SL |title=Acute retinal necrosis features, management, and outcomes |journal=Ophthalmology |volume=114 |issue=4 |pages=756–62 |year=2007 |pmid=17184841 |doi=10.1016/j.ophtha.2006.08.037 |url=}}</ref>
 
===Prognosis===
*Without treatment, the prognosis for Acute retinal necrosis (ARN) varies:<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
**Mild ARN: Usually self-limited and will resolve itself without treatment; risk of permanent [[vision loss]] is very low.
**Fulminant ARN: Will usually progress to complications such as [[progressive outer retinal necrosis]] and has a worse prognosis.
***[[Retinal detachment]] will usually occur without treatment, leading to permanent [[vision loss]].
***Spread of infection through the [[anterior]] chamber to the [[brain]] has particularly poor prognosis if [[encephalitis]] or [[meningitis]] develops.
*With treatment, the prognosis for ARN is good if the therapy is administered in the early stages and sustained until symptoms resolve.
**Uncommonly, prognosis can worsen if the patient is [[immunocompromised]] and experiences a subsequent infection due to vulnerability from prolonged topical [[corticosteroid]] use.


==Diagnosis==
==Diagnosis==
[[Acute retinal necrosis diagnostic criteria|Diagnostic Criteria]] | [[Acute retinal necrosis history and symptoms|History and Symptoms]] | [[Acute retinal necrosis physical examination|Physical Examination]] | [[Acute retinal necrosis laboratory findings|Laboratory Findings]] | [[Acute retinal necrosis electrocardiogram|Electrocardiogram]] | [[Acute retinal necrosis chest x ray|Chest X Ray]] | [[Acute retinal necrosis CT|CT]] | [[Acute retinal necrosis MRI|MRI]] | [[Acute retinal necrosis echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Acute retinal necrosis other imaging findings|Other Imaging Findings]] | [[Acute retinal necrosis other diagnostic studies|Other Diagnostic Studies]]
===Diagnostic Criteria===
The diagnosis of acute [[retinal]] [[necrosis]] is made when the following criteria are met:<ref name="pmid8172275">{{cite journal |vauthors=Holland GN |title=Standard diagnostic criteria for the acute retinal necrosis syndrome. Executive Committee of the American Uveitis Society |journal=Am. J. Ophthalmol. |volume=117 |issue=5 |pages=663–7 |year=1994 |pmid=8172275 |doi= |url=}}</ref>
*One or more discrete foci of peripheral [[retinal]] [[necrosis]], located outside of the major [[temporal]] [[vascular]] [[Arterial arcades|arcades]]
*Circumferential spread if [[Antiviral drug|antiviral therapy]] has not been administered
*[[Occlusion|Occlusive]] [[retinal]] vasculopathy
*A prominent [[vitreous]] or [[anterior chamber]] [[inflammation]]
*Rapid disease progression in the absence of therapy
 
===History===
Patient history of prior or concurrent diseases, particularly those associated with Acute retinal necrosis pathogens, or sources of [[immunocompromise]] should be considered in the diagnosis of Acute retinal necrosis:<ref name="pmid1397473">{{cite journal |vauthors=Moutschen MP, Scheen AJ, Lefebvre PJ |title=Impaired immune responses in diabetes mellitus: analysis of the factors and mechanisms involved. Relevance to the increased susceptibility of diabetic patients to specific infections |journal=Diabete Metab |volume=18 |issue=3 |pages=187–201 |year=1992 |pmid=1397473 |doi= |url=}}</ref>
*History of [[diabetes mellitus]]
*History of prolonged [[corticosteroid]] use<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
*History of [[Herpes simplex|genital or oral herpes infection]]
*History of [[Chickenpox|chickenpox]] or [[shingles]]
*History of [[Mononucleosis|mononucleosis]]
*History of [[HIV]] infection
 
===Symptoms===
Symptoms of Acute retinal necrosis include the following:<ref name="pmid17504853">{{cite journal |vauthors=Muthiah MN, Michaelides M, Child CS, Mitchell SM |title=Acute retinal necrosis: a national population-based study to assess the incidence, methods of diagnosis, treatment strategies and outcomes in the UK |journal=Br J Ophthalmol |volume=91 |issue=11 |pages=1452–5 |year=2007 |pmid=17504853 |pmc=2095441 |doi=10.1136/bjo.2007.114884 |url=}}</ref>
*[[Vision loss]]
**[[Blindness]] may be present in more severe cases
*[[Photophobia|Excessive sensitivity to light]]
*[[Ocular]] pain
*[[Flu]] symptoms
*[[Erythema|Redness]] of the affected eye
*[[Floaters]]<ref name="pmid24336545">{{cite journal |vauthors=Ford JR, Tsui E, Lahey T, Zegans ME |title=Question: Can you identify this condition? Acute retinal necrosis |journal=Can Fam Physician |volume=59 |issue=12 |pages=1307; 1308–10 |year=2013 |pmid=24336545 |pmc=3860929 |doi= |url=}}</ref>
*[[Flashes]]<ref name="urlAmerican Academy of Ophthalmology">{{cite web |url=http://www.aao.org/ |title=American Academy of Ophthalmology |format= |work= |accessdate=}}</ref>
 
===Physical Examination===
Physical examination for acute retinal necrosis is remarkable for the following:<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
*[[Erythema]] and [[hyperaemia]] of the [[retina]]<ref name="pmid17504853">{{cite journal |vauthors=Muthiah MN, Michaelides M, Child CS, Mitchell SM |title=Acute retinal necrosis: a national population-based study to assess the incidence, methods of diagnosis, treatment strategies and outcomes in the UK |journal=Br J Ophthalmol |volume=91 |issue=11 |pages=1452–5 |year=2007 |pmid=17504853 |pmc=2095441 |doi=10.1136/bjo.2007.114884 |url=}}</ref>
*White and yellow [[necrosis|necrotic]] [[lesions]] in the [[retina]]
**[[Pus|Purulent]] [[exudate]] can also be found in the periphery of the [[retina]]<ref name="pmid24385671">{{cite journal |vauthors=Flaxel CJ, Yeh S, Lauer AK |title=Combination systemic and intravitreal antiviral therapy in the management of acute retinal necrosis syndrome (an American Ophthalmological Society thesis) |journal=Trans Am Ophthalmol Soc |volume=111 |issue= |pages=133–44 |year=2013 |pmid=24385671 |pmc=3868412 |doi= |url=}}</ref>
**Opaque [[vitreous]] from the coalescence of [[necrotic]] [[tissue]]
*[[Anterior chamber]] [[inflammation]]
*[[Vitreous]] [[inflammation]]
*[[Scleritis]]
 
===Laboratory Findings===
Laboratory findings associated with Acute retinal necrosis are those used to determine the [[viral]] pathogen, obtained from [[aqueous humor]] or the [[vitreous]].<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
*Qualitative and Real-time [[Polymerase chain reaction]]<ref name="pmid25356955">{{cite journal |vauthors=Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D |title=Clinical manifestation of self-limiting acute retinal necrosis |journal=Med. Sci. Monit. |volume=20 |issue= |pages=2088–96 |year=2014 |pmid=25356955 |pmc=4226315 |doi=10.12659/MSM.890469 |url=}}</ref>
**PCR-tests for Acute retinal necrosis patients will produce [[genomic]] evidence of the causative [[virus]].
**It is the preferred test due to the 90% specificity in detecting [[Herpes simplex virus]] (HSV), [[Varicella-zoster virus]] (VZV), and [[Cytomegalovirus]] (CMV).
*Viral cultures may reveal positive results for HSV-1, HSV-2, VZV, or CMV.<ref name="pmid23052715">{{cite journal |vauthors=Silva RA, Berrocal AM, Moshfeghi DM, Blumenkranz MS, Sanislo S, Davis JL |title=Herpes simplex virus type 2 mediated acute retinal necrosis in a pediatric population: case series and review |journal=Graefes Arch. Clin. Exp. Ophthalmol. |volume=251 |issue=2 |pages=559–66 |year=2013 |pmid=23052715 |doi=10.1007/s00417-012-2164-8 |url=}}</ref>
*[[Immunoflourescence]] may reveal [[antibodies]] indicative of Acute retinal necrosis pathogens.<ref name="pmid18159535">{{cite journal |vauthors=Singh A, Preiksaitis J, Ferenczy A, Romanowski B |title=The laboratory diagnosis of herpes simplex virus infections |journal=Can J Infect Dis Med Microbiol |volume=16 |issue=2 |pages=92–8 |year=2005 |pmid=18159535 |pmc=2095011 |doi= |url=}}</ref>
*Detection of indicative [[antibodies]] via Goldmann-witmer coefficient.<ref name="pmid16458686">{{cite journal |vauthors=De Groot-Mijnes JD, Rothova A, Van Loon AM, Schuller M, Ten Dam-Van Loon NH, De Boer JH, Schuurman R, Weersink AJ |title=Polymerase chain reaction and Goldmann-Witmer coefficient analysis are complimentary for the diagnosis of infectious uveitis |journal=Am. J. Ophthalmol. |volume=141 |issue=2 |pages=313–8 |year=2006 |pmid=16458686 |doi=10.1016/j.ajo.2005.09.017 |url=}}</ref>
 
===Imaging Findings===
====Key CT Findings for Acute Retinal Necrosis====
CT imaging may reveal indicators of [[inflammation]] and infection by the causative pathogen for Acute retinal necrosis (ARN).<ref name="pmid15569737">{{cite journal |vauthors=Bert RJ, Samawareerwa R, Melhem ER |title=CNS MR and CT findings associated with a clinical presentation of herpetic acute retinal necrosis and herpetic retrobulbar optic neuritis: five HIV-infected and one non-infected patients |journal=AJNR Am J Neuroradiol |volume=25 |issue=10 |pages=1722–9 |year=2004 |pmid=15569737 |doi= |url=}}</ref>
*Hypoattenuation along the [[optic tract]] indicative of [[Varicella-zoster virus]] (VZV) infection.
*Hyperattenuation along the [[optic tract]], [[retina]], [[sclerae]], and [[lateral geniculate body]], indicating presence of lesions indicative of ARN.<ref name="pmid4026646">{{cite journal |vauthors=Sergott RC, Belmont JB, Savino PJ, Fischer DH, Bosley TM, Schatz NJ |title=Optic nerve involvement in the acute retinal necrosis syndrome |journal=Arch. Ophthalmol. |volume=103 |issue=8 |pages=1160–2 |year=1985 |pmid=4026646 |doi= |url=}}</ref>
*Infection-caused shrunken left globe.
 
====Key MRI Findings for Acute Retinal Necrosis====
MRI imaging may reveal the following indicators of Acute retinal necrosis:<ref name="pmid15569737">{{cite journal |vauthors=Bert RJ, Samawareerwa R, Melhem ER |title=CNS MR and CT findings associated with a clinical presentation of herpetic acute retinal necrosis and herpetic retrobulbar optic neuritis: five HIV-infected and one non-infected patients |journal=AJNR Am J Neuroradiol |volume=25 |issue=10 |pages=1722–9 |year=2004 |pmid=15569737 |doi= |url=}}</ref>
*Increased T2 signal intensity in the optic pathway: [[optic nerves]], [[optic chiasm]], [[lateral geniculate bodies]], [[optic radiations]], [[visual cortex]], [[midbrain]] structures, [[trigeminal nerves]], and [[meninges]].
**The increased intensity reveals lesions that may be indicative of [[Herpes simplex virus]] or [[Cytomegalovirus]] infection.
*[[Contrast-enhanced|Contrast enhanced CT]] T1-weighted images may reveal enhancement of [[optic nerve]], [[optic chiasm]], [[optic tracts]], [[optic radiation]], semilunar ganglion–Meckel cave, [[meninges]], and [[midbrain]].
 
====Electrocardiogram====
*There are no diagnostic electrocardiogram findings associated with Acute retinal necrosis.
 
====Chest X Ray====
*There are no diagnostic chest x ray findings associated with Acute retinal necrosis.
 
====Echocardiography or Ultrasound====
*There are no diagnositic echocardiography or ultrasound findings associated with Acute retinal necrosis.
 
====Other Imaging Findings====
=====Fundus Autoflourescence=====
Fundus Autoflourescence (FAF) is an imaging technique that examines [[flourophores]] in the [[neurosensory retina]] and the retinal pigment [[epithelium]], presenting with the following findings indicative of Acute retinal necrosis:<ref name="pmid7890502">{{cite journal |vauthors=Delori FC, Dorey CK, Staurenghi G, Arend O, Goger DG, Weiter JJ |title=In vivo fluorescence of the ocular fundus exhibits retinal pigment epithelium lipofuscin characteristics |journal=Invest. Ophthalmol. Vis. Sci. |volume=36 |issue=3 |pages=718–29 |year=1995 |pmid=7890502 |doi= |url=}}</ref>
*Hypoautoflourescence in the [[retina]], in conjunction with hyperflourescent borders, is indicative of Acute retinal necrosis and atrophy of retinal [[pigment]] [[epithelium]].<ref name="FreundMrejen2013">{{cite journal|last1=Freund|first1=K. Bailey|last2=Mrejen|first2=Sarah|last3=Jung|first3=Jesse|last4=Yannuzzi|first4=Lawrence A.|last5=Boon|first5=Camiel J. F.|title=Increased Fundus Autofluorescence Related to Outer Retinal Disruption|journal=JAMA Ophthalmology|volume=131|issue=12|year=2013|pages=1645|issn=2168-6165|doi=10.1001/jamaophthalmol.2013.5030}}</ref>
**Posterior extension of the hyperflourescent borders may be indicative of spreading [[inflammation]] and Acute retinal necrosis.
**Hyperflourescence may also be indicative of reduced ability to block flourophores into the [[retina]] due to damage and degradation.<ref name="pmid26120371">{{cite journal |vauthors=Ward TS, Reddy AK |title=Fundus autofluorescence in the diagnosis and monitoring of acute retinal necrosis |journal=J Ophthalmic Inflamm Infect |volume=5 |issue= |pages=19 |year=2015 |pmid=26120371 |pmc=4477008 |doi=10.1186/s12348-015-0042-3 |url=}}</ref>
*FAF is advantageous to color photos due to the ability to more starkly contrast lesions with unaffected [[retinal]] tissue.
 
=====Fluorescein Angiography=====
Fluorescein angiographic images may indicate evidence of Acute retinal necrosis by displaying [[retinal]] [[vasculature]] and potential [[retinal]] [[hemorrhages]], as well as white-yellow [[necrotic]] lesions.<ref name="pmid12063045">{{cite journal |vauthors=Takei H, Ohno-Matsui K, Hayano M, Mochizuki M |title=Indocyanine green angiographic findings in acute retinal necrosis |journal=Jpn. J. Ophthalmol. |volume=46 |issue=3 |pages=330–5 |year=2002 |pmid=12063045 |doi= |url=}}</ref><ref name="urlFluorescein angiography: MedlinePlus Medical Encyclopedia">{{cite web |url=https://medlineplus.gov/ency/article/003846.htm |title=Fluorescein angiography: MedlinePlus Medical Encyclopedia |format= |work= |accessdate=}}</ref>
*Fluorscein angiography can reveal [[optic nerve head]] leakage caused by intraocular [[inflammation]] from the pathogent responsible for ARN.<ref name="pmid20404987">{{cite journal |vauthors=Abu El-Asrar AM, Herbort CP, Tabbara KF |title=Differential diagnosis of retinal vasculitis |journal=Middle East Afr J Ophthalmol |volume=16 |issue=4 |pages=202–18 |year=2009 |pmid=20404987 |pmc=2855661 |doi=10.4103/0974-9233.58423 |url=}}</ref>
*Imaging may reveal [[occlusion|occlusive]] vasculopathy and periarterial vascular sheathing.
 
=====Optical Coherence Tomography=====
Optical Coherence Tomography (OCT) imaging may indicate Acute retinal necrosis with the following:<ref name="pmid16766400">{{cite journal |vauthors=Suzuki J, Goto H, Minoda H, Iwasaki T, Sakai J, Usui M |title=Analysis of retinal findings of acute retinal necrosis using optical coherence tomography |journal=Ocul. Immunol. Inflamm. |volume=14 |issue=3 |pages=165–70 |year=2006 |pmid=16766400 |doi=10.1080/09273940600672198 |url=}}</ref>
*Reflective inner layers of the [[retina]], indicative of white-yellow [[necrotic]] [[lesions]].
**Abnormalities and disorganization in the [[retinal]] structure indicative of [[inflammation]].
*[[Retinal]] [[exudate]]
*Diminished thickness of the [[retina]].
 
===Other Diagnostic Studies===
There are no other diagnostic studies associated with Acute retinal necrosis.


==Treatment==
==Treatment==
===Medical Therapy===
:*''' Empiric antimicrobial therapy'''
::*Preferred regimen: [[Acyclovir]] 10 mg/kg IV q8h for 1-2 weeks followed by [[Acyclovir]] 400 mg PO bid for chronic maintenance
::*Alternative regimen (1): [[Acyclovir]] 10 mg/kg IV q8h for 1-2 weeks followed by [[Valacyclovir]] 1 g IV q8h for 6 weeks to several months followed by [[Acyclovir]] 400 mg PO bid for chronic maintenance
::*Alternative regimen (2), unresponsive: [[Foscarnet]] 1.2-2.4 mg/0.1 mL intravitreal injection 1-3 times per week {{and}} ([[Ganciclovir]] 5 mg/kg IV q12 for 2 weeks followed by 5 mg/kg q24h for 5-7 weeks {{or}} [[Foscarnet]] 60 mg/kg IV q8h for 2 weeks followed by 90-120 mg/kg IV q24h {{or}} [[Cidofovir]] 5 mg/kg IV for 2 weeks followed by 5 mg/kg IV q2weeks) followed by ([[Acyclovir]] 400 mg PO bid for chronic maintenance {{or}} [[Valganciclovir]] 900 mg PO qd for chronic maintenance)
::*Note: [[Ganciclovir]] is administered for patients with suspected CMV acute retinal necrosis. Whereas [[Foscarnet]] is administered for patients who are not immunocompromised
:*''' Pathogen-directed antimicrobial therapy'''
::*'''HSV or VZV'''
:::*Preferred regimen: [[Acyclovir]] 10 mg/kg IV q8h for 1-2 weeks followed by [[Acyclovir]] 400 mg PO bid for chronic maintenance
:::*Alternative regimen: [[Acyclovir]] 10 mg/kg IV q8h for 1-2 weeks followed by [[Valacyclovir]] 1 g IV q8h for 6 weeks to several months followed by [[Acyclovir]] 400 mg PO bid for chronic maintenance
::*''' Cytomegalovirus'''
:::*Preferred regimen: [[Foscarnet]] 1.2-2.4 mg/0.1 mL intravitreal injection 1-3 times per week {{and}} [[Ganciclovir]] 5 mg/kg IV q12 for 2 weeks followed by 5 mg/kg q24h for 5-7 weeks followed by [[Valganciclovir]] 900 mg PO qd for chronic maintenance
===Surgery===
Surgery is not the first-line treatment option for patients with Acute retinal necrosis; it is primarily indicated when there is risk of complications, including [[retinal detachment]] and tissue atrophy.<ref name="pmid26035758">{{cite journal |vauthors=Shantha JG, Weissman HM, Debiec MR, Albini TA, Yeh S |title=Advances in the management of acute retinal necrosis |journal=Int Ophthalmol Clin |volume=55 |issue=3 |pages=1–13 |year=2015 |pmid=26035758 |pmc=4567584 |doi=10.1097/IIO.0000000000000077 |url=}}</ref>
====Vitrectomy====
*[[Vitrectomy]] may be indicated both before and after occurrence of [[retinal detachment]] to improve visual prognosis.<ref name="pmid22937510">{{cite journal |vauthors=Luo YH, Duan XC, Chen BH, Tang LS, Guo XJ |title=Efficacy and necessity of prophylactic vitrectomy for acute retinal necrosis syndrome |journal=Int J Ophthalmol |volume=5 |issue=4 |pages=482–7 |year=2012 |pmid=22937510 |pmc=3428546 |doi=10.3980/j.issn.2222-3959.2012.04.15 |url=}}</ref>
**[[Prophylactic]] [[vitrectomy]] can be effective in removing [[inflammation]] factors, preventing [[retinal detachment]] by removing or preventing the spread of pre-existing [[lesions]] and [[necrotic]] tissue.<ref name="pmid18584565">{{cite journal |vauthors=Kawaguchi T, Spencer DB, Mochizuki M |title=Therapy for acute retinal necrosis |journal=Semin Ophthalmol |volume=23 |issue=4 |pages=285–90 |year=2008 |pmid=18584565 |doi=10.1080/08820530802111192 |url=}}</ref>
**Remedial [[Vitrectomy]] in patients experiencing [[retinal detachment]] can lead to improved visual prognosis by [[retinal]] reattachment.<ref name="pmid1873262">{{cite journal |vauthors=McDonald HR, Lewis H, Kreiger AE, Sidikaro Y, Heckenlively J |title=Surgical management of retinal detachment associated with the acute retinal necrosis syndrome |journal=Br J Ophthalmol |volume=75 |issue=8 |pages=455–8 |year=1991 |pmid=1873262 |pmc=1042429 |doi= |url=}}</ref>
*The success of [[vitrectomy]] in improving outcomes is dependent on the onset of Acute retinal necrosis relative to the time the procedure is performed.<ref name="pmid22937510">{{cite journal |vauthors=Luo YH, Duan XC, Chen BH, Tang LS, Guo XJ |title=Efficacy and necessity of prophylactic vitrectomy for acute retinal necrosis syndrome |journal=Int J Ophthalmol |volume=5 |issue=4 |pages=482–7 |year=2012 |pmid=22937510 |pmc=3428546 |doi=10.3980/j.issn.2222-3959.2012.04.15 |url=}}</ref>
**Increased extent of [[necrosis]] and larger size, as well as posterior located, [[lesions]] were associated with worse visual prognosis despite [[prophylactic]] or remedial [[vitrectomy]].
**[[Prophylactic]] [[vitrectomy]] is often encouraged to maximize efficacy, performed in the early stages of ARN.
====Prophylactic Laser Retinopexy====
*Prophylactic laser retinopexy may be indicated to prevent [[retinal detachment]] by [[Laser photocoagulation|photocoagulation]], creating posterior chorioretinal adhesions.<ref name="pmid18723739">{{cite journal |vauthors=Park JJ, Pavesio C |title=Prophylactic laser photocoagulation for acute retinal necrosis. Does it raise more questions than answers? |journal=Br J Ophthalmol |volume=92 |issue=9 |pages=1161–2 |year=2008 |pmid=18723739 |doi=10.1136/bjo.2008.147181 |url=}}</ref>
**The procedure is contraindicated if there is [[vitreous]] [[inflammation]] or obstructed view and access to the [[posterior pole]].
*Due to reported occurrences of [[retinal detachment]] from prophylactic laser photocoagulation, more research is necessary to determine the ideal indications for the procedure.<ref name="pmid18723739">{{cite journal |vauthors=Park JJ, Pavesio C |title=Prophylactic laser photocoagulation for acute retinal necrosis. Does it raise more questions than answers? |journal=Br J Ophthalmol |volume=92 |issue=9 |pages=1161–2 |year=2008 |pmid=18723739 |doi=10.1136/bjo.2008.147181 |url=}}</ref>
**If performed on patients with excessive [[inflammation]] and [[vitreous]] opacity, there is evidence of photocoagulation worsening prognosis of Acute retinal necrosis, leading to [[retinal detachment]] and [[blindness]].<ref name="pmid18584565">{{cite journal |vauthors=Kawaguchi T, Spencer DB, Mochizuki M |title=Therapy for acute retinal necrosis |journal=Semin Ophthalmol |volume=23 |issue=4 |pages=285–90 |year=2008 |pmid=18584565 |doi=10.1080/08820530802111192 |url=}}</ref>
===Prevention===
====Primary Prevention====
Preventing onset of Acute retinal necrosis is dependent on preventing the causative infection from [[Herpes simplex virus]] (HSV), [[Varicella-zoster virus]] (VZV), and [[Cytomegalovirus]] (CMV). Measures to prevent viral infection include the following:<ref name="urlWHO | Herpes simplex virus">{{cite web |url=http://www.who.int/mediacentre/factsheets/fs400/en/ |title=WHO &#124; Herpes simplex virus |format= |work= |accessdate=}}</ref><ref name="Charkoudian2011">{{cite journal|last1=Charkoudian|first1=Leon D.|title=Acute Retinal Necrosis After Herpes Zoster Vaccination|journal=Archives of Ophthalmology|volume=129|issue=11|year=2011|pages=1495|issn=0003-9950|doi=10.1001/archophthalmol.2011.320}}</ref><ref name="urlCMV | Overview | Cytomegalovirus and Congenital CMV Infection | CDC">{{cite web |url=http://www.cdc.gov/cmv/overview.html |title=CMV &#124; Overview &#124; Cytomegalovirus and Congenital CMV Infection &#124; CDC |format= |work= |accessdate=}}</ref>
*Avoiding oral and genital contact with individuals infected with [[Herpes simplex virus|HSV]]
*Avoiding proximity to individuals infected with [[Varicella-zoster virus|VZV]] to avoid contact with pathogenic respiratory droplets and fluid contact
*Avoiding fluid contact with individuals infected with [[Cytomegalovirus|CMV]]
====Secondary Prevention====
While recurrence of Acute retinal necrosis is not completely preventable presently, administration of topical and [[intravitreal]] [[antiviral]] therapy targeted to the specific etiological cause of the disease can reduce the chance of recurrence.<ref name="pmid24385671">{{cite journal |vauthors=Flaxel CJ, Yeh S, Lauer AK |title=Combination systemic and intravitreal antiviral therapy in the management of acute retinal necrosis syndrome (an American Ophthalmological Society thesis) |journal=Trans Am Ophthalmol Soc |volume=111 |issue= |pages=133–44 |year=2013 |pmid=24385671 |pmc=3868412 |doi= |url=}}</ref>
*Application of [[antiviral]] therapy is more effective for prevention when administered as close to disease onset as possible.
**Extensive, prolonged therapy is important in preventing spread of the disease to the unaffected eye.
Further [[prophylactic]] measures, such as [[vitrectomy]], may be used in current Acute retinal necrosis patients to minimize the possibility of complications, including [[retinal detachment]].<ref name="pmid26035758">{{cite journal |vauthors=Shantha JG, Weissman HM, Debiec MR, Albini TA, Yeh S |title=Advances in the management of acute retinal necrosis |journal=Int Ophthalmol Clin |volume=55 |issue=3 |pages=1–13 |year=2015 |pmid=26035758 |pmc=4567584 |doi=10.1097/IIO.0000000000000077 |url=}}</ref>
==See also==
* [[Cytomegalovirus retinitis]]
* [[Progressive outer retinal necrosis]]


[[Acute retinal necrosis medical therapy|Medical Therapy]] | [[Acute retinal necrosis surgery|Surgery]] | [[Acute retinal necrosis primary prevention|Primary Prevention]] | [[Acute retinal necrosis secondary prevention|Secondary Prevention]] | [[Acute retinal necrosis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Acute retinal necrosis future or investigational therapies|Future or Investigational Therapies]]
==External links==
* http://www.iceh.org.uk/files/tsno8/text/18.htm
* http://www.eyepathologist.org/disease.asp?IDNUM=301330


==Case Studies==
==References==
[[Acute retinal necrosis case study one|Case #1]]
{{reflist|2}}


[[Category:Ophthalmology]]
[[Category:Ophthalmology]]
[[Category:Disease]]
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Faizan Sheraz, M.D. [2]; Luke Rusowicz-Orazem, B.S.

Overview

Acute retinal necrosis is a type of retinitis which can be associated with viral infections.

It was first characterized in 1971.[1][2]

One study indicated an incidence of 1 per 1.6 to 2.0 million.[3]

Historical Perspective

Classification

  • Acute retinal necrosis (ARN) may be classified by staging and severity into the following:[7]
    • Acute stage: Occurs at onset of disease and usually progresses past acute classification after a few weeks.
      • Presents with coalescence of white, necrotic tissue in the peripheral retina.
      • Vaso-occlusive retinal vasculitis is usually present.
      • The optic nerve head of the affected eye will appear swollen, but the posterior pole will usually not be affected during the acute stage.
    • Late stage: Is the natural progression of the disease and will present differentiating characteristics after a few weeks up to a few months.
      • Characterized by a regression of the coalesced necrosis in the peripheral retina, presenting starkly contrasted necrotic/non-necrotic tissue and mild pigmentation scarring and increased vitreous debris
      • Retinal detachment, severe vision loss, and potential blindness in the affected eye is indicative of late stage ARN.
      • If the infection is bilateral, the second eye will usually present signs of ARN in the weeks and months following the initial symptom manifestation in the first eye.
  • Acute retinal necrosis can also be classified by severity into the following:[8]
    • Mild: Is used to characterize ARN that is stable and non-progressive.
    • Fulminant: ARN that is progressive and will usually lead to retinal detachment and further complications if untreated.

Pathophysiology

Pathogenesis

Genetics

  • There is evidence of genetic predisposition to Acute retinal necrosis:
    • For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens are correlated to genetic predisposition to ARN.[12]
    • For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.[8]
  • Possession of the above antigens in their respective demographics are correlated to impaired immunity and increased predisposition to infection.

Associated Conditions

Causes

Differentiating Sandbox:Acute retinal necrosis from Other Diseases

Epidemiology and Demographics

Incidence

  • Research in the United Kingdom resulted in an estimated incidence of approximately 6.3 per 100,000 individuals.[23]
    • There is evidence that this incidence is underestimated due to biases in case adjudication and under-reporting of data.[3]
  • Worldwide, the increase of immunocompromised and aged populations in most countries evidences an increase in Acute retinal necrosis.

Age

  • Acute retinal necrosis (ARN) developed from Herpes simplex virus 1 and Varicella-zoster virus is most common among patients older than 50 years.[8]
  • Herpes simplex virus (HSV) 2 infection is more common among children and adolescents; the incidence of HSV-2 caused ARN is highest in children and young adults between age 9 and 22 years.

Gender

  • There is no gender predisposition to Acute retinal necrosis.

Race

  • There is no racial predisposition to Acute retinal necrosis.

Risk Factors

  • Risk factors for the development of Acute retinal necrosis (ARN) include the following:
    • For caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens are correlated to genetic predisposition to ARN.[12]
    • For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.[8]
    • Experiencing encephalitis from herpes simplex virus[24]
    • Immunocompromise from prior or concurrent disease.[25]
    • Immunosuppresion from extended corticosteroid therapy.[26]

Screening

  • There is no established, diagnostic screening process for Acute retinal necrosis.

Natural History, Complications, and Prognosis

Natural History

  • Symptoms of Acute retinal necrosis (ARN) develop rapidly upon onset of pathogenic infection.[8]
  • The natural progression of ARN depends on whether the case is mild or fulminant.
  • Without treatment, ARN will usually progress to Bilateral acute retinal necrosis (BARN) within weeks to a few months.[7]
    • There are exceptions in which the disease spread from the affected to the previously unaffected eye occurred up to 17 years later, due to reactivation of latent viral infection.[28]

Complications

Prognosis

  • Without treatment, the prognosis for Acute retinal necrosis (ARN) varies:[8]
  • With treatment, the prognosis for ARN is good if the therapy is administered in the early stages and sustained until symptoms resolve.
    • Uncommonly, prognosis can worsen if the patient is immunocompromised and experiences a subsequent infection due to vulnerability from prolonged topical corticosteroid use.

Diagnosis

Diagnostic Criteria

The diagnosis of acute retinal necrosis is made when the following criteria are met:[33]

History

Patient history of prior or concurrent diseases, particularly those associated with Acute retinal necrosis pathogens, or sources of immunocompromise should be considered in the diagnosis of Acute retinal necrosis:[25]

Symptoms

Symptoms of Acute retinal necrosis include the following:[3]

Physical Examination

Physical examination for acute retinal necrosis is remarkable for the following:[8]

Laboratory Findings

Laboratory findings associated with Acute retinal necrosis are those used to determine the viral pathogen, obtained from aqueous humor or the vitreous.[8]

Imaging Findings

Key CT Findings for Acute Retinal Necrosis

CT imaging may reveal indicators of inflammation and infection by the causative pathogen for Acute retinal necrosis (ARN).[39]

Key MRI Findings for Acute Retinal Necrosis

MRI imaging may reveal the following indicators of Acute retinal necrosis:[39]

Electrocardiogram

  • There are no diagnostic electrocardiogram findings associated with Acute retinal necrosis.

Chest X Ray

  • There are no diagnostic chest x ray findings associated with Acute retinal necrosis.

Echocardiography or Ultrasound

  • There are no diagnositic echocardiography or ultrasound findings associated with Acute retinal necrosis.

Other Imaging Findings

Fundus Autoflourescence

Fundus Autoflourescence (FAF) is an imaging technique that examines flourophores in the neurosensory retina and the retinal pigment epithelium, presenting with the following findings indicative of Acute retinal necrosis:[41]

  • Hypoautoflourescence in the retina, in conjunction with hyperflourescent borders, is indicative of Acute retinal necrosis and atrophy of retinal pigment epithelium.[42]
    • Posterior extension of the hyperflourescent borders may be indicative of spreading inflammation and Acute retinal necrosis.
    • Hyperflourescence may also be indicative of reduced ability to block flourophores into the retina due to damage and degradation.[43]
  • FAF is advantageous to color photos due to the ability to more starkly contrast lesions with unaffected retinal tissue.
Fluorescein Angiography

Fluorescein angiographic images may indicate evidence of Acute retinal necrosis by displaying retinal vasculature and potential retinal hemorrhages, as well as white-yellow necrotic lesions.[44][45]

  • Fluorscein angiography can reveal optic nerve head leakage caused by intraocular inflammation from the pathogent responsible for ARN.[21]
  • Imaging may reveal occlusive vasculopathy and periarterial vascular sheathing.
Optical Coherence Tomography

Optical Coherence Tomography (OCT) imaging may indicate Acute retinal necrosis with the following:[46]

Other Diagnostic Studies

There are no other diagnostic studies associated with Acute retinal necrosis.

Treatment

Medical Therapy

  • Empiric antimicrobial therapy
  • Preferred regimen: Acyclovir 10 mg/kg IV q8h for 1-2 weeks followed by Acyclovir 400 mg PO bid for chronic maintenance
  • Alternative regimen (1): Acyclovir 10 mg/kg IV q8h for 1-2 weeks followed by Valacyclovir 1 g IV q8h for 6 weeks to several months followed by Acyclovir 400 mg PO bid for chronic maintenance
  • Alternative regimen (2), unresponsive: Foscarnet 1.2-2.4 mg/0.1 mL intravitreal injection 1-3 times per week AND (Ganciclovir 5 mg/kg IV q12 for 2 weeks followed by 5 mg/kg q24h for 5-7 weeks OR Foscarnet 60 mg/kg IV q8h for 2 weeks followed by 90-120 mg/kg IV q24h OR Cidofovir 5 mg/kg IV for 2 weeks followed by 5 mg/kg IV q2weeks) followed by (Acyclovir 400 mg PO bid for chronic maintenance OR Valganciclovir 900 mg PO qd for chronic maintenance)
  • Note: Ganciclovir is administered for patients with suspected CMV acute retinal necrosis. Whereas Foscarnet is administered for patients who are not immunocompromised
  • Pathogen-directed antimicrobial therapy
  • HSV or VZV
  • Preferred regimen: Acyclovir 10 mg/kg IV q8h for 1-2 weeks followed by Acyclovir 400 mg PO bid for chronic maintenance
  • Alternative regimen: Acyclovir 10 mg/kg IV q8h for 1-2 weeks followed by Valacyclovir 1 g IV q8h for 6 weeks to several months followed by Acyclovir 400 mg PO bid for chronic maintenance
  • Cytomegalovirus
  • Preferred regimen: Foscarnet 1.2-2.4 mg/0.1 mL intravitreal injection 1-3 times per week AND Ganciclovir 5 mg/kg IV q12 for 2 weeks followed by 5 mg/kg q24h for 5-7 weeks followed by Valganciclovir 900 mg PO qd for chronic maintenance

Surgery

Surgery is not the first-line treatment option for patients with Acute retinal necrosis; it is primarily indicated when there is risk of complications, including retinal detachment and tissue atrophy.[47]

Vitrectomy

Prophylactic Laser Retinopexy

Prevention

Primary Prevention

Preventing onset of Acute retinal necrosis is dependent on preventing the causative infection from Herpes simplex virus (HSV), Varicella-zoster virus (VZV), and Cytomegalovirus (CMV). Measures to prevent viral infection include the following:[51][52][53]

  • Avoiding oral and genital contact with individuals infected with HSV
  • Avoiding proximity to individuals infected with VZV to avoid contact with pathogenic respiratory droplets and fluid contact
  • Avoiding fluid contact with individuals infected with CMV

Secondary Prevention

While recurrence of Acute retinal necrosis is not completely preventable presently, administration of topical and intravitreal antiviral therapy targeted to the specific etiological cause of the disease can reduce the chance of recurrence.[5]

  • Application of antiviral therapy is more effective for prevention when administered as close to disease onset as possible.
    • Extensive, prolonged therapy is important in preventing spread of the disease to the unaffected eye.

Further prophylactic measures, such as vitrectomy, may be used in current Acute retinal necrosis patients to minimize the possibility of complications, including retinal detachment.[47]

See also

External links

References

  1. ↑ "eMedicine - Acute Retinal Necrosis : Article by Andrew A Dahl, MD". Archived from the original on 16 February 2008. Retrieved 2008-02-05.
  2. ↑ 2.0 2.1 Urayama A, Yamada N, Sasaki T: Unilateral acute uveitis with retinal periarteritis and detachment. Jpn J Clin Ophthalmol 1971; 25: 607.
  3. ↑ 3.0 3.1 3.2 3.3 Muthiah MN, Michaelides M, Child CS, Mitchell SM (2007). "Acute retinal necrosis: a national population‐based study to assess the incidence, methods of diagnosis, treatment strategies and outcomes in the UK". Br J Ophthalmol. 91 (11): 1452–5. doi:10.1136/bjo.2007.114884. PMC 2095441. PMID 17504853.
  4. ↑ 4.0 4.1 Young NJ, Bird AC (1978). "Bilateral acute retinal necrosis". Br J Ophthalmol. 62 (9): 581–90. PMC 1043304. PMID 708676.
  5. ↑ 5.0 5.1 5.2 5.3 Flaxel CJ, Yeh S, Lauer AK (2013). "Combination systemic and intravitreal antiviral therapy in the management of acute retinal necrosis syndrome (an American Ophthalmological Society thesis)". Trans Am Ophthalmol Soc. 111: 133–44. PMC 3868412. PMID 24385671.
  6. ↑ Hayasaka S, Asano T, Yabata K, Ide A (1983). "Acute retinal necrosis". Br J Ophthalmol. 67 (7): 455–60. PMC 1040094. PMID 6860612.
  7. ↑ 7.0 7.1 Gartry DS, Spalton DJ, Tilzey A, Hykin PG (1991). "Acute retinal necrosis syndrome". Br J Ophthalmol. 75 (5): 292–7. PMC 1042358. PMID 1645179.
  8. ↑ 8.00 8.01 8.02 8.03 8.04 8.05 8.06 8.07 8.08 8.09 8.10 8.11 Brydak-Godowska J, Borkowski P, Szczepanik S, Moneta-Wielgoś J, Kęcik D (2014). "Clinical manifestation of self-limiting acute retinal necrosis". Med. Sci. Monit. 20: 2088–96. doi:10.12659/MSM.890469. PMC 4226315. PMID 25356955.
  9. ↑ 9.0 9.1 Ganatra JB, Chandler D, Santos C, Kuppermann B, Margolis TP (2000). "Viral causes of the acute retinal necrosis syndrome". Am. J. Ophthalmol. 129 (2): 166–72. PMID 10682968.
  10. ↑ Grose C (2012). "Acute retinal necrosis caused by herpes simplex virus type 2 in children: reactivation of an undiagnosed latent neonatal herpes infection". Semin Pediatr Neurol. 19 (3): 115–8. doi:10.1016/j.spen.2012.02.005. PMC 3419358. PMID 22889540.
  11. ↑ Whitley, Richard; Kimberlin, David W.; Prober, Charles G. (2007). Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge, UK: Cambridge University Press. ISBN 978-0511545313.
  12. ↑ 12.0 12.1 Holland GN, Cornell PJ, Park MS, Barbetti A, Yuge J, Kreiger AE, Kaplan HJ, Pepose JS, Heckenlively JR, Culbertson WW (1989). "An association between acute retinal necrosis syndrome and HLA-DQw7 and phenotype Bw62, DR4". Am. J. Ophthalmol. 108 (4): 370–4. PMID 2801857.
  13. ↑ 13.0 13.1 Coisy S, Ebran JM, Milea D (2014). "Progressive outer retinal necrosis and immunosuppressive therapy in myasthenia gravis". Case Rep Ophthalmol. 5 (1): 132–7. doi:10.1159/000362662. PMC 4036147. PMID 24926266.
  14. ↑ 14.0 14.1 14.2 "Facts About Uveitis | National Eye Institute".
  15. ↑ 15.0 15.1 "CMV retinitis: MedlinePlus Medical Encyclopedia".
  16. ↑ 16.0 16.1 16.2 Davis JL (2012). "Diagnostic dilemmas in retinitis and endophthalmitis". Eye (Lond). 26 (2): 194–201. doi:10.1038/eye.2011.299. PMC 3272204. PMID 22116459.
  17. ↑ Pikkel YY, Pikkel J (2014). "Acute retinal necrosis in childhood". Case Rep Ophthalmol. 5 (2): 138–43. doi:10.1159/000363130. PMC 4049010. PMID 24932179.
  18. ↑ Dart JK (1986). "Eye disease at a community health centre". Br Med J (Clin Res Ed). 293 (6560): 1477–80. PMC 1342247. PMID 3099921.
  19. ↑ Leibowitz HM (2000). "The red eye". N Engl J Med. 343 (5): 345–51. doi:10.1056/NEJM200008033430507. PMID 10922425.
  20. ↑ University of Michigan Eyes Have it (2009)http://kellogg.umich.edu/theeyeshaveit/red-eye/
  21. ↑ 21.0 21.1 Abu El-Asrar AM, Herbort CP, Tabbara KF (2009). "Differential diagnosis of retinal vasculitis". Middle East Afr J Ophthalmol. 16 (4): 202–18. doi:10.4103/0974-9233.58423. PMC 2855661. PMID 20404987.
  22. ↑ Witmer MT, Pavan PR, Fouraker BD, Levy-Clarke GA (2011). "Acute retinal necrosis associated optic neuropathy". Acta Ophthalmol. 89 (7): 599–607. doi:10.1111/j.1755-3768.2010.01911.x. PMID 20645925.
  23. ↑ Cochrane TF, Silvestri G, McDowell C, Foot B, McAvoy CE (2012). "Acute retinal necrosis in the United Kingdom: results of a prospective surveillance study". Eye (Lond). 26 (3): 370–7, quiz 378. doi:10.1038/eye.2011.338. PMC 3298997. PMID 22281865.
  24. ↑ Vandercam T, Hintzen RQ, de Boer JH, Van der Lelij A (2008). "Herpetic encephalitis is a risk factor for retinal necrosis". Neurology. 71 (16): 1268–74. doi:10.1212/01.wnl.0000327615.99124.99. PMID 18852442.
  25. ↑ 25.0 25.1 Moutschen MP, Scheen AJ, Lefebvre PJ (1992). "Impaired immune responses in diabetes mellitus: analysis of the factors and mechanisms involved. Relevance to the increased susceptibility of diabetic patients to specific infections". Diabete Metab. 18 (3): 187–201. PMID 1397473.
  26. ↑ Yamamoto JH, Boletti DI, Nakashima Y, Hirata CE, Olivalves E, Shinzato MM, Okay TS, Santo RM, Duarte MI, Kalil J (2003). "Severe bilateral necrotising retinitis caused by Toxoplasma gondii in a patient with systemic lupus erythematosus and diabetes mellitus". Br J Ophthalmol. 87 (5): 651–2. PMC 1771672. PMID 12714420.
  27. ↑ Matsuo T, Nakayama T, Koyama T, Koyama M, Matsuo N (1988). "A proposed mild type of acute retinal necrosis syndrome". Am. J. Ophthalmol. 105 (6): 579–83. PMID 2837090.
  28. ↑ Okunuki Y, Usui Y, Kezuka T, Takeuchi M, Goto H (2011). "Four cases of bilateral acute retinal necrosis with a long interval after the initial onset". Br J Ophthalmol. 95 (9): 1251–4. doi:10.1136/bjo.2010.191288. PMID 21242577.
  29. ↑ Liang ZG, Liu ZL, Sun XW, Tao ML, Yu GP (2015). "Viral encephalitis complicated by acute retinal necrosis syndrome: A case report". Exp Ther Med. 10 (2): 465–467. doi:10.3892/etm.2015.2557. PMC 4509005. PMID 26622338.
  30. ↑ Vukojević N, Popovic Suić S, Sikić J, Katusić D, Curković T, Sarić B, Jukić T (2006). "[Acute retinal necrosis]". Acta Med Croatica. 60 (2): 145–8. PMID 16848208.
  31. ↑ 31.0 31.1 McDonald HR, Lewis H, Kreiger AE, Sidikaro Y, Heckenlively J (1991). "Surgical management of retinal detachment associated with the acute retinal necrosis syndrome". Br J Ophthalmol. 75 (8): 455–8. PMC 1042429. PMID 1873262.
  32. ↑ 32.0 32.1 Lau CH, Missotten T, Salzmann J, Lightman SL (2007). "Acute retinal necrosis features, management, and outcomes". Ophthalmology. 114 (4): 756–62. doi:10.1016/j.ophtha.2006.08.037. PMID 17184841.
  33. ↑ Holland GN (1994). "Standard diagnostic criteria for the acute retinal necrosis syndrome. Executive Committee of the American Uveitis Society". Am. J. Ophthalmol. 117 (5): 663–7. PMID 8172275.
  34. ↑ Ford JR, Tsui E, Lahey T, Zegans ME (2013). "Question: Can you identify this condition? Acute retinal necrosis". Can Fam Physician. 59 (12): 1307, 1308–10. PMC 3860929. PMID 24336545.
  35. ↑ "American Academy of Ophthalmology".
  36. ↑ Silva RA, Berrocal AM, Moshfeghi DM, Blumenkranz MS, Sanislo S, Davis JL (2013). "Herpes simplex virus type 2 mediated acute retinal necrosis in a pediatric population: case series and review". Graefes Arch. Clin. Exp. Ophthalmol. 251 (2): 559–66. doi:10.1007/s00417-012-2164-8. PMID 23052715.
  37. ↑ Singh A, Preiksaitis J, Ferenczy A, Romanowski B (2005). "The laboratory diagnosis of herpes simplex virus infections". Can J Infect Dis Med Microbiol. 16 (2): 92–8. PMC 2095011. PMID 18159535.
  38. ↑ De Groot-Mijnes JD, Rothova A, Van Loon AM, Schuller M, Ten Dam-Van Loon NH, De Boer JH, Schuurman R, Weersink AJ (2006). "Polymerase chain reaction and Goldmann-Witmer coefficient analysis are complimentary for the diagnosis of infectious uveitis". Am. J. Ophthalmol. 141 (2): 313–8. doi:10.1016/j.ajo.2005.09.017. PMID 16458686.
  39. ↑ 39.0 39.1 Bert RJ, Samawareerwa R, Melhem ER (2004). "CNS MR and CT findings associated with a clinical presentation of herpetic acute retinal necrosis and herpetic retrobulbar optic neuritis: five HIV-infected and one non-infected patients". AJNR Am J Neuroradiol. 25 (10): 1722–9. PMID 15569737.
  40. ↑ Sergott RC, Belmont JB, Savino PJ, Fischer DH, Bosley TM, Schatz NJ (1985). "Optic nerve involvement in the acute retinal necrosis syndrome". Arch. Ophthalmol. 103 (8): 1160–2. PMID 4026646.
  41. ↑ Delori FC, Dorey CK, Staurenghi G, Arend O, Goger DG, Weiter JJ (1995). "In vivo fluorescence of the ocular fundus exhibits retinal pigment epithelium lipofuscin characteristics". Invest. Ophthalmol. Vis. Sci. 36 (3): 718–29. PMID 7890502.
  42. ↑ Freund, K. Bailey; Mrejen, Sarah; Jung, Jesse; Yannuzzi, Lawrence A.; Boon, Camiel J. F. (2013). "Increased Fundus Autofluorescence Related to Outer Retinal Disruption". JAMA Ophthalmology. 131 (12): 1645. doi:10.1001/jamaophthalmol.2013.5030. ISSN 2168-6165.
  43. ↑ Ward TS, Reddy AK (2015). "Fundus autofluorescence in the diagnosis and monitoring of acute retinal necrosis". J Ophthalmic Inflamm Infect. 5: 19. doi:10.1186/s12348-015-0042-3. PMC 4477008. PMID 26120371.
  44. ↑ Takei H, Ohno-Matsui K, Hayano M, Mochizuki M (2002). "Indocyanine green angiographic findings in acute retinal necrosis". Jpn. J. Ophthalmol. 46 (3): 330–5. PMID 12063045.
  45. ↑ "Fluorescein angiography: MedlinePlus Medical Encyclopedia".
  46. ↑ Suzuki J, Goto H, Minoda H, Iwasaki T, Sakai J, Usui M (2006). "Analysis of retinal findings of acute retinal necrosis using optical coherence tomography". Ocul. Immunol. Inflamm. 14 (3): 165–70. doi:10.1080/09273940600672198. PMID 16766400.
  47. ↑ 47.0 47.1 Shantha JG, Weissman HM, Debiec MR, Albini TA, Yeh S (2015). "Advances in the management of acute retinal necrosis". Int Ophthalmol Clin. 55 (3): 1–13. doi:10.1097/IIO.0000000000000077. PMC 4567584. PMID 26035758.
  48. ↑ 48.0 48.1 Luo YH, Duan XC, Chen BH, Tang LS, Guo XJ (2012). "Efficacy and necessity of prophylactic vitrectomy for acute retinal necrosis syndrome". Int J Ophthalmol. 5 (4): 482–7. doi:10.3980/j.issn.2222-3959.2012.04.15. PMC 3428546. PMID 22937510.
  49. ↑ 49.0 49.1 Kawaguchi T, Spencer DB, Mochizuki M (2008). "Therapy for acute retinal necrosis". Semin Ophthalmol. 23 (4): 285–90. doi:10.1080/08820530802111192. PMID 18584565.
  50. ↑ 50.0 50.1 Park JJ, Pavesio C (2008). "Prophylactic laser photocoagulation for acute retinal necrosis. Does it raise more questions than answers?". Br J Ophthalmol. 92 (9): 1161–2. doi:10.1136/bjo.2008.147181. PMID 18723739.
  51. ↑ "WHO | Herpes simplex virus".
  52. ↑ Charkoudian, Leon D. (2011). "Acute Retinal Necrosis After Herpes Zoster Vaccination". Archives of Ophthalmology. 129 (11): 1495. doi:10.1001/archophthalmol.2011.320. ISSN 0003-9950.
  53. ↑ "CMV | Overview | Cytomegalovirus and Congenital CMV Infection | CDC".
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