Sandbox:Acute retinal necrosis
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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
- Acute retinal necrosis was first officially classified as bilateral acute retinal necrosis in 1978 by N.J. Young and A.C. Bird.[4]
- 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.[5]
- The first extension of the classification of acute retinal necrosis to unilateral cases was given in 1983 by Hayasaka S. et al.[6]
- They identified that cases of bilateral acute retinal necrosis and cases of Kirisawa-type uveitis presented nearly identical characteristics:[2][4]
- Periarteritis
- Opaque, dense vitreous
- Peripheral retinal exudates
- Retinal detachment
- Vision loss
- Resistance to antibiotic therapy
- Negative test results for bacterial infection
- They identified that cases of bilateral acute retinal necrosis and cases of Kirisawa-type uveitis presented nearly identical characteristics:[2][4]
- 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 (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 stage: Occurs at onset of disease and usually progresses past acute classification after a few weeks.
- 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.
- 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.
- Mild: Is used to characterize ARN that is stable and non-progressive.
Pathophysiology
Pathogenesis
- The pathogenesis of Acute retinal necrosis is characterized by retinal inflammation due to ocular viral infection:[9]
- 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:[10]
- Epithelial penetration of the skin: transmitted through the 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 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 latency, reactivate, and cause retinal inflammation.[11]
- Retinal inflammation is caused by the up-regulated production of cytokines.
- 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:[10]
Genetics
- There is evidence of genetic predisposition to Acute retinal necrosis:
- Possession of the above antigens in their respective demographics are correlated to impaired immunity and increased predisposition to infection.
Associated Conditions
- Acute retinal necrosis is associated with the following ocular conditions:
Causes
- Acute retinal necrosis (ARN) is usually caused by the reactivation of the following pathogenic viruses in the Herpesviridae family:[17]
- 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.[9]
- VZV and 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.[8]
- HSV-2 is usually the cause of ARN in individuals younger than 25 years.
Differentiating Sandbox:Acute retinal necrosis 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.[16][18][19][20]
- 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[22]
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]
- 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.[27]
- 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.[7]
Complications
- Complications resulting from Acute retinal necrosis occur due to retinal tissue damage and subsequent infection from the causative pathogen, including the following:[8][5]
- Retinal detachment
- Neurological conditions, such as encephalitis[29] or meningitis
- Optic neuropathy
- Occlusive retinal vasculopathy
- Proliferative vitreoretinopathy[30]
- Macular pucker[31]
- Vitreous hemorrhage
- Neovascularization[32]
- Phthisis bulbi[32]
Prognosis
- Without treatment, the prognosis for Acute retinal necrosis (ARN) varies:[8]
- 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
Diagnostic Criteria
The diagnosis of acute retinal necrosis is made when the following criteria are met:[33]
- One or more discrete foci of peripheral retinal necrosis, located outside of the major temporal vascular arcades
- Circumferential spread if antiviral therapy has not been administered
- 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:[25]
- History of diabetes mellitus
- History of prolonged corticosteroid use[8]
- History of genital or oral herpes infection
- History of chickenpox or shingles
- History of mononucleosis
- History of HIV infection
Symptoms
Symptoms of Acute retinal necrosis include the following:[3]
- Vision loss
- Blindness may be present in more severe cases
- Excessive sensitivity to light
- Ocular pain
- Flu symptoms
- Redness of the affected eye
- Floaters[34]
- Flashes[35]
Physical Examination
Physical examination for acute retinal necrosis is remarkable for the following:[8]
- Erythema and hyperaemia of the retina[3]
- White and yellow necrotic lesions in the retina
- 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.[8]
- Qualitative and Real-time Polymerase chain reaction[8]
- 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.[36]
- Immunoflourescence may reveal antibodies indicative of Acute retinal necrosis pathogens.[37]
- Detection of indicative antibodies via Goldmann-witmer coefficient.[38]
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]
- 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.[40]
- Infection-caused shrunken left globe.
Key MRI Findings for Acute Retinal Necrosis
MRI imaging may reveal the following indicators of Acute retinal necrosis:[39]
- 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 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:[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]
- 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
Medical Therapy
- Empiric antimicrobial therapy
- 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
- Vitrectomy may be indicated both before and after occurrence of retinal detachment to improve visual prognosis.[48]
- 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.[49]
- Remedial Vitrectomy in patients experiencing retinal detachment can lead to improved visual prognosis by retinal reattachment.[31]
- The success of vitrectomy in improving outcomes is dependent on the onset of Acute retinal necrosis relative to the time the procedure is performed.[48]
- 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 photocoagulation, creating posterior chorioretinal adhesions.[50]
- 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.[50]
- 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.[49]
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
- http://www.iceh.org.uk/files/tsno8/text/18.htm
- http://www.eyepathologist.org/disease.asp?IDNUM=301330
References
- ↑ "eMedicine - Acute Retinal Necrosis : Article by Andrew A Dahl, MD". Archived from the original on 16 February 2008. Retrieved 2008-02-05.
- ↑ 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.
- ↑ 3.0 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.
- ↑ 4.0 4.1 Young NJ, Bird AC (1978). "Bilateral acute retinal necrosis". Br J Ophthalmol. 62 (9): 581–90. PMC 1043304. PMID 708676.
- ↑ 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.
- ↑ Hayasaka S, Asano T, Yabata K, Ide A (1983). "Acute retinal necrosis". Br J Ophthalmol. 67 (7): 455–60. PMC 1040094. PMID 6860612.
- ↑ 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.
- ↑ 8.00 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.
- ↑ 9.0 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.
- ↑ 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.
- ↑ Whitley, Richard; Kimberlin, David W.; Prober, Charles G. (2007). Human Herpesviruses: Biology, Therapy, and Immunoprophylaxis. Cambridge, UK: Cambridge University Press. ISBN 978-0511545313.
- ↑ 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.
- ↑ 13.0 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.
- ↑ 14.0 14.1 14.2 "Facts About Uveitis | National Eye Institute".
- ↑ 15.0 15.1 "CMV retinitis: MedlinePlus Medical Encyclopedia".
- ↑ 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.
- ↑ 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.
- ↑ Dart JK (1986). "Eye disease at a community health centre". Br Med J (Clin Res Ed). 293 (6560): 1477–80. PMC 1342247. PMID 3099921.
- ↑ Leibowitz HM (2000). "The red eye". N Engl J Med. 343 (5): 345–51. doi:10.1056/NEJM200008033430507. PMID 10922425.
- ↑ University of Michigan Eyes Have it (2009)http://kellogg.umich.edu/theeyeshaveit/red-eye/
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 25.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 31.0 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.
- ↑ 32.0 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.
- ↑ 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.
- ↑ 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.
- ↑ "American Academy of Ophthalmology".
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 39.0 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ "Fluorescein angiography: MedlinePlus Medical Encyclopedia".
- ↑ 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.
- ↑ 47.0 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.
- ↑ 48.0 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.
- ↑ 49.0 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.
- ↑ 50.0 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.
- ↑ "WHO | Herpes simplex virus".
- ↑ 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.
- ↑ "CMV | Overview | Cytomegalovirus and Congenital CMV Infection | CDC".