Acute retinal necrosis: Difference between revisions

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**The increased intensity reveals lesions that may be indicative of [[Herpes simplex virus]] or [[Cytomegalovirus]] infection.
**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]].
*[[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.


====Other Imaging Findings====
====Other Imaging Findings====

Revision as of 16:04, 19 August 2016

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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 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]

Symptoms

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.

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

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

Prevention

See also

External links

References

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