Sandbox:Acute retinal necrosis

# Overview
Acute retinal necrosis is a type of retinitis which can be associated with viral infections.
It was first characterized in 1971.
One study indicated an incidence of 1 per 1.6 to 2.0 million.

# Historical Perspective
- Acute retinal necrosis was first officially classified as bilateral acute retinal necrosis in 1978 by N.J. Young and A.C. Bird.
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.
- 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.
- The first extension of the classification of acute retinal necrosis to unilateral cases was given in 1983 by Hayasaka S. et al.
They identified that cases of bilateral acute retinal necrosis and cases of Kirisawa-type uveitis presented nearly identical characteristics:
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:
Periarteritis
Opaque, dense vitreous
Peripheral retinal exudates
Retinal detachment
Vision loss
Resistance to antibiotic therapy
Negative test results for bacterial infection
- 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.

# Classification
- Acute retinal necrosis (ARN) may be classified by staging and severity into the following:
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.
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.
- 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.
- 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:
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.
There is usually no sign of retinal detachment.
- 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.

# Pathophysiology

## Pathogenesis
- The pathogenesis of Acute retinal necrosis is characterized by retinal inflammation due to ocular viral infection:
Particles from Herpes simplex virus 1 (HSV-1), Herpes simplex virus 2 (HSV-2), and Varicella zoster virus (VZV) infiltrate the retina via various modes of transmission:
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.
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:
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.
- 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.
Retinal inflammation is caused by the up-regulated production of cytokines.
- Retinal inflammation is caused by the up-regulated production of cytokines.

## 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.
For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.
- For Caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens are correlated to genetic predisposition to ARN.
- For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.
- 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:
Progressive outer retinal necrosis
Uveitis
Cytomegalovirus retinitis
Toxoplasmic chorioretinitis
Endophthalmitis
- Progressive outer retinal necrosis
- Uveitis
- Cytomegalovirus retinitis
- Toxoplasmic chorioretinitis
- Endophthalmitis

# Causes
- Acute retinal necrosis (ARN) is usually caused by the reactivation of the following pathogenic viruses in the Herpesviridae family:
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.
- 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.
- 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.
- The majority of the ARN cases for individuals older than 50 years are caused by VZV and HSV-1.
- 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.
Progressive outer retinal necrosis
Uveitis
Uveitis
Endophthalmitis
Toxoplasma chorioretinitis
Cytomegalovirus retinitis
Conjunctivitis
Scleritis
Corneal abrasion
Glaucoma
Corneal ulcer
Retinal vasculitis
- Progressive outer retinal necrosis
- Uveitis
- Uveitis
- Endophthalmitis
- Toxoplasma chorioretinitis
- Cytomegalovirus retinitis
- Conjunctivitis
- Scleritis
- Corneal abrasion
- Glaucoma
- Corneal ulcer
- Retinal vasculitis
- 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
- Acute papillitis

# Epidemiology and Demographics

## Incidence
- Research in the United Kingdom resulted in an estimated incidence of approximately 6.3 per 100,000 individuals.
There is evidence that this incidence is underestimated due to biases in case adjudication and under-reporting of data.
- There is evidence that this incidence is underestimated due to biases in case adjudication and under-reporting of data.
- 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.
- 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.
For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.
Experiencing encephalitis from herpes simplex virus
Immunocompromise from prior or concurrent disease.
Immunosuppresion from extended corticosteroid therapy.
- For caucasian populations: possessing the HLA-DQw7, HLA-Bw62, and HLA-DR4 antigens are correlated to genetic predisposition to ARN.
- For Japanese populations: possessing the HLA-Aw33, HLA-B44, and HLA-DRw6 antigens are correlated to genetic predisposition to ARN.
- Experiencing encephalitis from herpes simplex virus
- Immunocompromise from prior or concurrent disease.
- Immunosuppresion from extended corticosteroid therapy.

# 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.
Initial signs and symptoms include conjunctivitis, vision loss and photophobia, and eye pain and pressure.
- 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.
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.
- Mild cases of ARN presents with white-yellow necrotic lesions that do not coalesce or lead to retinal detachment; the disease is self-limited.
- 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.
- 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.
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.
- 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.

## Complications
- Complications resulting from Acute retinal necrosis occur due to retinal tissue damage and subsequent infection from the causative pathogen, including the following:
Retinal detachment
Neurological conditions, such as encephalitis or meningitis
Optic neuropathy
Occlusive retinal vasculopathy
Proliferative vitreoretinopathy
Macular pucker
Vitreous hemorrhage
Neovascularization
Phthisis bulbi
- Retinal detachment
- Neurological conditions, such as encephalitis or meningitis
- Optic neuropathy
- Occlusive retinal vasculopathy
- Proliferative vitreoretinopathy
- Macular pucker
- Vitreous hemorrhage
- Neovascularization
- Phthisis bulbi

## Prognosis
- Without treatment, the prognosis for Acute retinal necrosis (ARN) varies:
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.
- 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.
- 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.
- 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:
- 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:
- History of diabetes mellitus
- History of prolonged corticosteroid use
- 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:
- Vision loss
Blindness may be present in more severe cases
- Blindness may be present in more severe cases
- Excessive sensitivity to light
- Ocular pain
- Flu symptoms
- Redness of the affected eye
- Floaters
- Flashes

## Physical Examination
Physical examination for acute retinal necrosis is remarkable for the following:
- Erythema and hyperaemia of the retina
- White and yellow necrotic lesions in the retina
Purulent exudate can also be found in the periphery of the retina
Opaque vitreous from the coalescence of necrotic tissue
- Purulent exudate can also be found in the periphery of the retina
- 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.
- Qualitative and Real-time Polymerase chain reaction
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).
- 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.
- Immunoflourescence may reveal antibodies indicative of Acute retinal necrosis pathogens.
- Detection of indicative antibodies via Goldmann-witmer coefficient.

## 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).
- 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.
- Infection-caused shrunken left globe.

### Key MRI Findings for Acute Retinal Necrosis
MRI imaging may reveal the following indicators of Acute retinal necrosis:
- 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.
- 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 ganglionMeckel 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 (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:
- Hypoautoflourescence in the retina, in conjunction with hyperflourescent borders, is indicative of Acute retinal necrosis and atrophy of retinal pigment epithelium.
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.
- 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.
- FAF is advantageous to color photos due to the ability to more starkly contrast lesions with unaffected retinal tissue.
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.
- Fluorscein angiography can reveal optic nerve head leakage caused by intraocular inflammation from the pathogent responsible for ARN.
- Imaging may reveal occlusive vasculopathy and periarterial vascular sheathing.
Optical Coherence Tomography (OCT) imaging may indicate Acute retinal necrosis with the following:
- Reflective inner layers of the retina, indicative of white-yellow necrotic lesions.
Abnormalities and disorganization in the retinal structure indicative of inflammation.
- 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
- 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.

### Vitrectomy
- Vitrectomy may be indicated both before and after occurrence of retinal detachment to improve visual prognosis.
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.
Remedial Vitrectomy in patients experiencing retinal detachment can lead to improved visual prognosis by retinal reattachment.
- 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.
- Remedial Vitrectomy in patients experiencing retinal detachment can lead to improved visual prognosis by retinal reattachment.
- The success of vitrectomy in improving outcomes is dependent on the onset of Acute retinal necrosis relative to the time the procedure is performed.
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.
- 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.
The procedure is contraindicated if there is vitreous inflammation or obstructed view and access to the posterior pole.
- 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.
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.
- 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.

## 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:
- 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.
- 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.
- 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.