Acute retinal necrosis (ARN) is a rare but serious inflammatory condition of the eye characterized by rapid, full-thickness death of retinal tissue, typically beginning in the peripheral retina and advancing toward the center. Patients often present with marked redness, pain, and vitritis (inflammation of the vitreous humor). If left untreated, ARN can lead to retinal detachment and permanent vision loss WikipediaEyeWiki.
Acute Retinal Necrosis (ARN) is a rapid, sight-threatening inflammation of the retina, most often caused by herpes viruses such as varicella-zoster virus (VZV) or herpes simplex virus (HSV). The condition typically begins in one eye and, if untreated, can progress to involve both eyes within days to weeks. Hallmark features include retinal whitening (necrosis), arterial inflammation (vasculitis), and inflammatory cells in the eye (vitritis). ARN can lead to permanent vision loss from retinal detachment, optic nerve damage, or widespread retinal scarring. Early diagnosis and prompt treatment are essential to preserve vision and prevent contralateral eye involvement.
In ARN, infection by herpes-family viruses triggers an intense immune response within the retina and surrounding ocular structures. This necrotizing retinitis is accompanied by occlusive vasculitis (inflammation and blockage of retinal arterioles), panuveitis (inflammation of all uveal layers), and risk of proliferative vitreoretinopathy. Prompt recognition and antiviral therapy are critical to preserve vision and prevent spread to the fellow eye NCBINature.
Types of Acute Retinal Necrosis
Classic Acute Retinal Necrosis
Classic ARN typically affects otherwise healthy, immunocompetent adults and presents unilaterally with peripheral multifocal areas of retinal whitening, vitritis, and occlusive arteritis. Over days to weeks, these lesions coalesce in a “scalloped” pattern, advancing centrally and risking retinal detachment. Early treatment with systemic or intravitreal antivirals (e.g., acyclovir, valacyclovir) can slow progression and improve outcomes EyeWikiWikipedia.
Progressive Outer Retinal Necrosis (PORN)
PORN is a variant seen almost exclusively in severely immunosuppressed patients, such as those with advanced HIV/AIDS. It features rapid, often bilateral outer retinal necrosis with minimal vitritis or anterior chamber inflammation. PORN lesions lack the typical occlusive vasculitis of ARN and can progress to central involvement within days, requiring aggressive antiviral and sometimes intravitreal therapy Wikipedia.
Causes of Acute Retinal Necrosis
Varicella-Zoster Virus (VZV)
VZV is the most common viral cause of ARN, reactivating from dorsal root or cranial nerve ganglia to infect the retina via axonal transport. The virus induces a strong inflammatory response, leading to peripheral retinal necrosis and vasculitis EyeWikiWikipedia.Herpes Simplex Virus Type 1 (HSV-1)
HSV-1 can reactivate from trigeminal ganglia and invade the retina, especially in older adults. ARN due to HSV-1 often presents with similar clinical features to VZV-associated cases but may have a slightly more indolent course EyeWikiWikipedia.Herpes Simplex Virus Type 2 (HSV-2)
HSV-2–related ARN is more frequently seen in younger patients and may follow neonatal or later systemic HSV infection. Like HSV-1, it causes multifocal retinitis and occlusive arteritis, requiring early antiviral therapy EyeWikiWikipedia.Cytomegalovirus (CMV)
Although CMV more commonly causes retinitis in immunocompromised hosts (e.g., HIV/AIDS), rare cases of CMV-driven ARN have been reported, usually in patients on immunosuppressive medications EyeWikiWikipedia.Epstein-Barr Virus (EBV)
EBV has been implicated in isolated ARN cases, confirmed by PCR of intraocular fluid. It may act alone or co-infect with other herpes viruses, complicating the inflammatory response EyeWikiWikipedia.Immunocompetent Host Status
Unlike many viral retinitides, ARN often occurs in immunocompetent individuals, indicating that a robust immune response may paradoxically contribute to retinal damage EyeWiki.HIV Infection
HIV-associated immunosuppression predisposes to ARN and especially to PORN. Low CD4 counts (<50 cells/µL) correlate with more severe presentations and bilateral involvement EyeWiki.Corticosteroid Therapy
Systemic or intraocular steroids can dampen antiviral immunity, triggering viral reactivation and ARN onset or exacerbation EyeWiki.Organ Transplantation
Solid-organ transplant recipients on immunosuppressive regimens (e.g., cyclosporine, tacrolimus) are at heightened risk for ARN due to impaired viral control EyeWiki.Bone Marrow Transplantation
Recipients of hematopoietic stem cell transplants face severe immunosuppression during engraftment, increasing ARN risk EyeWiki.Postpartum Period
Hormonal changes and transient immunosuppression in the immediate postpartum period have been associated with ARN development EyeWiki.Prior Herpetic Encephalitis
A history of HSV encephalitis may indicate viral persistence in the central nervous system, with potential spread to the retina via neural pathways EyeWiki.HLA-DQw7 Genetic Marker
Certain HLA types, including DQw7, have been linked to increased ARN susceptibility in Caucasians, suggesting a genetic predisposition EyeWiki.HLA-Bw62 Genetic Marker
Bw62 expression correlates with ARN risk, indicating immune-genetic factors in disease pathogenesis EyeWiki.HLA-DR4 Genetic Marker
DR4 has also been associated with ARN in North American populations, highlighting the role of antigen presentation in disease susceptibility EyeWiki.
Symptoms of Acute Retinal Necrosis
Acute Onset Vision Loss
Patients typically notice a sudden decrease in vision in the affected eye, ranging from mild blurring to near-complete vision loss, depending on lesion location and extent WikipediaEyeWiki.Eye Redness (Conjunctival Injection)
Intense inflammation causes blood vessel dilation, producing visible redness of the white part of the eye WikipediaEyeWiki.Photophobia (Light Sensitivity)
Inflammation of the uvea and cornea irritates light-sensitive retinal cells, causing discomfort or pain in bright environments WikipediaEyeWiki.Ocular Pain
Patients often report a dull ache or sharp pain behind the eye, reflecting scleritis or episcleritis associated with ARN EyeWiki.Floaters
Inflammatory cells and debris in the vitreous humor appear as dark spots or strands that drift across the visual field WikipediaEyeWiki.Flashes of Light (Photopsia)
Retinal traction and necrosis can stimulate photoreceptors, leading to brief, bright flashes perceived by the patient WikipediaEyeWiki.Vitreous Haze
Diffuse clouding of the vitreous impairs visualization of the retina and contributes to overall vision blurring EyeWiki.Anterior Chamber Cells and Flare
Inflammatory cells and protein in the front chamber cause a “smoky” appearance under slit-lamp examination, often accompanied by keratic precipitates on the corneal endothelium EyeWiki.Scleritis/Episcleritis
Inflammation of superficial or deep scleral tissues produces focal redness and pain, distinguishable by blanching response to topical vasoconstrictors EyeWiki.Risk of Retinal Detachment
Progressive necrosis and tractional membranes can lead to rhegmatogenous detachment, presenting as a shadow or curtain across the visual field EyeWikiNature.
Diagnostic Tests for Acute Retinal Necrosis
Physical Examination Tests
Visual Acuity Testing
Measures the clarity of vision using standardized charts (e.g., Snellen, LogMAR) to quantify central visual function. Reduced acuity correlates with lesion proximity to the macula WikipediaSimple Wikipedia.
Slit-Lamp Biomicroscopy
A high-intensity, adjustable beam and microscope allow detailed inspection of anterior and posterior segments, revealing keratic precipitates, anterior chamber cells, vitritis, and retinal necrosis margins WikipediaVerywell Health.
Ophthalmoscopy (Fundus Examination)
Using a handheld or indirect ophthalmoscope, the examiner visualizes the fundus to identify multifocal peripheral whitening, occlusive arteritis, and hemorrhages. Both direct and indirect techniques are employed for magnification and field of view adjustments WikipediaEyeWiki.
Dilated Fundus Examination
Pharmacologic pupil dilation enhances visualization of the retina and optic nerve. Dilating drops (e.g., tropicamide, phenylephrine) permit detection of necrotic foci, vascular occlusions, and early detachments WikipediaEyeWiki.
Manual Tests
Amsler Grid Test
A simple square grid used to detect central visual field defects. Patients report wavy, missing, or distorted lines when fixating on a central dot, indicating macular or optic nerve involvement WikipediaNCBI.
Confrontation Visual Field Testing
Examiner compares the patient’s peripheral vision against their own, detecting gross field defects suggestive of peripheral necrosis or scotomas Wikipedia.
Color Vision Testing
Ishihara plates or similar tests evaluate optic nerve and macular function; deficits may accompany ARN due to photoreceptor loss Wikipedia.
Pupillary Light Reflex
Assessment of afferent and efferent pathways; a relative afferent pupillary defect (Marcus Gunn pupil) may indicate extensive retinal necrosis Wikipedia.
Laboratory and Pathological Tests
Polymerase Chain Reaction (PCR) of Aqueous/Vitreous Fluid
Highly sensitive and specific for HSV, VZV, CMV, and EBV DNA, confirming viral etiology and guiding targeted antiviral therapy EyeWikiPMC.
Viral Culture of Ocular Fluid
Traditional method for viral isolation; slower than PCR but can identify viable virus and antiviral sensitivities EyeWiki.
Serologic Testing for Herpes Viruses
Measurement of serum antibodies (IgM, IgG) can support recent or past infection but lacks intraocular specificity Wikipedia.
Complete Blood Count (CBC) with Differential
Assesses systemic immunocompetence and may reveal leukocytosis or lymphopenia, informing prognosis and management EyeWiki.
Electrodiagnostic Tests
Full-Field Electroretinography (ERG)
Records global retinal electrical responses to light stimuli; decreased amplitudes reflect widespread photoreceptor dysfunction Wikipedia.
Multifocal ERG
Measures localized retinal function in multiple regions, detecting areas of preserved or lost activity in necrotic zones Wikipedia.
Pattern ERG (PERG)
Assesses macular and ganglion cell layer integrity by recording responses to patterned visual stimuli, sensitive to central retinal damage Wikipedia.
Visual Evoked Potentials (VEP)
Evaluates post-retinal visual pathway integrity; delayed latencies or reduced amplitudes can result from severe retinal inflammation Wikipedia.
Imaging Tests
Optical Coherence Tomography (OCT)
Provides high-resolution cross-sectional images of retinal layers, revealing thinning, necrosis, and secondary cystoid changes WikipediaWikipedia.
Fundus Photography
Color and autofluorescence images document extent and progression of necrotic lesions, arteriolar sheathing, and retinal detachment WikipediaWikipedia.
Fluorescein Angiography (FA)
Dynamic imaging of retinal circulation using intravenous fluorescein dye; identifies areas of non-perfusion, vessel leakage, and neovascularization risk Wikipedia.
Indocyanine Green Angiography (ICGA)
Visualizes choroidal vasculature with infrared-excited dye, complementing FA when choroidal involvement is suspected Wikipedia.
B-Scan Ocular Ultrasound
Useful when media opacities (e.g., dense vitritis) obscure fundus view; detects retinal detachment, vitreous opacities, and choroidal thickening Nature.
Non-Pharmacological Treatments
Below are supportive, adjunctive therapies for patients recovering from or at risk of ARN. Each is described with its purpose and underlying mechanism.
Physiotherapy & Electrotherapy Therapies
Low-Vision Rehabilitation Exercises
Description: Customized visual training sessions to improve the use of residual vision.
Purpose: Enhance visual field awareness and contrast sensitivity to maximize remaining sight.
Mechanism: Through structured eye-movement tasks (e.g., scanning patterns), neural plasticity is engaged to optimize the brain’s interpretation of limited retinal input.Oculomotor Training
Description: Eye-movement control exercises, such as smooth pursuit and saccade drills.
Purpose: Improve coordination between eyes and reduce visual distortions from irregular retinal scarring.
Mechanism: Repeated practice strengthens supranuclear pathways controlling eye muscles, allowing better tracking and fixation.Transcorneal Electrical Stimulation (TES)
Description: Low-level electrical currents delivered via a corneal electrode in therapy sessions.
Purpose: Promote retinal cell survival and reduce inflammation after necrosis.
Mechanism: TES upregulates neurotrophic factors (e.g., BDNF), enhancing photoreceptor and retinal ganglion cell health.Photobiomodulation (Low-Level Light Therapy)
Description: Exposure of the retina to near-infrared light (∼670 nm) using specialized goggles.
Purpose: Accelerate tissue repair and reduce oxidative stress.
Mechanism: Cytochrome c oxidase in mitochondria absorbs infrared light, boosting ATP production and lowering reactive oxygen species.Pulsed Electromagnetic Field Therapy (PEMF)
Description: Non-invasive application of pulsed magnetic fields around the orbit.
Purpose: Support retinal microcirculation and anti-inflammatory processes.
Mechanism: PEMF modulates nitric oxide pathways in endothelial cells, improving blood flow and inhibiting pro-inflammatory cytokines.Iontophoresis-Assisted Ocular Delivery
Description: Use of mild electric currents to drive therapeutic ions (e.g., antioxidants) across ocular tissues.
Purpose: Enhance local delivery of supportive nutrients without injections.
Mechanism: Electric fields increase permeability of scleral and conjunctival tissues, boosting transscleral diffusion of charged molecules.Ultrasound-Mediated Microbubble Therapy
Description: Low-intensity ultrasound pulses in combination with microbubble contrast agents.
Purpose: Open the blood-retinal barrier transiently for drug-free antioxidant or stem cell support.
Mechanism: Acoustic cavitation induces microstreaming that transiently loosens tight junctions, facilitating nutrient exchange.Orbital Compression Therapy
Description: Mild mechanical pressure applied intermittently to the closed eyelid using a specialized device.
Purpose: Reduce intraocular inflammation and encourage fluid outflow.
Mechanism: Cyclical compression promotes lymphatic drainage in orbital tissues and lowers pro-inflammatory cell infiltration.Magnetostimulation of Optic Nerve
Description: Transcranial magnetic stimulation targeted at the visual cortex/optic radiations.
Purpose: Support central visual processing when retinal input is compromised.
Mechanism: Magnetic pulses induce small electric currents in neural tissue, enhancing synaptic efficacy in visual pathways.Microcurrent Cranial Nerve Stimulation
Description: Very low-amplitude currents applied via skin electrodes around the eyelids.
Purpose: Modulate ocular neuroinflammation and pain.
Mechanism: Microcurrents activate endogenous opioid pathways and inhibit pro-inflammatory glial activation.
Exercise Therapies
Guided Saccadic Training
Description: Rapid eye-shift exercises between fixed targets.
Purpose: Sharpen residual eye-movements for efficient scanning of the visual scene.
Mechanism: Enhances coordination in the frontal eye fields and superior colliculus, improving visual search capabilities.Contrast Sensitivity Drills
Description: Exercises using graded contrast images (e.g., letters or objects).
Purpose: Train the brain to detect low-contrast stimuli in areas of retinal damage.
Mechanism: Repetitive exposure increases sensitivity of surviving photoreceptors and adaptation of visual cortex neurons.Head Tracking and Stabilization
Description: Coordinated head-and-eye movement drills while fixating on moving targets.
Purpose: Minimize dizziness and oscillopsia from irregular retinal signals.
Mechanism: Vestibulo-ocular reflex pathways are recalibrated to stabilize gaze during head motion.Peripheral Awareness Expansion
Description: Exercises to consciously direct attention to peripheral visual fields.
Purpose: Compensate for central scotomas by maximizing peripheral field usage.
Mechanism: Cognitive-perceptual training increases cortical representation of peripheral inputs.Neck and Posture Alignment
Description: Simple postural exercises to align head, neck, and spine.
Purpose: Reduce musculoskeletal strain from compensatory head tilt to view through intact retina.
Mechanism: Correct posture decreases tension in cervical muscles, easing ocular motility.
Mind-Body Therapies
Guided Imagery for Visual Comfort
Description: Relaxation scripts that involve “seeing” calming scenes internally.
Purpose: Reduce anxiety, eye strain, and improve adaptation to vision loss.
Mechanism: Activates parasympathetic nervous system, lowering intraocular inflammation.Mindfulness Meditation
Description: Focused attention on present-moment experiences (e.g., breath).
Purpose: Alleviate psychological stress, which can exacerbate inflammatory cascades.
Mechanism: Downregulation of HPA-axis and NF-κB signaling reduces systemic cytokine levels.Biofeedback-Assisted Ocular Relaxation
Description: Real-time feedback of eyelid muscle tension via surface electrodes.
Purpose: Teach patients to consciously relax periocular muscles to ease eye discomfort.
Mechanism: Operant conditioning leads to sustained reduction in muscular spasm and ocular pressure.
Educational & Self-Management
Structured Patient Education Modules
Description: Written and multimedia resources covering ARN pathogenesis, warning signs, and care steps.
Purpose: Empower patients to recognize symptom progression and adhere to follow-up schedules.
Mechanism: Knowledge reinforcement enhances self-efficacy and timely healthcare utilization.Digital Monitoring Apps
Description: Smartphone apps for logging vision changes, medication adherence, and symptoms.
Purpose: Maintain continuous patient-clinician communication and early detection of complications.
Mechanism: Automated alerts and data tracking support proactive management and rapid intervention.
Key Pharmacological Agents
Below are the cornerstone drugs for ARN, each with dosage, drug class, timing, and notable side effects.
Intravenous Acyclovir
As the first-line antiviral for ARN, acyclovir (class: nucleoside analogue) is given at 10 mg/kg every 8 hours for 7–10 days. Early initiation within 24–48 hours of symptom onset reduces viral replication and retinal necrosis. Side effects include reversible nephrotoxicity and, rarely, neurotoxicity (e.g., confusion) at high doses.Oral Valacyclovir
A prodrug of acyclovir (class: nucleoside analogue), dosed at 1 g three times daily, is often used to complete a 6-week course after IV therapy. Advantages include better bioavailability, but patients should hydrate well to reduce renal strain. Side effects: headache, nausea.Intravenous Foscarnet
A pyrophosphate analogue reserved for acyclovir-resistant cases, 90 mg/kg every 12 hours for 14–21 days. It inhibits viral DNA polymerase directly. Side effects include electrolyte disturbances (hypocalcemia, hypomagnesemia) and potential renal impairment; close monitoring is essential.Intravitreal Ganciclovir
Intraocular injection of 2 mg/0.1 mL ganciclovir (class: guanine analogue) may be given weekly for 2–4 weeks alongside systemic therapy. Provides high local concentrations to halt retinal viral load. Side effects: mild local inflammation; rare retinal toxicity if overdosed.Intravitreal Foscarnet
A 2.4 mg/0.1 mL injection (class: pyrophosphate analogue) weekly can be combined with systemic antivirals. Useful for sight-saving in severe necrosis. Minimal systemic side effects; local discomfort at injection site.Systemic Prednisone
A corticosteroid used adjunctively to reduce immune-mediated retinal damage, typically 1 mg/kg/day orally after 48 hours of antiviral therapy, then tapered over 4–6 weeks. Side effects: hyperglycemia, hypertension, osteoporosis with prolonged use.Valganciclovir
Oral prodrug of ganciclovir (class: guanine analogue) at 900 mg twice daily for 21 days, then once daily for maintenance. Offers convenience but can cause bone marrow suppression (neutropenia).Cidofovir (Intravitreal)
Acyclic nucleotide analogue injected at 5 µg/0.1 mL, usually a single dose. Reserved for refractory cases; risk of intraocular inflammation and hypotony.Famciclovir
Oral prodrug of penciclovir (class: nucleoside analogue), dosed at 500 mg three times daily for 21 days. Alternative for outpatient therapy; side effects include mild gastrointestinal upset and headache.Ganciclovir Implant
An intraocular sustained-release device delivering 0.4 mg/day for up to 5 months. Minimizes systemic toxicity. Surgical implantation risks include endophthalmitis and device migration.
Dietary Molecular Supplements
Adjunctive oral supplements may support retinal health and reduce oxidative damage in ARN recovery.
Omega-3 Fatty Acids (DHA/EPA)
Dosage: 1 g twice daily.
Function: Anti-inflammatory; supports photoreceptor membrane integrity.
Mechanism: Inhibits NF-κB and COX pathways, lowering cytokine-mediated damage.Lutein & Zeaxanthin
Dosage: 10 mg lutein + 2 mg zeaxanthin daily.
Function: Filter blue light; antioxidant.
Mechanism: Concentrated in macula, they neutralize free radicals and reduce phototoxicity.Vitamin C
Dosage: 500 mg twice daily.
Function: Water-soluble antioxidant.
Mechanism: Scavenges reactive oxygen species, regenerates vitamin E.Vitamin E (α-tocopherol)
Dosage: 400 IU daily.
Function: Lipid-soluble antioxidant.
Mechanism: Protects cell membranes from peroxidation.Zinc
Dosage: 40 mg elemental zinc daily.
Function: Cofactor for antioxidant enzymes.
Mechanism: Supports superoxide dismutase and metallothionein, reducing oxidative stress.Selenium
Dosage: 100 µg daily.
Function: Component of glutathione peroxidase.
Mechanism: Catalyzes reduction of peroxides, protecting retinal cells.N-Acetylcysteine (NAC)
Dosage: 600 mg twice daily.
Function: Precursor to glutathione.
Mechanism: Boosts intracellular glutathione, enhancing detoxification.Astaxanthin
Dosage: 4 mg daily.
Function: Strong antioxidant and anti-inflammatory.
Mechanism: Quenches singlet oxygen and inhibits pro-inflammatory enzymes.Resveratrol
Dosage: 150 mg daily.
Function: Activates sirtuins; anti-inflammatory.
Mechanism: Modulates NF-κB and COX-2, reducing retinal inflammation.Alpha-Lipoic Acid
Dosage: 300 mg daily.
Function: Recycles other antioxidants; anti-glycation.
Mechanism: Regenerates vitamins C/E and glutathione; chelates metal ions.
Advanced Regenerative & Viscosupplementation Therapies
These emerging treatments aim to repair or protect retinal tissue after necrosis.
Mesenchymal Stem Cell (MSC) Intravitreal Injection
Dosage: 1×10⁶ cells in 0.1 mL, single or repeated.
Function: Promote tissue repair and immunomodulation.
Mechanism: MSCs secrete neurotrophic factors (e.g., GDNF) and anti-inflammatory cytokines.Induced Pluripotent Stem Cell (iPSC)-Derived RPE Transplant
Dosage: Transplant of a monolayer sheet (~2 × 2 mm).
Function: Replace damaged retinal pigment epithelium.
Mechanism: Restores RPE support to photoreceptors, improving metabolic exchange.Intravitreal Hyaluronic Acid Viscosupplement
Dosage: 50 µL of 1.5% solution monthly.
Function: Provide mechanical support and hydration to vitreoretinal interface.
Mechanism: HA binds water, stabilizes vitreous gel, and may reduce traction on necrotic retina.Recombinant Neurotrophic Factor Injections
Dosage: BDNF 50 µg/0.1 mL intravitreally quarterly.
Function: Enhance neuronal survival.
Mechanism: BDNF binds TrkB receptors on retinal ganglion cells, activating anti-apoptotic pathways.Gene Therapy with CRISPR-Based Antiviral Constructs
Dosage: Single subretinal injection of viral vector encoding HSV-targeting guide RNA.
Function: Directly degrade viral DNA in retinal cells.
Mechanism: CRISPR/Cas9 system cleaves viral genome, halting replication.Platelet-Rich Plasma (PRP) Intravitreal Injection
Dosage: 0.1 mL of autologous PRP monthly for 3 months.
Function: Deliver concentrated growth factors.
Mechanism: PDGF, VEGF, and TGF-β in PRP stimulate angiogenesis and tissue repair.
Surgical Interventions
Surgery is reserved for complications such as retinal detachment or epiretinal membrane.
Vitrectomy
Procedure: Removal of vitreous gel and membranes; fluid-air exchange.
Benefits: Relieves traction, clears inflammatory debris, and allows direct laser retinopexy.Pars Plana Lensectomy
Procedure: Removal of cataractous lens through pars plana approach.
Benefits: Improves visualization for vitrectomy and reduces light scattering in inflamed eye.Retinal Detachment Repair with Silicone Oil Tamponade
Procedure: Placement of silicone oil after vitrectomy.
Benefits: Provides long-term internal support to reattached retina, lowering redetachment risk.Scleral Buckling
Procedure: Placement of an external band to indent sclera beneath a retinal break.
Benefits: Reinforces retinal adherence and reduces fluid accumulation under retina.Epiretinal Membrane Peeling
Procedure: Delicate removal of scar tissue on retinal surface via microforceps.
Benefits: Restores retinal contour, reducing metamorphopsia and improving vision.
Prevention Strategies
Reducing risk of ARN or its bilateral spread involves:
Prompt Shingles/HSV Treatment: Early antiviral therapy for herpes zoster or simplex infections.
Vaccination: Use of VZV vaccine in older adults to lower zoster risk.
Regular Ophthalmic Exams: Follow-up every 1–2 weeks during acute phase to catch early complications.
Protective Eyewear: UV-blocking glasses during outdoor exposure to reduce phototoxic stress.
Optimized Glycemic Control: In diabetic patients, maintain HbA1c < 7% to improve immune response.
Smoking Cessation: Smoking increases oxidative stress; quitting reduces inflammatory mediators.
Nutrition Optimization: Diet rich in antioxidants (fruits, leafy greens) to support retinal health.
Stress Management: Chronic stress impairs immunity; mind-body techniques lower systemic inflammation.
Avoid Ocular Trauma: Wear protective goggles in high-risk activities to prevent viral reactivation from injury.
Adherence to Follow-Up: Strict compliance with scheduled visits ensures early detection of fellow-eye involvement.
When to See a Doctor
Seek immediate ophthalmic evaluation if you experience any of the following—ideally within 24 hours:
Sudden onset of floaters or “cobweb” vision.
Photopsia (flashes of light) in peripheral or central vision.
Rapid decrease in visual acuity.
Eye redness with pain or headache.
New onset of a dark “veil” over vision.
Delays beyond 48 hours significantly raise the risk of severe vision loss or fellow-eye involvement.
What to Do & What to Avoid
Do:
Keep all antiviral appointments and medication refills on schedule.
Rest in a dimly lit environment to minimize phototoxic stress.
Use preservative-free lubricating drops to ease ocular dryness.
Apply cold compresses (10 minutes, 3×/day) to lessen eyelid swelling.
Report any new floaters or flashes immediately.
Avoid:
Rubbing or pressing the eye, which can worsen inflammation.
Over-the-counter steroid eye drops without physician approval.
Smoking or secondhand smoke exposure.
High-impact activities that raise intraocular pressure (e.g., heavy lifting).
Skipping scheduled optical coherence tomography (OCT) or fundus exams.
Frequently Asked Questions
What causes Acute Retinal Necrosis?
ARN is most often triggered by reactivation of dormant herpes viruses (VZV, HSV) in retinal cells, leading to necrotizing retinitis.Can ARN affect both eyes?
Yes. Without prompt treatment, contralateral eye involvement occurs in up to 70% of cases within weeks.How is ARN diagnosed?
Diagnosis is clinical—based on retinal whitening, vasculitis, and vitritis—and confirmed by PCR testing of aqueous or vitreous samples for viral DNA.Is vision loss permanent?
Delayed treatment increases risk of permanent scarring and detachment. Early antivirals and close monitoring can preserve vision in many cases.What is the role of steroids?
Systemic corticosteroids, started 48 hours after antivirals, reduce immune-mediated damage but require careful tapering to avoid viral resurgence.How long is the treatment course?
Initial IV antivirals last 7–10 days, followed by oral antivirals for 4–6 weeks. Intravitreal injections may continue for several weeks.Are there side effects of intravitreal injections?
Transient pain, mild inflammation, or hemorrhage can occur at the injection site, but serious complications are rare.Can ARN recur?
Recurrences are uncommon with adequate antiviral prophylaxis but possible, especially if immune suppression occurs.Should family members be tested?
ARN is not contagious through casual contact; family testing is not required unless they develop ocular symptoms.Is there a vaccine to prevent ARN?
No specific ARN vaccine exists, but VZV vaccination reduces zoster risk, indirectly lowering ARN likelihood due to VZV.Can ARN present with painless vision loss?
Yes; while pain is common, some patients report painless floaters or blurriness initially.How frequently should I follow up?
Weekly exams during the acute phase, then monthly until inflammation fully resolves.What is the prognosis for children?
Children may have more aggressive disease; early diagnosis and therapy are critical to prevent bilateral involvement.Are there lifestyle changes to support recovery?
A balanced diet rich in antioxidants, regular sleep, and stress reduction exercises can support retinal health.When can I resume normal activities?
Light activities (reading, walking) are permitted once vision stabilizes; avoid strenuous exertion until your ophthalmologist clears you.
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: July 10, 2025.
