Herpes Zoster Ophthalmicus: Recognition, HIV-Associated Risk and Emergency Eye Care

Herpes zoster ophthalmicus: emergency recognition, HIV-associated risk, eye complications and treatment

Herpes zoster ophthalmicus (HZO) is reactivation of varicella-zoster virus (VZV) in the ophthalmic division of the trigeminal nerve (V1). A painful unilateral forehead rash may be the first clue, but the cornea, uvea, retina, optic nerve, orbit and cranial nerves can also be affected. Disease may threaten sight at presentation or recur after the skin has healed. In people living with HIV, HZO can occur at younger ages, may be atypical or extensive, and can progress to severe retinal disease.

Learning outcomes

After this guide, learners should be able to explain VZV reactivation in V1; identify the rash and Hutchinson sign; assess the skin, eye and nervous system safely; recognize common and sight-threatening ocular complications; start appropriate systemic antiviral treatment without delaying for tests; apply a lower threshold for escalation in HIV; counsel about contagion and delayed recurrence; and arrange follow-up after the rash resolves.

Coverage of the supplied 35-slide presentation

This article follows the full 35-slide SlideShare deck. Some slides present clinical photographs or duplicate images without additional text; their relevant clinical content is represented in the case, localization, examination and complication sections. The source’s adult case is anonymized and updated. Drug doses and steroid directions from older slides are treated as historical teaching material, not copied as unsupervised prescriptions.

1. Cause and pathophysiology

VZV is an enveloped double-stranded DNA virus in the herpesvirus family. Primary infection causes varicella (chickenpox). After the acute illness resolves, VZV becomes latent in sensory ganglia, including the trigeminal ganglion. Years later, declining VZV-specific cellular immunity can permit reactivation. Virus travels along a sensory nerve to the skin and sometimes into ocular tissues. The result is shingles, usually a painful unilateral rash in one or adjacent dermatomes.

When reactivation affects the ophthalmic branch of cranial nerve V, it can involve the forehead, scalp, upper eyelid and ocular surface. The rash usually stays on one side of the face and does not cross the midline. It may be preceded by burning, tingling, allodynia, itching or deep pain. Fever, malaise, headache and fatigue can occur. Vesicles emerge in crops, then pustulate and crust; healing may leave pigment change, scars or lid-margin damage. In immunocompromised people, new lesions may continue longer or involve multiple dermatomes.

Why HIV changes the risk

HIV is associated with more frequent zoster, particularly when HIV is viraemic or CD4 counts are low. Zoster can also appear during the months after antiretroviral therapy (ART) starts, possibly as an immune reconstitution inflammatory syndrome (IRIS). An HZO presentation should prompt a respectful review of known HIV status, ART use, adherence, recent treatment changes, CD4 count and viral load when clinically available. If status is not known, testing should follow local consent, counselling and confidentiality requirements. HZO alone does not diagnose HIV, and a person with well-controlled HIV can still develop shingles.

In HIV, watch for multidermatomal or disseminated rash, persistent new lesions, necrotic or haemorrhagic lesions, visceral or central nervous system symptoms, ocular inflammation, and retinal necrosis. A rash confined to one dermatome in an otherwise stable patient can still be treated orally; severe or complicated disease needs hospital-based assessment and often intravenous treatment.

2. Recognize HZO at the bedside

V1 distribution

Map the rash rather than describing only “facial shingles.” V1 supplies the forehead, upper eyelid and scalp. The nasociliary branch also supplies the tip and side of the nose and parts of the eye. Vesicles on the tip of the nose are known as Hutchinson sign and increase concern for ocular involvement. The sign is a risk clue, not a diagnostic requirement: its absence does not rule out keratitis, uveitis or later eye disease.

Check for lesions on the eyelid margin, conjunctival injection or discharge, corneal haze, photophobia, ptosis, facial oedema and globe displacement. Eye involvement can be present before the skin eruption is fully developed or emerge later. Some patients have VZV eye disease without a typical rash (zoster sine herpete); specialist assessment is needed when the history and ocular findings suggest it.

Do not mistake VZV for HSV

HZO and herpes simplex virus (HSV) can both cause painful vesicles and epithelial keratitis. VZV more often follows a unilateral V1 dermatome with substantial neuralgic pain and reduced corneal sensation; HSV can recur in the same area and cause classic branching epithelial dendrites with terminal bulbs. VZV pseudodendrites are often raised, irregular and less likely to have terminal bulbs. These are patterns rather than rules. Clinical overlap is real, and recurrent vesicles in the same small area, atypical lesions or treatment failure should trigger reconsideration of HSV and other diagnoses.

3. Emergency assessment

History

• Establish onset of pain, rash and eye symptoms; whether vision is changing; and whether new skin lesions are still appearing.
• Ask about previous chickenpox or zoster, previous HZO, prior eye disease, contact lenses, eye surgery and treatment already taken.
• Screen for photophobia, foreign-body sensation, tearing, redness, blurred vision, floaters, flashes, a curtain or field defect, diplopia, ptosis and pain on eye movement.
• Ask about headache, confusion, weakness, numbness, facial palsy, hearing symptoms, fever, neck stiffness, vomiting, urinary symptoms, abdominal pain, cough or shortness of breath.
• For HIV: document ART, recent ART initiation or restart, adherence, latest CD4/viral load if available, prior opportunistic infections and immunosuppressive treatment. Also ask about cancer, transplant, chemotherapy, pregnancy and renal disease.

Examination

1. Visual acuity: measure each eye separately with habitual correction and pinhole when appropriate. In children or patients who cannot read a chart, document fixation, following and age-appropriate response. A new reduction is an urgent finding.
2. Skin and lids: map each involved dermatome, laterality, midline crossing, lesion stage, distribution on the nose and eyelid margin, scarring, secondary infection and evidence of dissemination. Look for Hutchinson sign, but do not use its absence to reassure.
3. Eye position and movement: inspect for ptosis, proptosis, lid oedema and globe displacement. Check extraocular movements, pain, diplopia, pupil size/reactivity and a relative afferent pupillary defect.
4. Conjunctiva and cornea: assess injection, discharge, epithelial defect, haze, ulcer, infiltrate and corneal sensation. Test sensation before applying anaesthetic. Use fluorescein if available and safe.
5. Anterior segment and pressure: look for anterior-chamber cells/flare, abnormal pupil, iris atrophy and signs of trabeculitis. Measure intraocular pressure only if equipment and expertise are available and there is no concern for open globe or another contraindication.
6. Posterior segment and neurology: fundoscopy if feasible, while remembering that a limited direct exam does not exclude retinitis. Assess cranial nerves and a brief neurologic examination; arrange dilated retinal examination urgently if floaters, field loss, reduced vision or immunosuppression raises concern.

Emergency examination identifies risk and establishes a handover. It does not replace slit-lamp examination, dilated fundoscopy, intraocular pressure monitoring or serial review by an eye specialist. A clear-looking cornea on day one does not rule out stromal keratitis or uveitis later.

4. Ocular and neurologic complications

VZV inflammation can affect nearly every ocular tissue. One patient can have more than one complication, and complications can appear at different times.

Retinal necrosis in HIV

VZV can cause acute retinal necrosis in immunocompetent or immunocompromised patients. Progressive outer retinal necrosis is strongly associated with advanced immunosuppression, including very low CD4 counts. PORN may begin with multiple pale outer-retinal lesions and comparatively little inflammation, then progress rapidly to full-thickness necrosis and retinal detachment. Both conditions can blind quickly. New floaters, flashes, field loss or rapid acuity decline in a patient with HIV and zoster is an eye emergency even if the skin rash is mild.

Postherpetic neuralgia

Pain may persist after skin lesions heal and can feel burning, electric, stabbing, numb, itchy or painful to light touch. It can interfere with sleep, appetite, mood, mobility and daily function. Older age, severe acute pain and extensive rash increase the risk. Ask specifically about function and distress. Analgesia can include simple pain relief when safe and, for neuropathic pain, clinician-selected medicines such as gabapentin, pregabalin or a low-dose tricyclic antidepressant with gradual titration. Account for renal function, sedation, falls, cardiac/anticholinergic effects, pregnancy and interactions with ART or other medicines. Avoid presenting the source deck’s high initial amitriptyline dose as a starting prescription.

5. Diagnosis and investigations

Typical unilateral V1 pain followed by a compatible vesicular rash is usually diagnosed clinically. Treat first when suspicion is high; laboratory confirmation should not delay antiviral therapy or urgent referral.

• VZV PCR: consider a swab from the base of a fresh lesion when the rash is atypical, disseminated, recurrent, difficult to distinguish from HSV, or occurring in a substantially immunocompromised patient. Follow local laboratory instructions for lesion sampling.
• Ocular PCR: aqueous or vitreous testing may be used by specialists for uncertain or severe intraocular disease, including suspected retinitis. It is not a routine emergency-department test.
• Serology: a blood antibody result generally does not establish that an acute rash or ocular inflammation is caused by VZV. A Tzanck smear does not reliably distinguish HSV from VZV.
• Eye assessment: slit-lamp examination with fluorescein, corneal sensation, pressure measurement and dilated retinal examination help localize disease. OCT, retinal photography, angiography or ultrasound may be added by ophthalmology.
• Systemic assessment: CBC, renal function and other tests depend on severity, medication choice, dehydration, HIV status and suspected visceral or CNS involvement. Renal function matters for acyclovir/valacyclovir dosing.

Consider HSV, allergic/contact dermatitis, impetigo, bacterial preseptal/orbital cellulitis, insect bites, other vesicular infections and zoster sine herpete. A painful red eye can also represent keratitis, uveitis, scleritis, acute angle-closure glaucoma or endophthalmitis; a rash should not distract from assessing these emergencies.

6. Treatment principles for emergency clinicians

Start systemic antiviral treatment promptly

Systemic acyclovir, valacyclovir or famciclovir reduces acute VZV replication. Treatment has its greatest benefit when started early, commonly within 72 hours of rash onset. Do not withhold treatment merely because 72 hours have passed when new lesions are appearing, the patient is immunocompromised, or eye, neurologic or visceral involvement is suspected. Current NIH HIV guidance recommends treatment for zoster in people with HIV as soon as possible and within one week of rash onset, or before all lesions have crusted.

These adult regimens are teaching references, not a substitute for the current national protocol, product information or patient-specific prescribing. Adjust antiviral doses to kidney function and consult a pharmacist or specialist when renal impairment, pregnancy, complex ART, intolerance or drug interactions are present. Children need weight-based paediatric advice.

Eye-directed treatment requires ophthalmology

• Topical corticosteroids: may be required for stromal keratitis or anterior uveitis, but only after an eye specialist has characterized the disease, with systemic antiviral treatment and pressure monitoring. They can worsen epithelial viral disease if used alone. Do not send a patient home with steroid drops for an undifferentiated red eye or dendritic lesion.
• Topical antiviral: is not routinely added to systemic therapy for the initial skin eruption. NIH guidance reserves topical antiviral treatment for selected late dendriform corneal epithelial lesions when the patient is not receiving oral antivirals; an ophthalmologist should decide.
• Raised intraocular pressure: may require aqueous-suppressant treatment selected and monitored by an eye clinician; steroids can also raise pressure.
• Surface protection: preservative-free lubrication, careful lid hygiene and specialist review may be needed for reduced corneal sensation or exposure. Avoid contact lenses while the eye is inflamed. Do not place calamine, skin creams or topical anaesthetic drops in the eye.
• Systemic steroids: are not routine treatment for shingles in people with HIV; NIH does not recommend adjunctive corticosteroids for HIV-associated zoster because benefit is unsupported. Any exceptional use for orbital, optic-nerve or CNS inflammation requires joint specialist care and effective antiviral therapy.
• Pain: provide appropriate acute analgesia and reassess control. Persistent neuropathic pain merits follow-up rather than repeated short courses of ineffective analgesics.

When admission or transfer is appropriate

• Any decline in vision, corneal ulcer/haze, anterior uveitis with high pressure, retinal symptoms, afferent pupillary defect, cranial nerve palsy or suspected orbital apex involvement.
• Disseminated/multidermatomal disease, extensive necrotic lesions, fever/toxicity, severe immunosuppression, visceral or CNS signs, inability to take oral medicines or uncontrolled pain.
• Unavailability of urgent ophthalmology when eye involvement is suspected, especially in a child, a person with advanced HIV or a patient with retinal symptoms.

7. Transmission, prevention and patient counselling

A person with shingles can transmit VZV to someone who has never had chickenpox or varicella vaccination; that person develops chickenpox, not shingles. VZV spreads from active lesions until vesicles dry and crust. Cover the rash when possible, perform hand hygiene, avoid touching or rubbing the eye, and avoid direct contact with people who are susceptible and at higher risk (including newborns, pregnant people without immunity and severely immunocompromised people) until lesions crust. Follow local infection-control precautions, especially for disseminated zoster or immunocompromised inpatients.

Explain that eye problems can begin after the rash, recur for months, or be present before it. Give clear return advice for increasing pain/redness, photophobia, blurred vision, flashes, floaters, a curtain, new double vision, severe headache, confusion, weakness or new skin lesions. Do not discharge with “return if worse” alone: identify where the patient should go and how urgently.

Recombinant zoster vaccine (RZV) can reduce future shingles. For people with HIV who have not received RZV, NIH advises vaccination after the acute episode resolves; active VZV-related keratitis or anterior uveitis is a reason to defer vaccination until inflammation is inactive. Coordinate timing with the HIV clinic and follow the current national immunization schedule and availability. RZV is non-live. Do not use a live zoster vaccine in a severely immunocompromised patient.

8. Follow-up is essential

Every patient with V1 zoster should receive ophthalmologic assessment. Patients with a normal initial examination still need planned follow-up because stromal keratitis and anterior uveitis can develop after forehead/scalp vesicles and can recur after the rash resolves. Follow-up frequency is set by the eye findings and treatment, ranging from close review during acute inflammation to periodic monitoring for delayed ocular hypertension, glaucoma, cataract, corneal scarring or recurrent keratitis. In HIV, establish a reliable handover to ophthalmology and the HIV/ART team; check that the patient can attend and has a means to return if symptoms change.

9. Case-based application

Case 1: early facial rash and mild red eye

A 28-year-old adult presents after one day of left forehead and eyelid pain followed by grouped vesicles on the forehead, upper and lower eyelids, and tip of the nose. Visual acuity is 6/6 in the right eye and 6/9 in the left. Pupils and eye movements are normal. The left conjunctiva is mildly injected; the cornea is clear and fluorescein examination shows no epithelial defect.

Interpretation: Typical V1 herpes zoster with Hutchinson sign and mild ocular-surface inflammation. A normal cornea today does not exclude later keratitis or uveitis.

Action: Start systemic antiviral treatment promptly after checking renal function and contraindications; contact ophthalmology for prompt review; document acuity and corneal findings; counsel about lesion coverage and transmission; arrange follow-up even if the first detailed eye examination is normal.

Case 2: shingles with advanced HIV and visual decline

A person with HIV, recent ART interruption and a low CD4 count reports forehead rash, photophobia and rapidly worsening vision. Several new lesions are appearing beyond the initial dermatome, and fundoscopy suggests pale peripheral retinal lesions.

Interpretation: Disseminated VZV with possible necrotizing retinitis/PORN is an immediate sight-threatening emergency.

Action: Arrange admission and same-day retinal/ophthalmology and infectious-disease consultation. Initiate hospital-based IV antiviral treatment according to the current protocol and renal function. Do not rely on oral outpatient treatment, topical eye drops or routine clinic follow-up.

Case 3: late recurrent red eye after the rash healed

A patient treated for facial shingles three months ago returns with photophobia and blurred vision. The skin is healed; slit-lamp examination shows stromal corneal haze and anterior-chamber inflammation.

Interpretation: Delayed or recurrent VZV stromal keratitis/anterior uveitis is possible. This is not simply “post-shingles irritation.”

Action: Urgent ophthalmology care. A specialist may use topical steroid with systemic antiviral cover, monitor pressure and consider long-term suppressive treatment, including the NIH-recommended valacyclovir course in HIV-associated recurrent disease.

Case 4: a red, painful eye in a person with facial vesicles

A patient with V1 vesicles has a red painful eye, marked photophobia, irregular pupil and elevated pressure.

Interpretation: Anterior uveitis/trabeculitis with ocular hypertension is possible, but other acute red-eye emergencies must be excluded.

Action: Same-day ophthalmology assessment, systemic antiviral therapy and pressure management directed by the eye service. Do not begin steroid drops without confirming the corneal epithelial status and arranging antiviral cover.

10. Knowledge check

1. What virus causes HZO, and where does it remain latent between episodes?
2. What does Hutchinson sign indicate? Why does its absence not make the eye safe?
3. Which ocular complications can appear after the rash has started to heal?
4. What is the usual adult oral antiviral regimen for localized zoster in a person with HIV, and what factors change dose or route?
5. When are topical ocular corticosteroids appropriate, and what must accompany them?
6. Why are floaters or a field defect urgent in a person with HIV and V1 zoster?
7. How is shingles transmitted to a susceptible contact, and what disease does that contact develop?
8. Why should a recurrent cluster of vesicles in exactly the same spot raise the possibility of HSV?

Answers

1. Varicella-zoster virus, which remains latent in sensory ganglia including the trigeminal ganglion.
2. Vesicles on the nose tip suggest nasociliary V1 involvement and increased risk of ocular disease. Ocular disease may occur without the sign, so every V1 zoster patient needs an eye examination.
3. Stromal keratitis, anterior uveitis, ocular hypertension, late dendriform epithelial lesions, corneal scarring, cataract and glaucoma.
4. Valacyclovir 1 g orally three times daily is preferred; famciclovir 500 mg orally three times daily or acyclovir 800 mg orally five times daily are alternatives. HIV guidelines use 7–10 days, longer if lesions resolve slowly. Renal impairment may require dose adjustment; severe/disseminated, CNS or visceral disease may require IV acyclovir and admission.
5. For specialist-confirmed stromal keratitis or anterior uveitis, alongside systemic antiviral therapy and pressure monitoring. Do not use them alone for epithelial disease or an undiagnosed red eye.
6. It can indicate acute retinal necrosis or progressive outer retinal necrosis, which can rapidly cause retinal detachment and irreversible vision loss.
7. Through active vesicular fluid until lesions crust; susceptible contacts develop chickenpox, not shingles.
8. VZV generally follows a dermatome and does not commonly recur in exactly the same small cutaneous site, whereas HSV often recurs in a fixed location.

Key takeaways for emergency practice

• V1 shingles is an eye-risk presentation: start systemic antivirals and arrange ophthalmology review.
• Hutchinson sign raises risk but is not required for ocular disease.
• Vision change, photophobia, red eye, floaters, field loss, abnormal pupil, cranial nerve signs or low CD4 warrants urgent escalation.
• Use oral antiviral therapy for stable localized disease; use IV therapy and admission for severe, disseminated, visceral, CNS or retinal disease.
• Topical steroids are specialist treatment for stromal keratitis/uveitis with antiviral cover; avoid unsupervised steroid treatment.
• Follow-up continues after the rash heals because ocular inflammation can be delayed or recurrent.
• In HIV, assess ART/CD4 context, support linkage to care and discuss RZV after acute disease resolves and ocular inflammation is inactive.

References and further reading

1. Herpes zoster ophthalmicus. Supplied 35-slide teaching presentation on SlideShare.
2. U.S. National Institutes of Health. Varicella-Zoster Virus Disease: Adult and Adolescent Opportunistic Infections guideline (updated 2026).
3. American Academy of Ophthalmology EyeWiki. Herpes Zoster Ophthalmicus.
4. Cohen EJ, et al. Low-Dose Valacyclovir in Herpes Zoster Ophthalmicus: The Zoster Eye Disease Study Randomized Clinical Trial. JAMA Ophthalmology. 2025.
5. Centers for Disease Control and Prevention. Clinical Overview of Shingles: clinical features and transmission.
6. World Health Organization. Shingles (herpes zoster).

Educational material for emergency medicine students. It supports, but does not replace, local referral pathways, specialist consultation, current national treatment protocols, renal-dose adjustment or patient-specific clinical judgement.