Eye damage from herpes zoster: symptoms and treatment

Ocular herpes zoster is a reactivation of the varicella-zoster virus (the same virus that causes chickenpox), affecting the first branch of the trigeminal nerve and ocular structures. Symptoms may begin with unilateral pain and tingling on the forehead, followed by a vesicular rash across the dermatome and involvement of ocular tissues, from the conjunctiva and cornea to the choroid and optic nerve. Without early treatment, the risk of persistent vision loss and nerve pain is high. [1]

Why "early start"? Systemic antiviral drugs started as soon as possible (ideally within 72 hours of rash onset) accelerate skin healing and reduce the incidence of ocular complications and postherpetic neuralgia. This is supported by clinical reviews, practice patterns, and studies, which underpin current recommendations. [2]

A key element of the strategy is prevention. The recombinant zoster vaccine (Shingrix) significantly reduces the risk of shingles and its ocular forms in adults: it is recommended for everyone aged 50 and over, and for those with compromised immune systems, as early as 19 years. The vaccine is not live, is well tolerated, and its effectiveness has been confirmed in real-world practice. [3]

Finally, in people with weakened immune systems, the course of the disease is more severe: deep keratitis, iridocyclitis, and nerve damage are more common. In these groups, the threshold for prescribing systemic antiviral drugs and the observation periods differ, with greater activity and duration. Therefore, the strategy is always individualized and based on a standard, but adapted to the patient. [4]

How the virus causes eye problems: What happens in the tissues

After chickenpox, the zoster virus permanently resides in the sensory ganglia. With age or weakened cellular immunity, it can reactivate: virus particles travel along the supraorbital, lacrimal, and nasociliary branches to the skin and eye. Initially, the corneal epithelium (pseudodendrites) is affected, followed by the stroma and endothelium. The iris and ciliary body (uveitis) can also be affected, and sometimes the optic nerve. [5]

Neuroimmune inflammation is key to the pathogenesis. This explains why HZO is often accompanied by severe, burning pain, tear film dysfunction, and prolonged hyperalgesia. Early antiviral therapy reduces viral replication and secondary inflammation, thereby lowering the risk of long-term neuralgia. [6]

Immune dysregulation can prolong the process: stromal keratitis and uveitis persist for weeks, requiring anti-inflammatory agents under the umbrella of antiviral protection. Early treatment shortens the active phase and reduces the likelihood of scarring and increased intraocular pressure. [7]

In immunocompromised patients, the risk of necrotic forms and associated lesions (e.g., keratoretinitis) is higher. In these cases, systemic medications are typically prescribed at full doses, with longer observation periods and a slower tapering of anti-inflammatory drops to prevent relapse. [8]

How HZO manifests: from the skin to the deep structures of the eye

The typical onset is a prodromal itching/burning sensation and pain on one side of the forehead and upper eyelid; after 1-3 days, a grouped vesicular rash appears across the dermatome. Unilaterality is a clue: involvement of the nasociliary nerve (vesicles on the tip of the nose) increases the likelihood of ocular involvement. At this stage, an ophthalmological examination is necessary. [9]

Ocular symptoms include redness, lacrimation, photophobia, blurred vision, and eye pain. Examination may reveal epithelial pseudodendrites, stromal infiltrates, endotheliitis with large precipitates, anterior uveitis, and elevated intraocular pressure. The severity of ocular symptoms does not always correlate with the severity of skin pain, so the diagnosis is based on examination rather than sensation alone. [10]

Rare but serious complications include scleritis, retinitis, and optic neuritis. These manifest as a sharp decrease in vision, including "flashes" and "blind spots"—an emergency. Early diagnosis and treatment reduce the risk of irreversible outcomes. [11]

After the rash subsides, some patients experience postherpetic neuralgia—a long-term, sometimes excruciating pain. The earlier antiviral treatment is started, the lower the risk and duration of neuralgia; for established pain, specific pain management and neuromodulation strategies are used. [12]

Table 1. Red flags requiring urgent inspection

Sign	Why is it dangerous?	What to do
Unilateral rash on forehead/eyelid + eye pain	High risk of HZO	Initiate systemic antivirals and ophthalmologist examination ≤72 hours
A sharp decrease in vision, "curtain", flashes	Possible stromal keratitis, uveitis, retinitis	See an ophthalmologist immediately for a comprehensive diagnosis.
Severe photophobia, lacrimation	Corneal involvement	Urgently evaluate the cornea, pressure, and begin treatment.
Pain persists/increases after skin heals	Postherpetic neuralgia	Connect pain relief and neuroprotocols

When to seek help and what not to do

You should seek medical attention immediately if a unilateral, painful rash appears in the forehead/upper eyelid area—this is the "window of effectiveness" for antiviral medications. Ideally, therapy should begin within the first 72 hours: the sooner, the better. If the rash has already formed, treatment is still indicated, especially if there are ocular symptoms. [13]

Don't "suppress" red eye with combined drops containing hormones without a diagnosis: topical steroids for corneal epithelial lesions without antiviral protection can worsen the condition. The decision regarding hormone therapy should be made by an ophthalmologist, and only with antiviral coverage. [14]

If pain and rash are severe, avoid contact lenses and makeup, as they can damage the surface and increase the risk of secondary infection. During the acute phase, it's best to use protective glasses to protect against light and wind, and preservative-free tear substitutes. [15]

If you have a weakened immune system, any suspicious symptoms are a reason to contact your doctor sooner. In these situations, the course of antiviral therapy may be longer, and monitoring may be more intensive. [16]

Diagnostics: step-by-step algorithm

The first step is a skin examination and interview: localization of pain and rash in the V1 dermatome often allows for a clinical diagnosis of HZO without laboratory testing. It is important to clarify the timeframe: when the symptoms began, at what time the blisters appeared, whether there have been similar episodes before, and whether there are any diseases or therapies that reduce immunity. [17]

The second step is a slit-lamp examination. This examination evaluates the corneal epithelium (pseudodendrites), stroma and endothelium (edema, precipitates), the anterior chamber (cells/flare), and intraocular pressure. This examination is the "gold standard" for the initial verification of ocular involvement. [18]

The third step is testing as indicated. Polymerase chain reaction (PCR) of conjunctival/corneal scrapings is helpful in atypical cases or in immunocompromised patients. If posterior segment involvement is suspected, optical coherence tomography is performed, and if necessary, angiography. General clinical tests are performed based on associated conditions. [19]

The fourth step is a dynamic assessment of the effect 24-72 hours after the start of therapy. When prescribing steroids, intraocular pressure must be monitored and the dose tapered slowly to avoid relapse. [20]

Table 2. Diagnostic "key"

Find	What does it mean	What's next?
Unilateral dermatomal rash	Zoster reactivation	Start of systemic antiviral drugs
Pseudodendrites in the epithelium	Epithelial keratitis HZO	Antiviral, without "self-steroids"
Stromal infiltrates/endotheliitis	Immune phase	Antivirals + steroids under control
Uveitis/high IOP	Anterior compartment involvement	Antivirals, steroids, blood pressure control

How HZO differs from other red eyes: differential diagnosis

HZO differs from bacterial keratitis by its association with a dermatomal rash and the absence of purulent stromal melting; bacteria more often have a pronounced infiltrate, pus, hypopyon, and an acute course without "dermatomal" skin. When in doubt, the diagnosis is based on the anamnesis and the rapid response of antiviral drugs. [21]

Herpes simplex ocular herpes simplex differs from herpes simplex ocular herpes by its skin "geography" and the type of epithelial defect: HSV has classic dendrites with beaded edges, while HZO has pseudodendrites and severe neuropathic pain. The treatment is similar in terms of antiviral therapy, but systemic therapy is the rule for HZO. [22]

Allergic conjunctivitis causes itching, lacrimation, and swelling, but lacks a dermatomal rash and typical corneal findings. Toxic keratopathies present with punctate erosions without a dermatomal pattern and systemic pain. A thorough history is often decisive. [23]

Rarely, "zoster without rash" occurs—unilateral pain along a dermatome with ocular symptoms. Polymerase chain reaction and antiviral therapy are helpful. In difficult cases, interdisciplinary consultation is necessary. [24]

Treatment

The mainstay of treatment is systemic antiviral medications at full doses, started as early as possible (ideally, ≤72 hours after the rash appears). Acyclovir, valacyclovir, or famciclovir are used for a 7-10-day course; the choice depends on availability and associated factors. Early initiation reduces the duration of the active phase and the risk of postherpetic neuralgia. [25]

In cases of epithelial corneal lesions, topical antiviral medications can complement systemic treatment, but oral medications remain the key. Steroids are contraindicated at this stage, as they suppress epithelialization and can worsen the defect. Decisions regarding topical therapy are made by an ophthalmologist. [26]

For stromal keratitis and endothelial keratitis, topical glucocorticosteroids are added to antiviral medications, tapering off gradually under pressure control. This combination is necessary to control immune inflammation and prevent scarring. Visit intervals at the beginning of treatment are short. [27]

Anterior uveitis is treated similarly: systemic antivirals plus topical steroids and cycloplegics as indicated, with regular tonometry. If pressure remains elevated, hypotensive drops are added. The goal is to prevent trabecular damage and secondary glaucoma. [28]

Pain management is a separate area. In the acute phase, stepped analgesia is used; if neuralgia is at risk, early use of neuromodulators is considered. Randomized trials of systemic antiviral agents show a reduction in the incidence and duration of postherpetic neuralgia with early onset. [29]

Immunocompromised patients often require longer courses and more frequent visits. In some cases, parenteral regimens and inpatient observation are considered for severe necrotic forms. Individualization is the key to safety and success. [30]

Protecting the ocular surface accelerates recovery: preservative-free tear substitutes, gentle protective lenses for neurotrophic lesions, and prevention of secondary bacterial infection in cases of severe epithelial defects. Eyelid hygiene and temporary avoidance of contact lenses are essential. [31]

Prevention of relapses after severe HZO is being actively studied. The role of long-term antiviral "maintenance" in certain subgroups is under discussion; preliminary data from the ZEDS (Zoster Eye Disease Study) indicate a potential benefit of long-term valacyclovir in reducing some outcomes, but interpretation of the data requires consideration of endpoints and risk group. Decisions are currently made on a case-by-case basis. [32]

Patient education is part of treatment: explain the difference between epithelial and stromal forms, the dangers of "self-steroids," the importance of starting pills early and adhering to the appointment schedule. This approach reduces anxiety and improves adherence, which directly impacts outcome. [33]

Finally, coordination with a general practitioner/neurologist is essential. Some patients require long-term management of neuralgia, correction of comorbidities, and vaccination after stabilization of the process to reduce the risk of recurrence in the future. [34]

Table 3. First-line drugs (guidelines)

Situation	Basic tactics	Comments
Acute HZO (skin ± eye)	Systemic antivirals 7-10 days	Start ≤72 hours, but later is also indicated for ocular forms
Epithelial keratitis	Systemic ± local antivirals	Avoid steroids without cover
Stroma/endothelium/uveitis	Antivirals + topical steroids	Slow "convergence", pressure control
Neuralgia	Stepwise analgesia, neuromodulators	Early initiation of antiviral therapy reduces the risk

Prevention: Vaccine and Everyday Measures

The recombinant zoster vaccine (Shingrix) is recommended for all adults 50 years and older—two doses, 2-6 months apart. For immunocompromised adults, it is recommended starting at age 19, sometimes with a shorter interval between doses for clinical reasons. The vaccine reduces the risk of herpes zoster and its ocular forms. [35]

Vaccination is recommended even for those who have already had ringworm: relapse is possible, and the vaccine reduces the likelihood of relapse and severe complications. It is most beneficial before the first episode, but even afterward, it is an important risk-reduction tool. [36]

Everyday measures include protecting the skin and eyes from excessive ultraviolet radiation (glasses, hats), caring for the surface of the eye when dry (tear substitutes), and careful handling of contact lenses. These steps do not replace the vaccine, but they help reduce triggers and improve treatment tolerance. [37]

Immunization is part of an overall strategy for older age groups and people with chronic illnesses. Discussing your vaccination schedule with your doctor is a simple way to effectively reduce the risk and burden of illness, including eye diseases. [38]

Table 4. Shingrix Vaccination: Quick Guide

To whom	Scheme	Notes
Adults ≥50 years	2 doses, 2-6 months between doses	Regardless of previous lichen or an old vaccine
Immunocompromised ≥19 years	2 doses; the interval may be shorter if indicated	This is decided with the attending physician.
I already had lichen/HZO	They vaccinate anyway	Reduces the risk of recurrence

Forecast: What it depends on and how to improve it

The best prognosis is achieved with early initiation of antiviral therapy and timely control of inflammation. Most patients respond well to therapy and return to normal activities; the earlier the course is started, the fewer complications and pain in the long term. [39]

Unfavorable factors include late presentation, severe uveitis/endotheliitis, necrotic forms in immunocompromised patients, and prolonged postherpetic neuralgia. Their impact can be partially mitigated by aggressive early management and subsequent follow-up. [40]

Vaccination is important for preventing recurrences and reducing population risk. Increased vaccination coverage in groups over 50 years of age is already associated with a reduction in morbidity and complications, as reflected in real-world cohorts and recommendations. [41]

Complex cases require interdisciplinary work (ophthalmologist, general practitioner/infectious disease specialist, neurologist). This approach not only improves outcomes but also reduces patient anxiety, especially if the treatment is explained in advance. [42]

Table 5. Common complications and how to prevent them

Complication	Why does it arise?	What reduces the risk
Corneal scarring, decreased vision	Treatment delay, immune inflammation of the stroma	Early antivirals + steroids for stroma
Secondary glaucoma	Uveitis, steroids	Pressure control, slow "convergence"
Postherpetic neuralgia	Neuroimmune cascade	Antiviral ≤72 hours, adequate pain relief
Neurotrophic keratopathy	Damage to sensory fibers	Protecting the surface of the eye

Frequently Asked Questions (FAQ)

Should I start taking medications if the rash appeared "yesterday" and the eye doesn't hurt yet?
Yes. Systemic antiviral medications taken within 72 hours reduce the risk of complications and accelerate healing, even if eye symptoms are still minimal. If eye complaints develop, consult an ophthalmologist immediately. [43]

Can I treat
HZO with drops alone? No. Systemic antiviral medications are the mainstay. Drops and ointments are optional, as indicated, especially in cases of stromal/endothelial involvement. [44]

Do hormonal eye drops help?
Yes, for stromal/endothelial inflammatory disease and uveitis, along with antiviral protection and under a doctor's supervision. Hormones are contraindicated for uncovered epithelial lesions. [45]

Is the vaccine necessary if I've already had shingles?
Yes. The virus remains in the body and can reactivate. Shingrix is recommended for everyone over 50 years of age and for immunocompromised individuals over 19 years of age, regardless of previous infection. [46]

Is it true that long-term antiviral therapy after HZO prevents relapses?
The data are still evolving. The ZEDS study examined prophylactic valacyclovir; interim reports suggest potential benefit for a range of outcomes, but the decision is currently individualized. Discuss this with your ophthalmologist. [47]

Table 6. A short “action navigator” for the patient

Situation	What to do today	What to discuss with your doctor
Unilateral rash on forehead/eyelid	Start systemic antiviral treatment	Timing and dosage, eye examination plan
Pain, photophobia, "fog"	See an ophthalmologist urgently	Are steroids and intraocular pressure control necessary?
The pain persists after healing	Pain relief, neuromodulators	Long-term management plan
Post-HZO, over 50 years old	Sign up for the Shingrix vaccination	2-dose schedule, compatibility with other vaccinations