Background: Herpes zoster ophthalmicus (HZO) is a reactivation of the varicella-zoster virus causing serious ocular and systemic complications, particularly in individuals with declining immunity.

Case report: A 74-year-old male with a history of various chronic conditions was referred to an eye clinic due to herpes zoster affecting his right forehead and eye. Initial treatment included acetaminophen-hydrocodone, valacyclovir, and ofloxacin, with hypotensive agent added to manage elevated intraocular pressure. Follow-up visits showed improvement in lid swelling and eye pain, although his visual acuity initially worsened before eventually improving to near complete resolution, with corneal edema resolving with topical steroid and IOP stabilizing. The patient's treatment regimen was adjusted accordingly, with instructions to return for continued care until resolution.

Conclusion: This case report highlights an unusual occurrence of HZO in an immunocompetent patient who had received Shingrix, emphasizing the need for awareness, early diagnosis, antiviral therapy, and tailored co-management approaches for effective care.

Keywords: herpes zoster ophthalmicus, shingles, shingrix, corneal edema, intraocular pressure, diabetes mellitus

Herpes zoster ophthalmicus (HZO) is a significant viral infection caused by the reactivation of the varicella-zoster virus within the ophthalmic branch of the trigeminal nerve. It poses serious ocular and systemic complications, often affecting patients with declining immunity, including the elderly and immunocompromised individuals.¹ Clinically, HZO manifests with a unilateral vesicular rash and can involve various ocular tissues, leading to conditions such as conjunctivitis, keratitis, uveitis, and neuropathic pain². Early diagnosis and prompt treatment with antiviral therapy are crucial in mitigating complications and improving patient outcomes³. This case report presents an unusual manifestation of HZO in an immunocompetent patient who received Shingrix (recombinant adjuvant zoster vaccine) shots a few years ago, emphasizing the need for awareness and timely management approaches. It underscores the importance of interdisciplinary care and prophylactic measures in susceptible populations. By providing detailed clinical insights, this report aims to assist clinicians in recognizing and managing various presentations of HZO.

A 74-year-old Caucasian American male was referred from urgent care clinic (UCC) because of herpes zoster affecting the right forehead and eye. He reported of a headache that started a week ago followed by worsening eye pain and lid swelling of the right eye over the past few days. The provider at UCC prescribed acetaminophen-hydrocodone (5 mg-325 mg) tablet q6h, valacyclovir 1g tablet three times a day (TID) for a week, and ofloxacin ophthalmic four times a day (QID) right eye (OD) before sending him to the eye clinic. He had no fever/chills, no nausea/vomiting, no shortness of breath/chest pain, no abdominal pain, no dysuria, no hematuria, no diarrhea/constipation, no swollen lymph nodes. Patient stated he has had his two shots for shingles a few years ago.

His last eye exam was about a years ago with early cataracts, vortex keratopathy secondary to taking amiodarone, and good vision in each eye. His problem list includes atrial fibrillation, coronary artery disease, COPD, HTN, hyperlipidemia, insomnia, and diabetes. The corresponding list of medication includes albuterol, amiodarone, amlodipine, apixaban, atorvastatin, fluticasone-salmeterol, losartan, metformin, metoprolol, nitroglycerin, and trazodone.

Best-corrected visual acuity (BCVA) was 20/60 PHNI OD and 20/20- left eye (OS). Right lid was swollen shut (Figure 1A). Shingle scabs were scattered across the right side of his forehead and head (Figure 1B). Extraocular muscle motility was limited OD because of severe swelling, confrontation fields were full OS, and pupils were equal, round, reactive to light without afferent pupillary defect. Anterior segment findings showed 1+ conjunctival hyperemia and edema once the lid was lifted open, diffuse corneal haze (Figure 2), and mild cataracts OU, and intraocular pressures (IOP) were 24 mmHg OD and 17 mmHg OS by Tonopen. No keratic precipitate and no pseudodendrites were seen in the cornea. Anterior chamber was hazy but no apparent cells OD. The patient was educated to continue with the medications that UCC prescribed above, and latanoprost was added qhs OD to lower the intraocular pressure. Return to clinic was ordered in a few days or sooner if the ocular symptoms got worse.

Figure 1A Severely swollen lids shutting the right eye.

Figure 1B Shingle scabs across the right forehead a few days after initial presentation.

Figure 2 Right eye after lifting open at initial presentation.

At the follow-up visit few days later, the right lid swelling, and eye pain were better, but his BCVA OD was worse 20/150 PHNI. Anterior segment findings showed resolving conjunctival hyperemia and edema, but the corneal edema was worsened with thicker cornea of 811 um and Descemet striae OD, 617 um OS (Figure 3A, B). IOP came down to 17 mmHg OD and 15 mmHg OS by Tonopen. Dilated fundus examination revealed relatively normal fundus with cup-to-disc (C/D) ratio of 0.25 round OD, OS. The fundus photo showed relatively normal retina OU, but hazy fundus view OD because of corneal edema (Figure 4A, B). Two drops of prednisolone acetate 1% (PF) were given in clinic about 5 min apart, and the patient was instructed to continue with ofloxacin qid, latanoprost qhs, and start PF q2h while awake, and return to clinic in a few days.

Figure 3A Resolving swollen right lid but worsening corneal edema showing Descemet striae.

Figure 3B Normal left eye after dilating drop.

Figure 4A Hazy view of the right fundus secondary to corneal edema.

Figure 4B Clear view of the left fundus.

A week later, lid and conjunctival edema continue to resolve. He felt better and vision in the right eye improved back to 20/60. IOP was lower at 12 mmHg OD and 13 mmHg OS by Tonopen. The corneal edema was resolving with less Descemet striae and thinner at 707 um OD, 601 um OS. PF was tapered down to qid OD, and Muro-128 gel qid was added to relieve corneal swelling. Patient was to return to clinic in a few days.

Ten days after initial presentation, lid and conjunctival edema continue to resolve. He felt better and vision in the right eye much improved to 20/25 (Figure 5). IOP remained normal at 14 mmHg OD and 14 mmHg OS by Tonopen. The corneal edema was resolving with less Descemet striae and thinner at 700 um OD, 598 um OS. Corneal sensitivity test with dental floss revealed moderately less sensitive right cornea. Patient was to continue PF qid OD, and Muro-128 solution qid.

Figure 5 Ten days after initial visit with BCVA recovering to 20/25.

Approximately three weeks after the initial presentation, he recovered almost completely with BCVA 20/20-2, IOP 14 mmHg and corneal pachymetry 613 um OD; his left eye remained healthy. He was recommended to continue taking artificial tears a few times a day for lubrication and consider booster shingle shots in the future.

The case of a 74-year-old male who developed herpes zoster ophthalmicus (HZO) despite prior immunization with the Shingrix vaccine raises pertinent questions about the systemic and ophthalmic challenges associated with this condition. HZO tends to occur predominantly in the elderly, which correlates with the natural decline in cell-mediated immunity, a key factor in varicella-zoster virus (VZV) reactivation⁴. This patient has multiple systemic diseases including COPD, HTN and diabetes that might weaken his immunocompetency. The development of HZO in this immunized patient highlights gaps in vaccine efficacy and or potential waning immunity secondary to his systemic conditions over time.

Ophthalmic manifestations of HZO are varied and can be severe, as demonstrated in this patient with significant scabs on the right forehead, swollen eyelids leading to eye closure, elevated intraocular pressure (IOP), conjunctival hyperemia, and corneal edema. These symptoms illustrate the extensive inflammatory response and potential ocular tissue involvement, including the risk of secondary ocular hypertension due to trabeculitis or severe uveitis.⁵ The corneal edema observed suggests endothelial cell dysfunction, likely secondary to the VZV infection and subsequent inflammation, which compromises corneal clarity and visual acuity.

Differential diagnoses for such a presentation encompass a range of infectious and inflammatory conditions. Primary considerations include acute anterior uveitis, bacterial keratitis, and autoimmune disorders like sarcoidosis and Behçet's disease, which can present with similar ocular inflammations and systemic signs.¹ However, the characteristic vesicular rash and history of prior varicella infection or vaccination strongly support the diagnosis of HZO. Table 1 provides a summary of key features of a few differential diagnoses that might present with similar ocular signs and symptoms.

Stromal zoster keratitis is an ocular condition caused by the reactivation of the varicella-zoster virus, which also triggers herpes zoster. The etiology involves the virus becoming latent in the sensory ganglia following an initial varicella infection (chickenpox) and subsequently reactivating later in life, often due to immunosuppression or aging. The reactivated virus can affect the cornea, leading to inflammation and scarring. Incidence rates of herpes zoster infections increase with age, particularly in those over 50 years old.

Clinical management of HZO involves a multi-modal approach aimed at addressing both the viral infection and its complications. Immediate administration of systemic antiviral therapy, such as oral acyclovir or valacyclovir, is crucial in reducing the viral load and preventing further complications.³ Adjunctive corticosteroids may be considered to control severe inflammation, albeit cautiously, due to the risk of exacerbating elevated IOP. Intraocular pressure should be monitored closely and managed with pressure-lowering medications as necessary. Additionally, supportive care for corneal edema, such as hypertonic saline drops, and measures to prevent secondary bacterial infections are integral to comprehensive care. Combining antiviral prophylaxis with corticosteroids can help in managing both the viral activity and the immune-mediated damage to the corneal stroma.⁶ Table 2 summarizes the clinical management of various ocular complications associated with HZO.⁶ Table 3 shares a reference for clinical management with oral antivirals and vaccine recommendations.^7,8

Some clinical pearls for this case report of herpes zoster ophthalmicus (HZO) are:

Vaccine awareness: Despite prior immunization with Shingrix, elderly patients may still develop HZO, indicating potential waning immunity or breakthrough infections. Continued monitoring and potential booster vaccinations may be necessary.

Timely treatment: Early administration of systemic antiviral therapy, such as acyclovir or valacyclovir, is crucial in managing HZO to reduce viral load and prevent severe complications.

Inflammation management: Adjunctive corticosteroids can help control severe ocular inflammation but must be balanced with the need to monitor and manage intraocular pressure (IOP) to prevent glaucoma.

Comprehensive ocular examination: A detailed ocular examination, including assessment of adnexa, conjunctiva, cornea, and posterior segment is essential to evaluate the extent of HZO involvement and guide treatment.

Multidisciplinary approach: Coordination with primary care provider and specialist is often necessary for comprehensive management, especially in cases with significant systemic symptoms or complications.

Patient Education: Educate patients about the signs and symptoms of HZO, the importance of early treatment, and the potential need for ongoing monitoring and follow-up to manage long-term complications.

This case underscores the importance of timely intervention and the necessity for continued vigilance even in vaccinated individuals, advocating for ongoing research into improved preventive and therapeutic interventions for HZO.

The authors would like to thank the medical assistants, optical and technical staff for the continued support in providing excellent eye care to our veterans.

The author declares that there are no conflicts of interest.

None.

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