A Short Review of Herpes Zoster Ophthalmicus

Basak Selin Kara

Introduction

Herpes zoster (HZ) is caused by reactivation of latent varicella zoster virus (VZV) within sensory ganglia. This reactivation is named as herpes zoster ophthalmicus (HZO) when it occurs in the ophthalmic branch (V1) of the trigeminal nerve. HZO begin with a typical dermatomal rash. However, it can progress to keratitis, anterior uveitis, secondary glaucoma, neurotrophic keratopathy, and rarely posterior segment involvement. It can cause permanent vision loss in severe cases. Early identification, systemic antiviral therapy, and appropriate follow up can reduce morbidity and visual impairment (1,2).

Epidemiology

Herpes zoster affects roughly one in three people during their lifetime. The incidence  of HZ increases significantly with age due to declining varicella zoster virus specific cellular immunity (3). Herpes zoster ophthalmicus accounts for a clinically significant proportion of cases. HZO accounts for approximately 8–15% of all herpes zoster presentations, and it is one of the most important complications of HZ because of its potential to cause visual morbidity (4).

It is demonstrated that the incidence of HZO has been increasing (5). Its incidence is estimated to be ranging from 20 to 35 per 100 000 person-years (6). Overall, the increasing incidence of HZO has shown the importance of prevention and early intervention (3,5).

Risk Factors

Risk factors for HZ has been widely studied. Increasing age is one of the most important risk factors. Immunosuppression due to disease or therapy is another major risk factor (7, 8).

Risk factors such as older age and immunocompromised state are also associated with more severe disease and poorer visual outcomes in HZO presentations (9). This justifies the need for having a lower threshold for early referral and closer follow-up for HZO in those with risk factors (9).

Clinical presentation

HZO is neurocutaneous disease with ocular involvement. It generally starts with unilateral neuropathic pain, paraesthesia, or dysaesthesia in the distribution of the ophthalmic (V1) branch of the trigeminal nerve. The pain is commonly followed by the characteristic vesicular eruption involving the forehead and upper eyelid. The vesicular eruption generally crust and heal between 2 to 6 weeks. In some patients, the prodromal phase can be longer making the diagnosis to be more challenging (1,10).

The patients can initially present with ocular involvement but ocular involvement can also develop in time. Patients commonly complain of red eye, photophobia, watery eyes, ocular pain, and blurred vision (1,2). Some patients can present with diplopia can when ocular motility or cranial nerves are affected (1,2).

Most common ocular presentation is an anterior segment disease. Its early findings include conjunctivitis and episcleritis.Keratitis and anterior uveitis may develop days to weeks later when inflammation progresses (1,10). HZO uveitis is often associated with secondary elevation of intraocular pressure and thus it requires close monitoring. An important long-term complication of trigeminal nerve involvement is reduced corneal sensation which can result in neurotrophic keratopathy, impaired epithelial healing, infection, scarring, and irreversible visual loss (9). HZO can progress after early improvement, theregore, ongoing review and safety-netting are crucial (7).

Prevention

Vaccination is the most effective method to reduce HZ and its complications. Vaccination reduces the risk of viral reactivation and reduces the severity of infection by enhancing VZV-specific immune responses (11,12).  It is shown to reduce the risk of HZO and prevent severe sight-threatening disease (13).

Management

Early suppression of viral replication limits inflammation and tissue damage. Therefore, initiation of systemic antiviral medication early in the disease course is a crucial part of the treatment. Current guidelines recommend oral aciclovir and valacyclovir for herpes zoster involving cranial nerves or eyes (2,14). Early initiation of antiviral therapy improves pain outcomes and may mitigate the risk of persistent symptoms.in addition to reducing the viral load (15).

Antiviral treatment is most effective when started within 72 hours of rash onset. However antiviral therapy is still indicated for HZO even if patient presents after 72 hour onset when new lesions are present or ocular involvement is identified (2).

Ophthalmologic management depends on the severity of eye involvement and focuses on protecting the ocular surface, controlling inflammation, and follow-up for complications such as increased intraocular pressure and corneal damage. Topical anti-inflammatory therapy such as corticosteroids, may be beneficial for treatment of stromal keratitis or uveitis. (1,2). Since the HZO can cause delayed or recurrent disease, follow-up should be arranged, and patients should be advised to seek help if they develop pain, photophobia, persistent redness, or any reduction in vision (7,9).

References

  1. Tuft S. How to manage herpes zoster ophthalmicus. Community Eye Health. 2020;33(108):71–72.
  2. Gross GE, Eisert L, Doerr HW, et al. S2k guidelines for the diagnosis and treatment of herpes zoster and postherpetic neuralgia. J Dtsch Dermatol Ges. 2020;18(1):55–78. doi:10.1111/ddg.14013.
  3. Johnson RW, Alvarez-Pasquin MJ, Bijl M, et al. Herpes zoster epidemiology, management, and disease and economic burden in Europe: a multidisciplinary perspective. Ther Adv Vaccines. 2015;3(4):109–120. doi:10.1177/2051013615599151.
  4. Curran D, Callegaro A, Fahrbach K, et al. Meta-regression of herpes zoster incidence worldwide. Infect Dis Ther. 2022;11(1):389–403. doi:10.1007/s40121-021-00567-8.
  5. Kawai K, Gebremeskel BG, Acosta CJ. Systematic review of incidence and complications of herpes zoster: towards a global perspective. BMJ Open. 2014;4(6):e004833. doi:10.1136/bmjopen-2014-004833.
  6. Kong CL, Thompson RR, Porco TC, Kim E, Acharya NR. Incidence rate of herpes zoster ophthalmicus: a retrospective cohort study from 1994 through 2018. Ophthalmology. 2020;127(3):324–330. doi:10.1016/j.ophtha.2019.10.001.
  7. Yawn BP, Wollan PC, St Sauver JL, Butterfield LC. Herpes zoster eye complications: rates and trends. Mayo Clin Proc. 2013;88(6):562–570. doi:10.1016/j.mayocp.2013.03.014.
  8. Marra F, Parhar K, Huang B, Vadlamudi N. Risk factors for herpes zoster infection: a meta-analysis. Open Forum Infect Dis. 2020;7(1):ofaa005. doi:10.1093/ofid/ofaa005.
  9. Niederer RL, Meyer JJ, Liu K, Danesh-Meyer HV. Herpes zoster ophthalmicus clinical presentation and risk factors for loss of vision. Am J Ophthalmol. 2021;226:83–89. doi:10.1016/j.ajo.2021.02.002.
  10. Cohen EJ, Jeng BH. Herpes zoster: a brief definitive review. Cornea. 2021;40(8):943–949. doi:10.1097/ICO.0000000000002754.
  11. Oxman MN, Levin MJ, Johnson GR, et al. A vaccine to prevent herpes zoster and postherpetic neuralgia in older adults. N Engl J Med. 2005;352(22):2271–2284. doi:10.1056/NEJMoa051016.
  12. Izurieta HS, Wernecke M, Kelman J, et al. Effectiveness and duration of protection provided by the live-attenuated herpes zoster vaccine in the Medicare population ages 65 years and older. Clin Infect Dis. 2017;64(6):785–793. doi:10.1093/cid/ciw854.
  13. Dooling KL, Guo A, Patel M, et al. Recommendations of the Advisory Committee on Immunization Practices for use of herpes zoster vaccines. MMWR Morb Mortal Wkly Rep. 2018;67(3):103–108. doi:10.15585/mmwr.mm6703a5.
  14. Hoang-Xuan T, Büchi ER, Herbort CP, et al. Oral acyclovir for herpes zoster ophthalmicus. Ophthalmology. 1992;99(7):1062–1071. doi:10.1016/S0161-6420(92)31849-4.
  15. Wood MJ, Kay R, Dworkin RH, Soong SJ, Whitley RJ. Oral acyclovir therapy accelerates pain resolution in patients with herpes zoster: a meta-analysis of placebo-controlled trials. Clin Infect Dis. 1996;22(2):341–347. doi:10.1093/clinids/22.2.341.

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