Table of Contents  
Year : 2013  |  Volume : 6  |  Issue : 3  |  Page : 292-293  

Herpes zoster ophthalmicus

Department of Ophthalmology, Padmashree Dr D Y Patil Medical College, Hospital and Research Centre, Dr D Y Patil Vidyapeeth, Pune, India

Date of Web Publication5-Jul-2013

Correspondence Address:
Kavita R Bhatnagar
B 4/21, Brahma Aangan, Off Salunke Road, Kondhwa, Pune - 411 048
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How to cite this article:
Bhatnagar KR. Herpes zoster ophthalmicus. Med J DY Patil Univ 2013;6:292-3

How to cite this URL:
Bhatnagar KR. Herpes zoster ophthalmicus. Med J DY Patil Univ [serial online] 2013 [cited 2021 May 14];6:292-3. Available from:

Varicella-zoster virus (VZV) causes two distinct syndromes and the primary infection, chickenpox, is a contagious and usually benign febrile illness. After this infection resolves, virus particles remain in the dorsal root or other sensory ganglion where they may lay dormant for years to decades.

As a result of aging, immunosuppressive illness, new stress, or medical treatments, the virus-specific cell-mediated immune responses may decline. Such conditions allow a reactivation of latent VZV and result in a localized cutaneous rash erupting in a single dermatome, called herpes zoster (HZ) or shingles.

Patients with HZ involving the first division of the trigeminal nerve has a disease process termed herpes zoster ophthalmicus (HZO). HZO was described long ago by Hippocrates; however, its relation to VZV was not elucidated until the advent of modern medical tools such as immune-histochemical assays.

HZO accounts for 10-25% of all cases of shingles. The sequelae of HZO can be devastating; they include chronic ocular inflammation, visual loss, and debilitating pain. [1],[2],[3]

By definition, HZO is reactivation of VZV in the ophthalmic division of the trigeminal nerve (V1). While HZO does not necessarily affect the structures of the eye, many of the acute and long-term complications associated with the disease are the result of direct viral toxicity to the eye or the ensuing inflammatory response within the eye. It is thought that approximately 50% of HZO will develop complications. Many of these poor outcomes can be prevented or ameliorated with early recognition, treatment, and referral.

Classically, HZO begins with flu-like symptoms including fever, myalgia, and malaise for approximately, 1 week. Typically, patients then develop a painful unilateral dermatomal rash in the distribution of one or more branches of V1: Supraorbital, lacrimal, and nasocilliary. The skin manifestations usually begin as an erythematous macular rash, progressing over several days into papules, vesicles, and then pustules. These eventually rupture and scab, and in immunocompetent individuals will resolve over the course of 2-3 weeks. In about 60% of cases, patients will complain of a painful dermatomal prodrome prior to the development of any rash. Ocular involvement is not invariable in HZO; however, in patients with nasocilliary nerve involvement (Hutchinson's sign) 100% go on to develop eye pathology. [4]

Physical exam should include a thorough ophthalmologic examination including external inspection, visual acuity, visual fields, extra ocular movements, pupillary response, fundoscopy, intraocular pressure; anterior chamber slit lamp exam, and corneal exam with and without staining. Classic ocular involvement is typified by dendritic or punctate keratitis. This pattern of infection occurs in approximately, 65% of patients with HZO; however, other eye findings are more frequent and range from simple conjunctivitis to retinal necrosis and detachment. Any structure in the eye may be involved.

Diagnostic testing is rarely indicated, as diagnosis can almost always be made by a combination of history and physical examination. It is possible to use a Tzanck smear or Wright stain to determine whether lesions contain herpes-type virus. Viral culture, direct immunofluorescence assay, or Polymerase chain reaction (PCR) may also be used to confirm the diagnosis.

Treatment consists of local wound care, pain control, initiation of antiviral medication, and antibiotics if needed. Acyclovir and other similar antivirals have been shown to significantly decrease adverse outcomes related to HZO if started within 72 h of initial symptoms. Studies report reduced pain during the outbreak, reduced likelihood of post-herpetic neuralgia, increased rate of skin healing, decreased duration of viral shedding, and decreased incidence of corneal involvement. Steroids (topical and systemic) may also play a role in the treatment of HZO. In some studies, systemic steroids have been shown to speed skin lesion healing and to decrease initial pain; however, there have been no definitive studies showing reduced long-term incidence of post-herpetic neuralgia or ocular complications. [4]

Oral opiate and non-steroidal anti-inflammatory medications are frequently indicated for pain and may be augmented by the use of cycloplegics in-patients who display features of iritis.

As regards Prognosis most patients with HZO have a single attack and do not go on to get further attacks. Visual outcome is generally good, with vision loss due to corneal problems rather than uveitis. Some patients, however, may develop chronic disease, including uveitis that requires long-term therapy and may persist for years.

  Research and Future Outlook Top

HZ is a common infection. Whether, the recently developed chicken pox vaccine will prevent or reduce the occurrence of the HZ later in life is currently unknown. Scientists are working to understand why the viral flares up in some patients and not in others. New antivirals that are more effective are also under development for the treatment of HZO. [5]

  References Top

1.Ang LP, Au Eong KG, Ong SG. Herpes zoster ophthalmicus. J Pediatr Ophthalmol Strabismus 2001;38:174-6.  Back to cited text no. 1
2.Cockburn DM, Douglas IS. Herpes zoster opthalmicus. Clin Exp Optom 2000;83:59-64.  Back to cited text no. 2
3.Gurwood AS, Savochka J, Sirgany BJ. Herpes zoster ophthalmicus. Optometry 2002;73:295-302.  Back to cited text no. 3
4.Shaikh S, Ta CN. Evaluation and management of herpes zoster ophthalmicus. Am Fam Physician 2002;66:1723-30.  Back to cited text no. 4
5.Catron T, Hern HG. Herpes zoster ophthalmicus. West J Emerg Med 2008;9:174-6.  Back to cited text no. 5


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