presentation of herpes zoster ophthalmicus

SAAD SHAIKH, M.D., AND CHRISTOPHER N. TA, M.D.

Am Fam Physician. 2002;66(9):1723-1730

A patient education handout on HZO, written by the authors of this article, is provided on page 1732 .

Herpes zoster ophthalmicus occurs when the varicella-zoster virus is reactivated in the ophthalmic division of the trigeminal nerve. Herpes zoster ophthalmicus represents up to one fourth of all cases of herpes zoster. Most patients with herpes zoster ophthalmicus present with a periorbital vesicular rash distributed according to the affected dermatome. A minority of patients may also develop conjunctivitis, keratitis, uveitis, and ocular cranial-nerve palsies. Permanent sequelae of ophthalmic zoster infection may include chronic ocular inflammation, loss of vision, and debilitating pain. Antiviral medications such as acyclovir, valacyclovir, and famciclovir remain the mainstay of therapy and are most effective in preventing ocular involvement when begun within 72 hours after the onset of the rash. Timely diagnosis and management of herpes zoster ophthalmicus, with referral to an ophthalmologist when ophthalmic involvement is present, are critical in limiting visual morbidity.

Herpes zoster is a common infection caused by the human herpesvirus 3, the same virus that causes varicella (i.e., chickenpox). It is a member of the same family (Herpesviridae) as herpes simplex virus, Epstein-Barr virus, and cytomegalovirus. Reactivation of the latent virus in neurosensory ganglia produces the characteristic manifestations of herpes zoster, commonly known as shingles. Normal aging, poor nutrition, and immunocompromised status correlate with outbreaks of herpes zoster, and certain factors such as physical or emotional stress and fatigue may precipitate an episode.

Herpes zoster ophthalmicus occurs when reactivation of the latent virus in the trigeminal ganglia involves the ophthalmic division of the nerve. The virus damages the eye and surrounding structures by secondary perineural and intraneural inflammation of sensory nerves. 1 Herpes zoster ophthalmicus represents approximately 10 to 25 percent of all cases of herpes zoster. 2 Although herpes zoster ophthalmicus most often produces a classic dermatomal rash, a minority of patients may have only ophthalmic findings, limited mainly to the cornea. Direct ocular involvement is not specifically correlated with age, gender, or severity of disease. Serious sequelae include chronic ocular inflammation, vision loss, and disabling pain.

Extraocular Manifestations of Herpes Zoster Ophthalmicus

The prodromal phase of herpes zoster ophthalmicus includes an influenza-like illness with fatigue, malaise, and low-grade fever that lasts up to one week before the rash over the forehead appears. 3 About 60 percent of patients have varying degrees of dermatomal pain in the distribution of the ophthalmic nerve. 4 Subsequently, erythematous macules appear along the involved dermatome, rapidly progressing over several days to papules and vesicles containing clear serous fluid and, later, pustules. These lesions rupture and typically crust over, requiring several weeks to heal completely. 5

Immunocompromised persons, particularly those with human immunodeficiency virus infection, have a much higher risk of developing herpes zoster ophthalmicus than the normal population. 6 These patients may have a generalized vesicular rash and become severely ill one to two weeks after disease onset. In addition, such patients develop more serious visual sequelae. 7

Viral transmission from patients with herpes zoster can occur, but it is less frequent than transmission from patients with chick-enpox. 7 Virus particles can be transmitted through direct contact with secretions from vesicles and secretion-contaminated articles.

Ocular Manifestations of Herpes Zoster Ophthalmicus

The skin manifestations of herpes zoster ophthalmicus strictly obey the midline with involvement of one or more branches of the ophthalmic division of the trigeminal nerve, namely the supraorbital, lacrimal, and nasociliary branches ( Figure 1 ) . Because the nasociliary branch innervates the globe, the most serious ocular involvement develops if this branch is affected. Classically, involvement of the tip of the nose (Hutchinson's sign) has been thought to be a clinical predictor of ocular involvement. Although patients with a positive Hutchinson's sign have twice the incidence of ocular involvement, one third of patients without the sign develop ocular manifestations. 8 A summary of ocular findings in patients with herpes zoster ophthalmicus is presented in Table 1 .

BLEPHARITIS AND CONJUNCTIVITIS

The eyelids are commonly involved in herpes zoster ophthalmicus ( Figure 1 , part b). Patients may develop blepharitis and present with ptosis secondary to edema and inflammation. A vast majority of patients will have vesicular lesions on the eyelids that resolve with minimal scarring.

Conjunctivitis is one of the most common complications of herpes zoster ophthalmicus. The conjunctiva appears injected and edematous, often with petechial hemorrhages. 9 The findings usually resolve within one week. However, secondary infection, usually Staphylococcus aureus , may develop and should be treated with broad-spectrum topical and/or systemic antibiotics.

CORNEAL DISEASE

Unlike eyelid or conjunctival involvement, corneal involvement can result in significant vision loss. The clinical features of corneal disease include direct viral infection, antigen-antibody reactions, delayed cell-mediated hypersensitivity reactions, and neurotrophic damage. 7 Patients with corneal disease present with varying degrees of decreased vision, pain, and light sensitivity. Corneal complications occur in approximately 65 percent of cases of herpes zoster ophthalmicus. 7

Epithelial Keratitis . The earliest corneal finding is punctate epithelial keratitis. 10 On slit lamp examination, this appears as multiple, focal, swollen lesions that stain with rose bengal or fluorescein dye. These lesions probably contain live virus and may either resolve or progress to dendrite formation. Punctate epithelial keratitis may present as early as one or two days after the initial skin rash, while dendrites often present at four to six days but can appear many weeks later. 11

Herpes zoster virus dendrites appear as elevated plaques and consist of swollen epithelial cells. They form branching or “medusa-like” patterns and have tapered ends ( Figure 2 , part a) in contrast to herpes simplex virus dendrites, which often have terminal bulbs. Dendrites also stain with rose bengal and fluorescein dye ( Figure 2 , part b) and can be viewed by Wood's lamp or slit lamp examination. Punctate and dendritic lesions can lead to anterior stromal corneal infiltrates. 11 , 12

Stromal Keratitis — Anterior Stromal Keratitis . The earliest finding of corneal stromal involvement presents during the second week of disease, occurring in 25 to 30 percent of patients with herpes zoster ophthalmicus. 13 The condition, known as anterior stromal keratitis or nummular keratitis, is characterized by multiple fine granular infiltrates in the anterior corneal stroma below the epithelial layer ( Figure 3 ) . Most of the infiltrates lie directly beneath pre-existing dendrites or areas of punctate epithelial keratitis. The infiltrates are thought to arise from antigen-antibody interaction resulting from viral proliferation in the overlying epithelium. 10 , 12 Anterior stromal keratitis may be prolonged and recurrent.

Stromal Keratitis—Deep Stromal Keratitis . This later stage of stromal keratitis is relatively uncommon and typically develops three to four months after the initial acute episode, but development can range from one month to many years later. 7 It is usually central and preceded by anterior stromal keratitis. The keratitis may present as a lesion consisting of a localized area of inflammation affecting all levels of the stroma, or as peripheral infiltrates that may have a surrounding immune ring. Corneal edema may be a prominent feature at this stage, usually with associated anterior chamber inflammation. A rare necrotizing form can also occur. A chronic relapsing course is not unusual, especially without timely and adequate treatment. Corneal neovascularization and lipid infiltrates may occur in patients with uncontrolled chronic disease. The pathogenesis of stromal disease probably involves a delayed cell-mediated hypersensitivity reaction.

Neurotrophic Keratopathy . Neurotrophic keratitis is the end result of decreased corneal sensation from herpes zoster virus-mediated destruction, including susceptibility to mechanical trauma, decreased lacrimation, and delayed epithelial healing. 7 Corneal thinning is a serious complication that may lead to corneal perforation. Such patients are at high risk for developing a secondary bacterial infection. Using preservative-free lubricating drops and ointment can prevent the development of epithelial defects.

Anterior uveitis, which is diagnosed by slit lamp examination, refers to inflammation of the iris and ciliary body and occurs frequently with herpes zoster ophthalmicus. It may be isolated or associated with keratitis. The inflammation is generally mild and transient, but it frequently causes a mild elevation in intraocular pressure. Zoster uveitis can result in iris atrophy and an irregular pupil. As with stromal keratitis, the course of disease may be prolonged, especially without timely, adequate treatment. Herpes zoster uveitis may cause glaucoma and cataract formation. Chronic inflammation can lead to endothelial cell injury, resulting in corneal edema.

EPISCLERITIS AND SCLERITIS

Findings of episcleritis include localized or diffuse redness, as well as pain and swelling of the conjunctiva and episclera. Scleritis is a more serious condition with involvement of the sclera. Both conditions may be accompanied by localized stromal keratitis.

ACUTE RETINAL NECROSIS AND PROGRESSIVE OUTER RETINAL NECROSIS SYNDROMES

Herpes zoster virus is considered the offending agent in most cases of acute retinal necrosis and progressive outer retinal necrosis syndromes. Compared with acute retinal necrosis, progressive outer retinal necrosis is a more severe viral retinitis observed in immunocompromised persons, often in patients with acquired immunodeficiency syndrome.

Symptoms include blurred vision and/or pain in one or both eyes. Acute retinal necrosis is characterized by peripheral patches of retinal necrosis that rapidly coalesce ( Figure 4 ) , occlusive vasculitis, and vitreous inflammation. Conversely, immunocompromised patients with progressive outer retinal necrosis are unable to mount a vitreous inflammatory response, leading to rapid involvement of the macula. Both conditions commonly cause retinal detachment. The prognosis is extremely poor in patients with progressive outer retinal necrosis; most patients have no light perception vision. 14 The visual prognosis in patients with acute retinal necrosis is better, with many patients achieving a visual acuity of 20/40. 15 Bilateral involvement in both forms is observed in one third of patients but may be as high as 70 percent in patients with untreated disease. 16 Treatment includes long courses of oral and intravenous acyclovir (Zovirax), and corticosteroids.

Postherpetic Neuralgia and Other Neurologic Complications

Postherpetic neuralgia affects about 7 percent of patients and is characterized by varying degrees of constant or intermittent pain in the distribution of the affected dermatome. 17 Increased age and prodromal symptoms are associated with a higher prevalence of post-herpetic neuralgia. It generally improves with time but may last for months to years. In severe cases, patients may be depressed and suicidal. Treatment includes topical capsaicin cream, over-the-counter analgesics, tricyclic antidepressants, and anticonvulsants. 18

Cranial nerve palsies involving the third (most common), fourth, and sixth nerves may occur rarely ( Figure 5 ) . A majority of the cases will have spontaneous resolution within six months. Optic neuritis has been noted in about one in 400 cases and may precede retinal disease or follow acute herpes zoster ophthalmicus infection ( Figure 6 ) . 17 , 19 , 20

Treatment of Herpes Zoster Ophthalmicus

Patients with herpes zoster ophthalmicus are treated with oral acyclovir (800 mg, five times daily) for seven to 10 days. Studies report alleviation of pain with oral acyclovir during the initial stages of the disease, especially if the drug is taken within the first three days of symptoms, and it may have a favorable effect on postherpetic neuralgia. 21 – 23 [Reference 22—Evidence level A, randomized controlled tiral (RCT). Reference 23—Evidence level A, RCT] Additionally, acyclovir administered within 72 hours of onset has been found to speed resolution of skin lesions, reduce viral shedding, and decrease the incidence of dendritic and stromal keratitis as well as anterior uveitis. 24 , 25

Valacyclovir (Valtrex) has higher bioavail-ability and has been shown to be equally safe and effective for the treatment of herpes zoster at a dosage of 1,000 mg three times daily for seven or 14 days. 26 [Evidence level A, RCT] Valacyclovir in a seven-day dosage regimen was recently shown to prevent ocular complications of herpes zoster ophthalmicus, including conjunctivitis, superficial and stromal keratitis, and pain. 27 [Evidence level A, RCT] Famciclovir (Famvir), 500 mg orally three times a day for seven days, may also be used. 28 Intravenous acyclovir is recommended in immunocompromised patients. 29 , 30 [Reference 29—Evidence level A, RCT] Acute pain control is achieved by local care and oral analgesics. Topical anesthetics should never be prescribed because of their corneal toxicity. A summary of treatment and management options for various ocular manifestations of herpes zoster ophthalmicus is presented in Table 2 .

Naumann G, Gass JD, Font RL. Histopathology of herpes zoster ophthalmicus. Am J Ophthalmol. 1968;65:533-41.

Ragozzino MW, Melton LJ, Kurland LT, Chu CP, Perry HO. Population-based study of herpes zoster and its sequelae. Medicine. 1982;61:310-6.

Goh CL, Khoo L. A retrospective study of the clinical presentation and outcome of herpes zoster in a tertiary dermatology outpatient referral clinic. Int J Dermatol. 1997;36:667-72.

Cobo M, Foulks GN, Liesegang T, Lass J, Sutphin J, Wilhelmus K, et al. Observations on the natural history of herpes zoster ophthalmicus. Curr Eye Res. 1987;6:195-9.

Burgoon CF, Burgoon JS, Baldridge GD. The natural history of herpes zoster. JAMA. 1957;174:265.

Sandor EV, Millman A, Croxson TS, Mildvan D. Herpes zoster ophthalmicus in patients at risk for the acquired immune deficiency syndrome (AIDS). Am J Ophthalmol. 1986;101:153-5.

Baratz KH, Goins K, Cobo M. Varicella-zoster viral infections. In: Kaufman HE, ed. The cornea. New York: Churchill Livingstone, 1988.

Harding SP, Lipton JR, Wells JC. Natural history of herpes zoster ophthalmicus: predictors of postherpetic neuralgia and ocular involvement. Br J Ophthalmol. 1987;71:353-8.

Arffa RC. Viral diseases. In: Arffa RC, Grayson M, eds. Grayson's Diseases of the cornea. 4th ed. St. Louis: Mosby, 1997.

Liesegang TJ. Corneal complications from herpes zoster ophthalmicus. Ophthalmology. 1985;92:316-24.

Jones DB. Herpes zoster ophthalmicus. In: Golden B, ed. Symposium on ocular inflammatory disease. Springfield, Ill.: Thomas, 1974.

Marsh RJ. Herpes zoster keratitis. Trans Ophthalmol Soc U K. 1973;93:181-92.

Womack LW, Liesegang TJ. Complications of herpes zoster ophthalmicus. Arch Ophthalmol. 1983;101:42-5.

Engstrom RE, Holland GN, Margolis TP, Muccioli C, Lindley JI, Belfort R, et al. The progressive outer retinal necrosis syndrome. A variant of necrotizing herpetic retinopathy in patients with AIDS. Ophthalmology. 1994;101:1488-502.

Blumenkranz M, Clarkson J, Culbertson WW, Flynn HW, Lewis ML, Young GA. Vitrectomy for retinal detachment associated with acute retinal necrosis. Am J Ophthalmol. 1988;106:426-9.

Palay DA, Sternberg P, Davis J, Lewis H, Holland GN, Mieler WF, et al. Decrease in the risk of bilateral acute retinal necrosis by acyclovir therapy. Am J Ophthalmol. 1991;112:250-5.

Kanski JJ. Herpes zoster ophthalmicus. In: Kanski JJ, Nischal KK, Milewski SA, eds. Ophthalmology: clinical signs and differential diagnosis. Philadelphia: Mosby, 1999.

Stankus SJ, Dlugopolski M, Packer D. Management of herpes zoster (shingles) and postherpetic neuralgia. Am Fam Physician. 2000;61:2437-48.

Lee MS, Cooney EL, Stoessel KM, Gariano RF. Varicella zoster virus retrobulbar optic neuritis preceding retinitis in patients with acquired immune deficiency syndrome. Ophthalmology. 1998;105:467-71.

Gunduz K, Ozdemir O. Bilateral retrobulbar neuritis following unilateral herpes zoster ophthalmicus. Ophthalmologica. 1994;208:61-4.

Peterslund NA. Management of varicella zoster infections in immunocompetent hosts. Am J Med. 1988;85:74-8.

Morton P, Thomson AN. Oral acyclovir in the treatment of herpes zoster in general practice. N Z Med J. 1989;102:93-5.

Huff JC, Bean B, Balfour HH, Laskin OL, Connor JD, Corey L, et al. Therapy of herpes zoster with oral acyclovir. Am J Med. 1988;85:84-9.

Liesegang TJ. Herpes zoster keratitis. In: Krachmer JH, Mannis MJ, Holland EJ, eds. Cornea. St. Louis: Mosby, 1997.

McGill J, Chapman C, Mahakasingam M. Acyclovir therapy in herpes zoster infection. A practical guide. Trans Ophthalmol Soc U K. 1983;103(pt 1):111-4.

Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrob Agents Chemother. 1995;39:1546-53.

Colin J, Prisant O, Cochener B, Lescale O, Rolland B, Hoang-Xuan T. Comparison of the efficacy and safety of valaciclovir and acyclovir for the treatment of herpes zoster ophthalmicus. Ophthalmology. 2000;107:1507-11.

Tyring SK. Efficacy of famciclovir in the treatment of herpes zoster. Semin Dermatol. 1996;15(2 suppl 1):27-31.

Balfour HH, Bean B, Laskin OL, Ambinder RF, Meyers JD, Wade JC, et al. Acyclovir halts progression of herpes zoster in immunocompromised patients. N Engl J Med. 1983;308:1448-53.

Balfour HH. Varicella zoster virus infections in immunocompromised hosts. A review of the natural history and management. Am J Med. 1988;85:68-73.

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Herpes Zoster Ophthalmicus

(herpes zoster virus ophthalmicus; ophthalmic herpes zoster; varicella-zoster virus ophthalmicus).

• Symptoms and Signs |
• Diagnosis |
• Treatment |
• Prevention |
• Key Points |

Herpes zoster ophthalmicus is a reactivated latent varicella-zoster virus (VZV) infection ( shingles ) involving the eye. Symptoms and signs, which may be severe, include unilateral dermatomal forehead rash and painful inflammation of all the tissues of the anterior and, rarely, posterior structures of the eye. Diagnosis is based on the characteristic appearance of the anterior structures of the eye plus ipsilateral zoster dermatitis of the first branch of the trigeminal nerve (V1). Treatment is with oral antivirals, mydriatics, and topical corticosteroids.

After the primary infection, latency is established in the sensory ganglion. VZV-specific T cell–mediated immunity maintains VZV in the latent state. Viral reactivation results when immunity declines due to age, illness, or immunosuppression. Herpes zoster of the forehead involves the globe in three fourths of cases when the nasociliary nerve is affected (as indicated by a lesion on the tip of the nose) and in one third of cases not involving the tip of the nose. Overall, the globe is involved in half of patients. Varicella zoster virus is highly contagious and transmission may occur by direct contact with an ulcerated skin lesion or airborne aerosols. 

Symptoms and Signs of Herpes Zoster Ophthalmicus

A prodrome of pain or tingling of the forehead may occur. During acute disease, in addition to the painful forehead rash, symptoms and signs may include severe ocular pain; marked eyelid edema; conjunctival, episcleral, and circumcorneal conjunctival hyperemia; corneal edema; and photophobia.

Complications

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Keratitis and/or uveitis may be severe and followed by scarring. Late sequelae—glaucoma, cataract, chronic or recurrent uveitis, corneal scarring, corneal neovascularization, and hypesthesia—are common and may threaten vision. Postherpetic neuralgia episcleritis (without increased risk of visual loss) and/or retinitis (with risk of severe visual loss).

Diagnosis of Herpes Zoster Ophthalmicus

Zoster rash on the forehead or eyelid plus eye findings

Diagnosis is based on either a typical acute herpes zoster rash on the forehead, eyelid, and tip of the nose, or on the characteristic pain plus signs of previous zoster rash (eg, atrophic hypopigmented scars). Both skin findings are unilateral (ie, do not cross the midline). Vesicular or bullous lesions in this distribution that do not yet obviously involve the eye should still prompt an ophthalmologic consultation to determine whether the eye is involved. Culture and immunologic or polymerase chain reaction studies of skin at initial evaluation or serial serologic tests are done only when lesions are atypical and the diagnosis uncertain.

Treatment of Herpes Zoster Ophthalmicus

Sometimes topical corticosteroids

Use of a brief course of high-dose oral corticosteroids to prevent postherpetic neuralgia in patients > 60 years who are in good general health remains controversial.

Prevention of Herpes Zoster Ophthalmicus

Recombinant is recommended for immunocompetent adults ≥ 50 years, regardless of whether they have had herpes zoster or been given the older, live-attenuated vaccine. This recombinant vaccine decreases the chance of getting herpes zoster by 97% for adults 50 to 69 years and 91% for adults ≥ 70 years.

The eye is affected in about half of cases of V1 varicella-zoster virus reactivation.

Keratitis and/or uveitis can be severe and cause morbidity.

Appearance of the typical herpes zoster rash is usually diagnostic.

Treatment is with oral antivirals and usually topical corticosteroids and pupillary dilation.

≥ 50 years.

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The CMGs offer information on the diagnosis and management of a range of conditions that present with varying frequency in primary and first contact care.

• Abnormalities of the Pupil
• Atopic Keratoconjunctivitis (AKC)
• Basal cell carcinoma (BCC) (periocular)
• Blepharitis (Lid Margin Disease)
• CL-associated Papillary Conjunctivitis (CLAPC), Giant Papillary Conjunctivitis (GPC)
• Cellulitis, preseptal and orbital
• Chalazion (Meibomian cyst)
• Concretions
• Conjunctival pigmented lesions
• Conjunctival scarring
• Conjunctivitis (Acute Allergic)
• Conjunctivitis (bacterial)
• Conjunctivitis (viral, non-herpetic)
• Conjunctivitis (seasonal & perennial allergic)
• Conjunctivitis, Chlamydial
• Conjunctivitis medicamentosa (also Dermatoconjunctivitis medicamentosa)
• Corneal (or other superficial ocular) foreign body
• Corneal Transplant Rejection
• Corneal abrasion
• Corneal hydrops
• Dacryocystitis (acute)
• Dacryocystitis (chronic)
• Dry Eye (Keratoconjunctivitis Sicca, KCS)
• Endophthalmitis (post-operative) (Exogenous endophthalmitis)
• Episcleritis
• Facial palsy (Bell's Palsy)
• Fuchs Endothelial Corneal Dystrophy (FECD)
• Glaucoma (chronic open angle) (COAG)
• Herpes Simplex Keratitis (HSK)
• Herpes Zoster Ophthalmicus (HZO)
• Keratitis (marginal)
• Keratitis, CL-associated infiltrative
• Microbial keratitis (Acanthamoeba sp.)
• Microbial keratitis (bacterial, fungal)
• Molluscum contagiosum
• Nasolacrimal duct obstruction (nasolacrimal drainage dysfunction)
• Ocular hypertension (OHT)
• Ocular rosacea
• Ophthalmia neonatorum
• Photokeratitis (Ultraviolet [UV] burn, Arc eye, Snow Blindness)
• Phthiriasis (pediculosis ciliaris)
• Pigmented fundus lesions
• Post-operative suture breakage
• Primary Angle Closure / Primary Angle Closure Glaucoma (PAC / PACG)
• Recurrent corneal epithelial erosion syndrome
• Retinal Vein Occlusion
• Steroid-related Ocular Hypertension and Glaucoma
• Sub-conjunctival haemorrhage
• Sub-tarsal foreign body (STFB)
• Trauma (blunt)
• Trauma (chemical)
• Trauma (penetrating)
• Uveitis (anterior)
• Vernal Keratoconjunctivitis
• Vitreomacular Traction and Macular Hole
• How to use the Clinical Management Guidelines

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Predisposing factors

Symptoms of herpes zoster ophthalmicus, signs of herpes zoster ophthalmicus, differential diagnosis, management by optometrist, management category, possible management by ophthalmologist, evidence base.

Herpes zoster ophthalmicus (HZO), also known as ophthalmic shingles, is caused by a localized reactivation of the varicella zoster virus (VZV) in the ophthalmic division of the trigeminal nerve. VZV is also known as human herpesvirus-3 (HHV-3). The features of herpes zoster in general are:

• previous systemic infection, typically in childhood (varicella, i.e. chickenpox)
• virus lies dormant (sometimes for decades) in dorsal root and cranial nerve sensory ganglia
• reactivation leads to herpes zoster (shingles)
• herpes zoster ophthalmicus (HZO) is defined by zoster involvement in the ophthalmic division of the trigeminal nerve
• herpes zoster affects 20-30% of the population at some point in their lifetime; 10-20% of these will develop HZO through involvement of the ophthalmic division of the trigeminal nerve. This represents a lifetime incidence of one in 100 individuals
• ocular involvement occurs in about 50% of HZO cases
• the most common sites of ocular involvement include conjunctivitis, followed by keratitis and uveitis.
• most cases of ocular involvement develop within three to four weeks of the initial primary care diagnosis
• HZO can result in moderate-to-severe loss of vision in a significant proportion of patients with ocular involvement, even with timely and appropriate management.
• Vaccination: the NHS offers routine herpes zoster vaccination for people aged 70-79 years. Vaccination has been shown to reduce the incidence rate of shingles and post-herpetic neuralgia. Two vaccines are available:  - Zostavax, a live vaccine given as 1 dose  - Shingrix, a non-live vaccine given as 2 doses, 2 months apart

Age: the peak incidence in healthy individuals is in the 5th to 7th decades, but one in three cases occur in people under the age of 50 Immune compromise: HIV infection, medical immunosuppression e.g. corticosteroids/chemotherapy

Pain and altered sensation (often described as “tingling“, “burning” or “shooting”) of the forehead on one side Rash affecting forehead and upper eyelid appears a day to a week later General malaise, headache, fever

Ocular symptoms in acute phase:

• photophobia

Skin features

• unilateral painful, red, vesicular rash on the forehead and upper eyelid, progressing to crusting after 2-3 weeks; resolution often involves scarring
• involvement of the skin supplied by the ophthalmic division of the trigeminal nerve (V1 dermatome). Does not cross the midline
• skin lesions on the side of the tip of the nose (Hutchinson’s sign, indicating nasociliary nerve involvement) indicates three to four times the usual risk of ocular complications, but these may also occur in one in three patients without the sign
• Zoster sine herpete is a rare variant which has no cutaneous manifestations
• periorbital oedema (may close the eyelids and spread to opposite side)
• lymphadenopathy (swollen regional lymph nodes)

Ocular lesions (variable in scope and severity, may be chronic or recurrent):

• ocular lesions may occur early or develop within one month after the onset of the skin rash and therefore patients may need to be monitored even after the rash starts to improve
• mucopurulent conjunctivitis (common), associated with vesicles on the lid margin; usually resolves within 1 week
• punctate epithelial – early sign, within 2 days (50% of cases)
• pseudodendrites – fine, multiple stellate lesions (around 4-6 days)
• nummular – fine granular deposits under Bowman’s layer
• disciform – 3 weeks after the rash (occurs in 5% of cases)
• reduced corneal sensation (neurotrophic keratitis), occurring in approximately 13% of HZ keratitis cases
• endothelial changes and KP
• episcleritis : occurs in around one third of cases
• scleritis : less common; usually develops after 1 week
• anterior uveitis
• secondary glaucoma (check IOP)
• rarely, posterior segment involvement: retinitis, acute retinal necrosis, choroiditis, optic neuritis, optic atrophy
• rarely, neurological complications: cranial nerve palsies, encephalitis
• post-herpetic neuralgia is defined as pain and/or itch lasting beyond 90 days after the onset of zoster. This affects around 25% of patients and is chronic and severe in about 7%

Complications can occur months or years after the acute phase

Ocular lesions: herpes simplex keratitis Cutaneous lesions: cellulitis, contact dermatitis, atopic eczema, impetigo

Practitioners should recognise their limitations and where necessary seek further advice or refer the patient elsewhere

Non pharmacological

Exclude uveitis, and posterior segment complications (following pupil dilatation, e.g. retinal necrosis ( GRADE*: Level of evidence=low, Strength of recommendation=strong)

Advise rest and general supportive measures (reassurance, support at home, good diet, plenty of fluids) (GRADE*: Level of evidence=low, Strength of recommendation=strong)

Advise avoidance of contact with elderly or pregnant individuals, also babies and children not previously exposed to VZV (who are non-immune) or immunodeficient patients (GRADE*: Level of evidence=low, Strength of recommendation=strong)

Pharmacological

Topical lubricants for relief of ocular symptoms (drops used during the day ± unmedicated ointment for use at bedtime)  Pain relief: aspirin , paracetamol or ibuprofen (check history for contraindications). Stronger analgesics (e.g. opiates) may be indicated (co-manage with GP) (GRADE*: Level of evidence=low, Strength of recommendation=strong)  

A1: for acute skin lesions: emergency referral (same day) to GP for systemic anti-viral treatment Early treatment with oral aciclovir (within 72 hours after rash onset) reduces the percentage of eye disorders in ophthalmic zoster patients from 50% to 20-30%. This early treatment also lessens acute pain.

(NB this recommendation, though representing conventional practice, is currently not evidence based. The on-going Zoster Eye Disease Study [ZEDS] may resolve this matter)

A3: first aid measures and urgent referral (within one week) to ophthalmologist if:

• untreated disciform keratitis can lead to scarring
• neurotrophic ulceration can lead to perforation
• anterior uveitis present

B3: management to resolution if co-managed with GP and keratitis mild and limited to epithelium Requires careful monitoring. Maintain low threshold for referral since HZO is associated with chronic and recurrent complications that may be sight threatening

Systemic anti-virals e.g. aciclovir, famciclovir, valaciclovir Topical anti-virals (off-licence use) Topical steroids Immunosuppressive therapy for scleritis Botulinum toxin-induced ptosis or surgical tarsorrhaphy for neurotrophic corneal ulceration Treat other ocular complications

*GRADE: Grading of Recommendations Assessment, Development and Evaluation ( www.gradingworkinggroup.org )

Sources of evidence

Chen N, Li Q, Yang J, Zhou M, Zhou D, He L. Antiviral treatment for preventing postherpetic neuralgia . Cochrane Database Syst Rev 2014;2:CD006866

Cohen EJ, Jeng BH. Herpes Zoster: A Brief Definitive Review . Cornea. 2021;40(8):943-949.

Civen R et al. The incidence and clinical characteristics of herpes zoster among children and adolescents after implementation of varicella vaccination. Ped Infect Dis J 2009;28:954-9

Cohen EJ. Management and prevention of herpes zoster ocular disease. Cornea. 2015;34 Suppl 10:S3-8

Davis AR, Sheppard J. Herpes Zoster Ophthalmicus Review and Prevention . Eye Contact Lens. 2019 ;45(5):286-291.

Gelb LD. Preventing herpes zoster through vaccination. Ophthalmology. 2008;115(2 Suppl):S35-8

Li JY. Herpes zoster ophthalmicus: acute keratitis. Curr Opin Ophthalmol. 2018;29(4):328-333

McDonald EM, de Kock J, Ram FS. Antivirals for management of herpes zoster including ophthalmicus: a systematic review of high-quality randomized controlled trials. Antivir Ther. 2012;17(2):255-64

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.

Opstelten W, Zaal M. Managing ophthalmic herpes zoster in primary care. BMJ 2005;331:147–51

Ting DSJ, Ghosh N, Ghosh S. Herpes zoster ophthalmicus . BMJ. 2019;364;k5234

Vadoothker S, Jeng BH. Management of chronic complications associated with herpes zoster ophthalmicus. Curr Opin Ophthalmol. 2018;29(4):334

What is Herpes Zoster Ophthalmicus?

Herpes Zoster Ophthalmicus (HZO) is a viral infection of the nerve that supplies sensation (touch and pain) to the eye surface, eyelids, skin of the forehead and nose (trigeminal nerve). The virus that affects it (Varicella Zoster Virus [VZV]) also causes chickenpox. Patients who develop HZO, like most people, have usually been exposed to chickenpox by the age of 16 and though they recover from that infection, the virus lies dormant in parts of the brain and spinal cord, with its activity suppressed by the body’s immune system. If, for some reason, that suppression weakens, viruses can become reactivated and travel down the trigeminal nerve, reaching the tissues that it supplies and causing inflammation. When the skin is involved, the condition is known as shingles. Shingles occurs more often and is likely to be more severe in older people whose immunity to VZV is weakening, and in people whose immune system is not functioning normally, as for example in HIV/AIDS, or is suppressed by medical treatment.

In HZO the skin of one side of the forehead and scalp is affected, along with the eye on the same side. Any part of the eye can be involved, but most commonly it is the eye surface, including the conjunctiva (the white of the eye) and the cornea (the clear window of the eye). The cornea reacts in various ways; the most serious long-term effects result from damage to the corneal nerves, causing loss of sensation.

How is Herpes Zoster Ophthalmicus managed?

When HZO first appears, patients benefit from anti-viral tablets prescribed as soon as possible, usually by the GP. Mild cases can be co-managed by the optometrist and the GP but more severe cases need to be referred to the ophthalmologist.

Public Health England has introduced shingles vaccination for certain people aged between 70 and 80. This is given once and provides a good measure of protection against the condition.

Herpes Zoster Ophthalmicus (HZO) Version 16 Date of search 04.05.23 Date of revision 29.06.23 Date of publication 01.09.23 Date for review 03.05.25 © College of Optometrists 

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Herpes zoster ophthalmicus

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• Peer review
• Darren Shu Jeng Ting , clinical research fellow in ophthalmology 1 2 ,
• Niru Ghosh , consultant general physician 3 ,
• Saurabh Ghosh , consultant ophthalmologist 1
• 1 Sunderland Eye Infirmary, Sunderland, UK
• 2 Academic Ophthalmology, Division of Clinical Neuroscience, School of Medicine, University of Nottingham, Nottingham, UK
• 3 Mayfield Medical Group, Jarrow, UK
• Correspondence to Darren Shu Jeng Ting ting.darren{at}gmail.com
• Accepted 2 November 2018

What you need to know

Offer patients systemic antiviral medication to reduce complications, notably corneal complications and potentially post-herpetic neuralgia

Herpes zoster ophthalmicus may directly involve the eye and/or the skin around the eye, or may occur without ocular involvement, where only the skin of the V1 dermatomal region is affected

Refer to ophthalmology if a patient has ocular symptoms or signs

A 70 year old man attended with a two day history of painful vesicular rash affecting the left forehead accompanied by a red, painful left eye. Three days before the onset of the rash, he had experienced a tingling sensation at the left forehead. A clinical diagnosis of herpes zoster ophthalmicus with ocular involvement was made.

Herpes zoster, or shingles, is a common infection caused by the reactivation of varicella zoster virus that lies dormant in the dorsal root nerve ganglion following primary chickenpox infection. Herpes zoster ophthalmicus accounts for 10-20% of cases of herpes zoster infection. 1 Patients usually present with painful, vesicular, dermatomal rashes affecting the ophthalmic division of the trigeminal nerve (V1). The diagnosis is usually made on clinical grounds but a viral swab can confirm the diagnosis.

Herpes zoster ophthalmicus may present with ocular involvement such as conjunctivitis, keratitis, iritis, and uveitis. It can also present without ocular involvement (where only the skin of the V 1 dermatomal region is affected). Herpes zoster infection may rarely present without any cutaneous manifestation, also known as “zoster sine herpete,” with or without ocular involvement, rendering the diagnosis more difficult. 2

This article aims to discuss the key points to cover in a history, examination, and initial management plan for a person attending primary care with a likely diagnosis of herpes zoster ophthalmicus.

What you should cover

Presenting complaint.

When did the rash start? Starting oral antiviral treatment within 72 hours of the onset of rash substantially reduces the risk of long term ocular complications such as corneal pseudo-dendrites, stromal keratitis, and uveitis. 3 However, a recent Cochrane review has shown that starting oral antiviral treatment within 72 hours may reduce the severity but not the incidence of post-herpetic neuralgia. 4 5

Is there any pain affecting the eye or the periocular skin? Many patients find it hard to distinguish between the pain affecting the eye and the pain around the eye. Eye pain, but not periocular pain, suggests ocular involvement.

Patients with “zoster sine herpete” describe neuropathic pain affecting the V1 dermatome without any rash.

Are there other ocular symptoms such as photophobia, discharge, visual loss/disturbance, floaters, flashing light, or diplopia?

Medical/ocular history

Is there any recent systemic illness? Active systemic illness can impair immunity increasing the risk of developing herpes zoster.

Is there any history of chickenpox or herpes zoster infection? Recurrent episodes should prompt investigation for any underlying immunosuppression.

Is the patient immunosuppressed, for instance, any history of HIV, organ transplantation, or malignancy? Immunosuppressed patients may present with a more aggressive clinical course that requires intravenous antiviral treatment.

Drug history

Is the patient on any immunosuppressive drug?

Has the patient received any shingles vaccination recently? Studies have shown that shingles vaccination, which contains live attenuated varicella zoster virus, may rarely result in reactivation of herpes zoster ophthalmicus. 6

Social history

Is there any recent contact with patients affected by chickenpox or herpes zoster infection? Is there any close contact with children, pregnant women, or immunosuppressed individuals? If the answer is yes, those who have been in contact with the patient are advised to look out for symptoms and signs of chickenpox or shingles and seek medical attention if affected.

Examination

General examination.

Pattern of rash—whether the vesicular rash follows the V1 dermatomal distribution and does not cross the midline of the face ( figs 1 and 2 ).

A patient with left herpes zoster ophthalmicus affecting the forehead and side of the nose (positive Hutchinson’s sign; yellow arrows ). The crusted skin rashes follow the V1 dermatomal distribution and do not cross the vertical midline

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A patient with left herpes zoster ophthalmicus affecting the forehead but not the nose (negative Hutchinson’s sign). The crusted skin rashes follow the V1 dermatomal distribution and do not cross the vertical midline

Presence of Hutchinson’s sign ( fig 1 ) —rash involving the tip, side, or root of the nose. This sign indicates the involvement of the nasociliary branch of the trigeminal nerve, and is a strong predictor of ocular inflammation and permanent corneal denervation in herpes zoster ophthalmicus (relative risk of 3-4 times). 7 This is because the eyes and the skin of the nose are supplied by the ciliary nerves and the anterior ethmoidal nerve, respectively, which are branches of the nasociliary nerve.

Unilateral or bilateral periorbital swelling—bilateral involvement is usually due to gravitational oedema, rather than because of spread of infection to the contralateral side of the face.

Signs of secondary bacterial infection purulent discharge or worsening, high grade fever. Secondary bacterial infection is usually restricted to the side affected by herpes zoster ophthalmicus.

General wellbeing—if the patient is confused, consider the possibility of coexisting encephalitis.

Ocular examination

Formally examine visual acuity using, for example, a Snellen chart. Examine the external eye for conjunctival redness. Consider instilling a drop of fluorescein 1% to check for corneal pseudo-dendrites using a blue light. Presence of fluorescein stained corneal changes requires a more urgent referral to ophthalmology

Consider viral swab cultures for herpes simplex virus and varicella zoster virus if there is diagnostic uncertainty about whether it is shingles.

Consider other causes of a rash around the eye:

Herpes simplex virus infection— typically presents as multiple vesicles on a raised, erythematous base, followed by ulceration at a later stage. Vesicles usually occur in clusters and do not follow the dermatomal pattern and cross the midline. A viral swab culture for herpes simplex virus and varicella zoster from fresh vesicles helps distinguish between the two infections.

Impetigo— a bacterial skin infection caused by staphylococcus or streptococcus, characterised by a cluster of small blisters or yellow golden crust that do not follow a dermatomal pattern and cross the midline. More common in children than in adults.

Contact dermatitis —an inflammatory skin condition that is caused by contact with either allergens or irritants. The diagnosis can usually be made through careful history taking.

Vaccinia dermatitis —an infective, blistering skin condition that occurs in patients with atopic dermatitis after receiving the smallpox vaccine. This vaccine became obsolete after the eradication of smallpox virus.

What you should do

The diagnosis is usually made on clinical grounds (ie, dermatomal rashes affecting the V1 region and stopping at the midline of the face). Take a viral swab from active vesicles if there is any uncertainty.

Initial stage

Start all patients with herpes zoster ophthalmicus, with or without ocular involvement, on systemic antiviral treatment within 72 hours of the onset of rashes. 8 Systemic antiviral treatment can be offered beyond 72 hours after the onset of rashes (if there are new blisters forming), because the risk of side effects of treatment is low. The first line treatment in the UK is oral aciclovir 800 mg five times a day for 7-10 days. Alternatively, oral famciclovir or valaciclovir may be used as a second line treatment. 8

If superimposed bacterial infection is suspected start an oral antibiotic.

Consider prescribing analgesia such as topical capsaicin cream, amitriptyline, or gabapentin, for neuropathic pain. Explain to the patients that there is a risk of post-herpetic neuralgia.

Consider prescribing lubricating eye drops for comfort if there are lesions near the eyelid. Topical aciclovir or antibiotic eye drops are usually not recommended acutely.

Stromal keratitis or uveitis requires topical steroids to treat the disease and alleviate the pain. Topical anaesthesia is not used as it prevents corneal healing and may worsen corneal denervation.

Advise patients to avoid contact with children, pregnant women, and immunosuppressed individuals, until the vesicles have crusted over (this usually takes 1-2 weeks).

When to refer

Refer to ophthalmology— refer patients with ocular symptoms such as eye pain and blurred vision, and/or signs, including red eye and positive corneal staining with fluorescein, to the ophthalmology team for further examination. This will include a comprehensive external eye examination and a dilated fundus examination.

Potential periocular, ocular, and extraocular complications of herpes zoster ophthalmicus

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Potential periocular, ocular, and extraocular complications of herpes zoster ophthalmicus are summarised in table 1. The commonest complications are conjunctivitis, corneal pseudo-dendrites, disciform keratitis, and uveitis. The most important complications that must not be missed are uveitis and acute retinal necrosis. 9 Uveitis causes pain and photophobia without any discharge. Acute retinal necrosis causes pain with loss of vision and/or floaters. oth conditions can only be confirmed on slit-lamp examination.

Most of the ocular complications can be managed in the outpatient setting, except for acute retinal necrosis —the most serious and blinding complication—which requires hospital admission for immediate intravenous and intravitreal antiviral treatment.

Acute medicine/infectious disease team— consider referring patients to secondary care in hospital for assessment and intravenous antiviral treatment in the following circumstances 8 :

involvement of central nervous system (eg, reduced mental status)

elderly patients with severe disease (eg, multi-dermatomal involvement)

immunosuppressed patients

those who cannot take oral medication.

those with acute retinal necrosis.

Pain team— refer patients to the pain team if post-herpetic neuralgia is not controlled by simple neuropathic pain killers.

Currently there is a shingles vaccination programme available in the UK for people over 70. 13 It has been shown to reduce the incidence rate of shingles and post- herpetic neuralgia. 10

Longer term complications — include corneal denervation, recurrent uveitis, and post-herpetic neuralgia. Patients with herpes zoster ophthalmicus have a substantially increased risk of developing a cardiac event, stroke, or dementia over periods of three months to more than a year after the onset. 11 12

Education into practice

Are you aware how to obtain ophthalmology advice for a patient with suspected herpes zoster ophthalmicus and ocular involvement?

How do you counsel the patients on the risk of post-herpetic complications, particularly post-herpetic neuralgia?

Do you routinely provide shingles vaccination to people in their 70s?

How this article was created

This article was written with the aim of improving the assessment and management of herpes zoster ophthalmicus in the primary care setting. A literature search was conducted in the electronic database PubMed to identify important evidence concerning herpes zoster infection, particularly herpes zoster ophthalmicus.

How patients were involved in the creation of this article

We consulted a patient who presented to the eye emergency department with left keratouveitis following a recent herpes zoster ophthalmicus infection. He was affected by ocular pain and photophobia as well as neuropathic pain at the V1 dermatome. His clinical problem has been taken into account during the writing of the “History” and “When to refer” sections. We highlighted the symptoms and signs of uveitis, and the importance of recognising and managing post-herpetic neuralgia in patients with herpes zoster ophthalmicus.

Facial photographs were obtained from two patients with written consent for illustrative purpose.

This is part of a series of occasional articles on common problems in primary care. The BMJ welcomes contributions from GPs.

Provenance and peer review: Commissioned, based on an idea from the author; externally peer reviewed.

Competing interests The BMJ has judged that there are no disqualifying financial ties to commercial companies. The authors declare the following other interests: None

Further details of BMJ policy on financial interests is here: https://www.bmj.com/about-bmj/resources-authors/forms-policies-and-checklists/declaration-competing-interests

• Liesegang TJ
• Foulks GN ,
• Liesegang T ,
• Barbarash RA ,
• Nahlik JE ,
• Collaborative Famciclovir Herpes Zoster Study Group
• Chouliaras G ,
• Spoulou V ,
• Quinlivan M ,
• Theodoridou M
• Völker-Dieben HJ ,
• Werner RN ,
• Nikkels AF ,
• Marinović B ,
• Matthews I ,
• Erskine N ,
• Vaccinations NHS

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Reactivation of endogenous latent varicella-zoster virus within the trigeminal ganglion with neuronal spread through the ophthalmic branch results in crops of grouped vesicles on the forehead and periocularly.

Patients typically present with periocular rash and an injected eye, along with a watery discharge. The most common corneal lesion is punctate epithelial keratitis, in which the cornea has a ground-glass appearance because of stromal edema. Pseudodendrites, also very common, form from mucous deposition, are usually peripheral, and stain moderate to poorly with fluorescein. These may be differentiated from the dendrites of HSV in that the pseudodendrites lack the rounded terminal bulbs at the end of the branches and are broader and more plaquelike. Anterior stromal infiltrates may be seen in the 2nd or 3rd week after the acute infection. Follicles (hyperplastic lymphoid tissue that appears as gray or white lobular elevations, particularly in the inferior cul-de-sac) and regional adenopathy may or may not be present. Iritis is seen in approximately 40% of patients.

FIGURE 2.54

Herpes Zoster Ophthalmicus. A vesicular rash in the distribution of the ophthalmic division (V1) of the trigeminal nerve is seen. The presence of the lesion near the tip of the nose (Hutchinson sign) increases the risk of ocular involvement. (Photo contributor: Lawrence B. Stack, MD.)

Treat patients with epithelial defects with topical broad-spectrum antibiotics to prevent secondary infection. Initiate oral antivirals within 72 hours of onset, and treat for 7 to 10 days. Use cycloplegics if an iritis is present. Artificial tears or ointment may be helpful, and narcotic analgesics may be required. Ophthalmologic consultation is indicated.

Ocular complications may follow the rash by many months to years. These complications have a highly variable presentation that can mimic almost any ophthalmic condition.

Recurrence is more common in the immunocompromised host.

Perform a careful eye exam with corneal staining. Nearly two-thirds of patients will develop ocular lesions.

Corneal hypesthesia and the appearance of dendrites with fluorescein staining are seen in both herpes zoster ophthalmicus and herpes simplex keratitis.

Patients with skin lesions on the tip of the nose (Hutchinson sign) are at high risk for ocular involvement. However, the eye may be involved without a nasal lesion.

FIGURE 2.55

Herpes Zoster Ophthalmicus. A large circular dendrite is seen in this patient with ocular involvement from herpes zoster virus. (Photo contributor: Alexandra Bingnear, RN.)

FIGURE 2.56

Herpes Zoster Ophthalmicus. Grouped vesicles on the forehead and eyebrow are seen with conjunctival injection indicating ocular involvement. (Photo contributor: Lawrence E. Heiskell, MD, FACEP, FAAFP.)

FIGURE 2.57

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INTRODUCTION

Herpes zoster, also known as shingles, results from activation of latent VZV from a sensory ganglion. The virus then travels down the associated sensory nerve to the skin, leading to a characteristic dermatomal rash, usually in association with dermatomal pain. Although herpes zoster can occur at any age, it is more commonly a disease of adults >50 years of age. In addition, the severity and complications of herpes zoster are much more common in this age group.

The treatment of herpes zoster will be reviewed here. The epidemiology, clinical manifestations, diagnosis, and prevention of herpes zoster are discussed elsewhere. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster" and "Varicella-zoster virus infection in pregnancy" and "Vaccination for the prevention of shingles (herpes zoster)" and "Prevention and control of varicella-zoster virus in hospitals" .)

DETERMINING EXTENT OF INFECTION

During the initial evaluation of a patient with herpes zoster, it is important to exclude signs and symptoms of complicated zoster. This includes disseminated disease or involvement of the eye, ear, or central nervous system ( table 1 ). As an example, if cutaneous lesions are present on the tip or side of the nose, patients are at risk for herpes zoster ophthalmicus. Such patients should be evaluated for any signs or symptoms of eye involvement (eg, tearing, ocular pain, blurred vision, conjunctival injection, swelling/erythema of the lid and periorbital structures); if these clinical features are present, the patient should be evaluated by an ophthalmologist. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Complications' and 'Ocular disease' below.)

Clinical Overview

Clinical features, complications, vaccination, transmission, epidemiology, herpes zoster in people who received varicella vaccine.

Herpes zoster, also known as shingles, is caused by reactivation of varicella-zoster virus (VZV), the same virus that causes varicella (chickenpox).

Primary infection with VZV causes varicella. After a person has varicella, the virus remains latent in the dorsal root ganglia. VZV can reactivate later in a person’s life and cause herpes zoster, a painful maculopapular and then vesicular rash.

People with herpes zoster most commonly have a rash in one or two adjacent dermatomes. The rash most commonly appears on the trunk along a thoracic dermatome or on the face and it usually does not cross the body’s midline.

The rash is usually painful, itchy, or tingly. A person can experience the following symptoms several days before the rash appears:

• Photophobia (sensitivity to bright light)

The rash develops into clusters of vesicles. New vesicles continue to form over 3 to 5 days, and the rash progressively dries and scabs over. The rash usually heals in 2 to 4 weeks. Permanent skin discoloration and scarring can occur.

Postherpetic neuralgia (PHN)

PHN is the most common complication of herpes zoster. PHN is pain that persists in the area where the rash once was located and continues more than 90 days after rash onset. PHN can last for months or even years.

A person’s risk of having PHN after herpes zoster increases with age. Older adults are more likely to have longer lasting, more severe pain. Approximately 10% to 18% of people with herpes zoster will have PHN. PHN is rare in people younger than 40 years old. The likelihood of PHN is also higher in people who experience more pain with the rash or have a large rash.

Herpes zoster ophthalmicus

Herpes zoster that affects the ophthalmic division of the trigeminal nerve is called herpes zoster ophthalmicus. This can result in acute or chronic ocular sequelae, including vision loss.

Disseminated zoster

Disseminated zoster can include generalized skin eruptions where the lesions occur outside of the primary or adjacent dermatomes. It can be difficult to distinguish from varicella. Visceral involvement of the central nervous system (meningoencephalitis), lungs (pneumonitis), and liver (hepatitis) can also occur. Disseminated zoster generally occurs in people with compromised or suppressed immune systems.

Other complications of herpes zoster include:

• Bacterial superinfection of the lesions, usually due to  Staphylococcus aureus  and, less commonly, due to group A  beta hemolytic streptococcus
• Cranial and peripheral nerve palsies

People with compromised or suppressed immune systems are more likely to have a severe, long-lasting rash and experience more severe complications from herpes zoster.

Recombinant zoster vaccine (RZV, Shingrix) is the recommended vaccine to prevent shingles and related complications. For information about vaccination recommendations see Shingles Vaccination .

People with active herpes zoster lesions can spread VZV , which causes varicella in people who never had varicella or never received varicella vaccine. Once varicella resolves, these people would be at risk for herpes zoster.

Active herpes zoster lesions are infectious through direct contact with vesicular fluid or through breathing in virus particles from the blisters until they dry and scab over. People with active herpes zoster lesions should cover their lesions and avoid contact with susceptible people in their household and in occupational settings until their lesions are dry and scabbed.

Also see Managing People at High Risk for Severe Varicella  and Preventing VZV Transmission from Herpes Zoster in Healthcare Settings

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Risk Factors

Anyone who had varicella can develop herpes zoster. Approximately 99.5% of people born before 1980 in the United States were infected with wild-type VZV. Children who receive varicella vaccine have a lower risk of herpes zoster compared with children who were infected with wild-type VZV.

Approximately 1 in 3 people in the United States will develop herpes zoster during their lifetime. Most people have only one episode; however, herpes zoster can recur.

A person’s risk for herpes zoster and related complications sharply increases after 50 years of age. The reasons why VZV reactivates and causes herpes zoster are not well understood. However, a person’s risk for herpes zoster increases as their VZV-specific cell-mediated immunity declines. This decline in immunity can result from increasing age and medical conditions or medications that suppress a person’s immune system. People with the following conditions that compromise or suppress their immune system have an increased risk for herpes zoster:

• Bone marrow or solid organ (renal, cardiac, liver, and lung) transplant recipients
• Cancer, especially leukemia and lymphoma
• Human immunodeficiency virus (HIV)
• Taking immunosuppressive medications, including steroids, such as for treatment of autoimmune diseases and other immune system deficiencies

Other potential risk factors for herpes zoster have been identified, but the findings are either inconsistent or unexplained. For example:

• More women than men develop herpes zoster.
• Herpes zoster is less common in Blacks than in Whites.

Disease Rates

An estimated one million cases of herpes zoster occur annually in the United States.

• The incidence of herpes zoster varies by age and is approximately 2–9 cases per 1,000 US population annually.

The precise incidence of recurrence is not known.

• Approximately 10% to 18% of people with herpes zoster will have PHN.
• Approximately 1% to 4% of people with herpes zoster are hospitalized for complications.
• Older adults and people with compromised or suppressed immune systems are more likely to be hospitalized. About 30% of people hospitalized with herpes zoster have compromised or suppressed immune systems.

One study estimated 96 deaths occur each year where herpes zoster was the underlying cause (0.28 to 0.69 per 1 million population). Almost all the deaths occurred in older adults or those with compromised or suppressed immune systems.

Herpes zoster rates among adults in the United States gradually increased over a long period of time. We do not know the reason for this increase. However, the rates across age groups have recently plateaued or declined.

CDC studies have found that herpes zoster rates started increasing before varicella vaccine was introduced in the U.S. and did not accelerate after the routine varicella vaccination program started.

Varicella vaccines contain live attenuated VZV, which results in latent infection. Although herpes zoster has always been uncommon among children, the rate of herpes zoster in U.S. children has declined since the routine varicella vaccination program started in 1996.

• Vaccinated children are less likely to become infected with wild-type VZV.
• The risk of reactivation of vaccine-strain VZV in children is lower compared with reactivation of wild-type VZV.
• Few older adults have received the varicella vaccine since it was licensed in 1995. There is very little information on the risk of herpes zoster in people who got varicella vaccine as adults.

CDC continues to monitor the impacts of the U.S. varicella and herpes zoster vaccination programs among adults and children.

• CDC. Use of Recombinant Zoster Vaccine in Immunocompromised Adults Aged ≥19 Years: Recommendations of the Advisory Committee on Immunization Practices — United States, 2022 . MMWR Recomm Rep . 2022;71(3):80-84.
• Leung et al. The Impact of Universal Varicella Vaccination on Herpes Zoster Incidence in the United States: Comparison of Birth Cohorts Preceding and Following Varicella Vaccination Program Launch . Journal of Infection Diseases . 2022.
• Harpaz and Leung. The Epidemiology of Herpes Zoster in the United States During the Era of Varicella and Herpes Zoster Vaccines: Changing Patterns Among Older Adults . Clin Infect Dis .2019;69(2):341-344.
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• Yih W, Brooks D, Lett S, et al. The Incidence of varicella and herpes zoster in Massachusetts as measured by the Behavioral Risk Factor Surveillance System (BRFSS) during a period of increasing varicella vaccine coverage . BMC Public Health . 2005;5(68).
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• Weinmann S, Chun C, Schmid DS, et al. Incidence and clinical characteristics of herpes zoster among children in the varicella vaccine era, 2005–2009 . Journal of Infection Diseases . 2013;208(11):1859-68.
• Hardy I, Gershon AA, Steinberg SP, LaRussa P. The incidence of zoster after immunization with live attenuated varicella vaccine. A study in children with leukemia. Varicella Vaccine Collaborative Study Group . N Engl J Med . 1991;325(22):1545-50.
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Herpes Zoster Ophthalmicus Clinical Presentation and Risk Factors for Lesion Recovery.

Author information, affiliations, orcids linked to this article.

• Xiao Z | 0000-0002-6633-8392

Clinical, Cosmetic and Investigational Dermatology , 29 Dec 2023 , 16: 3767-3773 https://doi.org/10.2147/ccid.s444766   PMID: 38170070  PMCID: PMC10759815

Abstract 

Patients and methods, free full text , herpes zoster ophthalmicus clinical presentation and risk factors for lesion recovery, zupeng xiao.

1 Department of Dermatology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China

Xiaoli Chen

Herpes zoster ophthalmicus (HZO) causes trouble in patients’ daily life and work. In severe cases, it may even lead to a decrease or loss of vision. To understand the demographic information and ocular symptoms of hospitalized patients with HZO, and to find potential factors related to improvement time of skin rash and duration of ocular symptoms at discharge, we design this study.

Patients and Methods

This is a retrospective study. All patients diagnosed with HZO who were hospitalized in the Department of Dermatology of a hospital in Chongqing, China from January 1, 2015 to December 30, 2021 were included in this study. A total of 189 patients were included in this study. Clinical manifestations of the disease during hospitalization, improvement time of ocular skin lesions, and whether ocular skin lesions disappeared completely at discharge were recorded.

The most common ocular symptom was eyelid swelling (92.6%), followed by eye pain (48.7%). The most common ocular sign was conjunctivitis (78.3%), followed by keratitis (15.9%). There were 149 cases without residual ocular symptoms and 40 cases with residual ocular symptoms. There was no statistically significant difference in demographic characteristics between the two groups (P>0.05). Age ≥70 years (B=0.381, −0.061~0.022, P=0.005), use of glucocorticoids (B=0.260, 0.024~0.496, P=0.031), and use of topical antiviral drugs (B=0.380, 0.054~0.705, P=0.023) were factors affecting the time interval from admission to improvement of skin rash. Tearing (HR, OR=4.827, 1.956~11.909, P<0.001) and blood urea nitrogen (OR=0.787, 0.620–1.000, P=0.050) were factors influencing residual ocular symptoms.

This study could help clinicians gain a deeper understanding of the clinical manifestations and partial influencing factors of HZO patients, which may contribute to future clinical work.

• Introduction

Herpes zoster (HZ), also known as shingles, is a contagious skin disease caused by the reactivation of the varicella-zoster virus (VZV), which lies dormant in spinal or cranial nerve ganglia after a previous infection with chickenpox. 1 With the accelerated aging process and increased stress in daily work and life, as well as decreased immunity, the incidence of HZ has shown a significant upward trend in China. 2 Herpes zoster ophthalmicus (HZO) is a special type of HZ, accounting for 10–20% of HZ cases, which involves the first division of the trigeminal nerve (ophthalmic division). 3 It often presents as unilateral eyelid swelling, erythema and blisters along nerve roots, tearing, photophobia, and ipsilateral headache, and can involve the eye, including conjunctivitis, keratitis, scleritis, uveitis, etc. 3 , 4 In recent decades, the incidence and related eye complications of HZO has increased according to some previous reports. 5 The most common complication of HZO is postherpetic neuralgia (PHN), which had a significant impact on patients’ physical, psychological, functional and social health. 6 HZO can also lead to severe complications such as depression secondary to postherpetic neuralgia, persistent pain severe vision loss and even permanent vision loss. 5 , 6 The main risk factors include advancing age, pain in the affected skin area, rash condition and eye involvement. 7 However, there are few studies on herpes zoster ophthalmicus.

This study aims to investigate the clinical manifestations and risk factors of rash recovery and eye symptoms after leaving hospital in patients with HZO.

• Materials and Methods

Inclusion Criteria for Participants

This study is a retrospective study approved by the Ethics Committee of the First Affiliated Hospital of Chongqing Medical University (ID: K2023-564). And it has the informed consent of the patient. To identify participants, this search was conducted in the discharge records of subjects reviewed at the Department of Dermatology, First Affiliated Hospital of Chongqing Medical University, between January 1, 2015, and December 31, 2021, using keywords “herpes zoster” or “herpes zoster ophthalmicus”. And they would generally be considered for discharge when the rash darkens in color, blisters dry up and form scabs without new skin lesions developing. Patients with HZO were selected according to the guideline of Werner RN if they had a typical rash of herpes zoster with primary diagnosis of HZO. 8 Patients without typical skin rash or non-v1 HZ were excluded. We identified 1105 participants through the search, of which 916 were excluded as they either did not have V1 nerve involvement or did not exhibit typical skin rash. Ultimately, a total of 189 participants were included in this study.

All hospitalized patients will receive standardized, sufficient dosage and duration of antiviral treatment. The dermatologists in the inpatient department will select appropriate antiviral medications and administration methods after evaluating the condition of patients. Topical ocular medication will be administered under the guidance of ophthalmologists.

Outcome Measures

We defined the improvement of rash as the relief of eye swelling, pain, tearing, vision problems after admission. Then we recorded the time interval from admission to the improvement of rash as the primary outcome. We defined patients who still had eye symptoms at discharge, such as pain, swelling, tearing, and photophobia, as having residual eye symptoms and used it as a secondary outcome. Patients were divided into two groups based on whether they had residual eye symptoms at discharge.

Methods Used in Statistical Analysis

Demographic data, medical history, clinical presentation, ocular signs, treatment, and outcomes of enrolled patients were reviewed and analyzed. Statistical analysis was performed using IBM/SPSS software version 23. Statistical analysis included independent sample t -tests and Chi-square test to compare baseline demographics and clinical characteristics between patients with residual eye symptoms and patients without residual eye symptoms at discharge. A linear regression model was established to evaluate the risk factors of the improvement time of ocular symptoms. Binary logistic regression model was used to analyze the factors influencing the presence of residual ocular symptoms. A two-sided P value <0.05 was considered statistically significant.

Demographic Characteristics and Underlying Diseases of Patients

A total of 189 patients with HZO were included in the analysis, and their demographic characteristics are shown in Table 1 . The median age at presentation was 61 years (mean 59.9±14.5 years), ranging from 14 to 93 years. 85 subjects (45.0%) were over 60 years old, while 19 cases (10.1%) were under 40 years old. The male-to-female ratio was 1.59. There were 47 current smokers (24.9%), 23 former smokers (12.1%), and 119 never smokers (63.0%). Fifty-four cases (28.6%) had hypertension or coronary heart disease, 34 cases (18.0%) had diabetes, 16 cases (8.5%) had hepatitis, 11 cases (5.8%) had cancer, 11 cases (5.8%) had kidney disease, and 4 cases (2.1%) had autoimmune diseases. None of the subjects had a record of previous vaccination against herpes zoster or HIV infection.

Patient Demographics

Abbreviations : CardiovasDis, Chronic cardiovascular disease; ChronKidnDis, chronic kidney disease; ChronInfecDis, Chronic infectious ocular signs and symptoms disease; COPD, chronic obstructive pulmonary disease; AutoimmuneDis, autoimmune disease.

Ocular Signs and Symptoms of Patients

The clinical manifestations of the study population are shown in Table 2 . The median time from the rash onset to ocular symptoms was 2 days (IQR 1–4 days), and the median time from rash onset to antiviral therapy was 4 days (IQR 3–6 days). The ratio of involvement between left and right sides was 1.84. All subjects presented with rashes on the head and face, with 164 cases (86.8%) having ocular symptoms, followed by 126 cases (66.7%) on the forehead, 103 cases (54.5%) on the cheeks, 82 cases (43.4%) on the scalp, and 32 cases (17.0%) at the nose and lips. Most subjects had eyelid edema (92.6%), 92 cases (48.7%) had eye pain, 35 cases (18.5%) had tearing, 25 cases (13.2%) had blurred vision, 19 cases (10.1%) had difficulty closing their eyes, 10 cases (5.3%) had photophobia, and 6 cases (3.2%) had a foreign body sensation in the eyes. The most common ocular presentation was conjunctivitis (78.3%), followed by keratitis (15.9%), scleritis (4.7%), and uveitis (1.1%). There were no cases of acute retinal necrosis or blindness among all patients.

Clinical Presentation of Individuals with Herpes Zoster Ophthalmicus

Types of Antiviral Drugs

The antiviral treatment status of this study is shown in Table 3 . All subjects received adequate antiviral therapy, with 109 cases receiving only oral administration, 44 cases receiving only intravenous administration, and 36 cases receiving intravenous treatment before oral administration. Among them, 148 patients used acyclovir or famciclovir, 29 cases used foscarnet sodium injection, and 12 cases used brivudine. Topical antiviral drugs were used by 161 patients. The median time from the rash onset to antiviral therapy was 4 days (IQR 3–6 days). The median duration of antiviral therapy was 7 days (IQR 5–8 days). There was no significant difference between the two groups in terms of antiviral treatment.

Treatment Profile of Patients with HZO

Data Analysis of Outcome Measures

Table 4 and Table 5 display the influencing factors for the gap from admin to rash recover and eye symptom leave. A linear regression model was used to examine the risk of time interval from hospital admission to resolution of rash caused by HZO. In the multivariate analysis, age (β=0.381, P=0.005), glucocorticoids (β=0.260, P=0.031) and topical antiviral (β=0.380, P=0.023) were found to be significant factors affecting the time interval from admission to resolution of rash. As age increases, the use of glucocorticoids and local antiviral drugs can increase the time interval. A logistic regression model was used to identify risk factors for residual ocular symptoms in HZO patients at discharge. In multivariate analysis, tearing (OR=4.827, P<0.001) and BUN (OR=0.787, P=0.050) were identified as significant factors affecting residual ocular symptoms at discharge.

Factors Associated with the Gap from Admin to Rash Recover

Note : *Indicates statistically significant.

Abbreviations : WBC, white blood cell; PLT, platelet; CRP, C-reactive protein.

Factors Associated with Eye Symptom Leave

Abbreviations : LOS, Length of Stay; BUN, Blood Urea Nitrogen.

HZO is a serious condition characterized by various symptoms and complications, including postherpetic neuralgia, conjunctivitis, keratitis, uveitis, and even retinal vasculitis and necrosis. 9 , 10 All HZO patients exhibited ocular manifestations in this study. Previous studies have reported an incidence rate of ocular symptoms in HZO patients ranging from around 50% to 80%. 7 , 11 , 12 This may be attributed to the fact that hospitalized patients generally have more severe symptoms. Patients with more pronounced and severe ocular involvement are more likely to be advised for hospitalization by doctors. Hence, the incidence rate of ocular symptoms among our patients is expected to be higher. Conjunctivitis, keratitis, and uveitis have been reported as the most common ocular manifestations of HZO. 4 , 7 In our study, conjunctivitis was the most frequent manifestation, followed by keratitis and scleritis. However, some of our patients did not undergo professional ophthalmic examinations, which may have resulted in certain ophthalmic symptoms being undetected in a timely manner.

Aging is a known risk factor for HZO. 7 This study identified advanced age as an independent risk factor for delayed skin lesion recovery. Emma et al’s study 13 analyzed HZO patients at the Massachusetts Eye and Ear Infirmary (MEEI), dividing the cases into two groups: 71 cases in 2007 vs 195 cases in 2013, with the average age of the latter group dropping significantly by almost six years. Carlos et al’s recent study 14 also analyzed the incidence rate of HZO in Columbia and found that its proportion increases with age in a total of 100,000 residents. We speculate that herpes zoster is showing a trend of getting younger. Additionally, the older a person is, the higher the likelihood of contracting the disease. More importantly, previous studies have shown that the specific cellular-mediated immunity to VZV may decrease with age, leading to an increasing incidence and severity of HZO. 15 And Anthony and Himal found that the herpes zoster vaccine can reduce the risk of developing herpes zoster and postherpetic neuralgia in individuals aged 50 and older, as well as those aged 70 and older. 16 , 17 Therefore, we believe that older adults with normal immune function should receive vaccination against herpes zoster.

Currently, there is a debate whether corticosteroids should be used in the treatment plan for HZO. Whitley and Han 18 , 19 analyzed 5 RCTs and conducted a Meta-analysis suggesting that early use of corticosteroids is ineffective for preventing HZO but can inhibit inflammation, alleviate acute phase pain, and accelerate skin lesion healing. Li et al’s study 20 suggested that prolonged steroid use may help with eye muscle paralysis recovery. And Langston’s study 21 indicated a noticeable acceleration in the recovery of rash recovery and acute pain relief for patients undergoing prednisone treatment, leading to an improvement in the quality of life. In our study, steroids were found to be meaningful in alleviating ocular skin lesions. Additionally, topical application of corticosteroid eye drops or ointments recommended by an ophthalmologist can be used. 1 The specific indicators for the use of corticosteroids, the selection of specific types, and the method of use still require further research.

It has been reported that topical acyclovir cream or penciclovir cream is ineffective in the treatment of HZ. 1 However, in our study, it was found that topical antiviral had a shortening effect on the improvement time of rash (P=0.005). This may be because the topical antiviral drug used in our hospital is interferon gel, which has been proved by Miyoshi et al 22 in eight cancer patients that while it did not relieve pain, it reduced the time it took for herpes to disappear. However, the sample size of this study was small and no statistical analysis was conducted. And it only studied the therapeutic effects of interferon gel in HZ, not in HZO. Whether external interferon gel can be effective in the treatment of HZO needs to be further designed and analyzed.

In addition, tearing (OR=4.827, 1.956–11.909, P< 0.001) and blood urea nitrogen (OR=0.787, 0.620–1.000, P=0.050) were the remaining influencing factors of ocular symptoms in our study. However, there is no literature on the relationship between tearing and urea nitrogen and herpes zoster. We speculate that tearing may be related to the involvement of the ophthalmic branch of the trigeminal nerve, affecting the lacrimal gland. Additionally, impaired BUN may suggest that it is not only the facial nerve that is affected. We should pay more attention to patients with renal impairment who have herpes zoster ophthalmicus. We hope to further validate this in the future.

The limitations of this study are retrospective analysis bias, as it only included HZO patients admitted to a hospital in Chongqing, China with relatively limited data collection, and some HZO patients might not have had their eye symptoms fully recognized. Additionally, some patients did not undergo complete ophthalmologic examinations, lack of relevant eye data, nor were they followed up afterwards. The main advantage of this study was that all patients were examined by at least one associate chief physician and chief physician, with diagnoses accurately determined beyond doubt. Patients’ basic information, clinical symptoms and laboratory indicators were recorded in an electronic medical record system, making comprehensive data and inflammatory indicators analysis of influencing factors for HZO possible.

• Conclusions

This study provides the demographics, clinical manifestations and some risk factors of HZO patients. HZO can lead to severe sequelae, most unfavorably involving the eyes, which may need more aggressive treatment for patients with severe rashes on the face. For those whose symptoms persist even after discharge, further studies and follow-up are necessary. This will help to gain a more comprehensive understanding of the long-term effects on patients with herpes zoster ophthalmicus and potential treatment options.

• Acknowledgments

The patients in this manuscript have given written informed consent to publication of their case details. The authors would like to thank the patients who participated in this study.

• Funding Statement

This study was supported by Special Foundation for Postdoctoral Research Projects of Chongqing (2021XM3080), Natural Science Foundation General Program of Chongqing (cstc2021jcyj-msxmX0182) and Natural Science Foundation General Program of China (81874238).

• Ethics Approval and Informed Consent

This study was approved by the Ethics Committee of the First Affiliated Hospital, Chongqing Medical University (ID: K2023-564). This article don’t involve the disclosure of patient privacy. Therefore, the ethics committee don’t require patient consent to review their medical records.

The authors declare that there is no conflict of interest regarding the publication of this paper.

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Bilateral Pupillary Involvement as a Clinical Presentation of Herpes Zoster Ophthalmicus

Affiliations.

• 1 Department of Neurology, Peking University Third Hospital, Bejing, China.
• 2 No.8 High School, Beijing, China.
• 3 Department of Ophthalmology, Daping Hospital, Army Medical University, Chongqing, China.
• 4 National Healthcare Group Eye Institute, Tan Tock Seng Hospital, Singapore, Singapore.
• 5 Singapore Eye Research Institute, Singapore, Singapore.
• 6 Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore.
• 7 Department of Ophthalmology, Peking University Third Hospital; Beijing Key Laboratory of Restoration of Damaged Ocular Nerve, Peking University Third Hospital, Bejing, China.
• PMID: 34637674
• DOI: 10.1080/09273948.2021.1986075

Purpose: Herpes zoster ophthalmicus (HZO) is traditionally considered as an unilateral disease. However, subclinical involvements in the contralateral eye structures are evidence, giving rise to a broader understanding of varicella-zoster virus (VZV) infection.

Methods: We enrolled 20 eyes of 10 patients with HZO and 12 eyes of healthy controls to investigate the bilateral features of HZO patients using a hand-held pupillometer and a Cochet-Bonnet esthesiometer.

Results: Maximum pupil size before constriction (INT) and minimum diameter when pupil constricts at peak (END) were significantly smaller in patients affected eyes compared with those in controls (p < .05). Interestingly, INT and END were significantly reduced in contralateral eyes of 20 affected patients and also in comparison to control group (p < .001 and p = .034 respectively).

Conclusion: The contralateral eyes may have subclinical involvement in patients with HZO based on significantly abnormal pupillary light reflex (PLR). Pupillometer provides a primary and convenient method to investigate the anatomy and pathology of the PLR.

Keywords: Bilateral pupillary involvement; Herpes zoster ophthalmicus; aricella-zoster virus infection; pupillary light reflex; pupilometer.

• Herpes Zoster Ophthalmicus*
• Herpesvirus 3, Human

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Multiple ocular manifestations in a patient diagnosed with herpes zoster ophthalmicus: case report

David-ionuț beuran.

* Department of Ophthalmology, „Dr. Carol Davila” Central Military University Emergency Hospital, Bucharest, Romania

Mioara-Laura Macovei

** „Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania

Ioana Ruxandra Boca

*** Clinical Emergency Eye Hospital, Bucharest, Romania

Objective: Our purpose was to present a case of a patient diagnosed with herpes zoster ophthalmicus with multiple ocular manifestations.

Case presentation: A 70-year-old Caucasian male presented to the hospital for headache and skin hyperesthesia on the scalp and forehead on the left side. The diagnoses of herpes zoster ophthalmicus and acute conjunctivitis were made for the left eye. The patient was followed up for 6 months and during that period the following diagnoses were made for the same eye: peripheral sterile corneal infiltrates, episcleritis, and hypertensive anterior uveitis.

Discussions: Herpes zoster ophthalmicus occurs when the reactivation of the dormant virus involves the ophthalmic division of the trigeminal nerve. The most frequent ocular presentations are conjunctivitis, keratitis, uveitis, episcleritis, and scleritis. The standard therapy consists of antivirals, such as acyclovir, valacyclovir, and famciclovir to limit the replication of the virus. The patient’s risk factors, the course of treatment, and the severity of the disease, all affect the prognosis, which is highly variable. Prevention of the disease consists of vaccination with one of the following two vaccines, Zostavax and Shingrix.

Conclusions: Final visual acuity for the left eye remained 1 despite numerous manifestations of the disease.

Abbreviations: VZV = Varicella-zoster virus, BCVA = best-corrected visual acuity, OU = both eyes, OD = right eye, OS = left eye, IOP = intraocular pressure, NCT = non-contact tonometer, ZVX = Zostavax vaccine

Introduction

Virus structure

Varicella-zoster virus (VZV) is a part of the Herpesviridae family and represents the etiologic agent of varicella (primary disease) and herpes zoster (secondary disease). The virus has an envelope, a double-stranded deoxyribonucleic acid, and establishes latency. Some precise glycoproteins mediate the cell and humoral immunity to VZV [ 1 ].

Transmission

VZV is very contagious and the virus is transmitted via respiratory tract or from direct contact with vesicular lesions, causing the primary infection, which is varicella. The incubation time ranges between 10-21 days [ 2 , 3 ].

Epidemiology

VZV occurs worldwide and is less frequent in some developed countries due to the vaccine. The incidence of varicella depends on the type of climate, for example in temperate climates the peak of the disease occurs before adolescence. There is also a higher incidence during winter and spring [ 4 ]. On the other side, herpes zoster also occurs worldwide, but the incidence increases with age and with the presence of risk factors such as immunosuppression, infections, and mental stress [ 2 ].

Primary infection

The primary disease manifests with cutaneous lesions that are in different developing stages. These are infectious until the vesicular lesions become dry, but the host is contagious up to 24-48 hours before the initial skin eruption [ 1 , 3 ].

Secondary infection

After the initial infection, the virus remains latent within the sensory ganglia for a variable amount of time. It can be reactivated, due to many factors (e.g. increased age, stress, immunosuppression) causing extraocular and ocular manifestations of herpes zoster [ 1 , 5 ].

Case presentation

A 70-year-old Caucasian male presented to the hospital for headache and skin hyperesthesia on the scalp and forehead on the left side. The symptoms started a week before the presentation. From personal history, we should mention chicken pox. Clinical examination revealed eruption on the scalp, forehead, and periocular (dermatome V1), on the left side, respecting the midline, currently represented by well-defined brown macules. Five days before, the lesions were represented by blisters.

Best-corrected visual acuity (BCVA) was 1 in both eyes (Oculus Uterque: OU) after correction of compound hyperopic astigmatism with the following refraction, right eye (Oculus Dexter: OD) +1,75/-1,00/2° and left eye (Oculus sinister: OS) +1,50/-0,75/59°. The intraocular pressure (IOP) in the right eye was 18 mmHg non-contact tonometer (NCT) and in the left eye 16 mmHg NCT. At anterior pole examination, both eyes presented pseudoexfoliative material at the level of the anterior lens capsule and cortical lens opacities. OS revealed eyelid edema, conjunctival hyperemia, and watery secretions. At posterior pole examination, OD presented small, white vitreous opacities and OS was without pathological changes.

After the initial examinations, the following diagnoses were established for OS: Herpes zoster ophthalmicus, acute conjunctivitis; for OD: asteroid hyalosis and for OU: age-related cataract, pseudoexfoliation syndrome, compound hyperopic astigmatism, presbyopia.

Blood was prelevated for the following: hemogram, fibrinogen, erythrocyte sedimentation rate, lipid profile, serum urea, uric acid, creatinine, blood glucose, alanine transaminase, and aspartate aminotransferase. Those outside normal limits were: fibrinogen 460 mg/dL, erythrocyte sedimentation rate 23 mm/1h, and blood glucose 185 mg/dL. Dermatology consultation confirmed the diagnosis of herpes zoster ophthalmicus and treatment was initiated for the skin lesions. Furthermore, the diabetology consultation confirmed the diagnosis of type II diabetes.

Considerations in the differential diagnosis of the rash included the eruption from the herpes simplex virus, which usually occurs in younger patients. The vesicles are grouped in a bouquet, situated on an erythematous background, with a limited distribution that does not respect the dermatomes.

A systemic treatment was initiated with oral acyclovir tablets, 800 mg five times daily for ten days. The local treatment for the skin lesions included fusidic acid ointment, 20 mg/g, applied externally on lesions twice a day for ten days. Topical treatment for OS contained ganciclovir ophthalmic gel 1,5 mg/g three applications daily for ten days and preservative-free artificial tears four times daily for ten days and later as needed.

On the 18th day of follow-up, the BVCA of OD remained 1, while the BVCA of OS was 0,8 with difficulty. IOP was within normal limits in OU, 14 mmHg NCT. Stromal, small infiltrates were observed at 6, 11, and 12 o’clock positions of the peripheral cornea ( Fig. 1 ). The diagnosis of peripheral sterile corneal infiltrates was made. The treatment with fluorometholone ophthalmic solution 2 mg/ml in OS was initiated, one drop four times daily for two weeks.

18 days after the first examination, peripheral sterile corneal infiltrates

After one week (approximately 3 weeks after the first examination), the BCVA of OU was 1 and IOP was maintained within normal limits. The infiltrates disappeared, leaving only one spot at the 12 o’clock position ( Fig. 2 ). The treatment was continued as follows: fluorometholone 2 mg/ml four drops per day for one week, three drops per day for one week, two drops per day for one week and finally one drop per day for one week.

Three weeks after initial presentation

Two months after the initial presentation, the patient came for follow-up. BCVA maintained 1 and IOP was slightly elevated in OS, 22 mmHg. At the level of the left eye conjunctiva, at the 11 o’clock position, a hyperemic, mobile nodule was observed ( Fig. 3A ). The epinephrine 10% test was positive ( Fig. 3B ). The diagnosis of nodular episcleritis was made. The treatment with fluorometholone was resumed as follows: 4 drops per day for two weeks then gradually decreased by one drop per week.

Two months after the initial presentation. Nodular episcleritis ( A ). Epinephrine 10% test ( B )

After approximately one month of resumed treatment, the patient presented with ocular discomfort and slightly decreased visual acuity of OS. Ophthalmological examination revealed dilated conjunctival and episcleral vessels, episcleral nodules at 11 and 3 o’clock positions ( Fig. 4A, B ), peripheral sterile corneal infiltrates mostly at 7-8 o’clock positions ( ​ C C ), and inferior endothelial precipitates ( ​ D D ).

Three months after the initial presentation. Episcleral nodule at 11 ( A ) and 3 ( B ) o’clock positions. Peripheral sterile corneal infiltrates mostly at 7-8 o’clock positions ( C ) and inferior endothelial precipitates ( D )

BCVA was 1 for OD and 0,9 for OS, IOP for OD was 15 mmHg adjusted at a pachymetry of 520 µm and for OS it was 24 mmHg adjusted at a pachymetry of 582 µm. The diagnoses made at that moment were episcleritis and hypertensive anterior uveitis. Treatment was initiated with dexamethasone 1 mg/ml ophthalmic solution 4 drops per day for 28 days, dorzolamide 20 mg/ml, and timolol 5 mg/ml combined ophthalmic solution 2 drops per day for 28 days, and acyclovir tablets 800 mg, 5 per day for 10 days.

The evolution was favorable, endothelial precipitates disappeared after five days. At one month, episcleral nodules were present ( Fig. 5A, B ). BCVA was 1 for OD and maintained 0,9 for OS. IOP was within normal limits. The patient continued treatment with dexamethasone and dorzolamide with timolol.

Four months after the initial presentation. Episcleral nodule at 11 and 3 o’clock positions ( A, B )

After two months, episcleral nodules disappeared ( Fig. 6A, B ). BCVA was 1 for both eyes.

Six months after initial presentation ( A, B )

Herpes zoster ophthalmicus

Herpes zoster ophthalmicus occurs when the reactivation of the dormant virus involves the ophthalmic division (V1) of the trigeminal nerve (V). The manifestations can only include the specific periocular rash and pain, but some patients present with direct ocular involvement [ 5 ].

Ocular manifestations

The spectrum of symptoms and signs affecting the eye may vary during different stages of the disease. Some of the most common symptoms are eye pain, red eye, tearing, blurry vision, and foreign body sensation [ 5 ]. The most frequent ocular presentations are conjunctivitis, keratitis, uveitis, episcleritis, and scleritis [ 2 , 6 ]. Corneal involvement includes epithelial, stromal, and endothelial keratitis. Uveitis can be anterior, posterior or panuveitis [ 7 ]. Some uncommon manifestations may be acute retinal necrosis, external ocular motor palsies, and optic neuritis [ 8 ].

It consists of antiviral therapy, to limit the replication of the virus. Acyclovir 800 mg is administrated five times per day orally, which should be initiated within 72 hours of the clinical presentation for at least 7 days [ 8 ]. Alternatives are valacyclovir 1000 mg and famciclovir 500 mg, both administrated three times per day orally for at least 7 days. The last two require renal dosing. Immunocompromised adults require intravenous administration of acyclovir, 10 mg/kg of ideal body weight, every eight hours for at least 7 days, or foscarnet 90 mg/kg every 12 hours [ 7 ]. The following treatment options for specific ocular manifestations are recommended: conjunctivitis requires topical lubrication and antibiotics for secondary bacterial infection prevention; epithelial keratitis requires topical lubrication; stromal keratitis requires topical steroids; episcleritis and scleritis require topical nonsteroidal anti-inflammatory agents and/or steroids; uveitis requires topical and oral steroids, oral antivirals (e.g. acyclovir) and cycloplegics; acute retinal necrosis and progressive outer retinal necrosis require intravenous antivirals (e.g. acyclovir) followed by oral antivirals (e.g. acyclovir) [ 5 , 9 ].

The variability is high, and it is based on the patient’s risk factors, treatment initiation time, and severity of the disease [ 7 ].

Complications

In a study of 869 patients, the complications were: corneal scar, neurotrophic keratopathy, band keratopathy, corneal melt, corneal perforation, iris transillumination defects, acute retinal necrosis, high intraocular pressure, glaucoma, moderate and severe vision loss. On multivariate analysis, factors associated with moderate visual loss (≤ 20/50) were: older age, white ethnicity, presenting visual acuity, and uveitis. On multivariate analysis, factors associated with severe visual loss (≤ 20/200) were: older age, immunosuppression, presenting visual acuity, and uveitis [ 10 ]. A frequent neurological complication is a postherpetic neuralgia. It is characterized by powerful pain that persists for three or more months after the onset of the disease [ 2 , 11 ]. The most vulnerable patients are the ones older than or equal to 50 years of age, resulting in an important correlation between increasing age and the occurrence of postherpetic neuralgia [ 11 ].

Vaccination

Prevention of the diseases is effective with the help of vaccines. Nowadays, two vaccines are available. The first one is the live attenuated Zostavax vaccine (ZVX), which is given as a subcutaneous injection and is a one-time vaccination. The second one is a non-live recombinant vaccine, named Shingrix, which is given as two intramuscular injections, 2 to 6 months apart [ 1 , 12 ]. The overall efficacy against the incidence of herpes zoster is 51.3% for ZVX and 97.2% for Shingrix. Both are recommended for immunocompetent adults aged ≥ 50 years. Shingrix is also recommended for adults aged ≥ 18 years, who are at increased risk of herpes zoster due to immunodeficiency or immunosuppression [ 13 ].

A 70-year-old patient diagnosed with herpes zoster ophthalmicus maintained a visual acuity of 1 despite numerous late ophthalmic manifestations.

Conflict of Interest Statement

The authors state no conflict of interest.

Informed Consent and Human and Animal Rights Statement

Informed consent has been obtained from the patient included in the case report.

Authorization for the use of human subjects

Not applicable.

Acknowledgments

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Disclosures