Varicella and zoster are identical viruses. Varicella is Latin for "little pox"; zoster is Greek for "girdle."

• Primary infection: Varicella (chicken pox)
• Secondary infection: Zoster (shingles). Shingles is a painful skin rash that develops on half the body, in a belt-like fashion; most often on chest starting in the middle of the back and wrapping around to the breast.

A vaccine for varicella-zoster virus is available in the US and is administered to infants.

Herpes Zoster Ophthalmicus (HZO)

Herpes zoster ophthalmicus varies widely in severity (unnoticed to globe destruction). Multiple complications may present as acute, chronic, or subacute and relapsing. Ten to 15 percent of all cases of HZO affect the ophthalmic division V (frontal, nasocilary, supraorbital, and supratrochlear branches). Ocular complications occur in 50 to 70 percent, and 40 percent of these with corneal lesions. Rarely disseminated systemic disease--severe immunosuppression.

The incidence increases with age and occurs most frequently in the 6th to 7th decade of life. In elderly, the signs and symptoms are more severe and last longer. Signs and symptoms also tend to be more severe in AIDS patients. There is no correlation between ocular complications and age, sex, or severity of the skin rash.

Clinical phases: Acute, chronic, and relapsing.

• Symptoms
• Signs
• Other Complications
• HZO Flow Chart
• Management and Treatment
• The Shingles Prevention Study

	URL: http://www.opt.indiana.edu/ce/virker/part3.htm Revised: November 28, 2005
	IU Optometry home page: http://www.opt.indiana.edu/ Comments (content): Dr. Vic Malinovsky at malinovs@indiana.edu or Dr. Jane Ann Grogg at jgrogg@indiana.edu Comments: Web Administrator Page design and coding: Terri Greene Copyright © 2005, The Trustees of Indiana University

Symptoms

• Prodromal: Flu-like illness with headache, mild fever, malaise, depression, and neck stiffness for up to one week before rash.
• Localized pain accompanied by hyperesthesia, superficial itching, tingling, burning sensation over the distribution of ophthalmic nerve. Pain may be severe, deep, boring, or lancing (constant or intermittent).
• Lymph node swelling.

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Signs Rash Blushing of the skin with localized pain followed in 3-5 days by maculas-papules-vesicles-pustules-burst and ulcerate then forming small, discrete to large lesions; hemorrhagic bullae may form Crusting after 6 days--may leave white scars in the area Varies in distribution, density, and severity Painful edema usually throbbing and burning Usually hemicranial distribution Scalp, forehead, upper lid, and side of nose

Click image for larger view. HZO: hemifacial skin lesions HZO: resolving skin lesions

Ocular involvement

• Hutchinson's rule: Vesicles on tip of nose (1/3 of the time) . . . signals ocular (possibly more serious) involvement--not infallible. 75% risk--Nasociliary branch of the ophthalmic nerve provides sensory supply to cornea, ciliary body, iris, conjunctiva, and tip of the nose.
• 50% with rash and lid edema only.
• Rash usually subsides within 2 weeks.
• Acute lesions of globe occur within 3 weeks of rash and often take a chronic course.
• Relapsing lesions up to 6 years; tendency to recur.
• Virus presumably reaches the eye via ciliary nerves.
• Ocular symptoms of pain, tearing, and foreign body sensation.

Upper eyelid involvement (early involvement)

• Ptosis due to severe edema and inflammation
• Vesicles of eyelid and lid margin; severe cases can result in scarring
• Complications of ectropion, ptosis, and loss of eyelashes

Conjunctiva involvement (early involvement)

• Conjunctivitis is a common manifestation with associated vesicles on lid margin; pseudomembranes can form.
• Subconjunctival hemorrhages
• Usually resolving in a week

Episclera and sclera involvement (early involvement)

• Episcleritis (35%) or scleritis often hidden by overlying conjunctivitis; tendency to recur
• Scleritis less common--may form sclerokeratitis, peripheral melting syndrome

Corneal complications Punctate epithelial keratitis (50%)--early Usually peripheral, multiple, raised, small, and focal Usually on average 2 to 4 days after rash Resolve or progress into pseudodendrite Felt to represent active viral replication Pseudodendrite--early Small, fine, multiple dendrites or stellate lesions Usually peripheral Stain moderately well with rose bengal and poorly with fluorescein Differs from HSV: more mucous plaque-like, broader, ropey, and lacks terminal bulbs; infiltrative vs. ulcerative Self limiting, no real response to steroids or antivirals Corneal hypoesthesia may occur-1 to 4 weeks Subepithelial haze or anterior stromal keratitis may follow

Click image for larger view. HZO: conjunctivitis HZO: punctate staining HZO: pseudodendrite

Anterior stromal infiltrates Usually underlying the epithelial lesions Single or multiple patches of hazy, granular deposits in anterior stroma Called nummular keratitis Appears 10 days after onset First white but later may be a brown discolor Most likely due to viral antigen diffusing into anterior stroma eliciting an immune response Fluctuate in density; similar to EKC

Click image for larger view. Nummular scars secondary to HZO

Disciform keratitis (5%) Deep central or peripheral disc-shaped stromal edema and infiltrates Occurs 1 to 2 months after rash Surrounding immune rings Associated iritis, KPs, and ocular hypertension Delayed hypersensitivity cell mediated response to viral antigens Response to steroids usually rapid, but rebound and recurrence are common. Dense opacification and vascularization may follow. Probably more common and severe in AIDS or other forms of immuno-suppression

Click image for larger view. Disciform stromal keratitis; note keratic precipitates

Neurotrophic keratitis

• Decreased corneal sensation initially (33%); a few in number will develop clinical signs
• Initially lack of corneal luster, an irregular corneal surface, and mild erosions
• May progress to persistent epithelial defects, sterile ulceration, vascularization, and perforation

Delayed corneal mucous plaques (5%)

• Elevated, coarse, opaque, gray-white linear or branching lesions on surface of cornea, stain with RB, usually occurs 3-4 months after rash
• Often confused with dendrites
• Can be wiped from surface
• Usually associated with neurotrophic keratitis
• Due to tear film instability and epithelial changes
• Self limiting; may need topical steroids

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Other Complications

• Iritis with or without corneal disease; may develop sectorial iris atrophy
• Glaucoma--trabeculitis
• Optic neuritis, disc edema
• Pupil anomalies--Horner's syndrome
• EOM palsies (3rd most common); spontaneous recovery in 6 months
• Cataracts
• Posterior segment involvement--chorioretinitis acute retinal necrosis syndrome and progressive outer retinal necrosis syndrome
• Post-herpetic neuralgia
  • Severe pain: increases dramatically in prevalence, severity, and duration with age, but not correlated with severity of skin rash or ocular involvement
  • 7%-17%
  • Pain may be constant or intermittent; worse at night; aggravated by touch and heat
  • Triggers: spontaneous or touching area
  • May last years: 50% resolve in 3 months; 20% continue to suffer beyond a year
  • May lead to suicide

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Management and Treatment

Effective treatment early in the disease with careful follow-up can prevent complications at later date. Hospital admission is only necessary in severe cases. If there is systemic spread, screen for malignancy. Segregate patient from people who have not had chicken pox or are immunocompromised.

Dermatitis

• Most cases of skin and lid dermatitis are self-limiting and benign.
• Optimal treatment is begun within 48-72 hours of the first skin eruption; may still be beneficial as late as 7 days.
• Oral antivirals:
  • Acyclovir (Zovirax) 800mg 5 times/day (generics)
  • Valacyclovir (Valtrex) 1000mg 3 times/day
  • Famciclovir (Famvir) 500mg 3 times/day for 7-10 days (faster healing time, shorter duration of post-herpetic neuralgia?)
• Use of antibiotic/steroid ointment applied to lesions?
• Amitriptyline is sometimes indicated in acute cases.

Skin and lid lesions

• Drying lotions should not be used.
• Oral antihistamines may prevent scratching.
• Warm compresses tid
• With severe lid involvement, use lubricating or antibiotic ointments to prevent complications from exposure or trichiasis.
• May need an oculoplastics consult
• Can use antibiotic oinments (e.g., bacitracin or erythromycin to skin lesions bid)

Acute neuralgia

• Acute neuralgia (severe at first) usually short-lived
• In addition to antivirals, oral analgesics are often recommended for pain. May need an opioid analgesic (e.g., Tylenol #3 [acetaminophen with codeine]).
• Role of oral steroids? 40-60mg prednisone daily with taper over 10 days? Contraindicated in immunosuppressed patients (e.g., HIV). No value in preventing post-herpetic neuralgia.

Post-herpetic neuralgia (PHN)

• Incidence of PHN is not decreased by the use of antivirals, but the duration is significantly shortened by the aggressive use of oral antiviral drug.
• Antidepressants (amitriptyline or newer selective serotonin re-uptake inhibitors such as Prozac, Paxil, Zoloft)
• Anticonvulsants
• Topical capsaicin (Zostrix) cream 4 times daily or doxepin (Zonalon) ointment
• Chronic pain management

Oral acyclovirs (or IV, especially in HIV) play a significant role in preventing or minimizing complications. They hasten resolution of signs and symptoms, reduce viral shedding and formation of new skin lesions, and decrease both the incidence and severity of ocular complications. They also reduce the corneal complications (i.e., dendriform keratitis, stromal keratitis, and anterior uveitis). Main side effect is intestinal disturbance (nausea and vomiting). If patient has kidney disease, it is important to consult patient's MD and adjust according to kidney function. Acyclovir (Zovirax) HZ: 800 mg 5x/day x 7-10 days HS: 400 mg 5x/day x 7-10 days Valacyclovir (Valtrex) HZ: two 500 mg tabs tid x 7-10 days HS: 500 mg tabs tid x 7-10 days Famciclovir (Famvir) HZ: 500 mg tid x 7-10 days HS: 500 mg bid x 7-10 days

Ocular involvement

Vision loss is a serious threat, but fortunately, an uncommon consequence. Oral therapy has been shown to influence the incidence and severity of eye complications. Topical antiviral agents are ineffective. Topical steroids with frequent applications at first and tapering carefully and slowly are of value in treatment of the immune phenomena. Be sure to monitor IOPs (use beta blockers/Alphagan P if elevated pressures). Artificial tears are helpful in neurotrophic keratitis. Cycloplegic drugs for management of secondary iritis and pain. Use penetrating keratoplasty for scarring.

• Conjunctival involvement: May use cool compresses and tears plus Erythromycin ointment bid?
• Epithelial disease (superficial punctate keratitis and pseudodendrites): Usually self-limiting. Questionable benefit of either topical antivirals or topical steroids (Pred Forte or Lotemax qid). Usually no treatment or just artificial tears and cool compresses for symptomatic relief.
• Stromal disease: Stromal infiltrates, disciform keratitis, interstitial keratitis, and sclerokeratitis all may respond to topical steroids. The minimum dose necessary to achieve the desired affects should be used (e.g., 1% prednisolone acetate [Pred Forte] qid or Lotemax with slow taper). Cycloplegic (e.g., 5% homatropine 2-3 times daily) can decrease pain and help to prevent or control uveitis and synechia. Make sure to rule out herpes simplex keratitis (HSK).
• Uveitis without stromal keratitis: Topical steroids (Pred Forte or Lotemax q 1-6 h). Cycloplegic (5% homatropine bid).
• Non-healing epithelial defects: Tears, ointments, antibiotic ointments (erythromycin), pressure patching, bandage soft contact lenses, tarsorrhaphy, or conjunctival flap.
• Mucous plaque keratitis: Usually resolve without treatment. Topical steroids, lubricants, and mucolytic agents (e.g., 10% acetylcysteine).
• Corneal scarring: If scarring affects vision, it is best treated with penetrating keratoplasty. May have a poor outcome because of recurrent or chronic inflammation, neovascularization, glaucoma, and poor tear film.
• Increased IOP: May be due to steroids or uveitis. If uveitis present, may increase steroid administration for a few days. If IOP still high, substitute with Lotemax and treat IOP with beta blockers (qd or Alphagan tid). Note: no prostaglandin.

The Shingles Prevention Study

Department of VA is studying an experimental shingles vaccine (more potent than vaccine used for children) to determine its safety and effectiveness in preventing shingles.

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