Herpes zoster (hz) presentation

HERPES ZOSTER

HERPES ZOSTER (HZ)

• An acute dermatomal infection associated with reactivation of VZV

• Characterized by Unilateral pain• A vesicular or bullous eruption limited to a dermatome(s) innervated by a corresponding sensory ganglion.

EPIDEMIOLOGYAge of Onset More than 66% are >50 years ofage; 5% of cases in children <15 years HIV/AIDSIncidenceIn one cohort, 5% of individuals with HZwere HIV-infected and 5% had cancer.Recurrent HZ < 1% of cases Occurs in 25% of HIV-infected individuals, an eight times higher incidence than the general population, ages 20–50 years;

• Renal and cardiac transplant recipients:7–9%• Recurrent HZ more common in immunocompromisedindividuals.• Immunization to VZV in childhood will alterthe epidemiology of HZ.

Risk Factors• Most common factor is diminishing immunityto VZV with advancing age, with mostcases occurring in those ≥55 years.• However, in most cases triggering factors arenot known.• Immunocompromise: MalignancyImmunosuppression, especially from lymphoproliferativedisorders and chemotherapy Radiotherapy.HIV/AIDS: eightfold increased incidence of HZ.

Pathogenesis• In varicella VZV passes from lesions in the skin and mucosa via sensory fibers centripetally to sensory ganglia.• In the ganglia the virus establishes lifelonglatent infection.• Reactivation occurs in those ganglia in which VZV has achieved the highest density and is triggered by immunosuppression, trauma, tumor, or irradiation (see risk factors).• Reactivated virus can no longer be contained.• Virus multiplies and spreads antidromically down the sensory nerve to the skin/mucosa where it produces the characteristic vesicles

Classification: HZ manifests in three distinct clinical stages: prodrome, active infection,chronic: postherpetic neuralgia (PNH). CLINICAL MANIFESTATIONSDuration of Symptoms• Prodromal stage: Neuritic pain or paresthesiaprecedes for 2–3 weeks (84% of cases).• Acute vesiculation: 3–5 days.• Crust formation: days to 2–3 weeks.• PHN: months to years. Chronic pain or PHN is that persisting after the lesions have healed or persisting 4 weeks after the onset of lesions, regardless of degree of healing.

Skin SymptomsProdromal Stage• Pain (stabbing, pricking, sharp, boring, penetrating,lancinating, shooting), tenderness,paresthesia (itching, tingling, burning, freeze burning)in the involved dermatome precedes the eruption. • Allodynia: heightened sensitivity to mildstimuli.Active Vesiculation Skin lesions may be pruriticbut in themselves are not painful.Zoster Sine Zoster Nerve involvement canoccur without cutaneous zoster.

Abdominal Zoster Presents with severeabdominal (or chest pain) that may precederash by hours to days.Chronic Stages PHN, described as “burning,”“ice-burning,” “shooting,” or “lancinating,” canpersist for weeks, months, or years after thecutaneous involvement has resolved. Constitutional Symptoms• Prodromal stage and active vesiculation: flulikesymptoms such as headache, malaise,fever.• Chronic stages: depression is very common inindividuals with PHN.

Mucocutaneous Lesions• Papules (24 h) → vesicles-bullae (48 h) → pustules (96 h) → crusts (7–10 days).• New lesions continue to appear for up to1 week.• Erythematous, edematous base with superimposed clear vesicles, sometimes hemorrhagic.• The vesicle-bulla is oval or round, may be umbilicated.• Vesicles erode forming crusted erosions Necrotic and gangrenous lesions sometimes occur.• Scarring is common after healing of HZ

Distribution• Unilateral, dermatomal .• Two or more contiguous dermatomes may beinvolved.• Noncontiguous dermatomal zoster is rare.• Hematogenous dissemination to other skinsites in 10% of healthy individualsSite of Predilection Thoracic (>50%), trigeminal(10–20%), lumbosacral and cervical (10–20%).Mucous Membranes Vesicles and erosionsoccur in mouth, vagina, and bladder, dependingon dermatome involved.

General ExaminationLymphadenopathy Regional nodes draining the area are often enlarged and tender.Sensory or Motor Nerve Changes Detectable by neurologic examination. Sensory defects(temperature, pain, touch) and (mild) motor paralysis, e.g., facial palsy. Eyes• In ophthalmic zoster, nasociliary involvement of V-1 (ophthalmic) branch of the trigeminal nerve occurs in about one-third of cases and is heralded by vesicles on the side and tip of the nose.• Complications include uveitis, keratitis, conjunctivitis,retinitis, optic neuritis, glaucoma,

proptosis, cicatricial lid retraction, and extraocular muscle palsies.• Acute retinal necrosis (rapidly progressive herpetic retinal necrosis) is more common in the immunocompromised hostDelayed Contralateral Hemiparesis• Occurs weeks to months (mean, 7 weeks) after an episode of HZ involving the first division of the trigeminal nerve (V-1).• Typical presentation is headache and hemiplegiaoccurring in a patient with recent history of HZ ophthalmicus.

thoracic zoster A 39-year-old female with HIV/AIDS hashad painful chest lesions for 3 weeks. Crusted and reepithelialized dermatomal erosions on the left back

Varicella zoster virus infection: disseminated cutaneous, in an immunocompromisedpatient

Varicella zoster virus infection: chronic herpes zoster in HIV disease

COURSE AND PROGNOSISIn immunocompetent host, rash usually resolves in 2 to 3 weeks. Complications can be:• Mucocutaneous Hemorrhage, gangrene Cutaneous dissemination Superinfection of skin lesions• SystemicNeurologic: meningoencephalitis, cerebral vascular syndromes, cranial nerve syndromes [trigeminal (ophthalmic) branch (HZ ophthalmicus), facial and auditory nerves (Ramsay Hunt syndrome)], peripheralmotor weakness, transverse myelitis

MANAGEMENTPreventionImmunization: Immunization with VZV vaccine may boost humoral and cell-mediated immunity and decrease the incidence of zoster in populations with declining VZV-specific immunity. Goals of management: Relieve constitutional symptoms; minimize pain; reduce viral shedding; prevent secondary bacterial infection; speed crusting of lesions and healing; ease physical, psychological, emotional discomfort; prevent viral dissemination or other complications; prevent or minimize PHN.

Antiviral therapy In individuals at high risk for reactivation of VZV infection, oral acyclovir can reduce the incidence of HZ. In prodromal stage: begin antiviral agent if diagnosis isconsidered likely; analgesics. With active vesiculation: antiviral therapy begun ≤72 h accelerates healing of skin lesions, decreases the duration of acute pain, and may decrease the frequency of PHN when given in adequate dosage.

Acyclovir 800 mg PO four times daily for 7–10 days. The 50% viral inhibitory concentration of acyclovir is three to six times higher for VZV than for HSV in vitro, and drugdose must be increased appropriately. The bioavailability of acyclovir is only 15–30% of the orally administered dose. For ophthalmic zoster and HZ in the immunocompromised host, acyclovir should be given intravenously. Acyclovir hastens healing and lessens acute pain if given within 48 h of the onset of the rash.∗Valacyclovir 1000 mg PO three times daily for 7 days, 70–80% bioavailable.

Famciclovir 500 mg PO three times daily for 7 days, 77% bioavailable. Reduce dose inindividuals with diminished renal function. Supportive therapy: for acute HZConstitutional symptoms Bed rest, nonsteroidal anti-inflammatory drugs.Sedation Pain often interferes with sleep. Sleep deprivation and pain commonly result indepression. Doxepin, 10–100 mg at bed time, is an effective agent.

Dressings Application of moist dressings (water, saline, Burow solution) to the involveddermatome is soothing and alleviates pain.Pain management Early control of pain with narcotic analgesics is indicated; failure to manage paincan result in failure to sleep, fatigue, and depression: Best to begin with more potent analgesics and then reduce potency as pain lessens.

Chronic stages (PHN)Pain management Pain is that of reflex sympathetic dystrophy. Severe prodromal pain or severe pain on the first day of rash is predictive of severe PHN.Gabapentin: 300 mg three times daily. Pregabalin.Tricyclic antidepressants such as doxepin, 10–100 mg PO at bed time.Capsaicin cream every 4 h.Topical anesthetic such as EMLA or 5% lidocaine patch for allodynia.Nerve block to area of allodynia.Analgesics.