HERPES ZOSTER

Definition:

Herpes zoster, or shingles, is a localized disease characterized by unilateral radicular

pain and a vesicular rash limited to the area of skin innervated by a single dorsal root or cranial
sensory ganglion. Whereas varicella, or chickenpox, results from primary exogenous varicella-
zoster virus (VZV) infection, herpes zoster is caused by reactivation of endogenous VZV that
has persisted in latent form within sensory ganglia following an earlier episode of chickenpox. In
contrast to recurrent herpes simplex, herpes zoster is commonly associated with severe pain:
prodromal pain often precedes the rash by several days; pain usually accompanies the
dermatomal rash of herpes zoster; and clinically significant pain and allodynia may persist for
weeks, months, or even years after the herpes zoster rash has healed, a debilitating
complication known as postherpetic neuralgia (PHN). The incidence and severity of herpes
zoster and PHN increase with age in association with an age-related decline in cell-mediated
immunity to VZV. The Shingles Prevention Study-a randomized double-blinded placebo-
controlled trial-sought to evaluate the capacity of a live attenuated VZV vaccine to protect older
adults from herpes zoster and PHN by boosting their waning cell-mediated immunity to VZV.
The study demonstrated that the zoster vaccine produced significant reductions in the incidence
of herpes zoster, in the burden of illness caused by herpes zoster, and in the incidence of PHN.

Predisposing Factors:

Infants who are unvaccinated

Eldelry people
Immunosuppressed people

Precipitating Factors

People who are having contacts with an object or a person having a herpes
zoster

People who are near in the room of a patient having herpes zoster

II. Pathologic Process

VZV infection gives rise to two distinct syndromes. The primary infection, chickenpox, is
a contagious and usually benign febrile illness. After this infection resolves, viral particles
remain in the dorsal root or other sensory ganglia, where they may lay dormant for years to
decades. In this latent period, host immunologic mechanisms suppress replication of the virus,
but VZV reactivates when the host mechanisms fail to contain the virus. Such failure may result
from a wide spectrum of conditions, ranging from stress to severe immunosuppression;
occasionally, it follows direct trauma. VZV viremia occurs frequently with chickenpox but also
may arise with herpes zoster, albeit with a lower viral load. Once VZV is activated at the spinal
root or cranial nerve neurons, an inflammatory response occurs that also encompasses the
leptomeninges; both plasma cells and lymphocytes are noted. This inflammation in the dorsal
root ganglion can be accompanied by hemorrhagic necrosis of nerve cells. The result is
neuronal loss and fibrosis. The frequency of dermatologic involvement is correlated with the
centripetal distribution of the initial varicella lesions. This pattern suggests that the latency may
arise from contiguous spread of the virus during varicella from infected skin cells to sensory
nerve endings, with subsequent ascent to the ganglia. Alternatively, the ganglia may become
infected hematogenously during the viremic phase of varicella, and the frequency of the
dermatome involvement in herpes zoster may reflect the ganglia most often exposed to
reactivating stimuli. The appearance of the cutaneous rash due to herpes zoster coincides with
a profound VZV-specific T-cell proliferation. Production of interferon alfa appears with the
resolution of herpes zoster. In immunocompetent patients, specific antibodies (immunoglobulins
G, M, and A [IgG, IgM, and IgA]) appear more rapidly and reach higher titers during reactivation
(herpes zoster) than during the primary infection. The patient has a long-lasting, enhanced, cell-
mediated immunity response to VZV. The anatomic location of the involved dermatome often
determines the specific manifestations. When cervical and lumbar roots are involved, motor
involvement, which is often overlooked, may be evident, depending on the virulence or extent of
migration. In at least 1 case of motor neuron involvement, lymphocytic infiltration and myelin
breakdown were observed with preservation of axons. This infection is contagious to persons
with no previous immunity to VZV. However, it is estimated to be only one third as contagious
as primary varicella. It is transmitted either via direct contact with the lesions or via the
respiratory route.

Clinical Manifestations:
The clinical manifestations can be divided into the following three phases: Preeruptive phase
(preherpetic neuralgia), Acute eruptive phase, Chronic phase (PHN). The preeruptive phase is
characterized by the following:
 Sensory phenomena along 1 or more skin dermatomes, lasting 1-10 days (average, 48
hours)
 Phenomena usually are noted as pain or, less commonly, itching or paresthesias [3]
 Pain may simulate headache, iritis, pleurisy, brachial neuritis, cardiac pain, appendicitis or
other intra-abdominal disease, or sciatica
 Other symptoms, such as malaise, myalgia, headache, photophobia, and, uncommonly,
fever

The acute eruptive phase is marked by the following:

Patchy erythema, occasionally accompanied by induration, in the dermatomal area of

involvement

Regional lymphadenopathy, either at this stage or subsequently

Grouped herpetiform vesicles developing on the erythematous base (the classic finding)

Cutaneous findings that typically appear unilaterally, stopping abruptly at the midline of the
limit of sensory coverage of the involved dermatome
 Vesicular involution: Vesicles initially are clear but eventually cloud, rupture, crust, and
involute

After vesicular involution, slow resolution of the remaining erythematous plaques, typically
without visible sequelae

Scarring can occur if deeper epidermal and dermal layers have been compromised by
excoriation, secondary infection, or other complications

Almost all adults experience pain, typically severe

A few experience severe pain without a vesicular eruption (ie, zoster sine herpete)

Symptoms tend to resolve over 10-15 days

Complete healing of lesions may require up to a month

PHN is characterized by the following:

 Persistent or recurring pain lasting 30 or more days after the acute infection or after all
lesions have crusted (9-45% of all cases) [4]

 Pain usually is confined to the area of original dermatomal involvement

 The pain can be severe and incapacitating

 Pain can persist for weeks, months, or years

 Slow resolution of pain is especially common in the elderly [5]

  PHN is observed more frequently after cases of herpes zoster ophthalmicus (HZO) and
in instances of upper-body dermatomal involvement

 Less common postherpetic sequelae include hyperesthesia or, more rarely,

hypoesthesia or anesthesia in the area of involvement

V. Diagnostic Tests

Diagnosis is based primarily on the history and physical findings. In most cases, confirming
the diagnosis via laboratory testing has no utility. In select patient populations, however—
particularly immunocompromised patients—the presentation can be atypical and may require
additional testing.

Laboratory studies for VZV include the following:

Direct fluorescent antibody (DFA) testing of vesicular fluid or a corneal lesion

Polymerase chain reaction (PCR) testing of vesicular fluid, a corneal lesion, or blood

Tzanck smear of vesicular fluid (lower sensitivity and specificity than DFA or PCR)

VI. Medical Management

Episodes of herpes zoster are generally self-limited and resolve without intervention; they tend
to be more benign and mild in children than in adults.

Conservative therapy includes the following:

Nonsteroidal anti-inflammatory drugs (NSAIDs)

Wet dressings with 5% aluminum acetate (Burrow solution), applied for 30-60 minutes 4-6 times
daily

Lotions (eg, calamine)

Primary medications for acute zoster–associated pain include the following:

Narcotic and nonnarcotic analgesics (both systemic and topical)

Neuroactive agents (eg, tricyclic antidepressants [TCAs])

Anticonvulsant agents

VII. Nursing Diagnosis

Acute/Chronic Pain related to Nerve pain as evidenced by Reports of burning, dull, or sharp
pain

Deficient Knowledge related to Complexity of treatment as evidenced by Inadequate follow-up

of instructions

Risk for Infection related to Skin lesions

Risk for Disturbed Body Image related to Preoccupation with changed body part

VIII. Nursing management

Assess the client’s description of pain or discomfort: severity, location, quality, duration,
precipitating or relieving factors.

Avoid rubbing or scratching the skin or lesion.

Apply cool, moist dressings to pruritic lesions with or without Burrow’s solution several times a
day. Discontinue once the lesions have dried.

Provide necessary information to the client and caregiver, including written information

Determine the client’s and caregiver’s understanding of the disease condition, treatment, and
complications.

Encourage herpes zoster vaccination (Zostavax).

Instruct the client to avoid contact with pregnant women and immunocompromised individuals.

Assist the client in articulating responses to questions from others regarding lesions and
infectious risk.