A 60-year-old patient with a compromised immune system presents for evaluation of a diffuse, primarily unilateral, vesicular, and bullous rash that started 3 days prior to presentation. The rash is pruritic in nature without drainage and the vesicles are not easily friable; little fluctuance is present in some vesicles and bullae.
The lesions have an erythematous base and some of the larger bullae appear hyperkeratotic in nature with a dark brown discoloration. The lesions extend from the area of the lumbar spine, over the left buttocks, and down the lateral, anterior, and medial upper leg to the level of the patella. Additionally, the lesions cross just beyond the midline in the lumbar region. There is no erythema or swelling of the surrounding skin. Scabbing and crusting are present on some lesions.
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Herpes zoster, commonly known as shingles, is caused by reactivation of the varicella zoster virus, which is stored in the sensory ganglia of the peripheral nervous system. Generally, the virus eludes detection by the immune system, allowing it to spread along nerve pathways.1 An estimate 1 million people in the United States develop shingles each year.2
The classic presentation of herpes zoster includes 1 to 2 dermatomes, and presentation of disseminated zoster encompasses 3 or more dermatomes. Traditionally, herpes zoster does not cross the midline, except when disseminated zoster is present. Vesicular clusters of herpes zoster lesions develop along the dermatome, following a distinct linear pattern and allowing for clinical diagnosis.1
Worldwide, the rate of herpes zoster cases continues to increase, and patients who are immunocompromised are particularly at risk.1 The likelihood of developing herpes zoster among patients who are immunocompetent is estimated at 4.8 per 1000 person-years in the United States. The incidence is highest among recipients of bone marrow or stem cell transplant (43 per 1000 person-years) and patients who have undergone solid organ transplant (17 per 1000 person-years).3
Immunocompromised patients are at increased risk for developing disseminated zoster as their weakened immune system allows for loss of varicella zoster virus T-cell immunity; this decreased immunity is more notable in older adults and immunocompromised individuals, which is why herpes zoster is typically seen in individuals older than 50 years of age.2,4
What Is Disseminated Herpes Zoster?
The clinical presentation of disseminated zoster is similar to that of classic herpes zoster but, because of the increased number of dermatomes involved, it is harder to distinguish a clear dermatomal path. Clinicians may also note that dissemination can lead to the vesicles crossing the dermatomal midline; this presentation is not seen in a typical localized herpes zoster case.1
Ultimately, disseminated zoster can infiltrate the central nervous system leading to ophthalmologic, neurologic, and internal organ complications. Additional complications may include bacterial superinfections (eg, Staphylococcus aureus) and postherpetic neuralgia (PHN).2 PHN is more likely to occur in patients who are immunocompromised and adults aged 60 years and older.2
The risk for PHN is correlated with the severity of pain reported during an acute herpes zoster outbreak and the number of lesions that develop.2 Although herpes zoster complications leading to mortality are rare, deaths do occur, primarily in patients who are immunosuppressed or 65 years of age or older.2 The US Centers for Disease Control and Prevention (CDC) reported that 30% of herpes zoster-related hospitalizations are attributed to patients who are immunocompromised or immunosuppressed.2
Treatment of Herpes Zoster
Preventive treatment with the recombinant zoster vaccine is recommended for adults aged 50 years and older. In patients who develop herpes zoster and require treatment, the treatment of choice is oral antiviral therapy, which should be initiated within 72 hours of symptom onset.5 Oral acyclovir, famciclovir, or valacyclovir or are all appropriate choices in the treatment of herpes zoster.5 Valacyclovir and famciclovir are both dosed 3 times a day, and acyclovir is dosed 5 times a day. For pregnant women, antiviral therapy should only be used in cases in which the potential benefits outweigh the risk to the fetus, in such cases acyclovir or valacyclovir are the treatments of choice.6,7
In immunocompromised individuals, Albrecht et al recommend intravenous acyclovir and inpatient hospitalization with close clinical monitoring.6 Renal insufficiency should be closely monitored with acyclovir administration. Although treatment should be initiated as soon as possible to promote the best outcomes, antiviral treatment should be initiated in all patients who are immunocompromised even if they present after 72 hours of symptom onset.6
Acute neuritis pain that is severe and disruptive to daily activities may require pain management in addition to antiviral treatment. Treatment can include topical analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and opioid analgesics.7
This patient received a clinical diagnosis of disseminated zoster based on an immunocompromised status, lesions across multiple dermatomes, and lesions crossing the midline. Because of the dissemination of herpes zoster, the patient was sent to a local hospital for further evaluation and management. The patient was not treated with intravenous acyclovir and was discharged home on oral valacyclovir therapy.
Amalia Gedney-Lose, DNP, ARNP, FNP-C, is a family nurse practitioner in Iowa City, Iowa and a clinical assistant professor at the University of Iowa.
1. Albrecht MA, Levin MJ. Epidemiology, clinical manifestations, and diagnosis of herpes zoster. UpToDate. 2019. https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster
2. Centers for Disease Control and Prevention. Shingles (herpes zoster). Clinical Overview for Health Care Professionals. CDC website. Updated October 5, 2020. Accessed February 4, 2021. https://www.cdc.gov/shingles/hcp/clinical-overview.html
3. Chen SY, Suaya JA, Li Q, et al. Incidence of herpes zoster in patients with altered immune function. Infection. 2014;42(2):325-334. doi:10.1007/s15010-013-0550-8
4. Weinberg A, Levin MJ. VZV T cell-mediated immunity. Curr Top Microbiol Immunol. 2010;342:341-357. doi:10.1007/82_2010_31
5. Fashner J, Bell AL. Herpes zoster and postherpetic neuralgia: prevention and management. Am Fam Physician. 2011;83(12):1432-1437.
6. Albrecht MA, Hirsch MS, Mitty J. Treatment of herpes zoster in the immunocompetent host. UpToDate. Updated March 11, 2020.
7. Dworkin RH, Johnson RW, Breuer J, et al. Recommendations for the management of herpes zoster. Clin Infect Dis. 2007;44 Suppl 1:S1-S26. doi:10.1086/510206