Clinical Challenge: Painful Eruptions on Face

Herpes zoster, commonly known as "shingles," is cause by reactivation of varicella zoster virus (VZV) — the virus that causes chickenpox. After the initial chickenpox infection, the virus remains latent in the dorsal root ganglion cells of sensory nerves. In zoster,...

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Herpes zoster, commonly known as “shingles,” is cause by reactivation of varicella zoster virus (VZV) — the virus that causes chickenpox. After the initial chickenpox infection, the virus remains latent in the dorsal root ganglion cells of sensory nerves. 

In zoster, the VZV virus becomes reactivated in selective dorsal root ganglia, travels down the length of nerve axon, and infects the skin in the region of the corresponding dermatome. Older age, immunosuppressive drugs, lymphoma, AIDS and radiation therapy are risk factors for reactivating the virus.^1-2

The risk for developing zoster is as high as 30% for whites aged older than 80 years. Blacks are four times less likely to develop zoster. The reason behind this variation is unknown. ^1-2

As many as 25% of patients with AIDS develop recurrent zoster; however, this risk is quite low in immunocompetent patients. ^1-2

Classically, herpes zoster occurs unilaterally within a dermatome. The adjacent dermatomes directly above and below the primary dermatome may also be affected. The most commonly involved dermatomes are the thoracic (60%) and cranial (20%, with the trigeminal nerve being the most common), followed by the lumbar and sacral.

The cutaneous eruption is frequently preceded by several days of pain in the affected dermatome. The eruption begins with red and sometimes edematous plaques involving some or all of the dermatome with vesicles of various sizes that may become purulent.  Crops of vesicles occur for one week and subsequently crust over. ^1-2 

As with our patient, lesions may develop in the mouth when the maxillary and/or mandibular branches of the trigeminal nerve are involved. Elderly and debilitated patients may have more severe presentations complicated by hemorrhagic blisters, eschar-like crust and significant scarring. ^1-2   

Cutaneous disseminated herpes zoster is defined as greater than 20 lesions outside of the primary and immediately adjacent dermatomes. It occurs primarily in elderly or debilitated patients, such as patients with AIDS or those with Hodgkins lymphoma. ^1-2      

Ophthalmic zoster occurs when the ophthalmic division of the trigeminal nerve is involved. Vesicles on the side and tip of the nose, known as Hutchinson’s sign, specifically indicate involvement of the nasociliary branch of the ophthalmic division. 

When Hutchinson’s sign is present, the risk for eye involvement is approximately 75%.  Involvement of the eyelid margin portends an almost 100% risk for eye involvement.  Prompt antiviral therapy reduces the risk for ocular complications from 50% to 25%.  An urgent referral to an ophthalmologist should be made in all suspected cases of ophthalmic zoster.^1-2  

Pain is one of the most troubling and common complications of herpes zoster. Pain may occur before, during and/or after the cutaneous eruption. Pain that persists after the resolution of skin lesions is termed post-herpetic neuralgia (PHN). In patients older than 70 years, 75% continue to have pain beyond one month. In some cases, this persistent pain can be quite disabling. ^1-2

Other herpes zoster complications include Ramsey-Hunt syndrome (involvement of facial and auditory nerves), motor nerve neuropathy, maxillary and mandibular alveolar bone necrosis, neurogenic bladder (involvement of sacral dermatomes), and vasculopathy of the central nervous system that can cause stroke.^1-2                 

Diagnosis

Herpes zoster is one of the most important diagnoses for health care workers to recognize, since prompt antiviral therapy can limit many of the sequelae of infection. 

Zoster diagnosis should be considered any time a patient presents with pain or a rash in a dermatomal distribution. The diagnosis is most frequently made on clinical grounds. 

When further workup is required, a Tzanck smear may be performed in which the base of a vesicle is scraped with a blade, spread on a glass slide and stained to evaluate for multi-nucleated giant cells. Viral culture has poor sensitivity. Direct fluorescent antibody (DFA) testing and PCR are more sensitive.^1-2

Metastatic squamous cell carcinoma would not present with an abrupt eruption of painful and crusted vesicles in a dermatomal distribution. 

Acute radiation dermatitis may occur one to four weeks following radiotherapy with pain and vesicles; however, the eruption would be limited to the radiation port, and it would not present in a dramatically dermatomal pattern as seen here.⁴

Chronic radiation dermatitis presents months to decades after radiotherapy with affected skin appearing dry, atrophic and fibrotic with overlying telangiectasias. ⁴

Treatment

Antiviral therapy consists mainly of valacyclovir, famciclovir or acyclovir, and should be instituted immediately upon suspecting the diagnosis. One of the major benefits of therapy is reducing the duration and severity of herpes associated pain and speeding the resolution of the skin lesions.

In complicated cases or in those with immunosupression, intravenous acyclovir is administered. Acyclovir is also the drug of choice for patients with significant renal failure. However, in uncomplicated cases, valacyclovir 1000 mg, three times daily by mouth for 7 days, is the treatment of choice and is likely more effective than oral acyclovir which must be given five times daily.^1-2

Pain management mainly consists of nonsteroidal anti-inflammatory medications (NSAIDs) and opioids. In cases of complicated post-herpetic neuralgia, serotonin reuptake inhibitors, tricyclic antidepressants and anticonvulsants are sometimes attempted.   

Topical lidocaine or capsaicin is occasionally beneficial.^1-2 Recent studies have shown that starting an oral gabapentin titration along with antiviral therapy at the time of diagnosis reduces the incidence of post-herpetic neuralgia.³

Adam Rees, MD, is a graduate of the University of California Los Angeles School of Medicine and a resident in the Department of Dermatology at Baylor College of Medicine in Houston.

References

1. Habif TP. “Chapter 12 – Warts, Herpes Simplex, and Other Viral Infections.” Habif: Clinical Dermatology a Color Guide to Diagnosis and Therapy. St. Louis: Mosby, 1996. Print.

2. James WD, Berger TG, Elston DM et al. “Chapter 11: Pityriasis Rosea, Pityriasis Rubra Pilaris, and Other Papulosquamous and Hyperkeratotic Diseases.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunders Elsevier, 2006.

3.  Lapolla W, Digiorgio C, Haitz K et al. “Incidence of postherpetic neuralgia after combination treatment with gabapentin and valacyclovir in patients with acute herpes zoster: open-label study.” Arch Dermotol. 2011;147(8):901-7.

4. James WD, Berger TG, Elston DM et al. “Chapter 3: Dermatoses Resulting from Physical Factors.” Andrews’ Diseases of the Skin: Clinical Dermatology. Philadelphia: Saunders Elsevier, 2006.