A Pruritic Vesicular Eruption
History
A 37-year-old man presented with a rash of 1-week duration. The rash was pruritic, and erythematous, with involvement of upper extremities, chest, and abdomen. One week prior to the eruption, the patient noted pain in his right chest and abdomen, for which he took ibuprofen.
The patient denied travel as well as new medications, soaps, detergents, sick contacts, pets, or foods. He smokes cigarettes and drinks alcohol occasionally; he denied any form of illicit drug use. He was sexually active. His medical history includes seasonal allergies for which he denied taking any medications. His family history is unremarkable. He works in retail.
Physical Examination
He was in no acute distress, appeared afebrile, and presented stable vital signs. His head had no signs of trauma. His pupils were equal, round, and reactive to light; they were nonicteric with noninjected sclera.
An intraoral exam revealed no erythema, lesions, or ulceration. His nose was without rhinorrhea. External inspection and palpation of neck showed no masses (lymphadenopathy) nor tenderness. Cardiac, pulmonary, genitourinary, and abdominal examinations were all within normal limits.
A large erythematous plaque—involving his chest and upper back—appeared in a dermatomal band with several small eroded and intact vesicles (Figure 1). He also had erythematous papules and vesicles extending from his distal forearm to the mid-brachial area (Figure 2) and abdomen. Some of these lesions were eroded, suggestive of excoriations.
The rest of the physical exam was unremarkable.
(Answer and discussion on next page)
Answer: Disseminated herpes zoster
The diagnosis of herpes zoster can be made clinically if the following elements are present:
1. Painful or abnormal sensory prodrome.
2. Dermatomal distribution of the rash.
3. Grouped vesicles.
4. Pain and allodynia in the area of the rash.
A Tzanck smear and/or direct fluorescent antibody staining can be obtained to confirm the diagnosis. In this patient, the diagnosis was confirmed by Tzanck smear. Additional laboratory tests include viral culture, serology, and polymerase chain reaction (PCR), but these may take several days (viral culture or serologies) and may be expensive (PCR). The diagnosis of disseminated herpes zoster requires a high degree of clinical suspicion, particularly in immunocompetent patients and the use of these additional tests may be needed.
Cause and Risk Factors
Varicella-zoster virus (VZV or human herpes virus-3) is the causative virus of varicella (chickenpox) and herpes zoster (shingles). The virus remains dormant in sensory dorsal root ganglia following primary infection. Herpes zoster represents reactivation of the dormant virus. During this process, the virus replicates in the affected dorsal root ganglion and produces a painful ganglionitis.1
Patients often experience a prodrome of mild fever, malaise, and myalgia that is followed by an eruption of pruritic, erythematous macules and papules, which quickly evolve to form clear vesicles. Subsequent neuronal inflammation and necrosis can result in severe neuralgia. The annual incidence of herpes zoster in the United States and Europe is 2.5 in 1000 persons (age 20-50), 5 in 1000 persons (age 51-79), and 10 in 1000 persons (patients older than 80).2,3
One percent of immunocompetent patients and 10% of immunocompromised patients2 will develop a generalized eruption or disseminated herpes zoster, defined as more than 20 vesicles outside the primary affected dermatome(s) or visceral involvement. In addition, up to 3% of patients with the disease will require hospitalization.1 Thus, early recognition and treatment is important to reduce serious sequelae from this illness.
The major risk factor for herpes zoster is increasing age. Other risks factors include mental and physical stress, immunocompromised status (eg, HIV), hematopoietic stem cell transplantation, and a family history of herpes zoster.2 Reactivation of the virus can occur spontaneously or provoked by stress, fever, cancer, immunosuppression, and radiation therapy.
Presentation
Clinically, herpes zoster may present with a prodrome of pruritus, hyperesthesia, pain, and tenderness to light touch 3 to 5 days prior to appearance of skin eruption. Most patients then proceed to develop a painful eruption of grouped vesicles in a dermatomal distribution. The condition usually resolves without sequelae in children and young healthy adults. However, older or immunocompromised patients may experience complications including postherpetic neuralgia, herpes zoster ophthalmicus, zoster oticus, visceral complications (pneumonia, hepatitis, myocarditis, or vasculitis), secondary bacterial infection, and meningoencephalitis.1,2
Furthermore, in immunocompromised patients, herpes zoster may present with unusual clinical findings, such as persistent verrucous lesions in HIV-infected patients or postherpetic hyperhidrosis.2 Of note, transmission of virus via contact with fluid from vesicles is estimated to be 15%.4
Treatment
Therapy for herpes zoster should be initiated within 72 hours of the development of skin lesions for optimal results. However, initiation up to 7 days after onset also appears to be beneficial. Treatment modalities that are FDA-approved include acyclovir, famciclovir, and valacyclovir—all of which result in decrease severity and duration of both skin lesions and pain.1
Differential Diagnosis
The differential diagnoses for this type of vesicular eruption include primary varicella infection, vesicular viral exanthems secondary to Coxsackievirus, pityriasis lichenoides et varioliformis acuta (PLEVA), ricketsialpox, drug eruptions, bullous insect bite reactions, bacterial skin infections (eg, cellulitis and bullous impetigo), and allergic contact dermatitis.3
Enteroviruses, such as Coxackievirus A and B viruses, can cause viral exanthems with a vesicular or zosteriform pattern. Patients tend to be young children and present with fever, malaise, and gray-white vesicular lesions on palms and soles. Occasionally, a more diffuse vesicular eruption with lesions in other areas may be present.
On the other hand, ricketsialpox, transmitted by the house-mouse mite, presents with the classic triad of eschar at site of the bite, fever, and rash. The skin eruption is composed of numerous, monomorphous, red papules with a small central vesicle. Unlike primary varicella infection, these lesions are less pruritic and more monomorphous in nature.
Pityriasis lichenoides is a spectrum of cutaneous eruptions that has acute and chronic forms. The acute form, PLEVA, is characterized by a polymorphous eruption that begins as asymptomatic to pruritic symmetrical with 2 mm to 3 mm red-brown papules and macules. The papules appear in successive crops and rapidly evolve into vesicular, necrotic, and sometimes purpuric lesions. These can involve the entire body and gradually resolve with or without a scar.
Finally, allergic contact dermatitis involves a type IV or delayed hypersensitivity reaction to external agents. It requires prior sensitization of the individual to the chemical in question. The acute eruption is typically vesicular and edematous while chronic lesions tend to be scaly or lichenified plaques.
Outcome of the Case
The patient was started on valacyclovir 1 g 3 times a day and given oxycodone-acetaminophen 5/325 mg for pain. He was seen 1-week later in the dermatology clinic, at which time the rash was resolving but the pain persisted. He was subsequently started on prednisone 40 mg for 5 days and continued on oxycodone-acetaminophen until the pain resolved approximately 1-month later.
A chest x-ray was ordered to monitor for possible lung malignancy and that HIV antibodies were also measured to assess for possible immunocompromised status. n
Bryan Baskin, DO, is the chief resident of Case Western Reserve University’s Emergency Medicine Residency Program at MetroHealth Medical Center and The Cleveland Clinic in Cleveland, OH.
Marjorie E. Montañez-Wiscovich, MD, PhD, is a resident in the department of dermatology at MetroHealth Medical Center and Case Western Reserve University in Cleveland, OH.
Stephen Somach, MD, is an associate professor in the department of dermatology at MetroHealth Medical Center and Case Western Reserve University in Cleveland, OH.
David Effron, MD, is an assistant professor of emergency medicine at Case Western Reserve University, attending physician in the department of emergency medicine at the MetroHealth Medical Center, and consultant emergency physician at the Cleveland Clinic Foundation in Cleveland, OH.
References:
1. Cohen JI. Clinical practice: herpes zoster. N Engl J Med. 2013;369:255-263.
2.Sengupta S. Cutaneous herpes zoster. Curr Infect Dis Rep. 2013;15:432-439.
3. Bader MS. Herpes zoster: diagnostic, therapeutic, and preventive approaches. Postgrad Med. 2013;125:78-91.
4. Bolognia JL, Jorizzo JL (ed), Schaffer JV (ed). Dermatology. 3rd ed. Philadelphia, PA: WB Saunders; 2012.