An 80-year-old male was admitted to the internal medicine ward with a 4-day history of diarrhea. On admission 1 week ago, he was dehydrated and hypotensive, but this resolved with intravenous fluids. He remains admitted to the hospital for rehabilitation with physiotherapy to return him to his normal functional baseline.
The patient now has a 4-day history of a burning and tingling sensation across one side of his back. A blistering rash, localizing to his back where he was complaining of pain, began 2 days ago. He otherwise has been feeling systemically well with no fevers or chills. The rash is extremely painful, and he has not found anything that improves the pain. It has not been spreading anywhere else on his body.
He has no history of significant skin disease other than chicken pox as a young child.
He takes no medications regularly and has no known medication allergies, and there is no family history of skin disease.
Vital signs: HR 75, BP 134/78, RR 18, SpO2 97% on room air, temp. 36.9oC.
Examination reveals a healthy-appearing elderly male in no significant distress. Head and neck exam is unremarkable. Cardiovascular exam reveals normal S1 and S2 heart sounds with no murmurs or extra heart sounds. Respiratory exam demonstrates normal breath sounds bilaterally with no crackles or wheezes. Abdomen is soft and nontender. Skin exam reveals well-defined erythema with overlying intact vesicles filled with cloudy fluid. There is also serous, purulent, and hemorrhagic crusting present on some of the lesions. The eruption is confined to the skin overlying the left T10 dermatome and stops abruptly at the midline. There are similar coalescing vesicles extending over the left flank on to the abdomen, also along the T10 dermatome distribution. It does not cross midline. The skin is tender to palpation over this eruption. Mucosal membranes are not involved.
Figure 49.1 shows skin eruption.
Complete blood count: normal white blood cell count, hemoglobin, and platelets.
Chemistry panel: normal sodium, potassium, bicarbonate, blood urea nitrogen, creatinine, and glucose.
A vesicle was deroofed and swabs were sent:
HSV polymerase chain reaction (PCR): negative for HSV-1 and HSV-2.
Varicella zoster virus PCR: positive.
Based on the clinical examination, the patient was empirically started on oral valacyclovir prior to the results of the PCR being available. As the patient is not immunocompromised, airborne and contact precautions were not needed. The lesions were completely covered with nonadherent dressings until they became dry and crusted. The burning pain and associated skin eruption improved over the next week.
Key Management Steps
1. Recognition of herpes zoster as the cause of a painful vesiculobullous eruption occurring in a dermatomal distribution.
2. Rule out severe drug reaction, such as SJS/TEN in any bullous condition, especially in the context of painful skin.
3. Initiation of antiviral treatment in patients within 72 hours of the onset of the cutaneous eruption to prevent postherpetic neuralgia. Also consider starting antivirals in those with ongoing new vesicle formation even if it is greater than 72 hours since onset of eruption.
4. Institute airborne and contact precautions in an immunocompromised patient with herpes zoster until disseminated disease is ruled out.
This patient presented with an acute onset, painful vesiculobullous eruption in a dermatomal distribution. The diagnosis of herpes zoster (shingles) was made by the clinical presentation of a generally systemically well patient with painful erythema, vesicles, and crusting along a single dermatome in the setting of prior exposure to varicella zoster virus as a child.
Apart from herpes zoster, the differential diagnosis of a painful vesiculobullous eruption includes SJS/TEN. These conditions are classically caused by exposure to a medication rather than infection. Patients with SJS/TEN will typically be systemically unwell with widespread erythema, painful skin, and mucosal membrane involvement. HSV can present with similar clinical features to varicella zoster virus but would be unusual to be localized to a dermatomal distribution. Varicella zoster (chicken pox) is also not typically seen in a dermatomal distribution and presents as widespread pruritic vesicles on an erythematous base (“dew drops on a rose petal”). Dissemination of cutaneous herpes zoster may present in immunocompromised patients, such as those with hematologic malignancy or a solid organ transplant. These patients may present with a generalized painful vesicular eruption involving multiple dermatomes and crossing the midline. Patients with disseminated cutaneous zoster may also be at risk of developing visceral involvement of herpes zoster.
Airborne and contact precautions are required in the setting of disseminated herpes zoster infection until all lesions are dry and crusted. In localized herpes zoster, these precautions are only required in immunocompromised patients until disseminated zoster has been ruled out. The lesions should be completely covered, though, in localized herpes zoster.
Varicella zoster virus is the cause of both varicella zoster (chicken pox), as well as herpes zoster (shingles). Once a patient is exposed to varicella zoster virus, either through primary infection or varicella zoster vaccination, he or she is at risk of developing herpes zoster. Following exposure, the virus travels to the dorsal root ganglion where it becomes dormant. Reactivation of the virus can occur in the setting of stress, fever, radiation therapy, local trauma, or immunosuppression. The incidence of herpes zoster is believed to be 2.5 in 1,000 patients aged 20 to 50 years old, 5 in 1,000 in those 51 to 79 years old, and 10 in 1,000 patients over 80 years of age.
Herpes zoster occurring on the face can potentially lead to significant complications. Approximately 50% of patients with involvement of the ophthalmic branch of the trigeminal nerve (V1) with will have ocular involvement, which could result in scarring and visual loss. Lesions of herpes zoster on the nasal tip, also known as Hutchinson’s sign, can indicate involvement of the V1 branch and warrants urgent ophthalmology consultation.
Treatment of uncomplicated herpes zoster with systemic antiviral medications is initiated with the goal of decreasing the duration and severity of the eruption. Antivirals can also reduce the risk of postherpetic neuralgia, which is the most common complication. Initiating treatment within 72 hours of the development of skin lesions is believed to be most effective in reducing postherpetic neuralgia; however, treating within 7 days has also shown beneficial effects. Postherpetic neuralgia is characterized by pain such as burning, stinging, or a stabbing sensation after the skin lesions have healed and can persist chronically.
Mendoza N, Madkan V, Sra K, Willison B, Morrison LK, Tyring S. Human herpesviruses. In: Bolognia J, ed. Dermatology. 3rd ed. Philadelphia, PA. Elsevier; 2012: 1321–1343.Find this resource:
Preventing varicella-zoster virus (VSV): transmission from zoster in healthcare settings. Centers for Disease Control and Prevention. May 1, 2014. https://www.cdc.gov/shingles/hcp/hc-settings.html
Tremaine AM, Bartlett B, Gewirtzman A, Tyring S. Herpes zoster. In: Lebwohl M, ed. Treatment of Skin Disease Comprehensive Therapeutic Strategies. 3rd ed. Philadelphia, PA. Saunders; 2010: 306–308.Find this resource: