When Varicella-Zoster Virus Masquerades as a Pressure Injury

Herpes simplex is a childhood disorder that is caused by the varicella-zoster virus (VZV).¹ The virus enters through the respiratory system and infects the tonsillar tissues, causing a T cell reaction.¹ The contaminated T cells spread throughout the body landing primarily in endothelial tissue, where replication occurs and inflammation ensues.¹

The result is the characteristic spotty rash otherwise known as chickenpox. Patients with herpes simplex typically present with prodrome symptoms of fever and malaise followed by a maculopapular rash that spreads to the scalp, face, trunk, and extremities.¹ It is not uncommon to develop between 250–500 itchy blisters as part of an active infection.¹ Initially an erythematous papule forms that rapidly develops into a vesicle. The vesicle ruptures to develop a wound that crusts over and resolves. Most infected individuals suffer from recurrent eruptions lasting anywhere from 7–10 days.¹

Although chickenpox is considered a mild self-limiting disease typically affecting children, the VZV persists within an infected individual for a lifetime. The latent virus lays dormant in the neurons of the peripheral ganglion.² The varicella-zoster virus can be reactivated years later during periods of stress or immunosuppression.² Outbreaks are more common in patients aged 60 and older.² The risk increases with age.

Typically, patients experience an eruption of erythematous and painful vesicles within the dermis. Generally known as shingles, outbreaks affect the skin supplied by nerves from a single spinal root known as a dermatome. Initial symptoms include pain and tingling 48–72 hours prior to the onset of the skin lesions.² Degenerative changes in the skin can last for 2–4 weeks.² Immunosuppressed individuals tend to present with more severe cases of shingles outbreaks. These lesions can become secondarily infected and may lead to prolonged neuralgic pain.

The remainder of this article will focus on a patient initially presenting with what was diagnosed as a pressure injury but was later determined to be an atypical wound caused by a severe case of VZV infection.

Case Report

A 74-year-old male was initially evaluated in his home for assessment of a chronic non-healing wound on the sacrum. Past medical history included hemiplegia following a spinal cord injury, gastroesophageal reflux disease (GERD), arthritis, benign prostatic hyperplasia (BPH), chronic obstructive pulmonary disease (COPD), hypertension, peripheral vascular disease (PVD) and obesity. The wound has been present for over 4 months. The patient was non-ambulatory and bedbound. Upon initial assessment, the wound measured 2cm x 3cm x 0.5cm (Figure 1). The wound base extends through subcutaneous tissue and is red and granular. The periwound tissue displays mild maceration and there is epibole of the tissue appreciated at the wound edge. No clinical signs and symptoms of infection were noted.

The diagnosis of a Stage 4 pressure injury was made. Treatment consisted of sharp debridement, followed by application of collagen to the wound base covered with boarded gauze. Offloading of the area was achieved with an alternating pressure mattress, ROHO cushion and turning education provided to the caregiver.

The patient was continuously followed for wound assessment and evaluation, but the wound continued to deteriorate despite offloading and advanced wound care. Two months into treatment the wound was larger, and the patient developed a satellite lesion on a non-pressure area of the buttocks (Figure 2).

Cultures were obtained to evaluate for increases in bacterial load as the cause of wound deterioration and new wound formation. Results showed heavy growth of Pseudomonas. Radiographs were ordered to evaluate for osteomyelitis. No underlying bone pathology was noted. Labs were also obtained. The patient had a slightly elevated WBC count at 12.2, his blood urea nitrogen (BUN)/creatinine ratio was high, and his total protein and albumin were low. The patient was placed on ciprofloxacin 500mg BID to treat the Pseudomonas and the wound was dressed with silver alginate and a bulky secondary dressing. The patient was placed on Juven (Abbott Nutrition) as a dietary supplement and the family was educated on the importance of proper nutrition in wound healing and the need for increase protein intake to support wound healing. Offloading was continued as ordered.

The wounds continued to deteriorate despite the addition of the dietary supplement and course of antibiotics (Figure 3). The wound had spread to the patient’s anal region, and he was experiencing extreme pain during bowel movements (Figure 3). Due to the rapid enlargement of the wound and the severity of patient discomfort the health care provider advised the patient and his family that he should seek care at the hospital to be worked up for sepsis and a tissue biopsy should be obtained to determine the wound etiology. He was admitted to the hospital later that day.

While hospitalized, the patient was taken to surgery for a debridement and biopsy of the wound. The histology report noted that the tissue specimen contained herpes viral inclusions. Immunohistochemical stains for VZV were positive. Acid-fast bacilli (AFB), Grocott methanamine silver (GMS) and Gram stains were negative for infectious organisms. The patient was treated with acyclovir IV and topic Lidex cream. The patient was eventually transferred to a skilled nursing facility, where he later died.  

Discussion

According to the Centers for Disease Control and Prevention, there are an estimated 1 million cases of shingles in the United States annually.³ Approximately 1 in every 3 adults will develop shingles at least once in their lifetime.³ The good news is with the advent of VZV vaccines the incidence is expected to decrease significantly.

The herpes zoster virus usually affects the thoracic and lumbar vertebra (T3–L3), while sacral herpes zoster is rare and has only been reported in 4–8% of cases.⁴ An atypical wound presentation such as this is a rare occurrence. The incidence of VZV increases in patients over the age of 60.⁵ A decrease in cellular immunity is a well-defined risk factor in the development of active cases of shingles and chronic non-healing wounds.⁵ It stands to reason that patient with multiple underlying chronic disease states would be at greater risk of developing more severe cases of shingles.

The immune system is important in the prevention of recurrent VZV attacks. In individuals with suppressed immune systems, such as illustrated in this case report, VZV virus infection may lead to viremia in addition to a more widespread and severe rash on the skin. Consequently, it should be kept mind that VZV, which develops in geriatric patients and individuals with weaker immune systems, may also appear with sacral region involvement, which is rarer, in addition to its typical regions of involvement.

Conclusion

Pathophysiology of atypical wounds caused by VZV, as described here, have unpredictable progression and are often refractory to standard of wound care therapies. No “gold standard” treatment exists due to the low incidence of occurrence. By utilizing a multidisciplinary approach that includes medical management, aggressive surgical intervention, and advanced wound care, health care providers will support better patient outcome with minimal patient morbidity.

Windy Cole, DPM, CWSP, is an Adjunct Professor and the Director of Wound Care at Kent State University College of Podiatric Medicine in Independence, Ohio. She is also the National Director of Clinical Safety, Quality and Education for Woundtech.

Acknowledgements
Case information was provided by Ann Whaley, FNP.

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References
1.    Chickenpox and herpes zoster (varicella-zoster virus), Editor(s): Bennett JE, Dolin R, Blaser MJ, Mandell D. Bennett's Principles and Practice of Infectious Diseases (Eighth Edition), W.B. Saunders, 2015, pp. 1731-1737.e2,
2.    National Institute on Aging. Shingles.
3.    Centers for Disease Control and Prevention. About shingles (herpes zoster).
4.    Hur J. Sacral herpes zoster associated with voiding dysfunction in a young patient with scrub typhus. Infect Chemother. 2015;47(2):133–136.
5.    Dworkin RH, Johnson RW, Breuer J, et al. Recommendations for the management of herpes zoster. Clin Infect Dis. 2007;44(Suppl 1):S1-26. http://dx.doi.org/10.1086/510206 PMid:17143845