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Puett, Lisa RN, BSN

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Journal of Pediatric Surgical Nursing: 4/6 2016 - Volume 5 - Issue 2 - p 34-35
doi: 10.1097/JPS.0000000000000093
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A 16-month-old male patient presented to the Emergency Department (ED) by ambulance with approximately 15% of total body surface area partial thickness burns to his entire back, flank, left chest, and left upper arm from a hot water heater explosion (Figure 1). The patient was sedated and debrided in the ED (Figure 2) and then admitted for fluid resuscitation, pain management, OT/PT, and caregiver education. The patient’s burns were dressed with antibiotic ointment and nonadherent dressings until postburn day 4 (PBD4), when he was transitioned to a silver-impregnated dressing. The patient was discharged on PBD4.

Figure 1
Figure 1:
Fifteen percent of total body surface area partial thickness scald burns to entire back, flank, left chest, and left upper arm; predebridement.
Figure 2
Figure 2:

On PBD6, the patient returned to the ED with complaints of fevers to 102°F and a rash over his healing burns, as well as lethargy and poor oral intake.

On examination, the patient appeared nontoxic and fussy but consolable by a caregiver. He was febrile to 39.0°C and tachycardic to 172. His breath sounds were clear. His conjunctiva was clear, and no oral lesions were noted. The lower back had 3–4 mm of clustered circular plagues with a crusted center and no active drainage. The left arm had four to five 3-mm vesicles/papules with crusting in the center (Figure 3). The sole of the right foot had a pigmented macule; otherwise, no other lesions were noted on the skin. Overall, his burns appeared to be healing well.

Figure 3
Figure 3:
Postburn day 6—rash over healing burns.

Blood, bacterial, and viral wound cultures were obtained. The burn dressings were changed back to antibiotic ointment and nonadherent. The patient was started on oral acyclovir and clindamycin, and he was admitted while awaiting culture results.


Herpes simplex virus (HSV).


This patient’s bacterial wound culture was positive for light Staphylococcus aureus, and the viral culture was positive for herpes simplex type 1 virus. The patient clinically improved with acyclovir and clindamycin, daily wound care, and supportive measures. His burns were healed upon discharge on PBD10.

Burn injuries have profound multisystem effects on the body. Immunosuppression occurs as a result of a massive inflammatory state, making infection and sepsis the leading cause of death in burn patients. HSV in burns may be a primary infection or reactivation of latent HSV. Regardless of the origin, activation of HSV can lead to increased risk for bacterial and fungal infections, resulting in prolonged burn recovery time and increased hospital length of stay (Williams, Erho, Hawkins, Herndon, & Lee, 2013).

HSV in burn-injured patients can vary in severity, from asymptomatic viral shedding to persistent fevers with cutaneous skin lesions and vesicles to visceral dissemination (McGill & Cartotto, 2000). In 2012, Sen, Szoka, Phan, Palmieri, and Greenhalgh reported cutaneous facial and neck lesions to be more prevalent in HSV infections. However, as in this case, cutaneous lesions may also occur on the trunk or extremities. The cutaneous lesions are most likely to occur over the burn-injured skin, including graft and donor sites.

HSV can be quickly identified by a Tzanck smear of the vesicular lesions, and immunofluorescence testing identifies the specific virus. Acyclovir is the pharmacological treatment of HSV, as well as meticulous wound care and actions to prevent spreading (Williams et al., 2013).

The direct interaction and reaction of HSV on bacteria is not known. In 2015, the University of Texas Medical Branch, Galveston, initiated a study to review the clinical differences among human herpes virus subtypes in order to establish therapy approaches and provide evidence for related mortality and morbidity in burn-injured patients.


McGill S. N., & Cartotto R. C. (2000). Herpes simplex virus infection in a paediatric burn patient: Case report and review. Burns, 26, 194–199.
Sen S., Szoka N., Phan H., Palmieri T., & Greenhalgh D. (2012). Herpes simplex activation prolongs recovery from severe burn injury and increases bacterial infection risk. Journal of Burn Care & Research, 33, 393–397.
University of Texas Medical Branch, Galveston. (2000). Review of human herpes viruses in burns. [Internet]. Bethesda, MD: National Library of Medicine (US). NLM Identifier: NCT02452229. Available from
    Williams F., Erho B., Hawkins H., Herndon D., & Lee J. (2013). Herpes simplex virus type 2 in a pediatric burned patient: A case report and review. Critical Care Medicine, 41, A300.

    burn; herpes; HSV; infection

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