An 81-year-old male patient with a history of well-controlled type 2 diabetes mellitus presented to the emergency room with a lesion on his left forehead, as well as periorbital swelling and erythema. Three days before presentation, he had injured his left forehead on a kitchen ventilator, resulting in a minor laceration. In the following days, he noticed a progressive rash and redness in the injured area, as well progressive left periorbital soft tissue swelling. Pain, itching, paraesthesia and vision impairment were absent.
On physical examination, the patient's vital signs including temperature were normal. Cardiopulmonary examination was without pathological findings. The skin on his left forehead showed a dark crusty erosion and there was pronounced periorbital redness and swelling on both sides (Figs. 1 and 2). There were singular papules on the chin and upper chest (Fig. 3), as well as multiple erythematous papules without vesicles on the back. The lesions were painless.
Trigeminal and facial palsies were absent. Blood tests showed an elevated C-reactive protein (36.1 mg/l, reference value <10.0 mg/l) with a normal white blood cell count with mild lymphopenia and monocytosis. Mild hyponatremia (129 mmol/l, reference value 135-145 mmol/l) and elevated creatinine (creatinine 115 mumol/l, reference value 49-97 mumol/l, corresponding to an estimated glomerular filtration rate of 51 ml/min/1.7) were present. A computed tomography scan of the head showed periorbital cellulitis on the left side without abscess formation (Fig. 4).
Our initial hypothesis was cellulitis resulting from the previous head injury and we started the patient on intravenous antibiotic treatment with amoxicillin/clavulanic acid 2.2 g three times a day. Due to the atypical presentation and extension of the skin lesions to the trunk, we suspected a possible viral aetiology and started concomitant treatment with intravenous acyclovir 500 mg three times a day. Within the next 24 hours the patient was febrile (38.3 C) and a vesicular rash had developed.
PCR testing of a swab of the vesicles on the forehead was positive for VZV (4,113,840,000 copies) and HSV-1 (396,500 copies). PCR testing of the vesicles on the trunk detected 312,000,000 copies of VZV and 600 copies of HSV-1. Serological studies were consistent with reactivation of the viruses (negative IgM, positive IgG antibodies for both VZV and HSV-1). Ophthalmological examination showed no evidence of herpes zoster ophthalmicus or acute retinal necrosis. We excluded underlying immunosuppressive diseases such as HIV infection and multiple myeloma. There were no clinical signs of reactivation of latent infections like cytomegalovirus or tuberculosis.
In summary, we established the diagnosis of disseminated VZV infection with concomitant reactivation of HSV-1, triggered by a minor head injury. The clinical picture was more consistent with VZV reactivation than HSV-1 reactivation, as there were no signs of herpes labialis or genitalis, and no herpetic whitlow. According to the guidelines , we increased the dose of acyclovir to 750 mg intravenously three times a day. Within 3 days, a favourable clinical course was observed with regression of the facial oedema and crusting of the vesicles.
After 7 days, we stopped therapy with both acyclovir and amoxicillin/clavulanic acid.