A rare case of herpes simplex virus encephalitis from viral reactivation following surgically treated traumatic brain injury

• Published in: Brain injury Vol. 38; no. 12; p. 1046
• Main Authors: Bhimani, Abhiraj D, Cummins, Daniel D, Kalagara, Roshini, Chennareddy, Sumanth, Hickman, Zachary L
• Format: Journal Article
• Language: English
• Published: England 14.10.2024
• Subjects: Acyclovir - therapeutic use; Adult; Antiviral Agents - therapeutic use; Brain Injuries, Traumatic - complications; Brain Injuries, Traumatic - surgery; Craniotomy - adverse effects; Encephalitis, Herpes Simplex - complications; Hematoma, Subdural, Acute - etiology; Hematoma, Subdural, Acute - surgery; Herpesvirus 1, Human; Humans; Male; Postoperative Complications; Virus Activation; herpes simplex virus; trauma; traumatic brain injury; HSV reactivation; Head injury; infectious disease
• ISSN: 1362-301X
• DOI: 10.1080/02699052.2024.2370834

Herpes simplex virus encephalitis (HSVE) is associated with significant morbidity and mortality. Here, we present the occurrence of HSVE in a 36-year-old immunocompetent patient following craniotomy for a traumatic acute subdural hematoma (ASDH). Imaging after four days of progressive headache following a fall with head-strike demonstrated a 1 cm thick left holohemispheric ASDH with significant cerebral compression, edema, and 8 mm of left-to-right midline shift, and an emergent craniotomy and ASDH evacuation were performed, with additional treatment needed for reaccumulation. Postoperatively, the patient developed a worsening leukocytosis, became febrile, and was hypotensive requiring vasopressor support. Despite empiric antibiotics, the patient remained persistently febrile with significant leukocytosis. Repeat head CT showed a new left insular hypodensity and a subsequent viral encephalitis panel was positive for HSV-1. The patient was then started on intravenous acyclovir, with progressive neurological exam improvement. Of note, the patient was noted to have a positive serum HSV-1 IgG antibody titer, indicative of prior infection. Given the known systemic immunosuppression in brain injury and the high prevalence of HSV seropositivity, clinicians should consider the possibility of HSVE from HSV reactivation in TBI patients with persistent fever, leukocytosis, and/or neurological deficits without an obvious etiology.