Abstract
A 44-year-old male with history of asplenia, provoked PE, and hyperlipidemia presented with ascending paralysis, bowel and bladder incontinence and altered mental status, and progressively developed acute hypoxic respiratory failure. Initial workup including CT head, magnetic resonance imaging (MRI) brain, and lumbar puncture which was concerning for herpes simplex virus (HSV) meningoencephalitis; out of caution he was started on multiple antibiotics consequently resulting in the development of Clostridium difficile (C.diff). He also received two doses of IVIG. He was transferred to our institution and after interval re-imaging via MRI brain and spinal surveys and repeat lumbar punctures, he was found to have a high CSF HSV titer and positive GAD 65 antibody, the latter likely a false positive due to IVIG administration. IVIG was not continued from the outside hospital due to the development of deep vein thrombosis (DVT), and the risks of plasmapheresis outweighed the benefits. The patient gradually improved after a prolonged course of acyclovir and was downgraded out of the Neuroscience ICU (NSICU), however decompensated due to rectal bleeding, and subsequently went into cardiac arrest. Though this patient underwent a splenectomy, his relative immunocompetency towards non-encapsulated organisms should have been preserved. It has not been clearly described in the literature how and why HSV encephalomyelitis takes a fulminant course in immunocompetent patients, including our asplenic patient. Furthermore, definitive treatment and management of this condition remains unclear. Severity of HSV encephalomyelitis has not been clearly described in the literature, particularly in immunocompetent patients (such as this asplenic patient).