October 2014, Vol 146, No. 4_MeetingAbstracts
Critical Care | October 2014
Posterior Reversible Encephalopathy Syndrome Associated With Hemorrhagic Fever With Renal Syndrome From Dobrava Virus Infection Blair Glasgo, MD; Nikunj Bhatt, MD; Sean Reilly, MD Walter Reed National Military Medical Center, Bethesda, MD
Chest. 2014;146(4_MeetingAbstracts):284A. doi:10.1378/chest.1992382
Abstract SESSION TITLE: Critical Care Student/Resident Case Report Posters I SESSION TYPE: Medical Student/Resident Case Report PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM INTRODUCTION: Dobrava is a hantavirus that causes a severe Hemorrhagic Fever with Renal Syndrome (HFRS) and can be associated with nonspecific CNS manifestations. Posterior Reversible Encephalopathy Syndrome (PRES) is a clinicoradiologic syndrome of headache, confusion, visual changes, and seizure with imaging findings of reversible posterior cerebral edema. We present the first known case of Dobrava virus HFRS complicated by PRES. CASE PRESENTATION: A healthy 37 year-old male US soldier in Kosovo presented with three days of fever, headache, vomiting, and diarrhea. Laboratory studies showed hyponatremia, thrombocytopenia, coagulopathy, and positive Dobrava IgG and IgM serologies. He was started on intravenous ribavirin and evacuated to the ICU of a US Army Hospital in Germany, where he developed nonoliguric renal failure and acute lung injury requiring noninvasive positive pressure ventilation. Neurologic examination revealed slowed speech, word finding difficulty, and decreased visual acuity with unremarkable ophthalmoscopic examination. His blood pressure increased from 120/75 on admission to 160/95 on illness day thirteen, when he suffered two generalized tonic clonic seizures. MRI/MRA revealed FLAIR signal hypodensities of the cerebellar, occipital, and parietal gray and white matter. PRES was diagnosed, and he was started on antihypertensive and antiepileptic medications. He had no further seizures, and his cognition, vision, and renal and pulmonary function improved. MRI six days and three months later showed near and complete resolution, respectively. DISCUSSION: The pathogenesis of PRES is poorly understood but thought to involve endothelial damage and/or cerebral autoregulatory dysfunction. Initially described in patients on immunosuppressants with acute hypertension and renal impairment, it is now recognized in conditions that cause endothelial dysfunction, including preeclampsia, cytotoxic chemotherapy, and viral encephalitis. Hantaviruses infect vascular endothelial cells and lead to an exaggerated immune response, causing capillary leakage and tissue edema, thus suggesting a possible mechanism for an association with PRES.
CONCLUSIONS: While the etiology of hantavirus infection-associated CNS manifestations is still unclear, PRES should be considered in the differential diagnosis of neurologic symptoms in order to treat and potentially prevent PRES with blood pressure monitoring and control.
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Reference #2: Pedraza R, Marik PE, Varon J. Posterior reversible encephalopathy syndrome: a review. Crit Care & Shock. 2009; 12:135 - 143. Reference #3: Abel Borges A, Figueiredo LT. Mechanisms of shock in hantavirus pulmonary syndrome. Current Opinion in Infectious Diseases. 2008;21(3):293-7.
DISCLOSURE: The following authors have nothing to disclose: Blair Glasgo, Nikunj Bhatt, Sean Reilly The patient in the above abstract was treated with ribavirin as part of an investigational protocol for hantavirus infection. However, the treatment of his hantavirus infection is not the point of the abstract. The fact that he developed PRES in the setting of hantavirus infection is the main topic of the abstract.