A 65‐year‐old man presented to the emergency department in late summer complaining of fever, cough, and decreased oral intake for the past 7 days. His symptoms were associated with blurry vision and nausea. His medical history included diabetes and hypertension. In the ED, he was alert and oriented. His temperature was 100.8°F. Physical and ocular exams were normal. The WBC count was 7.6 × 103 /μL. Chest X‐ray and electrocardiogram were unremarkable. Blood cultures were drawn and intravenous ceftriaxone and azithromycin were started. Over the next 24 hours, he became increasingly lethargic and his temperature was greater than 103°F. Acyclovir was started. A Head CT was unremarkable. A lumbar puncture revealed colorless CSF, 4 RBCs/mm3, 29 WBC/mm3 (68% lymphocytes, 31% neutrophils, 1% monocytes), glucose 115 mg/dL (serum level: 219 mg/dL), and protein 195 mg/dL. Bacterial and fungal stains were negative. Herpes simplex virus PCR of the CSF was negative. Blood cultures and Lyme antibodies were negative. A transthoracic echocardiogram revealed an ejection fraction of 50%–55% with abnormal left ventricular relaxation and a dilated left atrium. An electroencephalogram demonstrated abnormal generalized background slowing, consistent with diffuse encephalopathy. During morning rounds the following day, the patient continued to be lethargic, yet arousable and responsive to questions. Moments later, he was found unresponsive. The electrocardiogram revealed asystole. Cardiopulmonary resuscitation was unsuccessful. Autopsy of the brain revealed microglial nodules, perivascular lymphocytic infiltrate, and focal leptomeningeal monovascular infiltrate consistent with viral meningoencephalitis. Polymerase chain reaction of the brain tissue and CSF was positive for West Nile virus. Autopsy of the heart demonstrated focal left ventricular scarring with lymphocytes and histiocytes, consistent with myocarditis.
The presence of neurologic involvement, positive West Nile virus (WNV) PCR from the CSF and brain, lymphohistiocytic myocardial infiltrate, and lack of evidence of acute infarction supports WNV‐associated myocarditis causing a fatal arrhythmia as the likely cause of the patient's death. Arrhythmia is not uncommon in viral myocarditis. The implications of this case are significant. West Nile virus is one of the most frequently reported etiologies of viral encephalitis in the United States. West Nile virus infections among hospitalized patients manifest most commonly as neuroinvasive disease.
Physicians who are caring for WNV‐infected patients need to be aware of the possibility of WNV‐related myocarditis. The question arises whether a patient with an established diagnosis of WNV meningoencephalitis should be under continuous cardiac monitoring, bearing in mind the rare but fatal complication of cardiac arrhythmia secondary to viral myocarditis. In addition, WNV should be considered with any case of acute myocarditis, particularly during the summer and fall, when mosquitoes are most prevalent.
A. Kushawaha, none; S. Jadonath, none, N. Mobarakai, none; N. Parikh, none.
To cite this abstract:Kushawaha A, Jadonath S, Mobarakai N, Parikh N. West Nile Virus Myocarditis Causing a Fatal Arrhythmia. Abstract published at Hospital Medicine 2009, May 14-17, Chicago, Ill. Abstract 171. Journal of Hospital Medicine. 2009; 4 (suppl 1). https://www.shmabstracts.com/abstract/west-nile-virus-myocarditis-causing-a-fatal-arrhythmia/. Accessed May 26, 2019.