Case Presentation: We report the case of a 63-year-old male with a history of alcoholism and congestive heart failure who was brought to the Emergency Department after being found unconscious. He was febrile at 102.5° F and tachycardiac with a heart rate of 123 beats per minute. He was found to be tremulous, which raised the concern for Delirium Tremens. He was initially treated with broad spectrum antibiotics, while receiving treatment for alcohol withdrawal. However, his mental status failed to improve, prompting a lumbar puncture, which showed a high WBC count (predominantly neutrophils), elevated glucose and increased protein. A comprehensive infectious workup of his Cerebrospinal Fluid (CSF) was performed, while his empiric antimicrobial coverage was broadened to include Vancomycin, Meropenem, Doxycycline and Acyclovir. On hospital day #2, the patient became hemodynamically labile, apneic and unresponsive, requiring endotracheal intubation. An MRI was unremarkable. An EEG showed diffuse background slowing, consistent with encephalopathy. CSF analysis revealed IgM antibodies to WN virus. He continued to be unresponsive and apneic with a Glasgow Coma Scale score of 3 despite being off sedatives. IVIG was administered, based on case reports documenting its efficacy in the treatment of WN encephalopathy1. Within 48 hours the patient showed significant improvement. He opened his eyes to voice, and responded to commands. While his mental status improved dramatically, he continued to have profound and persistent neuromuscular weakness. He was eventually discharged to a long term facility for rehabilitation.
Discussion: West Nile (WN) virus is an arthropod-borne virus which can lead to a wide range of clinical symptoms, ranging from asymptomatic disease to severe meningitis, encephalitis, and acute flaccid paralysis. This variability in its presentation, in addition to a lack of proven therapies make it a difficult condition to diagnose and treat. Although there is a lack of treatment options for WN virus infection, the use of IVIG, interferon and Ribavirin have been described. In a case series published by Shimoni et al, IVIG administration was noted to result in complete recovery in a few patients. However, a greater number experienced improvement only in their degree of encephalopathy, without improvement of their flaccid paralysis2.
Conclusions: Our case contributes to a growing body of evidence suggesting that while IVIG may be beneficial in the treatment of WN encephalitis, it may have less of an impact on WN induced flaccid paralysis. It also suggests that the pathophysiological mechanisms responsible for behind WN virus encephalopathy may be different than those responsible for flaccid paralysis. Further investigation into the pathophysiology and treatment of WN encephalitis and paralysis is warranted.
REFERENCES:
1. Walid MS, Mahmoud FA. Successful Treatment with Intravenous Immunoglobulin of Acute Flaccid Paralysis Caused by West Nile Virus. The Permanente Journal. 2009;13(3):43-46.
2. Shimoni Z, Bin H, Bulvik S, et al. The clinical response of West Nile virus neuroinvasive disease to intravenous immunoglobulin therapy. Clinics and Practice. 2012;2(1):e18. doi:10.4081/cp.2012.e18.