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A case of West Nile virus encephalitis accompanied by diabetic ketoacidosis and rhabdomyolysis

INTRODUCTION: We present here a case of West Nile Virus (WNV) encephalitis that initially presented with diabetic ketoacidosis and rhabdomyolysis. CASE PRESENTATION: A 35-year-old male with no past medical history presented to the emergency department complaining of polydipsia, generalized weakness,...

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Detalles Bibliográficos
Autores principales: Burden, Zachary, Fasen, Madeline, Judkins, Benjamin L., Isache, Carmen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378900/
https://www.ncbi.nlm.nih.gov/pubmed/30815360
http://dx.doi.org/10.1016/j.idcr.2019.e00505
Descripción
Sumario:INTRODUCTION: We present here a case of West Nile Virus (WNV) encephalitis that initially presented with diabetic ketoacidosis and rhabdomyolysis. CASE PRESENTATION: A 35-year-old male with no past medical history presented to the emergency department complaining of polydipsia, generalized weakness, lightheadedness, and visual disturbances of one week duration. He was found to be in diabetic ketoacidosis. His hemoglobin A1c was 11%. The patient was appropriately treated for diabetic ketoacidosis and it resolved on hospital day 1. On hospital day 2, the patient developed a fever of 101.6 °F and his mental status became severely altered. He developed auditory and visual hallucinations. IgM and IgG antibodies to West Nile Virus were positive in the cerebral spinal fluid (CSF). The patient's creatine kinase level rose to 118,400 U/L during his hospitalization and eventually returned to baseline. The patient made a full recovery with no residual neurologic deficits after an 11 day hospital course. DISCUSSION: In this patient, neuroinvasive WNV was confirmed with positive CSF IgM. The patient’s newly diagnosed diabetes likely contributed to his susceptibility to neuroinvasive disease. Furthermore, WNV encephalitis in a background of DKA has not been previously described in the literature and this case demonstrates WNV neuroinvasive disease should be in the differential diagnosis for patients presenting with unexplained neurological symptoms. CONCLUSION: Diagnosis of neuroinvasive WNV is imperative to stop unnecessary therapies, limit further diagnostic evaluation, help predict patient outcomes, direct public health prevention measures, and further provide investigations into the clinical conditions that define the spectrum of WNV disease.