Unveiling the West Nile Virus's Sodium Surprise: A Unique Case of Hyponatremia

Introduction: West Nile virus (WNV) is a vector-borne flavivirus typically transmitted by the Aedes and Anopheles mosquitos. WNV infection typically manifests with symptoms consistent with viral meningitis and is typically self-resolving, lasting anywhere from 3-10 days. Although uncommon, 30% of patients with WNV encephalitis can be afflicted with hyponatremia, although the etiology is unclear. It can be speculated that because of encephalitis, neuroinflammation may be involved in the deterioration of adrenal signalling, leading to salt wasting. Case Description: We present a 75-year-old man who presented with meningeal signs and viral illness symptoms. He was found to be hyponatremic with a sodium of 117 mmol/L and was started on 3% saline, fluid restriction, and salt tablets. After ruling out more organic causes of hyponatremia, there was ongoing concern for SIADH in the setting of positive WNV titers. CSF analysis was fairly bland. A paraneoplastic panel was negative, copeptin levels were elevated, and an MRI of the brain revealed the absence of the posterior pituitary bright spot, suggesting a SIADH pathology. He continued to do well with IVF resuscitation and salt tablets, and eventually, his sodium returned to normal levels, with the most recent measure at 138 mmol/L. Discussion: WNV infection typically manifests with symptoms consistent with viral meningitis and encephalitis. Although there have been cases of mosquito-borne infections with subsequent encephalitis, this is the first known reported case of SIADH related to WNV infection reported to date. The association between WNV and SIADH resulting in hyponatremia adds a new dimension to our understanding of the neurological consequences of mosquito-borne illnesses. The negative paraneoplastic panel, elevated copeptin levels, and the established pathophysiology of WNV encephalitis suggest that SIADH occurred because of neuroinflammation and neuroendocrine disruption. These findings, coupled with supporting imaging demonstrating the loss of the pituitary bright spot, which suggests alterations in the posterior pituitary’s functional integrity, support our proposed pathophysiology of WNV-induced encephalitis causing SIADH. This case underscores the intricate interplay between WNV encephalitis, neuroinflammation, and hormonal dysregulation, emphasizing the diagnostic complexity and management challenges in this and other similar clinical scenarios.