A50-11 More Than Just Low Sodium: Unmasking Neuroborreliosis Behind Hyponatremia

Abstract Introduction Lyme disease, caused by the spirochete Borrelia burgdorferi, is a tick-borne infection with multisystem involvement, commonly affecting the skin, joints, heart, and nervous system. Neuroborreliosis, though less frequent, may manifest with meningitis, cranial neuropathies, or radiculopathies. Older adults can present atypically, leading to diagnostic delay. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a rare complication of neuroborreliosis, attributed to inflammatory disruption of hypothalamic-pituitary signaling. We report a diagnostically challenging case of Lyme neuroborreliosis presenting with recurrent tremors and profound SIADH-induced hyponatremia, initially suggestive of a primary metabolic or endocrinologic disorder. Case A 72-year-old man with hypertension, hyperlipidemia, type 2 diabetes, and prostate carcinoma status-post resection presented with tremors and progressive generalized weakness. He reported decreased appetite, constipation, and increased fluid intake (∼3 L/day). Notably, he had a similar admission three weeks earlier for tremors and weakness that resolved with electrolyte repletion. During that hospitalization, Lyme and California encephalitis Immunoglobulin G were positive, but treatment was deferred as results returned post-discharge. On arrival, he was afebrile, normotensive, and alert. Laboratory tests revealed serum sodium 115 mmol/L, potassium 2.7 mmol/L, magnesium 1.52 mg/dL, and WBC 16.1 × 109/L. CT head was unremarkable. He was admitted to the ICU for management of severe hyponatremia and hypokalemia. Workup suggested SIADH versus hypovolemia. Following cautious correction with hypertonic saline, D5W, and desmopressin, sodium normalized without neurologic sequelae. Cerebrospinal fluid analysis demonstrated lymphocytic pleocytosis with elevated protein and glucose, confirming neuroborreliosis secondary to untreated Lyme disease. The patient completed a 28-day course of intravenous ceftriaxone per infectious disease recommendations and was discharged neurologically improved on fluid restriction. Discussion This case deviates from the typical presentation of neuroborreliosis, as the patient exhibited neither meningismus nor cranial neuropathies, but rather recurrent tremors with profound hyponatremia. The observed SIADH likely reflected cytokine-mediated inflammation within the hypothalamic-posterior pituitary axis, where interleukin-6 and tumor necrosis factor-α may trigger non-osmotic ADH release, leading to water retention and euvolemic hyponatremia. The prompt normalization of sodium after ceftriaxone therapy supports a reversible, inflammation-driven neuroendocrine process rather than primary hypothalamic or pituitary dysfunction. This case underscores the diagnostic complexity of Lyme neuroborreliosis in older adults, where subtle neurologic findings may obscure recognition. Clinicians should maintain a high index of suspicion when evaluating unexplained hyponatremia in endemic areas, as timely antimicrobial therapy can prevent lasting neurologic or neuroendocrine complications. This abstract is funded by: None