A case of severe asymptomatic hyponatremia mimicking cerebrospinal fluid leak: a diagnostic challenge in polytrauma rehabilitation

Case Diagnosis: Severe asymptomatic hyponatremia after a motor vehicle collision (MVC) and polytrauma

Case Description or Program Description: A 39-year-old female in an inpatient rehabilitation facility (IRF) after a MVC with multiple traumatic injuries (including a right parietal subdural collection, Le Fort I fracture, left acetabular fracture, and open tibia-fibula fracture) developed clear nasal drainage and severe hyponatremia (120mmol/L). Given her maxillofacial trauma and repair, concern for cerebrospinal fluid (CSF) leak prompted neurosurgery and otolaryngology consultations.

Setting: IRF

Assessment/Results: CT showed no skull base fractures, and fiberoptic nasopharyngoscopy found no leakage along the cribriform plate. Neurosurgery and otolaryngology found no concerns, attributing the clear secretions to nasal congestion. The primary rehabilitation, internal medicine, and nephrology teams determined multifactorial causes, including syndrome of inappropriate antidiuretic hormone secretion (SIADH) and fluid imbalance. Sodium levels improved with fluid restriction and dietary modifications.

Discussion (relevance): CSF leaks, a known complication of skull base fractures, often present with clear rhinorrhea. This case highlights severe asymptomatic hyponatremia initially raising concern for a CSF leak, emphasizing the diagnostic complexity of hyponatremia in trauma. Hyponatremia in polytrauma is commonly attributed to SIADH or cerebral salt wasting. Symptomatic patients typically have lower sodium levels (mean 124.8mmol/L) than asymptomatic ones (mean 126.6mmol/L), suggesting severe hyponatremia ( < 125mmol/L) is usually symptomatic. In TBI, severe asymptomatic hyponatremia is rare. About 20% of neurotrauma patients develop severe hyponatremia, often with seizures and elevated intracranial pressure. In this case, the patient had severe hyponatremia (120mmol/L) but was surprisingly asymptomatic. However, the frequency of symptomatic vs. asymptomatic cases in TBI remains unclear in literature. Early identification, imaging, and a broad differential are key to distinguishing CSF leaks from other causes of hyponatremia.

Conclusions: Nasal drainage after polytrauma can lead to unnecessary workup if not correlated clinically. This case emphasizes the importance of a systematic approach using labs, imaging, and multidisciplinary evaluation to guide management.