Resident Physician University of California, Los Angeles Los Angeles, California, United States
Introduction: Recent work in traumatic spinal cord injury (SCI) has demonstrated that intraspinal pressure and spinal cord perfusion pressure affect functional outcomes by mechanisms analogous to intracranial pressure and cerebral perfusion pressure in traumatic brain injury. Serum sodium control is a critical component of forestalling post-traumatic cerebral edema. Curiously, there is no analogous literature on sodium control in spinal cord injury. To find evidence for hyponatremia-mediated exacerbation of secondary injury, we investigated the relationship between serum sodium and early functional decline in patients with isolated incomplete spinal cord injury.
Methods: We performed a retrospective analysis of patients admitted to Harbor-UCLA Hospital with isolated, incomplete traumatic spinal cord injury between 11/2017-10/2020. Data were extracted by chart review. Analysis was performed by custom scripts written in MATLAB.
Results: We identified 35 patients with isolated incomplete injury. Mean patient age was 52.5 years; patients were 74% male. On average, development of hyponatremia was associated with 22% lower ASIA motor scores compared to patients with stable serum sodium (p = 0.0027). This was not explained by admission sodium (p = 0.19). Severity of injury did not predict subsequent hyponatremia (p = 0.06) nor were there differences in hospital length of stay (p = 0.97), time to surgical intervention (p = 0.45), or injury level (p = 0.50).
Conclusion : Our pilot data establish that decline in serum sodium following incomplete SCI correlates with worsened motor strength at discharge. This warrants further study, and may represent an opportunity to improve neurologic outcomes through serum sodium management.
