RESUMO
Osmotic demyelination syndrome (ODS) is a clinical syndrome seen following aggressive correction of severe hyponatremia. Chronic alcohol use, malnutrition, and electrolyte derangement are additional risk factors promoting the demyelination in ODS. A 49-year-old female with a history of untreated mood disorder, hypertension, alcohol, and tobacco abuse presented to the emergency department (ED) with a three-month history of generalized body weakness. She also had a history of recurrent falls, difficulty walking, inadequate food and water intake, progressively worsening jaundice, and confusion which started about the same time. Her vital signs were normal; some of the significant physical examination findings were: sclera icterus, abdominal distension, bilateral pedal edema, hand tremors, rotary nystagmus, paraparesis, 1+ bilateral knee jerk, and absent bilateral ankle jerk. She had moderate hyponatremia, mild hypokalemia, deranged liver function test with a cholestatic pattern and transaminitis, hypoalbuminemia, elevated ammonia, lipase, in keeping with alcoholic liver disease and acute pancreatitis. In the ED, she received a normal saline infusion, and her serum sodium rose by just 6 mmol/L within the first 24 hours. She had drainage of her ascitic fluid and treatment with thiamine, folic acid, prednisone, lactulose, rifaximin, furosemide, spironolactone, and Ceftriaxone with improvement in clinical and laboratory abnormalities. Her lower extremity weakness persisted despite physical therapy, prompting neurologic evaluation. MRI of the lumbar spine showed an old compression fracture and lumbar spinal stenosis, while MRI brain findings were consistent with Osmotic demyelination. At the time of discharge to a rehabilitation facility, her serum sodium was 132 mmol/L, but her leg weakness persisted. Although rare, ODS can occur in the setting of moderate hyponatremia if there are additional risk factors that lower the threshold for demyelination.
