Osmotic Demyelination Syndrome Secondary to Hypernatremia and Hypokalemia: A Case Report of Complete Recovery

Osmotic demyelination syndrome (ODS) presents as quadriplegia with pseudobulbar palsy, and most cases occur with rapid correction of hyponatremia. It is due to demyelination of the pons without any inflammation. Other causes include chronic malnutrition, alcoholism, and underlying medical illnesses such as post-liver transplant. Here, we present a case report of a patient with hypernatremia and hypokalemia leading to ODS, whose early diagnosis and effective treatment resulted in complete recovery of the patient.

A 33-year-old female patient presented with vomiting followed by confusion and weakness of all four limbs. On admission, the patient was drowsy, obeying oral commands, mildly dyspneic, dehydrated, weakness of all four limbs. Deep tendon reflexes were present, and the bilateral plantar reflex showed no response. Her vitals were stable. On evaluation, arterial blood gas (ABG) showed hyperchloremic normal anion gap metabolic acidosis. Serum potassium level was very low, and serum sodium level was significantly high. MRI brain T2-FLAIR image showed hyperintensity in the central pons with peripheral sparing. Pons appeared swollen and edematous, suggestive of ODS. On further evaluation, she was found to have distal renal tubular acidosis. With this presentation and in the background of renal tubular acidosis, autoimmune disease was considered. It was negative in our case. In view of hypernatremia, after calculating the water deficit, she was given IV 5% dextrose and free water through the nasogastric tube, along with potassium supplements. She was also given steroids and other supportive measures. The patient recovered completely.

There was no evidence of hyponatremia during admission. Here, we consider that the osmotic demyelination could have occurred due to hypernatremia. The cause for hypernatremia in this case would have been hypokalemia. Moreover, hypokalemia leads to hypernatremia through a combination of increased sodium reabsorption in the kidneys, aldosterone-mediated effects, impaired renal concentrating ability, cellular electrolyte shifts, and associated volume depletion and dehydration. These mechanisms explain the complex relationship between sodium and potassium. Early diagnosis with MRI brain imaging and treatment allowed our patient to recover completely.