Osmotic Demyelination Syndrome due to Rhabdomyolysis and Hyperosmolar Hyperglycemic Syndrome following Cardiogenic Shock

Osmotic demyelination syndrome (ODS) is a relatively rare disease that causes rapid demyelination, resulting in pontine and central nervous system damage with various symptoms, including impaired consciousness. It often occurs when hyponatremia is rapidly corrected. However, it can also occur when a normonatremic patient suddenly develops hypernatremia. A 51-year-old man developed cardiogenic shock with impaired consciousness, hyperCKemia, hypernatremia, and hyperglycemia. Osmotic demyelination syndrome secondary to rhabdomyolysis and hyperosmolar hyperglycemic syndrome was suspected. The patient’s fluid volume decreased because of osmotic diuresis caused by hyperglycemia, and the blood sodium level increased rapidly. The latter resulted in ODS, which in turn resulted in a prolonged disturbance of consciousness, from which he has not yet recovered. ODS has been reported as a serious complication of rapid correction of hyponatremia, although it also occurs when normonatremia leads to hypernatremia. This disease is difficult to diagnose, as magnetic resonance imaging (MRI) of the brain is often unremarkable several weeks after its onset. This case of ODS occurred when normonatremia led to hypernatremia, as a result of rhabdomyolysis and hyperosmolar hyperglycemic syndrome. Diagnosis was made based on the MRI brain findings.

Osmotic demyelination syndrome following slow correction of hyponatraemia

Hyponatraemia is the most common electrolyte disturbance observed in hospital inpatients. We report a 90-year-old woman admitted generally unwell following a fall with marked confusion. Examination revealed a tender suprapubic region, and investigations observed elevated inflammatory markers and bacteriuria. Admission investigations demonstrated a serum sodium of 110 mmol/L with associated serum osmolality 236 mmol/kg and urine osmolality 346 mmol/kg. She was treated for hyponatraemia secondary to syndrome of inappropriate antidiuretic hormone (SIADH) and urosepsis. However, her serum sodium failed to normalise despite fluid restriction, necessitating treatment with demeclocycline and hypertonic saline. Despite slow reversal of hyponatraemia over 1 month, the patient developed generalised seizures with pontine and thalamic changes on MRI consistent with osmotic demyelination syndrome (ODS). This case highlights the risk of ODS, a rare but devastating consequence of hyponatraemia treatment, despite cautious sodium correction.