Endocrine Abstracts

Introduction: Central pontine myelinolysis (CPM) is a rare and potentially life-threatening complication of a sudden rise in serum osmolality. Along with extrapontine myelinolysis, it is part of the osmotic demyelination syndrome (ODS). Known risk factors include severe hyponatremia, alcoholism, thiazide use, hypokalemia, and malnourishment.

Case report: We report the case of a 31-year-old-male with history of alcohol and cannabis dependence, who had attended a private clinic two weeks earlier for gastric balloon placement, he was admitted to the emergency-department reporting nausea and vomiting with oral intolerance, nervousness, and agitation. He was initially detected to have hypo-osmolar hyponatremia (osmolality: 261 mmol/l, sodium: 114 mmol/l), and hypokalemia. His urine analysis revealed a urine osmolality of 279 mmol/l with a sodium level of 13 mmol/l supposedly because of hypovolemia due to inadequate fluid intake. The patient received intravenous potassium and was to be given 2000 ml of NaCl 0.9% in the first 24 h; Also, thiamine was prophylactically started to prevent Wernicke encephalopathy. Approximately 16 h after admission, the sodium levels increased to 123 mmol/l. The patient received glucose 5% infusion when sodium levels increased to 125 mmol/l within the first 24 h. In the following week the sodium levels normalized with a daily increase of 1-3 mmol/l. The potassium levels normalized quickly as well. During this period, the patient developed ataxia and resting tremors. Vitamin doses were switched to therapeutic because Wernicke encephalopathy was suspected. In the following days the patient’s neurological status deteriorated leading to a ‘locked in’ state when he was only able to open and move his eyes. An MRI of the brain showed a hyperintense signal in the central pontine region. Following the diagnosis of CPM, he was rehabilitated with occupational and physiotherapy.

Discussion: Our case, a patient with history of alcohol and cannabis dependence syndrome, complicated by central pontine myelinolysis probably due to an overly rapid correction of plasma osmolality. Given the fact that our patient had multiple risk factors and severe hyponatremia (<120 mmol/l) he would have benefited from a more intensively controlled rise in serum sodium levels or more aggressive lowering of sodium levels when overcorrection became apparent.

Conclusion: CPM is a rare complication of a rapid correction of serum osmolality, and we should always be aware of this complication. In patients with multiple risk factors, CPM might be prevented by frequent control of electrolytes and osmolality in combination with volume status and urinary output.