Refractory Hypernatremia and Osmotic Demyelination Syndrome After Liver Transplantation: A Case Report

• Osmotic demyelination syndrome is one of the most severe neurological complications associated with liver transplantation. • Management of postoperative serum sodium in patients with chronic hyponatremia previous to the liver transplant can present a significant clinical challenge. • This case highlights the importance of careful measurement and control of postoperative sodium in patients who undergo liver transplantation, as well as the potential pitfalls that can lead to the development of osmotic demyelination syndrome. • The case reported is remarkable for the development of refractory hypernatremia despite early and aggressive treatment for lowering serum sodium, as well the rapid onset of symptoms after liver transplantation. Osmotic demyelination syndrome is an uncommon neurologic condition, characterized by noninflammatory demyelination involving the pons and other areas of the central nervous system. As chronic hyponatremia is frequently associated with cirrhosis, patients undergoing liver transplantation are at an increased risk for developing this condition. We report the case of a patient who developed refractory hypernatremia and osmotic demyelination syndrome after liver transplantation. The patient was a 40-year-old man, who underwent liver transplantation for the treatment of cryptogenic cirrhosis, and had a preoperative sodium level of 128 mmol/L. Although there were no intraoperative complications, the patient showed signs of mental confusion and drowsiness in the second postoperative day, and we noticed an increase to 136 mmol/L in his serum sodium. Treatment with 5% dextrose and desmopressin was initiated, but his serum sodium continued to increase steadily, while his neurologic condition gradually worsened. Serum sodium rose to 157 mmol/L, and a magnetic resonance imaging of the brain showed extensive lesions consistent with osmotic demyelination syndrome. The clinical condition of the patient continued to deteriorate until his death 17 days after the transplant. Although the occurrence of this syndrome after liver transplantation is well described, the steady increase in serum sodium despite early treatment, as described in this case, is highly unusual, and highlights the great attention that must be taken with monitoring and control of serum sodium in patients who undergo liver transplant in the context of chronic hyponatremia. This manuscript is compliant with the Helsinki Congress and the Istanbul Declaration.