View Abstract

A3379 - A Rare Cause of Central Pontine Myelinolysis
Author Block: A. Khan1, M. Lough1, D. Dave1, H. E. Mohamed2; 1West Virginia University School of Medicine, Charleston Campus, Charleston, WV, United States, 2West Virginia Universtiy School of Medicine, Charleston Campus, Charleston, WV, United States.
Introduction: Central pontine myelinolysis (CPM) is a syndrome characterized by noninflammatory loss of myelin, classically due to rapid correction of hyponatremia. In recent years, there have been very few case reports of CPM due to hyperglycemic hyperosmolar states. Most of these cases report concurrent derangements in other plasma electrolytes. Here we describe a case of CPM due to hyperglycemia without serum sodium abnormalities. Case Presentation: A 60 year old male with poorly controlled, type 2 diabetes mellitus presented to the emergency department with a blood glucose >550 mg/dL at home. The patient denied acute complaints at presentation. He was lethargic with generalized weakness but oriented to person and time. During his ED course he became progressively somnolent and unresponsive, required intubation, and was admitted to the intensive care unit. Workup including arterial blood gas, urine drug screen, urinalysis, and CT head was unremarkable. Initial laboratory studies showed serum sodium of 143 mmol/L, potassium 3.4 mmol/L, and calculated serum osmolality of 319.5 mOsm/kg. He was treated with IVFs and insulin infusion protocol. He was extubated the following day, but his mental status continued to fluctuate. Serum sodium remained within normal limits. Serum potassium dropped to 2.9 mmol/L. Because of the fluctuation of his mental status, an MRI brain was obtained which revealed CPM. With supportive management the patient's mental status improved slowly and he was later discharged.Discussion: Though CPM is classically associated with rapid correction of hyponatremia, hyperglycemic states (most often associated with concurrent hypernatremia) have been shown to be associated with development of CPM, especially in metabolically susceptible patients. Patients with liver cirrhosis (often alcoholics), or liver transplant recipients, as well as chronically malnourished patients have traditionally been considered predisposed to developing CPM. Associations with hypokalemia and hypophosphatemia have also been described. Our patient had fluctuating serum potassium levels, with a low of 2.9 mmol/L, which conceivably contributed to the development of CPM. The pathogenesis of CPM is not well understood, but proposed mechanisms include damage to oligodendrocytes and astrocytes that ultimately results in osmotic shrinkage and apoptosis. This damage is thought to be due to a relative hypertonic insult that most commonly occurs after rapid correction of hyponatremia, but is also rarely due to primary hyperosmolar states. Previous case reports of CPM associated with hyperglycemia overwhelmingly also show concurrent hypernatremia. Ours was a rare case of CPM due to a hyperglycemic state without serum sodium derangements.