Osmotic Demyelination Syndrome Occurs Early in The Course of Hyperosmolar Hyperglycemic State.

Abstract

Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycaemic state (HHS) has been seldom reported. The aim of this study was to show that Osmotic Demyelination Syndrome occurs early in the course of Hyperosmolar I. BackgroundOsmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome, which usually occurs in the setting of a rapid correction of severe chronic hyponatremia 1,2 .ODS is a clinical syndrome characterized by altered mental status, quadriparesis, dyspnoea, dysarthria, and dysphagia which all occur characteristically five to seven days after the correction of serum sodium 3 . The pathogenesis is still to be clearly understood, it is known that rapidly increasing serum osmolality shifts water out of the cells as a response to correct solute imbalance resulting in shrinkage of glial cells that can consequently lead to disruption of the blood-brain barrier allowing inflammatory mediators to enter the central nervous system damaging oligodendrocytes and myelin 4-7 . Even though ODS has been classically thought to be exclusively secondary to a rapid correction of hyponatremia, it has also been described, even though rarely, in various other situations such as malnutrition, liver transplantation, alcoholism, hypokalemia, hypophosphatemia, AIDS, lithium toxicity, hypoglycemia, and folate deficiency, among others [8][9][10][11][12][13][14][15] . In all cases a growing body of evidence demonstrates that more than sodium per se, the key factor, in ODS pathogenesis, is a rapid change in serum osmoles. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported with less than five cases in the literature [16][17][18][19][20] . Previous cases have been in the clinical scenario of concomitant hypernatremia, chronic hyperglycemia/epilepsy, and after HHS treatment.Herein we present the case of a patient with HHS who presented with ODS early in the course of her illness. A review of previous cases and pathophysiological mechanisms involved in ODS secondary to HHS will be presented and discussed. Case PresentationA 45 year old female with poorly controlled Type2 Diabetes Mellitus came to the emergency room due to loss of consciousness. She was a known case of Type2 Diabetes Mellitus on Tab.Glipizide 5mg and Metformin 500mg for 10years and long acting Isophane Insulin(30:70) for 5years and she was a known Hypertensive on Tab Amlodipine 5mg for 5 years. She had irregular Medication.On Physical examination, her BP was 100/60 mmHg. Heart rate was 140/min and SpO 2 was 90% in Room air. Her BMI was 27.2. Mucus membranes were dry. ECG showed Right Axis Deviation. She had a Glasgow Coma Scale of 3/15 and muscle power was 0/5 in all the limbs and plantars were flexor B/L.There was no neck rigidity. Blood Glucose levels were 600mg%. Plasma and urinary ketones were negetive. ABG analysis showed pH 7.31. HbA1C was 14.1%, Serum Calcium 7.9mg/dL. Serum creatinine was 4.5mg/dL. Her eGFR

Serial Magnetic Resonance Imaging Findings in a Patient with Hyperglycemia-Related Osmotic Demyelination Syndrome: A Case Report

“…It is widely accepted that the most common cause of ODS is hyperosmotic stress resulting from rapid correction of severe hyponatremia [7]. Other conditions related to ODS include alcoholism, malnutrition, prolonged diuretic use, burns (in the context of hypernatremia), post-liver transplant, AIDS, folate deficiency, and hypoglycemia [6,8,9]. The association of ODS secondary to HHS has seldom been reported.…”