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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 Hyperglycaemic state and the pathophysiological mechanisms involved in ODS secondary to HHS. A 45 year old female with poorly controlled Type2 Diabetes Mellitus came to the emergency room due to loss of consciousness. She had a Glasgow Coma Scale of 3/15 and muscle power was 0/5 in all the limbs and plantar were flexor bilaterally. Blood Glucose levels were 600mg%. Plasma and urinary ketones were negetive. Arterial Blood Gas analysis showed pH 7.31. HbA1C was 14.1%, Serum Calcium 7.9 mg/dL. Serum creatinine was 4.5 mg/dL. NCCT Brain came to be Normal at the time of admission. Supportive therapy was started subsequently and she was put on Insulin infusion and blood glucose was closely monitored. She regained consciousness but she was disoriented and had irrelevant talks. Muscle power came normal. One week after admission MRI Brain was taken which showed focal areas of T2 Hypersensitivities in pons and subcortical white matter of bilateral parietal lobes suggestive of osmotic demyelination syndrome.In conclusion, the association of ODS with HHS is extremely rare. The exact mechanism by which HHS produces ODS still needs to be elucidated, but we favor a rapid hypertonic insult as the most probable mechanism. I. Background Osmotic 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 8-15 . 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 16-20 . 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 Presentation A 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 Osmotic Demyelination Syndrome Occurs Early In The Course Of ... DOI: 10.9790/0853-1603072529 www.iosrjournals.org 26 | Page was calculated to be 22.5mL/min/1.73m 2 . NCCT Brain came to be Normal at the time of admission. Fundus study showed Moderate NPDR.Sodium, Potassium, Phosphorous, Magnesium, Hemoglobin, WBC and Platelets were all within normal limits. Serum Albumin was 2.5mg/dl, SGOT 85 IU, SGPT 42 IU, Alkaline Phosphatase 316 IU and Total Bilirubin 0.3mg %. Supportive therapy was started subsequently and she was hydrated with normal saline, was put on Insulin infusion and blood glucose was closely monitored.. She regained consciousness but she was disoriented and had irrelevant talks. Muscle power came normal in 3 days. Blood sugar was poorly controlled. One week after admission MRI Brain was done which showed focal areas of T2 hypersensitivities in pons and subcortical white matter of bilateral parietal lobes suggestive of osmotic demyelination syndrome. During all her admission serum sodium was documented to be within normal range. ODS was diagnosed. Serum creatinine improved slowly Table 1: Laboratory measures during hospitalization. Day 2 5 7 9 11 Normal range Glucose 368 346 294 289 256 70–100 mg/dL Sodium 148 156 150 151 149 135–145 mmol/L Potassium 3.5 3.7 3.5 3.8 4.3 3.5–5 mmol/L Chlorine 118 114 106 107 106 101–111 mmol/L Creatinine 4.5 3.0 2.4 2.0 1.7 0.6–1.4 mg/dL MRI Brain showing focal areas of T2 hypersensitivities in pons and subcortical white matter of bilateral parietal lobes suggestive of osmotic demyelination syndrome.

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