Incidence of osmotic demyelination syndrome in Sweden: A nationwide study

Abstract

Objective To report the incidence rate of osmotic demyelination syndrome (ODS), associated risk factors, treatment, and long‐term outcomes in a nationwide cohort. Methods We conducted a retrospective study of individuals diagnosed with central pontine myelinolysis (ICD‐10 code G37.2) in the Swedish National Patient Register during 1997‐2011. Results During the study period, we identified 83 individuals with ODS, 47 women and 36 men. Median age at diagnosis was 55 years. The incidence rate of ODS for the entire study period was 0.611 (95% CI: 0.490‐0.754) per million person‐years and increased during the study period from 0.271 (95% CI: 0.147‐0.460) in 1997‐2001 to 0.945 (95% CI: 0.677‐1.234) individuals per million person‐years in 2007‐2011. Most cases (86.7%) were hyponatremic with a median sodium level at admission of 104 mmol/L. All hyponatremic cases were chronic. The cause of hyponatremia was multifactorial, including drugs (56.9%), polydipsia (31.9%), and vomiting or diarrhea (41.7%). A majority of patients (69.9%) were alcoholics. Hyponatremic patients were predominantly treated with isotonic saline (93.1%) and only 4.2% with hypotonic fluids. The median correction rate was 0.72 mmol/L/h. Only six patients were corrected in accordance with national guidelines (≤8 mmol/L/24/h). At three months, 7.2% had died and 60.2% were functionally independent (modified Rankin Scale 0‐2). Interpretation We found an increasing incidence during the study period, which could partly be explained by increased access to magnetic resonance imaging. ODS occurs predominantly in patients with extreme chronic hyponatremia which is corrected too fast with isotonic saline. Most patients survived and became functionally independent.

Osmotic Demyelination Syndrome following Correction of Hyponatremia by ≤10 mEq/L per Day

“…Characteristics of this group were similar to those identified in a nationwide study of 83 patients diagnosed with ODS in Sweden; in that study, most patients (86.7%) were hyponatremic (all chronic) with a median serum sodium of 104 mEq/L (IQR 99.5 -110.5); 69% of the patients were alcoholic, and 67.5% were hypokalemic 6 . Of note, Swedish national guidelines set a correction limit of SNa to ≤ 8 mEq/L in 24 hours, and all but 6 of the 83 patients (7%) exceeded this rate of correction.…”

The osmotic demyelination syndrome: the resilience of thalamic neurons is verified with transmission electron microscopy

“…29 In the old and current literature, number of reports of regional CPM and EPM ODS defects showed as consequences of abrupt adjustment of a temporary or chronic deficiency of the homeostatic sodium gradient. Its etiology can be found in a series of diverse afflictions, 30 such as in these exemplary list of clinical studies: alcoholism and/or combined with malnutrition, 1,19,[31][32][33][34][35][36][37][38][39][40] craniofacial and neurosurgeries, 41,42 diarrhea with AIDS, 43 excessive vomitus alone 44 or associated with pregnancy, 45,46 hyper glycemia, 47 pediatric diabetes, 48 diabetes insipidus due to cancer treatments, 49 folate deficiency, and kidney defect, 50 Grave's disease, 51 diuretic unbalance, and heart failure, [52][53][54][55] heat exhausting exercise, 56,57 liver cirrhosis, 58,59 or liver transplantation. 29,60,61 Disorders of sodium and osmotic homeostasis have been found in diverse small mammals.…”

Uremia Preventing Osmotic Demyelination Syndrome Despite Rapid Hyponatremia Correction

“…[6][7][8][9] Most occurred among subjects with a serum sodium <120 mEq/L and a sodium correction of >10 to 12 mEq/L in the initial 24 hours of presentation. [8][9][10][11][12] Despite its low incidence, given significant morbidity and mortality associated, it is still recommended to avoid the rapid correction of hyponatremia. The recommended rate of hyponatremia correction is 4 to 6 mEq/L in 24 hours.…”