Risk Factors and Outcomes of Rapid Correction of Severe Hyponatremia

Abstract

Background and objectives Rapid correction of severe hyponatremia can result in serious neurologic complications, including osmotic demyelination. Few data exist on incidence and risk factors of rapid correction or osmotic demyelination. Design, setting, participants, & measurements In a retrospective cohort of 1490 patients admitted with serum sodium ,120 mEq/L to seven hospitals in the Geisinger Health System from 2001 to 2017, we examined the incidence and risk factors of rapid correction and osmotic demyelination. Rapid correction was defined as serum sodium increase of .8 mEq/L at 24 hours. Osmotic demyelination was determined by manual chart review of all available brain magnetic resonance imaging reports. Results Mean age was 66 years old (SD=15), 55% were women, and 67% had prior hyponatremia (last outpatient sodium ,135 mEq/L). Median change in serum sodium at 24 hours was 6.8 mEq/L (interquartile range, 3.4-10.2), and 606 patients (41%) had rapid correction at 24 hours. Younger age, being a woman, schizophrenia, lower Charlson comorbidity index, lower presentation serum sodium, and urine sodium ,30 mEq/L were associated with greater risk of rapid correction. Prior hyponatremia, outpatient aldosterone antagonist use, and treatment at an academic center were associated with lower risk of rapid correction. A total of 295 (20%) patients underwent brain magnetic resonance imaging on or after admission, with nine (0.6%) patients showing radiologic evidence of osmotic demyelination. Eight (0.5%) patients had incident osmotic demyelination, of whom five (63%) had beer potomania, five (63%) had hypokalemia, and seven (88%) had sodium increase .8 mEq/L over a 24-hour period before magnetic resonance imaging. Five patients with osmotic demyelination had apparent neurologic recovery. Conclusions Among patients presenting with severe hyponatremia, rapid correction occurred in 41%; nearly all patients with incident osmotic demyelination had a documented episode of rapid correction.

Cotrimoxazole-Induced SIADH—A Unique Challenge during Treatment of Pulmonary Nocardiosis

“…Effective serum osmolality is determined by serum sodium concentration. Hypotonic hyponatremia, if acute and severe, can lead to the entry of water into brain cells and ultimately, to cerebral edema [13,14]. The brain adapts to such a level of hypotonicity by losing intracellular solutes, principally potassium and organic solutes called osmolytes.…”

“…Overt rapid correction of hyponatremia can induce Osmotic Demyelination Syndrome (ODS) [13]. However, rapid correction in acute and severe hyponatremia does not induce ODS because the cerebral adaptation is still in its early stage [14].…”

The use of mannitol in cardiopulmonary bypass prime solution—Prospective randomized double‐blind clinical trial

“…It has been shown that hyponatremia is a potentially dangerous condition associated with the risk of brain edema . Another serious condition, central pontine myelinolysis, may occur when hyponatremia is treated rapidly . Minimizing the risk of hyponatremia may benefit the outcome after cardiac surgery, and preventing hyponatremia during CPB is most important.…”

Normal Correction of Sodium Leading to Central Pontine Demyelinosis: A Rare Occurrence

“…Although the precise pathogenesis remains unclear, the most frequent trigger of myelinolysis in clinical practice is the rapid correction of chronic hyponatremia [ 2 ]. Osmotic demyelination has also been observed in other settings in the absence of rapid serum correction, such as hyperosmolar hyperglycemia, hyperammonemia, hypoxia, severe liver disease, and chronic alcoholism [ 4 ]. It is postulated that the brain adapts to chronically low levels of the intracellular osmolyte, and the subsequent iatrogenic hypertonic stress owing to rapid correction of hyponatremia causes the ions and water to quickly re-enter the intracellular space.…”