When Normonatremia Isn't Safe: Late Onser Osmotic Demyelination Causing Locked-In Syndrome in Alcoholic Cirrhosis With Wenicke's

Document Type

Conference Proceeding

Publication Date

5-2025

Publication Title

American Journal of Respiratory and Critical Care Medicine

Abstract

Serum sodium is a key determinant of tonicity in states of low tonicity, the brain adapts by modifying solute transport to maintain normal cerebral volume. This is particularly relevant in patients with conditions like alcoholism, malnutrition, and liver failure. In such patients, rapid correction of low serum sodium can cause a sudden influx of free water into brain cells, leading to cerebral edema. A safe threshold for sodium correction is typically 5 to 8 mEq over 24 hours/4-8 mmol/day. Osmotic demyelination is often observed when serum sodium levels drop below 120 mEq/L. This case describes a patient who developed osmotic demyelination without severe hyponatremia with normal correction41-year-old female with past medical history of alcohol use disorder and subsequent acute liver failure presented with fatigue, dysarthria, tremors nystagmus, and ataxia, hypertensive urgency and sinus tachycardia.. Labs: Elevated direct bilirubin at 13.4, normal serum sodium (135 mmol/L), and non anion gap acidosis (bicarbonate 12 mmol/l).NCCT scan of the head was unremarkable. Patient was started on IV thiamine lorazepam and lactulose. An MRI later revealed osmotic demyelination in the pons. Patient had been discharged from the outside facility 2 days prior to presentation. On , her sodium was 121 mmol/L (2 weeks prior). Her sodium was corrected from 121 to 128 mEq/L over 24hours with 2.5 liters of 0.9% saline and 0.5 liters of lactated ringer’s solution. Despite supportive care, the patient’s condition worsened, and on day five, she developed loss of gag reflex and shortness of breath, requiring supplemental oxygen. A repeat MRI showed worsening pontine demyelination. The patient was started on an NG tube for nutrition and to reduce the risk of aspiration. After discussions with her family, she transitioned to inpatient hospice care and passed away about four weeks later. Osmotic demyelination typically presents 2 to 3 days after rapid correction. Our patient developed symptoms two weeks later despite the normal rate of correction. Her differential diagnosis at presentation included symptomatic hyponatremia from Acute liver failure, alcohol withdrawal, and possible Wernicke’s encephalopathy. Bilirubin elevation can alter the brain blood barrier; furthermore alcoholic neurodegeneration predisposes this cohort to further damage . For such patients, fluid management should be approached cautiously, aiming for a sodium correction threshold of 4 to 5 mEq/L over 24 hours, with frequent sodium monitoring every 2 hours.

Volume

211

First Page

A5721

Comments

American Thoracic Society (ATS) International Conference, May 16-21, 2025, San Francisco, CA

Last Page

A5721

DOI

10.1164/ajrccm.2025.211.Abstracts.A5721

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