Abstract: FR-PO699
Overcorrection of Severe Hyponatremia in a Chronic Alcoholism Patient: A Case Report of Osmotic Demyelination Syndrome
Session Information
- Electrolytes and Cancer Trainee Case Reports
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid and Electrolytes: Clinical
Authors
- Ratanasrimetha, Praveen, Texas Tech University Health Sciences Center, Lubbock, Texas, United States
- Khampalikit, Inthira, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, Thailand
- Nugent, Kenneth, TTUHSC, Lubbock, Texas, United States
Introduction
Patient with chronic alcoholism can have chronic hyponatremia from multiple mechanisms. Both chronic alcoholism and severe hyponatremia predispose patient to the osmotic demyelination syndrome. Rapid correction of serum sodium can lead to severe neurological damage.
Case Description
45-year-old man with chronic alcoholism presented with confusion, generalized weakness, nausea, and vomiting for 3 days. He had history of heavy alcohol drinking for 3 years. Initial labs showed serum sodium level of 99 mmol/L. He was given intravenous 3% NaCl of the rate of 30 ml/hr to correct hyponatremia. Three hours later lab result showed a sodium level of 113 mmol/L. The patient was more lethargic and was found to have anisocoria. CT head showed diffuse atrophy but no acute abnormality. FLAIR MRI showed hyperintensity of supratentorial white matter, likely due to mild chronic microangiopathy. He was given intravenous 5%Dextrose at 100 ml/hr for overcorrection of hyponatremia. Later in hospital course he was more alert. His sodium level later increased to 127 mmol/L over the next 4 days. Patient was discharged to the nursing facility. He presented to hospital again with dysphagia, generalized weakness and spastic quadriparesis. His sodium level is 134 mmol/L. MRI showed abnormal restricted diffusion in the pons and bilateral thalami. There was subtle abnormal enhancement in the abnormal area in the pons which suggested osmotic demyelination syndrome.
Discussion
Patients who are high-risk for osmotic demyelination syndrome should raise awareness when correcting hyponatremia. Rapid sodium correction in this group of patients may lead to deterioration of neurological status due to neuronal shrinkage. The rate of sodium correction should not exceed 6-8 mEq/L in 24 hours period. Clinical manifestations of osmotic demyelination syndrome includes lethargy, dysarthria, dysphagia and seizure. Patients usually presented 2-6 days after correction. Our patient developed symptoms during the next 8 days. Even though it was later than the average onset, the risk factors and his symptoms are typical. MRI may not become positive until four weeks after onset. If the initial MRI is negative, it does not exclude osmotic demyelination syndrome.