OSMOTIC CENTRAL PONTINE DEMYELINATION SYNDROME IN A EUNATREMIC ELDERLY MAN Y Zhang BS 1 , Y Yang MD 2 1 Department of Internal Medicine, Tulane University School of Medicine, New Orleans, LA 2 Department of Internal Medicine, Fudan University School of Medicine Affiliated Hospital, Shanghai, China CASE:
A 76-year-old male with hypertension, type II diabetes mellitus, and transient ischemia attack presents with cough, fatigue, and headache for four days. A chest radiograph revealed a right middle lobar opacity with concern for community-acquired pneumonia (CAP). Intravenous antibiotics were started for CAP and the patient was admitted for monitoring. Complete blood count (CBC) and comprehensive metabolic panel (CMP) were within normal limits, showing a sodium of 136mmol/L and a creatinine of 0.74 mg/dL. On hospital day five, creatinine was found to be 1.12 mg/dL and 1 liter of normal saline was given as bolus to address prerenal acute kidney injury (AKI). Over the next two days, an additional 2 liters of normal saline was administered, which resulted in a return of creatinine to baseline. Upon finishing antibiotics on hospital day seven, the patient’s CAP symptoms resolved, and he was discharged to home. Two weeks later, the patient returned with his wife, who reported that he was more somnolent than usual and was slower to react. On presentation, the patient was alert and oriented but visibly fatigued. He denied dysarthria, dysphagia, or paresis. CBC and CMP were unremarkable and consistent with baseline, showing a sodium of 138mmol/L. Magnetic Resonance Imaging of the brain showed hyper densities and features consistent with mild central pontine myelinolysis. Lowering serum sodium was not attempted due to prolonged duration since symptom onset. The patient was subsequently discharged with instructions to follow-up with neurology. DISCUSSION: Osmotic Demyelination Syndrome (ODS) classically occurs due to rapid over-correction of serum sodium by more than 8 mEq/L over a 24-hour period in the setting of brain adaptation to hyponatremia. Brain hypoxia and diabetes mellitus has also been posited as risk factors for ODS, although the mechanisms are still under investigation. In this case, despite being eunatremic, a patient with a history of T2DM and TIA received intravenous fluid boluses during his hospital course and developed ODS. A complex interplay of these risk factors may have ultimately resulted in this unorthodox case of eunatremic ODS. Clinicians should carefully consider the possibility of ODS when replacing volume or electrolytes in high- risk patients.
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