OSMOTIC DEMYELINATION SYNDROME - IS SODIUM THE SOLE CULPRIT? Anisha Memdani, Bharatsimha Toutireddy, Ausef Amir, Catalina R. Negulescu; Baton Rouge General, Baton Rouge, LA.
Introduction: Osmotic demyelination syndrome (ODS) involves the myelin in the oligodendrocyte- rich areas of the pons (central pontine myleinosis, CPM) and sometimes extrapontine areas. It is a rare and sometimes fatal diagnosis associated with rapid correction of serum sodium >12 mEq/ 24hrs. Case: A 33-year-old woman with systemic lupus erythematosus on belimumab and chronic alcohol use presented with nausea, vomiting, lower extremity weakness, and numbness with difficulty ambulating. Initial CT scan of the abdomen revealed suspected gastric outlet obstruction and pancreatitis. The blood work noted: sodium of 128mmol/L and potassium of 5.3mmol/L. The day prior sodium was 135mmol/L on another visit. Other significant laboratory findings were alcoholic ketoacidosis, thiamine, folate deficiency (2.2 ng/ml) and B12 deficiency (240 pg/ml), and subsequent progressive hypokalemia as low as 2.1 mmol/L. Clinically she was noted to have bilateral lower extremity areflexia, unsteady gait, progressive encephalopathy attributed to delirium tremens and Wernicke’s encephalopathy. Despite appropriate correction of the electrolytes/ketoacidosis and thiamine, B12 and folic acid replacement, the patient had minimal clinical improvement hence an lumbar puncture was obtained that revealed albumin-
cytologic dissociation. An MRI of the brain was found to be unremarkable. She was empirically treated for Guillain-Barre syndrome (Miller-Fischer variant) which might have been present on admission. About 1 week later the patient had worsening of her quadriparesis and developed dysarthria. A repeat MRI of the brain revealed findings consistent with CPM. Given her underlying autoimmune status a second lumbar puncture was performed, and the autoimmune workup was unremarkable. Concomitantly, given her underlying autoimmune condition, pulse dose steroids course was given. Reevaluation of her overall clinical course and laboratory pattern revealed appropriate sodium correction with concomitant potassium replacement. Discussion: Rapid correction of chronic hyponatremia is the most common cause of ODS. However, our case presents a much less talked about cause of ODS: multiple electrolyte abnormalities can likely contribute to similar osmotic disturbance-induced demyelination and apoptosis. Our case highlights the need to still suspect ODS despite appropriate sodium correction in chronic alcohol users and associated acid-base and electrolyte imbalances, especially hypokalemia.
DUAL MYCOBACTERIUM MARGERITENSE AND NOCARDIA INFECTION OF A CRT-D POCKET: DIAGNOSTIC AND THERAPEUTIC CHALLENGES. Rakin Areef, Apryl Cronley, Fouad Chaban; Ochsner Clinic Foundation, New Orleans, LA.
Introduction: Infections involving cardiac implantable electronic devices (CIEDs), particularly by non-tuberculous mycobacteria (NTM) and rare pathogens like Nocardia, are uncommon but can lead to significant diagnostic and therapeutic challenges. Case: A 77-year-old male with a history of atrial fibrillation, coronary artery disease, heart failure with reduced ejection fraction (EF 10-15%), and chronic kidney disease underwent a cardiac resynchronization therapy defibrillator (CRT-D) upgrade in April 2024 following device malfunction. Post-operatively, the patient developed a pocket
infection. Initial cultures identified Mycobacterium margeritense, an uncommon NTM pathogen, and treatment was started with ciprofloxacin. In early September, the patient was readmitted with worsening symptoms and evidence of infection. A subsequent wound culture revealed a co-infection with Nocardia species, however this resulted after the patient expired. Due to pericardial calcification and high-risk embedding of the device, complete device extraction was deferred. Despite ongoing antimicrobial therapy, the patient’s condition deteriorated, presenting with septic and cardiogenic shock requiring vasopressor and respiratory support. 30
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