B52-30 Beyond the Bypass: Cardiac Arrest Following Weight Loss Surgery

Abstract Introduction Gastric bypass is a frequently seen intervention for morbidly obese patients who are unable to lose weight with conservative measures. Patients may experience short-bowel syndrome or dumping syndrome post-operatively, which manifests as nutrient malabsorption. This can lead to vitamin deficiencies and malnutrition, and metabolic derangements. Cardiac arrest is uncommonly seen after gastric bypass surgery, especially outside of the immediate postoperative period. We present a case of cardiac arrest due to malabsorptive syndrome resulting from a gastric bypass. Case Presentation A 41-year-old male with a significant past medical history of gastric bypass two years prior to admission found to be in ventricular fibrillation arrest outside along the beach. Return of spontaneous circulation (ROSC) was achieved en route to the hospital. Post-ROSC EKG showed normal sinus rhythm, flattened T-waves in leads I and V4-6, and prolonged QTc 544 ms. Labs showed hypokalemia (3.0 mmol/L) and severe high-anion gap metabolic acidosis (anion gap 31). Emergent cardiac catheterization revealed no obstructive coronary artery disease with an ejection fraction of 20%. His hypokalemia was aggressively repleted with over 240 mEq of potassium. Despite aggressive repletion, he would recurrently become mildly hypokalemic. The patient was discharged with continued potassium supplementation. Discussion Although the initial hypokalemia was mild, the severity was likely masked by the degree of the acidosis, as it is typically associated with hyperkalemia. There are certain scenarios hypokalemia can be seen in acidosis. With renal tubular acidosis or gastrointestinal losses (i.e. diarrhea), hypokalemia is frequently seen, but those present without an anion gap. In this case, his elevated anion gap suggests a different etiology. It is likely the acute component of this patient’s acidosis promoted extracellular shift of potassium, but he required over 240 mEq of repletion to normalize his potassium, suggesting the hypokalemia was more severe than how it presented. Hypokalemia can also be seen in chronic acidosis due to an upregulation in aldosterone secretion, thus promoting potassium secretion. However, this does not explain the severity of hypokalemia in this patient. It is also influenced by volume status and dietary intake. Given the prior gastric bypass and being in the heat and sun, there are multiple reasons as to why the patient’s hypokalemia became so critical. Conclusion Although frequently seen, potential complications after bariatric surgery can be grave if nutrition is not properly maintained. This case highlights the importance of monitoring and maintaining proper nutritional status in patients after bariatric surgery. This abstract is funded by: None