SESSION TITLE: Medical Student/Resident Cardiovascular Disease Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Although digoxin use has declined, its per patient toxicity incidence perhaps has not. Digoxin toxicity should be considered early in the patient presenting with gastrointestinal symptoms as they are at risk for renal dysfunction that may worsen cardiac function. CASE PRESENTATION: A 77-year-old male with a history of diabetes mellitus, atrial fibrillation, coronary artery disease, and ischemic cardiomyopathy presented with nausea, vomiting, diarrhea, and generalized fatigue worsening for one month. Presenting vitals: BP 80/60 mmHg, HR 60 bpm, temp. 34.2 C and pulse ox 99%. The patient was fully alert and oriented. Physical exam was largely unremarkable with clear lung exam, non-tender abdomen, no peripheral edema, and cardiac exam showing regular rhythm at 60 bpm. Labs showed K of 6 mmol/L, BUN of 79 mg/dL, Cr of 4.40 mg/dL, LA of 8.0 mmol/L, BNP 42000 pg/mL, and a normal CBC. Medication review significant for digoxin, amiodarone, and metformin use. Subsequently, digoxin level was found to be 6.0mcg/L and EKG showed ventricular paced rhythm. Given digoxin toxicity with hyperkalemia, digibind was administered. Patient was also found to have refractory metabolic acidosis in the setting of metformin toxicity, and so emergent sustained low efficiency dialysis was initiated. Right heart catheterization demonstrated low output heart failure, cardiac index 1.8L/min on dobutamine and norepinephrine. This low output was likely related to his renal failure and medication toxicities. The patient was sustained on inotropic agents and his pacemaker rate was increased. The patient had an aortic balloon pump placed while he and his family considered LVAD. Ultimately, the patient sustained further clinical deterioration at which time he and his family chose to pursue comfort measures. DISCUSSION: Advance heart failure is a challenging insidious disease. This is compounded by the fact that its treatments carry significant toxicities. In our case, the patient had recently reinitiated his prior amiodarone prescription. Both the prior medication discontinuation and subsequent re-initiation were unknown to his medical providers. The increase in digoxin levels when administered with amiodarone has long been observed and described. Digoxin toxicity presents with gastrointestinal symptoms as seen in our patient. Prolonged poor intake placed him at risk for renal dysfunction and perhaps subsequent worsening of his cardiac function due to the bidirectional relationship of cardiorenal syndrome. Frequent monitoring of digoxin levels is necessary in this patient population. Medication toxicities, interactions, and reconciliation are critical pieces of information in the critically ill patient. CONCLUSIONS: Drug interactions, such as the increase in serum digoxin when co-administered with amiodarone, can lead to the worsening of renal function which in the advanced heart failure patient, portends a poor prognosis. Reference #1: Haynes K, Heitjan D, Kanetsky P, Hennessy S. Declining public health burden of digoxin toxicity from 1991 to 2004. Clin Pharmacol Ther 2008;84:90-4. 10.1038/sj.clpt.6100458 Reference #2: Koonlawee Nademanee, et al. Amiodarone-digoxin interaction: Clinical significance, time course of development, potential pharmacokinetic mechanisms and therapeutic implications, Journal of the American College of Cardiology, Volume 4, Issue 1, 1984, Pages 111-116, ISSN 0735-1097. Reference #3: Forman DE, Butler J, Wang Y, Abraham WT, O’Connor CM, Gottlieb SS, Loh E, Massie BM, Rich MW, Stevenson LW, Young JB, Krumholz HM: Incidence, predictors at admission, and impact of worsening renal function among patients hospitalized with heart failure. J Am Coll Cardiol 43: 61–67, 2004 DISCLOSURES: No relevant relationships by Dustin Slagle, source=Web Response