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• W4303984685 abstract "SESSION TITLE: Lessons Learned from Critical Care CasesSESSION TYPE: Rapid Fire Case ReportsPRESENTED ON: 10/18/2022 12:25 pm - 01:25 pmINTRODUCTION: Digoxin is one of the oldest, most widely used drugs in cardiology. Despite this, many clinicians today still have difficulty with its use and monitoring. Here we present a 66-year-old female with both liver and renal dysfunction, who presented with severe digoxin toxicity despite mildly elevated serum levels.CASE PRESENTATION: Patient is a 66-year-old female with a history of end stage renal disease on hemodialysis, decompensated cirrhosis who presented to our hospital for altered mental status. She was hospitalized 3 weeks prior to this presentation for upper gastrointestinal bleeding. It was complicated with atrial fibrillation with rapid ventricular response. She couldn't tolerate beta blocker, so digoxin 0.125 mg/day was initiated. Digoxin level was checked and found to be elevated to 2.3 ng/ml, higher than the reference range, 0.8 - 2.0 ng/ml. Digoxin was reduced to 0.0625 mg/day. However, following serum concentration increased to 3.7 ng/ml, so digoxin was discontinued. The level trended down to 3.1 ng/ml and she was discharged 3 days prior to this presentation. After discharge, she developed altered mental status. On arrival, she was confused with bradycardia and hypotension. ECG showed sagging ST segment, biphasic T wave and atrial fibrillation with slow ventricular response. Laboratory/imaging work ups, including cerebrospinal fluid analysis, were unrevealing. Digoxin level was checked, showing 2.2 ng/ml. Given ECG findings and no other evident etiologies, digoxin toxicity was diagnosed. She was intubated and dopamine infusion was initiated. After 4 vials of digoxin immune fab were given, bradycardia and hypotension improved. Dopamine was discontinued on day 2. On day 3 bradycardia recurred, requiring dopamine again. Bradycardia was resolved the following day. Mental status also improved, and she was extubated on day 6.DISCUSSION: This case underscores three important messages. Firstly, digoxin is mainly excreted by the kidney, but a small fraction of digoxin is excreted by the liver. [1] The use of digoxin in the setting of renal and liver dysfunction necessitates significant caution and monitoring. Secondly, digitalis toxicity may develop even within widely accepted therapeutic” range, 0.8 - 2.0 ng/ml. It is not widely recognized that the latest guidelines recommended the serum concentration should target lower value, 0.7 - 0.9 ng/ml. [2] Lastly, toxicity might re-develop as a rebound” toxicity after an initial response to digoxin-specific antibody fragments. This occurs about 2% of patients even after a full neutralizing dose. This usually develops 12-24 hours after treatment, however, can develop up to 10 days. [3]CONCLUSIONS: This highlights the importance of new understanding of a drug that has been used for the last century. Clinicians should target a lower serum digoxin level of 0.7 to 0.9, especially in the setting of kidney and liver failure.Reference #1: Jeong, H.J., S.H. Lee, and H.E. Kang, Changes in digoxin pharmacokinetics associated with hepatic P-glycoprotein upregulation in rats with non-alcoholic fatty liver disease. Fundam Clin Pharmacol, 2021. 35(6): p. 1100-1108.Reference #2: Lindenfeld, J., et al., HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail, 2010. 16(6): p. e1-194.Reference #3: Pincus, M., Management of digoxin toxicity. Australian prescriber, 2016. 39(1): p. 18-20.DISCLOSURES: No relevant relationships by Christian CastanedaNo relevant relationships by Koichi Keitoku SESSION TITLE: Lessons Learned from Critical Care Cases SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: Digoxin is one of the oldest, most widely used drugs in cardiology. Despite this, many clinicians today still have difficulty with its use and monitoring. Here we present a 66-year-old female with both liver and renal dysfunction, who presented with severe digoxin toxicity despite mildly elevated serum levels. CASE PRESENTATION: Patient is a 66-year-old female with a history of end stage renal disease on hemodialysis, decompensated cirrhosis who presented to our hospital for altered mental status. She was hospitalized 3 weeks prior to this presentation for upper gastrointestinal bleeding. It was complicated with atrial fibrillation with rapid ventricular response. She couldn't tolerate beta blocker, so digoxin 0.125 mg/day was initiated. Digoxin level was checked and found to be elevated to 2.3 ng/ml, higher than the reference range, 0.8 - 2.0 ng/ml. Digoxin was reduced to 0.0625 mg/day. However, following serum concentration increased to 3.7 ng/ml, so digoxin was discontinued. The level trended down to 3.1 ng/ml and she was discharged 3 days prior to this presentation. After discharge, she developed altered mental status. On arrival, she was confused with bradycardia and hypotension. ECG showed sagging ST segment, biphasic T wave and atrial fibrillation with slow ventricular response. Laboratory/imaging work ups, including cerebrospinal fluid analysis, were unrevealing. Digoxin level was checked, showing 2.2 ng/ml. Given ECG findings and no other evident etiologies, digoxin toxicity was diagnosed. She was intubated and dopamine infusion was initiated. After 4 vials of digoxin immune fab were given, bradycardia and hypotension improved. Dopamine was discontinued on day 2. On day 3 bradycardia recurred, requiring dopamine again. Bradycardia was resolved the following day. Mental status also improved, and she was extubated on day 6. DISCUSSION: This case underscores three important messages. Firstly, digoxin is mainly excreted by the kidney, but a small fraction of digoxin is excreted by the liver. [1] The use of digoxin in the setting of renal and liver dysfunction necessitates significant caution and monitoring. Secondly, digitalis toxicity may develop even within widely accepted therapeutic” range, 0.8 - 2.0 ng/ml. It is not widely recognized that the latest guidelines recommended the serum concentration should target lower value, 0.7 - 0.9 ng/ml. [2] Lastly, toxicity might re-develop as a rebound” toxicity after an initial response to digoxin-specific antibody fragments. This occurs about 2% of patients even after a full neutralizing dose. This usually develops 12-24 hours after treatment, however, can develop up to 10 days. [3] CONCLUSIONS: This highlights the importance of new understanding of a drug that has been used for the last century. Clinicians should target a lower serum digoxin level of 0.7 to 0.9, especially in the setting of kidney and liver failure. Reference #1: Jeong, H.J., S.H. Lee, and H.E. Kang, Changes in digoxin pharmacokinetics associated with hepatic P-glycoprotein upregulation in rats with non-alcoholic fatty liver disease. Fundam Clin Pharmacol, 2021. 35(6): p. 1100-1108. Reference #2: Lindenfeld, J., et al., HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail, 2010. 16(6): p. e1-194. Reference #3: Pincus, M., Management of digoxin toxicity. Australian prescriber, 2016. 39(1): p. 18-20. DISCLOSURES: No relevant relationships by Christian Castaneda No relevant relationships by Koichi Keitoku" @default.
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• W4303984685 title "THE DANGER OF DIGOXIN: TOXICITY WITHIN THE THERAPEUTIC” RANGE" @default.
• W4303984685 doi "https://doi.org/10.1016/j.chest.2022.08.874" @default.
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