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Electrocardiographic changes in loperamide toxicity: Case report and review of literature

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AbstractIntroductionLoperamide, an antidiarrheal agent, is a µ‐opioid receptor agonist increasingly abused to prevent opioid withdrawal or to produce euphoric effects. At supra‐therapeutic doses, loperamide can cause cardiac toxicity due to blockade of Na and IKr channels, resulting in wide QRS rhythms, severe bradycardia, prolonged QTc, polymorphic ventricular tachycardia, cardiac arrest, and death. There are limited data on the cardiotoxic effects of high dose loperamide.Methods and ResultsA case report of loperamide toxicity is presented and then added to a contemporary review of the literature. In total, the presentation and management of 36 cases of loperamide cardiotoxicity are summarized. The overall median daily dose (interquartile range) of loperamide was 200 (134‐400) mg. The median QRS duration was 160 (125‐170) ms. The median QTc duration was 620 (565‐701) ms. Ventricular tachycardia was experienced by 24/36 (67%) of patients, 20 of which were specified to be polymorphic. Treatment was supportive, providing advanced cardiopulmonary life support and aggressive electrolyte repletion. Isoproterenol infusion or overdrive pacing was employed in 19/36 (53%) of cases. The median time to electrocardiogram normalization or hospital discharge, whichever came first, was 5 (3.5‐10) days.ConclusionLoperamide overdose is a toxidrome that remains underrecognized, and in patients with unexplained cardiac arrhythmias, loperamide toxicity should be suspected. Prompt recognition is critical due to the delayed recovery and high risk for life‐threatening arrhythmias.
Title: Electrocardiographic changes in loperamide toxicity: Case report and review of literature
Description:
AbstractIntroductionLoperamide, an antidiarrheal agent, is a µ‐opioid receptor agonist increasingly abused to prevent opioid withdrawal or to produce euphoric effects.
At supra‐therapeutic doses, loperamide can cause cardiac toxicity due to blockade of Na and IKr channels, resulting in wide QRS rhythms, severe bradycardia, prolonged QTc, polymorphic ventricular tachycardia, cardiac arrest, and death.
There are limited data on the cardiotoxic effects of high dose loperamide.
Methods and ResultsA case report of loperamide toxicity is presented and then added to a contemporary review of the literature.
In total, the presentation and management of 36 cases of loperamide cardiotoxicity are summarized.
The overall median daily dose (interquartile range) of loperamide was 200 (134‐400) mg.
The median QRS duration was 160 (125‐170) ms.
The median QTc duration was 620 (565‐701) ms.
Ventricular tachycardia was experienced by 24/36 (67%) of patients, 20 of which were specified to be polymorphic.
Treatment was supportive, providing advanced cardiopulmonary life support and aggressive electrolyte repletion.
Isoproterenol infusion or overdrive pacing was employed in 19/36 (53%) of cases.
The median time to electrocardiogram normalization or hospital discharge, whichever came first, was 5 (3.
5‐10) days.
ConclusionLoperamide overdose is a toxidrome that remains underrecognized, and in patients with unexplained cardiac arrhythmias, loperamide toxicity should be suspected.
Prompt recognition is critical due to the delayed recovery and high risk for life‐threatening arrhythmias.

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