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Introduction Loperamide, 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 Results A 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. Conclusion Loperamide 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.

A woman in her 40s with a medical history of infective endocarditis and hepatitis C secondary to ongoing intravenous drug use presented to the emergency department with severe back pain and evidence of vertebral osteomyelitis/diskitis. She was hospitalized and treated for Staphylococcus aureus bacteremia. Transesophageal echocardiography findings revealed pulmonic valve vegetations and severe tricuspid valve regurgitation secondary to a flail leaflet. She underwent 6 weeks of intravenous antibiotic treatment and subsequent tricuspid valve replacement with a 29-mm bioprosthetic Carpentier-Edwards valve complicated by transient third-degree heart block. Two days after pacemaker placement, she had episodes of light-headednessandchestpainwithheartratesbetween150and190beats per minute. Her blood pressure was 94/60 mm Hg. The electrocardiogram during tachycardia is presented in Figure 1.Question: What is the rhythm demonstrated on the electrocardiogram? InterpretationThe P waves are upright in leads II, III, and aVF, suggesting an origin in the sinus node with a rate of 96 beats per minute. Grouped beating is apparent, with 1 P wave producing 2 QRS complexes, giving rise to the regularly irregular rhythm. This pattern is diagnostic of dual atrioventricular (AV) nonreentrant tachycardia.

Background. In previous reports with a majority of Caucasian patients, peritoneal dialysis (PD) before kidney transplantation has been associated with poor outcomes and higher rates of graft thrombosis and infectious complications than hemodialysis (HD). We report our experience on the outcomes of prerenal transplant peritoneal dialysis in predominantly (73%) African American patient population. Methods. A retrospective data analysis of 401 kidney transplants performed at our center from 2000 to 2006 was performed. Adult recipients with at least three months of pretransplant HD or PD were included. Results. There were 339 patients on HD and 62 patients on PD. There was no difference in graft (P = 0.51) and patient survival (P = 0.52) at 1, 3, and 5-years. Patients on HD were more likely to experience delayed graft function than PD (38.8% versus 17.7%, P < 0.005). There was no difference in the incidence of vascular thrombosis or posttransplant infectious complications. When only the African American patients in the two groups were compared, there were no differences in graft or patient survival. Conclusions. Pretransplant peritoneal dialysis is associated with excellent patient and renal allograft outcomes in African Americans and does not predispose them to an increased risk of infectious or thrombotic complications.

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