Critical care explorations · 2026
Severe Diltiazem Poisoning Managed With CytoSorb Hemoadsorption and Supportive Therapies: A Case Report.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Cox Juul M, Verwaaijen Julia A M, Hendriks Ruben M F, Smeets Dorien, van Rijswijk Suzanne, Bosch Tessa M
Аннотация
BACKGROUND: Severe intoxication with nondihydropyridine calcium channel blockers, such as diltiazem, is associated with high morbidity and mortality. Evidence supporting extracorporeal treatment strategies remains limited. This case integrates serial toxicokinetic measurements with adjunctive hemoadsorption in sustained-release diltiazem poisoning.
CASE SUMMARY: A 73-year-old man presented with coma, complete atrioventricular block, refractory hypotension, and severe lactic acidosis. Despite optimized supportive therapy including vasopressors, calcium supplementation, hyperinsulinemic-euglycemic therapy, and continuous renal replacement therapy, he remained hemodynamically unstable. CytoSorb hemoadsorption was initiated 6 hours after ICU admission. Shortly thereafter, sinus rhythm was restored, serum lactate rapidly declined, and vasopressor and insulin requirements were progressively reduced, allowing discontinuation of extracorporeal support. The patient recovered and was discharged home.
CONCLUSIONS: Retrospective analysis demonstrated elevated diltiazem concentrations with delayed, capacity-limited elimination. This case supports considering hemoadsorption in unstable patients with severe diltiazem poisoning despite conventional measures and highlights the need for systematic pharmacokinetic evaluation in future studies.
CASE SUMMARY: A 73-year-old man presented with coma, complete atrioventricular block, refractory hypotension, and severe lactic acidosis. Despite optimized supportive therapy including vasopressors, calcium supplementation, hyperinsulinemic-euglycemic therapy, and continuous renal replacement therapy, he remained hemodynamically unstable. CytoSorb hemoadsorption was initiated 6 hours after ICU admission. Shortly thereafter, sinus rhythm was restored, serum lactate rapidly declined, and vasopressor and insulin requirements were progressively reduced, allowing discontinuation of extracorporeal support. The patient recovered and was discharged home.
CONCLUSIONS: Retrospective analysis demonstrated elevated diltiazem concentrations with delayed, capacity-limited elimination. This case supports considering hemoadsorption in unstable patients with severe diltiazem poisoning despite conventional measures and highlights the need for systematic pharmacokinetic evaluation in future studies.