A Case of Multidrug Intoxication Including Calcium Channel Blocker Treated with Plasmapheresis

Introduction: Amlodipine, a dihydropyridine calcium channel blocker (CCB), has a large volume of distribution and is primarily hepatically metabolized with an extended half-life. Despite amlodipine being highly protein bound, there is a paucity of evidence for the potential role of plasmapheresis (PLEX) in toxicity management. We present an overdose case with refractory shock necessitating both ECMO and PLEX treatment. Case Description: A 47 year old male with HTN, DMII, prostate cancer, gout, and PTSD presented following an intentional overdose of 900mg of amlodipine and a large quantity of an unknown medication, reportedly either triamterene-hydrochlorothiazide or amitriptyline. He presented with profound distributive shock and acute hypoxemic respiratory requiring several vasopressors and eventually intubation. Labs were notable for potassium 1.7, phosphorous <0.7, bicarb 9, Cr 2.32, glucose 597, anion gap 18, lactic acid 6.6 (peaked at 15.3), AST 57, ALT 71, WBC 29.4, VBG 7.26/30/40/13, CPK 6718, troponin 0.33 (peaked at 1.59). EKG demonstrated anterolateral ST depressions but no evidence of QT prolongation and TTE without wall motion abnormalities and EF >70%. He was seen by toxicology and started on insulin, glucagon, calcium chloride, sodium bicarb, lipid, and methylene blue infusions. In addition to electrolyte supplementation, he was started on VA-ECMO and underwent one session of PLEX followed by CRRT given persistent oliguric AKI and severe metabolic derangements. His course was further complicated by lower limb ischemia and ARDS, and the family elected for comfort measures. Discussion: Although dihydropiridine CCBs have affinity for the L-type calcium channels within the vascular smooth muscle, this pharmacological selectivity can be altered in the setting of toxicity. In addition to the profound cardiovascular repercussions, CCB also inhibit beta islet cells, leading to hyperglycemia. This finding has been described to associate with the severity of the intoxication. Conventional treatment includes hemodynamic support and calcium administration. Given CCBs are highly protein bound, hemodialysis is not recommended, but there may be some utility in PLEX in select cases. Previous case studies have demonstrated a reduction in amlodipine plasma concentrations of approximately 36%. In the setting of profound CCB overdose and associated vasoplegia, PLEX should be considered.