Abstract Introduction Amlodipine, a dihydropyridine calcium channel blocker (CCB), is a commonly prescribed antihypertensive in the United States. At therapeutic doses, non-dihydropyridine CCBs preferentially target vascular smooth muscle L-type calcium channels. In an overdose, this effect manifests as lactic acidosis secondary to impaired mitochondrial activity and ATP hydrolysis, hyperglycemia due to blunted insulin release, and severe vasodilation leading to non-cardiogenic pulmonary edema. Additionally, the distinction between dihydropyridine and non-dihydropyridine diminishes at toxic doses, leading to cardiovascular dysfunction and refractory shock. Case A 61-year-old patient with history of type 2 diabetes, hypertension, and schizoaffective disorder presented with purulent penile drainage and hyperglycemia to the 800s. He was admitted to the ICU for septic shock on three vasopressors. The patient became progressively more hypotensive and bradycardic despite additional vasopressors and broad-spectrum antibiotics. Upon further questioning the patient admitted to intentionally ingesting a large quantity of amlodipine the night before in a suicide attempt. Inpatient toxicology was consulted. An IV insulin bolus of 1u/kg was administered followed by a continuous infusion of insulin at 0.5u/kg and dextrose-containing fluid. Calcium chloride pushes and a continuous infusion were titrated to a goal level of 1.5x normal. The max dose of vasopressors was liberalized. On day 2, vasopressor requirements increased with lactate in the 10s, urine output decreased, and patient was intubated for respiratory distress. Methylene blue was trialed without improvement. A point of care ultrasound demonstrated grossly preserved cardiac squeeze but reduced compared to that on admission. Continuous renal replacement therapy was initiated to remove volume after a failed diuretic challenge and was kept until day 9. All vasopressors were discontinued by day 10. Patient was extubated on day 13 and downgraded to med/surg on day 20. Importance Understanding the physiology of CCB toxicity is crucial to management. Volume must be tightly monitored given low functional cardiac reserve. High dose insulin acts as a pressor to induce myocardial uptake of glucose in the CCB-induced insulin-resistant state. Calcium chloride reverses the CCB-induced decreased myocardial contractility. Given that much of the literature recommends initiating Venoarterial Extracorporeal Membrane Oxygenation (VA-ECMO) due to the amlodipine’s negative inotropy, it was discussed as part of the medical decision-making. However, this patient was DNR, and the medical team did not believe VA-ECMO would align with his goals. This case shows that the management of CCB overdose without VA-ECMO is feasible, which is important given under-resourced medical centers may lack VA-ECMO capabilities. This abstract is funded by: None
Mittal et al. (Fri,) studied this question.