A Survival Case in a Severe Amlodipine Intoxication

Calcium channel blockers (CCBs) are prescribed in a wide variety of cardiovascular conditions. Nevertheless, they remain a major cause of cardiovascular drug overdose that often leads to a lethal outcome. We report the case of an intoxication with amlodipine, which caused severe hypotension, in a young woman. The patient was initially treated with fluids, calcium gluconate, and Dobutamine without effect. She then received hyperinsulinemia euglycemia therapy. A rise in blood pressure (BP) was observed two hours after insulin was started. The next day, the insulin infusion was stopped and seven days later the patient was discharged from the hospital after psychiatric consultation. The positive inotropic effect of insulin therapy in our patient supports previous findings that suggest its use as a first-line therapy in the management of CCBs overdose. 1. Introduction Calcium channel blockers (CCBs) are the first cause of cardiovascular drug overdose death [1]. In the 28th Annual Report of the American Association of Poison Control Centers, cardiovascular drugs caused 128 cases of fatalities with 24 deaths (18.75%) due to amlodipine [2]. Amlodipine is a dihydropyridine calcium channel blocking agent used in the treatment of essential hypertension and angina pectoris. It is prescribed with a daily dose of 5–10？mg. Unlike other calcium channel blockers, amlodipine has a very low metabolic clearance with the advantage of using a once-daily dosage to maintain a near-constant plasma concentration [3]. There are several cases of amlodipine overdoses reported with several of them having a lethal outcome. We report a survival case in a severe amlodipine intoxication. 2. Case Report A 27-year-old woman with no known illnesses or history of psychiatric disorders was admitted approximately 6 hours after attempting suicide by ingesting 150？mg of amlodipine. She was newly married and had a conjugal conflict. On admission, the patient was conscious but lethargic with cold extremities. Her blood pressure was 75/49？mmHg and the pulse rate was 105？bpm. She received gastric lavage and still complained of nausea. The patient was started on intravenous fluids and transferred to the intensive care unit. On physical examination, the patient was slightly lethargic and had the following vital signs: systolic blood pressure, 80？mmHg; pulse, 125？bpm; respiratory rate, 26 breaths/min; and temperature, 36.5°C, pulse oximetry displayed 98% oxygen saturation under oxygen supplement. The head and neck exams were unremarkable. The cardiac examination found normal heart sounds without any