Abstract:Amlodipine, a dihydropyridine calcium channel blocker (CCB), is commonly prescribed for hypertension and anginal chest pain. An overdose of this medication can result in life-threatening complications such as vasodilatory shock and pulmonary edema. Noncardiogenic pulmonary edema in this setting is rare and not well understood. We report the case of a 57-year-old female with a complex medical history, including diffuse large B-cell lymphoma (DLBCL) in remission, asthma, and depression, who presented after ingesting approximately 87 tablets (870 mg) of amlodipine in a suicide attempt. The patient developed distributive shock requiring vasopressor support and acute hypoxic respiratory failure due to noncardiogenic pulmonary edema requiring intubation and mechanical ventilation and \ intensive care unit (ICU) admission. Her course was complicated by prolonged mechanical ventilation and ventilator-associated pneumonia (VAP), acute kidney injury (AKI), and metabolic derangements. With aggressive supportive therapy, including vasopressors, diuresis, antibiotics, and mechanical ventilation, the patient made a full recovery. This case highlights a rare but severe manifestation of amlodipine toxicity with noncardiogenic pulmonary edema requiring intubation. Early recognition and multidisciplinary management are critical to survival.Introduction:Calcium channel blocker (CCB) toxicity is a potentially fatal condition that requires prompt identification and aggressive management. CCBs are classified into two broad categories: non-dihydropyridines and dihydropyridines. The latter, including amlodipine, predominantly cause peripheral vasodilation and are less likely to affect myocardial conduction and contractility than non-dihydropyridines such as verapamil or diltiazem(1,2). Amlodipine has a prolonged half-life and a high affinity for vascular smooth muscle, which makes overdose particularly dangerous due to the sustained vasodilatory effects that can lead to significant hypotension and shock(3).While CCB overdose is mostly characterized by hypotension and bradycardia, complications like pulmonary edema, arrhythmias, and even multi-organ failure can also occur(4). Noncardiogenic pulmonary edema, in particular, is an uncommon but serious manifestation that can mimic acute respiratory distress syndrome (ARDS) in critically ill patients(5). The pathophysiology behind noncardiogenic pulmonary edema in amlodipine overdose remains unclear, but it is thought to result from increased pulmonary capillary pressure and endothelial dysfunction due to vasodilation(6). In this case report, we describe a severe overdose of amlodipine leading to profound vasodilatory shock, respiratory failure, and noncardiogenic pulmonary edema requiring ICU admission, mechanical ventilation, and a prolonged recovery period. This case underscores the need for early recognition and prompt management to prevent life-threatening complications in patients presenting with CCB overdose.Case Report A 57-year-old woman with a medical history significant for asthma, thoracic aortic aneurysm, diverticulitis, recently treated diffuse large B-cell lymphoma (DLBCL) in remission, major depressive disorder, and chronic tobacco abuse with 41 pack years was brought to the emergency department (ED) following a suicide attempt. The patient reportedly ingested approximately 85-87 tablets of her husband’s 10 mg amlodipine with suicidal intent. Additionally, she had made two suicide attempts via self-inflicted superficial knife wounds to her wrist within the preceding 24 hours, which were treated by her husband with bandages. She stated that she was started on fluoxetine about a week ago, after which she started developing suicidal ideations. On presentation, her BP was 82/48mm Hg, and her HR was 112 bpm. Initial laboratory evaluation revealed a leukocytosis of 16,000/µL, a bicarbonate level of 20 mmol/L, and a mildly elevated troponin of 17 ng/L. Presenting Chest Xray demonstrated prominent interstitial markings suggestive of pulmonary edema (figure 1). Serum toxicology screening was negative for acetaminophen, aspirin, and alcohol. Urine toxicology was negative for amphetamines, barbiturates, benzodiazepines, cannabinoids, cocaine, fentanyl, methadone, opiates, oxycodone, and phencyclidine. A chest radiograph demonstrated mild pulmonary vascular congestion. Electrocardiogram (ECG) showed sinus tachycardia with a normal axis, intervals, and ST-T segments, but poor R-wave progression. Her serum acetaminophen and aspirin levels for coingestants were negative, as was her urine toxicology.Poison Control, contacted promptly, recommended a single dose of activated charcoal and whole bowel irrigation, trending fingerstick blood glucose every hour to monitor for hyperglycemia, and supportive care with intravenous (IV) fluid resuscitation, calcium gluconate administration, and vasopressor support as needed. She was immediately started on aggressive IV fluid resuscitation and calcium gluconate. Refractory hypotension unresponsive to fluid therapy necessitated the initiation of a norepinephrine infusion. Due to ongoing hemodynamic instability, she was admitted to the intensive care unit (ICU) for escalation of care. The patient reluctantly agreed to nasogastric tube placement for the administration of polyethylene glycol and consented to ingest activated charcoal, both of which she had initially refused. She was started on management for amlodipine-induced distributive shock with non-cardiogenic pulmonary edema secondary to calcium channel blocker overdose.
