Background: Clenbuterol is a long-acting β 2-adrenergic agonist used outsidethe United States for treating pulmonary disorders and within the United States in veterinary medicine. Due to itspromotion of muscle growth and lipolysis ( β 3 effects), clenbuterol is illicitly exploited for livestock growth promotion and by bodybuilders. Recently, there have been reports of clenbuterol contamination of heroin and cocaine, resulting in prolonged tachycardia, hypokalemia, hypophosphatemia, and myocardial injury. We report a case of clenbuterol toxicity causing pulmonary edema and respiratory failure. Case report: The patient was a 33-year-old man who inhaled an unknown white powder and developed immediate onset of chest pain, palpitations, tremors, headache, nausea and vomiting. He presented to the emergency department, where the following initial vital signs were recorded: sinus tachycardia, 146 bpm; wide pulse pressure, 116/27 mm Hg; respiratory rate, 20/min; room air oxygen saturation, 99%. He was diaphoretic with a fine tremor and enlarged, reactive pupils. His electrocardiogram showed 1-millimeter ST depressions laterally. A working diagnosis of cocaine toxicity was made, and he was treated with 5 milligrams of intravenous lorazepam and 3 liters of normal saline without significant change in vital signs. Laboratory results were as follows: hypokalemia, 1.9 mmol/L; hypophosphatemia, 0.4 mg/dL; hyperglycemia, 230 mg/dL; lactate, 7.2 mmol/L; anion gap, 18. The patient was admitted to the intensive care unit, and treated with benzodiazepines and haloperidol for agitation, chest pain, and persistent tachycardia. Six hours after presentation, he desaturated to 64% on 100% oxygen. He was intubated for respiratory failure and CXR showed bilateral pulmonary edema. Ultrasound revealed bilateral oculated pleural effusions; creatinine kinase, 8880 U/L (normal rate, 25-185 U/L); creatinine kinase myocardial band, 57 ng/mL (normal rate, <5 ng/mL); troponin I, 1.18 ng/mL (normal rate, <0.4 ng/mL). He was extubated on hospital day 4 and discharged 9 days after initial presentation. His toxicology screen was negative for cocaine. His serum and urine analysis confirmed the presence of clenbuterol, at 6 and 874 ng/mL, respectively. Conclusion: Pulmonaryedema is a known complication of intravenous β 2-adrenergic agonists with a reported incidence of 5% in the obstetrics literature. The etiology is unknown but likely multifactorial, and can include cardiogenic mechanisms such as fluid overload and catecholamine-induced myocardial necrosis, and noncardiogenic mechanisms such as direct toxicity and increased pulmonary vessel permeability. This is the first documented case of pulmonary edema after inhalational β 2-adrenergic agonist exposure. Based on the recent epidemic of clenbuterol exposure, clinicians should be aware of the possibility of pulmonary edema and consequent respiratory failure.
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