ABSTRACT
Adverse cardiovascular events comprise a large portion of the morbidity and mortality in drug overdose emergencies. Adverse cardiovascular events encountered by emergency physicians treating poisoned patients include myocardial injury, hemodynamic compromise with shock, tachydysrhythmias, and cardiac arrest. Early signs of toxin-induced cardiovascular failure include bradycardia, tachycardia, and specific ECG findings. Treatment of toxicologic tachycardia relies on rapid supportive care along with proper use of benzodiazepines for sedation. Treatment of toxicologic bradycardia consists of the use of isotonic fluids, atropine, calcium salts, and glucagon. High-dose insulin euglycemia should be used early in the course of suspected severe poisoning and intravenous lipid emulsion given to patients who suffer cardiac arrest.
Subject(s)
Adrenergic beta-Agonists/poisoning , Calcium Channel Agonists/poisoning , Cardiovascular Diseases/chemically induced , Drug Overdose/complications , Emergency Medical Services/methods , Poisoning/complications , Cardiovascular Diseases/therapy , Drug Overdose/therapy , Humans , Poisoning/therapy , United StatesABSTRACT
OBJECTIVE: To study clinical features, treatment and curative effects in children with acute clenbuterol poisoning, in order to provide a basis for early diagnosis and treatment. METHODS: Clinical data of 28 hospitalized children with acute clenbuterol poisoning in April 2011 were retrospectively studied. RESULTS: Of the 28 patients, there were 15 males and 13 females, aged 1 to 13 years (mean age 6.5±4.8 years). Vomiting, palpitations and limb shaking were found as main clinical manifestations in the patients. Main changes of blood biochemical included hypokalemia, lactic acidosis, hyperglycemia, hypsocreatinkinase. Snus tachycardia and S-T segment depression were observed on ECG. Patients' symptoms were gradually alleviated after 12-78 hours by use of beta blockers, potassium supplement, protecting the heart and other symptomatic and supportive treatment. Blood biochemical indexes were improved after 48 hours of admission. All of the patients were cured after 5 days. The symptoms of the patients do not longer occur during a follow up of half a month. CONCLUSIONS: Acute clenbuterol poisoning is characterized by vomiting, palpitations, limb shaking, hypokalemia, lactic acidosis and tachycardia in children. An early effective treatment of this disease can improve prognosis in children.
Subject(s)
Adrenergic beta-Agonists/poisoning , Clenbuterol/poisoning , Acute Disease , Adolescent , Child , Child, Preschool , Electrocardiography , Female , Humans , Infant , Male , Retrospective StudiesABSTRACT
OBJECTIVE: To report the clinical manifestations and analytical findings in an epidemic outbreak of acute food poisoning with clenbuterol. MATERIALS AND METHODS: The clinical manifestations, physical examination findings and results of complementary tests are reported of fifteen patients performed by veal liver contaminated with clenbuterol. The clinical course of patients at 72 hours is reported. A quantitative measurement of clenbuterol in urine specimens from patients and in a veal liver specimen was performed by high pressure liquid chromatography (HPLC). RESULTS: The male/female distribution of patients was 7/8 respectively, with age ranging from 6 to 44 years. Symptoms appeared after 30 minutes to 2 hours of having ingested veal liver in 93% of cases. Patients presented at the Emergency Department with tremors, palpitations, anxiety, malaise, nausea, and pruritus as the most common complaints. On physical examination tachycardia was noted in 100% of cases. The analytical data included mild hypokaliemia (66%) and leukocytosis (28%). Only one patient required hospital admission on account of an hypertensive crisis. After 72 hours, 67% of patients were asymptomatic. The remaining patients had mild symptoms which included headache, myalgia, asthenia and anorexia. Serum potassium values returned to normality (p < 0.05). Urine measurements of clenbuterol were positive for all analyzed cases (50 +/- 42 ng/ml). The concentration of clenbuterol in a veal liver sample was 500 ppb. CONCLUSION: Clenbuterol poisoning should be suspected when symptoms of adrenergic hyperstimulation occur after the ingestion of meal, usually liver. Common symptoms include tachycardia and mild hypopotasemia. Diagnosis is confirmed by quantitative measurement of clenbuterol in urine. Most patients improve spontaneously shortly afterwards.