Journal of toxicology. Clinical toxicology
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J. Toxicol. Clin. Toxicol. · Jan 2001
Epidemiology of acute carbon monoxide poisoning in a Spanish region.
In Spain, as in most of the world, the incidence of acute carbon monoxide poisoning is probably underestimated. ⋯ Compared with previous Spanish series or with the antecedent year, acute carbon monoxide poisoning has a high prevalence in our region. Two factors appear to be essential to the accurate diagnosis of acute carbon monoxide poisoning: 1) the ability of emergency room physicians to recognize the clinical symptoms of carbon monoxide poisoning and 2) access to a carbon monoxide-oximeter.
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J. Toxicol. Clin. Toxicol. · Jan 2001
Case ReportsClenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels.
Clenbuterol is a long acting beta2-adrenergic agonist used in the treatment of pulmonary disorders. Acute clenbuterol toxicity resembles that of other beta2-adrenergic agonists. Most previously reported cases of clenbuterol toxicity describe patients who ate livestock illicitly treated with clenbuterol. ⋯ We report a case of human clenbuterol toxicity confirmed and correlated with qualitative and quantitative serum clenbuterol assays. This poisoned patient, a 28-year-old woman, developed sustained sinus tachycardia at 140/min, hypokalemia (2.4 mEq/L, 2.4 mmol/L), hypophosphatemia (0.9 mg/dL, 0.29 mmol/L), and hypomagnesemia (1.52 mg/dL, 0.76 mmol/L) after ingesting a reportedly small quantity of clenbuterol. The patient received repeated doses of metoprolol to treat her cardiovascular stimulation and potassium chloride to treat her hypokalemia. She remained symptomatic for more than 20 hours after the ingestion. Analysis by enzyme-linked immunosorbent assay and liquid chromatography/mass spectrometry revealed a serum clenbuterol concentration of 2.93 mcg/L 3 hours after the ingestion and an undetectable serum concentration 20 hours after ingestion. It is noteworthy that at a serum concentration below the limit of detection by liquid chromatography/mass spectrometry, the patient remained symptomatic. Acute clenbuterol toxicity is rarely reported following illicit use in humans, and this is the first such case to provide confirmatory toxicological analysis.
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J. Toxicol. Clin. Toxicol. · Jan 2001
Case ReportsCardiac damage in pediatric carbon monoxide poisoning.
Cardiovascular disorders including myocardial ischemia and heart failure have been described in both laboratory animals and humans following carbon monoxide poisoning. Carbon monoxide cardiotoxicity may be clinically occult and often remains undiagnosed because of the lack of overt symptoms and specific ischemic changes in the electrocardiogram. Routine myocardial necrosis markers have low diagnostic efficiency, particularly in patients with concomitant skeletal muscle necrosis or multiple organ failure complicating carbon monoxide poisoning. Carbon monoxide-induced cardiotoxicity has been investigated rarely in children. ⋯ This case report supports that a prolonged carbon monoxide exposure can cause cardiac damage in children even in the absence of specific symptoms, cerebral failure and high carboxyhemoglobin concentrations.
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J. Toxicol. Clin. Toxicol. · Jan 2001
Ethylene glycol toxicity: the role of serum glycolic acid in hemodialysis.
To correlate serum glycolic acid levels with clinical severity and outcome in ethylene glycol poisoning and to determine if glycolic acid levels are predictive of renal failure and the need for hemodialysis. ⋯ We propose glycolic acid > 8 mmol/L as a criterion for the initiation of hemodialysis in ethylene glycol ingestion. Patients with glycolic acid < 8 mmol/L probably do not need dialysis, regardless of the ethylene glycol concentration, when metabolism of ethylene glycol is therapeutically inhibited. In the absence of glycolic acid values, an anion gap > 20 mmol/L or pH < 7.30 predicts acute renal failure.
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Cardiac dysfunction including arrhythmias and myocardial ischemia have often been reported in carbon monoxide poisoning; scattered punctiform hemorrhages throughout the heart have been documented in autopsy samples. An appropriate diagnostic approach is crucial to assess carbon monoxide cardiac damage. This evaluation may be confounded by several factors, including the absence of overt symptoms and of specific ischemic changes in the electrocardiogram. ⋯ These investigations, as well as others performed in vitro, provide support for a direct action of carbon monoxide on the heart, in addition to systemic hypoxia produced by carboxyhemoglobin formation. This review focuses on the diagnostic aspects of carbon monoxide cardiotoxicity. Experimental results obtained in animals and in vitro models are also discussed.