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Ann Emerg Med 2002 Jul;40(1):73-8
California Poison Control System, San Diego Division, San Diego, CA, USA.
STUDY OBJECTIVE: We determine the incidence of clinically important bleeding in children with superwarfarin rodenticide ingestions not treated with gastrointestinal decontamination or prophylactic vitamin K. METHODS: We prospectively studied patients younger than 6 years of age who reported to our poison center with acute unintentional superwarfarin ingestions. Patients who received gastrointestinal decontamination or prophylactic vitamin K were excluded. Forty-eight- to 96-hour prothrombin time or international normalized ratio (INR) blood tests were recommended, and telephone contact was attempted at least 3 days after ingestion. RESULTS: A total of 595 consecutive patients were enrolled during the 16-month study period. Fifty patients were excluded: 8 who were known to have ingested 1 pellet or less; 25 who received activated charcoal; 15 who were treated with induced emesis; and 2 who received prophylactic vitamin K. The resulting study group contained 545 patients. Eighty-two patients were lost to follow-up. Follow-up was obtained for 463 patients, including 222 by telephone contact alone, 62 by 48- to 96-hour INR, and 179 by both methods. None of the patients had clinically important coagulopathy. Two patients had an INR of 1.5 or greater (1.5 and 1.8) without symptoms. Single nosebleeds were reported in another 2 patients with normal 48-hour INRs. Another child had a small amount of blood crusted in the nose with no other symptoms and no laboratory work available. One child with a normal 48-hour INR had blood-streaked stools that were thought to be caused by an anal fissure. CONCLUSION: Children with acute unintentional superwarfarin ingestions of less than 1 box may be managed without gastric decontamination or prophylactic vitamin K. Laboratory testing for coagulopathy should be reserved for cases involving clinically evident bleeding abnormalities.
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PMID: 12085076, UI: 22078954
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J Toxicol Clin Toxicol 2002;40(2):145-55
Vanderbilt University Medical Center, Nashville, Tennessee, USA. donna.seger@mcmail.vanderbilt.edu
The incidence of clonidine overdose is increasing, yet there is a paucity of new information regarding treatment options for clonidine toxicity. Reported treatment approaches vary widely, demonstrating the lack of science on which current treatment is based. Available research needs to be reassessed. Neurotransmitters, receptors, endogenous opioids, and baseline sympathetic tone determine the clinical response to clonidine as well as the potential response to drug therapy following clonidine overdose. This article reviews aspects of clonidine toxicity that need to be further investigated. Multicenter research trials will be required to evaluate new treatment options.
PMID: 12126186, UI: 22121189
J Toxicol Clin Toxicol 2002;40(2):129-35
Emergency Department, Hospital Clinic, Barcelona, Spain. omiro@clinic.ub.es
BACKGROUND: Previously used as a general anesthetic, gamma-hydroxybutyrate is now used as a recreational drug. Not surprisingly, an increasing number of acute overdose cases requiring emergency medical care have been reported and described, especially in the United States. OBJECTIVES: To determine the number and percentage of gamma-hydroxybutyrate overdoses over a 15-month period and to describe the clinical hallmarks and course of this new drug in overdose. METHODS: All toxicological emergencies, including those caused by illicit drug consumption, were recorded for 15 months in an urban public hospital emergency department. Accurate toxicological history was obtained from the patients and, if gamma-hydroxybutyrate was suspected, confirmation was performed by urine mass spectrometry. The study data were compared with data recorded in the same emergency department in 1989. RESULTS: The total number of toxicological emergencies attended in our emergency department have remained unchanged during the last decade, with a significant decrease in number of opiate overdoses and an increase in the number of cocaine, amphetamine, and gamma-hydroxybutyrate overdoses. During the study period, 104 gamma-hydroxybutyrate overdoses presented to the emergency department (3.1% of all toxicological emergencies), ranking second in illicit drugs requiring emergency consultation. The profile of a patient with gamma-hydroxybutyrate intoxication is well defined: a young individual (23 +/- 5 years), male (64%), emergency department presentation on weekends (90%), with simultaneous ethanol consumption (73%) and ingestion of additional illicit drugs (86%), decrease of consciousness being the main complaint in all cases [16% with Glasgow Coma Scale (GCS) = 3]. Complete recovery without sequelae occurred in all cases. CONCLUSION: Health authorities must be aware of the hazards of recreational gamma-hydroxybutyrate, and physicians must be cognizant of this recent cause of coma among youths presenting to the emergency departments.
PMID: 12126184, UI: 22121187
J Toxicol Clin Toxicol 2002;40(2):115-20
Branch of Medical Genetics, Istanbul Medical Faculty, Istanbul University, Turkey. sozturk@istanbul.edu.tr
OBJECTIVE: The object of this study was to investigate the genotoxic effect of acute overexposure to combustion products originating from coal or wood stoves in patients presenting with acute carbon monoxide intoxication. STUDY DESIGN: In a prospective study, we analyzed the frequency of sister chromatid exchange and the carboxyhemoglobin concentration in 20 consecutive patients without a history of smoking or drug use who had been treated in the Emergency Care Unit of Istanbul Medical Faculty due to acute carbon monoxide intoxication. All of these cases were domestic accidents due to dysfunctioning coal or wood stoves. The results were compared with a control group of 20 nonsmoking, nondrug-using healthy individuals matched for age, sex, and absence of other chemical exposure. RESULTS: The mean sister chromatid exchange frequency per metaphase was significantly higher in the study group compared to the control group: 8.11 +/- 2.39 vs. 6.33 +/- 1.60 (p = 0.008). We found that there was no positive correlation between the blood carboxyhemoglobin concentration and sister chromatid exchange frequency. CONCLUSIONS: These results suggest that acute exposure to combustion products of wood or coal is genotoxic to DNA. Potential causes of genotoxicity include known mutagenic compounds present in coal or wood smoke and ash, oxygen radicals formed during combustion, as well as hypoxic and reperfusion injury mechanisms initiated by carbon monoxide intoxication. Additional studies on separate carbon monoxide exposure from smoke and ash are needed to understand individual genotoxic contributions and mechanisms.
PMID: 12126182, UI: 22121185
Pediatr Emerg Care 2002 Apr;18(2):97-100
Missouri Regional Poison Center and Saint Louis University Division of Toxicology, St. Louis, Missouri 63117, USA. tominack@slu.edu
PMID: 11973502, UI: 21970181
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