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Cellular phone interference as a cause of acute epinephrine poisoning.
Hahn IH, Schnadower D, Dakin RJ, Nelson LS.
Publication Types:
PMID: 16126144 [PubMed - in process]
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Intentional self-poisoning with the chlorophenoxy herbicide 4-chloro-2-methylphenoxyacetic acid (MCPA).
Roberts DM, Seneviratne R, Mohammed F, Patel R, Senarathna L, Hittarage A, Buckley NA, Dawson AH, Eddleston M.
South Asian Clinical Toxicology Research Collaboration, Medical School, Australian National University, Acton, Australian Capital Territory, Australia. dmroberts@iprimus.com.au
STUDY OBJECTIVE: Data on poisoning with MCPA (4-chloro-2-methyl-phenoxyacetic acid) are limited to 6 case reports. Our objective is to describe outcomes from intentional self-poisoning with MCPA in a prospective case series of 181 patients presenting to hospitals in Sri Lanka. METHODS: Patient information was collected by on-site study physicians as part of an ongoing prospective cohort study of poisoned patients. Medical history, clinical details, and blood samples were obtained prospectively. RESULTS: Overall clinical toxicity was minimal in 85% of patients, including mild gastrointestinal symptoms in 44% of patients. More severe clinical signs of chlorophenoxy poisoning reported previously, such as rhabdomyolysis, renal dysfunction, and coma, also occurred but were uncommon. Eight patients died (4.4%). Most deaths occurred suddenly from cardiorespiratory arrest within 48 hours of poisoning; the pathophysiological mechanism of death was not apparent. The correlation between admission plasma MCPA concentration and clinical markers of severity of toxicity (physical signs, symptoms, and increased creatine kinase level) was poor. CONCLUSION: Intentional self-poisoning with MCPA generally causes mild toxicity, but cardiorespiratory arrest and death may occur. All patients should receive routine resuscitation and supportive care. It seems reasonable to correct acidosis and maintain an adequate urine output, but there is insufficient evidence to support other specific interventions. Our data do not support a clinical role for measurement of plasma MCPA in the acute management of poisoning, and insufficient data were available to fully examine the utility of measured electrolytes and creatine kinase levels.
PMID: 16126140 [PubMed - in process]
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A risk quantification instrument for acute acetaminophen overdose patients treated with N-acetylcysteine.
Sivilotti ML, Yarema MC, Juurlink DN, Good AM, Johnson DW.
Department of Emergency Medicine, Queen's University, Kingston, Ontario, Canada. sivilotm@meds.queensu.ca
STUDY OBJECTIVE: The risk of hepatotoxicity after acute acetaminophen overdose varies with timed serum acetaminophen concentration and delay to treatment. The ability to accurately predict hepatotoxicity is needed to reduce confusion about the optimal treatment regimen for individual patients and the effects of risk modifiers such as ethanol. We quantitatively estimate the risk of hepatotoxicity based on the degree and duration of pretreatment exposure to supratherapeutic concentrations of acetaminophen. METHODS: We examined all hospitalizations for acute acetaminophen overdose within a retrospective multicenter Canadian registry. We used a previously developed composite measure incorporating timed serum acetaminophen concentration and time to N-acetylcysteine treatment into a single parameter. We then modeled hepatotoxicity on this parameter, as well as age, sex, and ethanol use. Hepatotoxicity was defined as peak aminotransferase level of 1,000 IU/L or greater at 24 hours or longer. RESULTS: Of 1,270 admitted patients treated mostly with intravenous N-acetylcysteine for less than 24 hours, our model accurately identified the 94 patients who developed hepatotoxicity (discriminatory index 0.93). Hepatotoxicity occurred in none of the 313 patients (95% confidence interval [CI] 0% to 1.0%) above the traditional 150 mug/mL treatment line who were classified as low risk (<1%) using our instrument. After adjustment for severity of exposure, the risk of hepatotoxicity was considerably higher in the absence of coingested ethanol (median hepatotoxic dose 16.5 mmol/L x hour [95% CI 8.74 to 31.0 mmol/L x hour] versus 27.1 mmol/L x hour [95% CI 11.1 to 66.3 mmol/L x hour]), particularly among alcoholics (4.79 mmol/L x hour [95% CI 2.13 to 10.8 mmol/L x hour]). CONCLUSION: Our risk prediction instrument identifies a large group of low-risk patients for whom 20-hour intravenous N-acetylcysteine therapy is sufficient. Our results suggest that acute and chronic ethanol use dramatically influences acetaminophen toxicity. This work may facilitate the evaluation of individualized treatment strategies for higher-risk patients.
PMID: 16126138 [PubMed - in process]
 
Anaphylaxis.
Sheikh A, Walker S.
Division of Community Health Sciences, GP Section, University of Edinburgh, Edinburgh EH8 9DX. aziz.sheikh@ed.ac.uk
Publication Types:
PMID: 16081446 [PubMed - indexed for MEDLINE]
Managing insect sting allergy. The ins and outs of venom immunotherapy.
Graft DF.
Park Nicollet Clinic, Minneapolis, MN 55416, USA.
Insect sting allergy can lead to severe, even fatal, reactions in susceptible persons. Although self-injection epinephrine often terminates the reaction, it is not always effective. In this article, Dr Graft explores the use of venom immunotherapy (VIT) in selected patients in whom successful treatment can produce psychosocial as well as physiologic benefits.
PMID: 16106918 [PubMed - indexed for MEDLINE]
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