Clinical toxicology : the official journal of the American Academy of Clinical Toxicology and European Association of Poisons Centres and Clinical Toxicologists
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Clin Toxicol (Phila) · Jan 2006
Practice GuidelineCamphor Poisoning: an evidence-based practice guideline for out-of-hospital management.
A review of national poison center data from 1990 through 2003 showed approximately 10,000 annual ingestion exposures to camphor-containing products. A guideline that determines the threshold dose for emergency department referral and need for pre-hospital decontamination could potentially avoid unnecessary emergency department visits, reduce health care costs, optimize patient outcome, and reduce life disruption for patients and caregivers. An evidence-based expert consensus process was used to create the guideline. ⋯ A benzodiazepine should be used to control convulsions (Grade C). 4) Patients who have been exposed to a camphor product and who remain asymptomatic after 4 hours can be safely observed at home (Grade C). 5) Induction of emesis with ipecac syrup should not be performed in patients who have ingested camphor products (Grade C). 6) Activated charcoal administration should not be used for the ingestion of camphor products. However, it could be considered if there are other ingredients in the product that are effectively adsorbed by activated charcoal or if other substances have been co-ingested. (Grade C). 7) For asymptomatic patients with topical exposures to camphor products, the skin should be thoroughly washed with soap and water and the patient can be observed at home for development of symptoms (Grade C). 8) For patients with topical splash exposures of camphor to the eye(s), the eye(s) should be irrigated in accordance with usual poison center procedures and that referral take place based on the presence and severity of symptoms (Grade D). 9) Patients with camphor inhalation exposures should be moved to a fresh air environment and referred for medical care based on the presence and severity of symptoms. It is unlikely that symptoms will progress once the patient is removed from the exposure environment (Grade D).
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Clin Toxicol (Phila) · Jan 2006
Randomized Controlled TrialSafety of hydroxocobalamin in healthy volunteers in a randomized, placebo-controlled study.
This randomized, double-blind, placebo-controlled, ascending-dose study was conducted in healthy volunteers to evaluate the safety of the investigational cyanide antidote hydroxocobalamin. ⋯ Timely intervention for acute cyanide poisoning could entail administration of an antidote in the prehospital setting based on a presumptive diagnosis. Results of this placebo-controlled study in healthy volunteers corroborate previous studies and French postmarketing experience in cyanide-exposed patients in suggesting that the safety profile of hydroxocobalamin is consistent with prehospital or hospital use.
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Clin Toxicol (Phila) · Jan 2006
Case ReportsMonitoring of verapamil enantiomers concentration in overdose.
A 52-year-old woman with a history of depression and personality disorders, hypertension, coronary disease and asthma was admitted to the Department of Clinical Toxicology after taking 60 tablets of Staveran (immediate release verapamil), and 4 tablets of acetaminophen. One and a half hours after ingestion her condition was critical. She required endotracheal intubation and artificial respiration. ⋯ Terminal elimination half-lives were 18.7 (21.3) and 17.0 (18.5) hours, respectively, for R-(+)- and S-(-)-verapamil. Monitoring of verapamil enantiomers concentrations in serum indicated a higher concentration of the less active form and slightly faster elimination of the more active enantiomer. The data-support a stereoselective difference between first pass clearance and later systemic clearance of verapamil, when taken in overdose.
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Clin Toxicol (Phila) · Jan 2006
Case ReportsThe role of calcium oxalate crystal deposition in cerebral vessels during ethylene glycol poisoning.
Ethylene glycol (EG) poisoning can lead to serious morbidity or death, which occurs following conversion of ethylene glycol to toxic metabolites. These metabolites affect multiple organ/systems leading to metabolic acidosis, cardiopulmonary depression, acute renal failure and central nervous system deficits. ⋯ We describe a case of fatal EG poisoning in which the development of rapid cerebral edema was documented by CT scan and was accompanied by definitive evidence of birefringent crystals within walls of CNS blood vessels, with associated inflammation and edema. This case and others in the literature suggest that cerebral edema, and perhaps injury to other organs, could result from oxalate crystal deposition in small blood vessels in the brain and other organs.
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Clin Toxicol (Phila) · Jan 2006
Comparative StudyA comparison of vasopressin and glucagon in beta-blocker induced toxicity.
We compared the efficacy of vasopressin and glucagon in a porcine model of beta-blocker toxicity. Our primary outcome was survival over 4 hours. ⋯ In this beta-blocker toxicity model, there were no differences in the survival curves between vasopressin- and glucagon-treated pigs during a 4-hour analysis period. No overall differences were noted in MAP, systolic BP, CO, HR, pH, or glucose levels, although vasopressin treatment yielded higher MAP and systolic BP early in resuscitation.