The management of methanol poisoning includes standard supportive care, the correction of metabolic acidosis, the administration of folinic acid, the provision of an antidote to inhibit the metabolism of methanol to formate, and selective hemodialysis to correct severe metabolic abnormalities and to enhance methanol and formate elimination. Although both ethanol and fomepizole are effective, fomepizole is the preferred antidote for methanol poisoning.

This Position Paper was prepared using the methodology agreed by the American Academy of Clinical Toxicology (AACT) and the European Association of Poisons Centres and Clinical Toxicologists (EAPCCT). All relevant scientific literature was identified and reviewed critically by acknowledged experts using set criteria. Well-conducted clinical and experimental studies were given precedence over anecdotal case reports and abstracts were not considered. A draft Position Paper was then produced and presented at the North American Congress of Clinical Toxicology in October 2001 and at the EAPCCT Congress in May 2002 to allow participants to comment on the draft after which a revised draft was produced. The Position Paper was subjected to detailed peer review by an international group of clinical toxicologists chosen by the AACT and the EAPCCT, and a final draft was approved by the boards of the two societies. The Position Paper includes a summary statement (Position Statement) for ease of use, which will also be published separately, as well as the detailed scientific evidence on which the conclusions of the Position Paper are based. Urine alkalinization is a treatment regimen that increases poison elimination by the administration of intravenous sodium bicarbonate to produce urine with a pH > or = 7.5. The term urine alkalinization emphasizes that urine pH manipulation rather than a diuresis is the prime objective of treatment; the terms forced alkaline diuresis and alkaline diuresis should therefore be discontinued. Urine alkalinization increases the urine elimination of chlorpropamide, 2,4-dichlorophenoxyacetic acid, diflunisal, fluoride, mecoprop, methotrexate, phenobarbital, and salicylate. Based on volunteer and clinical studies, urine alkalinization should be considered as first line treatment for patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization cannot be recommended as first line treatment in cases of phenobarbital poisoning as multiple-dose activated charcoal is superior. Supportive care, including the infusion of dextrose, is invariably adequate in chlorpropamide poisoning. A substantial diuresis is required in addition to urine alkalinization in the chlorophenoxy herbicides, 2,4-dichlorophenoxyacetic acid, and mecoprop, if clinically important herbicide elimination is to be achieved. Volunteer studies strongly suggest that urine alkalinization increases fluoride elimination, but this is yet to be confirmed in clinical studies. Although urine alkalinization is employed clinically in methotrexate toxicity, currently there is only one study that supports its use. Urine alkalinization enhances diflunisal excretion, but this technique is unlikely to be of value in diflunisal poisoning. In conclusion, urine alkalinization should be considered first line treatment in patients with moderately severe salicylate poisoning who do not meet the criteria for hemodialysis. Urine alkalinization and high urine flow (approximately 600 mL/h) should also be ...

Introduction. Datura species, especially Datura stramonium (e.g., jimsonweed), are the focus of scores of case reports that chronicle the toxidrome of anticholinergic toxicity. Mechanisms of toxicity. Toxicity occurs because of the presence of up to 28 belladonna alkaloids, predominated by atropine and scopolamine. There are significant interspecies differences in the ratio of the belladonna alkaloids, atropine to scopolamine, and the presence of at least 26 other related alkaloids will vary, even between and among specimens of the same species. The differences may account for unexpected dose-response effects that are observed in some patients and even different profiles of toxicity. All parts of the Datura species contain belladonna alkaloids; in decreasing order, the belladonna alkaloid content is generally the greatest in the petioles (flowers), stem, fruit (seeds), leaves, and roots. Features. The most prominent symptoms are due to the blockade of peripheral muscarinic receptors that innervate exocrine glands, smooth muscle, and cardiac tissue. Therefore, the primary toxic manifestations include mydriasis, which is due to the blockade of papillary sphincter muscle and iris muscle; dry mouth, secondary to parasympathetic blockade of salivary secretion; tachycardia, caused by competition at muscarinic receptors in postganglionic parasympathetic neurons and blockade of receptors in the SA node; and fever and erythema, because of vasodilation and inhibition of sweating. Direct ocular exposure. Well known to produce mydriasis after ingestion, Datura is also notorious for producing maladies such as "gardeners eye" and "cornpickers eye," which is a testament to the high concentrations of belladonna alkaloids in the entire plant. When the sap or dried plant material from a member of the Datura species enters the eye directly, the papillary sphincter and ciliary muscles are affected resulting in mydriasis and cycloplegia. Pupil dilation is sudden in onset and often profound. In a dose-response fashion, the mydriasis and its persistence will be dependent on the alkaloidal content and quantity of the sap. The mydriasis can be bilateral, but most commonly it is unilateral, which is frightening to the victim and to the clinician and suggestive of significant cerebral pathology. Management. As with any toxic exposure, the foundation of patient management is supportive care and patient reassurance. Because of the central nervous system effects of the belladonna alkaloids, the patient may be agitated, combative, confused, and disoriented. Initial intervention focuses on addressing those issues that protect the patient and their caregivers. In severe cases, physostigmine, a cholinesterase inhibitor, should be used to reverse anticholinergic toxicity. Physostigmine should be given intravenously to an adult in a dose of 0.5-2.0 mg at a rate of no more than 1 mg/min; a second dose may be administered if necessary. Children should receive 0.02 mg/ kg intravenously and the rate should not exceed 0.5 mg/min. Extracorporeal eliminat...