Document Detail


Position Paper on urine alkalinization.
MedLine Citation:
PMID:  15083932     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 considered in patients with severe 2,4-dichlorophenoxyacetic acid and mecoprop poisoning. Administration of bicarbonate to alkalinize the urine results in alkalemia (an increase in blood pH or reduction in its hydrogen ion concentration); pH values approaching 7.70 have been recorded. Hypokalemia is the most common complication but can be corrected by giving potassium supplements. Alkalotic tetany occurs occasionally, but hypocalcemia is rare. There is no evidence to suggest that relatively short-duration alkalemia (more than a few hours) poses a risk to life in normal individuals or in those with coronary and cerebral arterial disease.
Authors:
A T Proudfoot; E P Krenzelok; J A Vale
Publication Detail:
Type:  Guideline; Journal Article; Practice Guideline; Review    
Journal Detail:
Title:  Journal of toxicology. Clinical toxicology     Volume:  42     ISSN:  0731-3810     ISO Abbreviation:  J. Toxicol. Clin. Toxicol.     Publication Date:  2004  
Date Detail:
Created Date:  2004-04-15     Completed Date:  2004-04-27     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8213460     Medline TA:  J Toxicol Clin Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1-26     Citation Subset:  AIM; IM    
Affiliation:
National Poisons Information Service (Birmingham Centre) and West Midlands Poisons Unit, City Hospital, Birmingham, UK.
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MeSH Terms
Descriptor/Qualifier:
Alkalies / urine*
Animals
Europe
Humans
Hydrogen-Ion Concentration
Poison Control Centers*
Practice Guidelines as Topic*
Societies, Medical
Toxicology / methods*
United States
Chemical
Reg. No./Substance:
0/Alkalies

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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