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      Extracorporeal Removal of Poisons and Toxins

      , ,
      Clinical Journal of the American Society of Nephrology
      American Society of Nephrology (ASN)

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          Abstract

          Extracorporeal therapies have been used to remove toxins from the body for over 50 years and have a greater role than ever before in the treatment of poisonings. Improvements in technology have resulted in increased efficacy of removing drugs and other toxins with hemodialysis, and newer extracorporeal therapy modalities have expanded the role of extracorporeal supportive care of poisoned patients. However, despite these changes, for at least the past three decades the most frequently dialyzed poisons remain salicylates, toxic alcohols, and lithium; in addition, the extracorporeal treatment of choice for therapeutic removal of nearly all poisonings remains intermittent hemodialysis. For the clinician, consideration of extracorporeal therapy in the treatment of a poisoning depends upon the characteristics of toxins amenable to extracorporeal removal ( e.g. , molecular mass, volume of distribution, protein binding), choice of extracorporeal treatment modality for a given poisoning, and when the benefit of the procedure justifies additive risk. Given the relative rarity of poisonings treated with extracorporeal therapies, the level of evidence for extracorporeal treatment of poisoning is not robust; however, extracorporeal treatment of a number of individual toxins have been systematically reviewed within the current decade by the Extracorporeal Treatment in Poisoning workgroup, which has published treatment recommendations with an improved evidence base. Some of these recommendations are discussed, as well as management of a small number of relevant poisonings where extracorporeal therapy use may be considered.

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          Most cited references42

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          2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report.

          This is the 34th Annual Report of the American Association of Poison Control Centers' (AAPCC) National Poison Data System (NPDS). As of 1 January 2016, 55 of the nation's poison centers (PCs) uploaded case data automatically to NPDS. The upload interval was 9.50 [7.33, 14.6] (median [25%, 75%]) min, facilitating a near real-time national exposure and information database and surveillance system.
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            Toxic alcohol ingestions: clinical features, diagnosis, and management.

            Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early.
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              Methanol outbreak in Norway 2002-2004: epidemiology, clinical features and prognostic signs.

              Knowledge on methanol poisoning does mainly come from clinical studies. We therefore report epidemiological, clinical and prognostic features from the large methanol outbreak in Norway in 2002-2004 where the new antidote fomepizole was the primary antidote in use. Combined prospective and retrospective case series study of 51 hospitalized patients who were confirmed poisoned with methanol, of whom nine died. In addition, eight patients died outside hospital. Most patients were admitted in a late stage and because of symptoms. Treatment consisted of alkali, fomepizole (71%) and haemodialysis (73%). The median serum methanol was 25.0 mmol L-1 (80 mg dL-1) (range 3.1-147.0 mmol L-1), median pH was 7.20 (6.50-7.50), and median base deficit 22 mmol L-1 (range 0-31). The most frequent clinical features reported were visual disturbances (55%), dyspnoea (41%), and gastrointestinal symptoms (43%). Twenty-four per cent were comatose on admission, of whom 67% died. There was a trend towards decreasing pCO2 with decreasing pH amongst the patients surviving. The opposite trend was demonstrated in the dying; the difference was highly significant by linear regression analyses (P 28 mmol L-1) upon admission were strong predictors of poor outcome. Early admission and ability of respiratory compensation of metabolic acidosis was associated with survival.
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                Author and article information

                Journal
                Clinical Journal of the American Society of Nephrology
                CJASN
                American Society of Nephrology (ASN)
                1555-9041
                1555-905X
                September 06 2019
                September 06 2019
                September 06 2019
                August 22 2019
                : 14
                : 9
                : 1408-1415
                Article
                10.2215/CJN.02560319
                6730523
                31439539
                04f756ba-9260-4280-a690-23ddb22eda04
                © 2019
                History

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