Severe metabolic acidosis early in paracetamol poisoning.

Zezulka, A. V.; Wright, N.

doi:10.1136/bmj.285.6345.851

Cited by 33 publications

(17 citation statements)

References 7 publications

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“…1 We found 4 reports 6,[11][12][13] in the literature of patients with acetaminophen levels .500 mg/L who died (1 of whom underwent hemodialysis), 12 and 3 patients with levels greater than 500 mg/L who underwent hemodialysis and survived. 2,5,14 The therapeutic value of hemodialysis in acetaminophen poisoning has historically been for a rapid acid-base correction and enhanced elimination of byproducts 15 ; however, these described benefits may be minimized and outweighed by the potential decreased efficacy of N-acetylcysteine due to its removal by hemodialysis. 16 This case represents the highest reported acetaminophen level treated solely with the N-acetylcysteine continuous infusion protocol approved by the US Food and Drug Administration in 2004.…”

Section: Discussionmentioning

confidence: 99%

A Gargantuan Acetaminophen Level in an Acidemic Patient Treated Solely With Intravenous N-Acetylcysteine

Zell-Kanter¹,

Coleman²,

Whiteley³

et al. 2013

American Journal of Therapeutics

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The objective of this report is to describe an acidemic patient with one of the largest recorded acetaminophen ingestions in a patient with acidemia who was treated with supportive care and intravenous (IV) N-acetylcysteine. A 59-year-old female with a history of depression was found comatose. In the Emergency Department, she was obtunded with agonal respirations and immediately intubated. Activated charcoal was given through a nasogastric tube. An initial acetaminophen serum level was 1141 mg/L. The patient was started on IV N-acetylcysteine. The acetaminophen level peaked 2 hours later at 1193 mg/L. She was continued on the IV N-acetylcysteine protocol. The next day her aspartate aminotransferase was 3150 U/L, alanine aminotransferase was 2780 U/L, and creatinine phosphokinase was 16,197 U/L. There was no elevation in bilirubin or international normalized ratio (INR). Transaminase levels decreased on day 3 and normalized by day 4 when she was transferred to a psychiatric unit. Few cases have been reported of strikingly elevated acetaminophen levels in poisoned patients who did not receive hemodialysis. These patients did have increased lactate levels, and some had normal liver function tests. All of these patients received N-acetylcysteine and survived the poisoning without sequelae. This patient in this report was unique in that she had the highest reported serum acetaminophen level with acidosis and was treated successfully with only IV N-acetylcysteine and supportive care.

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Section: Discussionmentioning

confidence: 99%

A Gargantuan Acetaminophen Level in an Acidemic Patient Treated Solely With Intravenous N-Acetylcysteine

Zell-Kanter¹,

Coleman²,

Whiteley³

et al. 2013

American Journal of Therapeutics

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“…L'augmentation de la lactatémie ( Il est décrit également que l'acidose contribue fortement à la dégradation de l'état neurologique du patient [11,18] et est responsable en partie de l'hypothermie. Dans la grande majorité des cas, dès l'admission aux urgences médicales, l'état mental du patient est altéré allant de la simple confusion au coma retrouvé chez 2 patients [2,3,10,11,13,14,16]. Avec un score sur l'échelle de Glasgow de 9/15, l'état mental du patient présenté était déjà fortement altéré à l'admission.…”

Section: Discussionunclassified

“…Le paracé-tamol est surtout connu pour sa toxicité hépatique retardée après métabolisation en N-acétyl-para-benzoquinone imine, lorsque les mécanismes de conjugaison sont saturés suite à l'ingestion de dose supra-thérapeutique. Cependant, depuis les années 1980, des cas d'acidose lactique associés à la prise de paracétamol sont décrits [2][3][4]. Nous présentons ici, le cas d'un homme de 60 ans, retraité.…”

Section: Introductionunclassified

L’acidose lactique précoce lors de l’intoxication massive au paracétamol : un trouble métabolique parfois méconnu

Grégoire

Bretonnière

Deslandes

et al. 2015

Toxicologie Analytique et Clinique

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“…Interestingly, there have been cases of "unexplained" metabolic acidosis occurring early in acetaminophen overdose, unrelated to lactic acidosis, renal or hepatic failure. 19,21 It is plausible that a number of these cases resulted from unrecognized pyroglutamic acidosis.…”

Section: Discussionmentioning

confidence: 99%

Profound metabolic acidosis from pyroglutamic acidemia: an underappreciated cause of high anion gap metabolic acidosis

Green

Bijlsma

Sweet

2010

CJEM

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The workup of the emergency patient with a raised anion gap metabolic acidosis includes assessment of the components of "MUDPILES" (methanol; uremia; diabetic ketoacidosis; paraldehyde; isoniazid, iron or inborn errors of metabolism; lactic acid; ethylene glycol; salicylates). This approach is usually sufficient for the majority of cases in the emer gen cy department; however, there are many other etiologies not addressed in this mnemonic. Organic acids including 5-oxoproline (pyroglutamic acid) are rare but important causes of anion gap metabolic acidosis. We present the case of a patient with profound metabolic acidosis with raised anion gap, due to pyroglutamic acid in the setting of malnutrition and chronic ingestion of acetaminophen.Keywords: pyroglutamic acid, 5-oxoproline, metabolic acidosis, acetaminophen, malnutrition, case report RÉSUMÉ L'investigation d'un patient à l'urgence présentant une acidose métabolique à trou anionique augmenté comprend l'évalua-tion des composantes de « MUDPILES » (mnémonique anglais pour méthanol; urémie; acidocétose diabétique; paraldéhyde; fer ou maladie enzymatique; acide lactique; éthylène glycol; salicylate). Cette approche suffit généralement pour la majorité des cas à l'urgence, mais ce mnémonique ne tient pas compte de nombreuses autres étiologies. CASE REPORTA 43-year-old woman was transported via ambulance to the emergency department (ED) after being found screaming incoherently in the hallway of her apartment building. On arrival she was restless and remained incoherent. She was accompanied by friends who confirmed that she had been in her usual state the previous day; however, she had recently received treatment at an addiction treatment centre for prescription narcotic dependence. She had lost 50 lb during the prior 6 months because of an eating disorder, and was likely malnourished. During her stay at the addiction treatment centre and in the days since her discharge, she had been ingesting large amounts of acetaminophen and a number of empty acetaminophen bottles were found in her apartment. Her medical history included recurrent nephrolithiasis and chronic lower back pain as well as a remote history of cocaine and alcohol abuse. Her other medications included quetiapine, trazodone, methadone, a stimulant laxative, docusate, gabapentin, furosemide and citalopram.Physical examination revealed a very thin woman with a body mass index of 18. Her temperature was 36.4°C, heart rate was 95 beats/min, blood pressure was 109/70 mm Hg, respiratory rate was 30 breaths/min and Glasgow Coma Scale score was 14 (eyes 4, verbal 4, motor 6). Her pupils were equal at 4 mm and reactive to light. Respiratory examination showed tachypnea, but was otherwise unremarkable. Her cardiovascular and abdominal examinations were normal. There were no focal neurologic findings and https://www.cambridge.org/core/terms. https://doi

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Severe metabolic acidosis early in paracetamol poisoning.

Abstract: M. After effects of sleeping drugs. In: Wheatley D, ed. Psychopharmacology of sleep. New York: Raven Press, 1981:177-97. 4 Clayton AB. The effects of psychotropic drugs on driving related skills.

Cited by 33 publications

References 7 publications

A Gargantuan Acetaminophen Level in an Acidemic Patient Treated Solely With Intravenous N-Acetylcysteine

A Gargantuan Acetaminophen Level in an Acidemic Patient Treated Solely With Intravenous N-Acetylcysteine

L’acidose lactique précoce lors de l’intoxication massive au paracétamol : un trouble métabolique parfois méconnu

Profound metabolic acidosis from pyroglutamic acidemia: an underappreciated cause of high anion gap metabolic acidosis

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