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      High-Anion-Gap Metabolic Acidosis During a Prolonged Hospitalization Following Perforated Diverticulitis: An Educational Case Report

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          Abstract

          Rationale:

          The metabolic acidoses are generally separated into 2 categories on the basis of an anion gap calculation: high-anion-gap and normal anion-gap metabolic acidosis. When a high-anion-gap metabolic acidosis (HAGMA) is not clearly explained by common etiologies and routine confirmatory testing, specialized testing can definitively establish rare diagnoses such as 5-oxoproline, d-lactate accumulation, or diethylene glycol toxicity.

          Presenting Concerns of the Patient:

          A 56-year-old woman had a prolonged hospital admission following perforated diverticulitis requiring sigmoid resection. Her hospitalization was complicated by feculent peritonitis and surgical wound dehiscence needing prolonged broad-spectrum antibiotics and wound debridements. She developed acute kidney injury and HAGMA in the hospital.

          Diagnoses:

          Chart review showed that she received a large cumulative dose of acetaminophen during her hospital stay. Laboratory studies showed markedly increased serum 5-oxoproline causing HAGMA.

          Interventions (Including Prevention and Lifestyle):

          Patient was admitted to the intensive care unit and treated with N-acetylcysteine and renal replacement therapy.

          Outcomes:

          After admission to the intensive care unit, the patient continued to require vasopressor and ventilatory support for septic shock and a ventilator-associated pneumonia. After an initial recovery and resolution of her HAGMA, she subsequently suffered recurrent aspirations which were fatal.

          Teaching points:
          • 1. The acronym GOLD MARK is useful when assessing patients with HAGMA and most causes of HAGMA can be established with routine testing.

          • 2. When the etiology of HAGMA remains unclear, additional testing can be required to diagnose rare causes of HAGMA.

          • 3. Rare causes of HAGMA are diethylene glycol, 5-oxoproline, and d-lactate accumulation.

          • 4. Acidosis secondary to 5-oxoproline accumulation can occur even with “therapeutic” doses of acetaminophen in patients receiving it regularly for a prolonged period and who have depleted glutathione stores.

          • 5. Risk factors for glutathione depletion include malnutrition, older age, sepsis, pregnancy, multiple chronic illnesses, and chronic kidney disease.

          Abrégé

          Justification:

          Les acidoses métaboliques sont généralement classées en deux catégories sur la base d’un calcul de trou anionique : les acidoses métaboliques à trou anionique élevé (HAGMA – High anion gap metabolic acidosis) et les acidoses métaboliques à trou anionique normal. Lorsque l’acidose métabolique à trou anionique élevé n’est pas clairement expliquée par des étiologies courantes et des tests de confirmation de routine, des tests spécialisés peuvent établir de façon définitive des diagnostics rares tels que l’accumulation de 5-oxoproline, l’accumulation de D-lactate ou une toxicité du diéthylène glycol.

          Présentation du cas:

          Une femme de 56 ans hospitalisée de façon prolongée à la suite d’une diverticulite perforée nécessitant une résection du sigmoïde. L’hospitalisation a été compliquée par une péritonite purulente et une déhiscence de la plaie chirurgicale ayant nécessité un débridement de la plaie et une antibiothérapie à large spectre prolongée. La patiente a développé une insuffisance rénale aiguë (IRA) et une HAGMA durant son séjour à l’hôpital.

          Diagnostic:

          L’examen du dossier a montré que la patiente avait reçu une dose cumulative importante d’acétaminophène pendant son séjour à l’hôpital. Des analyses en laboratoire ont montré une augmentation marquée de la 5-oxoproline sérique ayant causé l’HAGMA.

          Interventions (y compris prévention et mode de vie):

          La patiente a été admise à l’unité des soins intensifs et traitée par N-acétylcystéine et thérapie de remplacement rénal (TRR).

          Résultats:

          Après son admission à l’USI, la patiente a continué d’avoir besoin de vasopresseur et d’assistance respiratoire en raison d’un choc septique et d’une pneumonie associée au ventilateur. Après un rétablissement initial et la résolution de son HAGMA, la patiente a ensuite dû subir des aspirations récurrentes qui lui ont été fatales.

          Enseignements tirés:

          1. L’acronyme GOLD MARK est utile lors de l’évaluation des patients atteints d’HAGMA; la plupart des causes d’HAGMA peuvent être établies avec des tests de routine.

          2. Lorsque l’étiologie de l’HAGMA reste incertaine, des tests supplémentaires peuvent être nécessaires pour diagnostiquer les causes rares de l’HAGMA.

          3. Les causes rares de HAGMA sont une accumulation de diéthylène glycol, de 5-oxoproline et de D-lactate.

          4. L’acidose secondaire à une accumulation de 5-oxoproline peut se produire même avec des doses « thérapeutiques » d’acétaminophène chez les patients qui l’ont reçu régulièrement pendant une période prolongée et qui ont épuisé leurs réserves de glutathion.

          5. Les facteurs de risque pour l’épuisement des réserves de glutathion incluent la malnutrition, l’âge plus avancé, la septicémie, la grossesse, les maladies chroniques multiples et l’insuffisance rénale chronique.

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          Most cited references18

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          • Abstract: found
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          Paracetamol: not as safe as we thought? A systematic literature review of observational studies

          Objectives We conducted a systematic literature review to assess the adverse event (AE) profile of paracetamol. Methods We searched Medline and Embase from database inception to 1 May 2013. We screened for observational studies in English, which reported mortality, cardiovascular, gastrointestinal (GI) or renal AEs in the general adult population at standard analgesic doses of paracetamol. Study quality was assessed using Grading of Recommendations Assessment, Development and Evaluation. Pooled or adjusted summary statistics were presented for each outcome. Results Of 1888 studies retrieved, 8 met inclusion criteria, and all were cohort studies. Comparing paracetamol use versus no use, of two studies reporting mortality one showed a dose–response and reported an increased relative rate of mortality from 0.95 (0.92 to 0.98) to 1.63 (1.58 to 1.68). Of four studies reporting cardiovascular AEs, all showed a dose–response with one reporting an increased risk ratio of all cardiovascular AEs from 1.19 (0.81 to 1.75) to 1.68 (1.10 to 2.57). One study reporting GI AEs reported a dose–response with increased relative rate of GI AEs or bleeds from 1.11 (1.04 to 1.18) to 1.49 (1.34 to 1.66). Of four studies reporting renal AEs, three reported a dose–response with one reporting an increasing OR of ≥30% decrease in estimated glomerular filtration rate from 1.40 (0.79 to 2.48) to 2.19 (1.4 to 3.43). Discussion Given the observational nature of the data, channelling bias may have had an important impact. However, the dose–response seen for most endpoints suggests a considerable degree of paracetamol toxicity especially at the upper end of standard analgesic doses.
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            Acetaminophen/paracetamol: A history of errors, failures and false decisions.

            Acetaminophen/paracetamol is the most widely used drug of the world. At the same time, it is probably one of the most dangerous compounds in medical use, causing hundreds of deaths in all industrialized countries due to acute liver failure (ALF). Publications of the last 130 years found in the usual databases were analyzed. Personal contacts existed to renowned researchers having contributed to the medical use of paracetamol and its precursors as H.U. Zollinger, S. Moeschlin, U. Dubach, J. Axelrod and others. Further information is found in earlier reviews by Eichengrün, Rodnan and Benedek, Sneader, Brune; comp. references. The history of the discovery of paracetamol starts with an error (active against worms), continues with a false assumption (paracetamol is safer than phenacetin), describes the first side-effect 'epidemy' (phenacetin nephropathy, drug-induced interstitial nephritis) and ends with the discovery of second-generation problems due to the unavoidable production of a highly toxic metabolite of paracetamol N-acetyl-p-benzoquinone imine (NAPQI) that may cause not only ALF and kidney damage but also impaired development of the fetus and the newborn child. It appears timely to reassess the risk/benefit ratio of this compound.
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              • Article: not found

              Lactic acidosis: an update.

              Lactate is one of the most crucial intermediates in carbohydrate and nonessential amino acid metabolism. The complexity of cellular interactions and metabolism means that lactate can be considered a waste product for one cell but a useful substrate for another. The presence of elevated lactate levels in critically ill patients has important implications for morbidity and mortality. In this review, we provide a brief outline of the metabolism of lactate, the pathophysiology of lactic acidosis, the clinical significance of D-lactate, the role of lactate measurement in acutely ill patients, the methods used to measure lactate in blood or plasma and some of the methodological issues related to interferences in these assays, especially in the case of ethylene glycol poisoning.
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                Author and article information

                Journal
                Can J Kidney Health Dis
                Can J Kidney Health Dis
                CJK
                spcjk
                Canadian Journal of Kidney Health and Disease
                SAGE Publications (Sage CA: Los Angeles, CA )
                2054-3581
                28 October 2022
                2022
                : 9
                : 20543581221129753
                Affiliations
                [1 ]Division of Nephrology, Department of Medicine, The University of Ottawa and Ottawa Hospital Research Institute, ON, Canada
                [2 ]Division of Biochemistry, Department of Pathology and Laboratory Medicine, The University of Ottawa and The Ottawa Hospital, ON, Canada
                Author notes
                [*]Edward G. Clark, Associate Professor, Division of Nephrology, Department of Medicine, The University of Ottawa and Ottawa Hospital Research Institute, 1967 Riverside Drive, Ottawa, ON K1H 7W9, Canada. Email: edclark@ 123456toh.ca
                Author information
                https://orcid.org/0000-0002-7488-5644
                https://orcid.org/0000-0002-6767-1197
                Article
                10.1177_20543581221129753
                10.1177/20543581221129753
                9619282
                36325264
                0c1abe37-315a-4f6f-8ed3-ff7dc830bd8c
                © The Author(s) 2022

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                : 15 June 2022
                : 7 September 2022
                Categories
                Educational Case Report
                Custom metadata
                January-December 2022
                ts1

                high-anion-gap metabolic acidosis,5-oxoproline,acetaminophen,d-lactate acidosis,glutathione

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