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      Acidose metabólica na infância: por que, quando e como tratá-la? Translated title: Metabolic acidosis in childhood: why, when and how to treat

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          Abstract

          OBJETIVO: Apresentar uma revisão atualizada e crítica sobre os mecanismos das principais patologias associadas e o tratamento da acidose metabólica, discutindo aspectos controversos quanto aos benefícios e riscos da utilização do bicarbonato de sódio e outras formas de terapia. FONTES DOS DADOS: Revisão da literatura publicada, obtida através de busca eletrônica com as palavras-chave acidose metabólica, acidose láctica, cetoacidose diabética, ressuscitação cardiopulmonar, bicarbonato de sódio e terapêutica nas bases de dados PubMed/MEDLINE, LILACS e Cochrane Library, entre 1996 e 2006, além de publicações clássicas referentes ao tema, sendo selecionadas as mais atuais e representativas, buscando-se consensos e diretrizes. SÍNTESE DOS DADOS: A utilização de bicarbonato de sódio não demonstra benefícios no quadro hemodinâmico, evolução clínica, morbidade e mortalidade nos quadros de acidose metabólica de anion gap elevado, relacionados à acidose láctica, cetoacidose diabética e ressuscitação cardiorrespiratória. Assim, a sua utilização rotineira não é indicada. Devem ser considerados os potenciais efeitos colaterais. O tratamento da doença de base é fundamental para reversão do processo. Outras terapias alternativas não demonstram efetividade comprovada em grande escala. CONCLUSÕES: Apesar dos efeitos conhecidos da acidemia em situações críticas no organismo, discute-se o papel protetor da acidemia nas células sob hipoxemia e os riscos da alcalemia secundária à intervenção medicamentosa. Existe consenso na reposição de álcalis e bicarbonato de sódio nos casos de acidose de anion gap normal; entretanto, nos casos de acidose de anion gap elevado, particularmente na acidose láctica, cetoacidose diabética e na ressuscitação cardiorrespiratória, o uso de bicarbonato de sódio não demonstra benefícios, além dos potenciais efeitos adversos, o que torna restrita sua indicação. Apesar da controvérsia, o único ponto concordante refere-se à abordagem mais precoce da doença de base e dos mecanismos geradores da acidemia metabólica. Outras alternativas terapêuticas são promissoras; entretanto, os efeitos adversos e a falta de trabalhos controlados em pediatria não determinam evidências suficientes que recomendem sua utilização de rotina.

          Translated abstract

          OBJECTIVES: To critically discuss the treatment of metabolic acidosis and the main mechanisms of disease associated with this disorder; and to describe controversial aspects related to the risks and benefits of using sodium bicarbonate and other therapies. SOURCES: Review of PubMed/MEDLINE, LILACS and Cochrane Library databases for articles published between 1996 and 2006 using the following keywords: metabolic acidosis, lactic acidosis, ketoacidosis, diabetic ketoacidosis, cardiopulmonary resuscitation, sodium bicarbonate, treatment. Classical publications concerning the topic were also reviewed. The most recent and representative were selected, with emphasis on consensus statements and guidelines. SUMMARY OF THE FINDINGS: There is no evidence of benefits resulting from the use of sodium bicarbonate for the hemodynamic status, clinical outcome, morbidity and mortality in high anion gap metabolic acidosis associated with lactic acidosis, diabetic ketoacidosis and cardiopulmonary resuscitation. Therefore, the routine use of sodium bicarbonate is not indicated. Potential side effects must be taken into consideration. Treating the underlying disease is essential to reverse the process. The efficacy of other alternative therapies has not been demonstrated in large-scale studies. CONCLUSIONS: Despite the known effects of acidemia on the organism in critical situations, a protective role of acidemia in hypoxic cells and the risk of alkalemia secondary to drug interventions are being considered. There is consensus regarding the advantages of alkali and sodium bicarbonate therapy in cases with normal anion gap; however, in the presence of high anion gap acidosis, especially lactic acidosis, diabetic acidosis and cardiopulmonary resuscitation, the use of sodium bicarbonate is not beneficial and has potential adverse effects, limiting its indication. The only points of agreement in the literature refer to the early treatment of the underlying disease and the mechanisms generating metabolic acidemia. Other promising treatment alternatives have been proposed; however, the side effects and absence of controlled studies with pediatric populations translate into lack of evidence to support the routine use of such treatments.

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          Most cited references87

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          Management of life-threatening acid-base disorders. First of two parts.

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            Effects of bicarbonate therapy on hemodynamics and tissue oxygenation in patients with lactic acidosis: a prospective, controlled clinical study.

            To determine whether correction of acidemia using bicarbonate improves hemodynamic variables and tissue oxygenation in patients with lactic acidosis. Prospective, randomized, blinded, cross over study. Each patient sequentially received sodium bicarbonate and sodium chloride. The order of the infusions was randomized. Ten patients with metabolic acidosis, increased arterial plasma lactate concentrations (greater than 2.45 mmol/L), and no severe renal failure (creatinine less than 250 mumol/L [less than 2.3 mg/dL]). Sodium bicarbonate (1 mmol/kg body weight) or equal volume of sodium chloride was injected iv at the beginning of two successive 1-hr study periods. Period order was randomized. Arterial and venous blood gas measurements, plasma electrolytes (sodium, potassium, chloride), osmolality and lactate, 2,3-diphosphoglycerate (DPG), and oxygen hemoglobin affinity, hemodynamic variables, oxygen delivery, and oxygen consumption measurements were obtained before and repeatedly during the 1-hr period after the injection of bicarbonate or sodium chloride. Sodium bicarbonate administration increased arterial and venous pH, serum bicarbonate, and the partial pressure of CO2 in arterial and venous blood. Hemodynamic responses to sodium bicarbonate and sodium chloride were similar. Tissue oxygenation (as estimated by oxygen delivery, oxygen consumption, oxygen extraction ratio, and transcutaneous oxygen pressure) was not modified. No changes in serum sodium concentration, osmolality, arterial and venous lactate, red cell 2,3-DPG levels, or hemoglobin affinity for oxygen were observed. Administration of sodium bicarbonate did not improve hemodynamic variables in patients with lactic acidosis, but did not worsen tissue oxygenation.
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              Lactic acidosis update for critical care clinicians.

              F C Luft (2001)
              Lactic acidosis is a broad-anion gap metabolic acidosis caused by lactic acid overproduction or underutilization. The quantitative dimensions of these two mechanisms commonly differ by 1 order of magnitude. Overproduction of lactic acid, also termed type A lactic acidosis, occurs when the body must regenerate ATP without oxygen (tissue hypoxia). Circulatory, pulmonary, or hemoglobin transfer disorders are commonly responsible. Overproduction of lactate also occurs with cyanide poisoning or certain malignancies. Underutilization involves removal of lactic acid by oxidation or conversion to glucose. Liver disease, inhibition of gluconeogenesis, pyruvate dehydrogenase (thiamine) deficiency, and uncoupling of oxidative phosphorylation are the most common causes. The kidneys also contribute to lactate removal. Concerns have been raised regarding the role of metformin in the production of lactic acidosis, on the basis of individual case reports. The risk appears to be considerably less than with phenformin and involves patients with underlying severe renal and cardiac dysfunction. Drugs used to treat lactic acidosis can aggravate the condition. NaHCO(3) increases lactate production. Treatment of type A lactic acidosis is particularly unsatisfactory. NaHCO(3) is of little value. Carbicarb is a mixture of Na(2)CO(3) and NaHCO(3) that buffers similarly to NaHCO(3) but without net generation of CO(2). The results from animal studies are promising; however, clinical trials are sparse. Dichloroacetate stimulates pyruvate dehydrogenase and improves laboratory values, but unfortunately not survival rates, among patients with lactic acidosis. Hemofiltration has been advocated for the treatment of lactic acidosis, on the basis of anecdotal experiences. However, kinetic studies of lactate removal do not suggest that removal can counteract lactate production in any meaningful way. The ideal treatment is to stop acid production by treating the underlying disorder.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                jped
                Jornal de Pediatria
                J. Pediatr. (Rio J.)
                Sociedade Brasileira de Pediatria (Porto Alegre )
                1678-4782
                May 2007
                : 83
                : 2 suppl
                : S11-S21
                Affiliations
                [1 ] Santa Casa de Misericórdia de São Paulo Brazil
                [2 ] Universidade Federal de São Paulo Brazil
                [3 ] Santa Casa de Misericórdia de São Paulo Brazil
                [4 ] Hospital Israelita Albert Einstein
                [5 ] Santa Casa de Misericórdia de São Paulo Brazil
                [6 ] Universidade de São Paulo Brazil
                [7 ] Universidade de São Paulo Brazil
                [8 ] Hospital Israelita Albert Einstein
                Article
                S0021-75572007000300003
                10.1590/S0021-75572007000300003
                b5eb5ae0-eee0-4db9-bb7b-1feeb28837b4

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0021-7557&lng=en
                Categories
                PEDIATRICS

                Pediatrics
                bicarbonato de sódio,criança,Acidosis,acidosis,lactic,diabetic ketoacidosis,sodium bicarbonate,acidose láctica,cetoacidose diabética,child,Acidose

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