Bicarbonato de sodio intravenoso ¿Cuándo, cómo y por qué utilizarlo? / Intravenous sodium bicarbonate. When, how and why to use it?

Severe metabolic acidosis is defined by a pH < 7.2 with HCO3− < 8 mE- q/L in plasma. Its best treatment is to correct the underlying cause. However, acidemia produces multiple complications such as resistance to the action of catecholamines, pulmonary vasoconstriction, impaired cardiovascular function, hyperkalemia, immunological dysregulation, respiratory muscle fatigue, neurological impairment, cellular dysfunction, and finally, it contributes to multisystemic failure. Intravenous NaHCO3 buffers severe acidemia, preventing the associated damage and gains time while the causal disease is corrected. Its indication requires a risk-benefit assessment, considering its complications. These are hypernatremia, hypokalemia, ionic hypocalcemia, rebound alkalosis, and intracellular acidosis. For this reason, therapy must be "adapted" and administered judiciously. The patient will require monitoring with serial evaluation of the internal environment, especially arterial blood gases, plasma electrolytes, and ionized calcium. Isotonic solutions should be preferred instead of hypertonic bicarbonate. The development of hypernatremia must be prevented, calcium must be provided for hypocalcemia to improve cardiovascular function. Furthermore, in mechanically ventilated patients, a respiratory response similar to the one that would develop physiologically, must be established to be able to extract excess CO2 and thus avoid intracellular acidosis. It is possible to estimate the bicarbonate deficit, speed, and volume of its infusion. However, the calculations are only for reference. More important is to start intravenous NaHCO3 when needed, administer it judiciously, manage its side effects, and continue it to a safe goal. In this review we address all the necessary elements to consider in the administration of intravenous NaHCO3, highlighting why it is the best buffer for the management of severe metabolic acidosis.

Alkali Therapy Attenuates the Progression of Kidney Injury via Na/H Exchanger Inhibition in 5/6 Nephrectomized Rats

Metabolic acidosis is a cause of renal disease progression, and alkali therapy ameliorates its progression. However, there are few reports on the role of renal acid-base transporters during alkali therapy. We evaluated the effect of sodium bicarbonate therapy and the role of acid-base transporters on renal disease progression in rats with a remnant kidney. Sprague-Dawley rats consumed dietary sodium bicarbonate (NaHCO3) or sodium chloride (NaCl) with 20% casein after a 5/6 nephrectomy. After being provided with a casein diet, the NaHCO3-treated group had higher levels of serum bicarbonate than the control group. At week 4, the glomerular filtration rate in the NaHCO3 group was higher than that in the NaCl group, and the difference became prominent at week 10. The glomerulosclerosis and tubulointerstitial damage indices in the NaHCO3 group were less severe compared with controls at week 4 and 10. The expression of the Na/H exchanger (NHE) was decreased, and apical reactivity was decreased in the NaHCO3 group, compared with the NaCl group. Endothelin-1 levels in the kidney were also decreased in the NaHCO3 group. Dietary sodium bicarbonate has the effects of ameliorating renal disease progression, which may be related to the altered expression of NHE in the remaining kidney.

Isoniazid Toxicity Presenting As Status Epilepticus and Severe Metabolic Acidosis.

Isoniazid (INH) is an integral component of treatment of tuberculosis. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents to emergency medical services (EMS) with the triad. We report a patient presenting with multiple generalised tonic clonic (GTC) convulsions with severe metabolic acidosis as a manifestation of INH toxicity. ©

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

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...

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...

Ethylene glycol poisoning following ingestion of brake fluid / Envenenamiento con glicol de etileno tras la ingestión de líquido de frenos

A 32-year old male, with a history of depression and previous suicide attempts, was brought to hospital comatose after ingestion of brake fluid. He developed severe metabolic acidosis with an increased anion gap, hypotension, seizures and mild renal impairment. He required intensive care treatment for ventilatory and inotropic support. The clinical features, diagnosis and treatment of this unusual poison are discussed.

Un sujeto masculino de 32 años de edad, con una historia de depresión y previos intentos de suicidio, fue llevado en estado comatoso al hospital, luego de haber ingerido líquido de freno. El paciente desarrolló una acidosis metabólica severa con aumento del gap aniónico, hipertensión, convulsiones, e insuficiencia renal moderada. Requirió tratamiento mediante cuidados intensivos con apoyo ventilatorio e inotrópico. El trabajo analiza las características clínicas, el diagnóstico y el tratamiento de este envenenamiento inusual.

Experiencia clínica con el uso de bicarbonato por vía oral en el manejo de pacientes con acidocis metabólica tardía / Clinic experience in the use of oral bicarbonate in management of patients with late onset metabolic acidosis

Objetivo. Evaluar la evolución de pacientes con acidosis metabólica tardía con el uso de bicarbonato por vía oral. Diseño. Estudio descriptivo observacional. Población. Siete recién nacidos de ambos sexos. Metodología. Se incluyeron todos los pacientes con detención de ganancia de peso, prematuros, de bajo peso a quienes se les diagnosticó acidosis metabólica tardía. Al diagnóstico se inició bicarbonato de sodio a 2 mEq/kg/día, dividido en siete tomas y se redujo el aporte protéico al 50 de la cantiad de proteína que estaba tomando, durante 48 horas. Los pacientes fueron controlados a través de gases arteriales y evolución clínica. Resultados. No hubo diferencia con relación al sexo. Ningún paciente menor de 14 días desarrolló acidosis metabólica tardía. El grupo más afectado fue el de niños con pesos entre 1001 y 1200 gramos y aquellos cuyo aporte protéico superó los 3 gms/kg/día. El 87 de los pacientes resolvió su acidosis después del tratamiento. Conclusiones. La acidosis metabólica tardía del prematuro puede resolverse utilizando bicarbonato por vía oral, sin ninguna complicación

Curso temporal de la acidosis metabolica durante el para cardiorrespiratorio engatos: tratamiento por medio de bicarbonato de sodio / Temporal course of metabolic acidosis during cardiorespiratory arrest in cats: treatment with sodiun bicarbonate

La correlación entre el tiempo de paro cardiorrespiratorio (10 min.) inducido experimentalmente en gatos con las modificaciones concomitantes de pH (0.16 unidades/min), déficit de exceso de base (0.97 mEp/L/min) y otros componentes sanguíneos, así como el análisis de regresión de los valores del déficit del exceso de base durante el paro cardiorrespiratorio permitieron calcular la dosis de bicarbonato de sodio adecuada para la corrección inmediata de la acidosis metabólica durante los procedimientos de reanimación correspondientes tras cinco minutos de paro cardiorrespiratorio en gatos, aunque también provocó hipopotasemia y hiperosmolaridad. En condiciones similares, la dosis de bicarbonato de sodio calculada sin tomar en cuenta la relación entre tiempo de paro cardiorrespiratorio y déficit de exceso de base fue insuficiente para normalizar el pH. Los resultados indican la importancia de dichos factores y la posibilidad de predeterminar la dosis adecuada de bicarbonato de sodio para el tratamiento del paro cardiorrespiratorio