Abstract:Background: The etiology of acute metabolic acidosis (aMA) is heterogeneous, and the consequences are potentially life-threatening. The aim of this article was to summarize the causes and management of aMA from a clinician's perspective. Summary: We performed a systematic search on PubMed, applying the following search terms: "acute metabolic acidosis," "lactic acidosis," "metformin" AND "acidosis," "unbalanced solutions" AND "acidosis," "bicarbonate" AND "acidosis" AND "outcome," "acute metabolic acidosis" AN… Show more
“…Buffering, e.g. with sodium bicarbonate, should be performed if the symptoms are clinically relevant (Matyukhin et al, 2020;Adeva-Andany et al, 2014). In the case of refractory acidosis, the administration of N-acetylcysteine can be considered (Hundemer and Fenves, 2017;Tummers et al, 2020).…”
Abstract. We report a case of a 64-year-old female patient with severe metabolic
acidosis. Inhibition of 5-oxoprolinase by flucloxacillin was found to be
the cause of the metabolic derailment.
“…Buffering, e.g. with sodium bicarbonate, should be performed if the symptoms are clinically relevant (Matyukhin et al, 2020;Adeva-Andany et al, 2014). In the case of refractory acidosis, the administration of N-acetylcysteine can be considered (Hundemer and Fenves, 2017;Tummers et al, 2020).…”
Abstract. We report a case of a 64-year-old female patient with severe metabolic
acidosis. Inhibition of 5-oxoprolinase by flucloxacillin was found to be
the cause of the metabolic derailment.
“…The exact definition of acute metabolic acidosis is controversial; however, the development of acidosis within hours to days after the causative factor insult is considered acute. Among the commonly described causes, the accumulation of organic acids is commonly encountered in clinical settings, and lactic acid is one of the most commonly accumulated organic acids in the pathogenesis of metabolic acidosis [ 3 ]. Accumulation of these organic acids leads to a high anion gap metabolic acidosis (HAGMA).…”
Section: Discussionmentioning
confidence: 99%
“…Accumulation of these organic acids leads to a high anion gap metabolic acidosis (HAGMA). If the acidosis is secondary to underproduction or overexcretion of bicarbonate, it leads to a state termed normal or non-anion gap metabolic acidosis [ 3 ].…”
Metabolic acidosis is a frequently encountered laboratory finding in daily clinical practice. Rapid pH correction is almost always preferred and necessary while performing workup to identify the causative factors. We present the case of a 73-year-old male presenting with progressive dyspnea and severe metabolic acidosis. He had a pH of 6.6, bicarbonate of 1.8 mg/dL, lactic acid of 18.1 mg/dL, and pCO
2
of 14.1 mmHg. The intensivist and nephrologist made a joint decision to rapidly correct the pH using bicarbonate and emergent hemodialysis. Subsequently, continuous renal replacement therapy (CRRT) was started, leading to a favorable outcome. Our patient’s most likely etiology of lactic acidosis was metformin because he had a very high lactic acid, high anion gap metabolic acidosis, and acute renal failure on presentation. From our case and literature review, we suggest using hemodialysis, CRRT, and bicarbonate replacement for a better prognosis in patients with critical acidosis in view of frank renal failure and concurrent metformin use.
“…Whether SB treatment to correct metabolic acidosis actually improves clinical outcomes is controversial [7,8]. In adults with severe metabolic acidemia, SB treatment has no effect on mortality or the SOFA score [9].…”
Background: Metabolic acidosis is a common acid-base imbalance in critically ill patients. Whether sodium bicarbonate (SB) can improve clinical outcomes in the treatment of metabolic acidosis is still controversial. The aim of this study was to determine the factors influencing the clinical efficacy of SB in the treatment of metabolic acidosis and the potential benefit to patients.
Methods: Patients with metabolic acidosis who were treated with or without SB were identified and grouped from a retrospective cohort (Pediatric Intensive Care Unit [PICU] database), from which the clinical data were extracted. The in-hospital mortality curves of the acid-base balance parameters of patients in the two groups were drawn and fitted using the locally-weighted scatter plot smoothing (LOWESS) method. The prevalence ratios (PRs) of in-hospital mortality were estimated by log-binomial regression based on the maximum likelihood method, and the potential confounders, such as age and disease category, were adjusted.
Results: A total of 6,167 children with metabolic acidosis were enrolled, of whom 2,626 (42.58%) were treated with SB. The overall analysis showed that there was no significant difference in the in-hospital mortality rates (9.71% vs. 10.56%, p = 0.275) between children in the SB treatment and non-treatment groups, adjusted PR = 0.929 (95% CI, 0.802-1.072). There was no significant difference in the in-hospital mortality rates as a function of pH and HCO3- between the two groups. The in-hospital mortality rate as a function of chloride was significantly different; specifically, the curve of the untreated group was U-shaped and the curve of the treated group was L-shaped. The curves of the two groups crossed at 110 mmol/L of chloride after LOWESS fitting. There was no statistically significant difference in the risk of death between the SB treatment and non-treatment groups at a chloride < 107 mmol/L and a chloride >113 mmol/L. In the chloride < 107 mmol/L subgroup, SB treatment had a 41.7% increased risk of in-hospital death (adjusted PR=1.417, 95% CI, 1.069−1.481) and a 35.9% increased risk of 28-day death (adjusted PR=1.359, 95% CI, 1.315−1.474). In the chloride≥113 mmol/L subgroup, SB treatment had a 61.1% reduced risk of in-hospital death (adjusted PR=0.389, 95% CI, 0.268−0.553) and a 56.4% reduced risk of 28-day death (adjusted PR=0.436, 95% CI, 0.295−0.631). The median length of stay in the PICU of children in the SB group was also shorter than children in the non-treatment group when the chloride concentration was ≥110 mmol/L.
Conclusions: The clinical outcomes of SB in the treatment of metabolic acidosis are associated with chloride. When the chloride concentration was high (> 110 mmol/L), children benefited from SB treatment and when the chloride concentration was low (< 107 mmol/L), the risk of death increased.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.