Management of acute metabolic acidosis in the ICU: sodium bicarbonate and renal replacement therapy.
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ABSTRACT:
SUBMITTER: Yagi K
PROVIDER: S-EPMC8406840 | biostudies-literature | 2021 Aug
REPOSITORIES: biostudies-literature
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Management of acute metabolic acidosis in the ICU: sodium bicarbonate and renal replacement therapy.
Critical care (London, England) 20210831 1
This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2021. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2021 . Further information about the Annual Update in Intensive Care and Emergency Medicine is available from https://link.springer.com/bookseries/8901 . ...[more]
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Project description:BackgroundMetabolic acidosis is a major complication of critical illness. However, its current epidemiology and its treatment with sodium bicarbonate given to correct metabolic acidosis in the ICU are poorly understood.MethodThis was an international retrospective observational study in 18 ICUs in Australia, Japan, and Taiwan. Adult patients were consecutively screened, and those with early metabolic acidosis (pH < 7.3 and a Base Excess < -4 mEq/L, within 24-h of ICU admission) were included. Screening continued until 10 patients who received and 10 patients who did not receive sodium bicarbonate in the first 24 h (early bicarbonate therapy) were included at each site. The primary outcome was ICU mortality, and the association between sodium bicarbonate and the clinical outcomes were assessed using regression analysis with generalized linear mixed model.ResultsWe screened 9437 patients. Of these, 1292 had early metabolic acidosis (14.0%). Early sodium bicarbonate was given to 18.0% (233/1292) of these patients. Dosing, physiological, and clinical outcome data were assessed in 360 patients. The median dose of sodium bicarbonate in the first 24 h was 110 mmol, which was not correlated with bodyweight or the severity of metabolic acidosis. Patients who received early sodium bicarbonate had higher APACHE III scores, lower pH, lower base excess, lower PaCO2, and a higher lactate and received higher doses of vasopressors. After adjusting for confounders, the early administration of sodium bicarbonate was associated with an adjusted odds ratio (aOR) of 0.85 (95% CI, 0.44 to 1.62) for ICU mortality. In patients with vasopressor dependency, early sodium bicarbonate was associated with higher mean arterial pressure at 6 h and an aOR of 0.52 (95% CI, 0.22 to 1.19) for ICU mortality.ConclusionsEarly metabolic acidosis is common in critically ill patients. Early sodium bicarbonate is administered by clinicians to more severely ill patients but without correction for weight or acidosis severity. Bicarbonate therapy in acidotic vasopressor-dependent patients may be beneficial and warrants further investigation.
| S-EPMC7851901 | biostudies-literature
Project description:Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.
| S-EPMC4227445 | biostudies-other
Project description:ObjectiveThis article aims to describe the epidemiology of decompensated metabolic acidosis, the characteristics of sodium bicarbonate (SB) administration and outcomes in emergency department (ED) patients.DesignThis is a retrospective cohort study.SettingED of a tertiary referral hospital in Melbourne, Australia.ParticipantsAdult patients presenting to the ED between 1 July 2011 and 20 September 2020 with decompensated metabolic acidosis diagnosed on arterial blood gas (ABG).Main outcome measuresWe compared characteristics between those treated with or without SB. We studied SB administration characteristics, change in laboratory variables, factors associated with use and dose, and clinical outcomes.ResultsAmong 753,613 ED patients, 314 had decompensated metabolic acidosis on ABG, with 17.8% receiving SB. Patients in the SB group had lower median pH, CO2, bicarbonate, and base excess (BE) levels compared with the No SB group (P < 0.01). The median number of SB doses in the SB group was one treatment. This was given at a median total dose of 100 mmol and at a median of 2.8 h after the diagnostic blood gas results. Only 42% of patients in the SB group had a subsequent blood gas measured. In such patients, there was no significant change in pH, bicarbonate, or BE. SB therapy was not independently associated with mortality.ConclusionsABG-confirmed decompensated metabolic acidosis was rare but associated with a high mortality. SB administration occurred in a minority of patients and in more acidaemic patients. However, SB dose was stereotypical and not tailored to acidosis severity. Assessment of SB effect was infrequent and showed no correction of acidosis. Systematic studies of titrated SB therapy are required to inform current practice.
| S-EPMC10581257 | biostudies-literature
Project description:Objective: This study aimed to explore the effectiveness of sodium bicarbonate (SB) infusion on mortality in elderly septic patients with acute metabolic acidosis (MA) and in other subgroups. Methods: Retrospective analysis of a large ICU database (MIMIC-IV) was performed. Elderly septic patients with acute MA were identified from MIMIC-IV. Propensity score analysis (PSA) was performed to explain for the baseline differences in the probability to receive SB or not. The marginal structural Cox model (MSCM) was developed to adjust for both baseline and time-varying confounding variables. The primary outcome was the ICU and hospital mortality. Results: A total of 869 elderly septic patients with acute MA were identified in this study, including 361 in the SB group and 508 in the non-SB group. In the PSA, SB infusion was not associated with reduced ICU (HR 0.82, 95% CI 0.62-1.10; p = 0.19) or hospital (HR 0.94, 95% CI 0.74-1.19; p = 0.60) mortality in overall elderly septic patients with acute MA. In the subgroup of severe metabolic acidosis, SB infusion could not improve the ICU (HR 0.82, 95% CI 0.62-1.10; p =0.19) and hospital (HR 0.94, 95% CI 0.74-1.19; p =0.60) mortality on elderly septic patients. However, In the subgroup of moderate metabolic acidosis, SB infusion could be found associated with improved ICU (HR 0.64, 95% CI 0.43-0.95; p <0.05) and hospital (HR 0.70, 95% CI 0.50-0.99; p <0.05) survival in elderly septic patients. In the MSCM, the results were similar with PSA. Conclusion: SB infusion could improve both ICU and hospital survival for elderly septic patients with acute metabolic acidosis.
| S-EPMC9513550 | biostudies-literature
Project description:Objective: This study aimed to explore the effectiveness of sodium bicarbonate (SB) administration on mortality in septic patients with acute moderate lactic acidosis (MLA). Methods: The large ICU database (MIMIC-IV) was retrospectively analyzed. Patients with sepsis and acute MLA were identified. Propensity score analysis (PSA) was performed to explain baseline differences in the probability of accepting or not accepting SB. The edge structured cox model (MSCM) was used to adjust for baseline and time-varying confounding variables. The primary outcome was the ICU and hospital mortality. The subgroup of septic shock was also investigated. Results: A total of 512 septic patients with acute MLA were identified in this study, including 160 in the SB group and 352 in the non-SB group. In the PSA, SB administration was associated with reduced ICU (HR .58, 95% CI 0.38-.89; p <.05) and hospital (HR .67, 95% CI 0.47-.95; p <.05) mortality in septic patients with acute MLA. In the subgroup, the results were similar with septic patients. In the MSCM, SB administration could also improve the ICU (HR .35, 95% CI 0.16-.75; p <.01) and (HR .50, 95% CI 0.28-.88; p <.05) mortality on septic patients. However, In the subgroup, SB administration could only be found associated with improved hospital (HR .44, 95% CI 0.20-.97; p <.05) survival in septic shock. Conclusion: SB administration treatment could reduce ICU and hospital mortality of septic patients with acute MLA. Meanwhile, it could also improve hospital survival in the subgroup of septic shock patients with acute MLA.
| S-EPMC9868412 | biostudies-literature
Project description:The purpose was to investigate the effects of one dose of NaHCO3 per day for five consecutive days on cycling time-to-exhaustion (Tlim) at 'Critical Power' (CP) and acid-base parameters in endurance athletes.Eight trained male cyclists and triathletes completed two exercise periods in a randomized, placebo-controlled, double-blind interventional crossover investigation. Before each period, CP was determined. Afterwards, participants completed five constant-load cycling trials at CP until volitional exhaustion on five consecutive days, either after a dose of NaHCO3 (0.3 g·kg-1 body mass) or placebo (0.045 g·kg-1 body mass NaCl).Average Tlim increased by 23.5% with NaHCO3 supplementation as compared to placebo (826.5 ± 180.1 vs. 669.0 ± 167.2 s; P = 0.001). However, there was no time effect for Tlim (P = 0.375). [HCO3-] showed a main effect for condition (NaHCO3: 32.5 ± 2.2 mmol·l-1; placebo: 26.2 ± 1.4 mmol·l-1; P < 0.001) but not for time (P = 0.835). NaHCO3 supplementation resulted in an expansion of plasma volume relative to placebo (P = 0.003).The increase in Tlim was accompanied by an increase in [HCO3-], suggesting that acidosis might be a limiting factor for exercise at CP. Prolonged NaHCO3 supplementation did not lead to a further increase in [HCO3-] due to the concurrent elevation in plasma volume. This may explain why Tlim remained unaltered despite the prolonged NaHCO3 supplementation period. Ingestion of one single NaHCO3 dose per day before the competition during multiday competitions or tournaments might be a valuable strategy for performance enhancement.Trial registration: ClinicalTrials.gov Identifier NCT01621074.
| S-EPMC3623762 | biostudies-literature
Project description:Objective: Metabolic acidosis often occurs in the paediatric intensive care unit (PICU). Although sodium bicarbonate (SB) has been widely used in paediatrics, data on the effect of SB on children with metabolic acidosis in the PICU are scarce. Methods: Patients with metabolic acidosis who were treated with SB within 48 h of PICU admission were screened. Multivariate logistic regression, subgroup analysis, and propensity score matching (PSM) were used to investigate the relationships between SB infusion and clinical outcomes. Results: A total of 1,595 patients with metabolic acidosis were enrolled in this study. In the multivariate logistic regression model, SB infusion was not correlated with in-hospital mortality (odds ratio (OR) 0.87, 95% confidence interval (CI) 0.47-1.63, p = 0.668), but was significantly correlated with hypernatraemia (OR 1.98, 95% CI 1.14-3.46, p = 0.016), hypokalaemia (OR 2.01, 95% CI 1.36-2.96, p < 0.001), and hypocalcaemia (OR 4.29, 95% CI 2.92-6.31, p < 0.001). In the pH value, lactate level, acute kidney injury level, age grouping, and anion gap level subgroups, the ORs for SB and in-hospital mortality were not statistically significant. After PSM, the results remained unchanged. Conclusion: SB infusion does not reduce the in-hospital mortality of severely ill children with metabolic acidosis and increases the risk of hypernatraemia, hypokalaemia, and hypocalcaemia. More effort should be focused on eliminating the causes of metabolic acidosis rather than SB infusion.
| S-EPMC8970597 | biostudies-literature
Project description:BackgroundAcidosis frequently occurs in severe acute kidney injury (AKI), and continuous renal replacement therapy (CRRT) can control this pathologic condition. Nevertheless, acidosis may be aggravated; thus, monitoring is essential after starting CRRT. Herein, we addressed the longitudinal trajectory of acidosis on CRRT and its relationship with worse outcomes.MethodsThe latent growth mixture model was applied to classify the trajectories of pH during the first 24 hours and those of C-reactive protein (CRP) after 24 hours on CRRT due to AKI (n = 1815). Cox proportional hazard models were used to calculate hazard ratios of all-cause mortality after adjusting multiple variables or matching their propensity scores.ResultsThe patients could be classified into 5 clusters, including the normally maintained groups (1st cluster, pH = 7.4; and 2nd cluster, pH = 7.3), recovering group (3rd cluster with pH values from 7.2 to 7.3), aggravating group (4th cluster with pH values from 7.3 to 7.2), and ill-being group (5th cluster, pH < 7.2). The pH clusters had different trends of C-reactive protein (CRP) after 24 hours; the 1st and 2nd pH clusters had lower levels, but the 3rd to 5th pH clusters had an increasing trend of CRP. The 1st pH cluster had the best survival rates, and the 3rd to 5th pH clusters had the worst survival rates. This survival difference was significant despite adjusting for other variables or matching propensity scores.ConclusionsInitial trajectories of acidosis determine subsequent worse outcomes, such as mortality and inflammation, in patients undergoing CRRT due to AKI.
| S-EPMC9792158 | biostudies-literature
Project description:The sodium-bicarbonate cotransporter NBCn1 (SLC4A7) is an acid-base transporter that normally moves Na(+) and HCO(3)(-) into the cell. This membrane protein is sensitive to cellular and systemic pH changes. We examined NBCn1 expression and localization in the brain and its response to chronic metabolic acidosis. Two new NBCn1 antibodies were generated by immunizing a rabbit and a guinea pig. The antibodies stained neurons in a variety of rat brain regions, including hippocampal pyramidal neurons, dentate gyrus granular neurons, posterior cortical neurons, and cerebellar Purkinje neurons. Choroid plexus epithelia were also stained. Double immunofluorescence labeling showed that NBCn1 and the postsynaptic density protein PSD-95 were found in the same hippocampal CA3 neurons and partially colocalized in dendrites. PSD-95 was pulled down from rat brain lysates with the GST/NBCn1 fusion protein and was also coimmunoprecipitated with NBCn1. Chronic metabolic acidosis was induced by feeding rats with normal chow or 0.4 M HCl-containing chow for 7 days. Real-time PCR and immunoblot showed upregulation of NBCn1 mRNA and protein in the hippocampus of acidotic rats. NBCn1 immunostaining was enhanced in CA3 neurons, posterior cortical neurons, and cerebellar granular cells. Intraperitoneal administration of N-methyl-d-aspartate caused neuronal death determined by caspase-3 activity, and this effect was more severe in acidotic rats. Administering N-methyl-d-aspartate also inhibited NBCn1 upregulation in acidotic rats. We conclude that NBCn1 in neurons is upregulated by chronic acid loads, and this upregulation is associated with glutamate excitotoxicity.
| S-EPMC2867381 | biostudies-literature
Project description:BackgroundMetabolic acidosis is associated with accelerated progression of chronic kidney disease (CKD). Whether treatment of metabolic acidosis with sodium bicarbonate improves kidney and patient survival in CKD is unclear.MethodsWe conducted a randomized (ratio 1:1). open-label, controlled trial (NCT number: NCT01640119. www.clinicaltrials.gov ) to determine the effect in patients with CKD stage 3-5 of treatment of metabolic acidosis with sodium bicarbonate (SB) on creatinine doubling (primary endpoint), all-cause mortality and time to renal replacement therapy compared to standard care (SC) over 36-months. Parametric, non-parametric tests and survival analyses were used to assess the effect of SB on these outcomes.ResultsA total of 376 and 364 individuals with mean (SD) age 67.8 (14.9) years, creatinine clearance 30 (12) ml/min, and serum bicarbonate 21.5 (2.4) mmol/l were enrolled in SB and SC, respectively. Mean (SD) follow-up was 29.6 (9.8) vs 30.3 (10.7) months in SC and SB. respectively. The mean (SD) daily doses of SB was 1.13 (0.10). 1.12 (0.11). and 1.09 (0.12) mmol/kg*bw/day in the first, second and third year of follow-up, respectively. A total of 87 participants reached the primary endpoint [62 (17.0%) in SC vs 25 (6.6%) in SB, p < 0.001). Similarly, 71 participants [45 (12.3%) in SC and 26 (6.9%) in SB, p = 0.016] started dialysis while 37 participants [25 (6.8%) in SC and 12 (3.1%) in SB, p = 0.004] died. There were no significant effect of SB on blood pressure, total body weight or hospitalizations.ConclusionIn persons with CKD 3-5 without advanced stages of chronic heart failure, treatment of metabolic acidosis with sodium bicarbonate is safe and improves kidney and patient survival.
| S-EPMC6821658 | biostudies-literature