Faculty Opinions recommendation of Bicarbonate therapy in severe metabolic acidosis.

Background Gastrointestinal (GI) perforation is a risk factor for mortality in very low birth weight (VLBW) infants. Little data exist regarding pretreatment factors and patient characteristics known to independently correlate with risk of death. Materials and Methods A retrospective review of all VLBW infants who sustained GI perforation between 2011 and 2018 was conducted. Birth, laboratory, and disease-related factors of infants who died were compared to those who survived. Results 42 VLBW infants who sustained GI perforations were identified. Eleven (26.19%) died. There were no significant differences in birth-related factors, hematological lab levels at diagnosis, presence of pneumatosis, or bacteremia. Portal venous gas ( P = .03), severe metabolic acidosis ( P < .01), and elevated lactate at diagnosis ( P < .01) were statistically more likely to occur among infants who died. Discussion Portal venous gas, severe metabolic acidosis, and elevated lactate were associated with an increased risk of mortality among VLBW infants who develop a GI perforation. Further research is required to better identify risk factors.

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Identifying prognostic factors of severe metabolic acidosis and uraemia in African children with severe falciparum malaria: a secondary analysis of a randomized trial

Malaria Journal ◽

10.1186/s12936-021-03785-0 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Grace Mzumara ◽

Stije Leopold ◽

Kevin Marsh ◽

Arjen Dondorp ◽

Eric O. Ohuma ◽

...

Keyword(s):

Prognostic Factors ◽

Metabolic Acidosis ◽

Falciparum Malaria ◽

Model Building ◽

Statistical Significance ◽

Severe Metabolic Acidosis ◽

African Countries ◽

Prognostic Features ◽

African Children ◽

Severe Falciparum Malaria

Abstract Background Severe metabolic acidosis and acute kidney injury are major causes of mortality in children with severe malaria but are often underdiagnosed in low resource settings. Methods A retrospective analysis of the ‘Artesunate versus quinine in the treatment of severe falciparum malaria in African children’ (AQUAMAT) trial was conducted to identify clinical features of severe metabolic acidosis and uraemia in 5425 children from nine African countries. Separate models were fitted for uraemia and severe metabolic acidosis. Separate univariable and multivariable logistic regression were performed to identify prognostic factors for severe metabolic acidosis and uraemia. Both analyses adjusted for the trial arm. A forward selection approach was used for model building of the logistic models and a threshold of 5% statistical significance was used for inclusion of variables into the final logistic model. Model performance was assessed through calibration, discrimination, and internal validation with bootstrapping. Results There were 2296 children identified with severe metabolic acidosis and 1110 with uraemia. Prognostic features of severe metabolic acidosis among them were deep breathing (OR: 3.94, CI 2.51–6.2), hypoglycaemia (OR: 5.16, CI 2.74–9.75), coma (OR: 1.72 CI 1.17–2.51), respiratory distress (OR: 1.46, CI 1.02–2.1) and prostration (OR: 1.88 CI 1.35–2.59). Features associated with uraemia were coma (3.18, CI 2.36–4.27), Prostration (OR: 1.78 CI 1.37–2.30), decompensated shock (OR: 1.89, CI 1.31–2.74), black water fever (CI 1.58. CI 1.09–2.27), jaundice (OR: 3.46 CI 2.21–5.43), severe anaemia (OR: 1.77, CI 1.36–2.29) and hypoglycaemia (OR: 2.77, CI 2.22–3.46) Conclusion Clinical and laboratory parameters representing contributors and consequences of severe metabolic acidosis and uraemia were independently associated with these outcomes. The model can be useful for identifying patients at high risk of these complications where laboratory assessments are not routinely available.

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Complete recovery from severe metabolic acidosis associated with isoniazid poisoning in a young boy

Pediatric Emergency Care ◽

10.1097/00006565-198912000-00018 ◽

1989 ◽

Vol 5 (4) ◽

pp. 257-258 ◽

Cited By ~ 4

Author(s):

LEHMAN E. BLACK ◽

SIMON P. ROS

Keyword(s):

Metabolic Acidosis ◽

Complete Recovery ◽

Severe Metabolic Acidosis

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Brain pH responses to sodium bicarbonate and Carbicarb during systemic acidosis

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.256.5.h1316 ◽

1989 ◽

Vol 256 (5) ◽

pp. H1316-H1321 ◽

Cited By ~ 7

Author(s):

J. I. Shapiro ◽

M. Whalen ◽

R. Kucera ◽

N. Kindig ◽

G. Filley ◽

...

Keyword(s):

Metabolic Acidosis ◽

Sodium Bicarbonate ◽

Ammonium Chloride ◽

Respiratory Acidosis ◽

Arterial Pco2 ◽

Bicarbonate Therapy ◽

Brain Ph ◽

Dose Dependent ◽

Intracellular Alkalinization

Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.

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Sodium Bicarbonate Therapy in Patients with Metabolic Acidosis

The Scientific World JOURNAL ◽

10.1155/2014/627673 ◽

2014 ◽

Vol 2014 ◽

pp. 1-13 ◽

Cited By ~ 37

Author(s):

María M. Adeva-Andany ◽

Carlos Fernández-Fernández ◽

David Mouriño-Bayolo ◽

Elvira Castro-Quintela ◽

Alberto Domínguez-Montero

Keyword(s):

Chronic Kidney Disease ◽

Metabolic Acidosis ◽

Kidney Disease ◽

Sodium Bicarbonate ◽

Negative Impact ◽

Qtc Interval ◽

Bicarbonate Therapy ◽

Proximal Tubular ◽

Acute Metabolic Acidosis ◽

Renal Proximal Tubular

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.

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Risk Potential for Organ Dysfunction Associated with Sodium Bicarbonate Therapy (SBT) in Critically Ill Patients with Hemodynamic Worsening

10.21203/rs.3.rs-182629/v1 ◽

2021 ◽

Author(s):

Tiehua Wang ◽

Lingxian Yi ◽

Hua Zhang ◽

Tianhao Wang ◽

Jingjing Xi ◽

...

Keyword(s):

Logistic Regression ◽

Metabolic Acidosis ◽

Sodium Bicarbonate ◽

Critically Ill ◽

Organ Dysfunction ◽

Critically Ill Patients ◽

Control Group ◽

Increased Risk ◽

Bicarbonate Therapy ◽

Risk Potential

Abstract Background: The role of sodium bicarbonate therapy (SBT) remains controversial. This study aimed to investigate whether hemodynamic status before SBT contributed to the heterogeneous outcomes associated with SBT in acute critically ill patients.Methods: We obtained data from patients with metabolic acidosis from the Medical Information Mart for Intensive Care (MIMIC)-III database. Propensity score matching (PSM) was applied to match the SBT group with the control group. Logistic regression and Cox regression were used to analyze a composite of newly “developed or exacerbated organ dysfunction” (d/eOD) within 7 days of ICU admission and 28-day mortality associated with SBT for metabolic acidosis.Results: A total of 1765 patients with metabolic acidosis were enrolled, and 332 pairs obtained by PSM were applied to the final analyses in the study. An increased incidence of newly d/eOD was observed in the SB group compared with the control group (54.8% vs 44.6%, p<0.01). Multivariable logistic regression indicated that the adjusted OR of SBT for this composite outcome was no longer significant [OR (95% CI): 1.39 (0.9, 1.85); p=0.164]. This effect of SBT did not change with the quintiles stratified by pH. Interestingly, SBT was associated with an increased risk of the composite of newly d/eOD in the subgroup of patients with worsening hemodynamics before SBT [adjusted OR (95% CI): 3.6 (1.84, 7.22), p< 0.001]. Moreover, the risk potential for this composite of outcomes was significantly increased in patients characterized by both worsening [adjusted OR (95% CI): 2.91 (1.54, 5.47), p< 0.001] and unchanged hemodynamics [adjusted OR (95% CI): 1.94 (1.01, 3.72), p=0.046) compared to patients with improved hemodynamics before SBT. Our study failed to demonstrate an association between SBT and 28-day mortality in acute critically ill patients with metabolic acidosis.Conclusions: Our findings suggested that SBT for metabolic acidosis was associated with an increased risk potential for subsequent d/eOD, while the hemodynamic status remained unstable during the acute phase of critical illness.

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Acute Butylglycol Intoxication: A Case Report

Human Toxicology ◽

10.1177/096032718900800307 ◽

1989 ◽

Vol 8 (3) ◽

pp. 243-245 ◽

Cited By ~ 34

Author(s):

F.P. Gijsenbergh ◽

M. Jenco ◽

H. Veulemans ◽

D. Groeseneken ◽

R. Verberckmoes ◽

...

Keyword(s):

Case Report ◽

Metabolic Acidosis ◽

Suicide Attempt ◽

Rare Case ◽

Severe Metabolic Acidosis ◽

Forced Diuresis ◽

Present On Admission

A rare case of butylglycol intoxication in a suicide attempt is reported. Coma and hypotension were present on admission and severe metabolic acidosis arose subsequently. Forced diuresis and haemodialysis led to an uneventful outcome.

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