596: Bicarbonate Therapy in Acute Diarrhea Having Severe Dehydration and Severe Metabolic Acidosis: RCT

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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