Sodium Bicarbonate for the Treatment of Severe Metabolic Acidosis With Moderate or Severe Acute Kidney Injury in ICU

2019 ◽  
Author(s):  
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Kidney Injury ◽  
Severe Metabolic Acidosis

The Use of Sodium Bicarbonate for Metabolic Acidosis in Patients With Acute Kidney Injury

2020 ◽  
Vol 48 (3) ◽  
pp. e251-e252 ◽  
Author(s):  
Hiroshi Yonekura ◽  
Yohei Kawasaki ◽  
Yuki Nakamori ◽  
Masataka Kamei
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Sodium Bicarbonate ◽  
Kidney Injury

scholarly journals Ethylene Glycol Intoxication Requiring ECMO Support

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Raphael Rosen ◽  
Shelief Robbins-Juarez ◽  
Jacob Stevens
Keyword(s):  
Acute Kidney Injury ◽  
Renal Failure ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Extracorporeal Membrane Oxygenation ◽  
Kidney Injury ◽  
Neurological Injury ◽  
Severe Metabolic Acidosis ◽  
Toxic Metabolites ◽  
Ethylene Glycol Intoxication

Ethylene glycol is commonly used in antifreeze, and ingestion of even a small amount can result in acute kidney injury, severe metabolic acidosis, and neurological injury. When cases are recognized early, treatment involves administration of alcohol dehydrogenase inhibitors to prevent conversion to toxic metabolites of glycolate, glyoxolate, and oxalate. In later presentations with more severe renal injury, hemodialysis may be required for clearance of toxic metabolites and supportive care for renal failure. We present the first reported case of severe ethylene glycol intoxication requiring support of extracorporeal membrane oxygenation (ECMO) due to refractory cardiopulmonary collapse.

scholarly journals Successful Resuscitation of a Patient with Life-Threatening Metabolic Acidosis by Hemodialysis: A Case of Ethylene Glycol Intoxication

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Ikuyo Narita ◽  
Michiko Shimada ◽  
Norio Nakamura ◽  
Reiichi Murakami ◽  
Takeshi Fujita ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Ethylene Glycol ◽  
Kidney Injury ◽  
University Hospital ◽  
Severe Metabolic Acidosis ◽  
Continuous Hemodiafiltration ◽  
Successful Resuscitation ◽  
Life Threatening ◽  
Ethylene Glycol Intoxication

Background. Ethylene glycol intoxication causes severe metabolic acidosis and acute kidney injury. Fomepizole has become available as its antidote. Nevertheless, a prompt diagnosis is not easy because patients are often unconscious. Here we present a case of ethylene glycol intoxication who successfully recovered with prompt hemodialysis. Case Presentation. A 52-year-old Japanese male was admitted to a local hospital due to suspected food poisoning. The patient presented with nausea and vomiting, but his condition rapidly deteriorated, with worsening conscious level, respiratory distress requiring mechanical ventilation, hypotension, and severe acute kidney injury. He was transferred to the university hospital; hemodialysis was initiated because of hyperkalemia and severe metabolic acidosis. On recovering consciousness, he admitted having ingested antifreeze solution. Thirty-seven days after admission, the patient was discharged without requiring HD. Conclusions. We reported a case of ethylene glycol intoxication who presented with a life-threatening metabolic acidosis. In a state of severe circulatory shock requiring catecholamines, hemodialysis should be avoided, and continuous hemodiafiltration may be a preferred approach. However, one should be aware of the possibility of intoxication by unknown causes, and hemodialysis could be life-saving with its superior ability to remove toxic materials in such cases.

scholarly journals Identifying Prognostic Factors of Severe Metabolic Acidosis and Acute Kidney Injury in African Children with Severe Falciparum Malaria: A Secondary Analysis of A Randomised Trial

2021 ◽  
Author(s):  
Grace Wezi Mzumara ◽  
Stije Stije Leopold ◽  
Kevin Marsh ◽  
Arjen Dondorp ◽  
Eric Ohuma ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Prognostic Factors ◽  
Metabolic Acidosis ◽  
Falciparum Malaria ◽  
Kidney Injury ◽  
Severe Anaemia ◽  
Severe Metabolic Acidosis ◽  
Prognostic Features ◽  
African Children ◽  
Severe Falciparum Malaria

Abstract IntroductionSevere metabolic acidosis and acute kidney injury are major causes of mortality in children with severe malaria but are often underdiagnosed in low resource settings. MethodsWe conducted a retrospective analysis of the ‘Artesunate vs Quinine in the treatment of severe falciparum malaria in African children’ (AQUAMAT) trial to identify clinical features of severe metabolic acidosis and acute kidney injury in 5425 children from nine African countries. Separate models were fitted for acute kidney injury and severe metabolic acidosis. Separate univariable and multivariable logistic regression were performed to identify prognostic factors for severe metabolic acidosis (SMA) and acute kidney injury (AKI). 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. ResultsThere were 2296 children identified with Severe metabolic acidosis and 1110 with Acute Kidney Injury. Prognostic features of SMA among them were: deep breathing (OR: 5.41, CI: 4.26 – 6.89), hypoglycaemia (OR: 5.22, CI: 3.80 – 7.18), AKI (OR: 3.99, CI: 3.30 – 4.81), coma ( OR: 1.79 CI: 1.36 – 2.35), respiratory distress (OR: 1.49, CI: 1.21 – 1.83), prostration (OR: 1.64 CI: 1.30 – 2.03) and severe anaemia (OR: 1.40, CI: 1.11 – 1.77). Features associated with AKI were; older children(OR: 1.20, CI: 1.15 – 1.25), coma (2.47, CI: 1.78 – 3.42), Prostration (OR: 1.52 CI: 1.14 – 2.02), decompensated shock (OR: 1.74, CI: 1.15 – 2.63), black water fever (CI: 1.81. CI: 1.22 – 2.69), jaundice (OR: 3.31 CI: 2.01 – 5.47), SMA (OR: 4.02 CI:3.30 – 4.89), mild anaemia (OR: 1.36, CI: 1.05 – 1.76), severe anaemia (OR: 1.48, CI: 1.11 – 1.96), hypoglycaemia (OR: 2.02, CI: 1.58 – 2.59), hypernatremia (OR: 5.74, CI: 2.69 – 12.26) and hyperkalaemia (OR: 5.31. CI: 4.15 – 6.80). ConclusionClinical and laboratory parameters representing contributors and consequences of severe metabolic acidosis and acute kidney injury 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.

Electrolyte and acid–base disorders in AKI

2015 ◽  
Author(s):  
Achim Jörres ◽  
Dietrich Hasper ◽  
Michael Oppert
Keyword(s):  
Acute Kidney Injury ◽  
Metabolic Acidosis ◽  
Renal Replacement Therapy ◽  
Sodium Bicarbonate ◽  
Kidney Injury ◽  
Medical Emergency ◽  
Acid Base ◽  
Compensatory Mechanisms ◽  
Electrolyte Disturbances ◽  
Underlying Pathology

Electrolyte disturbances are common in patients with acute kidney injury (AKI) and should be corrected. In particular, hyperkalaemia above 6–6.5 mmol/L (especially with electrocardiogram changes) constitutes a medical emergency and warrants immediate intervention. Both hypo- and hypernatraemia may occur during AKI. Chronic changes in serum sodium need to be corrected bearing in mind the underlying pathology; however, when severe and evolving rapidly they should be corrected faster, irrespective of the cause. Acid–base disorders are also common in AKI and need to be treated in the context of underlying problems and physiological compensatory mechanisms. In metabolic acidosis, a bicarbonate deficit may be corrected by sodium bicarbonate administration. Of note, whilst patients with AKI tend to retain electrolytes such as potassium and phosphate, this might be reversed during renal replacement therapy and even substitution of these losses may be required.

scholarly journals Metabolic acidosis as a risk factor for the development of acute kidney injury and hospital mortality

2017 ◽  
Vol 13 (5) ◽  
pp. 2362-2374 ◽  
Author(s):  
Jiachang Hu ◽  
Yimei Wang ◽  
Xuemei Geng ◽  
Rongyi Chen ◽  
Xialian Xu ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Risk Factor ◽  
Metabolic Acidosis ◽  
Hospital Mortality ◽  
Kidney Injury

Sodium Bicarbonate and Renal Function after Cardiac Surgery

2015 ◽  
Vol 122 (2) ◽  
pp. 294-306 ◽  
Author(s):  
Michael Bailey ◽  
Shay McGuinness ◽  
Michael Haase ◽  
Anja Haase-Fielitz ◽  
Rachael Parke ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Serum Creatinine ◽  
Sodium Bicarbonate ◽  
Replacement Therapy ◽  
Primary Outcome ◽  
Artery Bypass ◽  
Kidney Injury ◽  
Acute Kidney Injury Network ◽  
Double Blind

Abstract Background: The effect of urinary alkalinization in cardiac surgery patients at risk of acute kidney injury (AKI) is controversial and trial findings conflicting. Accordingly, the authors performed a prospectively planned individual patient data meta-analysis of the double-blind randomized trials in this field. Methods: The authors studied 877 patients from three double-blind, randomized controlled trials enrolled to receive either 24 h of intravenous infusion of sodium bicarbonate or sodium chloride. The primary outcome measure was a postoperative increase in serum creatinine concentration of greater than 25% or 0.5 mg/dl (> 44 μm/L) within the first five postoperative days. Secondary outcomes included the raw change in serum creatinine, greater than 50% and greater than 100% rises in serum creatinine, developing AKI (Acute Kidney Injury Network criteria), initiation of renal replacement therapy, morbidity, and mortality. Results: Patients were similar in demographics, comorbidities, and cardiac procedures. Sodium bicarbonate increased plasma bicarbonate (P < 0.001) and urine pH (P < 0.001). There were no differences in the development of the primary outcome (Bicarbonate 45% [39–51%] vs. Saline 42% [36–48%], P = 0.29). This result remained unchanged when controlling for study and covariates (odds ratio [OR], 99% confidence interval [CI]: Bicarbonate vs. Control, 1.11 [0.77–1.60], P = 0.45). There was, however, a significant study-adjusted benefit in elective coronary artery bypass surgery patients in terms of renal replacement therapy (Bicarbonate vs. Control, OR: 0.38 [99% CI: 0.25–0.58], P < 0.0001) and the development of an Acute Kidney Injury Network grade = 3 (Bicarbonate vs. Control, OR: 0.45 [99% CI: 0.43–0.48], P < 0.0001). Conclusions: Urinary alkalinization using sodium bicarbonate infusion is not associated with an overall lower incidence of AKI; however, it reduces severe AKI and need for renal replacement therapy in elective coronary artery bypass patients.

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