China
Africa
Explore chapters and articles related to this topic
Fluid and electrolyte balance in the newborn
Published in Prem Puri, Newborn Surgery, 2017
Judith Meehan, Joseph Chukwu, Winifred A. Gorman, Eleanor J. Molloy
Acute metabolic acidosis is common in the critically ill newborn. Treatment requires management of the underlying cause. Sodium bicarbonate may be used for severe acidosis by giving a dose of 1–2 mmol/kg of 4.2% sodium bicarbonate diluted in equal volume of water. There is currently no evidence from randomized controlled trials to support its routine use in neonatal resuscitation.69 Its effect on morbidity and mortality has not been well demonstrated. There is controversy about the value of intravenous sodium bicarbonate for correction of metabolic acidosis.70 It is no longer recommended for resuscitation in newborn infants, and although it may correct acidosis in hypotensive shocked infants, this has not been shown to result in improvement in blood pressure or perfusion.71 Sodium bicarbonate infusion has potential side effects. Myocardial function may be depressed from the osmolar load with severe acidosis. Paradoxical intracellular acidosis may occur as well as a reduction in cerebral blood flow and increased risk of IVH. Use of sodium bicarbonate is therefore discouraged unless the infant has prolonged acidosis not responsive to other therapies including adequate ventilation.
Case 83: Shivering at the Station
Published in Layne Kerry, Janice Rymer, 100 Diagnostic Dilemmas in Clinical Medicine, 2017
The patient was warmed to 34°C using a Bair hugger. Intravenous sodium bicarbonate was given until the base excess reached −3. Insulin and dextrose treatment helped to correct the hyperkalaemia. Intravenous co-amoxiclav was commenced for possible sepsis of unknown source. Intravenous pabrinex was started for possible alcohol misuse. She was admitted directly to the high dependency unit.
Blood gas interpretation
Published in Philip Woodrow, Nursing Acutely Ill Adults, 2015
Severe acidosis is often fatal, so in the past was treated with aggressive infusion of intravenous sodium bicarbonate. However bicarbonate, like sodium, does not significantly enter cells (where metabolic acids are produced). Paradoxically, bicarbonate can dissociate into carbon dioxide and a hydrogen and oxygen radical; carbon dioxide can diffuse freely into cells, worsening intracellular acidosis. The Resuscitation Council (2010) therefore advise not to ‘routinely’ give sodium bicarbonate.
Sodium bicarbonate treatment for QRS widening in bupropion overdoses
Published in Clinical Toxicology, 2023
Michael Simpson, Linda Johnson, Charlotte Goldfine
To maximize results from the query tool, three queries were performed. Each query identified patients over 17 years of age with documented administration of intravenous sodium bicarbonate during a hospital encounter between January 2010 and June 2022. The first query included patients with a “Reason for Visit” of “Drug Overdose” within the same encounter where they received sodium bicarbonate. The second query included patients with ICD10 codes T43.291A, T43.292A, T43.293A, T43.294A, or T43.295A for the same encounter for which they received sodium bicarbonate. The third query included patients with a discharge summary that included the phrases “bupropion overdose,” “bupropion ingestion,” “bupropion toxicity,” “Wellbutrin overdose,” “Wellbutrin ingestion,” “Wellbutrin toxicity,” “Wellbutrin XL overdose,” “Wellbutrin XL ingestion,” or “Wellbutrin XL toxicity,” within the same encounter where the patient received sodium bicarbonate.
Severe and prolonged flecainide intoxication treated by extracorporeal life support: possible role of cytochrome P450 2D6 polymorphism?
Published in Clinical Toxicology, 2019
Philippe Hantson, Claire Wuidart, Vincent Haufroid
An 18-year-old woman was admitted six hours after the ingestion of a maximal estimated dose of 18,000 mg of extend-release flecainide that was her chronic treatment for supraventricular tachycardia. On arrival, she had a Glasgow Coma Scale score 3 that progressed from 3 to 6/15. Arterial blood pressure was 96/79 mm Hg, heart rhythm was 63/min, irregular. The electrocardiogram (ECG) revealed irregular rhythm with broad QRS complexes (220 ms). The initial laboratory investigation has revealed: arterial pH 7.21, bicarbonate 14 mmol/L, lactate 10.6 mmol/L, creatinine 1.4 mg/dL. The patient received 100 mmol of intravenous sodium bicarbonate and 1000 mL of fluids. After the development of a refractory shock, advanced cardiac life support was commenced with epinephrine and norepinephrine, external cardiac massage, and electric shocks for ventricular tachycardia and ventricular fibrillation. An additional dose of 300 mmol of sodium bicarbonate was administered without any change on the ECG. A single dose of activated charcoal had also been administered after intubation, even if the delay from ingestion was probably too long. Intravenous lipid emulsion (ILE) therapy was also given according to the following regimen: 1.5 mL/kg as a bolus, followed by 0.25 mL/kg/min over 30 min; there was no change in hemodynamic conditions. Extracorporeal cardiac life support (ECLS) was initiated less than 35 min after the failure of pharmacological resuscitation. Cardiac echography showed a depressed left ventricular function (ejection fraction 35%). The complete intensive care management is detailed in Figure 1.
Incidence of rebound salicylate toxicity following cessation of urine alkalinization
Published in Clinical Toxicology, 2023
Mary O’Keefe, Matthew Stanton, Ryan Feldman, Jillian Theobald
This was a single-center, retrospective study of adult and pediatric cases with a primary ingestion of acetylsalicylic acid and sodium bicarbonate infusion listed as a part of the patient’s treatment reported to the local poison center from 1 January 2015 through 31 December 2019. All data were queried from ToxSentry, the program at the local poison center used by the Specialists in Poison Information to input information received over the phone regarding cases. Cases were excluded if the salicylate product was not listed as the primary ingestion or if there was no serum salicylate concentration documented after discontinuation of intravenous sodium bicarbonate infusion. A “rebound serum salicylate concentration” was defined as any increase in serum salicylate concentration after discontinuation of the intravenous sodium bicarbonate infusion. “Salicylate toxicity” was defined as a serum salicylate concentration greater than 300 mg/L (2.17 mmol/L). “Rebound salicylate toxicity” refers to an increase in serum salicylate concentration greater than 300 mg/(2.17 mmol/L) after discontinuation of the intravenous sodium bicarbonate infusion. The local poison center recommends an endpoint of two decreasing serum salicylate concentrations less than 300 mg/L (2.17 mmol/L) as the internal guideline for cessation of alkalinization of the urine. However, due to a lack of a universal standard on when urine alkalinization should be stopped as described previously, cases were still included and analyzed even if they did not follow this internal guideline. The primary outcome was incidence of rebound salicylate toxicity following discontinuation of intravenous sodium bicarbonate infusion. This study was approved by the institutional review board.