Sodium bicarbonate therapy in severe diabetic ketoacidosis

doi:10.1016/0002-9343(83)91203-2

The American Journal of Medicine

Volume 75, Issue 2, August 1983, Pages 263-268

https://doi.org/10.1016/0002-9343(83)91203-2 Get rights and content

Abstract

Rates of recovery of plasma glucose and bicarbonate levels, arterial pH, and level of consciousness were determined in a retrospective analysis of 95 episodes of severe diabetic ketoacidosis in patients treated with conventional regimens including low-dose insulin, saline, and potassium administration. No significant differences were found between 73 episodes in 52 patients treated with sodium bicarbonate and 22 episodes in 21 patients not undergoing such treatment. In view of these observations, the potential hazards of sodium bicarbonate replacement therapy, and the fact that sodium bicarbonate is still frequently given, the use of intravenous sodium bicarbonate treatment in patients with severe diabetic ketoacidosis requires reevaluation.

References (20)

TDR Hockaday et al.
Diabetic coma
Clin Endocrinol Metab
(1972)
GJ Addis et al.
Bicarbonate therapy in diabetic acidosis
Lancet
(1964)
MA Bureau et al.
Cerebral hypoxia from bicarbonate infusion in diabetic acidosis
J Pediatr
(1980)
AJ King et al.
Acid-base changes during treatment of diabetic ketoacidosis
Lancet
(1974)
NG Soler et al.
Potassium balance during treatment of diabetic ketoacidosis with special reference to the use of bicarbonate
Lancet
(1972)
H Wang et al.
Effects of changes in coronary blood pH on the heart
Circ Res
(1965)
PH Gerst et al.
A quantitative evaluation of the effects of acidosis and alkalosis upon ventricular fibrillation threshold
Surgery
(1966)
DM Phear
PZ Zimmet et al.
Acid production in diabetic acidosis; a more rational approach to alkali replacement
Br Med J
(1970)
NY Smith et al.
Myocardial resistance to metabolic acidosis
Arch Surg
(1966)

There are more references available in the full text version of this article.

Cited by (122)

A Review of Bicarbonate Use in Common Clinical Scenarios
2023, Journal of Emergency Medicine
The use of sodium bicarbonate to treat metabolic acidosis is intuitive, yet data suggest that not all patients benefit from this therapy.
In this narrative review, we describe the physiology behind commonly encountered nontoxicologic causes of metabolic acidosis, highlight potential harm from the indiscriminate administration of sodium bicarbonate in certain scenarios, and provide evidence-based recommendations to assist emergency physicians in the rational use of sodium bicarbonate.
Sodium bicarbonate can be administered as a hypertonic push, as a resuscitation fluid, or as an infusion. Lactic acidosis and cardiac arrest are two common scenarios where there is limited benefit to routine use of sodium bicarbonate, although certain circumstances, such as patients with concomitant acute kidney injury and lactic acidosis may benefit from sodium bicarbonate. Patients with cardiac arrest secondary to sodium channel blockade or hyperkalemia also benefit from sodium bicarbonate therapy. Recent data suggest that the use of sodium bicarbonate in diabetic ketoacidosis does not confer improved patient outcomes and may cause harm in pediatric patients. Available evidence suggests that alkalinization of urine in rhabdomyolysis does not improve patient-centered outcomes. Finally, patients with a nongap acidosis benefit from sodium bicarbonate supplementation.
Empiric use of sodium bicarbonate in patients with nontoxicologic causes of metabolic acidosis is not warranted and likely does not improve patient-centered outcomes, except in select scenarios. Emergency physicians should reserve use of this medication to conditions with clear benefit to patients.
Euglycemic diabetic ketoacidosis: Etiologies, evaluation, and management
2021, American Journal of Emergency Medicine
Diabetic ketoacidosis is an endocrine emergency. A subset of diabetic patients may present with relative euglycemia with acidosis, known as euglycemic diabetic ketoacidosis (EDKA), which is often misdiagnosed due to a serum glucose <250 mg/dL.
This narrative review evaluates the pathogenesis, diagnosis, and management of EDKA for emergency clinicians.
EDKA is comprised of serum glucose <250 mg/dL with an anion gap metabolic acidosis and ketosis. It most commonly occurs in patients with a history of low glucose states such as starvation, chronic liver disease, pregnancy, infection, and alcohol use. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, which result in increased urinary glucose excretion, are also associated with EDKA. The underlying pathophysiology involves insulin deficiency or resistance with glucagon release, poor glucose availability, ketone body production, and urinary glucose excretion. Patients typically present with nausea, vomiting, malaise, or fatigue. The physician must determine and treat the underlying etiology of EDKA. Laboratory assessment includes venous blood gas for serum pH, bicarbonate, and ketones. Management includes resuscitation with intravenous fluids, insulin, and glucose, with treatment of the underlying etiology.
Clinician knowledge of this condition can improve the evaluation and management of patients with EDKA.
Diabetic ketoacidosis: A consensus statement of the Italian Association of Medical Diabetologists (AMD), Italian Society of Diabetology (SID), Italian Society of Endocrinology and Pediatric Diabetoloy (SIEDP)
2020, Nutrition, Metabolism and Cardiovascular Diseases
Diabetic ketoacidosis (DKA) is a serious medical emergency once considered typical of type 1 diabetes (T1DM), but now reported to occur in type 2 and GDM patients as well. DKA can cause severe complications and even prove fatal. The aim of our study was to review recent international and national guidelines on diagnosis, clinical presentation and treatment of diabetic ketoacidosis, to provide practical clinical recommendations.
Electronic databases (MEDLINE (via PUB Med), Scopus, Cochrane library were searched for relevant literature. Most international and national guidelines indicate the same accurate flow chart to diagnose, to evaluate from clinical and laboratory point of view, and treat diabetic ketoacidosis.
Prompt diagnosis, rapid execution of laboratory analysis and correct treatment are imperative to reduce the mortality related to diabetic ketoacidosis. These recommendations are designed to help healthcare professionals reduce the frequency and burden of DKA.
Evaluation and Management of the Critically Ill Adult With Diabetic Ketoacidosis
2020, Journal of Emergency Medicine
Citation Excerpt :
Several professional societies recommend the use of sodium bicarbonate for those with pH < 6.9 or serum bicarbonate < 5 mEq/L (10,33). However, sodium bicarbonate bolus administration has not demonstrated improved clinical outcomes, including mortality, time to DKA resolution, or reduced length of stay, and it may lead to cerebral edema and hypokalemia (108–113). A retrospective study of 86 patients found no improvement in time to resolution of acidemia, hospital discharge, requirement for i.v. insulin, and potassium requirement with i.v. sodium bicarbonate (114).
Diabetic ketoacidosis (DKA) is a hyperglycemic emergency that presents commonly to the emergency department. Severe DKA has the potential for significant morbidity and mortality if not recognized early and treated appropriately. It is incumbent on the emergency clinician to be vigilant in the management of these critically ill patients.
This narrative review evaluates the emergency medicine management of the adult patient with severe DKA.
DKA is a condition found most commonly in patients with insulin-dependent diabetes, often due to nonadherence with diabetic medications or an inciting event, such as infection or ischemia. The severity of DKA is classified based on the level of acidosis present rather than absolute glucose level. The management of severe DKA involves assessing and treating the inciting event, fluid hydration, insulin, and potassium repletion. Close monitoring is necessary to prevent the complications that can occur.
DKA is a medical condition that has the potential for significant morbidity and mortality if not recognized and managed appropriately.
Diabetes Mellitus
2020, Sperling Pediatric Endocrinology: Expert Consult - Online and Print
Diabetes mellitus (DM) is a syndrome of disturbed energy metabolism, conveniently defined by the degree of hyperglycemia, resulting from an absolute or relative deficiency of insulin action. These concepts are the basis of the current classification as type 1 DM (T1DM), type 2 DM (T2DM), and other predominantly genetic forms. T1DM is a disease of insulin deficiency associated with autoimmune destruction of functional beta cells, a process begun by environmental insults in genetically determined susceptible hosts; it is the most common form of DM in childhood. In this chapter, we discuss the advances in understanding the genetics, pathophysiology, evolution, and treatment of all forms of DM, increasingly driven by technologic advances in glucose sensing, continuous glucose monitoring, and algorithmically regulated pumps that constitute an “artificial pancreas,” together with newer insulin preparations that facilitate simulating normal basal and bolus patterns in normal persons. T2DM is increasing in adolescents, particularly with obesity and prevalence in minority populations; obesity with insulin resistance has unmasked genetic defects in the regulation of insulin synthesis and secretion. For these individuals, lifestyle modification and weight loss remain the cornerstone of prevention and treatment. However, if this approach fails, newer modalities of treatment, such as a variety of incretin hormones, inhibitors of its destruction, agents that promote glucose excretion, and rarely bariatric surgery are revolutionizing treatment. Several of the genes involved in T2DM cause specific syndromes of monogenic diabetes at birth (neonatal DM) and during adolescence (maturity onset-diabetes of youth [MODY]), often misdiagnosed as T1- or T2DM and for which oral treatments rather than insulin injections are available and effective. Together, these advances are associated with better quality of life, less complications, and the promise of potential prevention of diabetes in childhood.
Sodium bicarbonate therapy for critically ill patients with metabolic acidosis: A scoping and a systematic review
2019, Journal of Critical Care
Citation Excerpt :
We did not undertake any sensitivity analysis. Of the 2037 citations identified from electronic and hand searches, 12 reports were included in the review [22-33] (Suppl Fig. 1, Suppl Table 1, Table 1). The number of patients who received NaHCO3 across the studies ranged from nine [22] to 195 [25].
We aimed to assess the biochemical and physiological effects, clinical efficacy, and safety, of intravenous NaHCO3 therapy in critically ill patients with acute metabolic acidosis.
We conducted a scoping review concerning the biochemical and physiological effects of NaHCO3 (PART A), and a systematic review regarding clinical efficacy (PART B). We searched MEDLINE in Part A and MEDLINE, EMBASE, Cochrane, the National Institute of Health Clinical Trials Register, and the WHOICTRP for randomised controlled trials in Part B.
Twelve studies in Part A and two trials in Part B fulfilled the eligibility criteria. Intravenous NaHCO3 increased blood pH, base excess, serum bicarbonate, sodium, and PaCO2 during and after administration and decreased anion gap and potassium value. For clinical efficacy, only one study contributed to the effect estimate. The risk ratio (RR) for all-cause mortality was 0.83 (95% confidence interval, 0.68 to 1.02), and the risk of hypocalcaemia was increased in the bicarbonate group (RR 1.65, 95% confidence interval 1.09 to 2.50). There were inadequate data on hemodynamic indices.
Given the lack of data on the effects of intravenous NaHCO3 therapy to support its clinical use and the frequency of bicarbonate therapy, a program of investigation appears justified.

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¹: From the Department of Medicine, University of Chicago, Chicago, Illinois.

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Clinical studySodium bicarbonate therapy in severe diabetic ketoacidosis

Abstract

Clin Endocrinol Metab

Lancet

J Pediatr

Lancet

Lancet

Effects of changes in coronary blood pH on the heart

Circ Res

A quantitative evaluation of the effects of acidosis and alkalosis upon ventricular fibrillation threshold

Surgery

Acid production in diabetic acidosis; a more rational approach to alkali replacement

Br Med J

Myocardial resistance to metabolic acidosis

Arch Surg

Clinical study
Sodium bicarbonate therapy in severe diabetic ketoacidosis