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Review
, 9 (11), 199-205

Use of Sodium Bicarbonate and Blood Gas Monitoring in Diabetic Ketoacidosis: A Review

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Review

Use of Sodium Bicarbonate and Blood Gas Monitoring in Diabetic Ketoacidosis: A Review

Mit P Patel et al. World J Diabetes.

Abstract

Diabetic ketoacidosis (DKA) is a severe and too-common complication of uncontrolled diabetes mellitus. Acidosis is one of the fundamental disruptions stemming from the disease process, the complications of which are potentially lethal. Hydration and insulin administration have been the cornerstones of DKA therapy; however, adjunctive treatments such as the use of sodium bicarbonate and protocols that include serial monitoring with blood gas analysis have been much more controversial. There is substantial literature available regarding the use of exogenous sodium bicarbonate in mild to moderately severe acidosis; the bulk of the data argue against significant benefit in important clinical outcomes and suggest possible adverse effects with the use of bicarbonate. However, there is scant data to support or refute the role of bicarbonate therapy in very severe acidosis. Arterial blood gas (ABG) assessment is an element of some treatment protocols, including society guidelines, for DKA. We review the evidence supporting these recommendations. In addition, we review the data supporting some less cumbersome tests, including venous blood gas assessment and routine chemistries. It remains unclear that measurement of blood gas pH, via arterial or venous sampling, impacts management of the patient substantially enough to warrant the testing, especially if sodium bicarbonate administration is not being considered. There are special circumstances when serial ABG monitoring and/or sodium bicarbonate infusion are necessary, which we also review. Additional studies are needed to determine the utility of these interventions in patients with severe DKA and pH less than 7.0.

Keywords: Acidosis; Blood gas analysis; Diabetic ketoacidosis; Hyperglycemia; Ketone bodies; Ketosis; Sodium bicarbonate.

Conflict of interest statement

Conflict-of-interest statement: No potential conflicts of interest. No financial support.

Figures

Figure 1
Figure 1
The pathophysiology of diabetic ketoacidosis. Decreased insulin sensitivity leads to increased concentrations of counter-regulatory hormones which promote catabolism of proteins and adipocytes. The production of free amino acids leads to the stimulation of gluconeogenesis and glycogenolysis leading to hyperglycemia. Free fatty acids undergo oxidation in the mitochondria and result in ketone production leading to acidosis. FFA: Free fatty acids.

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