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Acid–Base Problems in Diabetic Ketoacidosis Kamel S The new england journal of medicine Review Article Disorders of Fluids and Electrolytes Julie R. Ingelfinger, M.D., Editor Acid–Base Problems in Diabetic Ketoacidosis Kamel S. Kamel, M.D., and Mitchell L. Halperin, M.D. From the Renal Division, St. Michael’s his review focuses on three issues facing clinicians who care for Hospital and University of Toronto, and patients with diabetic ketoacidosis; all of the issues are related to acid–base Keenan Research Center, Li Ka Shing Knowledge Institute of St. Michael’s disorders. The first issue is the use of the plasma anion gap and the calculation Hospital, University of Toronto, Toronto. T of the ratio of the change in this gap to the change in the concentration of plasma Address reprint requests to Dr. Halperin bicarbonate in these patients; the second concerns the administration of sodium bi- at the Department of Medicine, Univer- sity of Toronto Keenan Research Center, carbonate; and the third is the possible contribution of intracellular acidosis to the Li Ka Shing Knowledge Institute of St. development of cerebral edema, particularly in children with diabetic ketoacidosis. In Michael’s Hospital, 30 Bond St., Rm. this article, we examine the available data and attempt to integrate the data with 408, Toronto, ON M5B 1W8, Canada, or at mitchell . halperin@ utoronto . ca. principles of physiology and metabolic regulation and provide clinical guidance. N Engl J Med 2015;372:546-54. DOI: 10.1056/NEJMra1207788 Plasma Bicarbonate and the Plasma Anion Gap Copyright © 2015 Massachusetts Medical Society. The accumulation of ketoacids in the extracellular fluid leads to a loss of bicarbonate anions and a gain of ketoacid anions. Because of hyperglycemia-induced osmotic diuresis and natriuresis, patients with diabetic ketoacidosis usually present with a marked contraction of the extracellular fluid volume. This factor affects the assess- ment of their acid–base status and in some cases their therapy. Determination of the severity of metabolic acidemia is usually based on the extent of the decrease in the plasma bicarbonate concentration. Nevertheless, as shown in the equation below, the plasma bicarbonate concentration may be only moderately reduced when there is both a large deficit of bicarbonate in the extracellular fluid and a severe contraction of the volume of extracellular fluid. The bicarbonate deficit be- comes evident during reexpansion of the volume of extracellular fluid when saline is administered: − Extracellular fluid bicarbonate concentration [HCO3 ] = extracellular fluid − HCO3 content ÷ extracellular fluid volume. The addition of new anions is reflected in an increase in the plasma anion gap,1,2 which is the difference between the concentration of the major cation in plasma (sodium) and the major anions in plasma (chloride and bicarbonate). This difference is due largely to the net anionic valence on plasma proteins, principally albumin. A pitfall in using the plasma anion gap is the failure to correct for the net negative valence attributable to plasma albumin.3 This correction must be made not only when the plasma albumin concentration decreases but also when it increases; the latter may occur in patients with diabetic ketoacidosis because of the marked contraction in the volume of extracellular fluid. For every decrease of 1 g per deciliter in the plasma albumin concentration from its normal value of 4 g per deciliter, one should add 2.5 mmol per liter to the calculated value of the plasma anion gap. For every increase of 1 g per deciliter in the plasma albumin level, one should subtract 2.5 mmol per liter from the calculated value of the plasma anion gap.4,5 Even with this adjustment, it appears that the net negative valence on albumin is increased when there is an ap- 546 n engl j med 372;6 nejm.org February 5, 2015 The New England Journal of Medicine Downloaded from nejm.org by DAVID KIRK on February 5, 2015. For personal use only. No other uses without permission. Copyright © 2015 Massachusetts Medical Society. All rights reserved. Acid–Base Problems in Diabetic Ketoacidosis preciable decrease in the effective arterial blood crease in the concentration of bicarbonate ions. volume, and hence there is a higher value for the This indirect loss of sodium bicarbonate may be plasma anion gap.6 the dominant (and occasionally the only) compo- The relation between the increase (Δ) in the nent of metabolic acidosis in some patients with plasma anion gap and the decrease (Δ) in the diabetic ketoacidosis.12,13 plasma bicarbonate concentration — which is commonly referred to as delta-delta (Δ-Δ) — is Treatment with Sodium used to provide an estimate of the magnitude of Bicarbonate the acid load and to detect the presence of coexist- ing metabolic acid–base disorders.7,8 Some studies9 The use of sodium bicarbonate to treat acute indicate that in diabetic ketoacidosis, the ratio of metabolic acidosis that is caused by the produc- the increase in the plasma anion gap to the de- tion of organic acids is controversial.14-18 Severe crease in the plasma bicarbonate concentration acidemia may be associated with decreased car- approximates 1. It is important to recognize that diac contractility,19,20 diminished responses to en- this ratio is based on “concentrations” and not dogenous and administered catecholamines, and “contents” and to take into account changes in the a predisposition to cardiac arrhythmias,21,22 all of volume of extracellular fluid when using this ratio which may contribute to hemodynamic instability. to gauge the magnitude of the acid load.10 For In addition, severe acidemia may interfere with the example, consider a woman with type 1 diabetes binding of insulin to its receptor,23 which may whose weight is 50 kg and whose steady-state impair the capacity of insulin to slow the rate of volume of extracellular fluid is 10 liters. She has a ketoacid production. plasma bicarbonate concentration of 25 mmol per In three randomized, controlled trials involving liter and a plasma anion gap of 12 mmol per liter. a combined total of 73 patients,24-26 investigators After the development of diabetic ketoacidosis, the examined the effect of the administration of so- plasma bicarbonate concentration decreases to 10 dium bicarbonate in adult patients with diabetic mmol per liter, and the plasma anion gap in- ketoacidosis.27 Patients with serious concomitant creases to 27 mmol per liter in this patient. Be- illnesses (e.g., acute myocardial infarction, gastro- cause of the hyperglycemia-induced osmotic di- uresis and natriuresis associated with diabetic ketoacidosis, the current volume of extracellular fluid is only 7 liters. Although the ratio between Liver the change in the plasma anion gap and the change in the plasma bicarbonate concentration is β-HB− + H+ 1:1, the bicarbonate deficit and the amount of ketoacids retained in the extracellular fluid are not equal. The decrease in the content of bicarbonate Extracellular fluid Na+ + HCO – ions is 180 mmol ([25 mmol per liter × 10 liters] compartment 3 − [10 mmol per liter × 7 liters]), whereas the gain of ketoacid anions is only 105 mmol ([approxi- mately 0 mmol per liter × 10 liters] + [15 mmol per β-HB− + Na+ loss CO2 + H2O loss liter × 7 liters]). through urine through the lungs These calculations suggest that another com- ponent of bicarbonate loss occurred when ketoac- Figure 1. Indirect Loss of Sodium Bicarbonate Early ids were added (i.e., some ketoacid anions were in the Course of Diabetic Ketoacidosis. excreted in the urine along with sodium ions or β-hydroxybutyric acid is produced in the liver. It dissoci- potassium ions); this created an indirect form of ates in the extracellular fluid into the β-hydroxybutyrate loss of sodium bicarbonate (Fig. 1) that is not re- anion (β-HB−) and hydrogen ion (H+). The loss of bi- − + vealed by the increase in the plasma anion gap.11 carbonate (HCO3 ) and sodium ions (Na ) occurs in- Once the volume of the extracellular fluid has directly through two different routes. The loss of bicar- bonate occurs after it reacts with H+ producing carbon been expanded with the administration of saline, dioxide (CO2) and water (H2O); the CO2 is lost the deficit in bicarbonate ions becomes evident to through the lungs. The loss of sodium occurs during the clinician, since the decrease in the plasma its excretion in the urine with β-hydroxybutyrate. anion gap will not be matched by a similar in- n engl j med 372;6 nejm.org February 5, 2015 547 The New England Journal of Medicine Downloaded from nejm.org by DAVID KIRK on February 5, 2015. For personal use only. No other uses without permission. Copyright © 2015 Massachusetts Medical Society. All rights reserved. The new england journal of medicine intestinal hemorrhage, chronic renal failure, or ingly, the liver cannot work hard enough to pro- intraabdominal sepsis) were excluded from all duce an adequate amount of ADP or, consequently, + three trials. On the basis of outcome measures to convert enough NADH to NAD (and FADH2 to such as the change in arterial pH, plasma bicar- FAD), thereby setting a limit on the rate of keto- bonate concentration, and levels of metabolites acid production.32 measured, the administration of sodium bicar- The observed rate of production of ketoacids bonate was not beneficial. Mean arterial blood during prolonged starvation (approximately 1500 pressure was reported in only one study.24 We have mmol per day)34,35 suggests that there are ways in been unable to find published results from con- which the liver can bypass the limit on ketoacid trolled trials that examined the effect of the ad- production created by an insufficient supply of ministration of sodium bicarbonate on mortality, ADP. One possibility is uncoupled oxidative phos- hemodynamic stability, or the incidence of com- phorylation, in which hydrogen ions reenter mito- plications such as acute myocardial infarction, chondria by means of hydrogen ion channels that acute kidney injury, or stroke in patients with se- are not linked to the conversion of ADP to ATP vere acidemia.
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