Bicarbonate Therapy Risky in Diabetic Ketoacidosis - Brief Article

/Home/Complications of Diabetes/Diabetic Ketoacidosis (DKA)/Alternative Medicine for Diabetic Ketoacidosis

Bicarbonate Therapy Risky in Diabetic Ketoacidosis - Brief Article

SANTA FE, N.M. -- Anew study suggests that bicarbonate should be avoided in treating children with diabetic ketoacidosis. Bicarbonate therapy was associated with a quadrupled risk for cerebral edema in the study of 416 patients, Dr. Nicole Glaser reported at a pediatric conference sponsored by Symposia Medicus.

Three other factors also could help predict the development of cerebral edema in children with diabetic ketoacidosis. The higher the initial BUN level (or the greater the patient's dehydration), the greater the risk of cerebral edema. The lower the initial level of arterial carbon dioxide pressure (reflecting increased hyperventilation), the greater the chance of developing cerebral edema. And failure of the serum sodium level to rise as glucose levels fall in response to treatment also predicted cerebral edema, reported Dr. Glaser of the University of California, Davis.

Children with new-onset diabetes present with diabetic ketoacidosis in 25%-40% of cases, and 1%-5% of the latter develop clinically evident cerebral edema. Ketoacidosis causes 83%-97% of child deaths due to diabetes; in most of these deaths (about 63%), the child dies from cerebral edema.

Dr. Glaser and her associates retrospectively reviewed data on diabetic ketoacidosis admissions to 10 pediatric referral centers over a 15-year period. They compared 61 children who had cerebral edema with two control groups: 181 randomly selected control patients with ketoacidosis but no cerebral edema; and 174 control patients matched to the cerebral edema patients by age, initial glucose and pH levels, and whether they had new or preexisting diabetes mellitus.

A handful of previous trials--most of them in adults--have generated controversy over the use of bicarbonate therapy for ketoacidosis. This therapy did not result in more rapid resolution of acidosis, "at least in anything beyond the very short term," Dr. Glaser noted. Bicarbonate therapy also can cause a paradoxical increase in CNS acidosis, increased hypokalemia, and increased production of ketones.

The current study's finding that bicarbonate therapy quadrupled the risk for cerebral edema may become the kiss of death for its use in most cases.

"The risks of bicarbonate therapy likely outweigh the potential benefits except in certain specific cases: for example, symptomatic hyperkalemia or severe cardiovascular instability," she said.

The initial BUN level and arterial carbon dioxide pressure readings predicted cerebral edema in both univariate and multivariate analyses in the current study.

The finding that the risk of cerebral edema increases if sodium levels don't increase as glucose levels fall during therapy echoes the results of a 1990 study of 20 patients with cerebral edema and 219 controls. Sodium failed to rise as glucose fell in 95% of cerebral edema patients and in only 54% of controls, the retrospective study found. The current study found no predictive value in the rate of change of serum glucose concentration, the rapidity of insulin infusion, the intravenous fluid rate, or the rate of sodium administration.

These results contradict at least one previous study: Results of a 1988 uncontrolled case series suggested an increased risk of cerebral edema with more rapid fluid administration.

The new data suggest that bicarbonate should be avoided in treating diabetic ketoacidosis but offer no other treatment insights, Dr. Glaser said.

Reasonable treatment for diabetic ketoacidosis, based on the small amount of data in the medical literature, consists of insulin therapy, perfusion restoration, hemodynamic stabilization, fluid and potassium replacement, and moderate phosphate replacement, she said.

COPYRIGHT 2000 International Medical News Group
COPYRIGHT 2001 Gale Group