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Serum glucose changes during insulin therapy in pediatric patients with diabetic ketoacidosis
Paul Bradley1, Joseph D Tobias
1School of Medicine, University of Missouri, Columbia, MO 65212, USA.
Insights
Common insulin dosing for pediatric diabetic ketoacidosis (DKA) may cause rapid glucose drops. Careful insulin titration is crucial to avoid risks like cerebral edema in DKA treatment.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Intensive Care Medicine
Background:
- Diabetic ketoacidosis (DKA) treatment requires careful insulin dosing to prevent complications.
- Limited data exist on optimal insulin regimens for pediatric DKA.
- Rapid serum glucose decreases can lead to adverse events, including cerebral edema.
Purpose of the Study:
- To retrospectively analyze insulin dosing schemes in pediatric DKA patients.
- To evaluate the relationship between insulin dosage and serum glucose decrease rate.
- To identify commonly used insulin regimens and their efficacy in a pediatric intensive care unit.
Main Methods:
- Retrospective review of DKA therapy in 35 pediatric patients over 10 years.
- Analysis of intravenous bolus and infusion insulin doses administered.
- Correlation of insulin dosage (units/kg and units/kg/h) with serum glucose decline (mg/dL/h).
Main Results:
- Commonly used insulin bolus (0.1 units/kg) followed by infusion (0.05-0.1 units/kg/h) frequently exceeded the target glucose decrease of 100 mg/dL/h.
- In 24% of infusion hours at 0.05-0.1 units/kg/h, glucose decreased by over 100 mg/dL.
- Lower infusion rates (<0.05 units/kg/h) were associated with a significantly lower risk of rapid glucose decline (P=0.05).
Conclusions:
- Current insulin dosing protocols for pediatric DKA may lead to excessive glucose reduction.
- Lower insulin infusion rates might be safer in preventing rapid serum glucose drops.
- Prospective studies are necessary to establish precise insulin dosing guidelines for pediatric DKA.
Abstract:
There are limited data on which to base insulin dosing schemes for diabetic ketoacidosis (DKA). The goal of therapy is to avoid excessive decreases in serum glucose (greater than 100 mg/dL/h) because of the risks of rapid changes in serum osmolarity and the potential risk of cerebral edema. We retrospectively reviewed the therapy of DKA in pediatric patients admitted to our Pediatric Intensive Care Unit over the past 10 years. There were 35 patients who received IV bolus insulin therapy (0.08 to 1.6 units/kg, 0.24 +/- 0.27 units/kg). The serum-glucose decrease was less than or equal to 100 mg/dL in 10 patients, 101 to 200 mg/dL in 13 patients, 201 to 300 mg/dL in 8 patients, 301 to 400 mg/dL in 2 patients, and more than 500 mg/dL in 2 patients. In patients who received 0.05 to 0.1 units/kg of insulin as a bolus dose, the decrease in serum glucose was greater than 100 mg/dL in 5 of 11 patients. An insulin infusion was administered to 91 patients. During the 243 hours of insulin infusion therapy, the decline in serum glucose was 0 to 100 mg/dL during 162 hours, 101 to 200 mg/dL during 49 hours, 201 to 300 mg/dL during 8 hours, and more than 300 mg/dL during 3 hours. Of the 193 hours of 0.05 to 0.1 units/kg/h insulin administration, there were 47 hours (24%) during which the serum-glucose decrease was greater than 100 mg/dL. Of the 21 hours of insulin administration at less than 0.05 units/kg/h, there was 1 hour (4.8%) where the serum-glucose decrease was greater than 100 mg/dL (P = 0.05 vs. insulin infusion at 0.05 to 0.1 units/kg/h). Commonly used insulin dosing regimens of a bolus of 0.1 units/kg followed by an infusion of 0.05 to 0.1 units/kg/h frequently resulted in a decrease in serum glucose of greater than 100 mg/dL/h. Prospective trials are needed to more accurately define appropriate insulin dosing regimens for pediatric patients with DKA.
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