Glargine co-administration with intravenous insulin in pediatric diabetic ketoacidosis is safe and facilitates transition to a subcutaneous regimen

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

<div class="section"> <a class="named-anchor" id="S1">  </a> <h5 class="section-title" id="d3633608e143">Background</h5> <p id="P1">Diabetes ketoacidosis (DKA) is a common presentation and complication of type 1 diabetes (T1D). While intravenous insulin is typically used to treat acute metabolic abnormalities, the transition from intravenous to subcutaneous treatment can present a challenge. We hypothesize that co-administration of glargine, a subcutaneous long acting insulin analogue, during insulin infusion may facilitate a flexible and safe transition from intravenous to subcutaneous therapy. </p> </div><div class="section"> <a class="named-anchor" id="S2">  </a> <h5 class="section-title" id="d3633608e148">Objective</h5> <p id="P2">To determine if the practice of administering subcutaneous glargine during intravenous insulin is associated with an increased risk of hypoglycemia, hypokalemia or other complications in children with DKA. </p> </div><div class="section"> <a class="named-anchor" id="S3">  </a> <h5 class="section-title" id="d3633608e153">Methods</h5> <p id="P3">Retrospective chart review of patients aged 2-21 years, presenting to our center with DKA between April 2012 and June 2014. Patients were divided into two groups: those co-administered subcutaneous glargine with intravenous insulin for over 4 hours (G+); and patients with less than two hours of overlap (G−). </p> </div><div class="section"> <a class="named-anchor" id="S4">  </a> <h5 class="section-title" id="d3633608e158">Results</h5> <p id="P4">We reviewed 149 DKA admissions (55 G+, 94 G−) from 129 unique patients. There was a similar incidence of hypoglycemia between groups (25% G+ vs. 20% G−, p=0.46). Hypokalemia (<3.5mmol/L) occurred more frequently in the G+ group (OR= 3.4, 95% CI 1.7-7.0, p=0.001). Cerebral edema occurred in 2/55 (3.6%) of the G− group and none of the G+ subjects. </p> </div><div class="section"> <a class="named-anchor" id="S5">  </a> <h5 class="section-title" id="d3633608e163">Conclusion</h5> <p id="P5">Co-administration of glargine early in the course of DKA treatment is well tolerated and convenient for discharge planning; however, this approach is associated with an increased risk of hypokalemia. </p> </div>

Related collections

Most cited references 15

Record: found
Abstract: found
Article: not found

Hyponatremia: evaluating the correction factor for hyperglycemia.

T A Hillier, R D Abbott, E J Barrett (1999)

There are no controlled experimental data that assess the accuracy of the commonly used correction factor of a 1.6 meq/L decrease in serum sodium concentration for every 100 mg/dL increase in plasma glucose concentration. The purpose of this study was to evaluate experimentally the hyponatremic response to acute hyperglycemia. Somatostatin was infused to block endogenous insulin secretion in 6 healthy subjects. Plasma glucose concentrations were increased to >600 mg/dL within 1 hour by infusing 20% dextrose. The glucose infusion was then stopped and insulin given until the plasma glucose concentration decreased to 140 mg/dL. Plasma glucose and serum sodium concentrations were measured every 10 minutes. Overall, the mean decrease in serum sodium concentration averaged 2.4 meq/L for every 100 mg/dL increase in glucose concentration. This value is significantly greater than the commonly used correction factor of 1.6 (P = 0.02). Moreover, the association between sodium and glucose concentrations was nonlinear. This was most apparent for glucose concentrations >400 mg/dL. Up to 400 mg/dL, the standard correction of 1.6 worked well, but if the glucose concentration was >400 mg/dL, a correction factor of 4.0 was better. These data indicate that the physiologic decrease in sodium concentration is considerably greater than the standard correction factor of 1.6 (meq/L Na per 100 mg/dL glucose), especially when the glucose concentration is >400 mg/dL. Additionally, a correction factor of a 2.4 meq/L decrease in sodium concentration per 100 mg/dL increase in glucose concentration is a better overall estimate of this association than the usual correction factor of 1.6.

0 comments Cited 130 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Predictors of acute complications in children with type 1 diabetes.

T H Chase, Mark G Roback, Todd A. MacKenzie … (2002)

Diabetic ketoacidosis and severe hypoglycemia are acute complications of type 1 diabetes that are related, respectively, to insufficient or excessive insulin treatment. However, little is known about additional modifiable risk factors. To examine the incidence of ketoacidosis and severe hypoglycemia in children with diabetes and to determine the factors that predict these complications. A cohort of 1243 children from infancy to age 19 years with type 1 diabetes who resided in the Denver, Colo, metropolitan area were followed up prospectively for 3994 person-years from January 1, 1996, through December 31, 2000. Incidence of ketoacidosis leading to hospital admission or emergency department visit and severe hypoglycemia (loss of consciousness, seizure, or hospital admission or emergency department visit). The incidence of ketoacidosis was 8 per 100 person-years and increased with age in girls (4 per 100 person-years in or =13 years; P or =13 years), the risk of ketoacidosis in younger children increased with higher hemoglobin A(1c) (HbA(1c)) (relative risk [RR], 1.68 per 1% increase; 95% confidence interval [CI], 1.45-1.94) and higher reported insulin dose (RR, 1.40 per 0.2 U/kg per day; 95% CI, 1.20-1.64). In older children, the risk of ketoacidosis increased with higher HbA(1c) (RR, 1.43; 95% CI, 1.30-1.58), higher reported insulin dose (RR, 1.13; 95% CI, 1.02-1.25), underinsurance (RR, 2.18; 95% CI, 1.65-2.95), and presence of psychiatric disorders (for boys, RR, 1.59; 95% CI, 0.96-2.65; for girls, RR, 3.22; 95% CI, 2.25-4.61). The incidence of severe hypoglycemia was 19 per 100 person-years (P or =13 years). In younger children, the risk of severe hypoglycemia increased with diabetes duration (RR, 1.39 per 5 years; 95% CI, 1.16-1.69) and underinsurance (RR, 1.33; 95% CI, 1.08-1.65). In older children, the risk of severe hypoglycemia increased with duration (RR, 1.34; 95% CI, 1.25-1.51), underinsurance (RR, 1.42; 95% CI, 1.11-1.81), lower HbA(1c) (RR, 1.22; 95% CI, 1.12-1.32), and presence of psychiatric disorders (RR, 1.56; 95% CI, 1.23-1.98). Eighty percent of episodes occurred among the 20% of children who had recurrent events. Some children with diabetes remain at high risk for ketoacidosis and severe hypoglycemia. Age- and sex-specific incidence patterns suggest that ketoacidosis is a challenge in adolescent girls while severe hypoglycemia continues to affect disproportionally the youngest patients and boys of all ages. The pattern of modifiable risk factors indicates that underinsured children and those with psychiatric disorders or at the extremes of the HbA(1c) distribution should be targeted for specific interventions.

0 comments Cited 85 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis.

Donald L. Hilton, Robert Hamersley, J Rees … (2011)

The Joint British Diabetes Societies guidelines for the management of diabetic ketoacidosis (these do not cover Hyperosmolar Hyperglycaemic Syndrome) are available in full at: (i) http://www.diabetes.org.uk/About_us/Our_Views/Care_recommendations/The-Management-of-Diabetic-Ketoacidosis-in-Adults; (ii) http://www.diabetes.nhs.uk/publications_and_resources/reports_and_guidance; (iii) http://www.diabetologists-abcd.org.uk/JBDS_DKA_Management.pdf. This article summarizes the main changes from previous guidelines and discusses the rationale for the new recommendations. The key points are: Monitoring of the response to treatment (i) The method of choice for monitoring the response to treatment is bedside measurement of capillary blood ketones using a ketone meter. (ii) If blood ketone measurement is not available, venous pH and bicarbonate should be used in conjunction with bedside blood glucose monitoring to assess treatment response. (iii) Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers. (iv) Intermittent laboratory confirmation of pH, bicarbonate and electrolytes only. Insulin administration (i) Insulin should be infused intravenously at a weight-based fixed rate until the ketosis has resolved. (ii) When the blood glucose falls below 14 mmol/l, 10% glucose should be added to allow the fixed-rate insulin to be continued. (iii) If already taking, long-acting insulin analogues such as insulin glargine (Lantus(®), Sanofi Aventis, Guildford, Surry, UK) or insulin detemir (Levemir(®), Novo Nordisk, Crawley, West Sussex, UK.) should be continued in usual doses. Delivery of care (i) The diabetes specialist team should be involved as soon as possible. (ii) Patients should be nursed in areas where staff are experienced in the management of ketoacidosis. © 2011 The Authors. Diabetic Medicine © 2011 Diabetes UK.