Publication date: August 2009; Volume 6, Number 8

Excerpt from the issue...

A four-year-old boy presents to the emergency department with chief complaints of abdominal pain and nausea. A history reveals that the progressive abdominal pain and new-onset nausea, as well as polyuria, have lasted for several weeks. On further questioning, the parents indicate their son has lost several pounds in recent weeks. The physical examination reveals a generally uncomfortable boy who is holding his belly and is in obvious pain. He appears moderately dehydrated, with tacky lips and decreased skin turgor but adequate perfusion. A pulmonary examination reveals a deep and labored breathing pattern with no other focal abnormalities. His abdomen is diffusely tender, but there are no peritoneal signs.

You’ve seen this syndrome before. It is most likely diabetic ketoacidosis. A reading of “unmeasurable” on a finger stick confirms your suspicion. But now comes the hard part. You recall a similar patient a few months ago who developed sudden neurologic deterioration upon transfer to the pediatric intensive care unit. The intensivists diagnosed cerebral edema and felt it could have been avoided with better initial management. As you think about management options for this patient, you begin to question yourself: Was I responsible for the other patient’s poor outcome? Are there clear right and wrong choices when it comes to fluids, insulin, and electrolyte supplementation?

Acute hyperglycemic crisis is the most common and most serious reason for emergency department (ED) evaluation of diabetic children.^1-4 In patients who are eventually diagnosed with type 1 diabetes mellitus (also called juvenile diabetes or insulin-dependent diabetes mellitus), approximately 25% to 30% initially present with diabetic ketoacidosis (DKA), one form of acute hyperglycemic crisis.⁵ In patients with known type 1 diabetes, DKA and DKA-related illnesses comprise the majority of acute presentations.⁶ While many of these patients do well, DKA carries an estimated mortality rate of 0.15% to 0.30%.7,8 The most common cause of mortality is cerebral edema.^1,7,9 While the mechanism of cerebral edema is not well understood, evidence suggests it occurs early in the course of DKA,^1,10 emphasizing the vital role of the ED clinician in the initial management of the disorder.

The correction of hyperglycemia and the prevention of morbidity and mortality in patients with DKA begin in the ED. In recent years, a large body of evidence has helped to elucidate the pathophysiology of the disorder and the appropriate management options for children with this and related illnesses. This issue of Pediatric Emergency Medicine Practice provides the most up-to-date guidelines and the results of evidence-based studies in order to assist the pediatric emergency clinician in caring for patients presenting with acute hyperglycemic crises.

Note: Acute hyperglycemic crisis refers to both diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). Although the term collectively describes the 2 disorders, the majority of this article will focus on DKA, as it is the more common disease process. A special section is also dedicated to the understanding of HHS.