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Diabetes is subclassified into several different forms. Type 1 diabetes, previously referred to as juvenile-onset diabetes because of its earlier onset, is characterized by an abrupt and frequently complete decline in insulin production. Type 2 diabetes, previously referred to as adult-onset diabetes, is marked by increasing insulin resistance and is most commonly found in obese adults. Type 2 diabetes now occurs in overweight adolescents with a strong genetic tendency toward the disease. Type 1 diabetes (no longer called insulin-deficient diabetes mellitus) is the most common pediatric endocrine disorder, with an estimated prevalence of 1 in 400. As many as 27% to 40% of children with new-onset type 1 diabetes present in diabetic ketoacidosis (DKA).1 In children with known diabetes, DKA is much less common and tends to be clustered in a small subset of patients, with 5% of children with diabetes accounting for nearly 60% of DKA episodes.2 DKA is the leading cause of mortality in patients with diabetes <24 years of age, and cerebral edema is the leading cause of mortality in DKA.3

See Chapter 218, Type 1 Diabetes Mellitus, and Chapter 219, Type 2 Diabetes Mellitus, for a detailed discussion of the pathophysiology of diabetes.

The fundamental cause of DKA is an absolute or relative insulin deficiency that results in the inability of cells to take up and utilize glucose. Levels of counterregulatory hormones (catecholamines, cortisol, growth hormone, and glucagon) are elevated, which drives many of the physiologic disturbances observed in DKA. These hormones increase glucose production by promoting glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis, and further decrease glucose utilization by antagonizing insulin.

As the serum glucose level exceeds the renal absorption threshold, an obligatory osmotic diuresis ensues, which results in the classic symptoms of polyuria and polydipsia. If not recognized early, this can lead to profound dehydration and electrolyte disturbances. Acidosis stems from the complex metabolic derangements induced by insulin deficiency and unopposed glucagon. The cellular milieu of the body is essentially in a state of functional starvation, unable to utilize the excess serum glucose. Decreased lipid uptake by adipose tissue and increased lipolysis results in an overabundance of circulating free fatty acids, which are converted by the liver into the ketoacids acetoacetate and β-hydroxybutyrate.

Despite this profound shift in substrate production, ketoacid utilization and renal elimination are both impaired, which results in a wide anion gap metabolic acidosis. In certain patients, the acid-base status may be more complex. Persistent vomiting and severe volume depletion may result in a superimposed metabolic alkalosis that may mask the severity of the acidosis by producing a relatively normal pH. Severe dehydration and poor perfusion further lead to lactic acidosis, which results in a superimposed anion gap acidosis. Alternatively, a patient who remains relatively well hydrated will lose sodium with keto anions in the urine while retaining chloride and demonstrate a significant non-anion gap acidosis.


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