Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a common complication among children with IDDM, accounting for 14 to 31 percent of all diabetes-related hospital admissions. 67 It is the single most common cause of death in diabetic patients under 24 years of age.7 DKA is considered to be present when there is hyperglycemia (i.e., blood glucose level >250 mg/dL), ketonemia (i.e., ketones >1:2 dilution of serum), and metabolic acidosis (i.e., pH <7.2 and plasma bicarbonate £15 meq/L)5 accompanied by glucosuria and ketonuria. The majority of patients are also moderately to severely dehydrated. Precipitating factors for the initial presentation or for DKA include stress such as trauma, infection, vomiting, and psychological disturbances.5

The basic cause of DKA is absolute or relative insulin deficiency ( Fig, 1,2.4.-1). There also are elevated levels of counterregulatory hormones (glucagon, cortisol, growth hormone, epinephrine, and norepinephrine), which antagonize insulin. 2 These hormonal abnormalities result in increased glucose production (promoting glycogenolysis, gluconeogenesis, lipolysis, and ketogenesis) and decreased utilization. With progressive insulin deficiency, glucosuria accompanies the hyperglycemia. The resultant osmotic diuresis produces polyuria, which can result in a profound loss of fluids and electrolytes, dehydration, and compensatory polydipsia. Hyperosmolality is commonly encountered as a result of progressive hyperglycemia, which contributes to the symptoms, especially cerebral obtundation, in DKA. Serum osmolality can be estimated with the following formula:

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FIG. 124-1. Pathophysiology of diabetic ketoacidosis.

The hormonal interplay of insulin deficiency and glucagon excess shunts free fatty acids into ketone body formation. The rate of formation of these bodies, principally b-hydroxybutyrate and acetoacetate, exceeds the capacity for peripheral utilization and for renal excretion. The combination of ketoacid formation and dehydration results in metabolic acidosis, and, for compensatory alkalosis, rapid deep breathing (Kussmaul respirations) may be manifested at advanced stages. Dehydration with decreased perfusion to the tissues leads to lactic acidosis, which contributes to more profound acidosis. Once patients are sufficiently ketotic and acidotic, they manifest the classic fruity breath odor of ketosis. The state of consciousness may vary from alertness to drowsiness or coma, depending on the severity of DKA. Other findings on physical examination include fever, vomiting, and exquisite abdominal pain with guarding and rigidity, which can mimic an acute abdomen. The clinical findings of acute abdomen usually resolve with the treatment of DKA, but if not, an underlying cause must be sought. DKA should be considered in children who are vomiting and appear dehydrated but continue to urinate excessively.

In known diabetic patients, DKA may be precipitated by acute infections or other stresses but is usually caused by omission of insulin. A thorough search for sources of infection is essential. It is important to note that the degree of hyperglycemia does not correlate with the degree of acidosis, and patients who are only minimally hyperglycemic may be severely acidotic. The early recognition and treatment of DKA should be well known to every emergency physician so that the morbidity and mortality rates associated with this complication of IDDM can be reduced.

Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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