Chapter 80. The Diabetic Child

Type 1 diabetes is characterized by an abrupt and frequently complete decline in insulin production. Type 2 diabetes is marked by increasing insulin resistance, and occurs in overweight adolescents with a strong genetic predisposition. Diabetic ketoacidosis (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.

DKA is much more common in patients with type 1 diabetes than in those with type 2, but patients with type 2 to diabetes may develop hyperglycemic, hyperosmolar nonketotic (HHNK) syndrome with acidosis, which can result in severe total body water, potassium, and phosphorus deficits. About 4% of children with newly diagnosed type 2 diabetes present with HHNK syndrome, which has a case fatality rate of 12%.

Polyuria, polydipsia, and polyphagia are the classic triad leading to the diagnosis of type 1 diabetes. Other common symptoms include weight loss, secondary enuresis, anorexia, vague abdominal discomfort, visual changes, and genital candidiasis in a toilet-trained child.

Premonitory symptoms of cerebral edema occur in as few as 50% and include severe headache, declining mental status, seizures, and papilledema. Cerebral edema typically occurs 6 to 12 hours after initiating therapy and presents as headache, mental status changes, seizure, or coma. Although the etiology of this complication is unknown, it is felt that several factors may contribute, including overly aggressive fluid therapy, rapid correction of blood glucose levels, bicarbonate therapy, and failure of the serum sodium level to increase with therapy.

Occasionally children with DKA present to the ED complaining primarily of abdominal pain, which may mimic acute appendicitis; Kussmaul breathing (hyperpnea from acidosis) may be mistaken for hyperventilation from anxiety or respiratory distress from pulmonary disease.

The diagnosis of diabetes is established by demonstrating hyperglycemia and glucosuria in the absence of other causes such as steroid therapy, Cushing syndrome, pheochromocytoma, hyperthyroidism, or other rare disorders. DKA is generally defined as a metabolic acidosis (pH < 7.25 to 7.30 or serum bicarbonate level of <15 mEq/L) with hyperglycemia (serum glucose level of >300 milligrams/dL) in the presence of ketonemia/ketonuria.

Cerebral edema in DKA is a clinical diagnosis based on altered mental status not attributed to hypovolemia and treatment should begin prior to obtaining head CT when suspected. CT imaging can confirm the diagnosis, and intracranial pressure monitoring may be indicated.

The treatment of DKA consists of judicious fluid resuscitation, insulin therapy, correction of electrolyte abnormalities, and close monitoring. Patients should be placed on a cardiac monitor, noninvasive blood pressure device, and pulse oximetry, and intravenous lines should be established.

1. Administer 10 to 20 mL/kg normal saline boluses until hemodynamic stability is achieved. Give an initial 20 mL/kg normal saline (NS) bolus of normal saline if the child is in shock and repeat if needed. Once vital signs have stabilized, resist the desire to correct the fluid deficit too rapidly, especially if there is a high calculated osmolarity (ie, > 340 mOsm/L).

2. Follow the initial bolus with NS at 1.5 times maintenance rate in the ED.

3. If [K+] is <5.5 mEq/L and patient is urinating, add 30 mEq potassium per L (half as KCl and half as potassium phosphate). If initial [K+] is 2.5 to 3.5 mEq/L, add 40 mEq [K+]/L; consider adding more if the [K+] is < 2.5 mEq/L.

4. Begin regular insulin at 0.05 to 0.1 unit/kilogram/h after IV fluid bolus (if given) is complete. Adjust dose to maintain glucose decline at 50 to 100 milligrams/dL/h. Do not decrease insulin infusion below 0.05 unit/kilogram/h until ketonuria has resolved. High-dose insulin therapy and insulin boluses increase the risk of complications and should not be given.

5. Add dextrose to IV fluids when blood glucose is < 200 to 250 milligrams/dL. Glucose levels correct faster than ketoacidosis, so supplement with dextrose and continue the insulin drip until ketoacidosis has resolved.

6. Measure serum electrolyte levels every 2 hours; measure serum glucose level every hour.

7. The use of bicarbonate in the treatment of DKA is contraindicated, as it dose not improve outcome and it has been associated with a fourfold increase in the development of cerebral edema.

8. Management of cerebral edema. Treat patients with altered mental status suggestive of cerebral edema with mannitol 0.5 to 1 gram/kilogram. Consider 3% hypertonic saline, 10 mL/kg over 30 min. Restrict additional IV fluids to minimum required to maintain IV access. Use caution if endotracheal intubation is required and avoid eucapnea as severe metabolic acidosis requires compensatory respiratory alkalosis and a rise in CO2 may worsen systemic and intracellular acidosis.

9. Most patients with DKA require admission to the intensive care unit, even when in stable condition, because of intensive monitoring needs. Furthermore, many hospitals restrict the use of insulin infusions to intensive care settings. Patients with cerebral edema require ICU admission and possible intracranial pressure monitoring. Consultation with the patient's primary care physician and a pediatric endocrinologist should be made early in the course of therapy.