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