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Type 1 diabetes, an autoimmune disease, 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 diabetes may develop hyperglycemic hyperosmolar nonketotic syndrome (HHNS) 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 HHNS, 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. Symptoms of DKA include excessive thirst, weakness, vomiting, loss of appetite, confusion, abdominal pain, shortness of breath, and a generally ill-appearance. 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.

Premonitory symptoms of cerebral edema occur in 50% of patients and include severe headache, declining mental status, and seizures. Cerebral edema is rare (0.5% to 1% of all children presenting with DKA) but typically occurs 6 to 12 hours after initiating therapy. Although the etiology of this complication is unknown, it is felt that several factors may contribute, including young age, severe hyperosmolality, severe acidosis, and failure of the serum sodium level to rise commensurately with the fall in glucose level during therapy.


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 <7.30 or serum bicarbonate level of <15 mEq/L) with hyperglycemia (serum glucose level of >200 mg/dL) in the presence of ketonemia or ketonuria. In adolescent patients without known diabetes, consider toxic ingestions of ethylene glycol, isopropyl alcohol, or salicylates.

Cerebral edema in DKA is a clinical diagnosis based on altered mental status not attributed to hypovolemia. 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 ...

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