الفهرس 
EpidemiologyOnly 14 pages are availabe for public view
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Abstract
Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus. DKA also can occur in children with type 2 diabetes mellitus, particularly in obese African-American adolescents.
DKA is diagnosed when patients with diabetes mellitus exhibit both hyperglycemia (blood glucose of >200 mg/dl [11 mmol/l]) and metabolic acidosis (venous pH <7.3 and/or plasma bicarbonate <15 mEq/l . These abnormalities are accompanied by hyperketosis (concentration of total ketone bodies >5 mmol/l) and hyperosmolality.
Hyperosmolar hyperglycemic state (HHS) is a hyperglycemia emergency which is distinguished from classic DKA by marked hyperglycemia (plasma glucose >600 mg/dl), serum CO2 >15 mmol/l, absent to small ketonemia and ketonuria, and effective serum osmolality >320 mOsm/L.
DKA is the presenting feature of new onset type 1 diabetes mellitus in approximately 30 to 40 % of cases. Children who are younger (e.g, under six years of age) or from a low socioeconomic status are more likely to have DKA when they present with type 1 diabetes mellitus.
Presenting symptoms of DKA in older children and adolescents include polyuria, polydipsia, and fatigue. Other findings include weight loss, nocturia (with or without secondary enuresis), daytime enuresis, and vaginal or cutaneous moniliasis. Infants tend to present with decreased energy and activity, irritability, weight loss, and physical signs of dehydration; a severe Candida diaper rash is common.
Initial laboratory testing should include serum testing for glucose, electrolytes, creatinine and urea nitrogen, blood gases, and hematocrit. Direct measurement of beta-hydroxybutyrate in the blood should also be performed if possible. The diagnosis of DKA is confirmed by the findings of hyperglycemia, a high anion gap acidosis, significant ketonemia, and metabolic acidosis.
The venous pH and serum bicarbonate concentration directly reflect the severity of the acidosis. Neurologic status should also be formally assessed at presentation and periodically during treatment, because cerebral edema is an important cause of morbidity and mortality in patients with DKA.
Cerebral edema is responsible for 50 to 80 % of deaths related to diabetic ketoacidosis in children. Among children with DKA who develop cerebral edema, the mortality rate is 20 to 25 %, and 15 to 35% of survivors have permanent neurologic sequelae.
Children who are younger, newly diagnosed with DKA, or who present with elevated BUN, more profound acidosis, or neurologic symptoms are at greatest risk for cerebral edema.
Careful evaluation and monitoring is recommended for signs and symptoms of cerebral edema in all children undergoing treatment for DKA. Specific signs of increased intracranial pressure and changes detectable by head computed tomography often occur too late for effective intervention. Therefore, monitoring is recommended for symptoms that may occur earlier in the development of cerebral edema. These symptoms include headache, recurrent vomiting, and altered level of consciousness, as outlined in the bedside evaluation protocol.
Changes detectable by head computed tomography occur late in the development of cerebral edema. Therefore, the decision to treat should be based on clinical evaluation. Imaging may be useful to exclude other causes of neurological deterioration, but should not delay treatment.
If cerebral edema is suspected, it is recommended to begin treatment promptly by reducing the rate of fluid administration and administering mannitol (0.25-1 g/kg) or hypertonic (3%) saline. Mechanical hyperventilation is generally not recommended. Treatment options have not been rigorously studied, but prompt and aggressive treatment is appropriate given the high morbidity and mortality of cerebral edema.