![]() Once cerebral edema develops, death occurs in some 20–25%, and significant morbidity, including pituitary insufficiency, occurs in 10–25% of survivors. The reported mortality rates in children with DKA are constant in national population-based studies varying from ∼0.15 to 0.3%. Because cerebral edema occurs in the context of DKA, reduction of the incidence of DKA should be a major goal of treating children with diabetes. Currently, the etiology, pathophysiology, and ideal treatment are poorly understood, but these are areas of intense investigation. Only a minority of deaths in DKA are attributable to other causes, such as sepsis, other infections (including mucormycosis), aspiration pneumonia, pulmonary edema, acute respiratory distress syndrome, pneumomediastinum, hypo- or hyperkalemia, cardiac arrhythmias, central nervous system (CNS) hematoma or thrombosis, and rhabdomyolysis. Hence, greater severity at presentation in younger children together with less maturity of autoregulatory systems combine to predispose children to cerebral edema, which occurs in ∼0.5–1% of all episodes of DKA in children and is the most common cause of mortality in children with DKA ( 9– 12). DKA, defined by blood bicarbonate 14 years but did not differ significantly by sex or ethnicity ( 6).ģ) Cerebral and other autoregulatory mechanisms may not be as well developed in younger children. Generally, the rates of DKA are inversely proportional to rates of diabetes in that community, but throughout the U.S., the overall rates of DKA at diagnosis have remained fairly constant at ∼25% ( 6). Even in developed countries, some 15–70% of all newly diagnosed infants and children with diabetes present with DKA ( 1– 8). ![]() Because the diagnosis of diabetes is not suspected as it evolves, the duration of symptoms may be longer, leading to more severe dehydration and acidosis and ultimately to obtundation and coma. Infants and toddlers in DKA may be misdiagnosed as having pneumonia, reactive airways disease (asthma), or bronchiolitis and therefore treated with glucocorticoids and/or sympathomimetic agents that only compound and exacerbate the metabolic derangements. 1) The younger the child, the more difficult it is to obtain the classical history of polyuria, polydipsia, and weight loss. ![]()
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