Neurologic deterioration associated with cerebral edema in diabetic ketoacidosis is typically sudden in onset, progresses rapidly, and requires emergent treatment. The utility of brain imaging by head CT in decisions to treat for cerebral edema has not been previously studied. The objective of this study was to describe the characteristics of pediatric patients with diabetic ketoacidosis who develop altered mental status and evaluate the role of head CT in this cohort.
Retrospective analysis of clinical, biochemical, and radiologic data.
Tertiary care children’s hospital (2004–2010).
Six hundred eighty-six admissions of patients (< 26 yr) with diabetic ketoacidosis.
Altered mental status was documented during 96 of 686 diabetic ketoacidosis admissions (14%). Compared with alert patients, those with altered mental status were younger (median, 12.0 vs 13.1 yr; p = 0.007) and more acidotic (pH, 7.04 vs 7.19; p < 0.001), with higher serum osmolality (328 vs 315 mOsm/kg; p < 0.001) and longer hospital length of stay (4.5 vs 3 d; p = 0.002). Head CT was performed during 60 of 96 diabetic ketoacidosis admissions with altered mental status (63%), 16 (27%) of which had abnormal results. Hyperosmolar therapy for cerebral edema was given during 23 of the 60 admissions (38%), during which 12 (52%) had normal head CT results, eight of these 12 (67%) after cerebral edema treatment and four (33%) before. Of the 11 admissions with abnormal head CT results that received hyperosmolar therapy, four head CT scan (36%) occurred after hyperosmolar treatment and seven (64%) before. For the 11 admissions with head CT before cerebral edema treatment, there was a median 2-hour delay between head CT and hyperosmolar therapy.
In this single-center retrospective study, there was no evidence that decisions about treatment of patients with diabetic ketoacidosis and suspected cerebral edema were enhanced by head CT, and head CT may have led to a significant delay in hyperosmolar therapy.
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1Division of Medicine Critical Care, Department of Medicine, Boston Children’s Hospital and Harvard Medical School, Boston, MA.
2Division of Endocrinology, Department of Medicine, Boston Children’s Hospital and Harvard Medical School, Boston, MA.
3Department of Cardiology, Boston Children’s Hospital, Boston, MA.
*See also p. 281.
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Research reported in this publication was supported by the National Institutes of Health (T32 HD 75727-1). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. The funding institutions did not contribute to the collection, management, analysis, and interpretation of the data; nor preparation, review, or approval of the article.
Dr. Soto-Rivera received support for article research from the National Institutes of Health (NIH). Dr. DeCourcey received support for article research from the NIH and her institution received funding from the National Research Service Award Training Grant (T32 HD 75727-1) and from Agency for Healthcare Research and Quality-funded Training Grant (K12 HS022986-01). The remaining authors have disclosed that they do not have any potential conflicts of interest.
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