Premium
An 18‐yr prospective study of pediatric diabetic ketoacidosis: an approach to minimizing the risk of brain herniation during treatment
Author(s) -
Fiordalisi Irma,
Novotny William E,
Holbert Donald,
Finberg Laurence,
Harris Glenn D
Publication year - 2007
Publication title -
pediatric diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.678
H-Index - 75
eISSN - 1399-5448
pISSN - 1399-543X
DOI - 10.1111/j.1399-5448.2007.00253.x
Subject(s) - medicine , diabetic ketoacidosis , ketoacidosis , prospective cohort study , diabetes mellitus , intensive care medicine , pediatrics , endocrinology , type 1 diabetes
Background: During the late 1900s, raised intracranial pressure (ICP) during treatment of pediatric diabetic ketoacidosis (DKA) surfaced as the most important cause of morbidity and mortality in pediatric DKA. The contribution of fluid and electrolyte therapy to neurologic deterioration during treatment remains controversial. Methods: We proposed a physiologic approach to treatment of DKA, incorporating the principles of rehydration of hypertonic states. Consecutive episodes of pediatric DKA were managed using continuous intravenous insulin, an individualized assessment of the degree of dehydration, and rehydration solutions of tonicity approximating that of the patient. Gradual replacement of the volume of deficit after correction of shock, if present, was planned over 48 h with special attention to changes in effective osmolality along with intensive cardiorespiratory, neurologic, and biochemical monitoring. Mannitol was given for signs or symptoms of raised ICP. Results: Six hundred and thirty‐five consecutive episodes of pediatric DKA were treated from January 1988 to September 2005. Means ± standard deviation (SD) for initial measured concentrations of total carbon dioxide, glucose, and urea nitrogen were 7.8 ± 3.3 mmol/L, 602 ± 271 mg/dL (33.4 ± 15 mmol/L), and 21 ± 1 mg/dL (7.4 ± 3.6 mmol/L), respectively. Pretreatment blood gases were available for 477 episodes. The mean initial partial pressures of arterial and venous carbon dioxide ± SD were 16.8 ± 7 mmHg (kP a CO 2 = 2.24 ± 0.93) for n = 308 and 26.6 ± 7 mmHg (kP v CO 2 = 3.54 ± 0.93) for n = 169, respectively. Although repair was planned to occur over 48 h, the mean time to achieve clinical rehydration and correction of DKA was 11.6 ± 6.2 h. Mannitol was given in 35 (5.5%) episodes. There was no neurologic morbidity or mortality. Conclusion: Management of pediatric DKA using this multifaceted physiologic approach and the principles of rehydration described is safe and appears to minimize the risk of brain herniation during treatment.