Pancreatic enzyme concentrations are frequently elevated in children with diabetic ketoacidosis (DKA). We sought to determine the clinical and biochemical characteristics associated with patients with these elevations. Our hypothesis was that pancreatic enzyme elevations would be associated with biochemical markers of hypoperfusion.
Prospective cohort study.
Three university-affiliated children’s hospitals.
We collected data on consecutive children <18 yrs of age hospitalized with the diagnosis of DKA.
Serum electrolyte and lactate concentrations and venous pH and Pco2 were measured every 3 hrs from hours 0 to 12 and then every 6 hrs until hour 24. Serum calcium, phosphate, and magnesium concentrations were measured every 6 hrs from hours 0 to 24. Serum amylase, lipase, and triglyceride concentrations were measured at hour 0 and then 12, 24, and 48 hrs after the initiation of therapy.
We performed multivariable analyses to test for associations between clinical variables and pancreatic enzyme elevation in 67 children with DKA. Lipase was elevated in 21 (31%) and amylase in 16 (24%) of the children. Pancreatic enzyme values peaked 12–24 hrs after admission. There was no significant correlation between pancreatic enzyme elevation and abdominal pain. In multivariable analyses, an elevated blood urea nitrogen (BUN) concentration was associated with elevated serum amylase (odds ratio 1.04 per unit increase; 95% confidence interval, 1.01–1.09; p = .02), and elevated BUN concentrations and hypophosphatemia were associated with elevated serum lipase (odds ratio 1.04 per unit increase; 95% confidence interval, 1.00–1.08; p = .04; and odds ratio 0.35 per unit increase; 95% confidence interval, 0.15–0.81; p = .01, respectively).
Elevation of pancreatic enzymes is common in children with DKA, but clinical pancreatitis is rare. Pancreatic enzyme levels reach a peak 12–24 hrs after initiation of treatment for DKA. Pancreatic enzyme elevation is associated with increased BUN concentrations at presentation but is not associated with abdominal pain.
From the Division of Gastroenterology (JAQ), Division of Critical Care (JPM, FN), Division of Endocrinology, Department of Pediatrics (NG), and Department of Emergency Medicine (NK), University of California Davis School of Medicine and the UC Davis Children’s Hospital; Department of Pediatrics, University of Colorado, School of Medicine (AR); and Department of Pediatrics, Stanford University School of Medicine (JD, EKN).
Presented, in part, at the North American Society of Pediatric Gastroenterology, Hepatology and Nutrition Annual Meeting, Salt Lake City, UT, October 2005.
The authors have not disclosed any potential conflicts of interest.
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