ESPEYB16 10. Type 1 Diabetes Mellitus (1) (20 abstracts)
10.6. Clinical trial of fluid infusion rates for pediatric diabetic ketoacidosis
Kuppermann N , Ghetti S , Schunk JE , Stoner MJ , Rewers A , McManemy JK , Myers SR , Nigrovic LE , Garro A , Brown KM , Quayle KS , Trainor JL , Tzimenatos L , Bennett JE , DePiero AD , Kwok MY , Perry CS 3rd , Olsen CS , Casper TC , Dean JM , Glaser NS & PECARN DKA FLUID Study Group
Departments of Emergency Medicine, Pediatrics, and Psychology, University of California Davis Health, University of California, Davis, School of Medicine, Sacramento, USA
To read the full abstract: N Engl J Med. 2018 Jun 14;378(24):2275–2287
Neurological complications of diabetic ketoacidosis (DKA) are still causes of significant mortality and morbidity in type 1 diabetes (T1D). Children are still being reported with acute cerebral infarction (CI) and extra pontine myelinolysis (EPM) at onset of T1D (1). Frequently, their clinical management had not been optimal and putative risk factors for such complications had been neglected. Not only cerebral edema (CE), but also other severe neurological complications such as CI should be suspected when neurological deterioration occurs during DKA, and these may still cause brain injuries ranging from mild to severe (1).
This large randomized, controlled trial, involving 13 US centers, tested the rate of fluid administration and sodium chloride content of intravenous fluids in relation to neurologic outcomes in children with DKA. Children were randomly assigned to one of four treatment groups in a 2-by-2 factorial design (0.9% or 0.45% sodium chloride content and rapid or slow rate of administration). The primary outcome was a decline in mental status as proven by two consecutive Glasgow Coma Scale (GCS) scores of <14. Secondary outcomes included clinically apparent brain injury during treatment for diabetic ketoacidosis, short-term memory during treatment for diabetic ketoacidosis, and memory and IQ two to six months after recovery from diabetic ketoacidosis. 1389 episodes of DKA were reported in 1255 children. GCS score declined to <14 in 3.5% (48 episodes), and clinically apparent brain injury occurred in 0.9% (12 episodes).
No significant difference between treatment groups was observed in: episodes of GCS score <14, the magnitude of decline in GCS score, duration of time spent with GCS<14; tests of short-term memory; or incidence of clinically apparent brain injury during treatment for DKA. Memory and IQ scores measured after recovery from DKA did not differ between groups. Serious adverse events other than altered mental status were rare and occurred with similar frequency in all groups.
In summary, neither the rate of administration nor the sodium chloride content of intravenous fluids influenced neurologic outcomes in children with DKA in tertiary care centers when treatment was otherwise conducted according to recommended guidelines.
In retrospect, one might agree that sodium chloride or fluid infusion rate alone were unlikely to be the single and most relevant risk factor for the development of neurological complications in DKA, Other risk factors might be of more relevance, such as initial conscious level, bicarbonate use, rate of blood glucose lowering, and lack of intensive care unit monitoring. It is still recommended that not only an exceeded rehydration therapy but also a rapidly reduced serum osmolality due to an unbalanced rapid blood sugar decrease and serum sodium increase should be avoided in order to prevent neurological complications. A structured and well-defined rehydration strategy in the first 6–12 hours of therapy following an in-house standard operation procedure protocol remains crucial for recovery and can reduce neurological complications of patients with DKA.
Reference: 1. Petzold S, Kapellen T, Siekmeyer M, Hirsch W, Bartelt H, Siekmeyer W, Kiess W. Acute cerebral infarction and extra pontine myelinolysis in children with new onset type 1 diabetes mellitus. Pediatr Diabetes. 2011;12:513–7.
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ESPE Yearbook of Paediatric Endocrinology
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