Fluid Management of Diabetic Ketoacidosis
Laurence Finberg MD1
Kenneth B. Roberts MD
1 Department of Pediatrics, University of California at San Francisco
In last August's issue (16:304, 1995), Roberts commented on recent recommendations for the fluid management of diabetic ketoacidosis (DKA). This issue has great importance because the older recommendations or "traditional" therapy begun in the 1960 to 1990 era was associated with occasional serious and sometimes fatal outcomes because of central nervous system (CNS) damage. One pedagogical problem results from calling the complication "cerebral edema"; a more accurate term is cerebral swelling because the excess water from therapy is largely in cells, not the interstitial fluids, as is true of edema. Imaging studies show the ventricles to be small, similar to the situation in lead poisoning or cerebral hypoxia. Understanding the mechanism for the swelling will make it easier for the therapist to monitor the administration of fluid.
The initial swelling may occur before therapy for reasons we can only surmise or that are unknown. We do know that osmoprotective molecules (myoinositol, taurine, and perhaps others) will enter or be produced in cells in a hyperosmolar state such as DKA. This increase in cellular solute will attract water by osmosis. When fluid that has a lower sodium chloride concentration than interstital fluid (Na, 150 mEq/L; Cl, 118 m/Eq/L) is administered rapidly, either intravenously or orally, the tight junctions of the CNS vasculature admit water molecules by diffusion more rapidly than sodium and chloride ions; there is about a 4-hour lag time in equilibrium.
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