MAINTAINING NORMAL INTRACRANIAL-PRESSURE IN A RABBIT MODEL DURING TREATMENT OF SEVERE DIABETIC KETOACIDEMIA

Citation
Gd. Harris et al., MAINTAINING NORMAL INTRACRANIAL-PRESSURE IN A RABBIT MODEL DURING TREATMENT OF SEVERE DIABETIC KETOACIDEMIA, Life sciences, 59(20), 1996, pp. 1695-1702
Citations number
28
Categorie Soggetti
Biology,"Medicine, Research & Experimental","Pharmacology & Pharmacy
Journal title
ISSN journal
00243205
Volume
59
Issue
20
Year of publication
1996
Pages
1695 - 1702
Database
ISI
SICI code
0024-3205(1996)59:20<1695:MNIIAR>2.0.ZU;2-R
Abstract
Increased intracranial pressure (ICP) resulting in death or neurologic morbidity continues to complicate traditional management of diabetic ketoacidemia (DKA) in pediatric patients. When ICP or cerebrospinal fl uid pressures have been measured, correction of hyperglycemia in anima ls and treatment of DKA in humans have consistently resulted in pathol ogic increases in ICP. We hypothesized that elevations in ICP can be m inimized if changes in effective osmolality (E(osm)) are controlled du ring treatment of DKA. During a six-hour study period, three groups of rabbits were studied: a normal control group of nondiabetic animals ( C-nor, n = 10), a control group of animals with DKA (C-DKA; n = 8), an d an experimental group of animals with DKA (E(DKA); n = 8). There was no significant difference between the two groups with DKA regarding p retreatment degree of dehydration, blood pressure, hyperglycemia, acid emia or ICP. During the treatment period, C-nor received maintenance f luids only. C-DKA received insulin and an assumed volume of deficit (1 50 ml/kg) along with maintenance fluids and urinary output replacement with 0.45% NaCl. E(DKA) received insulin and one-half the volume of d eficit calculated by the weight lost with 0.9% NaCl plus maintenance f luids. There was no significant difference between C-DKA and E(DKA) re garding the rate at which DKA was corrected. While C-DKA demonstrated a progressive and statistically significant increase in ICP, E(DKA) ex hibited no such increase in ICP compared to normal, nondiabetic contro ls (C-nor) during treatment. Changes in E(osm) during treatment in C-D KA compared to C-nor and in C-DKA compared to E(DKA) were significantl y greater (p < .01); however, changes in E(OSM) in E(DKA) compared to C-nor were not significant. These data support the clinical observatio n that decreasing E(osm) during treatment of DKA is associated with in creased ICP and suggest that DKA can be treated effectively with i.v. fluids and insulin without increasing ICP.