title: The effect of resuscitative moderate hypothermia following epidural brain compression on cerebral damage in a canine outcome model.
abstract: A canine model of temporary epidural cerebral compression and standardized intensive care was developed to evaluate the effect of resuscitative (postinsult) moderate systemic hypothermia. A balloon was inflated over the temporal region to maintain contralateral intraventricular pressure (IVP) at 62 mm Hg for 90 minutes. For a 66-hour period after initiation of brain compression, the intubated dogs received controlled ventilation and standard intensive care. From 66 to 90 hours postinjury, the extubated dogs were evaluated as to functional outcome. Morphological brain damage was evaluated at 90 hours or earlier if brain death occurred. Eight dogs in a control group were maintained at a body of temperature of 38 degrees C. Eight treated dogs had core body temperature reduced by surface cooling starting 15 minutes after balloon inflation, first to 31 degrees C for 5 hours and then to 35 degrees C from 5 to 62 hours after insult. Intraventricular pressure increased to 20 mm Hg or greater in the control group at a mean of 2.9 hours (range 2 to 4 hours) following the insult, and in the hypothermic group at a mean of 14.8 hours (range 5 to 30 hours)--that is, during the time period when the body temperature was 35 degrees C, not 31 degrees C (p = 0.01). There was no difference in peak pressures between the two groups. Brain death occurred in four of the eight dogs in the normothermic group at 18, 24, 24, and 48 hours (mean +/- standard deviation 28 +/- 13 hours) and in three of the eight in the hypothermic group at 27, 42, and 45 hours (mean 38 +/- 10 hours) (not significant). The animals surviving 90 hours (four in the normothermic and five in the hypothermic group) were neurologically near normal. The total mean macroscopically damaged brain volume was 2584 +/- 1890 cu mm in the normothermic versus 765 +/- 611 cu mm in the hypothermic group (p = 0.03). The mean necrotic volume was 741 +/- 599 cu mm in the normothermic versus 263 +/- 346 cu mm in the hypothermic group (p = 0.07). Microscopically, the damaged regions consisted of ischemic neurons, reactive glia, edema, vascular endothelial hypertrophy, and erythrocyte extravasation. It is concluded that, in this model, immediate postinsult hypothermia of 31 degrees C (not 35 degrees C) for 5 hours prevents a rise in IVP and significantly decreases cerebral tissue damage, but does not prevent brain herniation during rewarming.
authors.affiliation: International Resuscitation Research Center, University of Pittsburgh Medical Center, Pennsylvania.
authors.forename: S
authors.initials: S
authors.lastname: Pomeranz
authors.forename: P
authors.initials: P
authors.lastname: Safar
authors.forename: A
authors.initials: A
authors.lastname: Radovsky
authors.forename: S A
authors.initials: SA
authors.lastname: Tisherman
authors.forename: H
authors.initials: H
authors.lastname: Alexander
authors.forename: W
authors.initials: W
authors.lastname: Stezoski
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000473:pathology / Q000503:physiopathology / Q000628:therapy*; D003422:Critical Care / Q000379:methods*; D004195:Disease Models, Animal; D004285:Dogs; D004388:Dura Mater; D005260:Female; D007036:Hypothermia, Induced / Q000379:methods*; D009336:Necrosis; D011312:Pressure; D011597:Psychomotor Performance; D016896:Treatment Outcome