POSTISCHEMIC HYPERTHERMIA EXACERBATES NEUROLOGIC INJURY AFTER DEEP HYPOTHERMIC CIRCULATORY ARREST

Citation
D. Shumtim et al., POSTISCHEMIC HYPERTHERMIA EXACERBATES NEUROLOGIC INJURY AFTER DEEP HYPOTHERMIC CIRCULATORY ARREST, Journal of thoracic and cardiovascular surgery, 116(5), 1998, pp. 780-791
Citations number
27
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiac & Cardiovascular System",Surgery
ISSN journal
0022-5223
Volume
116
Issue
5
Year of publication
1998
Pages
780 - 791
Database
ISI
SICI code
0022-5223(1998)116:5<780:PHENIA>2.0.ZU;2-X
Abstract
Background: Aggressive surface warming is a common practice in the ped iatric intensive care unit, However, recent rodent data emphasize the protective effect of mild (2 degrees-3 degrees C) hypothermia after ce rebral ischemia, This study evaluates different temperature regulation strategies after deep hypothermic circulatory arrest with a survival piglet model. Methods: Fifteen piglets were randomly assigned to 3 gro ups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15 degrees C, Brain temperature was maintained at 34 degrees C for 24 hours after cardiopulmonary bypass in group I, 37 degrees C in group II, and 40 degrees C in group III. Neurobehavioral recovery w as evaluated daily for 3 days after extubation by neurologic deficit s core (0, normal; 500, brain death) and overall performance category (1 , normal; 5, brain death). Histologic examination was assessed for hyp oxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Re sults: All results are expressed as mean +/- standard deviation. Recov ery of neurologic deficit score (12.0 +/- 17.8, 47.0 +/- 49.95, 191.0 +/- 179.83; P = .05 for group I vs III), overall performance category (1.0 +/- 0,0, 1.4 +/- 0.6, 2.8 +/- 1.3; P < .05 for group I vs IU), an d histologic scores (0.0 +/- 0,0, 1.0 +/- 1.2, 2.8 +/- 1.8; P < .05 fo r group I vs III cortex) were significantly worse in hyperthermic grou p III. These findings were associated with a significantly lower cytoc hrome aa, recovery determined by near-infrared spectroscopy in group I II animals (P = .0041 for group I vs III). No animal recovered to base line electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthe rmic group III animals, with a lower amplitude 14 hours after the oper ation, which gradually increased with time (P < .05 for group III vs g roups I and II). Conclusions: Mild postischemic hyperthermia significa ntly exacerbates functional and structural neurologic injury after dee p hypothermic circulatory arrest and should therefore be avoided.