TY - JOUR
T1 - Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest
AU - Shum-Tim, D.
AU - Nagashima, M.
AU - Shinoka, T.
AU - Bucerius, J.
AU - Nollert, G.
AU - Lidov, H. G.W.
AU - Du-Plessis, A.
AU - Laussen, P. C.
AU - Jonas, R. A.
AU - Swain, J. A.
AU - Murphy, D. A.
AU - Sano, S.
AU - Spray, T. L.
PY - 1998
Y1 - 1998
N2 - Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2°-3°C) hypothermia after cerebral 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 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15°C. Brain temperature was maintained at 34°C for 24 hours after cardiopulmonary bypass in group I, 37°C in group II, and 40°C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean ± standard deviation. Recovery 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 III), and histologic scores (0.0 ± 0.0, 1.0 ± 1.2, 2.8 ± 1.8; P < .05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P < .05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.
AB - Background: Aggressive surface warming is a common practice in the pediatric intensive care unit. However, recent rodent data emphasize the protective effect of mild (2°-3°C) hypothermia after cerebral 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 groups. All groups underwent 100 minutes of deep hypothermic circulatory arrest at 15°C. Brain temperature was maintained at 34°C for 24 hours after cardiopulmonary bypass in group I, 37°C in group II, and 40°C in group III. Neurobehavioral recovery was evaluated daily for 3 days after extubation by neurologic deficit score (0, normal; 500, brain death) and overall performance category (1, normal; 5, brain death). Histologic examination was assessed for hypoxic-ischemic injury (0, normal; 5, necrosis) in a blinded fashion. Results: All results are expressed as mean ± standard deviation. Recovery 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 III), and histologic scores (0.0 ± 0.0, 1.0 ± 1.2, 2.8 ± 1.8; P < .05 for group I vs III cortex) were significantly worse in hyperthermic group III. These findings were associated with a significantly lower cytochrome aa3 recovery determined by near-infrared spectroscopy in group III animals (P = .0041 for group I vs III). No animal recovered to baseline electroencephalographic value by 48 hours after deep hypothermic circulatory arrest. Recovery was significantly delayed in the hyperthermic group III animals, with a lower amplitude 14 hours after the operation, which gradually increased with time (P < .05 for group III vs groups I and II). Conclusions: Mild postischemic hyperthermia significantly exacerbates functional and structural neurologic injury after deep hypothermic circulatory arrest and should therefore be avoided.
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U2 - 10.1016/S0022-5223(98)00449-8
DO - 10.1016/S0022-5223(98)00449-8
M3 - Article
C2 - 9806385
AN - SCOPUS:0031796577
SN - 0022-5223
VL - 116
SP - 780
EP - 792
JO - Journal of Thoracic and Cardiovascular Surgery
JF - Journal of Thoracic and Cardiovascular Surgery
IS - 5
ER -