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POSTISCHEMIC HYPERTHERMIA EXACERBATES NEUROLOGIC INJURY AFTER DEEP HYPOTHERMIC CIRCULATORY ARREST.
Shum-Tim, Dominique MD a; Nagashima, Mitsugi MD a; Shinoka, Toshiharu MD a; Bucerius, Jan MD a; Nollert, Georg MD a; Lidov, Hart G. W. MD b; du-Plessis, Adre MD c; Laussen, Peter C. MD d; Jonas, Richard A. MD a
[Miscellaneous Article] Journal of Thoracic & Cardiovascular Surgery. 116(5):780-792, November 1998.

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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[degrees]-3[degrees]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[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 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.