POSTISCHEMIC HYPERTHERMIA EXACERBATES NEUROLOGIC INJURY AFTER DEEP HYPOTHERMIC CIRCULATORY ARREST

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.