Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest

• Published in: The Journal of thoracic and cardiovascular surgery Vol. 116; no. 5; pp. 780 - 792
• Main Authors: Shum-Tim, Dominique, Nagashima, Mitsugi, Shinoka, Toshiharu, Bucerius, Jan, Nollert, Georg, W. Lidov, Hart G., du-Plessis, Adre, Laussen, Peter C., Jonas, Richard A.
• Format: Journal Article
• Language: English
• Published: United States Mosby, Inc 01.11.1998; AATS/WTSA
• Subjects: Animals; Brain - pathology; Brain Damage, Chronic - pathology; Electroencephalography; Electron Transport Complex IV - metabolism; Heart Arrest, Induced; Hemoglobins - metabolism; Hypothermia, Induced; Hypoxia, Brain - pathology; Neurologic Examination; Neurons - pathology; Oxyhemoglobins - metabolism; Rewarming - adverse effects
• ISSN: 0022-5223; 1097-685X
• DOI: 10.1016/S0022-5223(98)00449-8

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 aa 3 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. (J Thorac Cardiovasc Surg 1998;116:780-92)