Postischemic hyperthermia exacerbates neurologic injury after deep hypothermic circulatory arrest.
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.
Shum-Tim
D
D
Department of Cardiovascular Surgery, Children's Hospital, Harvard Medical School, Boston, Mass 02115, USA.
Nagashima
M
M
Shinoka
T
T
Bucerius
J
J
Nollert
G
G
Lidov
H G
HG
du Plessis
A
A
Laussen
P C
PC
Jonas
R A
RA
D000818:Animals; D001921:Brain / Q000473:pathology; D001925:Brain Damage, Chronic / Q000473:pathology*; D004569:Electroencephalography; D003576:Electron Transport Complex IV / Q000378:metabolism; D006324:Heart Arrest, Induced; D006454:Hemoglobins / Q000378:metabolism; D007036:Hypothermia, Induced; D002534:Hypoxia, Brain / Q000473:pathology*; D009460:Neurologic Examination; D009474:Neurons / Q000473:pathology; D010108:Oxyhemoglobins / Q000378:metabolism; D017694:Rewarming / Q000009:adverse effects*
D006454:Hemoglobins; D010108:Oxyhemoglobins; C100003:deoxyhemoglobin; D003576:Electron Transport Complex IV