Moderate controlled cortical contusion in pigs: effects on multi-parametric neuromonitoring and clinical relevance.
Over the last decade, routine neuromonitoring of ICP and CPP has been extended with new on-line techniques such as microdialysis, tissue oxygen (ptiO(2)), acid-base balance (ptiCO(2), pH) and CBF measurements, which so far have not lead to clear-cut therapy approaches in the neurointensive care unit. This is partially due to the complex pathophysiology following a wide-range of brain injuries, and the lack of suitable animal models allowing simultaneous, clinically relevant neuromonitoring under controlled conditions. Therefore, a controlled cortical impact (CCI) model in large animals (pig) has been developed. After placement of microdialysis, ptiO(2), temperature and ICP catheters, an unilateral CCI injury (2.6-2.8 m/sec velocity, 9 mm depth, 400 ms dwell time) was applied and neuromonitoring continued for 10 h. CCI caused a rapid drop in CPP, ptiO(2) and glucose, whereas ICP, glutamate and lactate increased significantly. Most parameters returned to baseline values within hours. Lactate stayed elevated significantly throughout the experiment, but the lactate-to-pyruvate ratio (LPR) changed only slightly, indicating no severely ischemic CBF. Contralateral parameters were not affected significantly. Evaluation of brain water content and histology (12 h post-CCI) showed ipsilateral brain swelling by 5% and massive cell damage underneath the injury site which correlated with changes of ICP, CPP, glutamate, lactate, and ptiO(2) within the first hours post-CCI. Moderate controlled cortical contusion in pigs induced a complex pattern of pathophysiological processes which led to 'early' histological damage. Thus, this new large animal model will enable us to investigate the effect of therapeutic interventions on multi-parametric neuromonitoring and histological outcome, and to translate the data into clinical practice.
Alessandri
Beat
B
Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University Mainz, Mainz, Germany. beat.alessandri@uni-mainz.de
Heimann
Axel
A
Filippi
Ronald
R
Kopacz
Laszlo
L
Kempski
Oliver
O
D000818:Animals; D001831:Body Temperature / Q000502:physiology; D001929:Brain Edema / Q000209:etiology; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D005947:Glucose / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D007427:Intracranial Pressure / Q000502:physiology; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D008991:Monitoring, Physiologic; D010101:Oxygen Consumption / Q000502:physiology; D019289:Pyruvic Acid / Q000378:metabolism; D013552:Swine
D019344:Lactic Acid; D018698:Glutamic Acid; D019289:Pyruvic Acid; D005947:Glucose