The Experimental And Preliminary Clinical Study Of Role Of Brain Tissue Oxygenation After Traumatic Brain Injuries

Although great progress has been made in basic and clinical study of traumatic brain injury (TBI) in the recent decade, the mortality is still high, especially the poor outcome in severe TBI. The secondary cerebral ischemia or hypoxia is the main factor that influences the outcome after brain injury. Now most of the study is still focusing on the prevention and treatment of the secondary brain damage after severe TBI. Cerebral ischemia is the major common pathway that causes the secondary brain damage, and oxygen is the key factor to the neuronal survival and function. Intracranial pressure(ICP) and cerebral perfusion pressure are the currently main therapeutic pillars in the treatment of severe head injury. The study of brain oxygenation has open a new window to learn more about the function of the brain and also been a new index to determine outcome or evaluate the effect of frequently used treatments.Intracranial hematoma in pig is used to simulate acute intracranial hypertention. Multi-parameter monitoring technique is applied to monitor the brain oxygenation and metabolism. The actual effect of four treatments (Hyperoxia, mannitol, hyperventilation and moderate hypothermia) on brain oxygenation and metabolism is also observed. Meanwhile, the brain oxygenation and metabolism of ten severe head injury cases are continuously monitored and the relationship to the outcome is tentatively studied. The research consists of three parts:Part I The changes of brain tissue P2> PtjCO2> pHtj during acute intracerebral hematoma in pigs.Objective: To investigate the changes of brain tissue oxygen pressure (PtjC^X brain tissue carbon dioxide pressure (PuCCfe)- pHtj and lactate during acute intracranialhypertention caused by intracerebral hematoma in pigs. Method: The model of acute intracerebral hematoma in pigs was established by micro-pump injection method. MRK Slice preparation and section staining are used to observe the formation of the intracerebral hematoma. Brain tissue PtjO2?PtiCC^, pHtj and brain temperature were continuously monitored by Neurotrend system. The arterial blood gas was analysed. The lactate was measured by magnetic resonance spectrascopy (MRS). Results:(\} After blood injection, ICP is rapidly increased to high level (> 5.33kPa), CPP decreased to 9.6kPa, PtiO2 remarkably decreased to ischemic level 1.33kPa (p<0.01) , PtiCO2 remarkably increased to 13.10 ?.16kPa (p<0.05), and pH decreased to 7.17 ?0.13 kPa (p<0.05). (2) There was closely negative correlation between ICP and CPP during the formation of intracerebral hematoma (rjcp-cpp= -0.80, p<0.01) . PtjC>2 was closely correlated to CPP (rp,jO2-cpp=0.775, pO.ODandlCP (rptico2-cpp=0.65,p<0.01). During blood injection, PtjCO2 was closely correlated to CPP (rptjco2-cpp=0.65, p<0.01) .pHtj is changed with PtjCO2 and there was also close correlation between them (r pH-ptico2=: ~~ 0.791, p<0.01) . (3) For the MRI, the hematoma was located in left frontal lobe. MRS examinations showed that there was no lactate peak in the normal animal brains. Two hours after blood injection, lactate peak was markedly increased in brain tissue around hematoma, with Lac/Cr ratio increased significantly (pO.Ol). Lactate peak appeared in contralateral brain tissue and Lac/Cr ratio is increased significantly as well (p<0.01) . (4) Macroscopic slice preparation verified that hematoma was totally located in the left frontal lobe. Blood was not found in the ventricular. Ventricular was compressed obviously and the midline was shifted to right. Light microscopic examinations showed that massive hemorrhage occured in the brain tissue around the hematoma. Cerebral parenchyma necrosed and the normal neural structure disappeared. Cellulosic necrosis was seen in the peri-hematoma small cerebral blood vessel. Arteriola distented and congested. A great deal of neutrophil granules infiltrated diffusely. The pathology of brain showed the changes of encephalitis and meningoencephalitis. Focal hemorrhage was also found in the adjacent cerebral parenchyma. There were no evid...