Exploring Short-term Effect Of Nimodipine In Severe Traumatic Brain Injury From Angle Of Cerebral Oxygen Metabolism

Objective: Severe closed trauma of head causes high mortality and mutilation, so the focus of clinic treatment is to save lives and improve the patients'living quality. The main reason in affecting prognostic is secondary brain injury, which, according to many researchers, results from a serial of factors, such as lipid peroxidation, prostacyclin, some neuropeptide and neurotransmitter. Among all the reasons, nerve cell calcium overload is one of the crucial factors in the injury. Experiments on animals showed, calcium in nerve cell intracytoplasm increases considerably, 10 times of the control group (CG) in half an hour since head injury took place; within the period of 6-72 hours, Ca2+ in nerve cells kept overload, more than 16 times of the CG; even 7 days later, it was still twice as high as the CG. In correspondence with the above mentioned facts, half an hour later, cerebral edema became obvious and achieved its peak in 6 hours. Meanwhile, researchers found out that 90% of the head injury death suffered from ischemic change. In recent years, with the continuous study on Ca2+ antagonist, Nimodipine was found effective in treating Severe Traumatic Brain Injury through lessening the calcium overload of nerve cells, easing the cerebral edema and acute intracranial hypertension, improving the secondary cerebral ischemia and hypoxia, thus death and mutilation rate can be reduced. Partial pressure of brain tissue oxygen(PbtO2) monitoring technology, matured in recent years, is a new monitoring technology in brain oxygen metabolism succeeding skull imaging examination, intracranial pressure and brain therm monitoring. It is safe, accurate and causes little trauma, and is of great significance for the treatment and analysizing prognosis in Severe Traumatic Brain Injury .This research, through analysizing the change of PbtO2 and the intracranial pressure in the Nimodipine treatment of Severe Traumatic Brain Injury patients, together with the GOS marks of the patients investigated after 3 months, aims to find out the short-term effect of such treatment and explore the clinic significance of brain PtO2 monitoring.Method: 30 Severe Traumatic Brain Injury patients who came to hospital within 24 hours since they were injured were under investigation, all the cases were in accordance with: came to hospital within 24 hours from the time they were injured, and were confirmed by head CT scanning; Glasgow coma score (GCS) was 5-8, no associated injury or complication when the patients first came to hospital; no organ illness or using Ca2+ antagonist history; the patients'family member signed informed consent. All the cases were divided into Nimodipine treatment group and control group at random. The CG were applied conventional therapy, mainly including removing the hematoma or decompression through skull-opening operation, using dehydrating agent, hormone, and haemostat, preventing infection and alimentary tract hemorrhage, application of vitamin and neurotrophy drugs. The patients in the Nimodipine treatment group, besides the conventional therapy, were treated with Nimodipine (Nimotop,Germany Bayer cooperation) 10mg as soon as they were admitted to hospital; micro pump venous pumping (>6h), once a day, 14 days as a course of treatment. Patients in both groups were under brain PbtO2 and ICP monitoring, stytatics in different stages were analysized and every patient was given a GOS mark 3 months later, and comparison on prognosis between the two groups were made to check the short-term curative effect of Nimodipine in treating Severe Traumatic Brain Injury.Results: (1)There were no obvious differences between the two groups in age, sex, injured time and GCS marks (p>0.05) when admitted to hospital. (2)There were no remarkable differences between the Nimodipine treated group and the CG in brain PtO2 when they were sent to hospital and 8 hours later since they received the treatment. (p>0.05); When treated for 24 hours, 48 hours, 72 hours, brain PtO2 of the patients in the former group were remarkably higher than that of the later group. (3)Intracranial pressure of the patients in both groups was higher than the normal value, and reached its peak point in 24 hours. Intracranial pressure of the patients in the Nimodipine treated group gradually lowered in 3 days, and became normal 5 days later; while in the CG, the pressure was higher than that in the former group and became normal in 7 days. (4)3 months later, the GOS score showed: in the Nimodipine treated group, there were 13 cases in good prognosis (including the well recovered cases and the partially disabled cases), there were 2 cases in bad prognosis (including seriously disabled cases and the cases in the vegetative state). in the CG, there were 8 cases in good prognosis, there were 7 cases in bad prognosis. There were no deaths in the two groups, but remarkable differences. (5) There were no hypotensive cases in the Nimodipine treated group; tardive intracranial hematoma, brain oxygen, inserted intracranial pressure exploring needle caused intracranial hematoma, or infected cases were not found in both groups.Conclusion: (1) treating Severe Traumatic Brain Injury with Nimodipine can improve brain tissue ischemia, raise brain PtO2, lower intracranial pressure, and thus lessen the bad- prognosis caused by Severe Traumatic Brain Injury. (2) Brain PtO2 monitoring is an ideal monitoring way on brain oxygen metabolism and it can reflect the short-term curative effect on Severe Traumatic Brain Injury.