脑挫裂伤（Contusion and laceration of brain）

脑挫裂伤（Contusion and laceration of brain） 脑挫裂伤(Contusion and laceration of brain) Contusion and laceration of brain Right temporal lobe cerebral contusion cerebral contusion of brain contusion and laceration of brain collectively, because pathological from brain injury, contusion and laceration is also often coexist, the only difference is that what is important or which is the light of the problem. Usually the surface of the brain contusion and laceration in site and hedge violence against the site, especially the latter, are more serious and often in the frontal and temporal front end and the bottom, which is caused by sliding and collision of brain tissue in the cranial cavity. Contusion and laceration of brain parenchyma is often caused by the deformation and shear stress of brain tissue. It is often seen between the structures of different media, and mainly contusion and spot bleeding. Diagnosis Patients with cerebral contusion and laceration often have disturbance of consciousness, which often bring difficulty to the nervous system examination. For patients with positive signs of the nervous system, the location and extent of the injury can be determined according to the location sign and the coma. It is difficult to identify patients with severe disturbance of consciousness and poor response to external stimuli, even if there are neurological deficits. In particular, there are many patients with brain contusion or deep brain injury, and the location diagnosis is difficult. It is often necessary to rely on the CT scan and other necessary auxiliary examinations to make a definite diagnosis. Edit the paragraph Contusion and laceration of brain The treatment of contusion and laceration when treated mainly by non surgery should minimize the occurrence of brain injury after a series of pathophysiological reactions, close observation of intracranial hematoma, there is no secondary maintenance of internal and external environment of the body's physiological balance and prevention of complication. Surgical treatment is usually not necessary unless there is secondary haematoma in the brain or intracranial hypertension that is difficult to contain. Nonoperative treatment When the brain contusion occurs, that is, secondary brain damage begins, the two are closely linked and cause and effect, so early and reasonable treatment is the key to reduce disability rate and reduce mortality. The purpose of non surgical treatment is to prevent a series of pathophysiological changes after brain injury and to increase brain damage, and then to provide a good internal environment to restore the function of some damaged brain cells. Therefore, the correct treatment should not only focus on the whole body, and intracranial general treatment: for light and small and medium-sized parts in response to the trauma brain contusion patients, mainly symptomatic treatment, prevention and treatment of cerebral edema, close observation, timely monitoring of intracranial pressure and / or re examination of CT scanning. In addition to non surgical treatment, intensive care should be taken for the patients with moderate or severe conditions in coma. When conditions are sent to ICU (intensive care unit), using a multichannel physiological monitor, continuous monitoring and nursing. The patient should be on the side, keep the airway unobstructed and give oxygen intermittently. If the patient is expected in the short term (3 ~ 5 days) can not awake, should be early tracheotomy, so that timely removal of secretions, reduce airway resistance and die cavity. At the same time, the head of the bed should be raised from 15 to 30 degrees, which is beneficial to the intracranial venous return and lower intracranial pressure. Daily intake and output should be balanced, in the absence of excessive sodium depletion, saline liquid 500ml/d physiological saline that has met the demand, too much can promote brain edema. Sugary liquid supply, should prevent excessive blood sugar, so as not to aggravate cerebral ischemia, hypoxia damage and acidosis. When necessary, the insulin should be corrected appropriately, and the dosage should be adjusted in time according to the blood glucose measurement. If the patient still can not eat after 3~4 days, can be placed nasal feeding tube, given liquid diet, maintain daily thermal energy, intracranial hematoma And nutrition. In addition, the biochemical and acid-base samples of blood should be examined regularly for the critically ill patients, so as to guide the treatment measures. At the same time, attention should be paid to the prevention and treatment of heart, lung, liver, kidney function and complications. Special treatment: the patients with severe contusion and laceration of the brain often suffer from the aggravation of the struggle, agitation, limbs rigidity, high fever and convulsions, and the reasons should be found out to give timely and effective treatment. The injury occurs early in central high fever, frequent decerebrate rigidity, diencephalic seizures or epilepsy seizures, suitable for hibernation cooling and / or pentobarbital treatment. Traumatic acute brain swelling, also called diffuse brain swelling (DBS), is an early enlargement of the brain in severe brain injury. It may be associated with cerebral palsy, dilatation, or acute edema after ischemia. As soon as possible, hyperventilation, barbiturates, hormones and strong dehydration should be used as early as possible, while hibernation, cooling and decompression can also reduce the role of vascular brain edema. Surgery is useless, but harmful. Disseminated intravascular coagulation (DIC) is secondary to coagulopathy after brain injury. The reason is that brain tissue is rich in thromboplastin, which is released into the bloodstream after trauma and activates the coagulation system. Because of the abnormal accumulation of platelets, thrombosis can occur in small vessels in the cerebral cortex, basal ganglia, white matter, brain stem, etc., and secondary hemorrhage is caused by the dissolution of fibrin. Delayed intracranial hematomas may also be relevant (Touho, 1986). Intravascular coagulation can only be diagnosed by laboratory examinations, i.e. thrombocytopenia, reduction of fibrin, and prolongation of thrombin time. Once occurred, We should actively treat brain injury while losing fresh blood, supplement coagulation factors and platelets. The authors also used heparin anticoagulant therapy or multiple brain contusion KanXian deep against excessive fibrinolysis tranexamic acid. Reduce intracranial hypertension: almost all patients with brain contusion and laceration have increased intracranial pressure in different degrees. The light can be given in bed, oxygen therapy, hormone and dehydration and other conventional treatment. Severe cases should be treated with hyperventilation, large doses of corticosteroids as early as possible, and dehydration therapy under the monitoring of intracranial pressure. Serious injuries are should be considered hibernation cooling and pentobarbital therapy in addition, serious brain trauma, blood rheology also showed obvious changes, whole blood viscosity and plasma viscosity and hematocrit, erythrocyte aggregation and fibrinogen were increased; and the erythrocyte deformability decreased, and the degree of injury was positively correlated. Because the accumulation of red blood cells increased, the deformation force decreased and even overlap each other and form a three-dimensional network combination, make the blood flow shear stress increases, the viscosity increases caused by microcirculatory stasis, micro thrombosis, however aggravate brain secondary damage. Therefore, we should pay attention to the change of Hemorheology and correct it in the treatment of severe contusion and laceration of brain. At present, the Department of Neurosurgery commonly used on blood rheology of mannitol dehydrating agent has biphasic effect, namely the input is early increased blood volume, blood dilution; while the latter is decreased blood volume, blood viscosity increased. If, after repeated repeated use of mannitol, it is bound to cause significant increase in blood viscosity, resulting in the so-called "rebound phenomenon", and even can aggravate the vascular brain edema. For this reason, the authors used red cell hematocrit as the index for the treatment of patients with brain injury, and the optimal hematocrit was 0.3 to 0.4". Using low molecular dextran (Dextranum-40) intravenous infusion of 0.5g/kg/d implementation capacity or high capacity blood dilution, maintain blood viscosity in the optimal hematocrit value level, to reduce brain edema and secondary brain injury. Fourth, the rehabilitation of brain function: the purpose is to reduce the disability rate, improve the quality of life, so that patients with traumatic brain injury in life, work and social ability as much as possible to achieve independence, self-reliance. Although brain function recovery is the treatment of paralysis, aphasia, epilepsy, mental and mental complications or sequelae in the later stage of traumatic brain injury, the importance of early preventive therapy must be emphasized. In the treatment of acute craniocerebral trauma, we should pay attention to protect brain function and minimize waste loss. When the dangerous period is over and the condition is more stable, the drugs for the recovery of the nerve function should be given. Also begin functional exercises, including physical therapy, massage, acupuncture, and passive or active exercise. Contusion and laceration of temporal lobe surgical treatment Primary brain contusion usually does not require surgical treatment, but when secondary damage causes intracranial hypertension or even herniation, it is necessary to perform the operation. On the above, the 30ml CT associated with intracranial hematoma showed space occupying effect, non surgical treatment or poor intracranial pressure monitoring pressure exceeds 4.0kPa (30mmHg) or poor compliance, should be promptly performed craniotomy to remove the hematoma. Contusion and laceration of brain tissue due to severe, broken down and brain edema of increased intracranial pressure, reduce the intracranial pressure treatment is invalid, 5.33kPa to intracranial pressure (40mmHg), should be craniotomy for removal of erosion, for internal and external decompression, placed basilar cistern or ventricle drainage; cerebral contusion late hydrocephalus. One should first ventricle drainage reasons after treated water. Edit the pathological changes in this section The pathological changes of brain contusion, with cerebral contusion and laceration were visible light frontotemporal brain surface blood stasis, edema, subpial a bit patchy hemorrhage, subarachnoid or piamater often rip, bloody cerebrospinal fluid. Severe cerebral cortex and white matter under broken down, local hemorrhage, edema, rupture, and even the formation of hematoma, brain cortex damaged vascular embolization, erosion, necrosis, laceration zone around a little flaky hemorrhage andmalacia, wedge-shaped into brain white matter. 4~5 days later, the necrotic tissue began to liquefy, the blood resolved, and the surrounding tissues were stained with rust like iron, which contained black coagulation fragments. Even after 1 ~ 3 weeks, local necrosis and liquefaction area gradually absorbed with cystic hyperplasia of glial cells to repair peripheral, near brain atrophy, arachnoid thickening and adhesion of dura and brain tissue, finally formed meningocerebral scar block. Traumatic progressive intracranial hemorrhage Early brain contusion was observed under the microscope neurons cytoplasm vacuolization, disappearance of Nissl bodies, nuclear pyknosis, fragmentation and dissolution, axonal swelling, rupture, disappearance of cortical gray matter structure, boundary is not clear, glial cell swelling, capillary hyperemia, edema of the extracellular space. After several days to several weeks, the contusion tissue gradually liquefied and entered the repair stage, and the lesion area appeared lattice cells to engulf the dissociated debris and myelin sheath, And there are glial cells proliferation, hypertrophy and fiber ingrowth, local nerve cells disappear, and eventually replaced by glial scar. Edit the clinical presentation of this paragraph The clinical manifestations of cerebral contusion and laceration due to injury factors and injury vary, the disparity is very big, the light can be no primary disturbance of consciousness, such as pure depression fracture, closed skull crush injury that is likely to belong to this situation. And the person that weigh can cause deep coma, serious waste is damaged, contusion of the brain Even death. Consciousness disorder It is one of the most prominent clinical manifestations of brain contusion. After the injury, the patients usually become unconscious immediately. Because of the different injuries, the duration of coma varies from minutes to hours, days, months, and even to a mild coma. Most of the long-term coma patients suffered from extensive cortical damage or brain stem injury. In general, it is more than 30 minutes after the coma, which is the reference time for judging the contusion and laceration of the brain. Symptoms of burn According to the site of injury and the extent is different, if only hurt the frontal and temporal lobes in front of the so-called "dumb", but no neurological defect; if the damage to the cerebral cortex, can appear corresponding paralysis, aphasia, visual field defect, sensory disturbance and focal epilepsy. In the early stage of contusion and laceration of brain, there is no positive sign of nervous system. If there is a new localization sign in the course of observation, we should take into account the possibility of secondary damage to the brain, and check it in time. Headache and vomiting Headache symptoms only in patients after sober to statements; if after the injury sustained severe headache, frequent vomiting; or improved once again after aggravating, should be the reason, when necessary auxiliary examinations, in order to clear the encephalic hematoma. In patients with coma, attention should be paid to brain contusion and laceration when vomiting [1] can inhale the risk of asphyxiation. Vital signs There are many obvious changes, early have decreased blood pressure, weak pulse and rapid shallow breathing, this is because the brain function inhibition caused by head injury, often soon after injury and gradually recovered, if sustained hypotension, should pay attention to whether the composite combined injury. On the contrary, if the short term immediately to restore the vital signs and blood pressure increase, pulse pressure increase, pulse loud strong, pulse rate slow, slow breathing also deepened, it should be wary of intracranial hematoma and / or cerebral edema and swelling. In patients with cerebral contusion, the body temperature can also be slightly elevated, generally about 38 degrees, if high fever is accompanied by lower hypothalamus injury. Meningeal irritation After cerebral contusion due to subarachnoid hemorrhage, patients often have meningeal signs of irritation, as closed eyes photophobia, curl and lie, early fever and nausea and vomiting are also associated with this. The resistance of neck will disappear gradually in about 1 weeks, and if there is no permanent improvement, attention should be paid to the injury of cranial cervical junction or secondary infection of the skull. Edit this paragraph to identify the diagnosis X-ray plain film In the condition of injury, the X-ray examination of skull is still of great value. It not only can understand the specific situation of fracture, but also has special meaning for analyzing the mechanism of injury and judging the injury. CT scan We can make a clear differential diagnosis of brain contusion and concussion, and clearly show the location, extent and secondary damage of brain contusion, such as hemorrhage and edema. At the same time, the intracranial pressure can be estimated indirectly according to the size, shape and displacement of the ventricles and the cerebral cisterns. Importantly, for some atypical cases, periodic CT scans can be performed to dynamically observe the evolution of brain edema or the occurrence of delayed haematoma. In recent years, CT has been used as a routine examination for acute head injuries in hospitals with this device, because it is difficult to make ultra early diagnosis by means of injury history or physical examination. Stein et al. (1990) pointed out that the positive rate of first CT was 18% in light head injuries which were less dangerous in GCS13 ~ 15, and 5% needed surgical treatment, emphasizing the necessity of early CT examination. MRI (magnetic resonance imaging) Generally less used for the diagnosis of acute craniocerebral injury. MRI imaging time is longer, some metal emergency equipment can not enter the computer room, restless patients difficult to cooperate, so more CT as the preferred inspection items. But in some special cases, MRI is superior to CT, such as contusion of brain stem, corpus callosum and brain The display of cranial nerve; display contusion, axonal injury and early cerebral infarction and cerebral small; in the display and differential diagnosis CT stage of hematoma density, MRI has its unique advantages, is less than CT. Lumbar puncture It is helpful to understand the blood flow in cerebrospinal fluid, which can be used for identification of cerebral concussion, and can measure intracranial pressure and drainage of hemorrhagic cerebrospinal fluid. But the obvious intracranial hypertension patients should be taboo in CSF, so as not to promote the development of cerebral hernia. Other auxiliary examinations Such as cerebral angiography, now less, but in no CT hospital or area, we have to rely on the diagnosis of cerebral angiography auxiliary; EEG, mainly used for judging the prognosis of epilepsy or monitoring; brainstem auditory evoked potential, It has important reference value for analyzing the degree of brain function damage, especially for the determination of brain stem injury plane. In addition, radionuclide examination is of great value for the late complications of cerebral contusion, such as vascular embolization, arteriovenous fistula, cerebrospinal fluid leakage and hydrocephalus.