The treatment of cerebral contusion should be based on non-surgical treatment, which should minimize a series of pathophysiological reactions after brain injury, closely observe whether there are secondary hematomas in the skull, maintain the physiological balance of the internal and external environments of the body, and prevent the occurrence of various comorbidities. Unless there is secondary hematoma in the cranium or there is difficult to contain intracranial hypertension surgery, generally do not need surgical treatment. I. Non-surgical treatment: When cerebral contusion injury occurs, that is when secondary brain damage begins, the two are closely related and mutually causative, so early and reasonable treatment is the key to reduce the disability rate and mortality rate. The purpose of non-surgical treatment is, firstly, to prevent a series of pathophysiological changes after brain injury from aggravating brain damage, and secondly, to provide a favorable internal environment to enable partially damaged brain cells to recover their functions. Therefore, the correct treatment should focus on intracranial and take into account the whole body. 1.General treatment: for light and partially traumatized patients with medium-sized cerebral contusion, the main treatment is symptomatic, prevention and treatment of cerebral edema, close observation of the condition, timely monitoring of intracranial pressure and/or review of CT scan. For medium and heavy patients in coma, in addition to non-surgical treatment, nursing care should be strengthened. When possible, they can be sent to ICU (intensive care unit), using multi-channel physiological monitors for continuous monitoring and specialized care. The patient should lie on the side, keep the airway open, and give oxygen intermittently. If it is expected that the patient can not be awake in a short period of time (3-5 days), it is advisable to perform tracheotomy early in order to remove secretions in a timely manner and reduce airway resistance and dead space. At the same time, the head of the bed should be elevated 15°～30° to facilitate intracranial venous return and reduce cranial pressure. Daily intake and output should be balanced, in the absence of excessive sodium loss, saline fluid 500 ml/d saline is enough to meet the needs, too much can promote cerebral edema. Sugar-containing fluid supplementation, should prevent high blood sugar to avoid aggravating cerebral ischemia, hypoxia damage and acidosis. If necessary, appropriate amount of insulin should be given to correct, and adjust the dose of medication according to the blood glucose measurement. If the patient is still unable to eat after 3~4 days, a nasal feeding tube can be placed and a liquid diet can be given to maintain daily calories and nutrition. In addition, patients with serious illnesses should be sent for regular blood biochemistry and acid-base specimens to guide the treatment measures, and at the same time, attention should be paid to the prevention and treatment of cardiac, pulmonary, hepatic and renal functions and comorbidities. 2.Special treatment: patients with severe cerebral contusion injury are often aggravated by struggling and restlessness, limb tonus, high fever and convulsions, so the cause should be identified and timely and effective treatment should be given. For early post-injury patients with centralized hyperthermia, frequent cerebral tonicity, mesencephalic seizures or epileptic seizures, hibernation hypothermia and/or barbiturate treatment is recommended. Traumatic acute brain swelling, also known as disseminated brain swelling (DBS), is an early widespread brain enlargement in heavy brain injury, which may be related to cerebral vascular paralysis and dilatation or acute edema after ischemia, and occurs in adolescents. Hyperventilation, barbiturates, hormones and strong dehydration should be used as early as possible once it occurs, while hibernation and hypothermia and hypotension also have a role in reducing vasogenic cerebral edema. Surgery is not helpful but harmful. Diffuse intravascular coagulation (DIC), a coagulation abnormality secondary to brain injury. It is caused by the enrichment of brain tissue with coagulation kinase, which is released into the bloodstream after trauma and activates the coagulation system. Due to the abnormal accumulation of platelets, thrombosis can occur in small blood vessels in the cerebral cortex, basal ganglia, white matter, and brainstem, followed by secondary hemorrhage due to fibrinogenolysis. Delayed intracranial hematomas may also be involved (Touho, 1986). The diagnosis of intravascular coagulation is based on laboratory tests, i.e. thrombocytopenia, decreased fibrinogen and prolonged prothrombin time. Once it occurs, it should be treated aggressively for craniocerebral injuries with transfusion of fresh blood and supplementation of coagulation factors and platelets. Some authors also use heparin anticoagulation or anti-fibrin deep cyclic acid to fight against excessive fibrinolysis. 3, reduce intracranial hypertension: almost all patients with cerebral contusion injury have different degrees of increased intracranial pressure. In mild cases, bed rest, oxygen, hormone and dehydration and other routine treatment can be given as appropriate. In severe cases, hyperventilation, high-dose hormones, and dehydration under intracranial pressure monitoring should be administered as soon as possible. Hibernation cooling and barbiturate therapy should be considered in severe fashion. In addition, there are obvious changes in blood rheology after severe traumatic brain injury, manifested as an increase in whole blood viscosity, plasma viscosity, erythrocyte pressure, erythrocyte aggregation, and fibrinogen; and a decrease in the deformability of erythrocytes, the extent of which is positively correlated with the degree of injury. Due to the increase of red blood cell aggregation and decrease of deformability, the red blood cells are superimposed on each other to form a three-dimensional mesh, which increases the tangential stress of blood flow and elevates the viscosity, causing stagnation of microcirculation and the formation of microthrombus, which aggravates the secondary damage of the brain. Therefore, in the treatment of severe cerebral contusion, blood rheologic changes should be noted and corrected. Currently, mannitol, a commonly used dehydrating agent in neurosurgery, has a biphasic effect on blood rheology, i.e., in the early stage of input, the blood volume is increased and the blood is diluted; while in the late stage, the blood volume is decreased and the blood viscosity is relatively elevated. If this is the case, after repeated use of mannitol, it is bound to cause a significant increase in blood viscosity to produce the so-called “rebound phenomenon”, or even, can aggravate vasogenic cerebral edema. For this reason, some authors have taken the erythrocyte pressure as an indicator when performing dehydration treatment for patients with brain injury, and the erythrocyte pressure of 0.3～0.4 is the “optimal erythrocyte pressure”. Using low molecular dextranum (Dextranum-40) 0,5g/kg/d intravenous drip to implement isovolumic or high volume hemodilution therapy, to maintain the viscosity of the blood at the level of the “optimal erythrocyte pressure product” value, in order to reduce cerebral edema and secondary damage to the brain. 4. Cerebral function recovery therapy: The purpose is to reduce the disability rate, improve the quality of life, and make the patients with craniocerebral trauma achieve autonomy and self-reliance in life, work and socialization as much as possible. Although the recovery of brain function is the treatment of paralysis, aphasia, epilepsy and mental intelligence and other complications or sequelae in the late stage of craniocerebral trauma, the importance of early preventive treatment must be emphasized. Attention should be paid to the protection of brain function and minimization of damage during the acute phase of craniocerebral trauma. When the dangerous period is over and the condition is more stable, drugs for neurological function recovery should be given. At the same time, functional exercise should be started, including physical therapy, massage, acupuncture and passive or active exercise training. Surgery: primary cerebral contusion generally does not need surgery, but when there is secondary damage causing intracranial hypertension or even brain hernia, surgery is necessary. When there is an intracranial hematoma of more than 30ml, CT shows that there is a space-occupying effect, and the effect of non-surgical treatment is not good, or the intracranial pressure monitoring pressure is more than 4,0kPa (30mmHg) or poor compliance, craniotomy should be performed in time to remove the hematoma. For severe cerebral contusion injury, due to fragmentation of tissue and cerebral edema, resulting in progressive intracranial pressure increase, reduce the cranial pressure treatment is ineffective, intracranial pressure reaches 5, 33kPa (40mmHg), should be craniotomy to remove vesiculobullous tissue, internal and external decompression surgery, placed in the cerebral basal pool or cerebral ventricular drainage; cerebral contusion injuries in the later stages of hydrocephalus, should be preceded by cerebral ventricular drainage to find out the cause of the water and then give the corresponding treatment.