Traumatic subdural fluid is defined as the accumulation of cerebrospinal fluid in the subdural space due to arachnoid tear during head trauma. According to the literature, traumatic subdural fluid accounts for 3.7% to 10.0% of craniocerebral injuries. Regarding the pathogenesis of traumatic subdural fluid, there are theories such as arachnoid rupture, arachnoid valve formation, blood-brain barrier disruption and brain atrophy. Traumatic subdural effusion typology 1. receding type: gradual reduction of effusion and improvement of clinical symptoms by CT dynamic observation. 2.Stable type: no increase or decrease of fluid within 4 weeks of CT dynamic observation, and no significant change of corresponding clinical symptoms. 3.Progressive type: CT dynamic observation of the fluid gradually increased, and the brain pressure or the corresponding clinical symptoms gradually increased. 4.Evolutionary type: CT dynamic observation of effusion evolved into chronic subdural hematoma, and chronic intracranial pressure increase symptoms appeared. Pathologic features: 1. Fading cases can be explained by the theory of arachnoid rupture, i.e., the arachnoid membrane, which is closely adherent to the lateral fissure, optic cross-sectional area and pterygoid crest, is torn during head trauma, resulting in cerebrospinal fluid outflow and accumulation in the subdural cavity, which is gradually absorbed and reduced later. 2, stable cases can be explained by the doctrine of cerebral atrophy, under normal circumstances, the subdural cavity is a potential cavity, after the occurrence of cerebral atrophy, the subdural cavity increases, the rupture of the arachnoid membrane during cranial injury causes the accumulation of cerebrospinal fluid in the subdural cavity, due to the presence of cerebral atrophy, the patient’s symptoms of increased intracranial pressure are not obvious. If observed for a long time this type can turn into a receding or evolving type. 3. Progressive cases can be explained by the theory of arachnoid valve formation or the theory of blood-brain barrier disruption. Craniocerebral injury causes damage to the arachnoid membrane on the surface of the brain, forming a one-way valve, causing cerebrospinal fluid to flow into the subdural cavity through the one-way valve of the arachnoid injury, and the fluid gradually increases; or the blood-brain barrier is damaged after craniocerebral injury, capillary permeability increases, and plasma components leak out and accumulate in the subdural cavity, because the protein content of the fluid is high, the osmotic pressure also increases, causing water from the surrounding brain tissue and subarachnoid cavity to leak into the fluid, and the fluid gradually increases. The effusion gradually increases. 4, Evolutionary cases, due to long-term subdural fluid formation and the gradual increase of the fluid, resulting in bridging vein rupture or bleeding in the wall of the pericardium, and hyperfibrinolysis in the fluid, coagulation dysfunction, so that the bleeding does not stop and a chronic hematoma is formed or the subdural fluid changes in character, its protein content is high or mixed with blood components, easily leading to the evolution of traumatic subdural fluid into a chronic subdural hematoma. This may also explain why the evolution of traumatic subdural effusion into chronic subdural hematoma often occurs after 1 month of effusion, i.e., after the formation of the pericardium. The subdural type is more common in young adults and usually has no obvious symptoms of increased intracranial pressure or only mild symptoms of increased intracranial pressure in the early stage, and then gradually improves without positive neurological signs. The stable type is predominant in the elderly, with headache, dizziness, nausea, vomiting, mental abnormalities (euphoria, apathy, depression, etc.), and memory loss as the main manifestations, usually without positive neurological signs associated with subdural effusion. The main manifestation is progressive intracranial pressure increase. Patients may have mild hemiparesis, aphasia or mental abnormalities, and infants may have hydrocephalus-like manifestations; if combined with brain parenchymal injury, it may be accompanied by impaired consciousness and pathological signs. The clinical characteristics of the evolutionary type are: (1) The age of onset is polarized, often occurring in children under 1O years of age or in elderly people over 60 years of age, which may be related to the larger subdural cavity in children and elderly people. (2) It often occurs within 22-100 d after effusion and in cases with small amount of effusion and conservative treatment. This is because during conservative treatment of small amount of effusion, the effusion can be transformed into hydatid tumor and chronic hematoma due to pericardial hemorrhage after pericardial formation; while early surgery interrupts the process of transformation of effusion into hydatid tumor and pericardial formation, so traumatic subdural effusion evolves into chronic (3) Combined craniocerebral injury (3) The combined cranial injury is often very mild, so there is no impairment of consciousness. (4) There are signs and symptoms of chronic intracranial pressure increase. Classification and treatment The regressive type generally does not require surgery, but observation and symptomatic treatment are sufficient. Stable type is preferred to conservative treatment, if the brain pressure or the corresponding clinical symptoms are obvious, surgical external drainage treatment should be performed. If the effusion is reduced or disappears and the clinical symptoms improve after external drainage, external drainage alone can solve the problem. If, after external drainage, the fluid does not decrease or increases again after removal of the drainage tube or the clinical symptoms worsen, then internal shunt is required. In principle, surgical external drainage should be performed for subdural effusion that evolves into chronic subdural hematoma. The prognosis is best for the regressive type, which generally does not leave any neurological abnormalities. The prognosis for the stable type is also generally good, with the majority of neurological functions recovering well. The evolutionary type is almost always cured by early surgical cranial drainage treatment, and there is usually no death and good neurological recovery. The progressive type may have some mortality due to combined brain parenchymal injury or postoperative complications. In the literature, the mortality rate of traumatic subdural effusion combined with parenchymal injury can reach 12%-25%. The cause of death is often a combination of cerebral contusion and postoperative infection and systemic failure.