Chronic subdural hematoma is a hematoma with an envelope located between the dura mater and the arachnoid membrane that begins to show symptoms more than 3 weeks after head injury. It occurs in children and the elderly, accounting for 10% of intracranial hematomas and 25% of subdural hematomas, with the incidence of bilateral hematomas reaching 14.8%. The disease is easily misdiagnosed because of its mild head injury, insidious onset, and lack of obvious clinical features. The time from injury to onset is generally 1-3 months, with up to 34 years reported in the literature. (1) Injury cause and pathology Chronic subdural hematoma occurs because most of them have a history of minor head trauma, especially in the elderly when the frontal or posterior occipital force is applied, the brain tissue is more mobile in the cranial cavity, and it is most likely to tear the bridging vein that converges into the superior sagittal sinus from the brain surface, followed by the venous sinus, arachnoid granule or subdural hydatid damaged bleeding. Non-invasive chronic subdural hematomas are very rare and may be associated with aneurysms, vascular malformations, or other cerebrovascular disease. There have been many hypotheses about the cause of chronic subdural hematoma enlargement in the past, such as the mechanism of high osmotic pressure in the hematoma cavity, which have now been rejected. Most current studies have demonstrated that the factors contributing to the expanding hematoma are related to the patient’s brain atrophy, decreased intracranial pressure, increased venous tone, and impaired coagulation mechanisms. Chronic subdural hematomas in pediatric patients are predominantly bilateral, often caused by birth injuries and less frequently by postpartum intracranial injuries, and generally occur most frequently in children less than 6 months of age and gradually decrease thereafter, although trauma is not the only cause, as some authors have observed that malnutrition, scurvy, intracranial and extracranial inflammation, and children with hemorrhagic qualities, even severely dehydrated infants, can also develop this disease. The source of hemorrhage is mostly due to rupture of the bridging veins on the surface of the brain that converge into the superior sagittal sinus, while in non-traumatic subdural hematomas, it may be due to systemic disease or intracranial inflammation causing changes in dural vascular permeability. The pathogenic mechanism of chronic subdural hematoma is mainly due to increased intracranial pressure caused by the occupying effect, local brain pressure, obstruction of cerebral circulation, brain atrophy and degeneration, and an epileptic incidence of up to 40%. In long-standing hematomas, the envelope may become calcified due to vascular embolism, necrosis and connective tissue degeneration, resulting in long-term compression of brain tissue, promoting epilepsy and aggravating neurological deficits. There are even reports of subcortical hematoma formation due to rupture of the endothelium from rebleeding. (2) Symptoms and signs The main manifestations are chronic intracranial pressure increase, neurological dysfunction and psychiatric symptoms. Most patients have headache, weakness, decreased intelligence, mild hemiparesis and fundus edema, and occasionally epilepsy or stroke-like seizures. In the elderly, dementia, psychiatric abnormalities and positive cone bundle signs are more common, easily confused with intracranial tumors or normal cranial pressure hydrocephalus; pediatric patients often have drowsiness, cranial enlargement, parietal bulge, hallux valgus, convulsions, spasms and retinal hemorrhage, which resemble hydrocephalus. or none; Grade II: poor orientation or blurred consciousness, with mild hemiparesis and other neurological deficits; Grade III: wood stiffness, appropriate response to painful stimuli, with severe neurological deficits such as hemiparesis; Grade IV: coma, unresponsive to painful stimuli, and de-cranialized or de-corticalized state. (3) Diagnosis and differentiation CT of the head can estimate the time of hematoma formation not only from the morphology of the hematoma, but also from the density of the hematoma to infer the stage age. Generally, it takes about 3-8 weeks to evolve from crescentic hematoma to biconvex hematoma, and the average age of hematoma is high density at 3.7 weeks, low density at 6.3 weeks, and isointense at 8.2 weeks. In addition, MRI is more advantageous and provides good image differentiation between hematoma or effusion when CT is isointense. The disease needs to be differentiated from chronic subdural effusion, hemispheric occupying lesions, normal intracranial pressure hydrocephalus, and cerebral atrophy. (4) Treatment and prognosis Surgical treatment: 1. minimally invasive hematoma removal 2. borehole or cone hole flushing and drainage 3. anterior hallux valgus subdural puncture (for pediatric patients) 4. bone flap craniotomy for chronic subdural hematoma removal Minimally invasive hematoma removal is preferred, with less trauma, lower cost, better results, and relatively low recurrence rate. The surgical efficacy is satisfactory and the prognosis is mostly good, but the recurrence rate of the disease is high, 3.7% – 38%. (5) Postoperative hematoma recurrence Common causes of recurrence include: brain atrophy in elderly patients, difficulty in postoperative brain expansion; thick hematoma envelope, subdural cavity cannot be closed; hematoma cavity with blood clots not completely removed; fresh bleeding and hematoma recurrence. Therefore, care should be taken to prevent the recurrence of hematoma. After surgery, it is advisable to adopt a low head position, lie on the affected side, drink more water, do not use strong dehydrating agents, and supplement hypotonic fluids appropriately if necessary; craniotomy should be performed to remove the thick envelope or calcification; if there is a solid blood clot in the hematoma cavity or fresh bleeding, a bone flap or window should be used to open the cranium and remove it completely. Postoperative drainage tube high exhaust, low drainage, are external closed drainage bag (bottle), while through the lumbar puncture or ventricular injection of saline; postoperative residual cavity fluid, gas absorption and brain tissue expansion takes 10-20 days, so should be dynamic CT observation, if the clinical symptoms are significantly improved, even if there is still subdural fluid, there is no need to rush to operate again.