Intraoperative brain bulge occurs in severe craniocerebral injury, large pieces of brain tissue herniated out of the bone window, resulting in contusions of brain tissue at the edge of the bone window and impaired blood return, which in turn aggravates the brain bulge, forming a vicious circle, so the authors believe that it must be handled quickly and carefully. (1) Preoperative treatment: the presence of factors that may cause intraoperative brain expansion in heavy craniocerebral injury, preoperative should be given timely and effective treatment. If preoperative hypotension exists, blood volume should be actively replenished and shock should be corrected. For those with respiratory distress, misaspiration and hypoxemia, tracheal intubation should be performed promptly to keep the airway open, supplemented with artificial ventilation if necessary. Those with fractures of the extremities should be given appropriate fixation. A detailed medical history and careful reading of CT films should also be taken before surgery to be aware of the possible occurrence of delayed hematoma. Particular attention should be paid to the presence of skull fractures on the contralateral side of the hematoma. For those with obvious midline displacement or brain herniation formation, preoperative rapid intravenous infusion of 20% mannitol 250ml and tachyzoites 40mg, and rapid preoperative preparation should be given to strive for early surgery. (2) Intraoperative management: ① Ask the anesthesiologist to control the depth of anesthesia, maintain the patient’s normal blood pressure and oxygen saturation, and try to avoid using anesthetic drugs that may increase intracranial pressure. Adequate cerebral perfusion pressure should be maintained, but excessive blood pressure should be avoided. Eliminate factors that can increase cerebral blood flow, correct neck distortions, relax neck braces and ensure that resistance in the airway is not high to ensure patency of venous return. Hypercapnia must be avoided and ventilation should be accelerated to maintain PCO2 at 28-30 mmHg. ② Surgery is performed with standard large bone flap treatment. During surgery, as much of the pterygoid crest and temporal bone as possible are removed, and the base of the middle cranial fossa and part of the base of the anterior cranial fossa are exposed. This not only achieves adequate relief of intracranial pressure, but also facilitates adequate decompression of the lateral fissure vessels, resulting in a certain degree of relief of cerebral vein compression, which is conducive to reducing the occurrence and improvement of cerebral bulge. It has been reported that the incidence of intraoperative cerebral bulge was significantly reduced by using standard large bone flap decompression. In our group, all 21 cases of subdural hematoma were treated with standard large bone flap surgery and achieved better results. The dura mater was suspended before the bone flap was lifted and the dura mater was cut. The operator could sense the tension of the subdural brain tissue with the left hand. If the subdural tension is too high, it is not advisable to cut the dura immediately and quickly. A rapid intravenous drip of 250 ml of 20% mannitol, supplemented by hyperventilation and controlled blood pressure lowering, may be used. However, the time should not be too long as it may aggravate cerebral ischemia. Cut the dura mater after the relative reduction of cerebral pressure. After turning the dura mater, quickly and gently remove the hematoma and necrotic brain tissue and stop the bleeding completely. During this time, care should be taken to protect normal brain tissue and important reflux veins. After there is no active bleeding, the dura and artificial meninges are sutured to fully expand the subdural space. Epidural drainage is placed, the bone flap is removed, and the scalp is sutured. ④When brain bulge occurs, do not panic, but pay attention to actively search for the cause. If the brain bulge occurs gradually after removal of the hematoma, the possibility of delayed hematoma should be considered. The possibility of late hematoma should be considered. It can be explored first for any hemorrhagic lesions around the operative field. In this group, there were 2 cases of cerebral bulging after removal of intracerebral hematoma, which was found to be a subdural hematoma formation next to the cerebral falx after investigation. After the removal of this hematoma, the cerebral bulge was rapidly relieved. The postoperative recovery was good. If other causes of cerebral bulge are ruled out and no hematoma is found, the cranial CT should be reviewed and the hematoma should be found elsewhere before returning to the operating room for hematoma removal. It is important to avoid forcible cranial closure by blindly removing large pieces of brain tissue for internal decompression when the cause is not known. Internal decompression should be used as an option of last resort. (3) Postoperative treatment: The condition of intraoperative brain expansion in severe craniocerebral injury is critical, and the disability and mortality rates are extremely high, so postoperative treatment is also very important. (1) Routine supervised treatment in the ICU. It is necessary to monitor intracranial pressure and central venous pressure, and guide dehydration and rehydration. Pay attention to blood glucose level control, correct acid-base and water-electrolyte imbalance to maintain the stability of the internal environment, and pay attention to nutritional support so that it can smoothly pass the acute phase and improve the prognosis. ②Keep the airway unobstructed. If the patient is considered difficult to wake up in a short time, tracheotomy should be performed as early as possible. Early tracheotomy is conducive to improving pulmonary ventilation, correcting hypoxia, controlling pulmonary infection, and preventing further aggravation of cerebral edema. ③Subhypothermia treatment. The use of subhypothermia treatment can inhibit the oxygen-demanding metabolism of brain tissues, reduce oxygen consumption (a 1°C decrease in temperature can reduce oxygen consumption by about 7%), and improve the tolerance of brain tissues to hypoxia, thus achieving the role of protecting brain tissues. Meanwhile, subcooling plays a role in protecting brain tissue by reducing the toxic effects of excitatory amino acids, reducing the generation of free radicals, inhibiting intracellular calcium ion overload, and reducing the permeability of the blood-brain barrier and other mechanisms. Attention should be paid to the administration of inotropic or sedative agents during hypothermia to prevent the emergence of chilling reactions that can cause an increase in intracranial pressure. ④ Prevention and control of complications. Pay attention to the prevention and treatment of upper gastrointestinal bleeding due to stress ulcer, pulmonary infection, and renal insufficiency to reduce the morbidity and mortality rate. If hydrocephalus formation is found, early ventriculo-abdominal shunt can be performed to help promote patient’s awakening. ⑤ Brain cell activator and hyperbaric oxygen therapy. Early application of brain cell activators, such as naloxone hydrochloride, gangliosides, cytidyl phosphorylcholine, nimrodipine, ATP, vitamin C, vitamin E, peptide brain extracts such as brain activator, nerve growth factor, etc., may help improve the prognosis of patients, reduce the morbidity and mortality rate, and decrease the disability rate. Hyperbaric oxygen improves the hypoxic state of brain tissue and promotes the recovery of brain function by rapidly increasing the blood oxygen content, oxygen partial pressure and blood oxygen diffusion in the body within a short period of time. After the patient’s condition is stabilized, hyperbaric oxygen therapy should be performed as soon as possible if possible.