Severe craniocerebral injury is an important cause of death in modern society, causing severe physical and psychological impairment and having a serious impact on individuals, families, and society. When a craniocerebral injury causes a patient to fall into a coma, it is often accompanied by increased intracranial pressure, hypoxia and hypotension, and these conditions can exacerbate and accelerate neurological damage and may lead to death. The changes that occur in the nerves at the time of impact to the head are primary injuries, and the physiological and metabolic changes that occur within minutes to days afterwards are secondary injuries. Secondary injuries are often the main cause of death in the hospital for patients with traumatic brain injury. Within hours of brain injury, fluid released from the blood vessels begins to accumulate in the brain parenchyma, causing cerebral edema, which in turn causes an increase in intracranial pressure, resulting in cerebral ischemia. Many current drugs, including free radical scavengers, antagonists of excitatory neurotransmitters, and calcium antagonists, are aimed at inhibiting secondary damage. In addition, systemic secondary damage, such as hypotension and hypoxia, tends to occur before arrival at the hospital, with hypotension having the greatest impact on poor prognosis. To reduce secondary damage to the brain, it is important to prevent the occurrence of hypotension. Systolic blood pressure below 90 mmHg may worsen the prognosis, and the cause and treatment should be identified as soon as possible. The “U.S. Prehospital Guidelines for the Management of Severe Brain Injury, 2000 Edition” recommends that special attention should be paid to the airway, ventilation, and circulatory system in the management of patients. Patients with traumatic brain injury who have a pneumothorax or hemothorax should be especially careful about hypoxia. Patients with impaired consciousness may lose their protective airway reflexes, so it is especially important to establish a patent airway; patients with a GCS coma index score less than or equal to 8 should be endotracheally intubated, which has been documented to reduce mortality; as these patients are prone to errors, aggressive sputum-clearing maneuvers and appropriate antibiotic therapy should be given. All secondary damages directly or indirectly cause cerebral ischemia, therefore, rapid monitoring after trauma to prevent the occurrence of cerebral hypoxia-ischemia is the most urgent task. The leading cause of death in patients with head trauma after hospital admission is, above all, uncontrollable intracranial hypertension. CT of the head can quickly reveal the etiology and tell us the possible circumstances of elevated intracranial pressure: midline deviation, compression or occlusion of the midbrain pool and subarachnoid hemorrhage, etc., providing guidelines for treatment. Intracranial pressure monitor placement indications: coma index less than or equal to 8, lesions that may cause cerebral edema. According to the American College of Surgeons guidelines for the treatment of severe head trauma, intracranial pressure monitoring should be placed if the patient has a coma index score of 3-8 and an abnormal CT. Whereas CT is normal, intracranial pressure monitoring should also be placed if the patient is older than forty years, has unilateral or bilateral abnormal motor posture, or has a systolic blood pressure less than 90 mm Hg. Intracranial pressure monitoring is generally not recommended for patients with head trauma with a coma index score between 9-13, but should also be considered if CT shows the presence of an intracranial clot that may require surgery. Management of elevated intracranial pressure, regulation of cerebral perfusion pressure, avoidance of ischemia, prevention of seizures, and improvement of nutrition. The most important of these is how to avoid ischemia. Body fluids should be maintained in at least a normal volume state, with a central venous pressure of 6 to 15 cmH2O and a cerebral perfusion pressure greater than 70 mmHg. Maintenance of body fluids should be maintained with isotonic crystalloid or colloidal solutions. Avoid the use of hypotonic solutions to avoid low intravascular osmolarity that could allow water to leak into the interstitial tissue of the brain and cause cerebral edema. If the partial pressure of oxygen in the blood is lowered or the partial pressure of carbon dioxide is greater than 45 mmHg, the cerebral blood vessels will dilate and the cerebral pressure will rise. The head of the bed should be elevated 30 degrees to promote venous return and reduce intracranial pressure. The patient’s neck should be placed in a median position to avoid compression of the jugular vein, which can affect venous return and lead to an increase in intracranial pressure. Also note that straps holding the endotracheal tube in the neck can interfere with venous return if they are too tight and special care should be taken. Since a 1 degree Celsius increase in body temperature increases the metabolic rate of the brain by 13-15%, the brain tissue is prone to ischemia. Therefore, fever should be treated aggressively. The body temperature must be kept normal or slightly low. When dealing with fever, it is recommended to start using ice packs or cooling blankets and to avoid using other strong analgesic and antipyretic agents as much as possible to avoid lowering the cerebral perfusion pressure due to lowered vasodilator blood pressure. The main thing is to bring the patient into a virtuous cycle with exquisite and delicate medical care to keep the patient away from danger and avoid entering a vicious cycle.