I. Overview Debridement decompression is the last resort and effective step to save life in patients with refractory cranial hypertension and ineffective cranial pressure reduction such as dehydration and diuresis in heavy craniocerebral trauma, but its efficacy is controversial. In particular, in April 2011, the New England Journal of Medicine published “Debulking flap decompression for diffuse traumatic brain damage” by Australian scholars Cooper et al, which has aroused great concern and hot debate among neurosurgeons at home and abroad. Their RCT study found that early treatment with bilateral frontotemporoparietal decompression flaps was effective in reducing intracranial pressure and shortening treatment time in the ICU, but did not improve patient prognosis. Should Chinese neurosurgeons continue to adhere to or abandon the use of debridement decompression technique to rescue critical craniocerebral trauma patients? We organized Chinese clinical experts in craniocerebral trauma, referred to the main literature at home and abroad, combined with Chinese national ethics and clinical experience, and formulated an expert consensus on debridement decompression for craniocerebral trauma in China, which will help Chinese neurosurgeons to correctly understand the indications, contraindications, timing and methods of debridement decompression and the management of related problems. The mechanism of intracranial hypertension in craniocerebral trauma patients After the closure of cranial suture, the volume of cranial cavity has been relatively fixed. The contents of the cranial cavity include brain tissue (1400g), cerebrospinal fluid (75ml) and blood (75ml). Under normal circumstances, the total volume of these three is in dynamic balance with the total volume of the cranium to maintain the intracranial pressure at a normal level. Since the volume of brain tissue is relatively constant and cannot be compressed especially during acute intracranial pressure increase, the regulation of intracranial pressure is kept in balance between cerebral blood volume and cerebrospinal fluid volume. Under normal conditions, the cerebral blood flow required to maintain the minimum metabolism of brain tissue is 32 ml/100g/min (normal is 54-65 ml/100g/min), the whole brain blood flow is 400 ml/min (normal is about 700-1200 ml/min), the cerebrovascular content should be kept above 45 ml, and the volume of cerebral blood volume that can be compressed accounts for about about 3%. Cerebrospinal fluid is the most variable component of the three intracranial contents. The amount of cerebrospinal fluid in the ventricles, brain pools and intracranial subarachnoid space is about 75 ml, accounting for about 5.5% of the volume of the cranial cavity. When intracranial hypertension occurs, it is first reduced by cerebrospinal fluid secretion, increased absorption and partially compressed out of the skull to relieve the elevated intracranial pressure, followed by recompression of cerebral blood volume. Therefore, the compensatory volume available for relieving intracranial hypertension is about 8% of the cranial cavity volume. Acute craniocerebral trauma patients with pathologies such as intracranial hemorrhage, extensive cerebral contusion, tSAH, cerebral edema, cerebral infarction, and diffuse brain swelling can develop intracranial hypertension when their increased volume exceeds the compensatory volume. If the increase of intracranial pressure exceeds the limit of intracranial compensatory function, the continuous rise of intracranial pressure can cause the dysfunction of cerebral blood flow regulation, serious cerebral tissue ischemia and hypoxia, aggravate cerebral edema, increase the volume of brain tissue, the intracranial pressure rises even more, can make brain tissue displacement to form brain herniation, and finally cause respiratory and circulatory center failure and death due to brainstem compression. The development process of intracranial hypertension in craniocerebral trauma patients is divided into four different stages: compensatory stage, early stage, peak stage and late stage (exhaustion stage) according to the clinical symptoms and pathophysiological characteristics. The stages are not clear for patients with extra heavy craniocerebral trauma. 1.Compensation stage: Although the lesion has begun to form, it is in the initial development stage. Since there is a compensatory volume in the cranial cavity accounting for less than 8-10% of the total volume, as long as the lesion itself and the volume occupied after pathological changes do not exceed this limit, the intracranial pressure can still remain within the normal range, and the symptoms and signs of increased intracranial pressure will not appear clinically, so early diagnosis is more difficult. The speed of progression in this period depends on the nature, location and speed of development of the lesion and other factors. 2.Early stage: the lesion develops and exceeds the compensatory volume of the cranial cavity, but the intracranial pressure is lower than 1/3 of the normal value of the mean body arterial pressure, less than 4.7Kpa (35mmHg), the cerebral perfusion pressure value is 2/3 of the normal value of the mean body arterial pressure, and the cerebral blood flow also remains about 2/3 of the normal cerebral blood flow, about 34~37ml/100g brain tissue/min, and the PaCO2 value is within the normal range . The cerebrovascular autoregulatory response and systemic vasopressure response were both still well maintained. However, brain tissue already has early ischemia and hypoxia and reduced cerebral blood flow, and the vascular diameter has also changed significantly, so the signs and symptoms of increased intracranial pressure such as headache, nausea and vomiting gradually appear, which are aggravated by the actions leading to increased intracranial pressure. In acute intracranial pressure increase, Cushing’s reaction of increased blood pressure, slowed pulse rate, increased pulse pressure, slowed respiratory rhythm and deepened amplitude can still occur. 3.Peak stage: The lesion has developed to a serious stage, the intracranial pressure is 1/2 of the normal value of the mean arterial pressure = 4.7-6.6 Kpa (35-50 mmHg), the cerebral perfusion pressure is also equal to half of the mean body arterial pressure value, and the cerebral blood flow is also half of normal about 25-27 ml/100g brain tissue/min. If the intracranial pressure approaches the level of arterial diastolic pressure, PaCO2>6.1 Kpa (46mmHg) and close to 6.6Kpa (50mmHg), cerebrovascular autoregulatory response and systemic vasopressure response can be lost and diffuse disorders of cerebral microcirculation can occur. At this time, the patient has severe headache, repeated vomiting, and gradually tends to coma, and may show symptoms of brain herniation such as fixed dilatation of the eyes and pupils or forced head position. 4. Late stage (failure stage): The condition has developed to the endangered stage, with intracranial pressure increased to the equivalent of mean body arterial pressure, perfusion pressure <2.6kpa (20mmhg)< span="">, vascular diameter is close to complete occlusion of the lumen, cerebral blood flow is only 18-21ml/100g brain tissue/min, cerebral metabolic oxygen consumption (CMRO2) <0.7ml/100g brain tissue/min (normal value is 3.3-3.9 ml/100g brain tissue/min), PaCO2 close to 6.6 Kpa (50 mmHg), PaO2 drops to 6.6 Kpa (50 mmHg), and SaO2 <60%< span="">. At this time, the patient is in deep coma, all kinds of reflexes can disappear, double pupils are dilated, deafferentation is tonic, blood pressure drops, heartbeat is fast and weak, breathing is shallow and fast or irregular or even stops. The main clinical evidence of debridement decompression for the treatment of craniocerebral trauma and cerebral contusion patients with cranial hypertension 1. The surgical guidelines for craniocerebral trauma prepared by the American Association of Neurological Surgeons: debridement decompression is a life-saving surgery for patients with acute craniocerebral trauma and malignant cranial hypertension for which medical treatment is ineffective. Indications for surgery: acute craniocerebral trauma patients with progressive impairment of clinical consciousness, CT scan showing obvious occupying effect of intracranial injury, persistent elevation of ICP >30mmHg which is ineffective by medical treatment such as dehydration, and even dilated pupils. 2. Australian debridement decompression technique RCT study (Level I evidence): Professor Cooper and others in Australia randomly divided 155 patients with acute craniocerebral trauma, ICP>20mmHg during 1h after post-injury medical treatment, intermittent or lasting more than 20 minutes into debridement decompression group and medical drug treatment group through 15 hospitals in 8 years. The results showed that the debridement decompression technique was effective in reducing intracranial pressure and shortening the treatment time in the ICU, but did not improve patient prognosis. 3.RCT study of debridement decompression at Royal Children’s Hospital, Melbourne, Australia (Level I evidence): RCT study of 27 patients with cranial hypertension in children with craniocerebral trauma. 6-month follow-up results showed that the recovery rate of patients in the debridement decompression surgery group was 53.8% and the prognosis was 46.1%; the recovery rate of patients in the non-surgical group was only 14.3% and the prognosis was 85.7%. 4. A retrospective study of debridement decompression in Chang Gung Hospital, Taiwan (Class II evidence): 201 patients with acute craniocerebral trauma underwent debridement decompression surgery to observe 30-day mortality and influencing factors. The results revealed that 26.4% of patients undergoing debridement and decompression at 30 days post-injury had a mortality rate of 26.4%. Of these patients, 79.2% died from uncontrollable brain swelling and large cerebral infarcts. Patient age and GCS score were independent factors affecting prognosis. 5.A retrospective study (Level II evidence) of surgical and non-surgical procedures in 85 patients with acute craniocerebral trauma and a mean GCS score of 9. 55 patients underwent craniotomy and 30 patients underwent non-surgery. 3-month follow-up results: the mortality rate was 33% and 30% in the surgical and non-surgical groups, respectively, and the recovery rate was 47% in both groups. 6. A controlled study of surgical versus non-surgical patients with cerebral contusion in Japan (Class II evidence): 21 patients with cerebral contusion and ICP > 40 mmHg had a mortality rate of 22% in the debridement and decompression patients and 88% in the non-surgical group. They recommended that surgical debridement decompression should be performed aggressively in patients with cerebral contusions with reduced consciousness, progressive increase in ICP, and significant occupancy effect on CT scan. 7. A controlled clinical study of different debulking flap decompression procedures in patients with severe cerebral contusions with malignant cranial hypertension in China (Class II evidence): 486 patients with severe frontotemporal lobe contusions combined with refractory intracranial hypertension with severe craniosynostosis were randomly divided into a standard trauma large bone flap craniotomy group (n=241) versus a conventional temporoparietal flap surgery group (n=245). The clinical follow-up results at 6 months after surgery showed that 39.8% of patients in the standard trauma large bone flap group recovered well and had moderate disability, 34.0% had severe disability and vegetative survival, and 26.2% died; 28.6% of patients in the conventional temporoparietal flap group recovered well and had moderate disability, 36.3% had severe disability and vegetative survival, and 35.1% died. V. Expert recommendation for decompression of debridement 1. Strongly recommended: ①Patients with brain herniation in heavy craniocerebral trauma with dilated pupils, CT showing brain contusion, hemorrhage, cerebral edema, brain swelling and cerebral infarction with obvious occupational effects (midline shift, basal pool compression); ②Patients with heavy craniocerebral trauma with progressive elevation of ICP, >30mmHg for 30 minutes. 2.Recommended: acute craniocerebral trauma patients with progressive impairment of consciousness, patients with significant occupying effects (midline shift, basal pool compression) such as cerebral contusion, hemorrhage, cerebral edema, brain swelling and cerebral infarction on CT, and patients whose cranial hypertension cannot be controlled by first-line treatment such as osmotic dehydration diuretics. 3.Not recommended: Patients with extra heavy craniocerebral trauma who are dying of late brain herniation such as bilateral pupil dilatation and fixation, loss of light reflex, GCS score 3, respiratory arrest and unstable blood pressure. 4, surgical method: unilateral cerebral hemisphere injury patients use one side of the standard trauma large bone flap decompression, bilateral cerebral hemisphere injury patients perform bilateral standard trauma large bone flap decompression or coronal anterior hemicranial decompression. Temporal floor decompression must be adequate. In patients with severe intraoperative cerebral contusion brain swelling that occurs with brain bulge, the inactivated brain tissue should be removed and decompressed internally as necessary. Depending on the degree of cranial hypertension, the temporalis muscle can be removed to increase the compensatory volume of the cranial cavity. The temporalis fascia is advocated to be sutured with the dura mater in a reduced manner, and artificial dura mater can also be used to perform the reduction suture (adhesion). It is recommended to perform intracranial pressure monitoring technique after debridement decompression to guide the postoperative treatment and prognosis judgment. Common complications and sequelae after debridement decompression and their management Common complications and sequelae after debridement decompression for patients with severe craniocerebral trauma include: subdural fluid, hydrocephalus, intracranial hemorrhage, infection, incisional impaction, epilepsy and skull defect. Most subdural effusions are self-absorbing and do not require surgical intervention. Subdural effusions with significant occupational effects require surgical treatment such as puncture drainage, lumbar pool drainage or shunting. Compensatory enlargement of the ventricles due to extensive cerebral atrophy does not require surgical management, while progressive and obstructive hydrocephalus require surgical shunting. Cranioplasty is recommended as soon as the patient’s intracranial pressure is reduced to normal values after debulking decompression and the condition permits. Prophylactic use of antiepileptic drugs is not recommended. 1. As the evidence-based medical evidence for the treatment of severe cranial hypertension in heavy craniocerebral trauma continues to increase, the Chinese Expert Consensus on Craniocerebral Trauma Decompression will be constantly revised and improved, and we will reflect the latest and most authoritative clinical scientific findings in a timely and objective manner for the benefit of craniocerebral trauma patients. 2. The Expert Consensus on Craniocerebral Trauma Debridement Decompression in China belongs to the recommended program of neurosurgery experts. Clinicians should refer to the implementation according to the actual condition of patients. 3.The Chinese Expert Consensus on Craniocerebral Trauma Debridement and Decompression is only applicable to adult acute craniocerebral trauma patients. 4.The Chinese Expert Consensus on Craniocerebral Trauma Debridement and Decompression is for the reference of neurosurgeons in China and does not have legal effect.