I. Cerebrospinal Fluid Leakage
(I) Overview
Cerebrospinal fluid leakage refers to the breakage of both the arachnoid and dura mater, so that cerebrospinal fluid can leak outside the dura mater through the breakage, and then leak outside the body through the fracture suture. Cerebrospinal fluid leakage through the nasal cavity, ear canal or open wound is a serious complication of craniocerebral injury and can lead to intracranial infection, the incidence of which is about 2% to 9%.
(B) Sites and types of cerebrospinal fluid leakage Lin Jinzhi, Department of Neurosurgery, Guangdong Second People’s Hospital
Cerebrospinal fluid leaks occur in skull base fractures, anterior cranial fossa fractures often lead to nasal leaks, and middle cranial fossa fractures are mostly ear leaks. In children, the incidence of traumatic cerebrospinal fluid nasal leakage is less than 1% because the skull is soft and elastic and the paranasal sinuses are not yet fully developed, but the development of the tympanic ventricle and mastoid airspace is earlier in children, so cerebrospinal fluid ear leakage is not uncommon. The timing of cerebrospinal fluid leakage varies widely, with most occurring immediately after injury or within a few days, which is the acute phase of cerebrospinal fluid leakage; however, there are a few patients who develop it as late as several months later, called delayed cerebrospinal fluid leakage. The former mostly closes and heals on its own within 1 week; the latter, once it appears, is often prolonged, stopping and leaking, often leading to secondary intracranial infections and recurrent meningitis.
(iii) Clinical manifestations
Cerebrospinal fluid nasal leakage is most often seen in anterior cranial recess fractures, with an incidence of 39%. In acute patients, there is often bloody fluid spillage from the nasal cavity, orbital subcutaneous bruising, submembranous hemorrhage, loss or loss of sense of smell, and occasionally injury to the optic or oculomotor nerve. The amount of cerebrospinal fluid leakage is related to the body position. The leakage increases when sitting or hanging the head and stops when lying down.
Cerebrospinal fluid leakage is often caused by fractures of the middle fossa of the skull involving the tympanic chamber, because the rock bone is located at the junction of the middle and posterior fossa of the skull, and blood cerebrospinal fluid can enter the tympanic chamber whenever the middle ear cavity is injured by a fracture of the rock bone or the posterior fossa. If there is a rupture of the eardrum, the fluid flows out through the external ear canal, and when the eardrum is intact, the cerebrospinal fluid can flow back to the pharynx through the Eustachian tube or even from the posterior nasal orifice to the nasal cavity and then spill out from the nostril. In addition, delayed subcutaneous bruising in the postauricular mastoid area (Battle’s sign) is also a common sign of temporal fracture.
Cerebrospinal fluid leakage is almost always the result of improper initial management of open cranial injuries, mostly due to firearm brain penetration injuries. It is caused by improper dural repair or by poor healing due to trauma infection.
(IV) Diagnosis and treatment
1. Diagnosis
The first step in the diagnosis of cerebrospinal fluid leak is to determine the nature of the leak. The cerebrospinal fluid contains high sugar content, so it can be measured by urine sugar test paper. Sometimes the leaking fluid is mixed with blood, and biochemical measurements are difficult to confirm the diagnosis, so the red blood cell count can be used to compare the blood cell count of the leaking fluid with that of the blood to determine. However, the exact diagnosis may still rely on special examination methods: cranial X-ray, CT scan and other methods to assist in the diagnosis.
2. Treatment
Most of the acute cerebrospinal fluid nasal or ear leaks caused by skull base fracture can be cured by non-surgical treatment, and only a few of them can be considered for surgery if they persist for more than 3~4 weeks.
(1) Non-surgical treatment
Generally, the head is elevated 30 degrees to the affected side, so that the brain tissue sinks at the leakage hole to facilitate the adhesion and healing. At the same time, the nasal or ear cavity should be kept clean and unobstructed. Avoid sieving the nose and ears, avoid coughing and holding the breath, protect the bowel movement, limit the amount of body fluid intake, and give appropriate amount of drugs to reduce cerebrospinal fluid secretion, such as acetazolamide or mannitol for dehydration. Approximately 85% of patients are cured after 1 to 2 weeks of conservative treatment.
(2) Surgical treatment
Cerebrospinal fluid leak repair is required only after a prolonged leak (more than 3 months) or repeated recurrences after self-healing. Cerebrospinal fluid nasal leak repair; cerebrospinal fluid ear leak repair; cerebrospinal fluid wound leak.
Cranial nerve injury
Cranial nerve injury is mostly caused by skull base fracture, or brainstem injury involving cranial nerve nuclei, or secondary to intracranial hypertension, meningitis and blood supply disorders, or occasionally caused by surgical malpractice.
(I) Olfactory nerve injury
More than half of the olfactory nerve injuries are caused by direct frontal violence and the olfactory nerve filaments are avulsed at the sieve plate, mostly accompanied by paranasal sinus fracture. If it is a partial olfactory impairment, it may improve later. Before recovery, abnormal smell like burnt odor often appears. If the loss of smell lasts for more than two months, it is difficult to recover and there is no good treatment plan.
(ii) Optic nerve injury
It is often caused by frontal or frontotemporal injuries, especially direct violence to the superior extraorbital rim, often accompanied by fractures of the anterior and middle cranial fossa. Treatment of optic nerve injury is difficult, and there is no cure for the severed optic nerve. In case of partial injury or secondary damage, neurotrophic drugs and vasodilators should be given on the basis of effective relief of intracranial hypertension. For patients with progressive visual impairment in the early post-injury period and with fracture deformation, stenosis or bone spur of the optic canal, optic nerve canal decompression surgery can be considered. Intracranial approach: 1. Intracranial approach: open the cranium through the affected forehead, peel off the dura mater at the top of the orbit, and follow the upper edge of the pterygoid crest to the upper wall of the optic canal, do not damage the olfactory nerve in the sieve plate area. 2. Extracranial approach: open the lateral wall of the sieve sinus through the orbit or nose, that is, the medial wall of the orbit up to the posterior sieve plate, then under the microscope, carefully grind or chisel open the medial wall of the optic canal to achieve decompression.
(iii) Articular nerve injury
It is commonly caused by a fracture of the anterior cranial fossa involving the pterygoid fossa, or by a fracture of the middle cranial fossa through the cavernous sinus, occasionally secondary to an intracranial artery cavernous sinus fistula, aneurysm or cavernous sinus thrombosis. In patients with complete articular nerve paralysis, there is ptosis, pupillary dilatation, loss of light reflex, and loss of eye movement and radial function with the eyeball deviating slightly laterally and upward, downward, and inward. At present, there is no good treatment plan for traumatic articular nerve injury, relying mainly on neurotrophic drugs and vasodilators.
(iv) Facial nerve injury
The incidence of craniocerebral injury with facial nerve injury is 3%, and 1/5 of the patients who have blood and fluid overflow from the external auditory canal after the injury can develop ipsilateral facial muscle weakness. The common cause of facial nerve injury is fracture of the middle fossa of the skull and the mastoid process. Patients with facial nerve injury present with facial muscle paralysis, loss of expression on the affected side, incomplete eyelid closure, and deviation of the corners of the mouth to the healthy side. If the facial nerve injury is proximal to the bulbar nerve, the ipsilateral anterior 2/3 of the tongue is lost. Early treatment should be mainly non-surgical, using dexamethasone and appropriate amount of dehydration to reduce the trauma reaction and local edema, giving neurotrophic drugs and calcium blockers to improve nerve metabolism and vascular blood supply, which can often promote the recovery of nerve skills. For persistent complete facial palsy, alternative repair surgery is often used. For example, facial-sublingual nerve anastomosis or facial-phrenic nerve anastomosis, facial-paraneoplastic nerve anastomosis. It can achieve better results.
(v) Auditory nerve injury
Unilateral or bilateral deafness caused by auditory nerve injury is an important complication of craniocerebral injury, and it is reported that about 0.8% of craniocerebral trauma is accompanied by rock bone fracture and involves the middle ear cavity. After the injury, some patients show tinnitus and vertigo symptoms, and the treatment of auditory nerve injury, there is no good strategy yet, and drug therapy is still the main treatment. For tinnitus and vertigo that persist in the later stages, it is necessary to rely on sedatives to suppress or reduce the symptoms, such as phenobarbital, chlorpromazine, chlorpromazine or isopromazine. For individual cases of severe tinnitus or vertigo that have not been treated for a long time, otologic surgery can be considered to destroy the vagus or selectively cut the vestibular nerve.
Traumatic hydrocephalus
(I) Etiology and pathogenesis
Traumatic hydrocephalus is mostly caused by subarachnoid hemorrhage after cranial trauma, and the large amount of bloody cerebrospinal fluid stimulates the meninges and causes aseptic inflammation. Adhesions occur between the arachnoid and the soft meninges, even blocking the arachnoid granules, resulting in impaired cerebrospinal fluid circulation and reabsorption, causing traffic or obstructive hydrocephalus; or due to ventricular penetrating injury or hematoma breaking into the ventricles, blocking the interventricular foramen, the aqueduct or the exit of the four ventricles, i.e., an intermediate foramen and two lateral foramina, forming obstructive hydrocephalus; or due to severe brain bulging and displacement after decompression of the debridement flap, resulting in obstructed cerebrospinal fluid circulation (ii) Typology and clinical findings
(II) Classification and clinical manifestations
Acute hydrocephalus occurs within two weeks after the injury, or as early as 1 to 3 days after the injury, due to blockage of the cerebrospinal fluid circulation by blood clots (obstructive type) or blockage of the arachnoid membrane by blood red blood cells, which prevents the absorption of cerebrospinal fluid (traffic type). The patient’s condition deteriorates rapidly, with a significant increase in intracranial pressure, often combined with severe cerebral contusions. The chronic type is seen 3 to 6 weeks or as late as 6 to 12 months after the injury and is mostly due to traffic hydrocephalus caused by impaired cerebrospinal fluid absorption. The clinical presentation is mostly normal cranial pressure hydrocephalus. Dementia, gait instability, unresponsiveness and abnormal behavior gradually appear. The disease progresses slowly, with fluctuations in symptoms, and also shows persistent shallow coma for several months, followed by gradual recovery.
(III) Diagnosis and treatment
Diagnosis:There is a clear history of trauma, manifestation of intracranial hypertension, and the diagnosis can be confirmed by cranial CT examination.
Treatment:Once the diagnosis is clear, external ventricular drainage or ventriculo-abdominal drainage should be performed early, and the efficacy is certain. The effect of conservative treatment is uncertain.
IV. Venous sinus injury
The above sagittal sinus injury is the most frequent, the transverse sinus, sinus confluence is the second, can be divided into two kinds of partial tear and complete rupture. During the operation, holes should be drilled around the fracture, and a circle of bone should be bitten off around it, and traction lines should be made on both sides of the sinus, and muscle or fascia pieces should be prepared, and then the bone pieces or metal foreign bodies pierced into the sinus should be removed, and the injury should be seen under attraction. If there is no more bleeding, it can be sutured and fixed in the dura mater. The anterior 1/3 of the superior sagittal sinus can be ligated if it is not easy to repair, and the middle or posterior 1/3 of the sinus can be repaired as much as possible by using artificial vessels or anastomosis of the autologous saphenous vein. It is best to avoid ligation of the transverse sinus.
V. Craniofacial injury
The main complications are cerebrospinal fluid leakage and intracranial infection. The incidence of intracranial hematoma at the entrance to the skull base is high. Among the air sinuses, the frontal sinus has a high chance of injury. mastoid sinus. X-rays, CT scans, etc., no fracture fragments are seen in the skull, and there is no urgent clinical indication for surgery, the condition should be closely observed. If there are bone fragments in the skull, the skull should be opened through the skullcap, and the entrance to the skull base should be explored to remove the intracranial hematoma, bone fragments and inactivated brain tissue. The bone fragments are removed from the sinus, the mucosa of the sinus wall is scraped, the sinus cavity is filled with muscle fragments, and the dura mater is sutured. In the case of pterygoid sinus injury, the mucous membrane of the sinus wall is scraped through the nasal approach and the sinus cavity is filled with muscle pieces. Facial injuries are also cleared at the same time.
Sixth, ventricular injury
There is often a large amount of cerebrospinal fluid flowing from the wound, intracerebroventricular hemorrhage, deep coma, persistent hyperthermia, neck ankylosis, and more serious injuries. The intracerebroventricular blood clots should be cleared, the moving metal foreign body should be removed, and the ventricle should be repeatedly flushed with saline.
VII. Traumatic internal carotid cavernous sinus fistula
The fracture of the skull base or foreign body directly injures the cavernous sinus segment of the internal carotid artery and its branches, and the arterial blood is injected directly into the cavernous sinus by the rupture. Typical symptoms: ① pulsating proptosis; ② intracranial murmur, compression of the carotid murmur is reduced or disappeared; ③ eye movement disorders; ④ edema and congestion of the conjunctival membrane. Treatment: Currently, endovascular interventional embolization is the first treatment option for traumatic CCF. If the catheter cannot be properly placed due to various reasons (such as arteriosclerosis, torsion, stenosis, etc.), other treatment methods will be considered. These include transarterial and transvenous approaches, with the femoral artery being the most commonly used route. The commonly used embolization materials are detachable balloons and microspring coils. The detachable balloon catheter is the best way to embolize the fistula and keep the internal carotid artery open. The “kite flying” method can also be used to embolize the fistula and keep the internal carotid artery open.
Traumatic arterial rhinorrhea
Fracture of the skull base and injury to the internal carotid artery, pterygopalatine artery or sieve artery can cause arterial rhinorrhea that is difficult to stop. The rupture of the cavernous sinus segment of the internal carotid artery causes rhinorrhea manifested as head injury, blindness of one or both eyes and severe epistaxis. Emergency treatment: nasal tamponade to stop bleeding, blood transfusion for those with shock, and fluid to replenish blood volume. In severe cases, surgical treatment is required: carotid ligation or isolation of pseudoaneurysm of the internal carotid artery or pterygoid sinus tamponade can be used. (2) Nasal bleeding caused by injury to the pterygopalatine artery or sieve artery. Ligation of the pterygopalatine artery or carotid artery can also be performed. All need to clarify the lesion site according to the clinical manifestations and carotid angiography before the operation in order to deal with it correctly and effectively.
Nine, brain bulge
Generally can be divided into early cerebral bulge and late cerebral bulge. (1) early cerebral bulge (within a week), mostly caused by extensive cerebral contusion, acute cerebral edema, intracranial hematoma or early concurrent intracranial infection and other factors. After symptomatic treatment, lifting the increased intracranial pressure, the bulging brain tissue can be returned to the cranial cavity, brain function does not cause significant damage, can be called benign brain bulge; (2) late brain bulge (more than a week). Mostly due to incomplete initial debridement, intracranial bone fragments foreign body retention, causing brain infection, brain abscess, or subacute, chronic hematoma, etc., so that the intracranial pressure increases. Inflated brain tissue such as embedding, infection, necrosis, can also affect the adjacent uninflated brain tissue blood circulation disorders, the formation of malignant brain bulge or intractable brain bulge. When dealing with brain bulge should be surrounded by a woolen circle, properly protected and treated with dehydration and antibacterial agents, due to hematoma or abscess should be removed.
Ten, brain abscess
It is one of the common complications and late causes of death in penetrating brain injury. The incidence of abscess is about 10-15% in case of incomplete debridement, so early and thorough debridement is the key measure to prevent abscess. Treatment: timely surgical treatment should be performed, and early abscesses should be treated by expanding and draining the wound channel and removing foreign bodies. Abscesses in important functional areas should be punctured and extracted first. Late abscesses can be removed together with foreign bodies and sinus tracts.
Eleven, traumatic epilepsy
It can occur at any time after penetrating cranial injury, but the incidence is highest from 3 to 6 months after injury. Early seizures are associated with cerebral contusion, cerebral edema, hematoma and depression fracture. Late onset attacks are mostly caused by brain abscesses, brain scars and brain atrophy. The main clinical problem is limited seizures, but also grand mal seizures. Phenobarbital, phenytoin sodium, methotrexate, and parkinson can be used as the main medical treatment. Surgical treatment can also be performed to address the cause.
Cranial osteomyelitis
Often caused by open fractures of the skull and incomplete or untimely debridement. In the early stage, there is local redness, swelling, heat and pain and purulent secretions. In the late stage, chronic sinus tracts are formed, epidural inflammatory granulation tissue or abscesses are formed, and X-rays show the presence of dead bone or destruction of the edges of bone defects. Management: In the acute stage, antimicrobial agents are applied to keep the infection under control and limited. In the late stage, the sinus tract should be removed, dead bone should be removed, and epidural granulation tissue and pus should be cleared.
XIII. Cranial defect
After open craniocerebral injury debridement or closed craniocerebral injury debridement office decompression, cranial defect can be left behind. Diameter of 3cm or more, clinical dizziness, headache, and sometimes also cause nausea, vomiting and epilepsy. The patient has a sense of insecurity such as fear of bruising. The frontal area affects the facial appearance, etc. All must be repaired. Generally, the wound can be repaired after 3 months of healing, and the infected wound must be delayed until more than half a year after the injury. Any recent infection, incomplete wound debridement, or intracranial pressure is still high and there is brain expansion are temporarily not suitable for repair.
XIV, post-cranial injury syndrome
After craniocerebral injury, many patients may have some neurological or mental disorders, collectively referred to as craniocerebral injury syndrome. Also known as post-traumatic brain injury sequelae, concussion sequelae, traumatic brain injury neurosis, the disease name varies, indicating that the lack of uniform understanding and diagnostic criteria. The pathogenesis of the disorder may be due to mild organic brain injury and pathological changes (cerebral hemorrhage, cerebral edema, small cerebral softening foci and mild cerebral atrophy) in addition to the patient’s mental and psychological factors. Patients often complain of dizziness, headache, nausea, anorexia, fatigue, agitation, tinnitus, excessive sweating, palpitations, memory loss, mental atrophy, insomnia, hypogonadism, and menstrual disorders. The symptoms are sometimes mild and sometimes severe, and are related to the mental and emotional state, and the patient’s complaints are often more than the positive neurological signs. Sometimes it is difficult to locate some minor signs, although they are detected. Some of these casualties may have mild or moderate EEG abnormalities, and CT brain scan may have mild brain atrophy, etc. Treatment: Prevention and treatment are equally important. In the acute phase of the injury, the casualty should rest quietly in bed, do not think too much about the problem, suspend reading long books, etc. After the acute period, the casualty can be allowed to move early. Give appropriate sedative and analgesic to the clinical symptoms, care for the pain of the wounded, in order to relieve the wounded of the tension and anxiety of the so-called “sequelae” that cannot be cured, and carry out some body therapy, qigong, taijiquan, etc., with the treatment of Chinese medicine to activate blood circulation and remove blood stasis, and encourage the wounded to gradually transfer to normal life, study and work once the symptoms have progressed. Once the symptoms improve, the injured person will be encouraged to gradually transfer to normal life, study and work.
Section 7: Treatment principles of craniocerebral trauma
I. Steps and methods of craniocerebral trauma treatment
Understand the key injuries, systematically and briefly examine the whole body of the injured person, immediately deal with life-threatening diseases, quickly leave the scene and transfer to hospital. For patients with severe brain trauma, one hour after the injury is the golden time for resuscitation treatment. Therefore, whether the scene resuscitation of craniocerebral injury patients is timely and correct is the key to the success or failure of resuscitation.
(A) Firstly deal with asphyxia and bleeding
For patients who are unconscious and unconscious immediately after the injury, two points should be noted.
1.Keep the airway unobstructed
2. quickly deal with active bleeding
(B) specialty treatment of neurosurgery in the emergency room
The brain is the nerve center, brain tissue is the most fragile, difficult to regenerate and repair. Craniocerebral injury is likely to cause death and disability. The main causes of death from craniocerebral injury are: intracranial hemorrhage, cerebral contusion, both of which are interrelated and can develop into brain herniation. The longer the time, the less chance of successful resuscitation, and if the brain herniation exceeds 6 hours, the chance of survival is slim. Cerebral hemorrhage is more effective than cerebral contusions, while epidural hematoma in cerebral hemorrhage is the most effective and can be fully recovered in time for resuscitation.
The medical staff in the hospital emergency room should deal with the condition in a timely and decisive manner, closely observe the changes in the patient’s mental status, pupils and other vital signs and give the patient a cranial CT examination to determine the condition of the cranial injury, and at the same time immediately carry out the corresponding therapeutic care with the neurosurgeon to ensure maximum recovery of brain function. The more timely the treatment for craniocerebral injury, the better the patient’s prognosis. While treating cranio-cerebral trauma, doctors should pay attention to checking the patient’s whole body injury situation, comprehensive treatment first contact to do cranial CT scan, and those with brain herniation should immediately do preoperative preparation in the emergency room. Hospitals with strength can set up operating rooms in the emergency department, cranio-cerebral injury surgery is done, and then send the casualty back to the neurosurgery department for further treatment.
Second, the principles of treatment
(a) the classification of the patient treatment
According to the injury and the situation at the time of consultation, the injury can be divided into the following four cases, respectively, treatment.
(1) emergency resuscitation acute closed head injury, continuous coma or had been awake and then coma, GCS 3-5 points, increased intracranial pressure, dilated pupils on one side or the opposite side also began to expand, the vital signs change obviously, the situation is too critical for further examination, should be based on the mechanism of injury and clinical characteristics of localization, direct drilling exploration, craniotomy rescue; if the brainstem primary injury, de-brain ankylosis, pupils If it is a primary brainstem injury, decerebrate ankylosis, pupils large and small, hyperthermia, disorder of vital signs, but no intracranial hypertension, then tracheal intubation or incision, hibernation and cooling, hyperventilation, dehydration, hormones and cranial pressure monitoring and other non-surgical treatment should be performed.
(2) Preparing for surgery If the injury is serious, coma for more than 6 hours or coma again, GCS 6-8 points, vital signs suggesting an increase in intracranial pressure change, the necessary auxiliary examinations should be performed immediately, such as CT scan, etc., to clarify the localization and arrange for emergency surgery; if intracranial hematoma is not found by auxiliary examination, non-operative treatment should be given, intracranial pressure monitoring should be placed and CT should be reviewed regularly for 12-24 hours; if it is open craniocerebral injury should be prepared for surgical debridement while correcting blood volume deficiency.
(3) hospitalization observation Injury is serious, coma time between 20 minutes and 6 hours, GCS 9 to 12 points, positive or suspicious neurological signs, mild changes in vital signs, auxiliary examination with limited cerebral contusion without hematoma, should be admitted to the hospital for observation, review CT if necessary, or intracranial pressure monitoring if there are signs of increased intracranial pressure.
(4) Emergency room observation If the injury is mild, the coma time is less than 20 minutes, GCS score is 13-15, the neurological examination is negative, the vital signs are basically stable, and there are no obvious positive findings in the auxiliary examination, the patient should be kept in the emergency room for observation for 4-6 hours; if the condition is aggravated, the patient should be admitted to the hospital for further examination or observation; if the condition is stable or improving, the patient can be asked to return home for rest, but if one of the following conditions is present, the patient should immediately (1) headache and vomiting increase. (2) Re-impaired consciousness. (3) Restlessness. ④ unequal pupil size. ⑤ Respiratory depression. (6) Slow pulse. ⑦Paralysis of limbs. ⑧Aphasia. ⑨ Seizures. ⑩Mental abnormality.
III. Surgical treatment
The principle of surgical treatment is to save the patient’s life, correct or preserve the important functions of the nervous system, and reduce the mortality and disability rate. Craniocerebral injury surgery is mainly aimed at open craniocerebral injury, closed injury with intracranial hematoma or comorbidities and sequelae caused by craniocerebral trauma. Surgery is only one part of the whole treatment, never only focus on surgery and ignore non-surgical treatment and care work.
The purpose of surgery is to remove intracranial hematoma and other occupying lesions to relieve increased intracranial pressure and prevent brain herniation from forming or to relieve brain herniation. Surgery includes: epidural hematoma removal, acute and chronic subdural hematoma removal, minimally invasive intracranial hematoma urokinase lysis drainage and brain tissue debridement and decompression. It should be noted that: 1. the site of surgical flap opening should be selected correctly after diagnosis. 2. the design of bone flap opening should be prepared before surgery to facilitate hematoma removal and hemostasis. 3. the possibility of multiple hematomas should be noted, and efforts should be made not to leave hematomas behind. 4. decompression surgery: decompression surgery should be performed for brain contusion and severe cerebral edema.
(A) Surgical treatment of acute epidural hematoma
1. Indications for surgery
Regardless of the patient’s GCS score, as long as the acute epidural hematoma volume exceeds 30 mm3, surgical removal of the hematoma should be performed. Patients with hematoma volume less than 30 mm3, hematoma thickness less than 15 mm and midline shift less than 5 mm, if the GCS score is higher than 8 and there is no focal functional deficit, can be treated non-operatively under dynamic imaging and close observation of the neurosurgery center.
2. Timing of surgery
It is strongly recommended that patients with acute epidural hematoma with coma (GCS score less than 9) and unequal pupil size should undergo hematoma removal as soon as possible.
3. Surgical procedure
There is insufficient evidence to support a better outcome. However, craniotomy provides more complete removal of the hematoma.
(B) Surgical treatment of acute subdural hematoma
1. Indications for surgery
Regardless of the GCS score of the patient with acute subdural hematoma, as long as the thickness of the hematoma exceeds 10 mm or the midline shift exceeds 5 mm on CT scan, the hematoma should be removed surgically. All patients with acute subdural hematoma in a comatose state (GCS score less than 9) should be monitored for intracranial pressure. Patients with acute subdural hematoma with a hematoma thickness of less than 10 mm, a midline shift of less than 5 mm, and a comatose state (GCS score of less than 9) should be surgically removed if the GCS score at admission is 2 or more points lower than that at the time of injury and/or the pupils are unequal or fixed and dilated and/or the intracranial pressure exceeds 20 mmHg.
2. Timing of surgery
Patients with acute subdural hematoma who have indications for surgery should undergo surgical hematoma removal as early as possible.
3. Surgical procedure
Comatose patients with acute subdural hematoma with indications for surgery (GCS score 1 cm, frontal sinus rupture, severe cosmetic disfigurement, clinical or imaging evidence of wound infection, pneumothorax or severe wound contamination) can be treated non-operatively.
Patients with closed (simple) depressed skull fractures may receive nonoperative treatment.
1. Timing of surgery
Early surgery is recommended to reduce the risk of infection.
2. Surgical method
Prying up the fracture fragment and wound debridement are recommended as surgical methods. If there is no wound infection, recovery of the original fracture fragment is a surgical treatment option. Patients with open (compound) skull depression fractures should be treated with antibiotics.
The principles of surgical treatment are to save the patient’s life, to correct or preserve vital neurological functions, and to reduce the mortality and disability rates. Surgery for craniocerebral injury is mainly aimed at open craniocerebral injury, closed injury with intracranial hematoma, or comorbidities and sequelae caused by craniocerebral trauma. Surgery is only a part of the whole treatment, never focus on surgery and ignore the non-surgical treatment and care work.
Fourth, non-surgical treatment
Craniocerebral injury patients require surgical treatment of only about 15%, in fact, the vast majority of light, medium and heavy in part to non-operative treatment. Even for surgical patients, postoperative also need to carry out more complex non-operative treatment than surgery, in order to make the whole treatment to be successful.
（Patients with deep coma, posterior tongue drop, coughing and swallowing dysfunction, and frequent vomiting may easily cause mechanical obstruction of the respiratory tract, so respiratory secretions should be removed promptly.
(B) close observation of the condition Every half hour or one hour within 72 hours after the injury to measure respiration, pulse, blood pressure, check the consciousness, pupil changes, pay attention to the emergence of new symptoms and signs.
(C) Prevention and treatment of cerebral edema and lowering intracranial pressure
1.Head elevation except for those in shock
2.Limit the amount of infusion
Infuse 1500-2000ml of fluid every 24 hours, keep the urine volume at least 600ml in 24 hours, correct the imbalance of water and salt metabolism on the basis of intravenous infusion of 5-10% glucose solution, and give enough vitamins, and nasal nutrition can be given after the recovery of intestinal sounds.
(iv) Dehydration treatment
At present, the commonly used dehydration drugs are osmotic dehydration drugs and diuretics. Commonly used drugs for oral administration are: 1. 25-50mg of dihydrochlorothiazide, 3 times a day; 2. 250mg of acetazolamide, 3 times a day; 3. 50mg of aminoglutethimide, 3 times a day; 4. 20-40mg of tachyphylaxis, 3 times a day; 5. 60ml of 50% glycerol saline solution, 2-4 times a day. Commonly used for intravenous injection preparations are: 1.20% mannitol 250ml, rapid drip, 2-4 times a day; 2.30% urea conversion sugar or urea sorbitol solution 200ml, intravenous drip, 2-4 times a day; 3. 20-40mg of tachyzoites, intramuscular or intravenous injection, 1 to 2 times a day, in addition, can also be concentrated 2 times the plasma 100-200ml intravenous injection; 20% Human serum albumin 20-40ml intravenous injection, effective for eliminating cerebral edema and reducing intracranial pressure.
(e) Continuous extraventricular drainage or intermittent release of a certain amount of cerebrospinal fluid in cases with intracranial pressure monitoring, or lumbar puncture to release an appropriate amount of cerebrospinal fluid after the condition is stabilized, etc.
(6) Hibernation hypothermia therapy The cooling of body surface is conducive to lowering the metabolism of brain, reducing the oxygen consumption of brain tissue, preventing the occurrence and development of cerebral edema, and playing a role in lowering the intracranial pressure.
(vii) Barbiturate therapy High-dose pentobarbital or thiopental sodium can reduce brain metabolism, reduce oxygen consumption and increase brain tolerance to hypoxia, and reduce intracranial pressure. The initial dose is 3-5mg/kg intravenously, and the blood concentration should be measured during the dosing period. The effective blood concentration is 25~35mg/L. If intracranial pressure is found to rise, the dose should be increased immediately, which can be calculated by 2~3mg/kg.
(H) Hormone therapy Dexamethasone 5-10mg intravenously or intramuscularly, 2-3 times a day; hydrocortisone 100mg intravenously, 1-2 times a day; prednisone 5-10mg orally, 1-3 times a day, which can help eliminate cerebral edema and relieve the increase of intracranial pressure.
（It is estimated that for every 0.13 kPa (1 mmHg) decrease in partial pressure of CO2 in arterial blood, cerebral blood flow can be reduced by 2%, resulting in a corresponding decrease in intracranial pressure.
(X) Application of neurotrophic drugs These drugs include: ketamine, glutamate, adenosine triphosphate (ATP), cytochrome C, coenzyme A, chlorine ester, cytidylcholine, γ-aminotyrosine and so on. They can be used or combined according to the condition. A more commonly used combination is: cytochrome C 15-20mg. coenzyme A 50μ, adenosine triphosphate 20-40mg, regular insulin 6-10μ, vitamin B650-100mg, vitamin C1g and potassium chloride 1g added to 10% glucose solution 500ml, called energy combination for intravenous infusion, 1 to 2 doses daily, 10-15 days as a course of treatment.
(xi) Prevent complications and strengthen nursing care In the early stage, prevention of pulmonary and urinary tract infections should be the main focus, while in the late stage, it is necessary to ensure nutritional supply, prevent decubitus ulcers and strengthen functional training, etc.