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
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. 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 and stops leaking from time to time, 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 inadequate dural repair or by poor healing of the wound 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 the diagnosis. 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-operative 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 fractures. If it is a partial olfactory impairment, it may improve later. Before recovery, abnormal smell like burnt odor often appears. If bilateral loss of smell persists for more than two months, recovery is often difficult and there is no good treatment option.
(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 nerve 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 fractures of the anterior cranial fossa involving the pterygoid fossa, or by fractures of the middle cranial fossa through the cavernous sinus, occasionally secondary to 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 flow from the wound, intracerebroventricular hemorrhage, deep coma, persistent hyperthermia, neck ankylosis, and more serious injuries. The ventricular blood clots should be cleared, the moving metal foreign body should be removed, the ventricle should be repeatedly flushed with saline, and the ventricle should be continuously drained after surgery, and the tube should be removed in about 3 days.
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, diminished or absent murmur of compressed carotid artery; 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 have progressed, the injured person is encouraged to gradually transfer to normal life, study and work.