closed head injury
Introduction
Introduction to closed head injury Headinjury refers to the damage caused by violence on the skull. Including head soft tissue injury, skull fracture and brain injury. Among them, the consequences of brain damage are serious and should be especially vigilant. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific people Mode of infection: non-infectious Complications: coma
Cause
Causes of closed head injury
Craniocerebral injury begins with the mechanical distortion of the skull, meninges, cerebrovascular and brain tissue caused by external forces acting on the head. The type of damage depends on where and how severe the mechanical deformation occurs. Primary brain injury is mainly the damage of nerve tissue and cerebral blood vessels, which is characterized by the breakage and efferent dysfunction of nerve fibers, different types of nerve cell dysfunction and even cell death. Secondary brain injury includes cerebral ischemia, cerebral hematoma, brain swelling, cerebral edema, elevated intracranial pressure, etc. These pathophysiological changes are caused by primary injury, which in turn can aggravate primary brain injury. Pathological changes.
Prevention
Closed brain injury prevention
The prognosis is mainly neurosis after brain damage, brain dysfunction and traumatic epilepsy.
The preventive measures are mainly for patients with moderate to severe head injury, and special attention should be paid to the prevention of pneumonia, urinary tract infections and hemorrhoids. To strengthen the care, turn over regularly, clean the mouth, remove respiratory secretions, indwell the catheter, regular bladder irrigation.
Complication
Complications of closed head injury Complications
Post-traumatic syndrome
There are still symptoms such as headache, insomnia, memory loss and fatigue after several months of head injury. Handling: 1 patiently and meticulously explain work and psychological counseling to eliminate concerns. 2 symptomatic treatment; 3 encourage patients to participate in physical exercise, restore daily life and work.
Intracranial hypotension syndrome
There is an upright headache and dizziness after a head injury. A diagnosis of lumbar intracranial pressure <0.49 kPa (50 mmH20) can be established. Treatment: 1 supine or head low foot high; 2 encourage patients to drink more water and intravenous supplement balance solution or 5% glucose saline 3500 ~ 4000ml / d; 3 lumbar penetration into the filtered air or oxygen 10 ~ 20ml, or infusion of physiological saline 10 ~ 20ml, daily or every other day; 4 intracranial hypotension caused by long-term failure of cerebrospinal fluid leakage, should be surgically repaired.
Internal carotid artery - cavernous fistula
1 After the injury, there are exophthalmos, conjunctival congestion and edema, eye movement disorder, intracranial murmur, and compression of the ipsilateral carotid artery murmur, which can be clearly diagnosed. 2 cerebral angiography to determine the extent of the lesion. Treatment: Endovascular embolization is the preferred method for this disease, including detachable balloon embolization and microcoil embolization; when embolization is ineffective, direct craniotomy can be considered, including electrocoagulation, cavernous sinus Internal arterial repair.
Traumatic cerebrospinal fluid leakage
After the skull base fracture, the cerebrospinal fluid flows out through the nasal cavity or the ear canal. The blood is often mixed in the acute phase, and the leakage of cerebrospinal fluid is significantly increased when the head is lowered. The following tests can help to confirm the diagnosis: 1 effluent sugar qualitative test: the test is positive for cerebrospinal fluid. 2 When the leaking liquid contains blood, the sugar test is unreliable. It can be dripped with a dry gauze or absorbent paper. The liquid outside the blood spot is leached to the surroundings and is cerebrospinal fluid. 3 skull X-ray or CT scan can be seen in the air skull. 4CT cerebral angiography helps determine leaks. Treatment: Most of them can heal themselves; non-surgical treatments are not cured for 3 to 4 weeks; patients with repeated leakage or complicated purulent meningitis undergo surgery. Surgical method: craniotomy to find the dural damage to repair and suture. If the cerebrospinal fluid leaks from the sphenoid sinus and should be repaired and sutured through the nasal sphenoid sinus, the muscle can be covered or drilled in the saddle nodule to fill the sphenoid sinus.
Long-term coma
At present, most scholars at home and abroad continue to coma for more than one month after a craniocerebral injury, which is called long-term coma. For patients with head injury, they continue to coma for more than 6 to 12 months, and they have a denervated state or a cortical state, but the vital signs are stable. If there is no certain effect after the brain resuscitation series treatment, it can be considered as the survival state of the plant, but it should be actively treated. To see the aftereffects. Treatment: 1 prevention and treatment of various complications. 2 termination of the use of phenytoin, barbiturates. 3 Use brain cell activators as early as possible, such as ATP, Coenzyme A, B vitamins, citicoline, gangliosides, naloxone, etc. 4 Chinese medicine and acupuncture treatment. 5 Let the patient listen to favorite songs, family talks, etc. as early as possible. 6 as early as possible for hyperbaric oxygen therapy, usually takes 2 to 3 courses or more.
Skull defect
1 Surgical indications: the skull defect diameter is more than 3cm, the patient is accompanied by unsafe fear, and there are obvious stereotypes of dizziness, headache and other skull defect syndrome or affect the appearance. 2 surgical contraindications: traumatic site infection, intracranial hypertension, extensive scarring of the scalp or poor blood supply, severe brain dysfunction, long-term bedridden patients. 3 timing of surgery: generally 3 to 6 months after the injury, if the wound has been infected, it should be repaired after the wound has healed for one year. 4 repair materials: can use autologous or allogeneic bone, metal materials (such as titanium alloy), plexiglass or silicone rubber.
Traumatic epilepsy
Focal or systemic seizures occur after craniocerebral injury. EEG examination is of great value in determining the diagnosis and location of epilepsy. Treatment, 1 for patients with epilepsy after craniocerebral injury should be treated with anti-epileptic drugs, usually for 1 to 3 years. Currently commonly used anti-epileptic drugs in the clinic include phenytoin, sodium valproate, and carbamazepine. 2 For regular drug treatment for 2 to 3 years, there are still frequent epilepsy authors, may consider surgical epileptic foci resection and drug treatment.
Symptom
Symptoms of closed head injury Common symptoms Brain-occupying lesions Secondary epilepsy convulsions Vomiting coma
1. Coma: It is an important indicator reflecting the severity of craniocerebral injury.
2, headache: head soft tissue injury, fracture, intracranial hemorrhage, cerebrovascular dysfunction and increased or decreased intracranial pressure.
3, vomiting: often caused by intracranial hemorrhage stimulated by the vagus nerve or vestibular system
4, pupil: more than one big and small, or poor light response, observation changes, for the estimation of the condition and prognosis have great value.
5, the position and movement of the eye: the same direction of gaze or restricted movement.
6, physical activity disorders: single sputum, hemiplegia.
7, paraplegia, seizures.
8, changes in vital signs, brain damage can occur in a short period of time, slow pulse, low blood pressure, slow breathing, and more serious damage.
9, the neck is straight.
10, traumatic neurosis: rickets may occur after injury, stupor state or fraud.
Examine
Examination of closed head injury
Head check
In the case of scalp injury, there is no congestion in the eyelids, conjunctiva and mastoids, bleeding in the ears, nose and throat, and cerebrospinal fluid outflow.
Vital signs focus on changes in breathing, pulse, and blood pressure.
Body check
There are no maxillofacial, chest and abdomen organs, pelvis, spine and limb injuries. More attention should be paid to combined injuries when there is hypotension and shock.
Skull X-ray examination
Suspected skull fractures should be taken positively and laterally. The occipital force was injured and the amount of the pillow (Tang's position) was taken. Suspected optic nerve injury, optic nerve hole film, eyelid fracture, Korot's patch.
Waist wear
Understand the degree of subarachnoid hemorrhage and intracranial pressure. Severe traumatic intracranial hypertension or obvious signs of cerebral palsy are contraindicated.
CT scan
It is an important basis for assisting diagnosis of craniocerebral injury. Can display skull fracture, brain contusion, intracranial hematoma, subarachnoid hemorrhage, ventricular hemorrhage, gas cranial, cerebral edema or brain swelling, cerebral cistern and ventricle compression displacement deformation, midline structure displacement. CT examination should be performed when the condition changes.
MRI
Patients with acute head injury usually do not have an MRI. However, MRI is often superior to CT scan in patients with stable axonal injury, cerebral hemisphere, brainstem, focal contusion and small hemorrhage, and islet subacute intracranial hematoma.
Diagnosis
Diagnosis and diagnosis of closed craniocerebral injury
The method is mainly applied to clinical diagnosis, based on the pathological changes of the brain injury site and injury. Firstly, according to the injury site, it is divided into two parts: skull injury and brain injury. The two are divided into open and closed injuries. Brain injury is classified into open craniocerebral injury and closed craniocerebral injury according to whether the dura mater is intact. The diagnosis of the former is mainly based on dural rupture, cerebrospinal fluid outflow, cranial cavity and external traffic. Skull base fracture combined with cerebrospinal fluid leakage is also called internal open brain injury. Closed brain injury can be divided into primary and secondary.
