Craniocerebral trauma is very common in both civilian and wartime, with high mortality and disability rates, and is one of the major life-threatening disorders. Basic and clinical neuroscientists have done fruitful work in exploring the pathogenesis of craniocerebral injuries and craniocerebral injury treatment. Since the 1980s, with the continuous progress of basic research on craniocerebral injury, many new techniques, concepts and therapies have been applied in clinical treatment and have achieved satisfactory clinical efficacy.
1, craniocerebral injury after hyperglycemia and rehydration principles
For a long time, clinicians have been using different concentrations of glucose solutions to treat heavy craniocerebral injuries, and using 50% hypertonic glucose osmotic dehydration to treat traumatic cerebral edema. Balancing solution or saline was considered a contraindication for treating patients with cerebral edema from heavy cranial injuries. However, after several years of extensive experimental and clinical studies, the above view was proved to be wrong. On the contrary, the recent view is that balanced fluids should be preferred in the early post-injury period for patients with heavy craniocerebral injuries, and that 5% or 10% glucose solutions should not be used, and that 50% hypertonic glucose solutions are contraindicated. The basis for this includes.
(1) the higher the blood glucose after craniocerebral injury, the higher the rate of death and disability.
(2) A comparative study between equilibrium solution and glucose solution for craniocerebral injury found that animals with glucose solution had a higher mortality rate than equilibrium solution.
(3) Insulin treatment improves the outcome of craniocerebral injury.
(4) Glucose solution treatment after craniocerebral injury can increase the accumulation of lactic acid in brain tissue and aggravate brain edema and neuronal damage.
Of course, clinicians should adjust the type and amount of rehydration fluid in time according to the dynamic monitoring of patient’s blood sugar and plasma electrolyte content.
2.Efficacy evaluation of glucocorticoids in the treatment of traumatic cerebral edema
Glucocorticoids have been used by clinicians to treat patients with traumatic cerebral edema, but their efficacy has been controversial so far. The classical view advocates the use of dexamethasone or hydrocortisone to treat patients with heavy cranial brain injury cerebral edema, which is still widely used in clinical patients. However, many scholars believe that the efficacy of glucocorticoids in traumatic cerebral edema is inaccurate. In the 1980s, it was found that the efficacy of methylprednisolone was better than that of dexamethasone or hydrocortisone. Because of the well-known side effects of glucocorticoids, non-glucocorticoids-21 aminosteroids have been developed, which not only have strong anti-lipid peroxidation and reduce brain edema, but also have any glucocorticoid side effects. 21-aminosteroids and their derivatives have been used in the clinical treatment of patients with heavy cranio-cerebral injuries, and have achieved significant efficacy.
The dose of glucocorticoids is controversial. The classical method is to use conventional doses of glucocorticoids, such as: hydrocortisone 100-200mg/day, dexamethasone 20-40mg/day, methylprednisolone 40-100mg/day. Some people at home and abroad advocate the use of high-dose glucocorticoids, such as: dexamethasone 5mg/Kg/6H×2 times, 1mg/Kg/6H×6 times, followed by gradual reduction of dosage. However, most domestic and foreign clinical bulk prospective randomized double-blind controlled studies have shown that high-dose glucocorticosteroids do not improve the treatment outcome of patients with heavy craniocerebral injuries. It has also been reported that high-dose dexamethasone can significantly improve the prognosis of patients with heavy craniocerebral injuries. Therefore, most scholars at home and abroad do not advocate the use of high-dose hormone treatment for patients with heavy craniocerebral injuries, and even do not advocate the use of hormones.
3.The advantages and disadvantages of decompression of large bone flap
For patients with severe cerebral contusion combined with intracerebral hematoma, clinicians have long adopted decompression of the large bone flap after intracranial hematoma removal. The reason is that decompression can make the brain tissue expand in the direction of the decompression window, so as to reduce the pressure of intracranial hypertension on important brain structures, especially the brainstem and hypothalamus, in order to save the patient’s life. However, more and more clinical practice has demonstrated that decompression of the greater trochanter not only does not reduce the death and disability rate of patients with severe craniocerebral injuries, but may also increase the disability and death rate of patients with severe craniocerebral injuries. The reasons for this include.
(1) decompression of the greater trochanter can lead to embedding of the bulging brain tissue at the decompression window, obstruction of venous return of the embedded brain tissue, ischemic edema and necrosis of the brain tissue, and the formation of cerebral penetration malformation in the long run.
(2) Decompression without suturing the dura mater increases postoperative seizures.
(3) Decompression of the greater trochanter can cause the flow of cerebrospinal fluid from the ventricles in the direction of the decompression window, resulting in interstitial cerebral edema.
(4) Debridement decompression without suturing the dura mater allows blood to leak from the surgical wound into the cerebral pool and ventricular system, which can easily cause hydrocephalus.
(5) Decompression of the greater trochanter without suturing the dura causes brain instability within the cranial cavity, which can lead to re-injury.
(6) decompression without suturing the dura mater will increase the chance of intracranial infection and incisional dehiscence, etc.
4.Efficacy evaluation of hyperventilation to reduce cranial pressure
Since the seventies, clinicians have been advocating the use of hyperventilation to treat uncontrollable high cranial pressure with drugs. According to the arterial CO2 content, hyperventilation is classified as mild hyperventilation (PaCO 35-30mmHg), moderate hyperventilation (PaCO 30-25mmHg), and severe hyperventilation (PaCO <25mmHg). Clinical observations from early experimental studies found that the lower the PaCO level, the more pronounced the cerebral vasoconstriction and the stronger the lowering effect of cranial pressure. However, as experimental studies continued to progress, it was found that persistently low arterial CO partial pressure would lead to cerebral vasoconstriction and even spasm, which would then aggravate the degree of cerebral ischemia and secondary brain damage. Therefore, in the early 1990s, some people began to advocate the use of short duration (<24 hours) mild hyperventilation (PaCO 35-30 mmHg), which not only can reduce intracranial pressure, but also will not cause and aggravate cerebral ischemia. Until the mid-1990s, due to the introduction of direct brain tissue oxygen measurement technology, it was found that short-duration mild hyperventilation could not improve the brain tissue oxygen content, but on the contrary, it would reduce the brain tissue oxygen content. Therefore, scholars at home and abroad no longer advocate any form of hyperventilation for the treatment of intracranial hypertension, but use normal assisted breathing to maintain the arterial blood CO partial pressure in the normal range. Wan Zhengqiang, Department of Neurosurgery, Yancheng First People's Hospital
5.Nutritional support for patients with heavy craniocerebral injuries
There is no ideal method for nutritional support in the early post-injury period for patients with severe craniocerebral injuries. Nutritional support mainly includes two ways, namely, gastrointestinal nutrition and extra-gastrointestinal nutrition. The advantage of gastrointestinal nutrition is that it is simple and inexpensive, but the disadvantage is that due to stress ulcers, early post-injury intestinal peristalsis disappeared, easily caused by reflux misabsorption, bloating and diarrhea, especially the application of ventilator patients should not use transgastrointestinal nutrition. The advantage of parenteral nutrition is comprehensive nutrition, but the disadvantage is that it is easy to cause hyperglycemia, infection, and excessive rehydration to aggravate cerebral edema. At present, clinicians mostly choose to use transgastrointestinal or extragastrointestinal nutrition according to the specific conditions of patients. The main basis for choosing the type of supplementation in the early post-injury period is to try not to use varieties that cause hyperglycemia, in addition to adequate calories and nutrients.
Long-term post-injury nutritional support is especially important for patients with severe craniocerebral injuries due to the long duration of coma and increased caloric consumption. In addition to glucose, fatty milk, amino acids, vitamins, electrolytes, trace elements, colloidal liquid, blood or blood products that are commonly used in clinical practice, gastrointestinal nutrition must be strengthened. Elemental diets with different concentrations of high-calorie, comprehensive nutrition that can promote brain cell recovery have been developed at home and abroad. It can not only effectively ensure the resupply of various nutritional components, reduce the incidence of low protein blood, but also help to promote brain function recovery and improve the effect of heavy cranio-cerebral injury rescue.
6.The effect of preventive use of antiepileptic drugs in patients with heavy craniocerebral injuries
As to whether heavy craniocerebral injury patients need to use prophylactic antiepileptic drugs is quite controversial. Many physicians in China still insist on using prophylactic antiepileptic drugs for 1-3 years. However, more and more clinical studies have shown that the use of prophylactic antiepileptic drugs not only does not reduce the incidence of epilepsy after craniocerebral injury, but also aggravates brain damage and causes serious toxic side effects. In recent years, the incidence of post-injury seizures has been reported to be higher in patients on prophylactic antiepileptic drugs than in patients in the placebo group, and the mechanism for this is unclear. However, in any case, long-term prophylactic antiepileptic drugs are harmful and should not be advocated. The routine use of prophylactic antiepileptic drugs after intracerebral hematoma removal for severe cerebral contusions is more controversial. Most clinicians favor the use of prophylactic antiepileptic drugs, but to date there are no clinical studies to support this view. A growing number of foreign scholars are beginning to advocate the non-use of prophylactic antiepileptic drugs. Of course, if a patient with cranial injury has epilepsy, he or she should be treated with regular antiepileptic drugs.
7.Improvement of intracranial pressure monitoring technology
Intracranial pressure monitoring is of great value in determining changes in the condition of patients with heavy craniocerebral injuries, guiding treatment and determining prognosis. For many years, clinicians have used ventricular puncture to connect pressure monitoring devices, or epidural placement of sensors to monitor intracranial pressure. However, there are shortcomings such as *working injury, low accuracy, and easy to cause intracranial infection. Therefore, there has been a lack of simple and accurate cranial pressure monitoring technology without side effects. Until the late 1980s, foreign countries developed fiber-optic cranial pressure monitoring technology. This method is simple, less invasive, accurate and without any side effects. Basically, it meets the requirements of clinical intracranial pressure monitoring and has been popularized and used abroad. This technology has been introduced in China for clinical use. Wan Zhengqiang, Department of Neurosurgery, Yancheng First People’s Hospital
8.The concept of delayed traumatic intracranial hematoma
Due to the introduction of CT scan technology, the concept of delayed traumatic intracranial hematoma has been proposed. That is, intracranial hematoma was not detected in the first CT scan after cranial injury, but the intracranial hematoma confirmed by CT scan again is called delayed traumatic intracranial hematoma. The clinical significance of delayed traumatic intracranial hematoma is to draw the clinician’s attention to the fact that the failure to detect intracranial hematoma on the first CT scan in the early post-injury period does not mean that intracranial hematoma will not occur again. Regular CT follow-up should be performed according to the patient’s condition, and if the condition deteriorates, CT scan should be performed immediately to diagnose and manage delayed traumatic intracranial hematoma as early as possible. Indicate the death or disability of the patient caused by delayed diagnosis and treatment.
9. Clinical efficacy of subcritical cerebral protection
Since the eighties, a large number of animal experimental studies have proved that 33-35℃ sub-cold temperature can significantly reduce the mortality of craniocerebral injury animals, reduce brain edema and protect the blood-brain barrier. This technology has been used in the clinical treatment of patients with heavy craniocerebral injuries at home and abroad, and has also achieved positive efficacy. It has been used in Europe, the United States, Japan and other countries. However, because subcritical treatment requires the use of inotropes and ventilators for continuous use, it is difficult to carry out this technique in small and medium-sized hospitals in China.