重型颅脑损伤诊治进展（Progress in diagnosis and treatment of severe craniocerebral injury）

1、重型颅脑损伤诊治进展（Progress in diagnosis and treatment of severe craniocerebral injury）In recent years, traumatic brain injury has become the leading cause of death among young people in developed countries. With the rapid development of national economy and traffic, the incidence rate, disability rate and

2、mortality rate of traumatic brain injury are increasing year by year. Epidemiological data show that the incidence of traumatic brain injury in China has exceeded 100/10 million people, of which heavy craniocerebral injuries (severe, traumaticbrain, injury, sTBI) accounted for 18% to 20%. The most c

3、ommon cause of injuries is traffic accidents, and about 50 thousand people die each year in china. In recent years, on the basis of craniocerebral trauma and the prevention and treatment of the application has made great progress, the new theory has been produced and developed, but the sTBI mortalit

4、y rate and disability rate is still high, the total mortality rate has been maintained at 30% 50%. This article gives a brief account of some problems in clinical diagnosis and treatment of sTBI.Surgical treatment: decompressive craniectomyAlthough great progress has been made in the diagnosis and t

5、reatment of brain injuries, traumatic brain swelling and intractable intracranial hypertension caused by brain edema are still the major factors affecting the prognosis of patients with traumatic brain injury. DeLuca study shows that reducing the intracranial pressure through various measures, such

6、as dehydration, hyperventilation, barbiturate coma, mild hypothermia therapy can control the intracranial pressure, CPP30mmHg, should consider decompressive craniotomy. The typical American professor Becker argues that used for acute unilateral supratentorial intracranial hematoma and severe brain c

7、ontusion and severe intracranial hypertension in patients with standard large trauma craniotomy (standard trauma craniotomy), this method has been widely used in European countries. The operation methods: incision began in the zygomatic arch, anterior ear 1cm, in direction on the auricle extending a

8、bove the midline to the top of the head, and then along the midline anterior to the frontal hairline, when necessary, may be extended to the level of the brow. This allows removal of approximately 20cm * 15cm, or even larger bone flaps, and sufficient exposure to the base of the frontal and temporal

9、 lobes as far as possible to reduce the bone window to the skull base. Some people believe that standard trauma craniotomy can achieve short-term results, but can not improve the long-term prognosis of patients. Recently at home and abroad are concerned in the center of standard large trauma craniot

10、omy and routine craniotomy surgery in the treatment of sTBI patients with malignant intracranial hypertension: a prospective clinical controlled study, preliminary results of standard large trauma craniectomy is simple and safe, the effect is superior to conventional bone flap.Two 、 mild hypothermia

11、 treatmentIn recent years, domestic and foreign scholars on the sub low temperature (3235 DEG C) in brain injury were studied, that the cerebral protective effect is significant, and can inhibit the formation and release of some of the damage factor, conducive to the prevention and treatment of seco

12、ndary brain injury, blocking the vicious cycle after brain injury. But prospective randomized clinical studies of large sample, multi center by Calpain, found that mild hypothermia therapy can only improve sTBI GCS6 to reach the level of patients with mild hypothermia in 8, aged 30mmHg effect is poo

13、r and the ICP60mmHg is invalid; for ICP patients with normal, mild hypothermia for 24 hours, but the complex temperature should be slow and steady.Three 、 drug therapy(1) drug treatment of brain edemaAccording to the clinical and laboratory research results at home and abroad in recent years, the dr

14、ugs for the treatment of cerebral edema to increase the plasma osmotic pressure, hormone drugs, calcium channel antagonists, free radical scavenger and endocrine therapy.1 drugs to increase plasma osmolality: these drugs increase blood osmotic pressure in the blood vessel and form a osmotic gradient

15、 between the plasma and cerebrospinal fluid, allowing brain tissue regions to dehydrate,Intracranial pressure reduction.11 mannitol: mannitol is the most promising and most widely used osmotic dehydrating agent at home and abroad, and its mechanism is to reduce the water content of brain tissue by o

16、smotic dehydration. In the previous dose, usually with 1g/Kg, and now both animal experiments and clinical studies have demonstrated that low dose (half) the curative effect of mannitol and application of high doses of the same side effects caused by the latter to reduce kidney damage etc. In repeat

17、ed administration, the water content of the brain decreased with a single mannitol, but the water content of the brain increased by 3% after 5 doses. This is probably due to the destruction of the blood-brain barrier lesion, mannitol into the lesion area of the brain, and with the increase of the nu

18、mber of applications in which the accumulation of mannitol concentration lesions in brain tissue is higher than in blood concentration, resulting in the formation of reverse osmosis pressure gradient without dehydration. Therefore, it is inappropriate to use mannitol for several days in the past. In

19、 reducing intracranial pressure (ICP) of the mechanism, in addition to osmotic dehydration effect, mannitol also increases in cerebral blood flow, blood dilution and blood viscosity decreased by temporary blood volume increased, improve erythrocyte deformability, promote tissue oxygen transport to c

20、erebral vascular albumin, reflex contraction, intracranial volume reduction ICP, drop.12 albumin: the effect of high-dose (1 to 2g/kg) albumin in the treatment of acute TBI has been affirmed, and its neuroprotective mechanism may be: (1) dilation. (2) reduce brain edema and brain swelling. (3) scave

21、nging free radicals. (4) binding action. (5) inhibiting platelet aggregation. Albumin is a component of colloid osmotic pressure in plasma. Early (within 30 minutes after ischemia) can alleviate cerebral edema and infarct volume, and by combining with metal ions in the blood to prevent the latter ca

22、talytic effect on lipid peroxidation, while the long-term application form the high colloid osmotic mechanism of pressure in the treatment of ischemic brain edema may be through large molecules of blood brain barrier damaged and alleviating vasogenic brain edema cleared.13 hypertonic saline:In recen

23、t years, great progress has been made in the study of sodium salt balance after traumatic brain injury. It is believed that brain injury should be added instead of sodium sodium restriction, and that the administration of hypertonic saline in the early period of severe brain injury (HS) plays an imp

24、ortant role in cerebral perfusion blood volume, pressure recovery and reduce the secondary damage of brain. Traumatic brain injury is the most common cause of early death in trauma patients, and mortality in patients with severe hemorrhagic shock is over 50%. Rapid recovery of effective circulating

25、blood volume and organ blood flow is required for these patients, while iatrogenic brain edema and intracranial hypertension are avoided. Hypertonic saline by increasing serum sodium and serum osmotic pressure, osmotic pressure gradient will produce intracellular and interstitial water transfer to c

26、erebral blood vessels, to alleviate brain edema and reduce the effect of ICP; at the same time, reduce the damage of vascular endothelial cells by local edema, reduce vascular resistance, so as to effectively improve the cardiac output and blood brain flow. Vialetet and other studies have found that

27、 7.5% of saline is more effective than 20% mannitol in the treatment of refractory intracranial hypertension in patients with traumatic brain injury. The basic and clinical research results show that hypertonic saline treatment with or without brain injury have significant effect of shock, there is

28、a clear reduction of brain edema and reduce the role of ICP, even of mannitol in the treatment of intracranial hypertension invalid also has obvious curative effect.1 the basis of timely sodium supplementation after craniocerebral traumaAfter traumatic brain injury, because of stress lead to anterio

29、r pituitary corticotropin releasing hormone increase, have certain effects on sodium excretion, but generally only sub clinical symptoms, only to be found in the blood sodium and urine sodium examination of patients. Mainly concentrated in the heavy and severe type of patients. May be due to the ren

30、in angiotensin aldosterone system - vasopressin and atrial natriuretic natriuretic factor (ANP) and brain natriuretic titanium titanium EDLS (BNP EDLS) system regulating the relationship between the damage caused by normal. In addition,After brain trauma, the use of a large number of water removal a

31、gent will lead to low sodium. In the past, sodium supplementation has been associated with increased brain edema due to elevated intracranial hydrostatic pressure. In recent years, many studies have shown that ischemia and hypoxia are the major causes of death and disability in severe traumatic brai

32、n injury. The key to treatment is to restore blood volume and cerebral perfusion pressure as soon as possible. Kelly think that the hypertonic saline decreased ICP and increased blood pressure, which can effectively restore blood volume as soon as possible to traumatic brain injury associated with h

33、emorrhagic shock, thus greatly reduce the fatality rate and disability rate, and that the treatment of craniocerebral trauma first step should be to restore the blood pressure and cerebral perfusion pressure (CPP), as long as the CPP70mmHg. Can add sodium salt. In addition, hypotonic conditions also

34、 exacerbate brain edema. This shows that most of the patients with craniocerebral trauma have hyponatremia, especially in severe cases. The application of sodium salt plays an important role in the recovery of effective blood volume, increasing cerebral perfusion pressure and decreasing ICP. At pres

35、ent, most scholars agree with this point of view, namely in the treatment of traumatic brain injury and the use of dehydrating agents should not emphasize the amount of sodium restriction, and should be added to ensure the electrolyte, blood pressure and cerebral perfusion pressure in the normal ran

36、ge, to prevent secondary brain injury in cerebral ischemia and hypoxia.The effect and mechanism of 2 hypertonic sodium saltOver the past 20 years, isotonic electrolytes have been used instead of hypotonic electrolytes when sodium salt is added to brain trauma patients. Zornow et al found that hypoto

37、nic saline could increase brain edema or increase ICP, and think isotonic saline was the most appropriate. In recent years, research has tended to use hypertonic saline in the treatment of traumatic brain injury accompanied with hemorrhagic shock. The effect of hypertonic saline can be summarized as

38、 follows: (1) reduce intracranial pressure. Horn et al found that hypertonic saline showed a significant decrease in ICP, elevated CPP, and less prone to rebound in patients who had no mannitol. Its mechanism of reducing ICP is similar to that of mannitol. (2) expansion. Severe traumatic brain injur

39、y often involves shock, which is caused by excessive blood loss or cardiovascular disorder caused by severe traumatic brain injury. This kind of patient may cause increased mortality due to cerebral ischemia and hypoxia. Therefore, it is very important to expand and restore blood pressure in time. H

40、ypertonic saline can increase hypertension by absorption of interstitial fluid and the release of ANP, increasing cardiac output. The microcirculation of the brain can be improved by shrinking the swollen microvascular endothelial cells, inhibiting the release of angiotensin and inhibiting the adhes

41、ion of leukocytes to the endothelium. (3) reduce secondary brain damage. After brain trauma, the increase of catecholamine and steroid hormone results in higher WBC count. Neutrophils can cross the blood-brain barrier damage, accumulate in the trauma area, the release of peroxidase and protein hydro

42、lase mediated cell death, the release of class four arachidonic acid like substances can aggravate vascular spasm, further aggravate brain damage. (4) improving the chemical environment of the brain. Excitatory amino acids increased after brain injury, local ischemia leads to reduced ATP caused decr

43、ease of Na+-K+-ATP enzyme on the cell membrane activity, the Na+ concentration of extracellular glutamate decreased, then Na+/ active transport function decreased, resulting in extracellular glutamate accumulation. In addition, the aggregation of glutamate will cause depolarization of the surroundin

44、g cells and form positive feedback, leading to apoptosis of the surrounding cells.Side effects of hypertonic saline(1) demyelination damage (ODS): pons is sensitive to hypertonic state, and ODS may occur when treated with HS. ODS is generally more common in the animal model of traumatic brain injury

45、 or the clinical treatment of chronic diseases of sodium, or sub acute hyponatremia fill sodium process, but as long as the daily blood sodium increase no more than 10 20mmol/L can be avoided. In the clinical use of HS to control ICP, attention was paid to the rate of sodium infusion without ODS rep

46、orted.(2) acute renal failure recovery: application of HS in burn patients when Huang found the damage to renal function compared with Ringer solution increased significantly.However, other animal experiments and clinical trials have not been reported.(3) coagulopathy: the expansion of HS may lead t

47、o hemodilution and coagulopathy, but there is no relationship between the two animals in the large number of animal experiments and clinical trials.(4) hemolysis: hypertonic saline may cause red blood cells to contract and cause hemolysis.(5) rebound of ICP: it is reported that rebound of ICP may oc

48、cur during the treatment of intracranial hypertension with HS, especially after rapid infusion or cessation of continuous intravenous infusion.(6) disorders of electrolytes and acid-base balance: the use of HS may lead to hypernatremia, hyperkalemia, and hyperkalemia.To sum up, the balance of water

49、and sodium should be kept in the treatment of traumatic brain injury, and the unified and limited water restriction and sodium restriction should not be adopted. Different treatment measures should be adopted according to different situations. For severe traumatic brain injury accompanied by hypoten

50、sion or even shock, hypertonic saline can be used to expand blood volume, reduce secondary brain damage, and reduce brain edema. Qureshi 24 believes that if it is in clinical in craniocerebral trauma combined with hemorrhagic shock with 7.5%HS250ml intravenous rapid infusion for intracranial hyperte

51、nsion and cerebral hernia; can rapid injection of 24.3%HS30 60ml to reduce intracranial pressure; in surgery can be topical application of 3%HS. The concentration of HS used in clinical trials ranged from 1.8% to 24.3%, and there was no agreement between the methods of rapid infusion and continuous

52、infusion. Therefore, the clinical indications and dosage, dosage forms and the time period of action should be studied further. The application of small dose of 7.2% sodium chloride can quickly keep the stability of the cardiovascular system, and in the ischemic brain edema, for treatment of stroke

53、caused by cerebral trauma and hemorrhage significantly, can significantly reduce the water content of brain tissue (especially around the injury). However, further research is needed to determine the optimal time for action.Osmotic pressure of common liquidsLiquid name osmotic pressure (mOsm/L)0.9%

54、physiological saline 3080.45% salt water 1545% glucose saline 406Sodium lactate Ringers solution 27320% mannitol 10985% albumin 290Plasma 2952 hormone therapy: a large dose of hormone is the main role in promoting the stability of its structure, various membrane membrane, thereby inhibiting lipid pe

55、roxidation, stable ion channels and increase the local blood flow and so on. Its function is summed up as following three points (1), because of the anti-inflammatory effect of hormone, can strengthen cell and cell membrane. (2) to prevent the invasion of the diseased vessel wall and the cell membra

56、ne; (3) to defend against the blood-brain barrier and to repair it. Dosage: the first choice is dexamethasone, because of its strongest anti-inflammatory effect. The first dose of 12mg, then every 6 hours 4mg, a week after the gradual withdrawal of drugs, children 0.5-1mg/kg every time, 3-6 times a

57、day. The side effects and precautions: 1, gastrointestinal bleeding, ulcer formation, so the conventional application of anti acid treatment; 2, should pay attention to maintenance medication time, maintain hormone content of brain wound, must be repeated administration, gradually reduced after discontinuation; 3, due to hormones inhibit fibroblast gro