亚低温对重型脑损伤后血清IL-18含量的影响

目的 观察重型创伤性脑损伤(TBI)患者血清白细胞介素18(IL-18)的含量变化.方法 60例患者随机分成常温治疗组和亚低温治疗组,两组均于伤后第1 d、3 d、7 d 和10d 采用酶联免疫吸附(ELISA)法测定血清中IL-18 含量.结果 两组IL-18 含量均高于对照组(P ＜ 0.01).亚低温治疗组IL-18 含量在3d、7 d、10d 低于常温治疗组(P ＜0.01),而在伤后第1 d 差异无统计学意义(P ＞0.05).结论 亚低温治疗能够降低sTBI 患者血清IL-18 含量.     

Mild hypothermia therapy for patients with severe brain injury

The authors present a group of patients with severe head injuries in which deliberate mild hypothermia was carried out together with the standard treatment protocol according to the European Brain Injury Consortium. Thirty patients with severe head injuries with Glasgow Coma Scale (GCS) score of 3–8 were enrolled into the study. The subjects were divided into two groups. The average age in the hypothermic group of 15 patients was 35 years. The average GCS was 4.5 at the site of accident. Eight patients (53%) sustained associated severe injuries of other organs. The average age of the 15 patients in the normothermic control group was 39 years with an average GCS of 4.3. All the patients in the normothermic group and 11 patients in the hypothermic group underwent neurosurgery, five of them also decompressive craniotomy. Artificial ventilation with continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), arterial blood pressure, jugular bulb oximetry and urinary bladder temperature were instituted in the ICU. Cooling to a core temperature of 34 °C in the hypothermic group was achieved by forced air cooling in combination with circulating-water mattress cooling (Blanketrol II, Cincinnati Sub-Zero) and maintained for 72 h. The difference in the Glasgow Outcome Scale (GOS) between the hypothermic and normothermic groups of patients after 6 months was not statistically significant (P value 0.0843). In the hypothermic group, however, good neurological outcome (GOS 4 and 5) was reached in 13 patients (87%), which represents a 40% increase compared with the normothermic control group in which good neurological outcome was reached in 7 patients (47%). Mean normothermia ICP value of 18±2 mmHg was significantly (P value 0.0007) reduced during mild hypothermia therapy to 12±2 mmHg. Mean normothermia CPP value of 72±3 mmHg significantly increased (P value 0.0007) during this time to 80±4 mmHg with unchanged systolic arterial pressure (P value 0.9013). There were no cardiac or coagulopathy-related complications. Our results showed that mild therapeutic hypothermia could be useful in improving the outcome and neurological recovery in patients with severe head injuries.     

Induced Normothermia Attenuates Intracranial Hypertension and Reduces Fever Burden after Severe Traumatic Brain Injury

Introduction

Hyperthermia following a severe traumatic brain injury (TBI) is common, potentiates secondary injury, and worsens neurological outcome. Conventional fever treatment is often ineffective. An induced normothermia protocol, utilizing intravascular cooling, was used to assess the impact on fever incidence and intracranial pressure (ICP) in patients with severe TBI.

Methods

A comparative cohort study of 21 adult patients with severe TBI (GCS ≤ 8) treated with induced normothermia [36–36.5°C rectal probe setting; intravascular cooling catheter (CoolLine^®, Alsius Corporation, Irvine, CA)] were matched by age, gender, and severity of injury to 21 historical control severe TBI patients treated with conventional fever control methods. ICP was measured via an external ventricular catheter and time duration for ICP > 25 mmHg was calculated for the initial 72-h monitoring period. Non-parametric rank tests were performed.

Results

Mean (±SD) or median [range] demographics did not differ between groups [total N = 42 (6 female, 36 male, age 36.4 ± 14.8 years and initial GCS 7 [3–8], median and range]. Fever burden in the first 3 days (time >38°C) in the induced normothermia versus control group was significantly less at 1.6% versus 10.6%, respectively (P = 0.03). Mean ICP for patients with induced normothermia versus control was 12.74 ± 4.0 and 16.37 ± 6.9 mmHg, respectively. Furthermore, percentage of time with ICP > 25 mmHg was significantly less in the induced normothermia group (P = 0.03).

Conclusion

Induced normothermia (fever prophylaxis via intravascular cooling catheter) is effective in reducing fever burden and may offer a means to attenuate secondary injury, as evidenced by a reduction in the intracranial hypertension burden.     

Immunomorphological sequelae of severe brain injury induced by fluid-percussion in juvenile pigs--effects of mild hypothermia

Severe traumatic brain injury (TBI) often leads to a bad outcome with considerable neurological deficits. Secondary brain injuries due to a rise of intracranial pressure (ICP) and global hypoxia-ischemia are critical and may be reduced in extent by mild hypothermia. A porcine animal model was used to study the effect of severe TBI, induced by fluid percussion (FP; 3.5+/-0.3 atm) in combination with a secondary insult, i.e., temporary blood loss with hypovolemic hypotension. Six-week-old juvenile pigs were subjected to this kind of severe TBI; one group was then submitted to moderate hypothermia at 32 degrees C for 6 h, starting 1 h after brain injury. Animals were killed after 24 h. TBI and hypothermia-associated alterations in the brains were investigated by immunohistochemistry with antibodies against microtubule-associated protein 2 (MAP-2) and beta-amyloid precursor protein (betaAPP). In addition, DNA fragmentation was investigated by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) method. Seven of the 13 normothermic TBI animals developed a secondary increase in ICP (TBI-NT-ICP) after an interval of several hours. None of the animals in the hypothermic trauma (TBI-HT) group exhibited a secondary ICP increase, indicating a protective effect of the treatment. TBI-HT animals showed significantly higher levels of MAP-2 immunoreactivity, lower levels of betaAPP immunoreactivity and less DNA fragmentation than the TBI-NT-ICP animals. Differences between the TBI-HT group and normothermic animals without an ICP increase (TBI-NT) were less marked. A considerable decrease in MAP-2 outside the site of TBI-FP administration was seen only in the TBI-NT-ICP animals. MAP-2 immunohistochemistry was thus a reliable marker of diffuse brain damage. Axonal injury was present in all TBI groups, indicating its special significance in neurotrauma. Thus, severe TBI caused by FP, combined with temporary blood loss, consistently produced traumatic axonal injury and focal brain damage. Mild hypothermia was able to prevent a secondary increase in ICP and its sequelae of diffuse hypoxic-ischemic brain injury. However, hypothermia did not afford protection from traumatic axonal injury.     

Relationship between brain temperature, brain chemistry and oxygen delivery after severe human head injury: the effect of mild hypothermia

We studied brain temperature and the effect of mild hypothermia in 58 patients after severe head injury (SHI). Brain tissue oxygen tension (ptiO2), carbon dioxide tension (ptiCO2), tissuie pH (pHti) and temperature (T.br) were measured using a multiparameter probe. Microdialysis was performed to measure glucose, lactate, glutamate, and aspartate in the extracellular fluid. Mild hypothermia (34 degrees-36 degrees C) was employed in 33 selected patients who had persistent increased intracranial pressure (ICP > 20 mmHg). Mild induced hypothermia decreased brain oxygen significantly from 33 +/- 24 mmHg to 30 +/- 22 mmHg (p < 0.05). The ptiCO2 (46 +/- 8 mmHg) was also significantly lower during mild hypothermia (40.4 +/- 4.0 mmHg), p < 0.0001). The pHti increased from 7.13 +/- 0.15 to 7.24 +/- 0.10 (p < 0.0001) under hypothermic conditions. Induced hypothermia may protect patients from secondary ischemic events by lowering the critical ptiO2 threshold, reducing anaerobic metabolism, and decreasing the release of excitatory aminoacids. However, patients with spontaneous brain hypothermia on admission (Tbr < 36.0 degrees C) showed significantly higher levels of glutamate as well as lactate, compared to all other patients, and had a worse outcome. Spontaneous brain hypothermia carries a poor prognosis, and was characterized by markedly abnormal brain metabolic indices.     

颅内压监测在重型颅脑损伤中的应用

目的探讨颅内压(ICP)监测在重型颅脑损伤中的作用及意义。方法应用颅内压监护仪对42例重型颅脑损伤患者进行颅内压监测,对颅内压的变化与临床特征进行比较分析。结果 ICP 5~15 mmHg 5例,16~20 mmHg 14例,21~40 mmHg 17例,40 mmHg 6例。ICP初值与患者病死率有关,且呈负相关,差异具有统计学意义。结论重型颅脑损伤患者进行ICP监测对及早判断病情、治疗方面有重要价值。     

重型颅脑损伤患者亚低温治疗的临床研究

目的 通过比较重型颅脑损伤患者亚低温治疗组与常温治疗组的预后来证实亚低温治疗的脑保护作用. 方法 选取重型颅脑损伤患者76例(GCS≤8分),分为亚低温治疗组(36例)和常温治疗组(40例).常温治疗组患者应用脱水降颅压、营养神经、止血、抑制胃酸分泌、营养支持等常规治疗.亚低温治疗组患者除常规治疗外,合并应用冰毯实行亚低温治疗(患者躺在冰毯垫上,通过体表散热使中心体温和脑温降至所需温度,通常为32～34℃,并根据病情需要维持3～14 d).结果亚低温治疗组患者预后优于常温组,差异有统计学意义(P<0.05). 结论 亚低温治疗对重型颅脑损伤患者具有脑保护作用,能提高临床疗效,值得推广应用.     

ICU重型颅脑损伤患者行血管内控制性降温治疗的疗效分析

目的探讨血管内降温治疗对重型颅脑损伤患者意识水平、脑氧代谢和颅内压（ICP）的影响。 方法选取2015年4月至2017年4月郑州大学附属郑州中心医院重症医学科收治的重型颅脑损伤术后患者100例,按照随机数字表法分为对照组和观察组,每组50例。对照组给予常规标准化治疗,观察组给予血管内降温治疗。观察并比较2组患者治疗前、治疗3 d后意识水平、ICP、脑氧代谢变化。 结果2组患者治疗后的意识水平、ICP、脑氧代谢等指标水平均较同组治疗前均显著提高,差异有统计学意义（P<0.05）,且治疗后观察组水平均显著高于对照组,差异有统计学意义（P<0.05）。 结论血管内降温治疗能明显改善重型颅脑损伤患者的意识水平,提高脑氧代谢水平,同时降低ICP,具有重要的临床实践价值。     

镇静镇痛对重型颅脑损伤患者术后颅内压的影响分析

目的探讨镇静镇痛对重型、特重型颅脑损伤（TBI）患者术后颅内压（ICP）的影响。 方法选取湖州市第一人民医院神经外科自2016年1月至2018年6月收治的重型TBI患者45例,根据GCS评分将患者分为重型TBI组（GCS评分6~8分,26例）与特重型TBI组（GCS评分3~5分,19例）,观察2组镇静镇痛下及撤除镇静镇痛/唤醒下ICP值波动情况。 结果特重型TBI患者在镇静镇痛前后ICP差异无统计学意义（P>0.05）,重型TBI患者撤除镇静镇痛/唤醒后,ICP前后变化差异有统计学意义（P<0.05）。 结论镇痛镇静与重型TBI开颅术后颅内压力波动有显著相关性,使用镇静镇痛可获得安全、平稳的ICP。     

Therapeutic Hypothermia for Traumatic Brain Injury

Experimental evidence demonstrates that therapeutic temperature modulation with the use of mild induced hypothermia (MIH, defined as the maintenance of body temperature at 32-35?°C) exerts significant neuroprotection and attenuates secondary cerebral insults after traumatic brain injury (TBI). In adult TBI patients, MIH has been used during the acute "early" phase as prophylactic neuroprotectant and in the sub-acute "late" phase to control brain edema. When used to control brain edema, MIH is effective in reducing elevated intracranial pressure (ICP), and is a valid therapy of refractory intracranial hypertension in TBI patients. Based on the available evidence, we recommend: applying standardized algorithms for the management of induced cooling; paying attention to limit potential side effects (shivering, infections, electrolyte disorders, arrhythmias, reduced cardiac output); and using controlled, slow (0.1-0.2?°C/h) rewarming, to avoid rebound ICP. The optimal temperature target should be titrated to maintain ICP <20?mmHg and to avoid temperatures <35?°C. The duration of cooling should be individualized until the resolution of brain edema, and may be longer than 48?h. Patients with refractory elevated ICP following focal TBI (e.g. hemorrhagic contusions) may respond better to MIH than those with diffuse injury. Randomized controlled trials are underway to evaluate the impact of MIH on neurological outcome in adult TBI patients with elevated ICP. The use of MIH as prophylactic neuroprotectant in the early phase of adult TBI is not supported by clinical evidence and is not recommended.     

Early decompressive craniotomy in children with severe traumatic brain injury

Introduction Decompressive craniectomy remains a controversial procedure in the treatment of raised intracranial pressure (ICP) associated with post-traumatic brain swelling. Although there are a number of studies in adults published in the literature on this topic, most commonly as a salvage procedure in the treatment of refractory raised ICP, there are few that investigate it primarily in children with head injuries.Aim Our aim was to report the experience with decompressive craniotomy in children with severe traumatic brain injury (TBI) at the Red Cross Children's' hospital.Methods This study reports five patients in whom decompressive craniectomy or craniotomy with duraplasty was used as an early, aggressive treatment of raised ICP causing secondary acute neurological deterioration after head injury. The rationale was to save the patient from acute cerebral herniation and to prevent exposure to a prolonged course of intracranial hypertension.Results All patients benefited from the procedure, demonstrating control of ICP, radiological improvement and neurological recovery. Long-term follow-up was available, with outcome assessed at a minimum of 14 months after injury.Discussion The early approach to the use of decompressive craniotomy in the treatment of severe traumatic brain injury (TBI) with secondary deterioration due to raised ICP is emphasised. A favourable outcome was achieved in all of the cases presented. The potential benefit of decompressive craniectomy/craniotomy in the management of children with severe TBI is discussed.     

低频rTMS对创伤性颅脑损伤患者颅内压影响的实验研究

目的探讨低频重复经颅磁刺激(rTMS)对创伤性颅脑损伤(TBI)患者颅内压(ICP)的影响。方法32例急性中重型TBI患者分为非手术组及手术组,再分别将其随机分为常规治疗组(A组)及低频rTMS治疗组(B组)。采用无创颅内压检测分析仪测定患者的IcP。结果非手术组中B组患者的IcP均低于A组(P0.05);手术组中,B组患者的IcP在第1天与A组相比差异无统计学意义(p0.05),但有下降趋势,在第3天、第7天、第9天均低于A组(P0.05)。结论低频rTMS可以降低TBI后患者的ICP,从而起到脑保护作用。     

Noninvasive study of critical thresholds of Intracranial pressure and cerebral perfusion pressure for cerebral circulation and brain function

To ascertain the critical thresholds of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) for cerebral circulation and brain function, the extra- and intracranial haemodynamics and electrical brain responses were evaluated noninvasively with Doppler ultrasonography and multimodality evoked potentials (MEP’s) in 50 patients with severe head injury. Both extra- and intracranial blood flow velocities changed monotonically depending on the changes in ICP and CPP. They were decreased when ICP increased to 20-30 mmHg and when CPP decreased to 40-50 mmHg. The changes in elasticity index of the pulse wave of the common carotid artery was proportional to those of blood flow velocities. The frequency and degree of abnormalities of MEP’s were proportionally increased with the rise of ICP and reduction of CPP. When ICP increased to higher than 31 mmHg, MEP’s were classified as moderately or severely abnormal in more than 76% of the recordings. These results indicate that noninvasive study by use of Doppler ultrasonography and MEP’s can provide valuable information on critical brain ischaemia and brain dysfunction in patients with acute intracranial hypertension.     

Chronic histopathological consequences of fluid-percussion brain injury in rats: effects of post-traumatic hypothermia

Early outcome measures of experimental traumatic brain injury (TBI) are useful for characterizing the traumatic severity as well as for clarifying the pathomechanisms underlying patterns of neuronal vulnerability. However, it is increasingly apparent that acute outcome measures may not always be accurate predictors of chronic outcome, particularly when assessing the efficacy of potential therapeutic regimens. This study examined the chronic histopathological outcome in rats 8 weeks following fluid-percussive TBI coupled with moderate post-traumatic brain hypothermia, a protocol that provides acute neuronal protection. Animals received a moderate parasagittal percussive head injury (2.01–2.38 atm) or sham procedure followed immediately by 3 h of brain hypothermia (30°C) or normothermia (37°C). Eight weeks following TBI, serial tissue sections were stained with hematoxylin and eosin or immunostained for glial fibrillary acidic protein. Tissue damage, gliosis and immunoreactive astrocytes were observed in the ipsilateral thalamus, hippocampus, and in the neocortex lateral to the injury site. Within the thalamus, focal necrosis was restricted to selective thalamic nuclei. Significant hippocampal cell loss was found in the ipsilateral dentate hilar region of both TBI groups. Quantitative volume measurements revealed significant decreases in cortical, thalamic and hippocampal volume ipsilateral to the impact in both TBI groups. Lateral ventricles were substantially enlarged in the TBI-normothermia group, an effect which was significantly attenuated by post-TBI hypothermia. The attenuation of lateral ventricular dilation by post-traumatic hypothermia is indicative of chronic neuroprotection in this TBI model. These data provide new information concerning the chronic histopathological consequence of experimental TBI and the relevance of this trauma model to chronic human head injury. Received: 10 May 1996 / Revised: 8 August 1996 / Revised, accepted: 11 September 1996     

亚低温治疗重型颅脑损伤患者的血清S-100B蛋白含量分析

目的 通过检测亚低温治疗后重型颅脑损伤患者血清S-100B蛋白含量的变化来证实亚低温治疗的脑保护作用,探讨其可能的作用机制.方法 选取100例正常体检者为对照组,选取100例重型颅脑损伤患者(GCS≤8分1并分为亚低温治疗组50例和常温治疗组50例,分别于伤后早期(2～6 h)及伤后不同时间(1 d、3 d、5 d、7 d、10 d)采血,检测血清中S-100B蛋白含量,比较其在伤后不同时期的血清S-100B蛋白含量.结果 正常体检者血清S-100B蛋白含量测定结果证实,正常人血清S-100B蛋白含量与年龄、性别无关.亚低温治疗组、常温治疗组患者伤后血清S-100B蛋白含量与对照组相比差异有统计学意义(P<0.01).伤后1 d、3 d、5 d、7 d、10 d时亚低温治疗组血清S-100B含量明显低于常温治疗组,差异有统计学意义(P(0.05).结论 血清S-100B蛋白在重型颅脑损伤的诊断巾有高度敏感性和特异性,是一种有效的生化指标.亚低温治疗对重型颅脑损伤具有脑保护作用.     

Influence of moderate hypothermia on cerebral oxygenation in pigs with intracranial hypertension

BACKGROUND: Moderate hypothermia is one of the effective therapeutic methods for head injury in recent years, there are many mechanisms of moderate hypothermia for brain protection, and its influence on cerebral oxygenation is also one of them. OBJECTIVE: To observe the influence of moderate hypothermia on cerebral oxygenation of animals with acute intracranial hypertension, and further investigate the protective mechanism of moderate hypothermia. DESIGN: A randomized controlled trial. SETTING: Department of Neurosurgery, Renji Hospital affiliated to the Medical College of Shanghai Jiao Tong University. MATERIALS: Twenty healthy little pigs, either male or female, weighing 4.5–5.5 kg, were used. Neurotrend-typed multiparameter monitoring system (Diametrics Company, British); CMA/100 micro-injection pump (Carnegie Company, Sweden). METHODS: The experiment was conducted in the Changzheng Hospital affiliated to the Second Military Medical University of Chinese PLA in November, 2001. The pigs were randomized into two groups: the normothermia group (control group, n =10) and moderate hypothermia group (n =10). ① Bilateral femoral arteries were separated, one was connected to pressometer for monitoring mean arterial pressure (MEP), and the other for analysis of blood gases [including peripheral blood pH value, arterial partial pressure of carbon dioxide (PaCO2), arterial partial pressure of carbon dioxide (PaCO2), HCO3–]. ② Rectal temperature was monitored with mercurial thermometer. ③ Intracranial pressure was monitored using Camino optic ICP probe placed in the subdural space. ④ Neurotrend multiparameter monitoring sensor was inserted into the white matter for about 4 cm to determine cerebral perfusion pressure (CPP, CPP=MAP(ICP), brain tissue partial oxygen pressure (PO2), partial pressure of carbon dioxide (PCO2), HCO3– and brain temperature. The rectal temperature of animals in the moderate hypothermia group was lowered to 34 ℃ using ice bags, and the body temperature was maintained at 33–35 ℃ for 2 hours. The changes of the parameters were observed continuously, and the pigs in the normothermia group were not treated with cooling. MAIN OUTCOME MEASURES: ① MAP, ICP, rectal temperature, CCP; Indexes of cerebral oxygenation detected with Neurotrend-typed multiparameter monitoring system; ② Results of blood gases analysis in the moderate hypothermia group. RESULTS: All the 20 pigs were involved in the analysis of results. ① MAP, ICP, rectal temperature, CCP and indexes of cerebral oxygenation: In the moderate hypothermia group, the ICP after cooling was obviously lower than that before cooling [(3.31±1.19), (5.33±0.95) kPa, P < 0.05], CCP was higher, brain tissue PCO2 [(12.03±1.73), (10.59±2.01) kPa, P < 0.05], and brain tissue pH value was higher [(7.03±1.63), (9.40±1.30) kPa, P < 0.05], whereas the brain temperature was decreased as compared with that before cooling [(34.9±0.3), (37.2±0.2) ℃, P < 0.05]. ② Results of blood gases analysis in the moderate hypothermia group: There were no significant differences in the parameters of peripheral arterial blood gases analysis before and after cooling in the moderate hypothermia group (P > 0.05) CONCLUSION: Moderate hypothermia will not impair the cerebral oxygenation, and it can reduce brain tissue CO2 and decrease brain tissue acidosis.     

CT测量视神经鞘直径与急性颅脑创伤开颅术后颅内压的相关研究

目的探讨急性重型颅脑创伤患者开颅术后视神经鞘直径(ONSD)与颅内压(ICP)的相互关系,评价ONSD推测ICP变化情况的效能。方法回顾性分析48例急性重型颅脑创伤患者数据,通过重建头部薄层CT来测量球后ONSD,采用有创ICP传感器监测颅内压等临床数据;患者数据按手术类型分类为开颅手术组和单纯ICP组,分别应用线性及Logistic回归分析ONSD与ICP相关性及ONSD的评价效能。结果 48例患者平均ONSD=6.6mm(SD 0.5 4),平均ICP=12mmHg(SD6.5),ONSD与ICP呈明显线性相关性,其中手术组的线性关系更加明显,AUC=0.964,cutoff=7.1 mm,敏感性=100%,特异性=8 9%,P0.0 0 1,ONSD用于推测ICP效能较高,有统计学意义;而ICP组两者间无明显线性相关性。结论急性重症颅脑创伤开颅术后患者ONSD与ICP线性关系明显,可通过ONSD是否大于7.1 mm来推测ICP20 mm Hg,为危急重症患者提供重要的参考意见。     

局灶性脑低温处理对大鼠创伤性脑损伤模型的保护作用

目的探讨局灶性低温处理对SD大鼠创伤性脑损伤（TBI）模型的保护作用并探讨其相关机制。 方法将15只雄性SD大鼠随机平均分成假手术组（sham）,非冷却组（non-cooling）和冷却组（cooling）。Non-cooling组和cooling组制作TBI模型,3组实验同步进行,创伤后低温处理3 h,复温3 h,过程中检测大鼠血气、皮层脑电。复温结束处死大鼠后,对脑组织进行TTC和HE染色以评价脑死亡和脑水肿情况,Western blot检测相关机制蛋白表达情况。 结果Sham组和non-cooling组受外部刺激脑组织代谢升高,cooling组较其他组脑组织代谢低,TTC和HE染色显示cooling组脑死亡的面积和细胞死亡数量均少于non-cooling组,差异均具有统计学意义（P<0.05）。大鼠TBI后局灶性低温处理能显著降低大脑皮层的癫痫样棘波,在回温时这种不完全抑制持续存在,且低温处理降低了GABA_B1R蛋白的表达,差异均具有统计学意义（P<0.05）。Cooling组的脑水肿情况较non-cooling组轻,且cooling组AQP4蛋白表达降低,差异均具有统计学意义（P<0.05）。 结论局灶性低温处理对TBI大鼠具有保护作用,能显著减轻TBI引起的脑水肿,抑制大脑皮层的癫痫样棘波,具体机制可能分别与GABA_B1R和AQP4相关。为临床治疗TBI提供了一种更加安全、简单有效的方法。     

去骨瓣减压治疗重型颅脑损伤术中ICP的动态变化

目的探讨去骨瓣减压术(DC)治疗重型颅脑损伤中颅内压(ICP)的动态变化,分析减压前ICP与预后的相关性。方法回顾性分析35例重型颅脑损伤病人的临床资料,给予ICP探头植入后再行DC治疗。测定减压术前、去除骨瓣后、硬脑膜切开后、硬脑膜减张缝合后和关颅后的ICP,并于术后持续监测。出院时和伤后6个月以格拉斯哥预后评分(GOS)评估病人的预后,并分析减压术前ICP与预后的相关性。结果减压术前、骨瓣去除后、硬脑膜切开后、硬脑膜减张缝合后和关颅后的平均ICP分别为(42±12)mmHg、(26±6)mmHg、(6±3)mmHg、(8±5)mmHg和(12±7)mmHg。与减压术前相比较,骨瓣去除后和硬脑膜切开后ICP均明显下降(均P<0.001)。减压前ICP<40 mmHg组和ICP≥40 mmHg组在出院时和伤后6个月的预后良好率无显著差异(均P>0.05)。结论 DC治疗重型颅脑损伤时,硬脑膜广泛切开才能获得最大程度的ICP降低。