去骨瓣减压术治疗脑挫裂伤的临床分析

目的分析去骨瓣减压术治疗脑挫裂伤的短期及跃期疗效，并进一步分析不同大小骨窗的疗效差别.方法对100例脑挫裂伤患者进行去骨瓣减压术治疗，观察手术前后颅内压变化及头颅CT中线移位和基底池形态改变以判定减压术的短期效果：分析3月后GOS预后评分以判定减压术的艮期效果；按骨窗范围大小分为大骨瓣组和中等骨瓣组，分析两组的疗效差异。结果脑挫裂伤患者进行去骨瓣减压术后，能有效的降低颅内压在270mmH2O以下，P〈0．05；术后第1、3、7天颅内压与术前颅内压相比，均有明显下降，P〈0．05；手术后颅脑CT显示的中线移位程度与基底池形态较术前CT均有明显改善，P〈0．05。大骨瓣组第1、3天颅内压较中等骨瓣组为低．P〈0．05；但第7天颅内压两组无明显差异（P〉0.05）；患者伤后3月随访结果：恢复良好52例（52．0％）、轻残16例（16．0％）、重残12例（12．0％）、植物生存4例（4．0％）、死亡16例（16．O％），而且统计分析得出大骨瓣组预后优于中等骨瓣组，P〈0．05；大、中等骨瓣组的常见手术并发症切口脑脊液漏、外伤性癫痫、颅内感染、外伤性脑积水均无明显差异，P〉0．05。结论脑挫裂伤患者进行去骨瓣减压术能有效地降低颅内压及改善CT影像学征象，能明显降低死亡率和重残率．从而改善脑挫裂伤患者的短期及长期疗效：早期进行大骨瓣减压术的疗效优于中等骨瓣减压组．     

创伤急性硬膜下血肿不同术式效果观察

目的 分析颅脑外伤所致急性硬膜下血肿患者接受急诊实施标准开颅血肿清除加去骨瓣减压术治疗的临床效果。方法 以2021年1月1日至2021年12月31日期间在本院接受急诊治疗的颅脑外伤所致急性硬膜下血肿患者72例为研究对象，将其凭借随机数字表法进行分组。观察组患者接受标准开颅血肿清除加去骨瓣减压术治疗，对照组患者接受血肿清除骨瓣回纳术治疗。对比术后颅内压减弱情况、手术安全性以及治疗效果。结果 术后1天、3天、1周的颅内压对比，观察组均低于对照组（P<0.05）；术后并发症发生率对比，为观察组更低（P<0.05）；术后治疗效果对比，为观察组更高（P<0.05）。结论 颅脑外伤所致急性硬膜下血肿患者接受急诊实施标准开颅血肿清除加去骨瓣减压术治疗取得了明显的治疗效果，患者颅内压明显降低，术后不良反应发生率较低，患者预后更佳。     

双侧同时开颅去骨瓣减压治疗广泛额颞叶脑挫裂伤及脑疝的临床观察

重型颅颅脑损伤患者的残死率仍较高，如何降低死亡率仍是神经外科医生关注的重要课题。一侧去大骨瓣减压手术能使重型脑损伤患者死亡率显著下降，尤其适用于广泛额颞叶脑挫裂伤和急性硬膜下血肿脑疝形成的患者。但在部分病例中可出现迟发性硬膜外或脑内血肿、局部脑水肿加重和术中脑膨出等并发症。我们于2002年6月开始采用双侧同时去大骨瓣减压术治疗广泛额颞叶脑挫裂伤和急性硬膜下血肿脑疝形成的患者，明显提高了手术的效果，回顾性对照研究表明，应用双侧同时减压能够克服单侧去大骨瓣减压术易出现的一些严重并发症。现报告如下，并对有关问题加以探讨。     

双侧去骨瓣减压在重型颅脑外伤术中急性脑膨出中的作用

目的探讨单侧为主的重型颅脑外伤患者术中发生急性脑膨出时，双侧去骨瓣减压的效果。方法回顾性分析2003年10月至2011年12月期间本院收治的83例单侧为主的特重型颅脑外伤患者，所有人选病例术中均出现急性脑膨出并发症，研究单、双侧去骨瓣减压术对该类患者颅内压及预后GOS评分的影响。结果双侧去骨瓣减压组预后良好率显著高于单侧去骨瓣减压组（P〈0．05）；双侧去骨瓣减压组术后ICP显著低于单侧去骨瓣减压组术后ICP（P〈0．05）；存活的病例中双侧去骨瓣减压组比单侧去骨瓣减压组手术前后ICP平均下降幅度大。结论对以单侧为主的重型颅脑损伤，术中出现急性脑膨出时行双侧去骨瓣减压术较单侧减压更能有效降低术中急性脑膨出所致高颅压，降低死亡率。     

标准去大骨瓣减压术治疗37例急性硬膜下血肿疗效分析

目的探讨标准去大骨瓣减压术治疗急性硬膜下血肿的效果。方法选取2016-06—2017-11间在许昌市中心医院接受手术治疗的74例急性硬膜下血肿患者。根据不同手术方案分为2组,各37例。观察组采取标准去大骨瓣减压术,对照组采取骨瓣开颅术。结果术前2组患者的颅内压差异无统计学意义(P 0. 05)。术后第1、3、5天2组患者的颅内压均较术前降低,但观察组的降低幅度优于对照组,差异有统计学意义(P 0. 05)。观察组并发症发生率低于对照组,差异有统计学意义(P 0. 05)。结论标准去大骨瓣减压术治疗急性硬膜下血肿,可有效降低患者的颅内压和术后并发症发生风险,安全、可行。     

急性重度颅脑外伤伴天幕裂孔疝的手术治疗

目的比较标准外伤大骨瓣开颅血肿清除去大骨瓣减压并天幕裂孔疝复位术与常规大骨瓣开颅血肿清除去大骨瓣减压术对急性重度颅脑损伤伴天幕裂孔疝的治疗效果。方法 40例急性重度颅脑伤伴天幕裂孔疝患者(GCS≤8分)随机分为两组,每组20例。研究组采用标准外伤大骨瓣开颅血肿清除去大骨瓣减压并脑疝腹位术,对照组采用常规大骨瓣开颅血肿清除大骨瓣减压术。术后1 d、3 d、7 d对两组GCS评分、颅内压、脑水肿范围和中线结构移位等指标进行比较。结果术后3 d、7 d研究组较对照组的GCS评分、颅内压、脑水肿范围和中线结构移位等指标有显著改善(P0.01)。术后1年随访,研究组和对照组生存率分别为85%和60%,重残及死亡率分别为25%和50%,组间比较有显著差异(P0.05或P0.01)。结论标准外伤大骨瓣开颅血肿清除去大骨瓣减压并天幕裂孔疝复位术能提高患者生存率,减少死残率,是手术治疗重度颅脑外伤伴天幕裂孔疝的有效方法。     

标准外伤去大骨瓣减压术治疗急性硬膜下血肿效果分析

目的观察对急性硬膜下血肿患者实施标准外伤去大骨瓣减压术的临床应用效果。方法随机将西平县人民医院2016-06-2019-06间收治的76例急性硬膜下血肿患者分为2组,各38例。对照组实施常规骨瓣开颅术,对观察组实施标准外伤去大骨瓣减压术。结果观察组患者术后的GCS评分高于对照组,并发症发生率低于对照组,术后第1、3、5天的颅内压低于对照组,差异均有统计学意义(P<0.05)。结论对急性硬膜下血肿患者实施标准外伤去大骨瓣减压术,与常规骨瓣开颅术比较,可有效改善患者的GCS评分,并发症少,颅内压的控制更为理想。     

用自家颅骨骨瓣移植修复颅骨缺损13例报告

我院自1982年以来应用自家颅骨骨瓣移植修补外伤性颅骨缺损13例,17个部位。收到了满意临床效果,特报告如下。临床资料本组颅脑损伤特重型4例,重型9例。原因以交通肇事最多(占6/13),颅脑损伤以硬膜下血肿合并脑挫裂伤最多(占8/13)。该组患者均行钻孔探查、血肿清除、去骨瓣减压及内外减压术。其中单侧额颞骨瓣(大骨瓣)减压9例;单侧额颞骨瓣合并脑内(切除额颞叶极部)减压5例,双额颞骨瓣(大骨瓣)减压4例,双侧额颞骨瓣加脑内减压4例。     

标准大骨瓣减压术治疗急性硬膜下血肿的效果

目的探讨标准去大骨瓣减压术在急性硬膜下血肿患者中的应用效果。方法选取郑州市第一人民医院2014-09—2018-02间收治的80例急性硬膜下血肿患者,依据不同术式分为2组,各40例。对照组行常规骨瓣开颅术,观察组行标准去大骨瓣减压术。观察2组手术前后GCS评分及术后1、3、5 d颅内压及并发症情况。结果术后观察组GCS评分高于对照组,术后1、3、5 d颅内压低于对照组,差异有统计学意义(P0.05)。观察组并发症发生率低于对照组,差异有统计学意义(P0.05)。结论对急性硬膜下血肿患者采用标准去大骨瓣减压术,可改善颅内压和昏迷状况,降低并发症发生率。     

重型颅脑损伤去骨瓣减压术加颅内压监护的临床研究

目的 研究颅内压监护置入及行去骨瓣减压术在重型颅脑外伤脑肿胀患者中的应用价值。方法 回顾性收集本院在2018年1月至2021年12月期间收治的64例重型颅脑外伤脑肿胀患者为研究对象，根据采用的治疗方式划分为去骨瓣减压组（对照组）32例和颅内压监护置入联合去骨瓣减压组（观察组）32例，比较分析两组数据指标。结果 观察组患者术后GCS评分较对照组（9.42±1.31分）高，差异显著（P<0.05）；观察组术后发生消化道出血1例、肺部感染1例、肾功能损害1例和电解质紊乱1例，术后并发症发生率（12.50%）较对照组（34.38%）低，差异有统计学意义（P<0.05）；观察组患者恢复良好7例，轻度残疾13例，重度残疾8例、植物生存3例和死亡1例，预后显著优于对照组，差异有统计学意义（P<0.05）。结论 颅内压监护探头置入及去骨瓣减压术在重型颅脑外伤脑肿胀患者的治疗中临床效果良好，减少术后并发症的同时明显改善了患者预后，为此类患者的诊治提供了临床新思路。     

Long-term complications of decompressive craniectomy for head injury

There is currently much interest in the use of decompressive craniectomy for intracranial hypertension. Though technically straightforward, the procedure is not without significant complications. A retrospective analysis was undertaken of 164 patients who had had a decompressive craniectomy for severe head injury in the years 2004 to 2009 at the two major hospitals in Western Australia. Eighty-six patients had a bifrontal decompression and seventy-eight had a unilateral decompression. Two patients died due to post-operative care issues. Complications attributable to the decompressive surgery were: herniation of the cortex through the bone defect (42 patients, 25.6%), subdural effusion (81 patients, 49.4%), seizures (36 patients, 22%), hydrocephalus (23 patients, 14%), and syndrome of the trephined (2 patients, 1.2%). Complications attributable to the subsequent cranioplasty included: sudden death due to massive cerebral swelling in 3 patients (2.2%), infection requiring removal of the bone flap in 16 patients (11.6%), and bone flap resorption requiring augmentation in 10 patients (7.2%). After excluding simple complications such as subdural effusion and brain herniation through the skull defect and some patients who died as a direct consequence of traumatic brain or extracranial injury, 81 patients (55.5%) had at least one complication after decompressive craniectomy. The occurrence of at least one complication after decompressive craniectomy was significantly associated with an increased risk of prolonged stay in the hospital or rehabilitation facility (odds ratio 2.54, 95%confidence interval 1.22,5.24, p=0.013), after adjusting for predicted risk of unfavorable outcome.     

Cerebral hemodynamic changes gauged by transcranial Doppler ultrasonography in patients with posttraumatic brain swelling treated by surgical decompression

OBJECT: The use of decompressive craniectomy has experienced a revival in the previous decade, although its actual benefit on patients' neurological outcome remains the subject of debate. A better understanding of the intracranial pressure dynamics, as well as of the metabolic and hemodynamic brain processes, may be useful in assessing the effect of this surgery on the pathophysiology of the swollen brain. The aim of this study was to use transcranial Doppler (TCD) ultrasonography to examine the hemodynamic changes in the brain after decompressive craniectomy in patients with head injury, in addition to examining the relationship between such hemodynamic changes and the patient's neurological outcome. METHODS: Nineteen patients presenting with traumatic brain swelling and cerebral herniation syndrome who had undergone decompressive craniectomy with dural expansion were studied prospectively. The TCD ultrasonography measurements were performed bilaterally in both the middle cerebral artery (MCA) and in the distal portion of the cervical internal carotid artery (ICA) immediately prior to and after surgical decompression. After surgery, the mean blood flow velocity (BFV) rose to 175 +/- 209% of preoperative values in the MCA of the operated side, while rising to 132 +/- 183% in the contralateral side; the difference between the mean BFV increase in in the MCA of both the decompressed and the opposite side reached statistical significance (p < 0.05). The mean BFV of the extracranial ICA increased to 91 +/- 119% in the surgical side and 45 +/- 60% in the opposite side. Conversely, the MCA pulsatility index (PI) values decreased, on average, to 33 +/- 36% of the preoperative value in the operated side and to 30 +/- 34% on the opposite side; the MCA PI value reductions were significantly greater in the decompressed side when compared with the contralateral side (p < 0.05). The PI of the extracranial ICA reduced, on average, to 37 +/- 23% of the initial values in the operated side and to 24 +/- 34%, contralaterally. No correlation was verified between the neurological outcome and cerebral hemodynamic changes seen on TCD ultrasonography. CONCLUSIONS: Decompressive craniectomy results in a significant elevation of cerebral BFV in most patients with traumatic brain swelling and transtentorial herniation syndrome. The increase in cerebral BFV may also occur in the side opposite the decompressed hemisphere; the cerebral BFV increase is significantly greater in the operated hemisphere than contralaterally. Concomitantly, PI values decrease significantly postoperatively, mainly in the decompressed cerebral hemisphere, indicating reduction in cerebrovascular resistance.     

Decompressive craniectomy for severe intracranial hypertension due to cerebral infarction or meningoencephalitis

We describe the clinical course and outcome following decompressive craniectomy in six patients. Five patients suffered from severe intracranial hypertension due to middle cerebral artery infarction. In one patient the cause was bacterial meningoencephalitis. Acute clinical and neuroradiological signs of intracranial hypertension were seen in all cases. Following ineffective conventional brain edema therapy, decompressive craniectomy was undertaken. In five cases intracranial pressure was sufficiently lowered. One patient developed transtentorial herniation with subsequent brain death. Four patients with middle artery infarction showed moderate neurological disorders and one patient with bacterial meningoencephalitis recovered completely after treatment. Craniectomy in malignant middle artery infarction should be taken into consideration if conventional brain edema therapy does not sufficiently reduce critically raised intracranial pressure. Craniectomy provides development of brain herniation. This treatment may reduce high lethality rate and high frequency of severe neurological disorders.     

Management of severe traumatic brain injury by decompressive craniectomy

OBJECTIVE: The beneficial effect of decompressive craniectomy in the treatment of head trauma patients is controversial. The aim of our study was to assess the value of unilateral decompressive craniectomy in patients with severe traumatic brain injury. METHODS: We retrospectively investigated 49 patients who underwent decompressive craniectomy. Intracranial pressure, cerebral perfusion pressure, therapy intensity level, and cranial computed tomographic scan features (midline shift, visibility of ventricles, gyral pattern, and mesencephalic cisterns) were evaluated before and after craniectomy. The gain of intracranial space was calculated from cranial computed tomographic scans. Patient outcome was graded using the Glasgow Outcome Scale. RESULTS: Thirty-one patients (63.3%) underwent rapid surgical decompression within 4.5 +/- 3.8 hours after trauma; in 18 patients (36.7%), delayed surgical decompression was performed 56.2 +/- 57.0 hours after injury. Patients younger than 50 years or patients who underwent rapid surgical decompression had a significantly better outcome than older patients or patients who underwent delayed surgical decompression. Craniectomy significantly decreased midline shift and improved visibility of the mesencephalic cisterns. The state of the mesencephalic cisterns correlated with the distance of the lower border of the craniectomy to the temporal cranial base. Alterations in intracranial pressure, cerebral perfusion pressure, and therapy intensity level were not significant. The overall mortality of the patients corresponded to the reports of the Traumatic Coma Data Bank (1991). CONCLUSION: Although there was a significant decrease in midline shift after craniectomy, this did not translate into decompressive craniectomy demonstrating a beneficial effect on patient outcome.     

亚低温对重型颅脑损伤术后脑血管痉挛的影响

目的探讨亚低温对重型颅脑损伤（severe traumatic brain injury,sTBI）术后脑血管痉挛（cerebral vasospasm,CVS）及远期预后的影响。方法36例sTBI患者（GCS≤8分）,随机分为对照组和亚低温组,各18例。用脑循环动力检测仪检测伤后0、1、3、7、10、14、21 d的脑循环动力学参数（CV-DI）。对照组维持正常体温,亚低温组在4-8 h内将肛温降至33℃左右,维持3-5d。分析比较两组CVDI变化规律和远期预后。同期筛选出24例正常人检测其CVDI,作为正常组。结果①与正常组比较,对照组伤后CVDI可划分为4个期,即低灌注期（0 d）、高灌注期（1-3 d）、CVS期（4-14 d）、好转期（〉15 d）;而亚低温组仅表现出三个期,即低灌注期（0 d）、好转期（1-3 d）、恢复期（〉4 d）,未出现高灌注期和CVS期。②随防3个月时,对照组预后不良率为61.1%（11/18）,亚低温组为33.3%（6/18）,两组比较无显著性差异（P〉0.05）;随防3年后,对照组预后不良率为55.6%（10/18）,亚低温组为22.2%（4/18）,两组比较差异显著（P〈0.05）。结论sTBI术后要注重CVS的防治。亚低温能稳定sTBI术后脑循环功能,减少CVS发生率,从而改善远期预后。     

External decompressive craniectomy including resection of temporal muscle and fascia in malignant hemispheric infarction

Decompressive craniectomy procedures are used for malignant hemispheric infarctions. However, the temporal muscle and fascia are significant limiting factors for external herniation of an edematous brain. Therefore, the authors performed a decompressive craniectomy and expansive duraplasty combined with resection of the temporal muscle and fascia for 15 patients with a malignant hemispheric infarction. The volume of the maximum external herniation that was measured on the basis of a CT volumetry study ranged from 130 to 300 ml (mean +/- standard deviation, 200 +/- 64 ml) on postoperative Day 3.2 +/- 1.5 (range 2-5 days postoperatively). The mean value represented a 2-fold volume expansion in comparison with the conventional decompressive craniectomy, and the greater the external herniation obtained by external decompression, the smaller the midline brain shift after surgery. The mortality rate, favorable outcomes (modified Rankin Scale Scores 1-3), and unfavorable outcomes were 20, 60, and 20%, respectively, and the masticatory function was only minimally affected. Furthermore, a cranioplasty involving reconstruction of the temporal muscle defect performed using a MEDPOR implant resulted in good cosmetic outcomes with no temporal hollow. Resection of the temporal muscle in a decompressive craniectomy was shown to provide greater decompression and better clinical outcomes for malignant hemispheric infarctions at an acceptable cost of minimal masticatory dysfunction and cosmetic disfigurement.     

Incidence and risk factors for post-traumatic hydrocephalus following decompressive craniectomy for intractable intracranial hypertension and evacuation of mass lesions

There continues to be a considerable interest in decompressive craniectomy in the management of severe traumatic brain injury (TBI). Though technically straightforward, the procedure is not without significant complications. In this study we assessed the incidence and risk factors for the development of subdural hygroma and hydrocephalus after decompressive craniectomy. A total of 195 patients who had had a decompressive craniectomy for severe TBI between 2004 and 2010 at the two major trauma centers in Western Australia were considered. Of the 166 patients who survived after the acute hospital stay, 93 (56%; 95% confidence interval [CI] 48,63%) developed subdural hygroma; 45 patients (48%) had unilateral and 48 patients (52%) had bilateral subdural hygromas. Of the 159 patients who survived more than 6 months after surgery, 72 (45%; 95% CI 38,53%) developed radiological evidence of ventriculomegaly, and 26 of these 72 patients (36%; 95% CI 26,48%) developed clinical evidence of hydrocephalus and required a ventriculoperitoneal (VP) shunt. Maximum intracranial pressure prior to decompression (p=0.005), subdural hygroma (p=0.012), and a lower admission Glasgow Coma Scale score (p=0.009), were significant risk factors for hydrocephalus after decompressive craniectomy. Hydrocephalus requiring a VP shunt was associated with a higher risk of unfavorable neurological outcomes at 18 months (odds ratio 7.46; 95%CI 1.17,47.4; p=0.033), after adjusting for other factors. Our results showed a clear association between injury severity, subdural hygroma, and hydrocephalus, suggesting that damage to the cerebrospinal fluid drainage pathways contributes to the primary brain injury rather than the margin of the craniectomy as the factor responsible for these complications.     

Outcome following decompressive craniectomy for malignant swelling due to severe head injury

OBJECT: The aim of this study was to assess outcome following decompressive craniectomy for malignant brain swelling due to closed traumatic brain injury (TBI). METHODS: During a 48-month period (March 2000-March 2004), 50 of 967 consecutive patients with closed TBI experienced diffuse brain swelling and underwent decompressive craniectomy, without removal of clots or contusion, to control intracranial pressure (ICP) or to reverse dangerous brain shifts. Diffuse injury was demonstrated in 44 patients, an evacuated mass lesion in four in whom decompressive craniectomy had been performed as a separate procedure, and a nonevacuated mass lesion in two. Decompressive craniectomy was performed urgently in 10 patients before ICP monitoring; in 40 patients the procedure was performed after ICP had become unresponsive to conventional medical management as outlined in the American Association of Neurological Surgeons guidelines. Survivors were followed up for at least 3 months posttreatment to determine their Glasgow Outcome Scale (GOS) score. Decompressive craniectomy lowered ICP to less than 20 mm Hg in 85% of patients. In the 40 patients who had undergone ICP monitoring before decompression, ICP decreased from a mean of 23.9 to 14.4 mm Hg (p < 0.001). Fourteen of 50 patients died, and 16 either remained in a vegetative state (seven patients) or were severely disabled (nine patients). Twenty patients had a good outcome (GOS Score 4-5). Among 30-day survivors, good outcome occurred in 17, 67, and 67% of patients with postresuscitation Glasgow Coma Scale scores of 3 to 5, 6 to 8, and 9 to 15, respectively (p < 0.05). Outcome was unaffected by abnormal pupillary response to light, timing of decompressive craniectomy, brain shift as demonstrated on computerized tomography scanning, and patient age, possibly because of the small number of patients in each of the subsets. Complications included hydrocephalus (five patients), hemorrhagic swelling ipsilateral to the craniectomy site (eight patients), and subdural hygroma (25 patients). CONCLUSIONS. Decompressive craniectomy was associated with a better-than-expected functional outcome in patients with medically uncontrollable ICP and/or brain herniation, compared with outcomes in other control cohorts reported on in the literature.     

Decompressive craniectomy for severe traumatic brain injury: The relationship between surgical complications and the prediction of an unfavourable outcome

Object

To assess the impact that injury severity has on complications in patients who have had a decompressive craniectomy for severe traumatic brain injury (TBI).

Methods

This prospective observational cohort study included all patients who underwent a decompressive craniectomy following severe TBI at the two major trauma hospitals in Western Australia from 2004 to 2012. All complications were recorded during this period. The clinical and radiological data of the patients on initial presentation were entered into a web-based model prognostic model, the CRASH (Corticosteroid Randomization After Significant Head injury) collaborators prediction model, to obtain the predicted risk of an unfavourable outcome which was used as a measure of injury severity.

Results

Complications after decompressive craniectomy for severe TBI were common. The predicted risk of unfavourable outcome was strongly associated with the development of neurological complications such as herniation of the brain outside the skull bone defects (median predicted risk of unfavourable outcome for herniation 72% vs. 57% without herniation, p = 0.001), subdural effusion (median predicted risk of unfavourable outcome 67% with an effusion vs. 57% for those without an effusion, p = 0.03), hydrocephalus requiring ventriculo-peritoneal shunt (median predicted risk of unfavourable outcome 86% for those with hydrocephalus vs. 59% for those without hydrocephalus, p = 0.001), but not infection (p = 0.251) or resorption of bone flap (p = 0.697) and seizures (0.987). We did not observe any associations between timing of cranioplasty and risk of infection or resorption of bone flap after cranioplasty.

Conclusions

Mechanical complications after decompressive craniectomy including herniation of the brain outside the skull bone defects, subdural effusion, and hydrocephalus requiring ventriculo-peritoneal shunt were more common in patients with a more severe form of TBI when quantified by the CRASH predicted risk of unfavourable outcome. The CRASH predicted risk of unfavourable outcome represents a useful baseline characteristic of patients in observational and interventional trials involving patients with severe TBI requiring decompressive craniectomy.