Journal of Clinical Neuroscience xxx (2016) xxx–xxx
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Review
Decompressive craniectomy in neurocritical care Jia-Wei Wang, Jin-Ping Li, Ying-Lun Song, Ke Tan, Yu Wang, Tao Li, Peng Guo, Xiong Li, Yan Wang, Qi-Huang Zhao ⇑ Department of Neurosurgery, Beijing Chao-Yang Hospital, Capital Medical University, 8 South Gongti Road, Beijing 100020, PR China
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Article history: Received 5 April 2015 Accepted 20 June 2015 Available online xxxx Keywords: Decompressive craniectomy Meta-analysis Neurocritical illness Randomized controlled trial Stroke Traumatic brain injury
a b s t r a c t Recently, several randomized controlled trials (RCT) investigating the effectiveness of decompressive craniectomy in the context of neurocritical illnesses have been completed. Thus, a meta-analysis to update the current evidence regarding the effects of decompressive craniectomy is necessary. We searched PUBMED, EMBASE and the Cochrane Central Register of Controlled Trials. Other sources, including internet-based clinical trial registries and grey literature, were also searched. After searching the literature, two investigators independently performed literature screening, assessing the quality of the included trials and extracting the data. The outcome measures included the composite outcome of death or dependence and the risk of death. Ten RCT were included: seven RCT were on malignant middle cerebral artery infarction (MCAI) and three were on severe traumatic brain injury (TBI). Decompressive craniectomy significantly reduced the risk of death for patients suffering malignant MCAI (risk ratio [RR] 0.46, 95% confidence interval [CI]: 0.36–0.59, P < 0.00001) in comparison with no reduction in the risk of death for patients with severe TBI (RR: 0.83, 95% CI: 0.48–1.42, P = 0.49). However, there was no significant difference in the composite risk of death or dependence at the final follow-up between the decompressive craniectomy group and the conservative treatment group for either malignant MCAI or severe TBI. The present meta-analysis indicates that decompressive craniectomy can significantly reduce the risk of death for patients with malignant MCAI, although no evidence demonstrates that decompressive craniectomy is associated with a reduced risk of death or dependence for TBI patients. Ó 2015 Elsevier Ltd. All rights reserved.
1. Introduction As a leading cause of mortality and morbidity in the neurointensive care unit, increased intracranial pressure (ICP) has received considerable attention in clinical practice [1,2]. Various neurocritical illnesses, including malignant middle cerebral artery infarction (MCAI) and severe traumatic brain injury (TBI), lead to increased ICP and may result in cerebral herniation, death or permanent disability [3,4]. Unfortunately, although the well-known deleterious effects of increased ICP have long been recognized, medical and surgical interventions remain limited, and advances in treatment have been modest. The current options for the management of increased ICP consist of conservative treatment or surgical decompression [5,6]. Generally, conservative treatment includes a set of medical
⇑ Corresponding author. Tel./fax: +86 10 8523 1761. E-mail address: [email protected] (Q.-H. Zhao).
interventions, including head elevation, sedation, hypothermia, hyperventilation, hyperosmotic agents, barbiturates and cerebrospinal fluid withdrawal [7,8]. However, although maximal conservative treatment is provided for patients with increased ICP in a variety of neurocritical illnesses, the risk of death and severe disability remains high and ranges from 50 to 80%, based on previous retrospective reviews or surgical decompression series [4,9]. This has led to increasing enthusiasm in exploring other potentially effective strategies, such as decompressive craniectomy, to obtain satisfactory ICP control and a favorable outcome for neurocritical care patients with refractory intracranial hypertension. In recent years, decompressive craniectomy, as a second-tier therapeutic measure, has been a focus and appears to be a promising approach to control ICP [5,10–12]. It is postulated that decompressive craniectomy can allow brain tissue to expand, consequently facilitating control of increased ICP and reducing the risk of herniation, which may improve the outcome of neurocritical care patients. A recent systematic review involving patients who were 60 years of age or younger has revealed that
http://dx.doi.org/10.1016/j.jocn.2015.06.037 0967-5868/Ó 2015 Elsevier Ltd. All rights reserved.
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J.-W. Wang et al. / Journal of Clinical Neuroscience xxx (2016) xxx–xxx
surgical decompression can reduce the risk of death or severe disability following malignant MCAI [13,14]; another metaanalysis, including only one trial, failed to show a significant advantage for decompressive craniectomy to reduce an unfavorable outcome following severe pediatric TBI [15]. Recently, with the completion of several randomized controlled trials (RCT) involving malignant MCAI in older patients or severe TBI in adults, it is necessary to further compare the effects of decompressive craniectomy with conservative treatment in the management of neurocritical care patients with refractory intracranial hypertension. The present meta-analysis was performed to determine whether decompressive craniectomy is effective in decreasing the risk of death or dependence when compared to conservative treatments in the treatment of neurocritical care patients with refractory intracranial hypertension, based on current evidence. 2. Materials and methods 2.1. Study identification We performed a systematic review of the published literature to identify all clinical RCT in which decompressive craniectomy had been compared to conservative treatment for patients with neurocritical illnesses, including malignant MCAI or severe TBI confirmed by CT scan or MRI. Studies that were either not RCT or that did not directly involve the effects of decompressive craniectomy in neurocritical care patients with evidence of increased ICP or cerebral swelling, were eliminated.
2.4. Quality assessment The quality of eligible studies was formally evaluated using the Cochrane Collaboration’s tool for assessing the risk of bias in randomized trials. Specifically, studies were judged on the following items: adequacy of random sequence generation, allocation concealment, blinding of outcome assessment, incompleteness of outcome data, possibility of selective outcome reporting and other biases. The risk of bias for each item was categorized as high, unclear or low and was scored as 0, 1, or 2, respectively. Studies with a total score of 66 were considered to be low-quality; studies with a total score of P10 were considered to be high-quality. 2.5. Data extraction We extracted the following data from each study: baseline characteristics, design and objective, number of patients, timing of measurements, main results of the study, and follow-up results. The primary outcome assessed was the composite outcome of death or dependence in activities of daily living (ADL) at the end of the follow-up period (at least 6 months). The secondary outcome was death at the end of the follow-up period. In the present study, the cut-off points for the various scales to define dependence in ADL were a score of 3 or more on the modified Rankin Scale, a score of 60 or less on the Barthel Index, a grade of 3 or less on the Glasgow Outcome Scale and a grade of 4 or less on the Extended Glasgow Outcome Scale [16–18]. 2.6. Statistical analysis
2.2. Search strategy Based on key words or medical subject heading terms, such as ‘‘decompressive craniectomy”, ‘‘intracranial hypertension”, ‘‘brain edema”, ‘‘neurocritical care”, ‘‘traumatic brain injury”, ‘‘stroke”, ‘‘cerebrovascular disorders”, ‘‘intracranial hemorrhage”, and ‘‘brain ischemia”, an electronic search for relevant articles up to July 2014 was conducted in PUBMED, EMBASE and the Cochrane Central Register of Controlled Trials (CENTRAL) without language limitation. Moreover, the OpenGrey database (a System for Information on Grey Literature in Europe) and the USA National Technical Information Service (NTIS) were searched for grey literature. Internet-based clinical trial registries, such as ClinicalTrials.gov, International Clinical Trials Registry Platform and International Standard Randomized Controlled Trial Number Register, were also searched for suitable studies. In addition, abstracts and conference proceedings from the Web of Science were searched where available; we also complemented this by using the ‘‘Related Articles” function on PUBMED and searched the reference lists of relevant articles. For full details of the search strategy, see Supplementary Figure 1. The search was performed independently by two investigators and was completed in July 2014. 2.3. Literature screening After the literature search, two investigators independently reviewed the titles and abstracts of all of the identified studies and excluded those that were obviously irrelevant or duplicates. The full articles of the remaining studies were then retrieved and independently reviewed using a structured form to determine eligibility and to extract data. Disagreements were resolved by discussion and consensus or by a third investigator if needed. We contacted the study authors for clarification and further information where necessary.
Considering the possibility that effectiveness may differ in different illnesses, statistical analyses were performed according to the types of neurocritical illness. A heterogeneity-based method of meta-analysis was performed using Review Manager (version 5.2, Cochrane Collaboration and Update Software) for prospective RCT. Heterogeneity between studies was assessed by means of the standard Cochran’s Q statistic and I2 statistic, which was prespecified as P < 0.10 or I2 >50% in the present study. A summary risk ratio (RR) was used as the effect parameter for the metaanalysis, and the 95% confidence interval (CI) was used to interpret the results. A fixed-effect model was used to merge the values of the RR to estimate the overall effect size when heterogeneity between studies was not obtained. Otherwise, a random-effect model was used in the statistical analysis. All of the tests were two-sided, and statistical significance was defined as a probability value of 60 years old.
Table 1 Baseline characteristics of the 10 included trials Study, year
Groups
No.
Age (years)
Male/ Female
Critical neurological illness
Injury onset to randomization (hours)
Neurological scales
Cooper 2011 [19]
DC CT DC
73 82 14
23.7 [19.4–29.6] 24.6 [18.5–34.9] 52.3 [45.5–59.0]
59/14 61/21 9/5
Traumatic brain injury
35.2 [23.3–52.8] 34.8 [25.8–45.4] 53.8 [27.7–80.4]
CT
10
57.9 [45.4–65.8]
6/4
DC CT DC CT DC CT DC CT DC
32 32 17 15 49 63 10 10 11
50 ± 8.3 47.4 9.8 43 (30–60) 46 (29–59) 70 (62–82) 70 (61–80) 33.20 ± 2.83
20/12 18/14 8/9 7/8 25/24 31/32 n/a
Malignant infarction Malignant infarction Malignant infarction Traumatic
57.2 (49–67)
n/a
Malignant middle cerebral artery infarction
CT
13
65 (49–81)*
Taylor 2001 [26]
DC CT
13 14
n/a
Traumatic brain injury
15.0 (6.3–23.2) 17.2 (3–29)
Vahedi 2007 [27]
DC CT DC
20 18 24
120.9 (13.6– 176.4) (months) 43.5 ± 9.7 43.3 ± 7.1 63.5 (29–78)
GCS: 5 [3–7] GCS: 6 [4–7] NIHSS: 21.5 [19.5–23.8] NIHSS: 23.0 [20.5–27.5] NIHSS: 23 [17–34] NIHSS: 24 [20–36] NIHSS: 21 (19–26) NIHSS: 24 (19–31)* NIHSS: 20 (15–40) NIHSS: 21 (15–38) GCS: 5 (3–7) GCS: 5 (4–8) NIHSS: 21.2 (16– 28) NIHSS: 20.8 (17– 24) GCS: 6 (3–11) GCS: 5 (4–9)
9/11 9/9 18/6
Malignant middle cerebral artery infarction Malignant middle cerebral artery infarction
n/a
CT
23
64 (32–80)
16/7
Frank 2014 [20]
Hofmeijer 2009 [21] Jüttler 2007 [22] Jüttler 2014 [23] Moein 2012 [24] Slezins 2012 [25]
Zhao 2012 [28]
Malignant middle cerebral artery infarction
52.5 [29.5–64.4] middle cerebral artery middle cerebral artery middle cerebral artery brain injury
41 [29–50] 45 [29–63] 24 (13.5–36.0) 22.5 (12.0–35.0) 25 (12–49) 26 (9–47) n/a 21 (8–36) 19 (6–34)
23.6 ± 6.4 24.1 ± 6.4
NIHSS: 22.5 ± 5.4 NIHSS: 23.4 ± 6.2 GCS (E + M): 8.5 (7–9) GCS (E + M): 8 (7–9)
Data are presented as mean ± standard deviation, median [interquartile range] or median (range). CT = conservative treatment, DC = decompressive craniectomy, GCS = Glasgow Coma Scale, GCS (E + M) = Glasgow Coma Scale (Eye + Motor), n/a = not available, NIHSS = National Institutes of Health Stroke Scale, No. = number of patients. * Indicated significant differences.
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Table 2 Risk of bias and quality assessment of the 10 included trials Study, year
Random sequence generation
Allocation concealment
Blinding of outcome assessment
Incomplete outcome data
Selective reporting
Other bias
Total score
Cooper 2011 [19] Frank 2014 [20] Hofmeijer 2009 [21] Jüttler 2007 [22] Jüttler 2014 [23] Moein 2012 [24]
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
12 12 12
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Unclear (1)
Low (2) Low (2) Low (2)
Low (2) Low (2) Unclear (1)
12 12 9
Slezins 2012 [25]
Unclear (1)
Unclear (1)
Unclear (1)
Low (2)
Unclear (1)
Taylor 2001 [26] Vahedi 2007 [27] Zhao 2012 [28]
Low (2) Low (2) Low (2)
Low (2) Unclear (1) Low (2)
Unclear (1) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Unclear (1) Unclear (1) Low (2) Low (2) Low (2)
7 11 11 12
Risk of bias is categorized as high, unclear or low and the score of each item is listed in parenthesis. The possible maximum score for each trial is 12.
Fig. 2. Forest plot of the effect of decompressive craniectomy on the composite outcome of death or dependence in malignant middle cerebral artery infarction. There was no significant difference in the risk ratio of being dead or dependent at the final follow-up between the decompressive craniectomy group and the conservative treatment group. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel, yrs = years.
3.4. Severe TBI As shown in Figure 4 and 5, all three included trials involving severe TBI reported the effect of decompressive craniectomy on death and/or dependence at the end of the follow-up period [19,24,26]. The pooled RR of death and dependence at the end of follow-up using decompressive craniectomy compared to conservative treatment was 0.76 (95% CI: 0.36–1.62, P = 0.48) and was associated with statistically significant heterogeneity (P = 0.0.004, I2 = 82%), indicating that a decompressive craniectomy does not reduce the risk of death and dependence for patients with severe TBI in comparison with conservative treatment (Fig. 4). Moreover, data on the risk of death only did not indicate a significant difference between the decompressive craniectomy group and the
conservative treatment group (RR: 0.83, 95% CI: 0.48–1.42, P = 0.49), which was associated with statistically non-significant heterogeneity (P = 0.42, I2 = 0%) (Fig. 5). In addition, subgroup analysis based on patient age indicated that decompressive craniectomy and conservative treatment had the same risk of death and/or dependence in both adult and pediatric TBI patients.
4. Discussion In the present meta-analysis of 10 RCT, we investigated the effects of decompressive craniectomy on death or dependence compared to conservative treatment in neurocritical care patients with refractory intracranial hypertension. The main findings are
Please cite this article in press as: Wang J-W et al. Decompressive craniectomy in neurocritical care. J Clin Neurosci (2016), http://dx.doi.org/10.1016/j. jocn.2015.06.037
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Fig. 3. Forest plot of the effect of decompressive craniectomy on the risk of death in malignant middle cerebral artery infarction (MCAI). Decompressive craniectomy significantly reduced the risk of death for patients with malignant MCAI in comparison with the conservative treatment. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel, yrs = years.
Fig. 4. Forest plot of the effect of decompressive craniectomy on the composite outcome of death or dependence in severe traumatic brain injury. There was no significant difference in the risk ratio of being dead or dependent at the final follow-up between the decompressive craniectomy group and the conservative treatment group. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel.
as follows. (1) Decompressive craniectomy can significantly reduce the risk of death for patients suffering malignant MCAI (either younger or older than 60 years of age) in comparison with the risk of death in TBI. (2) There was no significant difference in the RR of death or dependence at the final follow-up between the decompressive craniectomy group and the conservative treatment group either in malignant MCAI or in severe TBI. As a rescue therapy, decompressive craniectomy is widely used in neurocritical care patients for whom maximal conservative
treatment has failed to control increased ICP [2,12]. However, some issues warrant further study. For example, although previous systematic reviews have reported that decompressive craniectomy is associated with a reduced risk of death or death or severe disability for patients with malignant MCAI, the evidence is based on a population that is younger than 60 years old [13,21]. Moreover, as for severe TBI, another common neurocritical illness, current evidence has failed to show a significant advantage for decompressive craniectomy in reducing an unfavorable outcome
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Fig. 5. Forest plot of the effect of decompressive craniectomy on the risk of death in severe traumatic brain injury (TBI). Decompressive craniectomy did not reduce the risk of death and dependence for patients with severe TBI in comparison with the conservative treatment. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel.
in the pediatric population [15]. In addition, several important research trials, including HeADDFIRST [20], DESTINY II [23] and DECRA [19], have recently been completed. Thus, it is necessary to re-evaluate the effect of decompressive craniectomy in the management of neurocritical care patients in light of emerging evidence. Our study may provides timely and substantial evidence for clinicians in the selection of appropriate treatment. In the present meta-analysis, the composite outcome of death or dependence in ADL after at least 6 months rather than death alone or other pathophysiological endpoints, such as ICP, was chosen as the primary outcome measure for the following reasons. On one hand, as clinically relevant outcomes, either death or dependence is important for patients with neurocritical illnesses, including malignant MCAI and severe TBI. A major goal of treatment is to ensure surviving patients are functionally independent in their ADL. In addition, data on death and dependence is reported in most studies. Thus, death and dependence in combination is most appropriate, and death alone is inadequate. On the other hand, generally speaking, pathophysiological parameters are more prone to measurement error or biased reporting compared to clinical outcomes. The potential for bias may be further amplified if a number of pathophysiological endpoints are collected in the study and may lead to striking treatment effects or even opposite results. Furthermore, previous studies indicate that a follow-up period of 6 months or longer is appropriate to evaluate outcomes in patients with brain injury [29–31]. A short follow-up period may not be enough to assess the long-term effect of decompressive craniectomy. Currently, as described in the included RCT, decompressive craniectomy is mainly used in two neurocritical illnesses: malignant MCAI and severe TBI. For malignant MCAI, our present meta-analysis updates the previous evidence that limits the population to patients younger than 60 years of age by including RCT that studied patients up to 80 years old. The results show that decompressive craniectomy can significantly reduce the risk of death for patients who are suffering malignant MCAI despite the absence of a substantial reduction in the composite outcome of death or dependence in these patients. Furthermore, in severe TBI, our results, which included data from adults with TBI, indicate that there is no evidence supporting that decompressive craniectomy is associated with a reduced risk of death or dependence in
comparison with conservative treatments. However, it must be noted that the CI are wide and should not exclude clinically significant differences. There are some limitations in the present study. First, although we attempted to bring together all of the relevant RCT in this metaanalysis and 10 trials were included, subgroup analyses based on patient age are limited by the small number of patients and trials, especially for severe TBI. It is probable that, in the near future, the results of an ongoing RCT (RESCUEicp study [32]) can shed light on this issue. Second, individual patient data, such as preoperative neurological status and timing of surgery, are absent; these have been proven to affect the outcome and the size of effects. A future meta-analysis that is stratified by these potential outcome factors may be of benefit to identify which patients are most likely to benefit from decompressive craniectomy. 5. Conclusions The present meta-analysis indicates that decompressive craniectomy can significantly reduce the risk of death for patients with malignant MCAI, although no evidence supports that decompressive craniectomy is associated with a reduced risk of death or dependence for TBI patients. Further well-designed trials are needed to identify which patients are most likely to benefit from decompressive craniectomy and to better evaluate the role of surgery in TBI patients. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. Acknowledgement This work was supported by Beijing Natural Science Foundation (7154200). Appendix A. Supplementary material Supplementary data associated with this article can be found, in the online version, at http://dx.doi.org/10.1016/j.jocn.2015.06.037.
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References [1] Di Ieva A, Schmitz EM, Cusimano MD. Analysis of intracranial pressure: past, present, and future. Neuroscientist 2013;19:592–603. [2] Rangel-Castillo L, Gopinath S, Robertson CS. Management of intracranial hypertension. Neurol Clin 2008;26:521–41. [3] Wartenberg KE. Malignant middle cerebral artery infarction. Curr Opin Crit Care 2012;18:152–63. [4] Stocchetti N, Maas AI. Traumatic intracranial hypertension. N Engl J Med 2014;370:2121–30. [5] Stocchetti N, Zanaboni C, Colombo A, et al. Refractory intracranial hypertension and ‘‘second-tier” therapies in traumatic brain injury. Intensive Care Med 2008;34:461–7. [6] Wijayatilake DS, Shepherd SJ, Sherren PB. Updates in the management of intracranial pressure in traumatic brain injury. Curr Opin Anaesthesiol 2012;25:540–7. [7] Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotraum 2007;24:S1. [8] Wijdicks EF, Sheth KN, Carter BS, et al. Recommendations for the management of cerebral and cerebellar infarction with swelling: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2014;45:1222–38. [9] Suarez JI, Zaidat OO, Suri MF, et al. Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team. Crit Care Med 2004;32:2311–7. [10] Bohman LE, Schuster JM. Decompressive craniectomy for management of traumatic brain injury: an update. Curr Neurol Neurosci Rep 2013;13:392. [11] Neugebauer H, Juttler E. Hemicraniectomy for malignant middle cerebral artery infarction: current status and future directions. Int J Stroke 2014;9:460–7. [12] Bor-Seng-Shu E, Figueiredo EG, Amorim RL, et al. Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. J Neurosurg 2012;117:589–96. [13] Cruz-Flores S, Berge E, Whittle IR. Surgical decompression for cerebral oedema in acute ischaemic stroke. Cochrane Database Syst Rev 2012;1:CD003435. [14] Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol 2007;6:215–22. [15] Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006;CD003983. [16] Balu S. Differences in psychometric properties, cut-off scores, and outcomes between the Barthel Index and Modified Rankin Scale in pharmacotherapybased stroke trials: systematic literature review. Curr Med Res Opin 2009;25:1329–41.
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[17] Hudak AM, Caesar RR, Frol AB, et al. Functional outcome scales in traumatic brain injury: a comparison of the Glasgow Outcome Scale (Extended) and the Functional Status Examination. J Neurotrauma 2005;22:1319–26. [18] Shih MM, Rogers JC, Skidmore ER, et al. Measuring stroke survivors’ functional status independence: five perspectives. Am J Occup Ther 2009;63:600–8. [19] Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011;364:1493–502. [20] Frank JI, Schumm LP, Wroblewski K, et al. Hemicraniectomy and durotomy upon deterioration from infarction-related swelling trial: randomized pilot clinical trial. Stroke 2014;45:781–7. [21] Hofmeijer J, Kappelle LJ, Algra A, et al. Surgical decompression for spaceoccupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 2009;8:326–33. [22] Juttler E, Schwab S, Schmiedek P, et al. Decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (DESTINY): a randomized, controlled trial. Stroke 2007;38:2518–25. [23] Juttler E, Unterberg A, Woitzik J, et al. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke. New Engl J Med 2014;370:1091–100. [24] Moein H, Sanati MA, Fard SA, et al. Outcome of decompressive craniectomy in patients with severe head injury: a pilot randomized clinical trial. Neurosurg Quart 2012;22:149–52. [25] Slezins J, Keris V, Bricis R, et al. Preliminary results of randomized controlled study on decompressive craniectomy in treatment of malignant middle cerebral artery stroke. Medicina (Kaunas) 2012;48:521–4. [26] Taylor A, Butt W, Rosenfeld J, et al. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst 2001;17:154–62. [27] Vahedi K, Vicaut E, Mateo J, et al. Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke 2007;38:2506–17. [28] Zhao J, Su YY, Zhang Y, et al. Decompressive hemicraniectomy in malignant middle cerebral artery infarct: a randomized controlled trial enrolling patients up to 80 years old. Neurocrit Care 2012;17:161–71. [29] Gabbe BJ, Simpson PM, Sutherland AM, et al. Evaluating time points for measuring recovery after major trauma in adults. Ann Surg 2013;257: 166–72. [30] Ardolino A, Sleat G, Willett K. Outcome measurements in major trauma– results of a consensus meeting. Injury 2012;43:1662–6. [31] Wade DT, Skilbeck CE, Hewer RL. Predicting Barthel ADL score at 6 months after an acute stroke. Arch Phys Med Rehabil 1983;64:24–8. [32] Hutchinson PJ, Corteen E, Czosnyka M, et al. Decompressive craniectomy in traumatic brain injury: the randomized multicenter RESCUEicp study (www. RESCUEicp.com). Acta Neurochir Suppl 2006;96:17–20.
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Review
Decompressive craniectomy in neurocritical care Jia-Wei Wang, Jin-Ping Li, Ying-Lun Song, Ke Tan, Yu Wang, Tao Li, Peng Guo, Xiong Li, Yan Wang, Qi-Huang Zhao ⇑ Department of Neurosurgery, Beijing Chao-Yang Hospital, Capital Medical University, 8 South Gongti Road, Beijing 100020, PR China
a r t i c l e
i n f o
Article history: Received 5 April 2015 Accepted 20 June 2015 Available online xxxx Keywords: Decompressive craniectomy Meta-analysis Neurocritical illness Randomized controlled trial Stroke Traumatic brain injury
a b s t r a c t Recently, several randomized controlled trials (RCT) investigating the effectiveness of decompressive craniectomy in the context of neurocritical illnesses have been completed. Thus, a meta-analysis to update the current evidence regarding the effects of decompressive craniectomy is necessary. We searched PUBMED, EMBASE and the Cochrane Central Register of Controlled Trials. Other sources, including internet-based clinical trial registries and grey literature, were also searched. After searching the literature, two investigators independently performed literature screening, assessing the quality of the included trials and extracting the data. The outcome measures included the composite outcome of death or dependence and the risk of death. Ten RCT were included: seven RCT were on malignant middle cerebral artery infarction (MCAI) and three were on severe traumatic brain injury (TBI). Decompressive craniectomy significantly reduced the risk of death for patients suffering malignant MCAI (risk ratio [RR] 0.46, 95% confidence interval [CI]: 0.36–0.59, P < 0.00001) in comparison with no reduction in the risk of death for patients with severe TBI (RR: 0.83, 95% CI: 0.48–1.42, P = 0.49). However, there was no significant difference in the composite risk of death or dependence at the final follow-up between the decompressive craniectomy group and the conservative treatment group for either malignant MCAI or severe TBI. The present meta-analysis indicates that decompressive craniectomy can significantly reduce the risk of death for patients with malignant MCAI, although no evidence demonstrates that decompressive craniectomy is associated with a reduced risk of death or dependence for TBI patients. Ó 2015 Elsevier Ltd. All rights reserved.
1. Introduction As a leading cause of mortality and morbidity in the neurointensive care unit, increased intracranial pressure (ICP) has received considerable attention in clinical practice [1,2]. Various neurocritical illnesses, including malignant middle cerebral artery infarction (MCAI) and severe traumatic brain injury (TBI), lead to increased ICP and may result in cerebral herniation, death or permanent disability [3,4]. Unfortunately, although the well-known deleterious effects of increased ICP have long been recognized, medical and surgical interventions remain limited, and advances in treatment have been modest. The current options for the management of increased ICP consist of conservative treatment or surgical decompression [5,6]. Generally, conservative treatment includes a set of medical
⇑ Corresponding author. Tel./fax: +86 10 8523 1761. E-mail address: [email protected] (Q.-H. Zhao).
interventions, including head elevation, sedation, hypothermia, hyperventilation, hyperosmotic agents, barbiturates and cerebrospinal fluid withdrawal [7,8]. However, although maximal conservative treatment is provided for patients with increased ICP in a variety of neurocritical illnesses, the risk of death and severe disability remains high and ranges from 50 to 80%, based on previous retrospective reviews or surgical decompression series [4,9]. This has led to increasing enthusiasm in exploring other potentially effective strategies, such as decompressive craniectomy, to obtain satisfactory ICP control and a favorable outcome for neurocritical care patients with refractory intracranial hypertension. In recent years, decompressive craniectomy, as a second-tier therapeutic measure, has been a focus and appears to be a promising approach to control ICP [5,10–12]. It is postulated that decompressive craniectomy can allow brain tissue to expand, consequently facilitating control of increased ICP and reducing the risk of herniation, which may improve the outcome of neurocritical care patients. A recent systematic review involving patients who were 60 years of age or younger has revealed that
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surgical decompression can reduce the risk of death or severe disability following malignant MCAI [13,14]; another metaanalysis, including only one trial, failed to show a significant advantage for decompressive craniectomy to reduce an unfavorable outcome following severe pediatric TBI [15]. Recently, with the completion of several randomized controlled trials (RCT) involving malignant MCAI in older patients or severe TBI in adults, it is necessary to further compare the effects of decompressive craniectomy with conservative treatment in the management of neurocritical care patients with refractory intracranial hypertension. The present meta-analysis was performed to determine whether decompressive craniectomy is effective in decreasing the risk of death or dependence when compared to conservative treatments in the treatment of neurocritical care patients with refractory intracranial hypertension, based on current evidence. 2. Materials and methods 2.1. Study identification We performed a systematic review of the published literature to identify all clinical RCT in which decompressive craniectomy had been compared to conservative treatment for patients with neurocritical illnesses, including malignant MCAI or severe TBI confirmed by CT scan or MRI. Studies that were either not RCT or that did not directly involve the effects of decompressive craniectomy in neurocritical care patients with evidence of increased ICP or cerebral swelling, were eliminated.
2.4. Quality assessment The quality of eligible studies was formally evaluated using the Cochrane Collaboration’s tool for assessing the risk of bias in randomized trials. Specifically, studies were judged on the following items: adequacy of random sequence generation, allocation concealment, blinding of outcome assessment, incompleteness of outcome data, possibility of selective outcome reporting and other biases. The risk of bias for each item was categorized as high, unclear or low and was scored as 0, 1, or 2, respectively. Studies with a total score of 66 were considered to be low-quality; studies with a total score of P10 were considered to be high-quality. 2.5. Data extraction We extracted the following data from each study: baseline characteristics, design and objective, number of patients, timing of measurements, main results of the study, and follow-up results. The primary outcome assessed was the composite outcome of death or dependence in activities of daily living (ADL) at the end of the follow-up period (at least 6 months). The secondary outcome was death at the end of the follow-up period. In the present study, the cut-off points for the various scales to define dependence in ADL were a score of 3 or more on the modified Rankin Scale, a score of 60 or less on the Barthel Index, a grade of 3 or less on the Glasgow Outcome Scale and a grade of 4 or less on the Extended Glasgow Outcome Scale [16–18]. 2.6. Statistical analysis
2.2. Search strategy Based on key words or medical subject heading terms, such as ‘‘decompressive craniectomy”, ‘‘intracranial hypertension”, ‘‘brain edema”, ‘‘neurocritical care”, ‘‘traumatic brain injury”, ‘‘stroke”, ‘‘cerebrovascular disorders”, ‘‘intracranial hemorrhage”, and ‘‘brain ischemia”, an electronic search for relevant articles up to July 2014 was conducted in PUBMED, EMBASE and the Cochrane Central Register of Controlled Trials (CENTRAL) without language limitation. Moreover, the OpenGrey database (a System for Information on Grey Literature in Europe) and the USA National Technical Information Service (NTIS) were searched for grey literature. Internet-based clinical trial registries, such as ClinicalTrials.gov, International Clinical Trials Registry Platform and International Standard Randomized Controlled Trial Number Register, were also searched for suitable studies. In addition, abstracts and conference proceedings from the Web of Science were searched where available; we also complemented this by using the ‘‘Related Articles” function on PUBMED and searched the reference lists of relevant articles. For full details of the search strategy, see Supplementary Figure 1. The search was performed independently by two investigators and was completed in July 2014. 2.3. Literature screening After the literature search, two investigators independently reviewed the titles and abstracts of all of the identified studies and excluded those that were obviously irrelevant or duplicates. The full articles of the remaining studies were then retrieved and independently reviewed using a structured form to determine eligibility and to extract data. Disagreements were resolved by discussion and consensus or by a third investigator if needed. We contacted the study authors for clarification and further information where necessary.
Considering the possibility that effectiveness may differ in different illnesses, statistical analyses were performed according to the types of neurocritical illness. A heterogeneity-based method of meta-analysis was performed using Review Manager (version 5.2, Cochrane Collaboration and Update Software) for prospective RCT. Heterogeneity between studies was assessed by means of the standard Cochran’s Q statistic and I2 statistic, which was prespecified as P < 0.10 or I2 >50% in the present study. A summary risk ratio (RR) was used as the effect parameter for the metaanalysis, and the 95% confidence interval (CI) was used to interpret the results. A fixed-effect model was used to merge the values of the RR to estimate the overall effect size when heterogeneity between studies was not obtained. Otherwise, a random-effect model was used in the statistical analysis. All of the tests were two-sided, and statistical significance was defined as a probability value of 60 years old.
Table 1 Baseline characteristics of the 10 included trials Study, year
Groups
No.
Age (years)
Male/ Female
Critical neurological illness
Injury onset to randomization (hours)
Neurological scales
Cooper 2011 [19]
DC CT DC
73 82 14
23.7 [19.4–29.6] 24.6 [18.5–34.9] 52.3 [45.5–59.0]
59/14 61/21 9/5
Traumatic brain injury
35.2 [23.3–52.8] 34.8 [25.8–45.4] 53.8 [27.7–80.4]
CT
10
57.9 [45.4–65.8]
6/4
DC CT DC CT DC CT DC CT DC
32 32 17 15 49 63 10 10 11
50 ± 8.3 47.4 9.8 43 (30–60) 46 (29–59) 70 (62–82) 70 (61–80) 33.20 ± 2.83
20/12 18/14 8/9 7/8 25/24 31/32 n/a
Malignant infarction Malignant infarction Malignant infarction Traumatic
57.2 (49–67)
n/a
Malignant middle cerebral artery infarction
CT
13
65 (49–81)*
Taylor 2001 [26]
DC CT
13 14
n/a
Traumatic brain injury
15.0 (6.3–23.2) 17.2 (3–29)
Vahedi 2007 [27]
DC CT DC
20 18 24
120.9 (13.6– 176.4) (months) 43.5 ± 9.7 43.3 ± 7.1 63.5 (29–78)
GCS: 5 [3–7] GCS: 6 [4–7] NIHSS: 21.5 [19.5–23.8] NIHSS: 23.0 [20.5–27.5] NIHSS: 23 [17–34] NIHSS: 24 [20–36] NIHSS: 21 (19–26) NIHSS: 24 (19–31)* NIHSS: 20 (15–40) NIHSS: 21 (15–38) GCS: 5 (3–7) GCS: 5 (4–8) NIHSS: 21.2 (16– 28) NIHSS: 20.8 (17– 24) GCS: 6 (3–11) GCS: 5 (4–9)
9/11 9/9 18/6
Malignant middle cerebral artery infarction Malignant middle cerebral artery infarction
n/a
CT
23
64 (32–80)
16/7
Frank 2014 [20]
Hofmeijer 2009 [21] Jüttler 2007 [22] Jüttler 2014 [23] Moein 2012 [24] Slezins 2012 [25]
Zhao 2012 [28]
Malignant middle cerebral artery infarction
52.5 [29.5–64.4] middle cerebral artery middle cerebral artery middle cerebral artery brain injury
41 [29–50] 45 [29–63] 24 (13.5–36.0) 22.5 (12.0–35.0) 25 (12–49) 26 (9–47) n/a 21 (8–36) 19 (6–34)
23.6 ± 6.4 24.1 ± 6.4
NIHSS: 22.5 ± 5.4 NIHSS: 23.4 ± 6.2 GCS (E + M): 8.5 (7–9) GCS (E + M): 8 (7–9)
Data are presented as mean ± standard deviation, median [interquartile range] or median (range). CT = conservative treatment, DC = decompressive craniectomy, GCS = Glasgow Coma Scale, GCS (E + M) = Glasgow Coma Scale (Eye + Motor), n/a = not available, NIHSS = National Institutes of Health Stroke Scale, No. = number of patients. * Indicated significant differences.
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Table 2 Risk of bias and quality assessment of the 10 included trials Study, year
Random sequence generation
Allocation concealment
Blinding of outcome assessment
Incomplete outcome data
Selective reporting
Other bias
Total score
Cooper 2011 [19] Frank 2014 [20] Hofmeijer 2009 [21] Jüttler 2007 [22] Jüttler 2014 [23] Moein 2012 [24]
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
12 12 12
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Unclear (1)
Low (2) Low (2) Low (2)
Low (2) Low (2) Unclear (1)
12 12 9
Slezins 2012 [25]
Unclear (1)
Unclear (1)
Unclear (1)
Low (2)
Unclear (1)
Taylor 2001 [26] Vahedi 2007 [27] Zhao 2012 [28]
Low (2) Low (2) Low (2)
Low (2) Unclear (1) Low (2)
Unclear (1) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Low (2)
Low (2) Low (2) Unclear (1) Unclear (1) Low (2) Low (2) Low (2)
7 11 11 12
Risk of bias is categorized as high, unclear or low and the score of each item is listed in parenthesis. The possible maximum score for each trial is 12.
Fig. 2. Forest plot of the effect of decompressive craniectomy on the composite outcome of death or dependence in malignant middle cerebral artery infarction. There was no significant difference in the risk ratio of being dead or dependent at the final follow-up between the decompressive craniectomy group and the conservative treatment group. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel, yrs = years.
3.4. Severe TBI As shown in Figure 4 and 5, all three included trials involving severe TBI reported the effect of decompressive craniectomy on death and/or dependence at the end of the follow-up period [19,24,26]. The pooled RR of death and dependence at the end of follow-up using decompressive craniectomy compared to conservative treatment was 0.76 (95% CI: 0.36–1.62, P = 0.48) and was associated with statistically significant heterogeneity (P = 0.0.004, I2 = 82%), indicating that a decompressive craniectomy does not reduce the risk of death and dependence for patients with severe TBI in comparison with conservative treatment (Fig. 4). Moreover, data on the risk of death only did not indicate a significant difference between the decompressive craniectomy group and the
conservative treatment group (RR: 0.83, 95% CI: 0.48–1.42, P = 0.49), which was associated with statistically non-significant heterogeneity (P = 0.42, I2 = 0%) (Fig. 5). In addition, subgroup analysis based on patient age indicated that decompressive craniectomy and conservative treatment had the same risk of death and/or dependence in both adult and pediatric TBI patients.
4. Discussion In the present meta-analysis of 10 RCT, we investigated the effects of decompressive craniectomy on death or dependence compared to conservative treatment in neurocritical care patients with refractory intracranial hypertension. The main findings are
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Fig. 3. Forest plot of the effect of decompressive craniectomy on the risk of death in malignant middle cerebral artery infarction (MCAI). Decompressive craniectomy significantly reduced the risk of death for patients with malignant MCAI in comparison with the conservative treatment. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel, yrs = years.
Fig. 4. Forest plot of the effect of decompressive craniectomy on the composite outcome of death or dependence in severe traumatic brain injury. There was no significant difference in the risk ratio of being dead or dependent at the final follow-up between the decompressive craniectomy group and the conservative treatment group. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel.
as follows. (1) Decompressive craniectomy can significantly reduce the risk of death for patients suffering malignant MCAI (either younger or older than 60 years of age) in comparison with the risk of death in TBI. (2) There was no significant difference in the RR of death or dependence at the final follow-up between the decompressive craniectomy group and the conservative treatment group either in malignant MCAI or in severe TBI. As a rescue therapy, decompressive craniectomy is widely used in neurocritical care patients for whom maximal conservative
treatment has failed to control increased ICP [2,12]. However, some issues warrant further study. For example, although previous systematic reviews have reported that decompressive craniectomy is associated with a reduced risk of death or death or severe disability for patients with malignant MCAI, the evidence is based on a population that is younger than 60 years old [13,21]. Moreover, as for severe TBI, another common neurocritical illness, current evidence has failed to show a significant advantage for decompressive craniectomy in reducing an unfavorable outcome
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Fig. 5. Forest plot of the effect of decompressive craniectomy on the risk of death in severe traumatic brain injury (TBI). Decompressive craniectomy did not reduce the risk of death and dependence for patients with severe TBI in comparison with the conservative treatment. CI = confidence interval, df = degrees of freedom, M-H = Mantel–Haenszel.
in the pediatric population [15]. In addition, several important research trials, including HeADDFIRST [20], DESTINY II [23] and DECRA [19], have recently been completed. Thus, it is necessary to re-evaluate the effect of decompressive craniectomy in the management of neurocritical care patients in light of emerging evidence. Our study may provides timely and substantial evidence for clinicians in the selection of appropriate treatment. In the present meta-analysis, the composite outcome of death or dependence in ADL after at least 6 months rather than death alone or other pathophysiological endpoints, such as ICP, was chosen as the primary outcome measure for the following reasons. On one hand, as clinically relevant outcomes, either death or dependence is important for patients with neurocritical illnesses, including malignant MCAI and severe TBI. A major goal of treatment is to ensure surviving patients are functionally independent in their ADL. In addition, data on death and dependence is reported in most studies. Thus, death and dependence in combination is most appropriate, and death alone is inadequate. On the other hand, generally speaking, pathophysiological parameters are more prone to measurement error or biased reporting compared to clinical outcomes. The potential for bias may be further amplified if a number of pathophysiological endpoints are collected in the study and may lead to striking treatment effects or even opposite results. Furthermore, previous studies indicate that a follow-up period of 6 months or longer is appropriate to evaluate outcomes in patients with brain injury [29–31]. A short follow-up period may not be enough to assess the long-term effect of decompressive craniectomy. Currently, as described in the included RCT, decompressive craniectomy is mainly used in two neurocritical illnesses: malignant MCAI and severe TBI. For malignant MCAI, our present meta-analysis updates the previous evidence that limits the population to patients younger than 60 years of age by including RCT that studied patients up to 80 years old. The results show that decompressive craniectomy can significantly reduce the risk of death for patients who are suffering malignant MCAI despite the absence of a substantial reduction in the composite outcome of death or dependence in these patients. Furthermore, in severe TBI, our results, which included data from adults with TBI, indicate that there is no evidence supporting that decompressive craniectomy is associated with a reduced risk of death or dependence in
comparison with conservative treatments. However, it must be noted that the CI are wide and should not exclude clinically significant differences. There are some limitations in the present study. First, although we attempted to bring together all of the relevant RCT in this metaanalysis and 10 trials were included, subgroup analyses based on patient age are limited by the small number of patients and trials, especially for severe TBI. It is probable that, in the near future, the results of an ongoing RCT (RESCUEicp study [32]) can shed light on this issue. Second, individual patient data, such as preoperative neurological status and timing of surgery, are absent; these have been proven to affect the outcome and the size of effects. A future meta-analysis that is stratified by these potential outcome factors may be of benefit to identify which patients are most likely to benefit from decompressive craniectomy. 5. Conclusions The present meta-analysis indicates that decompressive craniectomy can significantly reduce the risk of death for patients with malignant MCAI, although no evidence supports that decompressive craniectomy is associated with a reduced risk of death or dependence for TBI patients. Further well-designed trials are needed to identify which patients are most likely to benefit from decompressive craniectomy and to better evaluate the role of surgery in TBI patients. Conflicts of Interest/Disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. Acknowledgement This work was supported by Beijing Natural Science Foundation (7154200). Appendix A. Supplementary material Supplementary data associated with this article can be found, in the online version, at http://dx.doi.org/10.1016/j.jocn.2015.06.037.
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References [1] Di Ieva A, Schmitz EM, Cusimano MD. Analysis of intracranial pressure: past, present, and future. Neuroscientist 2013;19:592–603. [2] Rangel-Castillo L, Gopinath S, Robertson CS. Management of intracranial hypertension. Neurol Clin 2008;26:521–41. [3] Wartenberg KE. Malignant middle cerebral artery infarction. Curr Opin Crit Care 2012;18:152–63. [4] Stocchetti N, Maas AI. Traumatic intracranial hypertension. N Engl J Med 2014;370:2121–30. [5] Stocchetti N, Zanaboni C, Colombo A, et al. Refractory intracranial hypertension and ‘‘second-tier” therapies in traumatic brain injury. Intensive Care Med 2008;34:461–7. [6] Wijayatilake DS, Shepherd SJ, Sherren PB. Updates in the management of intracranial pressure in traumatic brain injury. Curr Opin Anaesthesiol 2012;25:540–7. [7] Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons. Guidelines for the management of severe traumatic brain injury. J Neurotraum 2007;24:S1. [8] Wijdicks EF, Sheth KN, Carter BS, et al. Recommendations for the management of cerebral and cerebellar infarction with swelling: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2014;45:1222–38. [9] Suarez JI, Zaidat OO, Suri MF, et al. Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team. Crit Care Med 2004;32:2311–7. [10] Bohman LE, Schuster JM. Decompressive craniectomy for management of traumatic brain injury: an update. Curr Neurol Neurosci Rep 2013;13:392. [11] Neugebauer H, Juttler E. Hemicraniectomy for malignant middle cerebral artery infarction: current status and future directions. Int J Stroke 2014;9:460–7. [12] Bor-Seng-Shu E, Figueiredo EG, Amorim RL, et al. Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. J Neurosurg 2012;117:589–96. [13] Cruz-Flores S, Berge E, Whittle IR. Surgical decompression for cerebral oedema in acute ischaemic stroke. Cochrane Database Syst Rev 2012;1:CD003435. [14] Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol 2007;6:215–22. [15] Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev 2006;CD003983. [16] Balu S. Differences in psychometric properties, cut-off scores, and outcomes between the Barthel Index and Modified Rankin Scale in pharmacotherapybased stroke trials: systematic literature review. Curr Med Res Opin 2009;25:1329–41.
7
[17] Hudak AM, Caesar RR, Frol AB, et al. Functional outcome scales in traumatic brain injury: a comparison of the Glasgow Outcome Scale (Extended) and the Functional Status Examination. J Neurotrauma 2005;22:1319–26. [18] Shih MM, Rogers JC, Skidmore ER, et al. Measuring stroke survivors’ functional status independence: five perspectives. Am J Occup Ther 2009;63:600–8. [19] Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011;364:1493–502. [20] Frank JI, Schumm LP, Wroblewski K, et al. Hemicraniectomy and durotomy upon deterioration from infarction-related swelling trial: randomized pilot clinical trial. Stroke 2014;45:781–7. [21] Hofmeijer J, Kappelle LJ, Algra A, et al. Surgical decompression for spaceoccupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 2009;8:326–33. [22] Juttler E, Schwab S, Schmiedek P, et al. Decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (DESTINY): a randomized, controlled trial. Stroke 2007;38:2518–25. [23] Juttler E, Unterberg A, Woitzik J, et al. Hemicraniectomy in older patients with extensive middle-cerebral-artery stroke. New Engl J Med 2014;370:1091–100. [24] Moein H, Sanati MA, Fard SA, et al. Outcome of decompressive craniectomy in patients with severe head injury: a pilot randomized clinical trial. Neurosurg Quart 2012;22:149–52. [25] Slezins J, Keris V, Bricis R, et al. Preliminary results of randomized controlled study on decompressive craniectomy in treatment of malignant middle cerebral artery stroke. Medicina (Kaunas) 2012;48:521–4. [26] Taylor A, Butt W, Rosenfeld J, et al. A randomized trial of very early decompressive craniectomy in children with traumatic brain injury and sustained intracranial hypertension. Childs Nerv Syst 2001;17:154–62. [27] Vahedi K, Vicaut E, Mateo J, et al. Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke 2007;38:2506–17. [28] Zhao J, Su YY, Zhang Y, et al. Decompressive hemicraniectomy in malignant middle cerebral artery infarct: a randomized controlled trial enrolling patients up to 80 years old. Neurocrit Care 2012;17:161–71. [29] Gabbe BJ, Simpson PM, Sutherland AM, et al. Evaluating time points for measuring recovery after major trauma in adults. Ann Surg 2013;257: 166–72. [30] Ardolino A, Sleat G, Willett K. Outcome measurements in major trauma– results of a consensus meeting. Injury 2012;43:1662–6. [31] Wade DT, Skilbeck CE, Hewer RL. Predicting Barthel ADL score at 6 months after an acute stroke. Arch Phys Med Rehabil 1983;64:24–8. [32] Hutchinson PJ, Corteen E, Czosnyka M, et al. Decompressive craniectomy in traumatic brain injury: the randomized multicenter RESCUEicp study (www. RESCUEicp.com). Acta Neurochir Suppl 2006;96:17–20.
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