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See the corresponding editorial in this issue, pp 587588.

J Neurosurg 117:589596, 2012

Decompressive craniectomy: a meta-analysis of influences


on intracranial pressure and cerebral perfusion pressure in
the treatment of traumatic brain injury
A review
Edson Bor-Seng-Shu, M.D., Ph.D.,1 Eberval G. Figueiredo, M.D., Ph.D.,1
Robson L. O. Amorim, M.D.,1 Manoel Jacobsen Teixeira, M.D., Ph.D.,1
Juliana Spelta Valbuza, Ph.D., 2 Marcio Moyses de Oliveira, M.D., Ph.D., 3
and Ronney B. Panerai, Ph.D. 4
Division of Neurological Surgery, Hospital das Clinicas, University of Sao Paulo School of Medicine;
Department of Medicine, Sao Paulo Federal University, Sao Paulo; 3Department of Morphology,
Maranhao Federal University, Maranhao, Brazil; and 4Department of Cardiovascular Sciences,
University of Leicester, United Kingdom
1
2

Object. In recent years, the role of decompressive craniectomy for the treatment of traumatic brain injury (TBI)
in patients with refractory intracranial hypertension has been the subject of several studies. The purpose of this review
was to evaluate the contribution of decompressive craniectomy in reducing intracranial pressure (ICP) and increasing
cerebral perfusion pressure (CPP) in these patients.
Methods. Comprehensive literature searches were performed for articles related to the effects of decompressive
craniectomy on ICP and CPP in patients with TBI. Inclusion criteria were as follows: 1) published manuscripts, 2)
original articles of any study design except case reports, 3) patients with refractory elevated ICP due to traumatic
brain swelling, 4) decompressive craniectomy as a type of intervention, and 5) availability of pre- and postoperative
ICP and/or CPP data. Primary outcomes were ICP decrease and/or CPP increase for assessing the efficacy of decompressive craniectomy. The secondary outcome was the persistence of reduced ICP 24 and 48 hours after the operation.
Results. Postoperative ICP values were significantly lower than preoperative values immediately after decompressive craniectomy (weighted mean difference [WMD] -17.59 mm Hg, 95% CI -23.45 to -11.73, p < 0.00001), 24
hours after (WMD -14.27 mm Hg, 95% CI -24.13 to -4.41, p < 0.00001), and 48 hours after (WMD -12.69 mm Hg,
95% CI -22.99 to -2.39, p < 0.0001). Postoperative CPP was significantly higher than preoperative values (WMD
7.37 mm Hg, 95% CI 2.32 to 12.42, p < 0.0001).
Conclusions. Decompressive craniectomy can effectively decrease ICP and increase CPP in patients with TBI
and refractory elevated ICP. Further studies are necessary to define the group of patients that can benefit most from
this procedure.
(http://thejns.org/doi/abs/10.3171/2012.6.JNS101400)

Key Words decompressive craniectomy traumatic brain injury


intracranial pressure cerebral perfusion pressure intracranial hypertension
meta-analysis

major principle in managing severe TBI is based


on strategies to control ICP and ensure adequate
CPP. The role of decompressive craniectomy in
the treatment of refractory posttraumatic intracranial hypertension remains controversial because of the absence
of randomized and controlled trials.
Although several publications have provided evidence that decompressive craniectomy can reduce
ICP,1,2,1014,1619 increase CPP,1,2,8,10,24,30 and favorably influence the outcome of patients with TBI, the small sample

size of the studies has limited further conclusions. This


is particularly true for CPP since some important studies have failed to demonstrate augmentation of CPP after
surgical decompression.16,27
The purpose of this review was to evaluate the efficacy of decompressive craniectomy in decreasing ICP
and increasing CPP by performing a systematic literature
search and quantitative analysis of the available scientific
studies.

Abbreviations used in this paper: CPP = cerebral perfusion pressure; ICP = intracranial pressure; TBI = traumatic brain injury;
WMD = weighted mean difference.

Search Strategy

J Neurosurg / Volume 117 / September 2012

Methods

An electronic search strategy was designed to iden589

E. Bor-Seng-Shu et al.
tify human TBI studies concerning changes in ICP and
CPP associated with decompressive craniectomy. This
search included papers published between January 1995
and December 2010. Two independent observers (E.B.
and R.L.O.A.) performed a systematic PubMed database
search using the keywords decompressive craniectomy,
cerebral decompression, brain decompression, and
decompression craniotomy. These subject headings
were also combined with head injury, head trauma,
traumatic brain injury, intracranial pressure, and cerebral perfusion pressure. Reference lists of recovered
articles were examined for additional suitable papers. The
Related Articles feature in PubMed was also used for
all selected studies to maximize the probability of finding
additional relevant studies. A third independent investigator (E.G.F.) resolved potential disagreement between
the 2 independent observers as regarded study identification. The authors of selected articles were contacted by
electronic mail to provide additional data not available
in their publications. Unpublished data were provided by
authors of selected papers who responded positively to
our request.
Inclusion Criteria and Data Extraction

The inclusion criteria for relevant research studies


were as follows: 1) published manuscripts, 2) original articles of any study design with prospective or retrospective
data, 3) patients with posttraumatic brain swelling and refractory intracranial hypertension, 4) decompressive craniectomy as a type of intervention, and 5) availability of
quantitative analysis of ICP and/or CPP estimations before and after decompressive craniectomy. Exclusion criteria were as follows: 1) incomplete data for quantitative
analysis (abstracts only, review articles, and case reports),
2) nonhuman models, 3) elevated ICP not associated with
TBI, and 4) non-English publications. Care was taken to
exclude articles with patients already used in other articles from the same institution to avoid corrupting the
population sample. Primary outcomes were ICP decrease
and/or CPP increase for assessing the efficacy of decompressive craniectomy. The secondary outcome was the
persistence of ICP reduction 24 and 48 hours after surgical decompression, as compared with preoperative levels.

Statistical Analysis

Two authors who were not involved in data collection (J.S.V. and M.M.O.) performed all statistical analysis. Data synthesis and analysis were performed using
The Cochrane Collaboration review manager software
RevMan version 4.2.8. For continuous variables, where
continuous scales of measurement are used to assess the
effects of treatment, the WMD was used with 95% CIs.

Results
Number of Studies Retrieved

Twenty-three studies were identified. Corresponding authors of 4 studies were contacted; however, only
1 replied and provided the requested data. Three studies

590

were excluded because of incomplete data for quantitative


analysis.13,18,31
Twenty studies (479 patients) assessed immediate
pre- and postoperative ICP values (Fig. 1). Eight of them
were prospective clinical studies,7,10,11,2426,30,32 and the remainder were retrospective studies.1,2,8,12,1417,22,23,27,28 Four
studies2,10,23,27 (79 patients) compared the ICP values measured 24 hours after decompressive craniectomy with the
preoperative values, and 3 studies7,10,27 (59 patients) compared the ICP values measured 48 hours after decompressive craniectomy with the preoperative values (Figs.
2 and 3). Cerebral perfusion pressure estimations before
and after decompressive craniectomy were performed in
8 studies (171 patients; Fig. 4).1,2,8,10,16,24,27,30
Study design, sample size, patient age, timing from
injury to craniectomy, ICP threshold for defining refractory intracranial hypertension, pre- and postoperative
ICP, type of ICP monitoring, surgical technique used, and
clinical outcome of the included studies are summarized
in Table 1.
Pooled Results

Postoperative ICP values were significantly lower


than preoperative values; this finding was observed immediately after decompressive craniectomy (WMD
-17.59 mm Hg, 95% CI -23.45 to -11.73, p < 0.00001;
Fig. 1), 24 hours after (WMD -14.27 mm Hg, 95% CI
-24.13 to -4.41, p < 0.00001; Fig. 2), and 48 hours after (WMD -12.69 mm Hg, 95% CI -22.99 to -2.39, p <
0.0001; Fig. 3).
Postoperative CPP was significantly higher than preoperative values (WMD 7.37 mm Hg, 95% CI 2.32 to
12.42, p < 0.0001; Fig. 4).

Discussion
Main Findings

Our pooled results demonstrated 1) a statistically significant immediate decrease in ICP, and 2) a sustained
reduction in ICP associated with decompressive craniectomy. Intracranial pressure was the lowest soon after
brain decompression and increased gradually over the
first 2448 hours; however, it remained stable and significantly lower than preoperative values. A decrease in both
the number and duration of high ICP episodes was also
demonstrated in some articles.26,27 In contrast, decompressive craniectomy failed to decrease ICP to acceptable
values in 8%20% of the cases, which was associated
with an unfavorable outcome.1,13,26,31,32
The pooled results also demonstrated a statistically
significant increase in CPP after decompressive craniectomy. Although this concept is quite intuitive, some relevant papers failed to show postoperative CPP augmentation.16,27
Implications for Surgical Management

Severe head trauma can lead to brain swelling, increased ICP, reduced cerebral blood flow, inadequate
O2 delivery, ischemia, metabolic failure, further brain
J Neurosurg / Volume 117 / September 2012

Effects of craniectomy on ICP and CPP

Fig. 1. Intracranial pressure values immediately before and after decompressive craniectomy. N = number of patients.

edema, and uncontrollable elevated ICP. Decompressive


craniectomy with dural augmentation enlarges the intracranial space, allowing the swollen cerebral hemisphere
to expand out of normal cranial limits while avoiding
brain herniation and brainstem compression.16 The gain
in intracranial volume as a result of the surgery results
in the improvement of cerebral compliance,9,27 a reduction in ICP,1,2,1014,1619 and an increase in CPP,1,2,8,10,24,30
favoring a rise in both cerebral blood flow and cerebral
microvascular perfusion,35,7,10,21 which can be accompanied by elevation in brain tissue PO211,20,25 as well as the
return of abnormal metabolic parameters to normal values in cases of cerebral ischemia.11 Experimental studies
have indicated that decompressive craniectomy prevents
posttraumatic ICP increase, significantly reduces contusion volume, and improves functional outcome.33,34 These
effects can, in part, be explained by ICP reduction and
CPP increase following decompressive craniectomy, as
demonstrated in our pooled results.
On the other hand, some studies have suggested that

decompressive craniectomy can worsen cerebral edema,


possibly associated with cerebral hyperemia as a result
of the conjunction of postoperative CPP increase, impairment of cerebrovascular pressure reactivity, and cerebral
inflammation.1,5,6,27,29 Therefore, avoiding postoperative
severe cerebral hyperemia by controlling CPP as well as
other factors, without worsening cerebral blood flow and
metabolism uncoupling, can potentially reduce the risk
of enhancing cerebral edema.4,5,17 In addition, cerebral
edema can also be aggravated and maintained by cerebral energy metabolism failure probably associated with
mitochondrial functional impairment.3
Limitations of the Study

There was considerable heterogeneity among the reviewed studies. First, the definition of refractory elevated
ICP varied; the ICP threshold was 20,1 25,28 30,16 or 40
mm Hg22 depending on the clinical series. Second, the
applied surgical technique varied as well: unilateral frontotemporoparietooccipital craniectomy, bifrontal crani-

Fig. 2. Intracranial pressure measured 24 hours after decompressive craniectomy as compared with preoperative values.

J Neurosurg / Volume 117 / September 2012

591

E. Bor-Seng-Shu et al.

Fig. 3. Intracranial pressure measured 48 hours after decompressive craniectomy as compared with preoperative values.

ectomy, bilateral frontotemporoparietal craniectomy, or


bitemporal craniectomy with or without dural opening.
Third, ICP monitoring involved either intraventricular
catheter monitoring or intraparenchymal gauge device
monitoring. Intraventricular catheter monitoring allows
CSF withdrawal for reducing ICP, delaying the need for
surgical decompression. Other factors that contributed to
methodological heterogeneity were a limited number of
patients, an arbitrary age limit within the inclusion criteria, a lack of stratification within the age groups, and
the absence of outcome end points. Another limitation of
this review was the absence of any randomized controlled
trial for examining the use of decompressive craniectomy
in reducing ICP and increasing CPP, except one paper
with a small sample size.26 As a consequence, we could
not compare the effect of decompressive craniectomy
against a comparable separate control group, as would be
preferred, and thus we assessed the changes in ICP and
CPP by using each patient as his or her own control. Although there was great heterogeneity among the reviewed
articles, most showed ICP reduction and CPP augmentation after decompressive craniectomy.
Of note, we have not performed a formal assessment
of reporting bias. Studies with negative results are less
likely to get published, and we have not been able to perform a search for unpublished studies. Our results could
suffer from the so-called drawer effect, and for this reason the WMD we obtained for ICP and CPP should be
approached with caution. This aspect can be improved

with more randomized controlled trials in this area because of the stricter controls on access to information
coming out of these trials.

Conclusions

In summary, decompressive craniectomy effectively


reduces ICP and increases CPP in TBI patients with uncontrollable intracranial hypertension; these effects may
lead to 1) a rise in both cerebral blood flow and cerebral
microvascular perfusionnot only in the decompressed
hemisphere, but also in the opposite hemisphere35,7,10,21
so that acceptable cerebral perfusion can be achieved at
lower arterial blood pressure levels, 5,27 2) an elevation in
brain tissue PO2 as well as the return of abnormal metabolic parameters to normal values in cases of cerebral
ischemia,11,20,25 and 3) potential benefits to functional
outcome (still being addressed by clinical trials). On the
other hand, the rise in CPP following decompressive craniectomy can result in 1) disturbed cerebral blood flow
(significant cerebral hyperemia in some cases)4 and 2) a
worsening of cerebral edema,1,6 mainly if impairment of
cerebral microvascular regulation occurs.27 Although our
results indicate that decompressive craniectomy seems to
be an effective treatment for reducing ICP and increasing
CPP, the correlation between these effects and clinical
outcome is uncertain. Most authors noticed that using decompressive craniectomy to control ICP does not always

Fig. 4. Cerebral perfusion pressure before and after decompressive craniectomy.

592

J Neurosurg / Volume 117 / September 2012

40

Whitfield et al.,
2001

Stiefel et al.,
2004
Aarabi et al.,
2006

J Neurosurg / Volume 117 / September 2012

Kim et al., 2009

28

40

16

21

4
9

R
R

Howard et al.,
2008

Olivecrona et
al., 2007
Ho et al., 2008

Heppner et al.,
2006
Kan et al., 2006
Skoglund et al.,
2006

26

13

Taylor et al.,
2001

Mnch et al.,
2000

Yoo et al., 1999

28.2 16.2, fa vorable out come group;


33.6 17.6,
unfavorable
outcome
group
52.3 10.3

38.0 15.7

37.6 1.7

10 (514)
22.1 10.8

27 (1750)

25.3

28.8 (2043)

23 (459)

ICP Threshold for


Indication

20 mm Hg

30 mm Hg plus
CPP <70 mm Hg
or ICP >35 mm
Hg
20 mm Hg w/ pla teau waves
20 mm Hg

9.6 6.9

28.2 9.6

68.5

45 (range 2157)

20 mm Hg

20 mm Hg for more
than 1 hr
20 mm Hg

20 mm Hg

8.7 (range 4.220) 25 mm Hg


105 79
20 mm Hg

11 6

115.2 (range
4.8384)
<48 (17 cases);
>48 (33 cases)

<48 (20 cases);


>48 (6 cases)

NR

Time From Injury


to Op (hrs)

surgery based on
CT scan & clini cal presentation
43.4 17.8
4.5 3.8 (63.3% 30 mm Hg for pe cases); 56.2 riod longer than
57 (36.7%
15 min
cases)
10 (1.1314.7) 17.3 (range
20 mm Hg
6.527.5)

27.6

Study No. of Mean Age in Yrs


Authors & Year Design Patients
(range)

37.9 15.9

35 13.5

25 6

36.4 3.4

47.5 9.5
29.2 3.5

35 8

24

26 4

37.5 10

26.4 7.9

22.1 11.1

31.7

Preop ICP
(mm Hg)

TABLE 1: Summary of characteristics in the clinical studies on decompressive craniectomy*

9.2 5.9

14.6 8.7

15.5 2

13.1 2.1

16.2 8.5
11.1 6

12 6

14.6

19 11

18.1 16

17.4 3.4

19.7 10.8

3.5

Postop ICP
(mm Hg)

IV

NR

IP

IV, IP

IV, IP
IV, IP

IP

IV, IP

IP

NR

IV, IP

NR

IV

ICP
Catheter

good outcome: 41%; poor out come: 59%

mean GOS Score 3.3; 1 patient


died

Outcome

GOS 45: 31%; GOS 13: 69%;


mortality: 37.5%
good outcome: 30%; survivors:
67% w/ good outcome; mortal ity: 55%

GOS 45: 71%; mortality: 14%

mortality: 75%
good outcome: 68%; mortality:
11%

GOS 45: 40%; PVS: 14%; se verely disabled: 9%; mortality:


28%
NR

NR

(continued)

hemicraniectomy (unilat good outcome: 57.1%; poor out or bilat)


come: 42.9%; mortality: 21.4%

hemicraniectomy (39
patients); bifrontal
craniectomy (1 case)
hemicraniectomy; bi frontal craniectomy
hemicraniectomy
hemicraniectomy (unilat
or bilat); bifrontal
craniectomy
hemicraniectomy; bi frontal craniectomy
hemicraniectomy; bi frontal craniectomy
hemicraniectomy

hemicraniectomy

bitemporal craniectomy; reduced risk of death, PVS, & se no duraplasty


vere disability at 6 mos postop:
0.54 (95% CI 0.291.07)
bifrontal craniectomy
good outcome: 69%; poor out come: 8%; mortality: 26%

hemicraniectomy

bifrontal craniectomy

Surgical Technique

Effects of craniectomy on ICP and CPP

593

594

43

62

36

100

Bao et al., 2010

Daboussi et al.,
2009

Eberle et al.,
2010
Schneider et
al., 2002
Soustiel et al.,
2010
Ucar et al.,
2005

29 13.2

35.1 16.6

36.6

35.7 15.0

35.3 15

38 9.4

17.1 6.8 (94


cases)

<24 (29 cases)

<24 (34 cases)


40.5 1.6

41 13.5

37 17

37 6.4

21.3 2.75

Preop ICP
(mm Hg)

20 mm Hg (7 cases 20.4 7.9


monitored)
25 mm Hg
29.8 5.2

20 mm Hg (19 cas es monitored)

20 mm Hg

30 mm Hg for more
than 15 min

25 mm Hg

ICP Threshold for


Indication

23.9 4.9

4.1 10.9

9.8 1.3

16.3 12.6

20 13

11.2 7.1

12.73 5.15

Postop ICP
(mm Hg)

IV

IV, IP

IV, IP

IP

IV, IP

IP

ICP
Catheter

GOS 45: 48%; GOS 23: 37%;


mortality: 15%

Outcome

GOS 45: 54.1%; PVS: 10.8%;


severe disability: 16.2%; mor tality: 18.9%
hemicraniectomy
good outcome & moderate dis ability: 42%; PVS: 27%; mor tality: 8%
hemicraniectomy biGOS 45: 41.9%; GOS 23:
frontal craniectomy
32.6%; mortality: 25.6%
GOS 23: 48.8%; GOS 45:
29.1%; mortality: 22.5%
hemicraniectomy (unilat good recovery: 7 times higher in
or bilat)
nonsurgical group
hemicraniectomy (unilat good outcome: 16%; poor out or bilat)
come: 84%; mortality: 54%

bifrontal craniectomy
(78% cases); hemi craniectomy (22%
cases)
bilat hemicraniectomy

Surgical Technique

* Values are expressed as the means SD unless indicated otherwise. Abbreviations: GOS = Glasgow Outcome Scale; IP = intraparenchymal gauge device monitoring; IV = intraventricular catheter
monitoring; NR = not reported; P = prospective study; PVS = persistent vegetative state; R = retrospective study.

26

37

<48 (15 cases);


72168 (12
cases)
26

72 (range 0240)

35 (1655)

Timofeev et al.,
2008

27

Time From Injury


to Op (hrs)

Study No. of Mean Age in Yrs


Authors & Year Design Patients
(range)

TABLE 1: Summary of characteristics in the clinical studies on decompressive craniectomy* (continued)

E. Bor-Seng-Shu et al.

J Neurosurg / Volume 117 / September 2012

Effects of craniectomy on ICP and CPP


result in a favorable clinical outcome. Certainly, this issue
deserves further research.
Disclosure
The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this
paper.
Author contributions to the study and manuscript preparation include the following. Conception and design: Bor-Seng-Shu,
Figueiredo, Teixeira, Amorim, Panerai. Acquisition of data: BorSeng-Shu, Figueiredo, Amorim. Analysis and interpretation of data:
Bor-Seng-Shu, Figueiredo, Amorim, Valbuza, de Oliveira, Panerai.
Drafting the article: Bor-Seng-Shu, Figueiredo, Amorim, Valbuza.
Critically revising the article: all authors. Reviewed submitted
version of manuscript: all authors. Approved the final version of
the manuscript on behalf of all authors: Bor-Seng-Shu. Statistical
analysis: Valbuza, de Oliveira. Study supervision: Teixeira, Panerai.

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Manuscript submitted August 16, 2010.


Accepted June 11, 2012.
Please include this information when citing this paper: published
online July 13, 2012; DOI: 10.3171/2012.6.JNS101400.
Address correspondence to: Edson Bor-Seng-Shu, M.D., Ph.D.,
Rua Loefgreen, 1272, CEP 04040-001, Sao Paulo, SP, Brazil. email:
edsonshu@hotmail.com.

J Neurosurg / Volume 117 / September 2012