J Neurosurg 118:757762, 2013

AANS, 2013

Predictors of cranioplasty complications in stroke and

trauma patients
Clinical article
Brian P. Walcott, M.D.,1 Churl-Su Kwon, M.D., M.P.H.,1
Sameer A. Sheth, M.D., Ph.D.,1 Corey R. Fehnel, M.D., 2 Robert M. Koffie, Ph.D.,1
Wael F. Asaad, M.D., Ph.D., 3 Brian V. Nahed, M.D.,1 and Jean-Valery Coumans, M.D.1
1
Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, Boston,
Massachusetts; 2Department of Neurology, Brown University Alpert Medical School and Rhode Island
Hospital; and 3Department of Neurosurgery and Brown Institute for Brain Science, Providence, Rhode Island

Object. Decompressive craniectomy mandates subsequent cranioplasty. Complications of cranioplasty may be

independent of the initial craniectomy, or they may be contingent upon the craniectomy. Authors of this study aimed
to identify surgery- and patient-specific risk factors related to the development of surgical site infection and other
complications following cranioplasty.
Methods. A consecutive cohort of patients of all ages and both sexes who had undergone cranioplasty following
craniectomy for stroke or trauma at a single institution in the period from May 2004 to May 2012 was retrospectively
established. Patients who had undergone craniectomy for infectious lesions or neoplasia were excluded. A logistic
regression analysis was performed to model and predict determinants related to infection following cranioplasty.
Results. Two hundred thirty-nine patients met the study criteria. The overall rate of complication following cra
nioplasty was 23.85% (57 patients). Complications included, predominantly, surgical site infection, hydrocephalus,
and new-onset seizures. Logistic regression analysis identified previous reoperation (OR 3.25, 95% CI 1.308.11, p
= 0.01) and therapeutic indication for stroke (OR 2.45, 95% CI 1.115.39, p = 0.03) as significantly associated with
the development of cranioplasty infection. Patient age, location of cranioplasty, presence of an intracranial device,
bone flap preservation method, cranioplasty material, booking method, and time interval > 90 days between initial
craniectomy and cranioplasty were not predictive of the development of cranioplasty infection.
Conclusions. Cranioplasty complications are common. Cranioplasty infection rates are predicted by reoperation
following craniectomy and therapeutic indication (stroke). These variables may be associated with patient-centered
risk factors that increase cranioplasty infection risk.
(http://thejns.org/doi/abs/10.3171/2013.1.JNS121626)

Key Words cranioplasty trauma infection complication

stroke decompressive craniectomy traumatic brain injury
vascular disorders

ecompressive craniectomy, while still controver

sial, is a potentially lifesaving procedure in se
verely brain-injured states, such as traumatic
brain injury, aneurysmal subarachnoid hemorrhage, and
malignant cerebral infarction.1,3,7,34,36,41,45 Growing evi
dence of its efficacy, particularly in the setting of malig
nant cerebral edema following ischemic stroke,15,17,42 has
been responsible for the increasing performance of the
procedure.44 For patients who survive, a subsequent cra
nioplasty operation is required. Given the rising use in
craniectomy and subsequent cranioplasty, it is necessary
to examine the complication rate of these procedures. In
particular, we seek to know whether cranioplasty compli
cations arise from factors specific to the procedure itself,

J Neurosurg / Volume 118 / April 2013

or whether they are affected by factors related to the ini

tial craniectomy.
Patient-specific and surgery-specific factors are his
torically reported to be the most important determinants
of complication following cranioplasty.2,5,12,31,48 While a
recent meta-analysis demonstrated no contribution from
surgery-specific factorssuch as method of bone flap
storage, implant material, time interval from cranioplasty
to infection, or overall complication rate following cra
nioplasty48there may be variables in certain patient
populations that are influential. We hypothesized that pa
tient- and surgery-specific risk factors are related to the
development of surgical site infection following cranio
plasty.
757

B. P. Walcott et al.
Methods

After obtaining institutional review board approval,

we retrospectively established a consecutive cohort of pa
tients who had undergone cranioplasty at a single institu
tion in the period from May 2004 to May 2012. Patients
were identified using an electronic operative scheduling
system that allowed identification of cases based on key
word query.
Men and women of all ages were included if they
had undergone a cranioplasty following a craniectomy
> 6 cm in diameter for either trauma or stroke. All pa
tients underwent cranioplasty at the Massachusetts Gen
eral Hospital. Occasionally, patients were included if they
had undergone initial treatment (craniectomy) at a refer
ring hospital, provided the necessary data elements were
available in the medical record.
Patients who had undergone craniectomy for infec
tious lesions, such as osteomyelitis, were excluded, as
were those who had undergone craniectomy for bone flap
infections following craniotomy for all causes. Patients
who had undergone craniectomy for neoplastic etiologies,
such as meningioma, were also excluded. And, finally, pa
tients who had undergone suboccipital cranioplasty were
excluded.
In addition to demographics, information regarding
the dates of all operations and the duration of follow-up
was recorded. Details of the initial craniectomy were re
viewed to identify the reason for craniectomy and its ur
gency. Urgency was extrapolated from the surgical sched
uling, categorized as elective (to be performed when
convenient), urgent (to be performed within 4 hours), or
emergent (to be performed within 15 minutes). Informa
tion about intracranial pressure monitoring and CSF di
version prior to cranioplasty was recorded as having no
device, having a fiberoptic parenchymal pressure monitor
and/or brain tissue oxygen monitor, having an external
ventriculostomy, or having a permanent CSF shunt. Com
plications from the initial craniectomy were recorded as
no complication, reoperation for any reason at the same
surgical site, persistent hydrocephalus (defined as the
need for permanent CSF diversion prior to or at the time
of cranioplasty), or an infection (based on the Centers for
Disease Control and Prevention standards for surgical
site infection).16
The location of the cranioplasty was classified as con
vexity, bifrontal, or bilateral convexity. The type of mate
rial used to reconstruct the cranial defect was classified
as autologous or synthetic. When autologous material was
used, the preservation method was described as in vi
vo subcutaneous storage, frozen at 80C, or sterilized.
Complications related to the cranioplasty were identified
as postoperative hematoma requiring reoperation, wound
healing disturbance, intracranial abscess or empyema re
quiring reoperation and discarding of the cranioplasty ma
terial, hydrocephalus (new need for permanent CSF diver
sion following cranioplasty), postoperative seizure (in the
absence of preexisting seizures), or death.
Statistical analysis was performed using the R pro
gramming environment and Prism 5 for Mac (GraphPad
Software, Inc.). Univariate logistic regression analyses
758

were performed to determine the variables associated

with infection following cranioplasty. Significance was
predefined at p < 0.05. Values represent the means stan
dard errors of the means, unless indicated otherwise.

Results

Two hundred thirty-nine patients met the study cri

teria. Patient demographics and surgical indications were
identified (Table 1). The mean time to cranioplasty was
183 15.1 days. The median follow-up was 440 days
(range 13681 days). The overall rate of complication fol
lowing cranioplasty was 23.85% (57 patients; Table 2).
Univariate logistic regression analysis identified previ
ous reoperation (OR 3.25, 95% CI 1.308.11, p = 0.01)
and therapeutic indication for stroke (OR 2.45, 95% CI
1.115.39, p = 0.03) as having a significant association
with the development of cranioplasty infection (Fig. 1
and Table 3). Age, location of cranioplasty, presence of an
intracranial device, bone flap preservation method (Fig.
2), cranioplasty material (Fig. 3), booking method, and
time interval > 90 days between initial craniectomy and
cranioplasty were not predictive of the development of
cranioplasty infection.
Special attention was paid to the subgroup of patients
who underwent reoperation (after the initial craniecto
my, before the cranioplasty), as it is possible that infec
TABLE 1: Summary of characteristics in 239 patients who
underwent cranioplasty
Parameter

No.

sex
M
F
mean age in yrs (range)
M
F
craniectomy booking
elective
urgent
emergent
location of cranioplasty
convexity
bifrontal
bilateral convexity
diagnosis
ruptured vascular lesion
hemorrhagic stroke
ischemic stroke
trauma
bone flap storage method
discarded
sterilized
frozen
subcutaneous

157
82
41.9 (5.872.8)
42.8 (0.487.0)
2
51
186
219
13
7
27
24
42
146
83
9
100
48

J Neurosurg / Volume 118 / April 2013

Cranioplasty complications
TABLE 2: Complications following cranioplasty
Complication

No. of Cases (%)

hematoma
wound healing disturbance
surgical site infection
hydrocephalus
seizure
death
overall

8 (3.35)
4 (1.67)
29 (12.13)
12 (5.02)
8 (3.35)
0 (0)
57 (23.85)

tion following craniectomy may predispose patients to

subsequent infection. Reoperation was performed in 25
trauma patients and 21 stroke patients for the following
indications: cerebral edema (10 patients), hematoma (16
patients), infection (17 patients), and other (negative ex
ploration for suspected infection [2 patients] and staged
treatment of a ruptured cerebral aneurysm [1 patient]).
Of these patients who underwent reoperation following
craniectomy, 10 went on to develop infection following
cranioplasty. Using a regression analysis in this reopera
tion group, we found no significant association with the
indication for reoperation (p = 0.214) or the indication
for initial craniectomy (p = 0.314). Even in a multivariate
model (equally weighted variables, p = 0.211) we found
no association with the development of subsequent cra
nioplasty infection.

Fig. 1. Bar graph showing that surgical indication predicts cranioplasty infection. In logistic regression analysis, the indication for craniectomy (stroke) predicted subsequent cranioplasty infection (OR 2.45,
95% CI 1.115.39, p = 0.03). n = number of cases; # = number.

Discussion

The 2 major aims of this retrospective analysis were

to identify all complications related to cranioplasty and to
evaluate the influence of specific risk factors on cranio
plasty infection rates. The overall complication rate was
higher (23.8%) than in other studies, as the criteria for
complication were rigorous and included the incidence
of outcomes not previously described in large series.5,31
These outcomes included the occurrence of new-onset
postoperative seizures and hydrocephalus. While the rate
of infection following cranioplasty is high,48 other com
plications must not be overlooked. We also uniquely lim
ited our analysis to patients with a primary diagnosis of
stroke or traumatic brain injury (excluding craniectomy

TABLE 3: Logistic regression analysis for predictors of infection following cranioplasty*

Factor

OR

95% CI

p Value

patient age
location of cranioplasty
convexity
bifrontal
bilateral convexity
presence of intracranial device
bone flap preservation method
not preserved
frozen
subcutaneous
cranioplasty material: autologous vs synthetic
prior surgical complication
none
previous reop
hydrocephalus
infection
craniectomy scheduling: emergent vs other
disease: stroke vs trauma
time to cranioplasty >90 days

1.01

0.991.03

0.41

REF
1.29
empty
0.70

REF
0.276.15

0.291.68

0.75

0.42

REF
1.95
1.82
1.78

REF
0.645.95
0.714.68
0.734.37

0.24
0.22
0.21

REF
3.25
1.65
0.72
1.42
2.45
0.85

REF
1.308.11
0.441.65
0.095.88
0.513.93
1.115.39
0.371.97

0.01
0.46
0.76
0.50
0.03
0.34

* REF = reference group to which the odds ratios for other outcomes were compared.
No infections associated with bilateral convexity location.
Significant.

J Neurosurg / Volume 118 / April 2013

759

B. P. Walcott et al.

Fig. 2. Bar graph indicating that the bone flap storage method does
not predict cranioplasty infection (frozen storage: OR 1.95, 95% CI
0.645.95, p = 0.24; subcutaneous storage: OR 1.82, 95% CI 0.71
4.68, p = 0.22).

performed primarily for infection or neoplasia) in an at

tempt to reduce confounding factors. Of the variables
examined, only 2 (previous reoperation and disease cat
egory of stroke) were significant in a univariate logistic
regression analysis. Our findings support a paradigm shift
in the understanding of infection following cranioplasty
that includes patient-specific factors as a major compo
nent of the risk propensity.
Timing of Surgery

The optimal timing of cranioplasty following crani

ectomy is intensely debated. Studies have been performed
that either support or refute its influence on postcranio
plasty infection.2,5,12,21,31 One hypothesis for a potentially
increased rate of infectious complications following ear
ly cranioplasty includes the retention of microorganisms
from the initial operation. Because microbial organisms
are present in a large proportion of elective operations,
both on the skin after its preparation and in the wound
immediately after incision,33 it is unlikely that microbes
from the initial craniectomy (even if present) would have
a preferential virulence over microorganisms inoculated
at the time of cranioplasty. There is evidence that an in
creased duration of hospitalization or nursing facility care
is associated with the colonization of organisms that have
a greater propensity for virulence, such as methicillin-re
sistant Staphylococcus aureus.4,22,26,43 In fact, it has been
shown that the majority of autologous bone flaps (and
possibly synthetic flaps) reimplanted are contaminated by
microorganisms with no effect on the risk of surgical site
infection.6
An alternative hypothesis is that a healing wound rep

Fig. 3. Bar graph indicating that the type of cranioplasty material

used does not predict cranioplasty infection (OR 1.78, 95% CI 0.73
4.37, p = 0.21).

760

resents a potential weak point in host defenses. Operating

on a wound in the early healing period has the potential to
dramatically alter the normal recruitment of leukocytes,
including neutrophils, macrophages, dendritic cells, and
lymphocytes, which are tightly regulated in a temporal
fashion by chemokines.11 Disturbing these patterns can
alter the normal progression of the epithelialization, col
lagen remodeling, and angiogenesis that are vital to host
defenses.35 Through this mechanism, reoperation may
have led to the observed increased risk of cranioplasty
infection, whereas the time interval to cranioplasty did
not. Note that the majority of cranioplasties in the present
study were performed in the maturation and remodeling
stage of wound healing.
A parallel hypothesis is that reoperation indirectly
selects for advanced disease severity and other patientspecific risk factors that contribute to the risk of infection,
congruent with our findings of time interval indepen
dence. For example, reoperation for intracranial hemor
rhage following craniectomy for subdural hematoma with
brainstem herniation may be indicative of a worse neuro
logical outcome. A worse neurological outcome and dis
orders of consciousness, in turn, may be associated with
a compromised nutritional status.23 While there are two
degrees of separation in this predictive model, there is
robust evidence that impaired nutrition is strongly asso
ciated with an increased surgical infection risk.14,18,25,27,37
This study also reveals stroke as a predictor of cra
nioplasty infection when compared with trauma. Patientspecific factors could be implicated in this finding as
well, since risk factors for stroke overlap with risk factors
for infection and include diabetes, cigarette smoking, and
elevated body mass index.810,13,24,28,38,39,47,50
Seizure and Hydrocephalus Following Cranioplasty

Cranioplasty is not merely a cosmetic operation. It

provides physical protection to the intracranial contents,
particularly as patients become more mobile following
brain injury. There is also preliminary evidence that cra
nioplasty can improve cerebral blood flow, thereby im
proving neurological status and recovery.19,29,32,49
Even though cranioplasty is considered an extra
dural procedure, a minimal amount of manipulation of
brain tissue during dissection of the extradural plane is
common. Moreover, there are instances in which brain
tissue is manipulated to facilitate the smooth contour of
the bony cranial construct. This manipulation may pre
cipitate seizure activity in already susceptible brain tis
sue. Since the conclusion of this study, we have instituted
a protocol for periprocedural seizure prophylaxis at the
time of cranioplasty. While robust evidence for its effi
cacy is unlikely due to clinical trial design limitations, it
is a low risk intervention that may limit the relatively high
incidence of new-onset seizures following cranioplasty.
While the avoidance of cranioplasty is recommended
in the setting of overt hydrocephalus, we sometimes per
form the procedure in patients with full cranial flaps
in the absence of cerebral edema. It is known that cra
nioplasty may play a significant factor in the need for
permanent CSF diversion following craniectomy.46 Some
patients do ultimately require CSF diversion, as occurred
J Neurosurg / Volume 118 / April 2013

Cranioplasty complications
among our series; however, we note that cranioplasty it
self was not specifically noted to precipitate communi
cating hydrocephalus. We were unable to determine in
our study whether hydrocephalus was the direct result of
the primary brain injury, the craniectomy, or the cranio
plasty. We suggest close surveillance for the development
of hydrocephalus following cranioplasty, particularly in
patients in whom the skin overlying the craniectomy site
is not significantly sunken. When overt hydrocephalus is
present during evaluation for cranioplasty, consideration
should be given to permanent CSF diversion either before
or at the time of cranioplasty.
Study Strengths and Limitations

One strength of the current study is the long-term fol

low-up, which allows time for indolent organisms to pre
sent with infection outside of the immediate perioperative
period.20 It is not uncommon for cranioplasty infections to
manifest months to even years later. Another strength is the
large size of the cohort allowing for meaningful analysis of
relatively rare complications. That said, retrospective stud
ies have inherent limitations. The use of a comprehensive
operative log, standardized definitions of variables, and a
detailed electronic medical record mitigated some of the
shortcomings of a retrospective design, such as selection
and recall bias. Our study was not powered to analyze pa
tient-specific factors in greater detail, such as the effects
of steroid use, body mass index, diabetes, obesity, and du
ration of surgery, all of which may contribute to postcra
nioplasty infection. A multivariate logistic regression was
not performed because of considerable controversy in the
literature over relevant variables.40
Cranioplasty has been performed for hundreds of
years.30 Despite a vast experience with different techniques,
materials, and protocols, the optimal combination is yet to
be elucidated. Mitigation of infection risk factors may be
possible by manipulation of patient-centered factors.

Conclusions

Cranioplasty infection rates are predicted by the

occurrence of reoperation and indication for surgery
(stroke). Complications following surgery include surgi
cal site infection, hydrocephalus, and new-onset seizures,
among others.
Disclosure
The authors report no conflict of interest concerning the mate
rials 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: Walcott, Fehnel,
Asaad. Acquisition of data: Walcott, Kwon, Fehnel, Koffie. Analysis
and interpretation of data: Walcott, Kwon, Sheth, Nahed, Coumans.
Drafting the article: Walcott, Kwon, Sheth. 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: Walcott. Statistical analysis: Walcott, Kwon, Sheth.
Administrative/technical/material support: Coumans. Study supervi
sion: Nahed, Coumans.

J Neurosurg / Volume 118 / April 2013

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Manuscript submitted August 20, 2012.
Accepted January 14, 2013.
Please include this information when citing this paper: pub
lished online February 8, 2013; DOI: 10.3171/2013.1.JNS121626.
Address correspondence to: Brian P. Walcott, M.D., Massachu
setts General Hospital, 55 Fruit Street, White Building Room 502,
Boston, Massachusetts 02114. email: walcott.brian@mgh.harvard.
edu.

J Neurosurg / Volume 118 / April 2013