15018752330
发表时间:2015-12-08 浏览次数:487次
Introduction
Cranioplasty implants, whether of autologous bone or biocompatible bone substitutes, are used primarily in cases of surgical cranial decompression following pathological elevations of intracranial pressure. These implants play roles in restoring both function and aesthetics, and thus, consideration of a custom-made solution as a first choice is in the best interest of the patient. Available bone substitutes include porous hydroxyapatite (HA), which favors regeneration (biomimetism) as well as reconstruction, and polymethylmethacrylate (PMMA), which should be reserved for severe cases of psychiatric disturbance, violent institutionalized patients, epileptics with frequent falling episodes, and the terminally ill. [1] Whichever material is used, however, prosthetic cranial implants are susceptible to intra- and postsurgical complications and even failure. The aim of this study was to investigate such occurrences in HA cranioplasty implants, seeking not only to determine the likely causes (whether correlated or not with the device itself) but also, where possible, to suggest countermeasures.
Methods
We analyzed information regarding failures or complications reported in
postmarketing surveillance and clinical studies of patients treated
worldwide with custom-made HA cranial implants (Custom Bone Service
Fin-Ceramica Faenza, Italy) during the period of 1997-2013. This
analysis was possible due to an agreement between the relevant parties
in the context of an academic study. No sensitive information was
collected during the research, which was limited to the processing of
data regarding adverse events according to the biomedical device
surveillance norms in force (MEDDEV-2). [2] Statistical interpretation of the data was performed using IBM SPSS (V19; Chicago, United States).
Results
In the study period, 2877 custom-made HA devices were implanted and all adverse events that arose were collated [Table 1]. The two most common complications were implant fractures (84 cases, 2.9% of the total fitted) and infections (51 cases, 1.77%). Of the fractures, 36 (1.25%) occurred postimplant (within 12 months of surgery, delayed fracture) and 48 (1.66%) occurred during the surgery itself (early fractures). A back-up was used to replace the primary implant in 43 of these cases. Fractures were not correlated with the size of the cranial defect. A correlation was noted between the occurrence of infection and the implantation site: frontoparietotemporal in 25 cases (49% of total infections), frontal-bifrontal in 17 (33.3%) temporoparietal in 6 (11.8%) and parietal in 3 (5.9%) [Table 2]. However, data analysis did not reveal a statistically significant difference regarding implantation site (Chi-square test; P = 0.1694; odds ratio = 1.65)[Table 3]. A further correlation between the time elapsed after surgery and the onset of infection was noted: less than 6 months in 32 (62.8%) cases, 6 months to 1 year in 3 cases (5.8%), and more than 1 year in 16 cases (31.4%). Analyzing data for the first postoperative year, it was observed that most infections occurred between 3 and 6 months (23 infections, 45%). It was also noted that infections were more common in cases of cranial trauma.
Discussion
Delayed posttraumatic prosthesis fracture (36/2877) occurred with an
incidence three-fold higher than that seen in normal population
(3.5-4.5/1000). The incidence of a second cranial trauma also seemed to
be greater than in normal population (2/1000), presumably due to the
clinical and neurological effects of the underlying primary pathology.
However, there was no discernable correlation between fracture and
defect size, so other issues need to be examined, most likely the
severity of the head trauma that fractured the skull or surgical error
stemming from a lack of careful planning, positioning, or fixing of the
implant. Regarding the planning, design, and validation phase, the
relevant persons (manufacturing technician and surgeon) should pay
particular attention to the following critical steps if such occurrences
are to be avoided: verification of suitable implant thickness and
uniformity of the density distribution of the prosthesis (micro- and
macro-pores and interconnection channels), ensuring that the prosthesis
perimeter engages the bone margin at all points, the latter being a type
of ledge upon which the implant should rest snugly all round, thereby
spreading the forces evenly. Thus, the prosthesis, in addition to
possessing suitable curvature, should be tailored to fit the cranial
lacuna precisely and without breaks. Indeed, if this does not occur, in
addition to a lack of osteointegration, the laws of mechanics dictate
that weaker areas with less resistance will arise. Regarding early
fracture (i.e. during surgery), if one implant breaks, it could be due
to manufacturing/design error, but if both the primary and back-up
devices break, surgical error is the more likely cause because the
possibility of a structural defect affecting two separate blocks of HA
is remote.
Infections were more frequent in trauma patients, not
surprisingly, because these represent the greater portion of the
population in which custom-made HA cranial implants are indicated. The
incidence of infection was 1.77%, a finding comparable to that reported
for titanium implants (1.18%) and slightly better than that for PMMA
prostheses (5.48%). [3],[4],[5],[6],[7] Of the infections, 73% occurred during the 1 st
year after fitting, confirming that infection risk is higher in the
postsurgical period. That being said, cranioplasty implants fitted in
the frontal sinus or mastoid can lead to airway fistulas and to acute
secondary infections that may arise at any time during the life of the
patient, even many years after surgery. [8],[9]
Infections were found to occur with particular frequency in cases of
large cranial implants (frontoparietotemporal), or those in the vicinity
of the paranasal sinuses (frontal/bifrontal). [10]
This could be due to at least two distinct factors: (1) skin coverage
is often insufficient in cases of large implants, due to tissue atrophy
arising from the surgical approach itself (sectioning of large arterial
blood vessels during the incision) and/or the time interval between
craniotomy and reconstruction, which can predispose a patient to
cutaneous lesions or ulcers that allow pathogenic agents to invade the
prosthesis; and (2) poor occlusion of the sinuses, in cases of frontal
or bifrontal cranioplasty, which effectively leaves the door open to any
invading pathogen. Moreover, the sometimes precarious clinical and
neurological conditions of trauma patients may reduce their immune
responses. A first statistical analysis of the data (Chi-square test)
did not reveal a difference between infection rates of HA implants that
either take or do not take relationship with the frontal sinus [Table 3].
Despite this finding, further in-depth, studies are warranted to
clarify a potential correlation between infection rates and implant
sites.
In almost all cases of infection, it is advisable to
cleanse the wound and remove the prosthesis to avoid intradural
propagation and the consequent severe risk as well as prolonged
hospitalization of the patient. [8],[11]
Indeed, in cases in which back-up devices have been used to replace
removed primary implants, infection rates are relatively low, presumably
due to the fact that these patients have already been administered
appropriate antibiotic treatment and have been scheduled for prompt
re-intervention without undue waiting times. Nevertheless, the need for
implant removal should be evaluated on a case-by-case basis, because in
certain cases conservation is possible. [12]
Indeed, we recently managed to salvage an infected HA cranial implant
by administering suitable antibiotic treatment over the course of a few
months. This experience showed that if the dura mater appears intact,
and if the pathogen can be isolated, identified, and targeted with
appropriate antibiotics, it is possible to opt for conservative
treatment provided that careful monitoring is implemented, which should
include regular blood tests and serial scintigraphy with labeled
leukocytes. It should not be forgotten that as long ago as 1948, 25% of
infected synthetic implants were salvaged by means of antibiotic therapy
and curettage. [8]
The relationship between the timing of surgery and infection lead us to
believe that this would be less frequent if the cranioplasty was
performed within the first 3 months or after 6 months. The time between 3
and 6 months is associated with the highest risk of complications, both
infectious and otherwise.
Another complication arising from
cranioplasty is the dislocation/mobilization of the implant, which can
be caused by poor planning, design and/or validation, and errors in the
surgical procedure. Thus, this type of occurrence is largely preventable
if a few simple precautionary steps are taken during the craniotomy
itself, such as use of the jigsaw technique and beveling the cranial
defect edge [Figure 1] and [Figure 2].
Furthermore, in cases of large lacunas requiring more than one implant,
these should be shaped so that their juncture mimics the natural
sutures of the skull and features slanted-S edges [Figure 3].
Other precautions include avoiding anchoring the prosthesis to the
temporal muscle; this muscle should instead be positioned over the
implant, which should be equipped with sufficient holes for anchorage [Figure 4]. [13]
Attempts should also be made to prevent the formation of a fluid
fistula, which can severely slow or impede cicatrisation and
osteomimesis. The main cause of fistulas is adhesion between the dura
mater, temporal muscle, and galea. [14]
Such scarring adhesions can prolong subsequent surgery times, cause
excessive blood loss, and increase the probability of an inadvertent
lesion to the dura mater or cerebral cortex due to the difficult
techniques required for their dissection. [15]
Nevertheless, these events can be averted by placing an inert,
nonresorbable membrane, such as a super-thin (0.1 mm) sheet of expanded
polytetrafluoroethylene (ePTFE; e.g. Preclude Peritoneal Membrane, W.L.
Gore and Associates. Inc.), between the dura and the soft tissues,
especially at the site of the temporal muscle. [16]
Extradural and extracranial pooling of fluid and subdural hematoma are
less frequent events in cranioplasties. The former can usually be
resolved by prompting parenchymal re-expansion (if viable) or by
increasing the number of dural suspension points and maintaining
subcutaneous drainage for a longer period of time. Adhesion of the scalp
to the cranial implant can be promoted by anchoring the latter to the
galea fascia using sutures.
The soft tissues overlying the
cranioplasty implant can also be subject to ischemia, necrosis, and/or
decubitus, and it is thus vital that cutaneous trophism and irrigation
is carefully evaluated in the presurgical phase. Moreover, a surgical
approach should be planned taking into account not only aesthetic
concerns (such as avoiding the incision encroaching below the hairline
and using the Simpson technique) but also seeking to avoid damage to the
main arterial trunks and temporal muscle. [13],[17]
In difficult cases featuring a paucity of viable soft tissue,
cranioplasty implant fitting could necessitate the use of cutaneous
expanders. Another useful surgical aid for improving cutaneous trophism
is dermal matrix (INTEGRA Dermal Regeneration Template Single Layer
film) [Figure 5]. [18]
Such matrices promote mesenchymal histoinduction and histoconduction,
serving to guide the formation of normal dermal tissue. The collagen and
glucosaminoglycans of these matrices provide structural support for the
infiltrating fibroblasts, macrophages, lymphocytes, and capillaries
that form the neurovascular network. In covering the implant, these
networks favor the development of better blood irrigation, important not
only for cutaneous tropism but also for the invasion of the porous HA
of the cranial implant by the organic bone matrix, promoting
osteoconduction and osteointegration of the prosthesis. The scalp is not
only necessary for implant coverage but it also supplies nutrients and
immune system components. Together with the dura, it also aids in the
osteomimesis process of the cranioplasty implant.
Indeed, another possible cause of HA cranial implant failure is lack of osteomimesis. If there is poor contiguity between the implant and the skull margin, osteoblast migration is compromised. To avoid this and to ensure the accurate design of the implant (which must fit perfectly along the entire border of its cranial housing), the surgeon must take certain factors into account during the surgery itself. In particular, the skull defect borders must be cleared completely of any scarring or inflammatory matrix, the dura on the border of the internal plate must be delaminated, and the craniectomy border drilled delicately. In addition, no material should be placed between the bone and implant, with the exception of HA granules or calcium phosphate paste [Figure 6]. Indeed, it has been demonstrated that more osteointegration occurs on a rough surface. [19] A prime concern of the surgeon, however, should be that the continuum is controlled and that the tissue exposed to drilling is adequately cooled. In fact, the threshold for damage to osteocytes is as low as 47 °C. [20] That being said, the limited clinical success of osteomimesis could also be explained by a lack of vascularization, which is affected by the tropism of the overlying skin, a critical process during bone growth and repair. [21]
In general, it appears that the majority of adverse events in cranioplasties are ascribable to human error, on the part of the manufacturer or the surgeon. Indeed, poor design or lack of adequate preparation is responsible for almost all custom-made HA cranioplasty implant failures. For this reason, a continuous exchange of information among surgeons and implant manufacturing technicians is essential, and should go some way to ensuring the continued success of this procedure.
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