Keywords
decompressive craniotomy - cranioplasty - complications - infection - bone flap resorption
- flap mobility - epidural fluid collection - extradural hemorrhage - flap subsidence
Introduction
Cranioplasty (CP) following decompressive craniotomy (DC)[1] is performed after the intracranial pressure subsides with the aim of improving
cosmesis and neurological function.[2]
[3] Conventionally done 3 to 6 months after DC, it is termed as “early” CP when done
within 12 weeks of DC and “late” if done after this period.[3]
Though commonly considered to be a “simple operation”[1] and often done by residents in training it has numerous complications. In a series
of 348 CPs, Zanaty et al[4] documented complications in 109 patients (31.32%) with a mortality rate of 3.16%,
while in 62 patients who underwent CP, Gooch et al[5] noted postoperative complications in 34%, with 16 patients (25.8%) needing reoperation.
In this article, we present a pictorial narrative of the complications (excluding
seizures) we have encountered over the past 18 years in a series of over 300 CPs along
with their management and suggested methods to avoid the same [[Table 1]].
Table 1
List of complications (excluding seizures) following cranioplasty and preventive measures
for the same
|
Complications
|
Preventive measures
|
|
Skin breakdown and flap exposure
|
Careful dissection
Tension free closure
Avoidance of excess use of cautery at the margins
|
|
Wound infection
Subgaleal pus
Intracranial empyema
Pyogenic osteomyelitis
|
Avoiding excessive tissue dissection
Eliminating dead space by placing a subgaleal drain, hitching the neo dura to the
superior surface of the CP flap, tenting sutures of the scalp from galea to pericranium
Strict maintenance of asepsis during surgery
Frequent imaging in cases of unexplained or persistent subgaleal collection.
|
|
Hematoma below the replaced flap
|
Optimization of bleeding parameters before surgery
Meticulous hemostasis
Placement of dural tenting sutures through the bone to eliminate dead space and/or
drain in the extradural space
Keeping some space at the margins of the base of the replaced flap for escape of collection
|
|
Intraparenchymal hemorrhage
|
Careful and sharp dissection of the skin flap from the neodura after identifying the
galeal-neodural plane avoiding dural breach
Ensure the screws which fix the mini plates to the bone margins of the craniotomy
defect do not violate the dura
|
|
Epidural fluid collection/hygroma below the flap
|
Avoidance of opening dura during dissection of the skin flap
Making small holes in the flap during CP to allow for egress of the collection into
the subgaleal space with placement of a subgaleal suction drain
|
|
Flap resorption
|
Consider using artificial substitutes during initial CP in those who are at a higher
risk of flap resorption – younger patients with larger, multifragmented flaps
|
|
Flap mobility
- poor fixation
- incompatible flap size due to absorption during storage
|
Fixing the flap firmly with a variety of commercially available devices rather than
sutures
Avoid replacing flaps that have decalcified and shrunk during storage in the body
and use artificial substitutes like titanium mesh or PMMA bone cement
|
|
Flap subsidence
|
Rigid fixation of flap during CP to obviate any inward migration later
|
|
Implant extrusion
|
Avoid using fixation devices at sites where the overlying skin and soft tissue is
thin
Bicortical purchase of screws may prevent back out.
|
Abbreviations: CP, cranioplasty; PMMA, polymethyl methacrylate.
List of Complications, Management, and Preventive Measures
Skin Breakdown and Flap Exposure
Skin breakdown with exposure of the bone flap can occur at the incision line of the
CP or even distant from it [[Fig. 1]] and at varying intervals following the CP. Thin skin with lack of subcutaneous
support, poor galeal closure, devitalized skin margins due to excessive use of cautery,
and tight sutures causing necrosis of the margins are possible causes of incision
line breakdown. Repaired lacerations in the middle of the skin flap that was raised
during DC lack subcutaneous support, adhere to the “neo dura” and may be devascularized
during dissection and elevation of the skin at CP and breakdown later. Most commonly,
skin breakdown follows the infection of the operative site.
Fig. 1 Clinical images showing delayed wound complications with bony exposure both away
from (A, C) and at the level of the incision (B).
Di Rienzo et al[6] classified wound complications as being one of three types – dehiscence, ulceration
,
or necrosis. Dehiscence, the commonest, is the separation of opposing margins along the suture
line while ulceration is defined as the loss of substance occurring inside the skin
flap distant from the line of suture and necrosis is a large, discolored area of nonviable
skin without exposure of the subjacent bone.[6] These need to be treated promptly as osteomyelitis and spreading infection may ensue.
In the absence of infection and if detected, early dehiscence can be managed by debriding
the margins until fresh bleeding occurs followed by secondary suturing but in cases
who present late there is retraction of the margins and tension free closure is difficult.
The conventional notion that an exposed CP must be removed (particularly in cases who present early) needs re-examination given the
availability of better antibiotics and improved surgical techniques such as flap coverage.[7] As all our cases presented late, the CP flap was removed and closure with either
pulley sutures or rotation flap was done.
Wound Infection
It is the most dreaded complication of CP and ranges from subgaleal pus, intracranial
pus below the bone flap (empyema), frank osteomyelitis, or a combination of all of
these [[Figs. 2]
[3]
[4]]. Infections may be classified into early (occurring within 4 weeks of CP) or late
(occurring after 4 weeks of CP).[8] Early infections usually present with fever, wound discharge, local swelling, redness
and tenderness, and elevated total counts and C reactive protein (CRP) on blood investigations.[8] These may be absent[9] in delayed infections that can even occur several months after the CP.
Fig. 2 Clinical image of a patient presenting with subgaleal collection (3 weeks after suture
removal) due to infection with pouting granulation at the incision site (A); axial CT scans (B, C) showing collection in the subgaleal plane with hypodensity in the collection (C) that is a strong marker of infection.
Fig. 3 Contrast-enhanced CT scans (A–C) showing abscess with enhancing walls both outside and inside the replaced bone flap.
Fig. 4 Clinical photographs (A, B) of a patient with delayed wound infection 8 months after the cranioplasty showing
granulation tissue with discharge at the incision site; noncontrast MR imaging (C–E) showing liquefied collection outside and granulation tissue inside the replaced
bone flap and (F) clinical image of the osteomyelitic eroded bone flap.
On plain computed tomography (CT) scan imaging, subgaleal pus may be confused with
a sterile subgaleal collection but the presence of air must be carefully looked for
and if present this hypodensity is often an indicator of infection.[10] Contrast-enhanced CT or magnetic resonance imaging (MRI) scans showing enhancement
of the walls of a single or multiseptate collection or restriction on diffusion-weighted
imaging are confirmatory for the presence of infection.[8]
Though it is difficult to identify osteomyelitis unless the bone is grossly eroded
because the avascular CP bone does not enhance on contrast we believe the treatment
in all cases is re-exploration and removal of the bone flap, thorough debridement
and closure to be followed by long-term antibiotics as per culture reports.
Hematoma Below the Replaced Flap
Collection of blood below the CP flap, which is thin and seen in only one to two cuts
in a postoperative CT scan is of no clinical consequence. However, on occasion, a
large collection may be seen below the replaced bone resulting in mass effect and
midline shift of the underlying brain.[11] Causative factors include bleeding diathesis, improper operative site hemostasis,
and a vascular “neo-dura” that is often found in early CPs.
These hematomas are usually extradural while subdural bleed post CP is rare due to
the tenuous but well-formed arachnoidal connections traversing the subdural space
between the brain and the overlying “neo-dura” that develop following DC essentially
obliterating the subdural space.
We have found extradural hematomas to be more frequent in cases where there is an
indwelling shunt [[Fig. 5]] or if a lumbar puncture (LP) is done preoperatively to slacken the brain prior
to CP as this decreases the natural tamponading effect the latter has on capillary
ooze from the dissected neo-dura and also in cases when bone cement used to fashion
an artificial bone flap obliterates the temporo-basal gap through which any collection
can egress to the subgaleal space.
Fig. 5 Pre-CP axial CT scan image (A) of a patient operated for left-sided acute subdural hematoma and contusions showing
contralateral (right sided) hygroma with external cerebral herniation and midline
shift; Axial images (B–D) showing concave flap after placement of a subduroperitoneal shunt and (E) extradural hemorrhage below the replaced flap after CP.
A “wait and watch” policy can be followed if the patient is asymptomatic but significant
neurological deficits mandates re-exploration, evacuation of the blood and replacement
of the bone flap after drilling a few small holes in it along with drains (in the
subgaleal and extradural planes).
Intraparenchymal Hemorrhage
Intraparenchymal hemorrhage after CP can occur due to iatrogenic injury to fragile
blood vessels formed following posttraumatic angiogenesis[12] while lifting the skin and galeal flap off the neodura dural cover during exposure
or due to screws used to fix the bone [[Fig. 6]]. The former etiology is likely to occur more frequently in cases where adequate
duraplasty is not done during the initial surgery.[13] Also, negative pressure suction drains might cause traction injury to these vessels.
Fig. 6 Pre-CP CT scan images (A, B) of a patient operated for left temporal intracerebral hemorrhage showing gliosis
at the site of surgery; post CP CT images (C, D) showing an intraparenchymal hemorrhage below the replaced flap but away from the
gliotic region and (E) coronal bone windows showing a screw used for fixation of the bone (orange arrow)
penetrating the full thickness and causing brain injury.
Hyperperfusion of underlying brain can cause sudden increase in cerebral blood flow
once atmospheric pressure is removed following CP and may lead to intraparenchymal
bleed particularly in patients with a sunken flap.[14] If the injury is small with no mass effect, midline shift or cisternal effacement
on CT scan, conservative treatment may be continued. Surgical evacuation is warranted
if the hemorrhage is large and life-threatening and then the bone flap should again
not be replaced.
Epidural Fluid Collection/Sub-flap Hygroma
The incidence of epidural fluid collections seen on CT scan below the replaced flap
varies from 6.1% to 37.3%.[15] The vast majority are asymptomatic resolving over time.[15]
[16] They are typically hypodense as opposed to extradural hematomas. Factors such as
dural stiffening preventing brain expansion after CP,[15] inflammatory response to artificial bone substitutes,[15] and intraoperative cerebrospinal fluid (CSF) leak have been implicated in its causation.[15]
[16]
When they are large enough to cause mass effect on the brain with fresh deficits [[Fig. 7]], treatment options include making a burr hole through the flap to let the fluid
out, or craniotomy and evacuation of the collection with placement of subgaleal drain
and dural tenting sutures.
Fig. 7 Pre-CP CT scan images (A) showing a “full” flap that necessitated LP to make space and seat the bone flap;
postoperative CT scans (B, C) showing sub-flap epidural fluid collection causing mass effect and midline shift.
Flap Resorption
It is a delayed complication of CP, previously called aseptic necrosis of the bone
flap and is of two types[17]–Type 1 where there is thinning of the bone or erosion at the margins of the flap
and Type 2 where there is complete lysis of both tables within the flap. The incidence
of this complication depends on the length of the follow-up and the attention with
which it is sought for and varies from 7.2% to 50%.[17]
Multifragmented bone flaps, late CP, larger flaps, younger age of the patient, CP
done for trauma, and the presence of a VP shunt have been implicated as predisposing
factors for the same.[17]
[18] Patients present with progressive softening of the operative site and rarely pain
and CT scans (with 3D reconstructions) show the extent of resorption [[Fig. 8]]. Management options include re-CP with cement or mesh or an expectant “wait and
watch” policy in children as re-calcification may occur.[19]
Fig. 8 Preoperative CT scans (A, B) showing a right-sided acute subdural hematoma with contusions causing mass effect
and midline shift; post DC CT image (C) showing decrease of mass effect; immediate post CP image (D) showing replaced bone flap and 3D reconstructed CT scan images after 2 years (E, F) showing significant resorption of the bone flap with only patchy islands remaining
intact.
Flap Mobility
A flap that is not firmly fixed (as with sutures instead of miniplates and screws)
may on occasion move with variations in intracranial pressure (occurring with coughing/sneezing)
or with posture too. While most patients will have non-serious complaints such as
a subjective fullness of the operative site on getting up from sleep which sinks inward
somewhat as the day progresses, abnormal mobility of the implanted bone may cause
symptoms and called the “Sinking Bone Syndrome.”[20] We have documented a case of reversible postural hemiparesis[21] where there was variation in MCA flow with flap movement [[Fig. 9]].
Fig. 9 Anteroposterior plain skiagrams of a post CP mobile flap in supine position with
full expiration (A) and sitting position with full inspiration (B) showing outward and inward mobility respectively. Transcranial doppler (C, D) showing increase in peak systolic velocity in the middle cerebral artery when the
flap drifts inwards compared with that in supine position.
Flap mobility can also occur due to incompatible flap size due to its absorption during
storage. We have encountered it in cases where we had placed the flap in a subcutaneous
abdominal pocket and when the patient underwent a delayed CP [[Fig. 10]]. It is probably due to absorption and decalcification of the bone during storage
in a metabolically active location.[22]
Fig. 10 Preoperative CT scan images (A–C) showing a spontaneous right sided parietal intracerebral hemorrhage; preoperative
digital subtraction angiography showed an arteriovenous malformation fed by branches
of the middle cerebral artery following excision of which bone flap was placed in
a subcutaneous abdominal pocket; pre CP CT scan image (D) and postoperative skiagrams after the patient complained of postural flap mobility
(E, F) showing incompatible flap size due to absorption in storage.
Flap Subsidence
A flap that is inadequately fixed during CP may sink into the brain if LP is done
to rule out meningitis [[Fig. 11]] or after ventriculoperitoneal shunting. Neurological deterioration may occur due
to disturbances in cerebral metabolism (documented using flurodeoxy glucose positron
emission tomography studies) due to decreased cerebral blood flow by the pressure
of the flap.[21]
Fig. 11 Plain skiagrams showing a replaced bifrontal CP flap initially created for hematoma
evacuation and clipping of a distal anterior cerebral artery aneurysm at first follow
up (A) and immediately following lumbar puncture 6 months later for meningitis (B) following which he became drowsy instantaneously and clinical photograph (C) after lumbar puncture before reinstallation of saline in the thecal sac.
Extrusion of Implants Used for Fixation
We encountered a previously unreported complication that occurred due to back out
of the miniplates and screws used to fix the bone flap during CP with erosion through
the skin [[Fig. 12]]. Treatment entails removal of the extruded screws and loosened plates and re-fixation
at another site if multiple fixation points are compromised or removal of just the
offending implant if localized to one level.
Fig. 12 Preoperative CT scans (A) of a patient with right sided extradural hematoma; postoperative CT scans (B) after DC and clot evacuation; post CP skiagram (C) showing the implants used to anchor the bone flap and clinical photographs (D,E) showing erosion of implant through the skin at one place and elevation of the wound
at two other places due to implant back out.
Conclusions
CP is a common but far from uncomplicated surgical procedure. Though we have not analyzed
the reason for every complication in each patient, it must be stressed that post-CP
complications are myriad and at times may be serious enough to threaten life or warrant
resurgery. Attention to small but basic surgical techniques will go a long way in
preventing unwanted postoperative events.
