Long-Term Complications of Decompressive Craniectomy for Head Injury

Abstract

There is currently much interest in the use of decompressive craniectomy for intracranial hypertension. Though technically straightforward, the procedure is not without significant complications. A retrospective analysis was undertaken of 164 patients who had had a decompressive craniectomy for severe head injury in the years 2004 to 2009 at the two major hospitals in Western Australia. Eighty-six patients had a bifrontal decompression and seventy-eight had a unilateral decompression. Two patients died due to post-operative care issues. Complications attributable to the decompressive surgery were: herniation of the cortex through the bone defect (42 patients, 25.6%), subdural effusion (81 patients, 49.4%), seizures (36 patients, 22%), hydrocephalus (23 patients, 14%), and syndrome of the trephined (2 patients, 1.2%). Complications attributable to the subsequent cranioplasty included: sudden death due to massive cerebral swelling in 3 patients (2.2%), infection requiring removal of the bone flap in 16 patients (11.6%), and bone flap resorption requiring augmentation in 10 patients (7.2%). After excluding simple complications such as subdural effusion and brain herniation through the skull defect and some patients who died as a direct consequence of traumatic brain or extracranial injury, 81 patients (55.5%) had at least one complication after decompressive craniectomy. The occurrence of at least one complication after decompressive craniectomy was significantly associated with an increased risk of prolonged stay in the hospital or rehabilitation facility (odds ratio 2.54, 95%confidence interval 1.22,5.24, p=0.013), after adjusting for predicted risk of unfavorable outcome.

Introduction

T he last two decades have seen a resurgence of interest in the use of decompressive craniectomy. A number of studies have demonstrated that the procedure is effective in reducing intracranial pressure in conditions such as severe head injury (Aarabi et al., 2006; Guerra et al., 1999; Howard et al., 2008; Kontopoulos et al., 2002; Morgalla et al., 2008; Polin et al., 1997), stroke (Hofmeijer et al., 2009; Jüttler et al., 2007), subarachnoid hemorrhage (Fisher et al., 1994), and infection (Adamo and Deshaies, 2008). While technically straightforward, the procedure is not without significant complications (Honeybul, 2010; Stiver, 2009; Yang et al., 2008). These complications relate not only to the decompressive procedure, but also to the subsequent cranioplasty (Gooch et al., 2009; Rish et al., 1979). There is, however, no consensus as to what is a complication of the surgical procedure as opposed to the primary pathology. In addition, most studies that have documented the complications of the procedure have used relatively short-term follow-up (Aarabi et al., 2006; Morgalla et al., 2008; Polin et al., 1997), with very few studies looking at outcome beyond 12 months (Kan et al., 2006).

The aim of this study was to document complications that occurred in a cohort of 164 patients for whom a minimum of 18 months of follow-up data were available. The clinical outcomes of most of these patients have been documented previously (Honeybul et al., 2010). In addition, an attempt has been made to define what constitutes a complication of the decompressive procedure rather than that of the primary traumatic brain injury.

Methods

After obtaining hospital ethics committee approval a retrospective analysis was undertaken of all patients who had had a decompressive craniectomy at the two major trauma hospitals in Western Australia between 2004 and 2009. These two major trauma hospitals together with a pediatric hospital are the only neurosurgical centers that provide neurotrauma services in Western Australia. These hospitals serve a population of about 2.1 million people. The literature was reviewed to determine complications that had previously been reported (Aarabi et al., 2006; Gooch et al., 2009; Morgalla et al., 2008; Polin et al., 1997; Stiver, 2009; Yang et al., 2008). For those patients that had been repatriated a telephone interview was performed with either the patient or their primary caregiver.

Indications for decompressive craniectomy, surgical technique, postoperative care, and cranioplasty

Decompressive craniectomy for diffuse cerebral swelling

The indications for decompressive surgery were based on the Brain Trauma Foundation guidelines for management of intracranial pressure (ICP) following traumatic brain injury (TBI; Bratton et al., 2007). This involves protocol-driven step-wise administration of sedation, ventilation, neuromuscular paralysis, super salt therapy, and cerebrospinal fluid (CSF) drainage where possible. Judicious doses of mannitol and hyperventilation were used to treat transient rises in ICP. All patients were managed in the intensive care unit and had a parenchymal ICP monitor inserted. The aim was to maintain the ICP below 20 mm Hg and the cerebral perfusion pressure (CPP) above 60 mm Hg. A decompressive craniectomy was considered if the ICP could not be maintained below 20 mm Hg despite maximal medical management. In the majority of cases the ICP was consistently above 30 mm Hg prior to surgery.

For bilateral cerebral swelling, a large bifrontal craniectomy was performed, extending posteriorly to approximately 1–2 cm in front of the coronal suture, and laterally to the floor of the middle fossa. The falx was routinely sectioned. When cerebral swelling was limited to one hemisphere, a unilateral craniectomy was performed.

Decompressive craniectomy following evacuation of a mass lesion

A unilateral decompressive craniectomy was performed following evacuation of a mass lesion when it was not possible to replace the bone flap because the ICP was greater than 20 mm Hg (all patients had a parenchymal ICP monitor placed for post-operative monitoring). At these two institutions, though there is much emphasis on performing large decompressive procedures, the size of the bone flaps is not formally measured.

Duraplasty and post-operative care

At these two institutions an onlay duraplasty is performed with a synthetic dural substitute. This is usually sutured in position; however, this is not a watertight closure. All patients are managed post-operatively in the intensive care unit and the ICP is routinely monitored with either a ventricular drain or a parenchymal monitor.

Cranioplasty

The bone flaps are stored in a sealed container in a designated refrigerator at a temperature of −40°C. They were not routinely cultured prior to storage or prior to implantation. The cranioplasty is performed as soon as possible after the decompression to restore both the cosmetic and protective functions. There is no specific time frame, but the clinical criteria that should be fulfilled were: resolution of brain swelling and adequate sinking of the scalp flap, no ongoing medical issues that needed to addressed, and no ongoing evidence of sepsis. CT scans are not routinely performed prior to cranioplasty unless there is clinical suspicion of potential problems such as hydrocephalus or non-resorbed effusions. For those patients that had seizures and were on anticonvulsant therapy, therapeutic serum levels were checked prior to surgery. Patients were otherwise not routinely placed on anticonvulsant therapy for a cranioplasty procedure.

The complications were divided into those attributable to the initial decompressive procedure, and those attributable to the subsequent cranioplasty (Table 1).

Table 1.

Overall Complications following Unilateral and Bifrontal Decompressive Craniectomy after Traumatic Brain Injury

	Bifrontal craniectomy (n=86)	Unilateral craniectomy (n=78)	Total number (%)
Complications following decompressive craniectomy (n=164)
Death
Traumatic brain injury	7	10	17 (10.4)
Thoracic aortic rupture	1	0	1 (0.6)
Fall onto unprotected cranium	1	0	1 (0.6)
Possible injury to unprotected cranium	1	0	1 (0.6)
Cardiac failure	1	0	1 (0.6)
Overwhelming sepsis	1	0	1 (0.6)
Palliative treatment withdrawal	3	0	3 (1.8)
Cortical herniation	28	18	42 (25.6)
> 1.5 cm herniation of the cortical surface outside of the line of the outer table of the craniectomized skull (Yang et al., 2008)
Damage to herniated cortex	2	4	6 (3.7)
Radiological evidence of new areas of hemorrhagic contusion relating to the edge of the craniectomy
Subdural/subgaleal effusion	44	37	81 (49.4)
> 1 cm maximal depth measured from the cortical surface to the inner aspect of the scalp
Requiring drainage	2	4	6 (3.7)
Hydrocephalus	16	7	23 (14)
Ventriculomegaly requiring placement of a shunt with subsequent clinical improvement
Post-operative epidural hematoma	1	0	1 (0.6)
Seizures	22	14	36 (22)
Subdural peritoneal shunt	1	0	1 (0.6)
Ventriculoperitoneal shunt malfunction	1 (infection)	1 (blockage)	2 (1.2)
Syndrome of the trephined	2	0	2 (1.2)
Clinical symptoms that were reversed following cranioplasty
Complications following cranioplasty (n=138)
Sudden death following cranioplasty	3	0	3 (2.2)
Infected cranioplasty	10	6	16 (11.6)
Requiring removal of the cranioplasty
Bone flap resorption
Requiring replacement
Clinically evident, not augmented	4	6	10 (7.2)
Radiologically-evident but not clinically-apparent	1	1	2 (1.4)
Includes only those patients who had had a repeat CT scan at least 6 months following autologous cranioplasty so that radiological resorption could be assessed	7	7	14 (10.1)
Structural failure	1	0	1 (0.7)

Statistical analysis

Descriptive statistics are used to describe the incidence rate and other characteristics of the complications. The relationships between the risk of flap infection and the timing of cranioplasty, and also between the occurrence of one complication other than subdural effusion or brain herniation through the skull defect and severity of TBI were assessed. We used the predicted risks of unfavorable outcome according to the CRASH prediction model as a surrogate of severity of TBI in this study (Perel et al., 2008). Categorical outcomes and continuous variables with skewed distributions were analyzed by the chi-square and Mann-Whitney U tests, respectively. Multivariate logistic regression was used to assess whether complications after decompressive craniectomy were independently associated with an increased risk of prolonged stay in hospital or rehabilitation facility. During this multivariate analysis, the predicted risk of unfavorable outcome was used to adjust for the severity of injury of the patients, and a prolonged stay in the hospital and rehabilitation facility was defined as a total length of stay greater than the median length of stay of the survivors (70 days). All statistical analyses were performed using SPSS for Windows (version 13.0; SPSS Inc., Chicago, IL), and p values < 0.05 were considered significant.

Results

Between 2004 and 2009 in Western Australia 164 patients required either a unilateral (n=78) or bilateral (n=86) decompressive craniectomy

Eight patients had either been repatriated or had left Perth. Of these, six patients were contacted and the patient or carergiver was interviewed by telephone. Long-term radiological examinations were unavailable for all these patients. Three patients were lost to 18-month follow-up but details at 6 months were available.

The patients were evenly distributed between the two hospitals and among the eight neurosurgeons that covered the on-call roster.

Of the 164 decompressive craniectomies performed there were: 68 unilateral procedures for which following evacuation of a mass lesion, it was not possible to replace the bone flap; 10 unilateral procedures for which cerebral swelling was predominantly unilateral; and 86 bifrontal procedures for which cerebral swelling was bilateral.

After excluding simple complications such as subdural effusion and brain herniation through the skull defect, and also patients who died as a direct consequence of traumatic brain or extracranial injury, 81 patients (55.5%) had at least one complication after decompressive craniectomy. These are shown in Table 1.

Having at least one complication other than brain herniation or effusion was significantly associated with an increased length of hospital stay (86 versus 45 days, p=0.001), and total duration of stay in all health institutions including rehabilitation facilities (147 versus 81 days, p=0.001). The risk of having at least one complication other than subdural effusion and brain herniation was significantly related to the severity of the underlying TBI (64 versus 56%, p=0.023), but not to age (p=0.23), or the presence of extracranial injuries (p=0.128). The occurrence of at least one complication after decompressive craniectomy was independently associated with an increased risk of prolonged stay in a hospital and rehabilitation facility (odds ratio [OR] 2.54, 95% confidence interval [CI] 1.22,5.24; p=0.013), after adjusting for the predicted risk of unfavorable outcome (OR 1.04 per percentage increment, 95% CI 1.02,1.06; p=0.01).

Of the 36 patients (22%) who developed seizures, 17 patients (10.3%) developed seizures following the head injury and prior to cranioplasty. Nineteen patients (11.7%) developed seizures following cranioplasty. Two patients developed seizures at 4 and 5 years following the initial injury.

The median time to cranioplasty after decompressive craniectomy was 94 days (interquartile range 44–127 days). Among the 138 survivors, 3 patients (2.2%) died suddenly following autologous cranioplasty. Most of the infections developed in the first post-operative month; however, 2 patients presented at 8 and 9 months. The infecting organism was staphylococcal in 14 cases (10.1%) and Propionibacterium in 2 cases (1.4%). The duration between decompressive craniectomy and cranioplasty was not related to the risk of infection (83 versus 95 days, p=0.353).

Fourteen patients (10.1%) had radiological evidence of bone flap resorption. However, not all patients had a repeat CT scan for which resorption could be assessed. Of the 138 patients who had had a cranioplasty procedure, 64 patients who had had an autologous cranioplasty also had a CT scan at least 6 months after reimplantation. The incidence of radiologically-evident but clinically-insignificant resorption could therefore be reported as 22%.

Discussion

There now appears little doubt that decompressive craniectomy will become a valuable tool in the management of severe head injury (Aarabi et al., 2006; Guerra et al., 1999; Howard et al., 2008; Honeybul et al., 2010; Kontopoulos et al., 2002; Morgalla et al., 2008; Polin et al., 1997). However, while the short-term complications occur over a fairly predictable time frame (Stiver, 2009; Yang et al., 2008), the long-term complications of the procedure have received less attention. In addition, there is no clear consensus as to what constitutes a complication of the decompressive procedure as opposed to that of the primary head injury.

There are two main categories to consider when discussing overall complications: those complications attributable to the initial decompressive procedure, and those attributable to the subsequent cranioplasty.

Complications of the decompressive surgery

Mortality

Of the 24 deaths that occurred following the decompressive surgery, 22 were due to either the primary TBI or extracranial injuries. Two patients died due to post-operative care issues. One patient died due to a fall (Honeybul, 2009); this patient was making an unexpectedly good recovery several days following the initial injury when he attempted to mobilize unaided, prior to fitting of a protective helmet, and he fell onto the unprotected craniectomy site. He suffered further cerebral injury and subsequently died. Following a detailed review of the case, a number of recommendations were made, and a specific post-decompressive craniectomy operational policy was implemented. While it is less clear as to the mechanism of injury in the second patient, it is likely that there may have been trauma to the unprotected cranium.

Herniation through the craniectomy defect and injury to the herniated cortex

Although there is no consensus as to how cortical herniation is defined, we have used the definition provided by Yang and associates (Yang et al., 2008). However, while this phenomenon has been reported as a complication (Aarabi et al., 2006; Csokay et al., 2001; Stiver, 2009; Yang et al., 2008), it occurs so commonly that it could almost be considered a natural sequela of the decompressive procedure. It was observed in 25.2% of our cohort. While the possibility of injury to the herniated cerebral cortex has been described (Aarabi et al., 2006; Csokay et al., 2001), differentiating maturation of a hemorrhagic contusion from actual injury to the cortex as it herniates through the craniotomy edge can be difficult (Stiver, 2009). In two cases in our cohort the size of the craniotomy was clearly too small, and there was obvious injury to the herniated cortex. In the remaining cases there was herniation with contusion maturation, but this was more widespread and not limited to the site of the craniectomy. In general, at these two centers there is an emphasis on performing extensive craniotomies for trauma surgery.

Subdural/subgaleal effusion

Post-traumatic subdural effusion is a well-recognized phenomenon following head injury, with a reported incidence of 6–21% (Lee et al., 1994; Lee, 1998). The pathogenesis has been attributed to traumatic rupture of the dura–arachnoid interface and trabeculae and the transient dynamic changes seen in CSF circulation (Fodstad et al., 1984; Haines et al., 1993; Lee, 1998). The development of a subdural effusion has been reported as a complication of decompressive craniectomy, with an incidence ranging from 26–60% (Aarabi et al., 2006; Guerra et al., 1999; Stiver, 2009; Yang et al., 2008). In this study, 81 patients (49.4%) developed some form of effusion. By using the CRASH outcome prediction model as a surrogate index of injury severity, it can be demonstrated that the development of an effusion can be related to the severity of the head injury (Honeybul et al., 2010). It may be that effusions are primarily a complication of TBI, and that removal of the bone flap merely provides space in which fluid can accumulate. Opening the dura provides a communication with the subgaleal space, and as the acute cerebral edema subsides, some form of effusion usually develops. While they can have a fairly impressive appearance, in most cases these effusions have little clinical significance (Aarabi et al., 2006; Stiver, 2009). They usually resorb once the bone flap is replaced.

Hydrocephalus

The incidence of symptomatic post-traumatic hydrocephalus varies from 0.7–29% (Grosswasser et al., 1988; Guyot and Michael, 2000; Licata et al., 2001). Differences in diagnostic criteria and classification have contributed to this wide variation in results. Among patients that have had a decompressive craniectomy, the incidence of post-traumatic hydrocephalus has been found to vary from 10–40% (Aarabi et al., 2006; Guerra et al., 1999; Howard et al., 2008; Kan et al., 2006; Kontopoulos et al., 2002; Morgalla et al., 2008; Polin et al., 1997; Stiver, 2009). In this study 24 patients had a ventriculoperitoneal shunt inserted. In one patient there was no clinical change and the diagnosis was amended to ventriculomegaly. As with subdural hygromas, by using the CRASH outcome prediction model as in index of injury severity, the development of hydrocephalus was also related to the severity of the head injury (Honeybul et al., 2010). The post-traumatic disturbance of CSF flow probably contributes to the development of subdural and subgaleal effusions, and presumably symptomatic hydrocephalus develops when CSF circulation fails to normalize. In the same manner as effusions, it may be that hydrocephalus should be regarded more as a primary complication of TBI rather than that of a decompressive craniectomy. However, it is possible that a decompressive craniectomy could alter CSF dynamics adversely and/or increase subarachnoid scarring, thereby placing this group of patients at greater risk of developing hydrocephalus (Kan et al., 2006).

Post-traumatic seizures

The incidence of post-traumatic seizures for all types of head injuries is 2–2.5% in civilian populations. This incidence increases to 5% in hospitalized neurosurgical patients. When only severe head injuries (brain contusion, intracranial hematoma, or loss of consciousness or post-traumatic amnesia for > 24 h) are considered, the incidence is 10–15% for adults and 30–35% for children (Annegers et al., 1998). Of those patients who have had a decompressive craniectomy (who presumably fall into the severe head injury category), the incidence of epilepsy has been found to vary from 7–20% (Guerra et al., 1999; Kan et al., 2006; Yang et al., 2008). In this study, 36 (22%) patients developed post-traumatic seizures. While it would appear that this complication develops primarily because of the severe head injury, the cerebral manipulation that occurs with the decompressive procedure and subsequent cranioplasty may have some influence. The fact that two cases presented with new onset of seizures at 4 and 5 years post-injury indicates the need for long-term follow-up when reporting complications.

Syndrome of the trephined

Several authors have described adverse symptoms related to the absence of the bone flap (Fodstad et al., 1984; Grant and Norcross, 1939; Yamaura and Makino, 1977). Syndrome of the trephined was first described by Grant and Norcross in 1939, and details the symptoms of headache, seizures, mood swings, and behavioral disturbances (Grant and Norcross, 1939). The term “syndrome of the sinking scalp flap” describes the neurological deficits that can occur due to cortical dysfunction caused by brain distortion under the scalp flap as the edema subsides (Yamaura and Makino, 1977).

To what degree patients are affected by these symptoms can be difficult to accurately determine because many of them are in recovery phase from a severe head injury. Patients frequently complain of headaches, mood swings, and behavioral disturbances, and it is difficult to establish to what degree these are merely a post-craniotomy phenomenon (Stiver, 2009). While there can be little doubt that certain individuals are more susceptible to the absence of skull coverage and the development of symptoms, there is wide variation in the degree to which the condition has been reported. Among our cohort two patients exhibited marked clinical improvement within 24 h of the cranioplasty procedure. In both cases the skull defect was bifrontal and both patients were young males. They were both initially making a slow recovery that had reached a plateau at approximately 4 months. Their clinical condition subsequently deteriorated such that they went from dependent but able to mobilize and to perform self-care with assistance, to drowsy and immobile, both requiring nasogastric supplementation to maintain adequate nutritional input. Following cranioplasty both patients dramatically improved within 24 h. They became alert, oriented, and independently mobile. They have subsequently progressed to achieve a good outcome. Another 4 patients whose autologous cranioplasty had significantly resorbed complained of severe postural headaches with associated vertigo. In all cases their symptoms resolved with insertion of a titanium cranioplasty.

Complications of cranioplasty

Sudden death following autologous cranioplasty

There have been three cases of sudden death following cranioplasty. All three patients were making a poor recovery following very severe head injuries and they had had significant complications. Following an uneventful cranioplasty procedure, they deteriorated in the first few hours following surgery. One patient had a witnessed seizure in the recovery room. All three patients had therapeutic serum levels of anticonvulsant medication, and all developed fixed and dilated pupils. Massive cerebral swelling was confirmed on CT scanning. They failed to recover despite removal of the bone flap. The mechanism behind this was not clearly established, but it may be related to failure of autoregulation (Czosnyka et al., 2001; Sviri et al., 2009). Further studies are needed to establish exactly which patients are at risk of this complication.

Infection

A number of reports have now documented the higher-than-expected incidence of infection following decompressive craniectomy and subsequent cranioplasty (Aarabi et al., 2006; Gooch et al., 2009; Guerra et al., 1999; Stiver, 2009; Yang et al., 2008). Within the Western Australian statewide neurosurgical service the overall infection rate for cranial procedures has been consistently audited at 1–2%; however, within our cohort, 16 (11.6%) of the 138 survivors who had a cranioplasty procedure had to have the bone flap removed because of infection.

The higher-than-expected infection rate may due to a number of factors (e.g., skin colonization while in hospital or immunocompromise following trauma and reoperation; Korinek et al., 1997, 2005; Stiver, 2009; Tokoro et al., 1989; Yang et al., 2008). While measures such as antibiotic prophylaxis, strict asepsis, and minimal handling are used to avoid infection, unfortunately among this group of patients the infection rate remains significantly higher than our baseline. In most cases the infection presented in the subsequent 2–4 weeks after surgery; however, two patients presented with infection at 8 and 9 months after the cranioplasty procedure. This again highlights the need for long-term follow-up. Fortunately all patients in this study recovered with no worsening of their neurological condition; however, there is little doubt that infection has the potential to significantly impair recovery.

Bone flap resorption

The incidence of bone flap resorption has been reported to be between 3 and 12% (Aarabi et al., 2006; Kan et al., 2006; Polin et al., 1997). Within the pediatric population it has been noted to occur in up to 50% of cases (Grant et al., 2004).

In our institution we do not routinely obtain CT scans 6 months following cranioplasty; however, in the 64 patients that did have a subsequent scan, 14 (22%) showed radiological evidence of bone flap resorption. In most cases this will have little clinical significance; however, given that most of these patients are young men, there may be implications when considering long-term cranial protection.

Summary

There appears to be little doubt that the use of decompressive craniectomy will become increasingly common, not only for severe head injury, but for other conditions such as stroke, subarachnoid hemorrhage, and infection. While the procedure is technically straightforward, there are a number of complications that can significantly impact patient recovery, and this study has demonstrated that long-term follow-up is required to capture the true clinical picture.

Footnotes

Author Disclosure Statement

No competing financial interests exist.

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