Over the past 2 decades there has been a resurgence of interest in the use of decompressive craniectomy in the management of neurological emergencies. While technically straightforward, the procedure is associated with a number of complications relating to the initial decompression and subsequent cranioplasty. One complication that has received relatively little attention relates to the management of the temporal muscle. Here, through an illustrative case, the author describes a novel method of minimizing dissection of the temporal muscle during a cranioplasty procedure. Rather than placing a synthetic material over the dura mater to prevent adhesions or dissecting the muscle off the dura, the dura was opened and reflected laterally, pedicled to the temporal muscle. The dural defect was closed with a dural substitute, and the bone flap was secured in a routine fashion. The temporal muscle was then secured in its anatomical position. At the 6-month follow-up, radiological and clinical examination confirmed the restoration of muscle volume with excellent cosmetic and functional results. Opening the dura on a temporal muscle pedicle does not represent a routine form of surgical reconstruction; however, the use of this technique may have some advantages especially in young patients who have made a good recovery and for whom facial aesthetics may be particularly important.
Stephen Honeybul, Courtney Janzen, Kate Kruger and Kwok M. Ho
The object of this study was to assess the long-term outcome and quality of life of patients who have survived with severe disability following decompressive craniectomy for severe traumatic brain injury (TBI).
The authors assessed outcome beyond 3 years among a cohort of 39 patients who had been adjudged either severely disabled or in vegetative state 18 months after decompressive craniectomy for TBI. Assessments performed included the Extended Glasgow Outcome Scale, modified Barthel Index (mBI), Zarit Burden Interview, and 36-Item Short-Form Health Survey (SF-36). The issue of retrospective consent for surgery was also assessed.
Of the 39 eligible patients, 7 died, 12 were lost to follow-up, and 20 patients or their next of kin consented to participate in the study. Among those 20 patients, 5 in a vegetative state at 18 months remained so beyond 3 years, and the other 15 patients remained severely disabled after a median follow-up of 5 years. The patients' average daily activity per the mBI (Pearson correlation coefficient [r] = −0.661, p = 0.01) and SF-36 physical score (r = −0.543, p = 0.037) were inversely correlated with the severity of TBI. However, the SF-36 mental scores of the patients were reasonably high (median 46, interquartile range 37–52). The majority of patients and their next of kin believed that they would have provided consent for surgical decompression even if they had known the eventual outcome.
Substantial physical recovery beyond 18 months after decompressive craniectomy for severe TBI was not observed; however, many patients appeared to have recalibrated their expectations regarding what they believed to be an acceptable quality of life.
Stephen Honeybul, Grant R. Gillett, Kwok M. Ho, Courtney Janzen and Kate Kruger
Stephen Honeybul, Kwok M. Ho, Christopher R. P. Lind and Grant R. Gillett
The goal in this study was to assess the validity of the corticosteroid randomization after significant head injury (CRASH) collaborators prediction model in predicting mortality and unfavorable outcome at 18 months in patients with severe traumatic brain injury (TBI) requiring decompressive craniectomy. In addition, the authors aimed to assess whether this model was well calibrated in predicting outcome across a wide spectrum of severity of TBI requiring decompressive craniectomy.
This prospective observational cohort study included all patients who underwent a decompressive craniectomy following severe TBI at the two major trauma hospitals in Western Australia between 2004 and 2012 and for whom 18-month follow-up data were available. Clinical and radiological data on initial presentation were entered into the Web-based model and the predicted outcome was compared with the observed outcome. In validating the CRASH model, the authors used area under the receiver operating characteristic curve to assess the ability of the CRASH model to differentiate between favorable and unfavorable outcomes.
The ability of the CRASH 6-month unfavorable prediction model to differentiate between unfavorable and favorable outcomes at 18 months after decompressive craniectomy was good (area under the receiver operating characteristic curve 0.85, 95% CI 0.80–0.90). However, the model's calibration was not perfect. The slope and the intercept of the calibration curve were 1.66 (SE 0.21) and −1.11 (SE 0.14), respectively, suggesting that the predicted risks of unfavorable outcomes were not sufficiently extreme or different across different risk strata and were systematically too high (or overly pessimistic), respectively.
The CRASH collaborators prediction model can be used as a surrogate index of injury severity to stratify patients according to injury severity. However, clinical decisions should not be based solely on the predicted risks derived from the model, because the number of patients in each predicted risk stratum was still relatively small and hence the results were relatively imprecise. Notwithstanding these limitations, the model may add to a clinician's ability to have better-informed conversations with colleagues and patients' relatives about prognosis.
Stephen Honeybul, David Anthony Morrison, Kwok M. Ho, Christopher R. P. Lind and Elizabeth Geelhoed
Autologous bone is usually used to reconstruct skull defects following decompressive surgery. However, it is associated with a high failure rate due to infection and resorption. The aim of this study was to see whether it would be cost-effective to use titanium as a primary reconstructive material.
Sixty-four patients were enrolled and randomized to receive either their own bone or a primary titanium cranioplasty. All surgical procedures were performed by the senior surgeon. Primary and secondary outcome measures were assessed at 1 year after cranioplasty.
There were no primary infections in either arm of the trial. There was one secondary infection of a titanium cranioplasty that had replaced a resorbed autologous cranioplasty. In the titanium group, no patient was considered to have partial or complete cranioplasty failure at 12 months of follow-up (p = 0.002) and none needed revision (p = 0.053). There were 2 deaths unrelated to the cranioplasty, one in each arm of the trial. Among the 31 patients who had an autologous cranioplasty, 7 patients (22%) had complete resorption of the autologous bone such that it was deemed a complete failure. Partial or complete autologous bone resorption appeared to be more common among young patients than older patients (32 vs 45 years old, p = 0.013). The total cumulative cost between the 2 groups was not significantly different (mean difference A$3281, 95% CI $−9869 to $3308; p = 0.327).
Primary titanium cranioplasty should be seriously considered for young patients who require reconstruction of the skull vault following decompressive craniectomy.
Clinical trial registration no.: ACTRN12612000353897 (anzctr.org.au)
Kwok M. Ho, Stephen Honeybul, Cheng B. Yip and Benjamin I. Silbert
The authors assessed the risk factors and outcomes associated with blood-brain barrier (BBB) disruption in patients with severe, nonpenetrating, traumatic brain injury (TBI) requiring decompressive craniectomy.
At 2 major neurotrauma centers in Western Australia, a retrospective cohort study was conducted among 97 adult neurotrauma patients who required an external ventricular drain (EVD) and decompressive craniectomy during 2004–2012. Glasgow Outcome Scale scores were used to assess neurological outcomes. Logistic regression was used to identify factors associated with BBB disruption, defined by a ratio of total CSF protein concentrations to total plasma protein concentration > 0.007 in the earliest CSF specimen collected after TBI.
Of the 252 patients who required decompressive craniectomy, 97 (39%) required an EVD to control intracranial pressure, and biochemical evidence of BBB disruption was observed in 43 (44%). Presence of disruption was associated with more severe TBI (median predicted risk for unfavorable outcome 75% vs 63%, respectively; p = 0.001) and with worse outcomes at 6, 12, and 18 months than was absence of BBB disruption (72% vs 37% unfavorable outcomes, respectively; p = 0.015). The only risk factor significantly associated with increased risk for BBB disruption was presence of nonevacuated intracerebral hematoma (> 1 cm diameter) (OR 3.03, 95% CI 1.23–7.50; p = 0.016). Although BBB disruption was associated with more severe TBI and worse long-term outcomes, when combined with the prognostic information contained in the Corticosteroid Randomization after Significant Head Injury (CRASH) prognostic model, it did not seem to add significant prognostic value (area under the receiver operating characteristic curve 0.855 vs 0.864, respectively; p = 0.453).
Biochemical evidence of BBB disruption after severe nonpenetrating TBI was common, especially among patients with large intracerebral hematomas. Disruption of the BBB was associated with more severe TBI and worse long-term outcomes, but when combined with the prognostic information contained in the CRASH prognostic model, this information did not add significant prognostic value.