It is a neurosurgical operation in which part of the skull is removed and the underlying dura opened to reduce brain swelling-related raised ICP, thereby preventing intracranial tissue shifts and life-threatening downward herniation.
It can be performed as a primary or secondary procedure.
Depending on the location of the affected area, different surgical decompression techniques have been developed. In the presence of diffuse brain edema without a midline shift, as commonly seen in traumatic brain injury, bilateral (eg, bifrontal) craniectomy has been advocated. Hemicraniectomy, or removal of a frontotemporoparietal bone flap, is suitable in patients with unilateral hemisphere swelling as seen after ischemic stroke 3).
Accumulating experience over the years has led to increasing refinement of the surgical technique. The size of the removed bone fragment has been recognized as a factor of crucial importance for generation of a sufficient decompressive effect 4).
Although it was still performed with some frequency prior to the twentieth century, its resurgence in modern form became possible only upon the development of precision cutting tools and sophisticated post-operative care such as antibiotics.
Though the procedure is considered a last resort, some evidence suggests that it does improve outcomes by lowering intracranial pressure (ICP).
A large frontotemporoparietal DC (not less than 12 x 15 cm or 15 cm diameter) is recommended over a small frontotemporoparietal DC for reduced mortality and improved neurologic outcomes in patients with severe TBI.
Data suggest that unilateral decompressive craniectomy (DC) has superiority in lowering ICP, reducing the mortality rate and improving neurological outcomes over unilateral routine temporoparietal craniectomy. However, it increases the incidence of delayed intracranial hematomas and subdural effusion, some of which need secondary surgical intervention. These results provide information important for further large and multicenter clinical trials on the effects of DC in patients with acute post-traumatic BS 5).
The unilateral decompressive craniectomy has an advantage over non-surgical treatment of children with severe brain injury and should be considered in their management 6).
Raised intracranial pressure is very often debilitating or fatal because it causes compression of the brain and restricts cerebral blood flow. The aim of decompressive craniectomy is to reduce this pressure.
After traumatic brain injury, secondary decompressive craniectomy is most commonly undertaken as a last-tier intervention in a patient with severe intracranial hypertension refractory to tiered escalation of ICP-lowering therapies. Although decompressive craniectomy has been used in a number of conditions, it has only been evaluated in randomized controlled trials after traumatic brain injury and acute ischemic stroke. After traumatic brain injury, decompressive craniectomy is associated with lower mortality compared to medical management but with higher rates of vegetative state or severe disability. In patients with stroke-related malignant hemispheric infarction, hemicraniectomy significantly decreases mortality and improves functional outcome in adults <60 years of age. Surgery also reduces mortality in those >60 years, but results in a higher proportion of severely disabled survivors compared to medical therapy in this age group. Decisions to recommend decompressive craniectomy must always be made not only in the context of its clinical indications but also after consideration of an individual patient's preferences and quality of life expectations 7).
Intracerebral hemorrhage is often complicated by secondary haematoma expansion and perihemorrhagic edema.
After few small previous studies had suggested advantages by the combination of decompressive hemicraniectomy with haematoma removal, decompression on its own has been investigated within the last 5 years. Two case series and one case-control study in altogether 40 patients with severe spontaneous intracerebral haemorrhage have shown mortality rates ranging from 13 to 25% and favourable outcome from 40 to 65%.
Decompressive hemicraniectomy appears to be a feasible and relatively well tolerated individual treatment option for selected patients with spontaneous intracerebral haemorrhage. Data are insufficient to judge potential benefits in outcome. A randomized trial is justified and mandatory 8).
After a craniectomy, the risk of brain injury is increased, particularly after the patient heals and becomes mobile again. Therefore, special measures must be taken to protect the brain, such as a helmet or a temporary implant in the skull. When the patient has healed sufficiently, the opening in the skull is usually closed with a cranioplasty. If possible, the original skull fragment is preserved after the craniectomy in anticipation of the cranioplasty.
In addition to reducing ICP, studies have found decompressive craniectomy to improve cerebral perfusion pressure and cerebral blood flow in head injured patients.
Decompressive craniectomy is also used to manage major strokes, associated with “malignant” edema and intracranial hypertension. The pooled evidence from three randomised controlled trials in Europe supports the retrospective observations that early (within 48 hours) application of decompressive craniectomy after “malignant” stroke may result in improved survival and functional outcome in patients under the age of 55, compared to conservative management alone.
The procedure is recommended especially for young patients in whom ICP is not controllable by other methods.
Age of greater than 50 years is associated with a poorer outcome after the surgery.
A minimum diameter of 12 cm has been widely accepted as mandatory for effective decompression for ICP control. Complete hemispheric exposure is frequently advocated to further reduce the risk of parenchymal shear stress, hemorrhage and swelling. At the same time, superior efficacy and comparable risk profile of a more extensive decompression have yet to be established.
Tanrikulu et al. reviewed 74 patients with comprehensive clinical data sets undergoing DHC from 2008 to 2013 at our institution. With a minimum threshold of 12 cm in AP diameter being observed in all cases, patients were grouped according to the absolute size of maximum AP diameter (<18 cm, ≥ 18 cm) and surface estimate (<180 cm(2), ≥ 180 cm(2)). Surgical technique, efficacy of ICP control, surgical complications and early clinical course were recorded.
Baseline demographics were comparable in both groups. Surgery was effective in relieving or preventing intracranial hypertension in all patients, irrespective of craniectomy size. With smaller craniectomies, immediate surgical and secondary complications such as parenchymal herniation, hemorrhage, or swelling did not occur more frequently.
Due to the heterogeneity of underlying disease, a conclusion as to effect of craniectomy size on long-term outcome cannot be made based on this study. However, if the obligatory lower threshold of 12 cm for DHC size and decompression to the temporal base are observed, a smaller craniectomy is equally effective in relieving intracranial hypertension. While not inadvertently associated with a more favorable surgical risk profile, it does not increase the risk for early secondary complications such as parenchymal shear stress, hemorrhage and swelling 9).
A retrospective study based on analysis of clinical and neurological outcome, using the Extended Glasgow Outcome Scale in 56 consecutive patients diagnosed with severe traumatic brain injury treated from February 2004 to July 2012. The variables assessed were age, mechanism of injury, presence of pupillary changes, Glasgow coma scale (GCS) score on admission, CT scan findings (volume, type and association of intracranial lesions, deviation from the midline structures and classification in the scale of Marshall classification and Rotterdam CT score.
96.4% of patients underwent unilateral decompressive craniectomy (DC) with expansion duraplasty, and the remainder to bilateral DC, 53.6% of cases being on the right 42.9% on the left, and 3.6% bilaterally, with predominance of the fourth decade of life and males (83.9%) 10).
Anterior and posterior circulation acute ischemic stroke carries significant morbidity and mortality as a result of malignant cerebral edema. Decompressive craniectomy has evolved as a viable neurosurgical intervention in the armamentarium of treatment options for this life-threatening edema 11).
The brain tissue deformation occurring in these patients is difficult to quantify. Twenty-six patients suffering from a large bone defect after craniectomy were examined in supine position. The third ventricle's axial diameter was measured by transcranial ultrasound. Subsequently, the patient was brought into a sitting position. After 5 minutes, another measurement was taken. This procedure was repeated about 7 days after cranioplasty. The patients were grouped according to “early cranioplasty” (cranioplasty within 40 days after craniectomy, median 30 days) and “late cranioplasty”, (cranioplasty more than 40 days, median 80 days). Data of 13 healthy volunteers were used as a reference standard. In the healthy volunteers, the third ventricle was enlarging after reaching the sitting position. The median diameter was 2.35 mm in the lying and 2.9 mm in the sitting position (p > 0.05). In the patients before early cranioplasty, a decrease of the diameter after reaching the sitting position was observed. The mean diameter was 7.0 mm in the lying and 5.9 mm in the sitting position (p > 0.01). This difference was not significant in patients before late cranioplasty (9.7 vs. 9.4 mm). After cranioplasty, the mean diameter was 6.6 and 6.2 mm in the early cranioplasty group and 9.2 mm and 9.4 mm in the late cranioplasty group (lying and sitting position, respectively). This data demonstrate for the first time that unphysiological orthostatic brain tissue deformation occurs in patients after craniotomy 12).
The stretching of axons may contribute to an unfavorable outcome in patients treated with DC.
The deformation of the brain tissue in the form of a Lagrangian finite strain tensor for the entire brain was obtained by a non-linear image registration method based on the CT scanning data sets of the patient. Axonal fiber tracts were extracted from diffusion-weighted images. Based on the calculated brain tissue strain tensor and the observed axonal fiber tracts, the deformation of axonal fiber tracts in the form of a first principal strain, axonal strain and axonal shear strain were quantified. The greatest axonal fiber displacement was predominantly located in the treated region of the craniectomy, accompanied by a large axonal deformation close to the skull edge of the craniectomy. The distortion (stretching or shearing) of axonal fibers in the treated area of the craniectomy may influence the axonal fibers in such a way that neurochemical events are disrupted. A quantitative model may clarify some of the potential problems with this treatment 13).
A total of 1,236 patients with TBI operated with a DC from January 2008 to December 2013 at a tertiary care hospital were included in the study. The data from the hospital computerized database was retrospectively analyzed and 324 (45%) patients were followed-up for a mean duration of 25.3 months (range 3-42 months) among the cohort of 720 alive patients. The institute's ethical committee clearance was obtained before the start of the study.
There were 81% males with a median age [interquartile range (IQR)] of 32 (23-45) years. The mortality rate and median (IQR) Glasgow outcome score (GOS) at discharge in patients presenting with minor, moderate, and severe head injury were 18%, 5 (4-5); 28%, 4 (1-5); and 47.4%, 2 (1-4), respectively. An overall favorable outcome (GOS 4 and 5) at discharge was observed in 46.5% patients and in 39% patients who presented with severe TBI. Only 7.5% patients were in a persistent vegetative state (PVS), while 78% had an overall favorable outcome at the last follow-up of surviving patients (P < 0.001). On multivariate analysis, the factors predictive of a favorable GOS at discharge were: a younger age (odds ratio (OR) 1.03, confidence interval (CI) = 1.02-1.04; P < 0.001), no pupillary abnormalities at admission (OR 2.28, CI = 1.72-3.02; P < 0.001), absence of preoperative hypotension (OR 1.91, CI = 1.08-3.38; P = 0.02), an isolated TBI (OR 1.42, CI = 1.08-1.86; P = 0.01), absence of a preoperative infarct (OR 3.68, CI = 1.74-7.81; P = 0.001), presence of a minor head injury (OR 6.33, CI = 4.07-9.86; P < 0.001), performing a duraplasty (OR 1.86, CI = 1.20-2.87; P = 0.005) rather than a slit durotomy (OR 3.95, CI = 1.67-9.35; P = 0.002), and, avoidance of a contralateral DC (OR 3.58, CI = 1.90-6.73; P < 0.001).
The severity of head injury, performing a duraplasty rather than a slit durotomy, avoidance of a contralateral DC, and the presence of preoperative hypotension, infarct, and/or pupillary asymmetry have the highest odds of predicting the short term GOS at the time of discharge, after a DC in patients with TBI. Although DC carries a high risk of mortality, the probability of the survivors having a favorable outcome is significantly more as compared to those who remain in a PVS 14).
From January 2006 to December 2009, 41 patients underwent DC after closed head injury. Study outcomes focused specifically on the development of hydrocephalus after DC. Variables described by other authors to be associated with posttraumatic hydrocephalus (PTH) were studied, including advanced age, the timing of cranioplasty, higher score on the Fisher grading system, low post-resuscitation Glasgow Coma Scale (GCS) score, and cerebrospinal fluid (CSF) infection. We also analyzed the influence of the area of craniotomy and the distance of craniotomy from the midline. Logistic regression was used with hydrocephalus as the primary outcome measure. Of the nine patients who developed hydrocephalus, eight patients (89%) had undergone craniotomy with the superior limit <25 mm from the midline. This association was statistically significant (p = 0.01 - Fisher's exact test). Logistic regression analysis showed that the only factor independently associated with the development of hydrocephalus was the distance from the midline. Patients with craniotomy whose superior limit was <25 mm from the midline had a markedly increased risk of developing hydrocephalus (OR = 17). Craniectomy with a superior limit too close to the midline can predispose patients undergoing DC to the development of hydrocephalus. We therefore suggest performing wide DCs with the superior limit >25 mm from the midline 15).
Two patients who underwent decompressive craniectomy after head trauma deteriorated secondary to paradoxical herniation, one after lumbar puncture and the other after ventriculoperitoneal shunting. They motivated the authors to investigate further provoked paradoxical herniation.
The authors reviewed the records of 205 patients who were treated at a single hospital with decompressive craniectomy for head trauma to identify those who had had lumbar puncture performed or a ventriculoperitoneal shunt placed after craniectomy but before cranioplasty. Among the patients who met these criteria, those with provoked paradoxical herniation were identified. The authors also sought to identify similar cases from the literature. Exact binomials were used to calculate 95% CIs. RESULTS None of 26 patients who underwent a lumbar puncture within 1 month of craniectomy deteriorated, whereas 2 of 10 who underwent a lumbar puncture 1 month afterward did so (20% [95% CI 2.4%-55.6%]). Similarly, after ventriculoperitoneal shunting, 3 of 10 patients deteriorated (30% [95% CI 6.7%-65.2%]). Timing of the procedure and the appearance of the skin flap were important factors in deterioration after lumbar puncture but not after ventriculoperitoneal shunting. A review of the literature identified 15 additional patients with paradoxical herniation provoked by lumbar puncture and 7 by ventriculoperitoneal shunting.
Lumbar puncture and ventriculoperitoneal shunting carry substantial risk when performed in a patient after decompressive craniectomy and before cranioplasty. When the condition that prompts decompression (such as brain swelling associated with stroke or trauma) requires time to resolve, risk is associated with lumbar puncture performed ≥ 1 month after decompressive craniotomy 16).