Last Updated: August 11, 2019
Rationale for the performance of a craniectomy was born out of the “rigid-box” illustration of the cranium devised by Alexander Monro and George Kellie, referred to as the Monro-Kellie doctrine. This concept is widely applicable to cerebral pathologies (eg, hematomas, expansive lesions, and cytotoxic cerebral edema) that can precipitate an intracranial hypertension or herniation syndrome.
This intervention can be applied in either a primary (prophylactic) or secondary (therapeutic) clinical setting. Primary performance of a craniectomy is considered when intracranial pressure (ICP) is anticipated to be a postoperative concern, as in the setting of acute epidural, subdural, or intraparenchymal hematoma (IPH) evacuation. Secondary performance of a craniectomy is common for patients who have had a cerebrovascular accident (CVA) or who have delayed posttraumatic cerebral edema, given that an initial attempt at medical management is often undertaken before surgical intervention is considered.
The goal of decompressive craniectomy is to reduce damage to healthy brain tissue by diverting injured tissue through the craniectomy defect to prevent a herniation syndrome.
Initial diagnosis of conditions that require consideration for decompressive craniectomy must involve an early cross-sectional imaging evaluation to determine the extent of intracranial pathology. Cerebral edema is a common imaging finding in patients with such a pathology.
Signs of cerebral edema on computed tomography (CT) images of the head include low-density parenchyma, decreased gray–white differentiation, effacement of the sulci and subarachnoid spaces, compressed ventricles, parenchymal herniation, vascular compression, and infarction.
With magnetic resonance imaging, features of cerebral edema include hypointensity on T1-weighted images and hyperintensity on T2-weighted images. The apparent diffusion coefficient intensity can differentiate between vasogenic (hyperintense) and cytotoxic (hypointense) edema.
In the setting of severe traumatic brain injury, cross-sectional imaging can reveal a combination of intracranial pathologies, including epidural or subdural hematoma, traumatic subarachnoid hemorrhage, cerebral contusion/IPH, and/or diffuse axonal shear injury. The intrinsic pathologies can precipitate delayed intracerebral abnormalities through resultant cerebral edema in the 2 to 3 days after trauma.
Patients with cytotoxic cerebral edema after a CVA that requires consideration for a decompressive craniectomy procedure are commonly those who have suffered a large-volume middle cerebral artery stroke.
Any changes in the clinical examination or baseline neurologic function prior to surgical intervention significantly affects the indication for a decompressive craniectomy and should be closely monitored during the preoperative stage. It is also important to perform a full laboratory evaluation to diagnose any preoperative coagulopathy, thrombocytopenia, or anemia that can affect the decision to pursue surgical intervention.
Indications for Surgery
The most difficult aspect of this form of craniectomy is the decision-making process to determine if the procedure is likely to be efficacious.
Decompressive craniectomy can involve different levels of decompression, depending on the pathology and brain region(s) involved. Surgical decompression options include hemicraniectomy, bifrontal craniectomy, bilateral craniectomy, hinge craniotomy, and suboccipital craniectomy.
Before surgery, it is important to discuss the anticipated outcome with the patient’s family, given the severity of brain injury generally present and aggressiveness of the intervention. The surgeon must ensure that the consenting party completely understands the deficits the patient will likely sustain as a result of the primary brain injury. The goal of this thorough discussion is to determine if intervention to preserve the patient’s life, despite a probable long-term limitation in function, is desired.
It is also important to remember that decompression should be carried out before the patient suffers from the herniation syndrome. In other words, considering the decompression emergently primarily at the time of herniation is not advised as this philosophy is associated with devastating and irreversible neurological outcomes that could have been prevented.
Widespread controversy exists in the literature regarding the overall outcomes and indications for surgical decompression compared to those of standard medical therapy for intracranial hypertension. The relevant literature regarding surgical indications for each type of major pathology, according to supratentorial or infratentorial location, is discussed below, and the surgical indications for decompressive craniectomy are summarized in Table 1.
Supratentorial Ischemic Stroke
The effectiveness of a decompressive craniectomy was evaluated by multiple randomized controlled trials and subsequent meta-analyses. The randomized controlled trials were designed to test the significance of surgical intervention within a certain time period after onset of ischemic stroke, specific neurologic criteria, and age.
The Decompressive Surgery for the Treatment of Malignant Infarction of the Middle Cerebral Artery (DESTINY) was one of the original randomized trials and demonstrated a survival benefit for surgery but the trial contained an insufficient number of patients to evaluate for functional outcomes.6 The trial enrolled patients up to 60 years of age suggesting that older patients may also benefit from surgical intervention.
The Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial (HAMLET)4 is a multicenter randomized trial published in 2009 and demonstrated that decompressive hemicraniectomy significantly reduced mortality but failed to reduce poor functional outcomes (mRS of 4 or greater).
The DEcompressive Craniectomy In MALignant middle cerebral artery infarction (DECIMAL) trial1 included patients randomized to surgical intervention within 30 hours of symptom onset. Outcomes were suggestive of increased survival but similar to some of the previous trials, improvement in functional outcome was demonstrated.
A Cochrane meta-analysis of the DECIMAL, DESTINY, and HAMLET trials was however suggestive of an improvement in good outcomes (mRS of 3 or less), improvement in survival, and no increase in patients with severe disability.3 More recent systematic analysis included 6 randomized trials and suggested a similar finding for improvement in survival and functional outcomes, however did suggest an increase in patients persistently remaining an mRS of 4. This poses an ethical dilemma given that the surgical intervention carries an improved rate of survival and possibly a favorable functional status, while also increasing the likelihood the patient will survive with a dependent neurologic status.
In general, a decompressive hemicraniectomy should be considered for patients after large MCA infarcts with malignant cerebral edema refractory to standard medical therapy, within 48-hours of ictus, to decrease mortality and increase the likelihood favorable neurological outcomes.
Multiple studies have evaluated the indications for surgical intervention for trauma-induced intracranial hypertension. The results of these studies suggest a likely benefit of surgical decompression for survival but also a compensatory increased rate of morbidity within the population of patients who survive.
The Decompressive Craniectomy (DECRA) study2 compared bifrontotemporoparietal decompressive craniectomy with standard medical therapy in the setting of traumatic brain injury. The authors compared medical management versus surgical management for patients with demonstrated diffuse cerebral edema and an ICP greater than 20 mm Hg for longer than 15 minutes in the setting of standard first-tier intensive care. The results indicate that, although ICP control was worse, patients in the medical management arm had outcomes 6 months after the trauma that were superior to those of patients in the surgical arm of the study.
The Randomized Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial Pressure (RESCU-ICP) trial5 demonstrated the affect that decompressive craniectomy had on mortality outcomes in patients 6 months after traumatic brain injury. The study revealed a 22% lower 6-month mortality rate for patients who underwent decompressive craniectomy compared to those who underwent only medical management. In compensation for their higher survival rate, patients in the surgical arm had a higher morbidity rate, with more patients surviving in a vegetative state or with severe disability. The proportions of patients with a good recovery were comparable between the 2 study arms.
The clinical equipoise of patients with a posterior fossa ischemic or hemorrhagic stroke has prevented randomized controlled study for surgical intervention. The literature is sparse on decompressive craniectomy for hemorrhagic posterior fossa stroke. A retrospective cohort study of 104 patients demonstrated an improved mortality for patients that underwent decompressive suboccipital craniectomy compared to medical treatment.8 The highest quality of evidence study was a retrospective matched case-control study including 28 surgical patients and 56 medical management controls.7 The study indicated that suboccipital decompressive craniectomy provided an improved clinical outcome in the absence of brainstem pathology.
In summary, the literature suggests that, based on non-randomized data, patients who deteriorate neurologically despite medical therapy, with a suitable neurologic status preoperatively and lack of intrinsic brainstem pathology (stroke or hemorrhage), should be considered for urgent surgical intervention.
Major randomized or prospective data on this topic are lacking, and the literature has relied on retrospective reviews and case series for guidelines. Outcomes are generally believed to benefit from early and aggressive surgical intervention if the patient’s preoperative neurological status justifies the intervention.
Contraindications to the procedure are broadly debated within the literature. Older age has been cited as a relative contraindication for decompression in the setting of trauma (cutoff of 50–65 years). Additional factors considered contraindications for decompression include severe coagulopathy and poor preoperative neurological status as evidenced by the Glasgow Coma Scale, unreactive pupils, or absent brainstem reflexes.
At the time of neurosurgical evaluation, the primary pathology inducing the elevated ICP should be identified. Implementation of maximal medical therapy for control of ICP before a decompressive craniectomy is advised.
Maximal medical therapy for elevated ICP involves a multimodal approach that can be applied in a tiered protocol.
Hyperosmolar therapy is a first-line therapy for elevated ICP. To implement this therapy appropriately, serum osmolality and sodium are monitored in a serial manner. Such therapy includes mannitol and/or hypertonic saline (3% or 23.4%). Hypertonic therapy should be reserved for those with a sodium level of <160 mEq/L or a serum osmolality of <320 mOsm/kg.
Removal of the cervical collar, applicable in the setting of trauma, preferably if CT images of the cervical spine are unremarkable, can serve as a palliative measure for patients with intracranial hypertension. Similarly, the head of the patient’s bed should be elevated to encourage cerebral venous return.
Hyperventilation can be considered for temporary ICP control by hypocapnia-induced cerebral vasoconstriction. This temporizing measure provides an immediate effect with a peak of impact approximately 30 minutes after the intervention. The effect of hyperventilation is implemented via a PaCO2level of 30 to 35 mm Hg. Prolonged hyperventilation confers multiple risks, including rebound vasodilation and ischemic injury.
Hypothermia as a therapy for elevated ICP is controversial; however, maintenance of normothermia is imperative. Fever should be treated aggressively via cooling blankets, ice packs, and acetaminophen, when applicable.
An external ventriculostomy catheter or an ICP monitor wire provides a quantitative measure for the success of medical therapy and accurately calculates cerebral perfusion pressure, the goal of which is >60 mm Hg.
If the patient’s ICP remains persistently elevated despite the abovementioned measures, he or she can be placed in a barbiturate-induced coma. This form of therapy is initiated by using sodium pentobarbital to suppress brain metabolism and will result in decreased cerebral metabolic demand and cerebral blood volume.
Persistently elevated ICP in the setting of maximal medical therapy, clinical examination decline, or radiographic progression of a herniation syndrome is an indication for decompressive craniectomy. Surgical intervention should ideally be performed within 48 hours of the inciting injury, given the propensity for progressive edema to the maximal swelling window in the setting of stroke or trauma.
Hemicraniectomy can also be referred to as a frontotemporoparietal craniectomy. The patient is positioned supine with optional placement of a sandbag under the ipsilateral shoulder. The head is placed in a rigid 3-point fixation or on a horseshoe head holder, depending on the surgeon’s preference, and rotated 45 to 60°. A reverse question-mark incision is planned to involve the zygomatic arch superior to the pinna and then posteriorly toward the inion, curving medially just lateral to the midline and then anteriorly to the hairline.
The scalp is then reflected along with the temporalis muscle as a single myocutaneous flap anteroinferiorly. Burr holes are then placed in the keyhole, frontal, parietal, and temporal regions. It is important to ensure that the frontal burr hole is at least 2 cm lateral to the midline to avoid the superior sagittal sinus.
After elevation of the bone flap, if the lesser wing of the sphenoid and the squamous segment of the temporal bone were not removed, a Leksell rongeur can be used to resect the excess bone in these regions. Adequate bony decompression over the lateral temporal lobe is paramount for maximizing the opportunity to decompress the brainstem.
A stellate durotomy is performed along the exposed dura, and a dural substitute or a large sheet of absorbable gelatin sponge can be placed overlying the stellate incision. This procedure will allow the brain to expand under the dural substitute.
Depending on the extent of parenchymal injury, medical management of external herniation can be performed intraoperatively. Cerebral edema can be so significant that the craniectomy must be extended to permit brain relaxation. In addition, noneloquent anterior temporal or frontal lobes can occasionally be removed to combat worrisome extracranial herniation.
Posterior Fossa Decompression
For details on suboccipital decompression, please refer to the Suboccipital Craniotomy chapter. The boney removal has to be wide and extend from 1 sigmoid sinus to the other and bounded by the transverse sinuses superiorly. The craniectomy should extend to the foramen magnum. Ultimately, the extent of craniectomy should be tailored to the extent of the involved cerebellum.
A sheet of dural substitute should be onlayed over the dura. I prefer the use of gelfilm for this purpose. Galea and skin should be closed in a meticulous manner to prevent the possibility of extracranial cerebral herniation or a cerebrospinal fluid leak.
The bone flap should be kept sterile and frozen or placed in the subcutaneous abdominal wall in preparation for a future cranioplasty, which is usually delayed for at least 6 weeks from the time of the craniectomy.
Patients might still require aggressive postoperative medical management of their ICP, which can be augmented via placement of an external ventriculostomy or ICP wire in the operating room. It is important to note that the waveform of ICP monitoring will be dampened significantly by decompression of the cranial vault.
A postoperative CT scan should be performed to assess the level of decompression and ensure that hemostasis is maintained. ICP monitoring and medical therapy should be continued in the postoperative phase; the goal ICP is <20 cm H2O.
Pearls and Pitfalls
- Patient selection is paramount for a successful outcome and should involve consideration of the extent of brain damage at the time of surgery and an honest discussion with the patient’s family regarding the likely functional outcome.
- Inadequate craniectomy is likely to lead to brain herniation and infarction of the herniated brain along the edges of the craniectomy. This process will lead to worsening infarction, edema, and mass effect.
Contributors: Benjamin K. Hendricks, MD, Kendall Burgett, BS
Bansal H, Chaudhary A, Singh A, et al. Decompressive craniectomy in malignant middle cerebral artery infarct: an institutional experience. Asian J Neurosurg 2015;10:203-206 (10.4103/1793-5482.161191).
Cooper JD, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011;364:1493-1502 (10.1056/NEJMoa1102077).
Cruz-Flores S, Berge E, Whittle IR: Surgical decompression for cerebral oedema in acute ischaemic stroke. Cochrane Database Syst Rev 1:CD003435, 2012.
Hofmeijer J, Kappelle LJ, Algra A, et al. Surgical decompression for space-occupying cerebral infarction (the Hemicraniectomy After Middle Cerebral Artery infarction with Life-threatening Edema Trial [HAMLET]): a multicentre, open, randomised trial. Lancet Neurol 2009;8:326-333 (10.1016/S1474-4422(09)70047-X).
Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med 2016;375:1119-1130 (10.1056/NEJMoa1605215).
Jüttler E, Schwab S, Schmiedek P, et al. Decompressive Surgery for the Treatment of Malignant Infarction of the Middle Cerebral Artery (DESTINY): a randomized, controlled trial. Stroke 2007;38:2518-2525 (10.1161/STROKEAHA.107.485649).
Kim MJ, Park SK, Song J, et al.: Preventive Suboccipital Decompressive Craniectomy for Cerebellar Infarction: A Retrospective-Matched Case-Control Study. Stroke 47:2565-2573, 2016
Luney MS, English SW, Longworth A, et al. Acute posterior cranial fossa hemorrhage—is surgical decompression better than expectant medical management? Neurocrit Care 2016;25:365-370 (10.1007/s12028-015-0217-7).
Pasternack JJ, Lanier WL Jr. Diseases affecting the brain. In Hines RL, Marschall KE (eds), Stoelting’s Anesthesia and Co-existing Disease, 7th Ed. Elsevier, Philadelphia, PA. 2018; pp 265-304.
Sims C, Mathew SJ. The management of traumatic brain injury. Curr Surg Ther 1145-1151.
Tamarit JG, Muns JA, Aboud ET, et al. Posterior fossa decompression for extraaxial and intraaxial cerebellar hematoma. In Nader R, Gragnaniello C, Berta S, et al (eds), Neurosurgery Tricks of the Trade: Cranial. Thieme, New York, NY. 2013.
Robertson C, Rangel-Castilla L. Critical care management of traumatic brain injury. In Winn HR (ed),Youmans and Winn Neurological Surgery, 7th Ed. Elsevier, Philadelphia, PA. 2017.
Please login to post a comment.