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Decompressive craniectomy

Decompressive craniectomy is a neurosurgical procedure in which a large portion of the skull is surgically removed to allow the swollen brain to expand beyond the rigid cranial vault, thereby reducing life-threatening intracranial pressure caused by conditions such as traumatic brain injury or stroke.^[1] This intervention is typically considered a last-resort measure after medical treatments like sedation, osmotherapy, and ventriculostomy fail to control refractory intracranial hypertension, which can lead to brain herniation and death if untreated.^[2] The procedure involves opening the underlying dura mater to maximize decompression and may be performed unilaterally (hemicraniectomy) or bilaterally (bifrontal craniectomy), depending on the location and extent of brain swelling.^[1] The primary indications for decompressive craniectomy include severe traumatic brain injury with elevated intracranial pressure, malignant middle cerebral artery infarction, acute subdural hematoma, and sometimes subarachnoid or intracerebral hemorrhage when conservative management is insufficient.^[1] During the surgery, the removed bone flap is typically stored in a freezer or abdominal subcutaneous pocket for future cranioplasty, which reconstructs the skull several months later to protect the brain and restore normal physiology.^[2] Timing is critical, with guidelines recommending intervention within hours of refractory pressure elevation to optimize outcomes, though early prophylactic use has shown limited benefits in randomized trials.^[3] Historically, decompressive craniectomy traces its roots to ancient trephination practices over 10,000 years ago, but its modern form was refined in the early 20th century by surgeons like Theodor Kocher and Harvey Cushing for wartime head injuries.^[3] While it significantly lowers mortality rates—for instance, from 48.9% to 26.9% at six months in patients with traumatic brain injury according to the RESCUEicp trial—survivors often face higher risks of severe disability, vegetative states, or dependency compared to medical management alone.^[2] Complications can include infection, hydrocephalus, syndrome of the trephined,^[4] and challenges during cranioplasty, underscoring the need for careful patient selection based on age, comorbidities, and injury severity.^[1] Current guidelines from organizations like the Brain Trauma Foundation endorse its use to improve mortality and favorable outcomes in patients with severe traumatic brain injury and refractory intracranial hypertension in select cases, while weighing long-term quality-of-life implications.^[5]

Overview

Definition

Decompressive craniectomy is a neurosurgical intervention that involves the surgical removal of a large portion of the skull, referred to as the bone flap, typically measuring at least 12 × 15 cm in size, without immediate replacement. This procedure is combined with a wide incision of the underlying dura mater to enable the expansion of brain tissue beyond the confines of the cranial vault, thereby reducing compressive forces on the brain.^[6]^[7] The primary goal of decompressive craniectomy is to create additional space for edematous or swollen brain tissue, preventing potentially fatal herniation and ischemia caused by unchecked intracranial hypertension.^[8]^[9] Two principal variants exist: unilateral hemicraniectomy, which targets focal lesions on one side of the brain, and bifrontal craniectomy, which addresses diffuse bilateral swelling across the frontal regions.^[9]^[10] This procedure is distinct from a craniotomy, where the bone flap is temporarily removed but replaced immediately to restore skull integrity, and from trephination (or burr hole drainage), which creates only a small opening in the skull for localized pressure relief or fluid evacuation rather than broad decompression.^[11]^[12]^[13]

Physiological rationale

Decompressive craniectomy addresses intracranial hypertension arising from cerebral edema, a condition where brain swelling elevates intracranial pressure (ICP), thereby compromising cerebral perfusion pressure (CPP). CPP is calculated as the difference between mean arterial pressure (MAP) and ICP, using the formula \text{CPP} = \text{MAP} - \text{ICP}.^[14] When ICP rises unchecked, CPP falls below critical thresholds (typically <60 mm Hg), leading to cerebral ischemia and potentially fatal herniation syndromes.^[14]^[1] This pathophysiology aligns with the Monro-Kellie doctrine, which posits that the intracranial compartment is a fixed-volume space containing brain tissue, blood, and cerebrospinal fluid (CSF), with their combined volumes remaining constant under normal conditions.^[1] Compensatory mechanisms, such as displacement of CSF or venous blood, initially mitigate volume increases from edema, but once exhausted, ICP escalates exponentially, further impairing cerebral blood flow and autoregulation.^[1] By removing a portion of the skull and dura, decompressive craniectomy creates an expandable space, permitting edematous brain tissue to herniate outward through the bony defect. This intervention normalizes ICP and enhances intracranial compliance, shifting the pressure-volume curve (where compliance is defined as C = \frac{dV}{dP}, the change in volume per unit change in pressure) to allow greater volume accommodation without proportional ICP rises.^[15]^[16] Supporting evidence from animal models, such as rat studies of malignant hemispheric infarction, demonstrates that early decompression restores cerebral blood flow by alleviating compressive forces on vasculature.^[17] Similarly, early human investigations, including those from the late 20th century, report increased cerebral blood flow velocities post-procedure in traumatic brain injury patients, correlating with improved perfusion dynamics.^[3]

Indications

Traumatic brain injury

Decompressive craniectomy serves as a primary surgical intervention for severe traumatic brain injury (TBI), particularly in cases of refractory intracranial hypertension where intracranial pressure (ICP) persists above 20-25 mmHg despite aggressive medical management.^[18] Maximal medical therapy typically encompasses tiered approaches such as osmotherapy using mannitol or hypertonic saline to draw fluid from brain tissue, controlled hyperventilation to induce vasoconstriction and lower cerebral blood volume, sedation, and cerebrospinal fluid drainage.^[19] This procedure is reserved for patients with diffuse brain swelling rather than localized lesions, as it physiologically permits outward herniation of swollen brain tissue to alleviate pressure, though the detailed mechanisms are outlined in the physiological rationale section.^[20] The Brain Trauma Foundation guidelines recommend decompressive craniectomy for adults with severe TBI, defined by a Glasgow Coma Scale (GCS) score of 3-8 accompanied by abnormal computed tomography (CT) findings such as cistern compression or midline shift, when ICP elevation proves unresponsive to medical interventions.^[18] Timing of the procedure varies: early intervention within 48 hours may be considered for diffuse injuries to preempt deterioration, while late salvage craniectomy is often employed beyond this window as a rescue measure for ongoing refractory hypertension.^[2] These recommendations stem from evidence balancing the risks of cerebral ischemia against the benefits of pressure reduction in non-penetrating, diffuse TBI patterns. Patient selection emphasizes younger adults under 40 years, who demonstrate better tolerance and potential for recovery due to greater physiological reserve, particularly in the context of diffuse axonal injury characterized by widespread white matter shearing without discrete mass effects.^[21] Focal mass lesions, such as epidural or subdural hematomas, are generally contraindicated for primary decompressive craniectomy, as evacuation via craniotomy is preferred to directly address the lesion.^[20] In clinical practice, decompressive craniectomy accounts for approximately 10-15% of surgical cases among patients with severe TBI requiring operative intervention, reflecting its role as a targeted rather than routine procedure.00338-3/fulltext)

Ischemic stroke

Decompressive craniectomy is indicated for patients with malignant middle cerebral artery (MCA) infarction, characterized by large hemispheric infarcts involving more than 50% of the MCA territory, accompanied by cerebral edema that leads to significant mass effect, such as midline shift greater than 5 mm or intracranial pressure (ICP) exceeding 20 mmHg.^[22] These infarcts typically manifest 2 to 4 days after stroke onset, resulting in life-threatening brain herniation if untreated.^[23] The procedure aims to alleviate intracranial hypertension by removing a large portion of the skull, allowing the swollen brain tissue to expand without further compression.^[24] Randomized controlled trials, including DECIMAL, DESTINY, and HAMLET, have provided robust evidence supporting decompressive craniectomy in this context. A pooled analysis of these trials demonstrated that early surgical intervention significantly reduces mortality, from 78% in medically managed patients to 29% in those undergoing craniectomy, particularly among individuals under 60 years of age.61172-1/fulltext) This analysis, involving 93 patients, also showed an increase in favorable functional outcomes, with more survivors achieving modified Rankin Scale scores of 0 to 3 at 12 months.61172-1/fulltext) The trials collectively enrolled patients with severe neurological deficits and radiological evidence of extensive infarction, confirming the procedure's role in preventing fatal outcomes from edema-related complications.61046-1/fulltext) Patient selection for decompressive craniectomy emphasizes age under 55 to 60 years, as older individuals may experience less benefit due to comorbidities and reduced neuroplasticity.^[22] Considerations for hemisphere involvement include potential language or sensory deficits in dominant hemisphere strokes, which historically raised concerns about quality of life; however, meta-analyses indicate comparable functional outcomes between dominant and non-dominant infarcts, supporting surgery in both cases when other criteria are met.^[25] Optimal timing is within 48 hours of symptom onset, as earlier intervention correlates with lower mortality and better survival with independence, based on trial data showing superior results compared to delayed procedures.61172-1/fulltext)

Other conditions

Decompressive craniectomy has been employed in cases of malignant cerebral edema arising from primary brain tumors such as glioblastoma, where rapid swelling leads to refractory intracranial hypertension despite medical management.^[26] In pediatric patients with glioblastoma, emergency hemicraniectomy has been performed to evacuate mass effect and alleviate pressure, allowing for subsequent tumor-directed therapies.^[26] Similar applications extend to infectious etiologies causing severe edema, including cerebral abscesses and malaria. For brain abscesses, decompressive craniectomy serves as an adjunct when abscess-related swelling causes life-threatening herniation, particularly in cases with extensive surrounding edema exceeding 2.5 cm in diameter.^[27] In cerebral malaria, particularly Plasmodium falciparum infections, decompressive procedures have been used to manage intracranial hypertension from diffuse edema and associated hematomas, though outcomes remain guarded due to the underlying systemic infection.^[28] Additionally, decompressive craniectomy addresses malignant edema in hypoxic-ischemic encephalopathy, often following global insults like near-drowning or asphyxia, by providing space for brain expansion in diffuse injury patterns.^[29] Decompressive craniectomy is also used in select cases of intracerebral or subarachnoid hemorrhage with malignant edema and refractory intracranial hypertension unresponsive to evacuation and medical therapy.^[30] Rare indications include fulminant hepatic failure with cerebral edema, where bilateral decompressive craniectomy has been reported to control intracranial hypertension in acute liver dysfunction, potentially bridging patients to transplantation. In refractory status epilepticus, decompressive craniectomy mitigates edema-induced pressure elevation when seizures contribute to secondary brain injury, as seen in case reports of invasive monitoring-guided interventions.^[31] For idiopathic intracranial hypertension unresponsive to ventriculoperitoneal shunting, cranial vault decompression offers a salvage option by expanding the calvarial volume and reducing pressure on optic nerves and brainstem structures.^[32] Case series demonstrate efficacy in pediatric abusive head trauma, where decompressive craniectomy reduces mortality in select cohorts with severe swelling, though nonaccidental mechanisms are associated with higher overall fatality rates compared to accidental injuries.^[33] In post-cardiac arrest cerebral swelling, early decompressive craniectomy has shown potential to lower mortality by up to 50% in small cohorts by interrupting herniation and ischemia cascades, particularly when combined with targeted temperature management.^[30] Relative contraindications for decompressive craniectomy include advanced age greater than 65 years, which is associated with poorer functional recovery due to reduced brain plasticity; bilateral fixed and dilated pupils indicating advanced herniation; and irreversible brainstem damage, often evidenced by Glasgow Coma Scale scores below 4 with absent brainstem reflexes.^[34]

Surgical procedure

Preoperative assessment

Preoperative assessment for decompressive craniectomy involves a multidisciplinary evaluation to confirm indications, optimize patient condition, and ensure informed decision-making, particularly in cases of refractory intracranial hypertension from traumatic brain injury (TBI) or ischemic stroke. This process typically includes neuroimaging to quantify mass effect, invasive monitoring to verify elevated intracranial pressure (ICP), correction of reversible physiological derangements, and detailed discussions of risks with patients or surrogates.^[5]^[24] Imaging plays a central role in assessing the extent of brain swelling and herniation risk. Non-contrast computed tomography (CT) of the head is the primary modality, used to identify midline shift greater than 5 mm, effaced basal cisterns, or significant mass effect from contusions, hematomas, or infarcts occupying more than 50-75% of the middle cerebral artery territory in stroke cases.^[24] In select instances, magnetic resonance imaging (MRI) may supplement CT to detect subtle ischemic changes or diffuse axonal injury not evident on initial scans, aiding in prognosis and contraindication identification such as extensive bilateral damage.^[5] For ICP monitor placement, CT also guides safe insertion sites, avoiding vascular structures or lesions.^[35] Invasive ICP monitoring is essential to document refractory hypertension before proceeding to surgery, as decompressive craniectomy is reserved for cases unresponsive to tiered medical management. The gold standard is an intraventricular catheter (external ventricular drain), which allows therapeutic cerebrospinal fluid drainage alongside pressure measurement, though intraparenchymal fiberoptic probes are alternatives when ventricular access is risky.^[35] Decompressive craniectomy is recommended for late refractory intracranial hypertension (>25 mmHg for 1-12 hours) despite maximal medical therapy (Level IIA evidence from RESCUEicp trial), but not for early refractory cases (>20 mmHg for >15 minutes; Level IIA from DECRA trial). The general ICP treatment threshold is <22 mmHg.^[5] Continuous monitoring of cerebral perfusion pressure (typically targeted at 60-70 mmHg) accompanies ICP assessment to guide preoperative optimization.^[36] Patient-specific factors must be addressed to minimize perioperative risks, involving input from neurosurgery, neurology, and intensive care teams. Coagulation status is evaluated and corrected if deranged; for instance, platelet counts should exceed 100,000/μL, and international normalized ratio (INR) below 1.4, with reversal of anticoagulants or antiplatelet agents where feasible, though recent evidence indicates no significant increase in hemorrhagic complications from preoperative antiplatelet use in TBI-related craniectomy.^[37] Sedation and ventilation are optimized to maintain stable hemodynamics and avoid exacerbating ICP, often using propofol or midazolam infusions titrated to minimize cerebral metabolic demand.^[38] Comorbidities such as hypertension or diabetes are managed aggressively, and baseline neurological status (e.g., Glasgow Coma Scale) is documented for outcome prognostication.^[38] Informed consent emphasizes the procedure's life-saving intent alongside substantial risks of disability, obtained from the patient if possible or surrogate decision-makers in impaired consciousness states. Discussions highlight potential outcomes, including a substantial risk of severe disability or vegetative state (approximately 40% of survivors in the RESCUEicp trial at 6 months), with reduced mortality but higher rates of poor functional outcomes compared to medical management alone.^[2] Ethical considerations include proxy involvement and alignment with advance directives, given prognostic uncertainties in severe cases.^[5]^[39]

Operative technique

The operative technique for decompressive craniectomy is performed under general anesthesia with strict adherence to sterile protocols to minimize infection risk.^[40] The patient is positioned supine with the head turned 30-45 degrees to the contralateral side and secured using a Mayfield three-pin skull clamp for rigid fixation, ensuring optimal access to the surgical site while maintaining cerebral venous drainage.^[24]^[41] A curvilinear or question-mark incision is made along the temporoparietal region for unilateral procedures or across the bifrontal area, sparing the pinna and extending sufficiently to allow wide exposure.^[42] Multiple burr holes are created using a high-speed drill, connected with a craniotome to remove a large bone flap: in unilateral hemicraniectomy, a fronto-temporo-parietal flap measuring at least 12 cm in diameter (ideally 15 cm) is excised down to the floor of the middle cranial fossa; for bifrontal craniectomy, the flap spans from the orbital roof to the coronal suture bilaterally, crossing the midline while carefully avoiding injury to the superior sagittal sinus.^[40] The bone edges are inspected and smoothed to prevent compression of the underlying brain. The dura is then managed with a wide durotomy, typically in a stellate or cruciate fashion, to allow herniation of swollen brain tissue without constriction.^[43] To facilitate expansion and prevent re-closure, a duraplasty is performed using autologous materials such as pericranium or galea aponeurotica, or synthetic grafts like bovine pericardium, sutured loosely around the dural edges.^[44]^[45] Closure involves multilayer approximation of the scalp without tension, while the bone flap is removed and stored either in the patient's subcutaneous abdominal pocket or in a freezer at -20°C for future cranioplasty.^[24] If not already placed preoperatively, an intracranial pressure probe may be inserted through a separate burr hole.^[46] The procedure typically lasts 1-2 hours, emphasizing meticulous hemostasis and sterile technique throughout to optimize outcomes.^[42]

Clinical outcomes

Reduction of intracranial pressure

Decompressive craniectomy rapidly reduces elevated intracranial pressure (ICP) in patients with severe brain injury, typically lowering mean ICP from levels exceeding 40 mmHg to below 20 mmHg within hours of the procedure.^[47] In one study of patients with refractory ICP, the mean ICP decreased from 36.4 mmHg (range 18–80 mmHg) immediately post-craniectomy to 12.6 mmHg (range 2–51 mmHg), with this effect observed across cases where preoperative ICP was often above 40 mmHg.^[47] The magnitude of reduction correlates with the size of the bone flap removed, where defects larger than 80 cm²—such as those spanning 70–160 cm² in frontotemporoparietal craniectomies—facilitate greater decompression and more effective ICP control compared to smaller flaps.^[48] Clinical studies report success rates of 70–90% in achieving ICP below 20 mmHg, with one series noting this threshold met in 85% of monitored patients post-decompression.^[49] The primary mechanism involves increasing intracranial compliance by removing a portion of the rigid skull, which allows the brain to expand outward without proportional rises in pressure, thereby accommodating swelling from edema or hemorrhage.^[50] This enhances the brain's ability to tolerate volume increases while maintaining cerebral perfusion, as evidenced by improved pressure-volume index measurements post-procedure.^[50] Continuous monitoring via ICP waveform analysis is essential to assess this effect, as the procedure alters waveform components—including pulse, respiratory, and slow waves—indicating changes in cerebrovascular reactivity and compensatory reserve.^[15] Waveform evaluation helps confirm sustained compliance improvements and guides adjustments in management. The ICP reduction is generally sustained for weeks to months, persisting until cerebral edema resolves, after which pressure typically normalizes within 4 weeks in many cases.^[51] However, failure rates approximate 10%, often attributable to incomplete decompression from inadequate bone flap size or persistent mass lesions requiring reoperation.^[52] As an adjunctive measure, decompressive craniectomy is frequently combined with ventricular drainage via external ventricular drain placement to facilitate cerebrospinal fluid (CSF) removal, further lowering ICP by creating additional space within the ventricular system.^[53] This multimodal approach enhances overall pressure control in refractory cases. The effects on ICP reduction have been confirmed in major trials such as DECRA and RESCUEicp.^[2]

Functional outcomes

Decompressive craniectomy (DC) substantially lowers mortality rates compared to medical management alone in patients with severe traumatic brain injury (TBI) or malignant middle cerebral artery (MCA) infarction, with systematic reviews indicating a relative risk reduction of 41-50% across adult populations.^[54]^[55] Among survivors, however, 30-50% experience significant disability, often requiring long-term care or assistance with daily activities.^[55] Functional recovery is typically evaluated using the Glasgow Outcome Scale (GOS) or its extended version (GOSE), which categorize outcomes from death (GOS 1) to good recovery (GOS 5). Favorable outcomes (GOS 4-5, indicating moderate disability or better) occur in approximately 40-60% of adults under 40 years, though rates vary by underlying condition and patient characteristics.^[56]^[55] Key factors influencing functional outcomes include patient age, with younger individuals (<60 years) achieving higher rates of independence (up to 39% good functional outcome overall) compared to older patients, who face elevated risks of moderate-to-severe disability (over 50%).^[55]^[57] Surgical timing also plays a role; early DC (within 48 hours of symptom onset) correlates with better recovery in ischemic stroke cases, potentially due to preempting irreversible brain herniation, while in TBI, outcomes improve with intervention before prolonged intracranial hypertension.^[54]^[55] Hemisphere involvement shows mixed results, with some evidence suggesting marginally better prospects for non-dominant hemisphere infarctions, though meta-analyses indicate comparable overall outcomes between dominant and non-dominant sides.^[58] Long-term, DC enhances survival rates but frequently results in increased dependency, with many survivors experiencing persistent neurological deficits that affect mobility, cognition, and self-care. A 24-month follow-up of the RESCUEicp trial (ages 10-65 years) confirmed sustained mortality reduction (33.5% vs. 54.0% with medical care) but similar rates of good recovery (extended GOSE 7-8: 11.0% vs. 10.9%) and higher severe or moderate disability in the craniectomy group.^[54]^[59] The net impact on quality-adjusted life years (QALYs) remains debated, as gains in lifespan are offset by reduced quality of life from disability; cost-utility analyses report variable QALY increments (0.14-0.35 per patient), highlighting the procedure's life-saving value alongside its disability burden.^[60]^[61]

Pediatric cases

Decompressive craniectomy in pediatric patients leverages the brain's greater neuroplasticity, resulting in higher rates of favorable outcomes compared to adults. Pooled data from 17 studies involving 186 children with traumatic brain injury who underwent hemicraniectomy showed a 6-month mortality rate of 21.1% and favorable outcomes (Glasgow Outcome Scale [GOS] scores 4-5) in approximately 78% of survivors (112 of 144).^[62] In contrast, the RESCUEicp trial (ages 10-65 years) reported favorable outcomes (extended GOSE 4-8) in 42.8% of the craniectomy group at 6 months. Children also experience lower complication rates, attributed to anatomical advantages such as thinner skull bones that facilitate surgical decompression with reduced blood loss and trauma, as well as more resilient dura that supports dural expansion. Recent analyses, however, suggest mixed results, with some evidence indicating DC may not reduce overall mortality or poor outcomes compared to medical management in pediatric TBI.^[63]^[2] Common indications for decompressive craniectomy in children include abusive head trauma, which accounts for up to 28% of cases requiring the procedure, and birth-related injuries such as subdural hemorrhages from perinatal trauma. Optimal timing is within 24-48 hours of injury to maximize cerebral protection, with early intervention (<24 hours) associated with improved functional recovery in pediatric series, though some studies show no significant difference between acute and subacute timing. Pediatric series and subgroup analyses, including a 2018 systematic review of 12 studies encompassing 260 patients, demonstrate reduced mortality with decompressive craniectomy compared to medical management alone (e.g., 0% vs. 34% in one series), without increasing rates of severe disability. The RESCUEicp trial, which included patients as young as 10 years, supports these findings in older children, though dedicated pediatric subgroups were not separately analyzed. A major consideration in pediatric cases is the impact of skull defects on cranial growth, as the craniectomy site can lead to asymmetric development and bone resorption if left unrepaired. To mitigate these issues, earlier cranioplasty is recommended, typically 3-6 months post-craniectomy, to accommodate ongoing skull expansion and reduce resorption risks, with delays beyond 6 weeks increasing complication rates in children.

Evidence from clinical trials

DECRA trial

The DECRA (Decompressive Craniectomy in Patients with Severe Traumatic Brain Injury) trial was a multicenter, randomized controlled trial conducted from December 2002 to April 2010 across 15 tertiary care hospitals in Australia, New Zealand, and Saudi Arabia. It enrolled 155 adult patients aged 15 to 59 years with severe diffuse traumatic brain injury, defined by a Glasgow Coma Scale score of 3 to 8 and refractory intracranial hypertension (intracranial pressure >20 mm Hg for more than 15 minutes per hour despite first-tier medical therapies). Patients were randomized to either early bifrontotemporoparietal decompressive craniectomy (n=73) or continued standard medical management (n=82), with the surgical intervention performed within 72 hours of injury, typically as an early prophylactic measure rather than salvage therapy.^[64]^[65] The primary outcome was the Extended Glasgow Outcome Scale (GOSE) score at 6 months post-injury, with an unfavorable outcome defined as GOSE 1 to 4. Results showed that decompressive craniectomy effectively lowered mean intracranial pressure (14.4 mm Hg in the surgery group vs. 19.1 mm Hg in the medical group; P<0.001) and reduced durations of mechanical ventilation, intensive care unit stay, and hospitalization. However, it was associated with worse functional outcomes, with 70% of the surgery group having unfavorable GOSE scores compared to 51% in the medical group (odds ratio for unfavorable outcome, 2.21; 95% CI, 1.14 to 4.26; P=0.02). Mortality rates were similar between groups at 6 months (19% vs. 18%).^[64] The trial faced several criticisms, including its relatively small sample size of 155 patients, which limited statistical power; exclusion of those with focal mass lesions, restricting generalizability to all traumatic brain injury cases; and early intervention timing (most surgeries within 40 hours of injury), which may not reflect typical salvage use for refractory hypertension. These limitations, along with baseline imbalances and lack of blinding, have been noted in subsequent analyses. Published in the New England Journal of Medicine in 2011, the DECRA trial influenced clinical guidelines, such as the 2020 Brain Trauma Foundation recommendations, which advise against early secondary decompressive craniectomy for refractory intracranial pressure elevation based on its findings of no mortality benefit and poorer functional outcomes, while favoring delayed approaches informed by later studies like RESCUEicp.^[64]^[65]^[59]^[18]

RESCUEicp trial

The RESCUEicp trial was an international, multicenter, parallel-group randomized controlled trial conducted from January 2004 to March 2014 across 52 centers in 20 countries, primarily led by the United Kingdom, enrolling 408 patients aged 10 to 65 years with traumatic brain injury (Glasgow Coma Scale score of 3–8) and refractory intracranial hypertension defined as intracranial pressure exceeding 25 mmHg for 1 to 12 hours despite first- and second-tier medical therapies per Brain Trauma Foundation guidelines, along with an abnormal computed tomography scan.^[2] Patients were randomly assigned to receive either decompressive craniectomy (performed in 92.6% of cases) or continued medical management (with barbiturate coma induced in 87.2% of cases).^[2] The primary outcome was the Extended Glasgow Outcome Scale (GOSE) score at 6 months after injury, with secondary outcomes including mortality, GOSE at 12 and 24 months, and intracranial pressure control.^[2] At 6 months, decompressive craniectomy reduced mortality to 26.9% compared to 48.9% in the medical management group (P<0.001), representing a 22 percentage point absolute reduction, though it increased rates of vegetative state (8.5% vs. 2.1%) and severe disability (37.3% vs. 22.4%).^[2] Favorable outcomes (GOSE scores 4–8, encompassing upper severe disability or better) occurred in 42.8% of the surgical group versus 34.6% of the medical group (P=0.12), showing no significant overall difference but highlighting a survival benefit that shifted more patients from death to less favorable states.^[2] Decompressive craniectomy also achieved superior intracranial pressure control, with fewer patients requiring additional interventions.^[2] Subgroup analyses, including by age (≤40 years vs. >40 years), indicated greater benefit from surgery in younger patients, where favorable outcomes reached 51.4% in the surgical group versus 36.2% in the medical group (absolute difference 15.2%, 95% CI 3.5–26.9%; interaction P=0.025).^[66] The trial results, published in 2016 in the New England Journal of Medicine, demonstrated that late decompressive craniectomy as salvage therapy after medical failure halves mortality in refractory cases, though at the cost of increased severe disability among survivors.^[2] These findings influenced updated Brain Trauma Foundation guidelines, which in their 2020 revision provide level-IIA recommendations supporting large decompressive craniectomies (≥12 × 15 cm) for late refractory intracranial hypertension to improve mortality and select outcomes in adult and select pediatric patients.^[67] By emphasizing delayed intervention over early prophylactic use, the trial addressed prior evidence gaps and shifted practice toward targeted salvage application in severe traumatic brain injury management.^[2]

Other studies

A pooled analysis of three randomized controlled trials—DECIMAL, DESTINY, and HAMLET—involving 93 patients aged 18–60 years with malignant middle cerebral artery infarction demonstrated that early decompressive craniectomy (within 48 hours of stroke onset) significantly reduced mortality to 22% compared to 71% in the control group, while achieving favorable functional outcomes (modified Rankin Scale [mRS] score ≤3) in 43% versus 21% of patients at one year.^[68] This analysis underscored the procedure's role in improving survival and moderate disability in younger stroke patients, though it highlighted the need for individualized decision-making due to potential severe impairments in survivors. Meta-analyses have synthesized evidence across various etiologies, confirming a consistent mortality benefit from decompressive craniectomy. The 2019 Cochrane systematic review on high intracranial pressure in traumatic brain injury, based on three randomized trials with 420 participants, found moderate-quality evidence of reduced death risk at six months (risk ratio 0.54, 95% CI 0.43–0.68), but low-quality evidence indicated uncertain effects on neurological outcomes, with possible increases in severe disability.^[69] Similarly, the 2022 Cochrane review on surgical decompression for malignant cerebral oedema after ischaemic stroke, drawing from trials like DECIMAL, DESTINY, and HAMLET, reported very low-certainty evidence for reduced mortality but emphasized caution regarding disability and quality of life.^[70] The RESCUE-ASDH trial (2023), a multicenter randomized study of 440 adults with traumatic acute subdural hematoma, compared decompressive craniectomy to craniotomy and found similar extended Glasgow Outcome Scale scores at 12 months (common odds ratio 0.85, 95% CI 0.60–1.21), indicating no clear superiority but comparable trends in mortality reduction alongside higher complication rates with craniectomy.^[71] Observational research has explored secondary decompressive craniectomy following initial hematoma evacuation. A 2025 retrospective cohort study of 101 patients who underwent primary decompressive craniectomy for severe traumatic brain injury found that secondary craniectomy was performed in 16 cases for refractory intracranial hypertension, with no significant differences in functional outcomes or complication rates compared to primary-only cases after adjustment, though predictors included higher preoperative ICP and smaller initial craniectomy area.^[72] Despite these advances, significant research gaps persist, particularly in elderly patients over 65 years and non-Western populations. A 2024 multicenter study of 223 patients noted poorer functional outcomes and higher mortality in older adults undergoing decompressive craniectomy for traumatic brain injury, underscoring the limited high-quality data guiding its use in this demographic.^[73] Reviews have similarly highlighted underrepresentation of non-Western cohorts, with most evidence derived from European and North American trials, potentially limiting generalizability to diverse global settings.

Complications

Surgical risks

Decompressive craniectomy carries significant intraoperative risks, primarily related to hemorrhage, often originating from venous sinuses or cortical veins during bone and dura removal.^[74] Brain exposure following dural opening can also lead to contusion expansion in up to 58% of patients, exacerbated by reperfusion edema and increased hydrostatic pressure gradients.^[74] These complications are mitigated through meticulous hemostasis techniques, such as bipolar coagulation and hemostatic agents, alongside continuous intracranial pressure (ICP) monitoring to guide the extent of decompression.^[75] In the early postoperative period (within the first 30 days), infections represent a major concern, with wound infections affecting about 5-10% of patients and meningitis or ventriculitis occurring in 2-5% due to cerebrospinal fluid leaks or duraplasty breaches.^[74] Subdural hygromas develop in roughly 10-27% of cases, typically within 10 days, resulting from cerebrospinal fluid accumulation in the subdural space.^[75] Paradoxical herniation, a rare but life-threatening event seen in 1-3% of patients, arises from rapid ICP reduction creating a negative pressure gradient, often if atmospheric pressure exceeds intracranial pressure.^[76] Overall, major perioperative complications occur in 20-30% of decompressive craniectomy cases, encompassing hemorrhage, infection, and hygroma, though rates can reach higher in select series.^[24] Prophylactic antibiotics, such as cefazolin, reduce infection risk, while vigilant ICP monitoring and serial imaging aid early detection.^[75] Management typically involves reoperation for hematoma evacuation or expanding contusions, and targeted antibiotic therapy for infections, often guided by cerebrospinal fluid cultures.^[74]

Long-term issues

One of the primary long-term complications following decompressive craniectomy is the syndrome of the trephined, also known as sinking skin flap syndrome, which affects approximately 10% of patients with traumatic brain injury. This condition arises months to years after surgery when the scalp flap sinks inward, leading to altered cerebral blood flow and cerebrospinal fluid (CSF) dynamics due to atmospheric pressure on the exposed brain. Common manifestations include persistent headaches, cognitive decline such as memory impairment and executive dysfunction, and motor weakness, often contralateral to the craniectomy site. Symptoms typically resolve promptly after cranioplasty, highlighting the reversible nature of this syndrome when addressed through skull reconstruction.^[77] Hydrocephalus represents another significant chronic issue, occurring in about 16% of adult patients post-decompressive craniectomy. It develops due to perturbed CSF flow pathways disrupted by the surgical defect and brain shifts, with higher rates observed in cases of ischemic stroke (around 26%) and hemorrhagic stroke (21%). This complication usually emerges after the first month and can lead to progressive ventricular enlargement, necessitating interventions like ventriculoperitoneal shunting in 15-20% of affected individuals overall. Early recognition through imaging and clinical monitoring is crucial, as untreated hydrocephalus can exacerbate neurological deficits.^[77] Seizures are a frequent long-term concern, with an incidence ranging from 20% to 40%.^[77] The underlying mechanism involves a lowered seizure threshold from cortical irritation, scar tissue formation, and altered intracranial dynamics, often manifesting within the first year but persisting as epilepsy in many cases. Prophylactic use of anticonvulsants remains controversial, as evidence on their efficacy in preventing late-onset seizures is mixed, though they are commonly initiated in high-risk patients. Additional long-term challenges include bone resorption when autologous bone flaps are used for eventual cranioplasty, affecting roughly 16% of adult cases and up to 39% in pediatric patients. This resorption, driven by factors such as delayed reconstruction and metabolic changes, can compromise structural integrity and necessitate revision surgery. Cosmetic deformities, such as scalp depression or contour irregularities, occur in about 3% of adults and are often linked to flap resorption or inadequate temporalis muscle preservation during initial surgery, impacting quality of life through visible asymmetry. These issues underscore the importance of timely cranioplasty to mitigate chronic morbidity.^[77]

Follow-up and recovery

Cranioplasty

Cranioplasty is the reconstructive surgery performed to repair the skull defect resulting from decompressive craniectomy, restoring cranial integrity and protecting the brain once acute swelling has resolved.^[78] This procedure is essential to prevent long-term complications associated with persistent skull defects, such as the syndrome of the trephined.^[79] The timing of cranioplasty is typically 3 to 6 months after decompressive craniectomy to ensure resolution of cerebral edema, confirmed by computed tomography (CT) imaging. Recent 2025 meta-analyses indicate that early cranioplasty (within 3 months) may be associated with lower complication rates in adults, though optimal timing remains debated.^[80] In pediatric cases, earlier timing—often within 6 weeks—is recommended to support skull growth and minimize developmental disruptions.^[81] Autologous bone is the preferred material for cranioplasty due to its biocompatibility and low rejection risk; it is commonly stored frozen or in a subcutaneous abdominal pocket during the post-decompressive period.^[82] Synthetic alternatives include polymethylmethacrylate (acrylic), titanium mesh for customizable shaping, and 3D-printed implants designed via computer-aided modeling for precise fit.^[78] The surgical technique involves elevating the scalp flap, dissecting the dura if necessary, positioning the bone flap or implant over the defect, and securing it with titanium plates and screws, akin to reversing the initial craniotomy.^[83] Complication rates range from 10% to 30%, with infection representing the most frequent issue, often necessitating implant removal.^[78] Cranioplasty improves cerebral hemodynamics by enhancing blood flow, particularly ipsilaterally, and alleviating symptoms of the trephined syndrome, such as headaches and motor deficits.^[84] Cranioplasty can lead to significant neurological improvements, including gains in cognitive and motor function, as demonstrated in a 2025 study.^[85]

Rehabilitation

Following decompressive craniectomy, the acute phase of rehabilitation begins in the intensive care unit (ICU) with close monitoring of neurological status, vital signs, and intracranial pressure to prevent secondary brain injury. Patients are gradually weaned from mechanical ventilation as respiratory stability improves, often within the first few days to weeks, depending on the underlying condition such as traumatic brain injury or stroke. To protect the exposed brain tissue from trauma during this period and prior to cranioplasty, custom-fitted helmets are routinely used, reducing the risk of injury during transfers and early movements.^[86]^[87]^[88] Rehabilitation involves a multidisciplinary team including physical therapists, occupational therapists, speech-language pathologists, and neuropsychologists to address motor deficits, aphasia (particularly in post-stroke cases), and cognitive impairments. Physical and occupational therapy focus on restoring strength, balance, and coordination through progressive exercises such as range-of-motion activities, gait training, and functional tasks to mitigate hemiparesis and spasticity. Speech therapy targets communication and swallowing difficulties, while neuropsychological interventions assess and rehabilitate attention, memory, and executive function to support overall independence.^[89]^[87] Intensive rehabilitation typically lasts 6-12 months, with inpatient phases emphasizing daily sessions of 1-2 hours and outpatient follow-up for sustained progress; goals center on achieving independence in activities of daily living (ADLs) such as self-care and mobility. Approximately 30-50% of patients attain moderate recovery, defined by favorable functional outcomes on scales like the Extended Glasgow Outcome Scale, enabling community reintegration with assistance.^[89]^[90]^[91] Challenges in rehabilitation include managing persistent disabilities like fatigue and hemiparesis, which require ongoing family support for emotional and practical aid in daily routines. A 2025 study supports the use of passive head-up tilt positioning as a safe early mobilization strategy in neurocritical care to enhance neurological recovery and reduce complications in patients with impaired consciousness.^[89]^[92]

History

Early history

The origins of decompressive craniectomy can be traced to ancient trepanation, a surgical practice involving the drilling or scraping of holes in the skull, dating back to the Neolithic era around 7000 BCE.^[93] This procedure was performed across various cultures, with archaeological evidence from healed trephined skulls found in Peru and Europe, indicating it was used to treat head trauma or alleviate perceived ailments such as headaches, epilepsy, or the release of "evil spirits."^[93] Approximately 5-10% of Neolithic skulls examined show signs of trepanation, with survival rates evidenced by bone healing estimated at 70-90% in many samples, suggesting a surprisingly effective primitive technique despite the absence of modern anesthesia or antisepsis.^[93] In the 19th century, decompressive craniectomy began to evolve as a more formalized neurosurgical intervention. Odilon Marc Lannelongue described linear craniectomy in 1890 as a method to address microcephaly in infants by relieving intracranial pressure through skull incisions, marking an early systematic approach to cranial decompression.^[94] Shortly thereafter, Thomas Annandale reported in 1894 on decompressive craniectomy as a palliative measure for inoperable brain tumors, expanding its application beyond congenital conditions to pathological states involving elevated intracranial pressure.^[95] Early 20th-century advancements were pioneered by Harvey Cushing, who in 1905 advocated subtemporal decompressive craniectomy for inaccessible brain tumors, performing subtotal skull resections to accommodate swelling and reduce mortality.^[95] This approach significantly lowered operative death rates in neurosurgery, with Cushing's overall tumor surgery mortality dropping from around 50-90% in prior eras to under 13% by 1910 through refined techniques and hemostasis.^[96] However, in the pre-antibiotic era before the 1940s, high postoperative infection rates—approaching 100% mortality in some intracranial infection cases—severely limited the procedure's widespread adoption due to risks of sepsis and osteomyelitis.^[97]

Modern developments

Decompressive craniectomy gained prominence in military medicine during World War I, refined by Harvey Cushing for severe head injuries in soldiers, and continued in World War II and conflicts like the Vietnam War, where rapid skull decompression was employed to mitigate intracranial pressure and facilitate debridement of fragments.^[98] This approach became a standard in forward surgical settings during conflicts like the Vietnam War, emphasizing early intervention to improve survival rates in combat casualties.^[99] In the 1970s, advancements in microsurgical techniques and intracranial pressure (ICP) monitoring, pioneered by Nils Lundberg, revolutionized the timing and precision of decompressive craniectomy.^[100] Lundberg's development of continuous ICP measurement via ventricular catheters allowed clinicians to detect refractory hypertension earlier, guiding surgical decisions and reducing risks associated with delayed intervention in severe TBI cases.^[101] During the 1990s and 2000s, randomized controlled trials (RCTs) began establishing a stronger evidence base for decompressive craniectomy, particularly in non-TBI contexts like stroke. Key stroke RCTs, such as DESTINY (2007) and DECIMAL (2007), demonstrated reduced mortality in patients with malignant middle cerebral artery infarction through hemicraniectomy, influencing broader adoption.^[24] Concurrently, the Eurotherm3235 trial (initiated in the 2000s and published in 2015) evaluated therapeutic hypothermia (32–35°C) as an adjunct to ICP control, including in conjunction with craniectomy, though it highlighted risks of poorer functional outcomes without clear mortality benefits.^[102] The 2016 publication of the RESCUEicp trial marked a pivotal shift, positioning decompressive craniectomy as a salvage therapy for refractory intracranial hypertension in TBI patients unresponsive to medical management.^[2] This international RCT showed that late craniectomy reduced mortality from 49% to 27% at 6 months compared to continued medical therapy, albeit with increased rates of severe disability, prompting its recommendation as a tier-3 intervention in guidelines.^[103] In the 2020s, research has emphasized minimally invasive variants, such as limited craniectomy, to balance ICP relief with reduced tissue disruption and complications.^[104] These approaches involve smaller bone flaps or endoscopic assistance, showing promise in select TBI cases for shorter recovery times. Parallel innovations in biomaterials for subsequent cranioplasty have improved outcomes, with regenerative options like hydroxyapatite composites and antimicrobial-modified implants reducing infection rates and promoting bone integration.^[105]^[106] As of 2025, AI-assisted imaging tools have enhanced patient selection for decompressive craniectomy by predicting outcomes from CT scans and trauma narratives, aiding in the identification of candidates likely to benefit and thereby optimizing resource use.^[107] Global guidelines, including those from the American Association of Neurological Surgeons (AANS) and Brain Trauma Foundation, have been refined for pediatric applications, weakly recommending craniectomy in cases of neurologic deterioration or refractory ICP while stressing individualized assessment.^[108]

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