Severe traumatic brain injury (TBI) due to focal or diffuse lesions leads to raised intracranial pressure (ICP). The normal ICP is less than 15 mm Hg; if the ICP remains persistently high, cerebral perfusion is compromised. Unrelieved intracranial hypertension culminates in irreversible neurological deterioration leading to fatal brain herniations. Raised ICP may be controlled by surgical evacuation of focal lesions when feasible and medical therapy including head end elevation, sedation, ventilation to normocarbia, osmotherapy, induced hypothermia, and metabolic suppression using barbiturate infusion. In refractory intracranial hypertension, a decompressive craniectomy (DC) is being increasingly performed, involving removal of a large segment of the skull and opening of the underlying dura mater.
It makes physiological sense to perform DC; if excessive pressure within the skull squashes the brain and leads to fatal herniation, opening the skull to relieve the pressure seems intuitive. Historically, the pressure-relieving effect of DC has been well known. In 1901, Kocher proposed DC for patients with raised ICP following TBI, followed by sporadic use of this technique over the years. Following its established efficacy in acute ischemic stroke,1 there has been an upsurge of interest in DC for severe TBI with intractable intracranial hypertension in recent times.
How does it work?
According to the Munro-Kellie hypothesis, the intracranial compartment in inelastic. Increase in volume of any of the intracranial contents (brain, blood, or cerebrospinal fluid), is compensated by a shift of the remaining contents out of the skull. However, when compensatory mechanisms fail, the ICP begins to rise. Opening the rigid skull allows room for the intracranial contents to expand, thus relieving pressure. Maintenance of ICP between 20–25 mm Hg improves outcomes following TBI.2,3
Technique of DC
DC is performed to reduce ICP and prevent brain herniation. Craniectomy must be extensive allowing enough room for the brain to expand. A unilateral frontotemporoparietal craniectomy is commonly carried out for a unilateral focal lesion. The incision is approximately 2 cm lateral to the midline to prevent injury to the superior sagittal sinus. The anteroposterior diameter of the bone flap must be more than 15 cm and descend down to the base of the temporal fossa to enable adequate decompression (Figure 1). Bifrontal craniectomy is performed for diffuse lesions with generalized cerebral edema. Through a bicoronal skin flap, a frontotemporal bone flap is removed including the bone over the superior sagittal sinus (Figure 2). The dura is opened after removal of the bone flap followed by augmentative duroplasty.
Does DC improve clinical outcomes?
Although relief of life-threatening intracranial hypertension may seem rational and intuitive, does it really improve clinical outcomes in TBI? Two randomized controlled studies have addressed this all-important question. The DECRA study recruited 155 patients with severe, diffuse TBI between 2002–2010.4 Patients with an ICP of more than 20 mm Hg for more than 15 min during a 1-h period, either continuously or intermittently, despite optimal first-tier medical management were enrolled. DC was performed within the first 72 h of injury in the study group, while standard medical care was continued in the control group. The surgical technique involved a bifrontotemporoparietal craniectomy with bilateral dural opening. Predictably, patients who underwent DC had significantly lower ICP compared to those who received standard medical management alone. The composite primary outcome comprised of death, vegetative state, or severe disability corresponding to a score of 1–4 on the extended Glasgow outcome scale (GOS-E). At 6-month follow-up, the composite unfavorableoutcome was significantly higher among patients who underwent DC compared to those who received standard medical therapy alone (70% vs. 51%). The study had several limitations including a higher number of patients with non-reactive pupils in the DC arm. The ICP threshold for DC was considered too low and out of tune with real-world care. Furthermore, bifrontal craniectomy without sectioning of the falx may not have been the most optimal DC technique. Notwithstanding these limitations, DECRA suggested that relief of ICP with DC may not translate to improved clinical outcomes.
The RESCUE-ICP study enrolled 398 patients with severe TBI between 2004–2014 who had an ICP of more than 25 mm Hg for 1–12 h in spite of stage I and II treatments.5 Patients were randomized to undergo DC or continued medical treatment, including barbiturate infusion. In contrast to the DECRA study, patients who had undergone evacuation of an intracranial hematoma were included if a craniectomy had not been performed previously. A large frontotemporoparietal DC was carried out for unilateral lesions and bifrontal DC was performed for diffuse lesions, based on the judgment of the operating surgeon. The primary outcome was assessed using the GOS-E at 6 months. Patients were followed up at for 24 months after randomization. In the DECRA study, a favorable outcome was defined as a score of 5 or higher on the GOS-E; however, in the RESCUE-ICP study, a score of 4 or higher was defined as a favorable outcome. (It is important to note this difference; a score of 4 on the GOS-E indicates that the patient is able to be alone at home, without assistance, for a period of up to 8 h). At 6 m follow-up, mortality was significantly lower with DC; however, there was a higher incidence of vegetative state, lower and upper severe disability compared to medical therapy. On sensitivity analysis, at 6 months, a favorable GOS-E (4 or higher) was not significantly different between patients who underwent DC and those who did not.
The RESCUE-ICP study suggests that DC improves survival at the expense of severely disabled life. However, the culture, beliefs, and values of the community may be crucial in determining what may be an acceptable level of functional ability. For instance, a GOS-E of 4 indicates the ability to be alone at home, but unable to travel or shop independently. Many patients and families may consider this an acceptable outcome, especially among the Indian population. Another important consideration is the validity of these studies in settings where ICP monitoring is not routine, with decision-making based primarily on clinical examination and CT imaging.
The bottom line
- DC as a relatively early intervention does not improve outcomes; it improves survival as a later intervention when first and second stage medical therapies fail.
- Improved survival with DC may result in a life with significant disability; however, the degree of acceptable disability varies among populations.
- A considered, patient and family-centered decision is important in deciding the most optimal therapy.
- A subset of patients may benefit from DC; it may be challenging to identify or study this subgroup in randomized controlled trials.
References:
- Vahedi K, Hofmeijer J, Juettler E, et al. Early decompressive surgery in malignant infarction of the middle cerebral artery: a pooled analysis of three randomised controlled trials. Lancet Neurol. 2007;6(3):215-222. doi:10.1016/S1474-4422(07)70036-4
- Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma. 2007;24 Suppl 1:S37-44. doi:10.1089/neu.2007.9990
- Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, et al. Guidelines for the management of severe traumatic brain injury. VIII. Intracranial pressure thresholds. J Neurotrauma. 2007;24 Suppl 1:S55-58. doi:10.1089/neu.2007.9988
- Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive Craniectomy in Diffuse Traumatic Brain Injury. N Engl J Med. 2011;364(16):1493-1502. doi:10.1056/NEJMoa1102077
- Hutchinson PJ, Kolias AG, Timofeev IS, et al. Trial of Decompressive Craniectomy for Traumatic Intracranial Hypertension. N Engl J Med. 2016;375(12):1119-1130. doi:10.1056/NEJMoa1605215
