Decompressive Hemicraniectomy: Update on Applications for Large Territory Stroke
Craniectomy has ancient roots in the trepanations of Neolithic Incas as well as classical Egypt and Greece, where it was first used as treatment for traumatic injuries.1,2 The modern era of cranial decompression began with Emil Kocher3, who proposed its use in traumatic brain injury, and Harvey Cushing4, who further defined the indication for intracranial hypertension. While neurosurgical technique, anesthesia, asepsis and medical management of traumatically injured and stroke patients improved dramatically throughout the 20th century, systematic evaluations regarding the efficacy and optimal timing of decompressive hemicraniectomy for large vessel ischemic stroke were first carried out during the early 2000s.
Decompression Improves Stroke Patient Survival
Large vessel occlusive ischemic stroke is an unfortunately high-incidence disease. In spite of the dramatic improvements in acute interventions (e.g. thrombolytics, endovascular techniques), many patients fail therapy or receive treatment after the onset of an irreversible large volume infarction. This results in the onset of malignant brain swelling and the potentially fatal secondary injuries associated with midbrain herniation syndromes. Middle cerebral artery (MCA) occlusions result in relatively predictable natural histories and have consequently provided the substrate for the study of decompressive hemicraniectomy via multiple randomized controlled trials (RCTs) and systematic reviews.
In 2007, the DECIMAL5 and DESTINY6 European multicenter randomized trial results were simultaneously published. These landmark publications randomized adults under 55 and under 60, respectively, with complete MCA infarcts to receive either early decompressive hemicraniectomy with durotomy or maximal medical treatment. Both trials demonstrated a large, beneficial effect size, with greater than two-fold improvements in mortality associated with surgical decompression (25% vs. 78% and 18% vs. 53%, respectively; via meta-analysis7 31% vs. 70%, RR=2.05 and 95%CI=1.54-2.72). Subsequent investigations, including the HAMLET8 trial and HeADD-FIRST9 pilot study, replicated these outcomes, with major variations in study design, including the stipulation that clinical deterioration be among the pre-specified inclusion criteria.
Mixed Results for Functional Outcome
In addition to the dramatic difference in survival offered by decompressive hemicraniectomy in these stroke patients, a meta-analysis provided information regarding functional outcomes. This showed a large proportion of patients shifted toward improvement in functional outcome after surgery. Unfortunately, it was also noted that a significant number of patients with anticipated mortalities shifted instead to a functionally devastated outcome. Survival without major disability (mRS?3) was significantly higher in the surgical group (27% vs. 14%, RR 1.58 and 95% CI 1.02-2.46), so too were patients with severe (mRS=4) and very severe (mRS=5) disability (32% vs. 10% and 11% vs. 4%). Of particular interest, the data also confirmed that patients older than 60 years rarely achieved a good neurological outcome (mRS?3), independent of treatment allocation, and in spite of the observation that the survival effect was observed in all age strata. Notably, the DESTINY-II10 randomized controlled trial confirmed a survival benefit for hemicraniectomy in patients older than 60 years, but no patient in either control or surgical arm survived without major disability (mRS?3). Although this finding was unsurprising given the natural history of MCA infraction, in contrast to analyses focused on younger patients, there was no evidence of a functional improvement in disability.
Regardless of the age group, it is fair to say that decompressive hemicraniectomy does result in an increase in the fraction of disabled patients — but it does so by keeping alive a number of patients that otherwise would have died, which is potentially offset in younger patients by parallel improvements in functional outcomes attributable to prevention of secondary injury.
Pre-emptive, Not Reactive
Prior to the reporting of these trials, standard-of-care in most institutions was to advise surgical decompression on the basis of clinical deterioration, with particular attention to signs of severe intracranial hypertension or impending herniation, including:
- Loss of consciousness
- New anisocoria
- Concerning imaging findings
Unfortunately, this practice likely resulted in avoidable injuries attributable to herniation events:
- Reduced cerebral perfusion
- Practical limitations and increased risks of emergent operations
- Hazard of initially undetected exam changes
- Increased risks of anesthesia and positioning after the onset of severe intracranial hypertension
Although supporting data are scant, it is both conceptually and experimentally11-13 reasonable to hypothesize that earlier surgery would improve outcomes. Perhaps the most compelling data is derived from the HAMLET trial, in which no statically significant benefit was observed in those patients allocated to surgery at a delay of >48 hours after infarction14. However, no additional benefit has been shown from operating prior to 24 hours, suggesting that an optimal window for treatment benefit may exist, allowing neurosurgical and critical care teams the opportunity to potentially conduct goals-of-care conversations with families prior to proceeding with an operation that may prolong life, but in some cases, with unacceptable disability.
Craniectomy size appears to be a major contributor to outcome in decompression after large-vessel occlusion or, by extrapolation, traumatic injury.15 To adequately reduce pressure on the involved hemisphere and avoid unnecessary venous congestion or craniectomy-associated hemorrhage, hemicraniectomy dimensions should be at least 12 cm anterior-to-posterior and extend from safely off-midline to the middle fossa floor, whenever technically feasible. Outcomes from contralateral or bilateral craniotomies are less studied, but may be indicated in uncommon clinical circumstances.
ICP Monitoring in Stroke Patients does not Impact Outcomes
The application of decompressive hemicraniectomy to large-vessel occlusion shares some common ground with malignant cerebral edema seen following a diffuse traumatic brain injury (TBI). Interestingly, although intracranial pressure monitoring is instrumental in many cases of TBI, it has failed to predict herniation in stroke patients, given that the unilateral nature of the cerebral edema frequently precipitates herniation and secondary injury without marked intracranial hypertension.16,17
Why are You Still Using Mannitol?
Shifting expert and emerging clinical evidence18,19 suggest that the use of small volume ultra-concentrated (e.g. 10-21%) intravenous sodium chloride should be considered first-line treatment once conservative measures are exhausted, as it reduces intracranial pressure while avoiding the diuresis and relative hypotension associated with mannitol — important considerations in trauma and stroke patients alike. It is also likely, that the rapid infusion and action of ultra-concentrated sodium chloride magnifies its rheological effect,20,21 while limiting the comparative increase in serum sodium or osmolarity associated with continuous infusion. Ultimately, case specific factors such as central access, medication availability, volume status, preexisting chronic hyponatremia (to avoid osmotic demyelination syndrome) and other medical comorbidities may also contribute to overall clinical decision-making.
We are at an inflection point in intensive care monitoring tools and imaging technology. Improvements in these tools and randomized, high-quality, clinical trials-based data are increasingly informing our collective knowledge regarding the best use of surgical decompressive techniques in massive infarction. In the interim, prophylactic early decompressive hemicraniectomy remains a beneficial tool for improving function and survival. No doubt, as we progress from the work of the pioneering neurosurgical Incans further into the 21st century, the role of craniectomy will continue to evolve.
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4. Cushing H: The establishment of cerebral hernia as a decompressive measure for inaccessible brain tumors: with the description of intermuscular methods of making the bone defect in temporal and occipital regions. Surg Gynecol Obstet 1:297-314, 1905
5. Vahedi K, Vicaut E, Mateo J, Kurtz A, Orabi M, Guichard J-P, et al: Sequential-design, multicenter, randomized, controlled trial of early decompressive craniectomy in malignant middle cerebral artery infarction (DECIMAL Trial). Stroke 38:2506-2517, 2007
6. Ju?ttler E, Schwab S, Schmiedek P, Unterberg A, Hennerici M, Woitzik J, et al: Decompressive surgery for the treatment of malignant infarction of the middle cerebral artery (DESTINY) a randomized, controlled trial. Stroke 38:2518-2525, 2007
7. Alexander P, Heels-Ansdell D, Siemieniuk R, Bhatnagar N, Chang Y, Fei Y, et al: Hemicraniectomy versus medical treatment with large MCA infarct: a review and meta-analysis. BMJ Open 6:e014390, 2016
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9. Frank JI, Schumm LP, Wroblewski K, Chyatte D, Rosengart AJ, Kordeck C, et al: Hemicraniectomy and durotomy upon deterioration from infarction-related swelling trial: randomized pilot clinical trial. Stroke 45:781-787, 2014
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13. Doerfler A, Forsting M, Reith W, Staff C, Heiland S, Schäbitz W-R, et al: Decompressive craniectomy in a rat model of “malignant” cerebral hemispheric stroke: experimental support for an aggressive therapeutic approach. J Neurosurg 85:853-859, 1996
14. Mitchell P, Gregson BA, Crossman J, Gerber C, Jenkins A, Nicholson C, et al: Reassessment of the HAMLET study. Lancet Neurol 8:602-603, 2009
15. Wagner S, Schnippering H, Aschoff A, Koziol JA, Schwab S, Steiner T: Suboptimum hemicraniectomy as a cause of additional cerebral lesions in patients with malignant infarction of the middle cerebral artery. J Neurosurg 94:693-696, 2001
16. Smith SE, Kirkham FJ, Deveber G, Millman G, Dirks PB, Wirrell E, et al: Outcome following decompressive craniectomy for malignant middle cerebral artery infarction in children. Dev Med Child Neurol 53:29-33, 2011
17. Schwab S, Aschoff A, Spranger M, Albert F, Hacke W: The value of intracranial pressure monitoring in acute hemispheric stroke. Neurology 47:393-398, 1996
18. Mangat HS, Wu X, Gerber LM, Schwarz JT, Fakhar M, Murthy SB, et al: Hypertonic Saline is Superior to Mannitol for the Combined Effect on Intracranial Pressure and Cerebral Perfusion Pressure Burdens in Patients With Severe Traumatic Brain Injury. Neurosurgery, 2019
19. Schwarz S, Georgiadis D, Aschoff A, Schwab S: Effects of hypertonic (10%) saline in patients with raised intracranial pressure after stroke. Stroke 33:136-140, 2002
20. Ogden AT, Mayer SA, Connolly Jr ES: Hyperosmolar agents in neurosurgical practice: the evolving role of hypertonic saline. Neurosurgery 57:207-215, 2005
21. Mangat HS, Chiu Y-L, Gerber LM, Alimi M, Ghajar J, Haertl R: Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury. J Neurosurg 122:202-210, 2015
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