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decompressive_craniectomy_for_severe_traumatic_brain_injury

Decompressive craniectomy for severe traumatic brain injury

The choice of acute surgical treatment of patients with traumatic brain injury (TBI) is a controversial subject. Primary decompressive hemicraniectomy is used as the first line surgical therapy in some institutions, whereas smaller craniotomies (with hematoma evacuation) are used in others 1) 2).

Decompressive craniectomy (DC), has been performed for the purpose of relieving intracranial hypertension with outcome improvement in specific TBI patients.

Most of the debate surrounding the role of decompressive craniectomy in the management of severe TBI results from a paucity of data coming from randomized controlled trials (RCTs) assessing this intervention.

There have been variations in neurosurgical techniques, timing, and patient populations in most of the observational studies published in the last 2 decades.

A new RCT, pending publication, will evaluate decompressive craniectomy as a secondary procedure after intracranial pressure (ICP) targeted medical therapies have failed, and will hopefully lend further evidence to support or not support this intervention.

RECOMMENDATIONS

Level of Evidence 1

There was insufficient evidence to support a Level I recommendation for this topic.

Level of Evidence 2A

Bifrontal decompressive craniectomy is not recommended to improve outcomes as measured by the Extended Glasgow Outcome Scale (GOS-E) score at 6 months post-injury in severe TBI patients with diffuse injury (without mass lesions), and with ICP elevation to values >20 mm Hg for more than 15 minutes within a 1-hour period that are refractory to first-tier therapies. However, this procedure has been demonstrated to reduce ICP and to minimize days in the intensive care unit (ICU).

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.

*The committee is aware that the results of the RESCUEicp study may be released soon after the publication of these Guidelines.

The results of this trial may affect these recommendations and may need to be considered by treating physicians and other users of these Guidelines. We intend to update these recommendations after the results are published if needed. Updates will be available at https://braintrauma.org/coma/guidelines.

EVALUATION OF THE EVIDENCE

The Class 2 studies either compared DC to medical management or compared DCs of different sizes, in terms of their effect on patient mortality and functional outcomes. Class 3 studies addressed these questions, and also comparison of DC to craniotomy and (4) assessment of the use of DC earlier or later in the course of treatment.

For the first two questions addressed by Class 2 evidence, the quality of the body of evidence was moderate. The RCT that compared DC to initial medical management was rated Class 1.

This study was high quality but was a single study, and replication is needed for high confidence in the results. Both RCTs that compared size of DCs were rated Class 2.

For the third and fourth questions for which only Class 3 evidence was identified, the body of evidence was rated as insufficient, primarily because the results were inconsistent, with different studies reporting positive, negative, and no effects. As the studies were of poor quality, it was not possible to reconcile these differing results or to use the studies to support Level III recommendations.

Applicability The applicability differs across questions and studies. The Class 1 study comparing DC to initial medical management was conducted in three countries over an 8-year period, and included 15 centers.

While this diversity may have limited the ability to detect an effect, it could increase the applicability of the study. The two studies rated Class 2 that compare size of DCs were both conducted in one country (China).15, 16 Incomplete reporting about these studies limited the ability to fully understand key elements such as the standard of care and characteristics of the populations.

SUMMARY OF THE EVIDENCE Process Of the 31 potentially relevant studies reviewed, 21 were excluded because they did not meet the inclusion criteria. Of the remaining 10 studies, one Class 114 and two Class 215, 16 studies were included as evidence to support recommendations for this topic. The remaining seven were rated Class 3.17-23

The DECRA trial, an RCT that compared bifrontotemporoparietal DC to initial medical management for refractory raised ICP, recruited patients in 15 tertiary care hospitals in Australia, New Zealand, and Saudi Arabia between December 2002 and April 2010.

This study found poorer GOS-E scores for patients in the DC group than those in standard care at 6 months post- injury, and lower ICP and fewer ICU days for patients in the DC group. Despite randomization, the proportion of patients in the DC group with reactivity in neither pupil on admission was higher (27% vs. 12%, p=0.04) than in controls. Planned baseline covariate adjustment did not change the results, but post hoc adjustment for this difference in pupil reactivity at admission resulted in outcome differences that were no longer significant. Based on this, the authors reported that “…the overall effect size did not change, although the harmful effect of craniectomy was no longer significant. A beneficial effect of craniectomy was excluded.”


The two studies that compared different sizes of DC were both conducted in China.

One was conducted at five medical centers, while the other was conducted at a single site. They differed in the requirements for inclusion; Jiang, 2005 et al. required refractory intracranial hypertension while Qiu, 200916 included patients based on a computed tomography (CT) scan showing a swollen hemisphere. Both studies found better outcomes with larger DCs; however, the differences in patients, procedures, and treatment, as well as the fact that these studies did not adjust for any covariates, limited the ability of these studies to provide a definitive answer to this question. Of importance, these studies did not make a comparison of different sizes with no decompression. Thus, the evidence did not allow an estimate of the effect of decompression compared with no decompression.

Both of the two Class 3 studies that compared DC to medical management reported no significant difference in mortality; however, one reported poorer functional outcomes with DC while the other found no difference in function.

The one Class 3 study comparing large and small DC reported lower mortality with larger DC.21 These results were similar to the Class 2 studies that addressed this question. For these questions, higher quality Class 2 evidence was available, and the Class 3 evidence was not used to inform the recommendations.

The studies that compared DC to craniotomy reported lower, but not statistically significant, mortality rates and conflicting findings about function and complications.

Similarly, the results of two studies of the timing of DC were inconsistent. One reported reduced mortality, and one reported no difference.

Given the quality of the studies and the inconsistency of the findings, the quality of the body of evidence was rated as insufficient and these studies were not used as the basis for recommendations.

REFERENCES

1. Xi G, Keep RF, Hoff JT. Pathophysiology of brain edema formation. Neurosurg Clin N Am. Jul 2002;13(3):371-383. PMID: 12486926. 2. Dunn LT. Raised intracranial pressure. J Neurol Neurosurg Psychiatry. Sep 2002;73 Suppl 1:i23-27. PMID: 12185258. 3. Farahvar A, Gerber LM, Chiu YL, et al. Response to intracranial hypertension treatment as a predictor of death in patients with severe traumatic brain injury.[Erratum appears in J Neurosurg. 2011 Jul;115(1):191 added Froelich, Matteus]. J Neurosurg. May 2011;114(5):1471-1478. PMID: 21214327. 4. Vik A, Nag T, Fredriksli OA, et al. Relationship of “dose” of intracranial hypertension to outcome in severe traumatic brain injury. J Neurosurg. Oct 2008;109(4):678-684. PMID: 18826355. 5. Bor-Seng-Shu E, Figueiredo EG, Amorim RLO, et al. Decompressive craniectomy: a meta-analysis of influences on intracranial pressure and cerebral perfusion pressure in the treatment of traumatic brain injury. J Neurosurg. Sep 2012;117(3):589-596. PMID: 22794321. 6. Eberle BM, Schnuriger B, Inaba K, Gruen JP, Demetriades D, Belzberg H. Decompressive craniectomy: surgical control of traumatic intracranial hypertension may improve outcome. Injury Sep 2010;41(9):894-898. PMID: 21574279. 7. Sahuquillo J, Arikan F. Decompressive craniectomy for the treatment of refractory high intracranial pressure in traumatic brain injury. Cochrane Database Syst Rev. 2006(1):1- 41. PMID: 16437469. 8. Bohman LE, Schuster JM. Decompressive craniectomy for management of traumatic brain injury: an update. Curr Neurol Neurosci Rep. Nov 2013;13(11):392. PMID: 24101348. 9. Huang X, Wen L. Technical considerations in decompressive craniectomy in the treatment of traumatic brain injury. Int J Med Sci. 2010;7(6):385-390. PMID: 21103073. 10. Ragel BT, Klimo P, Jr., Martin JE, Teff RJ, Bakken HE, Armonda RA. Wartime decompressive craniectomy: technique and lessons learned. Neurosurg Focus. May 2010;28(5):E2. PMID: 20568936. 11. Quinn TM, Taylor JJ, Magarik JA, Vought E, Kindy MS, Ellegala DB. Decompressive craniectomy: technical note. Acta Neurol Scand. Apr 2011;123(4):239-244. PMID: 20637010. 12. Hutchinson PJ, Kolias PJ, Timofeev I, et al. Update on the RESCUEicp decompressive craniectomy trial. Crit Care. 2011;15(Suppl 1):P312. 13. Hutchinson P. Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of intracranial pressure (RESCUEicp). ISRCTN66202560. DOI 10.1186/ISRCTN66202560. ISRCTN Registry 2005; http://www.isrctn.com/ISRCTN66202560. 14. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury.[Erratum appears in N Engl J Med. 2011 Nov 24;365(21):2040]. N Engl J Med. 2011;364(16):1493-1502. PMID: 21434843. 34

15. Jiang JY, Xu W, Li WP, et al. Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: a multicenter, prospective, randomized controlled study. J Neurotrauma. 2005;22(6):623-628. PMID: 15941372. 16. Qiu W, Guo C, Shen H, et al. Effects of unilateral decompressive craniectomy on patients with unilateral acute post-traumatic brain swelling after severe traumatic brain injury. Crit Care. 2009;13(6):R185. PMID: 19930556. 17. Huang AP, Tu YK, Tsai YH, et al. Decompressive craniectomy as the primary surgical intervention for hemorrhagic contusion. J Neurotrauma. Nov 2008;25(11):1347-1354. PMID: 19061378. 18. Soukiasian HJ, Hui T, Avital I, et al. Decompressive craniectomy in trauma patients with severe brain injury. Am Surg. Dec 2002;68(12):1066-1071. PMID: 12516810. 19. Akyuz M, Ucar T, Acikbas C, Kazan S, Yilmaz M, Tuncer R. Effect of early bilateral decompressive craniectomy on outcome for severe traumatic brain injury. Turk Neurosurg. 2010;20(3):382-389. PMID: 20669113. 20. Wen L, Wang H, Wang F, et al. A prospective study of early versus late craniectomy after traumatic brain injury. Brain Inj. 2011;25(13-14):1318-1324. PMID: 21902550. 21. Lu LQ, Jiang JY, Yu MK, et al. Standard large trauma craniotomy for severe traumatic brain injury. Chin J Traumatol. Oct 2003;6(5):302-304. PMID: 14514369. 22. Olivecrona M, Rodling-Wahlstrom M, Naredi S, Koskinen LO. Effective ICP reduction by decompressive craniectomy in patients with severe traumatic brain injury treated by an ICP-targeted therapy. J Neurotrauma. Jun 2007;24(6):927-935. PMID: 17600510. 23. Soustiel JF, Sviri GE, Mahamid E, Shik V, Abeshaus S, Zaaroor M. Cerebral blood flow and metabolism following decompressive craniectomy for control of increased intracranial pressure. Neurosurg. 2010;67(1):65-72. PMID: 20559092.

Case series

2017

Tapper et al. conducted a single-center retrospective study on adult blunt TBI patients admitted to a neurosurgical intensive care unit during 2009-2012. Patients were divided into three groups based on their initial treatment - decompressive craniectomy, craniotomy, and conservative. Primary outcome was 6-month Glasgow Outcome Scale (GOS) dichotomized to favorable outcome (independent) and unfavorable outcome (dependent). The association between initial treatment and outcome was assessed using a logistic regression model adjusting for case-mix using known predictors of outcome.

Of the 822 included patients, 58 patients were in the craniectomy group, 401 patients in the craniotomy group, and 363 patients in the conservatively treated group. Overall, 6-month unfavorable outcome was 48%. After adjusting for case-mix, patients in the decompressive craniectomy group had a statistical significantly higher risk for poor neurological outcome compared to patients in the conservative group (OR 3.06, 95% CI 1.45-6.42) and craniotomy group (OR 3.61, 95% CI 1.74-7.51).

In conclusion, patients requiring primary decompressive craniectomy had a higher risk for poor neurological outcome compared to patients undergoing craniotomy or were conservatively treated. It is plausible that the poor prognosis is related to the TBI severity itself rather than the intervention. Further prospective randomized trials are required to establish the role of decompressive craniectomy in the treatment of patients with TBI 3).

2006

During a 48-month period (March 2000-March 2004), 50 of 967 consecutive patients with closed TBI experienced diffuse brain swelling and underwent decompressive craniectomy, without removal of clots or contusion, to control intracranial pressure (ICP) or to reverse dangerous brain shifts. Diffuse injury was demonstrated in 44 patients, an evacuated mass lesion in four in whom decompressive craniectomy had been performed as a separate procedure, and a nonevacuated mass lesion in two. Decompressive craniectomy was performed urgently in 10 patients before ICP monitoring; in 40 patients the procedure was performed after ICP had become unresponsive to conventional medical management as outlined in the American Association of Neurological Surgeons guidelines. Survivors were followed up for at least 3 months posttreatment to determine their Glasgow Outcome Scale (GOS) score. Decompressive craniectomy lowered ICP to less than 20 mm Hg in 85% of patients. In the 40 patients who had undergone ICP monitoring before decompression, ICP decreased from a mean of 23.9 to 14.4 mm Hg (p < 0.001). Fourteen of 50 patients died, and 16 either remained in a vegetative state (seven patients) or were severely disabled (nine patients). Twenty patients had a good outcome (GOS Score 4-5). Among 30-day survivors, good outcome occurred in 17, 67, and 67% of patients with postresuscitation Glasgow Coma Scale scores of 3 to 5, 6 to 8, and 9 to 15, respectively (p < 0.05). Outcome was unaffected by abnormal pupillary response to light, timing of decompressive craniectomy, brain shift as demonstrated on computerized tomography scanning, and patient age, possibly because of the small number of patients in each of the subsets. Complications included hydrocephalus (five patients), hemorrhagic swelling ipsilateral to the craniectomy site (eight patients), and subdural hygroma (25 patients).

Decompressive craniectomy was associated with a better-than-expected functional outcome in patients with medically uncontrollable ICP and/or brain herniation, compared with outcomes in other control cohorts reported on in the literature 4).

1)
Kolias AG, Belli A, Li LM, Timofeev I, Corteen EA, Santarius T, et al. Primary decompressive craniectomy for acute subdural haematomas: Results of an international survey. Acta Neurochir 2012;154:1563-5.
2)
Kolias AG, Scotton WJ, Belli A, King AT, Brennan PM, Bulters DO, et al. Surgical management of acute subdural haematomas: Current practice patterns in the United Kingdom and the Republic of Ireland. Br J Neurosurg 2013;27:330-3.
3)
Tapper J, Skrifvars MB, Kivisaari R, Siironen J, Raj R. Primary decompressive craniectomy is associated with worse neurological outcome in patients with traumatic brain injury requiring acute surgery. Surg Neurol Int. 2017 Jul 11;8:141. doi: 10.4103/sni.sni_453_16. eCollection 2017. PubMed PMID: 28781918; PubMed Central PMCID: PMC5523471.
4)
Aarabi B, Hesdorffer DC, Ahn ES, Aresco C, Scalea TM, Eisenberg HM. Outcome following decompressive craniectomy for malignant swelling due to severe head injury. J Neurosurg. 2006 Apr;104(4):469-79. PubMed PMID: 16619648.
decompressive_craniectomy_for_severe_traumatic_brain_injury.txt · Last modified: 2017/08/08 08:28 by administrador