Patients may sustain fractures of the sacrum, a largely cancellous bony spinal segment, through either low or high energy trauma. Associated nerve root compression and neurologic injuries can be associated with stable or unstable sacral injuries and may be missed more frequently than injuries affecting lumbar roots because of the predominance of bowel and bladder symptoms unless the S1 nerve roots are affected. This is especially true in patients who have urinary catheters placed which precludes recognition of urinary symptoms.
Sacral fractures have been classified several times in the past but without consideration of the presence or absence of neurologic injury as a component of the classification system. The most widely used classification is the Denis system1 that divides zones of injury according to the location of the fracture line with respect to the neural foramina. Zone 1 injuries are common, pass lateral to the foramina, and have a low risk of neurologic injury of approximately 6%. Zone 2 injuries pass through the foramina and an intermediate risk of neural injury of about 28%, whereas zone 3 injuries are rare, occur medial to the foramina, and are associated with neurological deficits in about half of cases. Subsequent proposals to classify sacral injuries are primarily concerned with fracture morphology and do not focus on neurologic injury as a major determinant of surgical management.2–6 Recently, efforts have begun to develop a comprehensive sacral fracture classification system that incorporates neurologic status as a major determinant of the need for surgical intervention.7
Current principles guiding treatment of traumatic neurologic injury in patients with ongoing neural element compression have been shaped substantially by the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) trial.8 This study demonstrated improved neurologic outcome with early decompressive surgery and was consistent with preclinical data which suggested that early decompression should optimize outcomes. Although extension of these findings to neurologic deficits associated with nerve root compression is attractive, the pathoanatomical differences between spinal cord compression and nerve root compression may lead to differences in the relative benefit of decompressive surgery. No similarly comprehensive study of the role of timing of decompression in determining neurologic outcome after traumatic nerve-root level injuries has been performed.
There are 2 principle methods for decompression of neural elements to relieve stenosis associated with fracture malalignment. Direct decompression of the nerve roots requires sacral laminectomy of the affected segments. In contrast, many authors have reported “indirect” decompression of the cauda equina using fracture reduction and associated restoration or improvement of spinal canal patency without laminectomy. It is unclear whether this surgical strategy is equivalent to formal decompression in terms of the likelihood of recovery from neurologic deficits.
Given the uncertainties regarding the importance of decompression of the cauda equina to treat sacral stenosis associated with fracture, we sought to perform a systematic review to answer the following questions: (1) Does formal sacral decompression provide improvement in outcome for patients with neurologic deficit after sacral fracture compared with patients treated with indirect decompression? (2) Does the timing of surgical decompression influence neurologic outcome?
MATERIALS AND METHODS
Electronic Database Search
A systematic review was performed of literature published between January 1, 1985 and July 1, 2015. Two authors independently performed a MEDLINE search via PubMed. Peer-reviewed articles related to sacral fractures were identified using combinations of the following search terms: “Sacral fracture,” “Traumatic Sacral fracture,” “Sacral fracture decompression,” “Sacral fracture time to decompression,” and “Sacral Decompression.” Results including English and non-English literature were reviewed and selected for their relevance. Only clinical studies on human subjects and in the English language were included. Papers cited in each article identified by this search strategy were reviewed by the same reviewers to ensure that all eligible articles were identified and included. All English-language studies, and non-English papers that had been translated into English, were included. Studies that did not provide sufficient detail to confirm the nature of the sacral injury, treatment rendered (formal decompression or indirect decompression), and neurologic outcome were excluded. Studies using subjects less than 18 years of age, cadavers, nonhuman subjects, or laboratory simulations were excluded. In addition, studies without a clear methodology were excluded. Any studies in which more than 10% of a cohort met the exclusion criteria were excluded.
All studies were assigned a level of evidence using the grading tool described by the Centre for Evidence-Based Medicine.9 Additionally, all studies were analyzed for bias using the criteria recommended by the Cochrane Back Review Group.10 (see Appendix A, Supplemental Digital Content 1, http://links.lww.com/JOT/A47).
Using the title and abstract, 95% (1362/1433) of all articles could be excluded (Fig. 1). The remaining articles could not be immediately eliminated so each was fully reviewed, leading to exclusion of 58% (41/71) of these articles. If there was disagreement between the 2 reviewers about the inclusion of an article, a more senior author reviewed the articles.
Both cohorts in articles comparing 2 groups of patients treated differently were included. Cohorts from studies treatment techniques (ie, indirect reduction vs. open reduction) were separated and each group was included in the appropriate group.
In addition to classifying neurologic recovery rate as complete and incomplete, the effect of the timing of decompression was identified when this information was available. As time thresholds for what was considered to represent early versus delayed decompression varied by study, we arbitrarily defined early decompression as before 72 hours. This was a common threshold used in the literature and allowed the best possible aggregation of data.
The effect of decompression technique and timing of decompression surgery on partial and complete neurologic recovery was estimated using a generalized linear mixed model (GLMM) to implement a logistic regression with a study-level random effect. This is similar to the implementation of a random-effects meta-analysis, the difference being that different treatments are not necessarily compared in the same study. The random effect controls for differences between studies such as patient population. All statistical analyses were carried out in the statistical platform R 3.1.1 (R Foundation for Statistical Computing, Vienna, Austria). The generalized linear mixed model was implemented using the “lme4” package within R and the estimates of event rates and confidence intervals were made using the “effects” package.
One thousand four hundred thirty-three articles were initially identified, and 1361 articles were excluded on the basis of their title and abstract alone (Fig. 1). The remaining 71 articles underwent a full review, and an additional 41 articles were excluded at this time.
In total, 30 articles and 309 patients with sacral fracture and neurologic deficit were included in this systematic review. This includes 41 patients (13%) who had no functional recovery, 125 patients (40%) who had partial recovery, 140 patients (45%) with complete recovery, and 3 patients (1%) whose recovery status could not be determined. Study-level data on recovery status are included in Table 1.
The rate of partial or full recovery after indirect decompression procedure was 97% versus 87.5% after formal laminectomy [Odds Ratio (OR) 5.18 favoring indirect decompression, P = 0.08] (Tables 2 and 3). The rate of full recovery after indirect decompression procedure was 60.8% versus 41.4% after formal laminectomy (OR 2.2 favoring indirect decompression, P = 0.18) (Tables 2 and 3).
Data to analyze the influence of timing of formal sacral decompression on recovery rate were available. Patients treated within 72 hours of the index injury made at least a partial recovery in 93.1% of cases and a full recovery in 35% of cases (OR 1.5 favoring surgery within 72 hours, P = 0.62) (Tables 4 and 5). Patients treated after 72 hours made at least a partial recovery in 90% of cases and a full recovery in 36.3% of cases (OR 1.85 favoring surgery after 72 hours, P = 0.25) (Tables 4 and 5). There were insufficient data to determine the effect of timing on patients treated with indirect decompression.
Treatment of patients with neurologic deficit after spinal trauma ongoing neural element compression often includes formal decompression to relieve associated stenosis and improve the prospects for recovery of function. The sacrum has a unique biomechanical environment because of the lack of segmental motion. For this reason, decompression of nerve roots can be accomplished either through formal laminectomy or through realignment of angulated or displaced fractures, resulting in indirect decompression. As many sacral fractures are treated by trauma surgeons without formal spine surgery training, indirect approaches may be an attractive option in cases that are amenable. Given these 2 disparate decompression strategies for patients with neurologic deficits after sacral fracture, the purpose of this review was to identify differences in recovery rate between the 2 treatments and describe the role of timing of decompression on the rate of neurologic recovery.
A clinically relevant point of comparison for recovery of bowel or bladder function after sacral injury is the impact of treatment on patients with cauda equina syndrome. Srikandarajah et al11 recently described 200 patients with bladder dysfunction in a retrospective study of cauda equina syndrome. Although patients with incomplete cauda equina syndrome (poor urinary stream, loss of desire to void, straining, altered sensation) demonstrated a benefit with respect to bladder function at an early time point around 3 months after surgery, those with complete urinary retention at presentation did not have outcomes that varied significantly based on the length of time before surgical decompression. This finding in consistent with the experience described above for treatment of neurologic injury after sacral fracture. Chau et al12 systematically reviewed the clinical and preclinical data describing timing of decompression in the treatment of cauda equina syndrome. Review of the clinical data did not demonstrate the benefits of surgical decompression thresholds of 24 or 48 hours after symptom onset and therefore a meaningful division with respect to timing of intervention and eventual bladder function could not be determined. Similar to the present study, however, the authors suggested that this finding may be due to heterogenous data sampling; there is little evidentiary basis to guide clinical decision making in the treatment of neurologic deficit associated with both cauda equina syndrome and sacral fracture and the presentation of patients is often clouded by delayed and uncertain diagnosis.
The Surgical Timing in Acute Spinal Cord Injury Study trial explored the effect of timing of surgery on recovery after traumatic spinal cord injury.8 Although the subject of that study is different with respect to the nature of the neural element compressed (spinal cord vs. cauda equina), the results of that study are frequently invoked in advocating for early decompression of neural elements after spinal trauma. The appropriateness of this analogy is unclear. The relative durability of nerve roots compared with spinal cord parenchyma, the differences in neural element perfusion, and the differential innervation patterns of visceral structures versus skeletal muscle may decrease the importance of early decompressive surgery.
We found no differences in recovery rate between indirect sacral decompression and formal laminectomy although there was a strong trend toward improved function with indirect decompression alone (OR 5.18, P = 0.08). These data suggest that open decompression is unnecessary in many cases to achieve recovery of function. The trend toward improved outcome after indirect decompression could be misleading if treatment biases led surgeons to attempt indirect reduction only in less severe cases or those without ongoing neural element compression. Ayoub13 evaluated 28 patients treated in a single surgeon series with and without direct decompression and found patients who underwent direct decompression had superior outcomes. Although this contrasts with the findings of this review, Ayoub also describes performing open decompression only when patients had evidence of ongoing neural element compression. Totterman et al reported the outcome of 31 patients treated with and without formal decompression. This series included 14 patients treated with laminectomy and 17 without. Decision to perform laminectomy is not well described but was indicated in awake patients with “significant neurotrauma” or unconscious patients with significant canal stenosis. Inclusion of such studies with an inherent selection bias driven by treatment stratification may explain the lack of improved outcome with formal decompression as more severe cases may have been treated in this manner.
This review is limited by the weaknesses of retrospective study as all included studies are Level IV evidence with the exception of one Level III study. Early decompression was defined with an arbitrary threshold (72 hours), which is longer than what some authors define (also arbitrarily) as the standard of care (24 or 48 hours). Use of this threshold largely reflects the available literature and lower historical urgency to perform early decompression. Finally, limitations in the available literature precluded inclusion of a group comprised of patients who did not undergo decompression.
As is frequently the case with literature reviews, the primary shortcoming that limits our ability to draw firm conclusions lies in the available literature. Most of the literature describing treatment of sacral fractures was published before high-quality literature demonstrated the importance of early decompression to optimize results. Given this limitation, it is unsurprising that we cannot provide sound guidance about the importance of decompression within 24 hours. Our review found no benefit to early decompression within 72 hours and no difference between formal laminectomy and indirect decompression. We caution surgeons against taking these findings to constitute clinical guidance as treatment selection biases may have influenced our findings; as other authors have recommended for the treatment of cauda equina syndrome, we recommend formal decompression when indirect decompression may not provide adequate canal patency and early surgery with 24 hours when possible in patients with neurologic deficits.
1. Denis F, Davis S, Comfort T. Sacral fractures: an important problem. Retrospective analysis of 236 cases. Clin Orthop Relat Res. 1988;227:67–81.
2. Roy-Camille R, Saillant G, Gagna G, et al. Transverse fracture of the upper sacrum. Suicidal jumper's fracture. Spine (Phila Pa.1976). 1985;10:838–845.
3. Sabiston CP, Wing PC. Sacral fractures: classification and neurologic implications. J Trauma. 1986;26:1113–1115.
4. Burgess AR, Eastridge BJ, Young JW, et al. Pelvic ring disruptions: effective classification system and treatment protocols. J Trauma. 1990;30:848–856.
5. Isler B. Lumbosacral lesions associated with pelvic ring injuries. J Orthop Trauma. 1990;4:1–6.
6. Strange-Vognsen HH, Lebech A. An unusual type of fracture in the upper sacrum. J Orthop Trauma. 1991;5:200–203.
7. Schroeder GD, Kurd MF, Kepler CK, et al. The development of a universally accepted sacral fracture
classification: a survey of AOSpine and AOTrauma members. Glob Spine J. 2016;6:686–694.
8. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the surgical timing in Acute Spinal Cord Injury Study STASCIS. PLoS One. 2012;7:e32037.
9. Centre for Evidence Based Medicine.OCEBM Levels of Evidence. 2016. Available at: http://www.cebm.net/ocebm-levels-of-evidence/
. Accessed November 20, 2016.
10. Furlan AD, Malmivaara A, Chou R, et al. Updated method guideline for systematic reviews in the Cochrane Back and Neck Group. Spine (Phila Pa.1976). 2015;40:1660–1673.
11. Srikandarajah N, Boissaud-Cooke MA, Clark S, et al. Does early surgical decompression in cauda equina
syndrome improve bladder outcome? Spine (Phila Pa.1976). 2015;40:580–583.
12. Chau AM, Xu LL, Pelzer NR, et al. Timing of surgical intervention in cauda equina
syndrome: a systematic critical review. World Neurosurg. 2014;81:640–650.
13. Ayoub MA. Displaced spinopelvic dissociation with sacral cauda equina
syndrome: outcome of surgical decompression with a preliminary management algorithm. Eur Spine J. 2012;21:1815–1825.
14. He S, Zhang H, Zhao Q, et al. Posterior approach in treating sacral fracture
combined with lumbopelvic dissociation. Orthopedics. 2014;37:e1027–e1032.
15. Aresti N, Murugachandran G, Shetty R. Cauda equina
syndrome following sacral fractures: a report of three cases. J Orthop Surg (Hong Kong). 2012;20:250–253.
16. Bellabarba C, Schildhauer TA, Vaccaro AR, et al. Complications associated with surgical stabilization of high-grade sacral fracture
dislocations with spino-pelvic instability. Spine (Phila Pa.1976). 2006;31(11 suppl):S80–S88; discussion S104.
17. Park YS, Baek SW, Kim HS, et al. Management of sacral fractures associated with spinal or pelvic ring injury. J Trauma Acute Care Surg. 2012;73:239–242.
18. Lee JH, Kim JU, Jang JS, et al. Delayed neurological insufficiency caused by transverse sacral fracture
after minor trauma in elderly patients. Neurol Med Chir (Tokyo). 2011;51:427–430.
19. Dussa CU, Soni BM. Influence of type of management of transverse sacral fractures on neurological outcome. A case series and review of literature. Spinal Cord. 2008;46:590–594.
20. Siebler JC, Hasley BP, Mormino MA. Functional outcomes of denis zone III sacral fractures treated nonoperatively. J Orthop Trauma. 2010;24:297–302.
21. Nork SE, Jones CB, Harding SP, et al. Percutaneous stabilization of U-shaped sacral fractures using iliosacral screws: technique and early results. J Orthop Trauma. 2001;15:238–246.
22. Ayoub MA. Vertically unstable sacral fractures with neurological insult: outcomes of surgical decompression and reconstruction plate internal fixation. Int Orthop. 2009;33:261–267.
23. Zelle BA, Gruen GS, Hunt T, et al. Sacral fractures with neurological injury: is early decompression beneficial? Int Orthop. 2004;28:244–251.
24. Kim MY, Reidy DP, Nolan PC, et al. Transverse sacral fractures: case series and literature review. Can J Surg. 2001;44:359–363.
25. Lykomitros VA, Papavasiliou KA, Alzeer ZM, et al. Management of traumatic sacral fractures: a retrospective case-series study and review of the literature. Injury. 2010;41:266–272.
26. Sapkas GS, Mavrogenis AF, Papagelopoulos PJ. Transverse sacral fractures with anterior displacement. Eur Spine J. 2008;17:342–347.
27. Dalbayrak S, Yaman O, Ayten M, et al. Surgical treatment in sacral fractures and traumatic spinopelvic instabilities. Turk Neurosurg. 2014;24:498–505.
28. Tan GQ, He JL, Fu BS, et al. Lumbopelvic fixation
for multiplanar sacral fractures with spinopelvic instability. Injury. 2012;43:1318–1325.
29. Taguchi T, Kawai S, Kaneko K, et al. Operative management of displaced fractures of the sacrum. J Orthop Sci. 1999;4:347–352.
30. Chen HW, Liu GD, Zhao GS, et al. Isolated u-shaped sacral fracture
with cauda equina
injury. Orthopedics. 2011;34.
31. Hunt N, Jennings A, Smith M. Current management of U-shaped sacral fractures or spino-pelvic dissociation. Injury. 2002;33:123–126.
32. Carlson JR, Heller JG, Mansfield FL, et al. Traumatic open anterior lumbosacral fracture dislocation. A report of two cases. Spine (Phila Pa.1976). 1999;24:184–188.
33. Mouhsine E, Wettstein M, Schizas C, et al. Modified triangular posterior osteosynthesis of unstable sacrum fracture. Eur Spine J. 2006;15:857–863.
34. Sapkas G, Makris A, Korres D, et al. Anteriorly displaced transverse fractures of the sacrum in adolescents: report of two cases. Eur Spine J. 1997;6:342–346.
35. Ebraheim NA, Biyani A, Salpietro B. Zone III fractures of the sacrum. A case report. Spine (Phila Pa.1976). 1996;21:2390–2396.
36. Gibbons KJ, Soloniuk DS, Razack N. Neurological injury and patterns of sacral fractures. J Neurosurg. 1990;72:889–893.
37. Taller S, Lukas R, Suchomel P, et al. Surgical treatment of dislocated transverse fractures of the sacrum. Acta Chir Orthop Traumatol Cech. 2003;70:151–157.
38. Bekmez S, Demirkiran G, Caglar O, et al. Transverse sacral fractures and concomitant late-diagnosed cauda equina
syndrome. Ulus Travma Acil Cerrahi Derg. 2014;20:71–74.
39. Ruatti S, Kerschbaumer G, Gay E, et al. Technique for reduction and percutaneous fixation of U- and H-shaped sacral fractures. Orthop Traumatol Surg Res. 2013;99:625–629.
40. Sabourin M, Lazennec JY, Catonne Y, et al. Shortening osteotomy and sacro-sacral fixation for U-shaped sacral fractures. J Spinal Disord Tech. 2010;23:457–460.
41. Totterman A, Glott T, Soberg HL, et al. Pelvic trauma with displaced sacral fractures: functional outcome at one year. Spine (Phila Pa.1976). 2007;32:1437–1443.
42. Phelan ST, Jones DA, Bishay M. Conservative management of transverse fractures of the sacrum with neurological features. A report of four cases. J Bone Joint Surg Br. 1991;73:969–971.
43. Hu X, Pei F, Wang G, et al. Application triangular osteosynthesis for vertical unstable sacral fractures. Eur Spine J. 2013;22:503–509.
44. Gribnau AJ, van Hensbroek PB, Haverlag R, et al. U-shaped sacral fractures: surgical treatment and quality of life. Injury. 2009;40:1040–1048.
45. Blanco JF, De Pedro JA, Hernandez P, et al. Zone III sacral fractures–two case reports. Injury. 2004;35:1311–1313.
46. Konig MA, Seidel U, Heini P, et al. Minimal-invasive percutaneous reduction and transsacral screw fixation for U-shaped fractures. J Spinal Disord Tech. 2013;26:48–54.