Cauda equina syndrome in patients with low lumbar fractures I T
Transcription
Cauda equina syndrome in patients with low lumbar fractures I T
Neurosurg Focus 16 (6):e6, 2004, Click here to return to Table of Contents Cauda equina syndrome in patients with low lumbar fractures ISSADA THONGTRANGAN, M.D., HOANG LE, M.D., JON PARK, MD., F.R.C.S.(C), AND DANIEL H. KIM, M.D. Department of Neurosurgery, Stanford University Medical Center, Stanford, California Object. Symptoms of cauda equina syndrome (CES) can include low-back pain, sciatica, lower-extremity weakness, sensory deficit, perineal hypesthesia or anesthesia, and loss of bowel or bladder function. Several causes of the syndrome are recognized, but its optimal treatment remains controversial and has been broadly based on data gathered from series involving herniated discs. Information on the treatment of CES caused by low lumbar traumatic injuries has not been well documented. Methods. Between January 2000 and December 2003, 17 consecutive cases of CES caused by low lumbar traumatic injuries at L2–5 were identified. The traumatic injuries consisted of gun shot wound in two cases, motor vehicle accident in 11, and a fall from height in four. Conus medullaris injuries causing CES were excluded from this review. Presenting symptoms, mechanisms of injury, radiographic images, timing of surgery, surgical approaches, and neurological status at the final follow up were documented. All patients underwent follow up of at least 12 months. Fourteen of 17 patients had satisfactory outcomes. Despite undergoing surgery within the first 24 hours postinjury, three patients had what was classified as a poor outcome given their residual deficits and included two cases with gunshot injuries. Recovery of leg weakness occurred within 4 months, whereas bladder and bowel function recovered within 3 months. All patients in this series underwent decompression within less than 48 hours after syndrome onset. Overall, the authors found no difference regarding timing of surgery between patients in the satisfactory outcome group and those in the poor outcome group. Conclusions. Based on the evidence in this study, the severity of a patient’s condition on initial presentation is the most crucial factor in predicting outcome following CES due to low lumbar injuries. Although the matter of the timing of surgery remains controversial, the authors of this study recommend that surgery be performed within 48 hours of syndrome onset. KEY WORDS • cauda equina syndrome • burst fracture • lumbar spine • spinal injury In an adult, the conus medullaris ends at the L1–2 intervertebral disc level and continues to taper finally to form the terminal filum. The nerves of the cauda equina provide sensory and motor function to the lower extremities and sensation to the perineum and genitalia as well as innervate the pelvic viscera. They also provide necessary pathways for coordinated activities such as micturition, defecation, and sexual function. Injury to the conus medullaris or the nerves of the cauda equina can result in CES, which in its triad can include lower extremity weakness, perineal sensory loss, and bowel and bladder dysfunction. Several causes of the syndrome have been reported in the literature and include acute traumatic injury,6,9,19 herniated disc,2,4,13,19,20 and metastatic lesion.16 Although reports of CES caused by large central disc herniations have been well documented, the literature on CES caused by traumatic lumbar fractures is sparse. Timing of treatment and recovery from the synAbbreviations used in this paper: CES = cauda equina syndrome; CT = computerized tomography; GSW = gunshot wound; MVA = motor vehicle accident. Neurosurg. Focus / Volume 16 / June, 2004 drome have been based mainly on information gathered from clinical series involving disc herniations. In this report, we reviewed a clinical series of patients with CES caused by acute traumatic lumbar fractures (L2–5) and analyzed outcomes based on surgical treatment. CLINICAL MATERIAL AND METHODS We retrospectively identified 17 patients (12 male and five female) with a mean age of 38.5 years (range 17–80 years) who had been diagnosed with low lumbar traumatic injuries from the L-2 to L-5 vertebrae and CES on arrival to Stanford University Medical Center between January 2000 and December 2003. We defined “CES” as “a complex of saddle hypesthesia, motor weakness in the lower extremities, and bowel or bladder dysfunction.” At least two of the three criteria were necessary for diagnosis and inclusion into our review. Mechanisms of injury and neurological status at presentation were documented. Radiographic studies including plain x-ray films and CT scans of the lumbar spine had been obtained in all patients. We excluded any fracture 28 I. Thongtrangan, et al. above L-2 to exclude CES from a conus medullaris injury. We defined “early decompression” as “treatment within 48 hours of the development of the full syndrome” and “late decompression” as treatment any time following this. All patients had undergone posterior stabilization with pedicle screw/rod instrumentation with or without an additional anterior procedure. The anterior procedure had been considered mainly for decompression purposes and performed via a left mini-retroperitoneal approach. Standard corpectomy and anterior column reconstruction by using a structural allograft or an expandable cage with or without anterior instrumentation had been performed in selected cases. All patients had been followed up for at least 12 months postoperatively, and the recovery of neurological function was documented. Radiographic images were also monitored for any instrumentation-related complications. We defined “satisfactory outcome” as “an absence of bowel and/or bladder dysfunction and an ability to ambulate independently by the time of the last follow up,” whereas “poor outcome” was “a residual neurological deficit in any subcategory.” RESULTS Traumatic injuries included GSW in two cases, MVA in 11, and fall from a height in four. The level of fracture was at L-2 (seven cases), L-3 (seven cases), and L-4 (three cases). No patient had involvement of L-5. Demographic and clinical details are featured in Table 1. Of the 17 patients, 14 were determined to have a satisfactory outcome at the final follow up. The remaining three were classified as having a poor outcome because of residual neurological deficit including paraplegia and bowel and/or bladder dysfunction. A CT scan demonstrated spinal canal compromise in all cases (range 55–90% compromise). Three cases also had fracture of the lamina and dural tearing. All patients underwent surgery for decompression and stabilization. An anterior procedure was performed in only one case, a posterior procedure in two cases, and a posterior–anterior approach in the remaining 14 cases in (Table 1). The mean follow up was 13.5 months (range 12–17 months). Timing of Surgery All patients underwent surgery within 48 hours of presentation, with a mean time to decompression and stabilization of 20.8 hours (range 8–48 hours). Fourteen patients underwent surgery within 24 hours, whereas the remaining three patients underwent surgery within 48 hours. Eleven of 14 patients who had undergone surgery within the first 24 hours had satisfactory outcomes; the other three patients with satisfactory outcomes underwent surgery within 48 hours. TABLE 1 Demographic and clinical data* Fracture of Lamina/ Dural Tearing Leg Weakness Saddle Paresthesia Bladder Dysfunction Age (yrs), Sex Mechanism of Injury Level of Injury % Spinal Canal Involvement 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 55, M 43, F 21, F 74, F 35, F 36, M 46, M 31, M 80, M 17, M 45, M 19, F 20, M 54, M 33, M MVA MVA MVA fall MVA MVA MVA MVA fall fall MVA fall MVA MVA MVA L-3 L-3 L-2 L-4 L-2 L-3 L-4 L-2 L-3 L-3 L-2 L-2 L-3 L-2 L-4 55 70 60 80 70 65 75 65 55 60 75 60 65 80 90 no no no no no no no no no no no no no no yes yes yes yes yes yes yes yes yes yes no yes yes no yes yes yes yes yes yes yes yes yes yes no yes no yes yes yes yes yes yes yes yes yes yes yes yes yes yes yes no yes yes yes yes yes yes yes yes yes yes yes no yes no yes yes yes yes 20 16 30 48 24 12 16 20 24 16 14 8 36 16 24 AP AP AP ant AP AP AP AP AP AP AP AP AP AP AP 17 12 15 12 14 14 12 13 15 12 16 12 14 14 13 16 20, M GSW L-2 retained bullet yes yes yes yes yes 12 pst 12 17 25, M GSW L-3 retained bullet yes yes yes yes yes 18 pst 13 Case No. Decreased Rectal Tone Timing of Surgery (hrs) Surgical Approach F/U (mos) Residual Bowel/ Bladder Dysfunction Ability to Ambulate no no no no no no no no no no no no no no partial recovery of bladder dysfunction paraplegia, complete bowel/ bladder dysfunction paraplegia, complete bowel/ bladder dysfunction * Ant = anterior; AP = anterior–posterior; F/U = follow up; pst = posterior. 29 Neurosurg. Focus / Volume 16 / June, 2004 yes yes yes yes yes yes yes yes yes yes yes yes yes yes yes no no Cauda equina syndrome in patients with low lumbar fractures Interestingly, all cases with a poor outcome in this series involved surgery performed within the first 24 hours. Among the three cases with poor outcomes, two patients suffered from GSWs with severe destruction of the posterior spinal elements and tearing of the dura mater. The remaining patient had an L-4 burst fracture in conjunction with a lamina fracture and dural tearing. The mean timing of surgery in the satisfactory outcome group was 21.4 hours, whereas that in the poor outcome group was 18.2 hours. Overall, we could not make a consistent conclusion in regard to timing of surgery and clinical outcome. Nonetheless, it appears that patients with GSWs and CES will have a worse overall clinical outcome compared with that in patients with CES from a traumatic fracture injury. Motor Weakness Fifteen of 17 patients in this series had leg weakness on initial presentation. The two patients with no leg weakness were younger than 20 years old. One had fallen from a height and the other had been involve in an MVA. Interestingly, in both cases there was an L-3 burst fracture with spinal canal involvement. Thirteen of 15 patients with leg weakness on presentation recovered to the point of being able to ambulate independently. Such recovery began at 8 weeks after surgery, and no further recovery was observed after 4 months. In the two cases involving GSWs the patients presented with complete paralysis of the lower extremities, which remained the same despite early decompression and stabilization within 20 hours. Bladder Function Sixteen of 17 cases involved bladder dysfunction, that is, urinary retention requiring catheterization. In the entire series, only one patient presented with normal bladder function. Among patients in the satisfactory outcome group (14 of 17 patients), there was no residual bladder dysfunction at the final follow up. Bladder function improved a mean of 9 days after surgery (range 3 days–3 months). No bladder recovery occurred after 3 months. Three of the 17 patients were classified as having a poor outcome based on residual bladder dysfunction at the final follow up. The two patients who suffered GSWs did not recover bladder function. The patient with an L-4 burst fracture experienced partial recovery with residual urinary retention at the final follow up. Bowel Function Of the 17 patients identified for inclusion in our review, 15 had decreased anal tone on presentation. Normal anal tone was recovered within a mean of 10 days after surgery in the group with a good outcome (range 5 days–3 months). No further recovery occurred after 3 months. Of the three patients with a poor outcome, two had significant residual anal sphincter dysfunction. Not surprisingly, these two had suffered GSWs, which required regular bowel evacuations either with the aid of laxatives or manually. Saddle Paresthesia Saddle paresthesia was documented in 15 cases on presentation, including those with GSWs. Recovery occurred Neurosurg. Focus / Volume 16 / June, 2004 in all cases except those involving GSW. Saddle paresthesia resolved a mean of 4 days after decompression and stabilization (range 24 hours–8 days). ILLUSTRATIVE CASES Case 1 This 33-year old man suffered an L-4 burst fracture after having been in an MVA during which the vehicle rolled over. Physical examination revealed weakness of the quadriceps muscles bilaterally, perineal hypesthesia, and urinary retention. Radiographic images (Fig. 1A) and CT scans (Fig. 1B and C) of the lumbar spine revealed an L-4 burst fracture with 90% canal involvement as well as fracture of the lamina. A combined posterior–anterior decompression and stabilization procedures were performed within 24 hours. A dural tear was noted at the time of the surgery. Postoperative x-ray films (Fig. 2) demonstrated posterior stabilization with pedicle screw/rod instrumentation, and expandable cage placement for anterior column reconstruction after corpectomy. He regained perineal sensation 72 hours after surgery, complete motor strength in the lower extremities within the first 2 months, and partial recovery of bladder function by the final follow up. He demonstrated postmicturition residual urinary retention at the final follow up. Case 2 This 20-year-old man was shot in the back. Physical examination revealed paraplegia with complete loss of sensation to light touch and pinprick below the thighs, no rectal tone, saddle anesthesia, and bladder incontinence. Radiographic images (Fig. 3A) and CT scans (Fig. 3B and C) revealed severe destruction of the L-3 posterior elements and an intraspinally retained bullet at the level of L3. The anterior and middle columns were intact. The patient underwent a posterior laminectomy, removal of the bullet, posterior stabilization, and fusion by using a pedicle screw/rod system. Not surprisingly, dural laceration was noted intraoperatively with severe injury to the cauda equina. Postoperatively, he has not recovered neurological function despite having undergone early surgery within 18 hours. As of the final follow up, he remains an L-3 paraplegic with bowel and bladder incontinence. DISCUSSION The incidence of CES ranges from 1 to 5% depending on the origin of the disease.2,5,8,19,20 Central disc herniations are the most common origins reported in the published literature.2,3,5,8,13,14 Acute trauma of the lower lumbar spine as a cause of CES is uncommon. In our series of patients with CES caused by traumatic lower lumbar injuries, 14 (82%) of 17 patients achieved satisfactory outcomes following surgical decompression. Timing of decompression in the treatment of CES remains controversial despite the traditional neurosurgical teaching of early surgical intervention. In several published papers, authors support the role of early decompression with good to excellent outcome.8,10,15,19 In addition, in a recent metaanalysis,1 researchers asserted that patients undergoing surgery less than 48 hours after onset of symp30 I. Thongtrangan, et al. Fig. 2. Case 2. Postoperative x-ray films demonstrating posterior stabilization performed using a pedicle screw/rod system and expandable cage placement following anterior and middle column reconstruction. The alignment was well maintained with satisfactory decompression. Fig. 1. Anteroposterior (left) and lateral (right) x-ray films demonstrating an L-4 burst fracture. B: Sagittal CT scans demonstrating an L-4 burst fracture with segmental deformity and bone retropulsion. C: Axial CT scans revealing an L-4 burst fracture with significant canal compromise and lamina fracture posteriorly. 31 toms of CES had better outcomes than those in whom surgery had been undertaken later. Despite this, other investigators have questioned the role of early decompression. Kostuik, et al.,13 retrospectively reviewed 31 patients with CES caused by lumbar disc herniations who demonstrated excellent outcomes and recovery of motor function with late decompression up to 3 days postonset. They found no correlation between the length of time from the onset of symptoms to surgery and the extent of neurological recovery. Delamarter, et al.,7 in an animal model, also found similar evidence. These investigators developed a canine model of CES and evaluated neurological recovery following immediate, early, and delayed decompression. No differences in somatosensory evoked potentials were noted between early and delayed decompression. In our series, the timing of surgery did not correlate well with neurological recovery. Nonetheless, all of the patients in our study had undergone decompression and stabilization within 48 hours. Factors affecting recovery may correlate more with the type and severity of initial injury. In our review, three patients had a poor outcome because of residual neurological impairment including motor weakness, bladder dysfunction, and bowel dysfunction. Of these three, two suffered a GSW to the lower lumbar area. The role of bullet removal in neurological recovery has been controversial. Analysis of recent data from a study performed by the Regional Model Spinal Cord Injury Systems21 indicates that laminectomy and bullet removal plays no role in a spinal cord level lesion, but is a worthwhile procedure in treating injury at the level of, as well as caudad to, the conus medullaris. This is probably based Neurosurg. Focus / Volume 16 / June, 2004 Cauda equina syndrome in patients with low lumbar fractures pressure. The concept that compressed neural tissue below a threshold pressure may retain the ability to recover indefinitely may describe the excellent recovery rates described in both clinical and experimental studies involving delayed decompression. In addition, potential peripheral nerve regeneration or repair plays a major role in recovery of the cauda equina. Once compression pressure exceeds the threshold, however, permanent damage might occur and the time to full recovery prolonged or unlikely. Data from most series indicate that motor recovery is complete by 1 year, but there are reports of improvement in bladder function after a considerably longer timeframe11,17 even up to 5 years later.4,12 In our study, 15 of 17 patients recovered motor strength in the lower extremities to the point that they were able to ambulate independently by 4 months. Bowel and bladder function fully recovered within three months. No further improvements were noted after 3 months. Our data demonstrate the potential recovery following surgical decompression in patients with CES caused by low lumbar traumatic injuries. The natural history of recovery from CES in patients treated with conservative therapy is unknown because the preferred treatment option remains surgical in nature. Note, however, that the initial mechanism of injury may be an important factor in predicting recovery, especially given the poor outcome in the patients with GSWs. Also, based on our experience, the severity of initial traumatic injury appears to play a major role in recovery rather than timing of surgery. Regardless, given the morbidity associated with continual bladder dysfunction, we remain advocates of early surgical decompression for CES caused by traumatic injuries. Full decompression may require the anterior approach for the most optimal outcome. Fig. 3. Case 2. Anteroposterior (left) and lateral (right) x-ray films revealing gunshot injuries, with the retained bullet at L-3. B: Sagittal CT scans revealing destruction of posterior spinal elements, with retained bullet in the spinal canal. C: Axial CT scans demonstrating severe fracture and destruction of lamina and posterior elements, with retained bullet in the spinal canal. on the regional anatomy of the spinal cord and the greater susceptibility of the spinal cord to injury compared with these factors in the spinal nerve roots. It is probable that root level lesions are associated with greater clinical improvement after decompression because of the relatively large number of lumbar and sacral roots that can be compressed by a bullet at this level and the potential for axons to regenerate. Nonetheless, the patients in the present study with complete CES failed to show any neurological improvements despite early decompression and stabilization. Thus, these results may indicate that the severity of the initial injury plays an important role in recovery. In the case of an L-4 burst fracture with associated lamina fracture, dural tear, and near complete obliteration of the spinal canal from the retropulsed bone fragment, the patient had severe compression of the cauda equina in both the dorsal and ventral directions at the time of injury. Rydevik, et al.,18 demonstrated the importance of threshold Neurosurg. Focus / Volume 16 / June, 2004 CONCLUSIONS In this paper we focus on the neurological recovery from CES following low lumbar traumatic injuries and show that direct decompression and stabilization within 48 hours offers a favorable chance of recovery. Most patients with lower extremity weakness recovered to the point that they were able to ambulate independently, except those with GSWs. Bowel and bladder function can be expected to recover within 3 months; thereafter recovery is unlikely. Severity of the initial injury appears to be the most important factor for recovery. References 1. Ahn UM, Ahn NU, Buchowski JM, et al: Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine 25:1515–1522, 2000 2. Buchner M, Schiltenwolf M: Cauda equina syndrome caused by intervertebral lumbar disk prolapse: mid-term results of 22 patients and literature review. Orthopedics 25:727–731, 2002 3. Busse JW, Hsu WS: Rapid progression of acute sciatica to cauda equina syndrome. J Manipulative Physiol Ther 24: 350–355, 2001 4. Chang HS, Nakagawa H, Mizuno J: Lumbar herniated disc presenting with cauda equina syndrome. Long-term follow-up of four cases. Surg Neurol 53:100–105, 2000 5. Choudhury AR, Taylor JC: Cauda equina syndrome in lumbar disc disease. Acta Orthop Scand 51:493–499, 1980 32 I. Thongtrangan, et al. 6. Cybulski GR, Stone JL, Kant R: Outcome of laminectomy for civilian gunshot injuries of the terminal spinal cord and cauda equina: review of 88 cases. Neurosurgery 24:392–397, 1989 7. Delamarter RB, Sherman JE, Carr JB: 1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression. Spine 16:1022–1029, 1991 8. Dinning TA, Schaeffer HR: Discogenic compression of the cauda equina: a surgical emergency. Aust N Z J Surg 63:927–934, 1993 9. Gertzbein SD, Court-Brown CM, Marks P, et al: The neurological outcome following surgery for spinal fractures. Spine 13: 641–644, 1988 10. Gleave JR, Macfarlane R: Cauda equina syndrome: what is the relationship between timing of surgery and outcome? Br J Neurosurg 16:325–328, 2002 11. Hellstrom P, Kortelainen P, Kontturi M: Late urodynamic finding after surgery for cauda equina syndrome caused by a prolapsed lumbar intervetebral disk. J Urol 135:308–312, 1986 12. Jennett WB: A study of 25 cases of compression of the cauda equina by prolapsed intervertebral discs. J Neurochem 19: 109–116, 1956 13. Kostuik JP, Harrington I, Alexander D, et al: Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am 68: 386–391, 1986 14. Lavyne MH: Cauda equina syndrome secondary to lumbar disc herniation. Neurosurgery 34:561, 1994 33 15. McLaren AC, Bailey SI: Cauda equina syndrome: a complication of lumbar discectomy. Clin Orthop 204:143–149, 1986 16. Nather A, Bose K: The results of decompression of cord or cauda equina compression from metastatic extradural tumors. Clin Orthop 169:103–108, 1982 17. Nielsen B, de Nully M, Schmidt K, et al: A urodynamic study of cauda equina syndrome due to lumbar disc herniation. Urol Int 35:167–170, 1980 18. Rydevik BL, Pedowitz R, Hargens AR, et al: Effects of acute, graded compression on spinal nerve root function and structure. An experimental study of the pig cauda equina. Spine 16: 487–493, 1991 19. Shapiro S: Cauda equina syndrome secondary to lumbar disc herniation. Neurosurgery 32:743–747, 1993 20. Shapiro S: Medical realities of cauda equina syndrome secondary to lumbar disc herniation. Spine 25:348–352, 2000 21. Waters RL, Sie IH: Spinal cord injuries from gunshot wounds to the spine. Clin Orthop 408:120–125, 2003 Manuscript received April 16, 2004. Accepted in final form May 2, 2004. Address reprint requests to: Daniel H. Kim, M.D., Department of Neurosurgery, Stanford University Medical Center, Room R-201, Edwards Building, 300 Pasteur Drive, Stanford, California 943055327. email: neurokim@stanford.edu. Neurosurg. Focus / Volume 16 / June, 2004