|
 
 |
| CASE REPORT |
|
| Year : 2020 | Volume
: 17
| Issue : 2 | Page : 61-64 |
|
Recurrent cauda equina syndrome due to recurrent disc prolapse at the same previously intervened level
Suresh S Pillai, Ali Shabith, PA Ramsheela
BMH Spine Centre, Calicut, Kerala, Baby Memorial Hospital, Kozhikode, Kerala, India
| Date of Submission | 05-Jan-2021 |
| Date of Decision | 05-Jan-2021 |
| Date of Acceptance | 05-Mar-2021 |
| Date of Web Publication | 08-Mar-2021 |
Correspondence Address:
Suresh S Pillai
Baby Memorial Hospital, Kozhikode, Kerala
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/joasis.joasis_1_21
A 42 year old lady presented with acute onset “recurrent” cauda equina syndrome (CES) as a result of repeated disc prolapse at L4-L5 level on the left side, which was operated 10 years earlier. The patient had a previous successful surgery for cauda equina syndrome at the same level(left sided prolapse) and a symptom free period of 10 years. She presented with acute onset left lower limb radicular pain, inability to walk and void urine. Revision surgery by Posterior decompression and Discectomy L4 - L5 with Instrumented Posterolateral Fusion (PLF) from L3 - L5 were performed. There was intra operative dural tear which was primarily repaired. She regained bowel and bladder control post operatively in 10 days time. She became completely ambulant without any residual deficit. Recurrent cauda equina syndrome due to disc prolapse at the previously prolapsed site after a surgical intervention is not reported in the literature, to the best of our knowledge.
Keywords: Cauda equina syndrome, IVDP, recurrent
How to cite this article:
Pillai SS, Shabith A, Ramsheela P A. Recurrent cauda equina syndrome due to recurrent disc prolapse at the same previously intervened level. J Orthop Assoc South Indian States 2020;17:61-4 |
How to cite this URL:
Pillai SS, Shabith A, Ramsheela P A. Recurrent cauda equina syndrome due to recurrent disc prolapse at the same previously intervened level. J Orthop Assoc South Indian States [serial online] 2020 [cited 2023 Apr 1];17:61-4. Available from: https://www.joasis.org/text.asp?2020/17/2/61/310979 |
| Introduction | |  |
Cauda equina has equal incidence among males and females and has been implicated in 1%–15% of lumbar disc prolapse.[1] Ninety percent of lumbar disc herniation occurs at L4-5 or L5-S1.[1] Bladder dysfunction is a hallmark of cauda equina syndrome. Recurrent cauda equina syndrome due to disc prolapse at same level after a previous intervention and prolonged latent period is very rare. Here, we present such a rare case of a 42-year-old female with recurrent disc herniation at the same level causing recurrent cauda equina syndrome after a period of 10 years after the first procedure. It is unique and first of its kind being reported. She recovered from cauda equina syndrome following intervention on both occasions.
| Case Report | | |
A 42-year-old female presented to the outpatient department on a trolley. She was unable to move due to severe left lower limb radicular pain, saddle anesthesia, constipation, and inability to pass urine. She came on a trolley in the lateral position with the left lower limb flexed at the hip and knee. Her symptoms started 2 days back. She resisted all her movements due to severe pain. On evaluation, she had weakness of the left toe dorsiflexion (Grade 2), left ankle dorsiflexion (Grade 3), great toe flexion (Grade 2) bilaterally, saddle anesthesia, perianal numbness, loss of anal tone and absent voluntary anal contraction, sensory dullness over L5 and S1 dermatomes on the left, absent ankle jerk on the left (plantar reflex-equivocal bilaterally and normal knee jerks bilaterally), and inability to urinate despite having a full bladder (has not passed urine since the night before). Ultrasound examination of the abdomen showed a distended bladder with 600 mL of urine. She was unable to void, so the postvoid urine could not be assessed. Then, the bladder was catheterized.
Ten years back, she had an episode of cauda equina syndrome of 3 days' duration with acute disc prolapse at L4-5. She was operated at that time by L4 hemilaminectomy (L), wide decompression, and L4-5 discectomy at the same institute by another surgeon. The patient had a gradual recovery of her bowel and bladder functions over 3 months after the surgery. She has been doing alright since then.
With the recent episode, she was evaluated with X-ray [Figure 1] and magnetic resonance imaging (MRI) [Figure 2] of the lumbosacral spine. Xray of the lumbosacral spine showed evidence of laminectomy and thinned out pars interarticularis on the left side.There was no listhesis at this previously intervened level. There was retrolisthesis at L3-4 and L4-5. MRI showed disc extrusion at L4-5 on the left side (same level and side as the previous episode) with inferior migration and severe compression of the thecal sac and nerve root [Figure 3]. | Figure 1: Magnetic resonance imaging LS spine showing disc prolapse at L4-5 and L3-4
Click here to view |
She was evaluated and taken up for revision surgery. The remaining parts of the posterior elements at L4-5 were removed (L4 lamina on the right side). Intraoperatively, there was severe adhesion of the thinned out dura with arachnoid exposed at some regions of the operated site. The dura was found adherent to disc annulus on the left side posterolaterally, upon retracting the root, which showed the possibility of previous dural tear during the first surgery. Attempted separation of the dura from the annulus resulted in CSF leak. The dura was repaired with 6-0 Prolene by gently retracting the dura over a cottonoid with a number 4 penfield then and there. The extruded fragment was removed. The dura and nerve roots were thoroughly decompressed. In view of the retrolisthesis at L3-4, along with disc degeneration, instrumented posterolateral fusion was done from L3-L5. A Valsalva maneuver was done to check for any CSF leak. Local fat graft was put over the dura to prevent future adhesion. Nibbled bone chips were used for fusion. The lumbar fascia was closed in a watertight fashion with a drain directed away from the site of dural repair.
Postoperative period was uneventful. Check X-ray showed acceptable implant position [Figure 4]. She was kept in bed for 6 days and then mobilized. The catheter was clamped and released three hourly to look for bladder sensation. Eighth postoperative day onward, she regained bladder sensation and voluntary anal contraction. By the 10th day, the urinary catheter was removed. She was able to pass urine by herself. Meanwhile, she was shown to the urologist and was prescribe alpha receptor agonist. Her constipation was relieved. Neurologically, she improved. Partial foot drop, weakness of dorsiflexion of the big toe and other toes of the left foot recovered completely. All the muscles of her lower limb became Grade 5/5. Sensory dullness persisted over the L5 and S1 dermatomes on the left side. She walked normally on 10th post operative day [Figure 1],[Figure 2],[Figure 3]. Post void residual urine estimation by ultrasound scanning of the abdomen did not reveal significant amount (10 ml in this case) at discharge of the patient.
| Discussion | | |
Cauda equina syndrome is a rare neurological disorder that results from dysfunction of lumbar and sacral nerve roots in the vertebral canal, resulting in impairment of bladder, bowel, or sexual function. Typical manifestations of cauda equina syndrome include low back pain, unilateral or bilateral sciatica, lower extremity weakness, saddle, or perianal anesthesia as well as rectal and bladder sphincter dysfunction.[2] Cauda equina has equal incidence among males and females and has been implicated in 2%–6% of lumbar disc operations.[3],[4],[5] The pathophysiologic mechanisms in the development of cauda equina syndrome may be related to direct mechanical compression, inflammation, venous congestion, or ischemia. Histological examination of compressed nerve roots has shown dilatation of intraradicular veins with an inflammatory cell infiltrate.[6] Rydevic et al. demonstrated mechanical compression of roots causing intraneural edema, resulting in increased intraneural pressure, and decreased perfusion as the likely cause of nerve root dysfunction.[7]
Bladder dysfunction is a hallmark of cauda equina syndrome. Compression of roots causes loss of sensation to the bladder and subsequent inability to detect bladder fullness. In addition, loss of detrusor muscle and sphincter innervation causes inability to voluntarily empty the bladder and eventually leads to overflow incontinence.
Any compressive lesion can cause cauda equina syndrome, most common being compression from central lumbar disc herniation at the L4-L5 or L5-S1 levels.[8],[9] It may also be caused by spinal stenosis, epidural abscess, neoplasm, trauma, infection, hematomas (postsurgical), lumbar punctures, and spinal or epidural anesthetics.[10],[11],[12]
Recurrent disc herniation is the occurrence of disc prolapse at the previously operated site. It can occur as late as 8 years in various literature. The incidence of recurrent lumbar disc herniation varies between 5% and 18%. It is the most common indication for reoperation after a lumbar discectomy. The analysis of data from spine patient outcome research trial has shown younger age, lack of sensorimotor deficit, high ODI scores as risk factors for recurrence of lumbar disc herniation. Smoking, obesity, and diabetes are sited as risk factors.[13] Kim et al. suggested that high disc height and increased range of segmental motion positively correlate with risk of recurrence. Surgical technique and instability at the site of the prolapse are also cited as possible reasons.[14]
Treatment with either repeat discectomy or instrumented fusion has comparable outcomes. The treatment should be individualized. Reoperation rate is sited as 5%–5.5% approximately in meta-analyses.[15] This is similar to the reherniation rate and would suggest that most of the reherniation lead to reoperation.
This case of a recurrent cauda equina syndrome due to disc prolapse at the same level after a previous intervention and latent period of 10 years is very rare. There is no similar case reported in the literature to the best of our knowledge. The patient had recovery from cauda equina syndrome on both the occasions. After the present surgery, she recovered her bowel and bladder function in 10 days after surgery.
| Conclusion | | |
Recurrence of cauda equina syndrome due to disc prolapse at the same level after an intervention is very rare. No similar case reports are found to the best of our knowledge.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Suk KS, Lee HM, Moon SH, Kim NH. Recurrent lumbar disc herniation: Results of operative management. Spine (Phila Pa 1976) 2001;26:672-6.  |
| 2. | Ma B, Wu H, Jia LS, Yuan W, Shi GD, Shi JG. Cauda equina syndrome: A review of clinical progress. Chin Med J (Engl) 2009;122:1214-22. |
| 3. | Gleave JR, Macfarlane R. Cauda equina syndrome: What is the relationship between timing of surgery and outcome? Br J Neurosurg 2002;16:325-8. |
| 4. | Harrop JS, Hunt GE Jr., Vaccaro AR. Conus medullaris and Cauda equina syndrome as a result of traumatic injuries: Management principles. Neurosurg Focus 2004;16:e4. |
| 5. | Gardner A, Gardner E. Cauda equina syndrome: A review of current clinical and medicolegal position. Eur Spine J 2011;20:690-7. |
| 6. | Gitelman A, Hishmeh S, Morelli BN, Joseph SA Jr., Casden A, Kuflik P, et al. Cauda equina syndrome: A comprehensive review. Am J Orthop (Belle Mead NJ) 2008;37:556-62. |
| 7. | Rydevik BL, Myers RR, Powell HC. Pressure increase in the dorsal root ganglion following mechanical compression. Closed compartment syndrome in nerve roots. Spine (Phila Pa 1976) 1989;14:574-6. |
| 8. | Lavy C, James A, Wilson-MacDonald J, Fairbank J. Cauda equina syndrome. BMJ 2009;338:b936. |
| 9. | Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina sydrome secondary to lumbar disc herniation: A meta-analysis of surgical outcomes. Spine (Phila Pa 1976) 2000;25:1515-22. |
| 10. | Loo CC, Irestedt L. Cauda equina syndrome after spinal anaesthesia with hyperbaric 5% lignocaine. Acta Anaesthesiol Scand 1999;43:371-9. |
| 11. | Jensen RL. Cauda equina syndrome as a post operative complication of lumbar spine surgery. Neurosurg Focus 2004;16:E7. |
| 12. | Haldeman S, Rubinstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine (Phila Pa 1976) 1992;17:1469-73. |
| 13. | Huwang W, Han Z, Liu J, Yu L, Yu X. Risk factors for recurrent lumbar disc herniation: A systematic review and meta-analysis. Medicine 2016;95:e2378. |
| 14. | Randall J.Hlubeck and Gregory M Mundis et al. Treatment of recurrent lumbar disc herniation. Curr Rev Musculoskelet Med 2017;10:517-20. |
| 15. | Ran J, Hu Y, Zheng Z, Zhu T, Zheng H, Jing Y, et al. Comparison of discectomy versus sequestrectomy in lumbar disc herniation: A meta-analysis of comparative studies. PLoS One 2015;10:e0121816. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
|
Search Pubmed for