Keywords
cauda equina syndrome - adjacent segment disease - spinal stenosis - decompressive - spine surgery
Palavras-chave
síndrome da cauda equina - doença do segmento adjacente - estenose espinhal - descompressiva - cirurgia da coluna
Introduction
Cauda equina syndrome (CES) is a rare and critical complication of lumbar disc herniation that typically presents with saddle anesthesia, acute onset bladder incontinence or retention, perineal numbness, bilateral leg pain, and/or lower limb weakness.[1]
[2] Rarely, CES can also occur as a complication following spine surgery, with a reported incidence varying between 0.08% to 0.5%.[1]
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[9] Whether this complication occurs as a result of compression from disc herniation or as a complication of spine surgery, surgical decompression remains the mainstay of management of true CES. In cases of partial CES, without motor symptoms, conservative management may also be considered as an option.[1]
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We describe a rare case of partial CES following surgical decompression of spinal stenosis, in a patient with adjacent segment disease (ASD), that was successfully managed conservatively, without surgical decompression. Additionally, we review and discuss the relevant literature on conservative management of partial CES and discuss possible causes as well as the role of ASD in such cases.
Illustrative Case
A 47-year-old man presented to our department with lower back pain and bilateral radicular leg pain 2 years following an L4-L5 posterior lumbar fixation performed at another hospital. Imaging revealed ASD at L3-L4 ([Fig. 1A and B]), and the patient underwent an L3-L4 decompression with posterior screw fixation to fuse this segment with the previously fused L4-L5. Decompression was achieved with the use of a surgical microscope and the procedure was uneventful with blood loss of more than 100 mL. Post-anesthesia recovery from anesthesia was also uneventful.
Fig. 1 (A) Sagittal and (B) axial views of the preoperative T2-weighted magnetic resonance imaging showing spinal stenosis due to adjacent level segment disease at L3-L4 in a 47-year-old male who previously underwent L4-L5 posterior lumbar fixation.
On postoperative day 1, the patient developed acute bladder retention associated with pinpoint anesthesia in the perineal area encompassing the entire scrotum and the penile surface. A physical exam revealed no sensory or motor deficits in the lower limbs. Emergent magnetic resonance imaging and computed tomography showed no neural compression or abnormality ([Fig. 2A–D]). The patient was then immediately started on dexamethasone, gabapentin, and tamsulosin, and underwent urinary catheterization. Urinalysis and laboratories, including erythrocyte sedimentation rate and c-reactive protein, were unremarkable. Electrophysiology showed normal peroneal motor and sural sensory nerve velocities and latencies; however, mildly reduced tibial compound muscle action potentials were noted bilaterally. Needle electromyography demonstrated mildly enlarged motor unit potentials in the L5 and S1 innervated muscles without fibrillation potentials, consistent with chronic bilateral lower lumbosacral radiculopathies ([Fig. 3]). On postoperative day 5, the patient began to regain sensation and bladder control, and by day 7 returned to baseline.
Fig. 2 (A) Sagittal and (B) axial views of the postoperative T2-weighted magnetic resonance imaging showing decompression of L3-L4. (C) Sagittal and (D) axial postoperative computed tomography showing correct screw placement.
Fig. 3 Needle electromyography showing mildly enlarged motor unit potentials in the L5 and S1 innervated muscles without fibrillation potentials, consistent with bilateral diffuse lumbar radiculopathies.
Discussion
Observations
Despite CES being a well-known clinical finding in patients with lumbar disc herniation, postoperative CES, especially partial CES, remains rare. The literature on postoperative CES is sparse and mainly consists of case reports or series with few patients.[1]
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[13] To our knowledge, this is the first report of partial CES as a complication of corrective surgery for ASD.
In cases of postoperative CES, several potential perioperative factors have been proposed or identified, including choice of anesthetic agent, the occurrence of compressive lesions including epidural hematomas or abscesses, mispositioning of fat pad grafts, or retained surgical Gelfoam or sponges.[1]
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Cases with no postoperative radiologic evidence of compression have also been described,[1]
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[10] and several studies have attempted to explain the pathophysiology of these cases. In 1977, Murphy proposed that, even in the presence of extrusion of disc material, it is not compression but rather tension on the nerve roots that cause CES.[19] The tenuous microvascular supply to the conus medullaris is also likely a contributing factor,[7]
[20] as an area of hypovascularity right below the conus medullaris has been identified. Dural tension in this hypovascular area could thus induce root ischemia resulting in CES.[5]
[18] Henriques et al. and Evins et al. have also proposed that postoperative edema may cause venous congestion, which can also lead to nerve root ischemia.[2]
[21] The role of venous congestion in CES is further supported by porcine models, wherein multi-level compression traps blood between the compression sites, inducing significant venous stasis.[22]
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[24] Additionally, Hoyland et al. further found, in a large cadaveric series, that 72% of observed disc herniations compressed or distorted the venous plexus or small veins within the intervertebral foramen.[3] As such, initial compression by any mechanism can be compounded by ensuing venous congestion, which can then result in ischemia and intraneural edema, further decreasing perfusion.
Furthermore, Duncan and Bailey found that patients who developed postoperative CES in the absence of compression shared several comorbidities known to disrupt microvascular supply, including hypertension and diabetes mellitus.[1] Furthermore, spinal decompression for CES in patients with no imaging evidence of compression has also been shown to be ineffective, further supporting the role of vascular etiology.[1]
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Lessons
CES following surgical decompression for lumbar stenosis is a rare but critical complication that likely results from either primary mechanical compression of the nerve roots or ischemia of the nerve roots secondary to venous congestion. Management of CES often depends on the presence of visible compression in imaging studies. In patients with ASD, increased force on the intervertebral disc—from the mechanical stress caused by the arthrodesis of the adjacent segment—initiates a biochemical cascade with activation of pro-inflammatory cytokines that can result in hypoxic injury to the disc itself.[20]
Thus, it is possible that this pro-inflammatory and hypoxic environment contributed to nerve root ischemia in the case presented herein. As such, the association of pro-inflammatory cytokines with ASD and their role in the development of CES warrants further study as a potential risk factor for CES.
