Non-compressive postoperative cauda equina syndrome following decompression and transforaminal interbody fusion surgery

Abstract

Postoperative cauda equina syndrome (CES) is a known rare complication following lumbar disc surgery. Seldom are they seen following decompression for spinal stenosis and may be actually more frequent and under-reported? Emergent surgical exploration remains the mainstay of management as the factors responsible for postop CES remains a variety of compressive forces. Yet many a time postoperative imaging or surgical exploration fails to identify a pathology and this leads to an ischaemic theory responsible for CES. Our article highlights conservative management in these selective group. We share our experience in two cases of incomplete CES during our routine transforaminal interbody fusion which we followed closely without re-exploration eventually ending in a favourable outcome. Key messages: The factors responsible for postop CES remains mostly a variety of compressive forces though in some instances postoperative imaging or surgical exploration fails to identify such in some cases. This leads to an ischaemic theory responsible for CES. The role of conservative management of postoperative CES in certain selective cases has a favourable outcome as illustrated in our cases.

Background

Cauda equina syndrome (CES) is compressive neuropathy of multiple lumbar and sacral nerve roots characterised by bilateral sciatica, lower-extremity weakness, saddle-type hypoesthesia and bowel and bladder dysfunction.¹ It can have complete or partial clinical presentations.² The cause is an extradural compression that arises from tumours, trauma, infection or disc herniation. But rarely CES is a postoperative complication following lumbar disc surgery and few reports are there following decompression for spinal stenosis.^3–5 Postoperative CES remains a surgical emergency even though compressive pathology has not been identified by many authors.^{6 7} We report two cases which were managed conservatively with a favourable outcome at the end.

Case presentation

Case 1

This 47-year-old woman had a 2-year progressive history of neurogenic claudication with claudication distance less than 200 m at final presentation. She was otherwise neurologically intact. An MRI demonstrated severe stenosis at L4–L5. The patient underwent a L4–L5 laminectomy, discectomy from the right side and a titanium banana cage of size 9 mm filled with bone graft was used as a spacer (figure 1). All the exiting nerve roots were traced. The procedure was uncomplicated and uneventful, and implants were confirmed in fluoroscopy. In the postop recovery room, the patient regained full strength in her lower extremities and was transferred to the ward. Following morning she complained of numbness in right side the perineum and upper back of the thigh (American Spinal Injury Association (ASIA) scores right 0/2 to S 2–5, reduced anal pressure) without any motor weakness in the limbs. When Foley catheter had been removed, she suffered from urinary retention. Emergent postoperative CT imaging was done and the radiologist confirmed the sections demonstrated only normal postoperative changes with well-placed screws and cage, and adequate decompression with no adjacent level stenosis (figure 2). She was treated with the aid of intermittent catheterisation. At 3-month follow-up, she regained complete sensation and bladder function, and anal tone.

Figure 1.

Preoperative sagittal and axial cuts with a postoperative radiograph of case 1.

Figure 2.

Postoperative CT scans (sagittal and axial cuts) of case 1 showing well-placed screws and cage, and no compression.

Case 2

A 52-year-old man with a 5-year history of severe back pain and left sided radiculopathy failed to all conservative management including root blocks. His MRI demonstrated L3–L4 and L4– L5 disc bulges with desiccated discs at both levels. The patient underwent an uncomplicated double level transforaminal lumbar interbody fusion left side with 2×9 banana cage and pedicle screws at L3–L5 (figure 3). Postoperatively, he was neurologically intact except some heaviness on the left perineum (ASIA score left 0/2 for S 3–5, reduced anal tone). Injection methylprednisolone was administered (32 mg/kg loading dose followed by 5.4 mg/kg/hour). CT scan was done to confirm placement of screws and cage, and also rule out epidural haematoma (compressive aetiology) but was normal. No attempts at exploration were done and by 3 days he regained full sensation of the perineum but had urinary retention, bowel incontinence and loss of erection.

Figure 3.

Preoperative sagittal and axial cuts MRI with postoperative radiograph of case 2.

An ultrasonography ruled out benign hyperplasia of prostate. The patient was ambulatory and at 24-week follow-up, he had regained his bladder/bowel and genital function.

Investigations

This has been detailed in the case itself.

Differential diagnosis

The factors implicated in postoperative CES include: inadequate decompression, epidural haematoma, retained disc fragments, fat pad grafts, gel foams, retained sponges and a variety of other compressive pathology like intradural masses.^{6 8} More recently vascular insufficiency, that is, tenuous vascular supply below the tip of conus medullaris leading to subsequent ischaemia of the cauda equine roots has been put forth.⁹

Outcome and follow-up

Emergent postoperative CT imaging was done in both cases to rule out any screw/cage malplacement, any compressive pathology and also confirm decompression has been adequately achieved. We found only normal postoperative changes with well-placed screws and cage, and satisfactory decompression. The patients were treated with the aid of intermittent catheterisation. At 3 to 6-month follow-up, the patients regained complete sensation and bladder function, and anal tone.

Discussion

CES is a well-documented clinical finding in patients with acute lumbar disc prolapse. Some present as hemi-CES with unilateral pain, sensory loss and sphincter disturbance.² However, the findings in postoperative lumbar surgery setting are rare with incidences ranging from 0.08% to 0.2% only.^{1 4–6}

The factors implicated in postoperative CES include: inadequate decompression, epidural haematoma, retained disc fragments, fat pad grafts, gel foams, retained sponges and a variety of other compressive pathology like intradural masses.^{6 7} More recently vascular insufficiency, that is, tenuous vascular supply below the tip of conus medullaris leading to subsequent ischaemia of the cauda equina roots has been put forth. This anatomical rationale of this neuro-ischaemia was studied by Parke et al in their study.⁹ Secondary ischaemia has also postulated a cause even in patients with compressive aetiology. Henrique et al have suggested that postoperative oedema can trigger venous congestion and lead to nerve ischaemia in patients with relative spinal stenosis.³ The finding of diseases/co morbidities which affect the microvasculature in four out of five cases by Duncan and Bailey also point towards ischaemic theory.⁷ Murphy was first to emphasise that the lumbar extruded disc material puts tension, rather than compression, on the nerve root, which can cause CES.¹⁰

Traditionally CES has been asserted as compressive neuropathy.⁷ Postoperative imaging in the form of MRI or CT scan is warranted at the earliest to find out any mass lesion but is negative in many circumstances.^{6 7} The general consensus is postop CES like preop CES, is a medical emergency and requires an immediate surgical re-explorations within 48 hours.⁶ Many authors believe that despite negative imaging for the mass effect the surgical exercise is beneficial and should be routinely done in a situation of CES^{3 6}; there are a group of authors have had a trip to operation theatre and retrospectively believe not all cases should be re-explored.^{1 7} The data on this conservative management is scarce and few did not have expected outcome.⁶ Thus, the pendulum automatic sways towards the surgical direction.

Duncan et al had five cases of CES in their review of 175 patients of decompression with an incidence of 2.8% and they believe postop CES is more common than reported. They observed that re-exploration in three of five patients did not help to ascertain any compressive pathology and hence, put forward their theory of increased dural tension postoperatively due to expansion could compromise the hypovascular roots leading to ischaemia and precipitating CES.⁷ We had two cases both of which were incomplete CES and though we did get immediate CT scans but did not find any compressive aetiology. The striking findings in both cases were ipsilateral hemi-CES from the side where the cage was approached which could be mere coincidence or some triggering factor to further vascular compromise. The transforaminal approach being more lateral and facet excising is safer; requiring minimal or no retraction of dural sac than the posterior approach for cage placement. Yet we had both cases going by the transforaminal approach.

When compared with a study by Duncan, both of our cases where partial CES and hence complete recovery was gained. The prognosis for postoperative CES depends on the extent of involvement. Patients with the motor deficits are more likely to recover after emergent surgery than is bladder function.⁶ Some authors relate the prognosis of bladder function to the extent of sensory loss in the so-called saddle area.^{1 11} The recovery of bladder function runs parallel to the return of sensation in the saddle area.¹² This prognosis is however slow and unpredictive taking several months to years.¹¹

Learning points.

• Our cases illustrates the risk of postoperative cauda equina syndrome (CES) arising as a complication of decompression surgery for spinal stenosis.

• Aetiology of postoperative CES can be attributed to compressive and non-compressive causes such as nuero-ischaemia as demonstrated in our cases.

• In our two cases, we found favourable prognosis with conservative treatment when findings are partial and thorough imaging ruled out any compressive aetiology.