Cauda Equina Syndrome following lumbar spine procedures

The cauda equina is the collection of nerve roots that leave the lower end of the spinal cord and provide movement and sensation in the lower part of the body, chiefly the legs and bowel, and bladder. Cauda equina syndrome (CES) is a compressive neuropathy of these nerve roots. The clinical presentation is variable and may be either complete or partial. While many of the signs and symptoms are non-specific, the condition is characterised by bilateral sciatica, weakness of the legs, numbness in the saddle area, and bowel, bladder and sexual dysfunction. Without prompt treatment permanent loss of function of bowel, and bladder or weakness of the lower limbs may occur. CES is usually caused by extradural compression arising from disc herniations, tumours, trauma, or infection. However, it is also a relatively unknown rare postoperative complication following lumbar disc surgery. The incidence of postoperative CES is reported to be very low, at between 0.08% and 0.2% of cases, but it is very likely that the condition is underreported and the real incidence could be much higher. This is partly because the symptoms of CES are poorly predictive of positive findings on imaging.

Most cases of postoperative CES are thought to arise due to compression in the dural area. There may be a number of reasons for this, including inadequate decompression during the initial surgery, the development of an epidural haematoma, retention of disc fragments, migration of fat pad grafts or gel foams, and the occurrence of an intradural mass. Migration of bone graft materials to the sacral canal has been demonstrated on computed tomography (CT) scans. Gravity may then cause these fragments to fall in to the end of the dural cavity, leading to the development of CES. It has also been suggested that patients with underlying spinal canal stenosis who have undergone a discectomy using a keyhole interlaminar approach are more likely to develop CES postoperatively. However, the rise in popularity of this procedure has not been accompanied by a similar increase in the incidence of CES.

Recently, an alternative cause of postoperative CES has been suggested. The blood supply to the cauda equina is tenuous and it has been postulated that vascular insufficiency below the tip of the conus medullaris may lead to subsequent ischaemia of the cauda equina roots. Furthermore, secondary ischemia may occur in patients where the primary aetiology is compression. Postoperative swelling and oedema can lead to venous congestion, resulting in nerve ischaemia. It is also likely that extruded lumbar disc material puts tension, rather than compression, on the nerve roots. This tension may also compromise the vascular supply to the nerves, leading to ischemia. The ischemia theory is supported by a study that found that most patients with postoperative CES had co-existing disease affecting the microvasculature. It may also explain why many patients with postoperative CES do not have indications of compression following magnetic resonance imaging (MRI) or CT scanning. However, MRI studies have demonstrated ischemic lesions of the cauda equina following lumbar procedures.

Whatever the cause, postoperative CES is a medical emergency. Therefore, any patient complaining of symptoms indicating the condition should undergo scanning by MRI  preferably, or CT as soon as possible. Even if the scan does not indicate compression, many doctors believe that surgical re-exploration is essential and should ideally be performed within 48 hours. However, it is important to realise that transient urinary retention is a common postoperative complication of lumbar spine surgery and does not necessarily indicate direct nerve damage. Therefore, in some patients a more conservative approach may be indicated, but the decision of whether or not to operate remains challenging.

The prognosis for postoperative CES depends on the severity of the symptoms. Motor function is more likely to recover than bladder function, particularly after repeat surgery. The prognosis of bladder function appears to be closely linked to the severity and extent of sensory loss in the saddle area, and recovery of both often runs in parallel. However, improvements are slow and unpredictable, and the course of recovery is likely to take several months, if not years. The timing of surgical re-exploration can also influence recovery. The best prognosis is associated with decompression surgery within 48 hours, with around 70% of these patients reporting recovery of urinary and bowel function. Patients who undergo late decompression also report improvements in function, but the chances of complete recovery are decreased. Within the group of patients who undergo repeat surgery, around 80% make a full or delayed partial recovery, while up to 20% make no recovery at all.

Postoperative CES can arise for a number of reasons and is a rare, but potential devastating complication following lumbar spine surgery. It is a medical emergency, and patients reporting indicative symptoms should undergo neuroimaging as soon as possible. If this reveals a compressive lesion, immediate surgical decompression is required. Even when evidence of compression is lacking, surgical exploration is still recommended as timely intervention offers the best outcome for the patient.