Conus medullaris syndrome after epidural steroid injection: Case report

Discussion

ESI is regarded as an effective and conservative means of treating low-back pain resulting from nerve root inflammation. Recent case reports of post-procedural conus medullaris syndrome after spinal vascular compromise raise the question regarding safety.^16–18 Our case represents a sixth patient in whom conus medullaris syndrome developed after sustaining an acute spinal cord infarct during ESI. In 5 other case reports (Table 1), this complication affected patients (aged 42–71 years) who had previous lumbar surgery and then underwent a transforaminal steroid injection.^16–18 Of note, findings of spinal cord injury were not detectable on the initial MRI study within the first 24 hours in 1 case.¹⁷ Permanent paraplegia with loss of sphincter tone was observed in 1 patient.¹⁸ Outcomes in the remaining 4 patients varied from complete to partial recovery.

Injections are typically evaluated first by aspiration and injection of contrast. A nonvascular penetrating injection of contrast media verifies safe needle placement. However, in a series of 761 lumbosacral transforaminal injections performed, Furman et al.²⁰ reported that the sensitivity of positive flash or actual aspiration was only 44.7%, because only 38 of 85 patients had shown either flash or actual aspiration before injection. Specifically, they showed that there was an 11.2% rate of vascular injection in their series. In evaluating correct placement of 316 caudal-approach ESIs, Renfrew et al.²¹ implicated aspiration as an errorprone method for verifying needle placement, reporting a 9.2% incidence of vascular violation despite negative findings on aspiration.

Blood is supplied to the caudal-most portion of the spinal cord by the anterior spinal artery, 2 posterior spinal arteries, segmental radiculomedullary arterial branches, and most importantly, the artery of Adamkiewicz.²² The location of the artery of Adamkiewicz, which is the primary blood supply to the conus medullaris, is fairly unpredictable. It travels with the nerve through the foramen at or near the level of its origin from the thoracolumbar segmental arteries. ²³ Lazorthes et al.²³ showed that the artery of Adamkiewicz originated from the left T9-12 posterior intercostal arteries in 75% of cases and from the L1-2 lumbar arteries in 10% of cases. In 31 cadavers Biglioli et al.²⁴ located this artery between T12 and L3 in 26 cases (83.9%). In a 2002 review of more than 4000 spinal angiograms, Lo et al.²⁵ examined the variability of the artery of Adamkiewicz, noting that it originated at L2 in 1% of cases and L4 in 0.075% of cases.

Of the proposed mechanisms by which spinal cord medullary infarction may occur, one explanation may be the combined effect of an undetected direct arterial injection into a low-lying artery of Adamkiewicz and the resultant embolic incident from the injectate. Houten and Errico¹⁶ proposed that the collaterals surrounding the cord at the level of this artery were proximal to the injection site and thus allowed direct passage of the injected material into the conus. However, as discussed by Lo et al.,²⁵ the occurrence of a low-lying artery of Adamkiewicz is extremely unlikely. Considering this observation, we believe that it is unlikely that our patient had this low-lying artery that could have then been injected with an epidural steroid at this precise location.

Another plausible explanation is that an inadvertent sacral radicular artery injection carried injection material distally to the spinal cord. Lazorthes et al.²³ reported that material injected into the abdominal aorta below the level of the artery of Adamkiewicz would appear in the conus through collateralization.¹⁶ The most likely cause is injection of steroid particulate through either the artery of Adamkiewicz or collateral radiculomedullary arterial branches. Prior lumbar surgery may lead to compromise of normal vascular supply to the spinal cord, thus making it more susceptible to vascular injury. Direct arterial injury has also been cited as a cause of injury.¹⁶ Subsequent thrombus formation would result in an embolic infarct in the spinal cord supplied by the affected artery.

Other complications of transforaminal ESI include needle- induced vasospasm. Studies have shown that cerebral arteries constrict in response to mechanical stimuli. Florey²⁶ noted that such vasoconstriction was a local effect lasting 5 seconds to 10 minutes at the site of injury only. Simeone et al.²⁷ found that fine needle (30-gauge) arterial puncture in rhesus monkeys induced intense vasospasm, typically lasting anywhere from 4 hours to 4 days. Many studies have examined mechanically induced vasospasm of the cerebral vasculature and may be indirectly suggestive that a similar phenomenon can occur in the spinal cord and conus medullaris.

Of the multiple recommendations made to avoid such devastating complications as paralysis, first and foremost is the strict adherence to the standard and widely accepted techniques of transforaminal ESIs. These guidelines include the use of multiplanar fluoroscopy or computed tomography guidance together with contrast material to prevent complications. If recovery of neurologic function fails to occur in a patient within a 2- to 3-hour time period after ESI, an initial MRI study may be obtained to exclude an epidural hematoma. Repeat MRI after 24 hours should be performed as well. In our patient, as well as 1 other reported case,¹⁷ a delayed effect was observed with MRI signal changes occurring after 24 hours.