A Case of Spinal Cord Infarction Following Lumbar Transforaminal Epidural Steroid Injection: MR Imaging and Angiographic Findings

Discussion

TF ESI is a common procedure used in the nonsurgical management of lumbosacral radiculopathy.^4,5 The transforaminal approach allows concentrated delivery of medication to the ventral neural foramen and anterior epidural space, the areas most likely affected by disk pathology. However, needle placement via a transforaminal approach makes inadvertent vascular penetration of the radicular artery possible.

Minor complications include headache, back pain, worsening leg pain, facial flushing, and vasovagal reaction and have a reported incidence of 9.6%.⁶ Serious complications (eg, epidural hematoma, abscess, arachnoiditis) are uncommon, with an incidence of 0.9%.⁷ One of the rarest, yet most devastating, complications is spinal cord ischemia, which has been reported 5 times in the literature following lumbosacral TF ESI.^1–3

The blood supply to the thoracic spinal cord is predominantly from the anterior spinal artery, and a poor collateral network with the smaller posterior spinal arteries places the cord at high risk of ischemia if the dominant blood supply is compromised. At every level in the thoracolumbar spine, radicular branches off the segmental intercostal or lumbar arteries supply the exiting nerve root and foraminal structures. At as many as 5–6 levels, the radicular arteries also contribute to the anterior spinal artery, termed “radiculomedullary arteries.” The dominant radiculomedullary artery is called the “artery of Adamkiewicz” and is the primary source of blood for the thoracic cord. The artery of Adamkiewicz originates between T9 and L2 on the left in 85% of people, though aberrant origins from every lumbar level and S1 have been reported.

Theories regarding the cause of the SCI after TF ESI implicate inadvertent penetration of the radicular artery within the neural foramen in combination with a low origin of the artery of Adamkiewicz. Penetration of the radicular artery could result in focal dissection and distal emboli. If the injured radicular artery was, in fact, the artery of Adamkiewicz, this could result in spinal cord ischemia. Another proposed mechanism of injury suggests that intra-arterial injection of steroid suspension results in a shower of thrombogenic particulates to the distal cord with resultant ischemia.⁸

The incidence of vascular penetration with transforaminal needle placement is reportedly 8.1% at lumbar levels.⁹ Additionally, the use of a “flash” or backbleeding is not a reliable predictor of inadvertent vascular penetration.⁹ In this case, a small amount of backbleeding was reported on initial needle placement, which apparently resolved with repositioning. Contrast injection before therapeutic injection reportedly demonstrated epidural opacification.

CT and MR imaging are primarily used to exclude surgically correctable pathology that may mimic cord ischemia clinically. In this case, CT demonstrated no evidence of epidural collection or explanation for the flaccid paralysis. Findings on T2-weighted MR images are often normal but may demonstrate cord expansion and hyperintense signal intensity in the central cord and/or gray matter.¹⁰ Diffusion-weighted imaging (DWI) can also be useful in the setting of acute cord ischemia, demonstrating restricted diffusion.^10,11 In this case, MR imaging of the spine performed 4 hours after injection demonstrated increased T2 signal intensity in the gray matter and restricted diffusion in the lower thoracic cord. These findings are clinically useful because transient paralysis following subarachnoid injection of anesthetic has been reported.¹²

Catheter-directed spinal angiography in the setting of acute SCI following TF ESI has not been previously reported and was performed to evaluate potentially treatable lesions. In this case, the steroid injection presumably penetrated the right L2 radicular artery. The right L2 segmental artery origin could not be selected; however, if it was thrombosed back close to its origin, its presence would not have been detectable due to the inability to opacify the lumen. Irregular attenuated opacification of the distal right L2 segmental and radicular arteries via collaterals suggests that there was also spasm and/or thrombosis involving these vessels. The artery of Adamkiewicz was not demonstrated and putatively arose from the right L2 and was thrombosed. With such widespread vascular irregularity, we believe the SCI was likely secondary to inadvertent intra-arterial injection of thrombogenic particulate steroid. Although a focal dissection could theoretically result in distal emboli to the cord, it is unlikely to cause such widespread alteration in the appearance of the branches of the L2 segmental artery.