Paraplegia after elective repair of an infrarenal aortic aneurysm

Paraplegia is a rare but devastating complication of thoracic/thoraco-abdominal aortic aneurysm repair. The incidence after repair of infrarenal aneurysms is lower, at 1.4-2.0% for emergency cases and 0.1-0.2% for elective cases.^1,2

CASE HISTORY

A man of 68 was seen in the outpatient department with a symptomatic abdominal aortic aneurysm. Ultrasound scanning showed a 6.9 cm infrarenal aneurysm with involvement of the right external iliac artery together with bilateral femoral aneurysms. He was fit and well with stable cardiorespiratory status. Elective aneurysmal repair was conducted under general anaesthesia. Aorta and groin vessels were dissected and controlled and heparin (5000 U) was infused intravenously. An aorto-bifemoral graft was sutured in place. The distal end of the aorta was oversewn and the two limbs of the graft were joined, end to end, to the distal common femoral arteries after resection of the femoral aneurysms. The operating time was 3 hours 15 minutes and the aorta cross-clamping time was 1 hour and 45 minutes. There was no significant hypotension during the operative procedure. The patient had an epidural catheter for analgesia.

On the first postoperative day the patient developed flaccid paraplegia and became incontinent of urine and faeces. The paralysis affected distal muscles more than proximal muscles. Deep tendon reflexes were absent and plantars were equivocal. Sensation was diminished from L4 to S1. The findings on distal vascular examination had not changed, with palpable femoral, dorsalis pedis and posterior tibial arteries. Initially we suspected that the paresis was due to the effects of epidural analgesia, which we discontinued. An MRI scan ruled out compression or infarction of the spinal cord. Next day there was no improvement, so we revascularized his left internal iliac artery by use of a jump graft from the right limb of the aorto-bifurcation graft. Electromyographic studies indicated axonal degeneration of peripheral motor and sensory nerves supplying the lower limbs, with the sciatic nerve more affected than the tibial nerves. These findings suggested an acute compressive axonotmetic lesion affecting the lumbosacral plexus. A subsequent MRI scan ruled out any compressive lesion in the pelvis. With intense physiotherapy the patient made slow but steady progress, becoming able to walk with a stick and recovering continence.

COMMENT

Understanding of the pathophysiology of this complication demands a brief account of the blood supply of the spinal cord (Figure 1). Three spinal arteries, one anterior and a pair of posterior spinal arteries from the vertebral arteries, supply the cord. The anterior spinal artery is the principal artery of the three, supplying the anterior two-thirds of the cord, including the critical motor area.³ Segmental arteries from subclavian, intercostal, upper lumbar and branches from the internal iliac and middle sacral arteries regularly feed the anterior spinal artery. The largest of these segmental arteries is the great radicular artery of Adamkiewicz or arteria radicularis magna, which originates as a branch from a left intercostal artery between T9 and T12 in 75% of patients, T5 and T8 in 15%, and L1 and L2 in 10%.⁴ Operative interference with this artery is implicated as one of the causes of paraplegia in thoracoabdominal repair. The inferior mesenteric artery and branches of the profunda femoris join the hypogastric artery and its branches to form the pelvic circulation. The pelvic circulation supplies some of the distal spinal cord. At present there are no angiographic techniques to display the entire cord supply in an individual patient; this limits our ability to avoid neurological complications completely during aortic operations. Gloviczki et al.² classified ischaemic injuries to the spinal cord and lumbosacral roots or plexus according to their location and extent (Table 1).

Figure 1.

Arterial supply of the spinal cord [Reproduced from Fitzgerald MJT, J Folan Curran. Clinical Neuroanatomy and Related Neuroscience. New York: Saunders, 2002]

Table 1.

Classification of ischaemic injuries to the spinal cord and lumbosacral roots or plexus

Classification	Site of ischaemia	Neurological deficit
I	Distal thoracolumbar cord	Bilateral flaccid paraplegia and sensory loss. Bowel and bladder dysfunction
II	Anterior two-thirds of the spinal cord	Bilateral flaccid paraplegia and loss of pain and temperature sensation; proprioception and vibratory sensation maintained
III	Lumbosacral roots with/without patchy infarcts of cord	Bilateral asymptomatic paraparesis with or without bowel and bladder incontinence
IV	Lumbosacral plexus	Bilateral asymmetric paraparesis with/without bowel and bladder incontinence. Preservation of paraspinal muscle innervation
V	Segmental infarction of spinal cord	Bilateral spastic paraplasia with sensory loss
VI	Posterior third of spinal cord	Loss of proprioception and vibratory sensation

Interference with pelvic blood supply, prolonged aortic cross-clamping, prolonged suprarenal clamping, intraoperative hypotension, thromboembolic phenomena and interference with a low-origin arteria radicularis magna have all been suggested as possible causes of spinal cord ischaemia.⁵ MRI should be done to rule out a compressive lesion, since this is potentially curable. Electromyographic studies, for indicating the exact site of the lesion, will help in prognosis: patients with an ischaemic injury to the lumbosacral roots or plexus recover best. In the present case the injury to the lumbosacral plexus was probably due to interruption of the collateral flow via the branches of the internal iliac arteries.