Ischaemic injury to the lumbosacral plexus after aorto-iliac reconstruction is rare. There are less than 80 patients reported in literature. The aetiology of ischaemic neuropathy is multifactorial, although the major single cause is the alteration in the blood supply to the spinal cord or the lumbosacral plexus. Hypoperfusion, interruption of critical arteries to the distal cord or lumbosacral roots or plexus may lead to permanent neurological deficit. Occlusion of the great radicular artery or the artery of Adamkiewicz, which supplies the anterior spinal artery in the thoracolumbar segment, has been mentioned in different studies.
1As proposed by others,
2 we believe that interruption of the pelvic circulation is a major aetiological factor in the development of ischaemic injury in our patient. Almost all of the blood supply to the sacral plexus derives from the internal iliac artery. Both the lateral sacral and iliolumbar arteries, which originate from the internal iliac artery, send small branches into the anterior sacral foramina to supply the cauda equina.
The lumbar plexus is embedded in the posterior part of the psoas major muscle. The vasa nervosa to the plexus are derived from the blood supply to this muscle, almost all from the lumbar arteries. It has been established that vasa nervosa are essential for peripheral nerves as they cannot be sustained by axonoplasmic flow from the cell bodies.
3 However, rich collaterals within the psoas usually protect the lumbar plexus from ischaemic injury even in the event of occlusion of most or all of the lumbar arteries.
Gloviczki
et al.
4 identified six types of injury resulting from partial or complete interruption of flow through the various components of the medullary blood supply. Differentiation between the types can be difficult and requires careful neurological evaluation supplemented by findings from MRI and EMG. Each type of injury has a different aetiology and a different prognosis.
Type I lesions involve complete infarction of the distal spinal cord and conus, supplied by the anterior and posterior spinal arteries. These injuries are characterised by flaccid paraplegia, corresponding sensory loss and poor recovery. Type II lesions correspond with anterior spinal artery syndrome in which the area supplied by the posterior spinal artery is preserved. Flaccid paraplegia is present with loss of pain and temperature sensations with intact proprioception and vibration senses. Type III lesions are due to bilateral root ischaemia with or without patchy distal cord and conus ischaemia. Most of the cord functions are preserved. Type IV injury is unilateral plexus ischaemia caused by infarction of the lumbar or sacral plexus. Both types III and IV have favourable prognosis. Type V injury shows segmental spinal cord infarction. Patients present with spastic paraplegia because of preserved cord function distal to the infarction. Both this type and type II injury might be seen after thoracic or thoraco-abdominal aortic reconstruction. Type VI injury occurs as a result of infarction of the area supplied by the posterior spinal artery. These patients are characterised by loss of vibration and proprioception sensations.
In our patient, it seems likely that pelvic exclusion was responsible for the development of neurological ischaemic injuries especially after extending the graft to the femoral artery. His clinical picture was consistent with type IV lesions. In one report,
5 simple interruption of one internal iliac artery during renal transplantation led to paraparesis. The other factor identified that may have played a role in the development of the neurological deficits in our patient was intra-operative hypotension.
