Neurological Deficit Secondary to Spinal Cord Ischaemia after Infrarenal Abdominal Aortic Repair for Aorto-Iliac Occlusive Disease: A Case Report☆
Article Outline
- Abstract
- Case Report
- Discussion
- Conflict of Interest Statement
- Sources of Financial Support
- References
- Copyright
Abstract
Neurological deficit after infrarenal abdominal aortic repair is rare. We report on a patient who had an infrarenal aorto-bifemoral bypass for claudication. Postoperatively, the patient developed a partial anterior spinal artery syndrome (ASAS).
Factors contributing to the development of ASAS were evaluated using contrast-enhanced magnetic resonance angiography of the spinal cord's blood supply. ASAS was probably caused by a temporarily inadequate blood flow to the cord due to intra-operative hypotensive episodes combined with generalised vascular disease. Since treatment options for ASAS are solely supportive, preventive measures are imperative to avoid neurological deficit.
Keywords: Abdominal aortic repair, Adamkiewicz artery, Anterior spinal artery syndrome, Aorto-iliac occlusive disease, Magnetic resonance angiography
Clinical neurological deficit following spinal cord ischaemia is rare after infrarenal abdominal aortic repair, with incidences ranging between 0.10% and 0.25% after elective aneurysm repair and 0.02% and 0.3% after reconstruction for aorto-iliac occlusive disease.1, 2
We report on the development of a partial anterior spinal artery syndrome (ASAS) in a patient treated for aorto-iliac occlusive disease employing elective infrarenal abdominal aortic repair. Of special interest is the application of contrast-enhanced magnetic resonance (MR) angiography to visualise the anterior spinal cord's blood supply, enabling evaluation of possible causes of ASAS development.
Case Report
A 62-year-old man presented with invalidating claudication of the lower limbs. His history revealed a cerebral vascular accident of the right hemisphere (1985), excision of a carcinoma from the left groin (1986), abdominal radical prostatectomy (2005) and hypertension. A disadvantage in motor control of the left extremities accompanied by a discrete sensory loss was noticed preoperatively. Femoral and pedal pulses were absent on both sides. Preoperative MR angiography (Fig. 1) showed an atherosclerotic and 80%-stenosed infrarenal abdominal aorta without aneurysmal widening. The left common, external and internal iliac artery were occluded, and the right common and external iliac arteries 80% stenosed. The right internal iliac artery was fragile but patent. Both profundal and superficial femoral arteries showed adequate filling.
Figure 1
Preoperative subtraction magnetic resonance (MR) angiography providing a right-anterior overview on the abdominal aorta and left and right iliac system. The 80% stenosis of the infrarenal abdominal aorta is depicted by an asterix. Furthermore, the left common, internal and external iliac arteries were occluded (arrowheads). This occlusion continued as far as the inguinal ligament. The right common iliac artery showed an 80% stenosis, the right external iliac artery was narrowed and the right internal iliac artery (IIA) was fragile, but patent (white arrow). The profundal and superficial femoral arteries showed adequate filling on both sides. Additionally, the middle sacral artery contributed to the femoral arteries by collateral flow.
An infrarenal aorto-bifemoral bypass was placed (Unigraft, Braun, Melsungen, Germany) via a median laparotomy under general anaesthesia with combined epidural anaesthesia. Heparin was administered before infrarenal clamping. The proximal and distal anastomoses were completed end to side with 30-min clamping time and 400
ml of blood loss. Intra-operatively, systolic blood pressure dropped below 90mmHg 3 times for 10min.
Absence of motor function in both legs, except for minimal movement of the right foot, was first noticed 7h postoperatively. Pain and temperature sensation were reduced from T10 on the left and T12 on the right downwards with intact proprioception and vibratory sense. Knee- and ankle-jerk reflexes were absent as well as rectal sphincter tone. Bladder function was not assessed because of an indwelling urinary catheter. Urgent MR imaging showed no signs of myelopathy or aortic dissection. The clinical features were consistent with partial ASAS development. Conservative management consisted of maintenance of a mean arterial pressure greater than 90mmHg. Neither cerebrospinal fluid drainage nor corticosteroid treatment was initiated.
Dedicated MR angiography was performed 4 months after surgery (Fig. 2a and b).3 It showed a patent anterior spinal artery (ASA) and Adamkiewicz artery (AKA), of which the direct segmental supplier arose from level T10 on the right side. No additional anterior supply to the ASA below the level of aortic cross-clamping could be identified. The right internal iliac artery was opacified on examination with contrast and contributed to the flow to the lumbar segmental arteries. Intramedullary ischaemic spinal cord lesions were detected from the mid-thoracic level downwards. The patient recovered partially, with an incomplete return of motor function 24 months after surgery.
Figure 2
Dedicated contrast-enhanced magnetic resonance angiography conducted 4 months after the onset of the partial anterior spinal artery syndrome. (a) Sagittal view providing an overview in which the prosthetic abdominal aorta (asterisk) is depicted. The patent right internal iliac artery (of which a segment is marked by an oblique white arrow) contributed to the segmental arteries (double arrowheads), which were bypassed by the prosthesis, by collateral circulation. Note that the segmental supplier (SA) of the Adamkiewicz artery (AKA) was located at vertebral level T10 and was well above the level of the prosthesis. (b) The direct segmental supply from the aorta to the anterior spinal artery (ASA) was not interrupted postoperatively, as shown in the curved multiplanar reformation.
Discussion
Spinal cord ischaemia during abdominal aortic repair can manifest itself in various clinical symptoms. Permanent or temporary interruption of the blood flow to the ASA might result in ASAS development, which is characterised by symptoms of paraplegia, bladder and/or rectal incontinence and loss of pain and temperature sensations with intact proprioception and vibratory sense.1, 2
The ASA supplies the anterior part of the spinal cord responsible for the motor function as well as pain and temperature sensation in the lower limbs.2, 4 The AKA is the largest and is, therefore, considered the most important supplier of the thoracolumbar spinal cord.3 However, the pelvic circulation can considerably contribute to the distal cord's blood supply when AKA is dependent on collateral segmental supply or originates unusually high.2, 3, 5
The risk factors for the development of ASAS are listed in Table 1.1, 2, 3, 4, 5 In this case, permanent interruption of the segmental supplier, the AKA or the right hypogastric artery was excluded by postoperative contrast-enhanced MR angiography (Fig. 2a and b). Most probably, the intra-operative hypotensive episodes resulted in a temporary reduction in blood flow to the ASA, especially when the combination with generalised vascular disease is considered.
Table 1. Risk factors for the development of ASAS after abdominal aortic repair
| Surgery-related risk factors | Non-surgery-related risk factors |
|---|---|
| Prolonged aortic cross-clamping (>45min) | Atherosclerosis |
| Diabetes mellitus | |
| Supraceliac aortic cross-clamping interrupting blood flow to AKA | Anatomical variant of the origin of AKA History of previous abdominal surgery |
| Lack of heparinisation | History of hypertension |
| Emergent surgery for ruptured abdominal aortic aneurysm | Perioperative systemic hypotension •SBP: ≤100 mmHg•MAP: ≤55 mmHg |
| Interruption of pelvic collateral circulation, e.g. by aorto-bifemoral bypass graft with end-to-end anastomoses | |
| Intra-operative aortic embolisation | |
| Excessive blood loss |
Treatment options for ASAS in thoracoabdominal aortic surgery comprise permissive systemic hypertension (by means of volume replacement and vasopressor support), cerebrospinal fluid drainage and pharmacological modulation.1, 2, 6 Data regarding their efficacy are conflicting, but these interventions may be able to diminish or reverse spinal cord ischaemia.1, 6 As treatment options for ASAS are poor, preventive measures are essential. They consist of avoidance of intra-operative hypotension, careful handling of the abdominal aorta, minimal duration of aortic cross-clamping, cerebrospinal fluid drainage, neuromonitoring, intra-operative heparinisation, moderate hypothermia and re-implantation or preservation of potential suppliers of the ASA.1, 2, 3, 5
In conclusion, the aetiology of ASAS is frequently multifactorial and consisted, in this patient, of a temporary inadequacy of blood flow to the spinal cord caused by systemic hypotension combined with generalised vascular disease. Since treatment options for ASAS are solely supportive, intra-operative preventive measures are imperative to avoid postoperative neurological deficits.
Conflict of Interest Statement
The authors have no conflict of interest.
Sources of Financial Support
None.
References
- Ischemic injury to the spinal cord or lumbosacral plexus after aorto-iliac reconstruction. Am J Surg. 1991;162:131–136
- . Spinal cord ischemia after abdominal aortic operation: is it preventable?. J Vasc Surg. 1999;30:391–397
- . Magnetic resonance angiography and neuromonitoring to assess spinal cord blood supply in thoracic and thoracoabdominal aortic aneurysm surgery. J Vasc Surg. 2007;45:71–77[discussion 77–8]
- . Ischemic damage to the spinal cord following end-to-side aortobifemoral bypass. Ann Vasc Surg. 1993;7:569–576
- . Spinal cord ischemia following operations on the abdominal aorta. J Vasc Surg. 1986;3:94–103
- . Management of neurologic complications of thoracic aortic surgery. J Clin Neurophysiol. 2007;24:336–343
☆ This report is based on a case that was presented at the case presentation session of the 22nd European Society for Vascular Surgery Meeting, September 2008, Nice, France.
PII: S1533-3167(08)00035-6
doi:10.1016/j.ejvsextra.2008.11.009
© 2008 European Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
Refers to article:
- Neurological Deficit Secondary to Spinal Cord Ischemia after Infrarenal Abdominal Aortic Repair for Aorto-iliac Occlusive Disease: A Case Report , 27 January 2009
