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J R Soc Med. 2005 February; 98(2): 59–60.
PMCID: PMC1079380

Embolic spinal cord infarction as a presentation of abdominal aortic aneurysm

J F Fairhead, MRCS, D Phillips, FRCS, and A Handa, FRCS FRCS(Ed)

Embolization to the legs is a well-known presentation of abdominal aortic aneurysm. Embolization can also lead to spinal cord infarction.


A man aged 72 experienced transient abdominal pain and became unable to move his legs. An ex-smoker, he had previously been fit and well apart from mild osteoarthritis. On examination his pulse and blood pressure were normal and he had a full complement of lower limb pulses. There was complete paralysis and paraesthesia in both legs below T12/L1. An erythematous, non-blanching, purpuric rash covered the entirety of both legs and extended circumferentially to 5 cm above the umbilicus. In the abdomen a non-tender aneurysm was palpable, shown by thoracic and abdominal CT to be 7.8 cm in anteroposterior diameter, infrarenal, with no evidence of leak or dissection. There was extensive mural thrombus. The clinical diagnosis was of cutaneous and spinal cord embolization from the aortic aneurysm, and he was deemed to be at risk of further embolization. He was transferred to the operating theatre without delay and the aneurysm was repaired with a tube graft. There was a large amount of gritty, semi-liquid thrombus within the sac, which was seen to occlude the lumbar vessels. After removal of the thrombus, there was brisk back-bleeding from six of these vessels, which were oversewn. Clamp time was 55 minutes.

His postoperative recovery was uncomplicated; he was extubated in theatre, had a routine 24-hour admission to the intensive care unit and was eating and drinking normally by day five. He began to regain both sensory and motor function to his legs almost immediately. On the advice of a neurologist MRI was performed to exclude other treatable causes of his motor and sensory loss. This revealed increased signal in the cord from T12 to L2, consistent with infarction. He underwent intensive physiotherapy and by eleven weeks he was able to walk a few steps. He was continent of faeces but on removal of his catheter he had urinary retention and incontinence despite bladder training; later he was successfully taught intermittent clean self-catheterization. At the National Spinal Injuries Centre he received inpatient treatment followed by outpatient physiotherapy. At one year follow-up he is walking with callipers.


Several other associations of aneurysms with spinal cord infarction have been described. Dormal et al. described cord infarction as a complication of aneurysm repair or rupture, and from the published work reckoned the incidence to be 1–2% in all infrarenal surgery. The associated mortality was 50% in both ruptured and unruptured aneurysms.1 Thoraco-abdominal dissection is a well-known association, the likely mechanism of infarction being occlusion of the origins of major arteries feeding the spinal vasculature, such as the great anterior artery of Adamkiewicz at T10/12. Joo and Cummings describe a case of transient neurological syndrome as the only presentation of thoraco-abdominal dissection, with complete recovery after medical therapy.2 Similarly, local dissection can be a complication of infrarenal aneurysm.3 Acute aortic thrombosis may present as a painless paraplegia. Bolduc et al. describe two cases of acute thrombosis initially mimicking stroke in one patient and with relief of pain from a vulval abscess in another. Both patients were later found to have unsalvageable lower limbs.4 Direct erosion by a large aneurysm of the lumbar vertebral bodies in the setting of rheumatoid arthritis, leading to spinal cord compression, has also been described.5

The presentation we describe is different. The sudden loss of neurological function and non-blanching rash occurred preoperatively but there was no evidence of rupture, dissection or lower limb large artery occlusion. The intra-operative findings of liquid thrombus within the aneurysm sac are consistent with massive cholesterol embolization to the distal vasculature. Prompt surgery may have been critical in the prevention of further embolization and thus subsequent recovery of neurological function. Sudden paralysis and paraesthesia in such a context should prompt investigation for abdominal aneurysm and, if necessary, prompt surgical intervention.


1. Dormal PA, Delberghe X, Roeland A. Infra-renal aortic aneurysm and spinal cord ischaemia. A new case and review of the literature. Acta Chir Belg 1995;95: 136–8 [PubMed]
2. Joo JB, Cummings AJ. Acute thoracoabdominal aortic dissection presenting as painless, transient paralysis of the lower extremities: case report. J Emerg Med 2000;19: 333–7 [PubMed]
3. Joseph MG, Langsfield MA, Lusby RJ. Infra-renal aortic aneurysm; unusual cause of paraparesis. Aust NZ J Surg 1989;59: 743–4 [PubMed]
4. Bolduc ME, Clayson S, Madras PN. Acute aortic thrombosis presenting as painless paraplegia. J Cardiovasc Surg 1989;30: 506–8 [PubMed]
5. Latif S, Wasti A, Grundy DJ, Isdale A, Iveson JM. Direct erosion of lumbar spine by an abdominal aneurysm resulting in lumbar paralysis: an unusual presentation. Case report. Paraplegia 1995;33: 480–1 [PubMed]

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