Discussion
Acute aortic occlusion is a rare vascular emergency with a mortality rate that approaches 75%.4-6 It results from numerous etiologies, including saddle embolism at the aortic bifurcation, acute thrombus formation, subsequent to aortic dissection, or other causes related to severe atherosclerotic disease or hypercoagulable states.4,7
A recent retrospective series of 29 cases of AAO found that thrombosis was the cause for 76% of cases, and > 40% of patients had a hypercoagulable state either because of antiphospholipid antibody syndrome (17%) or malignancy (24%).6 The most common presentation of AAO is the abrupt onset of painful bilateral paresis or paraplegia.5,6 While some studies have suggested that the major determinant of mortality is time elapsed until revascularization,7 other studies have reported that the neurologic status of the extremities is more closely related with mortality.2
The anterior spinal artery is the major independent provider of blood flow to the anterior two-thirds of the spinal cord, including the anterior horns, the anterior commissure, the anterior funiculi, and to a variable extent, the lateral funiculi. The largest segmental posterior radicular branch of the anterior spinal artery is the artery of Adamkiewicz, which arises from the T9 to T12 level on the left in 75% of cases and provides perfusion to the lumbar spinal cord and the conus medullaris. Obstruction of blood flow in this region has been implicated in the clinical picture of anterior cord syndrome characterized by abrupt onset of radicular pain, flaccid paresis or paralysis, sphincter dysfunction with urinary and fecal incontinence, and decreased pain and temperature sensation below a sensory level with spared proprioception and vibratory sensation.3, 8-10
Aortography is the gold standard procedure for diagnosis of AAO, but it is a time-consuming procedure, and preoperative testing is controversial. Contrast-enhanced CT is useful for evaluation as it can be quickly accomplished and is more available in general hospitals. Moreover, CT scanning may reveal aortic dissections or aneurysms as the cause of occlusion. Deep Doppler ultrasonography also has demonstrated utility as a noninvasive and rapidly performed diagnostic procedure. Magnetic resonance angiography or CT should be performed for all cases unless the patient’s clinical condition prevents this evaluation. Imaging not only confirms diagnosis, but also is valuable for assessment and planning management.11-14
Once the diagnosis of AAO is made, management with IV fluid hydration, heparin administration, and optimizing cardiac function are essential. However, conservative management with anticoagulation alone is associated with high mortality, and unless the ischemia is irreversible or unless the patient is in a dying state, surgery is appropriate.5,7 Depending on the etiology of the AAO, anatomic considerations, and other patient factors, urgent revascularization with thrombo-embolectomy, direct aortic reconstruction, or anatomic or extra-anatomic bypass procedures may be employed. Aortic reconstruction has been advocated for all patients with infrarenal aortic occlusion given the concern for propagation of thrombosis at the distal aorta proximally to the renal and mesenteric arteries.7 Axillary-bifemoral bypass has been advocated as a rapid revascularization strategy with good patency and less physiologic strain for critically ill AAO patients.6
The patient in this study had a constellation of risk factors for developing AAO due to thrombosis and consequently sustaining spinal cord infarction. Echocardiography ruled out embolism of a mural thrombus. She had cardiac dysfunction due to atrial fibrillation and left ventricular failure causing a low-flow state (LVEF 30%). She also had a hypercoagulable state due to bladder malignancy in addition to severe atherosclerotic disease. She was not on systemic anticoagulation therapy because of her high fall risk. Hence, her risk for thrombosis was quite high. Despite expedient revascularization surgery, her postoperative course was complicated as a result of severe mesenteric ischemia due to chronic SMA occlusion, which caused her death.