Delayed permanent paraplegia after endovascular repair of abdominal aortic aneurysm

Abstract

Spinal cord ischemia is a rare complication after abdominal aortic surgery and has been attributed to surgical devascularization of the spinal cord, atheroembolization of the cord circulation, or hypoperfusion of cord structures secondary to hypotension or cord edema. We present a diabetic, hypertensive 75-year-old male with endstage renal disease who presented with a 5.5 cm asymptomatic infrarenal abdominal aortic aneurysm, and concomitant 3.5 cm right common iliac artery aneurysm. After undergoing successful endovascular repair with an aorto-uni-iliac device, unilateral hypogastric artery embolization, and femoral-femoral bypass, he was discharged to a rehabilitation facility neurologically intact with a stage 2 decubitus ulcer. He returned on postoperative day 21 with a large stage 4 septic decubitus ulcer, fever, leukocytosis, hypotension, and paraplegia. We hypothesize that the compromised blood flow from the initial reconstruction, combined with the delayed hypotension imposed by sepsis, resulted in spinal cord infarction. He was eventually discharged to a nursing facility with no improvement in his neurologic status. We report the first case of significantly delayed permanent paraplegia after endovascular abdominal aortic aneurysmorrhaphy.

The significance of the pelvic collateral circulation in aorto‐iliac disease

“…The present study also mentions the growing popularity of endovascular repair for treating not only Type A and Type B atheromatous lesions, as per the Trans-Atlantic Inter-Society Consensus II (TASC II) guidelines (Norgren et al, 2007a(Norgren et al, , 2007b, but also for the more extensive Type C and D lesions, alongside other techniques such as a combined hybrid endarterectomy (Piazza et al, 2011). However, despite this, there have also been many reports of paraplegia following endovascular repair (Reid et al, 2003;Kotelis et al, 2008;Goldstein et al, 2010).…”

“…These include prolonged aortic cross-clamp time in open repairs (Svensson et al, 1994), reduced patent blood flow through an aortofemoral or femoral-femoral bypass graft (Goldstein et al, 2010), technical difficulties associated with emboli development following femoral cannulation in preparation for a bypass mechanism (O'Connor and Rothenberg, 1995) and systemic factors predisposing to hypotension such as sepsis. These include prolonged aortic cross-clamp time in open repairs (Svensson et al, 1994), reduced patent blood flow through an aortofemoral or femoral-femoral bypass graft (Goldstein et al, 2010), technical difficulties associated with emboli development following femoral cannulation in preparation for a bypass mechanism (O'Connor and Rothenberg, 1995) and systemic factors predisposing to hypotension such as sepsis.…”

“…Although difficult to ascertain the exact mechanism causing spinal cord paraplegia, it is likely that a combination of iatrogenic and systemic patient factors is involved. These include prolonged aortic cross-clamp time in open repairs (Svensson et al, 1994), reduced patent blood flow through an aortofemoral or femoral-femoral bypass graft (Goldstein et al, 2010), technical difficulties associated with emboli development following femoral cannulation in preparation for a bypass mechanism (O'Connor and Rothenberg, 1995) and systemic factors predisposing to hypotension such as sepsis. These factors should be taken into consideration prior to and during procedures.…”

Spinal Cord Ischemia Following Endovascular Repair of Infrarenal Abdominal Aortic Aneurysm

“…The authors reported that secondary hypotension might induce further reduction in spinal cord perfusion and contribute to the development of delayed paraplegia. 10) The precise pathophysiology in Case 3 could not be determined.…”

<p>Successful reversal of isolated delayed spinal cord ischemia following endovascular abdominal aneurysm repair</p>

“…EVAR and open repair result in different mechanisms of SCI, including endovascular exclusion of vital arterial supply to the spinal cord, perioperative hypotensive episodes, and atheroembolization of debris into pelvic circulation following endovascular instrumentation 5,6,7. Three important mechanisms contribute to delayed SCI; reperfusion injury with the flux of inflammatory and neurochemical mediators, spinal cord edema, and lastly arterial hypotension 7,8,9. Recently, Awad et al unveiled the importance of spinal cord edema in the development of SCI, suggesting a multifactorial process of development 10.…”