Spinal Cord Ischemia in the Setting of Acute Type B Aortic Dissection: Successful Rescue with Thoracic Endovascular Aortic Repair

Introduction

In contemporary guidelines,^1,2 optimal medical treatment is recommended as the gold standard for uncomplicated acute type B aortic dissection (ABAD). Emergent surgical or endovascular interventions are required for complicated ABAD in lieu of a high in-hospital mortality rate of 23.5–29.3% reported in complicated ABAD.^3,4 A majority of those cases were ruptured complications as opposed to organ malperfusion. The incidence of spinal cord ischemia (SCI) was relatively low (2–4%) in the setting of organ malperfusion,^5,6 but paraplegia resulting from SCI, remains a devastating complication, adversely impacting patient outcomes, including quality of life (QOL). We report successful thoracic endovascular aortic repair (TEVAR) for 2 patients with SCI secondary to complicated ABAD.

Case Report

Case 1. A 70-year-old man presented with acute onset back pain and left lower extremity hypoesthesia. Upon emergent transfer to our institution, enhanced computed tomography (CT) revealed an ABAD with occluded false lumen, extending from the left subclavian artery (LSCA) to the terminal aorta (Figure 1A). Optimal medical management was initiated with continuous intravenous of calcium antagonist and beta-blocker, but his left lower extremity hypoesthesia worsened despite palpable dorsalis pedis pulses bilaterally. The dynamic obstruction of the segmental arteries responsible for the spinal cord hypoperfusion was assessed, confirming the diagnosis of SCI; CT revealed a small primary entry in the proximal descending aorta. Although the 11th intercostal arteries (ICA) and the 1^st lumbar arteries (LA) were enhanced, the 12th ICAs were not seen (arrowhead) (Figure 1B and 1C). Cerebrospinal fluid drainage (CSFD) was initiated followed by emergent TEVAR. Under general anesthesia, the right common femoral artery (CFA) was exposed and a delivery system with a 24F Dryseal introducer (W. L. Gore & Associates, Inc, Flagstaff AZ, USA) was inserted through the abdominal aorta. A 37 × 150 mm of conformable TAG thoracic endoprosthesis (W. L. Gore & Associates, Inc, Flagstaff, AZ, USA) was deployed just below the LSCA up to the T7 level and included the primary entry. No amplitude reduction of motor evoked potentials (MEPs) occurred during the procedure. After the TEVAR, the mean blood pressure could be maintained as high as 100 mmHg using continuous norepinephrine infusion with concomitant administration of spinal cord protective agents such as naloxone and prostaglandin E1, in the intensive care unit for 3 days. During the hospitalization, the SCI symptoms improved completely, and postoperative CT showed complete exclusion of the primary entry with true lumen dilatation by the stent graft (Figure 2A). The 12th ICAs that were not demonstrated on the preoperative CT were clearly enhanced (arrow) (Figure 2B and 2C). He was then discharged home on postoperative day 23.

OPEN IN VIEWER

Figure 1.

Preoperative computed tomography demonstrating acute type B aortic dissection with the false lumen occluded (A), and the 11th intercostal artery and 1st lumbar artery are contrasted, while the 12th intercostal arteries is not opacified obviously (arrowhead) (B, C).

OPEN IN VIEWER

Figure 2.

Postoperative computed tomography showing endoprothesis deployed from left subclavian artery to the descending aorta (A). And the dilatation of the true lumen. The 12th intercostal arteries, which had not been demonstrated preoperatively, is opacified (arrow) (B, C).

Case 2. A 52-year-old man who presented with acute onset back pain was diagnosed as ABAD by CT scan at a nearby hospital. Upon transfer to our institution, an enhanced CT confirmed an uncomplicated ABAD with patent false lumen, extending from the LSCA to the bilateral common iliac artery (Figure 3A). Optimal medical management was immediately initiated, but he complained of the right lower extremity hypoesthesia 5 hours after admission despite palpable dorsalis pedis pulses bilaterally. The CT demonstrated occlusion of almost all ICAs and true lumen compression of the distal descending aorta secondary to the dilated false lumen (arrowhead) (Figure 3B and 3C). SCI was diagnosed the result from the dynamic obstruction of the segmental arteries responsible for the spinal cord perfusion. Primary entry closure by emergent TEVAR was performed to dilate the true lumen and restore sufficient perfusion to the spinal cord. Under general anesthesia, the left CFA was exposed, and a 22F Dryseal introducer (W. L. Gore & Associates, Inc, Flagstaff AZ, USA) was inserted through the abdominal aorta to the descending thoracic aorta. A 31 × 150 mm of conformable TAG thoracic endoprosthesis (W. L. Gore & Associates, Inc, Flagstaff, AZ, USA) was deployed just below the LSCA to the T7 level, which included the primary entry. Even after the TEVAR, MEPs did not resume sufficiently so CSFD was initiated immediately. The mean blood pressure was also maintained as high as 100 mmHg with continuous norepinephrine injection with concomitant naloxone/prostaglandin E1 administration along with a one-time-methylprednisolone injection. As a result, his right lower extremity hypoesthesia remarkably improved 2 hours after initial treatment. Rectal bladder disturbance developed temporarily, but resolved prior to discharge. Postoperative CT showed sufficient true lumen dilatation with complete exclusion of the primary entry (Figure 4A). The seventh–ninth ICAs, not demonstrated on preoperative CT, were clearly enhanced postoperatively (arrow) (Figure 4B and 4C). Upon achieving clinical stability, he was finally transferred to a rehabilitation facility on postoperative day 35.

OPEN IN VIEWER

Figure 3.

Enhanced computed tomography demonstrating acute type B aortic dissection with the false lumen patent, which causes the compression of the true lumen of the distal descending aorta (A), and the occlusion in almost all intercostal arteries of the descending aorta (B, C).

OPEN IN VIEWER

Figure 4.

Postoperative computed tomography (CT) showing endoprothesis deployed from left subclavian artery to the descending aorta (A), the true lumen is sufficiently dilatated and the seventh–ninth intercostal arteries, which had not been demonstrated on the preoperative CT, are opacified (arrow) (B, C).

Discussion

In cases with uncomplicated ABAD, rest and antihypertensive therapy are indicated because when this optimal medical treatment is introduced, a much lower mortality rate (0–7.4%) is observed in contrast to surgery, which carries a much higher mortality risk.^7-9 The annual survival rate of uncomplicated ABAD is over 80%. ¹⁰

However, approximately 25% of ABADs are complicated upon admission or after, resulting in early death or permanent physical disability.^11,12 The 30-day mortality rate of complicated ABAD was reported as 23.5–29.3%.^3,4 Complicated ABAD is defined as acute aortic rupture or impending rupture, malperfusion involving visceral, renal, spinal cord or extremities, uncontrolled hypertension, persistent or recurrent pain, or rapid expansion evident on CT. ¹³ During the initial medical management, clinical signs of organ malperfusion manifesting as chest and abdominal pain, motor or sensor deficits, oliguria, or absent femoral pulsation, should be promptly assessed and managed. Moreover, primary and secondary entry locations, true and false lumens diameters, visceral and renal artery branching origins, and the presence of organ contrast effect should be evaluated on CT precisely and serially with great cautions.

Spinal cord ischemia has a very low incidence rate of 2–4% in the setting of all acute aortic dissections.^5,6 The current guidelines recommend emergent surgical or endovascular interventions for complicated ABAD,^1,2 and recently, it has been reported that TEVAR may be useful for improving kidney, bowel or lower extremity ischemia.^14-16 However, in contemporary guidelines, there have been no detailed descriptions on adequate treatments for spinal cord malperfusion because TEVAR cases for SCI are extremely rare due to its low incidence.

Three mechanisms of organ malperfusion have been proposed in ABAD: dynamic, static, and mixed obstruction of the organ perfusion. Dynamic obstruction is caused by true lumen compression and/or compression of the arterial branches by a dilated and higher pressure false lumen in the settings of a larger entry and a smaller re-entry. SCI has been reported to be mostly due to dynamic obstruction secondary to the intimal flap motion within the aortic lumen; the intimal flap itself can obstruct the orifices of segmental arteries. ¹⁶

Dynamic obstruction could be managed by prompt TEVAR to restore organ perfusion and prevent irreversible organ ischemia.^14,15 TEVAR for ABAD eliminates antegrade flow into the false lumen by coverage of the primary entry,^16-18 thereby expanding the stenotic true lumen and restoring branch vessel perfusion. ¹⁶ In the present cases, several ICAs that were not detected on preoperative CT were visualized on CT postoperatively.

Prompt TEVAR has another advantage for managing ABAD with organ ischemia. The primary entry closure by TEVAR shrink the false lumen and decrease the risk of fatal aortic rupture; it can allow us to maintain the mean blood pressure around 100 mmHg in order to provide sufficient organ perfusion.

A collateral network concept was proposed by Griepp. et al in 1996; there exists an axial network of small arteries in the spinal canal, the peri-vertebral tissues, and the paraspinous muscles around the spinal cord. It is supplied not only by ICAs and lumber arteries but also by the subclavian and the hypogastric arteries and their branches. ¹⁹ Moreover, the etiology of paraplegia is multifactorial, as it may include perfusion failure of Adamkiewicz artery and occlusion of the collateral arterial sources. In addition, systemic hypotension and previous abdominal aortic surgery should be considered among other etiologies.^20,21

Therefore, paraplegia can be prevented by maintaining sufficiently high blood pressure without causing fatal aortic rupture.

Conclusion

We report successful prompt TEVARs for SCI complicated with ABAD. Primary entry closure and true lumen dilatation by TEVAR with postoperative hypertensive management is a key management option to relieve SCI secondary to dynamic obstruction in ABAD.