Acute type B aortic dissection after ruptured thoracoabdominal aortic aneurysm repair resulting in thoracoabdominal branch endoprosthesis collapse and malperfusion

Abstract

We report the case of a patient who developed an acute Stanford type B aortic dissection 4 days after thoracoabdominal branch endoprosthesis repair for a ruptured thoracoabdominal aortic aneurysm. The dissection caused complete endograft collapse and profound malperfusion. Emergent salvage endovascular repair successfully re-expanded the graft; however, the patient ultimately died because of the severity of the systemic injuries. This case highlights the potential for acute type B aortic dissection to occur in a recently stented thoracic aorta segment following thoracoabdominal branch endoprosthesis repair and emphasizes the need for urgent recognition of malperfusion and meticulous computed tomography evaluation of the aortic injury pattern.

Thoracoabdominal aortic aneurysms (TAAA) have an incidence of roughly 6 to 10 cases per 100,000 persons per year.^1,2 Until recently, repair was limited to open, hybrid endovascular/surgical repair, or endovascular repair with physician modified or investigational devices. In January 2024, the Thoracoabdominal Branch Endoprosthesis (TAMBE; W. L. Gore & Associates) received US Food and Drug Administration approval for the treatment of complex aneurysmal disease involving the visceral aorta.³ The TAMBE is an off-the-shelf device that enables TAAA repair with a supraceliac seal and incorporation of four visceral and renal arteries with preloaded inner branches, with promising preliminary outcomes.³ Endovascular repair for ruptured TAAAs may be reasonable in hemodynamically stable patients at centers with endovascular expertise.⁴

Aortic dissections are a potentially fatal event with an incidence of approximately six cases per 100,000 individuals per year.⁵ Acute Stanford type B aortic dissection (TBAD), or DeBakey type III, dissections account for ∼29% of all aortic dissections and originate distal to the left subclavian artery.⁵ Standard management consists of anti-impulse therapy unless complications arise, such as malperfusion, persistent pain, aneurysmal expansion, or impending rupture—in which case endovascular repair is indicated.⁶ Endovascular repair can rapidly restore true lumen blood flow, stabilize the aneurysmal sac, and promote favorable aortic remodeling.⁶

Thoracic endograft collapse is a rare complication of thoracic endovascular aortic repair (TEVAR), typically associated with severe aortic arch angulation, small native aortic diameters, device oversizing, or inadequate radial force.⁷ However, TAMBE endograft collapse precipitated by an acute TBAD is exceedingly uncommon. Informed consent for publication of this case report and accompanying images was obtained from the patient’s next of kin. We present a case of post-TAMBE acute TBAD resulting in complete endograft collapse and catastrophic malperfusion.

Case report

A 77-year-old woman with hypertension and a history of tobacco use was transferred to our facility with a ruptured TAAA. She underwent emergent endovascular repair with a 31-mm GORE EXCLUDER TAMBE device (W. L. Gore & Associates), representing 14.8% oversizing relative to the proximal aortic diameter. Device delivery was facilitated by left axillary cutdown, a right common iliac conduit (10-mm Dacron), and percutaneous left common femoral artery access. At completion, the aneurysm was excluded; all four branch grafts were patent, and there was no evidence of endoleak. The right common iliac conduit was converted to a right iliofemoral bypass.

On postoperative day 1, she developed new-onset left-sided hemiparesis. This was presumed to be cardioembolic, and anticoagulation was initiated. Routine, postoperative computed tomography angiography (CTA) at approximately 9:30 am on postoperative day 4 demonstrated a patent TAMBE endograft without evidence of dissection or endoleak. A suspected contained rupture of a small atherosclerotic ulcer was noted in the mid-descending thoracic aorta (Fig 1).

Fig 1.

Computed tomography angiography (CTA) obtained on postoperative day (POD) 4 following thoracoabdominal branch endoprosthesis (TAMBE) repair of a ruptured thoracoabdominal aortic aneurysms (TAAA). A, Axial image showing complete expansion of the endograft with penetrating aortic ulcer (black arrow). B, Sagittal reconstruction demonstrating a patent TAMBE device with penetrating aortic ulcer (black arrow).

Later that evening, she developed severe back pain and profound hemodynamic instability. She became progressively obtunded, required intubation, and was started on vasopressors. Repeat CTA obtained at approximately 10:00 pm demonstrated a new acute TBAD originating at the left subclavian artery, with complete collapse of the TAMBE endograft, which appeared crescent-shaped on axial imaging (Fig 2).

Fig 2.

Computed tomography angiography (CTA) obtained following clinical deterioration demonstrating new Stanford type B aortic dissection with collapse of the thoracoabdominal branch endoprosthesis (TAMBE) device. A, Axial image showing near-complete, crescent-shaped collapse of the endograft lumen (black arrow) resulting in critical malperfusion. B, Sagittal reconstruction demonstrating severe compression of the endograft by the false lumen (FL).

The patient was emergently taken for salvage TEVAR to address the acute TBAD, re-expand the TAMBE, and restore visceral and lower-extremity perfusion. A 37-mm C-TAG GORE thoracic aortic stent graft (W. L. Gore & Associates) was deployed just distal to the origin of the left common carotid artery, followed by a second device bridging the TEVAR graft and TAMBE. Completion aortography (Fig 3) and intravascular ultrasound confirmed TAMBE re-expansion.

Fig 3.

Completion angiography following salvage thoracic endovascular aortic repair (TEVAR). A, Deployment of a proximal thoracic stent graft (black arrow) with restored expansion of the collapsed thoracoabdominal branch endoprosthesis (TAMBE; white arrow). B, Re-established visceral and lower-extremity circulation.

During device advancement, the right iliofemoral anastomosis was disrupted by the large sheath, necessitating repair with an interposition graft. Massive transfusion (10 units packed red blood cells, six fresh frozen plasma, and one platelet pack) was required for hemorrhage and diffuse arterial fragility. She subsequently developed ventricular fibrillation but achieved return of spontaneous circulation after one defibrillation and a single round of cardiopulmonary resuscitation.

Given concern for abdominal compartment syndrome from visceral malperfusion, a decompressive laparotomy was performed, which revealed dusky, but viable bowel. She was transferred to the intensive care unit, where she developed worsening shock and coagulopathy despite maximal vasopressor support. Despite continued efforts, her condition deteriorated, and care was ultimately withdrawn.

Discussion

This case illustrates two major postoperative complications following TAMBE repair of a ruptured TAAA: an early postoperative ischemic stroke and subsequent acute TBAD resulting in complete TAMBE collapse and catastrophic malperfusion. Similar events have been reported following endovascular aortic repair (EVAR), in which acute dissection leads to abdominal endograft collapse and aortic occlusion.8, 9, 10, 11 Postendovascular TBADs have been successfully managed with further endovascular and hybrid techniques; however, treatment should be individualized on the basis of anatomy, disease pattern, and clinical presentation.⁹

Postendovascular TBADs carry substantial morbidity and mortality from dynamic branch vessel obstruction, endograft collapse, aneurysm rupture, and visceral or lower-extremity malperfusion.7, 8, 9 Unlike uncomplicated spontaneous TBAD, dissections occurring after EVAR may compromise the integrity and function of the implanted endograft.7, 8, 9 These cases should prompt an urgent evaluation for evidence of malperfusion, endoleak, aneurysm expansion, or graft instability, which constitute clear indications for endovascular or open intervention.¹²

The etiology of postendovascular stent graft placement dissection is often multifactorial. Anatomical risk factors include severe aortic angulation,¹¹ a fragile or ulcerated aortic wall, and heavy atherosclerotic burden near the proximal landing zone.¹³ Technical and device-specific factors include excessive graft oversizing, aggressive wire or catheter manipulation, and anchoring stent barbs,¹³ which may directly injure the aortic intima. Although described primarily after EVAR, these mechanisms likely extend to TAMBE through similar device-aorta interactions.

Our patient’s severely diseased aorta, evidenced by her ruptured TAAA, may have been especially susceptible to intimal injury and dissection propagation. Endograft collapse resulted in near-complete cessation of distal perfusion, causing rapid hemodynamic instability and multiorgan ischemia. Hemorrhage from disruption of the right iliofemoral bypass likely further exacerbated her hemodynamic instability. An alternative index strategy would have been treatment of a longer thoracic aortic segment to cover potentially vulnerable native aorta. However, greater aortic coverage carries an increased risk of spinal cord ischemia, requiring a careful balance between aortic protection and neurologic risk.

The dissection appeared more consistent with a delayed metachronous proximal dissection than an unrecognized iatrogenic dissection from the index procedure. CTA approximately 12 hours before deterioration demonstrated no dissection, whereas repeat imaging after symptom onset demonstrated a new dissection originating near the left subclavian artery, proximal to the TAMBE. Although device sizing and procedural manipulation remain potential contributors to aortic wall injury, the interval imaging and proximal origin favor a newly developed dissection rather than one directly induced during TAMBE deployment. Despite successful endovascular salvage and TAMBE re-expansion, the severity and duration of malperfusion likely exceeded the patient’s physiologic capacity for recovery.

Conclusions

We describe a rare acute TBAD occurring 4 days after TAMBE repair of a ruptured TAAA, resulting in complete TAMBE collapse and severe malperfusion. This case highlights the vulnerability of recently treated aortas to additional injury and importance of prompt recognition of malperfusion. Awareness of anatomical, technical, and device-related risk factors is critical when performing and monitoring TAMBE procedures.

Funding

No sponsors were used in the creation of this study.

Declaration of generative AI and AI-assisted technologies in the writing process

During the preparation of this work, the authors used ChatGPT (OpenAI) to assist with language refinement. After using this tool, the authors reviewed and edited the content and take full responsibility for its accuracy and integrity.

Disclosures

M.J.C. serves as a consultant for Endologix. S.J.M. reports no conflicts of interest.