Endovascular stenting of a chronic ruptured type B thoracic aortic dissection, a second chance: a case report

Abstract

Medical therapy has been the mainstay of treatment for uncomplicated Stanford type B aortic dissection for many years 1. However, more recently, endovascular aortic stenting of dissecting thoracic aneurysm has also become a well recognised treatment option 2. Ongoing studies are currently investigating the long-term safety and efficacy of this technique. The complications of thoracic aortic stenting are also well recognised and graft perforation following endovascular stenting is a known entity 3,4. The best treatment modality for the treatment of these complications remains controversial. We report the first case in the English literature of an endovascular repair of a previously stented, ruptured chronic Stanford type B aortic dissection. Our report highlights both the need for awareness of the late complications of endovascular thoracic aortic repair as well as the feasibility of re-stenting in this difficult scenario.

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Case presentation
An 82-year-old man, who had previously undergone the first successful endovascular repair of a ruptured chronic type B dissection, presented to us again five years after his first procedure 5.

His original diagnosis of a Stanford type B aortic dissection had been made in 1994. He was initially managed medically with antihypertensive medication alone, however seven years later, he suffered sudden collapse and chest pain. A ruptured false lumen thoracic aneurysm was diagnosed by spiral computed tomographic angiography (SCTA). The aortic dissection extended distally from the left subclavian artery to the left common iliac artery. The coeliac axis appeared to have a common origin from both the true and false lumens, whereas the left renal and inferior mesenteric arteries originated from the false lumen.

He was deemed to be unsuitable for open surgery due to significant medical co-morbidity, including atrial fibrillation, ischaemic heart disease and chronic obstructive airways disease so therefore endovascular treatment of his condition was undertaken 5. The challenge was to exclude the rupture while maintaining perfusion of his gut and kidneys. This was undertaken using a total of four Gore Excluder endografts (WL Gore & Associates, Flagstaff, Ariz.). This has been previously described 5.

After a stormy post-operative course, he was discharged home with regular clinical and radiological follow-up, but after two years he declined to attend further review.

Four years after his original procedure, he re-presented to a nearby hospital with a one-month history of increasing chest and back pain associated with shortness of breath. Chest X-Ray showed left lower zone shadowing and he was treated for pneumonia. His respiratory symptoms improved, but his chest and back pain continued. Further laboratory investigations revealed that he was hypercalcaemic with a corrected calcium of 2.77 mmol/l. SCTA revealed a haematoma in the left mid-thoracic cavity associated with vertebral body erosion. The hypercalcaemia was attributed to this bony erosion and it was postulated that this had been caused by the pulsatile haematoma giving rise to his symptoms of chest & back pain. The patient was transferred to the vascular unit at our institution. Three dimensional SCTA reconstruction revealed a probable defect at the junction between the middle two of the four stents (adjacent to the haematoma), which appeared to have only 5 mm of overlap. Above the level of the haematoma, an apparent perforation of the second thoracic stent was seen. The haematoma was thought to be originating from either or both of these structural defects. These defects therefore constituted a type III endoleak Figure 1, 2/>/>/>/>/>/>/>/>/>

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References
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