Chronic mesenteric ischemia (CMI) is a relatively uncommon disorder, accounting for <1 per 100,000 hospital admissions in the United States. Prophylactic revascularization is not recommended in patients with either renal or mesenteric artery disease. Treatment is indicated in select patients who present with symptoms of chronic mesenteric ischemia, such as intestinal angina, weight loss, and fear of eating. This occurs because of the after-meal pain associated with the condition. The combination of angioplasty and stenting has become the first line of treatment and is associated with lower mortality and morbidity compared with open surgical reconstruction. Open surgical reconstruction is currently relegated to patients who are not candidates or fail endovascular therapy and those with recalcitrant, recurrent in-stent stenosis, or occlusion. The aim of this chapter is to summarize the most common intraprocedural and postoperative complications of mesenteric angioplasty and stenting for mesenteric and renal artery disease.
Mesenteric Angioplasty and Stenting
Selection of open versus endovascular approach is based on careful review of preprocedure computed tomography angiography and clinical risk. The superior mesenteric artery (SMA) is the primary target for revascularization and, as such, the anatomy of the SMA is the most important determinant of choice of therapy. The ideal lesion for angioplasty and stenting is a short, focal stenosis or occlusion with minimal to moderate calcification or thrombus, but interventions can be indicated in patients with more complex lesions. Celiac axis angioplasty and stenting carries a higher risk of restenosis and should not be performed if there is active compression by the median arcuate ligament, unless this has been surgically released. Intraprocedural complications may occur more frequently with severely calcified lesions and occlusions.
Despite the minimally invasive approach, mesenteric angioplasty and stent placement carry a risk of significant morbidity. The rate of intraoperative complications is poorly reported in the literature. Our group reported intraoperative complications in 18% of the patients , including residual stenosis in 9%, stent dislodgement or dissection in 5% each, and vessel occlusion, perforation, or mesenteric hematoma in <1%–2%. Distal embolization occurs in 8% of patients treated by SMA stenting without embolic protection, with higher rates among patients with subacute symptoms, occlusion, long lesions (>30 mm), and severe calcification. Finally, access-related complications range between 3% and 16%.
Brachial approach offers excellent access in patients with acute angles at the vessel origin, occlusions, or long lesions. Nevertheless, brachial punctures are more prone to access-related complications, including potentially disabling neuropraxia of the median nerve from developing hematoma.
Branch Perforation and Mesenteric Hematoma
Branch perforations may result from inadvertent catheter manipulations or excessive guidewire advancement into small branches. Therefore, the guidewire should ideally be placed in the main trunk of the SMA and should be visualized at all times ( Fig. 30.1 ).
Dissections and Thrombosis
Problems such as dissections ( Fig. 30.2 ) may also occur with small or larger profile devices. Excessive catheter and guidewire manipulation, fragile vessel wall or excessive dilatation, or oversizing of the stent can all cause dissection. Dissections occur more frequently adjacent to the distal edge of the stent, but also distally or within side branches. It is important to maintain guidewire access, which facilitates management. If the origin and extension of dissection is unclear, intravascular ultrasound helps identify the entry and end-point. Treatment can be done by distal extension using self-expandable stent ( Fig. 30.2 ), avoiding dilatation. If guidewire access has been lost, management can be difficult. If the dissection is flow-limiting, regaining access to the true lumen can be attempted and then stenting can be continued. However, if the main trunk is occluded and guidewire access cannot be achieved, open surgical revision is necessary ( Fig. 30.3 ). In these cases, proximal control can be obtained by balloon inflation, the dissection flap is excised and the arteriotomy is closed over a patch ( Fig. 30.3 ). Less frequently, bypass may be necessary.
Stent Dislodgement, Fracture, and Compression
The incidence of stent dislodgement has been reported up to 8% in the past with hand-mounted stents but is now rare; dislodgement can also be caused by incorrect measurement of the target diameter and stent downsizing. This complication can occur with covered stents (stent slippage) or in patients with recalcitrant lesions that are prone to “watermelon seed” the stent ( Fig. 30.4 ) during deployment. It is critical to maintain guidewire access. The stent can be locked with a balloon and relocated into a normal arterial segment within the mesenteric or iliac arteries. Finally, the SMA lesion can be restented. If access has been lost, the stent can be compressed against the arterial by placement of a second stent.
Stent fracture is an uncommon cause of recurrent stenosis or occlusion ( Fig. 30.5 ); stent fractures have been well documented in other areas and are more prevalent in arteries that cross flexion points, such as the popliteal artery. Flow-limiting stent fractures can often be addressed endovascularly.
Stent compression or in-folding can be seen in patients treated by fenestrated endografts, or when the delivery system of the aortic device compresses the leaflets of a balloon expandable stent ( Figs. 30.6 and 30.7 ). Reballooning the stent or overlap address the issue.