Inherent risks of stenting include restenosis and thrombosis. Recently, stent fractures have been recognized as a complication that may result in thrombosis, perforation, restenosis, and migration of the stent resulting in morbidity and mortality. Stent fractures were originally seen in the superficial femoral arteries but have since then been reported in almost all vascular sites including the coronary, renal, carotid, iliac, and femoropopliteal arteries. Fractures are the result of the complex interplay between stent manufacturing, the stented segment, pulsatile and nonpulsatile biomechanical forces, and plaque morphology at a particular vascular site. The presentation of a patient with a fracture is highly variable, ranging from asymptomatic in nature, detected on routine screening without any sequelae, to sudden cardiac death related to a thrombosed coronary artery. Despite being recognized as an important complication, consensus on routine surveillance and diagnostic methods to detect fractures continues to be lacking. Fortunately, most cases are relatively benign and can be managed conservatively if detected. In the setting of recurrent symptoms, further intervention is usually sought. In review of the literature most cases are managed with placement of a stent over the fractured area, the stent-in-stent technique, but several other alternatives may be available. As the knowledge of the variables that make stents prone to fracture are identified, better technologies and techniques can be employed to minimize the risk of this complication. This article reviews the available literature on stent fractures and complications using data found on PubMed, MEDLINE, the Manufacturer and User Facility Device Experience (MAUDE) database, and the Cochrane databases.

PSA of 0.3 ng/mL. Pre-operatively, 32% of men underwent a bone scan; this decreased slightly to 22% post-treatment. CT use was more common than bone scan both before and after treatment, while MRI was the least common. The majority (63%) of bone scans was obtained in men who did not receive adjuvant or salvage ADT at a median PSA 0.13 ng/mL (Figure). Median PSA at time of post prostatectomy bone scan was 0.24 ng/mL. On multivariable modeling, increased bone scan use was associated with D'Amico risk category (OR 1.3, 95% CI [1.2-1.4]) and receipt of adjuvant or salvage treatment (OR 3.1, 95% CI [2.9-3.3]), but not with pre-treatment PSA (OR 1.0, 95% CI [1.0-1.0]) or comorbidity (OR 1.1, 95% CI [0.9-1.2]).CONCLUSIONS: We found a substantial rate of bone scan utilization after radical prostatectomy, comparable to the pre-operative setting. The majority was performed for PSA <1ng/mL where likelihood of a positive test is miniscule. More judicious use of imaging seems warranted in this population.