Abstract
Splenic Artery Aneurysm (SAA) is the third most common abdominal aneurysm and accounts for 60% of all visceral aneurysms. The incidence of SAA in liver cirrhosis is increased and has been reported to be between 7-17%. The pathogenesis of SAA in the liver transplant (LT) population is poorly understood but is thought to have an increased risk of rupture following surgery. A large national database was used to identify whether SAA development following surgery had a worse disposition compared to the general population and if certain etiologies of liver disease carry a higher risk of development of SAA. The Nationwide Inpatient Sample (NIS) database was employed to examine all adult patients diagnosed with SAA from 2005-2014. The data was then further divided into those who also underwent liver transplantation . The rates of surgical and endovascular intervention, complication rates, mortality, hospital length of stay and cost were then compared to the general population as well as between transplant recipients who did and did not undergo repair of their SAA. The incidence of SAA with respect to liver disease was also examined. A total of 27,848 subjects with a diagnosis of splenic artery aneurysm were included. 182 (0.65%) were identified as also having underwent LT. The cohort was mostly white (81.8%, p=0.004) and female (F=70.9%, M=29.1%) with a mean age of 64. LT recipients tended to be younger on average (mean 52.7 vs. 64.4, p< 0.001) and were more likely to be male (M=53.3% vs. F=46.7%, p<0.001). There were higher rates of Chronic Hepatitis C (8.2% vs 3.1%, p<0.001) and Alpha-1 antitrypsin deficiency (5.5% vs 0.01%, p=0.001) in the LT group. SAA repair versus no repair after LT showed similar complication rates but mortality was significantly higher when SAA was not repaired (9.4% vs. 0% p=0.006). LT patients with concomitant SAA were younger and more likely male when compared to all patient’s with SAA, suggesting a difference in aneurysm pathology in this unique population. Also, a higher mortality rate was observed in the LT population who did not undergo repair of their SAA, reaffirming the current consensus that preemptive or simultaneous repair of SAA should be performed. HCV and alpha-1 antitrypsin disease were more likely to be associated with SAA in the transplant population, though not all transplant patients in our data set included a diagnosis for their liver failure, and thus an association of risk could not be established.
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