Splenic Artery Embolization: Tips, Tricks, and Current Standards of Practice.

Objective To study the use of contrast-enhanced ultrasound in diagnosing splenic arterial steal syndrome (SASS) after liver transplantation, and to compare the curative effect, safety and follow-up results of the different embolization methods in the treatment of SASS after liver transplantation. Methods From January 2005 to December 2017, 41 patients after liver transplantation in our hospital developed splenic artery steal syndrome and were treated with splenic arterial embolization. All these patients underwent ultrasound, and in 19 patients contrast-enhanced ultrasonography was also done to detect the presence of splenic artery steal. The findings were confirmed by angiography. These patients then underwent splenic arterial embolization. In 32 patients coil embolization was done (group A) and in 9 patients embolization was assisted with Amplatzer occluders (group B). Results In all the 41 patients with SASS, angiography after splenic artery embolization showed the second and third order arterial branches in the liver increased in number and in diameter with good blood flow compared with those before treatment. The postoperative blood flow and pattern on ultrasound returned to normal. In group A, 12 patients (12/32, 37.5%) developed splenic infarction, including 11 patients with partial splenic infarction, and 1 patient developed a splenic abscess after complete splenic infarction. In group B, two patients developed partial splenic infarction (2/9, 22.2%). All the patients with splenic infarct had no clinical symptoms. No treatment was required except for the patient who developed splenic abscess after complete splenic infarction. The patient recovered well after treatment with antibiotics and splenic abscess drainage. There was no other complications. Conclusions Contrast-enhanced ultrasound provided early diagnosis of splenic artery steal after liver transplantation. Interventional splenic artery embolization was safe and effective to treat splenic arterial steal syndrome after liver transplantation. Coil embolization assisted with Amplatzer occluders was better than the traditional coil embolization with more accurate embolization site and fewer complications. Key words: Liver transplantation; Splenic artery steal syndrome; Contrast-enhanced ultrasound; Interventional treatment; Splenic arterial embolization

ObjectiveThis retrospective study reports our experience using splenic arterial particle embolization and coil embolization for the treatment of sinistral portal hypertension (SPH) in patients with and without gastric bleeding.MethodsFrom August 2009 to May 2012, 14 patients with SPH due to pancreatic disease were diagnosed and treated with splenic arterial embolization. Two different embolization strategies were applied; either combined distal splenic bed particle embolization and proximal splenic artery coil embolization in the same procedure for acute hemorrhage (1-step) or interval staged distal embolization and proximal embolization in the stable patient (2-step). The patients were clinically followed.ResultsIn 14 patients, splenic arterial embolization was successful. The one-step method was performed in three patients suffering from massive gastric bleeding, and the bleeding was relieved after embolization. The two-step method was used in 11 patients, who had chronic gastric variceal bleeding or gastric varices only. The gastric varices disappeared in the enhanced CT scan and the patients had no gastric bleeding during follow-up.ConclusionsSplenic arterial embolization, particularly the two-step method, proved feasible and effective for the treatment of SPH patients with gastric varices or gastric variceal bleeding.

Various minimally invasive, surgical, and laparoscopic interventions are performed for treatment and management of splenic artery steal syndrome in liver transplant and cirrhotic patients. Common approaches include splenic artery banding, ligation, stenting, and embolization to increase hepatic arterial flow. Splenic artery embolization has undergone further development to facilitate timely diagnosis, increase efficacy, decrease adverse outcomes, and improve patient selection. We review the current diagnostic modalities and technical advancements of splenic artery embolization to improve hepatic arterial perfusion in patients with splenic artery steal syndrome.

Educational Exhibit Abstract No. 373 - Splenic artery embolization as treatment for splenic artery steal syndrome after liver transplantation

Background: Management of blunt spleen injuries has evolved from mandatory splenectomy to non-operative man-agement (NOM) allowing for splenic salvage, Splenic artery embolization (SAE) has been shown to be an effective treat-ment for hemodynamically stable patients with high-grade blunt splenic injury. However, there are no local estimates of how much treatment costs. Aim of Study: The aim of this study was to evaluate the cost of providing SAE to patients in the setting of blunt abdominal trauma with splenic injury and to determine if the costs of an added, preventative procedure (SAE) early in management of blunt splenic injury would be offset by added utility by avoiding splenectomy. Patients and Methods: This study was a retrospective cohort study from a tertiary institution (50 patients in King Khaled Hospital Trauma Center, Hail, KSA and 9 patients in Al Hussein University Hospital, Cairo, Egypt). A total of 59 patients were treated with embolization in this period for blunt trauma, and however 39 cases were excluded given the presence of multiple concomitant injuries. Isolated splenic injury treated with SAE were identified in 20 patients and included for final analysis. Of these 10 patients, none required subsequent splenectomy following SAE. Results: The mean total angiography costs were 1837.94± 405.368 $, the costs of post-procedure management of patients including all hospital costs prior to discharge with associated length of stay. Conclusion: Splenic embolization is a low-cost procedure for management of blunt splenic injury. The cost to provide SAE at our center was much lower than previously modelled data from overseas studies. Further research is advised to directly compare the cost of SAE and splenectomy in other countries.

04:12 PM Abstract No. 256 Splenic embolization for splenic arterial steal syndrome

Splenic artery steal syndrome (SASS) is a cause of graft hypoperfusion leading to the development of biliary tract complications, graft failure, and in some cases to retransplantation. Its management is still controversial since there is no universal consensus about its prophylaxis and consequently treatment. We present a case of SASS that occurred 48 hours after orthotopic liver transplantation (OLTx) in a 56-year-old male patient with alcoholic cirrhosis and severe portal hypertension, and who was successfully treated by splenic artery embolization. A literature search was performed using the PubMed database, and a total of 22 studies including 4,789 patients who underwent OLTx were relevant to this review. A prophylactic treatment was performed in 260 cases (6.2%) through splenic artery ligation in 98 patients (37.7%) and splenic artery banding in 102 (39.2%). In the patients who did not receive prophylaxis, SASS occurred after OLTx in 266 (5.5%) and was mainly treated by splenic artery embolization (78.9%). Splenic artery ligation and splenectomies were performed, respectively, in 6 and 20 patients (2.3% and 7.5%). The higher rate of complications registered was represented by biliary tract complications (9.7% in patients who received prophylaxis and 11.6% in patients who developed SASS), portal vein thrombosis (respectively, 7.3% and 6.9%), splenectomy (4.8% and 20.9%), and death from sepsis (4.8% and 30.2%). Whenever possible, prevention is the best way to approach SASS, considering all the potential damage arising from an arterial graft hypoperfusion. Where clinical conditions do not permit prophylaxis, an accurate risk assessment and postoperative monitoring are mandatory.

No. 117: Non-Operative Management of Blunt Spleen Trauma BST

3:27 PM Abstract No. 159 Endovascular treatment of splenic artery steal in pediatric liver transplant patients

Splenic Artery Embolization for Splenic Artery Steal Syndrome After Living Donor Liver Transplantation: A Case Report

Introduction: Liver transplantation is a definitive treatment for patients with end-stage liver disease and liver neoplasms. Vascular complications remain an important cause of morbidity and mortality in these patients. Splenic artery embolization is an alternative to improve the clinical and hemodynamic conditions of such patients. Methods: The research was conducted in October 2025 on the PubMed and Literatura Latino-Americana e do Caribe em Ciências da Saúde (LILACS) platforms, based on the descriptors: “Splenic artery,” “Embolization, therapeutic,” and “Liver Transplantation”; 15 articles were selected based on eligibility criteria. Results: Seven case reports and eight cohort studies, or retrospective case series were found, reflecting the current level of evidence on the application of splenic artery embolization in patients undergoing liver transplantation. Analysis of the articles allowed the data to be synthesized into three central thematic categories: indications for the procedure, techniques used, and clinical outcomes, including complications. Conclusion: Splenic artery embolization is a minimally invasive, safe, and effective therapeutic strategy for the management of selected complications after liver transplantation, such as splenic artery steal syndrome, refractory ascites, hydrothorax, and hypersplenism

The use of splenic artery embolization to maintain adequate hepatic arterial inflow after hepatic artery thrombosis in a split liver transplant recipient

Effect of Splenic Artery Embolization for Splenic Artery Steal Syndrome in Liver Transplant Recipients: Estimation at Computed Tomography Based on Changes in Caliber of Related Arteries

INTRODUCTION: The following case series analyzes patients that received a splenic artery embolization (SAE) following an orthotopic liver transplant (OLT). SAE following OLT is performed to correct splenic artery steal syndrome (SASS), where the splenic artery experiences an increase in blood flow at the expense of the hepatic artery. Normal hepatic artery blood flow is needed to ensure a successful transplant. CASE DESCRIPTION/METHODS: Four patients presented for OLT; three with living donors and one standard donor. The indications for OLT were alcoholic cirrhosis, cryptogenic cirrhosis with pancytopenia, NASH, and primary sclerosing cholangitis. The average MELD scores were 18 [11-26]. Two patients had previous history of CT diagnosed thrombosis in the right hepatic and portal veins. One patient had an intraoperative portal vein thrombectomy. Three patients had good size matched anastomotic connections for the hepatic arteries, while one patient’s recipient arteries were smaller than the donors. Upon post-transplant ultrasound, each patient had an increased hepatic artery resistivity index (RI) in the proximal, middle and distal parts of the artery. This indicates decreased blood flow to the liver as part of SASS. The relevant laboratory values immediately preceding SAE showed an average AST of 171.5 [45-301], ALT of 378.25 [249-458], alkaline phosphate of 176.75 [46-368], total bilirubin of 3.9 [1.9-6.6], direct bilirubin of 2.6 [1.4-4.4], and creatinine of 0.9 [0.73-1.05]. To correct this, all patients received an SAE on average 96.5 hours [20-213] following OLT to re-establish adequate blood flow to the liver. This is confirmed through a follow up ultrasound, which reveals decreased hepatic artery RI in all patients. The patient with primary sclerosing cholangitis received a re-do hepatojujenoctomy, however the other three patients did not have any strictures based on MRCP. None of the patients had graft rejection and are currently 6 months to 1 year post-transplant. DISCUSSION: SAE following OLT serves as a viable option for treating SASS. This procedure re-stored proper blood flow through the hepatic artery to the transplanted liver, which prevents graft rejection.

Splenic artery embolization (SAE) improves hepatic artery (HA) flow in liver transplant (OLT) recipients with so-called splenic artery steal syndrome. We propose that SAE actually improves HA flow by reducing the HA buffer response (HABR). Patient 1: On postoperative day (POD) 1, Doppler ultrasonography (US) showed patent vasculature with HA resistive index (RI) of 0.8. On POD 4, aminotransferases rose dramatically; his RI was 1.0 with no diastolic flow. Octreotide was begun, but on POD 5 US showed reverse diastolic HA flow with no signal in distal HA branches. After SAE, US showed markedly improved flow, RI was 0.6, diastolic flow in the main artery, and complete visualization of all distal branches. By POD 6, liver function had normalized. RI in the main HA is 0.76 at 2 months postsurgery. Patient 2: On POD 1, RI was 1.0. US showed worsening intrahepatic signal, with no signal in the intrahepatic branches and reversed diastolic flow despite good graft function. On POD 7, SAE improved the intrahepatic waveform and RI (from 1.0 to 0.72). Patient 3: Intraoperative reverse diastolic arterial flow persisted on PODs 1, 2, and 3, with progressive loss of US signal in peripheral HA branches. SAE on POD 4 improved the RI (0.86) and peripheral arterial branch signals. Patient 4: US on POD 1 showed good HA flow with a normal RI (0.7). A sudden waveform change on POD 2 with increasing RI (0.83) prompted SAE, after which the wave form normalized, with reconstitution of a normal diastolic flow (RI 0.68). In conclusion, these reports confirm the usefulness of SAE for poor HA flow but suggest that inflow steal was not the problem. Rather than producing an increase in arterial inflow, SAE worked by reducing portal flow and HABR, thereby reducing end-organ outflow resistance. Evidence of this effect is the marked reduction of the RI after the SAE to 0.6, 0.72, 0.86, and 0.68, in patients 1-4, respectively. SAE reduces excessive portal vein flow and thereby ameliorates an overactive HABR that can cause graft dysfunction and ultimately HA thrombosis.