Splenic Artery Steal Syndrome Research Articles

Modulation of graft vascular inflow guided by flowmetry and manometry in liver transplantation

Survival of the partial graft after living donor liver transplantation owes much to its tremendous regenerative ability. With excellent venous outflow capacity, a graft within a wide range of graft-to-standard-liver-volume ratios can cope with portal hypertension that is common in liver transplant recipients. However, when the ratio range is exceeded, modulation of graft vascular inflow becomes necessary for graft survival. The interplay between graft-to-standard-liver-volume ratio and portal pressure, in the presence of portosystemic shunt or otherwise, requires individualized modulation of graft portal and arterial inflows. Boosting of portal inflow by shunt ligation can be guided by transonic flowmetry, whereas muting of portal inflow by splenic artery ligation can be monitored by portal electronic manometry. We describe four cases to illustrate the above. One patient had hepatic artery thrombosis resulting from splenic artery steal syndrome which was the sequela of small-for-size syndrome. Emergency splenic artery ligation and re-anastomosis of the hepatic artery successfully muted the portal inflow and boosted the hepatic arterial inflow. Another patient with portal vein thrombosis underwent thrombendvenectomy. Portal inflow was boosted with ligation of portosystemic shunt, which is often present in these patients with portal hypertension. The coexistence of splenic aneurysm and splenorenal shunt required ligation of both in the third patient. The fourth patient, with portal pressure and flow monitoring, avoided ligation of a coronary vein which became a main portal inflow after portal thrombendvenectomy. Management of graft inflow modulation guided selectively by transonic flowmetry or portal manometry was described.

Case Report of Splenic Artery Steal Syndrome: Demonstration of Portal Hyperflow Mechanism by Anatomic Variant of the Splenic Artery and Correlation With Doppler Rates

We report the case of a liver transplant recipient who developed a “splenic artery steal syndrome” (SASS) successfully treated by partial splenic embolization (PSE). Interestingly, because the patient presented an anatomic variant of the splenic artery (SA) originating from the superior mesenteric artery (SMA), improvement was observed in hepatic artery (HA) flow following PSE that could only be explained by decreased portal perfusion and not by the derivation from the SA.

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

Purpose To estimate the effect of splenic artery embolization (SAE) on blood flow in orthotopic liver transplantation (OLT) recipients with splenic artery steal syndrome (SASS) based on changes in caliber of related arteries upon serial computed tomography (CT) scans. Methods Between 2004 and 2007, nine OLT recipients with SASS underwent SAE. They had CT scans before and after SAE: short-, mid-, and long-term, ie, approximately 1 week, 1 month, and 1 year, respectively. The diameters of the celiac axis (CA), common hepatic artery (CHA), and splenic artery (SA) were measured with arterial phase of each CT scan and the ratios of SA to CHA diameter (SA/CHA) calculated to analyze their changes during the follow-up period. Results The diameters of celiac axis, CHA, and SA and SA/CHA changed most rapidly during the short-term period. The CHA diameter significantly increased short-term post-SAE by CT and slightly decreased thereafter. However, the mid-term and long-term post-SAE CT values were still significantly greater than those on the pre-SAE CT. The SA diameter steadily decreased throughout the follow-up. The SA/CHA decreased until the mid-term. The SA diameter and SA/CHA were significantly smaller upon mid-term and long-term post-SAE CT compared with those at pre-SAE CT. Conclusions The effect of SAE to improve hepatic arterial flow in OLT recipients with SASS might be expected for at least approximately one year. The effect maximally occurred during the short-term after SAE on the basis of changes in the caliber of related arteries upon CT.

彩色多普勒超声在动态监测原位肝移植术后脾动脉盗血综合征中的应用

肝移植术后脾动脉盗血综合征(splenic artery steal syndrome,SASS)是肝移植术后发生的粗大的脾动脉和肝动脉争夺血流,从而引起肝动脉灌注不良和肝组织缺氧,导致肝和胆管缺血性损伤为特征的综合征.肝移植术后SASS发生率较低,但可导致严重后果,如得不到及时处理,患者会因移植物功能丧失而需再次肝移植[1]。

Utility of the Amplatzer Vascular Plug in Splenic Artery Embolization: A Comparison Study with Conventional Coil Technique

To retrospectively evaluate the role of the Amplatzer Vascular Plug (AVP) in proximal splenic artery embolization (SAE) compared with coils. Forty patients had proximal SAE performed with AVP(s) or coils as the primary embolic agent for splenic artery steal syndrome (n=23), trauma (n=5), portal hypertension (n=5), bleeding due to pancreatic pathology (n=4), and pre-splenectomy (n=3). Comparisons were made of occlusion and procedure time, cost, and radiation dose. Eighteen proximal SAE procedures were successfully performed with AVP. Twenty-two procedures were performed with coils, including one failed AVP attempt, which was completed with coils. Precise deployment without migration was achieved in all 18 AVP cases. Seven of 22 (31.8%) coil procedures had distal migration without consequence. There was no statistically significant difference in mean occlusion time (24.4 min for AVP vs. 31.5 min for coils, P=0.13), procedure time (43.7 min for AVP vs. 53.8 min for coils, P=0.16), or cost ($1474.13 for AVP vs. $1722.51 for coils, P=0.69). There was significant difference in radiation dose (842 mGy for AVP vs. 1,309 mGy for coils, P=0.04). Fourteen of the 18 (78%) AVP devices required additional embolic material. AVP with additional embolic agents is a useful alternative for proximal SAE because of precise deployment, resistance to migration, and radiation reduction. AVP use may be limited by vessel tortuosity. The occlusion time, procedure time, and cost were reduced but this was not statistically significant due to the need for additional embolic material.

Multidetector computed tomography for preoperative assessment of hepatic vasculature and prediction of splenic artery steal syndrome in patients with liver cirrhosis before transplantation

The purpose of this study was to evaluate the accuracy of MDCT for preoperative assessment of hepatic vascular anatomy and the identification of liver-transplantation (OLT) patients at risk of developing subsequent splenic artery steal syndrome (SASS). A total of 145 patients with liver cirrhosis who had undergone OLT and had pre-operative three-phase MDCT (4- to 64-rows) within 100 days before OLT were enrolled retrospectively. MDCT and 3Ds were reviewed by two independent blinded observers (O1/O2). Pre-operative imaging findings were correlated with intra-operative results; findings indicative for SASS were correlated with clinical data and DSA. Among all 145 patients, 16 patients (11%) showed accessory hepatic arteries (accuracy O1/O2, 97%; with 3Ds, 100%); 32 (22%) patients had replaced hepatic arteries (accuracy O1, 97%; O2, 95%; with 3Ds, 100%; kappa = 0.87 and 0.89, P < 0.001). Among 119 patients, 12 patients developed SASS after OLT. The logistic regression model revealed the spleen volume (P = 0.0105) as a predictive factor of SASS. With spleen volumes >or=829 ml, an accuracy of 75% for prediction of SASS was obtained. MDCT with three-dimensional post-processing (3Ds) was highly accurate for pre-operative hepatic vessel evaluation in patients before OLT. In addition, spleen volume was a predictive factor for developing SASS after OLT.

Splenic Artery Steal Syndrome After Liver Transplantation: An Alternative Technique of Embolization

Arterial steal syndrome after orthotopic liver transplantation (OLT) is characterized by arterial hypoperfusion of the graft, which is caused by a shift in blood flow into the splenic or gastroduodenal arteries. It causes hepatic hypoperfusion with attendant clinical manifestations of elevated liver function enzymes, allograft dysfunction, and cholestasis. Left untreated, the condition has a significant potential risk for postoperative morbidity and graft loss. Herein we have reported the case of a 68-year-old woman who developed splenic artery steal syndrome (SASS) after deceased donor liver transplantation. She was diagnosed by duplex Doppler ultrasonography and celiac trunk angiography, and subsequently treated with splenic artery embolization.

Role of Imaging in the Management of Splenic Artery Steal Syndrome

The purpose of this study is to discuss the etiology and role of imaging in the management of splenic artery steal syndrome (SASS) following orthotropic liver transplantation (OLT). Hepatic arterial thrombosis and stenosis have been the most commonly recognized arterial complications following OLT. Splenic artery steal syndrome is a recently described entity in the transplant literature and thought to be an under-recognized cause of graft ischemia. It is characterized by hepatic arterial hypoperfusion accompanied by splenic arterial and portal venous hyperperfusion and leads to various vascular and biliary graft complications. Because the clinical manifestations of SASS are so non-specific, imaging plays a key role in the diagnosis of this condition. This article discusses the role of imaging in the management of this potentially reversible cause of graft ischemia. Awareness of the imaging features and having a high index of suspicion are essential for the early diagnosis and prompt management of this condition.

“Splenic artery steal syndrome” is a misnomer: The cause is portal hyperperfusion, not arterial siphon

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.

Splenic Artery Steal Syndrome in Living Donor Liver Transplantation: A Case Report

Splenic artery steal syndrome (SASS) has only recently been recognized as a potential threat to transplanted livers. We report a case of SASS with progressive liver dysfunction that developed after living donor right lobe liver transplantation. SASS suspected by serial pre- and postoperative computed tomographic (CT) scans was diagnosed by celiac trunk angiography. It was successfully salvaged by splenic artery embolization. In this case, serial examinations of CT scans were useful to diagnose SASS. This case showed that portal hyperperfusion injury is a cause of liver graft dysfunction in SASS. The splenic artery embolization technique is a safe procedure that can be applied to treat such injury.

Splenic Embolization in Liver Transplant Recipients: Early Outcomes

Clinical improvement has been reported following splenic embolization for a wide variety of indications. Improvement following splenic embolization has been described in cirrhotic patients awaiting hepatic transplantation who are not candidates for surgical splenectomy. Occasionally, patients who have undergone hepatic transplantation have conditions that may also benefit from nonsurgical intervention with splenic embolization. Indications include persistent hypersplenism and pancytopenia precluding optimal treatment with antiviral therapy or chemotherapy, risk for persistent gastroesophageal variceal hemorrhage, and splenic artery steal syndrome attenuating hepatic arterial perfusion. Limited data is available on the outcome of splenic embolization in liver transplant recipients. We present the early outcomes of liver transplant recipients who were treated with splenic embolization. A retrospective chart review of all liver transplant recipients who underwent splenic embolization between 1997 and 2006 was performed, under minimal-risk study approval by the institutional review board. Five liver transplant recipients received splenic embolization: 3 for persistent hypersplenism, 1 for increased risk of gastroesophageal variceal hemorrhage, and 1 for splenic artery steal syndrome. The patients with hypersplenism demonstrated hematologic improvement, the patient with gastroesophageal varices did not experience any hemorrhage on follow-up, and the patient with splenic artery steal experienced resolution of the steal phenomenon. Postembolization syndrome was observed but no splenic abscess or death occurred. Mean follow-up was 20.2 months. In conclusion, splenic embolization is a safe and effective nonsurgical alternative for a variety of indications in liver transplant recipients.

Multidetector Computed Tomographic Angiography Findings of Splenic Artery Steal Syndrome in Liver Transplantation

Aims Splenic artery steal syndrome, a common complication in liver transplantation, is diagnosed by conventional angiography showing an enlarged splenic artery and by dynamic findings. The aim of this study was to determine multidetector computed tomographic angiography (MDCTA) findings of splenic artery steal syndrome to develop diagnostic criteria. Materials and Methods Ten patients were diagnosed as displaying splenic artery steal syndrome among 198 liver transplant patients. The diagnosis was confirmed by celiac angiography. In eight of them, MDCTA was performed. Axial and coronal maximum-intensity projection images were obtained in arterial and portal phases. We measured the diameter of the celiac trunk and of the splenic, left gastric, common hepatic, superior mesenteric artery, and transplant hepatic arteries. We also measured the diameter of the proximal and the distal segments of the abdominal aorta, along with the size of the spleen, the ratio of the splenic artery to the common hepatic artery, the ratio of splenic artery to transplant hepatic artery, the diameter of portal vein and superior mesenteric vein. The control group consisted of liver transplant patients with normal liver enzyme levels. We performed Student t test for statistical examination. Results The diameter of the splenic artery ( P < .05), the size of the spleen ( P < .01), and the ratio of the splenic to the transplant hepatic arteries ( P < .05) was significant between the two groups. The diameter of the splenic artery was larger than 4 mm in all patients in the study group. Conclusions Conventional angiography was mandatory for the diagnosis of splenic artery steal syndrome. MDCTA is a noninvasive method. Some computed tomography criteria are important for early diagnosis and treatment.

Arterial Steal Syndrome After Orthotopic Liver Transplantation

Arterial steal syndrome after orthotopic liver transplantation (OLT) is characterized by arterial hypoperfusion of the graft, which is caused by a shift in blood flow into the splenic or gastroduodenal arteries. In this report, we present mechanisms by which this syndrome caused ischemia in our patients. Steal was suspected by elevated levels of liver enzymes and the results of Doppler ultrasonography and computed tomographic angiography; it was confirmed by celiac angiography. Patients with established hepatic arterial thrombosis before angiography were excluded from this study. Steal was treated by embolization with a coil or by placement of an endoluminal narrowing stent. Ten patients at our institution (seven men and three women; mean age, 24.7 ± 11 years; range, 6 to 40 years) exhibited biochemical evidence of liver ischemia and graft failure at 1 to 170 days after having undergone orthotopic liver transplantation. Nine of those patients had splenic steal, and one had both splenic and left gastric artery steal syndrome. None of the patients had gastroduodenal artery steal syndrome. The eight patients with splenic steal syndrome and the patient with both splenic and left gastric steal syndrome were treated by transcatheter occlusion with a coil. The remaining patient with splenic steal syndrome was treated with an endoluminal narrowing stent placement. All patients improved clinically within 24 hours after treatment, exhibiting significant changes in their biochemical and radiological parameters. Follow-up ranged from 1 to 22 months (mean, 6.7 ± 6.6 months). One patient died from sepsis 1 month after having undergone coil embolization. He had no vascular anomalies at the time of death. We conclude that steal is a significant problem after OLT. Embolization and stenting are minimally invasive and successful treatments for steal, usually resulting early clinical improvement.

Improved graft function in liver‐transplanted patients after partial splenic embolization: reversal of splenic artery steal syndrome?

To describe the functional effect of partial splenic embolization (PSE) in liver-transplanted (LT) patients with hypersplenism and hepatitis C virus (HCV) recurrence. From May 2002 to May 2005, five LT patients with persistent hypersplenism, viral recurrence and graft dysfunction underwent PSE prior to pegylated interferon/ribavirin (peg-IFN/RBV). The mean splenic size was 19.5 cm (16-21) and there was evidence of an enlarged splenic artery (10.7+/-1 mm). PSE produced a median splenic infarction of 90% and a significant reduction in the splenic artery diameter to 5.8+/-0.4 mm (p=0.04). PSE significantly improved hematologic parameters, bilirubin levels, prothrombin activity, international normalized ratio and the Model for End-stage Liver Disease (MELD) score despite high HCV-RNA (6.2 log10 IU/mL). It was demonstrated histologic amelioration of ischemic changes in all subjects. PSE allowed the safe use of full-dose peg-IFN plus RBV in all subjects. In HCV LT patients with chronic graft dysfunction and cholestasis the improvement in the liver function following PSE might be due to the reversal of an undiagnosed splenic artery steal syndrome related to chronic hypersplenism masked by HCV recurrence.

Splenic Arterial Interventions: Anatomy, Indications, Technical Considerations, and Potential Complications

Splenic arterial interventions are increasingly performed to treat various clinical conditions, including abdominal trauma, hypersplenism, splenic arterial aneurysm, portal hypertension, and splenic neoplasm. When clinically appropriate, these procedures may provide an alternative to open surgery. They may help to salvage splenic function in patients with posttraumatic injuries or hypersplenism and to improve hematologic parameters in those who otherwise would be unable to undergo high-dose chemotherapy or immunosuppressive therapy. Splenic arterial interventions also may be performed to exclude splenic artery aneurysms from the parent vessel lumen and prevent aneurysm rupture; to reduce portal pressure and prevent sequelae in patients with portal hypertension; to treat splenic artery steal syndrome and improve liver perfusion in liver transplant recipients; and to administer targeted treatment to areas of neoplastic disease in the splenic parenchyma. As the use of splenic arterial interventions increases in interventional radiology practice, clinicians must be familiar with the splenic vascular anatomy, the indications and contraindications for performing interventional procedures, the technical considerations involved, and the potential use of other interventional procedures, such as radiofrequency ablation, in combination with splenic arterial interventions. Familiarity with the complications that can result from these interventional procedures, including abscess formation and pancreatitis, also is important.

Comparison of Two Different Percutaneous Splenic Artery Interventions in the Treatment of Hypersplenism: Preliminary Report

Background Splenomegaly and hypersplenism occur in patients with chronic liver disease and liver transplant recipients. The traditional treatment for hypersplenism is surgical removal. Percutaneous interventional methods, such as partial splenic embolization, are alternatives to surgery for hypersplenism. This article gives preliminary findings for a new percutaneous technique in which a narrowed stent is placed in the splenic artery. Methods The study focused on 10 patients (eight males and two females) who were treated for hypersplenism. Partial splenic embolization was performed in six patients (age range, 1–43 years) who were waiting for liver transplantation, and narrowed stents were placed in four patients (age range, 12–47 years) who had undergone either orthotopic two patients) or heterotopic two patients) liver transplantation. For embolization, the splenic artery was catheterized and polyvinyl alcohol particles were infused to the distal branches, reducing blood flow in the spleen by 40% to 50%. In the other cases, a narrowed stent was deployed to the middle portion of the splenic artery. Results Hypersplenism was successfully treated in all 10 cases. Compared with partial splenic embolization, placement of narrowed stents was associated with lower frequencies of postintervention fever and pain, shorter hospital stay, and decreased need for antibiotics. In addition to treating hypersplenism, narrowed-stent placement also completely resolved splenic artery steal syndrome in the two patients (orthotopic liver transplant recipients) with this condition. Conclusion Percutaneous placement of a narrowed stent in the splenic artery is a promising new technique for treating hypersplenism and splenic arterial steal syndrome.

COMPARISON OF TWO DIFFERENT PERCUTANEOUS SPLENIC ARTERY INTERVENTIONS IN THE TREATMENT OF HYPERSPLENISM: PRELIMINARY REPORT

Abstract Background Splenomegaly and hypersplenism occur in patients with chronic liver disease and liver transplant recipients. The traditional treatment for hypersplenism is surgical removal. Percutaneous interventional methods, such as partial splenic embolization, are alternatives to surgery for hypersplenism. This article gives preliminary findings for a new percutaneous technique in which a narrowed stent is placed in the splenic artery. Methods The study focused on 10 patients (eight males and two females) who were treated for hypersplenism. Partial splenic embolization was performed in six patients (age range, 1–43 years) who were waiting for liver transplantation, and narrowed stents were placed in four patients (age range, 12–47 years) who had undergone either orthotopic two patients) or heterotopic two patients) liver transplantation. For embolization, the splenic artery was catheterized and polyvinyl alcohol particles were infused to the distal branches, reducing blood flow in the spleen by 40% to 50%. In the other cases, a narrowed stent was deployed to the middle portion of the splenic artery. Results Hypersplenism was successfully treated in all 10 cases. Compared with partial splenic embolization, placement of narrowed stents was associated with lower frequencies of postintervention fever and pain, shorter hospital stay, and decreased need for antibiotics. In addition to treating hypersplenism, narrowed-stent placement also completely resolved splenic artery steal syndrome in the two patients (orthotopic liver transplant recipients) with this condition. Conclusion Percutaneous placement of a narrowed stent in the splenic artery is a promising new technique for treating hypersplenism and splenic arterial steal syndrome.

Successful minimally invasive management of late portal vein thrombosis after splenectomy due to splenic artery steal syndrome following liver transplantation: a case report

Portal vein thrombosis (PVT) after liver transplantation (OLT), which occurs in 1% to 2.7% of cases, can compromise patient and graft survival. Percutaneous transhepatic portal vein angioplasty offers an option to treat PVT, diminishing surgically related morbidity and the need for retransplantation. We describe a case of late PVT after OLT, which was successfully treated by a minimally invasive percutaneous transhepatic approach using both mechanical fragmentation and pharmacologic lysis of the thrombus followed by anticoagulation. The patient has had a good clinical course with normal graft function and patent portal blood flow at 6-month follow-up. This case report confirms the possibility of successful recanalization of the portal vein in a patient with late PVT after liver transplantation. Sustained anticoagulation/antiaggregation therapy for at least 6 months after the procedure is advisable.

Editorial on “diagnosis and treatment of arterial steal syndromes in liver transplantation recipients”

Liver TransplantationVolume 9, Issue 6 p. 603-604 EditorialFree Access Editorial on “diagnosis and treatment of arterial steal syndromes in liver transplantation recipients” Olivier Farges, Olivier Farges Department of Hepato-Pancreato-Biliary Surgery and Transplantation, Hospital Beaujon, Clichy, FranceSearch for more papers by this authorJacques Belghiti, Corresponding Author Jacques Belghiti [email protected] Department of Hepato-Pancreato-Biliary Surgery and Transplantation, Hospital Beaujon, Clichy, FranceDepartment of Digestive Surgery, Hospital Beaujon, 100 Boulevard du Général Leclerc, 92110, Clichy-France. Telephone: 331-4087-5895; FAX: 331-4087-1724Search for more papers by this author Olivier Farges, Olivier Farges Department of Hepato-Pancreato-Biliary Surgery and Transplantation, Hospital Beaujon, Clichy, FranceSearch for more papers by this authorJacques Belghiti, Corresponding Author Jacques Belghiti [email protected] Department of Hepato-Pancreato-Biliary Surgery and Transplantation, Hospital Beaujon, Clichy, FranceDepartment of Digestive Surgery, Hospital Beaujon, 100 Boulevard du Général Leclerc, 92110, Clichy-France. Telephone: 331-4087-5895; FAX: 331-4087-1724Search for more papers by this author First published: 30 December 2003 https://doi.org/10.1053/jlts.2003.50127Citations: 10AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Manner M, Otto G, Senninger N, Kraus T, Goerich J, Herfarth C. Arterial steal: An unusual cause for hepatic hypoperfusion after liver transplantation. Transpl Int 1991; 4: 122– 124. 2 Langer R, Langer M, Scholz A, Felix R, Neuhaus P, Keck H. Splenohepatic steal syndrome and gastroduodenal steal syndrome in patients before and after liver transplantation. Aktuelle Radiol 1992; 2: 55– 58. 3 Bolognesi M, Sacerdoti D, Bombonato G, Merkel C, Sartori G, Merenda R, et al. Change in portal flow after liver transplantation: Effect on hepatic arterial resistance indices and role of spleen size. Hepatology 2002; 35: 601– 608. 4 Marcos A, Olzinski AT, Ham JM, Fisher RA, Posner MP. The interrelationship between portal and arterial blood flow after adult to adult living donor liver transplantation. Transplantation 2000; 70: 1697– 1703. 5 Smyrniotis V, Kostopanagiotou G, Kondi A, Gamaletsos E, Theodo K, Kehagias K, Contis J. Hemodynamic interaction between portal vein and hepatic artery flow in small-for-size split liver transplantation. Transpl Int 2002; 15: 355– 360. 6 Boillot O, Delafosse B, Mechet I, Boucaud C, Pouyet M. Small-for-size partial liver graft in an adult recipient; A new transplant technique. Lancet 2002; 359: 406– 407. 7 De Carlis L, Sansalone CV, Rondinara GF, Belli LS, Rimoldi P, Romani F, et al. Splenic artery steal syndrome after orthotopic liver transplantation: Diagnosis and treatment. Transplant Proc 1993; 25: 2594– 2596. 8 Cherqui D, Riff Y, Rotman N, Julien M, Fagniez PL. The recipient splenic artery for arterialization in orthotopic liver transplantation. Am J Surg 1994; 167: 327– 330. Citing Literature Volume9, Issue6June 2003Pages 603-604 ReferencesRelatedInformation

Transcatheter splenic artery occlusion for treatment of splenic artery steal syndrome after orthotopic liver transplantation.

To review some aspects of the problem of splenic artery steal syndrome as cause of ischemia in transplanted livers and treatment by selective splenic artery occlusion. Eleven liver transplant patients from a group of 350 patients, nine men and two women, ranging in age from 40 years to 61 years (mean 52 years), presented with biochemical evidences of liver ischemia and failure, ranging from one to 60 days following orthotopic liver transplantation. Diagnosis of splenic artery steal syndrome was suspected by elevated enzymes, Doppler ultrasound and confirmed by celiac angiogram. Patients with confirmed hepatic artery thrombosis before angiography were excluded from the study. Embolization with Gianturco coils was performed. All patients were treated by splenic artery embolization with Gianturco coils. The 11 patients improved clinically within 24 hours of the procedure with significant change in the biochemical and clinical parameters. Followup ranged from one month to two years. One of the 11 patient initially improved, but developed hepatic artery thrombosis within 24 hours of the embolic treatment, requiring surgical repair. Splenic artery steal syndrome following liver transplantation surgery can be diagnosed by celiac angiography, and effectively treated by splenic artery embolization with coils. Embolization is one of the treatments available, it is minimally invasive, and leads to immediate clinical improvement. Hepatic artery thrombosis is a possible complication of the procedure.