Characteristics and Management of Splenic Artery Aneurysms in Adult Living Donor Liver Transplant Recipients

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1 LIVER TRANSPLANTATION 15: , 2009 ORIGINAL ARTICLE Characteristics and Management of Splenic Artery Aneurysms in Adult Living Donor Liver Transplant Recipients Deok-Bog Moon, 1 Sung-Gyu Lee, 1 Shin Hwang, 1 Ki-Hun Kim, 1 Chul-Soo Ahn, 1 Tae-Yong Ha, 1 Gi-Won Song, 1 Dong-Hwan Jung, 1 Gi-Young Ko, 2 and Kyu-Bo Sung 2 1 Division of Hepatobiliary Surgery and Liver Transplantation, Department of Surgery, and 2 Department of Diagnostic Radiology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea Splenic artery aneurysms (SAAs), occurring in 7% to 17% of patients with cirrhosis, often result in catastrophic rupture after liver transplantation. We had experienced 3 cases of ruptured SAAs after adult living donor liver transplantation (LDLT), and we then performed this study to find risk factors for coexisting SAAs in liver transplant candidates with cirrhosis and to propose ideal approaches for them. Preoperative and postoperative computed tomography angiograms and axial views were reviewed for 310 adult LDLT recipients who had cirrhosis from January 2004 to August The recorded variables were the preoperative diagnosis, the presence of SAA and its characteristics, the splenic artery (SA) diameter, and the presence and size of portosystemic collaterals. Devastating SAA rupture accompanied by hypovolemic shock occurred on postoperative days 6, 82, and 8, respectively, and it was treated emergently by embolization in cases 1 and 2 and by splenectomy in case 3. Cases 1 and 3 recovered well, but case 2 died of an unrelated cause with a long hospital stay. The incidence of SAA during the study period was 14.2% (44/310), and the size was mm. Most SAAs were single (70.6%, 31/44) and were located in the distal one-third of the SA (82.4%, 36/44). Large portosystemic collaterals demonstrating longstanding severe portal hypertension were significantly correlated with the occurrence of SAAs. Nine patients with SAAs were preventively treated by proximal ligation (n 4) intraoperatively and by embolization (n 5) 1 day before or after LDLT. No patient showed severe postembolization syndrome. In conclusion, a careful preoperative evaluation of SAAs by high-resolution 3-dimensional computed tomography in liver transplant candidates, especially in those showing large portosystemic collaterals, is merited. Preventive treatment should be encouraged regardless of the size in order to avoid severe morbidity and mortality related to SAA rupture, and methods such as radiological and surgical interventions need to be individualized according to the location and number of SAAs. Liver Transpl 15: , AASLD. Received February 8, 2009; accepted July 14, Splenic artery aneurysm (SAA) is an uncommon finding in the general population. 1 The true incidence is likely close to 0.8% of the population, 2 but the incidence of SAA rises in adult patients with cirrhosis and has been reported to be between 7% and 17%. 3-5 This increased incidence has been attributed to the increased splenic blood flow associated with portal hypertension. Blood flow in the splenic system increases in response to the volume demands of portosystemic shunts, which have been developed to decrease portal outflow resistance. 6 Positive correlations have been established between splenic blood flow and splenic artery (SA) diameter and between SA diameter and aneurysm size. 7,8 Although spontaneous rupture in patients with cirrhosis is uncommon, the incidence of rupture increases around 3% to 4% after liver transplantation, with most ruptures occurring in the immediate postoperative period and with a mortality rate of 50%. 3,9,10 The classical therapy Abbreviations: CI, confidence interval; CT, computed tomography; HBV; hepatitis B virus; HBV-LC, hepatitis B virus related liver cirrhosis; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; LDLT, living donor liver transplantation; LT, liver transplantation; POD, postoperative day; SA, splenic artery; SAA, splenic artery aneurysm. Address reprint requests to Sung-Gyu Lee, M.D., F.A.C.S., Division of Liver Transplantation and Hepatobiliary Surgery, Department of Surgery, Asan Medical Center, University of Ulsan College of Medicine, Pungnap-dong, Songpa-gu, Seoul , Korea. Telephone: ; FAX: ; sglee2@amc.seoul.kr DOI /lt Published online in Wiley InterScience ( American Association for the Study of Liver Diseases.

2 1536 MOON ET AL. TABLE 1. Description of Patients with Ruptured SAAs SAA Liver Disease Extrasplenic Intrasplenic Case Sex/Age Duration Diagnosis n Size n Size Treatment 1 Female/47 21 years HBV-LC 1 15 mm Splenic artery ligation at the time of LDLT, but the intrasplenic SAA ruptured on day 6. Coil embolization was performed. 2 Female/43 10 years HBV-LC, Multiple 20 mm 1 12 mm Splenic artery ligation HCC at the time of LDLT, but the intrasplenic SAA ruptured on day 82. Coil embolization was performed. 3 Male/44 11 years HBV-LC 1 24 mm The SAA ruptured on day 8. Splenectomy was performed. Outcome Alive Dead by 8 months because of an unrelated cause Alive Abbreviations: HBV-LC, hepatitis B virus related liver cirrhosis; HCC, hepatocellular carcinoma; LDLT, living donor liver transplantation; SAA; splenic artery aneurysm. for SAAs has been surgical treatment. With laparotomy, either ligation of the SA or excision of the aneurysms is performed with or without splenectomy. Recently, percutaneous embolization has also become one of the treatment options, depending on indications. 11 Ruptured SAAs after adult living donor liver transplantation (LDLT) for patients with liver cirrhosis occurred in 3 cases of this reported series. All the patients recovered with prompt treatment (Table 1). We retrospectively performed this study to determine the incidence and risk factors of SAAs in adult LDLT patients and to propose reasonable preventive measures. the normal portion of the SA. For the location of the SAA, the SA was divided into proximal, intermediate, and distal thirds. The 3-month and 1-year multidetector CT angiograms were investigated to detect any changes in the size and number of the known SAAs and to determine if any SAAs had newly formed. All data are expressed as means and standard deviations; comparisons between means were made with the Student t test, and comparisons between categorical variable were performed with the 2 test. Logistic regression was used for multivariate analysis. A P value less than 0.05 was considered significant. PATIENTS AND METHODS From January 2004 to August 2005, 327 adult-to-adult LDLT procedures were performed in 327 patients at our institute. Seventeen patients with fulminant hepatic failure were excluded from this study because they did not have liver cirrhosis or manifestation of portal hypertension, including the development of collateral vessels. The mean age was years, and 89 of the patients were female (28.7%). The primary liver disease was recorded, and the preoperative and postoperative multidetector computed tomography (CT) angiograms were assessed with respect to the presence, number, location, and diameter of the SAAs. Simultaneously, the size of the SA and the presence and size of venous collaterals, which are indirect severity parameters of patients with cirrhosis, were evaluated to reveal the relationship between the portal hypertension and the presence of SAAs in 278 adult LDLT patients with hepatitis B virus related liver disease. SAA was defined as a permanent and localized dilatation of the SA, with at least a 50% increase in the diameter in comparison with RESULTS Incidence of SAA Forty-four of the 310 adult LDLT patients with cirrhosis and portal hypertension (14.2%) were found to have SAAs. The mean age of the SAA patients was years, and 19 of the patients were female (40.9%). Except for 1 patient with Wilson s disease, 43 SAA patients (15.5%) were encountered among the 278 patients with hepatitis B virus related cirrhosis, whereas no SAAs were found in patients with other primary liver diseases (Table 2). Case Presentation of Posttransplant SAA Rupture Among 3 cases of devastating SAA rupture, rupture of an intrasplenic artery aneurysm occurred in cases 1 and 2, presumably because of maintained filling pressure through the accessory SA and right gastroepiploic artery on postoperative days 6 and 82, respectively, although they underwent proximal SA ligation during

3 SPLENIC ARTERY ANEURYSMS IN ADULT LDLT 1537 TABLE 2. Preoperative Diagnoses Number of Patients HBV-related cirrhosis with/ 278 without HCC HCV-related cirrhosis 11 Secondary biliary cirrhosis 4 Alcoholic cirrhosis 5 Cryptogenic cirrhosis 3 Autoimmune liver disease 6 Wilson s disease 2 Polycystic liver disease 1 Total 310 Abbreviations: HBV; hepatitis B virus; HCC; hepatocellular carcinoma; HCV, hepatitis C virus. Figure 2. Large spontaneous portosystemic collateral vessels demonstrating longstanding severe portal hypertension have a significant relation to the development of a splenic artery aneurysm. The arrowhead indicates large coronary collateral vessels, and the white arrow indicates a splenic artery aneurysm. Figure 1. Rupture of an intrasplenic arterial aneurysm due to persistent filling pressure via collateral arteries. In (A1,A2) case 1 and (B1,B2) case 2, a ruptured intrasplenic arterial aneurysm and a perisplenic hematoma were visible on computed tomography and angiography, respectively, and they were treated by coil embolization via (A3) the accessory splenic artery and (B3) the right gastroepiploic artery, respectively. the operation in order to reduce the SAA filling pressure. We successfully managed them with prompt coil embolization through collateral arteries to the SAAs, despite an episode of hypovolemic shock, because the vital signs of the patients could be maintained by resuscitation, and the bleeding rate and amount from the ruptured intrasplenic artery aneurysm were not too severe (Fig. 1). In case 3, we performed LDLT using a right lobe graft without recognition of a preexisting SAA; the patient had a sudden onset of profuse blood drainage and abdominal distension followed by uncontrollable hypovolemic shock on postoperative day 8, and we performed emergency splenectomy. He recovered from this operation but had a prolonged hospital stay. Case 1 had a 5.2-mm intrasplenic artery aneurysm only, and case 2 had 4 extrasplenic artery aneurysms ( mm) located at the splenic hilum and a mm intrasplenic aneurysm too. Case 3 had 3 extrasplenic artery aneurysms ( mm). All 3 patients had evidence of severe portal hypertension showing splenomegaly and large portosystemic collaterals. The diameters of the collateral vessels were 11.7, 12.9, and 19.6 mm in cases 1, 2, and 3, respectively. An intrasplenic artery aneurysm is prone to rupture regardless of small size and intraoperative ligation of the SA proximal to the SAA, which can decrease the SAA filling pressure, because it might be related to the maintained filling pressure of the intrasplenic SAA by the augmented collateral blood flow draining to the splenic hilum through the accessory SA and right gastroepiploic artery. However, the rupture of an extrasplenic artery aneurysm seems to be related to the size of the SAA under the maintained filling pressure of the SA (eg, case 3). Characteristics of SAAs Single SAAs were more common (70.6%, 31/44) than multiple SAAs (29.4%, 13/44). The most common location of SAAs was the distal third of the SA (82.4%, 36/44), and the incidence of SAAs of the intrasplenic and middle thirds of the SA was 11.8% (5/44) and 6.0% (3/44), respectively. All the SAA patients had visible portosystemic shunts on CT angiograms, but 82.4% of the non-saa patients had visible collateral vessels (P 0.014; Fig. 2). The diameter of the collateral vessels was mm in SAA patients and mm in non-saa patients (P 0.001). It was a significant indicator for the pres-

4 1538 MOON ET AL. TABLE 3. Indicators for the Presence of SAAs Univariate Multivariate SAA (n 44) No SAA (n 266) P Value P Value Hazard Ratio (95% CI) Splenic artery diameter mm mm ( ) Portosystemic collateral mm mm ( ) vessel diameter Presence of collateral vessels 44 (100%) 46 (17.3%) Abbreviations: CI, confidence interval; SAA; splenic artery aneurysm. Preoperative TABLE 4. Fates of SAAs According to the Management Methods Time of Patient* Detection Treatment Treatment Fate of SAA (Months) 1 Yes Intraoperative Proximal ligation Decrease in size Alive (52) 2 Yes POD 1 Embolization Disappearance Alive (49) 3 Yes POD 1 Embolization Disappearance Alive (47) 4 Yes POD 1 Embolization Disappearance Alive (46) 5 Yes Intraoperative Proximal ligation No change Alive (40) 6 No POD 1 Embolization Disappearance Alive (35) 7 Yes Intraoperative Proximal ligation No change Alive (34) 8 Yes Preoperative Embolization Disappearance Alive (33) 9 Yes Intraoperative Proximal ligation No change Alive (32) Abbreviations: POD, postoperative day; SAA, splenic artery aneurysm. *Ruptured cases (3) were excluded. Patient 7 was the first patient after the introduction of the established treatment protocol for SAA patients. Outcome ence of SAA in univariate and multivariate analysis. The diameter of the SA was mm in SAA patients and mm in non-saa patients, but there was no significant difference (P 0.098; Table 3). Indications of Preventive Measures for SAAs During the study period, we treated SAAs in 9 patients, except for 3 rupture cases. The first 6 cases were treated because the diameter of the SAA was much larger than 20 mm; this is the usual criterion for the treatment of SAAs, and it is easily identifiable on a preoperative CT scan. Until then, we had not fully recognized the risk of SAA rupture because there fortunately had been no episodes of SAA rupture in transplanted patients. After the experience of 3 rupture cases, we routinely treated SAAs regardless of the size, and the preventive measures were proximal ligation only, proximal and distal ligation, and embolization of SAAs. In the case of an extrasplenic single aneurysm apart from the splenic hilum, proximal and distal SA ligation of SAA was basically tried, but proximal ligation only was performed more often because the location of the SAA was close to the splenic hilum on intraoperative findings. Furthermore, poor accessibility related to (1) a thickened and fibrotic peritoneum that resulted from previously repeated spontaneous bacterial peritonitis or (2) severe retroperitoneal edema that resulted from a patient s poor intraoperative condition led us to perform proximal ligation only or SA embolization within 24 hours after liver transplantation. In the case of an intrasplenic aneurysm, an aneurysm located at the splenic hilum, or multiple splenic aneurysms, coil embolization of the SAAs was performed just before the operation day because of the postoperative experience with ruptured intrasplenic aneurysms despite proximal ligation only and because of the difficulty of intraoperative management of SAAs. Four underwent ligation of the SA during LDLT proximal to the SAA, and the SAA persisted on a follow-up CT scan. The other 5 were blocked at both the proximal and distal portions of the SAA with coil embolization preoperatively or postoperatively, and the SAA completely disappeared on a follow-up CT scan in all patients (Table 4). The degree of splenic infarction after the treatment of SAAs was diverse according to the procedure site of the SA. Intraoperative ligation of the SA mostly resulted in less than 50% of the volume of the spleen being infarcted on the postoperative day 7 follow-up CT scan. However, the infarcted volume after coil embolization of the SAA was wider than the ligation of the SA and was mostly less than 70%, but nearly total infarction was reached in 1 patient. Splenic abscess did not occur in the patient with nearly total infarction of the spleen. During the poststudy period, however, we experienced

5 SPLENIC ARTERY ANEURYSMS IN ADULT LDLT case of splenic abscess after coil embolization for multiple SAAs at the splenic hilum. Natural Posttransplant Course of Untreated SAAs When we reviewed follow-up CT scans for the 32 untreated SAA patients, except for 3 rupture cases, the size of the SAAs was mm (range, mm) before LDLT and mm 3 months after LDLT without significant changes. However, the size significantly decreased to mm by 1 year after LDLT (P 0.034); these are the first long-term follow-up results for SAAs after LDLT. DISCUSSION Since Beaussier 12 first described SAAs in 1770, more than 1000 cases have been reported in the literature. Brockman 13 published the first surgical case of such an aneurysm in Two years later, the first angiographic picture of an SAA (by Lindboe) appeared. 14 In 1974, Stanley and Fry 2 described various causes of SAAs, such as arterial dysplasia, portal hypertension with splenomegaly, focal arterial inflammatory processes, and hormonal and hemodynamic events in multiparous females, as well as SAAs in men with no clearly recognizable pathogenic factors. The clinical significance of SAAs is related to the fact that although SAAs are rare, the complication of rupturing is often fatal. 15,16 This study was performed in order to assess the characteristics and results from the management of SAAs in our 310 consecutively transplanted adult-to-adult LDLT recipients with cirrhosis. The overall incidence of SAA in our adult-to-adult LDLT population was 14.2%, and the SAAs were found most often in the hilum of the spleen in the distal third of the SA. These results coincided with Kobori et al. s report. 3 The incidence slightly increased to 15.5% in patients with hepatitis B virus related cirrhosis. In the 242-patient study by Kobori et al., a viral hepatitis prevalence of only 17% existed; however, the prevalence of viral hepatitis in SAA patients was 83% to 93% in other reports. 4,17 Because 89.7% (278/310) of the adult-to-adult LDLT patients in our series had hepatitis B virus related cirrhosis, the high prevalence of hepatitis B virus in our SAA patients (97.7%, 43/44) seems to be comparable to that of previous reports. 4,17 The female-to-male ratio of patients with SAA has been reported to be 4:1 in the general population. 2 This figure is affected by the high prevalence of SAA in multiparous women. Our study also yielded a higher incidence of SAA in females (21.3%, 19/89) than males (11.3%, 25/221), but the gender discrepancy was decreased in patients with cirrhosis. In patients with cirrhosis and portal hypertension, as in our patients, SAAs usually develop in the distal third of the main SA close to the hilum of the spleen, or they may be multiple and intrasplenic, generally at bifurcations of small arteries. Patients may have both intrasplenic and extrasplenic aneurysms. 4,5,8,18 The most common site in our series was the distal third of the SA (82.4%, 36/44). The major pathogenic factor underlying the development of SAAs in patients with cirrhosis and portal hypertension seems to be the high flow rate in the SA. 6,7,8 This increased flow is allowed by portosystemic shunting and a reactionary increase in the splenic arterial vasculature. 5 Increased splenic flow combined with portal hypertension places outward strain on the already weakened SA, predisposing patients to SAA formation and rupture. 17 A survey of 33 centers reporting 21 SAA ruptures showed that 29% occurred prior to transplantation. 19 However, none of our patients experienced SAA rupture prior to transplantation. Following liver transplantation, hemodynamic and proteolytic changes occur that predispose patients to SAA rupture. 17 Although the portal hypertension improves after liver transplantation, splenic arterial flow increases much more than before liver transplantation as seen after portocaval shunting. 9 It may further increase and predispose the SAA to rupture. 4 The high incidence of visceral artery aneurysm rupture after laparotomy was related to increased collagen lysis, and it was greatest within the first postoperative week 20 ; this corresponds to the course of posttransplant SAA rupture cases 1 and 3. Positive correlations have been established between splenic blood flow and splenic SA diameter and between SA diameter and aneurysm size. 7,8 SAA patients revealed a tendency of a larger SA diameter than non-saa patients, but it had no significance in our series. Avalon et al. 4 described how an end-to-side portocaval shunt may contribute to an increase in the SA flow and even SAA rupture in pregnant patients. This report makes the assumption that the presence of large spontaneous portosystemic shunts before liver transplantation might be a risk factor for SAA development. From our series, we obtained corresponding results and the first objective results of univariate and multivariate analysis: all the SAA patients had spontaneous portosystemic collaterals, and the diameter was mm, much larger than that of non-saa patients. This may be related to characteristics of large spontaneous portosystemic collaterals, which reflect longstanding severe portal hypertension in patients with cirrhosis. The indications for the treatment of SAAs remain an area of some controversy. Because of the increased rupture risk and high mortality during pregnancy and after liver transplantation, most clinicians would agree that for patients of child-bearing potential or those undergoing liver transplantation, SAA repair is warranted independently of its size. 11 Avalon et al. 4 recommended ligation of the SA proximal to the SAA, which reduces the filling pressure of this aneurysm. Preservation of the spleen is a clear advantage of SA ligation in view of the increased risk of severe infections after splenectomy in immunosuppressed patients. 21 However, the filling pressure of the SAA could be maintained through the accessory SA and right gastroepiploic artery in our series. The ruptured intrasplenic SAAs in cases 1 and 2 were related to

6 1540 MOON ET AL. Figure 3. Treatment methods for splenic artery aneurysms. (A) Proximal ligation only of a splenic artery aneurysm, which is not effective for an intrasplenic artery aneurysm because of sustaining blood filling pressure by collateral vessels. However, it is effective for preventing the rupture of a single extrasplenic splenic artery aneurysm, except for the splenic hilum. (B) Proximal and distal ligation of a splenic artery aneurysm, which is an ideal approach to a single extrasplenic splenic artery aneurysm, except for the splenic hilum, because of no blood filling pressure. (C) Coil embolization of multiple splenic artery aneurysms or a single splenic artery aneurysm located at the splenic hilum, which has no blood filling pressure but sometimes predisposes patients to splenic or portal vein thrombosis, pancreatitis, and severe splenic infarction or abscess. unrelieved filling pressure of the SAAs, regardless of intraoperative SA ligation proximal to the SAAs. Heestand et al. 17 recommended splenectomy and aneurysm ligation at transplantation. Splenectomy in patients with end-stage cirrhosis during liver transplantation, however, might cause life-threatening complications such as massive bleeding intraoperatively, portal vein thrombosis, and overwhelming sepsis postoperatively. As a result, intraoperative ligation at the proximal and distal sites of SAAs might be the most appropriate treatment for a single extrasplenic SAA apart from the splenic hilum. SA ligation is a feasible procedure in many liver transplant candidates with cirrhosis because the SA is already enlarged and tortuous. However, it is often a painstaking procedure and sometimes technically impossible in the setting of a history of recurrent spontaneous bacterial peritonitis, which might have thickened and hardened the peritoneum, or severe retroperitoneal edema resulting from the patient s poor intraoperative condition. In these situations, we intraoperatively converted our attempt from proximal and distal ligation of the SAA to proximal ligation only to decrease the filling pressure of the SAA. During the study period and until now, SAA rupture did not occur, and the size of the SAA was static or decreased after proximal ligation only for the extrasplenic single SAA patients. Hence, proximal ligation only is also a recommendable treatment for these patients. In our experience, percutaneous transarterial coil embolization of SAAs is an effective and easy method to get rid of SAAs, particularly when an SAA has multiplicity or is located in the distal or intrasplenic portion of the SA (Fig. 3). A specific problem with the embolization of SAAs is the development of a postembolization syndrome characterized by a combination of fever, abdominal pain, ileus, and pancreatic inflammation. This syndrome can be observed in 30% to 80% of patients 22,23 and resolves within 4 to 5 days after the procedure. However, postembolization syndrome has not been an issue in liver transplant recipients at our institution because most embolizations have been performed selectively to the proximal and distal SA of the SAA and also within 24 hours before or after liver transplantation in order to avoid or minimize the deteriorating effect. As a result, the infarcted volume of the spleen does not exceed 50% to 70% in most cases, and specific symptoms of postembolization syndrome are rarely conspicuous during the immediate posttransplant period. According to the report by Heestand et al., 17 embolization of SAAs can result in complicated postoperative courses related to massive necrosis of the spleen. We also experienced 1 case of nearly total infarction of the spleen after embolization for the multiple-saa patients, but the patient recovered without related complications. However, we recently experienced 1 case of splenic abscess, and there was another case of splenic vein thrombosis after coil embolization for multiple SAAs at the splenic hilum. Thereafter, when we have performed embolization of multiple SAAs, extreme care has been taken during the procedure in order to avoid total infarction of the spleen. With respect to treatment complications of SAAs, SA ligation is a much safer procedure because we have not experienced any complications such as severe splenic infarction or abscess, portal or splenic vein thrombosis, or sepsis, which might occur after splenectomy and coil embolization of the SA, during the study period and until now. 17 In our series, the SAA size increased without significance in our 32 untreated SAA patients for 3 months after LDLT. However, the SAA size significantly decreased by 1 year after LDLT, and these are the first long-term follow-up results of SAAs after LDLT; correspondingly, SAA rupture has been reported as late as 90 days post-transplant. 18

7 SPLENIC ARTERY ANEURYSMS IN ADULT LDLT 1541 Figure 4. Treatment algorithm for SAAs in liver transplant candidates with cirrhosis at the Asan Medical Center. Abbreviation: CT, computed tomography; LT, liver transplantation; SA, splenic artery; SAA, splenic artery aneurysm. In view of the high incidence and the significant morbidity and mortality associated with SAA rupture after liver transplantation, all liver candidates should be evaluated with imaging techniques capable of diagnosing SAA. 17 We perform 3-dimensional CT preoperatively for all recipient candidates for liver transplantation, and we carefully examine whether SAAs are present or not, particularly when the recipient has large spontaneous portosystemic collaterals. SAAs can be treated before, during, and immediately after the operation according to the number, location, and accessibility at our institution (Fig. 4). After the application of the proposed algorithm, SAA rupture was effectively prevented during the study period and also until now. In conclusion, our results suggest that routine preoperative surveillance for SAAs in recipient candidates should be done, and aggressive treatment with surgical or radiological interventions should be recommended within 24 hours before or after liver transplantation in order to avoid SAA rupture and untoward postembolization syndrome afterwards. REFERENCES 1. Moore SW, Lewis RJ. Splenic artery aneurysm. Ann Surg 1961;153: Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysms. Surgery 1974;76: Kobori L, van der Kolk MJ, de Jong KP, Peeters PM, Klompmaker IJ, Kok T, et al. Splenic artery aneurysms in liver transplant patients. Liver Transplant Group. J Hepatol 1997;27: Avalon A, Wiesner RH, Perkins JD, Tominaga S, Hayes DH, Krom RA. Splenic artery aneurysm in liver transplant patients. Transplantation 1988;45: Manenti F, Williams R. Injection studies of the splenic vasculature in portal hypertension. Gut 1966;7: Nishida O, Moriyasu F, Nakamura T, Ban N, Miura K, Sakai M, et al. Hemodynamics of splenic artery aneurysm. Gastroenterology 1986;90: Ohta M, Hashizume M, Ueno K, Tanoue K, Sugimachi K, Hasuo K. Hemodynamic study of splenic artery aneurysm in portal hypertension. Hepatogastroenterology 1994:41: Puttini M, Aseni P, Brambilla G, Belli L. Splenic artery aneurysm in portal hypertension. J Cardiovasc Surg (Torino) 1982;23: Lee PC, Rhee RY, Gordon RY, Fung JJ, Webster MW. Management of splenic artery aneurysms: the significance of portal and essential hypertension. J Am Coll Surg 1999; 189: Trastek VF, Pairolero PC, Joyce JW, Hollier LH, Bernatz PE. Sepenic artery aneurysms. Surgery 1982;91: Berceli SA. Hepatic and splenic artery aneurysms. Semin Vasc Surg 2005;18: Beaussier M. Sur un anevrisme de l artere splenique dont les parois se sont ossifiees. J Med Clin Pharm 1770;32: Brockman RL. Aneurysm of splenic artery. Br J Surg 1930;17: Abbas MA, Stone WM, Fowl RJ, Gloviczki P, Oldenburg WA, Pairolero PC, et al. Splenic artery aneurysm; two decades experience at Mayo Clinic. Ann Vasc Surg 2002; 16: Park H. Rupture of splenic artery aneurysm. Am J Forensic Med Pathol 1992;13: Mines D. Splenic artery aneurysm rupture. Am J Emerg Med 1991;9: Heestand G, Sher L, Lightfoote J, Palmer S, Mateo R, Singh G, et al. Characteristics and management of splenic artery aneurysm in liver transplant candidates and recipients. AmSurg2003;69: javascript:PopUpMenu2_ Set(Menu ); 18. Mattar SG, Lumsden AB. The management of splenic artery aneurysms: experience with 23 cases. Am J Surg 1995;169: Gitlin N, Grahame GR, Kreel L, Williams HS, Sherlock S. Splenic blood flow and resistance in patients with cirrhosis before and after portocaval anastomosis. Gastroenterology 1970;59: Swanson RJ, Littooy FN, Hunt TK, Stoney RJ. Laparotomy as a precipitating factor in the rupture of intra-abdominal aneurysms. Arch Surg 1980;115: Schwartz PE, Sterioff S, Mucha P, Melton LJ III, Offord KP. Postsplenectomy sepsis and mortality in adults. JAMA 1982;248: Carr JA, Cho JS, Shepard AD, Nypaver TJ, Reddy DJ. Visceral pseudoaneurysms due to pancreatic pseudocysts: rare but lethal complications of pancreatitis. J Vasc Surg 2000;32: Guillon R, Garcier JM, Abergel A, Mofid R, Garcia V, Chahid T, et al. Management of splenic artery aneurysms and false aneurysms with endovascular treatment in 12 patients. Cardiovasc Intervent Radiol 2003;26: