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.     

Evolving experience with prevention and treatment of splenic artery syndrome after orthotopic liver transplantation

Impaired hepatic arterial perfusion after orthotopic liver transplantation (OLT) may lead to ischemic biliary tract lesions and graft‐loss. Hampered hepatic arterial blood flow is observed in patients with hypersplenism, often described as arterial steal syndrome (ASS). However, arterial and portal perfusions are directly linked via the hepatic arterial buffer response (HABR). Recently, the term ‘splenic artery syndrome’ (SAS) was coined to describe the effect of portal hyperperfusion leading to diminished hepatic arterial blood flow. We retrospectively analyzed 650 transplantations in 585 patients. According to preoperative imaging, 78 patients underwent prophylactic intraoperative ligation of the splenic artery. In case of postoperative SAS, coil‐embolization of the splenic artery was performed. After exclusion of 14 2nd and 3rd retransplantations and 83 procedures with arterial interposition grafts, SAS was diagnosed in 28 of 553 transplantations (5.1%). Twenty‐six patients were treated with coil‐embolization, leading to improved liver function, but requiring postinterventional splenectomy in two patients. Additionally, two patients with SAS underwent splenectomy or retransplantation without preceding embolization. Prophylactic ligation could not prevent SAS entirely (n = 2), but resulted in a significantly lower rate of complications than postoperative coil‐embolization. We recommend prophylactic ligation of the splenic artery for patients at risk of developing SAS. Post‐transplant coil‐embolization of the splenic artery corrected hemodynamic changes of SAS, but was associated with a significant morbidity.     

肝移植术后脾动脉盗血综合征的诊断与治疗

目的 探讨肝移植术后脾动脉盗血综合征(SANS)的诊断和治疗.方法 回顾性分析1012例肝移植受者的临床资料,观察受者SASS的发生情况,并应用统计学方法分析受者性别、原发疾病、术前血小板水平及移植肝与受者的重量比(GRWR)等指标对SANS发生率的影响.SASS的诊断采用B型超声筛查与动脉造影检查相结合的方法.治疗均采用超选择性盗血动脉介入栓塞方法.术后对受者进行了8～36个月的随访,观察治疗效果.结果 有11例肝移植受者术后确诊为SANS,均发生于肝移植术后1个月内,平均(13.63±10.93)d,其发生率为1.09%(11/1012);受者的性别、原发疾病或术前血小板计数对肝移植术后SASS发生率的影响,差异均无统计学意义(P＞0.05),而GRWR较低者,SASS发生率较高(P＜0.01).经介入治疗后,11例受者存活情况良好,移植肝血流恢复正常,肝功能基本恢复正常,无血栓、缺血性胆道并发症发生.1例受者经介入治疗后脾脏周边部出现小片状梗死灶,其余10例受者脾脏无明显异常.结论 肝移植术后发生的SANS无明显特异性表现,应重视对GRWR较低受者的排查;采用B型超声筛查与动脉造影检查可以早期确诊;确诊后对盗血动脉进行超选择性介入栓塞治疗效果理想.     

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.     

Intrahepatic artery pseudoaneurysm associated with a metallic biliary stent after living donor liver transplantation: report of a case

An intrahepatic artery pseudoaneurysm (IHAA) is a very rare but potentially lethal complication occurring after liver transplantation. This report presents a case of an IHAA associated with a metallic biliary stent after liver transplantation. A 40-year-old male underwent living donor liver transplantation (LDLT) using a left lobe graft. The bile duct reconstruction was performed with Roux-en-Y hepaticojejunostomy. He developed obstructive jaundice 5 years after LDLT, and had biliary stricture of the anastomosis area, therefore, the two metallic biliary stents were finally positioned at the stricture of the biliary tract. He suddenly developed hematemesis 8 years after LDLT, and computerized tomography scan showed an IHAA. Although seven interlocking detachable coils were placed at the neck of the aneurysm, hematemesis recurred 3 days after the initial embolization. Therefore, retransplantation was successfully performed 25 days after the embolization of IHAA using a right lobe graft from his son. In conclusion, metal stent insertion can lead to the fatal complication of HAA. The placement of a metallic stent could have been avoided in this case. Percutaneous metallic stent insertion for biliary stenosis after liver transplantation should therefore only be performed in carefully selected patients.     

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.     

Stent placement in pediatric patients with hepatic artery stenosis or thrombosis after liver transplantation

Hepatic artery stenosis (HAS) and thrombosis (HAT) after orthotopic liver transplantation remain significant causes of graft loss. Postoperative HAT follows approximately 5% to 19% of orthotopic liver transplantation. It is seen more frequently in pediatric patients. In the past, repeat transplantation was considered the first choice for therapy. Recently, interventional radiological techniques, such as thrombolysis, percutaneous transluminal angioplasty, or stent placement in the hepatic artery, have been suggested, but little data exist related to stent placement in the thrombosed hepatic artery during the early postoperative period in pediatric patients. Between March 2000 and March 2005, percutaneous endoluminal stent placement was performed in seven pediatric liver transplant patients. HAT or HAS initially diagnosed in all cases by Doppler ultrasound then confirmed angiographically. We intervened in four cases of hepatic artery stenosis and three cases of hepatic artery occlusion. Stents were placed in all patients. Three ruptures were seen during percutaneous transluminal angioplasty of the hepatic artery using a covered coronary stents on the first, fifth day, or 17th postoperative day. In one patient, dissection of the origin of the common hepatic artery developed owing to a guiding sheath, and a second stent was placed to cover the dissected segment. The other two hepatic artery stents remained patent. In one stent became occluded at 3 months after the intervention with no clinical problems. Follow-up ranged from 9 to 40 months. In conclusion, early and late postoperative stent placement in the graft hepatic artery was technically feasible.     

Ischemic preconditioning prior to aortic cross-clamping protects high-energy phosphate levels,glucose uptake,and myocyte contractility

BACKGROUND: Atheroembolization following aortoiliac stent placement is uncommon. The purpose of this study was to examine the management and risk factors of lower extremity atheroembolization following aortoiliac stent placement for occlusive disease. MATERIALS AND METHODS: From March 1993 to February 2001, the hospital records of all patients who developed thromboembolic events following aortoiliac stent placement were reviewed. Risk factor analysis was performed by comparing with the control group, which consisted of 493 patients treated with aortoiliac stents during the study period who did not develop atheroembolic complications. Patients with cardiac etiologies or aortic aneurysms as the source of embolization as well as those who developed acute embolization following stent deployment (<30 days) were excluded. RESULTS: Atheroembolization occurred in eight patients (12 iliac artery stents and 1 aortic stent) at intervals ranging from 9 to 43 months (mean 22 months) following aortoiliac stent placement. Arteriography in all patients implicated the stented artery as the source of atheroembolism. Five corrective operations (two aorto-bifemoral bypasses, one ileofemoral bypass, and two aortoiliac endarterectomies) along with two concomitant femoropopliteal thrombectomies were performed successfully in five patients. The remaining three patients were treated with either thrombolysis and/or additional stent placement, which resulted in either iliac occlusion or recurrent embolic symptoms (P < 0.05). All 3 patients subsequently underwent bypass procedures (one ileofemoral and two femorofemoral bypasses). There was no perioperative mortality. During a mean follow-up of 16 months (range 3 to 45 months), two patients required minor amputations, whereas one required major leg amputation. No further episodes of atheroembolism occurred in the involved limbs following surgical bypass procedures. Risk factor analysis failed to identify potential variables that correlated with atheroembolism following aortoiliac stent placement. CONCLUSION: Patients with atheromatous embolization following aortoiliac stent placement should be evaluated aggressively. The treatment of choice is surgical correction or bypass with exclusion of the offending embolic source. Although intra-arterial stent placement in the atheroembolic stented iliac artery is feasible, it may provide a less durable result.     

原发性肝癌合并脾功能亢进的外科治疗

目的 探讨原发性肝癌合并脾功能亢进的合理治疗方法。方法 1994年1月至2004年12月我院收治67例原发性肝癌合并脾功能亢进患者，17例行肝切除联合脾切除，7例行单纯肝切除，43例行肝动脉栓塞化疗联合脾动脉栓塞。结果 肝切除联合脾切除组术后30d患者脾功能亢进症状消失，外周血细胞恢复正常。单纯肝切除组术后脾功能亢进症状加重，其中6例于术后3～7个月分别行脾动脉栓塞治疗。肝动脉栓塞化疗联合脾动脉栓塞组治疗后30 d 79％（34／43）的病例脾功能亢进症状改善，外周血细胞恢复正常。结论 原发性肝癌合并脾功能亢进的处理应争取行肝切除联合脾切除治疗，如肝癌不能切除，则应争取行肝动脉栓塞化疗联合脾动脉栓塞治疗。     

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

AIM: To describe the functional effect of partial splenic embolization (PSE) in liver-transplanted (LT) patients with hypersplenism and hepatitis C virus (HCV) recurrence. PATIENTS AND METHODS: 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). RESULTS: 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. CONCLUSIONS: 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.     

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.     

Emergency splenic arterial embolization for massive variceal bleeding in liver recipient with left-sided portal hypertension.

Splenic vein thrombosis with gastric variceal bleeding is difficult to manage, and splenectomy may be necessary to stop variceal bleeding. The authors report the case of a post-orthotopic liver transplant patient with bleeding gastric varices secondary to splenic vein thrombosis treated by partial splenic artery embolization. Successful embolization was performed via transcatheter approach depositing Gianturco coils into the intrasplenic artery resulting in immediate cessation of variceal bleeding. No recurrence of bleeding was noted postembolization. In conclusion, splenic artery embolization can be used as treatment for postliver transplant variceal bleeding with hypersplenism.     

经皮经肝胆道支架术在肝移植术后胆管狭窄中的应用

目的 评价经皮经肝胆道支架术治疗肝移植术后胆管狭窄的疗效.方法 肝移植术后胆管狭窄患者23例,其中吻合口狭窄7例,肝门区狭窄6例,多发性狭窄10例.确诊后均行经皮经肝胆道支架术.术前均给予经皮经肝胆管引流术(percutaneous transhepatic biliary drainage,PTBD),同时对狭窄部位...     

Ureteral stents: a risk factor for polyomavirus BK viremia in kidney transplant recipients undergoing protocol screening

Background

Polyomavirus BK nephropathy (BKN) remains a common cause of early renal transplant dysfunction and graft loss. To date, little has been reported on the role, if any, of transplant ureteral stents in the development of polyomavirus BK viremia (BVK) and BKN.

Methods

We performed a single-center, retrospective analysis of renal transplant recipients who underwent renal transplantation followed by monthly BKV screening at Albany Medical Center between January 1, 2006, and December 31, 2009. A transplant ureteral stent was placed at the discretion of the surgeon. The immunosuppression protocol employed for deceased donor and unrelated living -donor recipients was antithymocyte antibody induction with methylprednisolone, mycophenolate mofetil, tacrolimus, and sirolimus.

Results

During the study period, 186 recipients were identified; 124 (67%) underwent intraoperative transplant ureteral stent placement, while 62 patients (33%) did not undergo stent placement. With our monthly screening protocol, we detected BKV in 32 of the 186 recipients (17%) following transplantation; 27 of the 32 (84%) viremic patients were stent recipients. In all patients who developed BKV, an immunosuppression dose reduction protocol was employed. Ureteral stent placement conferred a statistically significant elevated risk of developing BKV (odds ratio = 3.17, 95% confidence interval 1.16–8.70). Patient gender, age, ethnicity, diabetes status, and retransplant status were not statistically significant factors in the development of BKV.

Conclusion

Our study demonstrated the elevated risk of BKV in recipients who undergo transplant ureteral stenting. Monthly BK polymerase chain reaction screening appears to be a useful tool for the early detection of BKV in this higher-risk group.     

Transcatheter treatment of splenic artery aneurysms (SAA). Report of two cases

Splenic artery embolization with steel coils was performed in two patients who both had large splenic artery aneurysms and hepatic cirrhosis complicated by hypersplenism. A good clinical effect was noticed after the procedure. It was concluded that this treatment is safe and effective and decreases the risk of splenic artery rupture. It also corrects hypersplenism. Transcatheter embolization appears to be a preferable alternative to surgery in such cases.     

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

Splenic artery steal syndrome (SASS) has been considered a life-threatening complication to liver transplant recipients. Herein we timely diagnosed a case of SASS with deteriorating liver function. SASS was screened by routine Doppler ultrasonography (DUS) and multidetector computed tomography and was ultimately diagnosed by selective celiac trunk angiography. The patient was rescued by splenic artery embolization. In this case, routine DUS was useful to screen SASS. Signs of high-resistance hepatic artery waveform and low diastolic flow were highly suspected of SASS. This case also indicated that portal hyperperfusion was a cause of graft dysfunction in SASS. The study was in accordance with the Helsinki Congress and the Declaration of Istanbul, no prisoners were used, and participants were neither paid nor coerced in this study. Furthermore, we reviewed the recent literatures on the advances in the diagnosis and treatment of SASS. These studies suggest that splenic artery embolization may be a safe and effective technique to treat SASS. In addition, identification of recipients at high risk of SASS with preoperative computed tomography scans and DUS is recommended. Banding or ligation the splenic artery may be useful to prevent SASS and other potential complications after liver transplantation.     

脾功能亢进患者肝移植术后脾功能恢复不良的原因分析

目的 探讨肝移植术后脾功能亢进恢复情况,分析脾功能亢进恢复不良的原因.方法 分析肝移植前存在脾功能亢进的93例患者,对术后脾功能亢进完全恢复正常的患者(正常组)和脾功能亢进不能完全恢复或不恢复的患者(异常组)进行比较,并对二组患者术后3个月的血小板计数进行相关性分析.结果 术后脾功能亢进完全恢复的正常组患者为60例(64.5%),脾功能亢进不完全恢复或未恢复的患者为33例(35.5%);正常组新肝期门静脉压力比异常组低(t=5.145;P＜0.01);正常组术后脾静脉血流较术前明显增加(t=2.295,P＜0.05),而异常组术前术后脾静脉血流没有差异;术后3个月血小板计数与术前血小板计数、术前脾大小、新肝期门静脉压力和术后脾脏大小有相关性.结论 肝硬化脾功能亢进患者在肝移植术后仍然存在脾功能亢进表现.术后早期各种原因引起的门脉压力下降不明显、脾血流量改善不良、脾脏缩小不明显等可能是导致脾功能恢复不良的因素.     

Percutaneous intracranial stent placement for aneurysms

OBJECT: Intracranial stent placement combined with coil embolization is an emerging procedure for the treatment of intracranial aneurysms. The authors report their results using intracranial stents for the treatment of intracranial aneurysms. METHODS: A prospectively maintained database was reviewed to identify all patients with intracranial aneurysms that were treated with intracranial stents. Ten lesions, including eight broad-based aneurysms and two dissecting aneurysms, were treated in 10 patients. Four lesions were located in the cavernous segment of the internal carotid artery, two at the vertebrobasilar junction, two at the basilar trunk, one at the basilar apex, and one in the intracranial vertebral artery. Attempts were made to place stents in 13 patients, but in three the stents could not be delivered. Altogether, intracranial stents were placed in 10 patients for 10 lesions. Results that were determined to be satisfactory angiographically were achieved in all 10 lesions. Two patients suffered permanent neurological deterioration related to stent placement. In two patients, the aneurysm recurred after stent-assisted coil embolization. In one case of recurrence a second attempt at coil embolization was successful, whereas in the second case of recurrence parent vessel occlusion was required and well tolerated. CONCLUSIONS: Intracranial stents can be a useful addition to coil embolization by providing mechanical, hemodynamic, and visual benefits in the treatment of complex, broad-based aneurysms.     

Arterial steal: an unusual cause for hepatic hypoperfusion after liver transplantation

Case reports of two patients with an unusual cause for a rapid increase in transaminases following liver transplantation are described. In the postoperative course, angiography revealed an arterial, hypoperfusion of the liver due to a steal phenomenon with blood shunting from the hepatic to the splenic artery. In one case, the underlying pathophysiology was a pre-existing filiform stenosis of the celiac trunk with insufficient recruitment of arterial blood from the superior mesenteric artery via the pancreatic arcade. Adequate liver perfusion was restored by simple ligation of the common hepatic artery. In the other case, angiography showed an arteriovenous fistula formation of the splenic vessels and minimal blood flow through the hepatic vessels. This was successfully corrected by angiographic embolization of the splenic artery with metal coils. After therapeutic intervention, both patients rapidly recovered with excellent liver function.     

Arterial steal: an unusual cause for hepatic hypoperfusion after liver transplantation

Abstract. Case reports of two patients with an unusual cause for a rapid increase in transaminases following liver transplantation are described. In the postoperative course, angiography revealed an arterial hypoperfusion of the liver due to a steal phenomenon with blood shunting from the hepatic to the splenic artery. In one case, the underlying pathophysiology was a pre-existing filiform stenosis of the celiac trunk with insufficient recruitment of arterial blood from the superior mesenteric artery via the pancreatic arcade. Adequate liver perfusion was restored by simple ligation of the common hepatic artery. In the other case, angiography showed an arteriovenous fistula formation of the splenic vessels and minimal blood flow through the hepatic vessels. This was successfully corrected by angiographic embolization of the splenic artery with metal coils. After therapeutic intervention, both patients rapidly recovered with excellent liver function.