|Year : 2017 | Volume
| Issue : 3 | Page : 101-106
Eighty percent partial splenic embolization is a safe and effective procedure in management of cirrhotic hypersplenism
Bor-Gang Wu1, Andy Shau-Bin Chou2, Guan-Jin Ho1, Ming-Che Lee1
1 Department of Surgery, Buddhist Tzu Chi General Hospital; School of Medicine, Tzu Chi University, Hualien, Taiwan
2 Department of Medical Imaging, Buddhist Tzu Chi General Hospital; School of Medicine, Tzu Chi University, Hualien, Taiwan
|Date of Submission||26-Sep-2016|
|Date of Decision||25-Oct-2016|
|Date of Acceptance||03-Nov-2016|
|Date of Web Publication||29-May-2017|
Department of Surgery, Buddhist Tzu Chi General Hospital, 707, Section 3, Chung-Yang Road, Hualien
Source of Support: None, Conflict of Interest: None
Background: Partial splenic embolization (PSE) has been proposed in patients with cirrhotic hypersplenism in cases when thrombocytopenia causes clinical manifestations or if there are contraindications to subsequent therapeutic procedures. We provide a retrospective review of the safety and favorable treatment results of 80% splenic embolization in patients with cirrhotic hypersplenism in our institute.
Methods: Thirteen consecutive patients with cirrhotic hypersplenism were included in a 4-year study period. The indications for PSE were as follows: percutaneous treatment of hepatocellular carcinoma (HCC) (n = 3), transarterial chemoembolization plus hepatic arterial infusion chemotherapy for HCC (n = 2), preparation for major surgery (n = 5), and severe purpura (n = 3). PSE was performed with up to 80% reduction of splenic blood flow by radiological intervention. A tight protocol of prophylactic antibiotics was introduced. Patient demographics, procedure-related complication, and efficacy of PSE were analyzed.
Results: The mean follow-up time was 26.1 ± 12.3 months. All the patients tolerated the procedure. The minor complication of postembolization syndromes such as fever and abdominal pain occurred in 38.5% and 61.5% of patients, respectively. Only a major complication of transient ascites needs diuretic therapy occurred in two patients. Pre-PSE platelet count was 35,077 ± 11,049/mm3, and it significantly increased 1 week after PSE, with a mean increase of platelet count to 384% of pre-PSE level (P < 0.001). The effect of PSE sustained to maintain the platelet count significantly at a mean level of 112,636 ± 33,341/mm3, 114,571 ± 30,696/mm3, and 118,000 ± 31,035/mm3 at 12, 24, and 36 months, respectively.
Conclusion: Our series demonstrated that 80% PSE is a safe and effective method to treat patients with cirrhotic hypersplenism. It could not only increase the platelet count within a short period of time but also maintain it at an acceptable level for a long duration. Under a tight protocol of prophylactic antibiotic and delicate technique of PSE, there was no any septic complication developed in our series.
Keywords: Cirrhosis, complication, hypersplenism, splenic embolization, thrombocytopenia
|How to cite this article:|
Wu BG, Chou AS, Ho GJ, Lee MC. Eighty percent partial splenic embolization is a safe and effective procedure in management of cirrhotic hypersplenism. Formos J Surg 2017;50:101-6
|How to cite this URL:|
Wu BG, Chou AS, Ho GJ, Lee MC. Eighty percent partial splenic embolization is a safe and effective procedure in management of cirrhotic hypersplenism. Formos J Surg [serial online] 2017 [cited 2020 Jan 22];50:101-6. Available from: http://www.e-fjs.org/text.asp?2017/50/3/101/207181
| Introduction|| |
Splenomegaly and hypersplenism, a related hematological syndrome resulting in thrombocytopenia, is frequent in patients with cirrhosis due to portal hypertension but is usually asymptomatic. However, in some patients, severe peripheral cytopenia may prevent clinical treatment of diseases, such as interferon therapy of chronic hepatitis or percutaneous ablation of hepatocellular carcinoma (HCC). Furthermore, severe bouts of purpura or painful splenomegaly may occur. Surgical splenectomy has been once performed to manage this cirrhotic complication but has been discouraged due to its high operative associated morbidity and mortality., Partial splenic embolization (PSE) has been proposed as an alternative treatment modality for the management of cirrhotic hypersplenism. After splenic arterial catheterization, embolization was performed until occlusion of about 50% of splenic arterial blood flow and it resulted in partial necrosis of the spleen. Many investigators had reported the feasibility of the procedure and claimed favorable results in the management of cirrhotic hypersplenism, usually followed by a significant increase in platelet counts., Progressive improvement in liver function following PSE has also been reported.,, However, severe complications such as venous thrombosis, splenic infarction resulting abscess formation, and even death after extensive PSE have been published in certain cases.,,,,, On the other hand, a less aggressive splenic embolization would have a higher recurrence of thrombocytopenia. The aim of the present study was to report both short-term and long-term results of an aggressive PSE, by means of 80% splenic embolization, in our patients with cirrhotic hypersplenism. The detail technique of PSE, patient demographics, and their clinical outcome could be demonstrated.
| Methods|| |
Patient population and clinical management
From December 2003 to December 2007, cirrhotic patients with hypersplenism and thrombocytopenia presented at our institute with at least one indication for PSE were included in this study. The indication for PSE included marked low platelet count <50,000/mm 3 resulting in a hemorrhagic disorder such as severe purpura and gingival bleeding and bleeding tendency in which preventing a percutaneous ablation of liver tumor or transarterial chemoembolization (TACE) of HCC or major surgeries. Only patients with active infection from spontaneous bacterial peritonitis were excluded from such an aggressive treatment protocol. Inform consent was obtained from all patients before the procedure. Patient characteristics, etiology of cirrhosis, Child-Pugh grading of liver function, platelet count before procedure, and indication of PSE were recorded. A tight protocol of prophylactic parenteral antibiotics was followed, with a 10-day course of intravenous injection of 1000 mg cefazoline at an interval of 6 h (3 days before PSE and 7 days thereafter). No pneumococcal vaccination was prescribed before the procedure. The procedure of PSE was done by the single radiologist (Dr. Andy Shau-Bin Chou) using a unique technique. All patients stayed in hospital after the procedure until the postembolization syndrome (PES) or any other significant complications had been disappeared or tolerable. Any complication developed after the procedure was recorded and treated conservatively, if indicated. Conservative management included appropriate hydroelectrolytic infusion and adequate analgesic treatment using acetaminophen, morphine, or nonsteroid anti-inflammatory drugs. No blood transfusion was prescribed during hospitalization. Peripheral blood count was intended to be checked at 1 week and 1, 3, 6, 12, 24, and 36 months after the procedure. A computed tomography (CT) was performed immediately after PSE and at the 2nd post-PSE month to assess the extent of splenic infarction and residual splenic volume semiquantitatively. All blood tests or image studies might be repeated if indicated clinically.
The study was conducted in accordance with the Declaration of Helsinki and was approved by the local ethics committee of the institute. Informed written consent was obtained from all patients prior to their enrollment in this study.
Procedure of partial splenic embolization
Under strict aseptic technique, a percutaneous femoral artery approach was used. The splenic artery was catheterized using 4-Fr RC-1 (Terumo, Tokyo, Japan) as a guiding catheter. The tip of the catheter was placed as distal to the hilus of the spleen as possible. A 2.7-Fr coaxial microcatheter system (Terumo, Tokyo, Japan) was introduced through the 4-Fr RC-1 catheter into the intrasplenic arterial branches. The middle and lower third intrasplenic branches were chosen for embolization. Infusion of polyvinyl alcohol dehydrated particles (Ultra-Drivalon, CatheNet-Science, France) with diameters of 400–600 μm into the selective branches was done. Then, the same branches were embolized by different sized of platinum microcoils (Boston Scientific, Cork, Ireland) according to vessel size. PSE was performed progressively by sequential and repeated injection of particles into each target branch of splenic artery combined with coil embolization until total splenic blood flow had been reduced down to 20% of their original flow with upper pole preserved [Figure 1]. The therapeutic end point was a splenic infarction ratio of 80%. The estimated value was obtained by visual inspection during angiography. The extent of splenic embolization was assessed by evaluation of the peripheral amputation of segmental branches on digital subtraction angiographic acquisition, and the postprocedure CT was also done to estimate the residual splenic volume. Residual splenic volume was defined as noninfarcted splenic tissue which was estimated in contrast-enhanced CT scan. It was obtained by adding enhanced volumes in serial transverse images.
|Figure 1: Procedure of partial splenic embolization. (a) Splenomegaly was shown in computed tomography, (b) A 4-Fr RC-1 Terumo catheter was placed as distal to the hilus of the spleen as possible, (c) sequential and repeated injection of particles into each target branch of splenic artery combined with coil embolization until total splenic blood flow had been reduced down to 20% of their original flow with upper pole preserved|
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Data were processed and analyzed using the SPSS 12.0 Statistical Software (SPSS 12.0 version for Windows, SPSS Inc., Chicago, IL, USA). Frequency and proportion were used to summarize the categorical variables in patient characteristics. The values of platelet count in different periods of following time were expressed as mean ± standard deviation. The paired t-test was performed to identify the difference of platelet count between pre- and post-PSE. P < 0.05 was considered statistically significant.
| Results|| |
Thirteen consecutive patients, included nine men and four women, underwent PSE and were followed with a mean duration of 26.1 ± 12.3 months (range: 1–44 months). The patients' age, gender, etiology of cirrhosis, Child-Pugh grading, and indications for PSE were summarized in [Table 1]. PSE was successfully performed in all patients, and all the immediate post-PSE CTs showed estimated 80% splenic infarction after embolization. In those nine patients who have performed CT at the 2nd post-PSE month, seven patients still maintained a residual splenic volume about 20% of pretreatment volume [Figure 2]. The other two patients were estimated to have 30% estimated residual splenic volume 1 month after PSE. Neither splenic rupture nor evidence of abscess could be found by CT image.
|Table 1: Partial splenic embolization in 13 cirrhotic hypersplenism patients: patient characteristics, indication, and complication|
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|Figure 2: The 2nd post-PES CT of abdomen from the same patient of Figure 1. (a) The spleen was infracted and liquefied. There was no perisplenic infiltration which indicated inflammatory process such as abscess formation could be identified. (b) About 20% splenic volume was preserved one month after PSE|
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Nine of 13 patients have experienced of PES in different degrees after PSE. Five patients (38.5%) were febrile and 8 patients (61.5%) complaint abdominal pain in whom medications were necessary to relief the symptom. Transient ascites was occurred in two patients (15.4%) and both of them need diuretic therapy to control the ascites. No significant change in serum bilirubin level and prothrombin activity could be observed in both patients with impaired liver function.
Five patients underwent either successful percutaneous radiofrequency ablation or TACE for their HCC, and another five major operations including three orthopedic surgeries and two laparoscopic surgeries were completed without hematological complication such as bleeding and coagulopathy. Four patients were dead during the study period. One patient died of terminal stage of metastatic squamous cell carcinoma with multi-organ failure in the 19th month after PSE. One patient died of esophageal bleeding associated with acute myocardial infarction in the 32nd month after PSE. The other two patients with HCC died of unknown etiology in the 18th and 28th month after PSE, respectively. None of the death was caused directly due to the procedure.
The change of platelet count during the 1st year after PSE is demonstrated in [Figure 3]. Platelet count dramatically increased soon at day 7 after PSE, with a mean level of 35,077 ± 11,049/mm 3 before the procedure up to 134,833 ± 48,585/mm 3 at 1 week, that is, a mean increase of platelet count to 384% of pre-PSE level (P < 0.001). A progressive decline in platelet count was observed from 1 to 3 months after PSE, and it was then constantly maintained thereafter up to 1 year. In those patients who be followed at least 12 months after PSE, 10 of 11 patients had a sustained platelet count >85,000/mm 3 at 12 months, with a mean level of 112,636 ± 33,341/mm 3. For those six patients who were followed for 36 months after PSE, the mean platelet count was still significantly increased as compared to pre-PSE count (118,000 ± 31,035 vs. 35,077 ± 11,049/mm 3, P = 0.001).
| Discussion|| |
Patients who have advanced liver disease can experience severe bleeding or thrombotic complications. Bleeding complications cause by both thrombocytopenia and impaired coagulation function, and thrombotic complications cause by impaired anticoagulant factors. The most common cause of thrombocytopenia in cirrhotic patients is hypersplenism. Cirrhotic hypersplenism can result in excessive trapping and clearing of the cellular blood elements by the enlarged and congested spleen. Several treatment modalities for the management of such complication of thrombocytopenia have been postulated. They included infusion of platelets, thrombopoietin or interleukin-11, splenic ablation, and shunt operation or transjugular intrahepatic portosystemic shunt (TIPS). Thrombocytopenia should not be considered as a primary indication for TIPS because of the risk associated with the procedure and its long-term side effects such as occlusion of shunt. In those treatment modalities, only shunt operation and splenic ablation have the long-term efficacy. PSE combined with repeated embolization in the treatment of ITP had also been reported.
The efficacy of PSE observed in our study confirms the results of previously published studies in the management of patients with cirrhotic hypersplenism.,,,, In particular, a marked increase in platelet count occurred in all our patients under such an aggressive PSE. The platelet count could be maintained over an acceptable level of 80,000/mm 3 at 1 year after PSE in most of the cases. Severe purpura of skin and gingival bleeding could be successfully controlled. All the patients could proceed to undergo either regular surgical intervention or percutaneous procedures without any hematological complication. Although the PES developed in 69.2% of our patients within 1 week after PSE, it would be resolved rapidly in almost patients after conservative treatment. Transient ascites occurred in two Child-Pugh grading B patients in this series. Such a complication could result either from hepatic decompensation secondary to splenic necrosis or peritoneal inflammation. In both cases, ascites was resolved after diuretic therapy. Other major complications of PSE such as rupture of the spleen, splenic abscess, pneumonia associated with pleural effusion, and septicemia have all been reported., Owman et al. demonstrated that a positive correlation between the risk of abscess and the volume of spleen necrosis. Therefore, the authors recommended that PSE must be strictly limited to reduce only 50% of the original splenic volume. The delayed occurrence of septic complication due to superimposed infection of splenic necrosis rather than contamination during the procedure has also been illustrated, and close clinical follow-up was suggested., In another review of 260 patients, the complication rate of 80% PSE was not necessarily higher than 50%. Hayashi et al. performed 70%–80% PSE without procedure-related death, and they concluded that the increase in platelet count was greatly dependent on the infarcted splenic volume. There were three patients (9.50%) developed pleural effusion in their series but none in ours. Our results revealed that pleural effusion might be preventable by the preservation of splenic upper pole. In our study, all patients underwent 80% PSE and no any septic complication developed in the long-term follow-up period. It may be contributed to the tight protocol of prophylactic antibiotics usage and the unique technique of splenic embolization using the sterile technique and materials for embolization.
Other major complication such as splenic vein thrombosis in which maybe asymptomatic in the initial presentation and would develop symptoms late after PSE was also illustrated. Hence, a monthly ultrasound examination was suggested at least 3 months after the procedure in those cases of splenic necrosis above 50%. In our study, we did CT image to evaluate the area of splenic necrosis at the 2nd post-PSE month. We could not find any patient that had either splenic or portal vein thrombosis at this period. Although we did not examine the patients by image so frequently, most of the patients who under regular followed in clinic were free of symptoms clinically.
Recurrence of thrombocytopenia was one of the major concerns for PSE in the management of cirrhotic hypersplenism. It may cause by revascularization or reperfusion of the embolized splenic arteries. The recanalization rate after endovascular embolization of visceral artery has been reported in the 0%–50% in the literature. In the most recent series, reperfusion after splenic artery embolization was estimated around 4.5%., To the present study, although the platelet count would decline 1 month after PSE, the level of platelet count could be maintained in a higher level than pre-PSE stage after 3 months of PSE without clinical symptoms. All the six patients who followed for more than 36 months could also maintain high platelet counts. Hence, the effect of revascularization or reperfusion of the embolized splenic arteries would develop 1 month after PES, but it did not have a significant impact on the long-term result of platelet count in patients with 80% PES.
| Conclusion|| |
PSE may resolve cytopenia and the clinical complications related to cirrhotic hypersplenism and splenomegaly. However, the indication of PSE has been limited to some selective cases due to its high risk of severe complications such as splenic abscess and septicemia. Furthermore, the extent of splenic necrosis should be strictly controlled during the procedure. In the present study, 80% PSE was performed in patients with cirrhotic hypersplenism complicated with bleeding tendency or ready for surgical or percutaneous procedure for their specific diseases. Our results revealed that 80% PSE was feasible and safe. It could not only increase the platelet count within in a short period but also would not increase the risk of septic complication such as splenic abscess or septicemia. The effect of PSE could be maintained for a long time after 80% reduction of splenic blood flow. Hence, our study of 80% PSE may provide a better result in the management of cirrhotic hypersplenism than previously published reports. Of course, a tight protocol of prophylactic antibiotics and delicate technique of splenic embolization is mandatory to such a better outcome.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Lisman T, Leebeek FW, de Groot PG. Haemostatic abnormalities in patients with liver disease. J Hepatol 2002;37:280-7.
Grassi CJ, Boxt LM, Bettmann MA. Partial splenic embolization for painful splenomegaly. Cardiovasc Intervent Radiol 1987;10:291-4.
Cao ZX, Chen XP, Wu ZD. Effects of splenectomy in patients with cirrhosis undergoing hepatic resection for hepatocellular carcinoma. World J Gastroenterol 2003;9:2460-3.
Wu CC, Cheng SB, Ho WM, Chen JT, Yeh DC, Liu TJ, et al.
Appraisal of concomitant splenectomy in liver resection for hepatocellular carcinoma in cirrhotic patients with hypersplenic thrombocytopenia. Surgery 2004;136:660-8.
Mozes MF, Spigos DG, Pollak R, Abejo R, Pavel DG, Tan WS, et al.
Partial splenic embolization, an alternative to splenectomy – Results of a prospective, randomized study. Surgery 1984;96:694-702.
N'Kontchou G, Seror O, Bourcier V, Mohand D, Ajavon Y, Castera L, et al.
Partial splenic embolization in patients with cirrhosis: Efficacy, tolerance and long-term outcome in 32 patients. Eur J Gastroenterol Hepatol 2005;17:179-84.
Tajiri T, Onda M, Yoshida H, Mamada Y, Taniai N, Kumazaki T. Long-term hematological and biochemical effects of partial splenic embolization in hepatic cirrhosis. Hepatogastroenterology 2002;49:1445-8.
Noguchi H, Hirai K, Aoki Y, Sakata K, Tanikawa K. Changes in platelet kinetics after a partial splenic arterial embolization in cirrhotic patients with hypersplenism. Hepatology 1995;22:1682-8.
Murata K, Shiraki K, Takase K, Nakano T, Tameda Y. Long term follow-up for patients with liver cirrhosis after partial splenic embolization. Hepatogastroenterology 1996;43:1212-7.
Vujic I, Lauver JW. Severe complications from partial splenic embolization in patients with liver failure. Br J Radiol 1981;54:492-5.
Sakai T, Shiraki K, Inoue H, Sugimoto K, Ohmori S, Murata K, et al.
Complications of partial splenic embolization in cirrhotic patients. Dig Dis Sci 2002;47:388-91.
Ohmoto K, Iguchi Y, Miyake I, Ohno S, Yamamoto S. Long-term evaluation of partial splenic embolization for liver cirrhosis and hepatocellular carcinoma accompanied by hypersplenism. Hepatol Res 1998;11:73-83.
Owman T, Lunderquist A, Alwmark A, Borjesson B. Embolization of the spleen for treatment of splenomegaly and hypersplenism in patients with portal hypertension. Invest Radiol 1979;14:457-64.
Alwmark A, Bengmark S, Gullstrand P, Joelsson B, Lunderquist A, Owman T. Evaluation of splenic embolization in patients with portal hypertension and hypersplenism. Ann Surg 1982;196:518-24.
Hadduck TA, McWilliams JP. Partial splenic artery embolization in cirrhotic patients. World J Radiol 2014;6:160-8.
Trotter JF. Coagulation abnormalities in patients who have liver disease. Clin Liver Dis 2006;10:665-78, x-xi.
Sanyal AJ. The use and misuse of transjugular intrahepatic portasystemic shunts. Curr Gastroenterol Rep 2000;2:61-71.
Kimura F, Itoh H, Ambiru S, Shimizu H, Togawa A, Yoshidome H, et al.
Long-term results of initial and repeated partial splenic embolization for the treatment of chronic idiopathic thrombocytopenic purpura. AJR Am J Roentgenol 2002;179:1323-6.
Sangro B, Bilbao I, Herrero I, Corella C, Longo J, Beloqui O, et al.
Partial splenic embolization for the treatment of hypersplenism in cirrhosis. Hepatology 1993;18:309-14.
Spigos DG, Jonasson O, Mozes M, Capek V. Partial splenic embolization in the treatment of hypersplenism. AJR Am J Roentgenol 1979;132:777-82.
Shah R, Mahour GH, Ford EG, Stanley P. Partial splenic embolization. An effective alternative to splenectomy for hypersplenism. Am Surg 1990;56:774-7.
Hayashi H, Beppu T, Masuda T, Mizumoto T, Takahashi M, Ishiko T, et al.
Predictive factors for platelet increase after partial splenic embolization in liver cirrhosis patients. J Gastroenterol Hepatol 2007;22:1638-42.
Carr SC, Mahvi DM, Hoch JR, Archer CW, Turnipseed WD. Visceral artery aneurysm rupture. J Vasc Surg 2001;33:806-11.
Abbas MA, Stone WM, Fowl RJ, Gloviczki P, Oldenburg WA, Pairolero PC, et al.
Splenic artery aneurysms: Two decades experience at Mayo clinic. Ann Vasc Surg 2002;16:442-9.
Saltzberg SS, Maldonado TS, Lamparello PJ, Cayne NS, Nalbandian MM, Rosen RJ, et al.
Is endovascular therapy the preferred treatment for all visceral artery aneurysms? Ann Vasc Surg 2005;19:507-15.
[Figure 1], [Figure 2], [Figure 3]