HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Figures Only Full Text (PDF) CME Test (opens in a new window) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Madoff, D. C. Articles by Hicks, M. E. Search for Related Content PubMed PubMed Citation Articles by Madoff, D. C. Articles by Hicks, M. E. Related Collections Vascular and/or Interventional Radiology Gastrointestinal Radiology

Splenic Arterial Interventions: Anatomy, Indications, Technical Considerations, and Potential Complications¹

¹ From the Division of Diagnostic Imaging, Interventional Radiology Section, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Unit 325, Houston, TX 77030-4009 (D.C.M., M.J.W., R.M., S.G., E.P.P., K.A., M.E.H.); and Department of Radiology and Interventional Radiology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland (A.D., B.B.). Recipient of a Cum Laude award for an education exhibit at the 2004 RSNA Annual Meeting. Received February 3, 2005; revision requested March 4 and received April 19; accepted April 25. The authors discuss an investigational or unlabeled use of a commercial product, device, or pharmaceutical that has not been approved for such purpose by the FDA. All authors have no financial relationships to disclose. Address correspondence to D.C.M. (e-mail: dmadoff{at}di.mdacc.tmc.edu).

	Abstract

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
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.

© RSNA, 2005

	LEARNING OBJECTIVES FOR TEST 6

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
After reading this article and taking the test, the reader will be able to:

• Identify the splenic vascular anatomy as it pertains to splenic arterial interventions.
  
• Describe the indications, contraindications, and technical considerations for splenic arterial interventions in various clinical situations.
  
• Discuss the pitfalls and complications associated with splenic arterial interventions.
  

	Introduction

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Splenic arterial interventions are increasingly used to treat various medical disorders and, when clinically appropriate, may be substituted for surgery. For example, embolization is often performed to treat posttraumatic splenic injuries and to improve hematologic parameters (ie, to treat pancytopenia, thrombocytopenia, leukopenia, or anemia) in patients with hypersplenism and in those who require high-dose chemotherapy or immunosuppressive therapy and who otherwise would be ineligible to receive that therapy. Embolization and/or stent-graft placement may be used also to exclude splenic artery aneurysms from the normal vessel lumen and thereby prevent aneurysm rupture. Further, embolization may be performed 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 manage neoplastic disease in the splenic parenchyma. As the use of interventions such as embolization and stent-graft placement in the splenic arteries becomes more widespread, clinicians involved in interventional radiology practice need to develop an understanding of the potential and limitations of these procedures. Toward that end, this article provides a succinct overview of the splenic vascular anatomy, the indications and contraindications for performing arterial interventions, the technical considerations that affect decisions about the target (proximal versus distal arterial segment) and the extent (partial vs complete) of embolization and other interventions, and possible complications of these procedures (eg, abscess formation and pancreatitis). Recent experience with transarterial irradiation for cancer of the spleen is summarized. The possible combination of interventions such as radiofrequency ablation with splenic arterial interventions also is discussed. Throughout, the results of clinical and experimental studies are reviewed to highlight the potential benefits and pitfalls of interventions for specific indications and to provide a glimpse of possible future trends in the use of these procedures.

	Splenic Vascular Anatomy

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
The splenic artery supplies the spleen and substantial portions of the stomach and pancreas (Fig 1) (1). The splenic artery courses superior and anterior to the splenic vein, along the superior edge of the pancreas. Near the splenic hilum, the artery usually divides into superior and inferior terminal branches, and each branch further divides into four to six segmental intrasplenic branches. The superior terminal branches are usually longer than the inferior terminal branches and provide the major splenic arterial supply. A superior polar artery usually arises from the distal splenic artery near the hilum, but it may originate from the superior terminal artery. The inferior polar artery usually gives rise to the left gastroepiploic artery, but the latter may also arise from the distal splenic or inferior terminal artery. The left gastroepiploic artery then runs along the greater curvature of the stomach. Numerous short gastric branches arise from the terminal splenic or left gastroepiploic artery to supply the gastric cardia and fundus.

View larger version (72K): [in this window] [in a new window] [Download PPT slide]   Figure 1.  Three-dimensional drawing of normal anatomy in the upper abdomen shows the main splenic artery and its branches.

	Splenic Trauma

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Background
The spleen is the solid organ most frequently injured in blunt abdominal trauma. In the past 3 decades, the treatment of traumatic splenic injuries has changed substantially, from surgical to nonsurgical management. The risk of fatal postsplenectomy sepsis or impaired resistance to certain infections later in life has motivated trauma physicians to adopt procedures that maximize splenic preservation (2). Nonsurgical management with bed rest and observation traditionally has been the treatment of choice for splenic injury in pediatric patients. The Eastern Association for the Surgery of Trauma Practice Management Guidelines Working Group has advocated the use of nonsurgical management as the first-line therapy also in adults (3). These recommendations, however, were based on the results of noncomparative prospective and retrospective controlled studies. Moreover, high failure rates (from 2% to 52%) with nonsurgical management in adults, with a resultant need for secondary splenectomy, have been reported (4,5).

Computed tomography (CT) may be useful for detecting extravasation of contrast material–enhanced blood or pseudoaneurysm suggestive of active hemorrhage and for classifying splenic injury according to its severity (Table). Velmahos et al (7) reported that the CT grade of splenic injury is an independent risk factor for failure of nonsurgical management, while investigators in a more recent study found that the risk of nonsurgical management failure was 44% in patients with splenic injury of grade 3 or higher (4). Splenic arterial embolization has been proposed to reduce the risk of nonsurgical management failure in both adults and children.

Technique of Splenic Arterial Embolization
At arteriography, frank extravasation is rare. More commonly, an arteriovenous fistula, pseudoaneurysm, or abrupt vessel truncation is depicted. A unique appearance characterized by punctate areas of parenchymal blush in the intra-splenic arteries (similar to the points of color in pointillist paintings) may be observed and is usually considered to indicate splenic contusion (11). A patient whose hemodynamic condition becomes unstable during the procedure may require immediate proximal embolization of the splenic artery. Extensive injury that involves multiple arterial branches renders individual lesion treatment impractical. Abnormalities identified on preprocedural CT scans may prompt an empiric proximal embolization.

The decision to use a particular embolic agent depends on the ability to access the target and on the nature of the lesion. When accessible, arteriovenous fistulas and pseudoaneurysms are treated with coils and/or gelatin sponges to augment hemostasis (Figs 2, 3). The incidence of segmental splenic infarction and intrasplenic air is increased with distal embolization (12). The presence of air in the spleen, unlike that in other organ systems, does not always indicate abscess formation. Splenic abscess occurs in a small percentage of patients and may be successfully managed percutaneously or intraoperatively (12,13). Salvage rates are similar whether embolization is performed in an artery segment distal or proximal to the splenic artery origin (14).

View larger version (167K): [in this window] [in a new window] [Download PPT slide]   Figure 2a.  Splenic arterial embolization for treatment of splenic laceration due to blunt abdominal trauma in a 26-year-old man. (a) Transverse contrast-enhanced CT scan shows active extravasation (arrow). (b) Splenic arteriogram obtained before intervention shows multiple pseudoaneurysms (arrows) in the upper pole of the spleen. (c) Postprocedural splenic arteriogram shows successful embolization with coils in the splenic artery.

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 2b.  Splenic arterial embolization for treatment of splenic laceration due to blunt abdominal trauma in a 26-year-old man. (a) Transverse contrast-enhanced CT scan shows active extravasation (arrow). (b) Splenic arteriogram obtained before intervention shows multiple pseudoaneurysms (arrows) in the upper pole of the spleen. (c) Postprocedural splenic arteriogram shows successful embolization with coils in the splenic artery.

View larger version (104K): [in this window] [in a new window] [Download PPT slide]   Figure 2c.  Splenic arterial embolization for treatment of splenic laceration due to blunt abdominal trauma in a 26-year-old man. (a) Transverse contrast-enhanced CT scan shows active extravasation (arrow). (b) Splenic arteriogram obtained before intervention shows multiple pseudoaneurysms (arrows) in the upper pole of the spleen. (c) Postprocedural splenic arteriogram shows successful embolization with coils in the splenic artery.

View larger version (154K): [in this window] [in a new window] [Download PPT slide]   Figure 3a.  Partial splenic arterial embolization in a 45-year-old man with blunt abdominal trauma from a motor vehicle accident. (a) Splenic arteriogram obtained before intervention shows multiple pseudoaneurysms (arrows) and reduced parenchymal blush in the upper pole of the spleen. (b) Splenic arteriogram obtained after embolization of the pseudoaneurysms with gelatin sponge pledgets shows continuation of blood flow to the inferior pole of the spleen (arrowheads).

View larger version (154K): [in this window] [in a new window] [Download PPT slide]   Figure 3b.  Partial splenic arterial embolization in a 45-year-old man with blunt abdominal trauma from a motor vehicle accident. (a) Splenic arteriogram obtained before intervention shows multiple pseudoaneurysms (arrows) and reduced parenchymal blush in the upper pole of the spleen. (b) Splenic arteriogram obtained after embolization of the pseudoaneurysms with gelatin sponge pledgets shows continuation of blood flow to the inferior pole of the spleen (arrowheads).

Use of Vaccination to Prevent Gram-Positive Sepsis
The development of overwhelming pneumococcal sepsis syndrome has been well established in the absence of splenic function or in the presence of decreased splenic function (17–19). Pneumococcal vaccination decreases the incidence of overwhelming pneumococcal sepsis syndrome (20). Surgical techniques for splenic preservation (partial splenectomy and reimplantation) and perioperative pneumococcal vaccination are thought to decrease the risk for overwhelming pneumococcal sepsis syndrome in asplenic patients. However, pneumococcal vaccination does not appear to be used routinely for the prevention of overwhelming pneumococcal sepsis syndrome in patients who undergo nonsurgical intervention. In a recent survey of 261 trauma surgeons, pneumococcal vaccine was reported to have been administered in 99.7% of patients who underwent splenectomy but in only 15.7% and 8.4% of patients who underwent splenorrhaphy and nonsurgical therapy, respectively (8). In addition, a little more than half of all surgeons surveyed had administered vaccinations against Haemophilus influenzae and Neisseria meningitidis concomitantly with the pneumococcal vaccine. To our knowledge, there are no published reports about the immunologic consequences of splenic arterial embolization and the role, if any, of vaccination in this setting.

	Hypersplenism

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Background
Surgical removal or transcatheter ablation of splenic parenchyma is often performed for the management of hypersplenism, a pathologic condition that is characterized by increased pooling or destruction of the corpuscular elements of the blood by the spleen (21). Hypersplenism may be seen in many disorders, including cirrhosis with portal hypertension (22,23); hematologic abnormalities such as idiopathic thrombocytopenic purpura, thalassemia major, and hereditary spherocytosis (24–27); and diffuse splenic infiltration from primary malignancies such as leukemia and lymphoma (28,29). Signs of hypersplenism include splenomegaly, thrombocytopenia, leukopenia, and anemia, and symptoms may include abdominal discomfort, pain, respiratory distress, and early satiety (30,31).

Rationale for Partial Embolization
Total splenectomy may be an effective treatment for hypersplenism, but it impairs the body’s ability to produce antibodies against encapsulated microorganisms and predisposes patients to sepsis. After splenectomy, the condition that was treated with this surgery may recur, with the possible result that a second surgical operation or additional transfusion will be needed. Patients who have comorbid conditions and severe cytopenia may not be considered candidates for this surgery. However, the removal of functional splenic tissue may improve hematologic abnormalities related to bone marrow suppression from systemic chemotherapeutic and immunosuppressive agents, so that optimal doses of such medications can be maintained (32,33).

The use of splenic arterial embolization also has been advocated for the intentional infarction of splenic tissue to reduce its consumptive activity. In 1973, Maddison (34) reported the initial clinical experience with splenic arterial embolization for this purpose, but severe complications of complete splenic infarction prevented its acceptance as a viable treatment option. Since then, many authors have advocated incomplete or partial splenic arterial embolization, in which a portion of the splenic parenchyma is left viable to preserve the spleen’s immunologic function.

Partial splenic arterial embolization evolved as initial attempts to treat hypersplenism with proximal splenic arterial occlusion proved unsuccessful. Treatment failures were attributed to abundant collateral circulation via short gastric and gastroepiploic arteries that reestablished the splenic blood supply around the occluded segment of the splenic artery (Fig 4). Although proximal arterial occlusion is ineffective for the management of hypersplenism, it is useful as a preoperative technique for reducing intraoperative blood loss in thrombocytopenic patients undergoing open or laparoscopic splenectomy (35,36).

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 4a.  Splenic arterial embolization in a 48-year-old woman with idiopathic thrombocytopenic purpura and splenomegaly. Because of comorbidity in this patient, embolization was preferred to splenectomy. (a) Splenic arteriogram obtained prior to treatment shows an enlarged spleen. (b) Splenic arteriogram obtained after embolization with microparticles (500–700 µm) and coils shows complete occlusion of the splenic artery. (c) Transverse contrast-enhanced CT scan obtained at follow-up shows a coil within the splenic artery (arrow), as well as complete infarction of the spleen, which is not contrast enhanced. After embolization, the platelet count returned to normal levels; 6 months later, however, symptoms recurred and embolization was repeated. (d) Arteriogram obtained after recurrence of symptoms and before second embolization shows a small pancreatic branch (arrow) that supplies blood to part of the lower pole of the spleen. Repeat embolization was performed with n-butyl-cyanoacrylate.

View larger version (128K): [in this window] [in a new window] [Download PPT slide]   Figure 4b.  Splenic arterial embolization in a 48-year-old woman with idiopathic thrombocytopenic purpura and splenomegaly. Because of comorbidity in this patient, embolization was preferred to splenectomy. (a) Splenic arteriogram obtained prior to treatment shows an enlarged spleen. (b) Splenic arteriogram obtained after embolization with microparticles (500–700 µm) and coils shows complete occlusion of the splenic artery. (c) Transverse contrast-enhanced CT scan obtained at follow-up shows a coil within the splenic artery (arrow), as well as complete infarction of the spleen, which is not contrast enhanced. After embolization, the platelet count returned to normal levels; 6 months later, however, symptoms recurred and embolization was repeated. (d) Arteriogram obtained after recurrence of symptoms and before second embolization shows a small pancreatic branch (arrow) that supplies blood to part of the lower pole of the spleen. Repeat embolization was performed with n-butyl-cyanoacrylate.

View larger version (162K): [in this window] [in a new window] [Download PPT slide]   Figure 4c.  Splenic arterial embolization in a 48-year-old woman with idiopathic thrombocytopenic purpura and splenomegaly. Because of comorbidity in this patient, embolization was preferred to splenectomy. (a) Splenic arteriogram obtained prior to treatment shows an enlarged spleen. (b) Splenic arteriogram obtained after embolization with microparticles (500–700 µm) and coils shows complete occlusion of the splenic artery. (c) Transverse contrast-enhanced CT scan obtained at follow-up shows a coil within the splenic artery (arrow), as well as complete infarction of the spleen, which is not contrast enhanced. After embolization, the platelet count returned to normal levels; 6 months later, however, symptoms recurred and embolization was repeated. (d) Arteriogram obtained after recurrence of symptoms and before second embolization shows a small pancreatic branch (arrow) that supplies blood to part of the lower pole of the spleen. Repeat embolization was performed with n-butyl-cyanoacrylate.

View larger version (150K): [in this window] [in a new window] [Download PPT slide]   Figure 4d.  Splenic arterial embolization in a 48-year-old woman with idiopathic thrombocytopenic purpura and splenomegaly. Because of comorbidity in this patient, embolization was preferred to splenectomy. (a) Splenic arteriogram obtained prior to treatment shows an enlarged spleen. (b) Splenic arteriogram obtained after embolization with microparticles (500–700 µm) and coils shows complete occlusion of the splenic artery. (c) Transverse contrast-enhanced CT scan obtained at follow-up shows a coil within the splenic artery (arrow), as well as complete infarction of the spleen, which is not contrast enhanced. After embolization, the platelet count returned to normal levels; 6 months later, however, symptoms recurred and embolization was repeated. (d) Arteriogram obtained after recurrence of symptoms and before second embolization shows a small pancreatic branch (arrow) that supplies blood to part of the lower pole of the spleen. Repeat embolization was performed with n-butyl-cyanoacrylate.

View larger version (134K): [in this window] [in a new window] [Download PPT slide]   Figure 5a.  Complete splenic arterial embolization performed in a 45-year-old man with acute myelogenous leukemia and refractory thrombocytopenia (platelet count, <10 x 109/L) after bone marrow transplantation. Embolization was performed immediately before splenectomy, to reduce intraoperative blood loss. (a) Splenic arteriogram obtained before embolization shows normal splenic anatomy. (b) Postembolization arteriogram shows complete occlusion of the splenic artery after infusion of polyvinyl alcohol particles (diameter range, 500–700 µm) and placement of a coil. Within 2 months of treatment, the platelet count returned to normal levels.

View larger version (141K): [in this window] [in a new window] [Download PPT slide]   Figure 5b.  Complete splenic arterial embolization performed in a 45-year-old man with acute myelogenous leukemia and refractory thrombocytopenia (platelet count, <10 x 109/L) after bone marrow transplantation. Embolization was performed immediately before splenectomy, to reduce intraoperative blood loss. (a) Splenic arteriogram obtained before embolization shows normal splenic anatomy. (b) Postembolization arteriogram shows complete occlusion of the splenic artery after infusion of polyvinyl alcohol particles (diameter range, 500–700 µm) and placement of a coil. Within 2 months of treatment, the platelet count returned to normal levels.

View larger version (77K): [in this window] [in a new window] [Download PPT slide]   Figure 6.  Three-dimensional drawing of selective partial splenic arterial embolization shows change in color (brown area) that represents absence of perfusion in the inferior portion of the spleen. PVA/EMBO = polyvinyl alcohol particles/embolization.

View larger version (154K): [in this window] [in a new window] [Download PPT slide]   Figure 7a.  Partial splenic arterial embolization in a 47-year-old woman with locally advanced pancreatic carcinoma and thrombocytopenia precluding further chemotherapy. (a, b) Arteriograms obtained before embolization show normal splenic anatomy (a) and the superior segment of the splenic artery (b) that was targeted for selective embolization with particles (diameter range, 300–500 µm). (c) Postembolization arteriogram shows complete occlusion of the targeted splenic artery segment. Within 1 month after embolization, the patient’s platelet count had increased to more than 400 x 109/L.

View larger version (148K): [in this window] [in a new window] [Download PPT slide]   Figure 7b.  Partial splenic arterial embolization in a 47-year-old woman with locally advanced pancreatic carcinoma and thrombocytopenia precluding further chemotherapy. (a, b) Arteriograms obtained before embolization show normal splenic anatomy (a) and the superior segment of the splenic artery (b) that was targeted for selective embolization with particles (diameter range, 300–500 µm). (c) Postembolization arteriogram shows complete occlusion of the targeted splenic artery segment. Within 1 month after embolization, the patient’s platelet count had increased to more than 400 x 109/L.

View larger version (151K): [in this window] [in a new window] [Download PPT slide]   Figure 7c.  Partial splenic arterial embolization in a 47-year-old woman with locally advanced pancreatic carcinoma and thrombocytopenia precluding further chemotherapy. (a, b) Arteriograms obtained before embolization show normal splenic anatomy (a) and the superior segment of the splenic artery (b) that was targeted for selective embolization with particles (diameter range, 300–500 µm). (c) Postembolization arteriogram shows complete occlusion of the targeted splenic artery segment. Within 1 month after embolization, the patient’s platelet count had increased to more than 400 x 109/L.

View larger version (77K): [in this window] [in a new window] [Download PPT slide]   Figure 8.  Three-dimensional drawing of nonselective partial splenic arterial embolization with gelatin sponge pledgets shows patchy changes in perfusion (brown areas) throughout the splenic parenchyma.

View larger version (120K): [in this window] [in a new window] [Download PPT slide]   Figure 9a.  Partial splenic arterial embolization performed to increase the white blood cell and platelet counts before additional chemotherapy in a 48-year-old man with pancreatic cancer and persistent neutropenia and thrombocytopenia. (a) Transverse CT scan of the abdomen shows splenomegaly before embolization. (b) Splenic arteriogram, obtained before embolization, shows normal anatomy and parenchymal enhancement pattern. (c) Splenic arteriogram, obtained after nonselective embolization with gelatin sponge pledgets, shows abrupt occlusion (arrows) of many splenic arterial branches and patchy remnants (10%–20%) of parenchymal blush. (d) Transverse CT scan, obtained 4 months after embolization, shows massive necrosis (arrows) of the splenic parenchyma. Within 2 weeks after embolization, the platelet count returned to a normal level (379 x 109/L).

View larger version (164K): [in this window] [in a new window] [Download PPT slide]   Figure 9b.  Partial splenic arterial embolization performed to increase the white blood cell and platelet counts before additional chemotherapy in a 48-year-old man with pancreatic cancer and persistent neutropenia and thrombocytopenia. (a) Transverse CT scan of the abdomen shows splenomegaly before embolization. (b) Splenic arteriogram, obtained before embolization, shows normal anatomy and parenchymal enhancement pattern. (c) Splenic arteriogram, obtained after nonselective embolization with gelatin sponge pledgets, shows abrupt occlusion (arrows) of many splenic arterial branches and patchy remnants (10%–20%) of parenchymal blush. (d) Transverse CT scan, obtained 4 months after embolization, shows massive necrosis (arrows) of the splenic parenchyma. Within 2 weeks after embolization, the platelet count returned to a normal level (379 x 109/L).

View larger version (167K): [in this window] [in a new window] [Download PPT slide]   Figure 9c.  Partial splenic arterial embolization performed to increase the white blood cell and platelet counts before additional chemotherapy in a 48-year-old man with pancreatic cancer and persistent neutropenia and thrombocytopenia. (a) Transverse CT scan of the abdomen shows splenomegaly before embolization. (b) Splenic arteriogram, obtained before embolization, shows normal anatomy and parenchymal enhancement pattern. (c) Splenic arteriogram, obtained after nonselective embolization with gelatin sponge pledgets, shows abrupt occlusion (arrows) of many splenic arterial branches and patchy remnants (10%–20%) of parenchymal blush. (d) Transverse CT scan, obtained 4 months after embolization, shows massive necrosis (arrows) of the splenic parenchyma. Within 2 weeks after embolization, the platelet count returned to a normal level (379 x 109/L).

View larger version (125K): [in this window] [in a new window] [Download PPT slide]   Figure 9d.  Partial splenic arterial embolization performed to increase the white blood cell and platelet counts before additional chemotherapy in a 48-year-old man with pancreatic cancer and persistent neutropenia and thrombocytopenia. (a) Transverse CT scan of the abdomen shows splenomegaly before embolization. (b) Splenic arteriogram, obtained before embolization, shows normal anatomy and parenchymal enhancement pattern. (c) Splenic arteriogram, obtained after nonselective embolization with gelatin sponge pledgets, shows abrupt occlusion (arrows) of many splenic arterial branches and patchy remnants (10%–20%) of parenchymal blush. (d) Transverse CT scan, obtained 4 months after embolization, shows massive necrosis (arrows) of the splenic parenchyma. Within 2 weeks after embolization, the platelet count returned to a normal level (379 x 109/L).

The techniques developed and used at different centers vary greatly, but general guidelines that are known collectively as the Spigos technique (41) have helped substantially to reduce complications. The protocol includes the administration of broad-spectrum antibiotics 8–12 hours before the procedure and for 1–2 weeks thereafter and of local antibiotics (such as gentamicin) suspended in the embolic solution, strict attention to sterility (whole-body povidoneiodine bath or wide surgical scrub at the site of catheter insertion), selective catheterization beyond the origin of major pancreatic artery branches to prevent their embolization, effective pain control with narcotics or epidural anesthetics for 48 hours (to prevent splinting and pulmonary complications such as atelectasis and pneumonia), and avoidance of excessive embolization (eg, infarction of more than 80% of the splenic mass). To help prevent pneumococcal infection, a polyvalent pneumococcal vaccine (Pneumovax 23; Merck Sharp & Dohme, Hoddesdon, England) was administered before the procedures (41).

More recently, Harned et al (42) evaluated the effect of partial splenic arterial embolization (infarction of 30%–40% of the splenic mass) and found that the reduced extent of embolization resulted in significantly lower morbidity, albeit with a less impressive correction of thrombocytopenia. Based on these results, a more conservative approach may be prudent at initial embolization, which may be followed by a second embolization procedure if necessary.

Complications of Embolization
The use of total splenic infarction has been limited because of the high incidence and severity of complications such as splenic abscess (Fig 10), splenic rupture, septicemia, splenic vein thrombosis, and unremitting bronchopneumonia (34). Several mechanisms may cause complications after complete splenic infarction: induced immunosuppression, anaerobic bacterial growth in the hypoxic tissue, percutaneous introduction of exogenous bacteria, and retrograde transport of enteric pathogens via a reversed portal flow.

View larger version (161K): [in this window] [in a new window] [Download PPT slide]   Figure 10a.  Splenic abscess in a 64-year-old man after splenic arterial embolization for grade III splenic trauma. (a) Transverse CT scan shows a large fluid collection (arrows) with air pockets in the splenic parenchyma after 2 days of percutaneous drainage. (b) Follow-up transverse CT scan obtained 3 weeks later shows that the fluid collection has almost completely disappeared.

View larger version (185K): [in this window] [in a new window] [Download PPT slide]   Figure 10b.  Splenic abscess in a 64-year-old man after splenic arterial embolization for grade III splenic trauma. (a) Transverse CT scan shows a large fluid collection (arrows) with air pockets in the splenic parenchyma after 2 days of percutaneous drainage. (b) Follow-up transverse CT scan obtained 3 weeks later shows that the fluid collection has almost completely disappeared.

View larger version (175K): [in this window] [in a new window] [Download PPT slide]   Figure 11.  Acute pancreatitis in a 62-year-old man after splenic arterial embolization with n-butyl-cyanoacrylate and coils (arrow) for a splenic artery aneurysm. Transverse abdominal CT scan shows moderate thickening (arrowheads) of the pancreatic tail with fat infiltration due to pancreatitis but without necrosis of the pancreas. The patient recovered spontaneously.

Numerous retrospective studies have demonstrated that partial splenic arterial embolization is an effective short-term therapeutic alternative to splenectomy for a wide spectrum of patients with hypersplenism. Kimura et al (44) reported the results of initial (n = 39) and repeat partial splenic arterial embolization (n = 12) in patients with chronic idiopathic thrombocytopenic purpura. The therapeutic effects of initial and repeat partial splenic arterial embolization were classified as complete response if the patient’s platelet count increased to more than 100 x 10⁹/L without steroids 1 year after the initial or repeat embolization, as partial response if the platelet count increased by 50–100 x 10⁹/L, or as no response. Twenty patients (51%) responded to initial partial splenic arterial embolization with a significantly higher peak platelet count (P =.029) after the intervention (11 with complete response, nine with partial response). Of 11 patients with complete response (median follow-up interval, 58 months; range, 21–156 months), one experienced a relapse after 32 months and underwent repeat partial splenic arterial embolization. Of the nine patients with a partial response, four maintained a platelet count of more than 50 x 10⁹/L without relapse (mean follow-up interval, 73 months; range, 14–142 months), and five experienced a relapse (mean follow-up interval, 34 months; range, 15–123 months). Repeat partial embolization resulted in partial response in four patients and in no response in one patient. Nineteen patients had no response to initial partial embolization (mean follow-up interval, 8 months; range, 3–22 months). Six of them underwent repeat partial embolization, and only one of the six had a partial response. Kimura and colleagues concluded that partial splenic arterial embolization with or without repeat embolization is an effective alternative to splenectomy in patients with chronic idiopathic thrombocytopenic purpura.

Nio et al (45) reported 41 partial splenic arterial embolization procedures performed in 36 children with liver disease and thrombocytopenia due to hypersplenism. The average splenic volume in which infarction was induced with embolization was 70.1% (mean follow-up interval, 71 months; range, 20 days to 182 months). Eleven patients (30.6%) had recurrent thrombocytopenia (<100 x 10⁹/L). There were no significant differences in the volumes of infarcted spleen or the platelet counts obtained before partial embolization between patients who experienced recurrent thrombocytopenia and those who did not. The peak platelet counts after partial embolization were significantly lower, however, in the patients with recurrent thrombocytopenia (P = .009).

	Portal Hypertension

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Background
The major sequelae of portal hypertension include variceal hemorrhage, hypersplenism, and hepatogenic ascites. A contributing factor to thrombocytopenia in patients with cirrhosis and portal hypertension is an increased platelet pool in the enlarged spleen (46). The combination of varices and a low platelet count puts these patients at high risk for catastrophic hemorrhage. Endoscopic obliteration of gastroesophageal varices and creation of a transjugular intrahepatic portosystemic shunt are the two most common options used to manage variceal hemorrhage. The endoscopic approach is used to directly treat varices, but such treatment does not address the underlying portal hypertension. Portosystemic shunt creation reduces the risk of hemorrhage by reducing the underlying portal pressure. Open or laparoscopic splenectomy has been proposed, but it has not gained wide acceptance because of the high risk of complications (approximately 10%), especially of portal vein thrombosis.

Results of Partial Embolization
The use of partial splenic arterial embolization to manage variceal hemorrhage in patients with portal hypertension (Fig 12) has been described in a limited number of reports (23,47–49). Embolization may be performed alone or in combination with other therapeutic interventions, such as endoscopic ligation (50,51) or retrograde transvenous variceal obliteration (52). The reduction of splenic volume results in a decrease in venous drainage and, thus, a reduction in portal venous flow and pressure. Xu et al (50) reported their experience with endoscopic variceal ligation and partial splenic arterial embolization in 41 patients in whom they evaluated the hemodynamic (blood flow rate and maximum flow velocity) effects of combination therapy. Esophageal varices and hypersplenism were well controlled, without recurrent hemorrhage (mean follow-up interval, 9.9 months), and there was a significant (P < .05) reduction in flow rate and maximum flow velocity in the main portal vein. Postembolization splenic abscess occurred in one patient, and another patient died of a pulmonary embolus. These results suggest a potential role for partial splenic arterial embolization in the spectrum of therapies used to manage morbid portal hypertension, especially in patients with advanced liver dysfunction and encephalopathy, conditions in which the use of a transjugular intrahepatic portosystemic shunt may be less desirable.

View larger version (131K): [in this window] [in a new window] [Download PPT slide]   Figure 12a.  Splenic arterial embolization for recurrent bleeding from gastric varices in a 58-year-old patient with cirrhosis of the liver after hepatitis C infection. A surgical shunt or transjugular intrahepatic portosystemic shunt could not be created because of the severity of cirrhosis (Child classification C). Since substantial splenomegaly was found at abdominal CT, splenic arterial embolization was performed with simultaneous monitoring of the portosystemic pressure gradient. (a) Angiogram shows balloon catheter (arrow) positioned in the right hepatic vein to monitor wedged hepatic venous pressure during the insertion of a microcatheter in the splenic artery. (b) Splenic arteriogram shows an enlarged splenic arterial trunk with a superior branch that originates at the approximate midpoint of the artery. (c) Follow-up arteriogram obtained after embolization with particles (500–700 µm) and coils shows occlusion of the splenic artery. The hepatic vein pressure decreased from 24 to 16 mm Hg after embolization.

View larger version (158K): [in this window] [in a new window] [Download PPT slide]   Figure 12b.  Splenic arterial embolization for recurrent bleeding from gastric varices in a 58-year-old patient with cirrhosis of the liver after hepatitis C infection. A surgical shunt or transjugular intrahepatic portosystemic shunt could not be created because of the severity of cirrhosis (Child classification C). Since substantial splenomegaly was found at abdominal CT, splenic arterial embolization was performed with simultaneous monitoring of the portosystemic pressure gradient. (a) Angiogram shows balloon catheter (arrow) positioned in the right hepatic vein to monitor wedged hepatic venous pressure during the insertion of a microcatheter in the splenic artery. (b) Splenic arteriogram shows an enlarged splenic arterial trunk with a superior branch that originates at the approximate midpoint of the artery. (c) Follow-up arteriogram obtained after embolization with particles (500–700 µm) and coils shows occlusion of the splenic artery. The hepatic vein pressure decreased from 24 to 16 mm Hg after embolization.

View larger version (144K): [in this window] [in a new window] [Download PPT slide]   Figure 12c.  Splenic arterial embolization for recurrent bleeding from gastric varices in a 58-year-old patient with cirrhosis of the liver after hepatitis C infection. A surgical shunt or transjugular intrahepatic portosystemic shunt could not be created because of the severity of cirrhosis (Child classification C). Since substantial splenomegaly was found at abdominal CT, splenic arterial embolization was performed with simultaneous monitoring of the portosystemic pressure gradient. (a) Angiogram shows balloon catheter (arrow) positioned in the right hepatic vein to monitor wedged hepatic venous pressure during the insertion of a microcatheter in the splenic artery. (b) Splenic arteriogram shows an enlarged splenic arterial trunk with a superior branch that originates at the approximate midpoint of the artery. (c) Follow-up arteriogram obtained after embolization with particles (500–700 µm) and coils shows occlusion of the splenic artery. The hepatic vein pressure decreased from 24 to 16 mm Hg after embolization.

Complications of partial splenic arterial embolization consisted mainly of fever, atelectasis, and abdominal pain, although two patients died as a result of more serious complications (severe hepatic insufficiency [n = 1] and complete splenic infarction with abscess, total portal vein thrombosis, and cardiac insufficiency [n = 1]). Thus, a standardized and graded partial embolization procedure is reasonably safe even in patients with advanced disease who are not candidates for surgery. Palsson and colleagues concluded that partial splenic arterial embolization produces durable effects on hematologic parameters, prevents esophageal variceal hemorrhage, and may substantially improve clinical status (53).

	Splenic Artery Aneurysm

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Background
Splenic artery aneurysms are the most common visceral artery aneurysms, with a reported prevalence of 0.8% at arteriography and 0.04%–0.10% at autopsy. Most aneurysms are small (<2 cm in diameter), saccular, and located at a bifurcation in a middle or distal segment of the splenic artery. Splenic artery aneurysms are multiple in 20% of cases. Splenic artery aneurysms are found most often in multiparous women: Hormonal and hemodynamic alterations specific to pregnancy likely contribute to intimal hyperplasia and fragmentation, which in turn may lead to aneurysm. The prevalence of splenic artery aneurysm is substantially increased in patients with portal hypertension and is estimated at 7%–20% in patients with cirrhosis. Splenic artery pseudoaneurysm secondary to digestion of the arterial wall by proteolytic pancreatic enzymes may be seen in patients with pancreatitis. Other uncommon causes of splenic artery aneurysm include fibromuscular dysplasia, infection, and congenital anomaly.

Most splenic artery aneurysms are detected incidentally during diagnostic imaging performed for other indications. Rupture of splenic artery aneurysms is rare; however, the rupture of splenic artery aneurysms that are left untreated is associated with a high mortality rate. Indications for treatment of splenic artery aneurysm or pseudoaneurysm include specific symptoms (eg, epigastric pain, left upper quadrant pain, back pain), female sex and childbearing age, presence of portal hypertension, planned liver transplantation, a pseudoaneurysm of any size, and an aneurysm with a diameter of more than 2.5 cm.

Treatment Options
Historically, the treatment for splenic artery aneurysm has been bipolar surgical ligation of the splenic artery, ligation of the aneurysm, or aneurysmectomy with or without splenectomy, depending on the aneurysm location. Surgery for splenic artery aneurysms is associated with a mortality rate of approximately 1%, but mortality is increased in patients with pancreatitis, in whom it is 16% for those with aneurysms in the pancreatic head and 50% for those with pancreatic body aneurysms. Splenic artery aneurysms also may be treated with percutaneous interventional techniques such as transcatheter embolization, placement of a covered stent-graft to exclude the aneurysm, or percutaneous injection of coils and/or thrombin.

Transcatheter embolization is associated with significantly lower morbidity and mortality than are surgical procedures (54,55). Precise selection of the occlusion site is necessary to preserve collateral blood flow to the spleen via the gastric, omental, and pancreatic vessels. Packing of the aneurysmal sac with embolic agents (most commonly with coils, but also with detachable balloons and inert particles) and exclusion of the aneurysmal neck with the "sandwich" method are the recommended techniques for treating splenic artery aneurysms (Figs 13–15). In a recent report, a large splenic artery aneurysm with a wide neck was successfully treated by packing the aneurysm with multiple detachable Guglielmi coils during occlusion of the aneurysmal neck with a balloon catheter. Embolization of intrasplenic lesions may be performed with microcatheter-based techniques, and success rates of 80%–90% have been reported for percutaneous transcatheter embolization.

View larger version (35K): [in this window] [in a new window] [Download PPT slide]   Figure 13a.  Drawings show techniques for splenic arterial embolization with multiple coils placed in the aneurysmal sac (a) and in splenic artery segments proximal and distal to the aneurysmal neck (the so-called sandwich method) (b).

View larger version (41K): [in this window] [in a new window] [Download PPT slide]   Figure 13b.  Drawings show techniques for splenic arterial embolization with multiple coils placed in the aneurysmal sac (a) and in splenic artery segments proximal and distal to the aneurysmal neck (the so-called sandwich method) (b).

View larger version (139K): [in this window] [in a new window] [Download PPT slide]   Figure 14a.  Treatment of splenic artery aneurysm secondary to atherosclerosis in a 68-year-old woman. (a) Celiac arteriogram shows a 2.4-cm-diameter saccular aneurysm (arrow) that arises from the splenic artery. (b) Fluoroscopic image shows multiple coils (arrow) deployed inside the aneurysmal sac. (c) Follow-up arteriogram shows treatment success; blood flow to the spleen (arrowheads) is preserved.

View larger version (131K): [in this window] [in a new window] [Download PPT slide]   Figure 14b.  Treatment of splenic artery aneurysm secondary to atherosclerosis in a 68-year-old woman. (a) Celiac arteriogram shows a 2.4-cm-diameter saccular aneurysm (arrow) that arises from the splenic artery. (b) Fluoroscopic image shows multiple coils (arrow) deployed inside the aneurysmal sac. (c) Follow-up arteriogram shows treatment success; blood flow to the spleen (arrowheads) is preserved.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 14c.  Treatment of splenic artery aneurysm secondary to atherosclerosis in a 68-year-old woman. (a) Celiac arteriogram shows a 2.4-cm-diameter saccular aneurysm (arrow) that arises from the splenic artery. (b) Fluoroscopic image shows multiple coils (arrow) deployed inside the aneurysmal sac. (c) Follow-up arteriogram shows treatment success; blood flow to the spleen (arrowheads) is preserved.

View larger version (142K): [in this window] [in a new window] [Download PPT slide]   Figure 15a.  Splenic arterial embolization for a splenic artery aneurysm of unknown origin in a 47-year-old man. (a) Splenic arteriogram shows a 2.5-cm-diameter aneurysm (arrow) that involves the midportion of the main splenic artery. (b) Arteriogram shows a microcatheter that was successfully inserted into the aneurysmal sac but that could not be advanced to the splenic artery downstream of the aneurysm. (c) Arteriogram shows embolization with placement of coils (arrow) in the bifurcation of the splenic artery to avoid retrograde filling from the splenic hilum via gastroepiploic collateral vessels and with deployment of n-butyl-cyanoacrylate and coils in the aneurysm. (d) Follow-up arteriogram shows exclusion of the aneurysm.

View larger version (147K): [in this window] [in a new window] [Download PPT slide]   Figure 15b.  Splenic arterial embolization for a splenic artery aneurysm of unknown origin in a 47-year-old man. (a) Splenic arteriogram shows a 2.5-cm-diameter aneurysm (arrow) that involves the midportion of the main splenic artery. (b) Arteriogram shows a microcatheter that was successfully inserted into the aneurysmal sac but that could not be advanced to the splenic artery downstream of the aneurysm. (c) Arteriogram shows embolization with placement of coils (arrow) in the bifurcation of the splenic artery to avoid retrograde filling from the splenic hilum via gastroepiploic collateral vessels and with deployment of n-butyl-cyanoacrylate and coils in the aneurysm. (d) Follow-up arteriogram shows exclusion of the aneurysm.

View larger version (108K): [in this window] [in a new window] [Download PPT slide]   Figure 15c.  Splenic arterial embolization for a splenic artery aneurysm of unknown origin in a 47-year-old man. (a) Splenic arteriogram shows a 2.5-cm-diameter aneurysm (arrow) that involves the midportion of the main splenic artery. (b) Arteriogram shows a microcatheter that was successfully inserted into the aneurysmal sac but that could not be advanced to the splenic artery downstream of the aneurysm. (c) Arteriogram shows embolization with placement of coils (arrow) in the bifurcation of the splenic artery to avoid retrograde filling from the splenic hilum via gastroepiploic collateral vessels and with deployment of n-butyl-cyanoacrylate and coils in the aneurysm. (d) Follow-up arteriogram shows exclusion of the aneurysm.

View larger version (165K): [in this window] [in a new window] [Download PPT slide]   Figure 15d.  Splenic arterial embolization for a splenic artery aneurysm of unknown origin in a 47-year-old man. (a) Splenic arteriogram shows a 2.5-cm-diameter aneurysm (arrow) that involves the midportion of the main splenic artery. (b) Arteriogram shows a microcatheter that was successfully inserted into the aneurysmal sac but that could not be advanced to the splenic artery downstream of the aneurysm. (c) Arteriogram shows embolization with placement of coils (arrow) in the bifurcation of the splenic artery to avoid retrograde filling from the splenic hilum via gastroepiploic collateral vessels and with deployment of n-butyl-cyanoacrylate and coils in the aneurysm. (d) Follow-up arteriogram shows exclusion of the aneurysm.

View larger version (33K): [in this window] [in a new window] [Download PPT slide]   Figure 16.  Drawing shows complete exclusion of an aneurysmal sac with a stent-graft while blood flow through the splenic artery is maintained.

View larger version (111K): [in this window] [in a new window] [Download PPT slide]   Figure 17a.  Stent-graft placement for a splenic artery aneurysm in a 69-year-old woman with duodenal adenocarcinoma and gastric outlet obstruction. (a) Transverse unenhanced CT scan shows a 2-cm-diameter splenic artery aneurysm (arrow) that required exclusion from the arterial lumen before duodenal resection. (b) Transverse CT scan obtained with intravenous contrast material shows contrast enhancement of the splenic artery aneurysm (arrow). (c) Transverse CT scan, obtained 4 months after placement of an 8 x 50-mm stent-graft (Viabahn; Gore, Flagstaff, Ariz) (white arrow) for exclusion of the aneurysm, shows a thrombus (black arrow) in the aneurysmal sac.

View larger version (157K): [in this window] [in a new window] [Download PPT slide]   Figure 17b.  Stent-graft placement for a splenic artery aneurysm in a 69-year-old woman with duodenal adenocarcinoma and gastric outlet obstruction. (a) Transverse unenhanced CT scan shows a 2-cm-diameter splenic artery aneurysm (arrow) that required exclusion from the arterial lumen before duodenal resection. (b) Transverse CT scan obtained with intravenous contrast material shows contrast enhancement of the splenic artery aneurysm (arrow). (c) Transverse CT scan, obtained 4 months after placement of an 8 x 50-mm stent-graft (Viabahn; Gore, Flagstaff, Ariz) (white arrow) for exclusion of the aneurysm, shows a thrombus (black arrow) in the aneurysmal sac.

View larger version (145K): [in this window] [in a new window] [Download PPT slide]   Figure 17c.  Stent-graft placement for a splenic artery aneurysm in a 69-year-old woman with duodenal adenocarcinoma and gastric outlet obstruction. (a) Transverse unenhanced CT scan shows a 2-cm-diameter splenic artery aneurysm (arrow) that required exclusion from the arterial lumen before duodenal resection. (b) Transverse CT scan obtained with intravenous contrast material shows contrast enhancement of the splenic artery aneurysm (arrow). (c) Transverse CT scan, obtained 4 months after placement of an 8 x 50-mm stent-graft (Viabahn; Gore, Flagstaff, Ariz) (white arrow) for exclusion of the aneurysm, shows a thrombus (black arrow) in the aneurysmal sac.

	Liver Transplantation

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Background
Increased blood flow to the spleen as a result of decreased splenic arteriolar resistance is a common finding in patients with chronic liver disease and portal hypertension. Definitive treatment of liver failure with orthotopic liver transplantation can be complicated by the diversion of arterial blood flow away from the donor liver. Concurrent disease in the recipient, such as hepatitis or transplant rejection, can lead to an increase in hepatic arterial resistance, which results in the shunting of even more blood from the celiac axis toward the spleen (Fig 18a ). The triad of liver failure, reduced hepatic arterial perfusion, and increased blood flow in the splenic circulation after liver transplantation is called splenic artery steal syndrome.

View larger version (72K): [in this window] [in a new window] [Download PPT slide]   Figure 18a.  Drawings show (a) splenic artery steal syndrome after liver transplantation, with substantial blood flow via the splenic artery to the spleen and with reduced blood flow to the transplanted liver, and (b) improved blood flow to the liver transplant after splenic arterial embolization.

View larger version (71K): [in this window] [in a new window] [Download PPT slide]   Figure 18b.  Drawings show (a) splenic artery steal syndrome after liver transplantation, with substantial blood flow via the splenic artery to the spleen and with reduced blood flow to the transplanted liver, and (b) improved blood flow to the liver transplant after splenic arterial embolization.

Treatment of Splenic Artery Steal Syndrome
Surgical and endovascular approaches that have been proposed for treatment of splenic artery steal syndrome include surgical splenectomy, splenic artery ligation, creation of a new vascular conduit from the aorta to the hepatic artery, and splenic arterial embolization (Fig 18b). Because liver transplant recipients are poor surgical candidates after transplantation, minimally invasive approaches to treating this syndrome are the most promising. Controversy exists, in the scarce literature on this subject, about whether or not repeat surgical ligation of the hepatic artery to the aorta or splenic arterial embolization should be considered the first-line therapy.

Uflacker et al (59) reported their findings of splenic artery steal syndrome in a series of 11 patients after liver transplantation. The diagnosis was confirmed with celiac artery angiography, and therapeutic embolization was performed with coils in the middle segment of the splenic artery. Immediate clinical improvement was noted in all patients. The authors reported only one procedure-related complication (hepatic artery thrombosis, which necessitated surgical repair). The authors noted that if hyperdynamic circulation to the spleen was observed intraoperatively, surgical anastomosis of the donor hepatic artery to the aorta should be performed to prevent splenic artery steal syndrome.

	Splenic Neoplasia

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Transarterial Splenic Irradiation
For years, splenic irradiation has been an effective treatment for lymphoma, leukemia, myelofibrosis, idiopathic thrombocytopenic purpura, and polycythemia vera with or without splenomegaly (60–64). Although radiation therapy in solid organ malignancies traditionally has involved the use of external-beam radiation, there is renewed interest in transarterial applications of irradiation, especially in patients with inoperable intrahepatic malignancy (65–67). The authors of two articles advocated the use of transarterial splenic irradiation with yttrium-90 microspheres (68,69). The first article was published in 1973 by Ariel and Padula (68), who treated the spleen in 13 patients, who had lymphosarcoma, leukemia, or Hodgkin disease, with a dose of 100 Gy administered via the splenic or celiac artery. Most patients in this series had only mild splenomegaly, if any. Reduction in splenic volume was not quantified exactly, and no serious side effects were noted. In 1995, Becker et al (69) reported the transarterial administration of yttrium-90 resin microspheres to treat congestive hypersplenism and thrombocytopenia in a patient. The dose to the spleen was 90 Gy, which is in the lower therapeutic range. Contrary to the expected observations after partial splenic arterial embolization, no segmental infarction was seen in this case, and the changes on CT scans were believed to represent fibrosis from irradiation rather than mechanically induced ischemia. Furthermore, the patient had considerably fewer side effects than are seen with standard partial splenic arterial embolization, but the peak platelet count was noticeably lower. Given the recent resurgence of interest in transcatheter therapies with administration of yttrium 90, further investigation of this alternative is warranted.

Combination Therapy
Another possibility for treatment of solid organ malignancies that has attracted recent interest is the combination of arterial embolization with therapeutic modalities such as radiofrequency ablation (70). It is hypothesized that this therapy combination helps to increase the ablation zone by reducing the heat sink effect, or the escape of thermal energy via moving blood. Recently, Liu et al (71) performed a study in 16 dogs to assess the feasibility and safety of radiofrequency ablation in the treatment of splenomegaly. Sixteen dogs were randomly divided into two groups, group 1 (n = 4) and group 2 (n = 12). Splenomegaly was induced with ligation of the splenic vein and its collateral branches in all dogs in both groups. After 3 weeks, radiofrequency ablation was performed in the spleen of the group 2 dogs. Complications of radiofrequency ablation were observed, CT was performed, the spleens were harvested, and the thermal lesions and histopathologic specimens from the spleen were examined. The authors observed segmental thermal lesions that had a hyperintense central zone of coagulative necrosis and a more extensive hypointense peripheral zone of infarction. The infarcted zone was absorbed and disappeared within 4–6 weeks after radiofrequency ablation, while the remaining spleen shrank. The fundamental histopathologic changes caused by radiofrequency-induced heating included the creation of lesions with a central zone of coagulative necrosis and peripheral zone of thrombotic infarction, subsequent tissue absorption and fibrosis in the zone of thrombotic infarction, the occlusion of vessels in the remnant of viable spleen, the deposition of extensive fibrous protein, and the disappearance of congestive splenic sinusoid. No complication or death occurred in either group. Liu and colleagues concluded that radiofrequency ablation of the spleen is feasible and safe. Although the results achieved in the two groups were similar, the use of partial splenic arterial embolization before radiofrequency ablation may help to improve both the experimental and the clinical results of ablation. Given the encouraging results described, further investigation of combination therapies for splenomegaly and primary and secondary splenic malignancies might be warranted.

	Conclusions

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 
Splenic arterial interventions may be used to treat a wide range of pathologic entities that are encountered in diverse areas of medical practice such as trauma surgery, vascular surgery, oncology, hematology, and organ transplantation. In this article, promising results of minimally invasive techniques used to manage splenic disease have been summarized. Further investigations are necessary to better define the role of the interventional radiologist in the management of splenic disease. As the demand for splenic arterial interventions increases, a thorough knowledge of the common techniques and their potential pitfalls will be required.

	References

Top Abstract LEARNING OBJECTIVES FOR TEST... Introduction Splenic Vascular Anatomy Splenic Trauma Hypersplenism Portal Hypertension Splenic Artery Aneurysm Liver Transplantation Splenic Neoplasia Conclusions References

 

1. Kadir S, Lundell C, Saeed M. Celiac, superior and inferior mesenteric arteries. In: Kadir S, ed. Atlas of normal and variant angiographic anatomy. Philadelphia, Pa: Saunders, 1991; 204–237.
2. Cullingford GL, Watkins DN, Watts AD, Mallon DF. Severe late postsplenectomy infection. Br J Surg 1991;78:716–721.[Medline]
3. Haller JA Jr, Papa P, Drugas G, Colombani P. Nonoperative management of solid organ injuries in children: is it safe? Ann Surg 1994;219:625–628.[Medline]
4. Velmahos GC, Toutouzas KG, Radin R, Chan L, Demetriades D. Nonoperative treatment of blunt injury to solid abdominal organs. Arch Surg 2003; 138:844–851.[Abstract/Free Full Text]
5. Albrecht RM, Schermer CR, Morris A. Nonoperative management of blunt splenic injuries: factors influencing success in age >55 years. Am Surg 2002;68:227–230.[Medline]
6. Moore EE, Cogbill TH, Jurkovich GJ, Shackford SR, Malangoni MA, Champion HR. Organ injury scaling: spleen and liver (1994 revision). J Trauma 1995;38:323–324.[Medline]
7. Velmahos GC, Chan LS, Kamel E, et al. Nonoperative management of splenic injuries: have we gone too far? Arch Surg 2000;135:674–679.[Abstract/Free Full Text]
8. Wahl WL, Ahrns KS, Chen S, Hemmila MR, Rowe SA, Arbabi S. Blunt splenic injury: operation versus angiographic embolization. Surgery 2004;136:891–899.[CrossRef][Medline]
9. Sclafani SJ, Shaftan GW, Scalea TM, et al. Nonoperative salvage of computed tomography-diagnosed splenic injuries: utilization of angiography for triage and embolization for hemostasis. J Trauma 1995;39:818–825.[Medline]
10. Link DP, Seibert JA, Gould J, Lantz BM. On-line monitoring of sequential blood flow reduction during splenic embolization. Acta Radiol 1989;30: 101–103.[Medline]
11. Levy JM, Wasserman PI, Weiland DE. Nonsuppurative gas formation in the spleen after trans-catheter splenic infarction. Radiology 1981;139: 375–376.[Free Full Text]
12. Killeen KL, Shanmuganathan K, Boyd-Kranis R, Scalea TM, Mirvis SE. CT findings after embolization for blunt splenic trauma. J Vasc Interv Radiol 2001;12:209–214.[Medline]
13. Haan J, Bochicchio G, Kramer M, Scalea T. Air following splenic embolization: infection or incidental finding? Am Surg 2003;69:1036–1039.[Medline]
14. Haan JM, Biffl W, Knudson MM, et al. Splenic embolization revisited: a multicenter review. J Trauma 2004;56:542–547.[Medline]
15. Haan J, Scott J, Boyd-Kranis RL, Ho S, Kramer M, Scalea TM. Admission angiography for blunt splenic injury: advantages and pitfalls. J Trauma 2001;51:1161–1165.[Medline]
16. Bessoud B, Denys A. Main splenic artery embolization using coils in blunt splenic injuries: effects on the intrasplenic blood pressure. Eur Radiol 2004;14:1718–1719.[Medline]
17. Morris DH. The importance of the spleen in resistance to infection. Ann Surg 1919;70:513–521.[Medline]
18. Whitaker AN. Infection and the spleen: association between hyposplenism, pneumococcal sepsis and disseminated intravascular coagulation. Med J Aust 1969;1:1213–1219.[Medline]
19. Bisno AL, Freeman JC. The syndrome of asplenia, pneumococcal sepsis, and disseminated intravascular coagulation. Ann Intern Med 1970;72:389–393.
20. Butler JC, Campbell JF, Lipman HB, Broome CV, Facklam RR. Pneumococcal polysaccharide vaccine efficacy: an evaluation of current recommendations. JAMA 1993;270:1826–1831.[Abstract/Free Full Text]
21. Peck-Radosavljevic M. Hypersplenism. Eur J Gastroenterol Hepatol 2001;13:317–323.[CrossRef][Medline]
22. Sangro B, Bilbao I, Herrero I, et al. Partial splenic embolization for the treatment of hypersplenism in cirrhosis. Hepatology 1993;18:309–314.[CrossRef][Medline]
23. Romano M, Giojelli A, Capuano G, Pomponi D, Salvatore M. Partial splenic embolization in patients with idiopathic portal hypertension. Eur J Radiol 2004;49:268–273.[CrossRef][Medline]
24. Stanley P, Chen TC. Partial embolization of the spleen in patients with thalassemia. J Vasc Interv Radiol 1995;6:137–142.[Medline]
25. Kimura F, Ito H, Shimizu H, et al. Partial splenic embolization for the treatment of hereditary spherocytosis. AJR Am J Roentgenol 2003;181: 1021–1024.[Abstract/Free Full Text]
26. Kumar S, Diehn FE, Gertz MA, Tefferi A. Splenectomy for immune thrombocytopenic purpura: long-term results and treatment of postsplenectomy relapses. Ann Hematol 2002;81:312–319.[CrossRef][Medline]
27. Miyazaki M, Itoh H, Kaiho T, et al. Partial splenic embolization for the treatment of chronic idiopathic thrombocytopenic purpura. AJR Am J Roentgenol 1994;163:123–126.[Abstract/Free Full Text]
28. Athale UH, Kaste SC, Bodner SM, Ribeiro RC. Splenic rupture in children with hematologic malignancies. Cancer 2000;88:480–490.[CrossRef][Medline]
29. Gardner RV, Warrier RP, Loe W, Ward K, Haymon M, Craver R. Splenic artery embolization as emergency treatment of splenic rupture in a child with T-cell acute lymphocytic leukemia having t(8;14) translocation. Med Pediatr Oncol 2003; 41:492–493.[CrossRef][Medline]
30. Pringle KC, Spigos DG, Tan WS, et al. Partial splenic embolization in the management of thalassemia major. J Pediatr Surg 1982;17:884–891.[CrossRef][Medline]
31. Jonasson O, Spigos DG, Mozes MF. Partial splenic embolization: experience in 136 patients. World J Surg 1985;9:461–467.[CrossRef][Medline]
32. Lokich J, Costello P. Splenic embolization to prevent dose limitation of cancer chemotherapy. AJR Am J Roentgenol 1983;140:159–161.[Free Full Text]
33. Gerlock AJ Jr, MacDonell RC Jr, Muhletaler CA, et al. Partial splenic embolization for hypersplenism in renal transplantation. AJR Am J Roentgenol 1982;138:451–456.[Abstract/Free Full Text]
34. Maddison FE. Embolic therapy of hypersplenism (abstr). Invest Radiol 1973;8:280.
35. Poulin EC, Mamazza J, Schlachta CM. Splenic artery embolization before laparoscopic splenectomy: an update. Surg Endosc 1998;12:870–875.[CrossRef][Medline]
36. Iwase K, Higaki J, Mikata S, et al. Laparoscopically assisted splenectomy following preoperative splenic artery embolization using contour emboli for myelofibrosis with massive splenomegaly. Surg Laparosc Endosc Percutan Tech 1999;9:197–202.[CrossRef][Medline]
37. Mozes MF, Spigos DG, Pollak R, et al. Partial splenic embolization, an alternative to splenectomy: results of a prospective, randomized study. Surgery 1984;96:694–702.[Medline]
38. Kumpe DA, Rumack CM, Pretorius DH, Stoecker TJ, Stellin GP. Partial splenic embolization in children with hypersplenism. Radiology 1985;155:357–362.[Abstract/Free Full Text]
39. Yoshioka H, Kuroda C, Hori S, et al. Splenic embolization for hypersplenism using steel coils. AJR Am J Roentgenol 1985;144:1269–1274.[Abstract/Free Full Text]
40. Hickman MP, Lucas D, Novak Z, et al. Preoperative embolization of the spleen in children with hypersplenism. J Vasc Interv Radiol 1992;3:647–652.[Medline]
41. Spigos DG, Jonasson O, Mozes M, Capek V. Partial splenic embolization in the treatment of hypersplenism. AJR Am J Roentgenol 1979;132:777–782.[Abstract]
42. Harned RK 2nd, Thompson HR, Kumpe DA, Narkewicz MR, Sokol RJ. Partial splenic embolization in five children with hypersplenism: effects of reduced-volume embolization on efficacy and morbidity. Radiology 1998;209:803–806.[Abstract/Free Full Text]
43. Watanabe Y, Todani T, Noda T. Changes in splenic volume after partial splenic embolization in children. J Pediatr Surg 1996;31:241–244.[CrossRef][Medline]
44. Kimura F, Itoh H, Ambiru S, 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;179:1323–1326.[Abstract/Free Full Text]
45. Nio M, Hayashi Y, Sano N, Ishii T, Sasaki H, Ohi R. Long-term efficacy of partial splenic embolization in children. J Pediatr Surg 2003;38:1760–1762.[CrossRef][Medline]
46. Kutti J, Weinfeld A, Westin J. The relationship between splenic platelet pool and spleen size. Scand J Haematol 1972;9:351–354.[Medline]
47. Hirota S, Ichikawa S, Matsumoto S, Motohara T, Fukuda T, Yoshikawa T. Interventional radiologic treatment for idiopathic portal hypertension. Cardiovasc Intervent Radiol 1999;22:311–314.[CrossRef][Medline]
48. Shimizu T, Onda M, Tajiri T, et al. Bleeding portal-hypertensive gastropathy managed successfully by partial splenic embolization. Hepatogastroenterology 2002;49:947–949.[Medline]
49. Sato T, Yamazaki K, Toyota J, Karino Y, Ohmura T, Suga T. Gastric varices with splenic vein occlusion treated by splenic arterial embolization. J Gastroenterol 2000;35:290–295.[CrossRef][Medline]
50. Xu RY, Liu B, Lin N. Therapeutic effects of endoscopic variceal ligation combined with partial splenic embolization for portal hypertension. World J Gastroenterol 2004;10:1072–1074.[Medline]
51. Taniai N, Onda M, Tajiri T, Toba M, Yoshida H. Endoscopic variceal ligation (EVL) combined with partial splenic embolization (PSE). Hepatogastroenterology 1999;46:2849–2853.[Medline]
52. Chikamori F, Kuniyoshi N, Kawashima T, Shibuya S, Takase Y. Combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration for complicated gastroesophageal varices. Hepatogastroenterology 2004;51:1506–1509.[Medline]
53. Palsson B, Hallen M, Forsberg AM, Alwmark A. Partial splenic embolization: long-term outcome. Langenbecks Arch Surg 2003;387:421–426.[CrossRef][Medline]
54. McDermott VG, Shlansky-Goldberg R, Cope C. Endovascular management of splenic artery aneurysms and pseudoaneurysms. Cardiovasc Intervent Radiol 1994;17:179–184.[CrossRef][Medline]
55. Guillon R, Garcier JM, Abergel A, et al. Management of splenic artery aneurysms and false aneurysms with endovascular treatment in 12 patients. Cardiovasc Intervent Radiol 2003;26:256–260.[CrossRef][Medline]
56. Arepally A, Dagli M, Hofmann LV, Kim HS, Cooper M, Klein A. Treatment of splenic artery aneurysm with use of a stent-graft. J Vasc Interv Radiol 2002;13:631–633.[Medline]
57. Brountzos EN, Vagenas K, Apostolopoulou SC, Panagiotou I, Lymberopoulou D, Kelekis DA. Pancreatitis-associated splenic artery pseudoaneurysm: endovascular treatment with self-expandable stent-grafts. Cardiovasc Intervent Radiol 2003;26:88–91.[CrossRef][Medline]
58. De Carlis L, Sansalone CV, Rondinara GF, et al. Splenic artery steal syndrome after orthotopic liver transplantation: diagnosis and treatment. Transplant Proc 1993;25:2594–2596.[Medline]
59. Uflacker R, Selby JB, Chavin K, Rogers J, Baliga P. Transcatheter splenic artery occlusion for treatment of splenic artery steal syndrome after orthotopic liver transplantation. Cardiovasc Intervent Radiol 2002;25:300–306.[CrossRef][Medline]
60. Galbraith PR. The mechanism of action of splenic irradiation in chronic myelogenous leukemia. Can Med Assoc J 1967;96:1636–1641.[Medline]
61. Abrams RA, Liu PJ, Ambinder RF, et al. Hodgkin and non-Hodgkin lymphoma: local-regional radiation therapy after bone marrow transplantation. Radiology 1997;203:865–870.[Abstract/Free Full Text]
62. Elliott MA, Chen MG, Silverstein MN, Tefferi A. Splenic irradiation for symptomatic splenomegaly associated with myelofibrosis with myeloid metaplasia. Br J Haematol 1998;103:505–511.[CrossRef][Medline]
63. Schratter-Sehn AU, Cerveny M, Simmel H, Schlogl E, Schratter A. Short-time splenic irradiation for splenomegaly. Onkologie 2003;26:21–24.
64. McFarland JT, Kuzma C, Millard FE, Johnstone PA. Palliative irradiation of the spleen. Am J Clin Oncol 2003;26:178–183.[CrossRef][Medline]
65. Herba MJ, Thirlwell MP. Radioembolization for hepatic metastases. Semin Oncol 2002;29:152–159.[CrossRef][Medline]
66. Salem R, Lewandowski R, Roberts C, et al. Use of yttrium-90 glass microspheres (TheraSphere) for the treatment of unresectable hepatocellular carcinoma in patients with portal vein thrombosis. J Vasc Interv Radiol 2004;15:335–345.[Medline]
67. Salem R, Thurston KG, Carr BI, Goin JE, Geschwind JF. Yttrium-90 microspheres: radiation therapy for unresectable liver cancer. J Vasc Interv Radiol 2002;13(9 pt 2):S223–S229.
68. Ariel IM, Padula G. Irradiation of the spleen by the intra-arterial administration of 90 yttrium microspheres in patients with malignant lymphoma: a preliminary report. Cancer 1973;31:90–96.[CrossRef][Medline]
69. Becker CD, Rosler H, Biasiutti FD, Baer HU. Congestive hypersplenism: treatment by means of radioembolization of the spleen with Y-90. Radiology 1995;195:183–186.[Abstract/Free Full Text]
70. Koda M, Ueki M, Maeda Y, et al. The influence on liver parenchymal function and complications of radiofrequency ablation or the combination with transcatheter arterial embolization for hepatocellular carcinoma. Hepatol Res 2004;29:18–23.[CrossRef][Medline]
71. Liu QD, Ma KS, He ZP, Ding J, Huang XQ, Dong JH. Experimental study on the feasibility and safety of radiofrequency ablation for secondary splenomagely and hypersplenism. World J Gastroenterol 2003;9:813–817.[Medline]

This article has been cited by other articles:

				A. R. Rasekhi, M. Naderifar, M. H. Bagheri, M. Shahriari, H. Foroutan, M. Karimi, and S. A. Nabavizadeh Radiofrequency Ablation of the Spleen in Patients with Thalassemia Intermedia: A Pilot Study Am. J. Roentgenol., May 1, 2009; 192(5): 1425 - 1429. [Abstract] [Full Text] [PDF]

				R. Sanyal and S. N. Shah Role of Imaging in the Management of Splenic Artery Steal Syndrome J. Ultrasound Med., April 1, 2009; 28(4): 471 - 477. [Abstract] [Full Text] [PDF]

This Article Abstract Figures Only Full Text (PDF) CME Test (opens in a new window) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Madoff, D. C. Articles by Hicks, M. E. Search for Related Content PubMed PubMed Citation Articles by Madoff, D. C. Articles by Hicks, M. E. Related Collections Vascular and/or Interventional Radiology Gastrointestinal Radiology