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DOI: 10.1148/rg.25si055504
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RadioGraphics 2005;25:S191-S211
© RSNA, 2005

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

David C. Madoff, MD, Alban Denys, MD, Michael J. Wallace, MD, Ravi Murthy, MD, Sanjay Gupta, MD, Edmund P. Pillsbury, BA, Kamran Ahrar, MD, Bertrand Bessoud, MD and Marshall E. Hicks, MD

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:


    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.



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Figure 1.  Three-dimensional drawing of normal anatomy in the upper abdomen shows the main splenic artery and its branches.

 
The splenic artery has many branches that supply the pancreatic body and tail. The first large branch is the dorsal pancreatic artery, and the second large branch is the greater pancreatic artery (or arteria pancreatica magna), which arises from the middle segment of the splenic artery. When embolization is planned, visualization of the pancreatic arteries is essential to reduce the risk of their unintended embolization.


    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.


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American Association for the Surgery of Trauma Organ Injury: Scale for the Spleen

 
Indications for Splenic Arterial Embolization
Surgery is usually performed in patients who have traumatic injuries to the spleen and unstable hemodynamics, whereas splenic injuries in patients with stable hemodynamics are treated with nonsurgical management. The objective of splenic arterial embolization is to improve the results of nonsurgical management (8). Indications for splenic arterial embolization vary, depending on local management protocols. The most widely accepted indication for this procedure is evidence of arterial injury on CT scans. In cases of arterial injury, embolization is performed with microcoils as distally as possible, in a small arterial branch that supplies the segment in which extravasation, pseudoaneurysm, or abrupt termination is depicted, to preserve perfusion to the remaining splenic parenchyma. Patients with a high risk for secondary rupture of the spleen should undergo embolization with coils in a more proximal segment of the splenic artery to reduce the pressure in the splenic parenchyma and help the spleen to heal (9). The placement of coils in a middle segment of the splenic artery allows reconstitution of the blood supply through collateral vessels, principally via the short gastric and gastroepiploic arteries, to the patent distal splenic, transgastric, and transpancreatic arteries. Proximal embolization performed exclusively with coils decreases the volume of splenic arterial blood flow and thereby produces relative hypotension in the splenic bed, which allows the spleen to repair itself without infarction (10).

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).



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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.

 


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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.

 


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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.

 


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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).

 


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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).

 
Results of Embolization
In 1995, Sclafani et al (9) reported the results of a study of blunt trauma–related splenic injuries in 172 patients, 60 of whom underwent splenic arterial embolization because of angiographic evidence of extravasation of contrast-enhanced arterial blood. Secondary splenectomy was required subsequently in only 7% of the 60 patients. Haan et al (15) analyzed the results of splenic arterial embolization in 40 patients in whom there was angiographic evidence of splenic vascular injury. In 92% of these 40 patients, nonsurgical salvage was successful; in 10%, repeat angiography was required for suspected rebleeding; and in half of these (5%), a second embolization procedure was necessary. Bessoud et al (16) recently proposed another treatment approach for all patients with splenic lacerations of grade III or higher and/or with evidence of extravasation on CT scans and stable hemodynamic status. The investigators in that study observed a 2.7% failure rate in a group of 37 patients who underwent treatment with this technique, compared with a failure rate of 10% for nonsurgical management in 30 patients. The group that underwent splenic arterial embolization had less morbidity, despite significantly higher CT grades of splenic trauma and a higher percentage of extravasation before intervention.

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 (1719). 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 (2427); 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).



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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.

 


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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.

 


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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.

 


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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.

 
Hematologic response and the severity of complications correlate with the amount of infarcted splenic tissue. Infarction of more than 80% of the splenic mass has been reported, but most interventionalists have attempted to achieve infarction in 60%–70% of the splenic mass (37,38). A lesser extent of infarction allows reduced sequestration and destruction of the blood elements (eg, red blood cells, platelets), maintenance of the spleen’s immunologic function, and preservation of ante-grade flow in the splenic vein. However, complete splenic infarction may be beneficial immediately before splenectomy in patients who have severe thrombocytopenia and who will receive platelet transfusions during surgery (Fig 5 ).



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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.

 


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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.

 
Methods of Partial Embolization
Partial splenic arterial embolization may be performed with one of two methods. With the first approach, selective partial embolization, a few distal branches of the splenic artery are selectively catheterized, and embolization is performed to achieve complete stasis in these branches while several other branches are left untreated (Figs 6, 7). Parenchymal phase angiograms may be used to estimate the volume of the remaining viable splenic tissue. Additional branches then may be catheterized, and embolization may be repeated, until the desired effect is achieved. With the second method, nonselective partial embolization, the working catheter tip is positioned more proximally in the main splenic artery but beyond the origin of major pancreatic branches (Figs 8, 9). Embolic particles are injected until the parenchymal blush is reduced. Contrast-enhanced CT may be used for follow-up examination.



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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.

 


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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.

 


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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.

 


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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.

 


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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.

 


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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).

 


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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).

 


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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).

 


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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 embolic agents most commonly used for splenic arterial embolization are gelatin sponge pledgets and polyvinyl alcohol particles. Yoshioka et al (39) showed excellent increases in platelet counts when coils were placed in the intrasplenic branches of the artery, and Hickman et al (40) successfully used gelatin sponge pledgets, polyvinyl alcohol particles, and/or coils for preoperative embolization.

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.



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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.

 


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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.

 
Like complete splenic ablation, partial splenic arterial embolization and proximal embolization (for splenic artery aneurysm) may entail complications and adverse effects, but these procedures are better tolerated than is complete splenic ablation (43). In addition, patients may develop pleural effusions that require thoracentesis; paralytic ileus; pancreatitis (Fig 11) (likely a result of non-target embolization of the dorsal pancreatic or greater pancreatic artery); or postembolization syndrome, which consists of fever, leukocytosis, and abdominal pain.



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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.

 
Results of Partial Embolization
Few studies have compared splenectomy with partial splenic arterial embolization in a randomized and prospective fashion. Mozes et al (37) studied 53 patients who were to undergo renal transplantation with azathioprine and either splenectomy (n = 25) or partial splenic arterial embolization (n = 28). The indications for the latter procedures were refractory leukopenia and thrombocytopenia. In patients in the group designated to undergo partial splenic arterial embolization, a mean of 65.4% ± 16.6 (standard deviation) of the splenic mass was ablated. Early postoperative morbidity rates and durations of hospital stay were similar in the two groups. Severe pancreatitis followed by death occurred in the splenectomy group (n = 2), and death from pneumococcal pneumonia occurred 3 months after partial splenic arterial embolization (n = 1). Renal transplantation was performed in equivalent numbers in both groups, with similar long-term graft survival (2.5–4.0 years) and similar long-term patient mortality (60% vs 66%). Splenic regeneration occurred in most patients after partial splenic infarction from embolization, and doubling of the splenic parenchyma was seen in 40% of those patients.

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 (23,4749). 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.



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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.

 


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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.

 


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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.

 
Palsson et al (53) reviewed the cases of 26 severely ill patients (mean age, 63.5 years) who underwent a total of 52 partial splenic arterial embolization procedures, mainly for thrombocytopenia due to bleeding from esophageal varices. The mean hemoglobin value, leukocyte count, and platelet count increased significantly after partial embolization, and the frequency of bleeding from esophageal varices decreased significantly. The hematologic parameters were improved in 19 patients, unchanged in five, and worse in two. Mean survival time was 50.5 months (range, 0.5–272.0 months).

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 1315). 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.



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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).

 


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