(Radiology. 2001;220:150-156.)
© RSNA, 2001
Vascular and Interventional Radiology |
Portal Venous Stent Placement in Patients with Pancreatic and Biliary Neoplasms Invading Portal Veins and Causing Portal Hypertension: Initial Experience1
Koichiro Yamakado, MD,
Atsuhiro Nakatsuka, MD,
Naoshi Tanaka, MD,
Ayumi Fujii, MD,
Shuji Isaji, MD,
Yoshifumi Kawarada, MD and
Kan Takeda, MD
1 From the Departments of Radiology (K.Y., A.N., N.T., A.F., K.T.) and First Surgery (S.I., Y.K.), Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. From the 1999 RSNA scientific assembly. Received June 13, 2000; revision requested July 24; final revision received November 28; accepted January 15, 2001. Address correspondence to K.Y. (e-mail: yama@clin.medic.mie-u.ac.jp).
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ABSTRACT
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PURPOSE: To evaluate the clinical usefulness of portal venous stent placement in patients with pancreatic or biliary neoplasms invading portal veins and causing portal hypertension.
MATERIALS AND METHODS: Thirteen patients underwent portal venous stent placement because of gastrointestinal bleeding (n = 8), risk of gastroesophageal varix rupture (n = 4), ascites (n = 4), thrombocytopenia (n = 3), and/or portal venous thrombosis (n = 3). The main portal vein or both the intrahepatic and main portal veins were invaded in six patients (group A). The main portal vein and splanchnic veins were involved in seven patients (group B). Stents were placed across the stenotic (n = 8) or occluded (n = 5) lesions after percutaneous transhepatic portography. Changes in portal venous pressure, stent patency, and survival were evaluated.
RESULTS: Mean portal venous pressure decreased significantly immediately after stent placement, from 24.9 mm Hg ± 5.9 (SD) to 15.8 mm Hg ± 4.6 (P < .001). In group A, blood flow through the stent was maintained and the symptoms had subsided at follow-up (mean, 12.5 months). In group B, symptoms were improved in five patients, but the stents were occluded in all but one patient at a mean follow-up of 1.5 months. There was a significant difference in stent patency between the patients with (14%) and those without (100%) splanchnic venous involvement (P < .01).
CONCLUSION: Stent placement helped to relieve portal hypertension symptoms. Splanchnic venous involvement was associated with worse stent patency.
Index terms: Bile ducts, neoplasms, 76.32 • Pancreas, neoplasms, 77.32 • Portography, 957.1242 • Stents and prostheses, 957.1268
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INTRODUCTION
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Portal venous hypertension caused by extrahepatic obstruction occurs when the portal vein is blocked at the site before blood reaches the liver. Patients with this condition comprise 5%–10% of all cases of portal hypertension (1–3). Neoplasms such as hepatocellular carcinoma, pancreatic cancer, and bile duct cancer are responsible for 15%–24% of cases with extrahepatic portal venous occlusion (1–4). Tumors directly invade or extrinsically compress the portal veins (1). Blockage of portal venous blood flow and associated thrombosis cause various symptoms (1–4). Development of varices in the stomach, esophagus, duodenum, and colon and bowel ischemia cause gastrointestinal bleeding, which can result in death (1–4). The development of ascites affects the patient’s quality of life. However, useful treatments have not been established.
Theoretically, resolving blockage of the portal venous blood flow leads to improvement in symptoms. We have already reported on the clinical usefulness of portal venous stent placement in patients with hepatocellular carcinoma invading the main portal vein (5). However, little is known about the clinical usefulness of stent placement for malignant portal venous stenosis or occlusion caused by pancreatic or biliary neoplasms. The purpose of this study was to evaluate the clinical usefulness of portal venous stent placement in patients with pancreatic or biliary neoplasms, and we describe our preliminary experience with this procedure in this article.
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MATERIALS AND METHODS
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Patients
From June 1997 to April 2000, 13 patients (three women, 10 men; mean age ± SD, 61.8 years ± 13.1; age range, 31–80 years) with pancreatic or biliary neoplasms underwent portal venous stent placement because of malignant portal venous stenosis or occlusion. The clinical characteristics of these patients are summarized in Tables 1 and 2. Seven patients had pancreatic cancer, and six had bile duct cancer. The diagnosis of primary tumor was established at laparotomic biopsy and previous surgery in eight patients. In the other five patients, the diagnosis was established by using radiologic procedures such as percutaneous cholangiography, endoscopic retrograde cholangiopancreatography, and abdominal computed tomography (CT); elevated values of tumor markers such as carcinoembryonic antigen and carbohydrate antigen 19-9; and brush bile cytology. Despite tumor resection, recurrent tumors invaded the portal veins in five patients. Stenosis or occlusion of the portal venous system surrounded by tumors was considered to be portal venous invasion. Primary tumors and lymph nodes involved the portal veins in the other eight patients.
Before portal venous stent placement, biliary-enteric bypass had been performed for biliary stenosis or occlusion in eight patients, and biliary stent placement had been performed in the other five patients. Portal venous involvement was found at contrast material–enhanced abdominal CT and ultrasonography (US) (including Doppler studies) and confirmed at transarterial portography. Portal veins were involved at the liver hilum in six patients (patients 1–6, group A). The main portal vein (n = 3) or the main and intrahepatic portal veins (n = 3) were invaded by tumors. In the other seven patients (patients 7–13, group B), the splanchnic veins were involved. In addition to the main portal vein, the splenic and superior mesenteric veins were invaded at the junction of both vessels in three of the seven patients (patients 7–9). In the other four patients (patients 10–13), the inferior mesenteric vein also was involved.
The backgrounds of the patients with and of those without splanchnic venous involvement are summarized in Table 2. Group A included five patients with bile duct cancer and one with pancreatic cancer. Group B included one patient with bile duct cancer and six patients with pancreatic cancer. The Child-Pugh score (6), Karnofsky performance status index (7), degree of anemia (ie, red blood cell count, hemoglobin level, and need for blood transfusion), and degree of portal venous invasion (ie, rate of occlusion and length of invaded lesions) were significantly worse in group B (Table 2). Endoscopic sclerotherapy was tried before portal venous stent placement in four patients with hemorrhagic gastroesophageal varices, but it failed to control bleeding. We previously reported on case 7 in the literature (8).
Portal Hypertensive Symptoms
The most common symptom was gastrointestinal bleeding, which was observed in eight (62%) patients. Hemorrhagic esophageal varices developed in four patients, and lower intestinal hemorrhage was suspected in the other four patients with melena. Blood transfusion was required in seven of the eight patients. Rapid development of gastroesophageal varices was seen in four patients. Ascites developed in four patients; thrombocytopenia, in three patients (mean platelet count, 4.2 x 104/µl [0.000042 x 109/L]); and portal venous thrombosis, in three patients. Abdominal pain was not assessed as a symptom of portal hypertension, because it was difficult to discriminate pain from underlying disease in some patients.
Stent Placement
Informed consent was obtained from either the patients or their families before portal venous stent placement. Stents were placed percutaneously by two radiologists (K.Y., A.N.) after transhepatic portography. The intact second-order portal branch was punctured with an 18-gauge percutaneous cholangiographic needle by using US guidance. A 5-F sheath was inserted into the portal vein, and a catheter was advanced beyond the stenotic (n = 8) or occluded (n = 5) lesions. Then, portography was performed. After the sheath was changed to 8 F, a 3,000-IU dose of heparin was injected in all except patient 7. Then, the stenotic or occluded lesions were dilated by using a balloon catheter. The stents were placed across the invaded lesions to increase the blood flow toward the liver and to decrease the venous pressure in the splanchnic veins. The diameter and length of the stents were determined according to the diameter and length of the involved vessels that were measured at portography after balloon dilation. After the stents were deployed, percutaneous transhepatic portography was repeated. When stenosis was still observed or the lesions were not fully covered by stents, either balloon dilation or a second stent placement was performed. A gelatin sponge was placed in the liver parenchymal tract through the sheath to prevent intraperitoneal hemorrhage when the sheath was withdrawn.
Anticoagulant therapy was initiated after stent placement. Heparin was given at a dose 6,000–10,000 IU per day for 3–5 days, followed by oral warfarin administration, unless bleeding occurred. Antibiotic agents were given before and 2–3 days after stent placement, unless complications such as liver abscess developed. Complications related to stent placement were evaluated.
Stent Data
Noncovered stents were placed through an 8- or 12-F sheath in nine patients. Stents with a diameter of 10 or 12 mm and a length of 3–6 cm (Z-stents; Cook, Bloomington, Ind) were placed in patients 7 and 10. Stents with a diameter of 10 or 20 mm and a length of 5–9 cm (Wallstent; Schneider, Tokyo, Japan) were placed in patients 2, 3, 5, 6, 8, 9, and 12. In four patients, stents covered with polyetetrafluoroethylene (Gore-Tex; W. L. Gore and Associates, Flagstaff, Ariz) were placed through a 12- or 15-F sheath: Covered stents with a diameter of 10 mm and lengths of 3 and 6 cm (Z-stents) were placed in patients 4 and 11; a covered stent with a diameter of 10 mm and a length of 5 cm (Wallstent), in patient 1; and a stent with a diameter of 10 mm and a length of 6 cm (NT Stent; Terumo, Tokyo, Japan), in patient 13.
Portal Venous Pressure, Stent Patency, and Survival
Portal venous pressure was measured beyond the stenotic or occluded lesions before and immediately after stent placement. The blood flow through the stent was evaluated by performing Doppler US at least every month and immediately after symptoms recurred. The patency period of the vein with a stent was defined as the interval between stent placement and occlusion. If blood flow through the stent was observed throughout the patient’s life, the patency period was considered to be equal to the survival period. The causes of stent occlusion were studied at autopsy. The clinical courses after portal venous stent placement and the causes of death (Table 3) were studied from clinical records.
Statistical Analyses
The data were expressed as means ± SD. Differences in patient background and stent patency between groups A and B were compared by performing the Student t test and the Fisher exact test. The cumulative survival rate was calculated by using the Kaplan-Meyer method, and the difference in prognosis between the two groups was compared by performing the log-rank test. A P value of less than .05 was considered to indicate a statistically significant difference.
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RESULTS
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Stent Placement
The results of portal venous stent placement are summarized in Table 3. In group A, initial percutaneous transhepatic portography depicted stenosis of the main portal vein in all patients (Fig 1a). Stents were placed in the main portal vein in three patients and from the intact intrahepatic veins to the main portal veins in the other three patients (Fig 1b).
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Figure 1a. Patient 1. Bile duct cancer invading the portal vein and causing thrombocytopenia and rapid development of gastroesophageal varices in a 70-year-old woman. (a) Frontal percutaneous transhepatic portogram shows severe stenosis (arrow) of the main portal vein. The left portal vein is completely occluded by tumor. Note the marked development of gastroesophageal varices (arrowheads). (b) Frontal portogram shows a covered stent (arrowheads) with a diameter of 10 mm and a length of 5 cm placed in the main portal vein. The image also shows that the main portal venous stenosis was eliminated; the portal venous pressure decreased from 36 to 15 mm Hg. The gastroesophageal varices also were eliminated. The platelet count increased from 26,000 to 153,000/µl (0.000026 to 0.000153 x 109/L) 2 weeks later. Symptoms did not recur during the patient’s survival of 11.2 months.
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Figure 1b. Patient 1. Bile duct cancer invading the portal vein and causing thrombocytopenia and rapid development of gastroesophageal varices in a 70-year-old woman. (a) Frontal percutaneous transhepatic portogram shows severe stenosis (arrow) of the main portal vein. The left portal vein is completely occluded by tumor. Note the marked development of gastroesophageal varices (arrowheads). (b) Frontal portogram shows a covered stent (arrowheads) with a diameter of 10 mm and a length of 5 cm placed in the main portal vein. The image also shows that the main portal venous stenosis was eliminated; the portal venous pressure decreased from 36 to 15 mm Hg. The gastroesophageal varices also were eliminated. The platelet count increased from 26,000 to 153,000/µl (0.000026 to 0.000153 x 109/L) 2 weeks later. Symptoms did not recur during the patient’s survival of 11.2 months.
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In group B, stents were placed on the basis of the hemodynamics of the mesenteric circulation and successful catheterization beyond the occluded or stenotic lesions. In patients 7–9, both the splenic and superior mesenteric veins were involved, but the inferior mesenteric vein was intact (Fig 2a, 2b). The superior mesenteric vein was occluded in all three patients. The splenic vein was stenotic in two patients and occluded in one. Stents were placed from the main portal vein to the splenic vein in these patients (Fig 2c). In the other four patients, three splanchnic veins were occluded (Fig 3a–3c). In two of them (patients 10 and 11), a catheter was successfully placed in the splenic and superior mesenteric veins (Fig 3b, 3c). After stents were placed in the splenic vein, additional stents were placed from the main portal vein to the superior mesenteric vein across the splenic vein with a stent (Fig 3c, 3d). In the remaining two patients (patients 12 and 13), a catheter was successfully placed in the splenic and inferior mesenteric veins, but it could not be advanced in the superior mesenteric vein. Stents were placed from the main portal vein to the inferior mesenteric vein across the splenic vein.
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Figure 2a. Patient 9. Recurrent bile duct cancer involving the splenic and superior mesenteric veins and causing esophageal varix rupture, refractory ascites, and portal venous thrombosis in a 51-year-old man. (a) Frontal percutaneous transhepatic portogram shows obstruction of the splenic vein (solid arrow). The superior mesenteric vein also is obstructed by tumor. The inferior mesenteric vein (open arrow) is intact and opacified retrogradely from the splenic vein. Gastroesophageal varices (arrowheads) also are shown. (b) Frontal portogram obtained after balloon dilation shows the occlusion of the splenic vein has improved, but stenosis (solid arrow) remains. The left portal vein is not opacified because of thrombosis. Note that the involved superior mesenteric vein (open arrow) is opacified. (c) Frontal portogram shows the portal venous pressure decreased, from 26 to 14 mm Hg, immediately after a noncovered stent with a diameter of 10 mm and length of 7 cm was placed from the main portal vein to the splenic vein. Hemorrhage from esophageal varices ceased, and refractory ascites improved; however, the tumor progressed and occluded the stent 1.3 months later. Note the blood flow in the left portal vein (arrow).
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Figure 2b. Patient 9. Recurrent bile duct cancer involving the splenic and superior mesenteric veins and causing esophageal varix rupture, refractory ascites, and portal venous thrombosis in a 51-year-old man. (a) Frontal percutaneous transhepatic portogram shows obstruction of the splenic vein (solid arrow). The superior mesenteric vein also is obstructed by tumor. The inferior mesenteric vein (open arrow) is intact and opacified retrogradely from the splenic vein. Gastroesophageal varices (arrowheads) also are shown. (b) Frontal portogram obtained after balloon dilation shows the occlusion of the splenic vein has improved, but stenosis (solid arrow) remains. The left portal vein is not opacified because of thrombosis. Note that the involved superior mesenteric vein (open arrow) is opacified. (c) Frontal portogram shows the portal venous pressure decreased, from 26 to 14 mm Hg, immediately after a noncovered stent with a diameter of 10 mm and length of 7 cm was placed from the main portal vein to the splenic vein. Hemorrhage from esophageal varices ceased, and refractory ascites improved; however, the tumor progressed and occluded the stent 1.3 months later. Note the blood flow in the left portal vein (arrow).
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Figure 2c. Patient 9. Recurrent bile duct cancer involving the splenic and superior mesenteric veins and causing esophageal varix rupture, refractory ascites, and portal venous thrombosis in a 51-year-old man. (a) Frontal percutaneous transhepatic portogram shows obstruction of the splenic vein (solid arrow). The superior mesenteric vein also is obstructed by tumor. The inferior mesenteric vein (open arrow) is intact and opacified retrogradely from the splenic vein. Gastroesophageal varices (arrowheads) also are shown. (b) Frontal portogram obtained after balloon dilation shows the occlusion of the splenic vein has improved, but stenosis (solid arrow) remains. The left portal vein is not opacified because of thrombosis. Note that the involved superior mesenteric vein (open arrow) is opacified. (c) Frontal portogram shows the portal venous pressure decreased, from 26 to 14 mm Hg, immediately after a noncovered stent with a diameter of 10 mm and length of 7 cm was placed from the main portal vein to the splenic vein. Hemorrhage from esophageal varices ceased, and refractory ascites improved; however, the tumor progressed and occluded the stent 1.3 months later. Note the blood flow in the left portal vein (arrow).
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Figure 3a. Patient 10. Pancreatic cancer involving the splenic veins and the superior and inferior mesenteric veins and causing refractory ascites and portal venous thrombosis in a 31-year-old man. (a) Frontal percutaneous transhepatic portogram shows complete occlusion of the main portal vein (arrow) and portal venous thrombosis (arrowheads). Note that the left portal vein is not opacified. (b) Frontal portogram shows a 5-F catheter that was advanced into the splenic vein (arrow) beyond the occlusion. (c) Frontal portogram shows that a 5-F catheter was also inserted into the superior mesenteric vein beyond the occlusion (arrow). (d) Frontal portogram shows that after noncovered stents with a diameter of 12 mm and a length of 6 cm were placed in the splenic vein, additional noncovered stents of the same size were placed from the main portal vein to the superior mesenteric vein across the splenic vein with a stent. The blood flow from the splenic vein to the liver was revived immediately after stent placement, and the portal venous pressure decreased from 28 to 16 mm Hg. The intrahepatic portal venous thrombosis (arrowhead) improved but remained. (e) Frontal portogram shows the blood flow from the superior mesenteric vein to the liver. Note the blood flow (arrow) in the left portal vein. Although symptoms improved after stent placement, occlusion was found and symptoms recurred 10 days later. Stents were occupied with thrombi at autopsy performed 3.3 months later.
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Figure 3b. Patient 10. Pancreatic cancer involving the splenic veins and the superior and inferior mesenteric veins and causing refractory ascites and portal venous thrombosis in a 31-year-old man. (a) Frontal percutaneous transhepatic portogram shows complete occlusion of the main portal vein (arrow) and portal venous thrombosis (arrowheads). Note that the left portal vein is not opacified. (b) Frontal portogram shows a 5-F catheter that was advanced into the splenic vein (arrow) beyond the occlusion. (c) Frontal portogram shows that a 5-F catheter was also inserted into the superior mesenteric vein beyond the occlusion (arrow). (d) Frontal portogram shows that after noncovered stents with a diameter of 12 mm and a length of 6 cm were placed in the splenic vein, additional noncovered stents of the same size were placed from the main portal vein to the superior mesenteric vein across the splenic vein with a stent. The blood flow from the splenic vein to the liver was revived immediately after stent placement, and the portal venous pressure decreased from 28 to 16 mm Hg. The intrahepatic portal venous thrombosis (arrowhead) improved but remained. (e) Frontal portogram shows the blood flow from the superior mesenteric vein to the liver. Note the blood flow (arrow) in the left portal vein. Although symptoms improved after stent placement, occlusion was found and symptoms recurred 10 days later. Stents were occupied with thrombi at autopsy performed 3.3 months later.
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Figure 3c. Patient 10. Pancreatic cancer involving the splenic veins and the superior and inferior mesenteric veins and causing refractory ascites and portal venous thrombosis in a 31-year-old man. (a) Frontal percutaneous transhepatic portogram shows complete occlusion of the main portal vein (arrow) and portal venous thrombosis (arrowheads). Note that the left portal vein is not opacified. (b) Frontal portogram shows a 5-F catheter that was advanced into the splenic vein (arrow) beyond the occlusion. (c) Frontal portogram shows that a 5-F catheter was also inserted into the superior mesenteric vein beyond the occlusion (arrow). (d) Frontal portogram shows that after noncovered stents with a diameter of 12 mm and a length of 6 cm were placed in the splenic vein, additional noncovered stents of the same size were placed from the main portal vein to the superior mesenteric vein across the splenic vein with a stent. The blood flow from the splenic vein to the liver was revived immediately after stent placement, and the portal venous pressure decreased from 28 to 16 mm Hg. The intrahepatic portal venous thrombosis (arrowhead) improved but remained. (e) Frontal portogram shows the blood flow from the superior mesenteric vein to the liver. Note the blood flow (arrow) in the left portal vein. Although symptoms improved after stent placement, occlusion was found and symptoms recurred 10 days later. Stents were occupied with thrombi at autopsy performed 3.3 months later.
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Figure 3d. Patient 10. Pancreatic cancer involving the splenic veins and the superior and inferior mesenteric veins and causing refractory ascites and portal venous thrombosis in a 31-year-old man. (a) Frontal percutaneous transhepatic portogram shows complete occlusion of the main portal vein (arrow) and portal venous thrombosis (arrowheads). Note that the left portal vein is not opacified. (b) Frontal portogram shows a 5-F catheter that was advanced into the splenic vein (arrow) beyond the occlusion. (c) Frontal portogram shows that a 5-F catheter was also inserted into the superior mesenteric vein beyond the occlusion (arrow). (d) Frontal portogram shows that after noncovered stents with a diameter of 12 mm and a length of 6 cm were placed in the splenic vein, additional noncovered stents of the same size were placed from the main portal vein to the superior mesenteric vein across the splenic vein with a stent. The blood flow from the splenic vein to the liver was revived immediately after stent placement, and the portal venous pressure decreased from 28 to 16 mm Hg. The intrahepatic portal venous thrombosis (arrowhead) improved but remained. (e) Frontal portogram shows the blood flow from the superior mesenteric vein to the liver. Note the blood flow (arrow) in the left portal vein. Although symptoms improved after stent placement, occlusion was found and symptoms recurred 10 days later. Stents were occupied with thrombi at autopsy performed 3.3 months later.
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Figure 3e. Patient 10. Pancreatic cancer involving the splenic veins and the superior and inferior mesenteric veins and causing refractory ascites and portal venous thrombosis in a 31-year-old man. (a) Frontal percutaneous transhepatic portogram shows complete occlusion of the main portal vein (arrow) and portal venous thrombosis (arrowheads). Note that the left portal vein is not opacified. (b) Frontal portogram shows a 5-F catheter that was advanced into the splenic vein (arrow) beyond the occlusion. (c) Frontal portogram shows that a 5-F catheter was also inserted into the superior mesenteric vein beyond the occlusion (arrow). (d) Frontal portogram shows that after noncovered stents with a diameter of 12 mm and a length of 6 cm were placed in the splenic vein, additional noncovered stents of the same size were placed from the main portal vein to the superior mesenteric vein across the splenic vein with a stent. The blood flow from the splenic vein to the liver was revived immediately after stent placement, and the portal venous pressure decreased from 28 to 16 mm Hg. The intrahepatic portal venous thrombosis (arrowhead) improved but remained. (e) Frontal portogram shows the blood flow from the superior mesenteric vein to the liver. Note the blood flow (arrow) in the left portal vein. Although symptoms improved after stent placement, occlusion was found and symptoms recurred 10 days later. Stents were occupied with thrombi at autopsy performed 3.3 months later.
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Stenosis or occlusion of the veins was eliminated immediately after stent placement and led to an increase or revival of blood flow toward the liver (Figs 1b, 2c, 3d, 3e). In all patients, the mean portal venous pressure decreased significantly immediately after stent placement, from 24.9 mm Hg ± 5.9 (SD) to 15.8 mm Hg ± 4.6 (P < .001). There was no substantial difference in portal venous pressure between groups A and B before or after stent placement.
Complications
After stent placement, all patients reported having abdominal pain related to the puncture site. Transient fever—that is, an elevation in body temperature of less than 38°C—developed in five patients. These symptoms subsided with symptomatic treatments. Liver abscess associated with high fever (40°C) developed at the puncture site in one patient with bile duct dilatation in whom a covered stent was placed by using a 12-F sheath. Percutaneous drainage was necessitated in this patient. Although intrahepatic portal venous thrombosis developed in the patient who did not receive heparin during the procedure (patient 7), it resolved after the administration of heparin and urokinase.
Improved Symptoms, Clinical Course, and Stent Patency
Symptoms improved in all patients in group A. Doppler US demonstrated that the blood flow through the vein with a stent was maintained, and the symptoms remained subsided during the mean follow-up period of 12.5 months (range, 2.0–28.0 months). Four patients with bile duct cancer received anticancer treatments after their symptoms improved. Three patients (patients 1–3) underwent brachytherapy, external-beam radiation therapy, and repeated hepatic arterial infusion chemotherapy by means of an implantable catheter and portal system. One patient (patient 6) received external-beam radiation therapy. All patients were discharged within 2 months after stent placement.
The stents remained patent during survival (2.1 months) in one patient (case 7) in group B. In the other six patients in group B, however, Doppler US depicted stent occlusion at a mean of 0.7 month (range, 0.2–1.3 months) after stent placement. The stents were obstructed within 1 month (mean, 0.4 month) in four patients in whom all three splanchnic veins were involved (patients 10–13). The symptoms improved in the 1st week after stent placement in five (71%) of seven patients but recurred following stent occlusion in four of these five patients. Despite stent placement, hemorrhage was not controlled in two debilitated patients (patients 11 and 13). Only patient 7 in group B was discharged—1 month later.
There was a significant difference in stent patency between the patients with and those without splanchnic venous involvement: The stents remained patent in one (14%) of seven patients in group B and in all six (100%) patients in group A (P < .01).
Autopsy was performed in seven of the 13 patients, and stent occlusion was confirmed in five patients in group B. The causes of stent occlusion were thrombosis in two patients (40%) (patients 10 and 11), tumor overgrowth in two patients (40%) (patients 8 and 9), and tumor ingrowth in one patient (20%) (patient 12). The endoluminal surface of the stent was not covered with neointima in two stents (patients 3 and 5), which were patent for 7.2 and 16.0 months, respectively.
Survival
At the time this article was written, 11 patients had died and two were living. Four patients died of recurrent gastrointestinal bleeding following stent occlusion, four died of cancer progression, and one patient each died of pneumonia, gastric ulcer, and associated acute myeloblastic leukemia.
In group A, three (50%) patients lived more than 1 year, and the 1- and 2-year survival rates were 60% and 20%, respectively. However, no patient in group B lived more than 4 months (1-year survival rate, 0%). There was a significant difference in mean survival between the two groups: 12.5 months ± 1.7 for group A versus 1.6 months ± 0.4 for group B (P < .001).
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DISCUSSION
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Clinical Usefulness of Stent Placement
Our study results showed that portal venous stent placement is useful in decreasing portal venous blood pressure in patients with malignant portal venous stenosis or occlusion caused by pancreatic or biliary neoplasms. The clinical outcomes, however, were quite different depending on the invasion site. When the portal venous blood flow was blocked at the main portal vein and the splanchnic veins were intact (group A), the stents remained patent and the portal hypertension symptoms subsided during survival (mean, 12.5 months). All patients were discharged, and half of them (three of six) lived for more than 1 year. In previously published literature (9,10), the same results are reported for two patients. On the other hand, when the splanchnic veins were involved (group B), the stents frequently (in six [86%] of seven patients) became occluded soon after stent placement. The outcomes were disappointing, particularly when all the splanchnic veins were occluded. At autopsy, the stents were occluded by thrombi in two (40%) of five patients, by tumor overgrowth in two (40%) patients, and by tumor ingrowth in one (20%) patient.
We previously reported on the clinical utility of portal venous stent placement in patients with hepatocellular carcinoma invading the main portal vein (5). Stents were occluded in six (29%) of 21 patients at a mean follow-up of 7 months. Tumor ingrowth, stent thrombosis, and liver failure were considered to be the causes of stent occlusion. We found stent placement to be contraindicated when liver failure occurred. Patients with splanchnic venous involvement by pancreatic and biliary neoplasms are usually debilitated, and the tumors are far advanced. It seems that the progressive nature of pancreatic cancer causes stent occlusion earlier, as compared with the occlusion associated with hepatocellular carcinoma. In addition, the decreased portal venous blood flow due to liver dysfunction causes stent thrombosis, although a small patient population prevented us from evaluating factors that might influence stent patency.
Autopsy findings showed also that stents were not covered by neointima 16 months after stent placement. Considering that the stent itself exhibits thrombogenicity, anticoagulant or antiplatelet therapy is essential (5,11).
The use of covered stents may help to prevent tumor ingrowth. We placed them in four patients in the present study. However, it is difficult to place covered stents in the portal veins. First, a large sheath is required. Use of large sheaths, however, is associated with bile duct dilatation in some patients and with ascites in others; therefore, a small sheath is preferable. Second, with covered stents, there is a risk of occlusion or stenosis of major patent portal branches such as the intrahepatic portal veins and splanchnic veins.
Indications for Portal Venous Stent Placement
On the basis of the good results in our study and data in previously published literature (9,10), we consider portal venous stent placement to be useful in patients with malignant stenosis or occlusion of the main portal vein. Furthermore, the results of this study show that portal venous stent placement can be one of the useful combined therapies in patients with malignant portal venous stenosis or occlusion. We combined brachytherapy, external-beam radiation therapy, and repeated hepatic arterial infusion chemotherapy for bile duct cancer in four patients after their symptoms improved. Combined therapies prevent or at least delay tumor overgrowth and ingrowth and improve prognosis (12,13). Three case reports (10,14,15) showed the clinical utility of portal venous stent placement, even in patients without symptoms. The stents were placed in the main portal vein to diminish the risk of gastrointestinal bleeding and to recover and ensure the function of transplanted and postoperative livers.
On the other hand, the poor results in group B do not strongly encourage us to perform portal venous stent placement when splanchnic veins are substantially involved. The clinical usefulness of arterial infusion chemotherapy and radiation therapy in increasing survival in patients with advanced pancreatic cancer has been reported on in some studies (16,17). These therapies combined may help to increase stent patency and survival in some patients.
In conclusion, when the splanchnic veins are intact, stent placement in the portal vein decreases portal venous pressure and helps to improve the patient’s quality of life and prognosis. In our study, however, involvement of the splanchnic veins was associated with worse stent patency and prognosis. Portal venous stent placement can be a useful part of a series of multimodal treatments in selected patients with advanced pancreatic and biliary neoplasms.
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FOOTNOTES
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Author contributions: Guarantor of integrity of entire study, K.Y.; study concepts, K.Y., Y.K.; study design, K.Y.; literature research, K.Y., A.F.; clinical studies, K.Y., A.N.; data acquisition, K.Y., A.N., N.T., A.F.; data analysis/interpretation, K.Y., K.T.; statistical analysis, K.Y.; manuscript preparation, K.Y.; manuscript definition of intellectual content, K.T.; manuscript editing, K.Y.; manuscript revision/review, K.T., S.I.; manuscript final version approval, K.T.
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ABSTRACT
INTRODUCTION
