Acute necrotizing pancreatitis is associated with a significant complication rate. The most serious are hemorrhagic complications. We report a case of surgically untreatable portal vein tear successfully treated by endovascular means in the form of stent-graft placement via a percutaneous transhepatic approach. Hemorrhagic necrotizing pancreatitis is a serious condition associated with mortality rates of 80%–90%. The most frequent source of bleeding is arterial erosion; erosion of the portal vein is very rare.
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A 36-year-old man was admitted in September 2007 with severe acute idiopathic necrotizing pancreatitis. He was an ex-smoker with no significant comorbidities other than obesity (body mass index, 34). After admission, several surgical abdominal revisions were performed to remove necrotic tissue; extensive necrosis occurred involving the portal vein and duodenal wall leading to duodenal perforation and acute peritonitis with bilateral pleural effusions, and the patient developed multiple organ failure and sepsis. Computed tomography (CT) at this stage showed erosion of all branches of the portal vein confluence, and on day 38 after admission the patient was transferred to our institution for further surgery. However, surgical repair of the vascular defect, measuring approximately 1 cm × 1.5 cm, was not possible because of extensive tissue necrosis and infection. Only splenic vein ligation and abdominal packing could be performed to control bleeding. Endovascular treatment was then suggested as the only other feasible option.
The procedure was performed under general anesthesia. Hemocoagulation tests revealed an International Normalized Ratio of 1.2 and an activated partial thromboplastin time of 33 seconds (ratio, 1.1), indicating sufficient hemostasis. An indirect portogram was acquired after selective superior mesenteric artery catheterization via inguinal approach, which showed patent superior mesenteric and portal veins and closed lienal vein (Figure, a). The defect in the portal vein was compressed by abdominal packing. The tenth intercostal space was punctured with micropuncture technique (Bile Duct Initial Set; Optimed, Karlsruhe, Germany) and percutaneous transhepatic access to the portal vein was established with a 6-F sheath (Cook, Bloomington, Indiana) under skiascopic control. The defect was found with use of a K2 catheter (Cook) and a Terumo standard 150-mm angled guide wire (Terumo, Somerset, New Jersey) through the portal vein access, and leakage of contrast material into the peritoneal cavity from the portal confluence was confirmed (Figure, b). The injury was ill-defined and hence was not suitable for glue or coil embolization, and stent-graft implantation was considered the best option. Calibration angiography with use of a calibration catheter was performed, with precise measurements of the superior mesenteric vein and portal vein at indirect portography. The portal vein measured 16 mm and the superior mesenteric vein 10 mm. An appropriate tapered iliac stent-graft measuring 9.5 × 16 mm in diameter was chosen (Stimcare; W.L. Gore and Associates, Flagstaff, Arizona) and the graft was implanted from the superior mesenteric vein to the portal vein. Completion angiography did not show any residual contrast agent extravasation (Figure, c). The liver tract was embolized with Gelaspon pieces (Chauvin Ankerpharm, Rudolstadt, Germany) without any sequelae. The patient was transferred to the operating room immediately after the procedure for the abdominal packing removal, which was done without any significant bleeding.
Nine further surgical procedures for minor bleeding episodes, duodenal perforation, and abdominal wall dehiscence including suture of the duodenum, drainage, changes of packing, hemostasis of other arterial bleeding events, and abdominal wall resuture were necessary after the intervention. The patient's clinical status slowly improved and he was transferred back to the referring hospital 63 days after admission. A CT angiogram obtained before transfer demonstrated a fully patent stent-graft and portal vein. Follow-up CT angiography performed 6 months after the procedure showed a patent stent-graft and patent superior mesenteric and portal veins (Figure, d). The patient had fully recovered from pancreatitis at that time.
Pancreatitis may cause a spectrum of vascular complications, ranging from asymptomatic venous thrombosis or incidentally detected pseudoaneurysm to catastrophic venous or arterial hemorrhage. The reported overall incidences of vascular complications in pancreatitis are 1%–6%. The incidence is three times higher in chronic pancreatitis versus acute pancreatitis (1). Hemorrhage is uncommon: Balthazar and Fisher (2) analyzed 1,910 patients with pancreatitis and reported an incidence of hemorrhagic complications of 1.3%. Hemorrhage is usually a result of vessel erosion or thrombosis of the portal, splenic, or upper mesenteric vein resulting in compartmental portal hypertension causing variceal bleeding. Venous thrombosis is not uncommon; Mortele et al (3) retrospectively reviewed 100 consecutive patients with acute pancreatitis. Arterial hemorrhage was seen in 5% of patients, and venous abnormalities, including splenic, superior mesenteric, and portal vein thrombosis, were seen in 19%, 14%, and 13% of patients, respectively.
Portal vein involvement occurs in approximately 10% of patients with chronic pancreatitis and may result in a fistula between the portal venous system and the pancreas (4). This complication is rare; only 33 patients with pancreaticoportal fistulas have been reported in the literature since 1966 to our knowledge. In the majority of cases, there was thrombosis of the portal venous system (4), and direct erosion of the portal vein is even less frequent. We know of only one case report of acute abdominal hemorrhage from portal vein erosion, which was successfully managed conservatively (5).
High-resolution CT is currently the modality of choice for the detection of major hemorrhage in inflammatory pancreatic disease. It confirms the site of bleeding and facilitates interventional planning. Patients in unstable condition with massive gastrointestinal bleeding should be taken directly to the angiography suite for diagnostic angiography and endovascular treatment (6).
In the present case, we successfully used techniques and tools with which we are familiar from procedures elsewhere. We chose a stent-graft because the vein wall defect was large. We know from the literature that a stent-graft can effectively cover portal vein bleeding in cases of such a defect in transjugular intrahepatic portosystemic shunt creation procedures. Lower pressure in the portal system causes slower bleeding and the size of the portal vein facilitates more frequent occurrence of larger defects in the vessel wall that require stent-graft placement as the best curative option. The iliac component of an aortic stent-graft is tapered in shape and wide enough to perform tamponade of the portal vein. We are familiar with a percutaneous transhepatic approach from portal vein embolization procedures. It was used in this case as a direct approach to the portal circulation suitable for placement of an 18-F sheath. The straight tract was also easy to embolize after the procedure. The present case demonstrates stent-graft placement to be a generally feasible treatment option for portal venous bleeding secondary to pancreatitis.
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