Biliopancreatic fistula with portal vein thrombosis caused by a pancreatic pseudocyst

We encountered a very rare case of biliopancreatic fistula with portal vein thrombosis caused by pancreatic pseudocyst. A 57-year-old man was referred to our hospital because of abdominal pain, obstructive jaundice, and portal vein thrombosis due to acute pancreatitis. Computed tomography showed a 7-cm-diameter pseudocyst around the superior mesenteric vein extending towards the pancreatic head, dilatation of the intrahepatic bile duct, and portal vein thrombosis. Endoscopic retrograde pancreatography revealed a main pancreatic duct with a pseudocyst communicating with the common bile duct. After pancreatic sphincterotomy, a 7-F tube stent was endoscopically placed into the pseudocyst. However, a 6-F nasobiliary tube could not be inserted into the bile duct because the fistula had a tight stenosis. Subsequently, the patient’s abdominal pain improved, the pancreatic cyst disappeared, and the serum amylase level normalized. Two months after the endoscopic retrograde cholangiopancreatography, percutaneous transhepatic biliary drainage was required because the patient’s jaundice became aggravated. Two weeks after the choledochojejunostomy, the patient left the hospital in good condition. A follow-up computed tomography showed cavernous transformation of the portal vein and no pancreatic pseudocyst. The patient remains asymptomatic for 2 years and 7 months after surgery. Biliary drainage may be necessary for biliopancreatic fistula with obstructive jaundice in addition to pancreatic cyst drainage. Biliopancreatic fistula can be treated by endoscopic procedure in some cases; however, surgical treatment should be required in cases that are impossible to insert a biliary stent because of hard stricture.     

Pancreatic pseudocyst causing portal vein thrombosis and pancreatico-pleural fistula.

Portal vein thrombosis and pancreatico-pleural fistula are unusual complications of chronic pancreatitis. We describe a patient with chronic alcoholic pancreatitis in whom erosion of the splenic vein led to portal vein thrombosis and to the development of a pancreatico-pleural fistula. We suggest that fistula formation may occur over a considerable time period as the portal vein thrombosis was diagnosed three years before the amylase-rich pleural effusions.     

The natural history of splenic vein thrombosis due to chronic pancreatitis: indications for surgery

Eleven patients with angiographically demonstrated splenic vein thrombosis associated with chronic pancreatitis were followed for an average of 6.5 yr to determine the natural history of this condition. Repeat angiography was performed in five patients. Significant gastric or gastroesophageal varices were noted in six cases. In another patient, peri-colonic varices and spleno-portal collaterals were demonstrated. Two patients bled massively during follow-up; one from gastric varices and one from colonic varices. Another patient, with known gastric varices, intermittent hematochezia and iron deficiency anemia, underwent surgery. All three patients responded well to splenectomy. Since three of the seven patients with splenic vein thrombosis and significant varices eventually required surgical correction, it may be that the long-term risk of gastrointestinal bleeding exceeds the risks of elective splenectomy in these patients.     

Gastrointestinal bleeding due to chronic portal vein thrombosis in ulcerative colitis

Summary The authors report the case of a patient suffering from ulcerative colitis, who had several episodes of digestive hemorrhage due to portal hypertension. Portal hypertension was secondary to chronic portal vein thrombosis. This diagnosis was made on the venous phase of celiac and mesenteric angiography. The authors review the published cases of ulcerative colitis with portal vein thrombosis and discuss the possible etiologic factors: hypercoagulability, thrombocytosis, and intraabdominal sepsis.     

部分脾动脉栓塞治疗慢性胰腺炎相关脾静脉血栓致区域性门静脉高压1例报告

区域性门静脉高压为门静脉某一分支障碍,导致血流异常及侧枝循环开放的临床较少见的疾病,据报道有多达37种原因可导致该类疾病,其中脾静脉血栓是最常见原因之一［1］。而胰腺炎是导致脾静脉血栓的主要原因之一［2］。早在1920年报道了第1例胰腺炎相关脾静脉血栓形成导致的区域性门静脉高压患者,如不及时诊治,患者会出现难治性胃底静脉曲张及出血。本文将报告因反复胰腺疾病所致脾静脉血栓形成,导致脾静脉部分堵塞,引发难治性胃底静脉曲张经部分脾动脉栓塞治疗患者1例。     

Spontaneous rupture of a pancreatic pseudocyst into the portal vein]

HISTORY AND ADMISSION FINDINGS: A 69-year-old woman complained of recurrent cramp-like symptoms in the upper abdomen. She admitted excessive alcohol intake. Physical examination revealed swelling and inflammation of both ankles. All other findings were unremarkable. INVESTIGATIONS: Sonography and computed tomography scan showed a cystic structure (5 cm) in the head of the pancreas. Biochemical testing revealed an anemia (Hb 7,5 mg/dl) and an elevated serum lipase (4494 U/l). Intestinal hemorrhage could not be confirmed by endoscopy. An involvement of parapancreatic structures with the pseudocyst could not be demonstrated by combination of endoscopic retrograde cholangiopancreatography (ERCP) and computed tomography (CT). COURSE: The patient died unexpectedly. Autopsy showed a rupture of the pancreatic pseudocyst into the portal vein leading to portal vein thrombosis. The cause of death was an embolism of the pulmonary arteries. Postmortal reevaluation of CT and ERCP clarified diagnostic features. CONCLUSION: Erosion of peripancreatic vessels is one of the life threatening complications in chronic pancreatitis. The complication is uncommon but should be included into differential diagnosis of recurrent intestinal bleeding.     

Acute mesenteric vein thrombosis and pancreatitis

Summary This article presents a case of acute mesenteric vein thrombosis with small bowel infarction associated with pancreatitis. Although a rare occurrence, the authors suggest this diagnosis should be considered as a possible complication of pancreatic inflammation.     

Marked hypervascularity and early arteriovenous shunting with portal vein filling in chronic relapsing pancreatitis

Angiography was performed in 2 patients with chronic relapsing pancreatitis. Marked hypervascularity and early arteriovenous shunting with portal vein filling were demonstrated. Increased capillary vessels in the thickened capsule due to inflammation were observed in the pathologic specimen. The angiographic findings we report here are quite similar to those of pancreatic arteriovenous malformation.     

Budd-Chiari syndrome and portal vein thrombosis due to essential thrombocytosis

Budd-Chiari syndrome secondary to essential thrombocytosis has been described in a few reports in the English literature. Associated portal vein thrombosis occurs very rarely. Herein, we report a case presented with ascites and finally diagnosed with hepatic and portal vein thrombosis, and essential thrombocytosis. We discussed the therapeutic approaches in the light of pertinent literature.     

Hepatocavopathy and isolated splenic vein thrombosis due to hypercoagulability state.

We report a patient with protein C and protein S deficiency and factor V Leiden mutation presenting with splenic vein thrombosis and with a web between the hepatic venous confluence and vena cava inferior. These two findings were thought to be due to the hypercoagulable state of the patient. Interestingly, there was no need for invasive procedures as the inferior accessory hepatic vein was patent. Hepatic venous flow was being maintained by the inferior accessory hepatic vein or a dominant collateral vein.     

Extensive portal and splenic vein thrombosis: differences in hemodynamics and management

BACKGROUND/AIMS: To assess the incidence of extensive portal and splenic vein thrombosis in patients with extrahepatic portal vein obstruction and determine the differences in presentation, portal hemodynamics and management as compared to patients with portal vein thrombosis alone. METHODOLOGY: 118 patients of extrahepatic portal vein obstruction presenting with variceal hemorrhage, having received no definitive treatment prior to presentation were divided into two groups--with portal and splenic vein thrombosis and with portal vein thrombosis, based on ultrasonography and splenoportography. Collateralization patterns on splenoportography were studied. Results of endoscopic variceal sclerotherapy were compared. RESULTS: Portal and splenic vein thrombosis was seen in 39 patients. Collateralization in case of portal and splenic vein thrombosis, in contrast to portal vein thrombosis, was predominantly left sided (74% vs. 9%, p < 0.0001). Fundal gastric varices were seen more often in patients with portal and splenic vein thrombosis (28% vs. 11%, p = 0.02), developing even after variceal obliteration, though obliteration was achieved in fewer sessions. Surgery for control of variceal bleed was performed more in the portal and splenic vein thrombosis group (33% vs. 15%, p = 0.02), especially for gastric varices (28% vs. 9%, p = 0.006). CONCLUSIONS: Portal and splenic vein thrombosis is present in 33% of patients with extrahepatic portal vein obstruction. Hemodynamic patterns differ, accounting for the preponderance of gastric varices on presentation in patients with portal and splenic vein thrombosis and an increased need for surgery.