Endovascular pseudoaneurysm repair after distal pancreatectomy with celiac axis resection

Erosive hemorrhage due to pseudoaneurysm is one of the most life-threatening complications after pancreatectomy.Here,we report an extremely rare case of rupture of a pseudoaneurysm of the common hepatic artery(CHA)stump that developed after distal pancreatectomy with en block celiac axis resection(DP-CAR),and was successfully treated through covered stent placement.The patient is a 66-year-old woman who underwent DP-CAR after adjuvant chemoradiotherapy for locally advanced pancreatic body cancer.She developed an intra-abdominal abscess around the remnant pancreas head 31 d after the surgery,and computed tomography(CT)showed an occluded portal vein due to the spreading inflammation around the abscess.Her general condition improved after CT-guided drainage of the abscess.However,19 d later,she presented with melena,and CT showed a pseudoaneurysm arising from the CHA stump.Because the CHA had been resected during the DP-CAR,this artery could not be used as the access route for endovascular treatment,and instead,we placed a covered stent via the inferior pancreaticoduodenal artery originating from the superior mesenteric artery.After stent placement,cessation of bleeding and anterograde hepatic artery flow were confirmed,and the patient recovered well without any further complications.CT angiography at the 6-mo follow-up indicated the patency of the covered stent with sustained hepatic artery flow.To our knowledge,this is the first reported case of endovascular repair of a pseudoaneurysm that developed after DP-CAR.     

Extrahepatic collaterals and liver damage in embolotherapy for ruptured hepatic artery pseudoaneurysm following hepatobiliary pancreatic surgery

AIM： To evaluate the effects of extrahepatic collaterals to the liver on liver damage and patient outcome after embolotherapy for the ruptured hepatic artery pseudoaneurysm following hepatobiliary pancreatic surgery.
METHODS： We reviewed 9 patients who underwent transcatheter arterial embolization （TAE） for the ruptured hepatic artery pseudoaneurysm following major hepatobiliary pancreatic surgery between June 1992 and April 2006. We paid special attention to the extrahepatic arterial collaterals to the liver which may affect post-TAE liver damage and patient outcome.
RESULTS： The underlying diseases were all malignancies, and the surgical procedures included hepatopancreatoduodenectomy in 2 patients, hepatic resection with removal of the bile duct in 5, and pancreaticoduodenectomy in 2. A total of 11 pseudoaneurysm developed： 4 in the common hepatic artery, 4 in the proper hepatic artery, and 3 in the right hepatic artery. Successful hemostasis was accomplished with the initial TAE in all patients, except for 1. Extrahepatic arterial pathways to the liver, including the right inferior phrenic artery, the jejunal branches, and the aberrant left hepatic artery, were identified in 8 of the 9 patients after the completion of TAE. The development of collaterals depended on the extent of liver mobilization during the hepatic resection, the postoperative period, the presence or absence of an aberrant left hepatic artery, and the concomitant arterial stenosis adjacent to the pseudoaneurysm. The liver tolerated TAE without significant consequences when at least one of the collaterals from the inferior phrenic artery or the aberrant left hepatic artery was present. One patient, however, with no extrahepatic collaterals died of liver failure due to total liver necrosis 9 d after TAE.
CONCLUSION： When TAE is performed on ruptured hepatic artery pseudoaneurysm, reduced collateral pathways to the liver created by the primary surgical procedure and a short postoperative interval may lead to an unfavorable ou     

Splenic artery ligature associated with endoscopic banding for schistosomal portal hypertension

AIM:To propose a less invasive surgical treatment for schistosomal portal hypertension.METHODS:Ten consecutive patients with hepatosplenic schistosomiasis and portal hypertension with a history of upper gastrointestinal hemorrhage from esophageal varices rupture were evaluated in this study.Patients were subjected to a small supraumbilical laparotomy with the ligature of the splenic artery and left gastric vein.During the procedure,direct portal vein pressure before and after the ligatures was measured.Upper gastrointestinal endoscopy was performed at the 30th postoperative day,when esophageal varices diameter were measured and band ligature performed.During follow-up,other endoscopic procedures were performed according to endoscopy findings.RESULTS:There was no intra-operative mortality and all patients had confirmed histologic diagnoses ofschistosomal portal hypertension.During the immediate postoperative period,two of the ten patients had complications,one characterized by a splenic infarction,and the other by an incision hematoma.Mean hospitalization time was 4.1 d(range:2-7 d).Pre-and post-operative liver function tests did not show any significant changes.During endoscopy thirty days after surgery,a decrease in variceal diameters was observed in seven patients.During the follow-up period(57-72mo),endoscopic therapy was performed and seven patients had their varices eradicated.Considering the late postoperative evaluation,nine patients had a decrease in variceal diameters.A mean of 3.9 endoscopic banding sessions were performed per patient.Two patients presented bleeding recurrence at the late postoperative period,which was controlled with endoscopic banding in one patient due to variceal rupture and presented as secondary to congestive gastropathy in the other patient.Both bleeding episodes were of minor degree with no hemodynamic consequences or need for blood transfusion.CONCLUSION:Ligature of the splenic artery and left gastric vein with supraumbilical laparotomy is a promising and less invasive method for treating presinusoidal schistosomiasis portal hypertension.     

Percutaneous portal venoplasty and stenting for anastomotic stenosis after liver transplantation

AIM： TO review percutaneous transhepatic portal venoplasty and stenting （PTPVS） for portal vein anastomotic stenosis （PVAS） after liver transplantation （LT）. METHODS： From April 2004 to June 2008, 16 of 18 consecutive patients （11 male and 5 female; aged 17-66 years, mean age 40.4 years） underwent PTPVS for PVAS. PVAS occurred 2-10 mo after LT （mean 5.0 mo）. Three asymptomatic patients were detected on routine screening color Doppler ultrasonography （CDUS）. Fifteen patients who also had typical clinical signs of portal hypertension （PHT） were identified by contrast- enhanced computerized tomography （CT） or magnetic resonance imaging. All procedures were performed under local anesthesia. If there was a PVAS 〈 75%, the portal pressure was measured. Portal venoplasty was performed with an undersized balloon and slowly inflated. All stents were deployed immediately following the predilation. Follow-ups, including clinical course, stenosis recurrence and stent patency which were evaluated by CDUS and CT, were performed. RESULTS： Technical success was achieved in all patients. No procedure-related complications occurred. Liver function was normalized gradually and the symptoms of PHT also improved following PTPVS. In 2 of 3 asymptomatic patients, portal venoplasty and stenting were not performed because of pressure gradients 〈 5 mmHg. They were observed with periodic CDUS or CT. PTPVS was performed in 16 patients. In 2 patients, the mean pressure gradients decreased from 15.5 mmHg to 3.0 mmHg. In the remaining 14 patients, a pressure gradient was not obtained because of 〉 75% stenosis and typical clinical signs of PHT. In a 51-year-old woman, who suffered from massive ascites and severe bilateral lower limb edema after secondary LT, PVAS complicated hepatic vein stenosis and inferior vena cava （IVC） stenosis. Before PTPVS, a self-expandable and a balloon- expandable metallic stent were deployed in the IVC and right hepatic vein respectively. The ascites and edema resolved gradually after treatment. The portosystemic collateral vessels resulting from PHT were visualized in 14 patients. Gastroesophageal varices became invisible on poststenting portography in 9 patients. In a 28-year- old man with hepatic encephalopathy, a pre-existing meso-caval shunt was detected due to visualization of IVC on portography. After stenting, contrast agents flowed mainly into IVC via the shunt and little flowed into the portal vein. A covered stent was deployed into the superior mesenteric vein to occlude the shunt. Portal hepatopetal flow was restored and the IVC became invisible. The patient recovered from hepatic encephalopathy. A balloon-expandable Palmaz stent was deployed into hepatic artery for anastomotic stenosis before PTPVS. Percutaneous transhepatic internal-external biliary drainage was performed in 2 patients with obstructive jaundice. Portal venous patency was maintained for 3.3-56.6 mo （mean 33.0 mo） and all patients remained asymptomatic. CONCLUSION： With technical refinements, early detection and prompt treatment of complications, and advances in immunotherapy, excellent results, can be achieved in LT.     

Stent-grafts placement for treatment of massive hemorrhage from ruptured hepatic artery after pancreaticoduodenectomy

AIM:To present a series of cases with life-threatening hemorrhage from ruptured hepatic artery pseudoaneurysm after pancreaticoduodenectomy(PD) treated with placement of stent-grafts.METHODS:Massive hemorrhage from ruptured hepatic artery pseudoaneurysm after PD in 9 patients(6 men,3 women) at the age of 23-75 years(mean 48 years),were treated with placement of percutaneous endovascular balloon-expandable coronary stent-grafts.All patients were not suitable for embolization because of a non-patent portal ve...     

Massive hepatic necrosis with toxic liver syndrome following portal vein ligation

Right portal vein ligation (PVL) is a safe and widespread procedure to induce controlateral liver hypertrophy for the treatment of bilobar colorectal liver metastases. We report a case of a 60-year-old man treated by both right PVL and ligation of the glissonian branches of segment 4 for colorectal liver metastases surrounding the right and median hepatic veins. After surgery, the patient developed massive hepatic necrosis with secondary pulmonary and renal insufficiency requiring transfer to the intensive care unit. This so-called toxic liver syndrome finally regressed after hemofiltration and positive oxygen therapy. Diagnosis of acute congestion of the ligated lobe was suspected. The mechanism suspected was an increase in arterial inflow secondary to portal vein ligation concomitant with a decrease in venous outflow due to liver metastases encircling the right and median hepatic vein. This is the first documented case of toxic liver syndrome in a non-cirrhotic patient with favorable issue, and a rare complication of PVL.     

Protein C deficiency related obscure gastrointestinal bleeding treated by enteroscopy and anticoagulant therapy

Obscure gastrointestinal bleeding is an uncommonly encountered and difficult-to-treat clinical problem in gastroenterology,but advancements in endoscopic and radiologic imaging modalities allow for greater accuracyin diagnosing obscure gastrointestinal bleeding.Ectopic varices account for less than 5% of all variceal bleeding cases,and jejunal variceal bleeding due to extrahepatic portal hypertension is rare.We present a 47-year-old man suffering from obscure gastrointestinal bleeding.Computed tomography of the abdomen revealed multiple vascular tufts around the proximal jejunum but no evidence of cirrhosis,and a visible hypodense filling defect suggestive of thrombus was visible in the superior mesenteric vein.Enteroscopy revealed several serpiginous varices in the proximal jejunum.Serologic data disclosed protein C deficiency(33.6%).The patient was successfully treated by therapeutic balloonassisted enteroscopy and long-term anticoagulant therapy,which is normally contraindicated in patients with gastrointestinal bleeding.Diagnostic modalities for obscure gastrointestinal bleeding,such as capsule endoscopy,computed tomography enterography,magnetic resonance enterography,and enteroscopy,were also reviewed in this article.     

A histologically proven case of progressive liver sarcoidosis with variceal rupture

Sarcoidosis is a chronic multi-systemic granulomatous disease,and liver involvement frequently occurs.in most cases,no evidence of liver dysfunction is ob-served,and portal hypertension due to sarcoid liver diseases is a rareoccurrence.Moreover,no case of liver sarcoidosis has ever been reported with confirma-tion of the disease progression.Herein we describe a patient having hepatic sarcoidosis with severe portal hypertension and liver dysfunction.The diagnosis was histologically confirmed from granulomatous status to established liver cirrhosis over 10 years.A 46-year-old woman developed massive hematemesis due to the rupture of gastric cardial varices.She underwent emer-gency endoscopic injection sclerotherapy,and clear evi-dence of chronic hepatic failure.Twelve years ago,she was diagnosed as having sarcoidosis with respiratoryclinicalsymptoms.Liver biopsy revealed asymptomatic incidental granulomas without fibrosis development.After a couple of years,features of liver dysfunction were manifest and progressed.Ten years after the first biopsy,a second liver biopsy was performed,and well established dense fibrosis was revealed.Although significant liver dysfunction with portal hypertension is rarely seen in sarcoidosis,this case indicates that we have to consider the possibility that sarcoidosis may cause end-stage liver cirrhosis.     

Hemobilia secondary to hepatic artery pseudoaneurysm: An unusual complication of bile leakage in a patient with a history of a resected Ⅲb Klatskin tumor

We report a case of a 74-year-old woman with a 16-year history of a double bilo-enteric anastomosis due to resected hilar cholangiocarcinoma [Type Ⅲb Klatskin tumor]. The patient presented with cholangitis secondary to benign anastomotic stenosis which resulted in a large intrahepatic biloma. In order to restore the patency of the anastomosis and overcome cholangitis, several attempts took place, including endobiliary stenting, balloon-assisted biloplasty and transhepatic billiary drainage. Anastomotic patency was achieved, complicated, however, by persistent upper gastro-intestinal bleeding, presented as hemobilia. A biloma-induced pseudoaneurysm of the left hepatic artery was diagnosed. This had ruptured into the biliary tract, and presented the actual cause of the hemobilia. Selective embolism of the pseudoaneurysm resulted in control of the hemorrhage, and was successfully combined with transhepatic dilatation of the anastomosis and percutaneous drainage of the biloma. The patient was ultimately cured and seems to be in excellent condition, 5 mo after treatment.     

Portal venous arterialization resulting in increased portal inflow and portal vein wall thickness in rats

AIM： To explore the influence of portal vein hemodynamic changes after portal venous arterialization （PVA） on peribiliary vascular plexus （PVP） morphological structure and hepatic pathology, and to establish a theoretical basis for the clinical application of PVA. METHODS： Sprague-Dawley rats were randomly divided into control and PVA groups. After PVA, hemodynamic changes of the portal vein and morphological structure of hepatohilar PVP were observed using Doppler ultrasound, liver function tests, ink perfusion transparency management and three-dimensional reconstruction of computer microvisualization, and pathological examination was performed on tissue from the bile duct wall and the liver. RESULTS： After PVA, the cross-sectional area and blood flow of the portal vein were increased, and the increase became more significant over time, in a certain range. If the measure to limit the flow in PVA was not adopted, the high blood flow would lead to dilatation of intrahepatic portal vein and its branches, increase in collagen and fiber degeneration in tunica intima. Except glutamic pyruvic transaminase （GPT）, other liver function tests were normal. CONCLUSION： Blood with a certain flow and oxygen content is important for filling the PVP and meeting the oxygen requirement of the bile duct wall. After PVA, It is the anatomic basis to maintain normal morphology of hepatohilar bile duct wall that the blood with high oxygen content and high flow in arterialized portal vein may fill PVP by collateral vessel reflux. A adequate measure to limit blood flow is necessary in PVA.     

Ectopic variceal bleeding after hepatobiliary surgery: A case report

Rationale:Jejunal varices are rare in portal hypertension and are often difficult to diagnose and treat. Herein, we present a case of gastrointestinal bleeding due to jejunal varices after hepatobiliary surgery.Patient concerns:A 69-year-old man presented with recurrent massive gastrointestinal bleeding. He underwent partial right hepatectomy and cholangiojejunostomy 2 years prior to the first onset of bleeding. Two sessions of endoscopic vessel ligation for esophageal varices were performed afterwards, and hematemesis resolved completely, but massive melena still recurred during the following 5 years.Diagnosis:The patient was diagnosed with jejunal varices caused by portal venous stenosis after hepatobiliary surgery.Intervention:Portal venous angioplasty using balloon dilation and stent implantation was performed.Outcomes:After the intervention procedure, the patient did not experience any onset of gastrointestinal bleeding during follow-up.Lessons:Hepatopancreatobiliary could lead to the formation of jejunal varices. The combined use of capsule endoscopy, contrast-enhanced computed tomography, and sometimes portal venography is a promising strategy to search for jejunal varices. Transcatheter angioplasty appears to be a safe and effective method for treatment of jejunal varices in certain appropriate cases.     

Effect of a portal venous stent for gastrointestinal hemorrhage from jejunal varices caused by portal hypertension after pancreatoduodenectomy

We report herein the case of a 64-year-old man successfully treated by portal venous stent placement for repeated gastrointestinal bleeding associated with jejunal varices. He was admitted to our hospital with melena 8 years after having a pancreatoduodenectomy for carcinoma of the papilla of Vater. From portogram findings showing severe portal vein (PV) stenosis and dilated collaterals through the jejunal vein of the Roux-en-Y loop, jejunal varices resulting from PV stenosis were suspected as the cause of the melena. A metallic stent was placed in the PV following percutaneous transhepatic PV angioplasty. Although the cure of hemorrhagic jejunal varices caused by PV stenosis is difficult in patients who have undergone major abdominal surgery, patency of the stent in this patient has been maintained for 32 months without gastrointestinal hemorrhage. Metallic stent placement is recommended as a useful treatment for PV stenosis that is less invasive than open surgery.     

Jejunal Varices as a Cause of Massive Gastrointestinal Bleeding

Jejunal varices are not a common manifestation of portal hypertension. This report describes a 46-yr-old man with recurrent massive gastrointestinal bleeding from jejunal varices arising in an area of adhesions between the intestine and the omentum. The bleeding site was identified by exploratory laparotomy. Medical therapy, including vasopressin infusion via the superior mesenteric artery, was of limited success for controlling acute variceal bleeding. However, jejunal resection and anastomosis resulted in complete resolution of the bleeding, and the patient has experienced no recurrent bleeding over a 3-yr follow-up period. A review of the literature shows that this syndrome is characterized by portal hypertension, generally due to liver cirrhosis; frequently, there is a history of abdominal surgery, and the syndrome presents with hematochezia but without hematemesis. Accurate preoperative diagnosis is often difficult. We propose that bleeding from jejunal varices, though uncommon, should be considered under such clinical conditions.     

Incidence,risk factors,and outcomes of jejunal varix of the afferent loop after pancreatoduodenectomy

BackgroundJejunal varix is a concerning late complication after pancreatoduodenectomy (PD) due to the risk of recurrent and intractable bleeding. Our aim was to investigate the incidence, risk factors, and outcomes of jejunal varix after PD.MethodsA total of 709 patients who underwent PD between 2007 and 2017 were included. Preoperative and postoperative CT images were reviewed to evaluate the development of portal vein (PV) stenosis (≥50%) and jejunal varices.ResultsJejunal varix developed in 83 (11.7%) patients at a median of 12 months after PD. Eighteen (21.7%) patients experienced variceal bleeding. PV stenosis (P < 0.001; odds ratio [OR] 33.2, 95% confidence interval [CI] 15.6–66.7) and PV/superior mesenteric vein resection (P = 0.028; OR 2.3, 95% CI 1.1–4.7) were independent risk factors for jejunal varix. Of the nine patients who underwent stent placement for PV stenosis before the formation of jejunal varices, none experienced variceal bleeding. By contrast, 18 (27.3%) of the 135 patients without PV stent placement experienced at least one episode of variceal bleeding.ConclusionsThe incidence of jejunal varix was substantial after PD. PV stenosis was a strong risk factor for jejunal varix. Early PV stent placement and maintaining stent patency could reduce the risk of variceal bleeding in patients with PV stenosis.     

Arterio-portal shunt in liver rescued by hepatectomy after arterial embolization

Arterio-portal shunts are generally treated with transcatheter arterial embolization, as a therapeutic measure for bleeding of esophageal varices. However, transcatheter arterial embolization is frequently associated with reestablishment of arterio-portal shunts. We now report our experience with partial hepatectomy to remove the arterio-portal shunt associated with esophageal varices, which recurred after transcatheter arterial embolization. The patient was a 60-year-old female, who had massive hematemesis caused by rupture of esophageal varices. Doppler sonography and arteriography demonstrated an arterio-portal shunt in the right anterior superior segment of the liver. Temporary hemostasis was achieved with transcatheter arterial embolization, however, hemorrhage recurred one month later. The second transcatheter arterial embolization failed to manage the shunt and varices. The patient developed hepatic coma. After recovery from coma, she was referred to our hospital. We carried out partial hepatectomy, which provided remarkable hemodynamic improvement; the portal vein flow changed from hepatofugal to hepatopetal. Esophageal varices and hepatic coma have totally disappeared. This patient has had no complaint and has remained free of esophageal varices, for 3 years postoperatively. She is having a normal life. The partial hepatectomy to remove the arterio-portal shunt induced complete resolution of the arterio-portal shunt, as well as dramatic improvement in portal flow and hepatic coma. Our experience in the present case suggests that partial hepatectomy should be considered as a radical therapy for arterio-portal shunt, without insistence on transcatheter arterial embolization.     

Injection Sclerotherapy for Esophageal Varices after Total Gastrectomy: Case Reports of Two Patients

Injection sclerotherapy was performed in two patients with esophageal varices who had undergone a total gastrectomy and Roux-en- Y esophagojejunostomy for gastric cancer. Both of the patients were diagnosed as having postnecrotic liver cirrhosis due to serum hepatitis. The first patient developed esophageal varices after surgery. The second patient had recurrent esophageal varices after surgery for both gastric cancer and the esophageal varices. Five percent ethanolamine oleate was the sclerosant used together with the contrast medium iopamidol (5% EOI). After intravariceal injection, the flow of the sclerosant was followed by fluoroscopy. The esophageal varices were fed by the branches of the jejunal vein of the arcade of the ascending jejunal limb. The esophageal varices and branches of the jejunal vein were destroyed by three consecutive sessions of sclerotherapy. No complications occurred during or after the therapy. Therefore, injection sclerotherapy, along with varicealography, is one of the most effective methods of treating esophageal varices arising after a total gastrectomy.     

Subtotal Splenectomy and Central Splenorenal Shunt for Treatment of Bleeding from Roux En Y Jejunal Loop Varices Secondary to Portal Hypertension

Purpose To present subtotal splenectomy and splenorenal shunt as a surgical option to treat severe bleeding from a Roux en Y jejunal loop varices secondary to portal hypertension. Method A 64-year-old white woman presented severe episodes of bleeding from varices inside a Roux en Y jejunal loop secondary to portal hypertension due to cirrhosis. Subtotal splenectomy was performed with preservation of the upper splenic pole supplied by the splenogastric vessels. This procedure was combined with a central splenorenal shunt to divert part of portal blood to systemic flow. Results This procedure was safely performed with no complications. A 2-year post-operative follow-up of the patient has been uneventful. No re-bleeding occurred during this period and she returned to her normal life. Conclusion Subtotal splenectomy combined with central splenorenal shunt seems to be a safe procedure useful for the treatment of enteral bleedings due to portal hypertension.     

Gastric variceal bleeding caused by an intrahepatic arterioportal fistula that formed after liver biopsy: a case report and review of the literature

An intrahepatic arterioportal fistula is a rare cause of portal hypertension and variceal bleeding. We report on a patient with an intrahepatic arterioportal fistula following liver biopsy who was successfully treated by hepatectomy after unsuccessful arterial embolization. We also review the literature on symptomatic intrahepatic arterioportal fistulas after liver biopsy. A 48-year-old male with bleeding gastric varices and hepatitis B virus-associated liver cirrhosis was transferred to our hospital; this patient previously underwent percutaneous liver biopsies 3 and 6 years ago. Abdominal examination revealed a bruit over the liver, tenderness in the right upper quadrant, and splenomegaly. Ultrasonographic examination, computed tomography, and angiography confirmed an arterioportal fistula between the right hepatic artery and the right portal vein with portal hypertension. After admission, the patient suffered a large hematemesis and developed shock. He was treated with emergency transarterial embolization using microcoils. Since some collateral vessels bypassed the obstructive coils and still fed the fistulous area, embolization was performed again. Despite the second embolization, the collateral vessels could not be completely controlled. Radical treatment involving resection of his right hepatic lobe was performed. For nearly 6 years postoperatively, this patient has had no further episodes of variceal bleeding.