Partial portal vein arterialization using right gastroepiploic artery: A novel solution for portal hypoperfusion

正To the Editor:Establishing dual arterial and portal inflow is essential for liver transplantation[1].Inadequate portal inflow compromises graft function and graft survival[2].Portal hypoperfusion is usually a consequence of spontaneous portosystemic shunt,ligation of which     

Late acute celiac and hepatic artery thrombosis with portal vein thrombosis resulting in hepatic infarction 12 years post orthotopic liver transplantation

Hepatic artery thrombosis (HAT) is relatively infrequent, but possibly a devastating complication of orthotopic liver transplantation (OLT). It often requires urgent retransplantation. Two main forms of HAT are recognized as early and late HAT (diagnosis within or after 30 days following LT). Early HAT typically results in graft failure. Late HAT features biliary obstruction, cholangitis, and hepatic abscess formation. We report here the case of a patient of Wilson’s disease who presented twelve years post-liver transplant symptoms typical of acute HAT and hepatic infarction. On diagnostic imaging, celiac axis and hepatic artery were thrombosed, resulting in ischemic necrosis of the left hepatic lobe. The resulting sepsis and transient hepatic insufficiency were managed conservatively, and repeat OLT was avoided. The patient remains stable more than one year later. To the best of our knowledge this case report is unique in the literature for the unusually long interval between OLT and late acute HAT, as well as celiac and portal vein occlusion. The acute presentation of sub massive hepatic necrosis is also uncharacteristic of late HAT and more typical of acute HAT. This report describes our experience in managing this and a literature review of the topic.     

A case of hepatic artery embolization and partial arterialization of the portal vein for intraperitoneal, hemorrhage after a pancreaticoduodenectomy

We report a case of hepatic artery embolization and partial portal vein arterialization for the treatment of a delayed massive hemorrhage after a pancreaticoduodenectomy. A 70-year-old male underwent a pancreaticoduodenectomy for the treatment of lower bile duct cancer. A slight discharge of pancreatic juice was recognized early during the postoperative period. A delayed massive hemorrhage occurred on postoperative day 34, resulting in hypotensive shock. Angiography and computed tomography examinations revealed bleeding from a pseudoaneurysm at the stump of the gastroduodenal artery and portal vein compression by the hematoma. Embolization of the stump of the gastroduodenal artery resulted in the total occlusion of the hepatic artery. We performed a partial portal vein arterialization via side-to-side anastomosis of a branch of the ileal artery and vein. The partial portal oxygen pressure increased from 70 mmHg to 90 mmHg. A liver abscess was recognized two weeks after the arterialization, but was successfully treated by percutaneous transhepatic drainage. The patient was discharged from hospital in good condition on postoperative day 69. Whether the partial portal vein arterialization was effective is unclear, but partial portal vein arterialization should be considered as an option in cases of total hepatic artery occlusion with impairment of portal blood flow.     

Spontaneous bacterial peritonitis in isolated splenic vein thrombosis with portal hypertension.

Spontaneous bacterial peritonitis (SBP) is a known complication of ascites due to cirrhosis; it has also been reported in some non-cirrhotic conditions with ascites. We report a 50-year-old lady with isolated splenic vein thrombosis who developed SBP due to E. coli .     

门静脉血栓的研究进展

近年来,随着诊断技术的进步,门静脉血栓检出率明显提高,而且在门静脉血栓的危险因素、对门脉系统的影响、临床表现、诊断方法及治疗等方面均有了新的认识,本文就以上几方面的研究进展做一综述。     

Extrahepatic portal vein thrombosis

Noncirrhotic, nontumoral portal vein thrombosis (PVT) is the second most-frequent cause of portal hypertension in the world. General thrombophilic factors can be identified in approximately 60% of patients. PVT may manifest as an acute process. However, the acute episode more frequently is asymptomatic or paucisymptomatic and portal vein thrombosis is misdiagnosed until the development of complications secondary to portal hypertension, such as variceal bleeding or portal biliopathy. Although no randomized controlled trials have been performed, after the diagnosis of acute PVT early initiation of anticoagulation (within 30 days of the onset of symptoms) is recommended to achieve recanalization. In patients with portal cavernoma, anticoagulation is aimed to prevent the progression and recurrence of thrombosis. Because of the lack of data in this specific population, variceal bleeding is managed as in cirrhotic patients. Ursodeoxycholic acid has been proposed empirically for the treatment of patients with symptomatic portal biliopathy. Choledocholithiasis might be present, complicating a bile duct stenosis. Accordingly, an endoscopic retrograde cholangiopancreatography with sphincterotomy, extraction with balloon catheter, and stent placement is indicated. Mortality among patients with PVT is low (5-year mortality rate of 5 to 10%) and is mainly related to associated diseases rather than to complications of portal hypertension.     

Pre-transplant portal vein thrombosis is an independent risk factor for graft loss due to hepatic artery thrombosis in liver transplant recipients

Background

Hepatic artery thrombosis is an uncommon but catastrophic complication following liver transplantation. We hypothesize that recipients with portal vein thrombosis are at increased risk.

Methods

Data on all liver transplants in the U.S. during the MELD era through September 2014 were obtained from UNOS. Status one, multivisceral, living donor, re-transplants, pediatric recipients and donation after cardiac death were excluded. Logistic regression models were constructed for hepatic artery thrombosis with resultant graft loss within 90 days of transplantation.

Results

63,182 recipients underwent transplantation; 662 (1.1%) recipients had early hepatic artery thrombosis; of those, 91 (13.8%) had pre-transplant portal vein thrombosis, versus 7.5% with portal vein thrombosis but no hepatic artery thrombosis (p < 0.0001). Portal vein thrombosis was associated with an increased independent risk of hepatic artery thrombosis (OR 2.17, 95% CI 1.71–2.76, p < 0.001) as was donor risk index (OR 2.02, 95% CI 1.65–2.48, p < 0.001). Heparin use at cross clamp, INR, and male donors were all significantly associated with lower risk.

Discussion

Pre-transplant portal vein thrombosis is associated with post-transplant hepatic artery thrombosis independent of other factors. Recipients with portal vein thrombosis might benefit from aggressive coagulation management and careful donor selection. More research is needed to determine causal mechanism.     

Changing perspectives in portal vein thrombosis

The aetiology of portal vein thrombosis (PVT) is heterogeneous. Important primary risk factors for PVT are cirrhosis, hepatobiliary malignancies and pancreatitis. Newly discovered thrombotic risk factors, such as latent myeloproliferative disorders and prothrombotic genetic defects, have also been identified as major risk factors for PVT. At least one-third of PVT patients demonstrate a combination of thrombotic risk factors. PVT, which does not have a detrimental effect on liver function, usually becomes manifest as a variceal haemorrhage in the oesophagus months to years after the development of thrombosis. Owing to intact coagulation variceal bleeding has a better prognosis among patients with PVT than cirrhotics. Endoscopic sclerotherapy or band ligation is the primary therapeutic option for variceal bleeding in patients with PVT. It is questionable whether anticoagulant therapy should be started, since it has not proven beneficial for most PVT patients. Therapy with anticoagulants is only recommended for those with acute PVT (especially in association with mesenteric vein thrombosis), those who recently underwent a portosystemic shunt procedure, and those with other thrombotic manifestations, particularly in case of proven hypercoagulability. Mortality of patients with PVT may be associated with concomitant medical conditions which lead to the PVT or with manifestations of portal hypertension, such as variceal haemorrhage. Multivariate analysis of a large Dutch PVT population has shown that age, malignancy, ascites and the presence of mesenteric vein thrombosis are independently related to survival. Death due to a variceal haemorrhage is rare. Poor outcome of PVT thus appears to be associated primarily with concomitant diseases which lead to PVT, and not the complications of portal hypertension. It is therefore uncertain whether surgical portosystemic shunting affects survival favourably.     

Spontaneous hepatic artery thrombosis with infarction of the liver.

Extensive infarction of the liver, initially thought to be halothane hepatitis, is described. The patient developed severe right upper quadrant abdominal pain and abnormal liver function tests after amputation of the leg. The correct diagnosis was made by percutaneous needle biopsy of the liver which demonstrated a large area of avascular necrosis. The patient recovered, indicating the remarkable ability of the liver to maintain function despite ischemic injury. The patient died later from an acute myocardial infarction, and at autopsy thrombosis of the hepatic artery and multiple hepatic infarcts were confirmed.     

Nonmalignant portal vein thrombosis in adults

Portal vein thrombosis (PVT) consists of two different entities: acute PVT and chronic PVT. Acute PVT usually presents as abdominal pain. When the thrombus extends to the mesenteric venous arches, intestinal infarction can occur. Chronic PVT is usually recognized after a fortuitous diagnosis of hypersplenism or portal hypertension, or when there are biliary symptoms related to portal cholangiopathy. Local risk factors for PVT, such as an abdominal inflammatory focus, can be identified in 30% of patients with acute PVT; 70% of patients with acute and chronic PVT have a general risk factor for PVT, most commonly myeloproliferative disease. Early initiation of anticoagulation therapy for acute PVT is associated with complete and partial success in 50% and 40% of patients, respectively. A minimum of 6 months' anticoagulation therapy is recommended for the treatment of acute PVT. For patients with either form of PVT, permanent anticoagulation therapy should be considered if they have a permanent risk factor. In patients with large varices, beta-adrenergic blockade or endoscopic therapy seems to prevent bleeding as a result of portal hypertension, even in patients on anticoagulation therapy. In patients with jaundice or recurrent biliary symptoms caused by cholangiopathy, insertion of a biliary endoprosthesis is the first treatment option. Overall, the long-term outcome for patients with PVT is good, but is jeopardized by cholangiopathy and transformation of underlying myeloproliferative disease into myelofibrosis or acute leukemia.