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Recent advances in chemotherapy and radiotherapy have led to an increase in the number of long-term survivors of pancreatic cancer. However, this has also increased the number of patients suffering from ectopic varices and bleeding owing to left-sided portal hypertension and thrombocytopenia caused by splenomegaly after pancreaticoduodenectomy combined with resection of the splenic vein. A 65-year-old woman with varices of the elevated jejunum due to left sided portal hypertension after pancreaticoduodenectomy had repeated melena, which started about 1 year before admission. We describe the first reported case of percutaneous transsplenic venous embolization using metallic coils, which successfully achieved hemostasis of refractory bleeding from the elevated jejunal varices after pancreaticoduodenectomy.
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Intestinal malrotation is a congenital rotational anomaly that results of abnormal rotation of the gut, said to occur in 1 in 6000 live births. Common mesentery predisposes to volvulus of the midgut and internal hernias due to the left position of the cecum and appendix. The association of this anomaly with acute left appendicitis is rarely reported in the literature. Occurrence of acute appendicitis on common mesentery is a source of diagnosis difficulties, which may lead to a surgical management delay. We report a case of a 10-year-old boy, admitted for a left-sided iliac pain whose radiological investigations confirmed a left acute appendicitis associated with complete common mesentery. The child underwent laparoscopic surgery with simple post-operative follow-up.
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Background & Aims: We aimed to evaluate long-term outcome of patients with chronic non-cirrhotic extrahepatic portal vein obstruction (CNC-EHPVO) who underwent portal vein recanalisation (PVR) without transjugular intrahepatic portosystemic shunt (TIPS) insertion and to determine factors predicting PVR failure and stent occlusion. Methods: This retrospective monocentric study included all patients who underwent PVR without TIPS insertion in the context of CNC-EHPVO between the years 2000 and 2019. Primary patency was defined by the absence of a complete stent occlusion on follow-up imaging. Results: A total of 31 patients underwent PVR with a median follow-up of 52 months (24-82 months). Indications were gastrointestinal bleeding (n = 13), abdominal pain attributed to CNC-EHPVO (n = 7), prior to abdominal surgery (n = 4), and others (n = 7). Technical success was obtained in 27 patients. PVR failure was associated with extension within the intrahepatic portal veins (p = 0.005) and recanalisation for abdominal pain (p = 0.02). Adverse events occurred in 6 patients with no mortality. Anticoagulation was administered in 21 patients after technical success of PVR. In patients with technical success, 5-year primary patency was 73% and was associated with improved muscle mass (p = 0.007) and decreased spleen volume (p = 0.01) at 1 year. Furthermore, 21 (78%) patients with PVR technical success were free of portal hypertension complication at 5 years. Conclusions: PVR without TIPS insertion was feasible and safe in selected patients with CNC-EHPVO and portal hypertension with past or expected complications. Primary patency at 5 years was obtained in 3 of 4 patients with technical success of PVR and was associated with a control of complications of CNC-EHPVO. PVR was associated with improvement of sarcopenia and decreased spleen volume at 1 year. Lay summary: Patients with chronic obstruction of the portal vein and without cirrhosis or malignancy can develop complications related to the high pressure in the venous system. The present study reports long-term favourable outcome of patients in whom the obstruction was treated with stents.
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Patients with cirrhosis of the liver are at high risk of developing portal vein thrombosis (PVT), which has a complex, multifactorial cause. The condition may present with a myriad of symptoms and can occasionally cause severe complications. Contrast-enhanced computed tomography (CT) is the gold standard for the diagnosis of PVT. There are uncertainties regarding the effect on PVT and its treatment outcome in patients with cirrhosis. The main challenge for managing PVT in cirrhosis is analyzing the risk of hemorrhage compared to the risk of thrombus extension leading to complications. All current knowledge regarding non-tumor PVT in cirrhosis, including epidemiology, risk factors, classification, clinical presentation, diagnosis, impact on natural history, and treatment, is discussed in the present article.
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Although stomal and parastomal varices are uncommon causes of variceal bleeding, the mortality rate might be as high as 40%. Timely intervention is essential for the management of these ectopic bleeding varices. Due to the rarity of such varices, no standard treatment guideline is available. We present three cases of bleeding stomal varices managed with an endovascular approach, one through percutaneous transhepatic and the other two through transjugular intrahepatic portosystemic shunt approach.
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Background: Proximal splenorenal shunt (PSRS) is one of the most commonly performed portosystemic shunt (PSS) in extrahepatic portal venous obstruction (EHPVO) for portal decompression. Sometimes various anatomical and surgical factors related to the splenic vein and/or left renal vein may make the construction of a PSRS difficult or impossible. Unconventional shunts are required to tide over such conditions. Methods: From January 2008 to December 2018, 189 patients with EHPVO underwent PSS, of which, the 10 patients who underwent unconventional shunts form the study group of this paper. Results: The ten unconventional shunts included 8 proximal splenoadrenal shunts, one collateral-renal shunt, and one inferior mesenteric vein to inferior vena cava (IMV-Caval) shunt. The mean percentage drop in omental pressure was 34.2% post-shunt with a mean anastomotic diameter of 13.7 ± 3.1 mm. Three patients experienced some form of postoperative complication. With a mean follow-up period of 32.3 months (maximum of 111 months) all patients had patent shunts on follow-up Doppler. None of the patients had variceal bleed, or features of biliopathy and hepatic encephalopathy in follow-up. Conclusion: Unconventional shunts can be used safely and effectively with good postoperative outcomes in EHPVO.
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BACKGROUND: Natural portosystemic shunt ligation practices in liver transplant vary widely across transplant centres and are frequently undertaken to prevent the serious consequence of portal steal phenomenon. No concrete indications have so far been convincingly identified for their management in living donor liver transplant. METHODS: We retrospectively studied the outcome of 89 cirrhotic patients who either did (n = 63) or did not (n = 25) undergo shunt ligation during living donor liver transplantation between 2017 and 2020. RESULTS: The incidence of early allograft dysfunction/nonfunction (P = 1.0) and portal venous complications (P = 0.555) were similar between the two groups. Although overall complications, biliary complications, and the composite of Grade III and IV complications were significantly higher in the nonligated group (P = 0.015, 0.052 and 0.035), 1- year graft and patient survival were comparable between them (P = 0.524). CONCLUSION: We conclude that shunt ligation in living donor liver transplantation may not always be necessary if adequate portal flow, good vascular reconstruction, and good graft quality have been ensured.
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A 60-year-old woman with Hepatitis C infection, cirrhosis, recurrent hepatic hydrothorax, and hepatocellular carcinoma was hospitalized with Coronavirus disease-2019 (COVID-19). After her initial discharge, she was re-admitted three weeks later with decompensated liver disease. Imaging revealed extensive thrombosis in the portal vein, superior mesenteric vein, splenic vein and bilateral brachial veins. Given the acute onset and extent of the thrombosis, the patient received therapeutic anticoagulation despite elevated prothrombin time/ international normalized ratio, thrombocytopenia and low fibrinogen. Cirrhotic patients with COVID-19 maybe at high risk of thrombosis, which can present with significant hepatic decompensation.
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Patients with liver cirrhosis frequently experience rectal variceal bleeding subsequent to portal hypertension. Unlike gastroesophageal variceal bleeding, a well-established guideline does not exist in terms of management of bleeding rectal varices. A 75-year-old male with non-alcoholic-steatohepatitis induced cirrhosis presented with a 3-day history of severe rectorrhagia. Considering patient's clinical history, TIPS was not performed and thus, a novel endovascular technique termed balloon-occluded antegrade transvenous obliteration was considered. Under conscious sedation, an occlusion was made through balloon catheter by sclerotic agents including air/sodium tetradecyl sulfate/Lipiodol. After the procedure, and in the 6 months follow up period the patient's hemodynamic status was stable and he recovered without any serious complications. Balloon-occluded antegrade transvenous obliteration is a feasible and safe modality for treating rectal varices bleeding and could be used as an alternative approach in patients with contraindications to traditional treatments.
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A 74-year-old male underwent laparoscopic radical cystectomy for invasive bladder cancer with open surgery for lymph node dissection and urinary diversion (ileal conduit). During the surgery, intestinal malrotation was diagnosed and Ladd procedure was performed. Ileal conduit was performed on the left side after considering the course of mesentery. Although a final diagnosis was reached during the surgery in this case, the presence of intestinal malrotation can be suspected based on the findings of contrast-enhanced computed tomography images obtained before the surgery. Images should be carefully inspected to detect intestinal malrotation when planning urinary diversion involving the intestinal tract.
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Occlusion of Portal Vein (PV) and Superior Mesenteric Vein (SMV) is a known effect of local infiltration by pancreatic or mesenteric neuroendocrine tumors. Venous occlusion leads to formation of collateral pathways to restore hepatopetal flow in main PV and these collateral pathways can be seen in the form of ectopic (duodenal or jejunal) varices. We present a case of bleeding duodenal varices secondary to SMV occlusion by a locally infiltrating pancreatic neuroendocrine tumor which was successfully treated by coil embolization of varices and SMV stenting of the occluded venous segment after failure of endoscopic glue injection. Various endovascular minimally invasive approaches have been described in literature for recanalization of SMV in such clinical scenarios which maybe challenging to treat for surgical methods. We recommend use of the retrograde transhepatic technique for recanalization of occluded SMV and embolization of associated varices as an alternate treatment option in such scenarios.
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AIMS: The natural history of portal cavernoma cholangiopathy (PCC) in patients with significant biliary obstruction (SBO) who cannot undergo shunt surgery, is not known. We therefore, analyzed data of patients of extra-hepatic portal venous obstruction (EHPVO) with PCC. METHODS: Prospectively recorded details of 620 (age 21.2 [11.4] years; 400 [65%] males) patients with primary EHPVO were reviewed. Outcomes (hepatic decompensation/mortality) of patients with PCC and SBO without shuntable veins were noted at follow up of 7 [4-11] years. RESULTS: Ninety-seven of 620 (15.6% [60 men]) EHPVO patients had PCC-SBO. Of these 57 did not have shuntable veins. The median duration from any index symptom to symptomatic PCC was 7 (0-24) years and from index bleed to symptomatic PCC was and 12 (5-24) years, respectively. Thirteen patients underwent endoscopic retrograde cholangiography; nine repeatedly over 7 (4-10) years. Decompensation was seen in 5 patients. Presentation other than variceal bleed was associated with hepatic decompensation (5/19 versus 0/38, P = 0.003). CONCLUSIONS: Majority of patients with PCC-SBO do not have shuntable veins, and may have good long-term outcomes. Patients presenting with variceal bleed have low chance of decompensation. Symptomatic PCC appears to be a late event in EHPVO.
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Portal vein thrombosis is an important cause of portal hypertension. PVT occurs in association with cirrhosis or as a result of malignant invasion by hepatocellular carcinoma or even in the absence of associated liver disease. With the current research into its genesis, majority now have an underlying prothrombotic state detectable. Endothelial activation and stagnant portal blood flow also contribute to formation of the thrombus. Acute non-cirrhotic PVT, chronic PVT (EHPVO), and portal vein thrombosis in cirrhosis are the three main variants of portal vein thrombosis with varying etiological factors and variability in presentation and management. Procoagulant state should be actively investigated. Anticoagulation is the mainstay of therapy for acute non-cirrhotic PVT, with supporting evidence for its use in cirrhotic population as well. Chronic PVT (EHPVO) on the other hand requires the management of portal hypertension as such and with role for anticoagulation in the setting of underlying prothrombotic state, however data is awaited in those with no underlying prothrombotic states. TIPS and liver transplant may be feasible even in the setting of PVT however proper selection of candidates and type of surgery is warranted. Thrombolysis and thrombectomy have some role. TARE is a new modality for management of HCC with portal vein invasion.
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Portal vein thrombosis (PVT) is being increasingly recognized in patients with advanced cirrhosis and in those undergoing liver transplantation. Reduced flow in the portal vein is probably responsible for clotting in the spleno-porto-mesenteric venous system. There is also increasing evidence that hypercoagulability occurs in advanced liver disease and contributes to the risk of PVT. Ultrasound based studies have reported a prevalence of PVT in 10-25% of cirrhotic patients without hepatocellular carcinoma. Partial thrombosis of the portal vein is more common and may not have pathophysiological consequences. However, there is high risk of progression of partial PVT to complete PVT that may cause exacerbation of portal hypertension and progression of liver insufficiency. It is thus, essential to accurately diagnose and stage PVT in patients waiting for transplantation and consider anticoagulation therapy. Therapy with low molecular weight heparin and vitamin K antagonists has been shown to achieve complete and partial recanalization in 33-45% and 15-35% of cases respectively. There are however, no guidelines to help determine the dose and therapeutic efficacy of anticoagulation in patients with cirrhosis. Anticoagulation therapy related bleeding is the most feared complication but it appears that the risk of variceal bleeding is more likely to be dependent on portal pressure rather than solely related to coagulation status. TIPS has also been reported to restore patency of the portal vein. Patients with complete PVT currently do not form an absolute contraindication for liver transplantation. Thrombectomy or thromboendovenectomy is possible in more than 75% of patients followed by anatomical end-to-end portal anastomosis. When patency of the portal vein and/or superior mesenteric vein is not achieved, only non-anatomical techniques (reno-portal anastomosis or cavo-portal hemitransposition) can be performed. These techniques, which do not fully reverse portal hypertension, are associated with higher morbidity and mortality risks in the short term.
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Portal cavernoma develops as a bunch of hepatopetal collaterals in response to portomesenteric venous obstruction and induces morphological changes in the biliary ducts, referred to as portal cavernoma cholangiopathy. This article briefly reviews the available literature on the vascular supply of the biliary tract in the light of biliary changes induced by portal cavernoma. Literature pertaining to venous drainage of the biliary tract is scanty whereas more attention was focused on the arterial supply probably because of its significant surgical implications in liver transplantation and development of ischemic changes and strictures in the bile duct due to vasculobiliary injuries. Since the general pattern of arterial supply and venous drainage of the bile ducts is quite similar, the arterial supply of the biliary tract is also reviewed. Fine branches from the posterior superior pancreaticoduodenal, retroportal, gastroduodenal, hepatic and cystic arteries form two plexuses to supply the bile ducts. The paracholedochal plexus, as right and left marginal arteries, run along the margins of the bile duct and the reticular epicholedochal plexus lie on the surface. The retropancreatic, hilar and intrahepatic parts of biliary tract has copious supply, but the supraduodenal bile duct has the poorest vascularization and hence susceptible to ischemic changes. Two venous plexuses drain the biliary tract. A fine reticular epicholedochal venous plexus on the wall of the bile duct drains into the paracholedochal venous plexus (also called as marginal veins or parabiliary venous system) which in turn is connected to the posterior superior pancreaticoduodenal vein, gastrocolic trunk, right gastric vein, superior mesenteric vein inferiorly and intrahepatic portal vein branches superiorly. These pericholedochal venous plexuses constitute the porto-portal collaterals and dilate in portomesenteric venous obstruction forming the portal cavernoma.
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BACKGROUND/AIMS: Duodenal varices (DV) are ectopic varices which can cause massive gastrointestinal bleeding. The diagnosis of DV may be difficult; sometimes they can be hidden behind duodenal folds. The aim of the study was to evaluate DV by endoscopic ultrasound. METHODS: Endoscopic ultrasound was done in patients detected or suspected to be having DV. The para duodenal varices were identified and subsequently hemodynamic evaluation of DV was done. RESULTS: Endoscopic ultrasound identified perforators in seven cases of DV. CONCLUSION: The endoscopic ultrasound can help in detection of DV underlying thickened folds. It can also help in hemodynamic evaluation of DV.
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Presence of portosystemic collateral veins (PSCV) is common in portal hypertension due to cirrhosis. Physiologically, normal portosystemic anastomoses exist which exhibit hepatofugal flow. With the development of portal hypertension, transmission of backpressure leads to increased flow in these patent normal portosystemic anastomoses. In extrahepatic portal vein obstruction collateral circulation develops in a hepatopetal direction and portoportal pathways are frequently found. The objective of this review is to illustrate the various PSCV and portoportal collateral vein pathways pertinent to portal hypertension in liver cirrhosis and EHPVO.
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Bleeding during endoscopic sphincterotomy is a common complication. Sometimes bleeding occurs as a late complication after endoscopic retrograde cholangiopancreatography (ERCP). We describe a case in which bleeding happened during ERCP but detection was done after the completion of the procedure. The detection of bleeding allowed further evaluation and detection of hemobilia in this case. The removal of blood clots from inside common bile duct by repeat ERCP however led to an uneventful recovery without any morbidity.