Steatotic liver disease after pancreatoduodenectomy occurs due to various factors, such as exocrine pancreatic insufficiency, impaired intestinal absorption, and malnutrition. The mechanism of steatogenesis differs to that of conventional steatotic liver disease associated with obesity and insulin resistance. We experienced a rare case of rapidly progressive steatotic liver disease accompanied by portal vein stenosis in the early postoperative period after subtotal stomach-preserving pancreaticoduodenectomy for distal cholangiocarcinoma. Although there was a complication due to postoperative drain infection, the patient was discharged from hospital with no nutritional problems. Two months postoperatively, the patient presented to the emergency room with dyspnea. CT showed a markedly steatotic liver, ascites, and portal vein stenosis. A portal vein stent was inserted transhepatically and the steatotic liver disease gradually improved. During the postoperative course, there were no problems indicated by nutritional markers; although the patient had diarrhea associated with postoperative pancreatic exocrine insufficiency, the symptoms were mild and improved after administration of oral pancrelipase. Before the intervention, the patient had intestinal edema, exacerbation of diarrhea, and a low serum zinc concentration, suggesting that impaired absorption caused by intestinal blood stasis and gut barrier dysfunction contributed to the development of steatotic liver disease.

BACKGROUND: Percutaneous transhepatic stent placement has become a common strategy for the postoperative treatment of portal vein (PV)/superior mesenteric veins (SMV) stenosis/occlusion. It has been widely used after liver transplantation surgery; however, reports on stent placement for acute PV/SMV stenosis after pancreatic surgery within postoperative 3 d are rare.
METHODS: Herein, we reported a case of intestinal edema and SMV stenosis 2 d after pancreatic surgery. The patient was successfully treated using stent grafts. Although the stenosis resolved after stent placement, complications, including bleeding, pancreatic fistula, bile leakage, and infection, made the treatment highly challenging. The use of anticoagulants was adjusted multiple times to prevent venous thromboembolism and the risk of bleeding. After careful treatment, the patient stabilized, and stent placement effectively managed postoperative PV/SMV stenosis.
CONCLUSIONS: Stent placement is effective and feasible for treating acute PV/SMV stenosis after pancreatic surgery even within postoperative 3 d.

OBJECTIVE: The incidence of post-transplant poral vein stenosis (PVS) is higher in pediatric liver transplantation, probably resulting from various portal vein (PV) reconstruction methods or other factors.
METHODS: 332 patients less than 12 years old when receiving liver transplantation (LT) were enrolled in this research. Portal vein reconstruction methods include anastomosis to the left side of the recipient PV trunk (type 1, n = 170), to the recipient left and right PV branch patch (type 2, n = 79), using vein graft interposition (type 3, n = 32), or end-to-end PV anastomosis (type 4, n = 50). The incidence of PVS was analyzed in terms to different PV reconstruction methods and other possible risk factors.
RESULTS: PVS occurred in 35 (10.5%) patients. Of the 32 patients using vein graft, 20 patients received a cryopreserved vein graft, 11 (55%) developed PVS, while the remaining 12 patients received a fresh iliac vein for PV interposition and none of them developed PVS. 9 patients whose liver donor was under 12 years old developed PVS, with an incidence of 18.8%.
CONCLUSIONS: Cryopreserved vein graft interposition and a liver donor under 12 are independent risk factors for PVS in pediatric LT.

BACKGROUND: Recurrent or locally advanced peri-hilar cholangiocarcinoma (PHCC) usually involves the portal vein (PV) leading to significant stenosis. With disease progression, clinical symptoms such as ascites, bleeding, and hepatic insufficiency are usually observed. Little is know about the benefit of PV stenting in relieving the symptoms associated to portal hypertension and allowing anticancer therapies. The aim of this study is to review our experience in PV stenting for PHCC patients.
METHODS: From 2014 to 2022, data from PHCC patients underwent PV stenting at Verona University Hospital, Italy, were reviewed. The indications were: gastrointestinal bleeding from esophagus-gastric varices, ascites not responsive to medical therapy, severe thrombocytopenia, liver insufficiency (hepatic jaundice, coagulopathy, and/or hyperammoniemia), or asymptomatic high-grade PV stenosis. Cavernous transformation and intrahepatic thrombosis in both sides of the liver were considered contraindication. Systematic anticoagulation therapy was not administered.
RESULTS: Technical success was achieved in all 16 (100 %) patients. The improvement of clinical symptoms were observed in 12 (75 %) patients. Anticancer therapy was administrated in 11 (69 %) patients. 2 (13 %) complications were observed: 1 biliary injury and 1 recurrent cholangitis that required a percutaneous trans-hepatic biliary drainage placement. Stent occlusion for tumor progression occurred in 1 patient and a re-stenting procedure was successfully performed. No case of thrombotic stent occlusion was observed during follow up. The 1-year stent patency was 86 % and the median patency period was 8 months (IQR, 4-12).
CONCLUSIONS: PV stenting is a feasible and safe palliative treatment that improves clinical condition, allow anticancer therapies, and provide a better quality of life.

Liver transplantation continues to rapidly evolve, and in 2020, 8906 orthotopic liver transplants were performed in the United States. As a technically complex surgery with multiple vascular anastomoses, stenosis and thrombosis of the venous anastomoses are among the recognized vascular complications. While rare, venous complications may be challenging to manage and can threaten the graft and the patient. In the last 20 years, endovascular approaches have been increasingly utilized to treat post-transplant venous complications. Herein, the evaluation and interventional treatment of post-transplant venous outflow complications, portal vein stenosis, portal vein thrombosis, and recurrent portal hypertension with transjugular intrahepatic portosystemic shunt (TIPS) are reviewed.

Other than rejection, hepatic artery and portal vein thrombosis are the most common complications in the immediate postoperative period with hepatic arterial thrombosis more common and more devastating. Hepatic artery stenosis is more common 1 month after transplantation, whereas portal and hepatic vein stenosis is more often seen as a late complication. Ultrasound is the first-line imaging examination to diagnose vascular complications with contrast-enhanced CT useful if ultrasound findings are equivocal. MR cholangiography is often most helpful in diagnosing bile leaks, biliary strictures, and biliary stones.

BACKGROUND: Hyperdynamic circulation in portal hypertension (PHT) depends on central neural activation. However, the initiating mechanism that signals PHT to the central neural cardiovascular-regulatory centers remains unclear. We aimed to test the hypothesis that oxidative stress in the gut initiates the signal that activates central cardiovascular nuclei in portal hypertensive rats.
METHODS: Two groups of rats were used. One had portal hypertension produced by partial portal vein ligation, while controls underwent sham operation. Hemodynamics including portal pressure, cardiac output, mean arterial pressure (MAP) and peripheral vascular resistance were measured. Activation of central cardiovascular nuclei was determined by immunohistochemical Fos expression in the paraventricular nucleus (PVN) of the hypothalamus. Myeloperoxidase activity, an oxidative stress marker, was measured in the jejunum. Hydrogen peroxide, the antioxidant N-acetyl-cysteine (NAC) or saline controls were administered for 12-14 days by gavage or osmotic minipumps placed in the peritoneal cavity.
RESULTS: Compared with controls, PHT rats showed increased cardiac output (54.2 ± 9.5 vs 33.6 ± 2.4 ml/min/100 g BW, p < 0.01), decreased MAP (96.2 ± 6.4 mmHg vs 103.2 ± 7.8, p < 0.01) and systemic vascular resistance (1.84 ± 0.28 vs 3.14 ± 0.19 mmHg/min/ml/100 g BW, p < 0.01). PHT rats had increased jejunal myeloperoxidase and PVN Fos expression. NAC treatment eliminated the hyperdynamic circulation, decreased jejunal myeloperoxidase and PVN Fos expression in PHT rats, but had no effect on sham controls. H2O2 significantly increased PVN Fos expression and decreased MAP.
CONCLUSIONS: These results indicate that in PHT, mesenteric oxidative stress is the initial signal that activates chemoreceptors and triggers hyperdynamic circulation by central neural cardiovascular-regulatory centers.

OBJECTIVE: To evaluate duplex US findings of the HA in all three postoperative vascular (HA, PV, HV and IVC) complications of paediatric LT for early detection and some helpful secondary signs to determine these vascular complications.
METHODS: We collected data from 44 post-LT paediatric patients who underwent daily duplex US for seven consecutive days and three months after LT during January 2017-June 2020. Four duplex US parameters of the HA (extrahepatic PSV, intrahepatic PSV, RI and AT) were compared in patients with and without complications.
RESULTS: The PSV of the extrahepatic HA in patients with HA complications was higher than that in patients without complications (P value = 0.019). The PSV at 107.7 cm/s is the optimal cut-off parameter associated with HA complications [a sensitivity of 88.9% and a specificity of 80.0% (ROC area is 0.84)]. The intrahepatic RI was higher on the first day than on the last day and gradually decreased in patients without vascular complications (P value = 0.000). The intrahepatic PSV significantly decreased with time when comparing the first and last days in patients without PV and HV-IVC complications (P value = 0.014 and 0.038). In contrast, patients with vascular complications showed no significant decrease.
CONCLUSIONS: The extrahepatic PSV relates to HA complications after paediatric LT but not PV and HV-IVC complications. Non-significantly decreased intrahepatic RI and PSV from the first day to the day of complication diagnosis may correlate with the occurrence of vascular complications.

Jejunal 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.
A 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.
Jejunal 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.
The 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.

It is well established that portal hypertension can occur in the absence of cirrhosis, as reported in patients with immune disorders, infections and thrombophilia. However, similar histological abnormalities primarily affecting the hepatic sinusoidal and (peri)portal vasculature have also been observed in patients without portal hypertension. Thus, the term porto-sinusoidal vascular disorder (PSVD) has recently been introduced to describe a group of vascular diseases of the liver featuring lesions encompassing the portal venules and sinusoids, irrespective of the presence/absence of portal hypertension. Liver biopsy is fundamental for PSVD diagnosis. Specific histology findings include nodular regenerative hyperplasia, obliterative portal venopathy/portal vein stenosis and incomplete septal fibrosis/cirrhosis. Since other conditions including alcohol-related and non-alcoholic fatty liver disease, or viral hepatitis, or the presence of portal vein thrombosis may occur in patients with PSVD, their relative contribution to liver damage should be carefully assessed. In addition to histology and clinical diagnostic criteria, imaging and non-invasive tests such as liver and spleen stiffness measurements could aid in the diagnostic workup. The introduction of PSVD as a novel clinical entity will facilitate collaborative studies and investigations into the underlying molecular pathomechanisms encompassed by this term.