OBJECTIVE: Portal hypertension resulting from non-cirrhotic extrahepatic portal vein obstruction (EHPVO) in children has been primarily managed with the Meso-Rex bypass, but only a few patients have a viable Rex recessus, required by surgery. This study reports a preliminary series of patients who underwent interventional radiology attempts at portal vein recanalization (PVR), with a focus on technical aspects and safety.
METHODS: A retrospective review of consecutive patients with severe portal hypertension due to non-cirrhotic EHPVO at a single institution from 2022, who underwent percutaneous attempts at PVR, was performed. Technical and clinical data including fluoroscopy time, radiation exposure, technical and clinical success, complications and follow-up were recorded.
RESULTS: Eleven patients (6 males and 5 females; median age 7 years, range 1-14) underwent 15 percutaneous transhepatic (n = 1), transplenic (n = 11), or simultaneous transhepatic/transplenic (n = 3) procedures. Rex recessus was patent in 4/11 (36%). Fluoroscopy resulted in a high median total dose area product (DAP) of 123 Gycm2 (range 17-788 Gycm2) per procedure. PVR was achieved in 5/11 patients (45%), 3/5 with obliterated Rex recessus. Two adverse events of grade 2 and grade 3 occurred without sequelae. After angioplasty, 4/5 patients required stenting to obtain sustained patency, as demonstrated by colour-Doppler ultrasound in all PVR after a median follow-up of 6 months (range 6-14).
CONCLUSIONS: Our preliminary experience suggests that 45% of children with non-cirrhotic EHPVO can restore portal flow even with obliterated Rex recessus. In non-cirrhotic EHPVO, PVR may be an option, if a Meso-Rex bypass is not feasible, although the radiation exposure deserves attention.
CONCLUSIONS: Innovative percutaneous procedures may have the potential to be an alternative option to the traditional surgical approach in the management of non-cirrhotic EHPVO and its complications in children not eligible for Meso-Rex bypass surgery.
CONCLUSIONS: Non-cirrhotic portal hypertension in children has been traditionally managed by surgery with Meso-Rex bypass creation. Percutaneous PVR may restore the patency of the native portal system even when the Rex recessus is obliterated and surgery has been excluded. Interventional radiological techniques may offer a minimally invasive solution in complex cases of EHPVO in children when Meso-Rex bypass is not feasible.

Portal cavernoma is a major cause of extrahepatic portal hypertension (EHPH) in children. It is a serious condition, due to the frequency and severity of digestive hemorrhages secondary to the rupture of esophageal varices (EV). Neonatal umbilical catheterization is a significant risk factor for the development of portal vein thrombosis (PVT) and portal hypertension. We report a case of a five-year-old male who presented with upper gastrointestinal (GI) bleeding on ruptured esophageal varices resulting from a portal cavernoma, complicating neonatal umbilical vein catheterization. This case illustrates the risk of severe vascular complications, particularly portal hypertension that can result from neonatal umbilical vein catheterization.

Portal vein thrombosis (PVT) poses significant therapeutic challenges due to its complex pathophysiology and diverse clinical presentations. Recent advancements have spurred the development of new therapeutic approaches to enhance treatment efficacy and safety. This review synthesized emerging therapies for PVT based on a comprehensive literature search across major databases such as PubMed, EMBASE, and Web of Science, among others, focusing on studies published in the last decade. Anticoagulation therapy, particularly with novel oral anticoagulants (NOACs), emerged as beneficial in personalized treatment regimens. Innovative surgical techniques and improved risk stratification methods were identified as crucial in the perioperative management of PVT. Additionally, advances in cell therapy and medical treatments for hepatocellular carcinoma in the context of PVT were explored. Promising outcomes were observed with modalities such as Yttrium 90 and liver transplantation combined with thrombectomy, particularly in complex PVT cases associated with hepatocellular carcinoma, albeit on a limited scale. The reviewed literature indicates a shift towards individualized treatment approaches for PVT, integrating novel anticoagulants, refined risk assessment tools, and tailored interventional strategies. While these emerging therapies show potential for enhanced efficacy and safety, further research is essential to validate findings across broader patient populations and establish standardized treatment protocols.

OBJECTIVE: Transjugular intrahepatic portosystemic shunt (TIPS) is an established procedure for the treatment of several complications of portal hypertension (PH), including non-neoplastic portal vein thrombosis (PVT). Selection criteria for TIPS in PVT are not yet well established. Despite anecdotal, cases of thromboembolic events from paradoxical embolism due to the presence of patent foramen ovale (PFO) after TIPS placement have been reported in the literature. Therefore, we aimed at describing our experience in patients with non-neoplastic splanchnic vein thrombosis (SVT) who underwent TIPS following PFO screening.
METHODS: We conducted a single-centre retrospective study, including consecutive patients who underwent TIPS for the complications of cirrhotic and non-cirrhotic portal hypertension (NCPH) and having SVT.
RESULTS: Of 100 TIPS placed in patients with SVT, 85 patients were screened for PFO by bubble-contrast transthoracic echocardiography (TTE) with PFO being detected in 22 (26%) cases. PFO was more frequently detected in patients with non-cirrhotic portal hypertension (NCPH) (23% in the PFO group vs. 6% in those without PFO, p = .04) and cavernomatosis (46% in the PFO group vs. 19% in those without PFO, p = .008). Percutaneous closure was effectively performed in 11 (50%) after multidisciplinary evaluation of anatomical and clinical features. No major complications were observed following closure.
CONCLUSIONS: PFO screening and treatment may be considered feasible for patients with SVT who undergo TIPS placement.

Portal vein thrombosis (PVT) is a challenging and controversial complication of cirrhosis. Experimental models that reproduce cirrhotic PVT and effective pharmacological therapies are limited. We aimed to investigate the nature course and mechanisms of PVT in cirrhosis. A novel PVT model was developed via two-step total portal vein ligation in healthy and thioacetamide (TAA)-cirrhotic rats. Circulating and liver-infiltrating neutrophils were isolated from individuals with cirrhosis to examine neutrophil extracellular traps (NETs) and explore their unique characteristics and implications in PVT-associated fibrosis in cirrhosis. We further validated macrophage-myofibroblast transition (MMT) via multiplex immunofluorescence and single-cell sequencing. In the experimental model, cirrhosis promoted PVT development and portal vein intimal thickening. Interestingly, cirrhosis promoted spontaneous resolution of PVT due to instability of thrombus structure, along with pulmonary and intrahepatic clots. NETs-MMT mediate cirrhotic PVT and PVT-associated fibrosis, including fibrotic thrombus remodeling and increased hepatic collagen deposition. Mechanistically, caspase-4-dependent activation of neutrophils and GSDMD mediated the formation of NETs. The extracellular DNA of NETs promoted TGF-β1/Smad3-driven MMT. Inhibiting GSDMD with disulfiram suppressed cirrhotic PVT and prevented associated fibrosis. The cirrhotic PVT model reflected the following three main characteristics of cirrhotic PVT: spontaneous resolution, immunothrombosis, and intimal fibrosis. Targeting NETs with GSDMD inhibitors may serve as a new therapeutic concept to treat cirrhotic PVT.

UNASSIGNED: Accidental foreign body ingestion is the most common hidden cause of abdominal pain. A high index of suspicion should be implemented in patients with unresolved abdominal pain. Here we reported a 54-year-old patient with vague abdominal pain who had a successful laparoscopic removal of a toothpick.
UNASSIGNED: Toothpicks and fish bones are considered one of the most common accidentally ingested foreign bodies. Fortunately, most patients are asymptomatic. About 80%-90% of ingested foreign bodies pass through the gut spontaneously within a week. We present a case of a 54-year-old female with chronic epigastric pain and fever found to have a foreign body (toothpick) that penetrated the stomach and migrated to the liver causing liver abscess with portal vein thrombosis. The patient was managed with laparoscopic removal of the foreign body with an uneventful postoperative course.

UNASSIGNED: Hypoalbuminemia, as defined by serum albumin (SA) levels ≤35 g/L, is associated to venous and arterial thrombosis in general population and in patients at risk of cardiovascular disease. It is unknown if SA ≤35 g/L is also associated to portal vein thrombosis (PVT) in cirrhosis.
UNASSIGNED: Cirrhotic patients enrolled in the Portal vein thrombosis Relevance On Liver cirrhosis: Italian Venous thrombotic Events Registry (PRO-LIVER) study (n = 753), were followed-up for 2 years to assess the risk of PVT, that was diagnosed by Doppler ultrasonography. Child-Pugh classes, Model for End-Stage Liver Disease score, presence of hepatocellular carcinoma and laboratory variables including SA, D-dimer, and high-sensitivity C-reactive protein (hs-CRP) were measured at baseline.
UNASSIGNED: SA ≤35 g/L was detected in 52% of patients. A logistic multivariate regression analysis showed that higher Child-Pugh class, hepatocellular carcinoma and thrombocytopenia were significantly associated to SA ≤35 g/L. In a subgroup of patients where data regarding hs-CRP and D-dimer were available, SA ≤35 g/L was inversely associated with hs-CRP and D-dimer. During the follow-up, a total of 61 patients experienced PVT. A Kaplan Meier survival analysis showed SA ≤35 g/L was associated to increased risk of PVT compared to SA >35 g/L (P = .005). A multivariate Cox proportional hazards regression analysis showed that male sex, lower platelet count, and SA ≤35 g/L remained associated to PVT after adjusting for confounding factors.
UNASSIGNED: Cirrhotic patients with SA ≤35 g/L are at higher risk of experiencing PVT compared to those with SA >35 g/L and could be considered as potential candidates to anticoagulant prophylaxis for PVT prevention.

Among the risk factors and underlying etiology of acute portal vein thrombosis, viral hepatitis is an extremely rare cause. We report a case of a young healthy 40-year-old male who was diagnosed with acute hepatitis A virus infection and presented with acute portal vein thrombosis. This article describes the possible pathophysiological mechanisms, clinical symptoms, and treatment of acute portal vein thrombosis in this patient. Based on this patient\'s history and treatment, we encourage testing for hepatitis A serological markers in the emergency department in a population with recent hepatitis A exposure risk factors and concurrent unexplained acute portal thrombosis.

BACKGROUND: Portal vein thrombosis in cirrhotic patients presents a significant clinical challenge. This study aims to (1) explore the impact of anticoagulation therapy on patient outcomes; (2) comparative outcomes in portal vein thrombosis treated between direct oral anticoagulant and Vitamin K Antagonist (VKA).
METHODS: We leveraged the TriNetX database to analyze a cohort comprising 4224 patients with liver cirrhosis and PVT who were treated with anticoagulation, alongside a comparison group of 15,300 patients with the same conditions but not receiving anticoagulation therapy.
RESULTS: The anticoagulated group showed a significant reduction in mortality (27.9 % vs. 34.2 %, HR = 0.723, 95 % CI: 0.678-0.770, P < 0.001). When comparing direct oral anticoagulant versus. VKA, in compensated liver cirrhosis, the direct oral anticoagulant group exhibited significantly lower mortality rates compared to VKA (17.7 % vs. 26.5 %, HR = 0.655, 95 % CI: 0.452-0.951, P = 0.025), with no significant difference in liver transplantation rates (4.0 % vs. 4.7 %, P = 0.080). In decompensated liver cirrhosis, the direct oral anticoagulant group exhibited lower mortality compared to the VKA group (23.6 % vs. 30.6 %, HR = 0.732, 95 % CI: 0.629-0.851, P < 0.001), and a higher frequency of liver transplantation was observed in the VKA group (10.6 % vs. 16.0 %, HR = 0.622, 95 % CI: 0.494-0.784, P < 0.001). Hospitalization rates were significantly lower in the direct oral anticoagulant group compared to the VKA group in decompensated cirrhosis (33.4 % vs. 38.3 %, HR = 0.830, 95 % CI: 0.695-0.992, P = 1.937).
CONCLUSIONS: Our study offers compelling evidence supporting the use of anticoagulation therapy in liver cirrhosis with portal vein thrombosis. The use of DOACs in patients with both compensated and decompensated liver cirrhosis showed a marked mortality benefit.

BACKGROUND: Although postoperative portal vein thrombosis (PVT) is a frequent complication of splenectomy, few studies have examined PVT after simultaneous hepatectomy and splenectomy (HS). The aim of this study was to clarify the risk factors for and characteristics of PVT after HS.
METHODS: This retrospective observational study included 102 patients, including 76 with liver cirrhosis (LC) and 26 without, who underwent HS between April 2004 and April 2021. The incidence and location of postoperative PVT detected on contrast-enhanced CT 1 week after surgery were analyzed. In addition, pre- and intraoperative parameters were compared between patients with postoperative PVT and those without in order to determine risk factors for PVT after HS.
RESULTS: Among the 102 patients, 29 (28.4 %), including 32.9 % with LC and 15.4 % without LC, developed PVT after surgery. Among the 29 patients with PVT, 21 (72.4 %), 4 (13.8 %), and 4 (13.8 %) developed thrombus in the intrahepatic portal vein only, extrahepatic portal vein only, and both the extra- and intrahepatic portal veins, respectively. Multivariable analysis showed that preoperative splenic vein dilatation was an independent risk factor for PVT after HS (odds ratio: 1.53, 95 % confidence interval: 1.156-2.026, P = 0.003).
CONCLUSIONS: Our results suggest that splenic vein dilatation is an independent risk factor for PVT after simultaneous HS, and that PVT after HS occurs more frequently in the intrahepatic portal vein. After HS for cases with dilated splenic veins, we should pay particular attention to the PVT development in the intrahepatic portal vein regardless of the type of liver resection.