Risk Factors for Esophageal Collateral Veins in Cirrhosis with and without Previous Endoscopic Esophageal Variceal Therapy

Background. Portosystemic collateral vessels are a sign of portal hypertension in liver cirrhosis. Esophageal collateral veins (ECVs) are one major type of portosystemic collateral vessels, which increase the recurrence of esophageal varices and bleeding after variceal eradication. However, the risk factors for ECVs were still unclear. Methods. We retrospectively screened cirrhotic patients who had contrast-enhanced computed tomography (CT) images to evaluate ECVs and upper gastrointestinal endoscopic reports to evaluate gastroesophageal varices at our department. Univariate and multivariate logistic regression analyses were performed to explore the independent risk factors for ECVs. Odds ratios (ORs) were calculated. Subgroup analyses were performed in patients with and without previous endoscopic variceal therapy which primarily included endoscopic variceal ligation (EVL) and endoscopic injection sclerotherapy (EIS). Results. Overall, 243 patients were included, in whom the prevalence of ECVs was 53.9%. The independent risk factors for ECVs were hepatitis C virus infection (OR = 0.250, p = 0.026), previous EVL (OR = 1.929, p = 0.044), platelet (OR = 0.993, p = 0.008), and esophageal varices needing treatment (EVNTs) (OR = 2.422, p = 0.006). The prevalence of ECVs was 60.8% (73/120) in patients undergoing EVL, 50% (10/20) in those undergoing EIS, and 47.5% (48/101) in those without previous endoscopic variceal therapy. The independent risk factors for ECVs were the use of nonselective beta-blockers (OR = 0.294, p = 0.042) and EVNTs (OR = 3.714, p = 0.006) in subgroup analyses of patients with and without previous endoscopic variceal therapy, respectively. Conclusions. The presence of ECVs should be closely associated with the severity of portal hypertension in liver cirrhosis. Risk of ECVs might be increased by previous EVL.

Risk Factors Regarding Portal Vein Thrombosis in Chronic Liver Disease

The portal vein thrombosis (PVT) is one of the most frequent vascular diseases of the liver, with a high rate of morbidity and mortality. The most common causes of the PVT are hepatic cirrhosis, hepatobiliary neoplasms, inflammatory and infectious abdominal diseases, and myeloproliferative syndromes.(1,2) The natural progress of the PVT has as a result portal hypertension which leads to splenomegaly and the formation of portosystemic collateral vessels, as well as gastroesophageal, duodenal and jejunal varices. Ultrasonography, especially Doppler ultrasound, is the most widely used imaging method to asses, supervise and diagnose PVT in patients with hepatopathies. The purpose of acute PVT treatment is to re-permeabilize the obstructed vessels; the endoscopic ligature of the varices in the eventuality of their rupture is safe and extremely efficient in chronic PVT. To conclude, PVT is the most common hepatic vascular disorder, and its prevalence has increased particularly among the patients with chronic hepatopathies.(3)

Portal vein thrombosis in Fontan-associated liver disease

A 25-year-old patient with signs of cirrhosis on ultrasound and CT presented with portal vein thrombosis on routine follow-up examinations; retrograde hepatic wedge angiography demonstrated only the right-sided portal vein branch. Development of a portosystemic collateral vessel to the left-sided renal vein prevented signs of hypersplenism. This unique complication of portal vein thrombosis should be considered during long-term surveillance.

Primary portal vein hypoplasia with portal hypertension in a young dog

A 5-month old Caucasian dog was presented with a 20-day history of abdominal distention along with inappetance, depression and vomiting of 24-hour duration. Physical examination findings included depression, ascites, mild inspiratory dyspnea and dehydration. Clinicopathological evaluation revealed hyperammonemia, hypoalbuminemia, hyperbilirubinemia, hypoglycemia and hyponatremia. Μicrohepatia and free abdominal fluid was detected with abdominal ultrasonography. During exploratory laparotomy, multiple acquired portosystemic collateral vessels were found, indicative of portal hypertension, along with a small liver of normal color and texture. Liver histopathology included features consistent with liver hypoperfusion. These findings supported the diagnosis of primary portal vein hypoplasia with portal hypertension. The animal recovered uneventfully postoperatively and was discharged with diuretics, hepatoprotectants and a low-protein diet and remains healthy two years after diagnosis. This case underscores that a favorable prognosis may be anticipated in cases of primary portal vein hypoplasia with portal hypertension, thus, justifying the long-term conservative management instead of considering euthanasia.

An Unusual Case of Portal Hypertension Secondary to Primary Hypoplasia of the Portal Vein

ABSTRACT Primary hypoplasia of the portal vein with secondary portal hypertension and acquired portosystemic collateral circulation is infrequently reported in the veterinary literature. Diagnosis of this condition requires documentation of abnormal hepatocellular function, the lack of intrahepatic or extrahepatic macroscopic congenital portosystemic shunts, and liver histopathology demonstrating portal hypoperfusion in the absence of hepatic inflammation or nodular regeneration. Due to a perceived poor prognosis, many patients with this condition are euthanized; however, those that are spared can be medically managed, in some cases for years. This case report describes the diagnosis and management of a patient with primary hypoplasia of the portal vein and secondary portal hypertension that presented with the severe but typical clinical manifestations of ascites and hepatic encephalopathy, normal liver enzyme concentrations, and normal serum bile acid concentrations.

N-butyl-2 cyanoacrylate (NBCA) embolus in the graft portal vein after portosystemic collateral embolization in liver transplantation recipient: what is the clinical significance?

Background An N-butyl-2 cyanoacrylate (NBCA) embolus in the graft portal vein was frequently observed after an intraoperative embolization of portosystemic collaterals performed to prevent portal steal in liver transplant (LT) recipients. The radiological and clinical features of NBCA emboli have not yet been described. Purpose To describe radiological and clinical features of NBCA embolus in graft portal vein after portosystemic collateral embolization in LT recipients. Material and Methods A total of 165 consecutive LT recipients who had undergone intraoperative NBCA embolization of varix were found in single institution’s computerized databases of a clinical cohort of LT. Patients were evaluated for NBCA emboli (categorized into major and minor emboli according to location) on first postoperative computed tomography (CT). All electronic medical records and radiologic studies including follow-up was evaluated to determine any radiological and clinical abnormality associated with NBCA embolus. Results NBCA emboli were found in 24% (39/165) of recipients. Although most patients had minor emboli (77%, 30/39) without remarkable ultrasonography (US) abnormalities, seven (78%) of nine recipients with major emboli showed intraluminal echogenic lesions in graft portal vein on grayscale US, and five of them (71%) showed partial portal flow obstruction, although none exhibited any abnormality on contrast-enhanced US. Recipients with NBCA portal emboli showed no significant clinical abnormalities and were discharged safely. NBCA embolus eventually disappeared mostly within six months (82%, 32/39). Conclusion NBCA emboli are frequently observed after portosystemic collateral embolization in LT recipients and are not associated with poor clinical outcome. They may mimic ordinary thromboemboli on US.