Quantitative CT Predictors of Portal Venous Intervention in Uncontrolled Variceal Bleeding.

OBJECTIVE. The purpose of this study was to quantify abdominal CT predictors of endoscopically refractory, uncontrolled variceal hemorrhage requiring portal venous intervention. MATERIALS AND METHODS. From 2009 to 2018, 64 patients with endoscopically refractory variceal hemorrhage requiring portal venous intervention (variceal hemorrhage group) and 67 patients without hemorrhage but with symptomatic, pressure gradient-proven portal hypertension (control group) underwent CT. CT scans were retrospectively reviewed for the following: varix size, variceal intraluminal protrusion, liver and spleen volumes, and portal vein diameter. RESULTS. Gastric variceal protrusion was found to be a strong CT parameter associated with refractory hemorrhage (mean depth, 0.75 mm in variceal hemorrhage group vs -2.91 mm in control group; p = 0.001). Gastric varix size was also associated with variceal hemorrhage (mean diameter, 8.03 vs 6.51 mm; p = 0.001). However, this trend was not observed in the sizes of the esophageal varices (mean diameter, 6.28 vs 6.43 mm; p = 0.370). Larger spleen volume (mean, 1312 vs 1152 cm3; p = 0.029) and liver volume (mean, 1514 vs 1143 cm3; p = 0.004) were also found to be predictors of variceal hemorrhage. Significant CT threshold findings included gastric variceal protrusion depth more than 0 mm (odds ratio [OR], 6.44), gastric varix size more than 6 mm (OR, 3.89), spleen volume more than 1000 cm3 (OR, 2.63), and liver volume more than 1000 cm3 (OR, 2.82). CONCLUSION. Quantitative imaging parameters on abdominal CT, such as intraluminal protrusion of gastric varices, gastric varix size, and larger spleen and liver volumes, were predictive of portal venous intervention, whereas esophageal varix size was not.

Post paracentesis deep circumflex iliac artery injury identified at angiography, an underreported complication.

BACKGROUND: Though injury to the inferior epigastric artery (IEA) is reported to be the most common source of hemorrhagic complications from paracentesis, we wish to present our experience involving deep circumflex iliac artery (DCIA) injuries that in our experience is the artery most frequently injured during paracentesis. METHODS: Sixteen patients with clinically significant hemorrhage following paracentesis were referred to our Interventional Radiology service for trans-catheter embolization. Patterns of hemorrhage from diagnostic cross-sectional imaging and subsequent angiographic findings and management were investigated. RESULTS: 8/16 patients (50%) had angiographic evidence of injury to the DCIA and 4/16 patients (25%) had evidence of injury to the IEA, with two of these patients demonstrating hemorrhage from both the DCIA and IEA; 3/16 patients had injuries to subcostal and/or intercostal arteries; while 3/16 patients had negative angiograms. All patients underwent embolization of the identified injured arteries, and empiric embolization was performed of the DCIA and/or IEA in the three patients with negative angiograms. Fourteen of sixteen patients stabilized post embolization, while two patients required a second embolization procedure to achieve hemostasis; all patients were subsequently discharged home in stable condition. CONCLUSION: Both the IEA and the lesser known DCIA need to be considered when performing paracentesis and at subsequent angiography for post paracentesis iatrogenic hemorrhage. Knowledge of both of these at-risk abdominal wall arteries may help minimize hemorrhagic complications from paracentesis.

Plasma fibronectin supports hemostasis and regulates thrombosis.

Plasma fibronectin (pFn) has long been suspected to be involved in hemostasis; however, direct evidence has been lacking. Here, we demonstrated that pFn is vital to control bleeding in fibrinogen-deficient mice and in WT mice given anticoagulants. At the site of vessel injury, pFn was rapidly deposited and initiated hemostasis, even before platelet accumulation, which is considered the first wave of hemostasis. This pFn deposition was independent of fibrinogen, von Willebrand factor, ß3 integrin, and platelets. Confocal and scanning electron microscopy revealed pFn integration into fibrin, which increased fibrin fiber diameter and enhanced the mechanical strength of clots, as determined by thromboelastography. Interestingly, pFn promoted platelet aggregation when linked with fibrin but inhibited this process when fibrin was absent. Therefore, pFn may gradually switch from supporting hemostasis to inhibiting thrombosis and vessel occlusion following the fibrin gradient that decreases farther from the injured endothelium. Our data indicate that pFn is a supportive factor in hemostasis, which is vital under both genetic and therapeutic conditions of coagulation deficiency. By interacting with fibrin and platelet ß3 integrin, pFn plays a self-limiting regulatory role in thrombosis, suggesting pFn transfusion may be a potential therapy for bleeding disorders, particularly in association with anticoagulant therapy.