From the SIR residents and fellows section (RFS)
Teaching Topic: Whether or Not to Use Free Hepatic Vein Pressure to Calculate the Portal Pressure Gradient in Cirrhosis.
Martin Rössle, MD, Philipp Blanke, MD, Benjamin Fritz, MD, Michael Schultheiss, MD, and Dominik Bettinger, MD. Free Hepatic Vein Pressure Is Not Useful to Calculate the Portal Pressure Gradient in Cirrhosis: A Morphologic and Hemodynamic Study. J Vasc Interv Radiol 2016; 27: 1130-1137
Click here for abstract
In a recent study published in JVIR, researchers from the University Hospital Freiburg investigated the role of using free hepatic vein pressure in calculating the hepatic venous pressure gradient. Diameter and pressure measurement were obtained in multiple locations within the hepatic vein, IVC, and right atrium on 30 hepatic venograms in 29 consecutive patients with planned TIPS creation. The authors found a wide range of pressure measurements and diameters across the length of the hepatic vein creating a significant amount of variability in measured pressure gradients that were not reflective of the hemodynamic changes occurring within the portal system. This challenges the current guideline recommendations of measurement in the hepatic vein or the IVC, disregarding the right atrium as an internal reference. The manuscript concludes that using the free hepatic vein pressure (FHVP) to calculate the hepatic vein pressure gradient (HVPG) is not recommended given changes with catheter tip position and vein morphology. However, the high agreement between the wedged hepatic vein/IVC pressure gradient (HCPG) and hepatic atrial pressure gradient (HAPG) suggest that both may be used.
What is the significance of the hepatic venous pressure gradient (HVPG)?
The HVPG is the calculated difference of the wedged hepatic vein pressure (WHVP) from the free hepatic vein pressure (FHVP). A value of more than 10 mm Hg is considered clinically significant portal hypertension. A reduction to less than 12 mm Hg or a reduction of more than 10% from the baseline value is associated with decreased risk of variceal hemorrhage and improved survival. Traditionally, FHVP should be measured close to the hepatic vein orifice within a distance of 4-5 cm of the IVC. When pressure measurement differences of more than 1-2 mm Hg exist between the hepatic vein and the IVC, the pressure measured at the IVC at the level of the entrance of the hepatic veins should be used in place of the FHVP.
This study sought to reevaluate the use of HVPG for several reasons. First, in patients with advanced cirrhosis, hepatic veins may be narrowed, irregular, or compressed. This may result in erroneous measurements with an apparently high FHVP and a low HVPG. Second, postprocedural measurement of the FHVP is difficult or impossible. Therefore, measurements are commonly performed in the IVC or right atrium, which is considered the “sea level” of the vascular system and therefore the natural reference for hemodynamic measurements.
What are the recommendations of the Baveno Consensus Workshop?
The most recent expanded Baveno VI Consensus recommends TIPS within 72 hours (ideally < 24 hours) in patients bleeding from esophageal or gastric varices at high risk of treatment failure (Child class C < 14 points or Child class B with active bleeding) after initial pharmacologic and endoscopic therapy (Class 1b; Level A). Persistent bleeding despite combined pharmacologic and endoscopic therapy is best managed by PTFE-covered TIPS (Class 2b; Level B). Rebleeding during the first five days may be managed by a second attempt at endoscopic therapy. If rebleeding is severe, PTFE-covered TIPS is likely the best option (Class 2b; Level B). New guidelines in this workshop now recommend TIPS for patients with refractory ascites who are intolerant to non-selective beta blockers (NSBB) (Class 5, Level D). TIPS can be considered in patients with transfusion-dependent portal hypertensive gastropathy in whom NSBB and/or endoscopic therapies fail (Class 4; Level C). The stepwise approach to management of Budd-Chiari syndrome/hepatic venous outflow tract obstruction is: anticoagulation, angioplasty/thrombolysis, TIPS, and orthotopic liver transplantation (Class 3b; Level B).
Morning Report Questions
What factors may contribute to the inaccuracy of FHVP measurement?
Aside from narrowed, irregular, or compressed veins in patients with cirrhosis, relative obstruction of a hepatic vein by a catheter may erroneously increase the measured FHVP. In this study, the percentage of vessel obstruction by the 8-F catheter (diameter, 2.4 mm) was 40% in the peripheral position and decreased to 10% in the central (proximal) position. Small hepatic veins with a diameter of < 6 mm have a considerable obstruction of 20% or more irrespective of the location of the tip of the catheter. This study found excellent correlation between the wedged hepatic vein/IVC pressure gradient (HCPG) and the hepatic atrial pressure gradient (HAPG), which justifies using either the IVC or right atrium as internal references to calculate the portosystemic pressure gradient, not the free hepatic venous pressure. If using the HAPG, the systemic difference of 2 mm Hg should be regarded by resetting the threshold for symptomatic portal hypertension at an HAPG of 14 mm Hg.
What concerns exist about the use of the right atrium as an internal reference when calculating the portosystemic pressure gradient?
The authors mention previous studies in which pressure measurement in the right atrium is neglected because changes in intraabdominal pressure may affect the portoatrial pressure gradient but not the portohepatic pressure gradient. Therefore, it can be argued that the portosystemic pressure gradient will be significantly higher when using right atrial pressure as an internal reference as compared to using the hepatic veins or IVC. These studies placed sandbags over the abdomen to mimic high intraabdominal pressure, which led to uniform increase in pressure downstream of the obstruction in the hepatic and portal veins but left the right atrium unaffected or even reduced. The authors argue that increased intraabdominal pressure in patients with true ascites reflects an “open” system and that such increased pressures result in a change in their respective blood pools but may have only a short and limited effect on the intravascular pressure.
De Franchis, Roberto. “Report of the Baveno VI Consensus Workshop: Stratifying Risk and Individualizing Care for Portal Hypertension.” Journal of Hepatology. 2015 September; 63(3): 743-752.
Rajat Chand, MD
Diagnostic Radiology Resident, PGY-2
John H. Stroger Hospital of Cook County