Indications, results and benefits of the measurement of hepatic venous pressure gradient

Transcription

1 Indications, results and benefits of the measurement of hepatic venous pressure gradient Poster No.: C-0976 Congress: ECR 2017 Type: Scientific Exhibit Authors: J. P. León Salinas 1, M. D. Ferrer-Puchol 2, E. Fernandez Torvisco 3, Keywords: DOI: G. Pacheco Del Río 3, E. Esteban 2, R. Ramiro 4 ; 1 Alzira (Valencia)/ ES, 2 Alzira/ES, 3 VALENCIA/ES, , Va/ES Neoplasia, Hemodynamics / Flow dynamics, Venous access, Diagnostic procedure, Catheters, Percutaneous, Fluoroscopy, Catheter venography, Oncology, Interventional vascular, Abdomen /ecr2017/C-0976 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 11

2 Aims and objectives Introduction Clinically significant portal hypertension is defined as an increase in the hepatic venous pressure gradient (HVPG) # 10 mmhg. The measurement of HVPG is currently the best method available to evaluate the presence and severity of portal hypertension (PHT). HVPG is defined as the difference between the wedged hepatic venous pressure (WHVP) (which reflects the sinusoid pressure) and the free hepatic venous pressure (FHVP). Although portal pressure is not measured directly, the two can be overlaid (1-2), which, added to its reliability and reproducibility, has made it the gold standard for PHT measurement. The measurement of direct portal pressure, which can be done transhepatically or transvenously, would be limited to selected cases with presinusoidal portal hypertension, such as cases of patients with esophageal varices, patent portal vein and normal WHVP (3). The measurement of HVPG is being increasingly used in clinical hepatology, as several studies have shown that this gradient is a reliable marker for a number of clinical endpoints. The main clinical applications of HVPG include diagnosis, risk stratification, the identification of patients with hepatocarcinoma who are candidates for hepatic resection, follow-up of the effectiveness of clinical treatment, and evaluation of PHT progression. The reduction of HVPG by more than 20% over the baseline value or a value below 12 mmhg is considered the therapeutic goal in treatment of portal hypertension (4). This leads to a marked reduction in the risk of bleeding (or rebleeding), ascites and spontaneous bacterial peritonitis (5). Objectives The objective of our study is to analyze the indications, results and benefits of measuring the hepatic venous pressure gradient (HVPG) to make clinical-surgical decisions. Methods and materials A retrospective study was performed on the HVPG measurements taken at our hospital from October, 2007 to August, Data were collected from patients' clinical histories. All of the measurements were taken in the vascular and interventional radiography room, equipped with a Philips Allura FD-20 angiography unit. Page 2 of 11

3 The selection of patients for HVPG measurement was made by consensus decision in a multidisciplinary clinical meeting. They were classified into four groups according to their indication: I: Patients with hepatocarcinoma, candidates for hepatic resection surgery to rule out portal hypertension (PHT) (25 measurements). II: HVPG control in patients on beta blocker therapy for esophageal varices (22 measurements). III: HVPG measurement prior to beginning beta blocker therapy for its later control (6 measurements). IV: Patients with uncertain diagnosis (5 measurements). In order to carry out the necessary procedures, if they were not already hospitalized, the patients were admitted on the morning of the intervention into the short-term hospitalization unit. All patients signed the informed consent at least 24 hours ahead of the procedure and had had recent laboratory tests to assess their kidney function, coagulation tests and platelet count. The procedures were performed in the vascular and interventional radiography room, under conscious sedation (if necessary) and non-invasive monitoring of patients' vital signs. The permeability of the right internal jugular vein was checked in the vascular radiology room. Following the injection of local anesthesia, an ultrasound-guided puncture of the right internal jugular vein was performed with an Abbocath-type 18 gauge needle. The Abbocath stylet was withdrawn, and a 0.035" hydrophilic guidewire was introduced through it, navigating by fluoroscopic guide to the inferior vena cava. A 5F introducer with a hemostasis valve was affixed. Next a 5F vertebral-type catheter was introduced over the guidewire, and using the catheter guidewire, a selective catheterization of the most accessible hepatic vein was performed. The FHVP was measured, keeping the distal end of the catheter in the hepatic vein, at 2-4 cm from where it drains into the inferior vena cava. The WHVP was measured positioning the catheter as distally as possible, occluding the vein, which was confirmed by injecting contrast and observing the hepatic parenchyma. In some cases a balloon was used to occlude the vein (Fig. 1 on page 4). The difference between these two measurements was interpreted as HVPG. Page 3 of 11

4 Following the procedure, the patients were prescribed absolute rest in a semi-sitting position for six hours. Meanwhile, their vital signs and the puncture site were monitored. If hospitalized in the short-term stay unit, the patient was discharged the same day, in the afternoon, if no issues arose. Images for this section: Fig. 1: Measurement of the hepatic venous pressure gradient. The FHVP is measured, keeping the distal end of the catheter in the hepatic vein, at 2-4 cm from where it drains into the inferior vena cava (Image A). The pressure of the wedged hepatic vein is measured by positioning the catheter more distally, occluding the vein (Image B). A balloon can also be used to occlude the vein (Image C). Proper occlusion can be confirmed by injecting contrast (Images B and C). Hospital Universitario de La Ribera - Alzira (Valencia)/ES Page 4 of 11

5 Results Between October, 2007 and August, 2015 a total of 58 measurements were taken on 52 patients. Measurements were more frequent in men (34) than women (18). The average age was 62. In Group I, the HVPG was normal in 20/25 cases, with surgery finally being performed in 12/20 cases, without any deaths due to hepatic decompensation in the 3 months following surgery. In the rest of patients who had high HVPG (8/20), following a re-evaluation in a multidisciplinary meeting, non-surgical alternatives were chosen. In Group II, 13/22 patients achieved the therapeutic goal of an HVPG <12 mm without upper digestive tract hemorrhages being produced in the year following the measurement. In Group III, the HVPG was high (HVPG >12 mmhg) in 6/6, with an average of 18.5 mmhg. Beta blocker therapy was begun for all of them, and response was checked 3-8 months after initiation. The therapeutic goal of reduction of HVPG >20% was achieved in all patients. The clinical data, results and potential usefulness of the hemodynamic study of portal hypertension in the patients of group IV are summarized in the table 1. Table 1: Summary of the 5 indications to measure HVPG for uncertain diagnosis (Group IV). PHT: Portal hypertension. WHVP: Wedged hepatic venous pressure. FHVP: Free hepatic venous pressure. HVPG: Hepatic venous pressure gradient: IVC: Inferior vena cava Clinical data Male patient, 17 years old, with immune thrombocytopenic purpura and posthepatic PHT. Female patient, 66 years old, with suspected PHT due to Budd-Chiari disease Portal hemodynamic study and/or treatment WHVP: 22 mmhg FHVP: 14 mmhg HVPG: 8 mmhg Thrombosis of suprahepatic veins was confirmed. Usefulness of measurement Confirmation of suspected posthepatic PHT diagnosis Confirmation of suspected Budd-Chiari diagnosis, and assistance in treatment of PHT, reducing Page 5 of 11

6 (Fig. 2 on page 6 and Fig. 3 on page 7) Male patient, 66 years old, with suspected prehepatic PHT due to portal cavernomatosis with portal thrombosis secondary to complicated cholecystitis Male patient, 63 years old, with chronic lymphoproliferative syndrome with suspected Budd-Chiari disease. Male patient, 58 years old with suspected essential PHT.. Stenosis angioplasty made to the suprahepatic IVC, reducing its pressure from 17 to 9 mmhg WHVP: 22 mmhg FHVP: 14 mmhg HVPG: 5 mmhg WHVP: 14 mmhg FHVP: 2 mmhg HVPG: 12 mmhg WHVP: 17 mmhg FHVP: 13 mmhg HVPG: 4 mmhg the pressure in the suprahepatic IVC. A sinusoidal component of the PHT was ruled out. Confirmation of presinusoidal and/or sinusoidal PHT, ruling out the suspected diagnosis The presence of sinusoidal PHT was ruled out. Images for this section: Page 6 of 11

7 Fig. 2: Budd-Chiari Syndrome in chronic phase. Images A: and B: Abdominopelvic CT with intravenous contrast. Image C: Ultrasound. Liver diminished in size, with compensatory hypertrophy of the caudate lobe. Inferior vena cava with a marked reduction of caliber, hepatic veins not visible and without flow in Doppler. Signs of portal hypertension with repermeabilization of the paraumbilical vein, splenomegaly and ascites. Hospital Universitario de La Ribera - Alzira (Valencia)/ES Page 7 of 11

8 Fig. 3: Same patient as Figure 2. The initial cavography was performed without identifying the arrival of hepatic veins (Image A), making catheterization impossible, and confirming thrombosis of the hepatic veins. An angioplasty was made of the most stenosed segment in the uppermost portion of the inferior vena cava (Image B). Although there was no modification in the control cavography (Image C), a reduction in the pressure of hepatic IVC from 17 to 9 mmhg was achieved. Hospital Universitario de La Ribera - Alzira (Valencia)/ES Page 8 of 11

9 Conclusion PHT is classified according to the affected anatomical localization into the categories of prehepatic, intrahepatic and posthepatic (3): 1.- Prehepatic portal hypertension: Portal thrombosis is the main cause of prehepatic portal hypertension, and can present acutely or chronically (portal cavernomatosis). It is diagnosed by imaging tests (6). 2.- Hepatic portal hypertension: Portal hypertension is divided into sinusoidal (cirrhosis) or presinusoidal. Presinusoidal hypertension is distinguished by having a normal or slightly high HVPG, with slightly high wedged hepatic venous pressure (WHVP) and normal free hepatic venous pressure (FHVP). Sinusoidal portal hypertension is the most frequent chronic liver disease, with cirrhosis being the main cause. It is distinguished by an increase WHVP and normal FHVP, which results in an increase in HVPG (3). 3.- Posthepatic portal hypertension In posthepatic (actually, postsinusoidal) portal hypertension, the HVPG is normal, with high WHVP and FHVP, and Budd-Chiari syndrome being the most frequent cause. In this syndrome, the obstruction can be present anywhere from the hepatic venules to the point where the inferior vena cava drains into the right auricle (6). The clinical and ultrasonographic suspicion of Budd-Chiari syndrome must be confirmed through angiographic study with catheterization of hepatic veins. The catheterization of hepatic veins enables confirmation of the existence and extension of the thrombotic lesion (7). Hepatic resection is contraindicated in cases of patients with hepatocarcinoma and HVPG >10 due to the high risk of irreversible hepatic decompensation within the three months following surgery (8, 9). In our study, the need to rule out clinically significant portal hypertension (HVPG>10) in patients with hepatocarcinoma was the most frequent indication for measuring HVPG. This enabled selection of patients who were candidates for resection, making it possible to operate on them, and in the case of those with high HVPG, offer them other, safer treatment alternatives. Our results were concordant with the evidence, and no deaths due to liver decompensation were registered in the three months following surgery. Page 9 of 11

10 Today, only pharmacological (non-cardioselective beta blockers) and endoscopic treatment (ligature of esophageal varices) are universally accepted for the prevention of the first variceal hemorrhage (10). In this context, pharmacological treatment with propranolol or nadolol reduces the incidence of the first variceal hemorrhage by 45%. The reduction of HVPG by more than 20% over the baseline value or achieving a value below 12 mmhg is considered the therapeutic goal in treatment of portal hypertension (4). When this goal is achieved, it has been shown that the risk of variceal bleeding or rebleeding, and other complications of PHT such as ascites, spontaneous bacterial peritonitis and hepatorenal syndrome is diminished, improving survival. Failure to achieve these therapeutic objectives is the strongest independent predictor for bleeding or rebleeding (11). In our study, concordantly with the evidence, there were no upper digestive tract hemorrhages over the follow-up of one year following the measurements, neither in the group that achieved the therapeutic goal (HVPG <12 mmhg) nor the group that showed a reduction greater than 20% of the HVPG. In our study, the least frequent indication was measurement of HVPG in patients with uncertain diagnosis (Group IV) allowing us not only to confirm, rule out and quantify the suspicions, but also assist in their treatment, as occurred in the case of the patient with Budd-Chiari syndrome (Figures 2 and 3). The limitations of our study were the low number of patients and the fact that it was retrospective. As a general conclusion, HVPG measurement is extremely helpful for the selection of patients who are candidates for surgical resection of hepatocarcinoma, for the control of beta blocker treatment to prevent upper digestive tract bleeding due to esophageal varices and for the differentiation of the different types of portal hypertension. Personal information References 1.- Perelló A, Escorsell A, Bru C, Gilabert R, Moitinho E, García-Pagán JC, et al. Wedged hepatic venous pressure adequately reflects portal pressure in hepatitis C virus-related cirrhosis. Hepatology.1999;30(6): Page 10 of 11

11 2.- Iwao T, Toyonaga A, Ikegami M, Sumino M, Oho K, Sakaki M, et al. Wedged hepatic venous pressure reflects portal venous pressure during vasoactive drug administration in nonalcoholic cirrhosis. Dig. Dis. Sci. 1994;39(11): Berzigotti A, Seijo S, Reverter E, Bosch J. Assessing portal hypertension in liver diseases. Expert Rev Gastroenterol Hepatol. 2013;7(2): Bosch J, Abraldes JG, Albillos A, Aracil C, Bañares R, Berzigotti A, et al. Hipertensión Portal: recomendaciones para su evaluación y tratamiento: documento de consenso auspiciado por la AEEH y el CIBERehd. Gastroenterol Hepatol. 2012;35: Bosch J, Abraldes JG, Berzigotti A, García-Pagan JC. The clinical use of HVPG measurements in chronic liver disease. Nat Rev Gastroenterol Hepatol. 2009;6(10): DeLeve LD, Valla D-C, Garcia-Tsao G. Vascular disorders of the liver. Hepatology. 2009;49(5): García-Pagán JC, Perelló A, Bosch J. Budd-Chiari síndrome. Gastroenterol Hepatol. 2000;23(10): Bruix J, Castells A, Bosch J, Feu F, Fuster J, Garcia-Pagan JC, et al. Surgical resection of hepatocellular carcinoma in cirrhotic patients: prognostic value of preoperative portal pressure. Gastroenterology. 1996;111(4): Llovet JM, Fuster J, Bruix J. Intention-to-treat analysis of surgical treatment for early hepatocellular carcinoma: resection versus transplantation. Hepatology. 1999;30(6): de Franchis R; Baveno V Faculty. Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension. J Hepatol.2010;53: Garcia-Tsao G, Bosch J. Management of varices and variceal hemorrhage in cirrhosis. N. Engl. J. Med. 2010;362(9), Page 11 of 11