DIRECT TRANSHEPATIC MEASUREMENT OF PORTAL VEIN PRESSURE USING A THIN NEEDLE

GASTROENTEROLOGY 72:584-589, 1977 Copyright 1977 by the American Gastroenterological Association Vol. 72, No.4, Part 1 Printed in U.S.A. DIRECT TRANSHEPATIC MEASUREMENT OF PORTAL VEIN PRESSURE USING A THIN NEEDLE Comparison with wedged hepatic vein pressre THOMAS D. BOYER, M.D., DAVID R. TRIGER, M.D., MASUMASA HORISAWA, M.D., ALLAN G. REDEKER, M.D., AND TELFER B. REYNOLDS, M.D. University of Sothern California School of Medicine and Liver Service, John Wesley Conty Hospital, Los Angeles, california A techniqe for the direct measrement of portal vein pressre in flly conscios patients is described. This ses a perctaneos transhepatic approach with a thin Chiba needle and is shown to be simple and safe. The techniqe has been applied to 123 patients with a variety of liver disorders and the pressre measrements have been compared with those obtained by the indirect techniqe of wedge hepatic vein catheterization. Close agreement was fond between portal vein pressre and wedged hepatic vein pressre in qiescent alcoholic liver disease and alcoholic hepatitis. In chronic active hepatitis, portal vein pressre tended to be higher than wedged hepatic vein pressre, indicating a presinsoidal component to the portal hypertension. This techniqe is shown to be sefl in assessing idiopathic portal hypertension and in demonstrating hepatofgal flow. The development of portal hypertension is one of the most serios complications of chronic liver disease. Measrement of portal vein pressre (PVP), therefore, is important in evalation and management of sch patients bt has been difficlt becase of the relative inaccessibility of the portal vein. Techniqes sed for assessment of portal pressre have inclded wedged hepatic vein pressre (WHVP),l splenic plp pressre,2 mbilical vein catheterization,3 and hepatic parenchymal pressre. 4,5 Only mbilical vein catheterization provides a direct measrement of the PVP withot resorting to a laparotomy. Dring the performance of transhepatic cholangiography with the Chiba needle, we fond that it was possible to enter portal vein branches within the liver and measre the PVP directly. This report describes the techniqe and the reslts in 123 patients with varios types of liver disease, and makes a comparison with WHVP measrements. Received Jly 16, 1976. Accepted October 11, 1976. This work was presented in part at the American Association for the Stdy of Liver Diseases Meeting in Chicago, November 4, 1975. Address reqests for reprints to: T. D. Boyer, M.D., Gastroenterology Section, Department of Medicine, University of California, San Francisco Medical Center, San Francisco, California 94143. Dr. Triger was the recipient of a Medical Research Concil Traveling Fellowship. Dr. Triger's present address is: Department of Medicine, University of Sothampton Medical School, Sothampton General Hospital, Sothampton, England. Dr. Horisawa's present address is: Second Department of Srgery, Nagoya University School of Medicine, Nagoya, Japan. Patients and Methods Patient Material Patients with different forms of liver disease of varying severity were stdied. All patients received a thorogh explanation of the procedre, and written consent was obtained. Patients with gross ascites, evidence of a bleeding tendency, or prothrombin activity ofless than 50% of control were exclded. The nmbers and categories listed below only inclde patients in whom sccessfl stdies were achieved. Alcoholic liver disease (ALD). This grop was composed of 29 patients with cirrhosis or varios degrees of fibrosis, with or withot steatosis. All patients had a liver biopsy, sally within 2 weeks of the portal pressre measrement. There was no clinical, biochemical, or histological evidence of active hepatic inflammation. Alcoholic hepatitis (AH). All 16 patients within this grop had a liver biopsy within 10 days of the procedre which showed the presence of alcoholic hyalin. The majority also had nderlying cirrhosis. Clinical and laboratory featres of AH were also freqently present,6 bt were not reqired for inclsion in this grop. Chronic active hepatitis (CAH). Twenty-five patients had biopsy-docmented CAH. These inclded 3 patients with a positive lps erythematoss cell test, 11 with a positive test for hepatitis B srface antigen, and 11 who had neither of these serological markers. Primary biliary cirrhosis (PBC). All 8 patients had clinical and histological featres consistent with PBC.7 Other hepatic disorders. The diagnoses in this grop of 15 patients (table 1) were based on established criteria for these entities. Unsal forms of portal hypertension. A frther 7 patients with nsal forms of portal hypertension are shown separately in table 2. 584

April 1977 PORTAL VEIN PRESSURE MEASUREMENT 585 Methods All patients were fasting and received meperidine (25 to 75 mg) and promethazine (50 mg) 112 hr before the procedre. They were placed on an X-ray table in the spine position. The WHPV was measred as previosly described, 8 and reslts were reported as millimeters of Hg above inferior vena caval pressre. Soon after the completion of the WHVP measrement, the transhepatic PVP was measred. The techniqe was similar to that described for transhepatic cholangiogr p hand y, the 9 Chiba needle (oter diameter 0.7 mm, inner diameter 0.5 mm) was sed throghot this stdy. In vitro stdies had proved that an accrate pressre cold be transmitted throgh this needle. The skin overlying the right lateral chest wall was cleansed with iodine. The pper abdomen was then floroscoped and a marker was placed on the sternm overlying the T Il - 12 interspace. The costophrenic slcs was identified and the first interspace below the slcs in the midaxillary line was selected for the point of entry. The skin and intercostal mscles were anesthetized with 2% xylocaine. With a scalpel, a small skin incision was made. The needle was then inserted parallel to the table dring apnea and was directed toward the T Il - 12 interspace. The needle was passed in one smooth motion to abot the right lateral vertebral margin. The patient was then allowed to breathe bt was reqested to avoid deep breaths throghot the remainder of the procedre. The stylet was removed and a syringe filled with 50% diatrizoate sodim (Hypaqe, Winthrop Laboratories, New York, N. Y.) was connected to the needle via polyethylene tbing. A small amont of contrast material was injected to confirm that the needle tip was within the hepatic parenchyma and the needle was then slowly withdrawn as contrast material was gently injected. When a vasclar channel is entered sing this techniqe, the portal and hepatic veins can easily be distingished by observing the direction of flow of the contrast material. In figre la, a portal vein is shown with contrast material flowing into the liver and filling sinsoids. In figre 1B, a hepatic vein is shown with rapid flow toward the inferior vena cava. After entering a vein and determining the direction of flow, the.needle was h connected e n to a Statham strain gage by tbmg filled WIth contrast material and the pressre was recorded. The position of the strain gage and patient were nchanged from the jst completed WHVP measrement. After pressre recording, 2 to 5 ml of contrast were injected and X-rays were taken. To ensre that valid pressres were obtained, the following criteria were established (fig. 2): the needle position shold be sch that (1) there is no parenchymal staining with injection of contrast material; (2) the pressre tracing shows a rapid rise followed by stable platea with slight respiratory variation; and (3) blood can easily be aspirated. The sal time between the measrement of WHVP and PVP was 30 min. In 14 patients, WHVP was measred before insertion of the transhepatic needle. With the catheter still in the hepatic vein, the transhepatic needle was inserted and WHVP and PVP recordings were again obtained within 1 to 2 min of each other. Reslts One hndred and twenty-six procedres were performed in 123 patients, and 101 were considered technically satisfactory for analysis. WHVP cold not be measred in 5 patients (4%), and a valid PVP was not obtained in 20 patients (16%). The major reasons for not obtaining a valid PVP were: pain reqiring discontination of the procedre before completion of the stdy (6 cases), inability to enter a portal vein (6 cases), and entrance into a hepatic artery (1 case). Review of the x rays or pressre tracing revealed that one of the above criteria had not been met in an additional 7 cases. The time reqired to obtain PVP was sally 10 min or less, and rarely exceeded 30 min. If a portal vein radicle was not entered dring for insertions of the needle, the procedre was discontined. In the 14 patients in whom simltaneos recordings of FIG. 1. A, Injection of contrast material into portal vein radicle with filling of sinsoids; B, similar injection into hepatic vein, showing contrast material draining toward the inferior vena cava.

586 BOYER ETAL. Vol. 72, No.4, Part 1 PORTAL VEIN FIG. 2. The left half of the figre is a diagrammatic representation of criteria necessary for good portal vein pressre (PVP) recording in contrast to that shown on the right. WHVP and PVP were performed, the entrance of the transhepatic needle into the liver cased no change in the WHVP. Reslts from the simltaneos and seqential pressre measrements were similar, and the data have therefore been combined. The correlations between WHVP and PVP for the patients with ALD, AH, CAH, and PBC are shown in figres 3 to 6, respectively. In the ALD patients an excellent correlation (r = 0.958) was fond between WHVP and PVP. A difference of 2 mm Hg or less between PVP and WHVP was recorded in 25 of 29, and the maximm difference observed was 4 mm Hg. Similar reslts were obtained in those with AH (r = 0.912), althogh in 1 patient a difference of 6.5 mm Hg (PVP less than WHVP) was recorded. Less agreement between the WHVP and PVP was fond in the CAH (r = 0.776) and PBC (r = 0.778) grops. In the latter two grops, WHVP and PVP differed by more than 4 mm Hg in 7 of33, with the PVP being higher in all bt 1 of those cases. A similar trend for the PVP to exceed the wedged pressre was also observed when the pressre differential was less than 4 mm Hg. Table 1 shows the pressre measrements obtained from a heterogeneos grop of patients. The nmber of patients with each disorder is small, so no conclsions can be reached abot the observed differences. Table 2 contains the data from 8 patients with nsal forms of portal hypertension. For patients (cases 17, 23, 75, and 126) had idiopathic portal hypertension, characteristically a presinsoidal lesion. to Case 45, stdied initially dring an episode of severe AH, was fond to have a PVP 10 mm Hg below WHVP, and the flow of contrast material appeared to be in a retrograde fashion, with visalization of portal vein, left gastric vein, and esophageal varices (fig. 7). Sperior mesenteric and splenic arteriography at that time show that 3 0 - - - - - - - - - - - - - - - - mm HQ. a: 20.!: :::I ;; co. Ot. 10 N=29 r =.96 2) 0 10 20 mmhq 30 Porlal Vein Pressre FIG. 3. Comparison of wedged hepatic vein pressre (WHVP)with portal vein pressre (PVP) in alcoholic liver disease (ALD). the majority of the portal venos otflow was throgh collaterals and not the liver. All evidence of hepatic inflammation sbsided after 3 months of abstention from alcohol; repeat WHVP and PVP then differed by only 3 mm Hg, and the observed flow was prograde. Two patients (cases 80 and 120) with spontaneos splenorenal shnts demonstrated on arteriography were also fond to have retrograde portal flow and to have portal vein pressres 3 and 8 mm Hg below the WHVP, respectively. Two additional patients inclded with the ALD

April 1977 PORTAL VEIN PRESSURE MEASUREMENT 587 grop also had spontaneos shnts on arteriography; however, PVP was eqal to WHVP in 1 and exceeded it by 2 mm Hg in the other, and only prograde flow of contrast material was seen after its injection into the portal vein. In 32 patients, PVP was measred in more than one portal vein radicle and the maximm observed difference was 3 mm Hg. Bile dcts of normal caliber were entered fortitosly in 15 cases (12%). Hepatic vein pressres with the Chiba needle were obtained in 46 stdies, and the pressres observed were similar to the 3 0 - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - mmhv /0.. : 20. S ;;. /0.. : c Q: 20 " Q..,., /0. N= 25 r =.78 0 /0 20 mmhg 30 Portal Vein Pressre FIG. 5. Comparison of wedged hepatic vein pressre (WHVP) with portal vein pressre (PVP) in chronic active hepatitis (CAH). 30r--------------------------------, mm tjv c : 20 OJ. /0 Porta I N-8 r -.78 20 mm 9 30 V.in Pr. r. FIG. 6. Comparison of wedged hepatic vein pressre (WHVP) with portal vein pressre in primary biliary cirrhosis (PBC). TABLE 1. Pressre measrements on a miscellaneos grop of patients with hepatic disorders Diagnosis Patient no. WHvp Pvpa Acte viral hepatitis 31 3 5.5 N= 16 r s.91 51 3 7 62 2 10 69 8 10 /0 20 mmhv 30 108 7.5 8 Portal Vein Prere Chronic persistent hepatitis 89 3.5 5 124 7 4.5 FIG. 4. Comparison of wedged hepatic vein pressre (WHVP) with Web lesion 15 4 (5)h 2 (4)b portal vein pressre (PVP) in alcoholic hepatitis (AH). Wilson's disease 21 5 7 Drg cholestasis 32 3 6 3 0 - - - - - - - - - - - - - - - - - - - - - - - - - - - - mm HV Cirrhosis after jejnoileal bypass Idiopathic fibrosis Metastatic cancer to the liver Hepatic artery-portal vein fistla Myelofibrosis 60 82 109 22 121 4 10.5 6 9 14.5 23 6 8 9 7 a WHVP, wedged hepatic vein pressre; PVP, portal vein pressre; vales given are millimeters of Hg above inferior vena caval pressre. b Vales in parentheses represent repeat stdy after web lesion was removed. free hepatic vein pressres recorded throgh the hepatic vein catheter. No significant complications were observed from the 126 stdies. Pain, centered in the midabdomen after intraparenchymal or intralymphatic injection of contrast material, was the most common complaint of the patients. The pain was sally short lived and well tolerated. A branch of the hepatic artery was entered in 3 cases and the gallbladder in 1. The procedre was discontined after the first entry into an artery, bt in the 2 sbseqent patients the remainder of the procedre was completed. No seqelae were observed in any of the patients. Antibiotics were not given to cover this procedre even if nobstrcted bile dcts were entered.

588 BOYER ET AL. Vol. 72, No.4, Part 1 Discssion Perctaneos transhepatic pnctre ofthe portal vein sing a relatively large needle has been previosly described,11 as has the cannlation of the portal vein for venography12 and limited pressre recording. 13 This is the first systematic stdy of perctaneos transhepatic PVP measrement sing the thin needle and comparison of the reslts to a simltaneosly measred WHVP. This techniqe is shown to be easy, safe, and accrate, and can be done repeatedly. Portal pressre measrement is performed with the patients flly conscios and reqires a minimm of time and patient discomfort. TABLE 2. Stdies on patients with nsal forms of portal hypertension. Diagnosis Patient no. WHVpa pvpa Idiopathic portal hypertension 17 1.5 13.5 23 7 19 75 4 21.5 126 7 14 Hepatofgal flow Alcoholic hepatitis 45 24 (16)b 14 (13)b ALD with spontaneos 120 19 16 shnt ALD with spontaneos 80 16 8 shnt ALD with hepatic artery- 54 20 25 portal vein fistal a WHVP, wedged hepatic vein pressre; PVP, portal vein pressre; vales given are millimeters of Hg above inferior vena caval pressre. b Vales in parentheses are repeat pressre 3 months after first stdy. Reslts in patients with ALD are similar to those in patients stdied in previos reports. An excellent correlation was fond between WHVP and PVP (fig. 3), entirely similar to the reslts obtained when the PVP was measred by mbilical vein catheterization. 8 14 In addition, we stdied patients with featres of AH and again fond good agreement between WHVP and PVP (fig. 4). The relationship between WHVP and PVP appears to be drlferent in those patients with nonalcoholic liver disease (PBC and CAH). In these disorders there is a measrable presinsoidal component to the portal hypertension in many patients (figs. 5 and 6). A normal WHVP (5 mm Hg or less) accompanied by an elevated PVP was fond in 2 patients with CAH and cirrhosis, a relationship not observed in or ALD patients. This presinsoidal portal hypertension might reslt from an inflow block similar to that thoght to exist in idiopathic portal hypertension shown in the 4 patients listed in table 1. 10 The above-noted differences in WHVP and PVP led to concern that the WHVP might have changed dring the corse of the procedre. In 14 patients, therefore, WHVP and PVP were determined simltaneosly, and no changes in WHVP after the insertion of the transhepatic needle were observed, sggesting that the reslts wold have been similar if all of the procedres had been done simltaneosly. The existence of the spontaneos reversal of portal venos blood flow has been controversial. Althogh seen dring hepatic vein catheterization l5 and mbilical portography,16 hepatofgal flow has not been observed sing flowmeters at srgery, and therefore its existence FIG. 7. Radiological demonstration ofhepatofgal blood flow (case 45). Contrast material can be seen in the portal vein (P.V.) and left gastric vein (L.G.V.). The tortos vessels faintly otlined above the left gastric vein are esophageal varices.

April 1977 PORTAL VEIN PRESSURE MEASUREMENT 589 in cirrhotic patients has been qestioned. 17 The presence of tre hepatofgal flow in the Bdd-Chiari syndome l8 and after side-to-side portacaval shnt l9 is generally acknowledged. In 2 of or patients with ALD (cases 80 and 120), spontaneos reversal of portal venos flow was sggested on contrast injection in portal vein branches. In these patients spontaneos splenorenal shnts were fond by angiography, and they presmably were hemodynamically similar to patients with side-to-side portacaval shnt. 19 Acte liver cell injry in patients with alcoholic liver disease has been fond to case transient elevation of the WHVP.20 Patients with AH have also been fond to have angiographic evidence of portal venos stasis when actely ill, which then resolves dring hospitalization. 21 Hepatic arterial flow may be increased. 22 The obliteration of the central veins that occrs as a part of acte AH6 in some patients may create a sitation similar to that fond in the Bdd-Chiari syndrome and reslt in temporary retrograde portal flow. Evidence of hepatofgal flow (fig. 7) was observed in 1 patient (case 45) with severe AH. Retrograde flow was also seen in this patient when contrast material was injected throgh a catheter in the wedge position. The failre to observe hepatofgal flow at srgeryl7 may reflect the fact that patients with severe alcoholic hepatitis are not sbjected to elective shnt srgery. In or stdy the contrast material was hand-injected throgh a small caliber needle into a free-flowing venos system. The artificial creation of hepatofgal flow seems nlikely nless there is portal venos stasis, in which case the possibility exists that the observed retrograde flow is an artefact of the procedre. For optimm assessment of portal pressre, an intraabdominal zero reference point is needed in order to measre the portal-hepatic vein pressre gradient accrately, 8 this is readily provided dring WHVP measrement. Measrement of PVP alone by the transhepatic techniqe leaves one dependent on an external zero reference point. However, it is often possible to record both portal and hepatic venos pressres by the transhepatic techniqe, and this circmvents the problem of an internal reference point. Direct portal pressre measrement is obviosly more meaningfl than WHVP when there is presinsoidal resistance increase. In some patients, hepatic vein catheterization and direct portal measrement are complementary procedres and shold be performed together. REFERENCES 1. Moyers JD, Taylor W J: An estimation of portal venos pressre by occlsive catheterization of the hepatic venle. J Clin Invest 30:662-663, 1951 2. Bolvin R, Chevalier M, Galls P, et al: Contribtion a l'etde d syndrome d'hypertension portale: etde cliniqe et portografiqe. Acta Gastroenterol Belg 14:795-805, 1951 3. Gonzales OC: Portography: a preliminary report of a new techniqe via the mbilical vein. Clin Proc Child Hosp DC 15:120-122, 1959 4. Vennes J: Intrahepatic pressre: an accrate reflection of portal pressre. Medicine 45:445-452, 1966 5. Orrego-Matte H, Amenabar E, Lara G, et al: Measrement of intrahepatic pressre as index of portal pressre. Am J Med Sci 247:278-282, 1964 6. Edmondson HA, Peters RL, Reynolds TB, et al: Sclerosing hyaline necrosis ofthe liver in the chronic alcoholic. Ann Intern Med 59:646-673, 1963 7. Klatskin G, Kantor F: Mitochondrial antibody in primary biliary cirrhosis and other diseases. Ann Intern Med 77:533-541, 1972 8. Reynolds TB, Ito S, Iwatski S: Measrement of portal pressre and its clinical application. Am J Med 49:649-657, 1970 9. Okda K, Tanikawa K, Emra T, et al: Nonsrgical, perctaneos transhepatic cholangiography. Diagnostic significance in medical problems of the liver. Am J Dig Dis 19:21-36, 1974 10. Sama SK, Bhargava S, Gopinath N, et al: Noncirrhotic portal fibrosis. Am J Med 51:160-169, 1971 11. Bierman HR, Steinbach HL, White LP, et al: Portal venipnctre: a perctaneos trans-hepatic approach. Proc Soc Exp BioI Med 79:550-552, 1952 12. Viamonte M, LePage J, Lndeqist A, et al: Selective catheterization of the portal vein and its tribtaries. Radiology 114:457-460, 1975 13. Nabseth D, Widrich W, O'Hara E, et al: Flow and pressre characteristics of the portal system before and after splenorenal shnts. Srgery 78:739-748, 1975 14. Viallet A, Joly J, Marlea D, et al: Comparison of free portal venos pressre and wedged hepatic venos pressre in patients with cirrhosis of the liver. Gastroenterology 59:372-375, 1970 15. Warren W, Fomon J, Viamonte M, et al: Spontaneos reversal of portal venos blood flow in cirrhosis. Srg Gynecol Obstet 126:315-323, 1968 16. Kessler R, Tice D, Zimmon D: Retrograde flow of portal vein blood in patients with cirrhosis. Radiology 92:1038-1042, 1969 17. Moreno A, Brchell A, Reddy R, et al: Spontaneos reversal of portal blood flow. The case for and against its occrrence in patients with cirrhosis ofthe liver. Ann Srg 181:346-357,1975 18. Pollard JJ, Nebesar RA: Altered hemodynamics of the Bdd Chiari syndrome demonstrated by selective hepatic and selective splenic angiography. Radiology 89:236-243, 1967 19. Redeker A, Knelis C, Yamamoto S, et al: Assessment of portal and hepatic hemodynamics after side-to-side portacaval shnt in patients with cirrhosis. J Clin Invest 43:1464-1471, 1964 20. Leevy C, Zinke M, Baber J, et al: Observations on the inflence of medical therapy on portal hypertension in hepatic cirrhosis. Ann Intern Med 49:837-851, 1958 21. Miller F, Maddrey W, Sheff R, et al: Hepatic venography and hemodynamics in patients with alcoholic hepatitis. Radiology 115:313-317, 1975 22. Cohn IN, Khatri 1M, Groszmann RJ, et al: Hepatic blood flow in alcoholic liver disease measred by an indicator diltion technic. Am J Med 53:704-714, 1972