Radionuclide hepatic perfusion index and ultrasonography: assessment of portal hypertension in clinical practice
Seidlová, V.; Hobza, J.; Pumprla, J.; Charouzek, J.
Acta Universitatis Palackianae Olomucensis Facultatis Medicae 122: 213-221
1989
ISSN/ISBN: 0301-2514 PMID: 2530818 Document Number: 331516
The final value of portal blood flow pressure depends on the degree of vascular obstruction, then on the resistance in collateral vessels and, last, on splanchnic blood flow. The initiating cause of portal hypertension most often lies in advancing anatomical damage leading to increased resistance and, consequently, to a reduction of portal blood flow, and simultaneous reciprocal development of extrahepatic collaterals. The determination of a true portal flow is a necessity particularly when deciding about a shunt surgery and its type, but it also supplies valuable information on the degree of portal flow restriction and, in this way, on the progress of pathophysiological changes, their extent and advance. The technique of radionuclide angiography and determination of the hepatic perfusion index (HPI) proposed by Sarper appears to be a profitable noninvasive method supplying well reproducible information on portal blood flow. Sarper proved it to be correlated with the degree of portal hypertension established by angiography. Ultrasonographic criteria of portal hypertension include dilatation of the portal vein in the region of the hilus hepatis exceeding 15 mm, and a more than 10 mm dilatation of the splenic vein above the spine. The mean HPI value obtained from the examination of 19 subjects without liver involvement was 0.6956 .+-. 0.0583. The group of chronic hepatopathies included 19 patients with bioptically verified chronic hepatitis without reconstruction and/or steatosis, and 32 patients with liver cirrhosis likewise confirmed by biopsy: portosystemic shunts could be demonstrated in 14 of the latter. The presence of collaterals was verified by x-ray proof of oesophageal varices, next by sequentional splenoportography and by In-MAA deposition in Lung bed after its intrasplenic application. The mean HPI value of 0.6739 .+-. 0.127 for chronic hepatitis without reconstruction did not differ significantly from the normal group. The cirrhotics had the HPI (0.45 .+-. 0.14) significantly reduced both against the normal subjects and patients with proved collaterals (0.39 .+-. 0.14), while cirrhoses without collaterals had their HPI 0.498 .+-. 0.119. There is a statistically significant difference between both the cirrhotic subgroups at 5% level. We could prove good reproducibility at repeated examination of patients after a brief time interval and of those with a stabilized picture. On the other hand, good correlation between unfavourable clinical progress and development of portal hypertension and HPI decrease could be demonstrated. Ultrasonography discovered manifestations of portal hypertension in the cirrhotic group for 56.2% of those examined, dilatation of the portal vein, simultaneous dilatation of the splenic vein in a total of 34.6%. Joining the methods of sonography and radionuclide determination of the hepatic perfusion index appears to be an addition to the existing examination methods in hepatology for the assessment of portal hypertension.