‘Latent’ Portal Hypertension in Benign Biliary Obstruction

Abstract

A prospective study was undertaken to evaluate the changes in portal venous pressure in patients with benign biliary obstruction (BBO) but without overt clinical, endoscopic or radiological evidence of portal hypertension. Portal venous pressure was measured at laparotomy in 20 patients (10 each with either benign biliary stricture or choledocholithiasis) before and after biliary decompression. Pressure was found to be on the high side in seven patients (>25 cm of saline in three patients and > 30 cm of saline in four). The mean fall of pressure was 3.4 cm of saline after biliary decompression. No correlation could, however, be found between portal venous pressure and duration of biliary obstruction, serum bilirubin or bile duct pressure. Liver histology showed mild to moderate cholestatic changes but maintained portal architecture in all. Benign biliary obstruction may therefore, lead to elevation of portal pressure, even though the patient may not necessarily have any clinical, endoscopic or radiological manifestations of portal hypertension. The pathogenesis of this ‘latent’ portal hypertension is probably multifactorial. If biliary obstruction is left untreated the development of overt portal hypertension may become a possibility in the future.

Liver histology in benign biliary stricture: Fibrosis to cirrhosis . . . and reversal?

“…In a previous study by our group, patients with benign obstructive jaundice, namely PCBDS and choledocholithiasis, were reported to have “latent portal hypertension” that was immediately reversed following relief of biliary obstruction. Liver biopsy showed cholangiohepatitis in the majority of these patients, although no specific grading system was used in that study 8 . On review, with the use of the scoring system in the present study, we observed that all the patients in the previous study did have varying degrees of fibrosis.…”

Correlations of portal pressure in post‐cholecystectomy benign biliary stricture

“…It has also been suggested that periportal fibrosis plays a pivotal role in the development of PH. However, other factors like hepatocyte hyperplasia and increased intraductal biliary pressure are also important . The duration of biliary obstruction is directly related to the reversal of microscopic and hemodynamic changes of PH caused by experimental ligation of the bile duct, and a similar association has been reported in two retrospective studies in humans …”

“…However, other factors like hepatocyte hyperplasia and increased intraductal biliary pressure are also important. [8][9][10] The duration of biliary obstruction is directly related to the reversal of microscopic and hemodynamic changes of PH caused by experimental ligation of the bile duct, 11,12 and a similar association has been reported in two retrospective studies in humans. 13,14 We measured the portal pressure (PP) in patients with post-cholecystectomy benign biliary stricture (PCBBS) and assessed its relationship with the injury repair interval (IRI), bile duct pressure (BP), severity of hepatic fibrosis (FS) and other factors.…”

“…The normal PP obtained by this method is controversial; on the basis of a study by Moreno et al . we considered a PP of up to 30 cm of saline (or 21.9 mmHg) to be normal; other authors have used a similar cut‐off …”

“…The normal PP obtained by this method is controversial; on the basis of a study by Moreno et al we considered a PP of up to 30 cm of saline (or 21.9 mmHg) to be normal; other authors have used a similar cut-off. 10,15,[42][43][44] In conclusion, PP in patients with PCBBS has a good positive correlation with IS and a fair positive correlation with both FS and IRI, whereas PP has no direct correlation with BP and OBPS. Prospective trials are needed to confirm this correlation and to evaluate the mechanism of fall in PP following biliary decompression.…”