NON-CIRRHOTIC PORTAL FIBROSIS CAUSING PORTAL HYPERTENSION

Portal hypertension is more prevalent in patients with liver cirrhosis and occurs infrequently in those without liver cirrhosis. Non-cirrhotic portal brosis (NCPF) and extrahepatic portal venous obstruction (EHPVO) are the two most common causes of non-cirrhotic portal hypertension. Unlike EHPVO, NCPF does not cause thrombosis of the extrahepatic portal vein. Sclerosis of the portal vein's medium and small branches occurs in NCPF. In NCPF, the hepatic venous pressure gradient (HVPG) is normal, in contrast to cirrhosis, where it is increased. Additionally, NCPF is referred to as non-cirrhotic intrahepatic portal hypertension (NCIPH), idiopathic portal hypertension, hepatoportal sclerosis, and benign intrahepatic portal hypertension. It is a disease with an unknown etiology that primarily affects middle-aged males and females and manifests as hematemesis and massive splenomegaly

New Classification of Gastric Varices: A Twenty-Year Experience

Objectives Gastric varices (GV) have been classified by the Sarin classification for over two decades. However, a subset of these varices does not fit into this classification. We share our experience on GV in past 20 years and propose a modification. Materials and Methods Consecutive patients with portal hypertension (PHT) posted for esophagogastroduodenoscopy were screened for GV between 1996 and 2016 at a tertiary-care hospital. GV were categorized as gastroesophageal varices (GOV1, GOV2) and isolated gastric varices (IGV1, IGV2) by Sarin’s classification. Patients with varices in esophagogastric region as well as distally in the stomach or duodenum, thus having efferent drainage into the superior as well as inferior vena cava simultaneously, remain unclassified and were coined as GOV3. Statistical Analysis Descriptive data was represented as mean (standard deviation) or median (interquartile range) or number (percentage). Chi-squared test, t-test, and logistic regression were done to compare groups and identify outcomes of interest. Results GV were recognized in 400 (11.5%) of 3,476 patients with PHT. Underlying disease was cirrhosis in 301 (75.2%), extrahepatic portal venous obstruction in 78 (19.5%), noncirrhotic portal fibrosis in 18 (4.5%) and Budd–Chiari syndrome in 3 (0.75%) patients with GV. GOV1, GOV2, IGV1, IGV2, and combined GOV1 with GOV2 were seen in 170 (42.5%), 154 (38.5%), 17 (4.3%), 5 (1.3%), and 12 (3.0%) patients; respectively. GOV3 were identified in 42 (10.5%) patients. Ninety-three patients with GV presented with gastrointestinal bleed and frequency of GOV2 was higher and GOV1 and GOV3 were lower among bleeders than non-bleeders. Conclusions A significant proportion of patients with GV remain uncategorized by current classification among PHT patients. Addition of GOV3 in Sarin’s classification will make it more comprehensive, uniform, and reproducible for future studies.

Endoscopic Biliary Stenting for Portal Biliopathy Perforating Paracholedochal Collateral: A Rare Complication

Extrahepatic portal venous obstruction (EHPVO) usually presents with upper gastrointestinal bleed in the first decade of life. Symptomatic portal hypertensive biliopathy is seen in a minority of patients with EHPVO. With use of endoscopic intervention, biliary drainage is maintained in these patients. Various procedural complications have been linked while performing endoscopic retrograde cholangiography and stenting; however, these are managed conservatively. Here, we are highlighting a case of EHPVO with symptomatic portal biliopathy in which the patient bled from paracholedochal collateral after biliary stenting and was managed successfully with a multidisciplinary approach.

Endoscopic Biliary Stenting for Portal Biliopathy Perforating Paracholedochal Collateral: A Rare Complication

ABSTRACTExtrahepatic portal venous obstruction (EHPVO) usually presents with upper gastrointestinal bleed in the first decade. Symptomatic portal hypertensive biliopathy is seen in minority of patients with EHPVO. With the use of endoscopic intervention, biliary drainage is maintained in these patients. Various procedural complications have been linked while performing endoscopic retrograde cholangiography and stenting; however, these are managed conservatively. Here, we are highlighting a case of EHPVO with symptomatic portal biliopathy who bled from paracholedochal collateral after biliary stenting and managed successfully with multidisciplinary approach.