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Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Ultrasonic evaluation of portosystemic collateral circulation in portal hypertension
S G Sheth1, D N Amarapurkar, K B Chopra
1TN Medical College, Bombay.
Insights
Portosystemic collateral circulation decompresses portal hypertension, preventing or reducing esophageal varices. This circulation is more common in non-cirrhotic patients and those treated with sclerotherapy, and does not cause ascites.
Area of Science:
- Gastroenterology
- Hepatology
- Vascular Medicine
Background:
- Portal hypertension is a serious condition characterized by elevated pressure in the portal vein system.
- Portosystemic collateral circulation develops as a compensatory mechanism to decompress the portal system.
- Understanding the role of collateral circulation is crucial for managing portal hypertension and its complications.
Purpose of the Study:
- To evaluate portosystemic collateral circulation in patients with portal hypertension.
- To assess the relationship between collateral circulation and etiological groups, esophageal varices, sclerotherapy, and ascites.
- To elucidate the decompressive role of portosystemic circulation in portal hypertension.
Main Methods:
- A prospective study involving 101 patients diagnosed with portal hypertension.
- Patients were categorized into four etiological groups: Alcoholic Cirrhosis (ALD), Non-alcoholic Cirrhosis (NALD), Non-cirrhotic Portal Fibrosis (NCPF), and Extrahepatic Portal Vein Obstruction (EHPVO).
- Esophageal varices were endoscopically graded, and other portosystemic collaterals were evaluated using ultrasonography.
Main Results:
- Portosystemic collaterals were observed in 26% of patients, being more frequent in non-cirrhotic groups (NCPF and EHPVO) than in cirrhotic groups (ALD and NALD).
- Collateral shunts were more prevalent in patients without esophageal varices and those who had undergone esophageal sclerotherapy.
- Gallbladder varices were the only ectopic varices identified, with an incidence of 3.96%.
Conclusions:
- Portosystemic collateral circulation plays a significant decompressive role in portal hypertension.
- This circulation appears to prevent the formation or progression of esophageal varices.
- Collateral circulation was not found to contribute to the development of ascites and was more common in non-cirrhotic patients and those treated with sclerotherapy.
Abstract:
The aim of the study was to evaluate portosystemic collateral circulation in relation to (1)individual etiological groups of portal hypertension., (2) Presence and size of esophageal varices, (3) esophageal sclerotherapy and (4) ascites. A prospective study of 101 patients of portal hypertension was carried out. Patients were divided into 4 etiological groups: Alcoholic cirrhosis (ALD) (38), Non-alcoholic cirrhosis (NALD) (35), non cirrhotic portal fibrosis (NCPF) (14) and extrahepatic portal vein obstruction (EHPVO) (14). Esophageal varices were assessed and graded endoscopically into 3 categories: no varix, small varices and large varices. Evaluation of portosystemic collateral circulation, other than esophageal varices was done ultrasonically. "Other" portosystemic collaterals (lienorenal, gastrorenal, dilated paraumbilical and umbilical veins, paraduodenal and gall bladdes varices) were seen in 26 out of 101 patients and more commonly in the non-cirrhotic groups (50%) [NCPF: 57.14%, EHPVO: 42.86%] than in the cirrhotic group (16.44%) [ALD: 13.5%, NALD: 20%]. Gall bladder varices were the only form of ectopic (extra esophagogastric) varices visualised with an overall incidence of 3.96%. Collateral shunts were seen more frequently in patients without varices (100%), than in patients with small varices (34.88%) or large varices (7.84%), and in patients having undergone esophageal sclerotherapy (57.14%). Collateral circulation did not contribute to the development of ascites. 37 patients with ascites did not have collateral shunts. We conclude portosystmic circulation plays a decompressive role in portal hypertension and prevents formation of esophageal varices or prevents them from increasing in size. It is seen more frequently in noncirrhotic patients and in those having undergone sclerotherapy and does not contribute to development of ascites.
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