Budd Chiari syndrome (BCS) is a condition arising from hepatic venous outflow tract obstruction (HVOTO) arising at the level of hepatic veins, inferior vena cava, right atrium or a combination of these. It can be classified as primary or secondary depending upon the underlying pathophysiology. Regardless of the cause of HVOTO, there is lack/complete absence of hepatic venous drainage leading to constellation of symptoms pertaining to portal hypertension with radiologically visible intrahepatic and extrahepatic porto-systemic collaterals. The presence of these collateral systems provide imaging diagnostic clue in chronic cases with cirrhosis labelled as chronic liver disease and thereby establishing the primary cause of cirrhosis to be BCS. Current essay aims to provide in depth knowledge of collateral pathways of BCS.

Budd Chiari syndrome (BCS) is a condition arising from hepatic venous outflow tract obstruction (HVOTO) arising at the level of hepatic veins, inferior vena cava, right atrium or a combination of these. It can be classified as primary or secondary depending upon the underlying pathophysiology. Epidemiologically the causes of primary BCS in western countries include the hepatic venous thrombosis/IVC thrombosis due to systemic disease in contrast to membranous or segmental obstruction of IVC in the Asian countries. Secondary causes by far remain similar like malignant obstructing masses or compressing mass lesions, etc. Regardless of the cause of HVOTO, there is lack/complete absence of hepatic venous drainage leading to constellation of symptoms pertaining to portal hypertension with radiologically visible intrahepatic and extra hepatic porto-systemic collaterals. The presence of these collateral systems provide imaging diagnostic clue in chronic cases with cirrhosis labelled as chronic liver disease and thereby establishing the primary cause of cirrhosis to be BCS. Therefore the knowledge of these collateral pathways is essential in order to achieve correct diagnosis of BCS so as to allow for timely intervention. The primary aim of this essay is to describe the collateral pathways seen on MDCT (Multi Detector Computed Tomography) venography of abdomen. We present the current essay from the case of a 25 year old female patient diagnosed as chronic liver disease (CLD) presenting with pain abdomen, ascites and deranged liver functions with a history of single episode of upper GI bleed. Viral markers were negative and diagnosis of cryptogenic CLD was sought for till the CECT abdomen revealed it to be case of chronic Budd Chiari syndrome with extensive venous collateralisation.

A CT examination was conducted on a 256 slice, dual source CTmodel SOMATOM Definition FLASH. CECT (contrast enhanced computed tomography) abdomen was performed from the dome of diaphragm till the pelvic outlet. NCCT (noncontrast computed tomography) scan was done prior to triple phase scan of the abdomen which consisted of arterial, porto venous and delayed phases. The phases were obtained with empirically timed scans using a bolus injector with arterial phase obtained between 20- 30 s, portovenous/hepatic venous phase 60-70 s and delayed phase at 120 s. The injection rate was between 3.5-4 ml/s and contrast injection was followed by saline chase 30 ml at the rate of 3 ml/s. 80 ml of contrast was given for the study.

With Regards,
Sara Giselle
Associate Managing Editor