Hemodynamic Complications of Liver Cirrhosis
Overview
Liver cirrhosis — the end-stage of progressive hepatic fibrosis — fundamentally disrupts portal haemodynamics. Perisinusoidal fibrosis increases resistance to portal venous flow, driving portal hypertension, which triggers a cascade of life-threatening sequelae including variceal haemorrhage, ascites, hepatic encephalopathy, and hepatorenal syndrome.
Portal Hypertension
Defined as a Hepatic Venous Pressure Gradient (HVPG) > 5 mmHg. Clinically relevant complications emerge at HVPG > 10 mmHg (varices form) and variceal bleeding risk increases sharply above 12 mmHg.
- Cause: Sinusoidal resistance increased by fibrosis + reduced endothelial nitric oxide = reduced intrahepatic vasodilatation.
- Splanchnic vasodilation: High portal flow increases nitric oxide, causing profound systemic and splanchnic vasodilation, reducing effective central blood volume.
- RAAS activation: Compensatory activation of RAAS and sympathetic system causes sodium and water retention, driving ascites and oedema.
Portosystemic Shunts and Varices
- Oesophageal varices: Formed via left gastric (coronary) vein into the azygous/hemiazygous system. Most dangerous site of bleeding.
- Gastric varices (GOV1/GOV2/IGV): Supplied by short gastric or left gastric veins. More difficult to treat with banding.
- Caput medusae: Via paraumbilical veins to the umbilicus.
- Anorectal varices: Via inferior mesenteric to iliac/pudendal veins.
- Splenorenal shunt: Via splenic vein to left renal vein — largest naturally-occurring spontaneous shunt.
WarningVariceal Haemorrhage: Life-Threatening Emergency
Variceal haemorrhage carries a 6-week mortality of 15-20% even with optimal management. Emergency management: IV terlipressin (reduces portal pressure), urgent endoscopy with banding/sclerotherapy, and antibiotic prophylaxis (prevents SBP and reduces rebleed risk). Consider Sengstaken-Blakemore tube for massive uncontrolled haemorrhage. TIPS as rescue therapy.
Imaging of Portal Hypertension
- Ultrasound Doppler: Portal vein diameter >13 mm, loss of respiratory variation, reversed (hepatofugal) portal flow, splenomegaly, ascites.
- CT: Nodular liver contour, caudate lobe hypertrophy (relative sparing), varices (enhancing serpiginous structures), splenomegaly, ascites.
- TIPS placement: Transjugular Intrahepatic Portosystemic Shunt — creates a direct channel between hepatic vein and intrahepatic portal vein using a covered metallic stent.
High Yield Facts
LightbulbFRCR / MD Prep Pearl
The caudate lobe (Segment I) has direct hepatic venous drainage to the IVC and is therefore relatively spared in cirrhosis, leading to apparent 'caudate lobe hypertrophy' on imaging. A caudate:right lobe ratio >0.65 suggests cirrhosis. The liver surface nodularity on ultrasound has a high specificity for cirrhosis.