Cirrhosis is a medical condition characterized by the scarring of the liver. This scarring occurs when the liver attempts to repair itself after long-term damage from various causes, such as chronic alcohol use or viral hepatitis. As scar tissue replaces healthy liver tissue, the liver’s ability to function normally becomes impaired. This progressive scarring also affects how blood circulates through the liver, leading to complications throughout the body.
How Cirrhosis Affects Blood Vessels
The liver receives a substantial portion of its blood supply from the portal vein, which carries blood rich in nutrients from the digestive organs. In a healthy liver, this blood flows freely through a network of small blood vessels called sinusoids. With cirrhosis, the accumulating scar tissue creates increased resistance and obstruction to this blood flow within the liver.
This obstruction causes pressure to build up in the portal vein and its tributaries, a condition known as portal hypertension. This elevated pressure forces blood to seek alternative pathways to return to the heart, bypassing the scarred liver.
The body responds by opening and enlarging pre-existing, smaller blood vessels that are not typically used for high-volume blood flow. These new pathways, known as collateral circulation, act as bypass routes for the blood, diverting it from the liver into the systemic circulation. However, these collateral vessels are not designed to handle the increased pressure and volume of blood, making them fragile and prone to swelling and rupture. This process is a primary mechanism by which cirrhosis leads to vein complications throughout the body.
Types of Affected Veins and Their Manifestations
The increased pressure from portal hypertension causes various veins to enlarge, forming structures called varices in different parts of the body. Esophageal varices are swollen veins in the esophagus, the tube connecting the throat to the stomach. These are concerning because they can rupture and cause severe, life-threatening bleeding, often manifesting as vomiting blood or dark, tarry stools. Patients with esophageal varices may not experience symptoms until bleeding occurs, making early detection important.
Gastric varices are enlarged veins found in the stomach lining, often occurring alongside or extending from esophageal varices. While less common than esophageal varices, bleeding from gastric varices can be more severe, requiring immediate medical attention. Symptoms of bleeding gastric varices include bright red blood in stool, dark, tarry stools, dizziness, or vomiting blood.
Rectal varices are dilated blood vessels that develop in the rectum, typically due to portal hypertension. Unlike common hemorrhoids, rectal varices are a direct consequence of the liver’s condition and may not cause pain until significant bleeding occurs. Signs can include painless rectal bleeding, blood in the stool, or symptoms of anemia such as fatigue and dizziness.
Caput medusae describes a pattern of visibly swollen veins radiating outwards from the navel across the abdomen. This appearance is due to the re-opening and enlargement of the umbilical and paraumbilical veins, which normally close after birth. These veins become engorged as they attempt to shunt blood away from the high-pressure portal system to systemic veins, serving as a visible sign of severe portal hypertension.
Detecting and Managing Vein Complications
Detecting vein complications in cirrhosis often involves a combination of diagnostic methods. Endoscopy, specifically an esophagogastroduodenoscopy (EGD), is frequently used to visualize and assess varices in the esophagus and stomach. For patients with cirrhosis, screening endoscopy is recommended to identify varices before they bleed. Imaging techniques, such as CT scans, MRI, and Doppler ultrasound, can also help identify dilated collateral vessels and assess blood flow patterns related to portal hypertension.
Managing these vein complications focuses on preventing and treating bleeding episodes. Medications like non-selective beta-blockers (e.g., propranolol or nadolol) are often prescribed to reduce pressure in the portal vein system and lower the risk of bleeding. Carvedilol is another beta-blocker that may be more effective in reducing portal pressure.
Endoscopic therapies are frequently employed for direct intervention. Endoscopic variceal ligation (EVL), or banding, involves placing small elastic bands around enlarged veins to cut off their blood supply, causing them to shrink. Endoscopic injection sclerotherapy (EIS) involves injecting a special chemical into the varix to induce scarring and close the vein, though EVL is generally preferred due to fewer complications.
For severe or refractory bleeding, shunting procedures like Transjugular Intrahepatic Portosystemic Shunt (TIPS) may be performed. TIPS creates a new pathway within the liver to divert blood flow and reduce portal pressure, thereby alleviating complications like bleeding varices and fluid buildup. Prompt medical attention is paramount for any suspected bleeding episode from these veins.