Liver disease, particularly when it advances to significant scarring known as cirrhosis, is a major cause of gastrointestinal (GI) bleeding. This life-threatening complication results from two primary issues: mechanical problems related to increased pressure and systemic issues involving the body’s inability to clot blood effectively. The damaged liver forces blood to find alternate, fragile routes that are prone to rupture, while simultaneously failing to produce the substances needed to stop the bleeding.
The Foundation: Understanding Portal Hypertension
The primary mechanism driving GI bleeding in liver disease is portal hypertension. The portal vein collects nutrient-rich blood from the entire digestive tract, spleen, and pancreas, carrying it directly into the liver for processing. This system is normally designed to handle a large volume of blood at a relatively low pressure.
In advanced liver disease, such as cirrhosis, the normal liver tissue is replaced by rigid, fibrous scar tissue. This dense scarring acts like a constricted filter, physically obstructing the smooth flow of blood through the liver’s internal pathways. The resistance to flow causes a significant and sustained backup of pressure in the portal vein system.
Portal hypertension is specifically defined as an elevated pressure gradient within the portal venous system. This occurs when the pressure difference between the portal vein and the systemic veins exceeds 5 millimeters of mercury (mm Hg). This pressure buildup is the direct cause of the mechanical complications that follow.
The increased pressure also triggers the release of chemicals that cause the blood vessels supplying the gut to widen, or vasodilate. This widening further increases the volume of blood flowing into the portal system, compounding the existing pressure problem. The resulting high pressure forces blood into fragile, high-risk vessels throughout the gastrointestinal tract.
The Direct Cause: Fragile Varices and Bleeding Sites
The body attempts to relieve the massive pressure of portal hypertension by redirecting the backed-up blood through alternative, low-resistance pathways. This involves enlarging small, pre-existing veins that bypass the blocked liver, creating collateral circulation. These new, abnormal vessels are known as varices, and they are the most dangerous source of GI bleeding.
Varices are swollen, convoluted veins that form where the portal system connects to the main systemic circulation. They are fragile because their walls are thin and not designed to withstand the high pressure forced through them. The most common and life-threatening sites for these varices are the lower esophagus and the stomach, leading to esophageal and gastric varices.
The intense portal pressure causes tension on the varix wall, eventually exceeding the tissue’s elastic limits and causing the vessel to rupture and bleed profusely. Variceal bleeding is an acute medical emergency and accounts for the majority of severe GI bleeding episodes in people with cirrhosis. Approximately 90% of individuals with cirrhosis develop varices, and up to a third will experience a bleeding event.
Another source of bleeding is portal hypertensive gastropathy. Chronic high pressure causes changes in the lining of the stomach and intestines, making capillaries dilated, congested, and prone to injury. This gastropathy typically results in slow, chronic blood loss that can lead to anemia.
Compounding the Problem: Deficiency in Clotting Factors
While mechanical issues initiate the bleeding, the impaired function of the damaged liver systemically hinders the body’s ability to stop the hemorrhage. The liver is primarily responsible for synthesizing almost all the proteins that make up the coagulation cascade, the sequence of steps required to form a stable blood clot.
When the liver is severely damaged, its synthetic capacity is dramatically reduced, leading to a deficiency in many coagulation factors. This deficiency results in impaired clotting, or coagulopathy, making any bleeding event difficult to control. The prolonged bleeding time further complicates the management of a GI bleed.
Liver disease also causes a low platelet count, known as thrombocytopenia. Portal hypertension causes blood to back up into the spleen, leading to its enlargement (hypersplenism). The enlarged spleen traps and sequesters an excessive number of platelets, removing them from circulation and weakening the body’s ability to form a clot.
The liver also produces thrombopoietin, a hormone that stimulates the bone marrow to produce platelets; liver dysfunction reduces this hormone’s production. The combination of reduced clotting factors and a lower platelet count means that systemic mechanisms to plug a leak are severely compromised. This often leads to massive and fatal hemorrhage once a fragile varix ruptures.