Oesophageal and Gastric Varices
Oesophageal and gastric varices are dilated, fragile veins that develop as a consequence of portal hypertension. They form when blood is diverted from the high-pressure portal system into low-pressure systemic veins. While this diversion temporarily reduces portal pressure, it creates vessels that are highly prone to rupture. Variceal bleeding is one of the most life-threatening complications of liver disease.
What You Need to Know
Oesophageal and gastric varices are a direct consequence of portal hypertension, where resistance to blood flow through the liver causes sustained elevation of pressure within the portal venous system. As this pressure rises, blood is diverted away from the liver through portosystemic collateral pathways that connect the portal and systemic circulations. One of the most clinically important sites of collateral formation is the gastro-oesophageal junction, where veins are thin-walled and structurally unsuited to accommodate high pressure or increased blood flow.
As portal hypertension progresses, veins in this region dilate and lengthen, forming varices that sit just beneath the mucosal surface. These vessels are exposed to both haemodynamic stress and mechanical irritation from swallowing, gastric distension, or vomiting. As the vessel walls stretch, they become increasingly fragile, meaning that relatively small changes in portal pressure can precipitate rupture. When bleeding occurs, it is often abrupt and severe, presenting as massive upper gastrointestinal haemorrhage with a high risk of haemodynamic instability.
Several factors influence the likelihood of bleeding, and these are important to understand when assessing risk and disease progression:
the degree of portal pressure elevation and ongoing splanchnic blood flow (increased blood flow to the gastrointestinal circulation)
the size and location of varices, with large oesophageal and fundal gastric varices carrying higher risk
underlying liver function, as worsening cirrhosis is associated with poorer vascular integrity and impaired haemostasis
Alcohol is a key driver in this process for many patients. Chronic alcohol exposure promotes hepatic fibrosis, increasing resistance within the liver, while also causing splanchnic vasodilation that increases blood flow into the portal system. Continued alcohol intake therefore compounds portal hypertension and substantially increases the risk of both first-time and recurrent variceal bleeding. Sustained abstinence plays a central role in slowing disease progression and reducing future bleeding risk.
Beyond the Basics
Portosystemic shunting at the gastro-oesophageal junction
Varices develop at anatomical sites where the portal and systemic circulations naturally communicate. At the gastro-oesophageal junction, blood from the left gastric vein, which normally drains into the portal venous system, is diverted into oesophageal veins that empty into the systemic circulation via the azygos system. When portal pressure rises, this pathway becomes a major route for decompression of the portal system. The oesophageal and gastric veins involved are thin-walled and lack the structural support required to tolerate sustained high pressure, making them vulnerable to progressive dilation.
As portal hypertension persists, these vessels become elongated and tortuous, forming varices that lie just beneath the mucosal surface. Their superficial location increases susceptibility to mechanical stress from swallowing, gastric distension, or reflux. Unlike arteries, these veins are not designed to regulate flow under pressure, so ongoing exposure to elevated portal pressure leads to gradual structural failure rather than adaptive remodelling.
Wall tension and risk of rupture
The risk of variceal rupture is determined by wall tension rather than vessel size alone. Wall tension refers to the force exerted on the vessel wall as a result of intraluminal pressure acting over the vessel radius. As varices enlarge, the radius increases while the vessel wall becomes thinner, creating a situation where even modest rises in pressure can produce a large increase in wall stress. This explains why some small-appearing varices may bleed and why not all large varices rupture predictably.
Acute increases in intra-abdominal pressure can act as immediate triggers for bleeding. Events such as coughing, vomiting, straining during defecation, or heavy lifting transiently increase pressure within the portal system. In a fragile varix with high baseline wall tension, these short-lived pressure spikes may be sufficient to cause rupture, leading to sudden and severe upper gastrointestinal haemorrhage.
Role of portal pressure thresholds
Clinically significant varices usually develop once portal pressure exceeds a critical threshold, commonly described using the hepatic venous pressure gradient. Below this level, collateral formation is limited and the risk of bleeding is low. Once the threshold is exceeded, collateral vessels enlarge rapidly and bleeding risk rises sharply. This pressure-dependent behaviour explains why portal hypertension severity correlates more closely with bleeding risk than liver disease stage alone.
Management strategies focus on lowering portal pressure rather than treating varices as isolated lesions. Pharmacological therapies aim to reduce portal inflow through splanchnic vasoconstriction (narrowing of blood vessels supplying the gut, which reduces blood flow into the portal system), while procedural interventions reduce resistance within the portal system or divert blood flow. Lowering portal pressure below the bleeding threshold reduces the likelihood of first-time and recurrent haemorrhage.
Impact of liver dysfunction and coagulopathy
Advanced liver disease commonly coexists with abnormalities of haemostasis (the body’s ability to form and maintain a stable clot). Reduced synthesis of clotting factors occurs due to impaired hepatocyte function, while thrombocytopenia develops as a result of hypersplenism, where an enlarged spleen sequesters platelets. Variceal bleeding is primarily driven by elevated pressure, but these haemostatic changes increase bleeding severity and make haemorrhage more difficult to control.
The combination of high-pressure venous rupture and reduced clot stability explains why variceal bleeding can be rapid, profuse, and life-threatening. Ongoing bleeding can also worsen coagulation through consumption of clotting factors and dilution from large-volume resuscitation, which adds to the difficulty of achieving haemostasis.
Alcohol and recurrent variceal bleeding
Alcohol accelerates disease progression by sustaining liver inflammation and fibrosis, which increases intrahepatic resistance and worsens portal hypertension. It also increases portal inflow through ongoing splanchnic vasodilation (widening of blood vessels supplying the gut, which increases blood entering the portal circulation). Continued alcohol use is strongly associated with recurrent variceal bleeding and increased mortality.
Even after successful control of an initial bleed, ongoing alcohol intake keeps portal pressure high and promotes re-bleeding. Sustained abstinence reduces ongoing liver injury, supports improvement in portal pressure over time, and remains one of the most effective strategies to reduce recurrence.
Clinical Connections
Variceal bleeding most commonly presents with haematemesis, melaena, or features of hypovolaemic shock such as tachycardia, hypotension, and altered level of consciousness. Bleeding is often sudden and severe because rupture occurs under high venous pressure and is compounded by impaired haemostasis in advanced liver disease. In people with known cirrhosis or established portal hypertension, variceal haemorrhage should be considered a likely cause of any upper gastrointestinal bleeding until proven otherwise. Diagnosis is confirmed with urgent upper gastrointestinal endoscopy, which allows direct visualisation of oesophageal or gastric varices and enables therapeutic intervention at the same time.
Clinical deterioration can occur rapidly, particularly when bleeding is ongoing or recurrent. Encephalopathy may develop or worsen due to hypovolaemia, reduced hepatic clearance of toxins, or increased nitrogen load from gastrointestinal bleeding. Airway compromise is a major risk in patients with active haematemesis, reduced consciousness, or agitation. Early recognition of physiological instability and complications is therefore central to improving outcomes.
Key clinical features that guide assessment and escalation include:
evidence of active bleeding, such as ongoing haematemesis or fresh melaena
signs of circulatory compromise, including hypotension, tachycardia, or rising lactate
neurological changes suggesting hepatic encephalopathy, particularly in the context of bleeding or infection
Screening plays a critical role in reducing first-bleed risk. In patients with cirrhosis, routine endoscopic screening is used to identify oesophageal or gastric varices before bleeding occurs. The presence, size, and appearance of varices inform the need for prophylactic therapy, such as non-selective beta blockers to reduce portal pressure or endoscopic band ligation for high-risk varices. These strategies target portal hypertension directly and have been shown to reduce the incidence of first-time haemorrhage and improve survival.
Long-term management focuses on preventing recurrence and addressing modifiable drivers of disease progression. Ongoing portal hypertension, poor liver function, and continued alcohol use markedly increase re-bleeding risk. Sustained alcohol abstinence, adherence to follow-up endoscopy, and optimisation of portal pressure–lowering therapies are central to reducing recurrence and improving long-term outcomes after an initial variceal bleed.
Concept Check
Why do varices commonly form at the gastro-oesophageal junction?
How does portal pressure influence variceal formation and rupture?
Why are varices prone to sudden, severe bleeding?
How does liver-related coagulopathy worsen variceal haemorrhage?
Why does continued alcohol intake increase recurrence risk?