What is Variceal Hemorrhage
Variceal hemorrhage is bleeding from dilated portosystemic collateral veins (varices) that develop in the esophagus or stomach as a consequence of portal hypertension, most commonly due to cirrhosis, and represents the most lethal complication of chronic liver disease with a 6-week mortality of at least 20%. 1
Pathophysiology and Development
Portal hypertension drives variceal formation when the hepatic venous pressure gradient (HVPG) reaches 10-12 mmHg, creating abnormal collateral vessels that divert portal blood into the systemic circulation. 1
The mechanism involves two key components:
- Increased intrahepatic resistance from architectural distortion due to fibrous tissue and regenerative nodules, plus active vasoconstriction accounting for 20-30% of resistance 1
- Increased portal blood inflow from splanchnic arteriolar vasodilation that occurs simultaneously with collateral formation 1
Types of Varices
Esophageal Varices
- Present in approximately 50% of all cirrhotic patients 1
- Prevalence correlates directly with disease severity: 40% in Child A patients versus 85% in Child C patients 1
- Develop at a rate of 8% per year in patients without existing varices 1
Gastric Varices
- Less common, occurring in 5-33% of patients with portal hypertension 1
- Classified as gastroesophageal varices (GOV) when extending from esophageal varices, or isolated gastric varices (IGV) when occurring independently 1
- GOV1 varices extend along the lesser curvature and are managed like esophageal varices 1
- GOV2 and fundal varices are more tortuous and have higher bleeding risk 1
Clinical Definition of Variceal Hemorrhage
A clinically significant variceal hemorrhage episode requires:
- Bleeding from an esophageal or gastric varix confirmed at endoscopy, OR large varices with blood in the stomach and no other identifiable bleeding source 1
- Transfusion requirement of ≥2 units of blood within 24 hours 1
- **Systolic blood pressure <100 mmHg** or postural change >20 mmHg, and/or pulse rate >100 beats/min at presentation 1
Risk Factors for Bleeding
The most critical predictor is variceal size, with large varices (>5 mm) carrying a 15% yearly bleeding risk. 1
Additional high-risk features include:
- Decompensated cirrhosis (Child B/C classification) 1
- Red wale marks (longitudinal dilated venules resembling whip marks on the variceal surface) 1
- Red spots (localized reddish mucosal areas on the varix surface) 1
- HVPG ≥20 mmHg measured within 24 hours of bleeding predicts failure to control bleeding (83% vs 29%) and higher 1-year mortality (64% vs 20%) 1
Natural History and Prognosis
Variceal hemorrhage occurs at a yearly rate of 5-15% in patients with varices. 1
Mortality and Rebleeding
- At least 20% mortality at 6 weeks despite modern therapy 1
- Spontaneous cessation occurs in up to 40% of patients, but this does not eliminate the need for definitive treatment 1
- Early rebleeding (within first week) occurs more frequently in patients with HVPG ≥20 mmHg 1
- Late rebleeding occurs in approximately 60% of untreated patients, mostly within 1-2 years of the index hemorrhage 1
Acute Management Principles
Variceal hemorrhage is a medical emergency requiring immediate intervention with a structured approach:
- Vasoactive drug therapy (terlipressin, somatostatin, or octreotide) should be initiated as soon as variceal bleeding is suspected, before endoscopic confirmation 1
- Antibiotic prophylaxis (ceftriaxone or norfloxacin) must be started immediately 1
- Restrictive transfusion strategy with hemoglobin threshold of 7 g/dL and target range of 7-9 g/dL 1
- Early diagnostic endoscopy within 12 hours for confirmation and endoscopic band ligation 1
- Vasoactive drugs continued for 3-5 days after bleeding control to prevent early rebleeding 1
Common Pitfall
Do not delay vasoactive drug therapy waiting for endoscopic confirmation—treatment should begin as soon as variceal bleeding is clinically suspected based on presentation in a cirrhotic patient with upper GI bleeding. 1