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Emergency and Acute Medicine: Varices
Esophageal varices develop as a consequence of Portal hypertension, where increased portal venous pressure leads to the formation of portal–systemic collateral vessels. At the gastroesophageal junction, these collaterals become fragile submucosal veins prone to rupture, resulting in life-threatening upper gastrointestinal bleeding.
Variceal bleeding accounts for approximately 10–30% of all upper GI hemorrhage and up to 90% of bleeding episodes in patients with cirrhosis. About 30% of cirrhotic patients will experience a variceal hemorrhage, with a mortality rate of around 30% per episode and a high recurrence rate of up to 70%. The most common underlying cause in adults is cirrhosis due to alcohol use or chronic hepatitis, although other causes include metabolic storage diseases such as Wilson disease or hemochromatosis. In certain regions, such as the Middle East, schistosomiasis is a major cause. In children, causes include biliary atresia, cystic fibrosis, and other intrahepatic obstructive disorders.
Patients typically present with signs of acute upper GI bleeding, including hematemesis, melena, or hematochezia (in severe cases). They may also show signs of hypovolemia such as tachycardia, hypotension, cool clammy skin, and altered mental status. Stigmata of chronic liver disease—such as jaundice, ascites, spider angiomata, and hepatosplenomegaly—are often present. In severe cases, patients may lose 20–40% of their total blood volume. Importantly, hematochezia in an unstable patient should be considered an upper GI bleed until proven otherwise.
Diagnosis is primarily clinical, supported by laboratory and endoscopic evaluation. Initial labs should include CBC, coagulation profile, renal function tests, and type and cross-match for transfusion. Hemoglobin may initially be normal despite significant blood loss, so serial measurements are essential. A BUN-to-creatinine ratio greater than 30 suggests significant upper GI bleeding. Definitive diagnosis and treatment are achieved via emergent endoscopy, which allows visualization and intervention.
Management in the emergency setting focuses on rapid stabilization and control of bleeding. Airway protection is critical, and early intubation is often recommended, especially in patients with altered mental status or massive bleeding. Two large-bore IV lines should be established for fluid resuscitation and blood transfusion, with a target hemoglobin around 8 g/dL. Overly aggressive fluid resuscitation should be avoided, as it may increase portal pressure and worsen bleeding.
Pharmacologic therapy should be initiated early. Octreotide is commonly used as first-line therapy (or somatostatin where available) to reduce portal pressure and control bleeding. Prophylactic antibiotics such as ceftriaxone or fluoroquinolones are essential, as they reduce the risk of infection and improve survival. Erythromycin may be given to improve gastric emptying prior to endoscopy.
Endoscopic therapy is the cornerstone of treatment. Endoscopic band ligation is preferred due to fewer complications compared to sclerotherapy. In cases of massive uncontrolled bleeding, balloon tamponade using devices such as the Sengstaken–Blakemore tube may be used as a temporary measure, though it carries significant risks including esophageal rupture. For refractory bleeding, a transjugular intrahepatic portosystemic shunt (TIPS) procedure or surgical intervention may be required.
All patients with active variceal bleeding require ICU admission due to the high risk of rebleeding and mortality. High-risk features include age over 60, renal failure, and low initial hemoglobin. Patients with nonbleeding varices may be managed as outpatients with close gastroenterology follow-up, including surveillance endoscopy and preventive therapy.
Key clinical points include the importance of early airway control, prompt initiation of vasoactive medications and antibiotics, and rapid involvement of gastroenterology for endoscopic management. Recognizing variceal bleeding early and initiating aggressive but targeted therapy significantly improves outcomes in this high-risk population.
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