## First-Line Pharmacotherapy for Acute Variceal Bleeding **Key Point:** Octreotide is the vasopressor of choice for acute esophageal variceal hemorrhage because it reduces portal pressure by causing splanchnic vasoconstriction while maintaining systemic hemodynamics. ### Mechanism of Action - Somatostatin analogue that causes selective splanchnic vasoconstriction - Reduces portal venous inflow and portal pressure gradient - Does NOT cause systemic vasoconstriction (unlike vasopressin) - Onset of action: 15–30 minutes ### Dosing & Duration - **Bolus:** 50 µg IV, then continuous infusion 50 µg/hour - **Duration:** Continue for 2–5 days after variceal bleeding control - Can be used as **bridge therapy** while awaiting endoscopic band ligation (EBL) ### Clinical Role in Acute Variceal Hemorrhage | Intervention | Timing | Role | |---|---|---| | **Octreotide** | Immediate (before/during endoscopy) | Pharmacological hemostasis; reduces rebleeding | | **Endoscopic band ligation** | Within 12 hours | Definitive local hemostasis | | **Propranolol** | After acute control | Secondary prophylaxis (prevents future bleeds) | **High-Yield:** Octreotide + EBL is the gold-standard combination for acute variceal hemorrhage. Octreotide alone achieves hemostasis in ~50% of cases; EBL achieves >90% hemostasis. **Clinical Pearl:** Octreotide is superior to vasopressin because it has fewer systemic side effects (no coronary vasospasm, no peripheral ischemia) and can be used safely in patients with cardiac comorbidities. **Mnemonic:** **OCTO** = Octreotide Controls Variceal Hemorrhage (splanchnic vasoconstriction) [cite:Harrison 21e Ch 307]
Sign up free to access AI-powered MCQ practice with detailed explanations and adaptive learning.