Endoscopic Hemostasis and Therapeutic Intervention
Hemostasis by lesion type
Endoscopic hemostasis starts with physiology: resuscitate, correct coagulopathy, and treat the underlying cause. For nonvariceal upper GI bleeding, Forrest classification drives therapy. High-risk stigmata-spurting (Ia), oozing (Ib), and visible vessel (IIa)-benefit from combination therapy: epinephrine injection to slow bleeding, followed by a mechanical or thermal method such as clips, thermal coagulation, or hemostatic powder. Adherent clot (IIb) may be washed off and treated if a high-risk stigma is exposed; flat pigmented spot (IIc) and clean base (III) do not need endoscopic therapy. Epinephrine alone is inadequate because it does not reduce rebleeding.
For ulcers, give high-dose proton pump inhibitor therapy (80 mg bolus then 8 mg/hour for 72 hours) for high-risk stigmata, test and treat H. pylori, and resume antithrombotics when bleeding is controlled after multidisciplinary discussion. Large ulcers (over 2 cm), posterior duodenal bulb location, and hemodynamic instability predict rebleeding.
Variceal bleeding requires a different approach: band ligation for esophageal varices, plus antibiotics (for example ceftriaxone) and vasoactive drugs. Gastric variceal bleeding is often treated with cyanoacrylate injection, not banding. Portal hypertensive gastropathy and GAVE are managed medically or with argon plasma coagulation.
Traps include banding a gastric varix, using epinephrine alone, and forgetting antibiotics in cirrhosis. Rule of thumb: for a spurting ulcer, inject dilute epinephrine, then place clips or thermal therapy, and start high-dose PPI.
Worked example: a 60-year-old with melena and a 2 cm posterior duodenal ulcer with a visible vessel receives epinephrine plus clip placement, high-dose PPI, H. pylori testing, and monitored resumption of aspirin.