Upper GI Bleeding: Diagnosis and Treatment
Definition and Epidemiology
Upper GI bleeding (UGIB) is bleeding originating proximal to the ligament of Treitz (esophagus, stomach, duodenum). Annual incidence is roughly 39-172 per 100,000 in Western countries. Bleeding stops spontaneously in about 80% of patients; of the 20% who continue or rebleed, mortality is 30-40%. Overall mortality for severe UGIB has remained at 5-10% since the 1970s, largely because more patients now have serious comorbidities and cirrhosis-related variceal bleeding - Sleisenger and Fordtran's Gastrointestinal and Liver Disease, Tintinalli's Emergency Medicine.
Causes
| Cause | Approx. Frequency |
|---|
| Peptic ulcer disease | ~35-40% (most common overall) |
| Esophageal/gastric varices | ~20-22% |
| Erosive gastritis/esophagitis | ~4-5% |
| Mallory-Weiss tear | ~4% |
| Angioectasia/telangiectasia | ~4% |
| Dieulafoy lesion | ~3% |
| Upper GI neoplasm | ~3% |
| Other (portal gastropathy, aortoenteric fistula, hemobilia, watermelon stomach) | remainder |
(UCLA CURE database, cited in Sleisenger and Fordtran's)
In cirrhotic patients, varices cause bleeding about 59% of the time, followed by peptic ulcer disease (~16%) - Tintinalli's Emergency Medicine.
Diagnosis
History
- Hematemesis or coffee-ground emesis strongly suggests an upper source; melena (even without hematemesis) in a patient under 50 also favors an upper source.
- Retching followed by hematemesis suggests a Mallory-Weiss tear.
- History of aortic graft raises concern for aortoenteric fistula.
- Review medications (NSAIDs, aspirin, steroids, anticoagulants) and alcohol use.
- Note: bright red/maroon rectal bleeding originates from an upper GI source in about 14% of cases, so absence of typical symptoms doesn't rule out UGIB - Tintinalli's Emergency Medicine.
Physical exam
- Inspect vomitus/NG aspirate directly.
- Vital signs: tachycardia, hypotension, orthostatic changes (but beta-blockers, young age, or baseline hypertension can mask these).
- Stigmata of liver disease: spider angiomas, palmar erythema, jaundice, ascites, gynecomastia.
- Rectal exam for stool color/consistency.
Laboratory
- Type and crossmatch, CBC (initial hematocrit may not reflect acute blood loss before hemodilution), coagulation studies, liver panel.
- An elevated BUN-to-creatinine ratio is a classic clue to UGIB (digested blood is a urea source) - Frameworks for Internal Medicine.
Bedside/confirmatory testing
- NG lavage: red blood or coffee-ground aspirate confirms UGIB when suspected but not clinically obvious.
Risk stratification tools
- Pre-endoscopy: Glasgow-Blatchford Score, Clinical Rockall Score, AIMS65 score - used to identify low-risk patients potentially suitable for outpatient management versus high-risk patients needing ICU-level care and urgent endoscopy.
Definitive diagnosis: Upper endoscopy (EGD)
- The diagnostic modality of choice; also allows immediate therapeutic intervention.
- Timing: after hemodynamic resuscitation, within 24 hours for most patients with overt bleeding; unstable patients may need it within 6-12 hours once resuscitated, stable patients within 12-36 hours.
- Forrest classification of ulcer stigmata predicts rebleeding risk: active spurting/oozing bleeding, non-bleeding visible vessel, adherent clot, flat pigmented spot, clean base (highest to lowest risk) - Sleisenger and Fordtran's.
- If bleeding is massive and the patient cannot be stabilized, urgent angiography or surgical exploration (with intraoperative endoscopy) may be required without waiting for elective EGD - Sleisenger and Fordtran's.
Treatment
1. Resuscitation and initial stabilization
- Two large-bore IV lines, crystalloid resuscitation, blood transfusion as needed (restrictive transfusion strategy targeting hemoglobin ~7-8 g/dL is generally favored in hemodynamically stable patients, per current evidence).
- Foley catheter for urine output monitoring; consider NG intubation.
- Correct coagulopathy/thrombocytopenia if actively bleeding and severe.
- ICU admission and surgical/GI consultation for high-risk patients (hypotension, tachycardia, altered mentation, significant comorbidity, anticoagulation, immunosuppression, or high-risk endoscopic findings such as active bleeding, visible vessel, varices, or suspected aortoenteric fistula) - Schwartz's Principles of Surgery.
2. Pharmacologic therapy
- Proton pump inhibitors (PPI): High-dose IV PPI (e.g., omeprazole 80 mg IV bolus then 8 mg/hr infusion) started empirically before endoscopy for suspected nonvariceal bleeding. Raises gastric pH above 6, which is needed for platelet aggregation and clot stability; reduces rebleeding, transfusion needs, and surgery rates - Tintinalli's Emergency Medicine.
- Octreotide (somatostatin analogue): For suspected variceal bleeding (or when the source is unclear) - 50 mcg IV bolus followed by 25-50 mcg/hr infusion (up to 5 days for confirmed variceal bleeding). Causes splanchnic vasoconstriction and lowers portal pressure; used as an adjunct to endoscopic therapy, not proven to improve mortality alone.
- Antibiotic prophylaxis in cirrhotic patients: IV ceftriaxone 1 g/day (or ciprofloxacin/levofloxacin) for ~7 days reduces bacterial infections, rebleeding, and mortality in variceal bleeders - Tintinalli's Emergency Medicine, Sleisenger and Fordtran's.
- Promotility agents (erythromycin, metoclopramide) before endoscopy can clear gastric blood/clot and improve visualization.
- Recombinant factor VIIa: reserved for severe bleeding with irreversible coagulopathy (e.g., advanced cirrhosis), given cost and thrombosis risk.
3. Endoscopic therapy (definitive for most cases)
- Nonvariceal lesions (ulcers, Mallory-Weiss, Dieulafoy): injection therapy (epinephrine), mechanical therapy (hemoclips, band ligation), thermal therapy (electrocoagulation, argon plasma coagulation), often combined for high-risk stigmata.
- Variceal bleeding: endoscopic variceal ligation (banding) is first-line; sclerotherapy is an alternative, particularly for gastric varices where banding is technically difficult.
- Doppler endoscopic probe can be used to confirm obliteration of underlying arterial flow and further reduce rebleeding risk in ulcer bleeding.
4. Rescue/second-line therapy
- Balloon tamponade (Sengstaken-Blakemore, Minnesota, or Linton-Nachlas tube): temporary bridge for massive variceal bleeding uncontrolled by endoscopy, achieving initial control in 85-98% of cases, but rebleeding occurs in 21-60% after deflation - used only as a bridge to definitive therapy given aspiration and perforation risks.
- Transjugular intrahepatic portosystemic shunt (TIPS): for variceal bleeding refractory to endoscopic/pharmacologic therapy, or early/pre-emptive TIPS in high-risk cirrhotic patients (e.g., Child-Pugh B/C) with active variceal bleeding.
- Angiographic embolization: for nonvariceal bleeding not controlled endoscopically, especially in high-surgical-risk patients.
- Surgery: reserved for bleeding refractory to endoscopic and angiographic measures, ongoing hemodynamic instability despite resuscitation, or specific surgical indications (e.g., perforated ulcer, aortoenteric fistula).
5. Long-term/secondary prevention
- Test and treat H. pylori in peptic ulcer disease.
- Discontinue or minimize NSAIDs/aspirin where possible; use PPI co-therapy if antiplatelet/anticoagulant therapy must continue.
- Nonselective beta-blockers (propranolol, nadolol) and repeat endoscopic banding for secondary prophylaxis of variceal bleeding in cirrhotic patients.
Recent evidence to note
A 2025 Canadian Association of Gastroenterology guideline update on endoscopic management of nonvariceal, nonpeptic-ulcer UGIB, and a 2025 Japanese guideline (2nd edition) on endoscopic management of nonvariceal UGIB have been published, refining hemostasis technique recommendations (PMID: 40778886, PMID: 40114631). A 2025 systematic review also reassessed prognostic scoring systems (Blatchford, Rockall, AIMS65) for ED risk stratification (PMID: 39093247). These are worth checking if you need the most current procedural recommendations, as guideline details can evolve faster than textbook editions.