Forrest classification of peptic ulcer bleeding is a universally accepted endoscopic staging system utilized to categorize peptic ulcers based on the presence and appearance of stigmata of recent hemorrhage (SRH) 1,4. Originally developed in 1974 by Forrest and colleagues to stratify patients entering clinical trials for acute upper gastrointestinal bleeding, the classification system remains the cornerstone for clinical decision-making, guiding the urgency and modality of endoscopic intervention, predicting the likelihood of recurrent hemorrhage, and determining overall patient disposition 2,3. Non-variceal upper gastrointestinal bleeding secondary to peptic ulcer disease continues to be a major medical emergency associated with significant morbidity and mortality, making rapid risk stratification essential for optimizing clinical outcomes 4.

Etiology & Risk Factors

  • Helicobacter pylori Infection: Chronic colonization by H. pylori induces mucosal inflammation, impairs defensive mechanisms, and accounts for a substantial proportion of gastric and duodenal ulcers complicated by hemorrhage 1,2.
  • Nonsteroidal Anti-inflammatory Drugs (NSAIDs) and Aspirin: Inhibition of gastric mucosal cyclooxygenase-1 (COX-1) reduces protective prostaglandin synthesis, predisposing patients to deep mucosal ulceration, submucosal vessel erosion, and acute bleeding.
  • Concomitant Antithrombotic Therapy: Dual antiplatelet therapy, therapeutic anticoagulation with direct oral anticoagulants (DOACs) or warfarin, and systemic corticosteroids exponentially increase the risk of ulcer progression and severe hemorrhage.
  • Critical Illness and Physiological Stress: Severe trauma, extensive burns (Curling ulcers), and central nervous system injury (Cushing ulcers) cause acute stress-related mucosal damage that can evolve into bleeding peptic ulcers.
  • Comorbid Medical Conditions: Advanced age, chronic kidney disease, hepatic cirrhosis, cardiovascular disease, and chronic obstructive pulmonary disease heighten both the incidence of bleeding ulcers and mortality rates following hemorrhagic events 1,2.

Pathophysiology

The pathogenesis of peptic ulcer bleeding begins with a breakdown of mucosal defense mechanisms relative to aggressive factors such as hydrochloric acid and pepsin 1,4. As the ulcer deepens through the lamina propria and submucosa, it directly exposes resident blood vessels—most commonly branches of the left gastric artery along the lesser curvature or the gastroduodenal artery in the posterior duodenal bulb. Depending on the depth of the vessel erosion, systemic blood pressure, and local hemostatic plug formation, distinct endoscopic stigmata evolve 4. Active arterial breach produces high-pressure spurting hemorrhage (Forrest Ia), whereas erosion of smaller venules or capillaries results in low-pressure oozing (Forrest Ib). If spontaneous hemostasis occurs, a protruding visible vessel (Forrest IIa) or an adherent clot (Forrest IIb) forms at the base. When the vessel undergoes complete thrombosis and subsequent fibrosis without visible remnants, a flat pigmented spot (Forrest IIc) or a clean, white fibrous base (Forrest III) remains 3,4.

Forrest classification of peptic ulcer bleeding — Pathophysiological Cascade & Clinical Flowchart 1 Mucosal Injury & Vessel Erosion NSAIDs, Helicobacter pylori, or acid hypersecretion breach the protective gastric or duodenal mucosal barrier, exposing submucosal arteries. 2 Vascular Breach & Hemorrhage Mechanical friction or enzymatic digestion erodes underlying submucosal blood vessels, leading to active bleeding or vessel wall weakening. 3 Endoscopic Stigmata Formation Visible arterial spurting, oozing, non-bleeding visible vessels, adherent clots, or flat pigmented spots develop at the ulcer base. 4 Clinical Presentation & Risk Stratification Patients manifest melena, hematemesis, or shock, and clinicians apply the Forrest classification to quantify rebleeding risk. 5 Therapeutic Intervention & Recurrence Prevention Urgent endoscopic thermal or mechanical therapy coupled with high-dose intravenous PPIs halts bleeding and prevents recurrence.

Clinical Presentation & Classic Clinical Signs

  • History & Cardinal Symptoms: Patients classically present with acute upper gastrointestinal bleeding manifestations, including hematemesis (bright red blood or "coffee-ground" emesis) and melena (dark, tarry, foul-smelling stools due to the degradation of blood by intestinal bacteria). Hematochezia may occur in the setting of rapid, massive hemorrhage with hyperperistalsis. Patients frequently report preceding epigastric burning pain, which may paradoxically lessen when the bleeding occurs due to the buffering effect of blood proteins on gastric acid. Symptoms of acute anemia and hypovolemia—such as dizziness, orthostasis, fatigue, syncope, and exertional dyspnea—are frequently reported.
  • Physical Examination & Named Clinical Signs: Physical examination focuses on evaluating hemodynamic stability. Tachycardia (heart rate greater than 100 beats per minute) is often the earliest sign of intravascular volume depletion, followed by hypotension, tachypnea, and altered mental status in severe hemorrhagic shock. Abdominal examination may reveal localized epigastric tenderness, though severe generalized peritonitis suggests concurrent hollow viscus perforation. Rectal examination confirms melena or dark red blood. Stigmata of chronic liver disease (e.g., jaundice, spider angiomata, ascites) or signs of systemic atherosclerosis should be systematically documented.

Diagnostic Workup & Interpretation (Laboratory, Imaging & ECG/Pathology)

Diagnostic Modality / Test Expected Clinical & Radiological / Laboratory Finding
Gold-Standard InvestigationUrgent esophagogastroduodenoscopy (EGD) performed within 24 hours of presentation (or within 12 hours for hemodynamically unstable patients after resuscitation) identifying the ulcer location, size, depth, and specific Forrest classification stigmata.
Laboratory PanelComplete blood count demonstrating normocytic or microcytic anemia (hemoglobin drop, though early acute bleeding may present with normal hemoglobin due to hemoconcentration). Elevated blood urea nitrogen (BUN)-to-creatinine ratio greater than 30:1 reflecting upper gastrointestinal blood digestion and intravascular volume depletion. Coagulation profile (PT/INR, aPTT, fibrinogen) and platelet count to identify coagulopathies.
Imaging / Radiology (X-ray, US, CT, MRI)Upright chest and abdominal radiographs to rule out free intraperitoneal air (pneumoperitoneum) indicating ulcer perforation. Multidetector CT angiography (CTA) in patients with ongoing massive hemorrhage where endoscopy is inconclusive or unsuccessful, demonstrating active contrast extravasation into the gastrointestinal lumen.
ECG / Histopathology / Procedural12-lead ECG to evaluate for myocardial ischemia or secondary ST-segment changes induced by severe acute anemic stress. Gastric mucosal biopsies obtained during EGD to evaluate for Helicobacter pylori infection (via rapid urease test, histology, or immunohistochemistry) and to rule out malignant gastric ulceration.

Staging, Classification & Clinical Scoring Systems

Criterion / Stage / Score Component Clinical Threshold, Points & Management Implication
Forrest IaActive spurting hemorrhage from the ulcer base. High rebleeding risk (approx. 55-90% if untreated). Requires immediate endoscopic therapy (combination of thermal/mechanical plus epinephrine injection).
Forrest IbActive oozing hemorrhage without spurting. High rebleeding risk (approx. 10-27%). Requires urgent endoscopic hemostasis and intravenous proton pump inhibitor therapy.
Forrest IIaNon-bleeding visible vessel (pigmented protuberance) at the ulcer base. Intermediate-to-high rebleeding risk (approx. 43-50%). Endoscopic hemostasis strongly recommended.
Forrest IIbAdherent clot covering the ulcer base. Intermediate rebleeding risk (approx. 22-33%). Careful targeted clot removal with water irrigation and cold guillotine snaring followed by treatment of underlying stigmata is standard.
Forrest IIcFlat pigmented spot (hematin base) without protrusion. Low rebleeding risk (approx. 5-10%). Routine endoscopic therapy is generally not mandatory; high-dose oral or IV PPI therapy suffices.
Forrest IIIClean, white fibrous ulcer base without blood stigmata. Very low rebleeding risk (less than 5%). No endoscopic therapy required; standard ulcer healing medical regimen.
Glasgow-Blatchford Score (GBS)Pre-endoscopy risk stratification score incorporating BUN, hemoglobin, systolic blood pressure, pulse, and comorbidities. A GBS of 0 to 1 identifies very low-risk outpatients who may be safely managed without hospital admission 1.

Differential Diagnosis

Differential Condition Distinguishing Clinical, Biochemical & Imaging Features
Esophageal Variceal BleedingHistory of chronic liver disease, portal hypertension, or cirrhosis. EGD reveals large tortuous esophageal or gastric varices rather than discrete mucosal peptic ulceration.
Mallory-Weiss SyndromeHistory of forceful retching or vomiting prior to hematemesis. EGD demonstrates linear mucosal tears at the gastroesophageal junction rather than chronic peptic ulcers.
Dieulafoy LesionAnomalous large submucosal tortuous arteriole eroding through normal gastric mucosa, typically presenting with sudden, massive, painless hemorrhage and a tiny mucosal defect on endoscopy.
Gastric Malignancy (Adenocarcinoma / GIST)Advanced age, weight loss, early satiety. EGD reveals an ulcerated mass with irregular, raised, firm edges; histopathology confirms malignancy rather than benign peptic disease.

Management & Treatment Protocol

  • Initial Stabilization & Resuscitation: Immediate assessment of airway, breathing, and circulation. Establish large-bore peripheral intravenous access (two 16-gauge or 18-gauge lines) or central venous access. Initiate restrictive red blood cell transfusion strategy targeting a hemoglobin threshold between 7 g/dL and 9 g/dL, reserving higher targets (greater than 10 g/dL) for patients with severe underlying ischemic cardiovascular disease 1. Correct severe coagulopathies with fresh frozen plasma, platelets, or reversal agents if antithrombotic therapy is active.
  • First-Line Medical / Pharmacological Therapy (with exact adult dosing): Administer high-dose intravenous proton pump inhibitors immediately upon presentation prior to endoscopy. Recommended adult dosing consists of a pantoprazole or esomeprazole 80 mg IV bolus followed by a continuous infusion of 8 mg per hour for 72 hours to maintain gastric pH above 6.0, promote platelet aggregation, and stabilize clot formation. Test and treat Helicobacter pylori infection with standard eradication regimens (e.g., bismuth quadruple therapy: PPI twice daily, bismuth subsalicylate 526 mg four times daily, metronidazole 500 mg three times daily, and tetracycline 500 mg four times daily for 14 days) once oral intake is resumed.
  • Endoscopic and Interventional Management: Perform diagnostic and therapeutic EGD. For active bleeding (Forrest Ia, Ib) or high-risk stigmata (Forrest IIa), apply dual endoscopic therapy combining local injection (dilute epinephrine 1:10,000) with thermal contact coagulation (BICAP or heater probe) or mechanical clipping (hemoclips). For persistent rebleeding refractory to endoscopic therapy, emergent transarterial embolization (TAE) via interventional radiology or surgical intervention (ulcer oversewing and vagotomy) is indicated 2,3.

Complications & Prognosis

  • Recurrent Hemorrhage: Occurs in 10% to 20% of high-risk Forrest Ia–IIa ulcers despite initial endoscopic therapy, significantly increasing inpatient morbidity and mortality.
  • Perforation and Obstruction: Deep ulcer erosion can lead to free perforation into the peritoneal cavity requiring emergent surgical exploration, or chronic scarring causing gastric outlet obstruction.
  • Prognostic Factors: Overall mortality from nonvariceal upper gastrointestinal bleeding ranges from 5% to 10%, driven primarily by advanced age, severe comorbidities, persistent or recurrent hemorrhage (Forrest Ia/Ib), and delayed endoscopic intervention 1,2.