A 23-year-old male patient presented with a two-day history of melena and associated fatigue. The patient reported a one-week history of intermittent NSAID use (ibuprofen 400 mg twice daily) for tension headache management. He denied regular aspirin, anticoagulant, or antiplatelet therapy. There was no prior history of peptic ulcer disease, gastrointestinal bleeding, or dyspepsia. Social history was notable for occasional alcohol consumption (1 - 2 drinks per week) and no tobacco use. The patient denied recent stress, corticosteroid use, or known hypersecretory states. Comorbidities were limited to intermittent tension headaches managed with over-the-counter analgesics. Family history was non-contributory for gastrointestinal disorders.

On presentation, the patient appeared pale and fatigued but was hemodynamically stable. Initial vital signs were as follows: blood pressure 98/62 mmHg, heart rate 108 beats/minute, respiratory rate 20 breaths/minute, temperature 36.8˚C, and oxygen saturation 97% on room air. Shock index was calculated at 1.1 (heart rate/systolic blood pressure), indicating hemodynamic compromise.

Key laboratory studies on admission revealed: hemoglobin 6 g/dL (severe anemia), hematocrit 18%, platelet count 230 × 10⁹/L, BUN 28 mg/dL, creatinine 0.9 mg/dL (BUN/Cr ratio 31.1), INR 1.0, and serum lactate 2.1 mmol/L. Liver function tests were within normal limits.

The patient was immediately resuscitated with intravenous crystalloid fluids. Two units of packed red blood cells were transfused during initial stabilization, with appropriate hemodynamic response (blood pressure improved to 110/70 mmHg, heart rate decreased to 92 beats/minute) [7]. Two large-bore peripheral intravenous lines (18-gauge) were secured, and continuous cardiac monitoring was initiated.

Formal risk stratification was performed at presentation. The Glasgow-Blatchford Score was calculated at 15 (indicating high risk requiring urgent intervention), and the pre-endoscopic Rockall Score was 4 (high-risk category) [8][9]. These scores supported the decision for urgent endoscopic evaluation within 12 hours and informed the need for close monitoring in an intensive care setting [10]. However, given the presence of active bleeding with hemodynamic compromise, urgent endoscopy was indicated regardless of risk score.

Urgent esophagogastroduodenoscopy was performed within 10 hours of presentation [11]. Endoscopy demonstrated a duodenal bulb ulcer with active oozing hemorrhage consistent with Forrest Ib classification [5]. The ulcer measured approximately 12 mm in diameter and was located on the posterior wall of the duodenal bulb—an anatomically high-risk region due to proximity to the gastroduodenal artery [12].

Following thorough water jet irrigation and suction clearance of pooled blood, no active spurting vessel was visualized; however, persistent low-pressure oozing from the ulcer base was observed. No large adherent clot requiring extraction was identified.

During the same endoscopic session, gastric mucosal biopsies were obtained from the antrum and body for histopathological evaluation, and a rapid urease test (CLO test) was performed [13]. Histology subsequently confirmed chronic active gastritis with H. pylori organisms identified on Giemsa staining. The rapid urease test was also positive for H. pylori.

A 23-gauge sclerotherapy needle was advanced through the working channel. Diluted epinephrine (1:10,000) was injected circumferentially around the bleeding site in four quadrants, with a total volume of approximately 8 - 10 mL. The needle was inserted 2 - 3 mm into tissue with slow injection until mucosal blanching was observed. Care was taken to avoid intravascular injection. The goals were temporary vasoconstriction, mechanical tamponade, improved visualization, and reduction in bleeding flow. Following injection, active oozing significantly decreased, allowing clear identification of the bleeding vessel [16].

Subsequently, a through-the-scope (TTS) hemoclip device was selected for definitive mechanical hemostasis [17]. The scope was positioned to achieve a perpendicular approach to the vessel axis. Stable scope position was achieved using torque steering and slight withdrawal. The bleeding point was centered in the visual field, and the clip jaws were opened fully prior to deployment.

Critical principles applied included capture of submucosa (not just superficial mucosa), avoidance of tangential placement, and ensuring vessel compression rather than edge approximation only. The clip was deployed directly across the visible bleeding point. Immediate cessation of bleeding was observed. No additional clips were required.

Hemostasis was confirmed by: 1) absence of active bleeding for more than 2 minutes, 2) no visible arterial pulsation, 3) stable clip positioning, and 4) clear field after irrigation. The patient remained hemodynamically stable throughout the procedure (Figure 1).

Figure 1. Endoscopic Images

Figure 1.(A) Active oozing hemorrhage from duodenal ulcer (Forrest Ib). (B) Post-hemoclip placement with complete hemostasis.

Given the positive rapid urease test and histologic confirmation of H. pylori infection, eradication therapy was initiated prior to discharge [13]. A 14-day bismuth-based quadruple regimen was prescribed: bismuth subsalicylate 524 mg four times daily, metronidazole 500 mg three times daily, tetracycline 500 mg four times daily, and omeprazole 20 mg twice daily.

Confirmation of eradication was planned via urea breath test at least 4 weeks after completion of antibiotics and 2 weeks after discontinuation of PPI therapy.

If H. pylori testing had been negative, the alternative management plan would have included: 1) comprehensive evaluation for ongoing NSAID or aspirin exposure, 2) assessment for Zollinger-Ellison syndrome if clinically suspected (elevated gastrin levels, multiple ulcers, refractory disease), and 3) counseling on avoidance of ulcerogenic medications including alcohol and NSAIDs.

Time from presentation to endoscopy was 10 hours. Total length of hospital stay was 4 days. Hemoglobin improved from 6 g/dL at admission to 9.2 g/dL at discharge. The reported hemoglobin of 13 g/dL was documented at the 6-week outpatient follow-up visit.

No outpatient rebleeding episodes were reported during the follow-up period. No repeat endoscopy was required. The patient reported full adherence to prescribed medications and completed the H. pylori eradication regimen without complications. Follow-up urea breath test at 6 weeks post-treatment confirmed successful eradication of H. pylori.

The Forrest classification categorizes ulcers based on endoscopic findings and guides management decisions [5]. Forrest Ib represents active oozing hemorrhage and carries a high risk of rebleeding if untreated. Risk stratification tools such as the Glasgow-Blatchford Score and Rockall Score assist in predicting outcomes and informing triage decisions, though they do not replace urgent endoscopic therapy in actively bleeding lesions [8][9].

Duodenal ulcers arise from an imbalance between mucosal defense mechanisms and luminal aggressive factors. Protective elements include mucus-bicarbonate barrier, prostaglandin-mediated mucosal blood flow, epithelial restitution, and tight junction integrity. Aggressive factors include gastric acid, pepsin, H. pylori-mediated inflammation, and NSAID-induced prostaglandin inhibition.

Helicobacter pylori colonization leads to chronic active gastritis and increased gastrin production, promoting acid hypersecretion [13]. In the duodenal bulb, acid exposure results in gastric metaplasia, allowing H. pylori colonization and local inflammatory damage. NSAIDs inhibit cyclooxygenase-1 (COX-1), reducing prostaglandin synthesis, which leads to reduced mucosal blood flow, impaired mucus secretion, and increased susceptibility to acid injury [19]. Concurrent H. pylori infection synergistically increases ulcer bleeding risk [3].

Ulcer bleeding occurs when erosion penetrates into submucosal or arterial vessels. In posterior duodenal ulcers, the gastroduodenal artery is particularly vulnerable. However, acidic pH destabilizes clot integrity by impairing platelet aggregation and fibrin polymerization. This explains why high-dose PPI therapy reduces rebleeding risk by maintaining intragastric pH above 6 [18].

Combination therapy significantly reduces rebleeding compared to injection alone [16][20]. Mechanical clipping provides durable vessel compression and is widely recommended in international guidelines [14][15]. Injection monotherapy has rebleeding rates of approximately 20% - 30%, while combination therapy reduces this to 5% - 10% [20].

Endoscopic therapy for acute non-variceal upper gastrointestinal bleeding has been extensively studied, with meta-analyses demonstrating significant reductions in rebleeding and mortality [21].

Through-the-scope (TTS) clips are mechanical compression devices deployed via standard working channels [17]. Mechanically, clips function by exerting radial compression across the vessel, collapsing the lumen and interrupting arterial inflow. Key technical principles include perpendicular orientation to vessel axis, adequate submucosal capture, avoidance of superficial mucosal-only grasp, and deployment on non-friable tissue margins.

Over-the-scope clip (OTSC) systems are larger nitinol-based devices mounted externally on the endoscope tip [22]. They provide full-thickness tissue capture, greater compression force, and wider span coverage. Randomized trials show OTSC superiority in recurrent bleeding after standard therapy [22]. Thermal probes achieve hemostasis via coaptive coagulation but carry risks of deep tissue necrosis and delayed perforation. Topical hemostatic powders provide temporary tamponade but do not offer definitive vessel compression.

The 2021 American College of Gastroenterology (ACG) guidelines provide strong recommendation for combination therapy for high-risk stigmata (Forrest Ia and Ib), discourage epinephrine monotherapy, recommend high-dose IV PPI for 72 hours following successful hemostasis, and advocate for a restrictive transfusion strategy [14].

The 2021 European Society of Gastrointestinal Endoscopy (ESGE) guidelines recommend combination therapy (strong recommendation, high-quality evidence), consider OTSC in refractory bleeding, and recommend repeat endoscopy for rebleeding [15]. The International Consensus Group recommends early endoscopy within 24 hours, combination therapy as preferred approach, and consideration of angiographic embolization before surgery in refractory cases [23]. The Asia-Pacific Consensus emphasizes risk stratification, supports early endoscopy, and advocates H. pylori eradication [24]. All major guidelines converge on definitive mechanical therapy as standard of care [25].

Current policies in acute NVUGIB management emphasize a structured approach to diagnosis, risk stratification, and treatment [26].

All major guidelines converge on definitive mechanical therapy as standard of care.

After successful endoscopic hemostasis and initiation of high-dose intravenous PPI therapy, routine scheduled second-look endoscopy is generally not indicated in the absence of clinical evidence of rebleeding [15]. Post-procedural management should instead emphasize close clinical monitoring and prompt repeat endoscopy if rebleeding is suspected.

Early repeat endoscopy should be triggered by clinical rebleeding, including recurrent hematemesis or fresh melena, hemodynamic instability (tachycardia, hypotension, rising shock index), hemoglobin drop (commonly ≥ 2 g/dL) or ongoing transfusion requirement, and persistent high nasogastric aspirate blood (if NGT used). Repeat endoscopy is typically performed urgently (same day/within 24 hours) once rebleeding is suspected, after immediate resuscitation.

At re-endoscopy, escalation follows a structured hierarchy: re-clip (additional TTS clips) if anatomy allows, add thermal therapy if clip placement is limited, consider OTSC for fibrotic ulcer base, failed standard clipping, or recurrent bleeding after initial combination therapy [22]. Randomized trials of endoscopic hemostatic techniques have established the superiority of combination therapy over monotherapy [27]. Endoscopic management strategies in peptic ulcer bleeding continue to evolve with advances in device technology and technique [28]. If endoscopic salvage fails, angiographic embolization is preferred before surgery in many settings.

This case underscores several critical clinical principles. First, age alone does not determine risk severity; young patients may present with life-threatening anemia despite preserved hemodynamics. Second, Forrest Ib lesions require definitive therapy despite the absence of spurting hemorrhage; oozing bleeding may represent unstable arterial erosion. Third, injection therapy should be viewed as an adjunct rather than definitive treatment. Fourth, mechanical compression remains the cornerstone of durable hemostasis. Fifth, anatomical awareness of posterior bulb vascular proximity guides therapeutic choice. Sixth, adherence to guideline-directed therapy reduces variability in outcomes [25]. Seventh, structured escalation algorithms reduce delays in definitive management. Eighth, acid suppression is mechanistically essential for clot stabilization. Ninth, H. pylori eradication is mandatory to prevent recurrence [13]. Tenth, multidisciplinary coordination between gastroenterology, interventional radiology, and surgery remains critical in refractory cases [29]. Cost-effectiveness analyses demonstrate that preventing rebleeding offsets procedural expense [30].