# Lecture 14: Gastrointestinal Bleeding
## Unit 2.2: Gastrointestinal System
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## Learning Objectives
By the end of this lecture, students will be able to:
1. Differentiate upper from lower GI bleeding by presentation
2. Describe the common causes of upper GI bleeding
3. Explain the management of variceal and non-variceal upper GI bleeding
4. Describe the causes and management of lower GI bleeding
5. Explain the approach to obscure GI bleeding
6. Describe risk stratification and transfusion strategies in GI bleeding
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## Overview of GI Bleeding
Gastrointestinal bleeding represents a common and potentially life-threatening clinical problem requiring systematic approach to localization, risk stratification, and management. Precise terminology facilitates communication and guides evaluation.
Anatomic localization divides bleeding into upper and lower sources based on the ligament of Treitz, the suspensory ligament at the duodenojejunal junction. Upper GI bleeding originates proximal to this landmark (esophagus, stomach, duodenum), while lower GI bleeding originates distally (jejunum, ileum, colon, rectum). This distinction carries practical importance because it determines the appropriate endoscopic approach and predicts likely etiologies.
Clinical presentations suggest bleeding location. Hematemesis, the vomiting of frank blood or coffee-ground material, localizes the source to the upper GI tract. The coffee-ground appearance results from gastric acid converting hemoglobin to hematin. Melena, black tarry stool with a characteristic foul odor, indicates upper GI bleeding in approximately ninety percent of cases, though proximal colonic sources occasionally produce melena when transit is slow. The black color results from bacterial degradation of hemoglobin during intestinal transit. Hematochezia, bright red or maroon blood per rectum, usually indicates lower GI bleeding but may result from brisk upper GI hemorrhage when bleeding is rapid enough to prevent hematinization.
Additional terminology distinguishes bleeding presentations. Overt bleeding is visible to the patient as hematemesis, melena, or hematochezia. Occult bleeding is not visible but detected by fecal occult blood testing or manifests as iron deficiency anemia. Obscure bleeding describes GI bleeding from a source not identified despite upper and lower endoscopy.
Epidemiologically, upper GI bleeding occurs more frequently than lower, with an incidence of 100 to 150 per 100,000 population annually compared to 20 to 30 per 100,000 for lower GI bleeding. However, upper GI bleeding carries higher mortality (five to ten percent) than lower GI bleeding (two to four percent), reflecting the typically larger volume of hemorrhage and greater hemodynamic compromise.
Hemodynamic assessment determines bleeding severity and guides resuscitation urgency. Mild bleeding manifests as hemoglobin above 10 g/dL with stable vital signs. Moderate bleeding presents with hemoglobin 7 to 10 g/dL, orthostatic hypotension (drop in systolic blood pressure greater than 20 mmHg or increase in heart rate greater than 20 beats per minute upon standing), or symptoms of hypovolemia. Severe bleeding involves hemoglobin below 7 g/dL, frank hypotension, or tachycardia at rest. Massive bleeding produces hemorrhagic shock requiring immediate transfusion and often intervention.
Panel A: Anatomical diagram with ligament of Treitz dividing upper GI sources (esophagus, stomach, duodenum) from lower GI sources (jejunum, ileum, colon, rectum) with common pathologies at each location. Panel B: Clinical presentations showing hematemesis (always upper), melena (90% upper), and hematochezia (usually lower but can indicate brisk upper bleeding) with source correlations. Panel C: Epidemiology comparison of upper GI bleeding (100-150 per 100,000, 5-10% mortality) versus lower GI bleeding (20-30 per 100,000, 2-4% mortality). Panel D: Hemodynamic severity classification from mild (hemoglobin above 10, stable vitals) through moderate (orthostatic changes), severe (hypotension at rest), and massive (hemorrhagic shock).
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## Upper GI Bleeding: Causes
Upper GI bleeding arises from sources proximal to the ligament of Treitz, with peptic ulcer disease representing the most common etiology. Understanding the spectrum of causes enables appropriate diagnostic suspicion and management planning.
Peptic ulcer disease accounts for thirty to forty percent of upper GI bleeding episodes. Duodenal ulcers bleed more commonly than gastric ulcers. Risk factors include Helicobacter pylori infection and NSAID use, often occurring together. Posterior duodenal ulcers are particularly prone to severe hemorrhage because of their proximity to the gastroduodenal artery; erosion into this vessel produces massive bleeding. The Forrest classification grades ulcer bleeding stigmata and predicts rebleeding risk, guiding endoscopic therapy decisions.
Erosive mucosal disease, including erosive esophagitis and erosive gastritis, causes fifteen to twenty percent of upper GI bleeding. These lesions typically produce low-volume bleeding and rarely require endoscopic intervention, though they may cause significant blood loss in aggregate.
Esophageal and gastric varices account for ten to twenty percent of upper GI bleeding overall but represent the most common cause in patients with cirrhosis and portal hypertension. Approximately thirty percent of patients with large varices experience hemorrhage within two years. Variceal bleeding carries fifteen to twenty percent mortality per episode, making it a true medical emergency.
Mallory-Weiss tears cause five to ten percent of upper GI bleeding, occurring as longitudinal mucosal lacerations at the gastroesophageal junction. The classic history involves forceful vomiting or retching preceding hematemesis, though this history is not always obtained. Most Mallory-Weiss tears stop bleeding spontaneously and require only supportive care.
Malignancy accounts for two to five percent of upper GI bleeding. Gastric adenocarcinoma, esophageal cancer, and GI stromal tumors may present with bleeding that is often chronic and occult but occasionally acute.
Vascular lesions, though less common, require recognition. Dieulafoy lesions are aberrant submucosal arteries, typically located in the proximal stomach along the lesser curvature, that erode through the overlying mucosa without an associated ulcer. They cause intermittent, sometimes massive arterial bleeding and can be difficult to identify endoscopically between bleeding episodes. Angiodysplasia, dilated mucosal vessels, may occur throughout the GI tract and cause chronic or acute bleeding.
Despite thorough evaluation, ten to fifteen percent of upper GI bleeding episodes have no source identified on endoscopy, potentially due to lesions that have healed or intermittent bleeding sources.
Panel A: Pie chart of upper GI bleeding etiologies showing peptic ulcer disease (30-40%), erosive disease (15-20%), varices (10-20%), Mallory-Weiss (5-10%), malignancy (2-5%), and no source identified (10-15%). Panel B: Peptic ulcer bleeding with posterior duodenal ulcer anatomy near gastroduodenal artery and Forrest classification (Ia-III) with rebleeding risk percentages. Panel C: Variceal bleeding showing portal hypertension pathophysiology, collateral formation at the esophagogastric junction, and endoscopic appearance with red wale signs. Panel D: Other causes including Mallory-Weiss tear at the GE junction, Dieulafoy lesion on the lesser curvature, and malignancy with ulcerated mass appearance.
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## Non-Variceal Upper GI Bleeding Management
Management of non-variceal upper GI bleeding follows a structured approach encompassing resuscitation, risk stratification, pharmacotherapy, endoscopic intervention, and post-endoscopic care.
Initial resuscitation takes priority in any patient with significant hemorrhage. Airway protection through intubation should be considered in patients with massive hematemesis, altered mental status, or inability to protect against aspiration. Intravenous access through two large-bore peripheral catheters enables rapid volume resuscitation. Crystalloid fluids restore circulating volume while blood products are being prepared. Patients with hemodynamic instability require intensive care unit admission.
Risk stratification guides disposition and timing of intervention. The Glasgow-Blatchford score, calculated at presentation before endoscopy, incorporates hemoglobin, blood urea nitrogen, blood pressure, heart rate, presentation with melena or syncope, and presence of liver disease or heart failure. A score of zero or one identifies very low-risk patients who may be safely managed as outpatients with elective endoscopy. The Rockall score, calculated after endoscopy, incorporates clinical variables plus endoscopic findings to predict mortality and rebleeding.
Pre-endoscopic medical management includes proton pump inhibitor therapy and consideration of prokinetics. Intravenous PPI at high dose (80 mg bolus followed by 8 mg/hour continuous infusion) may downstage high-risk lesions before endoscopy, reducing the appearance of active bleeding and improving visualization. Erythromycin (250 mg IV) given before endoscopy promotes gastric emptying and improves visualization in patients with significant blood or clot in the stomach. Anticoagulation should be held; reversal agents are indicated for life-threatening hemorrhage but should not delay endoscopy.
Timing of endoscopy balances adequate resuscitation against delays that might allow rebleeding. Most patients should undergo esophagogastroduodenoscopy within 24 hours of presentation. High-risk patients with hemodynamic instability, active hematemesis, or bloody nasogastric aspirate may benefit from earlier endoscopy within 12 hours, though resuscitation should not be compromised for procedural speed.
Endoscopic therapy for high-risk lesions employs multiple modalities. Injection therapy with dilute epinephrine (1:10,000 or 1:20,000) provides temporary hemostasis through vasoconstriction and tamponade but should not be used as monotherapy because rebleeding rates are high. Thermal therapy using bipolar coagulation or heater probe coagulates the bleeding vessel. Mechanical therapy with endoscopic clips provides direct vessel closure. Combination therapy (injection plus thermal or mechanical) is more effective than any single modality. Hemostatic powders (such as TC-325/Hemospray) provide temporary hemostasis and are useful as adjunctive or bridge therapy.
The Forrest classification determines which lesions require endoscopic therapy. High-risk stigmata mandating treatment include active bleeding (Forrest Ia spurting, Ib oozing), non-bleeding visible vessel (IIa), and adherent clot (IIb, after clot removal if possible). Low-risk stigmata (flat pigmented spot IIc, clean ulcer base III) do not require endoscopic therapy.
Post-endoscopic management continues PPI therapy. High-risk stigmata warrant continuation of high-dose intravenous PPI infusion for 72 hours, followed by twice-daily oral PPI. Low-risk stigmata may be managed with oral PPI from the outset. All patients with peptic ulcer bleeding should be tested for H. pylori and treated if positive. NSAID discontinuation is essential; if NSAIDs cannot be avoided, a PPI should be co-prescribed. Rebleeding occurs in approximately ten to twenty percent of high-risk lesions and should prompt repeat endoscopy. Persistent or recurrent bleeding despite endoscopic therapy may require interventional radiology (transarterial embolization) or surgical intervention.
Panel A: Initial resuscitation with airway assessment, two large-bore IV access, crystalloid resuscitation, and ICU admission criteria alongside Glasgow-Blatchford score components and low-risk discharge criteria. Panel B: Pre-endoscopic management including IV PPI (80 mg bolus plus 8 mg/hr infusion), erythromycin (250 mg IV), and anticoagulation management with endoscopy timing within 24 hours. Panel C: Endoscopic therapy modalities showing injection (epinephrine, not monotherapy), thermal (bipolar/heater probe), mechanical (clips), and hemostatic powder, with Forrest classification determining treatment. Panel D: Post-endoscopic care with PPI continuation protocols, H. pylori testing and treatment, NSAID counseling, and rebleeding management (repeat endoscopy, IR embolization, surgery).
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## Variceal Bleeding Management
Variceal hemorrhage represents a distinct clinical entity requiring specialized management that differs fundamentally from non-variceal bleeding. The combination of portal hypertension, coagulopathy, and underlying liver disease creates unique challenges.
Acute resuscitation in variceal bleeding follows specific principles. Fluid resuscitation should be more conservative than in non-variceal bleeding because aggressive volume expansion increases portal pressure and may worsen bleeding. Transfusion should maintain hemoglobin in the 7 to 8 g/dL range rather than normal values; higher targets are associated with increased rebleeding and mortality. Airway protection through intubation is frequently necessary given the massive volume of hematemesis typical of variceal bleeding.
Vasoactive drug therapy reduces portal pressure and splanchnic blood flow. Octreotide, a somatostatin analog, is administered as a 50 microgram intravenous bolus followed by 50 microgram per hour continuous infusion, continued for two to five days. Terlipressin, a vasopressin analog with longer half-life and fewer side effects, is preferred where available. These agents should be initiated at presentation, before endoscopy.
Prophylactic antibiotics have proven to reduce mortality, rebleeding, and infection in variceal bleeding. Ceftriaxone 1 gram intravenously daily for seven days is the preferred regimen, particularly effective against the spontaneous bacterial peritonitis that frequently complicates variceal hemorrhage in cirrhotic patients.
Endoscopic therapy should occur within 12 hours of presentation. Band ligation is the first-line treatment for esophageal varices, achieving hemostasis through mechanical strangulation of the varix. Sclerotherapy with injection of sclerosant agents provides an alternative when banding is technically not feasible. Gastric varices, which have different anatomic characteristics, are treated with cyanoacrylate (glue) injection rather than banding.
Rescue therapies are employed when endoscopic therapy fails to control bleeding. Balloon tamponade using a Sengstaken-Blakemore or Minnesota tube provides temporary hemostasis through direct pressure but carries significant risks including aspiration, esophageal rupture, and rebleeding upon deflation. It serves as a bridge to definitive therapy rather than a definitive treatment. Transjugular intrahepatic portosystemic shunt (TIPS) creates a connection between the portal and hepatic veins, decompressing the portal system. Early TIPS, performed within 72 hours (ideally within 24 hours) of presentation in high-risk patients (Child-Pugh class C with score 10 to 13, or class B with active bleeding on endoscopy), improves survival compared to standard endoscopic management.
Secondary prophylaxis after variceal bleeding aims to prevent recurrence, which occurs in approximately sixty percent of patients within one to two years without intervention. Band ligation is repeated every two to four weeks until varices are eradicated. Non-selective beta-blockers (propranolol, nadolol, or carvedilol) reduce portal pressure through reduction of cardiac output and splanchnic vasoconstriction. Combination therapy with both band ligation and beta-blockers provides superior protection. TIPS is considered for patients who rebleed despite combined medical and endoscopic therapy.
Panel A: Resuscitation principles with conservative fluid management, restrictive transfusion (hemoglobin target 7-8 g/dL), airway protection, and pharmacotherapy (octreotide, ceftriaxone prophylactic antibiotics). Panel B: Endoscopic therapy showing band ligation technique for esophageal varices, sclerotherapy as alternative, and cyanoacrylate injection for gastric varices. Panel C: Rescue therapies including balloon tamponade (Sengstaken-Blakemore tube as bridge) and TIPS procedure with early TIPS criteria for high-risk patients. Panel D: Secondary prophylaxis with band ligation protocol (every 2-4 weeks until eradication), beta-blocker options (propranolol, nadolol, carvedilol), combination therapy, and TIPS for refractory bleeding.
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## Lower GI Bleeding: Causes and Management
Lower GI bleeding originates distal to the ligament of Treitz and presents differently than upper GI hemorrhage. Most lower GI bleeding stops spontaneously, and mortality is lower than with upper GI bleeding, but significant hemorrhage requiring intervention occurs in a substantial minority.
Diverticular bleeding represents the most common cause of lower GI bleeding, accounting for thirty to forty percent of cases. Bleeding occurs when the vasa recta, the straight arteries supplying the colonic wall, erode at the dome of a diverticulum. The classic presentation is painless, large-volume hematochezia. Despite the predominance of diverticula in the left colon, right-sided diverticula are more commonly responsible for bleeding. Approximately eighty percent of diverticular bleeding stops spontaneously, though recurrence rates of twenty-five to forty percent necessitate consideration of definitive management after stabilization.
Angiodysplasia (arteriovenous malformations) causes ten to twenty percent of lower GI bleeding. These lesions consist of dilated, tortuous submucosal vessels that communicate directly with veins, bypassing the capillary bed. The right colon is the most common location. An association with aortic stenosis (Heyde syndrome) exists through mechanisms involving acquired von Willebrand factor deficiency. Chronic kidney disease also increases risk. Endoscopic treatment with argon plasma coagulation or other thermal methods provides hemostasis.
Hemorrhoids cause five to twenty percent of lower GI bleeding presentations, typically manifesting as small-volume bright red blood on tissue or dripping into the toilet bowl. Internal hemorrhoids are the usual source, as they overlie the superior hemorrhoidal venous plexus.
Inflammatory conditions including inflammatory bowel disease, ischemic colitis, and infectious colitis cause ten to fifteen percent of lower GI bleeding. Ischemic colitis characteristically presents with crampy abdominal pain followed by bloody diarrhea, affecting watershed areas such as the splenic flexure.
Colorectal neoplasia accounts for ten to fifteen percent of cases. Right-sided tumors often present with occult bleeding and iron deficiency anemia, while left-sided lesions may cause overt hematochezia or obstruction.
Post-polypectomy bleeding represents a recognized complication, occurring in approximately five percent of polypectomies, sometimes delayed by one to two weeks.
Initial assessment of lower GI bleeding includes hemodynamic evaluation and resuscitation as needed. Digital rectal examination confirms the presence of blood and may identify hemorrhoids or masses. A nasogastric aspirate, though controversial, may be considered when clinical presentation leaves uncertainty about upper versus lower source.
Risk stratification using tools such as the Oakland score helps identify patients safe for outpatient management versus those requiring admission. Factors predicting severe bleeding include hemodynamic instability, low hemoglobin, prior lower GI bleeding, and absence of isolated rectal bleeding.
Colonoscopy is the primary diagnostic and therapeutic modality. Urgent colonoscopy within 24 hours is indicated for hemodynamically significant bleeding. Rapid bowel preparation (4 to 6 hours) improves visualization and diagnostic yield. Endoscopic therapy with clips, thermal coagulation, or injection treats identified bleeding sources. When bleeding is not localized endoscopically and is ongoing, CT angiography identifies active extravasation and guides subsequent intervention. Angiographic embolization provides nonsurgical hemostasis when a bleeding vessel is identified. Tagged red blood cell scanning may help localize intermittent bleeding before angiography. Surgical resection is reserved for massive or recurrent bleeding when the source is localized.
Panel A: Pie chart of lower GI bleeding etiologies with diverticular (30-40%), angiodysplasia (10-20%), hemorrhoids (5-20%), colitis (10-15%), colorectal neoplasia (10-15%), and post-polypectomy (5%). Panel B: Diverticular bleeding anatomy showing vasa recta at diverticulum dome, predominantly right-sided bleeding, 80% spontaneous cessation, and 25-40% recurrence rate. Panel C: Angiodysplasia panel with AVM anatomy, right colon predilection, Heyde syndrome association with aortic stenosis, and argon plasma coagulation treatment. Panel D: Management algorithm from initial assessment and risk stratification through urgent colonoscopy, CT angiography for unlocalized bleeding, angiographic embolization, and surgery for massive or recurrent bleeding.
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## Obscure GI Bleeding
Obscure GI bleeding refers to bleeding from a source not identified after complete upper and lower endoscopy. This challenging clinical scenario typically involves bleeding from the small bowel, the portion of the GI tract not visualized by standard endoscopy. Obscure bleeding may be overt (visible) or occult (manifesting as iron deficiency anemia).
Small bowel sources account for the majority of obscure bleeding. Angiodysplasia is the most common cause, responsible for thirty to forty percent of cases. These lesions may be multiple and distributed throughout the small bowel. Small bowel tumors, including adenocarcinoma, carcinoid tumors, GI stromal tumors, and lymphoma, cause five to ten percent. Crohn's disease with small bowel involvement causes five to ten percent. NSAID enteropathy, producing small bowel ulcers and erosions, accounts for a similar proportion. Meckel's diverticulum, containing ectopic gastric mucosa that produces acid and causes ulceration, is an important cause in younger patients. Dieulafoy lesions, though typically gastric, may occur in the small bowel.
Video capsule endoscopy has become the first-line diagnostic modality for obscure bleeding. The patient swallows a small capsule containing a camera, light source, and transmitter. The capsule traverses the entire small bowel over eight to twelve hours, capturing images that are recorded and later reviewed. Diagnostic yield for obscure bleeding ranges from forty to sixty percent. Limitations include inability to perform biopsy or therapy, inability to control the capsule's position or speed, and contraindication in patients with strictures or obstruction where the capsule might become lodged.
Push enteroscopy allows examination of the proximal jejunum using a long endoscope inserted orally. While limited in reach (typically 50 to 100 cm beyond the ligament of Treitz), it enables biopsy and therapeutic intervention for proximal small bowel lesions.
Balloon-assisted enteroscopy (single-balloon or double-balloon) enables deeper small bowel examination and therapeutic intervention. The technique uses overtube balloons to pleat the small bowel over the endoscope, allowing sequential advancement. Antegrade (oral) and retrograde (anal) approaches together can achieve complete small bowel visualization. This modality is typically employed after capsule endoscopy identifies a lesion requiring intervention.
CT enterography or MR enterography provides cross-sectional imaging of the small bowel, particularly useful for identifying masses or inflammatory changes in Crohn's disease.
Technetium-99m pertechnetate scintigraphy (Meckel scan) detects ectopic gastric mucosa and should be considered in younger patients with obscure bleeding, as Meckel's diverticulum is a treatable cause.
Angiography may identify actively bleeding lesions, with embolization providing therapeutic option, but requires bleeding rates of at least 0.5 to 1 mL per minute for detection.
Intraoperative enteroscopy, performed during laparotomy with the surgeon assisting passage of the endoscope through the entire small bowel, represents the most invasive option and is reserved for patients with recurrent obscure bleeding in whom other modalities have failed.
Panel A: Definition and classification of obscure GI bleeding (no source after EGD and colonoscopy) with overt-obscure versus occult-obscure subtypes and small bowel sources pie chart (angiodysplasia 30-40%, tumors, Crohn's, NSAID enteropathy, Meckel's diverticulum). Panel B: Video capsule endoscopy showing device components (camera, LED, transmitter, battery), passage through small bowel, and 40-60% diagnostic yield with contraindications. Panel C: Evaluation algorithm from capsule endoscopy through balloon-assisted enteroscopy, CT/MR enterography, Meckel scan, angiography, and intraoperative enteroscopy as last resort. Panel D: Balloon-assisted enteroscopy technique showing balloon inflation and small bowel pleating with therapeutic intervention capabilities for identified lesions.
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## Special Considerations in GI Bleeding
Several clinical situations require modified approaches to GI bleeding management.
Anticoagulation management presents a common dilemma. For warfarin-anticoagulated patients, reversal with vitamin K, fresh frozen plasma, or prothrombin complex concentrate is appropriate for severe or life-threatening bleeding, with prothrombin complex concentrate providing more rapid and complete reversal. For direct oral anticoagulants (DOACs), specific reversal agents are available: idarucizumab for dabigatran and andexanet alfa for factor Xa inhibitors (rivaroxaban, apixaban). These should be reserved for life-threatening hemorrhage given their cost and the usually self-limited nature of most GI bleeding. Antiplatelet agents present nuanced decisions: aspirin for secondary cardiovascular prevention should generally be continued (or resumed within 3 to 5 days) given the mortality benefit, while aspirin for primary prevention can be held. Dual antiplatelet therapy after coronary stenting presents particularly high-stakes decisions requiring cardiology input.
Resumption of anticoagulation after bleeding must balance rebleeding risk against the indication for anticoagulation. For patients with high thrombotic risk (mechanical heart valves, recent venous thromboembolism, atrial fibrillation with high CHA2DS2-VASc score), anticoagulation should generally be resumed within seven days after hemostasis is achieved. Endoscopic therapy to reduce rebleeding risk facilitates earlier resumption.
Transfusion strategy significantly impacts outcomes. Restrictive transfusion targeting hemoglobin of 7 to 8 g/dL has proven superior to liberal transfusion (targeting 9 to 10 g/dL) in most GI bleeding settings, with lower mortality and rebleeding rates. This benefit is particularly pronounced in variceal bleeding, where overtransfusion raises portal pressure and increases bleeding risk. Liberal transfusion thresholds may be appropriate for patients with massive hemorrhage, active myocardial ischemia, or severe coronary artery disease. Platelet transfusion is indicated when platelet count is below 50,000 per microliter and active bleeding is present.
Proton pump inhibitor use in upper GI bleeding deserves clarification. Pre-endoscopic PPI administration may downstage high-risk lesions, potentially reducing the need for endoscopic intervention, though it does not reduce mortality, rebleeding, or surgery. Post-endoscopic high-dose PPI infusion (80 mg bolus plus 8 mg/hour for 72 hours) is indicated for high-risk stigmata and reduces rebleeding.
GI bleeding in cirrhotic patients requires recognition of unique physiology. Coagulopathy in cirrhosis reflects both procoagulant and anticoagulant factor deficiency; INR does not reliably indicate bleeding risk, and routine correction with fresh frozen plasma is not indicated. Varices should always be suspected and ruled out in a bleeding cirrhotic patient. Hepatic encephalopathy may be precipitated by the protein load of blood in the GI tract.
ICU patients commonly develop stress-related mucosal disease. Prophylaxis with PPI or H2 receptor antagonist is indicated for high-risk patients (mechanical ventilation greater than 48 hours, coagulopathy, severe illness), though routine prophylaxis in low-risk floor patients is not recommended due to lack of benefit and potential adverse effects.
Panel A: Anticoagulation management showing warfarin reversal (vitamin K, FFP, PCC), DOAC reversal (idarucizumab, andexanet alfa), antiplatelet decisions, and timing of anticoagulation resumption by thrombotic risk. Panel B: Transfusion strategy comparing restrictive (hemoglobin 7-8) versus liberal (hemoglobin 9-10) targets, with restrictive preferred especially in variceal bleeding, and platelet transfusion threshold (below 50,000 with active bleeding). Panel C: PPI role showing pre-endoscopic use (may downstage lesions, no mortality benefit) and post-endoscopic high-dose infusion for high-risk stigmata reducing rebleeding. Panel D: Special populations including cirrhosis (unreliable INR, always suspect varices, hepatic encephalopathy risk from blood protein) and ICU patients (stress ulcer prophylaxis indications).
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## Prevention Strategies
Prevention of GI bleeding encompasses primary prophylaxis for at-risk patients and strategies to minimize procedural bleeding risk.
Primary prophylaxis for variceal bleeding applies to patients with cirrhosis and varices who have not yet bled. All patients with cirrhosis should undergo screening esophagogastroduodenoscopy at diagnosis to assess for varices. Patients without varices should have repeat endoscopy in two to three years. Patients with small varices may receive non-selective beta-blocker therapy (propranolol, nadolol, or carvedilol) or undergo surveillance endoscopy annually. Patients with medium or large varices require primary prophylaxis with either non-selective beta-blockers or endoscopic band ligation. Non-selective beta-blockers reduce cardiac output and cause splanchnic vasoconstriction, lowering portal pressure. The choice between beta-blockers and band ligation depends on patient preference, tolerance, and adherence considerations.
Stress ulcer prophylaxis prevents stress-related mucosal disease in critically ill patients at high risk. Indications include mechanical ventilation exceeding 48 hours, coagulopathy, severe sepsis, and other high-risk states. Either proton pump inhibitors or H2 receptor antagonists provide effective prophylaxis. Prophylaxis should continue only while risk factors persist. Stress ulcer prophylaxis is not indicated in general floor patients without risk factors.
Prevention of NSAID-related GI complications requires risk stratification and appropriate co-therapy. All NSAID users with risk factors for GI complications (history of ulcer, age greater than 65, high-dose NSAID, concurrent anticoagulation or corticosteroids) should receive concomitant PPI therapy. Patients with history of ulcer bleeding should be tested and treated for H. pylori and should avoid NSAIDs if possible; if NSAIDs are necessary, a selective COX-2 inhibitor with PPI co-therapy provides the lowest risk. Patients who can avoid NSAIDs entirely should be encouraged to use acetaminophen for pain relief.
Post-polypectomy bleeding prevention incorporates technical and patient factors. Cold snare polypectomy for small polyps (less than 10 mm) produces lower bleeding rates than hot snare techniques. Prophylactic clip placement may reduce bleeding risk for large polyps (greater than 2 cm) or right-sided polypectomies. Anticoagulation management follows established guidelines, with temporary cessation based on the procedure's bleeding risk and the patient's thrombotic risk. Patients should be counseled that delayed bleeding may occur up to two weeks after polypectomy.
Panel A: Variceal prophylaxis algorithm from cirrhosis diagnosis through screening EGD to management of no varices (repeat in 2-3 years), small varices (beta-blockers or surveillance), and medium/large varices (beta-blockers or band ligation) with NSBB mechanism diagram. Panel B: Stress ulcer prophylaxis showing indications (mechanical ventilation over 48 hours, coagulopathy, severe sepsis), agents (PPI or H2RA), and note that floor patients without risk factors do not need prophylaxis. Panel C: NSAID-related bleeding prevention with risk factors requiring PPI co-therapy, H. pylori test-and-treat, NSAID alternatives, and COX-2 selective plus PPI for high-risk patients. Panel D: Post-polypectomy bleeding prevention with cold snare for small polyps, prophylactic clips for large or right-sided polyps, anticoagulation management, and patient counseling about delayed bleeding.
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## Summary
Upper GI bleeding originates proximal to the ligament of Treitz and presents with hematemesis or melena. Peptic ulcer disease is the most common cause (thirty to forty percent). Management includes resuscitation, risk stratification with the Glasgow-Blatchford score, pre-endoscopic PPI, and esophagogastroduodenoscopy within 24 hours. High-risk stigmata (active bleeding, visible vessel, adherent clot) require endoscopic therapy with combination modalities. Post-endoscopic high-dose PPI infusion continues for 72 hours for high-risk lesions.
Variceal bleeding requires specific management: restrictive transfusion targeting hemoglobin 7 to 8 g/dL, vasoactive drugs (octreotide 50 microgram bolus plus 50 microgram per hour infusion), prophylactic antibiotics (ceftriaxone 1 gram daily for 7 days), and endoscopic band ligation within 12 hours. TIPS is indicated for refractory bleeding and should be considered early (within 72 hours) in high-risk patients. Secondary prophylaxis combines band ligation with non-selective beta-blockers.
Lower GI bleeding most commonly results from diverticular bleeding, presenting with painless hematochezia. Colonoscopy after rapid bowel preparation provides diagnosis and therapy. CT angiography and embolization address ongoing bleeding not controlled endoscopically.
Obscure GI bleeding (no source after EGD and colonoscopy) typically originates in the small bowel, with angiodysplasia being the most common cause. Video capsule endoscopy is the first-line diagnostic test, followed by balloon-assisted enteroscopy for therapeutic intervention.
Transfusion should be restrictive (hemoglobin 7 to 8 g/dL) in most patients, particularly variceal bleeding. Anticoagulation should be held during active bleeding and reversed only for life-threatening hemorrhage. Resumption of anticoagulation depends on thrombotic risk.
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## Key Terms
| Term | Definition |
|------|------------|
| Hematemesis | Vomiting of blood or coffee-ground material, indicating upper GI source |
| Melena | Black tarry stool from upper GI bleeding (ninety percent) or proximal colon |
| Hematochezia | Bright red blood per rectum, usually lower GI source |
| Forrest classification | Endoscopic grading of ulcer bleeding stigmata guiding therapy and prognosis |
| Glasgow-Blatchford score | Pre-endoscopic risk stratification for upper GI bleeding |
| TIPS | Transjugular intrahepatic portosystemic shunt for portal decompression |
| Obscure GI bleeding | Bleeding without identified source after EGD and colonoscopy |
| Capsule endoscopy | Swallowed camera for small bowel visualization |
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