GI Bleeding — Upper and Lower

Acid-peptic / mucosal injury (most common UGIB category)

• Peptic ulcer disease: duodenal > gastric; driven by H. pylori urease-mediated mucosal injury and NSAID inhibition of COX-1–derived protective prostaglandins. Posterior duodenal bulb ulcers erode the gastroduodenal artery; high lesser-curvature gastric ulcers erode the left gastric artery.
• Erosive gastritis/esophagitis: stress-related mucosal disease in ICU patients (mechanical ventilation, coagulopathy, burns — Curling ulcer; head injury with vagal hyperstimulation — Cushing ulcer), alcohol, and reflux.

Portal hypertensive

• Esophagogastric varices and portal hypertensive gastropathy: any cause of cirrhosis, plus non-cirrhotic portal hypertension (portal/splenic vein thrombosis — isolated gastric varices, schistosomiasis).

Mechanical and traumatic

• Mallory-Weiss tear after retching; Boerhaave if transmural. Aortoenteric fistula after aortic graft repair, classically bleeding into the third portion of the duodenum.

Vascular

• Angiodysplasia (right colon, small bowel), Dieulafoy lesion, hereditary hemorrhagic telangiectasia, radiation proctopathy.

Structural / inflammatory / neoplastic (LGIB)

• Diverticulosis (left colon most prevalent, right-sided diverticula bleed more), ischemic colitis, IBD, infectious colitis, colorectal neoplasia, post-polypectomy bleeding, hemorrhoids/fissures, and Meckel diverticulum with ectopic gastric mucosa in children.

Modifiable risk factors

• NSAIDs and aspirin, anticoagulants (warfarin, DOACs) and P2Y12 inhibitors, SSRIs (impair platelet serotonin uptake), corticosteroids combined with NSAIDs, H. pylori infection, alcohol use, smoking, and inadequately treated portal hypertension (non-adherence to or under-dosing of non-selective beta blockers, which are titrated to heart rate/HVPG response rather than to systemic blood pressure).

Non-modifiable risk factors

• Age >60, prior GI bleed (the strongest single predictor), cirrhosis with large varices or red wale signs, chronic kidney disease and uremic platelet dysfunction, aortic stenosis with acquired von Willebrand disease (Heyde syndrome), left ventricular assist devices, and hereditary vascular syndromes.
• USPSTF now frames low-dose aspirin for primary prevention around this bleeding risk, no longer recommending routine initiation in adults ≥60.

Upper GI Bleeding Mechanisms

• Mucosal ulceration and erosion: Disruption of protective mucus layer and bicarbonate secretion allows gastric acid to breach epithelial tight junctions, creating full-thickness defects that expose submucosal and muscular vessels. Most commonly occurs in peptic ulcer disease from Helicobacter pylori infection or NSAIDs.
• Portal hypertension and variceal rupture: Cirrhosis and advanced liver disease cause increased hepatic vascular resistance, leading to portosystemic collateral formation. Esophageal varices develop in response to portal pressures >12 mmHg (hepatic venous pressure gradient), and mechanical shear stress from increased blood flow causes mucosal rupture and uncontrolled hemorrhage.
• Mucosal tears from severe vomiting: Mallory-Weiss tears result from forceful vomiting or retching, causing longitudinal mucosal lacerations in the distal esophagus and gastric cardia due to rapid pressure increases during straining.
• Vascular abnormalities: Dieulafoy lesions are aberrant arteries in the submucosa that erode through the epithelium; angiodysplasias involve abnormal venous collections and telangiectasia prone to bleeding.

Lower GI Bleeding Mechanisms

• Diverticular bleeding: Small penetrating arteries run on the medial aspect of colonic diverticula; bleeding occurs when these vessels erode from mechanical trauma or inflammatory processes, typically painless and often self-limited.
• Inflammatory ulceration: Inflammatory bowel disease (IBD) causes transmural inflammation with crypt abscess formation and ulceration that breaches the lamina propria and muscularis mucosae, exposing bleeding vessels.
• Internal hemorrhoids: Increased venous pressure from straining or portal hypertension causes vascular dilation in the superior hemorrhoidal venous plexus; bleeding occurs when the overlying mucosa erodes or during defecation.
• Colonic polyp pathology: Adenomatous polyps develop dysplastic epithelium with abnormal vascular proliferation; bleeding occurs when surface ulceration exposes dysplastic vessels or during polypectomy.
• Ischemic colitis mechanism: Reduced mesenteric perfusion causes mucosal ischemia, necrosis, and ulceration, typically at "watershed" areas (splenic flexure, rectosigmoid junction) with limited collateral blood supply.

Upper GI Bleeding Presentations

• Hematemesis (vomiting of blood): Direct evidence of active proximal bleeding; "coffee-ground" emesis indicates older, partially digested blood (acidified hemoglobin), suggesting slower bleeding or delayed gastric emptying.
• Melena (black, tarry stools): Results from oxidation of hemoglobin in the acidic stomach; indicates minimum 50 mL of blood loss and suggests bleeding above the ligament of Treitz.
• Hemodynamic instability: Tachycardia (>100 bpm), hypotension (<90 mmHg systolic), cool extremities, and altered mental status indicate significant intravascular volume loss (>30% blood volume); orthostatic vital signs (drop >20 mmHg systolic or >10 mmHg diastolic upon standing) suggest ≥15% volume loss.
• Variceal bleeding specifics: Massive hemoptysis-like presentation; patient may have known cirrhosis, jaundice, spider angiomas, gynecomastia, or ascites.
• Dyspepsia and abdominal pain: May precede bleeding in peptic ulcer disease; Mallory-Weiss tears typically occur after forceful vomiting (often alcohol-related).

Lower GI Bleeding Presentations

• Hematochezia (bright red or maroon stools): Indicates lower source; brisk bleeding may present as bright red blood per rectum (BPRPR), while slower bleeding results in darker, maroon-colored stools mixed with stool.
• Pain patterns: Diverticular bleeding is typically painless; IBD-associated bleeding accompanied by crampy abdominal pain, diarrhea, and tenesmus; ischemic colitis presents with severe abdominal pain out of proportion to findings.
• Bleeding without systemic symptoms: Hemorrhoids and internal bleeding from polyps often present with isolated blood on toilet paper or in stool without hemodynamic changes.
• Age-related presentations: Diverticular bleeding more common in elderly (>60 years); IBD in younger patients; angiodysplasia in elderly with chronic renal disease or aortic stenosis.

Important Clinical Pearls

• Melena always indicates upper source bleeding (proximal to ligament of Treitz); bright red blood can originate from lower sources or rarely rapid upper bleeding.
• Hemodynamic stability does not exclude serious bleeding; repeated episodes may rapidly destabilize.
• Concurrent use of anticoagulants or antiplatelet agents dramatically worsens outcomes and alters management strategy.

Initial Assessment and Risk Stratification

• Vital signs and orthostatics: Baseline heart rate, blood pressure, respiratory rate, and oxygen saturation; orthostatic measurements (lying and standing) quantify volume loss (≥20 mmHg systolic or ≥10 mmHg diastolic drop = significant loss).
• Complete blood count (CBC): Establishes baseline hemoglobin/hematocrit; note that hemoglobin may be falsely reassuring early in acute bleeding (equilibration takes 24–48 hours); platelet count identifies thrombocytopenia as bleeding risk.
• Metabolic panel and coagulation studies: Assess electrolytes, renal function (elevated BUN suggests upper GI source or dehydration; BUN:Cr ratio >30 suggests UGIB), liver function tests, PT/INR (cirrhosis, anticoagulation), aPTT, and fibrinogen.
• Type and crossmatch: Critical before transfusion; type and screen acceptable if stable; reserve blood if high-risk features present.
• Lactate measurement: Elevated lactate (>2 mmol/L) indicates tissue hypoxia and poor prognosis; useful prognostic marker.

Risk Stratification Scores (Upper GI Bleeding)

• Glasgow-Blatchford Score: Outpatient-based scoring system using age, sex, syncope, melena, hemodynamic parameters, and baseline comorbidities; score ≤0 identifies very low-risk patients suitable for outpatient management; score ≥1 warrants admission.
• APACHE II and SOFA scores: Assess severity of illness and sepsis risk; higher scores correlate with mortality and need for intensive care.
• Child-Pugh score (for cirrhotic patients): Predicts mortality in variceal bleeding; combination of albumin, INR, bilirubin, ascites, and encephalopathy grades risk.

Endoscopic Diagnosis (Gold Standard)

• Upper endoscopy (esophagogastroduodenoscopy, EGD): Allows direct visualization, identification of bleeding source, and therapeutic intervention; should be performed within 12 hours of admission (after stabilization); diagnostic accuracy >90% for identifying source.
• Colonoscopy for lower bleeding: Requires adequate bowel preparation (polyethylene glycol or sodium phosphate); can be performed in acute setting if bleeding controlled and risk of aspiration minimal; identifies source in 60–85% of cases.
• Stigmata of recent hemorrhage (Forrest classification for ulcers): Ia = spurting artery (active), Ib = oozing (active), IIa = nonbleeding visible vessel (high risk of rebleeding), IIb = adherent clot (

Immediate stabilization (before any endoscopy)

• Two large-bore peripheral IVs, crystalloid resuscitation, continuous monitoring, and airway protection — intubate for ongoing hematemesis or encephalopathy to prevent aspiration.
• Restrictive transfusion: per ACG, transfuse packed RBCs at a hemoglobin threshold near 7 g/dL (a higher threshold is reasonable in acute coronary syndrome). Over-transfusion in cirrhosis raises portal pressure and worsens variceal rebleeding.
• Reverse anticoagulation without delaying endoscopy: vitamin K plus 4-factor prothrombin complex concentrate for warfarin; idarucizumab for dabigatran; andexanet alfa for factor Xa inhibitors. Routine FFP to "correct" the INR of cirrhosis is not recommended — the INR does not reflect bleeding risk in liver disease.

Pharmacologic first line

• Proton pump inhibitor, e.g., IV pantoprazole as a bolus then infusion: raising intragastric pH above ~6 stabilizes clot by preventing pepsin-mediated fibrinolysis and platelet disaggregation.
• Splanchnic vasoconstrictor for suspected variceal bleed: octreotide infusion, started before endoscopy (AASLD).
• Prophylactic antibiotic in any cirrhotic with GI bleeding: third-generation cephalosporin, e.g., ceftriaxone — reduces infection, rebleeding, and mortality (AASLD).
• Prokinetic erythromycin before EGD may clear the stomach and improve visualization.

Endoscopic therapy

• EGD within 24 hours of presentation for UGIB (ACG). Epinephrine injection must never be used alone — combine with a second modality (clips, thermal coagulation, or hemostatic powder).
• Variceal band ligation for esophageal varices; cyanoacrylate injection for gastric varices.
• Colonoscopy after rapid PEG purge for LGIB (ACG); clip or coagulate the culprit diverticulum or vessel.

Escalation and definitive care

• CT angiography then transcatheter embolization for brisk bleeding that precludes prep or defeats endoscopy.
• TIPS for refractory or recurrent variceal bleeding (pre-emptive TIPS in high-risk cirrhotics per Baveno consensus); balloon tamponade only as a temporizing bridge.
• Surgery (oversew, resection) for failed endoscopic/angiographic control or perforation.

Emergencies (disease-related)

• Hypovolemic shock and exsanguination: loss of >30–40% blood volume overwhelms compensatory tachycardia; narrow pulse pressure, cool mottled extremities, rising lactate, and oliguria signal decompensation. Emergency.
• Aspiration pneumonitis: hematemesis with depressed consciousness; new hypoxemia and a right lower lobe infiltrate after the bleed. Emergency — the reason to intubate before EGD.
• Type 2 (demand) myocardial infarction: anemia plus tachycardia reduces coronary supply while raising demand; look for a troponin rise with ST depression in an elderly patient. Emergency.
• Rebleeding: highest with Forrest Ia/Ib and visible vessels; heralded by recurrent hematemesis, fresh melena, tachycardia, or a hemoglobin drop after apparent hemostasis. Emergency — repeat endoscopy.

Cirrhosis-specific consequences

• Hepatic encephalopathy: intraluminal blood is a large nitrogen load metabolized to ammonia; asterixis and confusion after a variceal bleed. Treat with lactulose.
• Spontaneous bacterial peritonitis and sepsis: bacterial translocation during hemorrhage — the rationale for ceftriaxone prophylaxis.
• Hepatorenal syndrome / acute kidney injury from renal hypoperfusion.

Treatment-related

• Transfusion complications: TACO (volume overload, pulmonary edema soon after transfusion), TRALI (non-cardiogenic pulmonary edema within 6 hours), citrate-induced hypocalcemia and dilutional coagulopathy with massive transfusion.
• Post-band ulceration or esophageal stricture/perforation; sclerotherapy carries higher stricture risk.
• Balloon tamponade: esophageal pressure necrosis and rupture, airway obstruction if the balloon migrates. Emergency.
• TIPS: new or worsened hepatic encephalopathy from portosystemic shunting, and shunt thrombosis.
• Angioembolization: bowel ischemia/infarction, contrast nephropathy, access-site hematoma.
• Colonoscopy/polypectomy: perforation (free air, peritonitis) and delayed post-polypectomy bleeding up to two weeks later. Perforation is an emergency.

• BUN:creatinine ratio >30 with a normal creatinine points to an upper source — absorbed hemoglobin nitrogen plus prerenal physiology. Paired with melena, this is the classic stem giveaway.
• Hematochezia plus hemodynamic instability = do EGD first. A brisk upper bleed transits too fast to be oxidized into melena; the reflexive "colonoscopy" answer is the trap.
• A negative nasogastric lavage does not exclude UGIB (a pyloric-channel or duodenal bleed may not reflux); NG lavage is no longer part of routine management. Similarly, an initially normal hemoglobin is expected early — equilibration takes 24–48 hours.
• Cirrhotic with hematemesis: two pre-endoscopic drugs improve outcomes — a splanchnic vasoconstrictor (octreotide in the US) and prophylactic ceftriaxone, with antibiotics carrying the clearest mortality benefit — both started before endoscopy, followed by band ligation within 12 hours (AASLD). Band ligation itself, and pre-emptive TIPS in selected high-risk patients (Baveno consensus), also affect survival. Do not delay antibiotics waiting for fever.
• Epinephrine injection alone is never the right answer — the ACG requires a second modality (clip or thermal) because epinephrine's effect is transient vasoconstriction, not vessel obliteration.
• Transfuse restrictively (threshold near 7 g/dL per ACG); in varices, over-transfusion raises portal pressure and provokes rebleeding.
• Named associations examiners love: aortic stenosis + colonic angiodysplasia + acquired type 2A von Willebrand disease = Heyde syndrome; painless massive rectal bleeding in a toddler = Meckel diverticulum, next step a technetium-99m pertechnetate scan; herald bleed weeks after aortic graft = aortoenteric fistula; retching then hematemesis in a drinker = Mallory-Weiss tear (usually self-limited).
• After a bleeding peptic ulcer, test and treat H. pylori and confirm eradication; a negative test during acute bleeding can be falsely negative and must be repeated.
• Crampy left-sided abdominal pain followed within 24 hours by bloody diarrhea in an older patient after a hypotensive/low-flow event = ischemic colitis at the splenic flexure or rectosigmoid watershed, with tenderness concordant with the pain; management is supportive (bowel rest, IV fluids, correct the perfusion deficit) unless peritonitis, gangrene, or perforation develops. Contrast this with acute mesenteric ischemia — severe pain out of proportion to a benign abdomen, usually without early hematochezia — which requires emergent CT angiography and revascularization.