Lower GI Bleeding

• Vascular mechanisms in diverticular bleeding: Diverticula form through herniation of mucosa and submucosa at points of weakness where blood vessels penetrate the colonic wall, particularly along the taeniae coli. The vasa recta run within the diverticular walls; progressive atherosclerotic disease and age-related loss of elastic fibers in vessel walls predispose to erosion of these vessels into the diverticular lumen. Bleeding occurs painlessly and may be voluminous due to the relatively large caliber of the penetrating vessels. This accounts for approximately 30-40% of lower GI bleeding in Western populations.

• Inflammatory mechanisms in infectious and idiopathic inflammatory bowel disease (IBD): Acute mucosal inflammation with edema, erosion, and ulceration of the bowel wall disrupts the epithelial barrier and exposes submucosal blood vessels. In infectious colitis, bacterial invasion triggers mucosal neutrophilic infiltration, production of pro-inflammatory cytokines (TNF-α, IL-1, IL-6), and increased intestinal permeability. In IBD, dysregulated Th1/Th17 T-cell immunity creates chronic transmural inflammation with crypt distortion and ulcer formation; bleeding typically accompanies other symptoms (diarrhea, abdominal pain, fever) reflecting the inflammatory milieu.

• Vascular malformations and angiogenesis pathology: Angiodysplasia (acquired vascular ectasia) and arteriovenous malformations (AVMs) represent focal abnormalities in vascular architecture, often in areas of chronic mucosal ischemia or associated with underlying conditions like aortic stenosis or renal failure. These lesions lack normal sphincter muscle surrounding vessels, predisposing to bleeding from trivial mucosal trauma. The pathogenic mechanism involves chronic low-flow states activating hypoxia-responsive transcription factors (HIF-1α), promoting aberrant neovascularization and loss of normal vascular pericyte coverage.

• Mechanical trauma in hemorrhoids and anal fissures: Internal hemorrhoids are submucosal vascular cushions at the rectoanal junction that enlarge through increased venous pressure (straining, portal hypertension) and disruption of supporting connective tissue. Direct mechanical trauma during defecation or passage of hard stool causes superficial erosion with brisk, typically self-limited bleeding. Anal fissures represent acute or chronic tears in the anoderm below the dentate line, causing bleeding with characteristic severe pain during and after defecation.

• Neoplastic mechanisms: Colorectal malignancies cause bleeding through invasion of submucosal and muscular vessels, ulceration of the mucosa overlying the tumor mass, and impaired hemostasis due to neoangiogenesis with immature, friable blood vessels lacking adequate perivascular support. Bleeding is typically slower and chronic rather than massive acute hemorrhage.

• Anticoagulation and coagulopathy effects: Therapeutic anticoagulation (warfarin, DOACs, heparin) impairs the coagulation cascade by inhibiting vitamin K-dependent factors, direct thrombin inhibition, or factor Xa inhibition, respectively. In patients with underlying structural colonic lesions (diverticula, angiodysplasia), anticoagulation lowers the hemostatic threshold, converting a minor mucosal defect into clinically significant bleeding. Platelet dysfunction and thrombocytopenia similarly compromise primary hemostasis at the mucosa.

• Diverticular disease (25-50% of cases in developed countries): Colonic diverticula are acquired herniations of mucosa through the muscular wall, with prevalence increasing with age (present in ~60% of those >80 years). Approximately 5-10% of patients with diverticula develop diverticulitis, but 10-15% experience painless lower GI bleeding. Diverticular bleeding is the most common cause of massive lower GI hemorrhage requiring transfusion. Risk factors include low dietary fiber intake, chronic use of NSAIDs, and possibly aspirin and anticoagulants.

• Hemorrhoids (40-50% of cases, particularly bright red blood per rectum without systemic symptoms): Internal hemorrhoids above the dentate line are extremely common (prevalence ~50% of population) and often asymptomatic; bleeding occurs with straining, hard stool passage, or prolonged sitting on toilet. External hemorrhoids, thrombosed or otherwise, present with acute pain and sometimes bleeding. Risk factors include chronic constipation, pregnancy, portal hypertension, and prolonged straining from any cause.

• Inflammatory bowel disease (10-15% of acute lower GI bleeding): Ulcerative colitis (UC) causes continuous mucosal inflammation starting at the rectum and extending proximally; disease severity correlates with bleeding risk. Crohn's disease can involve any segment of bowel and presents with more focal ulceration and potentially deeper inflammation, though gross bleeding is less common than in UC. Extraintestinal manifestations (arthritis, uveitis, primary sclerosing cholangitis) may offer diagnostic clues.

• Infectious colitis (3-5% of cases): Bacterial pathogens (Campylobacter jejuni, Shigella, Salmonella, enteroinvasive E. coli), viral agents (norovirus, rotavirus, cytomegalovirus in immunocompromised patients), and parasites (Entamoeba histolytica, schistosomiasis in endemic regions) cause acute mucosal inflammation with diarrhea and hematochezia. Distinguishing features include recent antibiotic exposure, travel history, or immunosuppression. Bloody diarrhea is most common with Shigella and Campylobacter.

• Angiodysplasia and vascular malformations (3-8% of cases): Acquired angiodysplasia accounts for ~5% of lower GI bleeding and increases with age, chronic kidney disease, and aortic stenosis. These lesions are often right-sided and may be multiple; they cause chronic intermittent bleeding or occult bleeding with anemia. Familial conditions like hereditary hemorrhagic telangiectasia (HHT) and Peutz-Jeghers syndrome predispose to diffuse vascular lesions and GI bleeding across all bowel segments.

• Colorectal and small bowel malignancy (5-10% of cases): Colorectal cancer typically presents with chronic occult bleeding and anemia rather than acute hemorrhage; left-sided lesions more commonly present with blood mixed in stool, while right-sided lesions often cause iron-deficiency anemia without obvious gross bleeding. Small bowel cancers are rare but are increasingly recognized as sources of obscure GI bleeding.

• Ischemic colitis (1-5% of cases, but increasing with age): Acute interruption of colonic blood supply from arterial occlusion, venous thrombosis, or low-flow states causes acute bloody diarrhea with left-sided abdominal pain, typically in patients >60 years with cardiovascular disease. Watershed areas (Griffith's point at splenic flexure, Sudeck's point at rectosigmoid junction) are vulnerable.

• Post-polypectomy syndrome: Delayed bleeding after colonoscopic polypectomy occurs in 0.3-6% of cases, typically within 2 weeks; thermal injury to the colonic wall causes transmural necrosis with subsequent vessel erosion and hemorrhage.

• Anticoagulation and antithrombotic therapy: Warfarin (INR >4), direct oral anticoagulants (apixaban, rivaroxaban, dabigatran), and antiplatelet agents (aspirin, clopidogrel, ticlopidine) substantially increase bleeding risk in patients with underlying colonic lesions. The relative risk increase is 1.5-3.0-fold depending on the agent and baseline bleeding risk.

• NSAIDs and aspirin: Both are independent risk factors for lower GI bleeding through mucosal erosion and impaired platelet function; the effect is dose- and duration-dependent.

• Hematochezia (bright red blood per rectum): Represents the most common presentation of lower GI bleeding, particularly with sources distal to the ligament of Treitz. The blood is characteristically bright red or maroon in color, reflecting minimal time for bacterial degradation of hemoglobin. Massive, rapid bleeding (>1000 mL/hr) may present as brisk hematochezia with hemodynamic compromise. The presence of hematochezia does not exclude proximal (upper) GI bleeding; in ~15% of cases with upper GI bleeding and rapid transit (as in variceal bleeding or right-sided colonic sources), bright red blood appears per rectum.

• Melena (black, tarry stools): Results from oxidation of hemoglobin to hematin by gastric acid and bacterial action; indicates slower bleeding or blood that has transited the proximal GI tract. While classically associated with upper GI bleeding, right-sided colonic bleeding or small bowel bleeding with slow transit may present as melena, creating diagnostic uncertainty. The presence of melena suggests ≥50 mL of blood in the GI tract.

• Occult GI bleeding: Microscopic blood loss without gross hematochezia or melena, detected by fecal occult blood testing, often reflects chronic bleeding from lesions like angiodysplasia or malignancy. Patients present with iron-deficiency anemia, fatigue, and dyspnea rather than acute bleeding symptoms.

• Hemodynamic compromise: Rapid blood loss exceeding 20-30% of blood volume triggers compensatory sympathetic activation with tachycardia, tachypnea, peripheral vasoconstriction, and eventual hypotension and altered mental status if bleeding continues. Orthostatic vital signs (systolic BP drop >20 mmHg or HR increase >20 bpm with standing) indicate ≥15% blood volume loss. Shock develops when >30-40% of circulating volume is lost.

• Associated abdominal pain: Absence of pain is the rule in diverticular bleeding and hemorrhoidal bleeding, helping differentiate these from inflammatory causes. Acute left lower quadrant or diffuse abdominal pain with bleeding suggests ischemic colitis, infectious colitis, or IBD flare. Chronic, intermittent bleeding with weight loss and altered bowel habits should raise concern for malignancy. Severe anal pain with bright red blood and small volume bleeding is characteristic of anal fissure.

• Diarrhea and systemic symptoms: Infectious colitis presents with acute diarrhea (often watery with blood and mucus), fever (often >38.5°C), and tenesmus. IBD presents with chronic diarrhea (often 4-6+ stools daily), weight loss, nocturnal symptoms, and extraintestinal manifestations. Absence of diarrhea argues against infectious and inflammatory causes.

• Physical examination findings: Vital signs assessment is paramount—tachycardia and hypotension indicate significant blood loss. Abdominal examination may reveal left lower quadrant tenderness in ischemic colitis or IBD, or be benign in diverticular or hemorrhoidal bleeding. Digital rectal examination (DRE) and anoscopy are essential to identify hemorrhoids, anal fissures, or rectal masses; visible blood in the anal verge or hemorrhoid is diagnostic of a distal source. In massive lower GI bleeding, bright red blood or clots in the rectum without identified source below mandates urgent evaluation for more proximal colonic or small bowel sources.

• Clinical variants by etiology: Diverticular bleeding is sudden-onset, painless, often voluminous (>500 mL), with hemodynamic compromise; hemorrhoidal bleeding is minimal volume, bright red, associated with defecation and visible on anoscopy; IBD bleeding accompanies diarrhea, abdominal pain, and systemic symptoms; ischemic colitis presents with abdominal pain, bloody diarrhea, and signs of systemic illness in an elderly patient with cardiovascular disease.

• Historical features guiding diagnosis: Onset and rapidity of bleeding—sudden painless massive hemorrhage suggests diverticular bleeding, while gradual chronic bleeding with anemia suggests angiodysplasia or malignancy. Associated symptoms are crucial: diarrhea and fever with bleeding suggests infectious colitis; chronic diarrhea, weight loss, abdominal pain with blood suggest IBD or malignancy; absence of symptoms with bright red blood suggests hemorrhoids or anal fissure. Medication history should specifically address anticoagulants (warfarin with target INR, direct oral anticoagulants), antiplatelet agents, and NSAIDs. Prior episodes of bleeding are common in diverticular disease (recurrence rate 20-30% after first episode) and angiodysplasia. Age is critical: >60 years makes diverticular disease, angiodysplasia, and malignancy more likely; <40 years makes IBD and hemorrhoids more probable.

• Laboratory assessment:
• Complete blood count: Establishes baseline hemoglobin/hematocrit and degree of anemia; acute brisk bleeding may show initially normal Hb due to acute volume contraction and compensatory hemodilution. Serial measurements track ongoing bleeding and transfusion requirements. Platelet count may reveal thrombocytopenia as a contributory factor.
• Coagulation studies (PT/INR, aPTT, fibrinogen): Essential if patient is on anticoagulation or has liver disease, bleeding disorder, or massive transfusion requirements (>6 units PRBC). Elevated INR in a patient on warfarin necessitates reversal with fresh frozen plasma, prothrombin complex concentrate (PCC), or vitamin K.
• Basic metabolic panel: Assesses renal function (baseline creatinine for contrast use in imaging), electrolytes (hypokalemia common with chronic diarrhea), and anion gap (metabolic acidosis indicates tissue hypoperfusion/shock).
• Type and crossmatch: Mandatory in all but the most trivial bleeding; crossmatched RBCs allow rapid transfusion.
• Fecal occult blood testing: Positive in occult GI bleeding but has poor positive predictive value (many false positives) and should not delay endoscopic evaluation.

• Nasogastric (NG) tube aspirate: Mandatory to exclude upper GI source in any patient with hematochezia or melena, as brisk upper GI bleeding can present with apparent lower GI hemorrhage. Clear, non-bloody NG aspirate excludes active upper GI bleeding with >90% sensitivity but does not exclude a non-bleeding upper GI source (e.g., esophageal varices that have stopped bleeding). Bilious NG aspirate rules out pyloric obstruction. Bloody or coffee-ground material mandates upper endoscopy rather than colonoscopy.

• Colonoscopy (gold standard for diagnosis and localization): Should be performed after stabilization and bowel preparation in hemodynamically stable patients, ideally within 12-24 hours of presentation (earlier if massive ongoing bleeding). Sensitivity for identifying bleeding source: 50-90% depending on the rate of bleeding at the time of examination; sources actively bleeding at the time of colonoscopy are identified in up to 95% of cases, while inactive bleeding sources may be missed. Preparation with polyethylene glycol (PEG) electrolyte solution is standard; in massive bleeding with ongoing transfusion requirements, rapid purge with 2 L PEG can be performed. Specific findings:
• Diverticula with active bleeding appear as a vessel spurting blood or with visible clot (Forrest Ia-Ib)

Immediate stabilisation (first 30 minutes)

• Resuscitation: two large-bore IVs, isotonic crystalloid, continuous monitoring. The ACG Clinical Guideline on acute lower GI bleeding endorses a restrictive transfusion strategy — transfuse red cells at a hemoglobin threshold near 7 g/dL, with a higher threshold (~8 g/dL) in patients with active coronary ischemia or massive ongoing hemorrhage. Liberal transfusion increases portal/splanchnic pressure and mortality in GI bleeding.
• Exclude an upper source first: in a hemodynamically unstable patient with hematochezia, upper endoscopy precedes colonoscopy, since brisk upper GI hemorrhage transits rapidly and masquerades as a lower source.
• Anticoagulation reversal: reserve for severe or life-threatening bleeding. Vitamin K antagonists — 4-factor prothrombin complex concentrate plus vitamin K (faster and lower volume than FFP). Dabigatran — idarucizumab. Factor Xa inhibitors — andexanet alfa. ACG advises that endoscopic hemostasis need not be delayed for complete correction of coagulopathy.

Definitive diagnosis-directed therapy

• Colonoscopy with hemostasis: the first-line therapeutic modality per ACG, after adequate polyethylene glycol purge. Through-the-scope clips are preferred for diverticular bleeding and post-polypectomy bleeding; band ligation is an alternative. Argon plasma coagulation (thermal) is the standard for angiodysplasia. Epinephrine injection is an adjunct only — never monotherapy, because vasoconstriction is transient and rebleeding is high.
• CT angiography for brisk, ongoing bleeding or hemodynamic instability, then catheter angiography with superselective microcoil embolization of the culprit vasa recta.
• Surgery (segmental colectomy) is reserved for failure of endoscopic and angiographic control, and should follow — not precede — localization.

Etiology-specific and contraindicated

• Hemorrhoids/fissure: fiber, sitz baths, topical therapy, rubber band ligation; fissures get topical nitrates or calcium channel blockers.
• Avoid: barium studies (obscure endoscopy/angiography), blind subtotal colectomy without localization, and resumption of non-aspirin NSAIDs. ACG recommends continuing aspirin prescribed for secondary cardiovascular prevention.

Complications of the hemorrhage itself

• Hemorrhagic shock (emergency): loss of >30–40% of circulating volume overwhelms sympathetic compensation; signalled by persistent tachycardia despite fluids, narrowed pulse pressure, hypotension, oliguria, and lactic acidosis on the metabolic panel.
• Type 2 myocardial infarction (emergency): anemia plus tachycardia creates supply–demand mismatch in patients with fixed coronary stenoses; look for chest pain, ST depression, and a rising troponin during active bleeding — a key reason for the slightly higher transfusion threshold in coronary disease.
• Acute kidney injury: prerenal hypoperfusion progressing to ischemic acute tubular necrosis; rising creatinine with muddy-brown casts.
• Recurrent bleeding: diverticular hemorrhage recurs in a substantial minority after a first episode, and risk rises further after a second.

Complications of treatment

• Transfusion reactions: TACO (volume overload — hypoxia with elevated JVP and B-lines) versus TRALI (non-cardiogenic pulmonary edema within 6 hours, normal filling pressures). Massive transfusion causes citrate-induced hypocalcemia (prolonged QT, perioral tingling) and dilutional coagulopathy.
• Colonoscopic perforation (emergency): mechanical or thermal injury; peritonitis with free air under the diaphragm.
• Post-polypectomy coagulation syndrome: transmural thermal burn without perforation — focal pain, fever, leukocytosis, but no free air; managed medically.
• Aspiration: from rapid large-volume PEG purge, especially in obtunded or elderly patients.
• Post-embolization colonic ischemia (emergency): the classic complication of angiographic therapy; new abdominal pain, bloody diarrhea, and segmental wall thickening on CT after the procedure. Contrast nephropathy and femoral access pseudoaneurysm are additional angiographic risks.
• Thromboembolism after anticoagulant reversal (emergency): stroke in atrial fibrillation or valve thrombosis; drives early re-initiation once hemostasis is secured.
• Surgical: anastomotic leak, stoma-related morbidity, and rebleeding after non-localized resection.

• Unstable hematochezia = upper endoscopy first: the single most tested next step. Roughly one in six brisk upper GI bleeds presents as bright red blood per rectum. A BUN:creatinine ratio >30 favors an upper source (absorbed blood as a protein meal plus prerenal azotemia).
• Painless, voluminous hematochezia in an elderly patient = diverticular bleeding, and it arises from the vasa recta — bleeding is arterial, right-sided diverticula bleed disproportionately, while diverticul*itis* is left-sided. Pain points away from diverticular bleeding.
• Heyde syndrome is the association examiners love: aortic stenosis + colonic angiodysplasia. High shear across the stenotic valve unfolds von Willebrand multimers for ADAMTS13 cleavage, producing acquired type 2A von Willebrand disease. Definitive treatment is aortic valve replacement, not repeated endoscopic ablation.
• Ischemic colitis: elderly patient, crampy left-sided pain then bloody diarrhea; CT shows segmental wall thickening at the splenic flexure (Griffiths point) or rectosigmoid (Sudeck point); thumbprinting on plain film. The rectum is spared by dual blood supply. Management is supportive — this is the classic trap for reflexive angiography.
• Painless massive rectal bleeding in a child = Meckel diverticulum; diagnose with technetium-99m pertechnetate scintigraphy (Meckel scan), which binds ectopic gastric mucosa.
• Unstable or brisk bleeding → CT angiography, not colonoscopy (no prep required, and it localizes for embolization). Tagged RBC scintigraphy detects slower bleeding but localizes poorly.
• Do not assume visible hemorrhoids are the source in an older patient with anemia or weight loss — a colonoscopy to exclude malignancy is still required.
• Common distractor: taking a patient to blind subtotal colectomy or stopping secondary-prevention aspirin. ACG advises continuing aspirin and localizing before resecting.