19.2 Upper & Lower Gastrointestinal Bleeding

Anatomical Distinction & Initial Clinical Differentiation

Acute gastrointestinal hemorrhage is a major medical emergency with an annual incidence of approximately 100 to 150 hospitalizations per 100,000 adults. The foundational principle of clinical evaluation is localizing the source relative to the Ligament of Treitz (the suspensory muscle of the duodenum at the duodenojejunal junction):

1. Upper Gastrointestinal Bleeding (UGIB):

   • Originates proximal to the ligament of Treitz (esophagus, stomach, or duodenum).
   • Cardinal Manifestations:
     • Hematemesis: Frank vomiting of bright red blood or clots, indicating active, brisk hemorrhage.
     • "Coffee-Ground" Emesis: Dark brown, granular vomitus resulting from the oxidation of red blood cell hemoglobin iron to acid hematin by gastric hydrochloric acid. Indicates either a slower rate of bleeding or bleeding that has temporarily arrested.
     • Melena: Passage of black, shiny, sticky, foul-smelling, tarry stools. Results from the digestive degradation of hemoglobin into hematin and other hemochromes by enteric bacteria over a prolonged intestinal transit time (typically requiring at least 50 to 100 mL of blood loss into the upper GI tract and >14 hours of colonic transit).
   • The High-Brisk Exception: A massive, torrential upper GI bleed (>1,000 mL) with hypermotile intestinal transit can present as bright red hematochezia accompanied by hemodynamic shock in 10% to 15% of severe lower GI presentations.

2. Lower Gastrointestinal Bleeding (LGIB):

   • Originates distal to the ligament of Treitz (jejunum, ileum, colon, rectum, or anus). In clinical practice, >90% of lower GI bleeding arises from the colon and anorectum.
   • Cardinal Manifestation:
     • Hematochezia: The passage of frank, bright red or maroon blood and clots per rectum. Reflects colonic or anorectal bleeding, or massive upper GI bleeding with accelerated transit.

The Diagnostic Utility of the BUN-to-Creatinine Ratio

A crucial, highly tested clinical distinction between UGIB and LGIB is the Blood Urea Nitrogen (BUN) to Serum Creatinine Ratio:

• In acute UGIB, blood entering the upper gastrointestinal lumen undergoes enzymatic digestion in the small intestine. The massive absorption of digested erythrocyte proteins, combined with hypovolemia-induced prerenal azotemia, produces a dramatic surge in BUN relative to serum creatinine, characteristically yielding a BUN/Creatinine ratio >20:1 to 30:1 (in the absence of underlying intrinsic renal failure).
• In acute LGIB, blood enters the gastrointestinal tract distal to the primary absorptive sites of the small bowel; consequently, systemic protein absorption does not occur, and the BUN/Creatinine ratio remains normal (<20:1) unless severe hypovolemic acute kidney injury supervenes.

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Resuscitation & Hemodynamic Stabilization Protocols

Initial management must focus entirely on hemodynamic resuscitation and airway protection prior to obtaining diagnostic imaging or endoscopy.

Airway Protection in Massive Hemorrhage

In patients presenting with active massive hematemesis, altered mental status (hepatic encephalopathy in cirrhotic patients), or severe agitation, early elective endotracheal intubation is mandatory before endoscopic evaluation. Intubation prevents catastrophic pulmonary aspiration of blood and gastric contents and guarantees a secured airway during urgent procedural interventions.

Vascular Access & Fluid Resuscitation

• Intravenous Access: Immediately establish two large-bore (16-gauge or 18-gauge) peripheral intravenous catheters in the upper extremities. Flow rate through a short, wide-bore peripheral line is dramatically superior to a standard triple-lumen central venous catheter (governed by Poiseuille's law: flow is inversely proportional to catheter length and directly proportional to the fourth power of the radius).
• Crystalloid Therapy: Infuse rapid boluses of isotonic balanced crystalloid solution (e.g., Lactated Ringer's or Plasmalyte) titrated to restore organ perfusion (mean arterial pressure ≥65 mm Hg, resolution of resting tachycardia, capillary refill <2 seconds, urine output ≥0.5 mL/kg/hour).

The Restrictive Red Blood Cell Transfusion Strategy

Historically, clinicians practiced "liberal" red blood cell (RBC) transfusions aiming for a normal hemoglobin concentration (>10 g/dL). Landmark randomized clinical trials fundamentally overturned this practice:

                    THE RESTRICTIVE VS LIBERAL TRANSFUSION PARADIGM

  ┌──────────────────────────────────────────────┐    ┌──────────────────────────────────────────────┐
  │     LIBERAL TRANSFUSION (Historical)         │    │      RESTRICTIVE TRANSFUSION (Modern)        │
  ├──────────────────────────────────────────────┤    ├──────────────────────────────────────────────┤
  │ • Threshold: Transfuse when Hb <9.0 g/dL     │    │ • Threshold: Transfuse when Hb <7.0 g/dL     │
  │ • Target Hemoglobin: 9.0 to 11.0 g/dL        │    │ • Target Hemoglobin: 7.0 to 8.0 g/dL         │
  │ • Overfills intravascular volume             │    │ • Prevents fluid overload & TRALI/TACO       │
  │ • Surges central venous & portal pressure    │    │ • Prevents portal hypertension spikes        │
  │ • Dislodges fresh fibrin-platelet clots      │    │ • Preserves vasoconstrictive clotting tone   │
  │ • Outcome: HIGHER REBLEEDING & MORTALITY     │    │ • Outcome: REDUCED 6-WEEK MORTALITY (5% vs 9%)│
  └──────────────────────────────────────────────┘    └──────────────────────────────────────────────┘

• The Villanueva Landmark Trial (NEJM 2013):
  • Randomized 921 patients with severe acute UGIB to a restrictive transfusion strategy (transfusion trigger: hemoglobin <7.0 g/dL, target 7.0–8.0 g/dL) versus a liberal transfusion strategy (trigger: hemoglobin <9.0 g/dL, target 9.0–11.0 g/dL).
  • Results: The restrictive group demonstrated a significant 45% relative reduction in 6-week all-cause mortality (5% vs 9%, p=0.02), a significant reduction in recurrent bleeding (10% vs 16%), fewer adverse events (cardiac overload, pulmonary edema, transfusion reactions), and shorter hospital stays.
• Pathophysiology in Cirrhotic Portal Hypertension: Over-transfusion expands the circulating intravascular volume, precipitating reflex splanchnic hypervolemia and sharp spikes in the hepatic venous pressure gradient (HVPG). Elevated portal venous pressure increases wall tension across fragile submucosal esophageal varices, blowing off immature fibrin-platelet thrombi and precipitating catastrophic secondary exsanguination.
• Guideline Transfusion Thresholds:
  • Hemodynamically Stable Patients without Acute Coronary Syndrome: Maintain a restrictive threshold—transfuse packed red blood cells only when hemoglobin falls <7.0 g/dL, titrating to a target of 7.0 to 8.0 g/dL.
  • Patients with Active Acute Coronary Syndrome (ACS) or Significant Symptomatic Cardiovascular Disease: Maintain a higher hemoglobin threshold of 8.0 to 10.0 g/dL to prevent supply-demand myocardial ischemia.

Coagulopathy & Anticoagulant Reversal in Life-Threatening Bleeding

• Thrombocytopenia: Transfuse platelets to maintain a platelet count >50,000/µL in active ongoing severe bleeding.
• Warfarin-Induced Coagulopathy: In patients on warfarin with life-threatening gastrointestinal hemorrhage, administer 4-Factor Prothrombin Complex Concentrate (4F-PCC) weight-adjusted (25–50 units/kg IV) PLUS Intravenous Vitamin K (10 mg IV slow infusion). 4F-PCC normalizes the INR within 15 to 30 minutes without the massive fluid volume and thawing delay associated with Fresh Frozen Plasma (FFP).
• Direct Oral Anticoagulant (DOAC) Reversal:
  • Dabigatran (Direct Thrombin Inhibitor): Administer Idarucizumab (Praxbind; 5 g IV in two 2.5-g boluses).
  • Oral Factor Xa Inhibitors (Apixaban, Rivaroxaban): Administer Andexanet alfa (if available) or weight-based 4F-PCC (50 units/kg IV).

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Clinical Risk Stratification Scores

Validated clinical prediction scores prevent unnecessary hospital admissions in low-risk patients while rapidly identifying high-risk individuals who require intensive care unit admission and emergent endoscopy.

The Glasgow-Blatchford Bleeding Score (GBS)

The Glasgow-Blatchford Score is the gold standard pre-endoscopic risk stratification tool, calculated entirely from bedside vital signs, clinical history, and initial laboratory data without requiring endoscopic visualization:

• Clinical Application & Triage Rules:
  • GBS Score 0 to 1 (Low Risk): Associated with <1% risk of requiring intervention (blood transfusion, endoscopic therapy, surgical intervention) or dying. Current international guidelines recommend that patients with a GBS of 0 or 1 can be safely discharged from the emergency department for outpatient follow-up and elective outpatient endoscopy, avoiding costly hospitalizations.
  • GBS Score ≥2 (High Risk): Mandates inpatient hospital admission, resuscitation, and inpatient endoscopy.
  • GBS Score ≥7: Highly predictive of active rebleeding and severe clinical outcome; warrants high-dependency unit or ICU admission.

The Rockall Score

Unlike the GBS, the complete Rockall Score combines pre-endoscopic clinical criteria (age, presence of shock, severe systemic comorbidities) with post-endoscopic findings (endoscopic diagnosis and stigmata of recent hemorrhage: clean ulcer vs. visible vessel or active spurting). A complete score ≤2 indicates low risk of rebleeding and mortality (<0.2%), while a score ≥8 carries a mortality exceeding 40%.

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Acute Upper Gastrointestinal Bleeding: Etiologies, Pharmacotherapy & Endoscopy

Common Upper GI Bleeding Etiologies

1. Peptic Ulcer Disease (PUD, ~50% of all UGIB):
   • Duodenal Ulcers: Predominantly located on the posterior duodenal bulb; deep erosion can penetrate into the gastroduodenal artery, producing catastrophic, rapid arterial exsanguination.
   • Gastric Ulcers: Predominantly located along the lesser curvature of the stomach; deep erosion can penetrate into branches of the left gastric artery.
   • Primary drivers: Helicobacter pylori mucosal colonization and extensive use of Nonsteroidal Anti-inflammatory Drugs (NSAIDs), including low-dose cardioprotective aspirin.
2. Gastroesophageal Varices (~15–20% of UGIB):
   • Severe portal hypertension (hepatic venous pressure gradient >10–12 mm Hg) drives the formation of dilated submucosal collateral vessels at the gastroesophageal junction and gastric fundus.
   • Carries the highest in-hospital mortality (15% to 20% at 6 weeks) and rebleeding rate (>30% within 5 days without treatment).
3. Mallory-Weiss Syndrome (~5–10% of UGIB):
   • Non-transmural, longitudinal mucosal and submucosal lacerations at the gastroesophageal junction or gastric cardia, classically precipitated by forceful retching, coughing, or vomiting following heavy alcohol bingeing.
   • Bleeding is self-limited and arrests spontaneously in >85% to 90% of cases.
4. Dieulafoy Lesion (~1–2% of UGIB):
   • A developmental vascular malformation characterized by an abnormally large, tortuous, caliber-persistent submucosal arteriole that fails to taper, protruding through a minuscule mucosal defect without surrounding ulceration, typically along the lesser curvature of the upper stomach.
   • Characterized by sudden, unpredictable, massive, recurrent arterial bleeding.
5. Gastric Malignancy / Neoplasm (~3–5%): Ulcerated gastric adenocarcinoma, lymphoma, or gastrointestinal stromal tumors (GIST).

Emergency Pharmacotherapy for Acute UGIB

1. High-Dose Intravenous Proton Pump Inhibitors (PPIs)

• Standard Regimen: Pantoprazole (or Esomeprazole) 80 mg IV bolus, followed by a continuous infusion of 8 mg/hour for 72 hours (or intermittent dosing of 40 mg to 80 mg IV twice daily).
• Physiologic Mechanism: Raises intragastric pH >6.0. Gastric acid and pepsin inactivate platelet aggregation, inhibit plasma coagulation factor activation, and rapidly dissolve existing fibrin clots. Maintaining pH >6.0 stabilizes the fibrin clot over the bleeding ulcer crater, downstages high-risk endoscopic stigmata prior to endoscopy, and significantly reduces the risk of recurrent ulcer rebleeding following endoscopic hemostasis.

2. Intravenous Octreotide (Somatostatin Analog)

• Standard Regimen: 50 mcg IV bolus, followed by a continuous infusion of 50 mcg/hour for 2 to 5 days.
• Indication: Mandatory immediate empiric administration in any patient with suspected or confirmed portal hypertensive variceal bleeding (history of cirrhosis, heavy alcohol use, stigmata of chronic liver disease).
• Mechanism: Selectively induces splanchnic arterial vasoconstriction by inhibiting the secretion of endogenous vasodilatory peptides (principally glucagon). Splanchnic vasoconstriction reduces splanchnic blood flow and portal venous inflow, decreasing portal venous pressures and diminishing variceal hemorrhage.

3. Prophylactic Intravenous Antibiotics in Cirrhosis

• Standard Regimen: Ceftriaxone 1 g IV daily for 7 days (or oral ciprofloxacin 500 mg PO BID once stable).
• CRITICAL EVIDENCE: Cirrhotic patients experiencing acute gastrointestinal bleeding have profound immune dysfunction and elevated rates of bacterial translocation across ischemic intestinal mucosa. Without antibiotic prophylaxis, >50% develop severe bacterial infections (spontaneous bacterial peritonitis, bacteremia, pneumonia). Bacterial infection triggers endogenous endothelin and nitric oxide release, surging portal pressures and causing early variceal rebleeding. Guideline-directed prophylactic ceftriaxone:
  • Reduces bacterial infections by >50%;
  • Reduces early variceal rebleeding by >50%;
  • Delivers a documented 9% absolute reduction in all-cause in-hospital mortality.
  • Exam Pearl: Prophylactic IV ceftriaxone must be ordered at the time of admission in all cirrhotic patients presenting with GI bleeding, regardless of whether ascites is clinically detected.

4. Pre-Endoscopic Prokinetic Agents

• Intravenous Erythromycin (250 mg IV infused over 30 minutes, administered 30 to 60 minutes prior to EGD): Acts as a motilin receptor agonist that accelerates gastric emptying, clearing retained blood, hematin, and large clots from the gastric fundus. Significantly improves endoscopic mucosal visualization and diagnostic yield while reducing the need for repeat "second-look" procedures.

Diagnostic & Therapeutic Esophagogastroduodenoscopy (EGD)

• Timing: Recommended within 24 hours of presentation for all admitted patients following hemodynamic stabilization. In high-risk patients with suspected variceal hemorrhage or persistent hemodynamic instability despite volume resuscitation, EGD should be performed within 12 hours.

Endoscopic Management of Peptic Ulcers: The Forrest Classification

[!IMPORTANT] THE DUAL THERAPY MANDATE: For high-risk peptic ulcers (Forrest Ia, Ib, and IIa), international guidelines strictly mandate dual endoscopic therapy combining:

1. Dilute epinephrine injection (1:10,000 or 1:20,000; provides immediate temporary arteriolar vasoconstriction and local mechanical tissue tamponade); PLUS
2. A second definitive mechanical or thermal modality: through-the-scope hemoclips (TTSC), bipolar electrocautery, heater probe coagulation, or over-the-scope clips (OTSC). Epinephrine injection monotherapy is clinically unacceptable due to unacceptably high rates of recurrent hemorrhage.

Endoscopic Management of Esophageal Varices

• Endoscopic Variceal Ligation (EVL / Band Ligation): The definitive treatment of choice. Elastic rubber bands are deployed around variceal cords starting at the gastroesophageal junction and proceeding proximally, inducing mechanical strangulation, local thrombosis, mucosal sloughing, and subsequent scar fibrosis. EVL is vastly superior to endoscopic sclerotherapy, with significantly higher initial hemostasis rates and lower risks of esophageal stricture or perforation.
• Refractory Variceal Hemorrhage & Salvage Pathways:
  1. Balloon Tamponade (Sengstaken-Blakemore or Minnesota Tube): Indicated for catastrophic, uncontrolled variceal bleeding refractory to endoscopic therapy. The gastric balloon is inflated with 250 to 300 mL of air and retracted against the gastroesophageal junction with 1 kg of external traction. Crucial Rule: Balloon tamponade is strictly a temporary rescue bridge (maximum 24 hours) due to high risks of esophageal pressure necrosis, mucosal gangrene, and lethal esophageal rupture.
  2. Transjugular Intrahepatic Portosystemic Shunt (TIPS): An expandable metallic stent placed endovascularly between a branch of the portal vein and the hepatic vein by interventional radiology, decompressing the portal system directly into the inferior vena cava. Early "pre-emptive" TIPS (performed within 24 to 72 hours of admission) significantly improves survival in high-risk cirrhotics (Child-Pugh Class C or Child-Pugh Class B with active bleeding at endoscopy).

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Acute Lower Gastrointestinal Bleeding: Differential & Diagnostic Workup

Acute LGIB is defined as bleeding arising distal to the ileocecal valve, accounting for ~20% to 30% of all major GI bleeding presentations.

Common Etiologies of Acute Lower GI Bleeding

                  SPECTRUM OF ACUTE LOWER GASTROINTESTINAL BLEEDING

  ┌─────────────────────────────────┐      ┌─────────────────────────────────┐
  │    DIVERTICULAR BLEEDING (30-50%)│      │     ISCHEMIC COLITIS (10-15%)   │
  ├─────────────────────────────────┤      ├─────────────────────────────────┤
  │ • Most common cause of massive  │      │ • Transient hypoperfusion state │
  │   painless lower GI hemorrhage  │      │ • Crampy lower abdominal pain   │
  │ • Ruptured nutrient arteriole   │      │   followed by bloody diarrhea   │
  │ • 80% stop spontaneously        │      │ • Watersheds: Splenic flexure & │
  │ • High recurrence rate (25-35%) │      │   rectosigmoid junction         │
  └─────────────────────────────────┘      └─────────────────────────────────┘
  ┌─────────────────────────────────┐      ┌─────────────────────────────────┐
  │    ANGIODYSPLASIA (5-15%)       │      │    ANORECTAL PATHOLOGY (~10%)   │
  ├─────────────────────────────────┤      ├─────────────────────────────────┤
  │ • Arteriovenous malformations   │      │ • Internal hemorrhoids: painless│
  │ • Cecum / right colon in elderly│      │   bright red blood dripping     │
  │ • Painless, episodic bleeding   │      │ • Anal fissures: sharp tearing  │
  │ • Heyde Syndrome: associated    │      │   pain on defecation with streak│
  │   with AORTIC STENOSIS & vWF    │      │   of bright red blood on tissue │
  └─────────────────────────────────┘      └─────────────────────────────────┘

1. Diverticular Hemorrhage (~30–50% of LGIB):
   • The single most common cause of acute, massive, overt lower GI bleeding in adults.
   • Pathophysiology: Penetrating nutrient arterioles (vasa recta) draped over the dome or neck of an isolated colonic diverticulum experience chronic asymmetric mechanical tensile stress and mucosal shear. This produces eccentric intimal thickening, medial thinning, and eventual arterial rupture into the diverticular lumen.
   • Clinical Hallmark: Sudden, abrupt onset of large-volume, painless, bright red or maroon hematochezia, frequently accompanied by an urge to defecate.
   • Natural History: Bleeding arrests spontaneously in 75% to 80% of patients with fluid resuscitation. However, recurrence occurs in 25% to 35% of individuals.
2. Angiodysplasia (Vascular Ectasias, ~5–15% of LGIB):
   • Dilated, tortuous, thin-walled submucosal arteriovenous malformations located predominantly in the cecum and ascending colon of elderly patients (>65 years of age).
   • Bleeding is characteristically painless, episodic, low-to-moderate volume, and may present as recurrent hematochezia, melena, or unexplained chronic iron deficiency anemia.
   • Heyde Syndrome (Aortic Stenosis & Angiodysplasia):
     • The well-established clinical association between severe calcific aortic valve stenosis, recurrent gastrointestinal angiodysplasia bleeding, and an acquired Type 2A von Willebrand syndrome.
     • Pathophysiology: High shear stress across the stenotic aortic valve uncoils and cleaves high-molecular-weight von Willebrand factor (vWF) multimers by the circulating metalloproteinase ADAMTS13. Depletion of functional vWF multimers impairs platelet adhesion at high shear rates, triggering persistent mucosal bleeding from preexisting colonic angiodysplasias.
     • Definitive Treatment: Surgical or transcatheter aortic valve replacement (AVR/TAVR) relieves aortic shear stress, restores normal circulating high-molecular-weight vWF multimers, and definitively cures the recurrent gastrointestinal hemorrhage in >80% to 90% of patients.
3. Ischemic Colitis (~10–15% of LGIB):
   • Caused by transient systemic hypoperfusion (hypotension, heart failure, shock, intense physical endurance exertion, or following abdominal aortic aneurysm repair) producing non-occlusive mesenteric microvascular ischemia of the large intestine.
   • Clinical Presentation: Sudden onset of mild-to-moderate, crampy, lower abdominal pain (predominantly LLQ) followed within 12 to 24 hours by mild-to-moderate hematochezia or bloody diarrhea.
   • Classic Watershed Zones:
     • Griffiths' Point (The Splenic Flexure): The junction between the superior mesenteric artery (via the middle colic artery) and the inferior mesenteric artery (via the left colic artery).
     • Sudeck's Point (The Rectosigmoid Junction): The junction between the inferior mesenteric artery (via the superior rectal artery) and the internal iliac artery (via the middle/inferior rectal arteries).
   • Diagnosis & Course: Abdominal CT demonstrates segmental colonic wall thickening and "thumbprinting" (submucosal edema and hemorrhage). Colonoscopy shows pale, edematous mucosa with petechial hemorrhages and dusky, longitudinal ulcerations. More than 90% of cases resolve spontaneously with supportive therapy (IV hydration and bowel rest).
4. Anorectal Disorders (~10% of LGIB):
   • Internal Hemorrhoids: Painless bright red blood dripping into the toilet bowl or coating the surface of formed stool.
   • Anal Fissures: Severe, sharp, "knife-like" or tearing rectal pain during defecation accompanied by small streaks of bright red blood on toilet paper.
5. Colorectal Neoplasia (~5–10% of LGIB): Colorectal adenocarcinoma and large polyps typically present with occult blood loss, altered bowel habits, and iron deficiency anemia, but occasionally manifest as intermittent overt hematochezia.
6. Post-Polypectomy Bleeding: May occur immediately or be delayed up to 7 to 14 days following colonoscopic snare polypectomy due to sloughing of the thermal eschar and exposure of underlying submucosal vessels.

Diagnostic & Interventional Algorithm for Acute LGIB

                  ACUTE LOWER GI BLEEDING DIAGNOSTIC DECISION TREE

                    ┌─────────────────────────────────────────┐
                    │ Patient Presenting with Acute Gross     │
                    │ Hematochezia (Bright Red Blood/Rectum)  │
                    └────────────────────┬────────────────────┘
                                         │
                     ┌───────────────────┴───────────────────┐
                     ▼                                       ▼
       ┌───────────────────────────┐           ┌───────────────────────────┐
       │   HEMODYNAMICALLY UNSTABLE│           │   HEMODYNAMICALLY STABLE  │
       │   (SBP <90, HR >100,      │           │   (SBP ≥90, HR <100,      │
       │    Syncope, Shock)        │           │    Responds to Fluids)    │
       └─────────────┬─────────────┘           └─────────────┬─────────────┘
                     │                                       │
                     ▼                                       ▼
       ┌───────────────────────────┐           ┌───────────────────────────┐
       │ RULE OUT MASSIVE UPPER GI │           │ RAPID COLONIC PURGE       │
       │ • Immediate NG Tube Lavage│           │ • 4 to 6 L Polyethylene   │
       │   or Urgent Emergent EGD  │           │   Glycol (PEG) Solution   │
       │ • 10-15% of brisk shock-  │           │ • Oral or via NG Tube     │
       │   level hematochezia is   │           └─────────────┬─────────────┘
       │   a massive upper GI bleed│                         │
       └─────────────┬─────────────┘                         ▼
                     │                         ┌───────────────────────────┐
                     ▼                         │ INPATIENT COLONOSCOPY     │
       ┌───────────────────────────┐           │ • Performed within 24 hrs │
       │ MULTIPHASE CT ANGIOGRAPHY │           │ • Localize & Treat:       │
       │ (CTA) OF ABDOMEN & PELVIS │           │   Hemoclips, Epinephrine, │
       │ • Rapid non-invasive test │           │   Bipolar Coagulation     │
       │ • Detects bleeding rates  │           └─────────────┬─────────────┘
       │   ≥0.3 to 0.5 mL/min      │                         │ If Inconclusive
       └─────────────┬─────────────┘                         │ or Recurrent
                     │ Extravasation                         ▼
                     ▼ Detected                ┌───────────────────────────┐
       ┌───────────────────────────┐           │ CATHETER ANGIOGRAPHY      │
       │ TRANSCATHETER ARTERIAL    │           │ or Tc-99m RBC SCINTIGRAPHY│
       │ EMBOLIZATION (TAE) by IR  │           │ (Scintigraphy detects     │
       │ • Superselective microcoil│           │  rates ≥0.1 mL/min)       │
       │ • High success, low bowel │           └───────────────────────────┘
       │   infarction risk (<2%)   │
       └───────────────────────────┘

• Triage Step 1: Rule Out Massive Upper GI Bleeding:
  • Any patient presenting with gross hematochezia accompanied by hemodynamic instability (systolic BP <90 mm Hg, heart rate >100 beats/min, postural syncope) must be evaluated for an upper GI hemorrhage before pursuing lower tract studies. Insert a nasogastric tube: aspiration of gross red blood or coffee-ground material confirms an upper source; aspiration of clear, yellow, bilious fluid reliably excludes active bleeding proximal to the ligament of Treitz. If aspirate is non-bilious or equivocal, proceed immediately to emergent EGD.
• Triage Step 2: Hemodynamically Stable Patient -> Inpatient Colonoscopy:
  • Rapid oral colonic preparation with 4 to 6 liters of polyethylene glycol (PEG) electrolyte lavage solution administered over 3 to 4 hours (clears blood, stool, and clots to allow safe mucosal visualization).
  • Inpatient Colonoscopy within 24 hours of presentation: Achieves high diagnostic accuracy and allows direct endoscopic hemostasis (through-the-scope hemoclips, bipolar coagulation, or band ligation).
• Triage Step 3: Ongoing Brisk Bleeding / Unstable -> Multiphase CT Angiography (CTA):
  • Biphasic/multiphase abdominopelvic CTA can detect active intraluminal contrast extravasation at arterial bleeding rates ≥0.3 to 0.5 mL/min.
  • Rapidly available without colonic preparation; pinpoints the precise anatomical vascular branch supplying the bleeding site.
• Triage Step 4: Transcatheter Arterial Embolization (TAE):
  • When CTA identifies active extravasation, the patient is transferred directly to the interventional radiology suite for catheter mesenteric angiography and superselective transcatheter microcoil or Gelfoam embolization. Modern microcatheter techniques achieve primary hemostasis in >85% to 90% of cases, with bowel infarction rates <2%.
• Technetium-99m Labeled RBC Scintigraphy (Nuclear Bleeding Scan):
  • High diagnostic sensitivity: detects low-volume extravasation at rates as low as ≥0.1 mL/min.
  • Limitation: Extremely poor anatomical spatial resolution (can indicate general abdominal quadrant but cannot reliably guide targeted segmental surgical resection). Best reserved for intermittent, obscure, or slow-rate bleeding when CTA and endoscopy are non-diagnostic.
• Emergency Segmental Colectomy:
  • Reserved as a last-resort intervention for life-threatening, persistent or recurrent hemorrhage that fails endoscopic and catheter angiographic therapies. Segmental colonic resection guided by precise preoperative angiographic localization is preferred; "blind" subtotal colectomy without localization carries an operative mortality exceeding 15% to 30%.