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Gastrointestinal Bleeding

Chapter 51 | Part 2: Cardinal Manifestations and Presentation of Diseases · Part 2 – Cardinal Manifestations & Presentation · Chapter 51


Key Clinical Points

  1. GIB is the most common gastrointestinal condition leading to hospitalization in the United States, accounting for ~530,000 admissions annually.
  2. The case fatality rate for GIB is approximately 2%; patients generally die from decompensation of underlying illnesses rather than exsanguination.
  3. Transfusion is recommended when hemoglobin falls below 7 g/dL in acute UGIB (restrictive strategy), which reduces rebleeding and death compared to a 9 g/dL threshold.
  4. Hemoglobin may remain normal or only minimally decreased at initial presentation of severe bleeding due to 'bleeding whole blood' (proportional loss of plasma and red cells); it falls as extravascular fluid enters the vascular space over up to 72 h.
  5. Glasgow-Blatchford score of 0–1 identifies patients with very low risk of requiring transfusion, hemostatic intervention, or death (~1% of such patients).
  6. High-dose PPI (80 mg bolus followed by 8 mg/h infusion OR 40 mg 2–4 times per day for 3 days) after endoscopic therapy reduces bleeding and mortality in high-risk ulcers.
  7. Cirrhotic patients with UGIB should receive an antibiotic (e.g., ceftriaxone) and IV vasoactive medication (e.g., octreotide) upon presentation.
  8. High-risk ulcer features include active bleeding, nonbleeding visible vessel, or adherent clot; 1/3 of these require urgent surgery if treated conservatively.
  9. Thalidomide is supported by evidence for reducing bleeding episodes, transfusions, and hospitalizations in small-intestinal vascular ectasias (multicenter double-blind randomized trial).
  10. Aspirin for secondary prevention should not be discontinued; it should be resumed immediately once hemostasis is confirmed.

DEFINITION & OVERVIEW

Overt GIB: Manifested by hematemesis (vomitus of red blood or 'coffee-grounds'), melena (black, tarry stool), and/or hematochezia (passage of red or maroon blood from the rectum). • Occult GIB: Absence of overt bleeding; presents as symptoms of blood loss (lightheadedness, syncope, angina, or dyspnea), iron-deficiency anemia, or a positive fecal occult blood test. • Classification by Site: ◦ Upper: Esophagus, stomach, or duodenum. ◦ Lower: Colon. ◦ Small Intestinal: Beyond the extent of standard upper endoscopy (approx. 75% of previously 'obscure' cases). ◦ Obscure: Source is not clearly identified.


EPIDEMIOLOGY

Hospitalization: Most common GI condition for hospitalization in the US (~530,000 annually). • Mortality: Case fatality rate of ~2%; deaths typically due to decompensation of underlying illnesses rather than exsanguination.


ETIOLOGY & PATHOPHYSIOLOGY

Upper Gastrointestinal Sources

Peptic Ulcers: Most common cause of UGIB (~50% of hospitalizations). ◦ High-risk features: Active bleeding, nonbleeding visible vessel (20%), or adherent clot. ◦ Prognosis: 1/3 of patients with high-risk findings require urgent surgery if treated conservatively. • Mallory-Weiss Tears: Account for ~2–10% of UGIB hospitalizations. • Esophageal Varices: Account for ~2–40% of UGIB hospitalizations, depending on population. • Erosions: Common in esophagus, stomach, or duodenum; account for up to ~30% of UGIB hospitalizations. Defined as mucosal-only breaks without arterial/venous involvement.

Lower Gastrointestinal Sources

Common Causes: Hemorrhoids (most common), anal fissures, diverticulosis (most common if local processes excluded). • Other Causes: Vascular ectasias (especially in patients >70 years), neoplasms (primarily adenocarcinoma), colitis (ischemic, infectious, Crohn's, ulcerative, NSAID-induced), postpolypectomy bleeding, and radiation proctopathy. • Diverticular Bleeding: Abrupt onset, often painless, frequently from right colon. Spontaneous resolution in ≥90% of patients; rebleeding ~15% over 4–5 years (higher in Asia). • Vascular Ectasias: Often chronic/occult; rarely hemodynamically significant.

Small-Intestinal Sources

Prevalence: ~75% of previously 'obscure' cases are estimated to originate in the small intestine. • Common Causes: Vascular ectasias, neoplasms (GIST, carcinoid, adenocarcinoma, lymphoma, metastases), and NSAID-induced erosions/ulcers. • Pediatric: Meckel's diverticulum is the most common cause of significant small-intestinal GIB in children. • Management: Initial endoscopic therapy; if rebleeding occurs, medical therapy (e.g., thalidomide or octreotide) is indicated.

Portal Hypertension Effects

Sources: Gastric varices, small/large intestinal varices, portal hypertensive gastropathy, and enterocolopathy. • Management: Endoscopic injection of tissue adhesive (e.g., n-butyl cyanoacrylate), TIPS, or retrograde transvenous obliteration.

Other Causes

Less Common UGIB: Neoplasms, Dieulafoy's lesion (aberrant vessel in mucosa), prolapse gastropathy, aortoenteric fistulas, hemobilia, or hemosuccus pancreaticus. • Heyde's Syndrome: Bleeding vascular ectasias + aortic stenosis; may benefit from aortic valve replacement.


CLINICAL FEATURES

Symptoms

Hematemesis: Indicates an UGIB source. • Melena: Indicates blood in GI tract for ≥14 h to 3–5 days; more common in proximal bleeding. • Hematochezia: Usually indicates LGIB; if present in UGIB, suggests rapid transit due to brisk bleeding and associated with hemodynamic instability.

Signs

Hemodynamics: Heart rate and blood pressure are primary indicators of clinical significance. ◦ Tachycardia → postural changes in BP → recumbent hypotension. • Hemoglobin Dynamics: Does not fall immediately due to 'bleeding whole blood' (proportional loss of plasma/RBCs). Fall occurs as extravascular fluid enters circulation, taking up to 72 h. • Other Indicators: Hyperactive bowel sounds, elevated BUN (due to volume depletion and protein absorption). • Nasogastric Aspirate: Nonbloody aspirate seen in ~15% of patients with serious hematochezia. Bile-stained appearance does not exclude UGIB (incorrect in ~50%). Testing for occult blood in non-grossly bloody aspirates is not useful.

Anemia

Chronic GIB: May present with low hemoglobin, low MCV, and increased RDW despite stable vitals.


DIFFERENTIAL DIAGNOSIS

UGIB vs LGIB Differentiation

Hematemesis: Indicates UGIB source. • Melena: Proximal source (blood in tract ≥14 h to 3–5 days). • Hematochezia: Usually LGIB; if present in UGIB, indicates rapid transit and hemodynamic instability.

Mimics

Nasogastric Aspirate: Nonbloody aspirate seen in ~15% of patients with serious hematochezia. Bile-stained appearance does not exclude UGIB (incorrect in ~50%).


INVESTIGATIONS & DIAGNOSIS

1. Initial Risk Assessment

Factors: Hemodynamic compromise (tachycardia/hypotension), age, and comorbidities. • Glasgow-Blatchford Score (Table 51-1): ◦ Blood urea nitrogen (BUN) (mg/dL): 18.2–22.4 (Score 2); 22.4–28.0 (3); 28.0–70.0 (4); ≥70.0 (6). ◦ Systolic blood pressure (mmHg): 100–109 (1); 90–99 (2); <90 (3). • Decision: Score of 0–1 → very low risk → outpatient management possible.

2. Endoscopy Timing

Pre-Endoscopic Meds: ◦ PPI infusion: Modestly reduces need for endoscopic therapy (reduces high-risk stigmata) but does not improve clinical outcomes. ◦ Erythromycin (250 mg IV, 30–90 min before): Improves visualization of features predicting risk. • Timing Logic: ◦ High-risk patients: Urgent endoscopy (6–12 h) does not improve outcome; may increase mortality in some cases. ◦ Low-risk patients: Early endoscopy identifies low-risk findings, allowing discharge in ≥40% of patients.

3. Angiography and CT

Angiography: Indicated for extrinsic extravasation. • CT Angiography: Used for workup of small intestinal/obscure bleeding sites. • Surgery: Indicated if bleeding persists or site is not identified.


MANAGEMENT & TREATMENT

1. UGIB Management

Peptic Ulcers: ◦ High-risk (Active bleeding, visible vessel, adherent clot) → Endoscopic therapy + High-dose PPI. ◦ Low-risk (Flat pigmented spot, clean base) → No endoscopic therapy + Once-daily PPI. • Esophageal Varices: ◦ Treatment: Endoscopic ligation + Vasoactive drug (e.g., octreotide) + antibiotic. • Mallory-Weiss Tear: Endoscopic therapy if active bleeding; otherwise, no endoscopic therapy. • Erosions: No endoscopic therapy + Once-daily PPI. • High-dose PPI Definition: 80 mg bolus followed by infusion (8 mg/h) OR intermittent oral or intravenous doses (e.g., 40 mg 2–4 times per day) for 3 days. • Prophylaxis: ◦ H. pylori eradication → reduces rebleeding to <5%. ◦ NSAIDs: Discontinue if bleeding occurs; use COX-2 selective + PPI if required. ◦ Aspirin (Secondary Prevention): Do not discontinue; restart immediately after hemostasis confirmed.

2. LGIB Management

Diverticular Bleeding: Spontaneous stop in ≥90%. Endoscopic therapy may be used if specific diverticulum is identified. • Vascular Ectasias: Initial endoscopic therapy; if rebleeding occurs, medical therapy (thalidomide/octreotide) or angiography. • Surgery: Required for major persistent/recurrent bleeding from colonic sources not treatable by other means.

3. Small-Intestinal Management

Initial Step: Endoscopic therapy. • Recurrent Bleeding: Medical therapy (thalidomide or octreotide) if endoscopic therapy fails. • Thalidomide: Multicenter trial showed marked reduction in bleeding, transfusion, and hospitalization.

4. Cirrhotic Patients

Immediate Action: Antibiotic (e.g., ceftriaxone) + IV vasoactive medication (e.g., octreotide).


PROGNOSIS & COMPLICATIONS

Rebleeding Rates

Colonic Diverticula: ≈15% over 4–5 years. • Vascular Ectasias (non-diverticular): ≈45% over ~2 years. • Small Intestinal: Pooled rebleeding rate of ≈45% over mean follow-up of ≈2 years.


SPECIAL CONSIDERATIONS

Aspirin & NSAID Management

Aspirin (Secondary Prevention): Do not discontinue; restart immediately after hemostasis. • Aspirin (Primary Prevention): Discontinue if UGIB develops. • NSAIDs: Discontinue if bleeding occurs; use COX-2 selective + PPI if required.


KEY PEARLS & CLINICAL TRAPS

Transfusion Threshold: 7 g/dL for acute UGIB. • Nasogastric Aspirate: Not useful for detecting occult blood; bile staining is often a false positive for presence of bile (incorrect in ~50%).


FLOWCHARTS

Flowchart 1: UGIB Management by Endoscopic Findings

Path A (Ulcer + Active bleeding/visible vessel): Ulcer → Active bleeding or visible vessel → Endoscopic therapy → High-dose PPI → Clear liquids for ≈2 days → Hospitalize 3 days. • Path B (Ulcer + Adherent clot): Ulcer → Adherent clot → May consider endoscopic therapy → High-dose PPI → Clear liquids for ≈2 days → Hospitalize 3 days. • Path C (Ulcer + Flat pigmented spot): Ulcer → Flat pigmented spot → No endoscopic therapy → Once-daily PPI → Clear liquids for ≈1 day → Hospitalize ≈1–2 days. • Path D (Ulcer + Clean base): Ulcer → Clean base → No endoscopic therapy → Once-daily PPI → Regular diet → Discharge after endoscopy. • Path E (Esophageal Varices): Esophageal Varices → Endoscopic ligation → Vasoactive drug (e.g., octreotide) + antibiotic → Clear liquids for ≈2 days → Hospitalize 3–5 days. • Path F (Mallory-Weiss Tear + Active bleeding): Mallory-Weiss Tear → Active bleeding → Endoscopic therapy → Antiemetic if nausea → Clear liquids for ≈1 day → Hospitalize ≈1–2 days. • Path G (Mallory-Weiss Tear + No active bleeding): Mallory-Weiss Tear → No active bleeding → No endoscopic therapy → Antiemetic if nausea → Regular diet → Discharge after endoscopy. • Path H (Erosions): Erosions → No endoscopic therapy → Once-daily PPI → Regular diet → Discharge after endoscopy.

Flowchart 2: LGIB Management

Pathway A (No Hemodynamic Instability): 1. Start → No Hemodynamic Instability → Colonoscopy. 2. Decision: Site identified? → Yes, bleeding stops → Discharge/Follow-up. → Yes, bleeding persists → Angiography → If bleeding persists → Surgery. → No (Site not identified) → Angiography → If bleeding persists → Surgery. • Pathway B (Hemodynamic Instability): 1. Start → Hemodynamic Instability → Upper GI source? 2. If Yes → Angiography. 3. If No (Upper GI source?) → CT angiography. 4. Decision: Extravasation? → Yes → Angiography. → No → Colonoscopy. 5. From Colonoscopy (under Hemodynamic Instability): → If Able to prep? (Yes) → Proceed to Site identified logic (same as Pathway A). → If Able to prep? (No) → Angiography. 6. Final Decision at Angiography: → If bleeding persists → Surgery. → If instability persists → Surgery with/without prior endoscopy if also not reached.


Reference Tables

TABLE 50-2 Assessment and Testing for Involuntary Weight Loss Indications 5% weight loss in 6 mo

Harrison's 22e, p.316

Indications Laboratory
5% weight loss in 6 mo Complete blood count
Body mass index <21 Thyroid function tests
51 Gastrointestinal
Bleeding
Loren Laine
Change in fit of clothing C-reactive protein
Abdominal pain, nausea, vomiting,
diarrhea, constipation, dysphagia
HIV testing, if indicated
Assessment Radiology
Medication review
Mini-Mental State Examinationa
Nutrition Screening Initiativea
Observation of eatinga
Instrumental activities of daily livinga

TABLE 51-1 Glasgow-Blatchford Score

Harrison's 22e, p.319

RISK FACTORS AT ADMISSION SCORE
Blood urea nitrogen (mg/dL)
18.2 to <22.4 2
22.4 to <28.0 3
28.0 to <70.0 4
≥70.0 6
Systolic blood pressure (mmHg)
100–109 1
90–99 2
<90 3