GI 16: GI Bleeds
❤🔥 Gastrointestinal (GI) Bleeding — Overview
📊 Incidence
390,000 principal hospitalizations per year
600,000 cases as secondary diagnosis
Mortality:
UGIB: 4.5–8.2%
LGIB: 3.0–8.8%
🧠 Remember: Upper bleeds are slightly more deadly due to risk of massive hematemesis and shock.
🧍♀ Clinical Presentation
🩺 History
Ask about:
New medications or recent exposures (NSAIDs, anticoagulants, steroids, alcohol)
Comorbidities: Liver disease, peptic ulcer disease, malignancy
Symptoms: Frequency, amount, color, timing of blood loss
Associated findings: Vomiting, melena, hematochezia, fatigue, syncope
🧠 Why this matters: History often points to location and cause of bleed (e.g., varices in cirrhosis vs ulcer from NSAIDs).
💓 Physical Examination
Look for:
Vital signs: Hypotension + tachycardia → hypovolemia
Skin: Cool, clammy (shock); petechiae or purpura (platelet/coagulopathy signs)
Signs of liver disease:
Spider angiomas 🕷
Palmar erythema ❤
Jaundice 💛
Abdomen: Distension, ascites, tenderness
Rectal exam:
Detects blood or melena
Persistent bleeding when pressure applied → active rectal bleeding
🧠 Mini-why: petechiae = small capillary bleeds (1–2 mm red dots). they indicate platelet issues, not big vessel rupture.
🧪 Laboratory Testing
Order ASAP:
Type and crossmatch → prep for transfusion
CBC (hemoglobin, platelets)
Electrolytes + glucose (hemodynamic stability)
LFTs (check for liver dysfunction)
🧠 Why: baseline labs show severity and guide transfusion thresholds.
💉 Key Symptoms — Determine Bleeding Site
Symptom | Description | Common Source |
|---|---|---|
Hematemesis | Vomiting blood (fresh red or coffee-ground) | Upper GI (esophagus, stomach, duodenum) |
Melena | Black, tarry, foul-smelling stool | Upper GI (slow bleed → blood digested by acid) |
Hematochezia | Bright red blood per rectum (with stool or alone) | Lower GI (colon, rectum, anus) |
🧠 Mnemonic tip:
👉 “Melena = Midnight tar” (black, digested)
👉 “Hematochezia = Cherry red, colon-fed.”
⚖ Differentiating Upper vs Lower GI Bleeds
Upper GI Bleed | Lower GI Bleed |
|---|---|
Peptic ulcer disease (most common) | Diverticulosis (most common) |
Esophageal or gastric varices | Malignancy or polyp |
Mallory–Weiss tear (esophageal tear from vomiting) | Colitis (inflammatory, infectious, or ischemic) |
Erosive esophagitis | Angiodysplasia (vascular lesion) |
🧠 Quick clue:
Upper = vomiting blood, black stool, liver disease link
Lower = fresh blood, often older adults, vascular or inflammatory cause
🩸 Anatomical Definitions
Type of Bleed | Location |
|---|---|
Upper GI bleed (UGIB) | Proximal to the ligament of Treitz (esophagus → duodenum) |
Lower GI bleed (LGIB) | Distal to the ligament of Treitz (jejunum → rectum) |
🧠 Mini-why: The ligament of Treitz marks the transition between duodenum and jejunum — a key landmark for bleed classification.
💊 Drug-Related Causes of GI Bleeding
Drug Class | Mechanism of Bleed Risk |
|---|---|
Aspirin | Irreversibly inhibits platelet aggregation + mucosal irritation |
Clopidogrel | Inhibits platelet aggregation (P2Y12 blockade) |
Warfarin | ↑ INR → impaired clotting → major bleed risk |
DOACs | Directly inhibit factor Xa or thrombin → ↓ coagulation |
NSAIDs | ↓ prostaglandins → ↓ mucosal protection → ulcers |
SSRIs | ↓ platelet serotonin → impaired platelet aggregation |
Corticosteroids | Cause mucosal thinning + ↑ ulcer risk (especially w/ NSAIDs) |
🧠 Mnemonic: “WAC N³S” = Warfarin, Antiplatelets, Corticosteroids, NSAIDs, SSRIs.
🔍 How to Suspect an Upper GI Bleed
💬 Historical Factors
Factor | Likelihood Ratio (LR) |
|---|---|
Prior UGIB | 6.2 |
Age < 50 years | 3.5 |
Warfarin use | 2.3 |
⚡ Symptoms
Symptom | LR |
|---|---|
Black, tarry stool | 5.1–5.9 |
Epigastric discomfort | 2.3 |
🩸 Physical Signs
Sign | LR |
|---|---|
Melena | 25 (very predictive) |
Blood in NG aspirate | 9.6 |
🧪 Labs
Finding | LR |
|---|---|
Urea:Creatinine ratio >30 | 7.5 (classic indicator of UGIB) |
🧠 Why Urea:Cr↑ in UGIB?
Blood digested in stomach → absorbed as protein → ↑ urea formation.
📈 Risk Stratification
Glasgow–Blatchford Score (GBS):
Score 0–1 → safe for outpatient management
Higher → admit + scope
🧠 Clinical pearl: Used to triage urgency — not to confirm the diagnosis.
🏥 Management of Upper GI Bleed
1⃣ Resuscitation
IV crystalloids ± blood transfusions
Monitor vitals + urine output
2⃣ Medications
PPI: Protect clot + stabilize pH (see below)
Octreotide: If variceal bleeding suspected
Hold anticoagulants/antiplatelets if clinically necessary
3⃣ Endoscopy
Diagnostic + therapeutic (done early)
💉 Blood Transfusions
Hgb may initially appear normal (hemodilution hasn’t occurred yet!)
Restrictive transfusion threshold:
→ Transfuse if Hgb < 70 g/L (some use < 80 g/L if cardiac disease)Expected effect:
1 unit PRBC ↑ Hgb by ≈10 g/L
🧠 If Hgb doesn’t rise after transfusion → suspect ongoing bleed or hemolysis.
⚗ Proton Pump Inhibitors (PPIs)
⚠ Why PPIs Are Critical in UGIB
Acidic environment:
↓ platelet aggregation
↑ pepsin activation → digests blood clots
↑ fibrinolysis → clot breakdown
👉 therefore, PPI = stabilizes clot and prevents rebleeding
🕐 Timing & Use
Step | PPI Role |
|---|---|
Pre-endoscopy | May downstage lesion + ↓ need for intervention |
Post-endoscopy | ↓ rebleeding + ↓ mortality in high-risk lesions (active bleed, visible vessel) |
🧠 Sequence to remember:
Suspect UGIB → give PPI → scope
💊 PPI Dosing Examples (recognize, not memorize)
Regimen | Notes |
|---|---|
Pantoprazole 80 mg IV bolus, then 8 mg/hr continuous IV infusion × 72h | Gold standard for high-risk bleeds |
Pantoprazole 80 mg IV bolus, then 40 mg IV q12h | Acceptable alternative |
Pantoprazole 40 mg IV q12h | For lower-risk patients |
🧠 Don’t confuse:
PPIs are superior to H₂RAs — they lower rebleeding, surgery, and mortality.
🩸 Variceal Bleeding
🧠 Definition:
Bleeding from dilated veins (varices) in the esophagus or stomach — usually due to portal hypertension from cirrhosis.
💀 High mortality if not managed fast.
💊 Pharmacologic Management
Drug | Dose | Role |
|---|---|---|
Octreotide | 50–100 mcg IV bolus, then 25–50 mcg/hr infusion for up to 5 days | ↓ splanchnic blood flow → ↓ portal pressure → ↓ variceal bleeding |
Antibiotics | Ciprofloxacin or Ceftriaxone × 4 days | Prevent infection in cirrhotic patients (bacterial translocation risk) |
🧠 Why antibiotics?
Cirrhosis + GI bleed = ↑ gut permeability → bacteria move from gut → bloodstream (↑ risk of sepsis).
→ Prophylaxis cuts mortality risk nearly in half.
🩺 Procedural Management
Step | Intervention | Purpose |
|---|---|---|
Endoscopy | Diagnostic + therapeutic (band ligation, sclerotherapy) | Visualize varices + stop bleeding |
Pharmacotherapy | PPI + Octreotide + antibiotics | Stabilize before/after scope |
🌈 Post-Bleed Management (after endoscopy)
After the gastroenterologist classifies the lesion:
Lesion Risk | PPI Regimen | Duration |
|---|---|---|
High-risk lesion (active bleed, visible vessel) | IV → switch to PPI BID x 14 days | 2 weeks |
Low-risk lesion (flat spot, clean base) | PPI QD x 14 days | 2 weeks |
After 14 days | PPI QD x 4–8 weeks | Longer if ulcer or other risk factors |
🧠 Why: Keeps gastric pH high enough for mucosal healing + clot stabilization.
💩 Lower GI Bleeding (LGIB)
Accounts for ~20% of all GI bleeds
Presents as hematochezia — maroon or bright red blood from the rectum
Usually less severe but still needs prompt assessment
💉 Common Causes
Cause | Note |
|---|---|
Diverticulosis | Most common |
Malignancy / Polyps | Tumor or erosion |
Colitis | Inflammatory, infectious, or ischemic |
Angiodysplasia | Fragile vascular lesions, esp. elderly |
🧠 Mnemonic: “Divert, Die, Dilate, Disease” = Diverticulosis, Malignancy, Angiodysplasia, Colitis.
🔬 Colonoscopy in LGIB
Test | Description | Purpose |
|---|---|---|
Colonoscopy | Scope through rectum to visualize lower tract | Identify + treat source of bleeding |
🚽 Bowel Preparation — Key for Clear Visualization
Inadequate prep can:
↑ procedural risk
↑ duration of insertion + total procedure time
↓ adenoma detection
↓ cecal intubation rate
Require repeat procedure sooner
🚫 Patient-Related Risk Factors for Poor Prep
Risk Factor | Why It Matters |
|---|---|
Prior inadequate prep | Predicts repeat issues |
Constipation | Stool retention limits visualization |
Constipating meds | Opioids, iron, anticholinergics |
Dementia or Parkinson’s | Poor compliance / slow motility |
Low health literacy / engagement | Improper prep timing or volume |
Obesity / Diabetes / Cirrhosis | Altered motility + slow transit time |
🧠 How to fix it: Reinforce prep instructions early, choose patient-friendly regimens, and manage constipation beforehand.
✅ End of Variceal & Lower GI Bleed Section Summary
🌟 EOB-Style Key Takeaways
Topic | Must-Know Point |
|---|---|
Octreotide | 50–100 mcg bolus → 25–50 mcg/hr infusion × 5 days |
Antibiotics | Ceftriaxone or Cipro × 4 days for cirrhotics |
Cirrhosis risk | ↑ bacterial translocation → infection prophylaxis essential |
PPI post-bleed | BID x 14d (high-risk) or QD x 14d (low-risk) → continue 4–8 weeks |
LGIB | 20% of bleeds; maroon/red stool; most often diverticulosis |
Poor bowel prep | Constipation, dementia, low literacy, obesity, diabetes, cirrhosis |
🚽 Bowel Preparation Pharmacology
💧 1⃣ Isosmotic Preparations (Polyethylene Glycol – PEG)
Feature | Details |
|---|---|
Mechanism | Osmotically balanced solution → mechanical lavage cleanses bowel by sheer fluid volume (not chemical irritation). |
Formulation | PEG with electrolytes — large-volume (4 L) or low-volume (paired with stimulant laxatives). |
Onset | ~1 hour after starting; take ≥ 2 h apart from other meds (to avoid absorption issues). |
ADR | Fullness, bloating, cramping, nausea, vomiting, dehydration, ↓ SBP < 20 mmHg, electrolyte imbalance, pulmonary aspiration, Mallory-Weiss tear, SIADH, pancreatitis. |
Key Point | Safest for renal or cardiac patients because it’s isosmotic (balanced electrolytes) and avoids major fluid shifts. |
🧠 Why large volume? it flushes everything out evenly without drawing or pushing water across the bowel wall — so minimal systemic effect.
⚗ 2⃣ Hyperosmotic Preparations
Feature | Details |
|---|---|
Mechanism | Pull water into the bowel lumen → ↑ peristalsis and evacuation. |
Volume | Smaller than PEG preps. |
Risks | Can cause transient electrolyte alterations and dehydration (since hyperosmotic). |
Example ingredients | Sodium phosphate, magnesium citrate (see below). |
Use with caution in | Elderly, renal insufficiency, CHF (risk of fluid/electrolyte imbalance). |
🧠 Why riskier? hyperosmotic solutions shift fluid into the gut — great for cleansing, but can worsen dehydration or electrolyte swings.
⚡ 3⃣ Stimulant Preparations
Feature | Details |
|---|---|
Mechanism | Directly stimulate colonic peristalsis to move stool. |
Patient Instructions | No solid food, but clear fluids allowed (helps prevent dehydration). |
Common brands | Pico-Salax, Picoflo, Purg-Odan (sodium picosulfate / magnesium oxide / citric acid). |
Onset | 3–6 hours. |
Adverse effects | Electrolyte imbalance, ↑ magnesium, dehydration, nausea, vomiting, diarrhea, abdominal pain, rash/hives, rare anaphylactoid reaction. |
🧠 Why combo works: magnesium oxide + citric acid = magnesium citrate in situ → adds osmotic pull + stimulant action.
🧴 4⃣ Magnesium Citrate (Citro-Mag)
Feature | Details |
|---|---|
Mechanism | Osmotic → draws water into intestines. |
Onset | 0.5 – 6 hours (fast!). |
ADR | Nausea, vomiting, hypermagnesemia, electrolyte disturbances, incontinence, dizziness, weakness, dehydration. |
Caution | Avoid in renal impairment (magnesium retention → toxicity). |
🌟 Quick Comparison Table
Type | Example | Volume | Mechanism | Major Concern |
|---|---|---|---|---|
Isosmotic | PEG w/ electrolytes | High | Lavage (balanced) | Nausea, fullness, rare SIADH |
Hyperosmotic | Na phosphate, Mg citrate | Low | Pulls water in | Electrolyte shifts |
Stimulant | Pico-Salax combo | Low | Stimulates colon | Dehydration, Mg↑ |
Combination | Low-vol PEG + stimulant | Moderate | Mixed | GI upset |
✅ End of Bowel Prep Section
💡 EOB-Tips Recap
PEG = safest for fragile pts (renal, elderly).
Hyperosmotic/stimulant = faster but riskier.
Always separate other oral meds by ≥ 2 h.
Watch for electrolyte and magnesium changes.
Encourage clear fluids to prevent dehydration.