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 hematocheziamaroon 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.