# Clinical Cases: Gastrointestinal Bleeding

## Case 1: Non-Variceal Upper GI Bleeding - Peptic Ulcer Disease

### Patient Presentation
**Demographics:** 68-year-old male

**Chief Complaint:** Vomiting blood and black tarry stools for 1 day

**History of Present Illness:** The patient developed nausea and vomited approximately 500 mL of bright red blood mixed with clots this morning. He subsequently noticed black, tarry, foul-smelling stools. He reports epigastric discomfort for the past 2 weeks that he attributed to "indigestion." He felt lightheaded when standing and nearly fainted in the bathroom.

**Past Medical History:** Osteoarthritis (takes ibuprofen 800 mg three times daily for 3 months), hypertension, hyperlipidemia, coronary artery disease with prior stent (on aspirin 81 mg and clopidogrel)

**Social History:** Former smoker (quit 10 years ago), social alcohol (2-3 beers weekly)

### Physical Examination
- **Vital Signs:** BP 92/58 mmHg (supine), HR 112 bpm; Standing: BP 74/50 mmHg, HR 138 bpm (positive orthostatic hypotension)
- **General:** Pale, diaphoretic male appearing anxious
- **Abdomen:** Soft, mild epigastric tenderness, no peritoneal signs, hyperactive bowel sounds
- **Rectal Exam:** Black, tarry, guaiac-positive stool

### Workup and Results
- **CBC:** Hemoglobin 7.2 g/dL (baseline 13.5), Platelets 185,000
- **BMP:** BUN 48 mg/dL (elevated due to blood in GI tract), Creatinine 1.1 mg/dL
- **Coagulation:** PT/INR normal
- **Type and Screen:** Performed; 4 units PRBCs crossmatched
- **Glasgow-Blatchford Score:** 14 (high-risk; hemoglobin, BUN, blood pressure, melena all contribute)
- **EGD (performed within 12 hours):** Large 2-cm posterior duodenal ulcer with visible vessel (Forrest IIa) at the base; no active bleeding at time of endoscopy

![Duodenal Ulcer Endoscopy](case_01_image.jpg)
*Endoscopic image of a duodenal ulcer with evidence of recent hemorrhage. The visible vessel (Forrest IIa classification) at the ulcer base indicates high risk for rebleeding and requires endoscopic therapy.*

**Image Source:** Wikimedia Commons. Samir, CC BY-SA 3.0

### Diagnosis
**Acute Upper GI Bleeding from Posterior Duodenal Ulcer (NSAID-induced) - Forrest IIa (High-Risk Stigmata)**

### Clinical Correlation
This case illustrates classic non-variceal upper GI bleeding from peptic ulcer disease, the most common cause of UGIB (30-40% of cases). Key teaching points include:

**Risk Factor Analysis:**
- **NSAID use**: Direct mucosal injury and prostaglandin inhibition reduce mucosal defense
- **Dual antiplatelet therapy**: Increases bleeding risk 3-5 fold when combined with NSAIDs
- **Location**: Posterior duodenal ulcers are particularly dangerous due to proximity to the gastroduodenal artery, which can cause massive hemorrhage if eroded

**Clinical Presentation:**
- **Hematemesis**: Frank blood indicates ongoing or recent active bleeding
- **Melena**: Black tarry stool from degraded blood (indicates at least 50-100 mL blood loss)
- **Orthostatic hypotension**: Indicates significant volume depletion (typically > 1L blood loss)
- **Elevated BUN:Creatinine ratio**: Blood protein absorbed in GI tract increases urea production

**Forrest Classification and Rebleeding Risk:**
- Forrest Ia (spurting): 55% rebleeding
- Forrest Ib (oozing): 43% rebleeding
- **Forrest IIa (visible vessel): 43% rebleeding** - requires therapy
- Forrest IIb (adherent clot): 22% rebleeding - consider clot removal and therapy
- Forrest IIc (flat pigmented spot): 10% rebleeding - no therapy needed
- Forrest III (clean base): 5% rebleeding - no therapy needed

### Treatment
**Resuscitation:**
- Two large-bore IV access
- Crystalloid resuscitation (Lactated Ringer's)
- **Restrictive transfusion strategy**: Target hemoglobin 7-8 g/dL (not normal range)
- ICU admission given hemodynamic instability

**Pre-Endoscopic Management:**
- IV PPI: Pantoprazole 80 mg bolus followed by 8 mg/hour infusion
- Hold antiplatelet agents temporarily (discuss with cardiology)
- Consider erythromycin 250 mg IV to promote gastric emptying before EGD

**Endoscopic Therapy (for Forrest IIa):**
- Combination therapy preferred: Epinephrine injection (1:10,000) followed by thermal coagulation (bipolar) OR endoscopic clips
- Epinephrine alone is not sufficient (high rebleeding rates)

**Post-Endoscopic Care:**
- Continue high-dose IV PPI infusion (80 mg bolus + 8 mg/hour) for 72 hours
- Test for H. pylori (stool antigen or biopsy urease test)
- Transition to oral PPI twice daily after 72 hours
- **NSAID cessation** - if pain management needed, use acetaminophen or consider COX-2 selective agent with PPI if NSAID absolutely required
- Cardiology consultation regarding timing of antiplatelet resumption (typically resume aspirin within 3-5 days; rebleeding risk vs. stent thrombosis)

---

## Case 2: Variceal Bleeding in Cirrhosis

### Patient Presentation
**Demographics:** 55-year-old male

**Chief Complaint:** Massive vomiting of blood for 2 hours

**History of Present Illness:** The patient experienced sudden onset of vomiting large amounts of bright red blood (estimated > 1 liter). He has a known history of alcoholic cirrhosis and was previously told he has "enlarged veins in his esophagus." He stopped taking his propranolol 2 weeks ago because he felt dizzy. He continues to drink alcohol daily.

**Past Medical History:** Alcoholic cirrhosis (Child-Pugh Class B), known esophageal varices (large, never bled), prior ascites requiring paracentesis, hepatic encephalopathy

**Social History:** Active alcoholism (1 pint of vodka daily), no IV drug use

### Physical Examination
- **Vital Signs:** BP 78/48 mmHg, HR 128 bpm, RR 24/min, Temp 37.8C
- **General:** Pale, confused male with active hematemesis, blood on gown and bed
- **HEENT:** Icteric sclerae, blood in oropharynx
- **Abdomen:** Distended with shifting dullness (ascites), caput medusae, splenomegaly
- **Extremities:** Palmar erythema, spider angiomata, muscle wasting
- **Neurologic:** Disoriented; asterixis present

### Workup and Results
- **CBC:** Hemoglobin 6.8 g/dL, Platelets 62,000, WBC 11,200
- **Coagulation:** INR 2.1, PTT 38 seconds
- **BMP:** Sodium 128 mEq/L, Creatinine 1.8 mg/dL (baseline 1.0)
- **LFTs:** Total bilirubin 4.2 mg/dL, Albumin 2.4 g/dL, AST 85 U/L, ALT 52 U/L
- **Child-Pugh Score:** 10 (Class C: bilirubin > 3, albumin < 2.8, INR > 2.3, ascites, encephalopathy)
- **MELD Score:** 24
- **EGD (within 12 hours):** Large esophageal varices (Grade III) with active spurting from one varix; red wale signs on remaining varices

![Endoscopic Banding for Esophageal Varices](case_02_image.png)
*Endoscopic image demonstrating esophageal varices. Large variceal columns are visible with red wale signs (red streaks on the varix surface), indicating high risk for bleeding. Endoscopic band ligation is the first-line treatment.*

**Image Source:** Wikimedia Commons. Jmarchn, CC BY-SA 3.0

### Diagnosis
**Acute Variceal Hemorrhage in Decompensated Cirrhosis (Child-Pugh C)**

### Clinical Correlation
Variceal bleeding is a life-threatening complication of portal hypertension, carrying 15-20% mortality per bleeding episode. This case highlights several critical concepts:

**Unique Physiology of Variceal Bleeding:**
- Portal hypertension causes collateral formation at sites of portosystemic anastomoses
- Esophageal varices develop when hepatic venous pressure gradient (HVPG) exceeds 10-12 mmHg
- Bleeding risk correlates with varix size, red wale signs, and severity of liver disease
- **Approximately 30% of patients with large varices will bleed within 2 years**

**Critical Differences from Non-Variceal Bleeding:**
- **Restrictive transfusion (Hgb 7-8 g/dL)** is even more important - overtransfusion increases portal pressure and worsens bleeding
- **Coagulopathy in cirrhosis is complex** - both pro- and anti-coagulant factors are depleted; INR does not reliably indicate bleeding risk; routine FFP is not indicated
- **Prophylactic antibiotics reduce mortality** - infection is common and worsens outcomes

**Why He Bled:**
- Discontinued propranolol (removes portal pressure-lowering effect)
- Ongoing alcohol use (continued liver injury)
- Large varices with red wale signs (high-risk stigmata)
- Child-Pugh C status (most severe liver disease)

### Treatment
**Immediate Resuscitation:**
- Airway protection: **Endotracheal intubation** (altered mental status + active hematemesis = high aspiration risk)
- Two large-bore IV access
- **Conservative fluid resuscitation** - avoid over-resuscitation
- Blood transfusion targeting Hgb 7-8 g/dL

**Pharmacotherapy (initiated immediately, before endoscopy):**
- **Octreotide**: 50 mcg IV bolus, then 50 mcg/hour continuous infusion for 3-5 days (reduces splanchnic blood flow and portal pressure)
- **Ceftriaxone 1 g IV daily for 7 days** - prophylactic antibiotics reduce infections, rebleeding, and mortality
- **Avoid nephrotoxic agents** - patient at high risk for hepatorenal syndrome

**Endoscopic Therapy (within 12 hours):**
- **Endoscopic band ligation (EBL)** - first-line for esophageal varices
- Band placed directly on actively bleeding varix, then on remaining large varices
- Superior to sclerotherapy with fewer complications

**Rescue Therapies (if endoscopy fails):**
- **Balloon tamponade** (Sengstaken-Blakemore or Minnesota tube) - temporary bridge, not definitive therapy; high complication rate
- **TIPS (Transjugular Intrahepatic Portosystemic Shunt)** - creates portosystemic shunt to decompress portal system

**Early TIPS Consideration:**
This patient is Child-Pugh C with score 10 - meets criteria for **early or "preemptive" TIPS** within 72 hours (ideally 24 hours). Studies show early TIPS in high-risk patients (Child-Pugh C 10-13, or Child-Pugh B with active bleeding) improves survival.

**Secondary Prophylaxis (after acute episode resolves):**
- Resume non-selective beta-blocker (propranolol, nadolol, or carvedilol)
- Serial band ligation every 2-4 weeks until varix eradication
- Combination of beta-blocker + band ligation provides best protection
- Alcohol cessation counseling and liver transplant evaluation