CASE B At the emergency room you attend to a 45 year old advertising executive who presents with the passage of black stools x 3 days and an associated lightheadedness. He complains that during that time, he developed easy fatiguability and generalized body weakness. Upon further questioning he states that his stools are not only black, but are sticky and malodorous. He further complains of recent worsening of a chronic epigastric burning which had been a problem off/on for years. He had doubled his usual dose of tums without significant relief of the burning. He takes NSAIDS as needed for back pain and recently started on one aspirin per day for cardiac prophylaxis. He smokes two packs of cigarettes per day and an occasional cigar. Past medical history: Hypertension, no history of coronary artery disease, no abdominal surgeries Family medical history: unremarkable Personal social history: 2-3 martinis at lunch and another cocktail before dinner Review of systems: no weight loss, good appetite, no easy bruisability Vitals: BP 120/80 supine, BP 90/60 standing, HR 110 RR 20 Temp 36.9%, 02 sat 95% room air alert, oriented, overweight male. He appears anxious and somewhat restless anicteric sclera, pale palpebral conjunctiva, no active dermatoses, cool extremities, symmetrical chest expansion, clear breath sounds distinct heart sounds, regular rhythm, no audible murmurs, Peripheral pulses are present but are rapid and weak abdomen: flat abdomen, soft, with direct tenderness in the epigastric area and the left upper quadrant, hyperactive bowel sounds, no palpable, no guarding or rebound tenderness, liver not enlarged, spleen not palpable, no masses appreciated rectal: good sphincteric tone, no palpable masses, black tarry stool no motor or sensory deficits LABORATORY TESTS: • CBC: Hemoglobin 9gm/dL, Hematocrit 27%, MCV 90, WBC 13 • PT/PTT – normal • BUN 45mg/dL • Creatinine 1.0 mg/dL • Chest x-ray – normal • X-ray of abdomen (kidney, ureter, bladder - KUB) is unremarkable. Points of Discussion 1. Diagnosis 2. Differential diagnosis and basis 3. Explain the different physical examination findings, how do you identify those physical examination findings? 4. Explain the laboratory findings 5. Types of gastrointestinal bleeding 6. Causes of the above type of gastrointestinal bleeding 7. Explain the pathophysiology of the disease 8. Algorithm in the management of GI bleeding based on endoscopic findings 9. History of Present illness 10. Ethiology

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CASE B - Full Case Analysis: Upper GI Bleeding / Peptic Ulcer Disease

1. DIAGNOSIS

Primary Diagnosis: Upper Gastrointestinal Bleeding (UGIB) secondary to Peptic Ulcer Disease (PUD)

This patient has a bleeding peptic ulcer, most likely a duodenal or gastric ulcer, on a background of NSAID/aspirin use, chronic alcohol consumption, and cigarette smoking. The black, sticky, malodorous (tarry) stools (melena), chronic epigastric burning refractory to antacids, and multiple mucosal risk factors point directly to this diagnosis.

2. DIFFERENTIAL DIAGNOSIS AND BASIS

Most Likely

Condition	Supporting Evidence
Bleeding peptic ulcer (gastric or duodenal)	Chronic epigastric burning, NSAID/aspirin use, smoking, alcohol, melena, epigastric tenderness
Gastritis / erosive gastropathy	Same risk factors; NSAID/alcohol-induced mucosal erosions

Other Causes of UGIB to Consider

Condition	Why Considered / Why Less Likely
Esophageal/gastric varices	Alcohol use raises concern; however, no hepatomegaly, no jaundice, no ascites, PT/PTT normal - against cirrhosis
Mallory-Weiss tear	No history of retching or vomiting preceding bleed
Esophagitis	Chronic reflux symptoms possible; however, typically causes less hemodynamic instability
Gastric malignancy	No weight loss, good appetite; less likely but should be excluded endoscopically
Dieulafoy lesion	Can present with massive sudden UGIB, but less common

Peptic ulcer is the most common cause of severe UGIB, accounting for approximately 35-40% of cases in large endoscopy databases. - Sleisenger and Fordtran's Gastrointestinal and Liver Disease

3. PHYSICAL EXAMINATION FINDINGS EXPLAINED

Vital Signs - Orthostatic Hypotension + Tachycardia

Supine BP 120/80, Standing BP 90/60 (drop of ≥20 mmHg systolic), HR 110 = Orthostatic (postural) hypotension with compensatory tachycardia
This indicates significant intravascular volume depletion. A drop in BP of ≥20 mmHg systolic and/or ≥10 mmHg diastolic upon standing, accompanied by tachycardia, signifies loss of approximately 15-20% of total blood volume (roughly 750-1000 mL)
How to identify: Measure BP and HR supine, then have patient sit or stand for 1-3 minutes, remeasure. Tachycardia and tachypnea are the first clinical signs of significant bleeding, followed by orthostatic changes. - Tintinalli's Emergency Medicine

Pale Palpebral Conjunctiva

Reflects anemia (Hgb 9 g/dL). The inner lower eyelid is everted; pallor rather than the normal pink-red color indicates reduced hemoglobin in the submucosal vessels
A reliable bedside indicator of anemia, especially when Hgb falls below 9-10 g/dL

Cool Extremities + Rapid/Weak Peripheral Pulses

Consequence of compensatory peripheral vasoconstriction. In response to reduced cardiac output from hypovolemia, catecholamine release causes peripheral arteriolar constriction, shunting blood to core organs. This reduces skin perfusion (cool, clammy extremities) and reduces pulse volume (weak, thready pulses) despite tachycardia
Indicates the patient is in compensated hypovolemic shock

Epigastric Tenderness + LUQ Tenderness

Direct tenderness (tenderness on direct palpation, without rebound) in the epigastrium reflects inflammation and ulceration of the gastric or duodenal mucosa
No guarding or rebound = no peritonitis, meaning the ulcer has NOT perforated
Hyperactive bowel sounds: blood in the GI lumen acts as a cathartic - the iron and protein content of blood stimulates intestinal motility

Anxious and Restless Appearance

Reflects early cerebral hypoperfusion and catecholamine excess due to hypovolemia. The brain begins to receive inadequate oxygen delivery, producing anxiety and agitation

Anicteric Sclera

Normal white sclera (no jaundice) argues against liver failure or biliary disease as a cause

Rectal Exam - Black Tarry Stool (Melena)

Melena is defined as black, tarry, sticky, malodorous stool resulting from degradation of hemoglobin to hematin by intestinal bacteria. It generally requires at least 50-100 mL of blood from a source proximal to the ileocecal valve. - Sleisenger and Fordtran's

4. LABORATORY FINDINGS EXPLAINED

Finding	Value	Interpretation
Hemoglobin 9 g/dL	Low (Normal: 13.5-17.5 g/dL in males)	Significant blood loss. Note: in acute bleeding, Hgb may underestimate true loss initially because hemodilution takes hours to equilibrate
Hematocrit 27%	Low (Normal: 41-53% in males)	Consistent with moderate-severe anemia from blood loss
MCV 90 fL	Normal (normocytic)	Suggests acute blood loss anemia (not chronic iron deficiency, which gives microcytic anemia with low MCV). Confirms this is an acute bleed on possibly a chronic background
WBC 13,000	Mildly elevated	Stress leukocytosis - a physiologic response to acute hemorrhage; also, digested blood proteins can stimulate WBC production
BUN 45 mg/dL	Elevated	Key finding: Digested blood in the small intestine is absorbed as urea, raising BUN. BUN:Creatinine ratio = 45:1.0 = 45 - a ratio >30 strongly suggests an upper GI source. - Frameworks for Internal Medicine; Sabiston Textbook of Surgery
Creatinine 1.0 mg/dL	Normal	Confirms the elevated BUN is from protein digestion (blood), NOT from renal failure. If creatinine were elevated, BUN:Cr ratio would be less discriminating
PT/PTT Normal	Normal	No coagulopathy; bleeding is from a structural/mucosal lesion, not a clotting defect
Chest X-ray Normal	Normal	Rules out free air under the diaphragm (which would indicate ulcer perforation)
KUB Normal	Normal	No free air, no obstruction, no perforation

BUN:Creatinine ratio >30 has sensitivity 39%, specificity 94%, LR+ 7.5 for upper GI source of bleeding. - Symptom to Diagnosis, 4th Edition

5. TYPES OF GASTROINTESTINAL BLEEDING

GI bleeding is classified anatomically and by presentation:

A. By Location

Upper GI Bleeding (UGIB) - source proximal to the ligament of Treitz (esophagus, stomach, duodenum)

Presents as hematemesis (vomiting blood or coffee grounds) and/or melena (black tarry stools)
Subcategories: esophageal, gastric, duodenal

Lower GI Bleeding (LGIB) - source distal to the ligament of Treitz (small bowel, colon, anorectum)

Presents as hematochezia (bright red or maroon blood per rectum)
Note: massive UGIB can also cause hematochezia in 10-15% of cases

Small Bowel Bleeding - between ligament of Treitz and ileocecal valve (a distinct intermediate category, often "obscure GI bleeding")

B. By Clinical Presentation

Type	Description
Overt bleeding	Visible - hematemesis, melena, hematochezia
Occult bleeding	Not visible to naked eye; detected only by fecal occult blood test (FOBT) or iron-deficiency anemia
Obscure bleeding	Persistent or recurrent bleeding with no source found after EGD and colonoscopy

C. By Severity

Mild: No hemodynamic compromise, Hgb >10
Moderate: Orthostatic changes, Hgb 7-10
Severe: Shock, requires ICU, Hgb <7

This patient has overt, moderate-to-severe UGIB.

6. CAUSES OF UPPER GI BLEEDING (the type in this patient)

The following table shows the frequency of causes in a large endoscopic database:

Cause	Frequency
Peptic ulcer	35.2% (most common)
Esophageal or gastric varices	21.9%
Portal hypertension-related lesions	4.6%
Esophagitis	4.6%
Angioectasia	4.0%
Mallory-Weiss tear	4.0%
Dieulafoy lesion	3.2%
UGI tract neoplasm	3.1%
Epistaxis (swallowed blood)	2.2%
Erosions	1.2%
Other / No cause found	~16%

- Sleisenger and Fordtran's Gastrointestinal and Liver Disease (UCLA CURE Database, n=968)

7. PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE WITH BLEEDING

Normal Mucosal Defense

The gastric mucosa is protected by a balance of:

Defensive factors: mucus-bicarbonate layer, mucosal blood flow, epithelial renewal, prostaglandins (PGE2, PGI2)
Aggressive factors: hydrochloric acid, pepsin

How Ulcers Form in This Patient

Step 1 - NSAIDs and Aspirin disrupt mucosal defense:

NSAIDs (including aspirin) inhibit cyclooxygenase (COX-1 and COX-2) enzymes
COX-1 is constitutively expressed in the gastric mucosa and produces protective prostaglandins (PGE2, PGI2)
Prostaglandins stimulate mucus secretion, bicarbonate secretion, mucosal blood flow, and epithelial cell proliferation
COX-1 inhibition by NSAIDs → reduced prostaglandin synthesis → decreased mucus/bicarbonate → mucosal vulnerability to acid
Aspirin also has a direct topical irritant effect (acid trapping in epithelial cells)

Step 2 - Alcohol:

Ethanol is directly toxic to gastric epithelium, disrupts the mucous barrier, increases back-diffusion of acid into the mucosa, and impairs mucosal healing

Step 3 - Cigarette smoking:

Reduces mucosal blood flow and healing; impairs prostaglandin synthesis; increases acid secretion; may promote H. pylori colonization

Step 4 - Acid injury:

With defensive mechanisms disrupted, gastric acid and pepsin penetrate the mucosal barrier
Mucosal erosion progresses through the epithelium, lamina propria, muscularis mucosae, and into the submucosa/muscularis propria = ulcer

Step 5 - Bleeding:

The ulcer erodes into submucosal blood vessels (arterioles)
Arterial erosion causes active spurting hemorrhage (high risk); venous erosion causes slower oozing
Blood enters the GI lumen, is digested by gastric acid and bacteria
Hemoglobin → hematin (black pigment) → melena

Summary of risk factors present in this patient:

NSAIDs (COX inhibition)
Aspirin (COX inhibition + topical acid)
Chronic alcohol use (direct mucosal toxin)
Cigarette smoking (2 packs/day - reduces healing, blood flow)
Chronic epigastric symptoms (pre-existing ulcer disease)
Hypertension (likely on antihypertensives that may affect splanchnic perfusion)

Source: Robbins & Kumar Basic Pathology; Sleisenger and Fordtran's

8. ALGORITHM: MANAGEMENT OF GI BLEEDING BASED ON ENDOSCOPIC FINDINGS

Initial Resuscitation (before endoscopy)

Two large-bore IV lines (≥18 gauge) or central cordis
Supplemental oxygen; consider intubation if hematemesis/altered mental status
IV fluid resuscitation immediately - do not delay for ICU transfer
Admit to ICU if hemodynamic instability or active bleeding
Type and screen / crossmatch
IV Proton Pump Inhibitor (PPI) - high-dose; continuous infusion or every 12 hours IV
Transfuse if Hgb <7 g/dL (restrictive strategy shown to reduce mortality and rebleeding vs. liberal strategy)

Endoscopy within 24 hours after adequate resuscitation in most patients with overt UGIB

Endoscopic Findings - Forrest Classification and Management

The Forrest classification stratifies ulcer risk based on endoscopic stigmata of recent hemorrhage (SRH):

Forrest Class	Appearance	Rebleeding Risk	Management
Ia	Active arterial spurting	~90%	Endoscopic hemostasis MANDATORY (combination therapy: epinephrine injection + thermal coagulation or clips) + high-dose IV PPI infusion
Ib	Active oozing	~10%	Endoscopic hemostasis + IV PPI
IIa	Non-bleeding visible vessel (NBVV)	~50%	Endoscopic hemostasis MANDATORY + IV PPI
IIb	Adherent clot	~33%	Endoscopic therapy (attempt clot removal + treat underlying vessel) + IV PPI
IIc	Flat pigmented spot	~7%	Medical management with oral PPI; outpatient follow-up acceptable
III	Clean ulcer base	~3%	Oral PPI; may be discharged early if no other high-risk features

Endoscopic Hemostasis Techniques

Injection therapy: Epinephrine injection (causes vasoconstriction + tamponade); never used alone - always combined
Thermal/contact therapy: Bipolar electrocoagulation, thermocoagulation (heater probe) - causes coaptive coagulation of bleeding vessel
Mechanical therapy: Hemostatic clips (over-the-scope or through-the-scope) - physically occludes vessel
Non-contact thermal: Argon plasma coagulation (APC)
Combination therapy (injection + thermal or injection + clips) is superior to monotherapy for high-risk stigmata

Post-Endoscopy Management

High-dose IV PPI after successful endoscopic hemostasis of high-risk ulcers (reduces rebleeding, transfusion, hospital stay)
H. pylori testing; eradicate if positive (reduces recurrence)
Stop NSAIDs and aspirin (if medically permissible); if aspirin must be continued, add PPI
Repeat endoscopy ("second look") is selective, not routine
Angiographic embolization for patients who fail endoscopic therapy
Surgery (oversewing of ulcer, vagotomy/pyloroplasty) for patients refractory to endoscopic + angiographic therapy

Sources: Sleisenger and Fordtran's; Sabiston Textbook of Surgery; Frameworks for Internal Medicine

9. HISTORY OF PRESENT ILLNESS (Reconstructed)

A 45-year-old male advertising executive with a background of hypertension and chronic intermittent epigastric burning presents to the emergency department with a 3-day history of passage of black, sticky, malodorous stools (melena), associated with:

Lightheadedness - consistent with orthostatic hypotension and cerebral hypoperfusion from blood loss
Easy fatiguability and generalized body weakness - symptoms of anemia and reduced oxygen delivery to tissues
Worsening epigastric burning - exacerbation of pre-existing peptic ulcer disease, now unresponsive to doubled doses of antacids (Tums/calcium carbonate)

Relevant exposure history:

Regular NSAID use for chronic back pain (COX inhibition, impaired mucosal defense)
Recently started low-dose aspirin for cardiac prophylaxis (additional COX inhibition)
Heavy cigarette smoking - 2 packs per day (impaired mucosal healing, reduced blood flow)
Alcohol use - 3-4 martinis/cocktails daily (direct mucosal toxin, portal hypertension risk)

Pertinent negatives: No hematemesis (blood did not reach the esophagus in significant quantity to trigger vomiting), no weight loss (against malignancy), good appetite, no easy bruisability (normal coagulation), no history of liver disease or abdominal surgery

10. ETIOLOGY (Causes - in this specific patient)

This patient has multiple concurrent etiologic factors all converging to produce peptic ulceration and hemorrhage:

Primary Etiologic Agents

Factor	Mechanism
NSAIDs (chronic use)	COX-1 inhibition → reduced prostaglandin synthesis → breakdown of mucus-bicarbonate barrier → acid injury. In the U.S., NSAID use is now the most common cause of gastric ulcers as H. pylori rates decline with aging population increasing aspirin use - Robbins Basic Pathology
Aspirin	Both topical acid injury AND systemic COX inhibition. Even low-dose aspirin disrupts the gastric mucosal barrier
Chronic alcohol consumption	Direct toxin to gastric epithelium; disrupts mucous layer; increases back-diffusion of H+ ions; impairs mucosal cell proliferation; causes erosive gastritis
Cigarette smoking	Reduces mucosal blood flow and prostaglandin synthesis; impairs ulcer healing; increases gastric acid secretion; may enhance H. pylori virulence

Contributing/Underlying Factors

Factor	Role
H. pylori infection (likely, not yet tested)	Present in >70% of PUD; causes chronic gastritis, impairs mucosal defenses; MUST be tested and eradicated
Stress / sympathoadrenal activation	Advertising executive with high-stress occupation; stress increases acid secretion, reduces mucosal blood flow
Pre-existing peptic ulcer diathesis	Years of chronic episodic epigastric burning suggest a pre-existing vulnerable mucosa
Hypertension medications	Some antihypertensives may affect splanchnic perfusion

Why the Bleed Occurred NOW

The combination of doubling NSAID dose + adding aspirin for cardiac prophylaxis simultaneously overwhelmed an already compromised mucosa (from years of alcohol and smoking), finally tipping the balance from chronic ulceration to frank hemorrhage with erosion into a submucosal vessel.

Summary Table

Item	Key Points
Diagnosis	UGIB from bleeding peptic ulcer (gastric or duodenal)
Key history	3 days melena, chronic epigastric burning, NSAIDs, aspirin, alcohol, heavy smoking
Key exam	Orthostatic hypotension, tachycardia, pale conjunctiva, cool extremities, epigastric tenderness, melena on rectal exam
Key labs	Hgb 9, Hct 27%, normocytic (acute), BUN 45 (BUN:Cr = 45 - confirms UGIB), normal PT/PTT, normal Cr
Type of GI bleed	Overt, moderate-severe, UPPER GI bleeding (melena)
Pathophysiology	NSAID/aspirin COX inhibition + alcohol + smoking → mucosal defense failure → acid injury → ulceration → arterial erosion → melena
Management	IV access, resuscitation, IV PPI, upper endoscopy within 24h, hemostasis based on Forrest class, stop NSAIDs, test and treat H. pylori

Sources: Sleisenger and Fordtran's Gastrointestinal and Liver Disease; Sabiston Textbook of Surgery; Frameworks for Internal Medicine; Robbins & Kumar Basic Pathology; Tintinalli's Emergency Medicine; Symptom to Diagnosis 4th ed.

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