STRESS-RELATED MUCOSAL DISEASE (SRMD) / STRESS ULCERS

🔷 I. DEFINITIONS

1. Stress-Related Mucosal Disease (SRMD)

  • Acute erosive and ulcerative gastritis occurring in critically ill patients.
  • Includes:
    • Stress erosions (superficial)
    • Stress ulcers (deep, bleeding lesions)

2. Stress Ulcers

  • Multiple shallow mucosal lesions in the gastric fundus and body, caused by hypoperfusion and acid-mediated injury.


🔷 II. PATHOPHYSIOLOGY

1. Gastric Mucosal Barrier Breakdown

  • Stress → splanchnic vasoconstriction → mucosal ischemia
  • Ischemia → ↓ bicarbonate/mucus, ↑ H⁺ back-diffusion → mucosal necrosis

2. Key Factors

Pathogenic Mechanism

Details

Ischemia

Hypoperfusion due to shock, sepsis, hypovolemia

Acid & Pepsin

Contribute to mucosal damage

Cytokines

TNF-α, IL-1 → impair mucosal integrity

Oxidative Stress

ROS during reperfusion injury

Bile Reflux

Disrupts epithelial tight junctions



🔷 III. RISK FACTORS

 Major Independent Risk Factors 

  • Mechanical ventilation ≥ 48 hours
  • Coagulopathy:
    • Platelets <50,000/mm³
    • INR >1.5 or aPTT >2× control

 Additional Risk Factors (Supportive):

  • Sepsis
  • ICU stay > 7 days
  • High-dose corticosteroids (>250 mg hydrocortisone/day)
  • Traumatic brain injury, spinal cord injury
  • Major burns (>35% BSA) – Curling’s ulcer
  • Multiple organ dysfunction syndrome (MODS)
  • Acute renal or hepatic failure
  • History of GI ulcer or bleeding within 1 year


🔷 IV. CLINICAL FEATURES

1. Usually Asymptomatic

  • Most cases are subclinical erosions

2. Overt Upper GI Bleeding

  • Hematemesis, coffee-ground emesis
  • Melena
  • Anemia
  • Hemodynamic instability (if severe bleeding)


🔷 V. DIAGNOSIS

A. Clinical Suspicion

  • In ICU patients with risk factors and unexplained blood loss

B. Endoscopy

  • EGD = gold standard
  • Findings:
    • Diffuse superficial erosions
    • Gastric body/fundus > duodenum
    • Rarely, visible vessels or active bleeding

C. Other Clues

  • Drop in hemoglobin
  • Positive nasogastric aspirate for blood
  • Occult blood in stool


🔷 VI. DIFFERENTIAL DIAGNOSIS

  • Peptic ulcer disease
  • Mallory–Weiss tear
  • Esophageal varices
  • Dieulafoy lesion
  • Gastric antral vascular ectasia (GAVE)


🔷 VII. PREVENTION

 Who Should Receive Prophylaxis? 

 Indicated If:

At least ONE major risk factor:

  • Mechanical ventilation >48 hr
  • Coagulopathy

OR
≥2 minor risk factors (institution dependent)


 NOT Indicated In:

  • General ward patients
  • ICU patients without risk factors
  • Patients tolerating enteral feeds & no risk factors

Overuse → harms > benefits.

B. Agents Used

Class

Example

Mechanism

PPIs

Pantoprazole, Esomeprazole

Irreversible H⁺/K⁺ ATPase inhibitor

H₂ Blockers

Ranitidine, Famotidine

Reversible H₂ receptor blocker

Sucralfate

Mucosal coating agent

Adheres to ulcer base, needs acidic pH

Antacids

Rarely used now

Neutralize gastric acid


C. Preferred Agent

  • PPI > H₂ Blocker (more potent, fewer failures)
  • IV Pantoprazole (40 mg OD/BID) common in ICU

D. Discontinuation

  • Stop when patient is off mechanical ventilation, has no bleeding risk, tolerates oral feeds

 Enteral Feeding as Natural Prophylaxis

Enteral nutrition:

  • Maintains mucosal perfusion
  • Stimulates prostaglandins
  • Buffers acid

🔷 VIII. COMPLICATIONS

  • Overt GI bleeding → hemorrhagic shock
  • Blood transfusion requirement
  • Prolonged ICU stay
  • Increased mortality



🔷  CONTROVERSIES & RECENT INSIGHTS

1. SUP Overuse

  • Many patients receive SUP unnecessarily → ↑ risk of infections (VAP, C. difficile)
  • Evaluate risk-benefit before starting

2. Infection Risk

  • PPIs → hypochlorhydria → ↑ VAP, C. difficile colitis

3. Choice of Agent

  • Recent guidelines suggest PPIs for high-risk patients
  • Avoid sucralfate in ventilated patients (aspiration risk)