STRESS-RELATED MUCOSAL DISEASE (SRMD) / STRESS ULCERS

πŸ”· 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.


πŸ”· II. PATHOPHYSIOLOGY

1. Gastric Mucosal Barrier Breakdown

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

2. Key Factors

Pathogenic Mechanism

Details

Ischemia

Hypoperfusion due to shock, sepsis, hypovolemia

Acid & Pepsin

Contribute to mucosal damage

Cytokines

TNF-Ξ±, IL-1 β†’ impair mucosal integrity

Oxidative Stress

ROS during reperfusion injury

Bile Reflux

Disrupts epithelial tight junctions



πŸ”· III. RISK FACTORS

 Major Independent Risk Factors 

  • Mechanical ventilation β‰₯ 48 hours
  • Coagulopathy:
    • Platelets <50,000/mmΒ³
    • INR >1.5 or aPTT >2Γ— 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


πŸ”· 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)


πŸ”· 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


πŸ”· VI. DIFFERENTIAL DIAGNOSIS

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


πŸ”· VII. PREVENTION

 Who Should Receive Prophylaxis? 

 Indicated If:

At least ONE major risk factor:

  • Mechanical ventilation >48 hr
  • Coagulopathy

OR
β‰₯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 β†’ harms > benefits.

B. Agents Used

Class

Example

Mechanism

PPIs

Pantoprazole, Esomeprazole

Irreversible H⁺/K⁺ ATPase inhibitor

Hβ‚‚ Blockers

Ranitidine, Famotidine

Reversible Hβ‚‚ receptor blocker

Sucralfate

Mucosal coating agent

Adheres to ulcer base, needs acidic pH

Antacids

Rarely used now

Neutralize gastric acid


C. Preferred Agent

  • PPI > Hβ‚‚ 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

πŸ”· VIII. COMPLICATIONS

  • Overt GI bleeding β†’ hemorrhagic shock
  • Blood transfusion requirement
  • Prolonged ICU stay
  • Increased mortality



πŸ”·  CONTROVERSIES & RECENT INSIGHTS

1. SUP Overuse

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

2. Infection Risk

  • PPIs β†’ hypochlorhydria β†’ ↑ VAP, C. difficile colitis

3. Choice of Agent

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