Rosen & Barkin's 5-Minute Emergency Medicine Consult (290 page)

• Inflammatory response of gastric mucosa to injury—“gastritis”
  
• 3 lines of defense of gastric mucosa:
  
  • Mucous layer that forms protective pH gradient
    
  • Surface epithelial cells that can repair small defects
    
  • Postepithelial barrier that neutralizes any acid that has traversed 1st 2 layers
    
• No definite link between histologic gastritis and dyspeptic symptoms
  
• Epithelial cell damage with no associated inflammation—“gastropathy”
  

• Common causes of gastritis: Infections, autoimmune, drugs (i.e., cocaine), hypersensitivity, stress
  
• Common causes of gastropathy: Endogenous or exogenous irritants, such as bile reflux, alcohol, or aspirin and NSAIDs, ischemia, stress, chronic congestion
  
• Acute gastritis:
  
  • Stress (sepsis, burns, trauma):
    
    • Decrease in splanchnic blood flow leading to decreased mucus production, bicarbonate secretion, and prostaglandin synthesis
      
    • Results in mucosal erosions and hemorrhage
      
  • Alcohol:
    
    • Induces production of leukotrienes that cause microvascular stasis, engorgement, and increased vascular permeability
      
    • Leads to hemorrhage
      
  • NSAIDs, including aspirin:
    
    • Interfere with prostaglandin synthesis, leading to similar cascade as induced by alcohol
      
    • Results in mucosal erosions
      
  • Steroids
    
• Chronic gastritis:
  
  • Produced by
    Helicobacter pylori
    
  • Mechanism of
    H. pylori
    unclear:
    
    • Gram-negative spiral bacteria found in gastric mucous layer
      
    • Contains enzyme urease that allows it to change pH level (alkaline) of its microenvironment
      

DIAGNOSIS

• Dyspepsia
  
• Bloating
  
• Nausea/vomiting
  
• Anorexia
  
• Epigastric tenderness
  
• Heartburn
  

• Dyspepsia
  
• Epigastric pain or discomfort (episodic and chronic)
  
• Bloating, indigestion, eructation, flatulence, and heartburn
  
• Anorexia, nausea/vomiting
  
• Hematemesis, melena
  

• Careful physical exam including stool Hemoccult testing and vital signs with orthostatics
  
• Dehydration, tachycardia (with vomiting)
  
• Pallor (hemorrhagic gastritis)
  
• Abdominal exam
  
• Nonspecific
  
• Epigastric tenderness
  

• ABCs
  
• Hematocrit determination
  
• Evaluation for dehydration/shock
  

• Normal lab values in uncomplicated gastritis
  
• CBC:
  
  • Anemia with acute hemorrhagic gastritis
    
  • Leukocytosis: Infection
    
• Electrolytes, BUN, creatinine, glucose
  
• Amylase/lipase for pancreatitis in differential
  
• Urinalysis:
  
  • Assess dehydration/ketosis (starvation)
    
  • Bilirubin present with hepatitis
    

• ECG:
  
  • For elderly patients
    
  • Myocardial ischemia in differential
    
• Endoscopy:
  
  • Outpatient unless significant hemorrhage
    
  • Allows for visualization of bleeding sites, histologic confirmation of mucosal inflammation, and detection of
    H. pylori
    
• Noninvasive
  H. pylori
  testing:
  
  • ¹³
    C and
    ¹⁴
    C urea breath tests
    
  • Stool antigen test
    
  • Serology to detect antibodies to
    H. pylori
    
  • Serum pepsinogen isoenzymes
    
    • The ratio of pepsinogen isozymes I and II in serum correlates with presence of metaplastic atrophic gastritis (principally autoimmune metaplastic atrophic gastritis and pernicious anemia)
      

• Peptic ulcer disease (PUD)
  
• Nonulcer dyspepsia (symptoms without ulcer on endoscopy)
  
• Gastroesophageal reflux
  
• Biliary colic
  
• Cholecystitis
  
• Pancreatitis
  
• Hepatitis
  
• Abdominal aortic aneurysm
  
• Aortic dissection
  
• Myocardial infarction
  

TREATMENT

• ABCs
  
• IV fluid resuscitation
  

• ABCs with acute erosive or hemorrhagic gastritis that presents with hemodynamic instability
  
• IV fluid resuscitation with lactated Ringer solution or 0.9% normal saline (NS) via 2 large-bore catheters
  
• NGT for gastric decompression and lavage when history of hematemesis or unstable vital signs
  
• Foley catheterization to assess volume replacement
  

• Pain control with:
  
  • Antacids
    
  • GI cocktail:
    
    • 30 mL antacids + 10–20 mL viscous lidocaine
      
  • H
    ₂
    antagonists
    
  • Proton pump inhibitors (PPIs)
    
  • Sucralfate
    
  • Avoid narcotics—may mask serious illness
    
• Acute hemorrhagic gastritis:
  
  • IV fluid resuscitation
    
  • Blood transfusion if low hematocrit
    
  • Reverse causes (alcohol, sepsis, NSAIDs, or trauma)
    
  • Prevent
    acute
    or
    erosive
    gastritis in critically ill:
    
    • Antacids hourly or IV PPI or H
      ₂
      antagonists
      
    • Goal is to keep pH level at >4
      
• Chronic gastritis—
  H. pylori
  therapy:
  
  • Treatment of
    H. pylori
    infection:
    
    • Invasive or noninvasive testing to confirm infection
      
    • Oral (PO) eradication antibiotic therapy options
      
  • Most common therapies for
    H. pylori
    infection:
    
    • PPI (omeprazole 20 mg or lansoprazole 30 mg), clarithromycin 500 mg BID for 2 wk, amoxicillin 1 g BID for 2 wk.
      
    • For penicillin-allergic patients: PPI + clarithromycin 500 mg BID + metronidazole 500 mg BID for 14 days
      
    • 4-drug therapy: H
      ₂
      blocker, bismuth subsalicylate (Pepto-Bismol) + either amoxicillin 1,000 mg BID or tetracycline 500 mg QID in combination with either metronidazole 250 mg QID or clarithromycin 500 mg BID for 14 days
      
  • Drug resistance in US:
    
    • Metronidazole: 30–48%
      
    • Clarithromycin: >10%
      
    • Amoxicillin: Uncommon
      
    • Bismuth: None
      
  • Treatment controversial for asymptomatic or nonulcer dyspepsia gastritis
    
• Vitamin B
  ₁₂
  supplementation for
  atrophic gastritis
  

• Bismuth subsalicylate: 525 mg tabs 2 PO QID not to exceed 8 doses in 24 hr
  
• Cimetidine (H
  ₂
  blocker): 800 mg PO at bedtime nightly (peds: 20–40 mg/kg/24 h) for 6–8 wk
  
• Famotidine (H
  ₂
  blocker): 40 mg PO at bedtime nightly (peds: 0.5–0.6 mg/kg q12h) for 6–8 wk
  
• Lansoprazole (PPI): 30 mg PO BID for 2 wk
  
• Maalox Plus: 2–4 tablets PO QID
  
• Misoprostol: 100–200 μg PO QID
  
• Mylanta II: 2–4 tablets PO QID
  
• Nizatidine (H
  ₂
  blocker): 300 mg PO at bedtime nightly for 6–8 wk
  
• Omeprazole (PPI): 20 mg PO BID (peds: 0.6–0.7 mg/kg q12–24 h) for 2 wk
  
• Pantoprazole (PPI): 40 mg PO/IV daily for 2 wk
  
• Ranitidine (H
  ₂
  blocker): 300 mg PO at bedtime nightly (peds: 5–10 mg/kg/24 h given q12h) for 6–8 wk
  
• Sucralfate: 1 g PO QID for 6–8 wk
  

• Triple therapy using a PPI with clarithromycin and amoxicillin or metronidazole given twice daily remains the recommended 1st choice treatment.
  
• Sequential 10-day therapy in high prevalence areas:
  
  • Double therapy for 5 days:
    
    • PPI
      
    • Amoxicillin
      
  • Followed by triple therapy for 5 days:
    
    • PPI
      
    • Clarithromycin
      
    • Metronidazole
      

• Bismuth-based quadruple therapies remain the best 2nd choice treatment.
  
• The rescue treatment should be based on antimicrobial susceptibility testing.
  

FOLLOW-UP

• Acute hemorrhagic or erosive gastritis that presents with upper GI tract bleeding, tachycardia, and hypotension
  
• Uncontrolled pain or vomiting
  
• Coagulopathy from medication or liver disease
  

• Unremarkable physical exam with normal CBC and heme-negative stools
  
• If heme-positive stools, discharge if stable vital signs, normal hematocrit, and negative NGT aspiration for upper GI tract hemorrhage:
  
  • Outpatient evaluation for endoscopy
    

• Outpatient referral for endoscopy and
  H. pylori
  testing
  
• Biopsy for gastric dysplasia and malignancy
  

Close follow-up with gastroenterologist for endoscopy with biopsy for diagnostic reasons.

• Gastritis/gastropathy is a common presentation to ED.
  
• Symptoms typically are dyspepsia, nausea, and vomiting.
  
• ED management depends on patient’s clinical symptoms, but should include diagnostic and therapeutic components.
  
• Therapeutic management usually involves treatment of
  H. pylori
  .
  
• Drug resistance of
  H. pylori
  to antibiotics is increasing.
  
• Close follow-up with gastroenterologist recommended for biopsy and to detect gastric cancers.