Gastritis

Section: UGI Sub-section: Gastric

Definition

• Inflammation of gastric mucosa

Aetiology

• Acute
  • H. Pylori
  • NSAIDs
  • Acids, Alkali or thermal injury,
  • Radiation,
  • Uremia,
  • Stress
• Chronic
  • H.Pylori
  • Pernicious anemia,
  • NSAIDs – associated with MALToma 10%

Pathology

• Acute
  • PMN, mucosal inflammation ± erosions,
  • Histology shows congested haemorrhagic mucosa
• Acute emphysematous
  • Gas-forming organisms seen
    • Endotoxin-producing Clostridium (C.perfringens etc)
    • Other anaerobes
      • Bacetroides
      • Anaerobic Streptococci
• Acute suppurative
  • streptococcus
• Chronic
  • chronic inflammatory cells
  • ± destruction of normal glandular tissue
• Superficial gastritis
  • Confined to gastric pits (and not the glands)

Atrophic Gastritis

• Extends into glands and full thickness lamina propria
• Type A
  • Due to Pernicious anaemia,
  • Auto-antibodies to parietal cells,
  • Profound atrophy,
  • Intestinal metaplasia (goblet & paneth cells, enterocytes),
  • Principally affects body,
  • Grossly flat with loss of rugae
• Type B
  • Commonest
  • Due to H.Pylori
  • Asymptomatic
  • Effects antrum
• Type C
  • Due to bile reflux or chronic NSAID use,
  • Deep gastric pits,
  • Oedema of lamina propria

Stress ulceration

• Pathophysiology
  • Mucosal ischemia resulting in break down of normal protective factors (mucus, bicarbonate secretion, prostaglandins, blood flow), exacerbated by presence of acid.
• Occurs within 1-2 days of stress event in 50% of pts
  • Physical trauma, shock, sepsis, haemorrhage, resp failure
• Stress related mucosal injury (superficial erosions)
  • Almost always in proximal portion of stomach (fundus)
  • Multiple superficial non-ulcerating erosions that can bleed.
• Only symptom may be painless UGI bleeding
  • Stress ulcer
  • Progression of mucosal injury with ulceration
  • High risk of GI bleeding.
    • Curling ulcer – stress ulcer after severe burns
    • Cushing’s ulcer – deep, post neurological illness
• PPI Prophylaxis
  • Only for those at high risk – critically ill with coagulopathy or prolonged ventilation
    • Unnecessary use can actually increase risk of vent-associated pneumonia and C.diff
• Begin enteral feeding as soon as possible
• Management
  • Most settle with PPI and correction of haemodynamics
  • If >3L or bleeding persists, consider anterior gastrotomy and oversew of bleeding areas

Curling’s ulcer

• Acute gastric erosion resulting as a complication of severe burns
  • Usually burns with >30% BSA
• Reduced plasma volume leads to ischaemia and necrosis of gastric mucosal cells
• Previously could result in haemorrhage or perforation with high risk of mortality
  • Less common now with PPI use

Cushing’s ulcer

• Gastric ulcer associated with elevated intracranial pressure
  • Can also be oesophagus or DU
• Mechanism
  • ? Direct vagal stimulation as a result of increased intracranial pressure
    • Tumour, trauma, or other intracranial processes
  • Leads to increased acetylcholine mediated parietal cell stimulation
  • Increased acid leads to ulceration
    • Usually deep ulcers
    • Risk of perforation or haemorrhage

Bile Reflux Gastropathy

• Definition
  • Endoscopic and histological signs of gastritis typically as a result of alteration in pyloric function (eg post-op)
  • Attributing symptoms is problematic, as most patients with bile reflux are asymptomatic
• Incidence
  • symptoms may occur months or years after an index operation
• Classification
  • Primary: de novo
  • Secondary: related to previous operation
• Etiology
  • Due to regurgitation of bile into the stomach because of:
    • An incompetent pyloric sphincter
    • Abnormal duodenal motility
    • Operative changes –
      • Gastric surgery (gastroenterostomy (especially Billroth II), pyloroplasty)
      • Even lap cholecystectomy
  • Concomitant infection with H.pylori can cause increased inflammation
• Clinical
  • Patients commonly asymptomatic
  • Abdo pain, bilious vomiting, weight loss
• Pathology
  • Bile salts and lecithin cause gastric mucosal injury
• Investigations
  • Endoscopy: Bx & CLO test
  • 24hr gastric pH &/or gastric bilirubin (or bile salt) monitoring
  • Scintigraphic detection of bile in stomach (bile reflux scan)
• Management
  • Test for and eradicate H. pylori
  • Medical management (limited success):
    • Ursodeoxycholic acid → improves Sx but not histology
    • Sucralfate → improves histology, but not Sx
    • Rabeprazole (same results as sucralfate)
    • PG E2
    • Cholestyramine and alginates
  • Definitive management is surgery (revision & Roux-en-Y)
    • Get improved symptoms in 50-90%
    • Uncommon to ‘cure’ pt of all symptoms
    • Surgery for primary reflux is rare: ‘duodenal switch’
• Prognosis / Natural Hx:
  • May be a risk factor the development of antral metaplastic gastritis
  • Improvement from surgery less likely in patients with delayed gastric emptying

Menetrier’s Disease

• Overview
  • Hypoproteinaemic Hypertrophic Gastropathy
  • Rare, acquired disease, Pre-malignant
  • Characterised by massive gastric folds in the fundus and body
  • Gives mucosa cobblestone or cerebriform appearance (looks like brain!)
• Pathology
  • Foveolar Hyperplasia
    • Expansion of surface mucous cells, and loss of parietal cells
    • Typical changes seen on endoscopy
  • Protein loss from the stomach
  • Excessive mucus production
  • Hypo or achlorhydria (gland atrophy)
• Aetiology
  • Unknown - ? CMV infection in children, ? H.Pylori in adults
• Presentation
  • Epigastric pain, vomiting, weight loss, anorexia, peripheral oedema
• Investigations
  • Gastroscopy and biopsy to R/O gastric carcinoma or lymphoma
  • Can do 24hr pH monitoring to detect low acid levels
• Management
  • Anticholinergics, PPIs, Octreotide, H.pylori eradication
  • Inconsistent results
  • Consider total gastrectomy if
    • Massive ongoing protein loss despite medical therapy
    • Dysplasia or carcinoma on biopsy