Dyspepsia

Definitions

• Peptic ulcer disease
  • Chronic illness with recurrent ulcerations in stomach and proximal duodenum
  • Acid and pepsin are crucial factors
  • Vast majority due to H. pylori (70-90%) or NSAID use
• Gastritis
  • Acute or chronic inflammation of gastric mucosa
• Dyspepsia
  • Continuous or recurrent upper abdominal pain or discomfort +/- nausea/bloating

introduction

• Uncomplicated peptic ulcer disease 5/1000 per year and 10% lifetime incidence in the West
• H. pylori affects 50% of the population
• Risk factors for ulcers not due to H. pylori or NSAID’s
  • Antiplatelets
  • Stress
  • Helicobacter heilmannii
  • CMV
  • Behcet’s disease
  • Zollinger-Ellison syndrome
  • Crohn’s
  • Cirrhosis with portal hypertension
  • Older age
  • African American

Introduction

• Dyspepsia
  • Affects 20-40% of population
  • No clear association with alcohol, sex, age, SES, smoking
  • More common in those infected with H. pylori or take NSAID’s

Pathophysiology

• Balance of mucus, blood flow, bicarbonate secretion vs. HCl, pepsin, urease, cytotoxins, proteases, gastrin levels and reduced mucus/bicarb secretion
• 1-10% (10-20% in de Alwis) of H. pylori infected individuals suffer peptic ulcers
• 90-95% of patients with duodenal ulcers have H. pylori
• 70% of patients with gastric ulcers have H. pylori
• Prevalence of H. pylori is lower in those with complicated duodenal ulcers than uncomplicated
• H. pylori negative ulcers have significantly worse outcomes, especially if eradication is performed despite negative testing
• H. pylori also causes mucosa-associated lymphoid tissue (MALT) lymphoma and eradication of bacterium causes remission in a large proportion of low-grade tumors
• Risk factor for adenocarcinoma of stomach also
• Diet and alcohol use do NOT cause peptic ulcer disease

Pathophysiology

• Endoscopy of dyspepsia patients shows:
  • 13% erosive oesophagitis
  • 8% peptic ulcer disease
  • <0.3% have gastric or oesophageal cancer
  • Gastritis, duodenitis and gastric erosions may be evident but it is unclear if these cause dyspepsia symptoms
  • 70-80% diagnosed as ‘functional dyspepsia’
  • Gastric ulcerations have greater morbidity and mortality than duodenal

Functional dyspepsia

• Patients show abnormal responses to stomach distension after a single meal, abnormal gastric emptying, abnormal sensitivity of duodenum to acid and abnormalities in acid clearance

Clinical presentation

• Burning epigastric pain, dull achge, empty feeling
• May be relieved by milk/antacids/food
• Pain recurs as gastric contents empty, with recurrent pain classically waking the patient at night
• Tends to occur daily for weeks, resolve and then recur in weeks to months
• Post-prandial pain, food intolerance, nausea, retrosternal pain and belching are not related to PUD
• Atypical presentations are common >65yo including:
  • No pain
  • Epigastric pain not relieved with food
  • Nausea
  • Vomiting
  • Anorexia
  • Weight loss
  • Bleeding

Clinical presentation

• Change in character of pain may herald complication
  • Acute epigastric pain may signify perforation
  • Back pain may indicate perforation into the pancreas causing pancreatitis
  • Nausea/vomiting may indicate gastric outlet obstruction due to oedema or scarring
  • Ulcer bleeding
• Gastritis
  • Most common presentation is GI bleeding
  • May have epigastric pain, nausea, vomiting

diagnosis

• Who needs an endoscopy?
  • Age >50 with new onset symptoms
  • Unexplained weight loss
  • Persistent vomiting
  • Dysphagia or odynophagia
  • Iron deficiency anaemia or GI bleeding
  • Abdominal mass or lymphadenopathy
  • FHx of upper GI malignancy

diagnosis

• H. pylori testing
  • Rapid urease test
    • Detects presence of urease on biopsy sample
    • >90% sensitive and >95% specific
  • Anti-H. pylori IgG antibodies serology
    • Sensitivity 85%, specificity 79%
    • Not useful as a test of cure as remain positive for years
  • Urea breast test
    • C-13 or C-14-labelled urea is ingested and broken down to labelled CO2 and ammonia
    • Sensitivity and specificity >95%
      Can be used as test of eradication also
  • Stool antigens
    • >90% sensitivity and specificity
    • Testing >4 weeks after eradication therapy is a good test of cure
  • Sensitivity of all tests is significantly decreased by PPI, H2-antagonists, antibiotics and bismuth compounds

treatment

• PPI + antacids for breakthrough pain and referral to primary care for further evaluation for H. pylori and eradication therapy
• Cessation of any causative agent e.g. NSAID
• Short-course of PPI seems better than H2-receptor antagonist for undiagnosed dyspepsia
• If alarm features evident (see prior slide), immediate referral for endoscopy is mandated
• Guidelines suggest if H. pylori positive, should undergo eradication and subsequent endoscopy only if symptoms persist or alarm features arise

ppi

• Irreversibly bind H+/K+ ATPase on gastric parietal cells, blocking H+ secretion
• Most effective if taken 30-60 minutes prior to a meal as require acidic compartments within stimulated parietal cells for activation
  • Work poorly when fasting or with other antisecretory agents e.g. H2 receptor antagonists
• Heal ulcers faster than H2-RA’s and have some effect against H. pylori
• Metabolised in liver by Cytochrome P450 and may decrease metabolism of other drugs
• May inhibit absorption of drugs that rely on gastric acidity

H2-receptor antagonists

• Competitively inhibit histamine action on H2 receptors of gastric parietal cells
• Needs renal dosing adjustment
• Side effects are rare but include headache, confusion, lethargy, depression and hallucinations

antacids

• Buffer gastric acid to allow ulcer healing
• Magnesium- and aluminium-containing compounds inhibit absoprtion of drugs and should be avoided in renal failure
• Mainly used for symptom relief PRN

H. Pylori eradication

• If diagnosed in the presence of PUD, eradication is clearly indicated
• Triple therapy – Omeprazole 20mg BD + Amoxicillin 1g BD + Clarithromycin 500mg BD for 7 days

complications

• Haemorrhage
  • PUD is the most common cause of upper GI non-variceal bleeding
  • 15% of peptic ulcers bleed with overall mortality rate of 10%
  • Actively bleeding ulcers on endoscopy have a 55% risk of re-bleeding and 11% mortality rate, whereas those with a clean base have  5% and 2% risk respectively
• Perforation
  • Resuscitation, Triple antibiotics, NG, erect CXR and surgical referral
  • Free air evident on CXR in 80-85% (not 100% sensitive)
  • Gastric perforation more common in Asians and duodenal perforation in Westerners
• Obstruction
  • Can occur due to oedema with active ulcer disease or scarring from chronic ulcer disease
  • Surgical correction is often necessary

Disposition and follow-up

• Most patients with uncomplicated dyspepsia can be discharged home with PPI course and primary care follow-up
• If alarm features, obtain consultation to arrange early endoscopy
• If complications apparent, admit
• Avoid alcohol, smoking, NSAID’s, steroids and any foods that appear to upset their stomach
• Follow-up in 1-2 days if not improving or 1-2 weeks if symptoms improving
• Advise of warning signs of complications

Last Updated on October 28, 2020 by Andrew Crofton