Dyspepsia
Neil C. Jackson
General
Common symptom with
extensive differential
diagnosis and heterogenous
pathophysiology.
Epidemiology
 25% of general population/year
 25% with evidence of organic cause
 75% without
Symptoms
 Chronic or recurrent pain or discomfort in the upper abdomen
 Ulcer-like or acid dyspepsia
 Burning pain, epigastric huger-like pain
 Relief with food/antacids/antisecretory agents
 Food-provoked dyspepsia or indigestion
 Postprandial epigastric discomfort and fullness
 Belching, early satiety, nausea, occasional vomiting
 Reflux-like dyspepsia
 Rome III Criteria
 Postprandial fullness
 Early satiation
 Inability to finish a normal sized meal
 Epigastric Pain or Burning
Organic dyspepsia
 PUD
 GERD
 GE malignancy
 Biliary
 Meds (NSAIDs)
 Other
 Celiac / chronic pancreatitis
 Infiltrative dz (Eosinophilic gastritis / crohn’s / sarcoid)
 DM radiculopathy / hypercalcemia / heavy metal toxicity
 Hepatoma / steatohepatitis / mesenteric ischemia
PUD
 A spectrum from gastritis to ulceration complicated by
bleeding, pain and perforation.
 Poor correlation with reported symptoms and EGD
findings
 Includes Duodenal and gastric ulcers
 Commonly due to H.Pylori and/or NSAID, tobacco, EtOH
 Treatment = H.pylori eradication and removal of inciting
agents
Duodenal vs. Gastric Ulcers
 Gastric ulcer
 Worse with meals
 Poor response to antacids/otcs
 Duodenal ulcer
 Pain when acid is secreted in absence of a food buffer
 Improves with meals, alkali, antisecretory agents
 Worse 3-5 hours after a meal
 Worse at night between 11pm – 2am
 Maximal circadian stimulation of acid secretion
GERD
 Some degree of reflux is physiologic
 Montreal classification:
 A condition that develops when reflux of stomach contents
causes troublesome symptoms and/or complications
 Prevalence= 10-20% in western world, <5% in Asia
 Heartburn = retrosternal burning, most common
 Regurgitation = gastric content into mouth/throat
 Dysphagia = common in longstanding GERD due to
 Reflux esophagitis
 Stricture
More GERD
 Globus sensation
 Almost constant perception of a lump in the throat
 Water brash (foaming at the mouth)
 Rare hypersalivation caused by reflux
 Chest pain
 Mimics angina, typically squeezing/burning
 Substernally with radiation to back/neck/jaw/arms
 Lasts minutes to hours
 Spontaneous resolution with antacids
 Occurs after meals, awakens from sleep
 Worse with emotional stress
GE Malignancy
 Uncommon cause of chronic dyspepsia in Western
Hemisphere
 More common in Asian, Hispanic, Afro-Caribbean
populations
 Increases with age
 Epigastric pain vague, mild in early disease – more
severe and constant with progression
 Weight loss from insufficient caloric intake
 Dysphagia related to esophageal or proximal gastric
malignancy
NSAIDs
 Direct effect
 Ionization upon absorption into gastric mucosa
 Topical epithelial injury
 Systemic effect
 Inhibition of GI mucosal COX activity (COX1)
 Decreased mucosal prostaglandin protection
History
 Association of symptoms with meals
 Heartburn / regurgitation / cough
 NSAID use ??
 Radiation to back, personal/fhx of pancreatitis
 Significant weight loss / anorexia / vomiting / dysphagia
/ odynophagia / fhx of GI malignancy
 Severe episodic epigastric / RUQ pain lasting more than
one hour
Exam
 Usually normal except for epigastric tenderness
 Jaundice, pallor, ascites, muscle wasting
 Palpable abdominal mass
 Palpable lymphadenopathy
 L supraclavicular = Virchow’s node
 Periumbilical = Sister Mary Joseph’s node
 Carnett sign
 Double straight leg raise or head raise while supine
 Finger presses point of tenderness
 + test = Increased pain with muscle tensing
Labs
 CBC
 Electrolytes + Calcium
 Hepatic Function Panel
Alarm Features
 Age > 55 yrs with new-onset dyspepsia
 FHx of upper GI malignancy
 Unintended weight loss
 GI bleeding
 Progressive dysphagia
 Odynophagia (painful swallowing)
 Unexplained Iron deficiency
 Persistent vomiting
 Palpable mass or node
 Jaundice
Diagnosis: Pt with alarm features
 Upper endoscopy within two weeks
 with stomach biopsy for H.pylori
 Yield of EGD increases with age
 Per meta-analysis of 9 studies, 5389 pts:
 6% erosive esophagitis
 8% PUD
 If normal, most will have functional dyspepsia
 Further evaluation warranted if alarm features
 Age cutoff controversial
 AGA suggests 60-65 yrs
 45-50 with Asian, Hispanic, Afro-Caribbean descent
Reflux Esophagitis
Barrett’s Esophagus
Gastric Ulcer
Esophageal Ulcer
Diagnosis: No alarm features
 Test and treat for H.pylori
 If local h.pylori prevalence >10 %
 Empiric PPI / H2blocker
 If local h.pylori presence <5%
Test and Treat for H.Pylori
 Urea breath test or stool Ag
 Serologic testing should not be used
 NNT is 14
H. Pylori eradication
 Quadruple Therapy
 Triple therapy + bismuth 525mg 4xdaily for 10-14 days
 With clarithromycin/metronidazole resistance > 15%
 With recent/repeated exposure to clarithro/flagyl
 Triple Therapy
 PPI (multiple options)
 Omeprazole 20mg bid
 Pantoprazole 40mg bid
 Amoxicillin: 1g BID 7-14 days
 Clarithromycin: 500mg BID 7-14 days
 Alternative antibiotics
 Doxycycline 100mg bid / Flagyl 250mg 4xdaily
Anti-Secretory Therapy
 PPIs > H2 blockers
 PPI (Omeprazole / pantoprazole / lansoprazole )
 Irreversibly binds/inhibits H/K atp pump on parietal cells
 Only effective in active parietal cells
 Must be taken 30-60 minutes before meals
 Twice daily dosing if :
 Failed standard therapy
 Large gastric ulcer
 H2 blockers (Ranitidine / cimetidine / famotidine)
 Inhibit Histamine H2 receptors on parietal cells
Functional Dyspepsia
 Presence of one or more:
 Postprandial fullness
 Early satiation
 Epigastric pain/burning
 Negative diagnostic evaluation for organic disease
 Symptoms for last three months
 Onset more than 6 months previously
Pathophysiology
 Gastric motility / compliance
 Delayed gastric emptying (30%)
 rapid gastric emptying (10%)
 Visceral hypersensitivity
 Increased pain with normal gastric stretching/compliance
 Independent of delayed gastric emptying
 H.pylori infection
 Unclear mechanism, ?smooth muscle dysfunction 2/2 inflammatory
modulation of enteric nervous system
 Altered gut microbiome
 Symptoms more likely after episode of AGE
 Psychosocial dysfunction
 Association with GAD, somatization, Major Depression
 Higher prevalence in pts with self-reported hx of child abuse
Treatment
 H.Pylori test and treat
 Tricyclic anti-depressants
 If persistent symptoms despite PPI x8wks
 PPI / H2 blockers
 Metoclopramide (Prokinetic)
 If failed above therapy
 5-10 mg TID half hour before meals and at night x4wks
References

Uptodate
 Approach to the Adult with Dyspepsia
 Functional dyspepsia in adults
 Clinical manifestations of peptic ulcer disease
 Clinical manifestations and diagnosis of GERD in adults
 Clinical features,diagnosis,staging of gastric cancer
 Epidemiology, pathobiology and clinical manifestations of esophageal cancer
 Differential diagnosis of abdominal pain in adults

AGA
 AGA medical position statement: evaluation of dyspepsia – Gastroenterology,
2005

AFP
 Evaluation and management of non-ulcer dyspepsia
 H.Pylori Infection