I. Definitions

  1. Dyspepsia: epigastric discomfort, in some cases related to meals and/or ass'd with nausea, vomiting, early satiety, belching, or bloating; sometimes also reflux sx
  2. Nonulcer dyspepsia: dyspepsia without peptic ulcer
  3. Functional dyspepsia: Dyspepsia for > 6mos without pathology seen on endoscopy

II. Etiology

  1. No clear association with H. pylori Infection in the absence of ulcer
  2. Differential diagnosis of Dyspepsia:
  1. Functional dyspepsia (60% of patients)
  2. Peptic Ulcer Disease (about 20% of pts w/o identifiable systemic or medication-related cause)
  3. GERD (about 25% of ditto)
  4. Gastritis (about 21% of ditto)
  5. Irritable bowel syndrome
  6. Inflammatory Bowel Disease
  7. Celiac Disease
  8. Cholelithiasis (n.b. gallstones may be present but not responsible for dyspepsia symptoms)
  9. Chronic cholecystitis
  10. Chronic pancreatitis
  11. Gastroparesis, e.g. Diabetic Gastroparesis
  12. Malabsorption syndromes
  13. Mesenteric Ischemia
  14. Alcohol use
  15. Intestinal parasitosis (e.g. Giardiasis, Strongyloides)
  16. Intra-abdominal neoplasm, particularly Gastric Cancer (almost always in pts > 45yo) and Pancreatic Cancer
  17. Non-gastroenterological causes
    1. Medications (especially Theophylline, Digitalis, NSAIDs, Iron, Potassium, Serotonin Reuptake Inhibitors, Bisphosphonates)
    2. Myocardial Ischemia
    3. Hyperparathyroidism
    4. Thyroid Disorders (both hypo- and hyperthyroidism)
    5. Pregnancy
    6. Collagen-vascular diseases
  1. Commonly cited "alarm" signs for pts with dyspepsia, suggesting possibility of serious etiologies:
    1. Unintended weight loss
    2. Odynophagia
    3. Dysphagia
    4. Vomiting
    5. Jaundice
    6. Hematemesis
    7. Hematochezia
    8. Melena
    9. Anemia
    10. Anorexia
    11. Palpable abdominal mass
    12. Lymphadenopathy
    13. Lack of response to therapy
    14. Chronic NSAID use
    15. Alcohol overuse
    16. Family history of gastric cancer
    17. Personal history of upper GI malignancy or peptic ulcer
    18. Age > 55yo

III. Evaluation of a patient with Dyspepsia

  1. In a prospective study in 2,741 pts with dyspepsia (by "Rome II" criteria) without "alarm symptoms" and without current NSAID use > 2d/wk, recent H. pylori tx, or sx of GERD all of whom underwent upper endoscopy, prevalence of cancer identified on endoscopy was 0.2% (only one in pts < 50yo) (Clin. Gastroent. Hepatol. 7:756, 2009-JW)
  2. The sx pattern & the presence/absence of epigastric tenderness do not reliably distinguish among the underlying causes of Dyspepsia (Scan J Gastroenterol 1997;32:118-25; Gastroenterology 1982;82:16-9. --Ref'd in UW Guidelines)
  3. Workup with esophagogastroduodenoscopy (EGD):
    1. Consider EGD for all who have no alterable systemic or medication-related cause, b/c of sig. incidence of ulcer
    2. Consider earlier EGD if older (60% of pts > 60yo w/dyspepsia will have PUD; Ann. Int. Med. 108:865, 1988; acommonly used cutoff is onset > 45yo)
    3. Consider EGD if any of the above "alarm" signs are present
    4. For pts at low risk of PUD (e.g. young, nonsmokers, no NSAID use) and malignancy can consider empiric tx, e.g. promotility agents (see below) before EGD
  4. Consider abdominal ultrasound or CT, particularly if biliary or pancreatic etiology is suspected
  5. H. pylori serology may be a useful "triage" tool in that pts < 45yo with dyspepsia but negative H. pylori serology, no NSAID use, and no "alarm" sx (persistent vomiting, dysphagia, odynophagia, evidence of GI bleed, unintentional weight loss, etc.) suggests a VERY low likelihood of ulcer (UW Guidelines)
  6. Labs-Consider:
    1. CBC (rule out anemia from slow GIB)
    2. Serum Calcium (rule out hyperparathyroidism)
    3. LFT's (look for hepatobiliary etiologies)
    4. Thyroid function tests
    5. Amylase and/or lipase (rule out chronic pancreatitis)
    6. H. pylori serology, for low-risk pts (to r/o need for EGD; see "C" above)

IV. Treatment of Dyspepsia

  1. In patients < 55yo with no "alarm" features (see above) consider two options (similar rates of symptomatic "cure" at 1y):
    1. "Test and treat" with noninvasive H. pylori testing and treatment if positive, and if symptoms persist, proton pump inhibitor for 4-8wks
      1. Preferable in populations with high prevalence of H. pylori infection
    2. Empiric treatment with proton-pump inhibitor x 4-8wks
  2. Promotility agents (e.g. metoclopramide 10mg TID-QID, domperidone) shown to be effective in sx control in randomized trials (Treatment of Functional Dyspepsia. Scand J Gastroenterol 1991;26:47-60)
  3. H2 Blockers & Proton-Pump Inhibitors
    1. Only a modest symptomatic benefit c/w placebo (meta-analysis done in J Clin Gastroenterol 1989;11:69-77--Ref'd in UW Guidelines)
    2. In a study in 224 primary care patients with "functional dyspepsia" (> 12wks in the last 12mos of upper abd pain/discomfort, no evidence of organic disease, and sx not releaved by defecation; no change in stool frequency or form) and normal EGD randomized to esomeprazole 40mg/d vs. placebo; at 4wks, active-tx pts had sig. greater incidence of sx relief (51% vs. 32%) but no sig. diff. at 8wks (Am. J. Gastroent. 101:2096, 2006--JW) 
  4. Tx of H. pylori infection in pts with dyspepsia who have not yet undergone EGD-Controversial, may not offer any cost benefit over proceeding straight to EGD
  5. Tx of H. pylori infection in pts with non-ulcer dyspepsia and H. pylori infection-Benefit is quite small
  1. Other treatment options for functional dyspepsia
    1. Small, frequent meals
    2. Avoid tobacco and excess alcohol and caffeine
    3. Avoid medications that may exacerbate (see above)
    4. Weight control if overweight
    5. Anti-emetics if have nausea and/or vomiting
    6. Tricyclic antidepresants may improve symtpoms when accelerated gastric emptying is present
(Sources include Core Content Review of Family Medicine, 2012)