Approach to Dyspepsia

Dr. Ghalia Abu Mohsen

 Definition
• Chronic or recurrent pain or discomfort
centered in the upper abdomen that is
episodic or persistent and can be
caused by a variety of conditions.
• often associated with belching, bloating,
heartburn, nausea or vomiting.
Your patient comes complaining of either/&:
 epigastric pain
 heartburn
 regurgitation
 nausea
 vomiting
 belching
 bloating (the sensation of abdominal fullness
without objective distention)
 Anorexia or early satiety.
 
 Epidemiology
• Dyspepsia affects up to 40 % of adults each
year, and about 10 % of those affected seek
medical care.
• Most cases in patients who seek care are
eventually diagnosed as functional
dyspepsia.
• dyspepsia is responsible for substantial
health care costs (medications and diagnostic
evaluations) and considerable time lost from
work.
Classification of Dyspepsia…
•   Functional dyspepsia (50-70%): also called non-ulcer dyspepsia. 
•   Non-functional dyspepsia, there is a structural or/& functional cause
such as:
 Gastroesophageal reflux disease (25%):Dx by 24 hour pH monitoring
 Peptic ulcer disease (20%): Dx by endoscopy
 Gastritis: infection by H.pylori, Dx by serology test and urea breath test
 Gastric or Esophageal cancer (1-2%): Dx by endoscopy & biopsy
 Acute/ chronic pancreatitis: Dx by Hx and elevated (3X) serum lipase &
amylase.
 Biliary and GB diseases.
• Non-GI causes such as:
 DM
 Thyroid diseases
 Medications: NSAID, antibiotics, estrogen and many others
 Severe kidney diseases
 Hyperparathyroidism.
 Etiology

• In about 50 to 70 % of patients, a specific etiology

is not identified (“functional” or non-ulcer
dyspepsia). Many of these patients are
hypothesized to have an augmented perception
of visceral pain.
• Structural conditions commonly associated with
dyspepsia include peptic ulcers and
gastroesophageal reflux disease (GERD). Gastric
or esophageal cancers are serious causes but
account for fewer than 2 % of cases
 Evaluation
• Evaluation of patients with dyspepsia includes a
thorough history and physical examination, with
special attention given to elements that suggest
the presence of serious disease. 

• Before any investigation is performed, the

physician must decide whether the patient is at
high risk for serious disease and should undergo
immediate endoscopy or whether the patient can
safely receive empiric drug therapy.
 History
• A thorough history is important in
evaluating the patient with dyspepsia,
although symptoms alone may not be
very useful in establishing a specific
diagnosis. 
• Location of discomfort
• Duration
• Quality of pain
• Severity
• Associated symptoms
• Exacerbating and relieving symptoms
• History of similar symptoms
• Family history
• Drugs
• Smoking
• Alarm symptoms (red flags)
 Alarm symptoms
• Age >55 yr
• Bleeding, melena, hematemesis
• Anemia
• early satiety
• Anorexia
• Fever
• unexplained weight loss
• dysphagia or odynophagia
• persistent vomiting
• Long standing reflux symptoms
• family history of gastrointestinal malignancy
• previous documented peptic ulcer
• abdominal mass
• lymphadenopathy
Questions to Ask When Determining Common Causes of Dyspepsia:
Peptic ulcers
• Does the patient have a personal history of ulcers?
• Does the patient have a strong family history of ulcers?
• Does the patient have risk factors associated with peptic ulcer?
• Does the patient report melena?
• Is the patient a smoker ? a chronic NSAIDs user?
Gastroesophageal reflux disease
• Does the patient complain of heartburn or regurgitation?
• Are symptoms worse when the patient is lying down?
• Does the patient have a chronic cough or hoarseness?
Biliary tract disease
• Does the patient report any history of jaundice?
• Does the patient report dark urine?
• is pain episodic and severe, and may last for hours?
• Does pain occur after meals especially after large fatty meal ?
• Is the pain associated with meals or belching ?
Pancreatitis
• Is the pain stabbing, and does it radiate to the patient's back?
• Is the pain abrupt, is it unbearable in severity and does it last for many hours without relief?
• Does the patient have a history of heavy alcohol use?
Gastroparesis: (Dysmotility-like dyspepsia)
• Does the patient complain of symptoms of bloating, abdominal distention,
flatulence and prominent nausea?.
• Does the patient tend to feel hungry but have premature satiety with resultant
epigastric heaviness or fullness even after the consumption of small meals?.
• Does the patient has diabetes mellitus, is there any peripheral neuropathy
present?.
Cancer
• Is the patient over 50 years of age?
• Has the patient had a recent significant weight loss?
• Does the patient have trouble swallowing?
• Has the patient had recent protracted vomiting?
• Does the patient have a history of melena?
• Is the patient a smoker?
Metabolic disorders
• Does the patient have a medical history of diabetes mellitus,
hypothyroidism or hyperthyroidism, or hyperparathyroidism?

Medications
• Is the patient currently taking medications commonly associated
with dyspepsia?
 Examination
• Physical examination is usually normal in patients with
uncomplicated dyspepsia.
• epigastric tenderness
•  hypotension or tachycardia may indicate significant blood loss from
gastrointestinal bleeding.
• The stool should also be tested for occult blood.
• dental erosions may be found in GERD
• Jaundice or a positive Murphy's sign suggests gall bladder disease.
• Signs of hypothyroidism or hyperthyroidism should also be
considered in the evaluation of dyspepsia.
• Weight loss, a positive fecal occult blood test, a palpable mass,
signal nodes (Virchow's nodes) and acanthosis nigricans are signs
of possible malignancy. 
• Clinical signs of anemia, such as brittle nails, cheilosis and pallor of
the palpebral mucosa or nail beds, may also suggest malignancy.
 Laboratory Evaluation
Specific investigations toward suggested condition by Hx &
Physical exam.
• The initial evaluation of dyspepsia should include a CBC to
rule out anemia.
• If the history and physical examination suggest the
presence of gallstones or another hepatobiliary condition,
liver function tests and sonographic evaluation should be
ordered.
• Likewise, if pancreatitis is suspected, serum lipase and
amylase levels should be obtained.
• Patients with nausea, vomiting and epigastric fullness may
also have generalized electrolyte imbalances. Therefore,
electrolyte measurements should be considered.
• H.pylori tests:
• Urea breath test (UBT)
• if H. pylori is present, the urease produced by the organism breaks down
ingested carbon 14–labeled urea into ammonia and labeled carbon
dioxide, which can be detected in the patient's breath. The UBT is more
sensitive and specific than serologic testing, it is useful for confirming
eradication of the organism, but it is more expensive. should be
performed 4 to 6 weeks after completion of eradication therapy. PPIs
must be stopped for at least two weeks before the test.
• Stool test : with a polymerase chain reaction (PCR) test or an antigen
enzyme immunoassay (EIA). Also useful for confirming eradication of the
organism with high sensitivity and specificity. cheaper than urea breath
tests. PPIs should be stopped for 2 weeks before testing, but stool
antigen tests are not as affected by PPI use as are urea breath tests.
• Antibody titers: H. pylori can also be detected in the serum with
antibody titers positive serology test (IgG), but it indicates previous
exposure to H. pylori,(cannot distinguish between an active infection and
a past infection). Thus, it is not useful for confirming eradication. Test is
not affected by PPI or antibiotic use  
• ENDOSCOPY WITH BIOPSY
• Endoscopy with biopsy is recommended to rule out cancer
and other serious causes in patients 55 years or older, or
with one or more alarm symptoms.
• In patients who have not been taking a PPI within one to
two weeks of endoscopy, or bismuth or an antibiotic within
four weeks, the rapid urease test performed on the biopsy
specimen provides an accurate, inexpensive means of
diagnosing H. pylori infection. Patients who have been on
these medications will require histology, with or without
rapid urease testing. Culture and polymerase chain
reaction allow for susceptibility testing.
 Management
• After a thorough clinical evaluation and
detailed history, conditions such as GERD,
biliary pain and medication-induced
dyspepsia can most likely be confirmed or
excluded.
• The remaining patients probably have ulcer-
like, or functional (nonulcer) dyspepsia.
• in the absence of warning signs for serious
disease, a test-and-treat strategy is
effective and cheaper than initial endoscopy.
Management of Dyspepsia
• Patients with the onset of dyspepsia at 56 years or
older, or those with alarm symptoms at any age
should undergo immediate upper endoscopy.
• Patients with reflux-predominant symptoms should be
treated as if they have GERD.
• The test-and-treat strategy should be pursued first,
followed by a trial of a proton pump inhibitor.
• If these strategies fail, upper endoscopy should be
considered according to the physician’s judgment.
However, the prevalence of ulcer or malignancy in H.
pylori–negative patients is low in this group.
Functional Dyspepsia
•  Functional (non-ulcer) dyspepsia is defined as the
presence of postprandial fullness, early satiety, or
epigastric pain or burning in the absence of causative
structural disease.
• There is no definitive pathophysiologic mechanism for
functional dyspepsia. Patients with functional dyspepsia
commonly have coexisting symptoms of irritable bowel
syndrome or other functional GI disorders, as well as
anxiety and depression .
• Symptoms should be for at least 12 weeks (not necessary
consecutive) within the previous 6 months.
 Pathophysiology
• Gastric dysmotility: delayed gastric
emptying
• Acid secretion: low PH
• Role of Helicobacter pylori infection
• Hypersensitivity to gastric distention
Rome III Diagnostic Criteria for Functional Dyspepsia
Presence of at least one of the following:
• Bothersome postprandial fullness
• Early satiation
• Epigastric pain
• Epigastric burning

and

• No evidence of structural disease (including at upper

endoscopy) that is likely to explain the symptoms
Diagnostic Approach of functional dyspepsia

• Functional dyspepsia is a diagnosis of exclusion;

therefore, physicians should focus on excluding
serious or specifically treatable diseases, without
spending too much time investigating symptoms.
• The physician should perform a detailed history and
physical examination at the initial presentation, noting
any findings that point to a diagnosis other than
functional dyspepsia. 
• If any cause is identified for the dyspepsia, the
diagnosis of functional dyspepsia is no longer valid.
 Treatment
• Treatment of functional dyspepsia can be
frustrating for physicians and patients
because few treatment options have proven
effective.
• Patients will need continued reassurance
and support from their physicians.
• Treatment is generally aimed at one of the
presumed underlying etiologies of functional
dyspepsia.
(1) PROKINETICS
(2) GASTRIC ACID SUPPRESSION:
(3) H. PYLORI ERADICATION
(4) PSYCHOTROPIC AND
PSYCHOLOGICAL INTERVENTIONS
PEPTIC ULCER DISEASE
 PEPTIC ULCER DISEASE
• An important cause of dyspepsia is (PUD), which
includes gastric and duodenal ulcers.
• Duodenal ulcers are approximately 3 times as
common as gastric ulcers.
• PUD is most commonly caused by Helicobacter
pylori  infection or use of non-steroidal anti-
inflammatory drugs (NSAIDs), a rare cause is
Zollinger-Ellison Syndrome.
 Pathophysiology of H. pylori
• H. pylori, a gram-negative, helical, rod-shaped
bacterium, colonizes the gastric mucosa of
approximately one-half of the world population.
• H. pylori is present in 95% of patients with
duodenal ulcers and in 70% of those with gastric
ulcers.
• It is typically transmitted via the fecal-oral route
during early childhood and persists for decades.
• The bacterium is a known cause of gastric and
duodenal ulcers and is a risk factor for mucosa-
associated lymphoid tissue (MALT) lymphoma and
gastric adenocarcinoma.
 History
• Epigastric discomfort or pain : is the most
common presenting symptom, occurs on
empty stomach in duodenal ulcer, and after
eating in gastric ulcer.
• Nausea or Vomiting
• Heartburn
• Loss of appetite
• Fullness , belching, bloating, flatulence
 Diagnosis
• During the initial evaluation, a test-and-treat strategy to
identify and eradicate Helicobacter pylori infection is more
effective than empiric treatment and more cost-effective than
initial endoscopy.
• The test-and-treat strategy for detecting H. pylori is
appropriate in patients with dyspepsia and low risk of gastric
cancer (age younger than 55 years and no alarm symptoms) 
• Eradication of H. pylori helps one out of 15 patients with
functional dyspepsia diagnosed by endoscopy, but may not
be cost-effective.
• Endoscopy is recommended for patients who are 55 years or
older, or who have alarm symptoms.
 Management
• Eradication of H. pylori is recommended in all
patients with PUD. “the only good H. pylori is
a dead H. pylori”.
• therapy must be chosen empirically based on
regional bacterial resistance patterns, local
recommendations, and drug availability.
• standard triple therapy is a reasonable initial
therapy where clarithromycin resistance is
low.
• Eradication heals most duodenal ulcers and greatly
diminishes the risk of recurrent bleeding.
• Current data suggest that increasing the duration of therapy
to 14 days significantly increases the eradication rate.

• When indicated, eradication testing should be performed at

least 4 weeks after completion of therapy.

• Indications for eradication test (by the urea breath test or

stool antigen test ):
 H. pylori–associated ulcer
 continued dyspeptic symptoms
 H. pylori–associated MALT lymphoma
 resection for gastric cancer.
 Complications
• Bleeding
• Perforation
• Gastric outlet obstruction
• Gastric cancer / malignant transformation
Gastroesophageal Reflux
Disease
(GERD)
 GERD is a chronic, relapsing condition with
associated morbidity and an adverse impact on
quality of life.
 The disease is common, with an estimated
lifetime prevalence of 25 to 35 % in the U.S.
population. though many persons with GERD may
not seek medical care
 The lower oesophageal sphincter tone is reduced
and there are frequent transient LOS relaxations
 Diagnosis
• In practice, the initial diagnosis of
GERD is based on the history.
• Diagnostic testing should be reserved
for patients who:
 present with warning signs and symptoms,
 have not responded to PPI therapy, or
 have disease duration of 5 to 10 years
 Diagnosis
(1) Clinical manifestations:
• The two classic symptoms that define this disorder are
heartburn and regurgitation.
• The epigastric burning sometimes radiates to the throat
and worsens when a patient eats, bends down or lies flat.
• Esophageal spasm from gastroesophageal reflux is
characterized by sharp, stabbing substernal pain (non
cardiac chest pain, mimic angina).
• Heartburn and esophageal reflux and spasm commonly
occur at night or after the consumption of a large meal.
 Symptoms
• Heartburn
• Acid regurgitation
• Nausea
• Belching
• Water brash (sour taste in mouth)
• Non cardiac chest pain
• Chronic hoarseness of voice/ Recurrent Laryngitis
• Asthma (bronchospasm)
• Chronic cough
• Dental enamel loss
• Globus sensation
• Recurrent sore throat
 Red flags
• Age >55
• Persistent dysphagea or odynophagia (possible
esophageal stricture)
• Early satiety
• Gastrointestinal bleeding
• Weight loss (possible cancer)
• Persistent vomiting
• chest pain (possible cardiac causes)
• Iron deficiency anemia
(2) RADIOLOGIC FINDINGS (Barium radiology )
• seldom useful for diagnosing GERD
• Only one third of patients with GERD have radiologic signs of
esophagitis.
• Findings include erosions and ulcerations, strictures, hiatal
hernia, thickening of mucosal folds and poor distensibility.
• Only a minority of patients with documented abnormal pH have
radiographically evident esophagitis. Consequently, a
radiographic study is NOT the test of choice for the diagnosis of
GERD.
(3) ENDOSCOPY
• Only 50 % of patients with GERD manifest macroscopic
evidence on endoscopy.
• While endoscopy lacks sensitivity for identifying GERD, it is the
gold standard for assessing esophageal complications of
GERD. such as Barrett's esophagus, esophagitis and strictures.
(4) AMBULATORY PH MONITORING
• Ambulatory pH monitoring is generally considered the
diagnostic gold standard for use in patients with GERD.
• In this study, a pH monitor is placed in the esophagus
above the lower esophageal sphincter, and the pH is
recorded at given moments in time.
• Over the 24-hour test period, the patient writes down the
time and situation in which symptoms occur, in the hope
that symptoms can be correlated with the lowering of
esophageal pH that occurs with reflux.
• Esophageal pH monitoring may not be available in some
areas. Furthermore, the test is time-consuming, and it
can be inconvenient for the patient. In addition, pH
monitoring requires good technical placement of the
probe and experienced interpretation of the results.
 Risk factors of Barrett's
esophagus
• Long standing reflux (>10 years)
• Male gender
• Obesity
• Middle age
• Tobacco smoking
• White race
• High socioeconomic status
 Management
• The primary treatment goals in patients with
GERD are relief of symptoms, prevention of
symptom relapse, healing of erosive esophagitis,
and prevention of complications of esophagitis.
• Includes:
 lifestyle modifications
 Pharmacologic agents
 Surgery  
LIFESTYLE MODIFICATIONS:include
• elevating the head of the bed by six inches
• decreasing meal size and fat intake
• stopping smoking
• reducing alcohol consumption
• losing weight
• avoiding recumbency for three hours postprandially and
not consuming large meals and certain types of food
• Avoid medications that may potentiate GERD symptoms,
including calcium channel blockers, beta agonists, alpha-
adrenergic agonists, and others
• Avoid wearing clothing that is tight around the waist.  
• Dietary Factors Associated with Increased Reflux
Symptoms*
• Caffeinated products
• Peppermint
• Fatty foods
• Chocolate
• Spicy foods
• Citrus fruits and juices
• Tomato-based products
• Onions, especially if uncooked.
• Alcohol
 Pharmacologic agents
• step-up therapy (treat initially with an
H2RA for 8 weeks; if symptoms do not
improve, change to a PPI)
• step-down therapy (treat initially with a
PPI for 8 weeks; then titrate to the
lowest effective medication type and
dosage).
 Proton pump inhibitors
(PPIs)
•  PPIs bind to proton pump in gastric parietal cells,
resulting in suppression of basal and stimulated acid
secretion
• PPIs include Lansoprazole , Omeprazole ,
Pantoprazole ,and Esomeprazole (Nexium). For these
agents, no significant differences have been
demonstrated in the symptomatic treatment of GERD
or the healing of erosive esophagitis.
• In patients with erosive esophagitis identified on
endoscopy, a PPI is the initial treatment of choice. 
• PPIs are taken by mouth. They are available as tablets or
capsules. Commonly, these medicines are taken 30 minutes
before the first meal of the day.
• Side effects from PPIs are rare. may include: headache,
diarrhea, abdominal pain, nausea, or itching.
• PPIs are possibly associated with increased incidence of
Clostridium difficile-associated diarrhea (CDAD); consider
diagnosis of CDAD for patients taking PPIs who have diarrhea
that does not improve
• Studies suggest that PPI therapy may be associated with an
increased risk for osteoporosis-related fractures of the hip,
wrist, or spine, particularly with prolonged (>1 yr), high-dose
therapy
• Daily long-term use (e.g., longer than 3 years) may lead to
malabsorption or a deficiency of cyanocobalamin (vitamin B12)
 ANTIREFLUX SURGERY
Indications for surgery include:
• failed medical management
• patient preference for surgery despite
successful medical management
• complications of GERD
• medical complications attributable to a large
hiatal hernia
• atypical symptoms with reflux documented on
24-hour pH monitoring.
 Nissen fundoplication
• Includes reduction of hiatal hernia, repair of
diaphragmatic hiatus, strengthening of the
gastroesophageal junction–posterior diaphragm
attachment, and strengthening of the antireflux
barrier through placement of a gastric wrap
around the gastroesophageal junction 
• long-term follow-up studies have found that
within three to five years of surgery, 52 % of
patients are taking antireflux medications again.
 Complications of GERD
Severity of symptoms doesn't necessarily correlate with the
presence or severity of these complication
• Esophagitis (tends to become a relapsing, chronic
condition )
• Strictures
• Ulcerations
• Barrett's esophagus (progressive replacement of
distal stratified squamous mucosa with metaplastic
columnar epithelium). The condition carries a risk
for progression to esophageal adenocacenoma