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Chapter 20 • Heartburn and Indigestion
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239
EVIDENCE-BASED PRACTICE
Can a Trial of
PPI Conrm the Diagnosis of GERD?
This meta-analysis included 15 studies that compared
clinical response to a short course of a PPI with an objective measure of GERD such as 24-hour pH monitoring.
Sensitivity of the trial response in detecting GERD was
78% (95% CI, 0.66 to 0.86), and specificity was 54%
(95% CI, 0.44 to 0.65). This analysis concluded that a PPI
trial in patients suspected of having GERD does not confidently establish or exclude the diagnosis of GERD. The
authors suggest that, despite diagnostic uncertainty, a PPI
trial might be reasonable in patients without alarm symptoms or other suspected complications of GERD.
Data from Numans ME, Lau J, de Wit NJ, Bonis PA: Short-term treat-
ment with proton-pump inhibitors as a test for gastroesophageal reflux
disease: A meta-analysis of diagnostic test characteristics, Ann Intern
140:518, 2004.
Med
Response to Antacids
A diagnosis of acid-induced heartburn can be indirectly
established through response to antacids; however, lack
of response does not exclude reux.
Trial of Proton Pump Inhibitors
A trial of proton pump inhibitors (PPI) for 4 to 6 weeks
may be useful in patients with classic symptoms of
reux without alarm symptoms. A negative trial does
not rule out GERD.
Sublingual Nitroglycerin
Both angina and reux may respond to the administra-
tion of nitroglycerin.
Helicobacter pylori Testing
Screening for Helicobacter pylori (H. pylori) infection
is not recommended in patients suspected of having
GERD. H. pylori testing may be useful in high preva-
lence areas or in patients with dyspepsia symptoms
that suggest peptic ulcer disease or gastritis. Labora-
tory methods for testing include antibody or antigen
testing with serology, urine, or stool, or urea breath
test.
Endoscopy
Upper endoscopy is the gold standard to determine
abnormal esophageal mucosal pathology. It is indi-
cated to evaluate for alarm symptoms: esophageal or
gastric malignancy, eosinophilic esophagitis, screening
of high-risk patients (family history of gastric cancer,
emigrated from a country with a high rate of gastric
cancer, or had a prior partial gastrectomy), and in patients unresponsive to PPI. The American College of
Gastroenterology recommends endoscopy to screen for
Barrett esophagus in patients who have chronic GERD
symptoms. Endoscopy is the procedure of choice in
cases where mucosal lesions or growths are suspected.
It is not useful for identifying hiatal hernia. Upper endoscopy is not required in the presence of typical
GERD symptoms without alarm features.
Esophageal pH Monitoring
Esophageal pH monitoring provides direct physiologic measurement of acid in the esophagus through
use of a probe or endoscopically placed capsule.
Twenty-four-hour esophageal pH monitoring is useful
in patients with atypical manifestations of GERD such
as chest pain or chronic cough. Esophageal pH monitoring with symptom recording may identify a relationship between heartburn and acid reux with a pH
lower than 4.
Esophageal Manometry
Esophageal manometry is indicated in patients with
refractory reux in whom surgical therapy is planned
to determine the functional capacity of the lower
esophageal sphincter (LES). It is not recommended for
GERD diagnosis.
Upper GI Series
An upper GI series (barium swallow) is useful in patients unwilling to have endoscopy or with medical
contraindications to the procedure. It is useful in diagnosing hiatal hernia. It can identify ulcerations and
strictures; however, it may miss mucosal abnormalities
and is not used to diagnose GERD.
Electrocardiography and Cardiac Enzymes
If the clinical history is suggestive of a cardiac origin,
coronary artery disease or MI should be excluded
through ECG and/or cardiac enzyme testing. The preferred biomarker is a cardiac troponin (T or I; cTnT, or
cTnI); creatinine kinase MB isoenzyme (CK-MB) is
less sensitive (see Chapter 8).
DIFFERENTIAL DIAGNOSIS
Gastroesophageal Reflux
Gastroesophageal reux (GER) is seen in all age
groups, but is most common in newborns and infants
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Chapter 20 • Heartburn and Indigestion
(younger than 6 months of age). In infants, GER occurs three to four times a day because of transient relaxation of an immature esophageal sphincter. This can
be a functional diagnosis and does not necessarily indicate pathology. This is sometimes referred to as the
“happy spitter”; the condition improves with age and
simple feeding techniques. In adults, GER generally
occurs after a meal, lasts for a few minutes, and has no
other symptoms.
Gastroesophageal Reflux Disease
or Reflux Esophagitis
Gastroesophageal reux disease (GERD) is dened as
symptoms and complications resulting from the reux
of gastric contents into the esophagus into the oral
cavity (including larynx) or into the lung. GERD can
be either erosive or nonerosive. The severity of esophageal damage does not correlate with the severity of
symptoms.
Classic symptoms include heartburn that is caustic
and stinging, typically without radiation to the back.
Regurgitation of gastric contents into the mouth
(acid regurgitation, water brash, or pyrosis) suggests
progressing GERD. Lying supine or leaning forward
provoke both heartburn and regurgitation.
Additional symptoms may include chronic cough
and bronchospasm, chest pain, hoarseness, early satiety, abdominal fullness, bloating with belching, and
dental erosion in children.
Causes of GERD include transient relaxation of
the lower esophageal sphincter (LES); medications
that lower LES pressure (calcium channel blockers,
alpha-adrenergic antagonists, anticholinergic drugs,
theophylline, nitrates, sildenal, albuterol sedatives,
and prostaglandins); foods that lower LES pressure
(chocolate, yellow onions, peppermint), tobacco abuse,
alcohol, coffee, pregnancy, and gastric acid hypersecretion. Hiatal hernia may or may not be a causative
factor. Obesity is associated with a signicant increase
in the risk for reux.
Complications of reux esophagitis include esophageal ulceration, hematemesis, melena, stricture development, and Barrett esophagus.
The presence of frequent and typical reux symptoms should lead to a provisional diagnosis of GERD
rather than dyspepsia. In the absence of alarm features,
diagnosis is typically made by careful history and
physical examination and a trial of medication with
antacids or PPI. Generally, when symptoms of gastroesophageal reux are typical, and the patient responds
to therapy, there is no need for further diagnostic tests
to verify a diagnosis of gastroesophageal reux disease
(GERD). However, overlap of GERD with dyspepsia
is probably frequent and needs to be considered when
symptoms do not respond to appropriate management
of GERD.
Upper endoscopy or 24-hour pH monitoring are
indicated for complicated or refractory cases.
Other Causes of Esophagitis
Esophagitis can cause pain with swallowing and weight
loss. Other causes of esophagitis include infective
esophagitis, allergic eosinophilic esophagitis, and
so-called “pill” esophagitis.
Infective Esophagitis
Infective esophagitis is caused by fungal agents, such
as Candida species and Torulopsis glabrata; viral
agents, such as herpes simplex, cytomegalovirus, HIV,
and varicella zoster; and rarely, bacterial infections
including diphtheria and tuberculosis. The typical
presenting signs and symptoms are odynophagia, dysphagia, and retrosternal pain. Patients may also experience fever, nausea, and vomiting. Diagnosis of infectious esophagitis is made by endoscopy (ulcerations,
exudates) and histopathology examination; adding
polymerase chain reaction, tissue viral culture, and
immunocytochemistry enhances the diagnostic sensitivity and precision.
Allergic Eosinophilic Esophagitis
Allergic eosinophilic esophagitis (AEE) occurs primarily in young children and adolescents with dyspepsia symptoms of reux such as vomiting, irritability, food refusal, and early satiation. Adults report
reux, epigastric or chest pain, and dysphagia. The
failure of high-dose PPI treatment and the absence of
acid reux are necessary for diagnosis. Patients often
have a personal or family history of other allergic
disorders. Most patients with AEE have atopic dermatitis, allergic rhinitis, asthma, or modest peripheral
eosinophilia. Diagnosis is made by classic ndings on
endoscopy, such as linear furrowing, and multiple
rings accompanied by biopsies that show eosinophilic
inltration.
Pill Esophagitis
Oral medications of any type can cause esophageal
injury by producing a caustic acid solution (e.g., ferrous sulfate), producing a caustic alkaline solution
Chapter 20 • Heartburn and Indigestion
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241
(e.g., alendronate), placing a hyperosmolar solution in
contact with the esophageal mucosa (e.g., potassium
chloride), or causing direct injury to the esophageal
mucosa (e.g., tetracycline). Medications that can cause
esophagitis include tetracycline, potassium chloride,
ferrous sulfate, NSAIDs, and bisphosphonates. The
patient may report taking the medication at bedtime
with insufcient water, and/or lying down directly af-
ter taking the medication. The patient may also report
acute discomfort followed by progressive retrosternal
pain. Ulcer formation can cause odynophagia, dyspha-
gia, and weight loss. Physical examination is normal.
Endoscopy shows a focal lesion.
Functional Heartburn
Functional heartburn (FH) is a gastrointestinal disorder
characterized by symptoms of heartburn not related
to gastroesophageal reux or other organic causes.
Findings include normal endoscopy ndings and
normal esophageal acid exposure during esophageal
pH monitoring.
The patient reports vague nonspecic symptoms
and obtains no consistent relief with medication. The
patient may report anxiety. Physical examination is
normal with no evidence of systemic disease or weight
loss. Box 20-1 describes a source for diagnostic criteria
for functional GI disorders.
Hiatal Hernia
Hiatal hernia is stomach herniation via esophageal hiatus of the diaphragm. It causes pain in the epigastrium
or lower chest that worsens on reclining and is relieved
on standing. The pain may be retrosternal with radiation down the left arm. Physical examination is generally normal. A large hernia may create dullness on
percussion over the left lung base, absent breath
sounds, or bowel sounds present in the chest. The
causal association of hiatal hernia with GERD is
Box 20-1
Diagnostic Criteria for Functional
GI Disorders
The Rome criteria is a system developed to classify functional gastrointestinal disorders. Functional disorders are
those in which symptoms cannot be explained by the presence of structural or tissue abnormality. The most recent
revision of the Rome III Criteria is available at www.rome-
criteria.org/criteria/.
unclear. Hiatal hernia is diagnosed by barium swallow.
Upper endoscopy is poor at identifying hiatal hernia.
Peptic Ulcer Disease
Peptic ulcer disease (PUD) includes gastric and duodenal ulcer disease. Uncomplicated PUD may have no
symptoms. PUD is characterized by episodic gnawing
or epigastric pain usually 2 to 5 hours after meals, or
on empty stomach; nighttime awakening as a result
of pain; and symptom relief with food intake, antacids,
or antisecretory agents. Other symptoms include fullness, bloating, early satiation, vomiting, indigestion,
loss of appetite, heartburn, hematemesis, back pain,
and unexplained weight loss. Children may present
with generalized abdominal pain. Older adults are
more likely to be asymptomatic but may also have
nonspecic complaints including confusion, restlessness, abdominal distention, and falls.
Most peptic ulcers are caused by H. pylori infection,
or NSAIDs, including aspirin. Other high risk medications include corticosteroids (in high doses or when
combined with NSAIDs), bisphosphonates, mycophenolate, potassium chloride, and uorouracil.
Diagnosis is made by endoscopy. In patients with
isolated dyspepsia who do not exhibit alarm symptoms
testing for and treating for H. pylori infection is effective and less expensive than initial endoscopy.
Also see Chapter 3 on Abdominal Pain for assessment of acute upper abdominal pain.
Esophageal Cancer
Carcinomas of the esophagus include both squamous
cell and adenocarcinoma. Patients are usually asymptomatic until advanced stage III or stage IV. They
typically present with alarm symptoms of dysphagia
(initially occurs with solid foods and gradually progresses to include semisolids and liquids), odynophagia, anorexia, and unintentional weight loss. Esophageal cancer is likely caused by repeated exposure to
irritants such as smoking, alcohol, or chronic GERD
in combination with genetic predisposition. There is
a strong association between Barrett esophagus and
development of esophageal adenocarcinoma.
Physical examination ndings that suggest advanced disease include cachexia, ipsilateral Horner
syndrome (miosis, ptosis, absence of sweating on ipsilateral face and neck), supraclavicular adenopathy,
hoarseness, and halitosis. Epigastric swelling or a mass
may be present on palpation. Patients may have anemia. Diagnosis is made with endoscopy.
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Chapter 20 • Heartburn and Indigestion
Gastric Cancer
The most common gastric cancer is adenocarcinoma.
The presenting symptoms are dyspepsia unrelieved by
antacids, epigastric discomfort (usually lessened by
fasting and exacerbated by food intake), and early satiation. Alarm symptoms include dysphagia, anorexia,
and weight loss. Symptoms occur late in the disease.
Physical examination ndings indicative of advanced disease include a palpable left supraclavicular
(Virchow) node and a palpable hard lymph node in the
umbilicus. An epigastric or abdominal mass may be
palpable. A hard, nodular liver generally indicates
metastatic disease. The patient may be pale from anemia. Ascites, lymphadenopathy, or pleural effusion
may indicate metastasis. Stools may be positive on
fecal occult blood testing.
Diagnosis is made with endoscopy.
Gastritis
Gastritis is caused by inammation of the lining of the
stomach that can be acute or chronic. Acute gastritis is
caused by irritation caused by excessive alcohol use,
chronic vomiting, stress, or the ingestion of aspirin,
NSAIDs, or steroids. The most common cause of
chronic gastritis is H. pylori infection. Other causes
include other bacterial, viral, fungal, or parasitic infection; bile reux; or pernicious anemia. Bile gastritis
can occur after a partial gastrectomy, truncal vagotomy
and pyloroplasty for peptic ulcer reux, or cholecystectomy. Bile reux can cause severe epigastric abdominal pain accompanied by bilious vomiting and
weight loss.
The most common gastritis symptoms are those of
dyspepsia. They include abdominal pain, indigestion,
heartburn, epigastric discomfort that is worse after
eating, loss of appetite, sense of fullness, nausea, occasional vomiting, and a burning or gnawing feeling in
the stomach between meals or at night.
On physical examination epigastric tenderness may
be present on palpation.
Endoscopy is indicated in patients with alarm features or persistent symptoms. Upper endoscopy demonstrates friable, beefy red mucosa. Additional workup
may include testing for H. pylori infection, a CBC to
assess for anemia, and fecal occult blood testing.
Dyspepsia
Dyspepsia refers to recurrent or chronic pain or discomfort in the upper abdomen without radiation
that occurs with eating or soon after a meal. Burning
pain conned to the epigastrium is a cardinal symptom
of dyspepsia. Other symptoms may include postprandial fullness, upper abdominal bloating, early satiation, belching, nausea, and vomiting. Heartburn may
occur as part of the symptom constellation, but when
heartburn is the predominant symptom, the patient
should be considered to have gastroesophageal reux
disease and not dyspepsia.
Dyspepsia can be caused by structural disease
such as gastroesophageal reux, peptic ulcer disease,
gastritis, and gastric cancer. American Gastroenterological Association (AGA) Guidelines recommend
endoscopy for patients older than age 55 with newonset dyspepsia symptoms, and for younger high risk
patients (those with weight loss, progressive dysphagia, recurrent vomiting, evidence of gastrointestinal
bleeding, or family history of cancer). Biopsy specimens should be obtained during endoscopy for
H. pylori.
Functional Dyspepsia (Nonulcer Dyspepsia)
In some patients with dyspepsia, diagnostic testing
shows no evidence of structural disease. Box 20-1 lists
diagnostic criteria for functional dyspepsia.
The etiology and pathophysiology of nonulcer dyspepsia include abnormalities of gastric motor function
(such as delayed gastric emptying and antral hypomotility), visceral hypersensitivity, H. pylori infection,
and psychosocial factors associated with anxiety and
depression. Risk factors include excessive amounts
of caffeine, alcohol, and smoking; taking steroids,
NSAIDs, or other medications; and living in a high
H. pylori prevalence area.
Gas and Gas Entrapment
Excessive abdominal gas can produce abdominal discomfort, vague feelings of indigestion, abdominal
bloating, belching, and chest pain. Excessive gas
comes from bacterial degradation of large intestine
contents as a result of ingestion of atulogenic foods,
GI stasis, constipation, malabsorption, gas in the
stomach from air swallowing (aerophagia), hurried
eating or drinking, smoking, chewing gum, poorly tting dentures, and dry mouth from anxiety or anticholinergics. Gas can become trapped in the hepatic or
splenic exures (hepatic or splenic exure syndrome).
Bending over or wearing tight garments intensies
pain, and pain is relieved by the passage of atus.
Physical examination ndings may include visible
abdominal distention on inspection. The abdomen may
be distended with hyperresonance on percussion and
diffuse tenderness on palpation.
Chapter 20 • Heartburn and Indigestion
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243
Cardiac Causes of Heartburn and Indigestion
(see Chapter 8)
Acute Coronary Insufficiency
Acute coronary insufciency refers to those situations
in which chest pain is caused by a lack of oxygen to
the myocardium, but there is no evidence of infarct.
The patient reports severe, oppressive, constricting,
retrosternal discomfort lasting longer than 30 minutes.
The patient may report prior history of MI or angina.
On physical examination, abnormal sounds, such as
paradoxical second heart sound (S2) during pain, are a
sign of coronary ischemia. A transient S3 (ventricular
gallop) or mitral regurgitation murmur at the apex can
occur occasionally with myocardial ischemia. An S4
(atrial gallop) typically indicates a stressed heart,
which can be the result of hypertension, MI, or CAD.
The ECG may show intermittent ischemic changes
or may be normal. Cardiac isozymes tests are normal.
Stable Angina
Stable angina refers to chest pain typically described as
substernal chest pressure or heaviness, radiating to the
left shoulder and arm, neck, or jaw. The pain onset is
usually gradual, brought on and exacerbated by exercise and stress; it is associated with nausea, diaphoresis, and shortness of breath and is alleviated with rest
and/or nitroglycerin. Pain typically lasts 2 to 10 minutes. Physical examination is usually normal with no
tenderness on palpation of the abdomen. An S4 gallop
can be transiently present during an episode of pain.
Tests for angina include performing an ECG during an
episode of pain, which can show ST segment depression and T wave inversions, or the ndings may be
normal. Administration of sublingual nitroglycerin
during an episode of pain relieves the pain.
Myocardial Infarction
The patient with an acute MI generally describes a
sudden onset of pain at rest. It is a persistent, often
severe, deep, central chest pain and can radiate, as
does angina, to the throat or neck, across both sides of
the chest to the shoulder, and/or down the medial aspect of either or both arms. Rest or nitroglycerin does
not relieve the pain. The chest pain is often associated
with shortness of breath, nausea, vomiting, and diaphoresis.
Patients can also express a sense of impending doom.
A review of risk factors include men 45 years and older
and women 55 years and older, cigarette smoker, hyperlipidemia, hypertension, diabetes, obesity, history of
CAD, and family history of CAD. Objective evidence of
an MI can include skin pallor, cool diaphoretic skin,
and transient paradoxical S2. The patient can be hypertensive or hypotensive. Abnormal rhythms include
tachycardia and bradycardia.
The patient with a suspected MI should be placed
on a cardiac monitor as soon as possible. Observe for
premature ventricular contractions and classic electrocardiographic changes that indicate MI, including ST
segment elevations, T wave inversions, and Q waves.
Performing a 12-lead ECG and determining levels of
cardiac isozymes will help conrm a diagnosis.
DIFFERENTIAL DIAGNOSIS OF
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
GER Infants: Spitting up 3-5 times a day
GERD Heartburn, pyrosis
Infective
esophagitis
Common Causes of Heartburn and Dyspepsia
Adults: Pain occurs after a meal
and lasts a few minutes
No other symptoms
Possible extraesophageal symptoms,
laryngitis, wheezing, cough
Infants: Weight loss, arching of
back, vomiting, irritability
Odynophagia, dysphagia, retrosternal
pain; possible fever, nausea,
and vomiting
None None
None
Possible wheezing with asthma
Obesity
Growth chart change
None
Possible fever
Trial of antacids
Trial of PPI
pH monitoring
Endoscopy for refractory
symptoms to rule out
erosions
Endoscopy: ulcerations,
exudates
Continued
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Chapter 20 • Heartburn and Indigestion
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Heartburn and Dyspepsia — cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
AEE Young children and adolescents:
Dyspepsia, heartburn, vomiting,
irritability, food refusal, early
satiation
Adults: Heartburn, epigastric or
chest pain, dysphagia, and
food impaction
Personal or family history of allergic
Pill esophagitis Medication history: tetracycline, po-
Functional
heartburn
Hiatal hernia Pain in epigastrium or lower chest
PUD Episodic gnawing or epigastric pain
disorders
tassium chloride, ferrous sulfate,
NSAIDs, and bisphosphonates
Takes medication at bedtime with
insufficient water, and/or lying
down directly after taking
Acute discomfort followed by
progressive retrosternal pain
Burning retrosternal discomfort
or pain
Symptoms present for the last 3 mo
that worsens on reclining; relieved
on standing
Pain may be retrosternal with radia-
tion down left arm
usually 2-5 hr after meals or on
empty stomach
Nighttime awakening because of
pain; symptom relief with food
intake, antacids, or antisecretory
agents
Fullness, bloating, early satiation,
vomiting, indigestion, loss of
appetite, heartburn, hematemesis,
back pain, and unexplained
weight loss
Medication history: NSAIDs, aspirin,
high dose corticosteroids, bisphosphonates, mycophenolate, potassium chloride, and fluorouracil
Children may present with general-
ized abdominal pain
Older patients may be asymptom-
atic, but may also present with
nonspecific complaints including
confusion, restlessness, abdominal distention, and falls
None
Possible allergic rhinitis, atopic
dermatitis
None Endoscopy: focal lesion
None Endoscopy
None
Large hernia may create dullness
on percussion over the left
lung base, absent breath
sounds, or bowel sounds
resent in the chest
None Endoscopy: ulcers;
Endoscopy: linear furrowing
and multiple rings
UGI
H. pylori testing
CBC if suspect anemia
FOBT for bleeding
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245
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Heartburn and Dyspepsia — cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Esophageal
cancer
Gastric cancer Dyspepsia unrelieved by antacids,
Gastritis
Dyspepsia Epigastric pain or burning with
Functional
dyspepsia
(nonulcer
dyspepsia)
Alarm symptoms: dysphagia (solids
or liquids), odynophagia, anorexia,
and unintentional weight loss
Repeated exposure to irritants such
as smoking, alcohol
History of Barrett esophagus
epigastric discomfort, usually
lessened by fasting, and exacerbated by food intake and early
satiation
Alarm symptoms of dysphagia,
anorexia, and weight loss
Dyspepsia with abdominal pain,
indigestion, heartburn, and
epigastric discomfort that is
worse after eating, loss of appetite, sense of fullness, nausea,
occasional vomiting, burning or
gnawing feeling in the stomach
between meals or at night
Excessive alcohol use, chronic
vomiting, stress, or the ingestion
of aspirin, NSAIDs, or steroid.
Bile gastritis can occur after partial
gastrectomy, truncal vagotomy
and pyloroplasty for peptic ulcer
reflux, or cholecystectomy
Bile reflux can cause severe epigas-
tric abdominal pain, accompanied
by bilious vomiting, and weight
loss
postprandial fullness, early
satiation
Symptoms for 3-6 mo
Risk factors: excessive amounts
of caffeine or alcohol, smoking,
steroids, NSAIDs, living in an area
with high prevalence of H. pylori
Advanced disease: cachexia,
ipsilateral Horner syndrome
(miosis, ptosis, absence of
sweating on ipsilateral face
and neck), supraclavicular
adenopathy, hoarseness,
halitosis
Epigastric swelling or mass may
be present on palpation
Advanced disease: cachexia,
palpable left supraclavicular
(Virchow) node, palpable hard
lymph node in umbilicus
A hard, nodular liver indicates
metastatic disease
May be pale from anemia
Ascites, pleural effusions may
indicate metastasis
Possible epigastric tenderness Endoscopy for patients
May have epigastric tenderness Endoscopy: for patients
None H. pylori testing
Endoscopy
Endoscopy
1FOBT
with alarm features or
persistent symptoms
Additional workup may
include testing for
H. pylori
CBC if anemia suspected
FOBT for bleeding
55 yr and older, those
with weight loss, progressive dysphagia, recurrent
vomiting, evidence of GI
bleeding, or family history
of cancer, new-onset
dyspepsia
H. pylori testing: patients
55 yr and younger without alarm features
Testing for structural
disease, negative
findings
Continued
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Chapter 20 • Heartburn and Indigestion
DIFFERENTIAL DIAGNOSIS OF
Common Causes of Heartburn and Dyspepsia — cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Gas/gas
entrapment
Acute coronary
insufficiency
Stable angina Chest pain typically described as
MI Sudden onset of pain at rest
AEE, Allergic eosinophilic esophagitis; CAD, coronary artery disease; CBC, complete blood count; ECG, electrocardiogram; FOBT, fecal occult blood
testing; GER, gastroesophageal reflux; GERD, gastroesophageal reflux disease; GI, gastrointestinal; MI, myocardial infarction; NSAID, nonsteroidal
antiinflammatory drugs; PPI, proton pump inhibitors; PUD, peptic ulcer disease.
Abdominal discomfort, vague feel-
ings of indigestion; abdominal
bloating, belching, chest pain
Ingestion of flatulogenic foods,
GI stasis, constipation, malabsorption, air swallowing (aerophagia), hurried eating or drinking,
smoking or chewing gum, poorly
fitting dentures, or dry mouth
from anxiety or anticholinergics
Pain worsens by bending over or
wearing tight garments and is
relieved by passage of flatus
Severe, oppressive, constricting,
retrosternal discomfort lasting
longer than 30 min
Possible prior history of MI or
angina
substernal chest pressure or
heaviness, radiating to the
left shoulder and arm, neck,
or jaw
Onset brought on and exacerbated
by exercise and stress; typically
lasts 2 to 10 min
Alleviated with rest and/or
nitroglycerin
Persistent, often severe, deep,
central chest pain; and may
radiate to the throat or neck,
across both sides of the chest
to the shoulder, and/or down the
medial aspect of either or both
arms
Nitroglycerin does not relieve the
pain
Possible sense of impending
doom
Risk factors: Men 45 yr and
older; women 55 yr and older;
cigarette smoker; hyperlipidemia;
hypertension; diabetes; obesity;
history of CAD; family history
of CAD
Possible distended abdomen
with hyperresonance on
percussion
Possible abnormal heart sounds
such as paradoxical S2 during
pain; transient S3 (ventricular
gallop) or mitral regurgitation
murmur at the apex; S4 (atrial
gallop)
Possible diaphoresis and
shortness of breath
Transient S4 gallop during an
episode of pain
Skin pallor, cool diaphoretic skin
Hypertensive or hypotensive
Possible transient paradoxical
S2 or abnormal rhythms
including tachycardia and
bradycardia
None
ECG: intermittent ischemic
changes or normal
Cardiac isoenzymes
normal
ECG during an episode
of pain: ST segment
depression and T wave
inversions, or the findings
can be normal
ECG: ST segment eleva-
tions, T wave inversions,
and Q waves
Cardiac enzymes elevated
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247
References and Readings
AGA Institute: American Gastroenterological Association Medical
Position Statement on the Management of Gastroesophageal
Reux Disease, Gastroenterology 135:1383, 2008.
American Gastroenterological Association Medical Position
Statement: Evaluation of dyspepsia, Gastroenterology 129:1753,
2005.
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CHAPTER
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21
oarseness is a disturbance of the normal voice
H
pitch by an abnormal vibration of the vocal cords.
It is a term used to describe an unnaturally rough,
harsh, or deep voice. Voice is the sound produced when
the vocal folds are approximated and expired airow
between the cords causes them to vibrate. The sound
produced by the larynx is amplied by the pharynx,
oral cavity, sinuses, and nasal cavity and is modied
by movements of the tongue, uvula, and soft palate.
Hoarseness may be an early sign of local disease or a
manifestation of a systemic illness. Hoarseness is a
cardinal symptom of laryngeal disease.
The larynx is a musculocartilaginous structure
lined with a mucous membrane connected superiorly
to the pharynx (below the tongue and hyoid) and
inferiorly to the trachea. It is the sphincter that
guards the entrance into the trachea and functions
secondarily as the organ of voice. Nine cartilages
connected by ligaments and eight muscles form the
larynx. The lower portion of the thyroarytenoid
muscle forms the true vocal fold, or folds, which are
highly elastic and account for the extraordinary versatility of the voice and the wide range of pitch,
volume, and quality. The glottis is the triangular
opening between the true vocal cords. The supraglottic area includes the ventricular folds (false
vocal cords), aryepiglottic folds, and the epiglottis
(Figure 21-1). The epiglottis is the lidlike cartilaginous structure that overhangs the entrance to the
larynx and serves to prevent food from entering the
larynx and trachea while swallowing.
Many benign conditions cause hoarseness such
as functional disorders from voice overuse and upper
respiratory infections. Acute laryngitis is the most
common cause of hoarseness. Functional causes are
unrelated to organic disease and may have a psychosocial component, such as restraint in expressing anger,
crying, or a history of psychological trauma.
However, persistent hoarseness for more than
2 weeks in an adult and 1 week in a child may indicate
secondary changes to the vocal cords. These changes
Hoarseness
may be caused by structural changes resulting from
palsies, polyps, or cysts; laryngeal neoplasm; or congenital disorders of the larynx. Hoarseness may also be
a symptom of systemic disease, such as hypothyroidism, or a symptom of inammation caused by a variety
of processes. Many forms of laryngitis that appear
alike on physical examination have very different
causes. Critical clues to the specic etiology of laryngitis depend on taking a careful history.
DIAGNOSTIC REASONING: FOCUSED
HISTORY
Is the hoarseness acute or chronic?
Key Questions
l
How long has the symptom been present?
l
Has this happened before? Is it recurrent?
l
Is it getting better or worse?
l
Have you noticed other symptoms?
Duration
Symptoms of less than 2 weeks’ duration are considered to be acute; the most likely cause is a viral upper
respiratory tract infection. Inammations secondary
to acute viral infection or voice overuse are the most
common causes of acute laryngitis. Chronic symptoms suggest structural change in the larynx or
hoarseness secondary to disorders, such as gastroesophageal reux disease (GERD), or systemic disease such as hypothyroidism. If the duration of
hoarseness is longer than 2 weeks, referral to an ear,
nose, and throat specialist is indicated to evaluate
for possible neoplasm, most often squamous cell
carcinoma, because chronic laryngitis rarely has an
infectious cause.
Recurrence
Recurrent episodes of hoarseness may indicate allergies or sinusitis with postnasal drip, laryngeal reux,
or systemic disease.
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