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TABLE 9.4.1 Differential Diagnosis of Acute and Chronic Diarrhea
Acute diarrhea
Infectious
Bacteria (Salmonella, Campylobacter, Shigella, Escherichia coli)
Virus (rotavirus, norovirus)
Protozoa (Cryptosporidium, Giardia, Entamoeba histolytica)
Noninfectious
Food intolerance
Medications
Inflammatory bowel disease
Carcinoid
Thyroid disease
Chronic diarrhea
Fatty
Intestinal malabsorption
Maldigestion
Inflammatory
Inflammatory bowel disease
Infection
Ischemia
Neoplasia
Secretory
Medications
Motility disorder
Neoplasia
Inflammatory bowel disease
Toxin
Osmotic
Carbohydrate malabsorption
Ingestion of magnesium, sulfates, or phosphates
REFERENCES
1. Feldman M, Friedman L, Brandt L (eds.) (2010). Sleisenger and Fordtran’s gastrointestinal and liver
disease: pathophysiology/diagnosis/management, 9th ed. Chapter 15: Diarrhea. Accessed online at
MDConsult.com.
2. Kellermayer R, Shulman RJ. Approach to the causes of chronic diarrhea in children. Accessed at
UpToDate.com (http://www.uptodate.com/contents/overview-of-the-causes-of-chronic-diarrhea-in-
children?source=see_link) on May 5, 2012.
3. Wanke CA (2011). Approach to the adult with acute diarrhea in developed countries. Retrieved from
UpToDate.com
4. Thielman NM, Guerrant RL. Clinical practice. Acute infectious diarrhea. N Engl J Med 2004;350:38.
5. DuPont HL. Guidelines on acute infectious diarrhea in adults. The practice parameters committee of
the American college of gastroenterology. Am J Gastroenterol 1997;92:1962.
6. Schiller LR. Chronic diarrhea. Gastroenterology 2004;127:287.
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Taylor’s DifferenTial Diagnosis Manual
9.5
Dysphagia
Susan M. Newman and Richard Fruehling
I. BACKGROUND. Dysphagia is defined as difficulty in swallowing. This is a common complaint
in primary care practices, especially in aging persons. Up to 10% of adults older than 60 years,
25% of hospitalized patients, and 30–40% of nursing home patients experience swallowing
problems; 7% of Americans will experience dysphagia in their lifetime.
II. PATHOPHYSIOLOGY. Organic swallowing problems occur at two primary sites: in the oro-
pharynx at the initiation of the swallow reflex or in the esophagus with propulsion of food.
Dysfunctional transfer of the food past the upper esophageal sphincter into the esophagus causes
oropharyngeal dysphagia symptoms, and disordered peristalsis or conditions that obstruct the
flow of a food bolus through the esophagus cause esophageal dysphagia symptoms. Mechanical
obstruction or neuromuscular motility disorders occur in both the oropharynx and the esopha-
gus. Common causes of oropharyngeal and esophageal dysphagia are listed in Table 9.5.1 (1).
TABLE 9.5.1 Differential Diagnosis of Dysphagia
Oropharyngeal dysphagia
Neuromuscular disease (diseases of the central nervous system)
Cerebrovascular accident
Parkinson’s disease
Brain stem tumors
Degenerative diseases
Amyotrophic lateral sclerosis
Multiple sclerosis
Huntington’s disease
Postinfectious
Poliomyelitis
Syphilis
Peripheral nervous system
Peripheral neuropathy
Motor end-plate dysfunction
Myasthenia gravis
Skeletal muscle disease (myopathies)
Polymyositis
Dermatomyositis
Muscular dystrophy (myotonic dystrophy, oculopharyngeal dystrophy)
Cricopharyngeal (upper esophageal sphincter), achalasia
Obstructive lesions
Tumors
Inflammatory masses
(Continued)
Chapter 9 • Gastrointestinal Problems
189
TABLE 9.5.1 Differential Diagnosis of Dysphagia
Trauma/surgical resection
Zenker’s diverticulum
Esophageal webs
Extrinsic structural lesions
Anterior mediastinal masses
Cervical spondylosis
Esophageal dysphagia
Neuromuscular disorders
Achalasia
Spastic motor disorders
Diffuse esophageal spasm
Hypertensive lower esophageal sphincter
Nutcracker esophagus
Scleroderma
Obstructive lesions
Intrinsic structural lesions
Tumors
Strictures
Peptic
Radiation-induced
Chemical-induced
Medication-induced
Lower esophageal rings (Schatzki’s ring)
Esophageal webs
Foreign bodies
Extrinsic structural lesions
Vascular compression
Enlarged aorta or left atrium
Aberrant vessels
Mediastinal masses
Lymphadenopathy
Substernal thyroid
From Castell DO. Approach to the patient with dysphagia. In: Yamada T, ed. Textbook of
gastroenterology, 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 1995.
III. EVALUATION. Choosing the best study depends on many factors including age, acuity of
onset, comorbidities, and availability of testing modalities in the community.
A. History. A careful history identifies 80–85% of causes by differentiating whether the
dysphagia is oropharyngeal or esophageal in location and whether it is obstructive or neuro-
muscular in nature. The onset, severity, and duration of dysphagia combined with questions
about associated symptoms can help narrow the differential diagnosis (see Table 9.5.2)
(3). Alcohol and tobacco consumption histories provide important information. It is also
(Continued)
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Taylor’s DifferenTial Diagnosis Manual
important to obtain a thorough past medical history to evaluate for gastroesophageal reflux
disease, cancer or radiation, immunocompromised states, and other medical problems asso-
ciated with dysphagia such as scleroderma. Medications can cause direct esophageal injury,
dysmotility, decreased lower esophageal sphincter tone with reflux, or xerostomia with
subsequent dysphagia (see Table 9.5.3) (4).
B. Physical Examination. Examination should focus on the head, eyes, ears, nose, and
throat (HEENT), neck, and neurologic systems. A pulmonary exam is also important
to evaluate for aspiration, a possible complication of dysphagia. However, physical exam
typically provides limited information unless the patient has experienced an obvious
cerebrovascular accident. Gag reflexes are also of little use because this is absent in up
to 13% of nondysphagic patients.
C. Testing. Few screening laboratory tests are indicated in the evaluation of dysphagia unless
history or clinical examination findings dictate otherwise. Imaging studies are often required for
TABLE 9.5.2 Associated Symptoms and Possible Causes of Dysphagia
Condition Diagnoses to consider
Progressive dysphagia Neuromuscular dysphagia
Sudden dysphagia Obstructive dysphagia, esophagitis
Difficulty in initiating swallow Oropharyngeal dysphagia
Food “sticks” after swallow Esophageal dysphagia
Cough
Early in swallow Neuromuscular dysphagia
Late in swallow Obstructive dysphagia
Weight loss
In the elderly Carcinoma
With regurgitation Achalasia
Progressive symptoms
Heartburn Peptic stricture, scleroderma
Intermittent symptoms Rings and webs, diffuse esophageal spasm,
nutcracker esophagus
Pain with dysphagia Esophagitis
Postradiation
Infectious: herpes simplex virus, monilia
Pill induced
Pain made worse by
Solid food only Obstructive dysphagia
Solids and liquids Neuromuscular dysphagia
Regurgitation of old food Zenker’s diverticulum
Weakness and dysphagia Cerebrovascular accidents, muscular dystrophies,
myasthenia gravis, multiple sclerosis
Halitosis Zenker’s diverticulum
Dysphagia relieved with repeated swallows Achalasia
Dysphagia made worse with cold foods Neuromuscular motility disorders
From Johnson A. Deglutition. In: Scott-Brown WG, Kerr AG, eds. Scott-Brown’s otolaryngology,
6thed. Boston, MA: Butterworth-Heinemann, 1997.
Chapter 9 • Gastrointestinal Problems
191
TABLE 9.5.3 Medications Associated with Dysphagia
Medications that can cause direct esophageal mucosal injury
Doxycycline (Vibramycin)
Tetracycline
Clindamycin (Cleocin)
Trimethoprim–sulfamethoxazole (Bactrim, Septra)
Nonsteroidal anti-inflammatory drugs
Alendronate (Fosamax)
Zidovudine (Retrovir)
Ascorbic acid
Potassium chloride tablets (Slow-K)
a
Theophylline
Quinidine gluconate
Ferrous sulfate
Medications, hormones, and foods associated with reduced lower esophageal sphincter
tone and reflux
Butylscopolamine
Theophylline
Nitrates
Calcium antagonists
Alcohol, fat, chocolate
Medications associated with xerostomia
Anticholinergics: atropine, scopolamine (Transderm Scop)
α-Adrenergic blockers
Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Antiarrhythmics
Disopyramide (Norpace)
Mexiletine (Mexitil)
Ipratropium bromide (Atrovent)
Antihistamines
Diuretics
Opiates
Antipsychotics
a
Especially the slow-release formulation.
From Boyce HW. Drug-induced esophageal damage: diseases of medical progress. [Editorial]
Gastrointest Endosc 1998;47:547–550; Stoschus B, Allescher HD. Drug-induced dysphagia.
Dysphagia 1993;8:154–159.
definitive diagnosis. According to the American College of Radiologist Appropriateness Criteria
for dysphagia, an X-ray biphasic esophagram is usually appropriate for evaluation of unexplained
oropharyngeal or substernal dysphagia. Videoradiography is also commonly done. In addition,
manometry and endoscopy (nasopharyngeal laryngoscopy or upper gastrointestinal endoscopy)
192
Taylor’s DifferenTial Diagnosis Manual
should be considered depending on various clinical factors, but is generally not advisable prior to
barium studies. Endoscopy is more sensitive (92% vs. 54%) and more specific (100% vs. 91%)
than double-contrast upper gastrointestinal radiography and also generally allows for biopsy of
lesions or therapeutic maneuvers such as dilation, but is also more expensive and invasive.
IV. DIAGNOSIS
A. Differential Diagnosis.
The diagnosis of dysphagia centers on the answers to two ques-
tions: is the dysphagia oropharyngeal or esophageal in location? Is it neuromuscular or
obstructive in nature (Table 9.5.1)? Patients with oropharyngeal dysphagia present with
difficulty in initiating swallowing and have associated coughing, choking, or nasal regurgi-
tation. Speech quality may have a nasal tone. Oropharyngeal dysphagia is associated with
stroke, Parkinson’s disease, or other long-term neuromuscular disorders. Local structural
lesions are less common. Esophageal dysphagia often causes the sensation of food sticking
in the throat or chest. Motility disorders and mechanical obstructions are common. Several
medications have been associated with direct esophageal mucosal injury, whereas others can
decrease lower esophageal sphincter pressures and cause reflux (Table 9.5.3) (4, 5).
B. Clinical Manifestations. Patients with neuromuscular dysphagia experience gradually
progressive difficulty in swallowing solid food and liquids. Cold foods often aggravate the
problem. Patients may succeed in passing the food bolus by repeated swallowing, by perform-
ing the Valsalva maneuver, or by making a positional change. They are more likely to experi-
ence pain when swallowing than patients with simple obstruction. Achalasia, scleroderma, and
diffuse esophageal spasm are the most common causes of neuromuscular motility disorders.
Obstructive pathology is typically associated with dysphagia of solid food but not liquids.
Patients may be able to force food through the esophagus by performing a Valsalva maneuver,
or they may regurgitate undigested food. Rapidly progressing dysphagia of a few months’ dura-
tion suggests esophageal carcinoma. Weight loss is more predictive of a mechanical obstructive
lesion. Peptic stricture, carcinoma, and Schatzki’s ring are the predominant obstructive lesions.
REFERENCES
1. ACR Appropriateness Criteria
®
dysphagia. 1998 (revised 2010). NGC:007921.
2. Castell DO. Approach to the patient with dysphagia. In: Yamada T, ed. Textbook of gastroenterology,
2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 1995.
3. Johnson A. Deglutition. In: Scott-Brown WG, Kerr AG, eds. Scott-Brown’s otolaryngology, 6th ed.
Boston, MA: Butterworth-Heinemann, 1997.
4. Koch WM. Swallowing disorder. Diagnosis and therapy. Med Clin North Am 1993;77:571.
5. Boyce HW. Drug-induced esophageal damage: diseases of medical progress [Editorial]. Gastrointest
Endosc 1998;47:547–550.
6. Stoschus B, Allescher HD. Drug-induced dysphagia. Dysphagia 1993;8:154–159.
9.6
I. BACKGROUND. Epigastric discomfort was a term initially used to describe an alteration in the
digestion of food; however, it can be caused by a wide array of conditions occurring in multiple
organs across the gastrointestinal, cardiovascular, and pulmonary systems. Serious causes, such
as gastric, esophageal, bowel, and pancreatic cancers, are rare but must also be considered.
Common reported symptoms are bloating and early satiety; nevertheless, overlapping symp-
toms make initial diagnosis difficult, and in many patients a definite cause is not established.
Pulmonary, cardiac, and vascular causes of epigastric discomfort are previewed in other chapters.
Epigastric Distress
Daniela Cardozo and Milton (Pete) Johnson
Chapter 9 • Gastrointestinal Problems
193
TABLE 9.6.1 Typical Historical, Physical Examination, and Laboratory
Findings for Gastrointestinal Etiologies of Epigastric Discomfort
History Physical examination Laboratory tests
GERD Heartburn, regurgitation, sour
belches, pain radiating
to throat, pain worsened
by lying supine, chronic
cough, hoarseness,
beneficial trial of treatment
with proton pump inhibitors
Dental erosions,
examination often
normal
Usually normal
PUD Personal or family history
of PUD, smoking history,
nonsteroidal anti-
inflammatory drug use,
pain reduced by the intake
of meals
Hypotension or
tachycardia (GI
bleeding), melena
Positive Helicobacter pylori
antibody testing, positive
urea breath test, stool
H. pylori testing, heme-
positive stools
GI malignancy Dysphagia, weight loss,
continuous pain, anorexia,
protracted vomiting, age
>50 y, smoking or alcohol
history, family history
Weight loss, palpable
mass, Virchow’s
nodes, hypotension
or tachycardia (GI
bleeding), melena,
acanthosis nigricans,
brittle nails, cheilosis,
conjunctival pallor
Anemia, heme-positive
stools
Pancreatitis Abrupt-onset pain, stabbing,
severe, and radiating to
back; history of alcohol use
Diffuse, severe pain Elevated amylase, lipase
II. PATHOPHYSIOLOGY
A. Etiology.
Up to 25% of the cases of epigastric discomfort are caused by peptic ulcer disease;
the most common cause encountered by primary care physicians is idiopathic, referred also as
functional dyspepsia. Gastroesophageal reflux disease (GERD) should be suspected when regur-
gitation and heartburn are primary complains. Esophagitis can be related to GERD but also can
be caused by hypersecretory conditions. Esophagitis and gastritis can also be primarily inflamma-
tory conditions, related to medications such as nonsteroidal anti-inflammatory drugs and toxins
such as alcohol. Most peptic ulcer diseases are related to Helicobacter pylori infection. Gallstones,
formed by supersaturation of bile, cause pain by obstructing the cystic duct. Obstruction of the
cystic duct by gallstones can cause cholecystitis, an acute inflammatory condition.
B. Epidemiology. Epigastric discomfort and dyspepsia occur in 25% of the population each
year, but most affected persons do not seek medical care. Patients at increased risk for gallstones
include the elderly, the obese (especially those who try a rapid weight loss), the pregnant, and
those on medications such as fibrates, estrogens, and contraceptives. Also at increased risk for
gallstones are certain ethnicities, those with maternal family history, the female gender, and
those with metabolic diseases such as diabetes, cirrhosis, and hypertriglyceridemia.
III. EVALUATION. Typical history, physical examination, and laboratory findings associated with
common causes of epigastric distress are listed in Table 9.6.1.
A. Genetics. Most causes of epigastric discomfort result from environmental factors, but
some, such as cholelithiasis, exhibit hereditary components. Colonic and esophageal malig-
nancies arise in certain inherited disorders. Hereditary pancreatitis is caused by a mutation
in the cationic trypsinogen gene.
(Continued)
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Taylor’s DifferenTial Diagnosis Manual
TABLE 9.6.1 Typical Historical, Physical Examination, and Laboratory
Findings for Gastrointestinal Etiologies of Epigastric
Discomfort
History Physical examination Laboratory tests
Cholelithiasis Rapid-onset pain, increasing
in intensity, <3 h duration,
radiation to scapula or
right shoulder, sweating,
vomiting, pain brought on
by meals, more common at
night, genetic component
No palpable mass Usually normal
Cholecystitis
>3 h duration of pain, shifts
from epigastrium to right
upper quadrant, acholic
stools, dark urine
Palpable mass
(30–40%), fever,
jaundice (15%),
positive Murphy’s sign
Leukocytosis (with left shift),
elevated sedimentation
rate, elevated
bilirubin, elevated
aminotransferases,
elevated alkaline
phosphatase, elevated
amylase
Irritable bowel Constipation and/or diarrhea,
pain relieved by defecation
Normal Normal
GERD, gastroesophageal reflux disease; GI, gastrointestinal; PUD, peptic ulcer disease.
From Bazaldua OV, Schneider FD. Evaluation and management of dyspepsia. Am Fam Physician
1999;60:1773–1788; Dyspepsia and GERD Practice Guideline. Institute for Clinical Systems
Improvement (ICSI); 2004 Jul; Marshall BJ. Gastritis and peptic ulcer disease. In: Rakel RE, ed.
Conn’s current therapy, 57th ed. Elsevier, 2005:600–603; Ahmad M, et al. Differential diagnosis of
gallstone induced complications. South Med J 2000;93:261–264.
(Continued)
IV. DIAGNOSIS
A. Clinical Approach.
1. The patient’s history, a thorough physical exam along with limited laboratory workup,
helps initially to put into evidence the most common causes of epigastric discomfort.
Complete blood count and a comprehensive metabolic panel can be ordered depend-
ing on the clinical presentation. These provide information regarding the presence
of alarm signs and might mandate further invasive testing. Recommendations made
by American Gastroenterological Association (AGA) suggest the test and treatment
approach that consists in a simple trial of treatment with a double-dosed proton
pump inhibitor, such as omeprazole in young patients less than 55 years of age with-
out alarm symptoms for 4–8 weeks along with H. pylori testing with stool antigen or
13c urea breath test and treating accordingly if positive. If symptoms remit, further
workup may not be necessary. If symptoms do not remit, then an upper endoscopy is
warranted. Patients 55 years or older and the presence of alarm symptoms irrespective
of age should prompt the clinician to proceed with more invasive diagnostic workup,
specifically upper gastrointestinal endoscopy.
2. The biliary colic of gallstones consists of epigastric or right upper quadrant pain of rapid
onset that increases in intensity over a 15-minute interval and lasts as long as 3 hours,
usually without any palpable mass. Pain may radiate to the interscapular region or to the
right shoulder. Associated sweating and vomiting are common. Attacks of biliary colic
are often brought on by eating, which stimulate contraction of gallbladder, especially a
fatty meal. Fever, tachycardia and a positive Murphy’s sign are usually absent.
Chapter 9 • Gastrointestinal Problems
195
TABLE 9.6.3 Differential Diagnosis of Gastrointestinal Causes of Epigastric
Discomfort
Esophagus
Esophagitis
Gastroesophageal reflux disease
Medications
Lung
Pneumonia
Pulmonary embolism
Pneumothorax
Acute cholecystitis causes epigastric or right upper quadrant tenderness or mass
and fever. The pain typically lasts longer than 3 hours and, over time, shifts from the
epigastrium to the right upper quadrant. In the elderly, localized tenderness may be the
only presenting sign. The gallbladder is palpable 30–40% of the time, and jaundice is
seen in about 15% of patients with acute cholecystitis. Leukocytosis and left shift in
complete blood count are usually present in cholecystitis. Elevation of serum alkaline
phosphatase and total bilirubin is not a prominent feature of cholecystitis. If present, it
could potentially represent more serious condition such as cholangitis, choledocolithiasis
or Mirizzi syndrome. Physical examination often cannot provide information about the
source of inflammation and pain, and that is the reason why it is mandatory to obtain
an ultrasound immediately when the aforementioned laboratory results are present (2).
3. Malignancies that cause epigastric discomfort are rare. Symptoms of gastric and esopha-
geal cancers are similar to those of other causes of epigastric distress. Alarm symptoms
such as progressive dysphagia, unexplained iron deficiency anemia, unintended weight
loss, history of gastrointestinal bleeding, odynophagia, lymphadenopathy, jaundice,
persistent emesis, or hematemesis can differentiate patients with a more serious disease.
Numerous medications induce nonulcer dyspepsia (see Table 9.6.2). Costly diagnostic
studies can be avoided by identifying medication-associated dyspepsia.
4. Irritable bowel syndrome is generally associated with chronic complex abdominal pain and
with abnormal bowel habits. There is significant overlap with functional dyspepsia.
5. It must be mentioned that the pain of ischemic heart disease may originate in the epi-
gastrium and must be ruled out. Metabolic disorders are a rare cause of epigastric dis-
comfort, but a complete differential should include malabsorption syndromes, collagen
vascular disorders, Zollinger-Edison syndrome, and Crohn’s disease.
B. Differential Diagnosis. The differential diagnosis of gastrointestinal causes of epigastric
discomfort is presented in Table 9.6.3.
TABLE 9.6.2 Medications Associated with Epigastric Discomfort
Acarbose
Bisphosphonates
Iron supplements
Nonsteroidal anti-inflammatory drugs
Oral antibiotics
Potassium supplements
Systemic corticosteroids
(Continued)
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Taylor’s DifferenTial Diagnosis Manual
TABLE 9.6.3 Differential Diagnosis of Gastrointestinal Causes of Epigastric
Discomfort
Pancreas
Pancreatitis
Heart
Cardiac ischemia
Pericarditis
Stomach
Gastritis
Peptic ulcer disease
Bleeding
Gastroparesis
Medications
Gallbladder
Cholelithiasis
Cholecystitis
Bowel
Irritable bowel syndrome
Bleeding
(Continued)
REFERENCES
1. Bazaldua OV, Schneider FD. Evaluation and management of dyspepsia. Am Fam Physician 1999;
60:1773–1788.
2. Ahmed A, Cheung RC, Keeffe EB. Management of gallstones and their complications. Am Fam
Physician 2000; 61:1673–1680, 1687–1688.
3. Singer AJ, McCracken G, Henry MC, et al. Correlation among clinical, laboratory, and hepatobiliary
scanning findings in patients with suspected acute cholecystitis. Ann Emerg Med 1996; 28:267.
4. Thompson W, Longstreth, Drossman D. Functional bowel disorders and functional abdominal pain.
Gut 1999; 45 Suppl 2: 1143
5. Klauser AG, Schindlbeck NE, Müller-Lissner SA. Symptoms in gastro-oesophageal reflux disease.
Lancet 1990; 335:205.
9.7
I. BACKGROUND. Upper gastrointestinal (GI) bleeding, defined as bleeding proximal to the
ligament of Treitz, is responsible for 400,000 hospital admissions in the United States, with a
mortality rate of 13%. It is seen twice as commonly in men than in women, and the prevelance
is noted to increase with age (1). Bleeding can be either acute or chronic, and the source can be
overt or occult. The patient may be either hemodynamically stable or unstable on presentation.
Upper Gastrointestinal
Bleeding
Lindsey M. Mosel and Milton (Pete) Johnson
Chapter 9 • Gastrointestinal Problems
197