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to thrive, choking or gagging, voice changes, immunocompromised state, history of intu-
bations, neck or thoracic surgery, neuromuscular disorder, prematurity, or congenital
syndromes. Congenital causes of stridor commonly present prior to 6 months of age. A
child older than 6 months of age with stridor lasting hours to days usually has viral croup
or foreign body aspiration, although if the child is toxic appearing, consider epiglottitis
or an abscess. Any history of smoking or alcohol abuse should raise suspicion for cancer
in adults (2–4).
a. Viral laryngotracheitis (croup) accounts for 90% of childhood cases of stridor. A
typical history is a nontoxic febrile child younger than 6 years of age with a 2–3 day
history of URI and barking cough with inspiratory stridor.
b. Laryngomalacia is the most common cause of stridor in infants. It presents with
intermittent inspiratory stridor worse when supine and feeding difficulties within
the first 2 weeks of life and usually resolves spontaneously in about 9 months.
Gastroesophageal reflux and neuromuscular disorders frequently accompany laryngo-
malacia (2, 4, 5).
c. Epiglottitis and bacterial tracheitis are life-threatening infections that are typically
associated with high fevers, rapid progression, drooling, voice changes, and marked
odynophagia in a toxic-appearing patient (4, 5).
d. An afebrile history of acute choking or gagging suggests aspiration or ingestion of a
foreign body.
B. Physical Examination
1. Focused physical examination
a. Include temperature, respiratory rate, heart rate, work of breathing and emphasize
general appearance. Also examine the neck, palate, tonsils, jaw, tongue size, lungs, ears,
and nose (fog on a mirror assesses patency).
b. Signs of respiratory distress may be present, including dyspnea, tachypnea, chest
retractions, or nasal flaring. Degree of retractions may be a better indicator of severity
than the stridor, as stridor can become quieter as the obstruction gets worse. Cyanosis
is an ominous sign.
TABLE 8.8.1 Common Causes of Stridor
Congenital
a
Inflammatory
Laryngomalacia
b
Laryngotracheobronchitis (croup)
Laryngeal cysts and webs Epiglottitis, bacterial tracheitis
Laryngeal hemangiomas Retropharyngeal abscess
Tumors Allergic edema
Subglottic stenosis
c
Diphtheria, tetanus
Vocal cord paralysis
c
Micrognathia Noninflammatory
Vascular ring Foreign body
Ectopic thyroid Gastroesophageal reflux disease
Cri du chat Hysterical stridor
Macroglossia Trauma
a
More common in children younger than 6 months of age.
b
Also found in older children or adults with neuromuscular disorders.
c
Commonly congenital but may be iatrogenic.
168
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2. Additional physical examination
a. A toxic-appearing child with high fever, drooling, severe respiratory distress, and a
preference for sitting and leaning forward with head in a “sniffing” position suggests
epiglottitis or pharyngeal abscess.
b. Look for features of known syndromes, which may suggest particular sources of
airway obstruction. Examples: micrognathia (Pierre Robin), macroglossia (Beckwith-
Wiedemann), or cutaneous hemangiomas (subglottic hemangiomas) (4, 5).
C. Testing
1. If epiglottitis or bacterial tracheitis is strongly suspected, or if the patient is unstable,
then further testing is not indicated prior to starting treatment. When further testing is
needed, endoscopy is the gold standard, but x-ray images may provide limited diagnostic
information. Chest or head/neck x-rays may show a foreign body or signs of one, such as
relative oligemia, mediastinal shift, or air trapping. Croup can be diagnosed on clinical
grounds, though a “steeple sign” may be present on posterior–anterior x-ray imaging of
the neck. Abscess is suggested by the presence of a retropharyngeal or retrotracheal space
(3, 4, 6, 7).
2. Computed tomography and magnetic resonance imaging of the neck may help in the
search for causes of persistent chronic stridor, though they are insensitive for identifying
airway stenosis. Vocal cord ultrasound is used when vocal cord paralysis is suspected (4).
3. Respiratory virus antibody panels or direct fluorescence antibody testing can be done. A
complete blood count can be useful in the acutely ill patient (bacterial infection being more
likely to have leukocytosis with neutrophil predominance). Arterial blood gas measurement
will reveal acid–base status. Carbon dioxide levels may be high in partial airway obstruction
despite reassuring pulse oximetry in a patient being given supplemental oxygen (3, 4).
IV. DIAGNOSIS. In making the diagnosis of stridor, three basic patterns exist: acute febrile, acute
nonfebrile, and chronic.
A. Acute Stridor
1. Laryngotracheobronchitis (croup) accounts for 90% of cases of stridor in children.
Generally, this diagnosis is made on clinical grounds (acute onset in a mildly febrile
child). It is due to a viral infection; most commonly parainfluenza virus but could be
respiratory syncytial virus, rhinovirus, adenovirus, or influenza virus. The entire illness
usually abates in 5 days. Hospitalization, unlike with epiglottitis, is rarely needed (3, 5).
2. Laryngomalacia can be confidently suspected in the right clinical setting (chronic, afe-
brile, less than 6 months old) and confirmed by endoscopy.
3. Epiglottitis is a medical emergency. A patient with epiglottitis classically appears as a
toxic young child with fever, respiratory distress, sore throat, or drooling. Haemophilus
influenzae was the most common cause of stridor (and epiglottitis) prior to the Hib
vaccine. Now streptococcus, staphylococcus, and viral agents are more likely causes. A
muffled voice suggests retropharyngeal abscess.
4. Foreign body aspiration can present acutely with symptoms similar to epiglottitis, but
without fever. Foreign body aspiration is common in 1- to 2-year-old children, although
it does occur in adults and can even be a cause of chronic stridor (3).
5. Acute allergic reaction can also cause stridor. The history should herald a possible offend-
ing noninfectious agent, and although respiratory collapse may be eminent, the patient
is afebrile.
6. Trauma causing acute stridor is readily identified by history.
B. Chronic stridor. Causes of chronic stridor typically occur in early childhood. Laryngeal
papillomas, tumors, and subglottic stenosis are typically congenital, whereas foreign body
aspiration and hysterical stridor can occur at any age. Laryngomalacia and laryngeal lesions
are caused by webs, hemangiomas, and cysts; they are usually identified early in life (5).
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
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169
REFERENCES
1. Marx JA, Hockberger RS, Walls RM, eds. Rosen’s emergency medicine, 7th ed. Philadelphia, PA: Mosby,
2009:2104–2105.
2. Rakel RE, Rakel DP, eds. Textbook of family medicine, 8th ed. Philadelphia, PA: WB Saunders,
2011:334–336.
3. Long SS, Pickering LK, Prober CG, eds. Principles and practice of pediatric infectious diseases revised
reprint, 3rd ed. Philadelphia, PA: Churchill Livingstone, 2009:172–177.
4. Flint PW, Haughey BH, Lund VJ, et al., eds. Cummings otolaryngology—head and neck surgery, 5th ed.
Philadelphia, PA: Mosby, 2010:2866–2868, 2896–2901.
5. Kliegman RM, Stanton BF, St. Geme III JW, Schor NF, Behrman RE, eds. Nelson textbook of pedi-
atrics, 19th ed. Philadelphia, PA: WB Saunders, 2011:283, 314, 1450–1451, 1445–1446, 1445.
e3–1445.e4.
6. Barratt GE, Koopmann CF Jr, Coulthard SW. Retropharyngeal abscess—a ten-year experience.
Laryngoscope 1984;94:455.
7. Stankiewicz JA, Bowes AK. Croup and epiglottitis: a radiologic study. Laryngoscope 1985;95:1159.
8.9
I. BACKGROUND. Wheezing is one of the most common respiratory complaints to present to
primary care physicians. Up to 25% of children under the age of 5 years present to their pri-
mary care manager with a wheezing illness (1).
II. PATHOPHYSIOLOGY AND ETIOLOGY. Expiratory wheezing is the sound heard on ausculta-
tion when air is rapidly passed through smaller, narrowed airways. Younger children and infants
have smaller airways than adults and thus have more frequent wheezing symptoms (2).
A. Wheezing in Infants. The most common cause for wheezing in this age group is infec-
tious lower respiratory tract illnesses, e.g., respiratory syncytial virus and coronavirus. Edema
in the smaller airways caused by the infection results in airway constriction, which can then
lead to small airway collapse and air trapping. If this process leads to wheezing in a child less
than 2 years, it is called bronchiolitis (1). Another common cause of wheezing in infants is
asthma. Many infants with recurrent wheezing and lower respiratory tract illnesses are very
likely to have asthma, even without evidence of ectopic disease and despite their young age
(3). Some common risk factors for asthma are second-hand smoke exposure, male sex, and
unclean living conditions. A third common cause (but often unrecognized) of recurrent
wheezing in infants is inhalation/aspiration of food and liquids, which is usually associated
with gastroesophageal reflux disease (GERD). A classic related symptom is coughing while
feeding; however, this may extinguish as the cough reflex is diminished from repeated lar-
ynx stimulation by foreign substances (1). Some of the more uncommon and rare causes of
wheezing in infants are listed in Table 8.9.1.
B. Wheezing in Children. The most common cause of recurrent wheezing in children is
asthma, and the prevalence is highly linked to elevated serum immunoglobulin E (IgE) lev-
els. As with infants, children with asthma have decreased lung function compared with those
without asthma, and second-hand smoke exposure increases the risk of developing a wheeze
(3). Likewise, another common cause of recurrent wheeze is repeated aspiration of foods and
liquids associated with GERD. An isolated, sudden episode of localized wheezing in children
may be due to foreign body inhalation. More common than aspiration, a swallowed foreign
body, if stuck in the esophagus, may cause a wheeze by compression of the trachea (1). Single
episodes of wheezing in children can also be caused by infections, with viruses being the most
common pathogens (e.g., respiratory syncytial and parainfluenza viruses) (Table 8.9.1).

Wheezing

Katrina N. Wherry
170
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C. Wheezing in Adults. Asthma is one of the most common causes of wheezing in adults,
with a prevalence of 10–12% in developed countries (4). While the majority of adults with
asthma are diagnosed in early childhood, asthma can develop in adulthood without a his-
tory of recurrent wheeze in childhood (4). The prevalence of asthma in adults is also highly
linked to elevated serum IgE levels (1). Chronic obstructive pulmonary disease (COPD)
is another cause of recurrent wheezing in adults who typically have a significant smoking
history. These patients will usually have other symptoms associated with wheezing, such as
cough, exertional dyspnea, and sputum production (4). Episodic wheezing in adults can
also be secondary to congestive heart failure (CHF) and pulmonary embolism (5). See
Table 8.9.1 for more diagnoses.
III. EVALUATION. Given that asthma is a common cause of wheezing in all age groups, the
initial evaluation of a wheezing patient should aim to exclude other diagnoses that can cause
wheezing (1).
A. Clinical History
a. Onset. If within the first few weeks of life, consider a congenital cause of wheezing. If it
started suddenly, foreign body aspiration may be more likely (1, 2).
b. Timing and Pattern. If the wheezing is episodic and recurrent, asthma may be more
likely. If the wheezing occurs during a certain time of the year, then infectious causes or
asthma that is triggered by certain environmental allergens may be more likely (1, 2).
c. Associated Symptoms. If there are cough and sputum production, fever, and upper
respiratory symptoms, then consider infectious causes and COPD. In an infant and
child, cough during feeding may be associated with aspiration and reflux. If there is poor
weight gain in the child or infant, then consider GERD and cystic fibrosis (CF) (2, 6).
d. Family and Social History. If there is a family history of the atopic triad, asthma,
eczema, and environmental allergies, then asthma may be more likely. If the patient has a
significant smoking history, or a parent smokes, consider asthma and COPD. Although
most patients with CF do not have a family history of the disease, recurrent infections
causing wheezing may be secondary to CF (6).
B. Physical Examination. Inspect the newborn for persistent cyanosis, as this can be associ-
ated with congenital anomalies. Inspect the adult and child for clubbing in the setting of
recurrent wheezing episodes, as this can be associated with CF. Palpate the chest of the infant
and child for a localized vibration consistent with wheezing in the setting of foreign body
aspiration. Dullness to percussion can be consistent with consolidation caused by signifi-
cant infection. Wheezes can be heard on auscultation, and their location should be noted
TABLE 8.9.1 Uncommon and Rare Causes of Wheezing by Age Group (1, 5)
Infants and Children Adults
Infectious pertussis and tuberculosis Pulmonary embolism
Bronchopulmonary dysplasia Benign and malignant tumors causing obstruction
Cystic brosis Eosinophilic pulmonary infiltration
Congestive heart failure Vocal cord dysfunction
Congenital vascular anomalies
Mediastinal masses
Bronchiolitis obliterans
Immune deficiency
Tracheobronchial anomalies
 
171
as localized wheezes are more consistent with foreign body aspiration. Other breath sounds
should also be noted: crackles can be present in infection or CHF, and stridor can be heard
in viral infections that also affect the upper airways (6).
C. Testing. The decision to order a test will depend on the differential diagnosis being con-
sidered after a careful history and physical is performed. For suspected asthma or COPD,
spirometry should be performed. Generally, patients older than 5 years will be able to follow
the necessary steps to perform spirometry. Infants may be tested by their response to treat-
ment with an inhaled beta agonist (1, 5). Chest x-ray findings may support infectious causes
of wheezing or rare causes such as masses or congenital malformations. A swallow study
may help identify patients with frequent aspiration or GERD, swallowed foreign objects, or
anatomic abnormalities. Bronchoscopy should be considered if other testing does not help
narrow the differential diagnosis (6). If CF is considered, genetic and sweat chloride testing
should be performed. When pertussis or tuberculosis is considered, testing for antibodies to
pertussis and purified protein derivative skin testing should be performed (1).
IV. DIAGNOSIS. The differential diagnosis will be created after a careful history is taken and
will be supported by physical exam findings and testing. One of the most common causes of
wheezing in all age groups is asthma, and an effort should be made to exclude the other causes
of wheezing especially in infants, where many other conditions (some rare) can produce similar
symptoms to asthma (1).
Disclaimer
The opinions and assertions contained herein are the private views of the author and are not to be
construed as official or as reflecting the views of the U.S. Air Force Medical Service, the U.S. Air
Force or the Department of Defense at large.
REFERENCES
1. Martinati LC, Boner AL. Clinical diagnosis of wheezing in childhood. Allergy 1995;50:701–710.
2. Weiss LN. The diagnosis of wheezing in children. Am Fam Physician 2008;77(8):1109–1114.
3. Martinez FD, Wright AL, Taussig LM, et al.; Group Health Medical Associates. Asthma and wheezing
in the first six years of life. N Engl J Med 1995;332:133–138.
4. Fauci AS, Braunwald E, Kasper DK, et al., eds. Harrison’s principles of internal medicine, 17th ed.
New York, NY: McGraw Hill Medical, 2008. Accessed at http://accessmedicine.com/resourceTOC.
aspx?resourceID=4 on May 1, 2012.
5. Summary report 2007 National Asthma Education and Prevention Program expert panel report 3:
Guidelines for the diagnosis and management of asthma. Accessed at http://www.nhlbi.nih.gov/guide-
lines/asthma/asthsumm.pdf on May 1, 2012.
6. Finder JD. Understanding airway disease in infants. Curr Probl Pediatr 1999;29:65–81.
172
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Gastrointestinal Problems

Richard Fruehling
CHAPTER 9
9.1
I. BACKGROUND. Abdominal pain is a common complaint and comprises up to 10% of
total visits to the emergency department. The etiology may be quite varied resulting from
extra-abdominal pathology or intra-abdominal sources. Physical findings are variable and
sometimes misleading, where life-threatening conditions may evolve from seemingly benign
presentations.
II. PATHOPHYSIOLOGY. The common reasons for intra-abdominal pain that causes concern
are presented in Table 9.1.1 (1). Selected causes of severe intra-abdominal pain are listed in
Table 9.1.2. Causes of extra-abdominal pain are listed in Box 9.1.

Abdominal Pain

Zachary W. Meyer and Richard Fruehling
TABLE 9.1.1 Common Causes of Abdominal Pain
Diagnosis Etiology Epidemiology
Gastric, esophageal, or
duodenal inflammation
Gastric hypersecretion,
breakdown of mucoprotective
barriers, infection, exogenous
source
All age groups. Gastroenteritis
may be seasonal, with travel
history and affected family
See peptic ulcer disease
Acute appendicitis Appendiceal lumen obstruction
leads to swelling, ischemia,
infection, and perforation
Adolescence to young adulthood
Higher perforation rate in
children, women, and elderly
Mortality rate of 0.1% (2–6%
with perforation)
Biliary tract disease Passage of gallstones causes
biliary colic
Impaction of a stone in cystic
duct or common duct causes
cholecystitis or cholangitis
Peak age of 35–60 y
Rare in patients <20 y of age
Female-to-male ratio of 3:1
Risk factors: multiparity, obesity,
alcohol intake, birth control pills
Ureteral colic Family history, dehydration,
urinary tract infections, gout,
certain medications
Average age of 30-40 y, primarily
in men, less common in
children
(Continued)
173
III. EVALUATION
A. History
1. The history should include the following: Palliative/alleviating factors, Quality of pain,
Radiation or referred pain pattern, Severity, and Time of onset/temporal relationships.
The character of pain is particularly helpful (e.g., colicky, steady, sharp, burning, tearing,
and gnawing). The associated symptoms should be identified (e.g., dysuria, hematuria,
melena, hematochezia, change in bowel habits, diarrhea, vomiting). The exact sequence
of symptoms may be especially helpful; for example, in acute appendicitis, generalized
pain and anorexia typically precede point tenderness.
2. A thorough gynecologic history should be performed in all women with abdominal pain,
and pregnancy (including ectopic pregnancy) should be considered.
3. Small bowel obstruction in patients with prior abdominal surgery should be considered.
Alarming symptoms generally involve escalating symptoms, fever, profound illness, and
extremes of age.
TABLE 9.1.1 Common Causes of Abdominal Pain
Diagnosis Etiology Epidemiology
Diverticulitis Diverticular infection or
inflammation or perforation
May develop peritonitis, fistulas,
or abscesses
Incidence increases with
advancing age; male > female
Recurrences are common
Called “left-sided appendicitis”
Peptic ulcer Sometimes associated with
Helicobacter pylori infection
Risk factors include nonsteroidal
anti-inflammatory drug use,
tobacco and alcohol use
Occurs in all age groups; peaks
at the age of 50 y
Men affected twice as much
as women. Severe bleeding or
perforation is rare
Bengiamin RN, Budhram GR, King KE, Wightman JM. Abdominal pain. In: Marx JA, ed. Rosen’s
emergency medicine: concepts and clinical practice, 7th ed. Philadelphia, PA: Mosby, 2010:
160–194.
TABLE 9.1.2 Selected Life-threatening Causes of Abdominal Pain
Diagnosis Etiology Epidemiology
Ruptured or
leakingaortic
aneurysm
Exact etiology undetermined.
Contributing factors:
atherosclerosis, genetic
predisposition, connective tissue
disease, infection
More frequent in men
Risk factors: hypertension, diabetes
mellitus, smoking, chronic obstructive
pulmonary disease, coronary artery
disease (CAD)
Acute pancreatitis Alcohol, gallstones, hypertriglyceridemia,
hypercalcemia, post endoscopic
retrograde cholangiopancreatography
(post-ERCP)
Peak age in adulthood, rare in
childhood
More frequent in males
Mesenteric
ischemia
Often multifactorial, including
transient hypotension in the
presence of atherosclerosis.
Occlusion occurs in 65% of cases
(75% embolic)
Most common in elderly people with
cardiovascular disease, congestive
heart failure (CHF), diabetes mellitus,
sepsis, dehydration
Mortality 70%
(Continued)
174
Taylor’s DifferenTial Diagnosis Manual
B. Physical Examination
1. Analysis of the general appearance of the patient is especially helpful. Patients with col-
icky (hollow viscus obstruction) pain often writhe about, seeking a comfortable position.
Peritonitis causes patients to be still and jarring the bed or heel tap may exacerbate the
pain. Check complete vital signs for evidence of sepsis/shock; identify fever, tachycardia,
or hypotension.
2. Inspect the abdomen for distension, pulsations, or ecchymosis (Grey Turner’s or
Cullen’s sign).
3. Auscultate for the presence of bowel sounds or bruits suggestive of aneurysms. Bowel
sounds are sometimes absent in appendicitis.
4. Palpation begins distal to areas of pain and should be gentle. Guarding and rigidity
should be noted. Masses and organomegaly should be assessed. Murphy’s sign may help
identify gallbladder pathology. The iliopsoas and obturator signs may indicate appendi-
citis. Genital examination is important to exclude hernia and a rectal examination may
help identify a retrocecal appendicitis.
C. Testing
1. Laboratory Evaluation. It is necessary to obtain a serum human chorionic gonadotropin
from any patient who could potentially be pregnant. Electrolytes can rule out metabolic
abnormalities such as hypercalcemia. A complete blood count should be considered in
infectious etiologies and for the purpose of monitoring hematocrit stability and plate-
let count. Elevated liver tests can identify hepatocellular or obstructive biliary disease.
Elevated amylase may be found in pancreatitis, salivary disease, mesenteric ischemia, and
fallopian pathology. Lipase is very specific to the pancreas. Urinalysis is useful to exclude
urinary tract infections. Hematuria is found in 90% of renal stones. Pyuria can be present
when an inflammatory mass (e.g., appendicitis) is close to the urinary tract (2).
2. Imaging. Plain film acute abdominal series (upright and supine) identify free air and
abnormal gas patterns. Plain films may identify calcifications associated with renal stones
(85%), biliary lithiasis (15%), and pneumonia as an extra-abdominal cause for pain.
Ultrasound is useful to rule out ectopic pregnancy, appendicitis, biliary tract disease,
abdominal aortic aneurysm, and hydroureter. Computed tomography (CT) scan has
largely replaced other modalities, because it provides a quick accurate imaging modality
to detect appendicitis, urolithiasis, cholecystitis, diverticulitis, and pancreatitis. In elderly
patients with abdominal pain, CT scan alters the initial diagnosis in 45% of cases and
affects admission decisions in 26% of cases (3).
IV. DIAGNOSIS
A. Differential Diagnosis.
This is usually broad and needs frequent reconsideration. If
a treatment modality is unsuccessful, the working diagnosis must be questioned and the
BOX 9.1 Important Extra-Abdominal Causes of Abdominal Pain
Thoracic: myocardial infarction/unstable angina, pneumonia, PE, pericarditis, herniated disk
Genitourinary: testicular torsion
Abdominal Wall: muscle spasm, muscle hematoma, herpes zoster
Infections: streptococcal pharyngitis (often in children), mononucleosis, Rocky Mountain spotted
fever
Systemic: diabetic ketoacidosis, alcoholic ketoacidosis, uremia, sickle cell disease, porphyria,
systemic lupus erythematosus, vasculitis, glaucoma, hyperthyroidism
Toxic: methanol poisoning, heavy metal toxicity, scorpion bite, snake bite, black widow spider bite
Bengiamin RN, Budhram GR, King KE, Wightman JM. Abdominal pain. In: Marx JA, ed. Rosen’s
emergency medicine: concepts and clinical practice, 7th ed. Philadelphia, PA: Mosby, 2010:
160–194.
Chapter 9 • Gastrointestinal Problems
175
differential expanded. Serial examination and close follow-up are needed if the diagnosis is
in question.
B. Clinical Manifestations. Patterns associated with the different types of abdominal pain
are presented in Table 9.1.3. Multiple causes necessitate a broad differential diagnosis.
Numerous diagnostic modalities exist, including physical examination, laboratory studies,
and ancillary studies.
REFERENCES
1. Bengiamin RN, Budhram GR, King KE, Wightman JM. Abdominal pain. In: Marx JA, ed. Rosen’s
emergency medicine: concepts and clinical practice, 7th ed. Philadelphia, PA: Mosby, 2010:159–169.
2. Kamin RA, Nowicki TA, Courtney DS, et al. Pearls and pitfalls in the emergency department evalua-
tion of abdominal pain. Emerg Med Clin North Am 2003;21:61–72.
3. Esses D, Birnbaum A, Bijur P, et al. Ability of CT to alter decision making in elderly patients with
acute abdominal pain. Am J Emerg Med 2004;22:270–272.
4. O’Brien MC. Chapter 74. Acute abdominal pain. In: Tintinalli JE, ed. Tintinalli’s emergency medicine,
7th ed. New York, NY: McGraw-Hill, 2011.
TABLE 9.1.3 Types of Abdominal Pain
Visceral pain Results from stretching unmyelinated nerve fibers surrounding an organ;
may be “crampy, dull, or achy,” can be either steady or intermittent. This
type of pain is often ill-defined and diffuse. Examples include appendicitis,
cholecystitis, bowel obstruction, and renal colic. Foregut structures often refer
to the epigastrium (stomach, duodenum, pancreatic-biliary tree), and midgut
structures (small bowel, ascending colon) refer to periumbilical area. Hindgut
structures (descending colon) often refer to the suprapubic area or the back
Somatic pain Arises from pain fibers in parietal peritoneum; usually sharper, localized, and
more constant; may develop after visceral pain. Usually, it represents perito-
neal inflammation from various sources (bleeding, chemical irritation, infec-
tious causes) and most often causes great concern. Patients prefer immobility
Referred pain Defined as pain felt at a distance from the diseased organ. Diaphragmatic irrita-
tion often radiates to shoulders, and ureteral colic often radiates to groin.
Referred pain is often localized to the developmental dermatome and can be
misleading in localizing the source. However, it is usually perceived on the
same side as the involved organ (4)
9.2

Ascites

Manoj Kumar and Milton (Pete) Johnson
I. BACKGROUND. Ascites involves an accumulation of fluid in the peritoneal cavity. It is known
as the most common major complication of cirrhosis. About 50% of patients with compensated
cirrhosis develop ascites in 10 years (1). The 1- and 5-year mortality among patients with ascites
due to cirrhosis is approximately 15% and 44%, respectively (2). Spontaneous bacterial perito-
nitis and hepatorenal syndrome are known complications of ascites, contributing to significant
morbidity and mortality, with a median survival of 25 years. Patients with ascites are commonly
176
Taylor’s DifferenTial Diagnosis Manual
referred for liver transplantation as the later improves the survival rate by approximately 40%
in this population (3).
II. PATHOPHYSIOLOGY. The widely accepted theory for ascites formation is peripheral arterial
vasodilatation hypothesis in cirrhosis patients. Portal hypertension (PH) in advanced stages
of cirrhosis causes increased sinusoidal pressure, which subsequently triggers vasodilatation in
splanchnic and peripheral arterial system mediated by nitric oxide. This vasodilatation activates
renin–angiotensin system, sympathetic nervous system, and antidiuretic hormone to maintain
fluid homeostasis (4). These factors activate salt and fluid retention and interrupt the balance
among the Starling forces. Thus, the fluid with the greater pressure displaces into the tissues
and then “weep” from the surface of the liver and collects in the peritoneal cavity in the form
of ascites. Elevated levels of epinephrine and norepinephrine along with hypoalbuminemia also
contribute to ascites formation in chronic liver disease patients. Hypoalbuminemia contributes
by decreasing plasma oncotic pressure and favors the extravasation of fluid from the plasma to
the peritoneal cavity. The low arterial pressure and reduced systemic vascular resistance induce
renal vasoconstriction and renal hypoperfusion and thus eventually trigger renal injury. The
renal system then loses its ability to clear free water and eventually develop dilutional hypona-
tremia and hepatorenal syndrome.
III. EVALUATION
A. History.
The history should cover questions about risk factors for liver disease. History
of alcoholism, transfusions, tattoos, HIV, and other risk factors for infectious hepatitis is
relevant. Other pertinent past medical history could be of cancers (leukemia, lymphomas),
heart failure, renal disease, and tuberculosis. In patients with no clear etiology of cirrhosis,
lifetime body weight, diabetes, and hyperlipidemia should be evaluated to include nonalco-
holic steatohepatitis in the differential diagnosis.
B. Physical Examination. Patients with full and distended abdomen should have their
flanks examined by percussion method. If flank dullness is significantly appreciated then,
shifting dullness should be tested. The presence of shifting dullness has sensitivity and
specificity of greater than 80% and 50%, respectively, in the diagnosis of ascites, and its
presence usually indicates at least 1500 cc of fluid in the peritoneal cavity (5). In obese
patients with liver disease, distinguishing ascites from obesity by physical examination can
frequently be a challenge and abdominal ultrasound may be required. Signs of PH and liver
failure include collateral veins over the abdominal wall, jaundice, palmar erythema, spider
angiomas, etc.
C. Testing. Once ascites is confirmed, diagnostic abdominal paracentesis should be done
in all patients. Bleeding is sufficiently uncommon and thus administration of fresh frozen
plasma or platelets is not recommended (6). Besides new-onset ascites, other indications for
abdominal paracentesis include ascites with fever, abdominal pain, tenderness, hypotension,
ileus, acidosis, azotemia, hypothermia, or encephalopathy and tense ascites. Cell count,
differential count, ascitic fluid total protein, and serum–ascites albumin gradient should be
checked as routine tests on ascitic fluid. If infection of the fluid is suspected, bedside culture
in blood culture bottles should be performed and then empiric antibiotic coverage should
be initiated and continued until infection is ruled out by routine laboratory investigation
of the fluid. Total serum CA125 is not helpful in the differential diagnosis of ascites of any
type (6). pH, lactate, cholesterol, fibronectin, and glycosaminoglycans testing is not help-
ful (7). The significance and interpretation of the laboratory findings from the ascitic fluid
are described in Tables 9.2.1 and 9.2.2.
IV. DIAGNOSIS.
A. Differential Diagnosis.
The differential diagnosis of ascites is listed in Table 9.2.3. Some
rare causes of ascites include trauma to lymphatics or ureters, chlamydia, coccidioides, gono-
coccus induced, nephrotic syndrome, serositis, hypothyroidism, acquired immunodeficiency
syndrome, Fitz-Hugh-Curtis syndrome, and peritoneal mesothelioma.
B. Clinical manifestation. The general symptoms include nausea, anorexia, heart
burn, dyspnea, abdominal distension, orthopnea, weight gain, and pedal edema.
Patients can also present with signs of spontaneous bacterial peritonitis and hepatic
Chapter 9 • Gastrointestinal Problems
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