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TABLE 9.2.2 Clinical Association of Paracentesis Fluid Results
Characteristic Association
Amylase Elevated in small bowel or pancreatic injury
LDH In uncomplicated ascites, LDH is fewer than half the serum
values. Peritonitis > SBP > serum LDH
Glucose concentration Mildly depressed in carcinomatosis and SBP. In bowel
perforation or late SBP, the glucose level may be as low as 0
Cytology This is of benefit when carcinomatosis is present. This test
requires the release of malignant cells into the ascitic fluid,
sensitivity 67% of all malignancy-related cases
Renal panel Assess for hepatorenal syndrome
LDH, lactate dehydrogenase; SBP, spontaneous bacterial peritonitis.
encephalopathy. Those with esophageal varices may present with signs of variceal hemor-
rhage. Hepatosplenomegaly, umbilical hernia, and scrotal edema are frequently seen as
well. Masses or lymphadenopathy suggest underlying malignancy. Distended neck veins,
cardiomegaly, S3 on auscultation support cardiac cause of ascites. Nephrotic syndrome
can present in the form of anasarca.
TABLE 9.2.1 Paracentesis Fluid Findings and Their Significance
Characteristic Specific findings Significance
Appearance Clear
Turbid/cloudy
Opalescent
Milky
Pink/bloody
Brown
Cirrhosis
Infection
Elevated triglyceride concentration
Traumatic tap, malignancy
Patient with jaundice, ruptured gallbladder,
duodenal ulcer
Cell count and differential Polymorphonuclear
leukocytes count
>250
Spontaneous bacterial peritonitis
Serum to ascites albumin
gradient (serum albu-
min–ascites albumin)
(g/dL)
>1.1
Portal hypertension: cirrhosis, alcoholic
hepatitis, compression from large liver
metastases, portal vein thrombosis, Budd-
Chiari syndrome, cardiac ascites, acute
fatty liver of pregnancy, myxedema, mixed
ascites
<1.1
No portal hypertension: peritoneal
carcinomatosis (most common),
tuberculosis, pancreatic or biliary ascites,
bowel infarction or obstruction, nephritic
syndrome
(Continued)
178
Taylor’s DifferenTial Diagnosis Manual
REFERENCES
1. Gines P, Quintero E, Arroyo V, et al. Compensated cirrhosis: natural history and prognostic factors.
Hepatology 1987;7:12–18.
2. Planas R, Montoliu S, Balleste B, et al. Natural history of patients hospitalized for management of
cirrhotic ascites. Clin Gastroenterol Hepatol 2006;4:1385–1394.
3. Gines P, Cardenas A, Arroyo V, et al. Current concepts: management of cirrhosis and ascites. N Engl
J Med 2004;350:1646–1654.
4. Schrier RW, Arroyo V, et al. Peripheral arterial vasodilation hypothesis: a proposal for the initiation of
renal sodium and water retention in cirrhosis. Hepatology 1988;8:1151–1157.
5. Cattau EL Jr, Benjamin SB, Knuff TE, Castell DO. The accuracy of the physical exam in the diagnosis
of suspected ascites. JAMA 1982;247:1164–1166.
6. Runyon BA, AASLD Practice Guidelines Committee. Management of adult patients with ascites due
to cirrhosis: an update. Hepatology 2009;49(6):2087.
7. Haubrich WS, Schaffner F, Brek J, et al. Bockus gastroenterology, 5th ed. Philadelphia, PA: WB
Saunders, 1994:2009.
TABLE 9.2.3 Differential Diagnosis of Ascites
Cause Comment
Cirrhosis
Etiology in ∼80% of ascites (3)
Alcoholic hepatitis
Carcinomatosis Two-thirds of malignancy-related ascites
Metastases One-third of malignancy-related ascites
Congestive heart failure History of heart failure or severe lung disease
Tuberculosis
Cause in ∼1% of ascites (3)
Hepatitis B and C Leads to cirrhosis
Pancreatic disease Ascites amylase is five times the serum values
Wilson’s disease Effects range from liver test abnormalities to hepatic failure
Hemochromatosis Iron deposition causes cirrhosis
Constrictive pericarditis Leads to hepatic congestion
Mixed ascites
∼5% (cirrhosis + another etiology)
9.3
Constipation
Timothy McAuliff and Richard Fruehling
I. BACKGROUND. Constipation is a common gastrointestinal complaint among the general
population. The definition varies from patient to patient, being described as stools that are too
hard, too small, too difficult, or too infrequent (1). To clarify and offer an objective diagnosis
for the clinician, an international panel in 2006 developed a consensus definition called The
Rome-III criteria (2) (see Table 9.3.1).
II. PATHOPHYSIOLOGY. The colon and rectum are responsible for both digestive and excre-
tive functions, including continued mixing of the output of the ileum, further processing of
undigested carbohydrate (including digestion and absorption), absorption of water to create
(Continued)
Chapter 9 • Gastrointestinal Problems
179
TABLE 9.3.1 Rome-III Criteria for the Diagnosis of Functional Constipation
Adults
• Two or more of the following symptoms are present for at least 3 months, with onset at least 6
months prior to diagnosis.
°
Straining during at least 25% of defecations.
°
Lumpy or hard stools in at least 25% of defecations.
°
Sensation of incomplete evacuation for at least 25% of defecations.
°
Sensation of blockage or obstruction in anus or rectum for at least 25% of defecations.
°
Use of manual maneuvers (e.g., digital expression of stool, pelvic floor support) to facilitate at
least 25% of defecations.
°
Fewer than three defecations per week
• Loose stools are rarely present without the use of laxatives.
• Symptoms do not meet the criteria for irritable bowel syndrome
Infants and young children
• Two or more weeks of one of the following symptoms:
°
Hard stools (pebblelike = scybalous) in most bowel movements
°
LESS THAN three FIRM stools per week
• Symptoms not explained by a metabolic, endocrine, or anatomic cause
Adapted with permission from Longstreth GF, Thompson WG, Chey WD, et al. Functional Bowel
Disorders. Gastroenterology 2006;130:1480–1491.
semisolid or solid stool, and ultimately evacuation of stool from the body. These processes are
coordinated through a variety of neurotransmitters, a parasympathetic neural plexus, and a
variety of other voluntary and involuntary mechanisms.
A. Etiology. Changes in the texture of the stool, the peristaltic function or internal diameter
of the colon, or the expulsive function of the rectum and pelvic floor can lead to constipa-
tion (3, 4). Risk factors are numerous and more common causes include a low-fiber diet,
inactivity, and medications (5) (see Table 9.3.2).
B. Epidemiology. Prevalence rates range between 2% and 28% and it is a more common
complaint among women and the elderly (6).
TABLE 9.3.2 Causes of Constipation (Rated by the Likelihood of Being a
Cause of Constipation)
Functional (common) Medications (less common)
Low-fiber diet Antacids Clonidine
Sedentary lifestyle Anticholinergics Diuretics
Dehydration Antidepressants Sinemet
Slow transit time Calcium channel blockers Narcotics
Outlet delay Cholestyramine Sympathomimetics
(Continued)
180
Taylor’s DifferenTial Diagnosis Manual
TABLE 9.3.2 Causes of Constipation (Rated by the Likelihood of Being a
Cause of Constipation)
Functional (common) Medications (less common)
Irritable bowel syndrome
Inflammatory bowel disease
Nonsteroidal anti- inflammatory
drugs
Psychotropics
Excessive milk intake
Stool withholding
Structural (less common) Neurogenic (rare) Endocrine/metabolic (rare)
Anal fissures Cerebrovascular events Diabetes mellitus
Hemorrhoids Multiple sclerosis Hypercalcemia
Colonic strictures Parkinson’s disease Hyperparathyroidism
Diverticulitis Hirschsprung’s disease Hypokalemia
Ischemia Spinal cord tumors or
abnormalities
Hypothyroidism
Radiation colitis Cerebral palsy Uremia
Adenocarcinoma Chagas disease Celiac disease
Imperforate anus Botulism Cystic fibrosis
Pelvic masses Down syndrome Pregnancy
Prune belly syndrome
Psychogenic (less common) Connective tissue (rare)
Anxiety Amyloidosis
Depression Scleroderma
Somatization Systemic lupus erythematosus
III. EVALUATION (see Figure 9.3.1)
A. History and Physical Examination. Initially, the patient should be screened for alarming
features that require more extensive testwork (hematochezia, >10 lb weight loss, obstipation,
family history of colon cancer). If these are absent, then evaluate via history and physical
(including rectal exam with hemoccult) to distinguish idiopathic constipation from second-
ary causes. (Table 9.3.3 presents findings in the history and physical examination that aid in
distinguishing idiopathic or functional causes from secondary causes.) If a secondary cause is
found, treat the underlying cause. If no cause is found on initial clinic visit, treat the patient
empirically with a trail of fiber, increased physical activity, and constipation medications. If
the patient fails conservative management, then further diagnostic testing is warranted (7).
Note: Obstipation (lack of flatus) may be indicative of a bowel obstruction, which
requires immediate surgical evaluation.
B. Testing. Laboratory tests include serum chemistries (including calcium and glucose),
complete blood count (for anemia), and thyroid function tests. Abdominal x-ray may show
fecal retention. Colon transit time may be measured using a “pill camera” or radiopaque
marker study. Anorectal or colonic manometry may provide information about colonic tone
and motility (8). Colonoscopy is indicated when any of the following are present: anemia,
rectal bleeding, hemoccult positive stools, obstructive symptoms, new onset of constipation,
unintended weight loss, a change in stool caliber, or if the patient is older than 50 years and
is due for colon cancer screening (9).
(Continued)
Chapter 9 • Gastrointestinal Problems
181
History/physical
examination/consideration for
secondary causes (see tables)
No cause identified
No cause identified
Colonoscopy-
if over age 50 (screening)
Colonic transit (marker) study plus
anorectal manometry/balloon expulsion test
All normal
Functional defecation
disorder
Slow transit
constipation
Slow transit
constipation with functional
defecation disorder
Symptomatic
treatment (see
algorithm for
normal transit
constipation)
See algorithm
for functional
defecation
disorder
See algorithm
for slow transit
constipation
Treat first for functional
defecation disorder.
If inadequate response,
also treat for slow
transit constipation
Figure 9.3.1. Diagnostic approach to chronic constipation unresponsive to conservative therapy.
Courtesy of Arnold Wald, MD. 2012 UpToDate “Etiology and evaluation of chronic constipation in adults”
TABLE 9.3.3 History and Physical Examination Findings
Component Finding Condition suggested
History
Age at onset Childhood onset Congenital causes
Duration Acute onset Correctable causes
Longer duration Functional cause
The most troubling symptom Straining
Need for manual maneuvers
for evacuation
Pelvic floor dysfunction
Cramping/bloating between
bowel movements
Irritable bowel syndrome
Medication history See the list of common
offenders in Table
9.3.2
Physical examination
Digital rectal examination Tender puborectalis Puborectalis spasm
Inability to expel rectal finger Pelvic floor dysfunction
(Continued)
182
Taylor’s DifferenTial Diagnosis Manual
IV. DIAGNOSIS
A. Differential Diagnosis.
A differential diagnosis of functional constipation is presented in
Table 9.3.2.
REFERENCES
1. Stewart WF, Liberman JN, Sandler RS, et al. Epidemiology of constipation (EPOC) study in the United
States: relation of clinical subtypes to sociodemographic features. Am J Gastroenterol 1999;94:3530.
2. Longstreth GF, Thompson WG, Chey WD, et al. Functional bowel disorders. Gastroenterology
2006;130:1480–1491.
3. Arce DA, Ermocilla CA, Costa H. Evaluation of constipation. Am Fam Physician 2002;65:2283–2290.
4. Faigel DO. A clinical approach to constipation. Clin Cornerstone 2002;4(4):11–21.
5. Leung FW. Etiologic factors of chronic constipation: review of the scientific evidence. Dig Dis Sci
2007,52(2):313–316.
6. Satish-Rao SC. Constipation: evaluation and treatment. Gastroenterol Clin North Am 2003;32:659–683.
7. Barnett JL, Hasler WL, Camilleri M. American Gastroenterological Association medical position
statement on anorectal testing techniques. American Gastroenterological Association. Gastroenterology
1999;116:732.
8. Rao SS, Singh S. Clinical utility of colonic and anorectal manometry in chronic constipation. J Clin
Gastroenterol 2010;44:597.
9. Qureshi W, Adler DG, Davila RE, et al. ASGE guideline: guideline on the use of endoscopy in the
management of constipation. Gastrointest Endosc 2005;62:199.
TABLE 9.3.3 History and Physical Examination Findings
Component Finding Condition suggested
Rectal mass, anal stricture Obstruction
Anal fissure Cause or effect?
Impacted stool Slow transit constipation
Simulated defecation Laxity of anal verge Neurogenic causes
Perineal function during simulated
expulsion and retention
Low activity Pelvic floor dysfunction
Vaginal examination (women) Observe for rectocele Pelvic relaxation
Neurologic examination Other focal neurologic deficits Neurogenic causes
Abdominal examination Masses, scars Causes of obstruction
9.4
I. BACKGROUND. Clinically, the most useful definition of diarrhea is the most vague and
patient-centric, that is, frequent, loose stools. Diarrhea can also be defined as daily stools cumu-
latively weighing over 200 g in teenagers and adults and weighing over 10 g/kg/d for infants and
young children (1, 2). Another way to characterize diarrhea is as a definite increase in frequency
and decrease in consistency of stools, relative to said individual’s baseline. The last definition is
more clinically useful in children.
Diarrhea
Safana Anna Makhdoom and Robert C. Messbarger
(Continued)
Chapter 9 • Gastrointestinal Problems
183
These stools are often watery, excessive, and can be uncontrolled. Diarrhea can be associ-
ated with fever, abdominal cramping, painful defecation, mucousy stools, and/or bloody stools.
Additionally, the duration of diarrhea is of significant clinical importance. Acute diarrhea is of
less than 14 days duration, while diarrhea beyond 30 days’ duration is termed chronic; persis-
tent diarrhea is diarrhea lasting beyond 14 days (3).
In selected clinical settings (e.g., impoverished or immunocompromised patients), this ail-
ment can be life threatening.
II. PATHOPHYSIOLOGY
A. Etiology
1. Acute diarrhea can be infectious or noninfectious. By and large, most acute diarrhea in
the developed world and developing world is infectious. The pathogenic organisms can
be bacteria, protozoa, and/or viruses. Noninfectious causes include food allergies, drugs,
and/or adverse drug effects, and other disease states including inflammatory bowel dis-
ease, thyrotoxicosis, and carcinoid syndrome.
For pediatric patients, acute diarrhea is also commonly due to infectious gastroen-
teritis. However, other etiologies in the pediatric population include other infections
(e.g., acute otitis media, urinary tract infection); life-threatening conditions (e.g., intus-
susception; toxic megacolon, appendicitis; hemolytic uremic syndrome); overfeeding;
starvation stools; antibiotic associated diarrhea (AAD). More rare etiologies can include
endocrinologic pathologies, anatomic abnormalities, and genetic disorders (e.g., con-
genital adrenal hyperplasia; blind loop syndrome; cystic fibrosis).
Large-volume stools result from a small bowel pathology, while smaller vol-
ume, bloody, and painful stools may be more likely to derive from distal, colonic
pathology.
2. Chronic diarrhea is categorized as one of four types: fatty, inflammatory, secretory, or
osmotic.
a. Fatty diarrhea contains excess stool fat, shown either by direct measurement or Sudan
staining.
b. Inflammatory diarrhea may contain mucous, blood, and/or fecal leukocytes in
the stool.
c. Secretory diarrhea is watery and has a low osmotic gap of <50 mOsm/kg (normal:
290 mOsm/kg).
d. Osmotic diarrhea is also watery but has an osmotic gap of over 125 mOsm/kg.
B. Epidemiology
1. The epidemiology of diarrhea in the United States has not been well studied, in contrast
to the developing countries. It is well established that acute diarrhea is the lead-
ing cause of childhood death worldwide. In the US population, viruses are likely
the most common cause, with bacterial infection producing most of the severe
cases. However, most studies show that less than 10% of stool cultures will show
a bacterial agent. In the United States, acute diarrhea rarely requires a significant
diagnostic evaluation and usually no more than symptomatic oral rehydration* and
reassurance.
2. Chronic diarrhea is a worldwide childhood problem, with infection being the most
common cause. In adults in developed countries, chronic diarrhea is most frequently
because of irritable bowel syndrome, inflammatory bowel disease, and malabsorption
syndromes. In developed countries, the common causes of chronic diarrhea in children
include malabsorption or maldigestion (2). Two common causes are chronic nonspecific
diarrhea and celiac disease.
III. EVALUATION. Most patients with acute diarrhea experience a mild, self-limited illness and
no laboratory testing is necessary. The challenge of the initial evaluation is to distinguish
these patients from the more serious disorders. “Red flags” associated with severe illness
include hypovolemia; bloody diarrhea; fever; more than five unformed stools in 24 hours;
184
Taylor’s DifferenTial Diagnosis Manual
severe abdominal pain; antibiotic use or hospitalization; or diarrhea in an infant, geriatric, or
immunocompromised patient (4).
Chronic diarrhea with the above “red flags” or with weight loss, systemic symptoms (fevers,
anorexia), abdominal masses, or other signs pointing to a malignancy should be worked up
beyond a physical exam.
Pediatric patients with acute diarrhea, if afebrile or febrile, and nonbloody stools usually
have viral enteritis, which do not usually require extensive lab workup. The afebrile or febrile
child with bloody diarrhea is most worrisome because of the possibility of bacterial enteritis
(usually febrile), HUS, intussusception or pseudomembranous colitis (the latter three listed
are usually afebrile), all of which warrant further evaluation.
Persistent or chronic diarrhea in the pediatric patient can warrant further evaluation.
Severe abdominal pain, dehydration, abdominal masses all may warrant further
evaluation.
A. History. Evaluation of acute diarrhea begins with a history of the onset, duration, pattern
(time of day; relation to dietary intake; urgency) and characteristics (bloody; malodorous;
floating; greasy) of the stools. Patients should be questioned regarding occupation (e.g.,
exposure to raw meat at work), travel (e.g., Mexico; mountains in the United States), sexual
practices (risk of human immunodeficiency virus and possible immunocompromise), pets,
and hobbies that could signal exposure to potential pathogens. Other key points include
inquiries regarding fevers, medication use (e.g., metformin), a dietary history, and a com-
plete past medical history (to determine risk of nosocomial infection or immunocompro-
mised status).
A concern of chronic diarrhea should thoroughly explore the onset, duration, pat-
tern, and characteristics of the stools. Major findings include significant weight loss,
diarrhea for longer than 1 year, nocturnal diarrhea, and straining with stool. Other
questions should focus on social and epidemiologic history (travel, foods, sexual
practices, living conditions, water sources), family history (e.g., inflammatory bowel
disease), associated symptoms (e.g., fever, fecal incontinence, abdominal pain, mouth
ulcers, joint pains), and aggravating or palliative factors (diet, stress, medication). A
detailed medical history evaluates for iatrogenic causes (e.g., medication; total paren-
teral nutrition in past; bowel resection; cholecystectomy; or other surgeries), immuno-
compromised state, and possible psychiatric pathology (e.g., laxative abuse; anorexia
nervosa). A thorough review of systems provides evidence of systemic processes that
can cause diarrhea such as diabetes mellitus, hyperthyroidism, rheumatologic disease,
and tumors.
In pediatric patients, in addition to the above questions, inquire about formula use,
recent feeding changes, appearance of stools, appearance of infant (“well” vs. “toxic”),
recent medications or hospitalizations, attendance at daycare, and exposure to sick
contacts.
B. Physical Examination. Examination should focus on signs of hypovolemia (e.g., dry
mucous membranes, orthostatic hypotension). Observation of fever or peritoneal signs can
indicate an invasive source (Shigella, Campylobacter) (3, 5). Abdominal signs (masses, asci-
tes, liver changes), anorectal signs (loss of tone, fissures, fistulas), lymphadenopathy, mouth
ulcers, rashes, and thyroid changes can provide diagnostic clues (6).
In pediatric patients, abdominal masses can indicate intussusception. Toxic-appearing
infants or children may be suffering from toxic megacolon, pseudomembranous colitis, or
intussusception. In children having purpuric rashes, consider HUS as a diagnosis. Peritoneal
signs may signal an appendiceal pathology.
C. Testing. See Figures 9.4.1 and 9.4. 2 for evaluation of acute and chronic diarrhea.
Threshold for imaging (e.g., ultrasound [U/S] or contrast enema for intussusception;
U/S or computed tomography for appendiceal pathology) for a pediatric patient with
bloody or febrile diarrhea should be lower, especially in a difficult to console child.
Chapter 9 • Gastrointestinal Problems
185
No
Yes
History and
Physical
Examination
Test for Fecal
Leukocytes or Fecal
Lactoferrin
InflammatoryNoninflammatory
Stool Culture
Consider Ova and
Parasite Testing
Consider
Clostridium
Difficile
No Further
Laboratory
Workup Indicated
No Further
Laboratory
Workup Indicated
“Red Flags”
Present?
Figure 9.4.1. Laboratory evaluation of acute diarrhea. (Adapted from Thielman NM, Guerrant RL.
Clinical practice. Acute infectious diarrhea. N Engl JMed 2004;350:38.)
IV. DIAGNOSIS
A. Differential Diagnosis.
See Table 9.4.1 for a differential diagnosis of diarrhea.
B. Clinical Manifestations
1. Acute diarrhea features a few well-described patterns. Traveler’s diarrhea commonly
begins 3–10 days after arrival in a foreign location where the patient is exposed to food
or water contaminated with enterotoxigenic E. coli, Salmonella, or Campylobacter,
among other bacteria. Diarrhea that develops within 6 hours of food ingestion is
commonly because of a preformed bacterial toxin (Staphylococcus aureus). Symptoms
that begin after more than 8 hours suggest either a bacterial (Clostridium perfringens
at 8–16 hours) or viral infection (3). Febrile diarrhea is suggestive of invasive bacteria,
enteric viruses, or a cytotoxic organism. If diarrhea occurs in the setting of a recent
course of antibiotic therapy or recent hospitalization, Clostridium difficile toxin should
be considered. C. difficile is being seen in those without recent hospitalizations or
recent antibiotic use and the threshold for testing for stool C. difficile toxin should also
be lower.
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Taylor’s DifferenTial Diagnosis Manual
2. Chronic diarrhea has a myriad possible underlying etiologies. However, crampy abdomi-
nal pain with bowel habits varying between diarrhea and constipation is common in
irritable bowel syndrome. Diarrhea with abdominal pain, weight loss, and fever is a
hallmark of inflammatory bowel disease. Finally, malabsorption classically presents with
weight loss and voluminous, fatty, malodorous stools. Flatulence is seen more commonly
with carbohydrate malabsorption, while pancreatic exocrine insufficiency can present
with pale stools.
*Note: Oral rehydration therapy solution can be made at home with 0.25 teaspoons
each of sodium chloride and sodium bicarbonate mixed in 1 L of water. To this, add 4
tablespoons of table sugar (3).
Figure 9.4.2. Laboratory evaluation of chronic diarrhea. ACTH, adrenocorticotropic hormone; CT,
computed tomography; O&P, ova and parasites; SPEP, serum protein electrophoresis; TSH, thyroid-
stimulating hormone. (Adapted from Fine KD, Schiller LR. AGA technical review on the evaluation and
management of chronic diarrhea. Gastroenterology 1999;116:1464.)
History and
Physical
Examination
Initial Testing: Complete Blood Count,
Chemistry, 48–72-Hour Stool Analysis
(Quantity, pH, Occult Blood, Fecal Leukocytes,
Osmotic Gap, Laxatives)
Fatty
Inflammatory
Secretory
Osmotic
Carbohydrate
Malabsorption
(Diet Review
H
2
Breath Test
Lactase Assay)
Laxative Levels
Structural Tests
(Small Bowel
X-ray, CT,
Colonoscopy)
Infection Tests
(Culture,
O&P, Viruses)
Structural Tests
(Small Bowel
X-ray, CT)
Pancreatic Tests
(Secretin,
Chymotrypsin)
Structural Tests (Small Bowel X-ray,
CT, Colonoscopy)
Infection Tests (Culture, O&P,
Giardia
)
Other Testing (Plasma Peptides, Urine
Catecholamines, TSH, ACTH
Stimulation, SPEP, Immunoglobulins,
Cholestyramine Trial)
Chapter 9 • Gastrointestinal Problems
187