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9.10
I. BACKGROUND. Jaundice refers to a yellowish discoloration of the skin, sclerae, and mucous
membranes caused by the deposition of bile pigments. Normal serum bilirubin in children and
adults is less than 1 mg/dL. Typically, physical examination is unable to detect elevations of
bilirubin until the serum level exceeds 2.0–3.0 mg/dL.
II. PATHOPHYSIOLOGY
A. Etiology.
Bilirubin is formed primarily through the metabolic breakdown of heme rings,
predominantly from the catabolism of red blood cells. Dysfunction of any of the phases of bil-
irubin metabolism (prehepatic, intrahepatic, or posthepatic) can lead to jaundice. Normally,
96% of plasma bilirubin is unconjugated (indirect). When the plasma elevation is caused
predominantly by unconjugated bilirubin, the defect is likely to be the result of overproduc-
tion, impaired hepatic uptake, or abnormalities in conjugation. When the plasma elevation
includes a substantial contribution from conjugated (direct) bilirubin, then hepatocellular
disease, defective canalicular excretion, and biliary obstruction are the more likely causes.
B. Epidemiology. Among adults presenting with jaundice, serious underlying disease is com-
mon. In one study, 20% of patients with jaundice had pancreatic or biliary carcinoma, 13%
experienced gallstone disease, and 10% suffered from alcoholic cirrhosis (1). Jaundice rarely
represents a medical emergency but can present as massive hemolysis, kernicterus, ascending
cholangitis, and fulminant hepatic failure.
III. EVALUATION
A. History
1. A careful history gives multiple clues to the etiology of jaundice. Sudden onset is consis-
tent with viral hepatitis, acute biliary obstruction, trauma, or toxin-mediated fulminant
liver failure. More gradual onset is indicative of chronic liver disease (including alcoholic
cirrhosis) or malignancy. A lifelong history suggests an inherited metabolic or hemolytic
cause. Acholic stools, dark urine, and right upper quadrant (RUQ) pain, especially fol-
lowing a fatty meal, should suggest cholestasis or cholelithiasis. A history of fever or prior
biliary surgery, especially if RUQ pain is present, points to cholangitis. Charcot’s triad
of cholangitis includes fever, RUQ pain, and jaundice. In the presence of a history of
anorexia, malaise, or myalgias, a viral etiology should be considered. Typically, pruritus
or weight loss is associated with noninfectious etiologies such as primary biliary cirrhosis
in which pruritus is commonly the initial symptom (2). Numerous medications can
induce hepatocellular injury or cholestasis (see Table 9.10.1).
2. Blood transfusions, intravenous drug use, sexual contacts, travel to endemic regions, or
ingestion of contaminated foods can also expose patients to viral-related hepatocellular
injury. Past medical history and surgical history, prior episodes of jaundice, and a history
of a rheumatologic disease or inflammatory bowel disease should be examined. Family
history may reveal an inherited defect in bilirubin conjugation or transport, Wilson’s
disease, α1-antitrypsin deficiency, or hemochromatoses.
B. Physical Examination. In addition to icterus, examination findings of ascites, splenomeg-
aly, spider angiomas, caput medusa, gynecomastia, testicular atrophy, palmar erythema, or
Dupuytren’s contracture suggest chronic liver disease and portal hypertension. An abdomi-
nal examination to assess liver size and tenderness is important. Altered consciousness and
asterixis point toward liver failure. Kayser-Fleischer rings are seen in Wilson’s disease, and
Courvoisier’s sign (a painless palpable gallbladder) is suggestive of pancreatic cancer.
C. Testing
1. Initial laboratory testing for a jaundiced patient includes a complete blood count (CBC)
and peripheral smear, a fractionated serum bilirubin (total and direct), and a urinalysis.
Jaundice
Vijaya Subramanian and John C. Huscher
208
Taylor’s DifferenTial Diagnosis Manual
Additional testing should include aspartate aminotransferase/alanine aminotransferase
(AST/ALT), γ-glutamyl transpeptidase, and alkaline phosphatase. Pure liver function
should be evaluated by obtaining an albumin and a prothrombin time.
2. Further laboratory testing and imaging are predicated on obtaining the initial results
and may include serologic testing for viral hepatitis, autoimmune markers (antimito-
chondrial antibodies: primary biliary cirrhosis, or anti-smooth muscle antibodies and
antimicrosomal antibodies: autoimmune hepatitis), serum iron, transferrin and fer-
ritin (hemochromatosis), ceruloplasmin (Wilson’s disease), and α1-antitrypsin activ-
ity (α
1
-antitrypsin deficiency). Ultrasound and computed tomography (CT) can help
distinguish obstructive disease from hepatocellular disease (3).
IV. DIAGNOSIS. Historical features corroborated by physical examination and laboratory studies
should distinguish obstructive causes from nonobstructive causes, differentiate acutely present-
ing conditions from more chronic diseases, and discriminate unconjugated and conjugated
sources of bilirubin (see Table 9.10.2). Dubin-Johnson and Rotor’s syndrome are inherited
disorders that affect transportation of conjugated bilirubin.
A CBC is useful in detecting hemolysis, which is indicated by the presence of schistocytes
and increased reticulocytes on the smear. Results of the patient’s aminotransferases further refine
the differential diagnosis. Hepatocellular injury is distinguished from cholestasis by substantial
TABLE 9.10.1 Medications Associated with the Development of Jaundice
Alcohol Antibiotics
Diuretics Diuretics
Acetaminophen Oral hypoglycemics
Cholesterol-lowering agents Inhaled anesthetics
Anticonvulsants Chemotherapy agents
Sex hormones Nonsteroidal anti-inflammatory drugs
Psychotropic medications Herbal compounds
TABLE 9.10.2 Differential Diagnosis of Jaundice
Disorders of unconjugated hyperbilirubinemia
Overproduction Impaired uptake Impaired conjugation
Intravascular hemolysis Congestive heart failure Crigler-Najjar syndrome, types
I and II
Extravascular hemolysis Cirrhosis Advanced cirrhosis
Dyserythropoiesis Gilbert’s disease Wilson’s disease
Extravasation of blood into
tissues
Medication—rifampin,
probenecid
Antibiotics, ethinyl estradiol
Neonates
Disorders of conjugated hyperbilirubinemia
Extrahepatic cholestasis Intrahepatic cholestasis Hepatocellular injury
Sclerosing cholangitis Viral hepatitis See Table 9.10.1
Choledocholithiasis Alcoholic hepatitis
Pancreatitis Nonalcoholic steatohepatitis
Tumors Biliary cirrhosis
AIDS cholangiopathy Toxins
(Continued)
Chapter 9 • Gastrointestinal Problems
209
9.11
I. BACKGROUND. Rectal bleeding is a common problem primary care physicians are faced with in
the outpatient and emergency department setting. The spectrum of rectal bleeding can range from
mild to severe: bright red blood per rectum, which can present as blood on the toilet paper, a small
amount of blood in the toilet bowl, or fresh blood on the stool. This mostly tends to be chronic
intermittent bleeding. Many patients with mild rectal bleeding do not seek health care for this
problem (1). Acute massive rectal bleeding with hematochezia or melena can be life threatening (2).
II. PATHOPHYSIOLOGY. Rectal bleeding is typically a sign of local mucosal or vascular disease,
but it can also signify proximal intestinal disease in the small or large bowel. Scant or minimal
rectal bleeding is a common problem present in up to 15% of the population. Constipation
traumatizes local venous and mucosal tissues. Pregnancy can inhibit venous blood flow in the
pelvis and lead to hemorrhoid formation. Bleeding from sources proximal to ligament of Treitz
tends to produce stools that are black and tarry because of metabolism of heme.
Rectal Bleeding
Nirmal Bastola and Robert C. Messbarger
elevations in the aminotransferases (AST/ALT). A ratio of AST/ALT of >2.0 suggests alcoholic
liver disease. Infectious causes of hepatitis cause greater elevations of ALT than AST. Levels
greater than 10,000 U/L usually occur with acute injury to the liver (e.g., acetaminophen or
ischemia). Normal aminotransferases argue against hepatocellular injury and increase the likeli-
hood that hemolysis or a disorder of bilirubin processing exists. However, this can be mislead-
ing in chronic liver disease when there is little liver parenchyma left for being injured. Alkaline
phosphatase and gamma glutamyltransferase are markers for cholestasis. Ultrasound is the most
sensitive imaging technique for detecting biliary stones. CT scan provides more information
about liver and pancreatic parenchymal disease. Further imaging may be done by a gastroen-
terologist or interventional radiologist such as endoscopic retrograde cholangiopancreatography
and percutaneous transhepatic cholangiography in case of extrahepatic obstruction (4).
REFERENCES
1. Reisman Y, Gips GH, Lavelle SM, et al. Clinical presentation of (subclinical) jaundice.
Hepatogastroenterology 1996;43:1190.
2. Leuschner U. Primary biliary cirrhosis-presentation and diagnosis. Clin Liver Dis 2003;7:741.
3. Namita Roy Chowdury, Jayan Roy Chowdury, Diagnostic approach to the patient with jaundice
or asymptomatic hyperbilirubinemia. Accessed at http://www.uptodate.com/contents/diagnostic-
approach-to-the-patient-with-jaundice-or-asymptomatic-hyperbilirubinemia?source=search_result&se
arch=jaundice&selectedTitle=1∼150.
4. Sean PR, Rebecca K. Jaundice in the adult patient. Am Fam Physician 2004;69(2):299–304.
TABLE 9.10.2 Differential Diagnosis of Jaundice
Disorders of unconjugated hyperbilirubinemia
Strictures Infiltrating diseases
Parasitic infections Total parenteral nutrition
Pregnancy
End-stage hepatic disease
AIDS, acquired immunodeficiency syndrome.
(Continued)
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Taylor’s DifferenTial Diagnosis Manual
III. EVALUATION
A. Initial Evaluation.
The initial evaluation should determine the acuity and hemodynamic
stability of the patient and establish the origin of the bleeding as upper or lower gastrointes-
tinal (GI) tract in nature. Potential hemodynamic compromise warrants volume resuscita-
tion with two large-bore intravenous lines, preferably in an intensive care setting involving a
gastroenterologist on the team. If rectal bleeding is minimal or has stopped, and the patient
is stable, evaluation can occur in the outpatient setting (3–5, 9).
B. History and Differential Diagnosis (2). By far, the most common anorectal bleeding
source is hemorrhoidal disease. Risks of hemorrhoids increase with advancing age, pregnan-
cy, prolonged sitting or standing, chronic diarrhea, or constipation. Associated complaints
from hemorrhoids include anal pruritus, pain, and prolapse. Other anorectal sources of
minimal bleeding include anal fissures, polyps, proctitis, rectal ulcers, and cancer (4). It is
also necessary to take the history of any use of blood thinners.
1. Upper GI tract
Peptic ulcer disease: Use of aspirin, nonsteroidal anti-inflammatory drugs, or tobacco
Esophageal varices: Alcohol abuse; jaundice; signs of portal hypertension, including asci-
tes, palmar erythema, spider angiomata, hepatomegaly, splenomegaly, and rectal varices
Mallory-Weiss tear: Bleeding preceded by vomiting, retching, or seizures
Gastric cancer: Left supraclavicular adenopathy; palpable mass; abdominal pain; weight
loss; cachexia
2. Lower GI tract
Diverticular disease: Age >60 years; painless bleeding; possible recent constipation
Arteriovenous malformations: Age >60 years; painless bleeding; chronic renal failure
Colonic neoplasms: Age >50 years; abdominal pain; weight loss; muscle wasting;
protein calorie malnutrition; right-sided colon cancer may be associated with palpable
right-sided abdominal mass; hepatomegaly; liver nodules; history of adenomatous polyps
or long-standing ulcerative colitis; prior exposure to ionized radiation; family history of
familial polyposis coli or cancer family syndrome (6).
3. Inflammatory bowel disease
Ulcerative colitis: starts in younger patients (20–40 years of age); usually involves the
rectum; associated with diarrhea mixed with blood and mucus
Crohn’s disease: starts in younger patients (20–40 years of age); perianal, peritoneal,
and/or abdominal wall fistulas may be associated
Radiation colitis: History of radiation treatment to abdomen and/or pelvis
Hemorrhoids: Perianal mass may be painful (external hemorrhoid) or painless (internal
hemorrhoid); commonly starts in younger patients; associated with constipation, preg-
nancy, or postpartum period
Anal fissures: More common in patients with history of constipation; associated with
severe sharp pain occurring with straining on defecation; pain resolves within an hour
after defecation; commonly starts at 20–40 years of age
Colon tuberculosis: History of pulmonary tuberculosis or past exposure to tuberculosis
Aortoduodenal fistula: History of abdominal aortic aneurysm surgically repaired with
synthetic vascular graft placement
C. Workup
1. Initial laboratory tests to assess hemodynamic stability and clotting ability are complete
blood count to assess for anemia, type and screen, stool hemoccult test, serum blood urea
nitrogen and creatinine, and coagulation panel (9).
2. Imaging studies can be directed at the most likely source of bleeding. Younger patients with
intermittent mild rectal bleeding can be evaluated with anoscopy or flexible sigmoidoscopy.
Persons older than 50 years of age with painless bleeding are assumed to have colon cancer
until proved otherwise by colonoscopy, even if the rectal examination is abnormal.
IV. DIAGNOSTIC PROCEDURES
A. Chronic Intermittent Rectal bleeding.
Colonoscopy is the diagnostic tool of choice
in a hemodynamically stable patient with a suspected lower GI source of bleeding (2, 7).
Double-contrast barium enema with sigmoidoscopy may be an alternative in patients
Chapter 9 • Gastrointestinal Problems
211
who have a relative contraindication to colonoscopy. Some physicians may consider a lim-
ited evaluation of the anorectosigmoid area with sigmoidoscopy in patients younger than 40
years because only 5% of colorectal cancer cases occur in this population (8). In addition,
the most common cause of rectal bleeding in patients younger than 30 years is anal pathol-
ogy such as hemorrhoids or fissures, which can be diagnosed with anoscopy (9). In cases
where the source of bleeding cannot be confirmed, or if bleeding and anemia continue, a
colonoscopy should be performed for complete evaluation of the large bowel (10). Small
bowel sources of GI bleeding are uncommon, accounting for only 2–10% of all cases.
Because of its location, evaluation is technically difficult. For these reasons, therefore, evalu-
ation of the small bowel is less commonly indicated (11, 12). However, when endoscopy is
nondiagnostic, the small bowel should be evaluated. Obscure GI bleeding is the recurrent
blood loss without an identifiable source of bleeding even after esophagogastroduodenos-
copy (EGD) and colonoscopy. When evaluation of the small bowel is considered necessary,
several procedures can be employed including barium-contrast upper GI series with small
bowel follow through (SBFT), capsule endoscopy, angiography (requires blood loss at a rate
of 1 mL/min), technetium radiolabeled RBC scan (requires blood loss at a rate of 0.1 mL/
min), and push enteroscopy (13).
B. Acute Massive Rectal Bleeding. Acute massive rectal bleeding frequently arises from
an upper GI source. The diagnostic workup begins with an EGD. If the patient is not
experiencing hematemesis and endoscopy is not immediately available, a nasogastric tube
may be placed for gastric lavage while awaiting endoscopy. If no blood is returned and bile
is identified, an upper GI source is much less likely, and the workup can focus on the large
bowel. Colonoscopy is one of two diagnostic tools of choice used to evaluate acute lower GI
bleeding. Colonoscopy may be performed urgently or electively, depending on the patient’s
hemodynamic status and risk stratification criteria (2, 7, 11, 14, 15).
REFERENCES
1. Talley NJ, Jones M. Self-reported rectal bleeding in a United States community: prevalence, risk fac-
tors, and health care seeking. Am J Gastroenterol 1998;93:2179–2183.
2. Maltz C. Acute gastrointestinal bleeding. Best Pract Med 2003;16:1–19. Accessed online March 11, 2005.
3. Bounds B, Friedman L. Lower gastrointestinal bleeding. Gastroenterol Clin 2003;32:1107–1125.
4. Gopal D. Diseases of the rectum and anus: a clinical approach to common disorders. Clin Cornerstone
2002;4:34–48.
5. Peter D, Dougherty J. Evaluation of the patient with gastrointestinal bleeding: an evidence based
approach. Emerg Med Clin North Am 1999;17:239–261.
6. Manning LL, Dimmitt, Dimmitt SG, Wilson GR. Diagnosis of gastrointestinal bleeding in adults.
Am Fam Physician 2005;71(7):1339–1346.
7. Eisen GM, Dominitz JA, Faigel DO, et al. An annotated algorithmic approach to acute lower gastro-
intestinal bleeding. Gastrointest Endosc. 2001;53:859–863.
8. Steele GD Jr. The National Cancer Data Base report on colorectal cancer. Cancer 1994;74:1979–1989.
9. Lewis JD, Brown A, Localio AR, Schwartz JS. Initial evaluation of rectal bleeding in young persons:
a cost-effectiveness analysis. Ann Intern Med 2002;136:99–110.
10. Fine KD, Nelson AC, Ellington RT, Mossburg A. Comparison of the color of fecal blood with the
anatomical location of gastrointestinal bleeding lesions: potential misdiagnosis using only flexible
sigmoidoscopy for bright red blood per rectum. Am J Gastroenterol 1999;94:3202–3210.
11. Fallah MA, Prakash C, Edmundowicz S. Acute gastrointestinal bleeding. Med Clin North Am
2000;84:1183–1208.
12. Ell C, Remke S, May A, Helou L, Henrich R, Mayer G. The first prospective controlled trial compar-
ing wireless capsule endoscopy with push enteroscopy in chronic gastrointestinal bleeding. Endoscopy
2002;34:685–689.
13.
Zuckerman GR, Prakash C, Askin MP, Lewis BS. AGA technical review on the evaluation and man-
agement of occult and obscure gastrointestinal bleeding. Gastroenterology 2000;118:201–221.
14. Wilcox CM, Clark WS. Causes and outcome of upper and lower gastrointestinal bleeding: the Grady
Hospital experience. South Med J 1999;92:44–50.
15. Zuccaro G Jr. Management of the adult patient with acute lower gastrointestinal bleeding. American
College of Gastroenterology. Practice Parameters Committee. Am J Gastroenterol 1998;93:1202–1208.
212
Taylor’s DifferenTial Diagnosis Manual
9.12
I. BACKGROUND. Steatorrhea results from fat malabsorption. It is quantitatively defined as the
presence of more than 7 g of fat in the stool during a 24-hour period while the patient is on
a diet containing no more than 100 g of fat per day. It manifests as a history of greasy, foul
smelling stools that leave an oily residue in the toilet bowl, increased flatulence, and weight loss.
Normally more than 90% of daily dietary fat is absorbed into the general circulation, but any
defects in the processes can reduce this uptake and lead to fatty diarrhea.
II. PATHOPHYSIOLOGY. This can result from defects in any of the three phases required for
proper digestion and absorption of fat.
A. Luminal Phase. This phase includes substrate (fat) hydrolysis by the help of digestive
enzyme, followed by fat solubilization in the presence of bile salts.
B. Mucosal Phase. This can be also called as absorptive phase where mucosal uptake and
reesterification occur. This phase is defective in celiac disease where changes occur in the
mucosal structure.
C. Postabsorptive process. During this phase, the chylomicrons are formed and transported
to the lymphatic system.
1. Etiology. Chronic pancreatitis is the most common cause of steatorrhea, which results
from ethanol abuse. It causes steatorrhea due to pancreatic lipase deficiency. Steatorrhea
is evident only when more than 90% of pancreatic exocrine insufficiency occurs (2).
Other causes are cystic fibrosis and pancreatic duct obstruction. Cirrhosis and biliary
obstruction may cause mild form of steatorrhea due to deficiency of intraluminal bile
acid concentration. Similar pathology can be seen in bacterial overgrowth in the small
intestine which may deconjugate bile acids and alter micelle formation, thus impairing
fat digestion. Bacterial overgrowth can be seen in stasis from a blind loop, small bowel
diverticulum, or dysmotility, which is very common in the elderly.
Mucosal malabsorption can result from a variety of enteropathies, the most common
being celiac disease. Celiac disease is characterized by villous atrophy and crypt hyperplasia
in the proximal small bowel; these mucosal changes can cause fatty diarrhea. Other causes
of fat malabsorption due to mucosal changes are tropical sprue, mycobacterium avium
intracellulare infection of the intestinal mucosa, and AIDS. Abetalipoproteinemia is a very
rare defect of chylomicron formation and fat malabsorption seen commonly in children.
Giardiasis is a protozoal infection that also causes fat malabsorption. Other miscellaneous
causes are neomycin, colchicine, and cholestyramine consumption. Amyloidosis and
chronic small bowel ischemia can also be considered as causes of steatorrhea (1).
Postmucosal malabsorption of fat can result from a very rare condition called intes-
tinal lymphangiectasia or acquired lymphatic obstruction secondary to trauma, cardiac
disease causing congestion of the mucosal lining. In these conditions, there is fat malab-
sorption and enteric losses of protein and there is associated lymphocytopenia. It is seen
that carbohydrate and amino acid absorption are preserved.
2. Epidemiology. The incidence and prevalence of steatorrhea are difficult to estimate because
this condition arises from an array of diverse underlying conditions that are difficult to
amass into an overall figure. These other conditions are nonreportable illnesses or surgical
procedures performed for other reasons and so are not readily tabulated in the literature.
III. EVALUATION
A. History.
A careful history often provides clues to probable diagnoses and guides the clinician to
do tests that are most likely to provide a definitive diagnosis or helps to narrow down the differ-
ential diagnosis for steatorrhea. Abdominal pain in the epigastric region will be seen in patients
Steatorrhea
Monica Sarawagi and Milton (Pete) Johnson
Chapter 9 • Gastrointestinal Problems
213
TABLE 9.12.1 Causes of Pancreatic Exocrine Insufficiency
Alcohol-induced liver diseases Cystic fibrosis
Chronic pancreatitis Zollinger-Ellison syndrome
Hypertriglyceridemia Gastrectomy
Cancer of the pancreas Vagotomy
Resection of the pancreas Hemochromatosis
Blockage of the pancreatic duct Shwachman-Diamond syndrome
Traumatic pancreatitis Trypsinogen deficiency
Hereditary pancreatitis
α
1
-Antitrypsin deficiency
Enterokinase deficiency Somatostatinoma
Graft vs. host disease
with chronic pancreatitis. Jaundice will be seen in cholestasis. Cramping, abdominal pain,
bloating, and flatulence in addition to steatorrhea will be seen in celiac disease and giardiasis.
B. Physical Examination. Physical findings associated with steatorrhea are limited. A thor-
ough examination of the abdomen to exclude palpable masses should be undertaken along
with a search for signs of alcoholic liver disease. There might be evidence of lack of subcuta-
neous fat, temporal wasting, signs suggestive of end-stage cirrhosis like palmar erythema and
telangiectasias. Other findings noted can be skin jaundice suggesting biliary obstruction.
C. Testing. The role of laboratory and radiologic investigation is
1. Confirmation of steatorrhea.
2. Determination of the type of steatorrhea.
3. Assessment for conditions that cause fat malabsorption.
Patients with suspected steatorrhea can be tested for fecal fat presence by any of these
methods:
a. Sudden stain of a random sample of homogenized stool.
b. Steatocrit is a quantitative measure of fat as a proportion of a whole centrifuged
homogenized stool sample. A spot acid steatocrit level (normal less than 10%) has
been reported as having a sensitivity of 100% and a specificity of 95% when compared
with 72-hour quantitative fat analysis.
c. The gold standard for diagnosis remains the quantitative determination of fecal fat
from stool samples collected over 72 hours while the patient ingests a diet with a
limited fat content. Once true steatorrhea is demonstrated, further testing helps deter-
mine the underlying disorder.
d. Measurement of fecal elastase-1 is a simple noninvasive test for pancreatic exocrine
insufficiency (3).
e. The d-xylose test measures the absorptive capacity of the proximal small bowel mucosa (4).
d-xylose does not require pancreatic exocrine function to be absorbed. Disorders of the
intestinal mucosa that impede absorption lead to low levels of the sugar in both serum
and urine samples. Inadequate renal function, dehydration, or hypothyroidism can also
depress urine levels, so determinations of serum thyroid-stimulating hormone, blood
urea nitrogen, and creatinine are warranted. Bacterial overgrowth of the small intestine
can also produce an abnormal d-xylose test. An abnormal d-xylose test should prompt
referral for small intestine biopsy to search for evidence of mucosal diseases including
gluten enteropathy, Whipple’s disease, giardiasis, tropical sprue, or intestinal lymphoma.
Some of these entities may also be diagnosed by their characteristic appearance on an
upper gastrointestinal series. A normal d-xylose test indicates proper mucosal function
and so the problem is usually the digestion of fats within the intestinal lumen. The most
frequent etiology is pancreatic insufficiency (see Table 9.12.1). A secretin test may be
required to measure pancreatic function. A therapeutic trial of pancreatic enzymes with
improvement in symptoms is considered presumptive proof of the diagnosis. The bile
214
Taylor’s DifferenTial Diagnosis Manual
salt breath test, a nuclear medicine study, measures bile acid absorption. Because the
terminal ileum is also the site of vitamin B12 absorption, the Schilling test may also be
utilized to search for disorders of absorption. Disorders of the terminal ileum (Crohn’s
disease, granulomatous ileitis, and prior ileal resection) result in poor absorption of bile
salts, which then pass into the colon where bacteria deconjugate them. Poor reabsorp-
tion depletes the supply of bile salts, resulting in maldigestion of fats. Noninvasive
testing for small bowel bacterial overgrowth (SBBO) is available by the c-xylose breath
test, the bile acid breath test, or the breath hydrogen test (6). A therapeutic trial of
oral tetracycline with resolution of steatorrhea is presumptive confirmation of bacte-
rial overgrowth, avoiding a more costly testing. The upper small intestine is normally
bacteriologically sterile except for contaminants from the mouth and upper respiratory
tract. Aspiration of fluid through an endoscope or a small intestine tube placed under
fluoroscopic guidance that yields a bacterial colony count greater than 100,000/mL is
diagnostic of SBBO. Abdominal computed tomography (CT) scan with oral and IV
contrast can be done to look for small bowel lymphoma, Crohn disease, or pancreatic
abnormalities. Alternatively, ultrasound of the pancreas can be helpful to look for any
structural abnormality of the pancreas in the absence of CT scan.
D. Genetics. Genetics plays little role in this disorder with the exception of those conditions
with familial tendencies such as cystic fibrosis, gluten enteropathy, and acanthocytosis. In
approximately 25% of cases, Zollinger-Ellison syndrome occurs in association with a genetic
syndrome, multiple endocrine neoplasia type 1 (5).
IV. DIAGNOSIS
A. Differential diagnosis.
The following conditions can be considered as some of the com-
mon causes of steatorrhea:
o Chronic pancreatitis
o Bacterial overgrowth syndrome
o Ileal disease
o Celiac disease
o Intestinal lymphangiectasia
o Graves disease
o Lipase inhibitors, for example, tetrahydrolipstatin (orlistat).
The degree of steatorrhea can lend clues to the source. Mild steatorrhea can occur with any disor-
der that causes rapid transit of intestinal contents, because the shortened exposure of the fats prevents
proper absorption. The explosive urgent diarrhea of irritable bowel syndrome can mimic steatorrhea,
but the fecal fat content does not usually meet the criteria for true steatorrhea. The proper workup
of this symptom frequently requires specialized testing and procedures, necessitating consultation
with a gastroenterologist if initial history and the more readily available tests fail to reveal its source.
Treatment
Patients with steatorrhea may or may not present with diarrhea; dietary restriction of fat plays a important
role in controlling episodes of diarrhea. Initial fat intake can be restricted to 50 g/d and then gradually
increased until diarrhea appears. Maximum allowed quantity is usually not more than 100 g/d distributed
equally among four meals. For patients with pancreatic insufficiency, pancreatic extract containing 30,000–
50,000 units of lipase can be given. This dose of lipase is distributed throughout each of four daily meals.
REFERENCES
1. Gruy-Kapral C, Little KH, Fordtran JS, et al. Conjugated bile acid replacement therapy for shortbowel
syndrome. Gastroenterology 1999;116:15.
2. Grigg AP, Angus PW, Hoyt R, et al. The incidence, pathogenesis and natural history of steatorrhea
after bone marrow transplantation. Bone Marrow Transplant 2003;31(8):701–703.
3. Beharry S, Ellis L, Corey M, et al. How useful is fecal pancreatic elastase 1 as a marker of exocrine
pancreatic disease? J Pediatr 2002;141(1):84–90.
4. Craig RM, Ehrenpreis ED. D-xylose testing. J Clin Gastroenterol 1999;29(2):143–150.
5. Domínguez-Muñoz JE. Pancreatic exocrine insufficiency: diagnosis and treatment. J Gastroenterol
Hepatol 2011;26(Suppl. 2):12–16.
6. Ziegler TR, Cole CR. Small bowel bacterial overgrowth in adults: a potential contributor to intestinal
failure. Curr Gastroenterol Rep 2007;9(6):463–467.
Chapter 9 • Gastrointestinal Problems
215
CHAPTER 10
Renal and Urologic Problems
David M. Quillen
10.1
I. BACKGROUND. Dysuria is defined as “painful urination.” Acute dysuria is a frequent problem
seen in ambulatory practices, accounting for >3 million office visits a year. The most common
diagnosis given for patients with dysuria is a urinary tract infection (UTI). The estimated cost
of traditional management of acute UTIs approaches $1 billion per year in the United States.
Although a UTI is the most common cause of dysuria symptoms, many other causes need to be
accurately diagnosed. The differential diagnosis for patients with dysuria can be separated into
broad categories. With a few notable exceptions, the differential diagnoses for men and women
are similar, although the incidences are greatly different and change with age (1, 2).
II. PATHOPHYSIOLOGY
A.
Causes of dysuria—female (3)
1. Infectious
a. Cystitis, lower UTI, with or without pyelonephritis
b. Urethritis caused by a sexually transmitted disease (STD): Chlamydia, Neisseria gonor-
rhoeae, herpes simplex virus (HSV)
c. Vulvovaginitis—bacterial vaginosis, trichomoniasis, yeast, genital HSV
2. Noninfectious—trauma, irritant, allergy, atrophy, sexual abuse
B. Causes of dysuria—male (4)
1. Infectious
a. Urethritis caused by Chlamydia, N. gonorrhoeae, yeast (uncircumcised → balanitis), HSV
b. Cystitis (if culture positive, possible anatomic abnormality, further workup indicated)
c. Prostatitis, acute more common than chronic (5)
2. Noninfectious
a. Penile lesions, trauma, sexual abuse
b. Benign prostatic hypertrophy (BPH) particularly in older men (1). Infection can be
evident but is primarily an obstructive process
III. EVALUATION
A. History.
A good general history is critical and can help direct further questions. Careful ques-
tioning about other associated symptoms and risk factors is the key to sorting out the diagnosis.
1. Internal Dysuria versus External Dysuria
a. Internal dysuria is where the discomfort seems to be centered inside the body and
begins before or with the initiation of voiding.
i. Inflammation of the bladder or urethra
b. External dysuria is when the discomfort appears after voiding has initiated.
ii. Vaginitis, vulvar inflammation, or external penile lesions
2. Other important history items
a. New sex partner → STD cause
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b. Diaphragm usage → bladder infection
c. Gradual onset → urethritis and external causes
d. Suprapubic pain, costovertebral angle tenderness, fever, and flank pain → pyelonephritis
e. Older men → questioning about BPH
B. Physical Examination. The examination is essential in narrowing the diagnosis.
1. Rule out pyelonephritis
a. Fever
b. Flank tenderness
c. Suprapubic tenderness
2. Genital examination
a. Speculum examination in women
b. Foreskin retraction in uncircumcised men
c. Prostate examination
3. Collection of samples for testing
a. HSV lesions
b. Discharge—yeast, bacterial vaginosis, gonorrhea, and trichomoniasis
c. Trauma
C. Testing
1. Urine analysis dipstick test—nitrates and leukoesterase (urea-fixing bacteria and leukocytes)
2. Direct microscopic examination of the urine can detect the following:
a. Leukocytes, bacteria, and blood
b. Pyuria (defined as white blood cell count >10/mm
3
of urine)
3. Urine culture: takes up to 48 hours
IV. DIAGNOSIS. Given the many causes of dysuria, an accurate diagnosis can be difficult without
a thorough approach to each patient. Because most causes have other associated symptoms
and findings, a diagnosis can usually be made with a carefully taken history, a focused physical
examination, and appropriate laboratory tests. Separating an uncomplicated UTI or STD from
the more serious pyelonephritis and other possible diagnoses is the challenge in these patients.
REFERENCES
1. Bremnor JD, Sadovsky R. Evaluation of dysuria in adults. Am Fam Physician 2002;65(8):1589–1596.
2. Johnson JR, Stamm WE. Diagnosis and treatment of acute urinary tract infections. Infect Dis Clin
North Am 1987;4(1):773–791.
3. Kurowiski K. The woman with dysuria. Am Fam Physician 1998;57(9):2155–2164, 2169–2170.
4. Ainsworth JG, Weaver T, Murphy S, et al. General practitioners’ immediate management of men
presenting with urethral symptoms. Genitourin Med 1996;72(6):427–430.
5. Roberts RO, Lieber MM, Rhodes R, et al. Prevalence of a physician-assigned diagnosis of pros-
tatitis: the Olmsted County study of urinary symptoms and health status among men. Urology
1998;51(4):578–584.
10.2
I. BACKGROUND. Hematuria, defined as “blood in the urine,” is frequently an outpatient com-
plaint. It can manifest as gross (macroscopic) hematuria with obvious reddish discoloration,
greater than 50 red blood cells/high power field (400×), or microscopic hematuria detected
with a dipstick followed by a microscopic examination. Although there is existing controversy
pertaining to what constitutes microhematuria, the American Urological Association defines
Hematuria
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