Steatorrhea
Steatorrhea: Excerpt from The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
Charles L. Bryner, Jr.
Steatorrhea, the third most common cause of chronic diarrhea, manifests as a history of greasy, foul-smelling stools that leave an oily residue in the toilet bowl, increased flatulence, and weight loss.
Approach
A simple diagnostic approach is to divide the causes of steatorrhea into two categories: Does the malabsorption result from intraluminal digestion abnormality or from mucosal disease blocking absorption? Although crossover occurs between the categories, this categorization is a clinically expedient starting point.
History
A careful history and physical examination provide clues to probable diagnoses and guides the astute clinician to tests most likely to provide a definitive diagnosis. How frequent are stools? How long have symptoms been present? Any recent travel or pancreatitis (ask about level of alcohol intake)? Weight loss (Chapter 2.13)? Are there food intolerances or family history of similar problems?
A. Liver disease. Does the patient have liver disease? Acute or chronic liver disease can cause steatorrhea. Impaired synthesis or excretion of conjugated bile salts results in a bile salt deficiency and maldigestion of fats. Hepatitis, primary biliary cirrhosis, alcohol-induced liver diseases, or extrahepatic biliary obstruction (including cancer of the head of the pancreas) may be culprits in steatorrhea (Chapter 9.8). Liver function testing and appropriate use of ultrasonography or computed tomography (CT) may delineate the problem. Prolonged, severe cardiac failure or hemochromatosis can cause cirrhosis, which can produce steatorrhea.
B. Medications. Has the patient been taking any medications? Laxative abuse occurs more frequently in women than in men. Laxative abuse hastens gastrointestinal (GI) transit and can preclude adequate absorption of fats. Other drugs that can cause steatorrhea include bile acid sequestering resins (cholestyramine and colestipol), colchicine, paraaminosalicylic acid, paromomycin sulfate (Humatin), and antibiotics (e.g., tetracycline and neomycin).
C. GI problems. Is there a history of GI surgery or disorder affecting gastrointestinal motility? The short bowel syndrome following gastrectomy is a well-known cause of steatorrhea (5). Pancreatic enzymes can be inactivated by exposure to gastric acids or by bacterial overgrowth secondary to stasis of intestinal contents in a blind loop. Segmental stasis of intestinal contents can occur in diabetes or scleroderma. Stasis permits bacterial overgrowth of the affected segment. The bacteria subsequently deconjugate and metabolize the bile acids in the small bowel rather than the colon.
D. Foods. Ingestion of certain foods has been shown to cause steatorrhea. Ingestion of a large amount of peanuts or using liquid paraffin to treat constipation can result in significant steatorrhea.
Physical examination
Physical findings associated with steatorrhea are limited. Thoroughly examine the abdomen to exclude palpable masses and search for signs of alcoholic liver disease. Testing of the stool for occult blood can be helpful.
Testing
The Sudan III spot test for stool fat or quantitative determination of fecal fat in the total stool collected over 72 hours confirms steatorrhea (1,2). More than 7 g/day of fat excreted while the patient consumes a diet containing no more than 100 g/day of fat defines steatorrhea.
How severe is the steatorrhea? More than 35 g/day of fat excreted is more likely maldigestion of fats from pancreatic disease than malabsorption disorders of the intestinal mucosa.
How can the clinician differentiate mucosal disease from intraluminal digestive problems? The D-xylose test measures the absorptive capacity of the proximal small bowel mucosa. D-xylose does not require pancreatic exocrine function to be absorbed. Disorders of the intestinal mucosa that impede absorption lead to low levels of sugar in both serum and urine samples. Inadequate renal function, dehydration, or hypothyroidism can also depress urine levels, which warrants determinations of serum thyroid-stimulating hormone, blood urea nitrogen, and serum creatinine. 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 celiac sprue (3), Whipple’s disease, giardiasis, tropical sprue, or intestinal lymphoma. A biopsy is more likely to detect diseases with diffuse rather than patchy involvement of the mucosa. Some of these entities can also be diagnosed by their characteristic appearance on an upper GI series.
Serum antibody testing can now identify celiac sprue (4). Sweat chloride testing is indicated in young children because cystic fibrosis is the leading cause of steatorrhea in this age group.
What if the D-xylose test is normal? A normal test indicates proper mucosal function and so the problem is the digestion of fats within the intestinal lumen. The most frequent cause is pancreatic insufficiency (Table 9.10). Confirmation once relied on intubation of the intestine to directly measure pancreatic secretions. The newer noninvasive NBT-PABA (bentiromide) test requires pancreatic enzymes to cleave a peptide, allowing its absorption and subsequent measurement when excreted in urine. Occasionally, a secretin test will be required to measure pancreatic function. A therapeutic trial of pancreatic enzymes with improvement in symptoms is considered presumptive proof of the diagnosis. Abdominal ultrasonography, CT, or endoscopic retrograde cholangiopancreatography can also be useful in the evaluation of suspected pancreatic disease.
Disorders of the terminal ileum (Crohn’s disease, granulomatous ileitis, prior ileal resection) result in poor absorption of bile salts which then pass into the colon where bacteria deconjugate them. Poor absorption depletes the supply of bile salts, resulting in maldigestion of fats (5). The bile 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 can also be used to search for disorders of absorption.
How to test for bacterial overgrowth in the intestine? The upper small intestine is normally bacteriologically sterile, except for contaminants from the mouth and upper respiratory tract. This is maintained by peristalsis. 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. Noninvasive testing is available by the C-xylose breath test, the bile acid breath test, or the breath hydrogen test. A therapeutic trial of oral tetracycline with subsequent resolution of steatorrhea is presumptive confirmation of bacterial overgrowth, which may avoid more costly testing.
Diagnostic assessment
The differential diagnosis for steatorrhea is extensive. The degree of steatorrhea can lend clues to the source. Mild steatorrhea can occur with any disorder that causes rapid transit of intestinal contents as the shortened exposure of the fats prevents proper absorption. The proper workup of this symptom will frequently require specialized testing and procedures necessitating consultation with a gastroenterologist when the initial history and more readily available tests fail to reveal its source.
References
1. Wilson FA, Dietschy JM. Differential diagnostic approach to clinical problems of malabsorption. Gastroenterology 1971;61:911–931.
2. Olsen WA. A practical approach to diagnosis of disorders of intestinal absorption. N Engl J Med 1971;285:1358–1361.
3. Pruessner HT. Detecting celiac disease in your patients. Am Fam Physician 1998;57:
1023–1034.
4. Murray JA. Serodiagnosis of celiac disease. Clin Lab Med 1997;17:445–464.
5. Toffolon EP, Goldfinger SE. Malabsorption following gastrectomy and ileal resection. Surg Clin North Am 1974;54:647–653.
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Book Source Details
- Book Title: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter
- Author(s): Robert B. Taylor (editor)
- Year of Publication: 2000
- Copyright Details: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, Copyright © 2000 Lippincott Williams & Wilkins.
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