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Updated: 12/26/06 02:17 PM |
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| HOME | HEAL | EDUCATE | RESEARCH | DIRECTORY | OUTREACH |
Authors: D.R. Saunders, C.E. Rubin, and J.D. Ostrow
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Download Chapter ♦ Download Lecture Slides & Notes
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U. Diagnosis of Small Intestinal Diseases
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1. History of Malabsorption
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Suspect malabsorption by subtle aspects of the history |
If a patient is emaciated although he or she overeats and if he or she complains of abdominal distension with bulky foul-smelling stools, then anybody would suspect malabsorption. The mark of the accomplished physician is to suspect malabsorption in a seemingly well-nourished patient with more subtle complaints. The tip off may be the fact that the patient eats far more than one would expect for a person of his or her weight. Since, dietary histories are tedious and notoriously inaccurate, the best approach to establish a disparity between weight and intake is a comparative one: Does the person eat more than his or her heavier mate, siblings, friends, or fellow students?
Malabsorption can present obscurely as a manifestation of a single deficiency. If a patient has iron lack anemia and is not bleeding, then iron malabsorption should be suspected, especially if the patient's anemia did not respond to oral iron treatment. If a patient develops edema (swelling), he or she may be found to have a low plasma protein (low intravascular oncotic pressure permits excess fluid to enter the extracellular compartment). If you exclude protein leak via a damaged kidney or inadequate protein synthesis by a damaged liver, then look to the small bowel; it may be losing protein for various pathologic reasons. If the patient has muscle twitching and cramps or bone pain, these may be symptoms of calcium or magnesium malabsorption. If a patient bruises easily, or bleeds too long after a cut, prothrombin deficiency may be the cause. Prothrombin manufacture depends on vitamin K absorption and this may rarely be the only clue to malabsorption. A patient may not enter puberty when expected and growth may be retarded. These findings may be caused by occult malabsorption or occult inflammatory bowel disease. |
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2. Physical Examination In Malabsorption
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A stool exam is mandatory in anyone with steatorrhea or diarrhea. |
The patient may have the characteristic celiac appearance with thin extremities and a swollen abdomen. Of all the physical findings in a patient with malabsorption, the most constant one is the typical odor of rancid fat on the speck of stool on the rectal examining finger, confirmed by a qualitative fecal fat stain (see below). |
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Malabsorption may cause myriad combinations of symptoms and signs |
Skin pallor and pale conjunctivae suggest anemia; if the tongue is smooth and red or if vibration sense has been lost in the legs, this suggests a vitamin B12 deficiency anemia. Dependent edema is ankle swelling after being up all day long or swelling over the sacrum after being in bed all night. This sign can be elicited by pressing the suspicious area firmly with the fingertips and seeing if a depression persists (pitting edema). Protein deficiency is one cause of dependent edema. Chvostek's sign is a facial twitch in response to tapping the facial nerve in front of the right ear lobe and Trousseau's sign is present when the hand flexes and goes into spasm after application of a blood pressure cuff to the upper arm; both signs suggest muscle irritability secondary to Ca++ or Mg++ deficiency. Many "black and blue" marks on the skin when the patient has had no trauma suggest clotting defects and may reflect prothrombin deficiency secondary to malabsorption of its precursor, vitamin K.
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3. Laboratory Methods for Confirming Malabsorption
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| Qualitative Sudan stain for fecal fat |
One should first look microscopically for excess fat in the stool. A pinhead speck of stool is emulsified by mixing it thoroughly with one drop of water on a slide; one drop of an ethanolic Sudan stain and another of glacial acetic acid are then added, and the whole suspension mixed and covered with the cover slip. The slide is heated gently over an alcohol lamp and brought to a boil three times. The acetic acid changes the soaps to fatty acids; the heat promotes dispersion of lipid globules in which the stain becomes dissolved and dissipates the ethanol. While warm, the slide should be examined microscopically under 40 and 100 magnifications. Only an obvious excess of fat globules means anything. Over 95% of patients with steatorrhea have a positive test.
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| Proof of malabsorption by quantitative fecal fat determination |
Definitive screening for steatorrhea involves chemical analysis of a 24-hour stool specimen, which can be best collected in a 1-gallon paint can. If the characteristic rancid odor is present and if its weight for 24 hours is obviously increased (300 gm/d), there may be little doubt of steatorrhea. The stool may be lighter colored than normal (custard appearance) and in pancreatogenous steatorrhea free oil may be evident (unhydrolyzed triglyceride). The grams of fat in the stool for 24 hours can be determined by analysis. On the usual American diet more than 6 grams of fat in the stool daily suggests steatorrhea.
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Accessory tests, to distinguish digestive from mucosal defects, are less definitive: Urinary d-xylose excretion Serum carotene |
Simple tests are used to screen for steatorrhea. Some use the blood carotene level and others use urinary d-xylose determinations. The accuracy of both of these tests in proving malabsorption is only 75%. They tend to miss mild malabsorption and they have other sources of error. Carotene is a nonpolar substance and requires micelle formation and an intact jejunal mucosa to be absorbed. Blood carotene levels may be normal in pancreatogenous steatorrhea because some micelles are formed and because the intestinal absorptive cell is intact. D-xylose is absorbed primarily by a passive mechanism and is slowly metabolized in the body; thus, its urinary excretion should reflect the ability of the mucosa to absorb it. This test has all of the defects of an oral tolerance test, i.e., urinary excretion may be spuriously low if gastric emptying is delayed, if renal function is impaired, if the extravascular space is expanded or if effective circulating blood volume is decreased. D-xylose may be metabolized by bacteria if there is proximal bacterial overgrowth in stasis syndrome. A very low blood carotene, or a low urinary d-xylose excretion after an oral dose of xylose, suggests significant loss of jejunal mucosal function. Small bowel biopsy is a much more direct and accurate method of determining mucosal injury and this is the method which we use.
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| Blood folate often low in jejunal disease |
Folic acid is absorbed in the proximal small intestine and therefore blood folate levels offer an indirect indication of jejunal absorption. Vitamin B12 is absorbed in the ileum and radioactive vitamin B12 absorption test will indicate ileal malfunction if it is abnormally low despite the addition of intrinsic factor to the test dose.
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| Lactase deficiency a common feature of mucosal disease |
If lactase deficiency is suspected as a cause of symptoms this can be determined by a simple screening test. Fifty grams of lactose are swallowed in 250 cc of water. The test is positive if the patient develops diarrhea several hours later (often with excess flatus), with a high content of glucose in the stool.
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4. Small Bowel Biopsy
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| Small bowel biopsy is definitive in diagnosing mucosal abnormalities causing malabsorption |
The small bowel mucosa can be biopsied during upper endoscopy without undue danger or discomfort. There are more than ten mucosal diseases which are now recognized as having specific diagnostic pathologic pictures which can be recognized by this method. There is a group of other diseases including celiac sprue where the pathologic picture is dramatic but nonspecific , i.e., the mucosa is flat and the villi are absent. In these diseases the diagnosis is made by some confirmatory clinical maneuver such as the response to a gluten-free diet in celiac sprue. Small bowel biopsy is particularly useful in distinguishing a mucosal cause of malabsorption from an intraluminal one. It should be used when suspicion is high for a mucosal abnormality causing malabsorption.
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Next Section (V): Crohn’s Disease » |
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