What is STEATORRHEA?

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stuart13
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What is STEATORRHEA?

Post by stuart13 » Sun Jan 31, 2010 12:59 pm

STEATORRHEA is distinctly different from diarrhea and loose bowels.

The following is lifted and edited from a medical web-site so that you may be better informed...................


Steatorrhea is not really a condition but a symptom in which fecal matter is frothy, foul-smelling and floats because of a high fat content. It is common in malabsorption syndromes.



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Steatorrhea is excessive excretion of fecal fat.

Causes & Development

Both digestive and absorptive disorders can cause steatorrhea. Digestive disorders affect the production and release of the enzyme lipase from the pancreas, or bile from the liver, which are substances that aid digestion of fats; absorptive disorders disturb the absorptive and enzyme functions of the intestine. Any condition that causes malabsorption or maldigestion is also associated with increased fecal fat. As an example, children with cystic fibrosis have mucus plugs that block the pancreatic ducts. The absence or significant decrease of the pancreatic enzymes, amylase, lipase, trypsin, and chymotrypsin limits fat, protein and carbohydrate digestion, resulting in steatorrhea due to fat malabsorption.

The underlying condition causes of steatorrhea include:

* Malabsorption
* Malabsorption of fats in small intestine
* Pancreatitis
* Celiac disease
* Sprue

Increased fecal fat levels are found in cystic fibrosis, malabsorption secondary to other conditions like Whipple's disease or Crohn's disease, maldigestion secondary to pancreatic or bile duct obstruction, and "short-gut" syndrome secondary to surgical resection, bypass, or congenital anomaly.

Signs & SymptomsSteatorrhea is suspected when the patient has large, "greasy", and foul-smelling stools. Signs of steatorrhea include:

* Foul-smelling feces
* Bulky stool
* Pale stools
* Loose stools
* Greasy stools

Diagnosis & Tests

Pancreatic and small intestinal diseases are the major causes of steatorrhea. In order to confirm the presence of pancreatic disease, a structural abnormality in the pancreas is sought by abdominal X-ray (calcification), ultrasound, CT scan, or ERCP.

When small intestinal disease is suspected as the source of steatorrhea, function tests of intestinal absorption may be performed. D-xylose absorption will test proximal small bowel function. The Schilling tests (I and II) and bile acid breath tests assess distal small bowel function. The Schilling test with antibiotics (part III) and the bile acid breath test will facilitate a diagnosis of bacterial overgrowth. Structural abnormalities of the small bowel are detected by barium studies and/or biopsy. Less common causes of steatorrhea require further diagnostic testing (e.g.duodenal aspiration for Giardia, serum gastrin for Zollinger-Ellison disease, etc.).

Treatment & Prevention

The dietary therapy of steatorrhea requires knowledge of the cause of the disease associated with the steatorrhea. Once the cause is established, then an approach to the dietary management can be adopted. Recommendations for either the treatment of the primary disease, limitation of fat intake, nutritional support, or pancreatic-enzyme replacement are made depending on the disease process.

In cases of chronic pancreatitis, a marked reduction in the secretion of pancreatic enzymes leads to steatorrhea. The first requirement in the treatment of steatorrhea is the ingestion of potent enzymes. A total of 30,000 units of lipase should be consumed with each meal. A few mouthfuls of the meal should be consumed priorto ingesting any enzymes in orderto protect enzymes against the harmful effects of gastric acid.

Therapy with potent pancreatic enzymes usually reduces the passage of bulky stools and permits significant weight gain. If this therapy is ineffective, however, the next important step in treatment of steatorrhea is the protection of enzymes against gastric acid. This protection can be achieved by either reducing the secretion of hydrogen ions with an H2 blocker (while continuing therapy with the same potent enzymes) or by ingesting pH-sensitive enteric-coated pancreatic enzymes. These enteric-coated preparations do not release enzymes until the milieu becomes alkaline (presumably within the duodenum).

The pH-sensitive enteric-coated enzymes may fail either because the pH within the stomach becomes alkaline prematurely (thereby permitting the premature release of enzymes which may then be exposed to a subsequent acid milieu) or because the size of the microspheres that contain the enzymes may be too large to be emptied in timely fashion from the stomach.

If pancreatic enzyme therapy with either an H2 blocker or enteric-coated preparation does not provide improvement, the next step is to decrease dietary fat to 50gm per day and to substitute medium-chain triglycerides (which do not require hydrolysis prior to absorption) for some dietary fat.

If steatorrhea persists, there may be excessive gastric secretion that requires a more potent H2 blocker. There appear to be factors other than acid that may prevent effectiveness of pancreatic enzymes. For example, even when sufficient pancreatic enzymes are instilled directly into the duodenum, steatorrhea may not be fully eliminated.

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