Steatorrhea overview: Difference between revisions
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** Preferred regimen (7) : [[Magnesium gluconate]] 1 to 4 g (54 to 216 mg elemental [[magnesium]]) q6h | ** Preferred regimen (7) : [[Magnesium gluconate]] 1 to 4 g (54 to 216 mg elemental [[magnesium]]) q6h | ||
** Preferred regimen (8) : [[Calcium carbonate]] 500 mg (elemental [[calcium]]) q12h | ** Preferred regimen (8) : [[Calcium carbonate]] 500 mg (elemental [[calcium]]) q12h | ||
=== Antidiarrheal agents === | |||
*Preferred regimen (1) : [[Loperamide]] 2 to 4 mg as needed, not to exceed 12 mg/day | |||
*Preferred regimen (1) : [[Diphenoxylate and Atropine|Diphenoxylate with atropine]] ([[Lomotil]]) 1 to 2 tabs after loose stool, not to exceed 8 per day | |||
*Preferred regimen (1) : [[Opium Deodorized|Deodorized opium tincture]] 10 percent (10 mg per mL) 0.3 to 0.6 mL q8h | |||
===Surgery=== | ===Surgery=== | ||
Revision as of 23:53, 11 February 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]
Overview
Steatorrhea is the formation of non-solid feces. Stools may also float due to excess fat from malabsorption, have an oily appearance and be foul smelling. An oily anal leakage or some level of fecal incontinence may occur. There is increased fat excretion, which can be measured by determining the fecal fat level. While definitions have not been standardized, fat excretion in feces in excess of 0.3 (g/kg) / day is considered indicative of steatorrhea.
Historical Perspective
Classification
Steatorrhea may be classified based on etiology into 3 types, intestinal, biliary, and pancreatic steatorrhea.
Pathophysiology
Normal fat absorption involves a complex mixture of digestive enzymes, bile salts, and an intact intestinal mucosa to enable uptake of these hydrophobic complexes.
- After ingestion, dietary lipids are initially emulsified in the stomach and then hydrolyzed by the action of gastric and pancreatic lipase and colipase.
- The hydrolyzed lipids are then aggregated into micelles or liposomes with the addition of bile salts in the duodenum and jejunum.
- These micelles are absorbed across the intact intestinal villi by both active and passive processes. Finally, they are packaged into chylomicrons within intestinal epithelial cells and transported to the circulation via the lymphatic system
- 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/ steatorrhea.
- The bulk of dietary lipid is neutral fat or triglyceride, composed of a glycerol backbone with each carbon linked to a fatty acid.
- Foodstuffs typically also contain phospholipids, sterols like cholesterol and many minor lipids, including fat-soluble vitamins.
- Finally, small intestinal contents contain lipids from sloughed epithelial cells and considerable cholesterol delivered in bile.
Causes
Common causes of steatorrhea
- Celiac disease
- Choledocholithiasis
- Cystic fibrosis
- Exocrine pancreatic insufficiency
- Hypolipidemic drugs
- Inflammatory bowel disease
- Small bowel bacterial overgrowth syndrome
Differentiating steatorrhea from other Diseases
Steatorrhea must be differentiated from Cystic fibrosis, Hartnup'sdisease, Whipple's disease, Zollinger Ellison syndrome, Acrodermatitis enteropathica, intestinal lymphangiectasia
Epidemiology and Demographics
The demographic measures of steatorrhea can be explained by independent causes of steatorrhea.
Small intestinal bacterial overgrowth syndrome
Epidemiology and demographics of small intestinal bacterial overgrowth is as follows:
Age
Gender
Race
- There is no racial predilection for small intestinal bacterial overgrowth (SIBO).
Cystic fibrosis
Cystic fibrosis (CF) is an autosomal recessive disorder whose incidence has long been estimated as 1/2500 live births in Caucasians.
Celiac disease
Incidence
- The incidence of celiac disease is approximately 10-13 per 100,000 individuals worldwide.
- In United States the incidence of celiac disease is approximately 10 per 100,000 individuals
Prevalence
- Worldwide, the prevalence of celiac disease is estimated to be 500 to 1000 per 100,000 individuals.
- In United States, the prevalence of celiac disease is approximately 710 per 100,000 individual
Age
- Celiac disease affects children and adults alike.
- In children celiac disease peaks in early childhood.
- In adults celiac disease is usually diagnosed around fourth and fifth decades of life.
Race
- Celiac disease usually affects individuals of the non-Hispanic white race (1000 per 100,000 individuals), Hispanics (300 per 100,000 individuals) and non-Hispanic blacks (200 per 100,000 individuals).
- HLA-DQ2 associated celiac disease is frequently found in white populations located in Western Europe.
Gender
- Women are more commonly affected by celiac disease than men.
- The female to male ratio is approximately 3:1.
- In contrast, patients over the age of 60 who are diagnosed with celiac disease are most commonly males.
Region
- Tthe highest prevalence of celiac disease has been reported in Algerian refugees. These individuals have a high rate of consanguinity and high frequencies of HLA-DQ2.
Risk Factors
Common risk factors in the development of steatorrhea include: Celiac disease, cystic fibrosis, exocrine pancreatic insufficiency, inflammatory bowel disease, small intestinal bacterial overgrowth, hypolipidemic drugs
Screening
There is insufficient evidence to recommend routine screening for steatorrhea
Natural History, Complications, and Prognosis
Natural History
The importance for the parthenogenesis of steatorrhea is deficiency of enzymes required for digestion of fatty food, or absorption of digested fatty food. The mechanism may be different for patients having steatorrhea and the microscopic picture of every pathology may be different but the effect of loosing fat in stool is similar in all patients. Steatorrhea was caused by the decreased enzymatic function of the pancreas, asynchronism of the food and bile supply to the intestinal lumen, disorders of absorption of lipolysis products.
Complications
The outcomes of steatorrhea are explained as below:
Adults:
Anemia,
Intestinal obstruction
Weight loss.
Children:
Failure to thrive
Anemia
Weight loss
Prognosis
Prognosis generally is good once the cause are treated and if replacement therapy is started . Most of the time it depend on the the cause of loosing fat in stool.
Diagnosis
Diagnostic study of choice
The 72 hr-fecal fat determination is the gold standard test for the diagnosis of steatorrhea
History and Symptoms
Mild steatorrhea can manifest as passage of frothy, foul smelling stool, greasy in appearance and difficult to flush, abdominal pain, bloating, heart burn. if severe it may cause malnutrition , dehydration,anemia, muscle weakness, weight loss, skin problems, neurological problems, osteoporosis.
Physical Examination
Patients with steatorrhea usually appear emaciated secondary to loss of subcutaneous fat. Physical examination of patients with steatorrhea is usually remarkable for distended abdomen, orthostatic hypo-tension and ecchymoses, Chvostek sign and Trousseau sign secondary to hypocalcemia
Laboratory Findings
Quantitative analysis of fat in the stool may be helpful in the diagnosis of steatorrhea. The various tests that may be helpful in the diagnosis are acid steatocrit, near-infrared reflectance analysis (NIRA) and sudan III stain.
Imaging Findings
X-ray
There are no x-ray findings associated with steatorrhea. However, there are x-ray findings depends on the underlying causes.
CT scan
There are no CT scan findings associated with steatorrhea. However, there are CT scan findings depends on the underlying causes
MRI
There are no MRI findings associated with steatorrhea. However, there are MRI findings depends on the underlying causes.
Other Diagnostic Studies
There are no other diagnostic studies associated with steatorrhea. However, there are no other diagnostic studies depends on the underlying causes.
Treatment
Medical Therapy
Management of steatorrhea include treatment of underlying etiology, control of diarrhea and correction of nutritional deficiencies.
Correction of Nutritional Deficiencies
- Oral supplementation with vitamins and minerals is usually well tolerated in patients who are are undergoing specified treatment for underlying etiology.
- Rapid recovery following the identification of a nutritional deficiency can be achieved by supplementation with 5 to 10 times the Recommended Dietary Allowance.
- Preferred regimen (1) : Vitamin A 40,000 to 50,000 units q12h
- Note : Maintenance: 8000 to 20,000 units/day (dosage ≥15,000 units can be teratogenic)
- Preferred regimen (2) : Vitamin D3 (cholecalciferol) 30,000 to 50,000 units q24h
- Preferred regimen (3) : Vitamin K 2.5 to 12.5 mg q24h
- Preferred regimen (4) : Folic acid 5 mg q24h during repletion
- Preferred regimen (5) : Vitamin B12 (cyanocobalamin) 1 mg subcutaneously
- Preferred regimen (6) : Ferrous sulfate 325 mg (65 mg elemental iron) q8h
- Preferred regimen (7) : Magnesium gluconate 1 to 4 g (54 to 216 mg elemental magnesium) q6h
- Preferred regimen (8) : Calcium carbonate 500 mg (elemental calcium) q12h
- Preferred regimen (1) : Vitamin A 40,000 to 50,000 units q12h
Antidiarrheal agents
- Preferred regimen (1) : Loperamide 2 to 4 mg as needed, not to exceed 12 mg/day
- Preferred regimen (1) : Diphenoxylate with atropine (Lomotil) 1 to 2 tabs after loose stool, not to exceed 8 per day
- Preferred regimen (1) : Deodorized opium tincture 10 percent (10 mg per mL) 0.3 to 0.6 mL q8h