Steatorrhea overview: Difference between revisions
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* In late 1960's case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.<ref name="pmid14797703">{{cite journal |vauthors=PROWSE CB |title=Idiopathic steatorrhoea |journal=Proc. R. Soc. Med. |volume=43 |issue=11 |pages=895–6 |year=1950 |pmid=14797703 |pmc=2081764 |doi= |url=}}</ref> | * In late 1960's case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.<ref name="pmid14797703">{{cite journal |vauthors=PROWSE CB |title=Idiopathic steatorrhoea |journal=Proc. R. Soc. Med. |volume=43 |issue=11 |pages=895–6 |year=1950 |pmid=14797703 |pmc=2081764 |doi= |url=}}</ref> | ||
* Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency ia an important land mark in the 21st century.<ref name="pmid25206255">{{cite journal |vauthors=Trang T, Chan J, Graham DY |title=Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency in the 21(st) century |journal=World J. Gastroenterol. |volume=20 |issue=33 |pages=11467–85 |year=2014 |pmid=25206255 |pmc=4155341 |doi=10.3748/wjg.v20.i33.11467 |url=}}</ref> | * Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency ia an important land mark in the 21st century.<ref name="pmid25206255">{{cite journal |vauthors=Trang T, Chan J, Graham DY |title=Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency in the 21(st) century |journal=World J. Gastroenterol. |volume=20 |issue=33 |pages=11467–85 |year=2014 |pmid=25206255 |pmc=4155341 |doi=10.3748/wjg.v20.i33.11467 |url=}}</ref> | ||
* The CFTR gene was discovered first in 1989. In 1990, scientists successfully added cloned normal gene to Cystic Fibrosis cells in the laboratory, which corrected the chloride | * The CFTR gene was discovered first in 1989. In 1990, scientists successfully added cloned normal gene to Cystic Fibrosis cells in the laboratory, which corrected the chloride transportation. | ||
==Classification== | ==Classification== | ||
Revision as of 01:58, 12 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
Steato means relating to fatty matter or tissue and rrhea means discharge; flow. So the word means flow of fatty matter. Malabsorption is a condition which is associated with impaired absorption of one or all dietary nutrients. There are multiple etiologies with diminished intestinal absorption. Many of them present with diarrhea, especially steatorrhea. Some of the main causes of steatorrhea are celiac disease, cystic fibrosis, pancreatic insufficiency, small inetestinal beacteraial overgrowth syndrome. The history of celiac disease dates back to late 1800's when an english scientist described celiac disease.
n October 1887, Samuel Gee, an English leading authority in pediatrics, gained the full credit of explanation of celiac disease, presenting a lecture named "celiac affection" to medical students; which was published next year. Gee mentioned that "If the patient can be cured at all, it must be by means of diet".[9] He also added that "the allowance of farinaceous food must be small".[10] He also found gluten-free diet relieved symptoms, which relapsed when gluten
- In 1950, Wim Dicke, a Dutch pediatrician, suggested in his doctoral thesis that elimination of wheat, rye, and oats from diet would result in reasonable cure of celiac disease. He found the pathological factor to be gluten.[1]
- At the same time, Wim Dicke's colleagues, Weijers and Van de Kamer, presented a way to diagnose celiac disease by using stool fat measurement.[2]
- In late 1960's case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.[3]
- Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency ia an important land mark in the 21st century.[4]
- The CFTR gene was discovered first in 1989. In 1990, scientists successfully added cloned normal gene to Cystic Fibrosis cells in the laboratory, which corrected the chloride transportation.
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
Bile acid binding resins
- Preferred regimen (1) : Cholestyramine 4 g three times daily
- Preferred regimen (1) : Colestipol granules 5 to 10 g three times daily
- Note: Administer ≥1 hour before or >4 hours after other drugs to prevent decreased absorption of other drugs.
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
Bile acid binding resins
- Preferred regimen (1) : Cholestyramine 4 g three times daily
- Preferred regimen (1) : Colestipol granules 5 to 10 g three times daily
- Note: Administer ≥1 hour before or >4 hours after other drugs to prevent decreased absorption of other drugs.
Pancreatic enzymes
- Preferred regimen (1) : Pancrelipase delayed-release capsules (Creon minimicrospheres)
- Preferred regimen (1) : Pancrelipase tablets and powder (Viokase) 1 g
- (equivalent to 20,000 units lipase component) with meals
- Note: Approximately 30,000 units (90,000 USP) (lipase component) with each meal.
Management of Underlying Etiologies
- For a detailed explanation of management of Crohn's disease click here
- For a detailed explanation of management of celiac disease click here
- For a detailed explanation of management of gallstones disease click here
- For a detailed explanation of management of cystic fibrosis disease click here
- For a detailed explanation of the management of small bowel bacterial overgrowth syndrome click here
Surgery
Surgical intervention is usually not recommended for the management of steatorrhea. Surgery is usually reserved for patients with refractory or pre-malignant complications, such as Enteropathy Associated T-cell Lymphoma (EATL) and ulcerative jejunitis (UJ). EATL patients presenting with ulcerative lesions, stenotic lesions, and perforation needs surgical intervention. Surgery also serves as a pre-therapy in order to prevent perforation of the small bowel during chemotherapy in case of EATL. After surgery patients receive immunotherapy, chemotherapy and/or stem cell transplantation.
Prevention
Primary Prevention
Effective measures for the primary prevention of steatorrhea include smoking cessation, alcohol cessation, minimizing the use of certain medications, such as antibiotics, that can alter normal bowel flora, and consuming diet rich in dietary fiber
Secondary Prevention
Secondary preventive measures of steatorrhea are similar to primary preventive measures.
References
- ↑ Dicke, W. K.; Weijers, H. A.; KAMER, J. H. v. D. (1953). "Coeliac Disease The Presence in Wheat of a Factor Having a Deleterious Effect in Cases of Coeliac Disease". Acta Paediatrica. 42 (1): 34–42. doi:10.1111/j.1651-2227.1953.tb05563.x. ISSN 0803-5253.
- ↑ Kamer, J. H. Van De; Weijers, H. A.; Dicke, W. K. (1953). "Coeliac Disease: An Investigation into the Injurious Constituents of Wheat in Connection with their Action on Patients with Coeliac Disease". Acta Paediatrica. 42 (3): 223–231. doi:10.1111/j.1651-2227.1953.tb05586.x. ISSN 0803-5253.
- ↑ PROWSE CB (1950). "Idiopathic steatorrhoea". Proc. R. Soc. Med. 43 (11): 895–6. PMC 2081764. PMID 14797703.
- ↑ Trang T, Chan J, Graham DY (2014). "Pancreatic enzyme replacement therapy for pancreatic exocrine insufficiency in the 21(st) century". World J. Gastroenterol. 20 (33): 11467–85. doi:10.3748/wjg.v20.i33.11467. PMC 4155341. PMID 25206255.