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==Overview==
==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.
'''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. Based on underlying etiology steatorrhea can be classified into 3 types, intestinal, biliary, and pancreatic steatorrhea.  Steatorrhea occurs as a result of either defect of the normal architecture of [[Gastrointestinal tract|digestive tract]] or defect of [[synthesis]] or [[secretion]] of [[enzymes]] required for metabolism fats. Steatorrhea may be caused by [[Celiac disease]], [[choledocholithiasis]], [[cystic fibrosis]], [[exocrine pancreatic insufficiency]], [[hypolipidemic drugs]], [[inflammatory bowel disease]], [[Small intestinal bacterial overgrowth syndrome|small bowel bacterial overgrowth syndrome]]. 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]]. If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include [[anemia]], [[intestinal obstruction]], [[weight loss]]. Prognosis of steatorrhea is generally good with appropriate treatment. The 72 hr-fecal fat determination is the gold standard test for the diagnosis of steatorrhea. Mild steatorrhea can manifest as passage of frothy, foul smelling stool, greasy in appearance and difficult to flush, [[abdominal pain]], [[bloating]], [[Heartburn|heart burn]]. if severe it may cause [[malnutrition]] , [[dehydration]], [[anemia]], [[muscle weakness]], [[Weight loss|weight loss,]] [[Dermatological lesions|skin problems]], [[Neurological disorder|neurological problems]], [[osteoporosis]]. Patients with steatorrhea usually appear emaciated secondary to loss of subcutaneous fat. Physical examination of patients with steatorrhea is usually remarkable for [[Distended abdomen|distended abdomen,]] [[Orthostatic hypotension|orthostatic hypo-tension]] and [[ecchymoses]], [[Chvostek's sign|Chvostek sign]] and [[Trousseau sign]] secondary to [[hypocalcemia]]. There are no specific laboratory findings associated with steatorrhea. Management of [[steatorrhea]] include treatment of underlying etiology, control of [[diarrhea]] and correction of [[nutritional deficiencies]]. Surgery is usually reserved for patients with refractory or pre-malignant complications, such as Enteropathy Associated T-cell [[Lymphoma]] (EATL) and ulcerative jejunitis (UJ).  Effective measures for the primary prevention of steatorrhea include [[smoking cessation]], [[Alcohol consumption|alcohol cessation]], minimizing the use of certain medications, such as [[antibiotics]], that can alter normal bowel flora, and consuming diet rich in [[dietary fiber]].


==Historical Perspective==
==Historical Perspective==
The history of celiac disease dates back to late 1800's when an english scientist described celiac disease. In October 1887, Samuel Gee, a pediatrician, was the first to describe in detail celiac disease and its association with fatty stools. In 1950, Wim Dicke's colleagues, Weijers and Van de Kamer, presented a way to diagnose mal-absorption syndromes by using [[stool]] [[fat]] measurement. In late 1960's case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.


==Classification==
==Classification==
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==Pathophysiology==
==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.
Stearorhea can be defined as loss of undigested fat in [[stools]]. The processes can be invoked by either defect of the normal architecture of [[Gastrointestinal tract|digestive tract]] or it may involve defect of [[synthesis]] or [[secretion]] of [[enzymes]] of GI tract which are needed to metabolize fatty content of food.  
* 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==
==Causes==
===Common causes of steatorrhea===
Steatorrhea may be caused by [[Celiac disease]], [[choledocholithiasis]], [[cystic fibrosis]], [[exocrine pancreatic insufficiency]], [[hypolipidemic drugs]], [[inflammatory bowel disease]], [[Small intestinal bacterial overgrowth syndrome|small bowel bacterial overgrowth syndrome]].
*[[Celiac disease]]
*[[Choledocholithiasis]]
*[[Cystic fibrosis]]
*[[Exocrine pancreatic insufficiency]]
*[[Hypolipidemic drugs]]
*[[Inflammatory bowel disease ]]
*[[Small bowel bacterial overgrowth syndrome]]


==Differentiating steatorrhea from other Diseases==
==Differentiating steatorrhea from other Diseases==
Steatorrhea must be differentiated from Cystic fibrosis, Hartnup'sdisease, Whipple's disease, Zollinger Ellison syndrome, Acrodermatitis enteropathica, intestinal lymphangiectasia
Steatorrhea must be differentiated from other causes of mal-absorption such as [[cystic fibrosis]], [[Hartnup disease|Hartnup'sdisease]], [[Whipple's disease]], [[Zollinger-Ellison syndrome|Zollinger Ellison syndrome]], [[acrodermatitis enteropathica]], [[Lymphangiectasia|intestinal lymphangiectasia]].


==Epidemiology and Demographics==
==Epidemiology and Demographics==
The demographic measures of steatorrhea can be explained by independent causes of steatorrhea.
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 ===
* Small intestinal bacterial overgrowth is more commonly observed among [[elderly]] [[patients]].
=== Gender ===
* Small intestinal bacterial overgrowth (SIBO) affects [[men]] and [[women]] equally.
=== 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 [[Adult|adults]] alike.
* In [[children]] celiac disease peaks in early [[childhood]].
* In [[Adult|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==
==Risk Factors==
Common [[risk factors]] in the development of steatorrhea include: [[Celiac disease|Celiac diseas]]<nowiki/>e, [[cystic fibrosis]], [[exocrine pancreatic insufficiency]], [[inflammatory bowel disease]], [[small intestinal bacterial overgrowth]], [[hypolipidemic drugs]]
Common [[risk factors]] in the development of steatorrhea include: [[Celiac disease|Celiac diseas]]<nowiki/>e, [[cystic fibrosis]], [[exocrine pancreatic insufficiency]], [[inflammatory bowel disease]], [[small intestinal bacterial overgrowth]], [[hypolipidemic drugs]]
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==Natural History, Complications, and Prognosis==
==Natural History, Complications, and Prognosis==
===Natural History===
If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include [[anemia]], [[intestinal obstruction]], [[weight loss]]. Prognosis of steatorrhea is generally good with appropriate treatment.
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==
==Diagnosis==
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===History and Symptoms===
===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.
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]], [[Dermatological lesions|skin problems]], [[Neurological disorders|neurological problems]], [[osteoporosis]].


===Physical Examination===
===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
Patients with steatorrhea usually appear emaciated secondary to loss of subcutaneous fat. Physical examination of patients with steatorrhea is usually remarkable for [[Distended abdomen|distended abdomen,]] [[Orthostatic hypotension|orthostatic hypo-tension]] and [[ecchymoses]], [[Chvostek's sign|Chvostek sign]] and [[Trousseau sign]] secondary to [[hypocalcemia]].


===Laboratory Findings===
===Laboratory Findings===
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===Other Diagnostic Studies===
===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==
==Treatment==
===Medical Therapy===
===Medical Therapy===
Management of [[steatorrhea]] include treatment of underlying etiology, control of [[diarrhea]] and correction of [[nutritional deficiencies]].


===Surgery===
===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]]
===Primary Prevention===
Effective measures for the primary prevention of steatorrhea include [[smoking cessation]], [[Alcohol consumption|alcohol cessation]], minimizing the use of certain medications, such as [[antibiotics]], that can alter normal bowel flora, and consuming diet rich in [[dietary fiber]].


===Prevention===
===Secondary Prevention===
Secondary preventive measures of steatorrhea are similar to [[Steatorrhea primary prevention|primary preventive measures]].


==References==
==References==

Latest revision as of 22:36, 26 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. Based on underlying etiology steatorrhea can be classified into 3 types, intestinal, biliary, and pancreatic steatorrhea. Steatorrhea occurs as a result of either defect of the normal architecture of digestive tract or defect of synthesis or secretion of enzymes required for metabolism fats. Steatorrhea may be caused by Celiac diseasecholedocholithiasiscystic fibrosisexocrine pancreatic insufficiencyhypolipidemic drugsinflammatory bowel diseasesmall bowel bacterial overgrowth syndrome. Common risk factors in the development of steatorrhea include Celiac diseasecystic fibrosisexocrine pancreatic insufficiencyinflammatory bowel diseasesmall intestinal bacterial overgrowthhypolipidemic drugs. If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include anemiaintestinal obstructionweight loss. Prognosis of steatorrhea is generally good with appropriate treatment. The 72 hr-fecal fat determination is the gold standard test for the diagnosis of steatorrhea. 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. 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 ecchymosesChvostek sign and Trousseau sign secondary to hypocalcemia. There are no specific laboratory findings associated with steatorrhea. Management of steatorrhea include treatment of underlying etiology, control of diarrhea and correction of nutritional deficiencies. Surgery is usually reserved for patients with refractory or pre-malignant complications, such as Enteropathy Associated T-cell Lymphoma (EATL) and ulcerative jejunitis (UJ). 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.

Historical Perspective

The history of celiac disease dates back to late 1800's when an english scientist described celiac disease. In October 1887, Samuel Gee, a pediatrician, was the first to describe in detail celiac disease and its association with fatty stools. In 1950, Wim Dicke's colleagues, Weijers and Van de Kamer, presented a way to diagnose mal-absorption syndromes by using stool fat measurement. In late 1960's case of idiopathic steatoeehea and reticulosis of the small bowel as a late complication was reported.

Classification

Steatorrhea may be classified based on etiology into 3 types, intestinal, biliary, and pancreatic steatorrhea.

Pathophysiology

Stearorhea can be defined as loss of undigested fat in stools. The processes can be invoked by either defect of the normal architecture of digestive tract or it may involve defect of synthesis or secretion of enzymes of GI tract which are needed to metabolize fatty content of food.

Causes

Steatorrhea may be caused by 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 other causes of mal-absorption such as 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.

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

If left untreated, steatorrhea can lead to severe malnutrition due to inability of gastrointestinal tract to absorb fat soluble vitamins and ultimately severe weight loss. Complication of steatorrhea include anemia, intestinal obstruction, weight loss. Prognosis of steatorrhea is generally good with appropriate treatment.

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.

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

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

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