Chronic Diarrhea

Chronic Diarrhea: Excerpt from The 5-Minute Pediatric Consult

Edisio Semeao, MD

Chronic Diarrhea - BASICS

Chronic Diarrhea - description

• Diarrhea lasting >2–4 weeks, whereas acute diarrhea, generally caused by enteric pathogens, is self-limiting and duration of symptoms <1 week
• Stool output >200 g/d in children and adults or 10 g/kg/d in infants is considered diarrhea.
• The initial focus is to establish the pattern of stool output with regards to:
  • Volume
  • Frequency
  • Consistency
  • Gross appearance

Chronic Diarrhea - epidemiology

• Chronic diarrhea seen in the tropics and developing countries is more likely infectious in nature than in the US.
• Gender and genetic factors do not play a significant role in most cases of chronic diarrhea.

Chronic Diarrhea - pathophysiology

The major categories are osmotic and secretory. Inflammatory and motility disorders are smaller but important subcategories to consider.

• Osmotic diarrhea occurs when unabsorbable solute accumulates in the lumen of the small intestine and colon:
  • This increases the intraluminal osmotic pressure and results in excessive fluid and electrolyte losses in stool.
  • Osmotic diarrhea will improve with fasting.
  • Osmotic diarrhea is usually related to malabsorption of dietary products or to the presence of congenital or acquired disaccharidase deficiency or glucose-galactose defects.
• Secretory diarrhea occurs when the net secretion of fluid and electrolyte is in excess of absorption in the intestine:
  • The intestinal mucosa is normally very active in both of these processes.
  • The diarrhea occurs independently of the osmotic load in the intestinal lumen and does not improve with fasting.
  • The mechanisms for secretory diarrhea include the activation of intracellular mediators such as cAMP, cGMP, and calcium-dependent channels.
  • These mediators stimulate active chloride secretion from the crypt cells and inhibit the neutral coupled sodium chloride absorption.
• Inflammation in the intestine can cause an alteration in mucosal integrity resulting in exudative loss of mucus, blood, and/or protein. Increased permeability and altered mucosal surface area may affect absorption and result in diarrhea owing to a malabsorptive process.
• Motility disorders will affect the intestinal transit time. Hypomotility states such as stasis from bacterial overgrowth can lead to diarrhea.

Chronic Diarrhea - DIAGNOSIS

Chronic Diarrhea - signs & symptoms

Chronic Diarrhea - history

• Evaluation of the stool pattern, including consistency, frequency, and appearance.
  • The history of blood and mucus in stool is strongly suggestive of inflammation.
  • Large volume stools (>750 mL/d) imply small bowel disease and/or a secretory process.
  • Watery stools tend to be more associated with carbohydrate malabsorption, small bowel processes, medications and functional processes.
  • Steatorrhea (fatty stools) can be greasy, oily, foul smelling and bulky and are usually associated with pancreatic disease, bacterial overgrowth, short bowel syndrome.
• Dietary intake including the types of food and the occurrence of diarrhea in close relationship to specific foods (e.g., dairy products) may be diagnostic. The amount and type of liquid ingested may also be helpful in diagnosis.
• Nutritional status and growth parameters need to be assessed. The presence of growth failure or malnutrition has considerable implications compared with a child with normal growth and no history of weight loss.
• Onset of diarrhea such as abrupt or gradual is important to determine. Overall duration of the diarrhea and pattern of intermittent vs. continuous may also help in determining the underlying process.
• Other symptoms associated with the diarrhea are important to assess and include abdominal pain, fever, bloating, tenesmus, soiling, rashes and joint complaints.
• Exposure to medications (antibiotics, laxatives, chemotherapeutic agents) or herbal therapies
• History of abdominal surgery
• Inquire about travel history
• Family history of certain disorders may raise the level of suspicion in the patient. These include: celiac disease, inflammatory bowel disease, cystic fibrosis and other pancreatic processes.

Chronic Diarrhea - physical exam

• Nutritional status: Compare height, weight, and head circumference with normal standards and previous exam measurements.
• Anthropometric measurements are important in assessing loss of body fat and muscle mass.
• Peripheral edema, ascites, rash, dystrophic nails, alopecia, chronic chest findings, and pallor may all be indicative of nutritional deficiencies secondary to chronic diarrhea.
• A rectal examination may reveal stool impaction with overflow diarrhea.
  • Is there blood in the stool?
  • Perianal disease (fistula, skin tags, abscess)
• Evidence of infection should be considered with symptoms such as fever, bloody diarrhea, and vital sign instability.
• Aphthous lesions, arthritis and clubbing
• The abdominal exam in most patients is generally nonspecific.

Chronic Diarrhea - tests

Chronic Diarrhea - lab

• Stool samples:
  • Stool should be tested for occult blood and for the presence of fecal leukocytes.
  • Stools pH and reducing substances: If stool is positive for reducing substances and/or the pH <5.5, carbohydrate malabsorption with or without proximal small bowel injury is likely. (Note: Sucrose is not a reducing substance. If sucrose malabsorption is suspected, stool sample has to be hydrolyzed with hydrochloric acid and heat before analysis.)
  • A positive Sudan stain of the stool is indicative of fat malabsorption. However, a 72-hour fecal fat collection remains the gold standard to diagnose fat malabsorption
  • Stool for fecal elastase to assess fat malabsorption.
  • Stool should be cultured for bacteria, ova and parasites, and viral organisms. Clostridium difficile toxins A and B are heat labile, and stool must be kept cool during transport. Collect stool in the correct containers to assure accurate and reliable analysis.
  • Stool may be collected for electrolyte and osmolality measurements. Osmotic gap >100 mOsm/kg is indicative of an osmotic diarrhea.
  • Spot or 24-hour collection for fecal alpha-1- antitrypsin to assess protein loss.
• Blood samples:
  • Hemoglobin and RBC
  • Prealbumin and albumin are good parameters of protein and overall nutritional status.
  • Electrolytes
  • Erythrocyte sedimentation rate, C-reactive protein (CRP) can serve as markers for inflammatory conditions.
  • Hormonal studies to assess for secretory tumors (vasoactive intestinal peptide (VIP), gastrin, secretin, urine assay for 5-HT)
  • In the evaluation for celiac disease, serum antitissue transglutaminase antibody and antiendomysial antibodies as long as the total serum IgA is normal.
  • Hepatic panel, coagulation profile and fat soluble vitamin levels (25 OH vitamin D, vitamins E, A, K) may be helpful to assess fat malabsorption.
  • Viral serologies such as human immunodeficiency virus and cytomegalovirus need to be considered in the immunocompromised host with diarrhea.
  • Thyroid studies in patients with large volume watery diarrhea
• Specialized studies:
  • A D-xylose absorption test is helpful in screening for small bowel injury. Timed serum D-xylose following oral ingestion is significantly lower in diseases causing diffuse mucosal damage to the small bowel (i.e., postviral enteropathy, celiac disease).
  • A hydrogen breath test may be helpful in evaluating for the possibility of small bowel bacterial overgrowth.
  • Sweat chloride if cystic fibrosis is suspected

Chronic Diarrhea - imaging

• Plain radiograph studies usually not helpful
• Upper GI series with small bowel follow through may show partial small bowel obstruction, strictures, or evidence of inflammatory bowel disease.
• Abdominal CT scan may help in assessing the pancreas for calcifications and inflammation.

Chronic Diarrhea - diag proced-surgery

• Endoscopy with small bowel biopsy and small bowel aspirate for culture to help diagnose certain congenital, immunologic, or infectious causes of diarrhea.
  • Small bowel disaccharidase studies will help detect carbohydrate malabsorption.
• Colonoscopy will diagnose colitis related to inflammatory bowel disease or infection.
• Video capsule endoscopy may also be used to further evaluate the small bowel for evidence of inflammation.

Chronic Diarrhea - differencial diagnosis

• Infants (<1 year of age):
  • Cow’s milk and/or soy protein intolerance
  • Intractable diarrhea of infancy is associated with diffuse mucosal injury beginning <6 months of age resulting in malabsorption and malnutrition.
  • Infectious/protracted postinfectious diarrhea
  • Microvillus inclusions disease
  • Autoimmune enteropathy
  • Hirschsprung disease with enterocolitis
  • Transport defects (e.g., congenital chloridorrhea)
  • Nutrient malabsorption (e.g., congenital glucose-galactose malabsorption and congenital lactase deficiency, sucrase-isomaltase deficiency)
  • Cystic fibrosis
  • AIDS enteropathy
  • Primary immune defects
  • Munchausen syndrome by proxy (factitious)
  • Drug, toxin induced
• Children (1–5 years of age):
  • Chronic nonspecific diarrhea of infancy (toddler’s diarrhea)
  • Infectious/postinfectious enteritis
  • Giardiasis
  • Eosinophilic gastroenteritis
  • Sucrase-isomaltase deficiency
  • Tumors (neuroblastoma, VIPoma with secretory diarrhea)
  • Inflammatory bowel disease
  • Celiac disease
  • Cystic fibrosis
  • Small bowel bacterial overgrowth
  • AIDS enteropathy
  • Constipation with (overflow) encopresis
  • Acquired short bowel syndrome
  • Shwachman syndrome
  • Factitious
• Children (>5 years of age):
  • Similar to above
  • Acquired lactose deficiency (early adolescent)
  • Inflammatory bowel disease
  • Celiac disease
  • Constipation with (overflow) encopresis
  • Irritable bowel syndrome (adolescent)
  • Laxative abuse (adolescents)
  • Infection
• Bacterial (Aeromonas, Plesiomonas, Campylobacter, Salmonella, Mycobacterium tuberculosis, Yersinia, recurrent Clostridium difficile)
• Viral (rotavirus, adenovirus, Norwalk virus)
• Parasites (amoeba, trichuris, cryptosporidium, giardia, schistosoma, cyclospora)
• Small bowel bacterial overgrowth
• Tumors (neuroblastoma, VIP oma with secretory diarrhea)
• Primary bowel tumors (rare, adolescent)
• Complex congenital heart disease with protein losing enteropathy
• Pancreatic insufficiency/chronic pancreatitis
• Hyperthyroidism
• Diabetes

Chronic Diarrhea - TREATMENT

Chronic Diarrhea - general measures

• The 1st goal is to ensure adequate nutritional intake to permit normal growth and development.
• Antibiotics when infection is suspected.
• Many causes of congenital diarrhea do not have specific therapy available, and treatment is supportive

Diet:

• If infection is severe or protracted, a predigested formula may be necessary early in the recovery phase
• If oral nutrition appears inadequate, the formula can be given in a slow, continuous fashion via a nasogastric/jejunal tube.
• Remove offending agent (e.g., cow’s milk protein, soy protein, lactose, or gluten).
• In cases in which there is increased motility and thus rapid transit time, such as in chronic nonspecific diarrhea, alterations in the diet can be very helpful.
• Elimination of sorbitol-containing juices, which increases the osmotic load and low-carbohydrate diet will help to lower the osmotic load delivered to the intestine. Furthermore, a high-fat diet will slow the intestinal transit time and increase the time available to absorb fluid, electrolytes, and nutrients from the intestinal tract.

Chronic Diarrhea - medication

• The use of antimotility agents such as loperamide and Lomotil and antisecretory agents, such as octreotide may have a role in noninfectious causes of diarrhea. However, identification and treatment of the underlying cause of diarrhea is always preferable.
• Pancreatic enzymes may be used in specific patients
• Luminal (nonabsorbed) antibiotics for small bowel bacterial overgrowth

• In certain cases in which the diet is altered as a therapeutic intervention, the physician must ensure that the patient is still absorbing adequate calories and micronutrients so that the nutritional status of the patient is not further compromised.
• Avoid the reinstitution of a regular diet too quickly following a severe and/or protracted insult to the gut since this may further exacerbate the diarrhea.
• The use of antimotility and antisecretory agents should be judicious and as an adjunct to other therapy, but not as the mainstay in the treatment regimen.
• In patients with cow’s milk and/or soy allergy, rechallenge should be after 12 months of age and should be in a controlled environment in case anaphylaxis occurs.

Chronic Diarrhea - bibliography

1. Ali SA, Hill DR. Giardia intestinalis. Curr Opin Infect Dis. 2003;16:453–460.
2. Lee SD, Surawicz CM. Infectious causes of chronic diarrhea. Gastroenterol Clin North Am. 2001;30:679–692, viii.
3. Salvilahti E. Food-induced malabsorption syndromes. J Pediatr Gastroenterol Nutr. 2000;30(suppl):S61–S66.
4. Vanderhoof JA. Chronic diarrhea. Pediatr Rev. 1998;19(Dec):418–422.

Chronic Diarrhea - CODES

Chronic Diarrhea - icd9

• 009.3 Diarrhea of presumed infectious origin
• 564.5 Functional diarrhea
• 787.91 Diarrhea   Diarrhea NOS

Chronic Diarrhea - FAQ

• Q: If my infant has cow’s milk allergy, when can he have cow’s milk?
• A: In patients with cow’s milk and/or soy allergy, rechallenge should be after 12 months of age and should be in a controlled environment in case anaphylaxis occurs. If the testing is negative, ingestion of cow’s milk can be recommended.
• Q: What are the best markers for success in management of chronic diarrhea?
• A: If weight and height normalize, the chances of continued malabsorption are unlikely.

Book Source Details

• Book Title: The 5-Minute Pediatric Consult
• Author(s): M. William Schwartz MD; et al.
• Year of Publication: 2008
• Copyright Details: The 5-Minute Pediatric Consult, Copyright © 2008 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: The 5-Minute Pediatric Consult Authors: M. William Schwartz MD; et al. Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7577-9

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