Diarrhea and Malabsorption

Diarrhea

I. Definition

There exists some controversy as to how best to define diarrhea. Classically diarrhea is defined as an increase in the quantity of stool in excess of 200 g per day diarrhea, malabsorption, malabsorbtion. Others feel it is more accurately defined as an increase in the liquidity of stool, though this is much more difficult to quantify.

II. Pathophysiology

From a pathophysiologic standpoint, diarrhea is separated into four basic mechanisms:

A. Osmotic: Caused by the presence, in the lumen of the gut, of large amounts of poorly absorbable, osmotically active solutes. These solutes draw large amounts of fluid into the lumen of the gut, because the GI mucosa is incapable of sustaining an osmotic gradient.

Frequent causes include 1) ingestion of non-absorbable salts (eg, magnesium containing laxatives) and sugars (lactulose) 2) malabsorption of osmotically active sugars (lactose intolerance).

B. Secretory: Refers to diarrhea caused by abnormal ion transport by enterocytes and may be subdivided as follows:

1) Congenital defects of ion absorption

2) Intestinal resection

3) Diffuse mucosal disease

C. Exudative/inflammatory: Disruption of the integrity of the mucosal barrier. Seen in enteroinvasive infections (amebiasis, enteroinvasive E. coli, Salmonella), inflammatory bowel disease, and ischemic colitis. Typically red cells or PMNs may be seen in the stool.

D. Deranged Motility

III. Acute Diarrhea

Refers to diarrhea of (<2-3 weeks duration)

A. Bacterial: Campylobacter, C. difficile, E. coli, Salmonella, Shigella

B. Parasitic: E. Histolytica, Giardia lamblia, Cryptosporidium, Cyclospora

C. Viral: Adenovirus, Norwalk virus, Rotavirus

D. Food Poisoning

E. Medication

F. Recent ingestion of poorly absorbed sugars

G. Fecal impaction

Diagnostic tests: Stool for leukocytes, Stool cx, Stool C. diff., Stool O&P w/Giardia ag, Flexible sigmoidoscopy.

IV. Chronic Diarrhea (>4 weeks duration)

Irritable bowel syndrome, Inflammatory bowel disease, parasitic infestations, radiation, malabsorption, medications, colon carcinoma, villous adenoma, lymphoma, gastrectomy, thyroid disease, diabetes, surreptitious laxative abuse, hormone secreting neuroendocrine tumor, amyloidosis, systemic mastocytosis, food allergy.

Diagnostic tests:

A. Stool for wbcs, guaiac, sudan stain, O&P w/Giardia ag, 72 hr stool fat, stool osmolarity and osmotic gap, stool magnesium

B. Serum for TFTs, ESR, VIP, gastrin, calcitonin, amebic serology, antiendomysial ab, antiglaidin ab, and laxative screen.

C. Urine for 5-HIAA, VMA and metanephrines

D. Colonoscopy

E. Abdominal CT

F. UGI/SI series

G. Small intestinal biopsy, quantitative cx, aspirate for Giardia

H. Carbohydrate Breath Tests

Maldigestion and Malabsorption

I. Mechanisms of Malabsorption

A. Intraluminal Malabsorption

1) defective lipolysis/proteolysis

• pancreatic insufficiency, ZE syndrome

2) impaired micelle formation

• biliary obstruction, bacterial overgrowth, ileal disease

B. Mucosal Malabsorption

1) Lactose intolerance

2) Giardia infestation

3) Celiac disease

4) Whipple's disease

5) Short bowel syndrome

C. Defective Transport

Lymphatic obstruction. Frequently associated with protein loosing enteropathy.

II. Diagnostic Tests for Malabsorption

A. Quantitative 72 hr. fecal fat. (abnormal if7g/24hr, on 100g fat diet) Abnormal if any of the stages of absorption are impaired. Utility affected by inconvenience of test.

B. D-Xylose test: tests specifically for the mucosal stage of absorption

C. Small bowel biopsy

D. Culture of SI aspirate: For bacterial overgrowth

E. Lactose/Hydrogen breath test

F. Schilling test: To evaluate B 12 malabsorption

G. Small bowel series: For detection of short gut, blind loops, giant diverticula, fistulae, diffuse mucosal abnormality.

III. Celiac Disease

A. AKA celiac sprue, gluten sensitive enteropathy, non-tropical sprue

B. Epidemiology:

• Northwestern European ancestry

• Two age peaks:

• Infancy

• 4^th -5^th Decade

• Environmental factors: Irish in Ireland >Irish in US

C. Pathogenesis

• Wheat Gluten (contains Glutenin and Gliadin)

• Villous injury occurs within hours of exposure

• T-Cell mediated response to gliadin

• Decreased absorptive surface area

• Loss of brush border enzymes

D. Clinical Features

• Diarrhea/Steatorrhea

• Weight loss

• Dermatitis Herpetiformis

• Single nutrient deficiency

• Asymptotic

E. Diagnostic Tests

• D-Xylose

• Small intestinal biopsy (gold standard)

• Antiendomysial and antigliadin antibodies:

Serum IgA antigliadin is specific but not sensitive

Serum IgA antiendomysial ab is most sensitive & specific (80-90%) Tests turn negative once patient on gluten-free diet

F. Pathology

• Endoscopically: "scalloped folds" in the duodenum

• Histologically:

• Absence/blunting of villi

• Crypt hyperplasia

• Expansion of lamina propria w/lymphocytes and plasma cells

• Features are non-diagnostic

G. Treatment

• Gluten withdrawal from diet: wheat, rye, barley, ?oat

• Limit milk products initially

• Vitamin repletion