Diarrhea, Constipation, and Malabsorption

NORMAL GASTROINTESTINAL FUNCTION

ABSORPTION OF FLUID AND ELECTROLYTES 

Fluid delivery to

the GI tract is 8–10 L/d,including 2 L/d ingested; most is absorbed in small

bowel. Colonic absorption is normally 0.05–2 L/d,with capacity for 6 L/d if

required. Intestinal water absorption passively follows active transport of Na_,

Cl_,glucose,and bile salts. Additional transport mechanisms include Cl_/

HCO3                                        

_ exchange,Na _/H_ exchange,H _, K_,Cl _,and HCO3

_ secretion,Na _- glucose cotransport,and active Na_ transport across the basolateral membrane

by Na_,K_-ATPase.

NUTRIENT ABSORPTION

1. Proximal small intestine: iron,calcium,folate,fats (after hydrolysis of triglycerides

to fatty acids by pancreatic lipase and colipase),proteins (after

hydrolysis by pancreatic and intestinal peptidases),carbohydrates (after hydrolysis

by amylases and disaccharidases); triglycerides absorbed as micelles

after solubilization by bile salts; amino acids and dipeptides absorbed

via specific carriers; sugars absorbed by active transport.

2. Distal small intestine: vitamin B12,bile salts, water.

3. Colon: water,electrolytes.

INTESTINAL MOTILITY Allows propulsion of intestinal contents

from stomach to anus and separation of components to facilitate nutrient absorption.

Propulsion is controlled by neural,myogenic,and hormonal mechanisms;

mediated by migrating motor complex,an organized wave of neuromuscular

activity that originates in the distal stomach during fasting and

migrates slowly down the small intestine. Colonic motility is mediated by local

peristalsis to propel feces. Defecation is effected by relaxation of internal anal

sphincter in response to rectal distention,with voluntary control by contraction

of external anal sphincter.

DIARRHEA

PHYSIOLOGY Formally defined as fecal output _200 g/d on low-fiber

(western) diet; also frequently used to connote loose or watery stools. Mediated

by one or more of the following mechanisms:

Osmotic Diarrhea Nonabsorbed solutes increase intraluminal oncotic

pressure,causing outpouring of water; usually ceases with fasting; stool osmolal

gap _ 40 (see below). Causes include disaccharidase (e.g.,lactase) deficiencies,

pancreatic insufficiency,bacterial overgrowth,lactulose or sorbitol ingestion,

polyvalent laxative abuse,celiac or tropical sprue, and short bowel syndrome.

Lactase deficiency can be either primary (more prevalent in blacks and Asians,

usually presenting in early adulthood) or secondary (from viral,bacterial, or

protozoal gastroenteritis,celiac or tropical sprue, or kwashiorkor).

Secretory Diarrhea Active ion secretion causes obligatory water loss; diarrhea

is usually watery,often profuse, unaffected by fasting; stool Na_ and K_

are elevated with osmolal gap _ 40. Causes include viral infections (e.g.,rotavirus,

Norwalk virus),bacterial infections (e.g., cholera, enterotoxigenic Escherichia

coli, Staphylococcus aureus),protozoa (e.g., Giardia, Isospora, Cryptosporidium),

AIDS-associated disorders (including mycobacterial and

HIV-induced),medications (e.g., theophylline,colchicine, prostaglandins, diuretics), Zollinger-Ellison syndrome (excess gastrin production), vasoactive intestinal peptide (VIP)-producing tumors,carcinoid tumors (histamine and serotonin), medullary thyroid carcinoma (prostaglandins and calcitonin), systemic

mastocytosis,basophilic leukemia, distal colonic villous adenomas (direct secretion

of potassium-rich fluid),collagenous and microscopic colitis, and cholerrheic

diarrhea (from ileal malabsorption of bile salts).

Exudative Inflammation,necrosis, and sloughing of colonic mucosa; may

include component of secretory diarrhea due to prostaglandin release by inflammatory cells; stools usually contain PMNs as well as occult or gross blood.

Causes include bacterial infections [e.g., Campylobacter, Salmonella, Shigella,

Yersinia,invasive or enterotoxigenic E. coli, Vibrio parahemolyticus, Clostridium

difficile colitis (frequently antibiotic-induced)],colonic parasites (e.g., Entamoeba

histolytica),Crohn’s disease, ulcerative proctocolitis, idiopathic inflammatory

bowel disease,radiation enterocolitis, cancer chemotherapeutic agents,

and intestinal ischemia.

Altered Intestinal Motility Alteration of coordinated control of intestinal

propulsion; diarrhea often intermittent or alternating with constipation. Causes

include diabetes mellitus,adrenal insufficiency, hyperthyroidism, collagen-vascular

diseases,parasitic infestations, gastrin and VIP hypersecretory states, amyloidosis,

laxatives (esp. magnesium-containing agents), antibiotics (esp. erythromycin),

cholinergic agents, primary neurologic dysfunction (e.g., Parkinson’s

disease,traumatic neuropathy),fecal impaction, diverticular disease, and irritable

bowel syndrome. Blood in intestinal lumen is cathartic,and major upper

GI bleeding leads to diarrhea from increased motility.

Decreased Absorptive Surface Usually arises from surgical manipulation

(e.g.,extensive bowel resection or rearrangement) that leaves inadequate absorptive

surface for fat and carbohydrate digestion and fluid and electrolyte

absorption; occurs spontaneously from enteroenteric fistulas (esp. gastrocolic).

EVALUATION History Diarrhea must be distinguished from fecal incontinence,

change in stool caliber, rectal bleeding, and small, frequent, but

otherwise normal stools. Careful medication history is essential. Alternating

diarrhea and constipation suggests fixed colonic obstruction (e.g.,from carcinoma)

or irritable bowel syndrome. A sudden,acute course,often with nausea,

vomiting,and fever, is typical of viral and bacterial infections, diverticulitis,

ischemia,radiation enterocolitis, or drug-induced diarrhea and may be the initial

presentation of inflammatory bowel disease. _90% of acute diarrheal illnesses

are infectious in etiology. A longer (_4 weeks),more insidious course suggests

malabsorption,inflammatory bowel disease, metabolic or endocrine disturbance,

pancreatic insufficiency,laxative abuse,ischemia, neoplasm (hypersecretory

state or partial obstruction),or irritable bowel syndrome. Parasitic and

certain forms of bacterial enteritis can also produce chronic symptoms. Particularly

foul-smelling or oily stool suggests fat malabsorption. Fecal impaction

may cause apparent diarrhea because only liquids pass partial obstruction. Several

infectious causes of diarrhea are associated with an immunocompromised

state (Table 52-1).

Physical Examination Signs of dehydration are often prominent in severe,

acute diarrhea. Fever and abdominal tenderness suggest infection or inflammatory

disease but are often absent in viral enteritis. Evidence of malnutrition

suggests chronic course. Certain signs are frequently associated with specific

deficiency states secondary to malabsorption (e.g.,cheilosis with riboflavin or

iron deficiency,glossitis with B12,folate deficiency).

Stool Examination Culture for bacterial pathogens,examination for leukocytes,

measurement of C. difficile toxin,and examination for ova and parasites

are important components of evaluation of pts with severe,protracted,or bloody

diarrhea. Presence of blood (fecal occult blood test) or leukocytes (Wright’s

stain) suggests inflammation (e.g.,ulcerative colitis, Crohn’s disease, infection,

or ischemia). Gram’s stain of stool can be diagnostic of Staphylococcus, Campylobacter, or Candida infection. Steatorrhea (determined with Sudan III stain

of stool sample or 72-h quantitative fecal fat analysis) suggests malabsorption

or pancreatic insufficiency. Measurement of Na_ and K_ levels in fecal water

helps to distinguish osmotic from other types of diarrhea; osmotic diarrhea is

implied by stool osmolal gap _ 40,where stool osmolal gap _ osmolserum _

[2 _ (Na_ _ K_)stool].

Laboratory Studies CBC may indicate anemia (acute or chronic blood loss

or malabsorption of iron,folate, or B12),leukocytosis (inflammation), eosinophilia

(parasitic,neoplastic, and inflammatory bowel diseases). Serum levels of

calcium, albumin,iron, cholesterol,folate,B 12,vitamin D, and carotene; serum

iron-binding capacity; and prothrombin time can provide evidence of intestinal

malabsorption or maldigestion.

Other Studies D-Xylose absorption test is a convenient screen for smallbowel

absorptive function. Small-bowel biopsy is especially useful for evaluating

intestinal malabsorption. Specialized studies include Schilling test (B12

malabsorption),lactose H2 breath test (carbohydrate malabsorption),[ 14C]xylose

and lactulose H2 breath tests (bacterial overgrowth),glycocholic breath test (ileal

malabsorption),triolein breath test (fat malabsorption), and bentiromide and

secretin tests (pancreatic insufficiency). Sigmoidoscopy or colonoscopy with

biopsy is useful in the diagnosis of colitis (esp. pseudomembranous,ischemic,

microscopic); it may not allow distinction between infectious and noninfectious

(esp. idiopathic ulcerative) colitis. Barium contrast x-ray studies may suggest malabsorption (thickened bowel folds),inflammatory bowel disease (ileitis or

colitis), tuberculosis (ileocecal inflammation),neoplasm,intestinal fistula, or

motility disorders.

TREATMENT

An approach to the management of acute diarrheal illnesses is shown in Fig.

52-1. Symptomatic therapy includes vigorous rehydration (IV or with oral

glucose-electrolyte solutions),electrolyte replacement, binders of osmotically

active substances (e.g.,kaolin-pectin),and opiates to decrease bowel motility

(e.g.,loperamide,diphenoxylate); opiates may be contraindicated in infectious

or inflammatory causes of diarrhea. An approach to the management of

chronic diarrhea is shown in Fig. 52-2.

MALABSORPTION SYNDROMES

Intestinal malabsorption of ingested nutrients may produce osmotic diarrhea,

steatorrhea,or specific deficiencies (e.g., iron; folate; B12; vitamins A,D,E, and

K). Table 52-2 lists common causes of intestinal malabsorption. Protein-losing

enteropathy may result from several causes of malabsorption; it is associated

with hypoalbuminemia and can be detected by measuring stool   1-antitrypsin

or radiolabeled albumin levels. Therapy is directed at the underlying disease.

CONSTIPATION

Defined as decrease in frequency of stools to _1 per week or difficulty in

defecation; may result in abdominal pain,distention,and fecal impaction, with

consequent obstruction or,rarely,perforation. A frequent and often subjective

complaint. Contributory factors may include inactivity,low-fiber diet, and inadequate allotment of time for defecation.

SPECIFIC CAUSES Altered colonic motility due to neurologic dysfunction

(diabetes mellitus, spinal cord injury,multiple sclerosis,Chagas’ disease,

Hirschsprung’s disease,chronic idiopathic intestinal pseudoobstruction, idiopathic

megacolon),scleroderma, drugs (esp. anticholinergic agents, opiates, aluminum-

or calcium-based antacids,calcium channel blockers, iron supplements,

sucralfate), hypothyroidism,Cushing’s syndrome,hypokalemia, hypercalcemia,

dehydration,mechanical causes (colorectal tumors, diverticulitis, volvulus, hernias,

intussusception), and anorectal pain (from fissures,hemorrhoids, abscesses,

or proctitis) leading to retention,constipation,and fecal impaction.

TREATMENT

In absence of identifiable cause,constipation may improve with reassurance,

exercise,increased dietary fiber,bulking agents (e.g., psyllium), and increased

fluid intake. Specific therapies include removal of bowel obstruction (fecolith, tumor),discontinuance of nonessential hypomotility agents (esp. aluminumor

calcium-containing antacids,opiates) or substitute magnesium-based antacids

for aluminum-based antacids. For symptomatic relief,magnesium-containing

agents or other cathartics are occasionally needed. With severe hypoor

dysmotility or in presence of opiates,osmotically active agents (e.g., oral

lactulose,intestinal polyethylene glycol–containing lavage solutions) and oral

or rectal emollient laxatives (e.g.,docusate salts) and mineral oil are most

effective.

Common Causes of Malabsorption

Maldigestion: Chronic pancreatitis,cystic fibrosis, pancreatic carcinoma

Bile salt deficiency: Cirrhosis,cholestasis,bacterial overgrowth (blind loop syndromes, intestinal diverticula, hypomotility disorders), impaired ileal reabsorption (resection,Crohn’s disease),bile salt binders (cholestyramine, calcium

carbonate,neomycin) Inadequate absorptive surface: Massive intestinal resection,gastrocolic fistula, jejunoileal bypass

Lymphatic obstruction: Lymphoma,Whipple’s disease, intestinal lymphangiectasia

Vascular disease: Constrictive pericarditis,right-sided heart failure, mesenteric

arterial or venous insufficiency Mucosal disease: Infection (esp. Giardia,Whipple’s disease, tropical sprue), inflammatory diseases (esp. Crohn’s disease),radiation enteritis, eosinophilic enteritis,ulcerative jejunitis,mastocytosis,tropical sprue, infiltrative disorders

(amyloidosis,scleroderma, lymphoma,collagenous sprue, microscopic colitis),

biochemical abnormalities (gluten-sensitive enteropathy, disaccharidase

deficiency,hypogammaglobulinemia, abetalipoproteinemia, amino acid transport

deficiencies),endocrine disorders (diabetes mellitus, hypoparathyroidism,

adrenal insufficiency,hyperthyroidism, Zollinger-Ellison syndrome, carcinoid

syndrome)