If it diarrhea-predominant IBS, then maybe this will really help....Dicetel
(pinaverium bromide). I don't know if it's available where you are, but it's
an intestinal calcium-channel blocker. It works like magic for me.

Lar

Try cutting out all wheat products and gluten containing products.

TC

If you are interested in trying nutritional products to help with your
condition, you might consider trying mangosteen. It has been used for
many years in Southeast Asia for diarrhea. There is a whole fruit
puree beverage
that is now available called XanGo. while no medical claims can be
made for
this product,it might be worth trying as others have had success with
the use
of mangosteen for diarrhea.

I'm not a big fan of using Bovine Colostrum for any of the
many things it is promoted for, however it is generally very
effective for chronic diarrhea.
You could also try Acidophilus (small amounts for a short
time only), or a Digestive / Pancreatic Enzyme product,
and you might want to be checked for folic acid, calcium,
or iron deficiency.

     

 


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The Merck Manual of Diagnosis and Therapy    
Section 3. Gastrointestinal Disorders    
Chapter 27. Diarrhea And Constipation  
Topics  
[General]  
Diarrhea  
Constipation  
 
Diarrhea
Increased frequency, fluid content, or volume of fecal discharge.

(See also Chs. 28, 30, and 31; Acute Infectious Neonatal Diarrhea in
Ch. 260; and Acute Infectious Gastroenteritis in Ch. 265.)

In Western society, the stool weight of healthy adults is 100 to 300
g/day, depending on the amount of unabsorbable dietary material
(mainly carbohydrates). Diarrhea occurs when stool weight is > 300
g/day, unless this weight is normal (eg, in persons whose diet is rich
in vegetable fiber). Diarrhea results mainly from excess fecal water
(ie, 60 to 90% of stool weight is water).

Etiology and Pathophysiology
Diarrhea has infectious, drug-induced, food-related, postsurgical,
inflammatory, transit-related, and psychologic causes. These many
causes produce diarrhea by four distinct mechanisms: increased osmotic
load, increased secretion, inflammation, and decreased absorption
time.

Osmotic diarrhea occurs when unabsorbable, water-soluble solutes
remain in the bowel, where they retain water. Osmotic diarrhea occurs
with sugar intolerance, including lactose intolerance caused by
lactase deficiency, and with the use of poorly absorbed salts (Mg
sulfate, Na phosphates) as laxatives or antacids.

Ingestion of large amounts of the hexitols (eg, sorbitol, mannitol),
which are used as sugar substitutes, causes osmotic diarrhea as a
result of their slow absorption and stimulation of rapid small-bowel
motility ("dietetic food" or "chewing gum" diarrhea). Even eating too
much of some foods, such as certain fruits, can produce osmotic
diarrhea.

Secretory diarrhea occurs when the small and large bowel secrete more
electrolytes and water than they absorb. Secretagogues include
bacterial toxins (eg, in cholera), enteropathogenic viruses, bile
acids (eg, after ileal resection), unabsorbed dietary fat (eg, in
steatorrhea), some drugs (eg, anthraquinone cathartics, castor oil,
prostaglandins), and peptide hormones (eg, vasoactive intestinal
peptide produced by pancreatic tumors). Microscopic colitis
(collagenous or lymphocytic colitis) causes 5% of secretory diarrhea.
It is 10 times more common in women, generally affecting persons >=
60. Nausea, vomiting, abdominal pain, flatulence, and weight loss may
occur, although the diarrhea is often without other symptoms. Symptoms
are often prolonged. Loperamide can be used to control symptoms, and
histologic changes may resolve with prednisone or sulfasalazine.

Exudative diarrhea occurs with several mucosal diseases (eg, regional
enteritis, ulcerative colitis, TB, lymphoma, cancer) that cause
mucosal inflammation, ulceration, or tumefaction. The resultant
outpouring of plasma, serum proteins, blood, and mucus increases fecal
bulk and fluid content. Involvement of the rectal mucosa may cause
urgency and increased stool frequency because the inflamed rectum is
more sensitive to distention.

Decreased absorption time occurs when chyme is not in contact with an
adequate absorptive surface of the GI tract for a long enough time so
that too much water remains in the feces. Factors that decrease
contact time include small- or large-bowel resection, gastric
resection, pyloroplasty, vagotomy, surgical bypass of intestinal
segments, and drugs (eg, Mg-containing antacids, laxatives) or humoral
agents (eg, prostaglandins, serotonin) that speed transit by
stimulating intestinal smooth muscle.

Malabsorption (see also Ch. 30) produces diarrhea by osmotic or
secretory mechanisms. The mechanism may be osmotic if the unabsorbed
material is abundant, water-soluble, and of low molecular weight.
Lipids are not osmotic, but some (fatty acids, bile acids) act as
secretagogues and produce secretory diarrhea. In generalized
malabsorption (eg, nontropical sprue), fat malabsorption causes
colonic secretion, and carbohydrate malabsorption causes osmotic
diarrhea.

Malabsorption-related diarrhea may also develop when the transport of
chyme is prolonged and fecal bacteria proliferate in the small bowel.
Factors that increase transit time and permit bacterial overgrowth
include strictured segments, sclerodermatous intestinal disease, and
stagnant loops created by surgery.

Paradoxical diarrhea results from oozing around a fecal impaction in
children and in debilitated or demented adults.

Complications
Fluid loss with consequent dehydration, electrolyte loss (Na, K, Mg,
Cl), and even vascular collapse may occur. Collapse may develop
rapidly in patients who are very young or old, are debilitated, or
have severe diarrhea (eg, those with cholera). HCO3 loss may cause
metabolic acidosis. Serum Na concentrations vary according to the
composition of diarrheal losses relative to plasma. Hypokalemia may
occur in severe or chronic diarrhea or if the stools contain excess
mucus. Hypomagnesemia after prolonged diarrhea may cause tetany.

Diagnosis
The history should note the circumstances of onset, including recent
travel, food ingested, source of water, and medication use; duration
and severity; associated abdominal pain or vomiting; blood in the
stool or change in color; frequency and timing of bowel movements;
consistency of stool; evidence of steatorrhea (fatty, greasy, or oily
stools with a foul odor); associated changes in weight or appetite;
and rectal urgency or tenesmus.

Fluid and electrolyte status should be evaluated. A full examination
with attention to the abdomen and a digital rectal examination are
important. Patients with prolonged or severe diarrhea should undergo
proctoscopic examination and (at sigmoidoscopy) biopsy of the rectal
mucosa for histologic examination (infectious, ulcerative, or
collagenous colitis).

Micro- and macroscopic stool examination may be helpful. The
consistency, volume, and presence of blood (apparent or occult),
mucus, pus, or excess fat in the stool should be noted. Microscopy may
confirm the presence of WBCs (indicating ulceration or bacterial
invasion), unabsorbed fat, meat fibers, or parasitic infestation (eg,
amebiasis, giardiasis). Stool pH, normally > 6.0, is decreased by
bacterial fermentation of unabsorbed carbohydrate and protein in the
colon. Alkalinization of the stool can reveal the pink color of
phenolphthalein, a commonly abused laxative. With large volume, stool
electrolytes can be measured to determine if diarrhea is osmotic or
secretory.

Generally, in diseases of the small bowel, stools are voluminous and
watery or fatty. In colonic diseases, stools are frequent, sometimes
small in volume, and possibly accompanied by blood, mucus, pus, and
abdominal discomfort. In diseases of the rectal mucosa, the rectum may
be more sensitive to distention, and diarrhea may be characterized by
frequent, small stools.

Acute diarrhea caused by dietary indiscretion or acute infection
resolves spontaneously; however, if general symptoms (fever, abdominal
pain) are prominent, fecal cultures are advisable, certainly before
empiric treatment with antibiotics. For chronic diarrhea, fecal
cultures and microscopy determine whether specific therapy is
indicated, and sigmoidoscopy and biopsies should follow to look for
inflammatory causes. When malabsorption is possible, fecal fat
excretion should be measured, followed by small-bowel x-ray
(structural disease) and biopsy (mucosal disease). If evaluation is
still negative, assessment of pancreatic structure and function
(pancreatic enzyme secretion, pancreatography) is needed.

Treatment
Diarrhea is a symptom; when possible, the underlying disorder should
be specifically treated, but more often symptomatic treatment will
also be necessary. Intestinal transit time may be increased by
diphenoxylate 2.5 to 5 mg (tablets or liquid) tid or qid, codeine
phosphate 15 to 30 mg bid or tid, paregoric (camphorated opium
tincture) 15 mL q 4 h, or loperamide hydrochloride 2 to 4 mg tid or
qid. Anticholinergics (eg, belladonna tincture, atropine,
propantheline) can decrease peristalsis. A psyllium or methylcellulose
compound provides bulk; although usually prescribed for constipation,
bulking agents in small doses decrease the fluidity of liquid stools.
Kaolin, pectin, and activated attapulgite adsorb fluid.

Severe acute diarrhea may require urgent fluid and electrolyte
replacement to correct dehydration, electrolyte imbalance, and
acidosis. NaCl, KCl, glucose, and fluids to counteract acidosis (Na
lactate, acetate, bicarbonate) may be indicated. Fluid balance and
estimated body fluid composition must be monitored (see Water and
Sodium Metabolism in Ch. 12). Associated vomiting or GI bleeding may
require additional measures.

An oral glucose-electrolyte solution may be given if nausea and
vomiting are not severe. Fluids containing glucose (or sucrose, as
table sugar), NaCl, and Na bicarbonate are easy to prepare and are
rapidly absorbed: 5 mL (1 tsp) table salt, 5 mL baking soda, 20 mL
table sugar, and flavoring are added to 1 L water (about 1 qt).

Parenteral fluids generally are required for more severe diarrhea. If
nausea or vomiting is present, oral intake should be restricted.
However, when water and electrolytes must be replaced in massive
amounts (eg, in epidemic cholera), an oral glucose-electrolyte
solution is sometimes given in addition to the more conventional IV
therapy with electrolyte (bicarbonate) fluids (see Cholera in Ch.
157). Dietary changes may help persons with chronic symptoms (see
Table 27-1).