Transcript Description

BY
DR: RAMY A. SAMY
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Definition:
abnormal increase in stool liquidity, stool
frequency, and stool weight (more than 200
grams per day).
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Diarrhea :
< 2 weeks: acute
> 2 weeks: chronic
Traveler’s diarrhea
 Infection: non-inflammatory
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Inflammatory
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Other medical disease:
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Drugs:
Acute diverticulitis, superior
mesenteric arterial/venous thrombosis, Ischemic bowel disease, IBD
Virtually all medications
◦ magnesium- or phosphate-containing antacids or supplements,
antiarrhythmics, broad-spectrum antibiotics, antineoplastics,
antihypertensives, bile acids, cholinergic agents, laxatives, NSAID,
potassium supplements, and prostaglandins.
◦ Medicinal elixirs contain high amounts of sorbitol, which can have a
cathartic effect on the bowel (1 dose….) eg. acetaminophen, theophylline,
and cimetidine (not listed)
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Immunocompromised and food allergy
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Whenever a person travels from one country
to another—particularly if the change involves
a marked difference in climate, social
conditions, or sanitation standards and
facilities—diarrhea is likely to develop within
2–10 days
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There may be up to ten or even more loose
stools per day, often accompanied by
abdominal cramps, nausea,
occasionally vomiting, and rarely fever. The
stools do not usually contain mucus or
blood,
and
aside
from
weakness,
dehydration, and occasionally acidosis, there
are no systemic manifestations of infection.
The illness usually subsides spontaneously
within 1–5 days, although 10% remain
symptomatic for a week or longer, and in 2%
symptoms persist for longer than a month .
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Bacteria cause 80% of cases of traveler's
diarrhea, with enterotoxigenic E coli,
Shigella species, and Campylobacter jejuni
being the most common pathogens.
Less common causative agents include
Aeromonas, Salmonella, noncholera vibrios,
Entamoeba histolytica, and Giardia lamblia.
Contributory causes may at times include
unusual food and drink, change in living
habits,
occasional
viral
infections
(adenoviruses or rotaviruses), and change in
bowel flora
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Watery, nonbloody diarrhea associated with
periumbilical cramps, bloating, nausea, or
vomiting (singly or in any combination)
suggests small bowel enteritis caused by
either
a
toxin-producing
bacterium
(enterotoxigenic
E
coli
[ETEC],
Staphylococcus aureus, Bacillus cereus, C
perfringens) or other agents (viruses,
Giardia) that disrupt the normal absorption
and secretory process in the small intestine.
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Prominent vomiting suggests viral enteritis
or S. aureus food poisoning.
Though typically mild, the diarrhea (which
originates in the small intestine) may be
voluminous (ranging from 10 to 200
mL/kg/24 h) and result in dehydration with
hypokalemia and metabolic acidosis due to
loss of HCO3– in the stool (eg, cholera).
Because tissue invasion does not occur,
fecal leukocytes are not present.
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A severe systemic illness manifested initially
by prolonged high fevers, prostration,
confusion, respiratory symptoms followed by
abdominal tenderness, diarrhea, and a rash is
due to infection with Salmonella typhi or
Salmonella
paratyphi,
which
causes
bacteremia and multiorgan dysfunction
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In over 90% of patients with acute diarrhea, the
illness is mild and self-limited and responds
within 5 days to simple rehydration therapy or
antidiarrheal agents
Patients with signs of inflammatory diarrhea
manifested by any of the following require
prompt medical attention:
high fever (> 38.5 °C),
bloody diarrhea,
abdominal pain, or
diarrhea not subsiding after 4–5 days.
Similarly,
patients
with
symptoms
of
dehydration must be evaluated (excessive
thirst, dry mouth, decreased urination,
weakness, lethargy)
Physical examination should note the
patient's general appearance, mental
status, volume status, and the
presence of abdominal tenderness or
peritonitis
 Peritoneal findings may be present in
C difficile and enterohemorrhagic E
coli.
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Hospitalization is required in patients
with severe dehydration, toxicity, or
marked
abdominal
pain.
Stool
specimens should be sent in all cases
for examination for fecal leukocytes
and bacterial cultures
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Most cases of acute diarrhea are selflimited, and specific therapy is not
necessary.
Preventing dehydration and restoring fluid
losses. IV/PO
Oral intake should be
encouraged to minimize the risk of
dehydration.
The misconception that the bowel needs
to be at rest or that oral intake will
worsen the diarrheal illness should be
abandoned.
Avoid milk and other lactose-containing
products, Caffeine-containing products
Glucose-containing electrolyte solutions
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Clostridium
difficile
¼
of
antibiotic-
associated diarrhea.
¾ no etiologic agent is identified, diarrhea–
mild– abdominal pain(-). respond to...
Antibiotics
:clindamycin,
ampicillin,
amoxicillin, and cephalosporins
The clinical presentation varies
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The diagnostic test:
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Treatment
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Prevention
? Pus cell, stool OB
? Gram stain
? Culture
? Tissue culture assay for the cytotoxicity of toxin
B
◦ ? ELISA: detect toxin
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◦ Oral metronidazole(500mg po tid or 250mg po
qid ) or oral vancomycin hydrochloride for 10 to
14 days
◦ oral metronidazole is preferred
◦ Approximately 15% of patients experience
relapse…
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Inflammatory, bloody diarrhea
Severe volume depletion
High fever
Sever abdominal pain
Duration > 3 days
Community outbreak
Impaired host
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Antibiotics
Antiretroviral agents
Antineoplastic agents
Anti-inflammatory agents (NSAIDs, gold, 5-ASA)
Antiarrhythmics (quinidine)
Antihypertensives (β blockers)
Oral hypoglycemics (metformin, acarbose)
Antacids (magnesium-containing)
Acid-reducing agents (H2 blockers, PPIs)
Colchicine
Prostaglandin analogs (misoprostol)
Theophylline
Vitamin and mineral supplements
Herbal products
Heavy metals
 Etiology
The causes of chronic diarrhea
may be grouped into six major
pathophysiologic categories
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As stool leaves the colon, fecal osmolality is
equal
to
the
serum
osmolality,
ie,
approximately 290 mosm/kg. Under normal
circumstances, the major osmoles are Na+,
K+, Cl–, and HCO3–. The stool osmolality
may be estimated by multiplying the stool
(Na+ + K+) × 2 (multiplied by 2 to account
for the anions)
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The most common causes of osmotic
diarrhea are disaccharidase deficiency
(lactase deficiency), laxative abuse, and
malabsorption syndromes .
Osmotic diarrheas resolve during fasting.
Osmotic diarrheas caused by malabsorbed
carbohydrates
are
characterized
by
abdominal
distention,
bloating,
and
flatulence due to increased colonic gas
production.
The major causes of malabsorption
are small mucosal intestinal diseases,
intestinal
resections,
lymphatic
obstruction, small intestinal bacterial
overgrowth,
and
pancreatic
insufficiency
 In
patients
with
suspected
malabsorption, quantification of fecal
fat should be performed
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Increased intestinal secretion or decreased
absorption results in a watery diarrhea that
may be large in volume (1–10 L/d) but with a
normal osmotic gap
Major causes include:
 endocrine tumors (stimulating intestinal or
pancreatic secretion),
 bile salt malabsorption (stimulating colonic
secretion), and
 laxative abuse
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Diarrhea is present in most
patients with inflammatory bowel
disease (ulcerative colitis, Crohn's
disease, microscopic colitis). A
variety of other symptoms may be
present,
including
abdominal
pain, fever, weight loss, and
hematochezia
 Abnormal
intestinal
motility
secondary to systemic disorders
or surgery may result in diarrhea
due to rapid transit or to stasis of
intestinal contents with bacterial
overgrowth
resulting
in
malabsorption
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Cyclospora, and the intestinal nematodes
Immunocompromised
patients,
especially
those with AIDS, are susceptible to a number
of infectious agents that can cause acute or
chronic diarrhea
Chronic diarrhea in AIDS is commonly caused by
Cryptosporidium, cytomegalovirus, Isospora belli,
Cyclospora, and Mycobacterium avium complex.
 Approximately
15% of patients
with chronic diarrhea have factitial
diarrhea caused by laxative abuse
or factitious dilution of stool
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Rome Criteria:
Recurrent abdominal pain or discomfort at least 3
days per month for the past 3 months, associated with
2 or more of:
- Improvement wih defecation
- Onset associated with a change in frequency of
stool
- Onset associated with a change in form
(appearance) of stool
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Periods of constipation common
Long history, passage of mucus, exacerbation by stress
Diarrhea during waking hours, urgency
Coexistence with other functional disorders
Against IBS: Recent onset, nocturnal diarrhea, bleeding,
weight loss, voluminous or greasy stool, abnormal blood
tests
Rule out celiac sprue!
Functional diarrhea: Recurrent loose stools without pain.
• History
• Physical examination
• Routine laboratory tests (CBC, albumin, ESR/CRP)
• Stool analysis
• Categorize:
• Watery diarrhea
• Inflammatory diarrhea
• Fatty diarrhea
Secretory
Osmotic
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Define patient’s complaint of diarrhea (change in
consistency, presence of urgency or incontinence)
Stool characteristics (blood, mucus, oil, pus, food
particles) and volume
Duration, pattern of onset
Relation to prandial state
Nocturnal diarrhea
Weight loss
Travel history
Risk factors for HIV infection
Dietary profile and medication review
Family history of IBD
Other
systemic
symptoms
Physical finding
Diagnosis
More helpful to determine severity rather than etiology 
Skin changes
Celiac sprue (dermatitis herpetiformis)
Hemodynamics, temperature,
signs ofpigmentosa)
toxicity 
Mastocytosis (urticaria
Amyloidosis (macroglossia,
purpura)
Helpful clues:
Addison’s disease (hyperpigmentation)
Glucagonoma (migratory necrolytic
erythema)
Carcinoid syndrome (flushing)
Degos’ disease (malignant atrophic
papulosis)
Peripheral neuropathy, orthostatic
hypotension
Amyloidosis
Thyroid nodule
Medullary carcinoma of the thyroid
Right-sided cardiac murmur,
hepatomegaly
Carcinoid syndrome
Arthritis
IBD, Whipple’s, infections
Lymphadenopathy
AIDS, lymphoma
Peripheral vascular disease/abdominal
bruits
Mesenteric vascular insufficiency
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Directed testing for confirmation based on
clinical suspicion, or “broad net” cast in difficult
cases
Categorize diarrhea into watery, inflammatory,
fatty
Timed collection is best, spot tests on random
stool sample more practical
- Occult blood
- White blood cells
- pH
- Sudan stain for fat
- Cultures
- Laxative screen
- Electrolytes, osmolality
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Occult blood and white blood cells:
- Primarily define inflammatory diarrhea
- Wright stain: Sensitivity 70%, specificity 50% for leukocytes
- Fecal calprotectin and lactoferrin less operator dependent,
but test characteristics in chronic diarrhea not well defined
pH:
- Low pH (<
malabsorption
6)
generally
indicative
of
carbohydrate
Sudan stain:
- Fatty diarrhea (steatorrhea)
- Gold standard: Quantitative estimation of stool fat on
collected specimen
- Qualitative estimation feasible on random sample,
- Semiquantitative methods (number and size of fat globules)
correlate well with quantitative collection
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Stool cultures:
- Infection: Usually inflammatory diarrhea
- Bacterial infection rarely cause of chronic diarrhea in
immunocompetent host - Routine cultures are low yield and not
recommended (but done anyway!)
- Special techniques for Aeromonas and Plesiomonas
- Ova and Parasites
- Always consider giardiasis (stool ELISA for Giardia antigen)
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Stool electrolytes:
Stool osmotic gap: 290 – 2([Na+] + [K+])
- Gap < 50 mOsm/Kg: Pure secretory diarrhea
- Gap > 125 mOsm/Kg: Pure osmotic diarrhea
- Gap 50-125 mOsm/kg: Mixed or mild carbohydrate
malabsorption
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Measured stool osmolality:
- Not used to calculate gap
- Useful in cases of unexplained diarrhea
- Low measured stool osmolality (< 290 mOsm/Kg)
suggestive of contamination with water or dilute urine