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Practice Essentials

Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to
secretion. The augmented water content in the stools (above the normal value of approximately 10
mL/kg/d in the infant and young child, or 200 g/d in the teenager and adult) is due to an imbalance
in the physiology of the small and large intestinal processes involved in the absorption of ions,
organic substrates, and thus water.
Signs and symptoms
Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day and lasts no longer
than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than 14
days. The distinction has implications not only for classification and epidemiologic studies but also
from a practical standpoint, because protracted diarrhea often has different etiologies, poses
different management problems, and has a different prognosis.
The clinical presentation and course of diarrhea therefore depend on its cause and on the host.
Consider the following to determine the source/cause of the patient’s diarrhea:
 Stool characteristics (eg, consistency, color, volume, frequency)
 Presence of associated enteric symptoms (eg, nausea/vomiting, fever, abdominal pain)
 Use of child daycare (common pathogens: rotavirus, astrovirus,
calicivirus;Campylobacter, Shigella, Giardia, and Cryptosporidium species [spp])
 Food ingestion history (eg, raw/contaminated foods, food poisoning)
 Water exposure (eg, swimming pools, marine environment)
 Camping history (possible exposure to contaminated water sources)
 Travel history (common pathogens affect specific regions; also consider rotavirus
and Shigella, Salmonella, and Campylobacter spp regardless of specific travel history, as
these organisms are prevalent worldwide)
 Animal exposure (eg, young dogs/cats: Campylobacter spp; turtles: Salmonellaspp)
 Predisposing conditions (eg, hospitalization, antibiotic use, immunocompromised state)
Signs and symptoms of diarrhea may include the following:
 Dehydration: Lethargy, depressed consciousness, sunken anterior fontanel, dry mucous
membranes, sunken eyes, lack of tears, poor skin turgor, delayed capillary refill
 Failure to thrive and malnutrition: Reduced muscle/fat mass or peripheral edema
 Abdominal pain/cramping
 Borborygmi
 Perianal erythema
See Clinical Presentation for more detail.
Diagnosis
Fecal laboratory studies include the following:
 Examination for ova and parasites
 Leukocyte count
 pH level: A pH level of 5.5 or less or the presence of reducing substances indicates
carbohydrate intolerance, which is usually secondary to viral illness
 Examination of exudates for presence/absence of leukocytes
 Cultures: Always culture for Salmonella, Shigella, and Campylobacter spp andY
enterocolitica in the presence of clinical signs of colitis or if fecal leukocytes are present; look
for Clostridium difficile in those with diarrhea characterized by colitis and/or bloody stools;
assess for Escherichia coli, particularly O157:H7, with bloody diarrhea and a history of eating
ground beef; screen for Vibrio andPlesiomonas spp with a history of eating raw seafood or
foreign travel
 Enzyme immunoassay for rotavirus or adenovirus antigens
 Latex agglutination assay for rotavirus
Other laboratory studies may include the following:
 Serum albumin levels: Low in protein-losing enteropathies from enteroinvasive intestinal
infections (eg, Salmonella spp, enteroinvasive E coli)
 Fecal alpha1-antitrypsin levels: High in enteroinvasive intestinal infections
 Anion gap to determine nature of the diarrhea (ie, osmolar vs secretory)
 Intestinal biopsy: May be indicated in the presence of chronic or protracted diarrhea, as well
as in cases in which a search for a cause is believed to be mandatory (eg, in patients with
acquired immunodeficiency syndrome [AIDS] or patients who are otherwise severely
immunocompromised)
See Workup for more detail.
Management
Acute-onset diarrhea is usually self-limited; however, an acute infection can have a protracted
course. Management is generally supportive: In most cases, the best option for treatment of acute-
onset diarrhea is the early use of oral rehydration therapy (ORT). [1]
Pharmacotherapy
Vaccines (eg, rotavirus) can help increase resistance to infection. Antimicrobial and antiparasitic
agents may be used to treat diarrhea caused by specific organisms and/or clinical circumstances.
Such medications include the following:
 Cefixime
 Ceftriaxone
 Cefotaxime
 Erythromycin
 Furazolidone
 Iodoquinol
 Metronidazole
 Paromomycin
 Quinacrine
 Sulfamethoxazole and trimethoprim
 Vancomycin
 Tetracycline
 Nitazoxanide
 Rifaximin
Background
Acute diarrhea is defined as the abrupt onset of 3 or more loose stools per day. The augmented
water content in the stools (above the normal value of approximately 10 mL/kg/d in the infant and
young child, or 200 g/d in the teenager and adult) is due to an imbalance in the physiology of the
small and large intestinal processes involved in the absorption of ions, organic substrates, and
thus water. A common disorder in its acute form, diarrhea has many causes and may be mild to
severe.
Childhood acute diarrhea is usually caused by infection of the small and/or large intestine;
however, numerous disorders may result in diarrhea, including a malabsorption syndrome and
various enteropathies. Acute-onset diarrhea is usually self-limited; however, an acute infection can
have a protracted course. By far, the most common complication of acute diarrhea is dehydration.
Although the term "acute gastroenteritis" is commonly used synonymously with "acute diarrhea,"
the former term is a misnomer. The term gastroenteritis implies inflammation of both the stomach
and the small intestine, whereas, in reality, gastric involvement is rarely if ever seen in acute
diarrhea (including diarrhea with an infectious origin); in addition, enteritis is also not consistently
present. Examples of infectious acute diarrhea syndromes that do not cause enteritis
include Vibrio cholerae– induced diarrhea and Shigella -induced diarrhea. Thus, the term acute
diarrhea is preferable to acute gastroenteritis.
Diarrheal episodes are classically distinguished into acute and chronic (or persistent) based on
their duration. Acute diarrhea is thus defined as an episode that has an acute onset and lasts no
longer than 14 days; chronic or persistent diarrhea is defined as an episode that lasts longer than
14 days. The distinction, supported by the World Health Organization (WHO), has implications not
only for classification and epidemiological studies but also from a practical standpoint because
protracted diarrhea often has a different set of causes, poses different problems of management,
and has a different prognosis.
Pathophysiology
Diarrhea is the reversal of the normal net absorptive status of water and electrolyte absorption to
secretion. Such a derangement can be the result of either an osmotic force that acts in the lumen
to drive water into the gut or the result of an active secretory state induced in the enterocytes. In
the former case, diarrhea is osmolar in nature, as is observed after the ingestion of nonabsorbable
sugars such as lactulose or lactose in lactose malabsorbers. Instead, in the typical active
secretory state, enhanced anion secretion (mostly by the crypt cell compartment) is best
exemplified by enterotoxin-induced diarrhea.
In osmotic diarrhea, stool output is proportional to the intake of the unabsorbable substrate and is
usually not massive; diarrheal stools promptly regress with discontinuation of the offending
nutrient, and the stool ion gap is high, exceeding 100 mOsm/kg. In fact, the fecal osmolality in this
circumstance is accounted for not only by the electrolytes but also by the unabsorbed nutrient(s)
and their degradation products. The ion gap is obtained by subtracting the concentration of the
electrolytes from total osmolality (assumed to be 290 mOsm/kg), according to the formula: ion gap
= 290 – [(Na + K) × 2].
In secretory diarrhea, the epithelial cells’ ion transport processes are turned into a state of active
secretion. The most common cause of acute-onset secretory diarrhea is a bacterial infection of the
gut. Several mechanisms may be at work. After colonization, enteric pathogens may adhere to or
invade the epithelium; they may produce enterotoxins (exotoxins that elicit secretion by increasing
an intracellular second messenger) or cytotoxins. They may also trigger release of cytokines
attracting inflammatory cells, which, in turn, contribute to the activated secretion by inducing the
release of agents such as prostaglandins or platelet-activating factor. Features of secretory
diarrhea include a high purging rate, a lack of response to fasting, and a normal stool ion gap (ie,
100 mOsm/kg or less), indicating that nutrient absorption is intact.
Mortality/Morbidity
Mortality from acute diarrhea is overall globally declining but remains high. Most estimates have
diarrhea as the second cause of childhood mortality, with 18% of the 10.6 million yearly deaths in
children younger than age 5 years.
Despite a progressive reduction in global diarrheal disease mortality over the past 2 decades,
diarrhea morbidity in published reports from 1990-2000 slightly increased worldwide compared
with previous reports. In the United States, an average of 369 diarrhea-associated deaths/year
occurred among children aged 1-59 months during 1992-1998 and 2005-2006. [6] The vast majority
of diarrhea-associated infant deaths were reported in 2005-2007, with 86% of deaths occurring
among low-birthweight (< 2500 g) infants. [7]
Furthermore, in countries in which the toll of diarrhea is highest, poverty also adds an enormous
additional burden, and long-term consequences of the vicious cycle of enteric infections, diarrhea,
and malnutrition are devastating. [4]
Sex
Most cases of infectious diarrhea are not sex specific. Females have a higher incidence
of Campylobacter species infections and hemolytic uremic syndrome (HUS).
Age
Viral diarrhea is most common in young children. Rotavirus and adenovirus are particularly
prevalent in children younger than 2 years. Astrovirus and norovirus usually infect children
younger than 5 years. Yersinia enterocolitis typically infects children younger than 1 year, and
the Aeromonas organism is a significant cause of diarrhea in young children.
Very young children are particularly susceptible to secondary dehydration and secondary nutrient
malabsorption. Age and nutritional status appear to be the most important host factors in
determining the severity and the duration of diarrhea. In fact, the younger the child, the higher is
the risk for severe, life-threatening dehydration as a result of the high body-water turnover and
limited renal compensatory capacity of very young children. Whether younger age also means a
risk of running a prolonged course is an unsettled issue. In developing countries, persistent
postenteritis diarrhea has a strong inverse correlation with age.

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