[General]
Gastroenteritis: Inflammation of the lining of the
stomach and intestines, predominantly manifested by upper GI tract
symptoms (anorexia, nausea, vomiting), diarrhea, and abdominal
discomfort.
(See also Food
Allergy and Intolerance under Disorders
with Type I Hypersensitivity Reactions in Ch. 148; Acute
Infectious Neonatal Diarrhea under Neonatal
Infections in Ch. 260; and Acute
Infectious Gastroenteritis under Bacterial
Infections in Ch. 265.)
The electrolyte and fluid loss associated with
gastroenteritis may be little more than an inconvenience to an
otherwise healthy adult but may be of grave significance to a person
less able to withstand this loss (eg, the elderly, very young, or
debilitated or those with certain concomitant illnesses).
Etiology and Epidemiology
Gastroenteritis may be of nonspecific, uncertain, or
unknown etiology or of bacterial, viral, parasitic, or toxic
etiology. When a specific cause can be identified, the specific
syndrome name can be used, thus avoiding the less specific term
"gastroenteritis."
Campylobacter infection is the most common
bacterial cause of diarrheal illness in the USA (see Campylobacter
Infections and Noncholera
Vibrio Infections in Ch. 157). Person-to-person
transmission is especially common with gastroenteritis caused by
Shigella, Escherichia coli O157:H7, Giardia,
Norwalk virus, and rotavirus. Salmonella infection may be
acquired through contact with reptiles (eg, iguanas, turtles).
Viral causes of gastroenteritis include Norwalk virus
and Norwalk-like viruses, rotaviruses, adenoviruses, astroviruses,
and caliciviruses. Epidemics of viral diarrhea in infants, children,
and adults are usually spread via contaminated water or food or via
the fecal-oral route. Norwalk virus infections occur year-round and
cause about 40% of outbreaks of gastroenteritis in children and
adults. During winter in temperate climates, rotaviruses are major
causes of serious diarrheal illnesses that result in hospitalization
of children < 2 yr old. Adults, whose infections tend to be
milder, probably have some immunity.
Certain intestinal parasites, notably Giardia
lamblia (see Giardiasis
under Intestinal
Protozoa in Ch. 161), adhere to or invade the intestinal mucosa
and cause nausea, vomiting, diarrhea, and general malaise.
Giardiasis is endemic in many cold climates (eg, Rocky Mountain
states, northern USA, Europe). The disease can become chronic and
can cause a malabsorption syndrome (see Ch.
30). It is usually acquired via person-to-person transmission
(eg, in day care centers) or from drinking contaminated water (eg,
from streams). Another intestinal parasite, Cryptosporidium
parvum, causes watery diarrhea that is sometimes accompanied by
abdominal cramps, nausea, and vomiting. In healthy persons the
illness is usually mild and self-limited, but in immunocompromised
patients the infection may be severe, causing substantial
electrolyte and fluid loss. Cryptosporidium is probably
most commonly acquired by drinking contaminated water. Although
Cryptosporidium oocysts are commonly found in municipal
water supplies, it is unknown what percentage of water supplies
contain viable, infectious oocysts.
Intestinal flu or grippe and some types of traveler's
diarrhea may be caused by bacterial enterotoxins or viral
infections.
Pathophysiology
Certain bacterial species elaborate
enterotoxins, which impair intestinal absorption
and can provoke secretion of electrolytes and water. In some
instances, a chemically pure toxin has been characterized (eg, the
enterotoxin of Vibrio cholerae); pure toxin alone produces
the voluminous watery secretion from the small intestine seen
clinically, thereby demonstrating an adequate pathogenic mechanism
for diarrhea. Enterotoxins are probably the mechanism of other
diarrheal syndromes (eg, E. coli enterotoxin may cause some
outbreaks of "nursery diarrhea" and traveler's diarrhea).
Some Shigella, Salmonella, and E.
coli species penetrate the mucosa of the small intestine or
colon and produce microscopic ulceration, bleeding, exudation of
protein-rich fluid, and secretion of electrolytes and water. The
invasive process and its results may occur whether or not the
organism elaborates an enterotoxin.
Gastroenteritis may follow ingestion of
chemical toxins contained in plants (eg, mushrooms,
potatoes, garden flora), seafood (fish, clams, mussels), or
contaminated food.
Heavy-metal (arsenic, lead, Hg, cadmium) ingestion may
cause acute nausea, vomiting, and diarrhea. Many drugs, including
broad-spectrum antibiotics, have major GI side effects. Various
mechanisms play a role, including the alteration of normal gut
flora.
Symptoms and Signs
The character and severity of symptoms depend on the
nature of the causative agent, the duration of its action, the
patient's resistance, and the extent of GI involvement. Onset is
often sudden and sometimes dramatic, with anorexia, nausea,
vomiting, borborygmi, abdominal cramps, and diarrhea (with or
without blood and mucus). Associated malaise, muscular aches, and
prostration may occur.
If vomiting causes excessive fluid loss, metabolic
alkalosis with hypochloremia occurs; if diarrhea is more prominent,
acidosis is more likely. Excessive vomiting or diarrhea may cause
hypokalemia. Hyponatremia may develop, particularly if hypotonic
fluids are used in replacement therapy. Severe dehydration and
acid-base imbalance can produce headache and muscular and nervous
irritability. Persistent vomiting and diarrhea may result in severe
dehydration and shock, with vascular collapse and oliguric renal
failure.
The abdomen may be distended and tender; in severe
cases, muscle guarding may be present. Gas-distended intestinal
loops may be visible and palpable. Borborygmi are audible with the
stethoscope, even without diarrhea (an important differential
feature from paralytic ileus). Signs of extracellular fluid
depletion (see Disorders
of Water and Sodium Metabolism in Ch. 12) may be present (eg,
hypotension, tachycardia).
Diagnosis
A history of ingestion of potentially contaminated
food, untreated surface water, or a known GI irritant; recent
travel; and contact with similarly ill persons may be important.
Stool examination for fecal WBCs and culture are indicated unless
symptoms subside within 48 h. Sigmoidoscopy helps diagnose
ulcerative colitis and amebic dysentery, although shigellosis and
E. coli O157:H7 may produce colonic lesions
indistinguishable from those of ulcerative colitis. Diagnosis may
also require culture of vomitus, food, and blood. Eosinophilia may
indicate parasitic infection.
The acute surgical abdomen is usually excluded by a
history of frequent stools, a low or normal WBC count, and lack of
muscle spasm and localized tenderness. However, diarrhea may occur
at times in acute appendicitis, incomplete small-bowel obstruction,
other acute intra-abdominal emergencies, and colonic
malignancy.
General Principles of Treatment
Supportive treatment is most important. Bed rest with
convenient access to a toilet or bedpan is desirable. When nausea or
vomiting is mild or has ended, oral glucose-electrolyte solutions
(see Diarrhea
in Ch. 27), strained broth, or salted bouillon may prevent
dehydration or treat mild dehydration. Even if vomiting, the patient
should take frequent but small sips of such fluids because the
vomiting may resolve with volume replacement. Children may become
dehydrated more quickly and should be given an appropriate
rehydration solution (several are available commercially). Commonly
used liquids, such as carbonated beverages or sports drinks, lack
the correct ratio of glucose to Na and thus are not appropriate for
children < 5 yr old. If vomiting is protracted or if severe
dehydration is prominent, IV replacement of appropriate electrolytes
is necessary (see Cholera
in Ch. 157).
If vomiting is severe and a surgical condition has
been excluded, an antiemetic (eg, dimenhydrinate 50 mg IM q 4 h,
chlorpromazine >= 25 to 100 mg/day IM) or prochlorperazine 10 mg
po tid (suppository 25 mg bid) may be beneficial. Meperidine 50 mg
IM q 3 or 4 h may be given for severe abdominal cramps. Morphine
should be avoided because it increases intestinal muscle tone and
may aggravate vomiting.
When the patient can tolerate fluids without vomiting,
bland food (cereal, gelatin, bananas, toast) may be added to the
diet gradually. If after 12 to 24 h, moderate diarrhea persists
without severe systemic symptoms or blood in the stool,
diphenoxylate 2.5 to 5 mg tid or qid in tablet or liquid form,
loperamide 2 mg po qid, or bismuth subsalicylate 524 mg (two tablets
or 30 mL) po six to eight times/day may be given.
The role of antibiotics is disputed,
even for specific infectious diarrheas, but most authorities
recommend treating symptomatic shigellosis (see Shigellosis
in Ch. 157). Antibiotics appropriate to sensitivity testing should
be given when systemic infection is evident. However, antibiotics do
not help patients with simple gastroenteritis, nor do they help
asymptomatic carriers to "clear" rapidly. In fact, antibiotics may
favor and prolong the carrier state of salmonellosis. Indiscriminate
use of antibiotics fosters the emergence of drug-resistant organisms
and is discouraged.
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