Page 975 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

706 PART 5: Infectious Disorders

TABLE 76-2 Features of Noninflammatory, Inflammatory, and Hemorrhagic Diarrhea
Noninflammatory Inflammatory Hemorrhagic
Clinical presentation Large volumes of watery stool; signs and symptoms Dysentery; small quantities of blood and mucus, often Grossly bloody bowel movements
of dehydration accompanied by fever
Laboratory findings Fecal leukocyte studies negative; acidosis; azotemia Fecal leukocyte studies positive Anemia; azotemia in the setting of hemolytic uremic
syndrome (HUS)
Typical pathogens Vibrio cholerae, enterotoxigenic Escherichia coli, Shigella species, Salmonella species, Campylobacter E coli type O157:H7
rotavirus, norovirus jejuni
Pathophysiology Toxin-mediated secretory diarrhea Compromise of the intestinal epithelium with varying Poorly understood
degrees of bacterial invasion
Approach to Rehydration and antimicrobial therapy Antimicrobial therapy if severely ill or Supportive therapy; antimicrobials may increase the
therapy immunocompromised risk of HUS

of food-borne gastroenteritis have been reported among hospitalized is rapid fluid replacement. Severely dehydrated patients may require
patients, in the absence of an identified cluster, the workup of the ICU replacement of 10% of their bodyweight within a 2 to 4-hour period.
17
patient with diarrhea usually need not include consideration of these The timely use of antibiotic treatment, usually with a fluoroquinolone,
pathogens. doxycycline, or azithromycin, is generally recommended. 19
However, it is in recognition of the relative infrequency with which the While V cholerae is the prototypical pathogen associated with nonin-
clinician in the ICU will encounter diarrhea that is not hospital acquired flammatory diarrhea, an array of other organisms can produce the same
that a review of these less familiar presentations is actually warranted. syndrome. While the diarrhea induced by these other pathogens tends
While the distinctions between these syndromes are somewhat arbitrary, to be less severe than that associated with cholera, the greater frequency
and there is considerable overlap between them, it is imperative that the with which these organisms cause infection in the developed world
clinician caring for critically ill patients at least be able to recognize these makes them more likely to be encountered as a cause of diarrhea in this
syndromes. In the sections that follow, inflammatory, noninflammatory, setting. Most important among these are the so-called enterotoxigenic
and hemorrhagic diarrheas are considered separately. Each is discussed strains of Escherichia coli. These isolates produce an extracellular toxin,
with respect to the most common clinical presentations and pathogens a component of which is similar to that produced by V cholerae. The
that could be expected in the ICU (Table 76-2). A general approach end result is comparable—profuse watery diarrhea that challenges the
to the diagnosis and treatment of diarrhea among patients in the ICU patient and clinician to maintain adequate hydration.
follows. The chapter concludes with an in-depth discussion of diarrhea Although viral causes of diarrhea tend to be more severe and com-
caused by C difficile—an organism whose central role as a cause of diar- mon in pediatric patients, rotavirus and norovirus do deserve mention.
rhea among patients in the ICU has already been noted. Both cause a noninflammatory diarrhea. Outbreaks of norovirus in the
■ NONINFLAMMATORY DIARRHEA intensive care unit have been described. In large measure because of
20
the especially high contagiousness of these pathogens, all ICU patients
In general, the noninflammatory diarrheal syndromes are character- with diarrhea should be placed on contact precautions for the duration
ized by the production of large volumes of watery stool devoid of gross of their illness. Prolonged viral shedding and infection can be seen
blood or inflammatory cells. By definition, stool examination for fecal in immunocompromised hosts. The most common mode of trans-
leukocytes in such patients will be negative. The typical presentation and mission is person-to-person contact via fecal or vomitus-oral route.
pathophysiology of noninflammatory diarrhea are best exemplified by Aerosolization as a mode of infection may occur and masks should be
infection with Vibrio cholerae. While this gram-negative bacillus is the worn when clearing areas of heavy soiling with vomitus and diarrhea.
most prevalent cause of dehydrating diarrhea throughout the world, it Management for norovirus and rotavirus is supportive with special
is rarely encountered as a pathogen causing serious disease in the devel- attention paid to avoiding volume depletion and maintaining electrolyte
oped world. That said, the metabolic sequelae of cholera are capable of balance. 20
generating systemic illness sufficiently severe as to require ICU admis- ■
sion in a returning traveler. INFLAMMATORY DIARRHEA
The diarrhea of cholera is secretory in nature. Having established Spanning a broad spectrum of clinical severity, inflammatory diarrhea is
itself in the lumen of the bowel, V cholerae releases an extracellu- strictly defined by the presence of fecal leukocytes when the stool from
lar protein that binds to the membrane of intestinal epithelial cells. affected patients is examined microscopically. In terms of pathophysiol-
The enterotoxin induces an increase in intracellular cyclic adenosine ogy, these infections are characterized by compromise of the integrity
monophosphate (cAMP). The high concentration of cAMP induces an of the intestinal epithelium. Depending on the causative organism,
increase in chloride secretion and a decrease in sodium absorption, pro- there may be varying degrees of bacterial invasion. As a result of this
ducing the massive fluid and electrolyte loss characteristic of cholera. 18 process, inflammatory cells, including both neutrophils and lympho-
While the diarrhea experienced by the patient infected with V cholerae cytes, are recruited to the affected area, where some are shed into the
is characteristic of the other noninflammatory diarrheal infections, the intestinal lumen.
severity of disease is unique to cholera. Diarrhea is voluminous, often In the most extreme cases, inflammatory diarrhea causes the clinical
described as “rice water” stool and patients can lose more than 1 L of syndrome commonly referred to as dysentery. The patient with dysen-
fluid every hour. Affected patients are at high risk for life-threatening tery presents with semisolid or liquid bowel movements that are not
dehydration. Vital signs will reveal tachycardia and hypotension. The as voluminous as those seen with noninflammatory diarrhea. In fact,
metabolic abnormalities can precipitate severe acidosis. To compensate, some patients report very scant production of fecal matter. For them,
the patient may become tachypneic. Skin evaluation in these individuals bowel movements are characterized by small quantities of gross blood
reveals decreased turgor. The mucous membranes, including conjuncti- and mucus. Fever is often present, but is usually not exceedingly high.
vae, appear dry. In extreme cases, the patient’s eyes will appear sunken, Patients with dysentery may experience severe cramping abdominal
producing a characteristic facies. If fluids are not replaced promptly and pain or tenesmus—pain with the passage of bowel movements. Because
in sufficient quantity, the infection will be fatal. The mainstay of therapy of the limited ability of many critically ill patients to report such

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