Page 976 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 76: Gastrointestinal Infections and Clostridium Difficile 707

complaints, clinicians should be alert for the presence of the unique TABLE 76-3 Diagnostic Approach to the Patient with Infectious Diarrhea
stool characteristics that identify the patient with dysentery and inflam-
matory diarrhea. A number of pathogens have been described in associ- History
ation with the clinical manifestations of inflammatory diarrhea, but the Timing and rapidity of onset
classical description of the syndrome is associated with infection with Associated signs and symptoms (fever)
Shigella species, particularly S dysenteriae. As was true for cholera and
other noninflammatory diarrheas, this association once again points to Nature and quantity of bowel movements
a shared pathophysiology. Pathogenic Shigella species elaborate an exo- Prior antibiotics or chemotherapy
toxin (Shiga toxin) that acts by inhibiting protein synthesis, damaging Physical examination
the intestinal mucosa. Analogous Shiga-like toxins have been detected in
association with other bacterial species linked to inflammatory diarrhea, Hemodynamic compromise (tachycardia or hypotension)
including both enteroinvasive and enterohemorrhagic strains of E coli. Signs of dehydration (orthostasis, skin tenting)
Like Shigella, the other bacterial species commonly identified in Rectal examination for gross or occult bleeding
cases of inflammatory diarrhea are generally acquired through fecal
oral transmission, often in the setting of food-borne outbreaks. In the Laboratory
United States, the most common such pathogens are members of the Stool for fecal leukocytes
Salmonella species. Outbreaks of food-borne salmonellosis, while most Testing for C difficile
commonly linked to undercooked poultry and dairy products, have Stool culture (especially in the setting of outbreak or community acquisition)
even been reported in the context of a deliberate release associated
with an episode of domestic bioterrorism. Other important pathogens Stool for ova and parasites (if travel related)
21
identified in association with inflammatory diarrhea include E coli and Endoscopy (reserve for persistent cases in which other tests are not revealing)
Campylobacter jejuni and are usually associated with undercooked or
cross-contaminated foodstuffs.
■ HEMORRHAGIC DIARRHEA of bowel movements (with particular emphasis on the presence or

Patients with hemorrhagic diarrhea, characterized by the presence of absence of bloody stools). Additional essential data include information
about recent travel, unusual dietary intake, and the presence of similar
frank blood in bowel movements, are increasingly being seen in the symptoms among companions with whom the patient has shared a meal.
setting of the ICU. In addition to the hemodynamic and metabolic Of course, a specific history of prior antibiotic therapy or cancer che-
complications that characterize other inflammatory diarrheas, patients motherapy will be needed to distinguish individuals at especially high
with hemorrhagic diarrhea have been found to be predisposed to sys- risk for C difficile colitis. By the end of this process, the clinician should
temic illness that can warrant admission to critical care. Infections with be able to characterize the diarrhea as acute or chronic, community
enterohemorrhagic E coli O157 : H7 and other serotypes have been epi- or hospital onset, and severe or mild. The last finding is of particular
demiologically linked to the development of the hemolytic uremic syn- importance in that supportive therapy to alleviate severe dehydration
drome and thrombotic thrombocytopenic purpura. 22,23 The mechanism should not be withheld pending further laboratory and microbiologic
linking infection and this syndrome is not yet completely understood. evaluation of severe cases.
It is likely that the interaction between the Shiga toxin, leukocytes, and Given the emphasis placed on distinguishing inflammatory from
platelets contributes to the resultant thrombotic events that are noted on noninflammatory diarrhea, it will come as no surprise that the initial
histopathology. The deposition of fibrin thrombi in the renal glomeruli laboratory workup of the critically ill patient with diarrhea should
24
can induce sufficient anemia, thrombocytopenia, and azotemia as to be include an objective measure of inflammation. Testing for fecal leuko-
life threatening. The hemolytic uremic syndrome typically follows the cytes offers a reliable means by which to do so. The test is performed
onset of diarrhea by about 1 week. While many of these patients will by mixing a drop of stool with methylene blue on a slide, followed by
require intensive supportive therapy, including blood transfusion and examination under a microscope. Testing for stool occult blood has
hemodialysis, for most the condition is reversible. Of particular concern been suggested as another useful tool to identify patients in the ICU
to clinicians caring for these patients is the observation that antimicro- with inflammatory diarrhea. Unfortunately, testing for occult blood,
bial treatment may contribute to the emergence of this syndrome. 25 even in the presence of a new fever in a critically ill patient, may be
■ EVALUATION OF THE CRITICALLY ILL PATIENT WITH DIARRHEA of little use in discriminating inflammatory infectious diarrhea from
other common, noninfectious causes of bloody bowel movements
The foremost consideration in the evaluation of the critically ill patient among such patients, including stress-induced gastric ulceration and
with diarrhea is the prompt recognition of infection with C difficile, as ischemic colitis.
is discussed in detail later. In the setting of prior exposure to antimi- In the setting of noninflammatory diarrhea, epidemiologic data must
crobials or antineoplastic therapy, most hospital-onset diarrhea can be be interpreted to assess the likelihood of infection with unexpected, but
presumptively attributed to C difficile infection until proven otherwise. potentially lethal pathogens such as V cholerae. For a traveler returning
Identification of these patients is critical not only for the initiation of from an endemic area presenting with signs and symptoms consistent
directed therapy, but to ensure that adequate infection control proce- with cholera, direct stool examination under darkfield or phase contrast
dures are followed to limit the spread of infection to other vulnerable microscopy can reveal the linear motility characteristic of V cholerae.
patients in the ICU. A comprehensive approach to the diagnosis of The organism will also grow on nonselective bacteriologic media, but
C difficile is provided at the end of this chapter. the preferred method is culture on thiosulfate-citrate-bile salts-sucrose
Whether or not C difficile infection can be excluded, the evaluation of agar. If infection with enterotoxigenic E coli is suspected, an assay to
diarrhea in the ICU must progress in a systematic fashion with respect to detect toxin is available from reference laboratories. Diagnosis of rotavi-
the microbiology of the most likely infecting organism (Table 76-3). The rus and norovirus is important in complicated cases, immunocompro-
initial assessment of these patients should include an accurate history of mised hosts, and for infection control purposes. The diagnostic test of
both the course of diarrhea and the presence of any precipitating factors choice for rotavirus is reverse-transcription polymerase chain reaction
that might suggest a causative organism. The patient, or for the uncom- on stool samples. This testing modality appears to be more sensitive
municative patient, a family member or friend, should be queried about than enzyme-linked immunoassays diagnosis. Testing for norovirus
the timing of onset of diarrhea, the progression of symptoms, associated can be done by antigen enzyme immunoassays or reverse-transcriptase
systemic complaints such as fever or chills, and the nature and quantity polymerase chain reaction on a patient’s stool. 20

section05_c74-81.indd 707 1/23/2015 12:37:29 PM