Diagnosis
A CDAD diagnosis is reached based on a number of clinical and laboratory findings such as
low-grade fever, median leukocytosis of around 16,000 WBCs/mm^3 , occasional hypoalbumi-
nemia secondary to a protein-losing enteropathy, and, in 5% of patients, even the dramatic
presentation of acute abdomen. Sigmoidoscopy, when performed in equivocal cases, will show
whitish or yellowish pseudomembranes overlying the mucosa in 41% of cases, and radiologic
studies, although nonspecific, will often show signs of inflammation such as cecal dilatation,
air–fluid levels, and mucosal thumbprinting. Even though diagnosis is often confirmed using
the enzyme-linked immunoassay, it is worth bearing in mind that these tests are only about
85% sensitive. Even polymerase chain reaction (PCR), culture, and the cytotoxicity assay—
considered to be the gold-standard in terms of specificity—are likewise imperfect; therefore, a
negative test result should not undermine the weight of sound clinical judgment when other
likely causes of nosocomial diarrhea have been ruled out (16,17).
Treatment and Prevention
Therapy for mild cases may consist only of discontinuing the offending antibiotics, or
switching to antibiotics less likely to perpetuate CDAD, such as aminoglycosides, macrolides,
sulfonamides, or tetracyclines: up to a quarter of cases will resolve following this step alone.
For moderate-to-severe cases, metronidazole, either orally or intravenously, is the first line of
therapy. In the 20% to 30% of patients who will relapse, a second course of metronidazole is
recommended, followed by vancomycin enema for persistent symptomatic infection. Other
treatments, such as intravenous immunoglobulin, cholestyramine that binds the bacterial
toxin, and probiotics such asLactobacillus, the yeastSaccharomyces boulardii, and even donor
feces or “stool transplantations” to seed the regrowth of normal gut flora, have all been tried
with success but as yet are not commonly done. Of course, prevention remains the most
effective means of addressing theC. difficile dilemma, and precautions such as contact
isolations for known carriers, conscientious handwashing, gloves, and bleach disinfection of
hospital surfaces, endoscopes, and other equipment should never be overlooked (16,17).
Acalculous Cholecystitis
Acalculous cholecystitis, with its difficulty in diagnosis and attendant high mortality, should
be a consideration in jaundiced postoperative patients. Although this disease occurs in only
about 0.19% of SICU patients, it nevertheless accounts for around 14% of all acute cholecystitis
patients, and the mortality ranges from 15% to 41% (18,19). With this in mind, physicians
caring for high-risk populations should carefully evaluate the signs and symptoms of this
disease, and even a low level of clinical suspicion should prompt more thorough investigation.
Risk Factors and Pathophysiology
Although the pathogenesis of acalculous cholecystitis has not been entirely elucidated, it is
apparent that the critically ill patient is particularly prone. Risk factors include recent trauma,
burn injury, or non–biliary tract operations, atherosclerosis, diabetes, hypertension, chronic
renal failure, hemodynamic instability such as congestive heart failure or shock, and use of total
parenteral nutrition (TPN) (18–21). One patient has been reported in the literature with
acalculous cholecystitis secondary to a diaphragmatic hernia mechanically obstructing the cystic
duct (19). Only about 13% have a history indicative of gallbladder disease (21). Given these
associations, it is likely that there are multiple triggering factors contributing to a common
disease state. An experimental form of the disease is produced by a combination of decreased
blood flow to the gallbladder, cystic duct obstruction, and bile concentration (21). It can be
conjectured that a partially ischemic state, together with the effects of stasis, creates a favorable
environment for the growth of enteric bacteria, ultimately leading to inflammation, often with
accompanying gangrene, empyema, perforation, and abscess at rates much higher than those
seen with calculous cholecystitis (18,20,21).E. coliis the organism most commonly isolated (19).
Presentation and Diagnosis
In addition to having one or more of the above risk factors, acalculous cholecystitis patients
frequently present with the classical signs and symptoms of the calculous form, such as right
Intra-abdominal Surgical Infections and Their Mimics in Critical Care 263