Chapter 26 ICU Infections

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SECTION II • Medical and Surgical Crises

Table 26-5.  Causes and Treatment of Endocarditis Patient Characteristic Likely Organisms

Initial Therapy

“Normal” host, community- acquired infection

Streptococcus (especially viridans) S. aureus Enterococcus

Nafcillin or oxacillin plus penicillin and gentamicin

Substitute vancomycin in penicillin allergic patients or if resistant Staphylococcus or Enterococcus recovered (daptomycin second “backup” alternative)

Vancomycin plus aminoglycoside As above for normals

Prosthetic valve disease

Early postoperative: S. epidermidis Gram-negative rods Diphtheroids Late postoperative: (as above for normals) S. epidermidis S. aureus including MRSA, Gram-negative rods Candida Same organisms and therapy as for IV drug users

Vancomycin plus aminoglycoside Amphotericin B (consider adding flucytosine and surgery)

Intravenous drug users

ICU acquired

Infectious Diarrhea Diarrhea developing in the ICU is an extremely common problem. Its etiology often is multifactorial and rarely caused by bacteria associated with usual outpatient infectious diarrhea (e.g., Salmonella, Shigella, Campylobacter, and Yersinia ). When diar- rhea is infection related, a much more common condition is antibiotic associated or “pseudomem- branous” colitis, more commonly known as “ C. dif- ficile ” colitis. Although it is entirely reasonable to perform stool cultures and to examine the stool for inflammatory cells, ova, and parasites in patients recently admitted and predisposed to such patho- gens, repeated culturing of patients with loose stools is cumbersome, expensive, and of very low yield. Pathophysiology Pseudomembranous colitis is caused by toxins pro- duced by Clostridium difficile . This hardy organism, often present in low numbers even in healthy per- sons, persists as the gut microbiome is narrowed by antibiotic pressure. As the organisms prolifer- ate, clostridial toxin is released to directly attack colonic mucosa, in some cases producing the areas of mucosal damage that form the characteristic but inconsistently observed ulcerations known as “pseu- domembranes.” Certain strains that have emerged in recent years (e.g., NAP1) are much more potent in generating toxins. Although classically described

after intravenous clindamycin therapy, C. difficile may overgrow the normal flora of patients receiv- ing essentially any parenteral or oral antibiotic and those inoculated by the infective spores of other patients transmitted in health care environments. Spores from C. difficile can persist in the local environment for weeks to months. Alcohol-based disinfecting liquids do not eradicate these spores, mandating strict handwashing protocols and iso- lation measures to be taken by health care work- ers in order to prevent spread and limit outbreaks. Less commonly, colonic overgrowth in response to antibiotic therapy by other microorganisms (e.g., Staphylococcus, Candida ) can give rise to a similar picture. Although years ago C. difficile colitis was an uncommon nuisance, now, mutations in the bacte- ria have made the disease potentially lethal. Signs and Symptoms C. difficile colitis typically presents with watery diarrhea on the fourth to ninth day of antibiotic therapy. Although usually guaiac positive, the stool is rarely bloody. However, bloody stools may result from one form of the disease localized to the hepatic flexure. Classically, crampy periumbilical and hypo- gastric pain and low-grade fever were common, and an “acute abdomen” was rare (see Chapter 37). Now, high fever, profound leukocytosis, and a pre- sentation suggestive of bowel ischemia or infarction (elevated lactate) are often seen. As experience has