The fact that >25–50% of nosocomial infections are due to the combined effect of the patient’s own flora and invasive devices highlights the importance of improvements in the use and design of such devices. Intensive education, “bundling” of evidence-based interventions (Table 17-4), and use of checklists to facilitate adherence have reduced infection rates (Table 17-3) through improved asepsis in handling and earlier removal of invasive devices. It is especially noteworthy that turnover or shortages of trained personnel jeopardize safe and effective patient care and have been associated with increased infection rates.
TABLE 17-4EXAMPLES OF EVIDENCE-BASED “BUNDLED INTERVENTIONS” TO PREVENT COMMON HEALTH CARE–ASSOCIATED INFECTIONS AND OTHER ADVERSE EVENTS ||Download (.pdf) TABLE 17-4 EXAMPLES OF EVIDENCE-BASED “BUNDLED INTERVENTIONS” TO PREVENT COMMON HEALTH CARE–ASSOCIATED INFECTIONS AND OTHER ADVERSE EVENTS
|Prevention of Central Venous Catheter Infections |
|Catheter insertion bundle: |
|Educate personnel about catheter insertion and care. |
|Use chlorhexidine to prepare the insertion site. |
|Use maximal barrier precautions and asepsis during catheter insertion. |
|Consolidate insertion supplies (e.g., in an insertion kit or cart). |
|Use a checklist to enhance adherence to the “insertion bundle.” |
|Empower nurses to halt insertion if asepsis is breached. |
|Catheter maintenance bundle: |
|Cleanse patients daily with chlorhexidine. |
|Maintain clean, dry dressings. |
|Enforce hand hygiene among health care workers. |
|Ask daily: Is the catheter needed? Remove catheter if not needed or used. |
|Prevention of Ventilator-Associated Events |
|Elevate head of bed to 30–45 degrees. |
|Decontaminate oropharynx regularly with chlorhexidine (controversial). |
|Give “sedation vacation” and assess readiness to extubate daily. |
|Use peptic ulcer disease prophylaxis. |
|Use deep-vein thrombosis prophylaxis (unless contraindicated). |
|Prevention of Surgical-Site Infections |
|Choose a surgeon wisely. |
|Administer prophylactic antibiotics within 1 h before surgery; discontinue within 24 h. |
|Limit any hair removal to the time of surgery; use clippers or do not remove hair at all. |
|Prepare surgical site with chlorhexidine-alcohol. |
|Maintain normal perioperative glucose levels (cardiac surgery patients).a |
|Maintain perioperative normothermia (colorectal surgery patients).a |
|Prevention of Urinary Tract Infections |
|Place bladder catheters only when absolutely needed (e.g., to relieve obstruction), not solely for the provider’s convenience. |
|Use aseptic technique for catheter insertion and urinary tract instrumentation. |
|Minimize manipulation or opening of drainage systems. |
|Ask daily: Is the bladder catheter needed? Remove catheter if not needed. |
|Prevention of Pathogen Cross-Transmission |
|Cleanse hands with alcohol hand rub before and after all contacts with patients or their environments. |
Urinary tract infections (UTIs) account for ~30–40% of nosocomial infections; up to 3% of bacteriuric patients develop bacteremia. Although UTIs contribute at most 15% to prolongation of hospital stay and may have an attributable cost in the range of only $1300, these infections are reservoirs and sources for spread of antibiotic-resistant bacteria. Most nosocomial UTIs are associated with preceding instrumentation or indwelling bladder catheters, which create a 3–7% risk of infection each day. UTIs generally are caused by pathogens that spread up the periurethral space from the patient’s perineum or gastrointestinal tract—the most common pathogenesis in women—or via intraluminal contamination of urinary catheters, usually due to cross-infection by caregivers who are irrigating catheters or emptying drainage bags. Pathogens come occasionally from inadequately disinfected urologic equipment and rarely from contaminated supplies.
Hospitals should monitor essential performance measures for preventing nosocomial UTIs (Table 17-4). Prompts to clinicians to assess a patient’s need for continued use of an indwelling bladder catheter can improve removal rates and lessen the risk of UTI. Guidelines for managing postoperative urinary retention (e.g., with bladder scanners) also may limit the use or duration of catheterization. Other approaches to the prevention of UTIs have included the use of topical meatal antimicrobial agents, drainage bag disinfectants, and anti-infective catheters. None of the latter three measures is considered routine.
Administration of systemic antimicrobial agents for other purposes decreases the risk of UTI during the first 4 days of catheterization, after which resistant bacteria or yeasts emerge as pathogens. Prophylactic antibiotic administration at the time of catheter removal has been reported to decrease the risk of UTI. Selective decontamination of the gut also is associated with a reduced risk. Again, however, none of these approaches is routine.
Irrigation of catheters, with or without antimicrobial agents, may actually increase the risk of infection. A condom catheter for men without bladder obstruction may be more acceptable than an indwelling catheter and may lessen the risk of UTI if maintained carefully. The role of suprapubic catheters in preventing infection is not well defined.
Treatment of UTIs is based on the results of quantitative urine cultures (Chap. 33). The most common pathogens are Escherichia coli, nosocomial gram-negative bacilli, enterococci, and Candida. Several caveats apply in the treatment of institutionally acquired infection. First, in patients with chronic indwelling bladder catheters, especially those in long-term-care facilities, “catheter flora”—microorganisms living on encrustations within the catheter lumen—may differ from actual urinary tract pathogens. Therefore, for suspected UTI in the setting of chronic catheterization (especially in women), it is useful to replace the bladder catheter and to obtain a freshly voided urine specimen. Second, as in all nosocomial infections, at the time treatment is initiated on the basis of a positive culture, it is useful to repeat the culture to verify the persistence of infection. Third, the frequency with which UTIs occur may lead to the erroneous assumption that the urinary tract alone is the source of infection in a febrile hospitalized patient. Fourth, recovery of Staphylococcus aureus from urine cultures may result from hematogenous seeding and may indicate an occult systemic infection. Finally, although Candida is now the most common pathogen in nosocomial UTIs among patients on intensive care units (ICUs), treatment of candiduria is often unsuccessful and is recommended only when there is upper-pole or bladder-wall invasion, obstruction, neutropenia, or immunosuppression.
Historically, pneumonia has accounted for ~10–15% of nosocomial infections; ventilator-associated pneumonia (VAP) occurred in 1 to >4 patients per 1000 ventilator-days, and these infections were reported as responsible for a mean of 10 extra hospital days and $23,000 in extra costs per episode. Most cases of bacterial nosocomial pneumonia are caused by aspiration of endogenous or hospital-acquired oropharyngeal (and occasionally gastric) flora. Nosocomial pneumonias are associated with more deaths than are infections at any other body site. However, attributable mortality rates suggest that the risk of dying from nosocomial pneumonia is affected greatly by other factors, including comorbidities, inadequate antibiotic treatment, and the involvement of specific pathogens (particularly Pseudomonas aeruginosa or Acinetobacter). Surveillance and accurate diagnosis of pneumonia have been problematic in hospitals because many patients, especially those in the ICU, have abnormal chest roentgenographs, fever, and leukocytosis potentially attributable to multiple causes. This diagnostic uncertainty has led to a refocus from VAP to “ventilator-associated events” (VAEs), conditions, and complications, for which worsening physiologic parameters, such as oxygenation, are key metrics. Early data suggest that ~5–10% of patients using mechanical ventilators develop VAEs. Viral pneumonias, which are particularly important in pediatric and immunocompromised patients, are discussed in the virology section and in Chap. 21.
Risk factors for nosocomial pneumonia include those events that increase colonization by potential pathogens (e.g., prior antimicrobial therapy, contaminated ventilator circuits or equipment, or decreased gastric acidity); those that facilitate aspiration of oropharyngeal contents into the lower respiratory tract (e.g., intubation, decreased levels of consciousness, or presence of a nasogastric tube); and those that reduce host defense mechanisms in the lung and permit overgrowth of aspirated pathogens (e.g., chronic obstructive pulmonary disease, extremes of age, or upper abdominal surgery).
Control measures for pneumonia (Table 17-4) are aimed at frequent testing of readiness for extubation, remediation of risk factors in patient care (e.g., minimizing aspiration-prone supine positioning), and aseptic care of respirator equipment (e.g., disinfecting or sterilizing all inline reusable components such as nebulizers, replacing tubing/breathing circuits only if required because of malfunction or visible soiling—rather than on the basis of duration of use—to lessen the number of breaks in the system, and teaching aseptic technique for suctioning). Although the benefits of selective decontamination of the oropharynx and gut with nonabsorbable antimicrobial agents and/or use of short-course postintubation systemic antibiotics have been controversial, a randomized multicenter trial demonstrated lowered ICU mortality rates among patients on mechanical ventilation who underwent oropharyngeal decontamination.
Among the logical preventive measures that require further investigation are placement of endotracheal tubes that provide channels for subglottic drainage of secretions, which has been associated with reduced infection risks during short-term postoperative use, and noninvasive mechanical ventilation whenever feasible. Use of silver-coated endotracheal tubes may lessen risk of VAP but is not considered routine. It is noteworthy that reducing the rate of VAP often has not reduced overall ICU mortality; this fact suggests that this infection is a marker for patients with an otherwise-heightened risk of death.
The most likely pathogens for nosocomial pneumonia and treatment options are discussed in Chap. 21. Several considerations regarding diagnosis and treatment are worth emphasizing. First, clinical criteria for diagnosis (e.g., fever, leukocytosis, development of purulent secretions, new or changing radiographic infiltrates, changes in oxygen requirement or ventilator settings) have high sensitivity but relatively low specificity. These criteria are most useful for selecting patients for bronchoscopic or nonbronchoscopic procedures that yield lower respiratory tract samples protected from upper-tract contamination; quantitative cultures of such specimens have diagnostic sensitivities in the range of 80%. Second, early-onset nosocomial pneumonia, which manifests within the first 4 days of hospitalization, is most often caused by community-acquired pathogens such as Streptococcus pneumoniae and Haemophilus species, although some studies have challenged this view. Late-onset pneumonias most commonly are due to S. aureus, P. aeruginosa, Enterobacter species, Klebsiella pneumoniae, or Acinetobacter. When invasive techniques are used to diagnose VAP, the proportion of isolates accounted for by gram-negative bacilli decreases from 50–70% to 35–45%. Infection is polymicrobial in as many as 20–40% of cases. The role of anaerobic bacteria in VAP is not well defined. Third, one multicenter study suggested that 8 days is an appropriate duration of therapy for nosocomial pneumonia, with a longer duration (15 days in that study) when the pathogen is Acinetobacter or P. aeruginosa. Finally, in febrile patients (particularly those who have endotracheal or gastric tubes inserted through the nares), occult respiratory tract infections, especially bacterial sinusitis and otitis media, should be considered.
SURGICAL WOUND INFECTIONS
Wound infections occur in ~500,000 patients each year, account for ~15–20% of nosocomial infections, contribute up to 7–10 extra postoperative hospital days, and result in $3000 to $29,000 in extra costs, depending on the operative procedure and pathogen(s). The average wound infection has an incubation period of 5–7 days—longer than many postoperative stays. For this reason and because many procedures are now performed on an outpatient basis, the incidence of wound infections has become more difficult to assess. These infections usually are caused by the patient’s endogenous or hospital-acquired skin and mucosal flora and occasionally are due to airborne spread of skin squames that may be shed into the wound from members of the operating-room team. True airborne spread of infection through droplet nuclei is rare in operating rooms unless there is a “disseminator” (e.g., of group A streptococci or staphylococci) among the staff. In general, the common risks for postoperative wound infection are related to the surgeon’s technical skill, the patient’s underlying conditions (e.g., diabetes mellitus, obesity) or advanced age, and inappropriate timing of antibiotic prophylaxis. Additional risks include the presence of drains, prolonged preoperative hospital stays, shaving of operative sites by razor the day before surgery, long duration of surgery, and infection at remote sites (e.g., untreated UTI).
The substantial literature related to risk factors for surgical-site infections and the recognized morbidity and cost of these infections have led to national prevention efforts and to recommendations for “bundling” preventive measures (Table 17-4). Additional measures include attention to technical surgical issues (e.g., avoiding open or prophylactic drains), operating-room asepsis, and preoperative therapy for active infection. Reporting surveillance results to surgeons has been associated with reductions in infection rates. Preoperative administration of intranasal mupirocin to patients colonized with S. aureus, preoperative antiseptic bathing, and intra- and postoperative oxygen supplementation have been controversial because of conflicting study results, but evidence seems mostly to favor these interventions.
The process of diagnosing and treating wound infections begins with a careful assessment of the surgical site in the febrile postoperative patient. Diagnosis of deeper organ-space infections or subphrenic abscesses requires a high index of suspicion and the use of CT or MRI. Diagnosis of infections of prosthetic devices, such as orthopedic implants, may be particularly difficult and often requires the use of interventional radiographic techniques to obtain periprosthetic specimens for culture. Cultures of periprosthetic joint tissue obtained at surgery may miss pathogens that are cloistered in prosthesis-adherent biofilms; cultures of sonicates from explanted prosthetic joints have been more sensitive, particularly for patients who have received antimicrobial agents within 2 weeks of surgery.
The most common pathogens in postoperative wound infections are S. aureus, coagulase-negative staphylococci, and enteric and anaerobic bacteria. In rapidly progressing postoperative infections manifesting within 24–48 h of a surgical procedure, the level of suspicion regarding group A streptococcal or clostridial infection (Chaps. 44 and 51) should be high. Treatment of postoperative wound infections requires drainage or surgical excision of infected or necrotic material and antibiotic therapy aimed at the most likely or laboratory-confirmed pathogens.
INFECTIONS RELATED TO VASCULAR ACCESS AND MONITORING
Intravascular device–related bacteremias cause ~10–15% of nosocomial infections; central vascular catheters (CVCs) account for most of these bloodstream infections. Past national estimates indicated that as many as 200,000 bloodstream infections associated with CVCs occurred each year in the United States, with attributable mortality rates of 12–25%, an excess mean length of hospital stay of 12 days, and an estimated cost of $3700 to $29,000 per episode; one-third to one-half of these episodes occurred in ICUs. However, infection rates have dropped steadily (Table 17-3) since the publication of guidelines by the Healthcare Infection Control Practices Advisory Committee (HICPAC) in 2002. With increasing care of seriously ill patients in the community, vascular catheter–associated bloodstream infections acquired in outpatient settings are becoming more frequent. Broader surveillance for infections—outside ICUs and even outside hospitals—will be needed.
Catheter-related bloodstream infections derive largely from the cutaneous microflora of the insertion site, with pathogens migrating extraluminally to the catheter tip, usually during the first week after insertion. In addition, contamination of the hubs of CVCs or of the ports of “needle-less” systems may lead to intraluminal infection over longer periods, particularly with surgically implanted or cuffed catheters. Intrinsic (during the manufacturing process) or extrinsic (on-site in a health care facility) contamination of infusate, although rare, is the most common cause of epidemic device-related bloodstream infection; extrinsic contamination may cause up to half of endemic bacteremias related to arterial infusions used for hemodynamic monitoring. The most common pathogens isolated from vascular device–associated bacteremias include coagulase-negative staphylococci, S. aureus (with ≥50% of isolates in the United States resistant to methicillin), enterococci, nosocomial gram-negative bacilli, and Candida. Many pathogens, especially staphylococci, produce extracellular polysaccharide biofilms that facilitate attachment to catheters and provide sanctuary from antimicrobial agents. “Quorum-sensing” proteins, a target for future interventions, help bacterial cells communicate during biofilm development.
Evidence-based bundles of control measures (Table 17-4) have been strikingly effective, eliminating almost all CVC-associated infections in one ICU study. Additional control measures for infections associated with vascular access include use of a chlorhexidine-impregnated patch at the skin-catheter junction; daily bathing of ICU patients with chlorhexidine; application of semitransparent access-site dressings (for ease of bathing and site inspection and protection of the site from secretions); avoidance of the femoral site for catheterization because of a higher risk of infection (most likely related to the density of the skin flora); rotation of peripheral catheters to a new site at specified intervals (e.g., every 72–96 h), which may be facilitated by use of an IV therapy team; and application of aseptic technique when accessing pressure transducers or other vascular ports.
Unresolved issues include the role of gut translocation rather than vascular access sites as a cause of primary bacteremia in immunocompromised patients and the implications for surveillance definitions; the best frequency for rotation of CVC sites (given that guidewire-assisted catheter changes at the same site do not lessen and can even increase infection risk); the appropriate role of mupirocin ointment, a topical antibiotic with excellent antistaphylococcal activity, in site care; the relative degrees of risk posed by peripherally inserted central catheters (PICC lines); and the risk-benefit of prophylactic use of heparin (to avoid catheter thrombi, which may be associated with increased risk of infection) or of vancomycin or alcohol (as catheter flushes or “locks”—i.e., concentrated anti-infective solutions instilled into the catheter lumen) for high-risk patients.
Vascular device–related infection is suspected on the basis of the appearance of the catheter site or the presence of fever or bacteremia without another source in patients with vascular catheters. The diagnosis is confirmed by the recovery of the same species of microorganism from peripheral-blood cultures (preferably two samples drawn from peripheral veins by separate venipunctures) and from semiquantitative or quantitative cultures of the vascular catheter tip. Less commonly used diagnostic measures include (1) differential (faster) time to positivity (>2 h) for blood drawn through the vascular access device than for a sample from a peripheral vein and (2) differences in quantitative cultures (a threefold or greater “step-up”) for blood samples drawn simultaneously from a peripheral vein and from a CVC, which should show the step-up if infected. When infusion-related sepsis is considered (e.g., because of the abrupt onset of fever or shock temporally related to infusion therapy), a sample of the infusate or blood product should be retained for culture.
Therapy for vascular access–related infection is directed at the pathogen recovered from the blood and/or infected site. Important considerations in treatment are the need for an echocardiogram (to evaluate the patient for endocarditis), the duration of therapy, and the need to remove potentially infected catheters. In one report, approximately one-fourth of patients with intravascular catheter–associated S. aureus bacteremia who were studied by transesophageal echocardiography had evidence of endocarditis; this test may be useful in determining the appropriate duration of treatment.
Detailed consensus guidelines for the management of intravascular catheter–related infections have been published and recommend catheter removal in most cases of bacteremia or fungemia due to nontunneled CVCs. When attempting to salvage a potentially infected catheter, some clinicians use the “antibiotic lock” technique, which may facilitate penetration of infected biofilms, in addition to systemic antimicrobial therapy (see www.idsociety.org/Other_Guidelines/).
The authors of the consensus treatment guidelines advise that the decision to remove a tunneled catheter or implanted device suspected of being the source of bacteremia or fungemia should be based on the severity of the patient’s illness, the strength of evidence that the device is infected, the presence of local or systemic complications, an assessment of the specific pathogens, and the patient’s response to antimicrobial therapy if the catheter or device is initially retained. For patients with track-site infection, successful therapy without catheter removal is unusual. For patients with suppurative venous thrombophlebitis, excision of affected veins is usually required.