Screening for Vancomycin-Resistant Enterococcus in the ICU
June 1, 2001 4 minutes read
Screening for Vancomycin-Resistant Enterococcus in the ICU
Abstract & Commentary
Synopsis: In this study of colonization and infection with vancomycin-resistant enterococcus (VRE) in the ICUs of a tertiary care hospital, twice-weekly rectal surveillance for VRE effectively stratified critically ill patients into low and high risk for the development of VRE infection.
Source: Hendrix CW, et al. Ann Surg. 2001;233(2):259-265.
Enterococcus has become an important nosocomial pathogen in the ICU, and the emergence of vancomycin resistance is a potentially devastating consequence of caring for complex critically ill patients. In 1993, 2.5% of approximately 9000 nosocomial enterococcal isolates tested for susceptibility were resistant to vancomycin. In comparison to susceptible isolates, vancomycin-resistant enterococcus seems to be associated with increased mortality, particularly when isolated from the blood. VRE bloodstream infection has been associated with a 52% mortality, which represents an approximate 2-fold increase in comparison to infection by vancomycin-sensitive strains.
Given the limited therapeutic options once VRE infection is established, infection control practices assume great importance in the prevention of attributable mortality and other complications. Strategies such as education and hand washing are relatively effective and do not require individual knowledge of colonization patterns or risk factors. In contrast, other strategies to minimize transmission between patients, such as cohorting, are also effective but require the identification of colonized patients. However, little is known about the ideal surveillance strategy and whether surveillance identifies patients who subsequently develop VRE infection and death.
During a 3-month period, Hendrix and colleagues studied a strategy of surveillance for VRE in high-risk patients admitted to critical care units at a tertiary referral hospital. Patients admitted to the ICU for at least 3 days, or who died and who had an appropriate culture performed, were prospectively enrolled. Specimens for surveillance cultures were obtained from the oropharynx, rectum, urine, gastric, and endotracheal tube aspirates, at admission to and discharge from the unit and also twice-weekly while in the ICU. Colonization was defined as growth of VRE in any of the surveillance cultures, and infection was defined by a positive culture in addition to clinical signs and symptoms of infection. Hendrix et al clearly described their culture techniques and conditions and defined vancomycin resistance by a minimum inhibitory concentration (MIC) of 16 mg/mL or higher. Strain determination was performed by restriction digestion of genomic DNA.
Of 139 enrolled patients, 117 met all inclusion criteria and were studied. Twenty-three of 117 (20%) were colonized during their ICU stay. In 11 patients (48% of the colonized patients and 9% of the entire study group), cultures obtained at the time of admission to the ICU were positive (prevalent colonization). Colonization developed in the remaining 12 (52%) at some later point while in the ICU (incident colonization). VRE infection was identified at ICU admission (n = 3) or developed during the ICU stay (n = 9) in 10% of the entire group.
Twice-weekly surveillance of the rectum alone identified 99% of the VRE-positive days that were identified by surveillance cultures obtained from all 5 sites (396 of 400 days). Surveillance cultures obtained at admission and once-weekly identified 20% fewer VRE-positive days. Hendrix et al determined that a positive rectal surveillance culture was followed by infection 44% of the time (positive predictive value). In contrast, a negative rectal surveillance culture was 99% predictive of not developing a VRE infection in the subsequent week. They also determined that the surveillance and infection isolates were identical in 8 of the 9 incident infections.
Hendrix et al concluded that twice-weekly rectal surveillance for VRE effectively stratifies critically ill patients into low and high risk for the development of VRE infection. They also conclude that such a surveillance strategy could optimize targeted infection control strategies that depend on identification of VRE colonization.
Comment by Grant E. O'Keefe, MD
This study provides useful information for critical care physicians who practice in areas where VRE is endemic. Because treatment options for infection are limited, strategies to prevent colonization are relatively more important. Hendrix et al have determined that a surveillance strategy incorporating surveillance cultures on admission followed by twice-weekly rectal cultures alone identified the vast majority of VRE-positive days, and detected 99% of the VRE-positive days that were identified by a more intensive and more costly strategy.
While these findings are important, some caveats must be considered. First, the predictive values of positive and negative surveillance cultures reported by Hendrix et al are dependent upon the prevalence of colonization and infection and may not apply to other hospitals or situations. It is possible that in situations of lower (or higher) prevalence, the ideal surveillance strategy may be different from that determined in this article. Second, this study includes a relatively small number of patients who ultimately became infected after a positive surveillance culture. Although Hendrix et al report an 89% sensitivity (8/9 infections preceded by rectal colonization), this is a small number of observations on which to base conclusions. In summary, and given the limitations of this relatively small study, the surveillance strategy proposed by Hendrix et al represents a reasonable approach to screening for VRE.
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