Although a number of studies have been performed regarding the prevention of CAUTI, most used the definition of CAUTI developed by the Centers for Disease Control of the National Healthcare Safety Network (CDC-NHSN), which includes ASB. However, approximately 75% to 90% of patients with ASB do not develop a systemic inflammatory response or other signs or symptoms that suggest infection [6
]. Additionally, the monitoring and treatment of ASB is not an effective prevention measure for symptomatic UTI (SUTI), because most cases of SUTI are not preceded by bacteriuria for more than a day [8
]. ASB treatment has not been shown to be clinically beneficial and is associated with the selection of antimicrobial-resistant organisms. This study only defined symptomatic UTIs requiring treatment as CAUTI; those uninfected before ICU admission who developed CAUTI within 48 hours of transfer to the ICU were designated as CAUTI occurring in the ICU during patient selection. The CDC definition of nosocomial infection was used as a reference in developing these definitions [9
]. Because the usual symptoms of UTI (e.g., dysuria, frequent urination, and urgency) are difficult to assess in CAUTI, the presence of fever during urine culture was used to determine SUTI.
Despite a marked reduction in the risk of bacteriuria since the introduction of the sterile, closed urinary drainage system in 1960 [12
], bacteriuria inevitably occurs over time either via breaks in the sterile system or via the extraluminal route [13
]. Microbial pathogens can enter the urinary tract either by the extraluminal route, via migration along the outside of the catheter in the periurethral mucous sheath, or by the intraluminal route via movement along the internal lumen of the catheter from a contaminated collection bag or catheter-drainage tube junction. The formation of biofilms by urinary pathogens on the surface of the catheter and drainage system occurs universally with prolonged durations of catheterization [14
]. Over time, the urinary catheter becomes colonized with microorganisms living in a sessile state within the biofilm, rendering them resistant to antimicrobials and host defenses and virtually impossible to eradicate without removing the catheter.
Not only does the urinary catheter invite biofilm formation, but the presence of the catheter itself impairs many of the normal defense mechanisms of the bladder. The urinary catheter connects the heavily colonized perineum with the normally sterile bladder, and it provides a route for bacterial entry along both its external and internal surfaces [15
]. Urine often pools in the bladder or in the catheter itself, and urinary stasis encourages bacterial multiplication [16
]. Obstruction of the catheter can lead to overdistension and ischemic damage of the bladder mucosa, thus increasing its susceptibility to bacterial invasion [17
]. The catheter also damages the bladder mucosa by triggering an inflammatory response and by mechanical erosion [18
Several risk factors have been cited to be associated with CAUTI. In this study, only two risk factors (duration of catheterization and diabetes) were found to be significantly associated with acquisition of infection.
Increased duration of catheterization was identified as a significant factor associated with acquiring CAUTI in this study and in several other studies [1
]. The occurrence of bacteriuria is inevitable while the urinary catheter is in place [13
]. In prospective studies by Garibaldi et al. [8
] and Warren et al. [22
], the daily risk of bacteriuria with catheterization ranged from 3% to 10% and approached 100% after 30 days, which is considered to be the delineation between short- and long-term catheterization. Of course, in most cases, it was just catheter-associated ASB, which is different from CAUTI. The relationship between catheter-associated ASB and CAUTI is unclear, but the presence of catheter-associated ASB is necessary for the development of CAUTI. The development of urinary symptoms must require some facilitating events, and as the duration of catheterization is increased, the possibility of events occurring is increased also. In addition, catheter-associated ASB represents a large reservoir of antimicrobial-resistant urinary pathogens that may be transmitted to other patients and frequently triggers inappropriate antimicrobial use. Therefore, the greatest impact of an intervention may be to reduce the frequent occurrence of ASB, and the reduction of inappropriate urinary catheter durations is important for that. According to the guidelines on Diagnosis, Prevention, and Treatment of CAUTI in Adults by the Infectious Diseases Society of America in 2009, indications for urinary catheter insertion are described as follows: clinically significant urinary retention, urinary incontinence, accurate urine output monitoring required, and patient unable or unwilling to collect urine [23
This study identified diabetes as a factor in the development of CAUTI, and diabetes as a factor in the development of UTIs has been confirmed in numerous other studies. Geerlings and Hoepelman [24
] noted that in patients with diabetes, impaired granulocyte function, increased adherence of uropathogens to bladder epithelial cells, and the effects of glucosuria on the growth of uropathogens in diabetic patients contribute to a higher UTI prevalence. Platt et al. also documented the presence of diabetes as a risk factor and proposed two possibilities for why diabetic patients are at increased risk of acquiring infection: an increased prevalence of perineal colonization by potential pathogens and an increased ability of the urine of some patients with diabetes to support microbial growth [20
]. These effects of diabetes promote the colonization of uropathogens on the catheter surface when urinary catheters are indwelled and affect the synthesis of biofilms. In addition, the immunocompromised state, which is a characteristic of these patients, allows bacteriuria to easily extend into the upper urinary tract. Patients with diabetes, especially those admitted to the ICU with indwelling catheters, are more susceptible to the development of urosepsis; thus, these patients require strict blood glucose monitoring to prevent CAUTI occurrence and progression.
According to the 2006 to 2007 statistics from the NHSN, the pathogens identified (in the order of frequency) were E. coli (21.4%), Candida spp. (21.0%), Enterococcus spp. (14.9%), P. aeruginosa (10.0%), K. pneumoniae (7.7%), and Enterobacter spp. (4.1%); this grouping is similar to the culture results from this study. However, this study had a smaller proportion of Candida spp. compared with the NHSN numbers, which is thought to be attributable to the fact that the NHSN study did not distinguish between SUTI and ASB, whereas this study specifically selected those with SUTI.
In the other studies, the risk factors associated with CAUTI included the duration of catheterization, diabetes mellitus, not receiving systemic antimicrobial therapy, female sex, catheter insertion outside the operating room, and older age [14
]. The different outcomes in present study may be because we distinguished between SUTI and ASB but could also be due to the limitations of this study.
A limitation of this study is that it included a relatively small number of patients in both the CAUTI and control groups, because it was a retrospective analysis that was conducted on the basis of data from a single hospital. Consequently, to complement this fact, a prospective analysis based on data from multiple institutions is necessary. The results from such studies will aid in the development of guidelines for the prevention of CAUTI in ICUs that are appropriate for Korean hospital settings.