Objective.To evaluate the epidemiology, outcomes, and importance of Clostridium difficile colonization pressure (CCP) as a risk factor for C. difficile–associated disease (CDAD) acquisition in intensive care unit (ICU) patients.Design.Secondary analysis of data from a 30-month retrospective cohort study.Setting.A 19-bed medical ICU in a midwestern tertiary care referral center.Patients.Consecutive sample of adult patients with a length of stay of 24 hours or more between July 1, 1997, and December 31, 1999.Results.Seventy-six (4%) of 1,872 patients were identified with CDAD; 40 (53%) acquired CDAD in the ICU, for an incidence of 3.2 cases per 1,000 patient-days. Antimicrobial therapy, enteral feeding, mechanical ventilation, vancomycin-resistant enterococci (VRE) colonization or infection, and CCP (5.5 vs 2.0 CDAD case-days of exposure for patients with acquired CDAD vs no CDAD; P = .001) were associated with CDAD acquisition in the univariate analysis. Only VRE colonization or infection (45% of patients with acquired CDAD vs 16% of patients without CDAD; adjusted odds ratio, 2.76 [95% confidence interval, 1.36-5.59]) and a CCP of more than 30 case-days of exposure (20% with acquired CDAD vs 2% with no CDAD; adjusted odds ratio, 3.77 [95% confidence interval, 1.14-12.49]) remained statistically significant in the multivariable analysis. Lengths of stay (6.1 vs 3.0 days; P < .001 by univariate analysis) and ICU costs ($11,353 vs $6,028; P < .001 by univariate analysis) were higher for patients with any CDAD than for patients with no CDAD.Conclusions.In this nonoutbreak setting, the CCP was an independent risk factor for acquisition of CDAD in the ICU at the upper range of exposure duration. Having CDAD in the ICU was a marker of excess healthcare use.
Objective.To evaluate 2 active surveillance strategies for detection of enteric vancomycin-resistant enterococci (VRE) in an intensive care unit (ICU).Design.Thirty-month prospective observational study.Setting.ICU at a university-affiliated referral center.Patients.All patients with an ICU stay of 24 hours or more were eligible for the study.Intervention.Clinical active surveillance (CAS), involving culture of a rectal swab specimen for detection of VRE, was performed on admission, weekly while the patient was in the ICU, and at discharge. Laboratory-based active surveillance (LAS), involving culture of a stool specimen for detection of VRE, was performed on stool samples submitted forClostridium difficiletoxin detection.Results.Enteric colonization with VRE was detected in 309 (17%) of 1,872 patients. The CAS method initially detected 280 (91%) of the 309 patients colonized with VRE, compared with 25 patients (8%) detected by LAS; colonization in 4 patients (1%) was initially detected by analysis of other clinical specimens. Most patients with colonization (76%) would have gone undetected by LAS alone, whereas use of the CAS method exclusively would have missed only 3 patients (1%) who were colonized. CAS cost $1,913 per month, or $57,395 for the 30-month study period. Cost savings of CAS from preventing cases of VRE colonization and bacteremia were estimated to range from $56,258 to $303,334 per month.Conclusions.A patient-based CAS strategy for detection of enteric colonization with VRE was superior to LAS. In this high-risk setting, CAS appeared to be the most efficient and cost-effective surveillance method. The modest costs of CAS were offset by the averted costs associated with the prevention of VRE colonization and bacteremia.
The authors studied blood lead levels of 226 randomly selected children, aged 6-92 mo, who lived in either a lead-mining area or a nonmining area, and 69 controls. The authors sought to determine to what extent mining activities contributed to blood lead levels in the children. The mean blood lead levels in the study and control groups were 6.52 microg/dl and 3.43 microg/dl, respectively. The corresponding proportions of children with elevated blood lead levels were 17% and 3%. Soil and dust lead levels were up to 10 times higher in the study than the control group. Elevated blood lead levels appeared to result from exposure to both lead-mining waste and lead-based paint. Mining waste was the cause of the higher prevalence of elevated blood lead levels in these children.
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