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Attributable mortality from extensively drug-resistant gram-negative infections using propensity-matched tracer antibiotic algorithms.

Authors :
Kadri SS
Strich JR
Swihart BJ
Hohmann S
Dekker JP
Palmore T
Bonne S
Freeman B
Raybould J
Shah NG
Patel D
Husson J
Jacobs MD
Duong L
Follmann D
Hooper DC
Timpone J
Danner RL
Source :
American journal of infection control [Am J Infect Control] 2019 Sep; Vol. 47 (9), pp. 1040-1047. Date of Electronic Publication: 2019 Feb 27.
Publication Year :
2019

Abstract

Background: Tracer antibiotic algorithms using administrative data were investigated to estimate mortality attributable to extensively drug-resistant gram-negative infections (GNIs).<br />Methods: Among adult inpatients coded for GNIs, colistin cases and 2 comparator cohorts (non-carbapenem β-lactams or carbapenems) treated for ≥4 consecutive days, or died while receiving the antibiotic, were separately propensity score-matched (1:2). Attributable mortality was the in-hospital mortality difference among propensity-matched groups. Infection characteristics and sepsis severity influences on attributable mortality were examined. Algorithm accuracy was assessed by chart review.<br />Results: Of 232,834 GNIs between 2010 and 2013 at 79 hospitals, 1,023 per 3,350 (30.5%) colistin and 9,188 per 105,641 (8.7%) β-lactam (non-carbapenem) comparator cases died. Propensity-matched colistin and β-lactam case mortality was 29.2% and 16.6%, respectively, for an attributable mortality of 12.6% (95% confidence interval 10.8-14.4%). Attributable mortality varied from 11.0% (7.5%-14.7%) for urinary to 15.5% (12.6%-18.4%) for respiratory (P < .0001), and 4.6% (2.1%-7.4%) for early (≤4 days) to 16.6% (14.3%-18.9%) for late-onset infections (P < .0001). Attributable mortality decreased to 7.5% (5.6%-9.4%) using a carbapenem comparator cohort but increased 9-fold in patients coded for severe sepsis or septic shock (P < .0001). Our colistin algorithm had a positive predictive value of 60.4% and sensitivity of 65.3%.<br />Conclusions: Mortality attributable to treatment-limiting resistance during GNIs varied considerably by site, onset, and severity of infection.<br /> (Published by Elsevier Inc.)

Details

Language :
English
ISSN :
1527-3296
Volume :
47
Issue :
9
Database :
MEDLINE
Journal :
American journal of infection control
Publication Type :
Academic Journal
Accession number :
30824387
Full Text :
https://doi.org/10.1016/j.ajic.2019.01.010