Impact of methicillin resistance on mortality in Staphylococcus aureus VAP: a systematic review.
The aim of the present study was to estimate the impact of methicillin resistance on mortality in ventilator-associated pneumonia (VAP) due to Staphylococcus aureus. PubMed, Scopus and the bibliographies of the eligible studies were searched. The DerSimonian-Laird random effects model was used to determine the effect of methicillin resistance on mortality. Eight articles were included. Crude in-hospital mortality was higher in patients with VAP due to methicillin-resistant S. aureus (MRSA) than in those with VAP due to methicillin-sensitive S. aureus (MSSA). This was also the case for crude intensive care unit mortality. However, three of the selected studies, which adjusted for potential confounding factors, including adequacy of empirical treatment and severity of illness, demonstrated no difference in in-hospital mortality between patients with MRSA and MSSA VAP. This was not the case for another eligible study that also made adjustment, but for confounders other than those shown above. The limited available evidence seems to suggest that methicillin resistance is associated with death among persons acquiring Staphylococcus aureus ventilator-associated pneumonia. However, although supported by even more limited data, adjustment for risk factors suggests that this association may not be causal, but probably due to confounders, such as the adequacy of empirical treatment and severity of illness.
Athanassa
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Alfa Institute of Biomedical Sciences, 9 Neapoleos Street, 151 23 Marousi, Greece.
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Falagas
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D017052:Hospital Mortality; D006801:Humans; D007362:Intensive Care Units / Q000706:statistics & numerical data; D016106:Methicillin Resistance; D053717:Pneumonia, Ventilator-Associated / Q000188:drug therapy / Q000401:mortality; D012121:Respiration, Artificial / Q000009:adverse effects; D013203:Staphylococcal Infections / Q000188:drug therapy / Q000401:mortality; D013211:Staphylococcus aureus / Q000187:drug effects / Q000472:pathogenicity