Am J Respir Crit Care Med 2002 Jan 1;165(1):41-6
Service de Reanimation Medicale, and Service de Microbiologie, Hopital Bichat-Cl-Bernard, Assistance Publique-Hopitaux de Paris, Paris, France.
Results of routine microbiologic cultures of specimens obtained before the onset of ventilator-associated pneumonia (VAP) in intensive care unit (ICU) patients might help to identify the causative microorganisms and thus to select effective initial antimicrobial therapy. To test this hypothesis, we prospectively studied 125 consecutive VAP episodes for which the causative microorganisms were determined using bronchoscopic techniques. Upon entry into the study, each patient's hospital chart was reviewed and culture results of all previously obtained microbiologic specimens were recorded (mean number +/- SD per patient, 45 +/- 38). A total of 220 microorganisms were cultured at significant concentrations (> or = 10(3)/10(4) colony-forming units [cfu]/ml) from bronchoscopic specimens and considered responsible for pneumonia. Of these 220 organisms, only 73 (33%) were recovered before VAP onset, sometimes from multiple sites in the same patient but mainly from prior respiratory secretion cultures (n = 53). Also previously isolated were 342 organisms that were not responsible for VAP, making prospective identifications of the true pathogens difficult. Among the 102 episodes for which prior respiratory secretion culture results had been obtained (mean time before VAP onset, 8 +/- 9 d), all the organisms ultimately responsible for pneumonia were previously recovered from only 36 (35%) of these specimens. Based on these data, the contribution of routine microbiologic specimens in guiding initial antimicrobial therapy decisions for patients with suspected VAP appears limited.
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PMID: 11779728, UI: 21637844
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Am J Respir Crit Care Med 2002 Jan 1;165(1):4-8
Cardiology Section, The Rhode Island Hospital, Providence, Rhode Island 02903, USA. Athena_Poppas@Brown.edu
PMID: 11779722, UI: 21637838
Anaesthesia 2002 Jan;57(1):21-6
Department of Anaesthesiology and Intensive Care Medicine, Charite, Humboldt University, Schumannstr. 20-21, D-10098 Berlin, Germany. dieter.beck@rz.hu-berlin.de
[Medline record in process]
A large proportion of intensive care unit patients are low-risk admissions. Mortality probabilities generated by predictive systems may not accurately reflect the mortality experienced by subpopulations of critically ill patients. We prospectively assessed the impact of low-risk admissions (mortality risk < 10%) on the mortality estimates generated by three prognostic models. We studied 1497 consecutive admissions to a general intensive care unit. The performance of the three models for subgroups and the whole population was analysed. The proportions of patients designated as low risk varied with the model and differences in model performance were most pronounced for these patients. The APACHE II mortality ratios (1.32 vs. 1.19) did not differ for low- and higher risk patients, but mortality ratios generated by APACHE III (2.38 vs. 1.23) and SAPS II (2.19 vs. 1.16) were nearly two-fold greater. Calibration for higher risk patients was similar for all three models but the APACHE III system calibrated worse than the other models for low-risk patients. This may have contributed to the poorer overall calibration of the APACHE III system (Hosmer-Lemeshow C-test: APACHE III chi(2) = 329; APACHE II chi(2) = 42; SAPS II chi(2) = 62). Imperfect characterisation of the large proportion of low-risk intensive care unit admissions may contribute to the deterioration of the models' predictive accuracies for the intensive care population as a whole.
PMID: 11843737, UI: 21832526
Crit Care Med 2002 Jan;30(1 2):S97-S123
[Record supplied by publisher]
PMID: 11839894
Crit Care Med 2002 Jan;30(1 Suppl):S74-9
Department of Surgery, University of Michigan, Ann Arbor, MI, USA. sarbabi@umich.edu
The cellular control switches are regulated through an extensive network of interactive intracellular signal transduction pathways, such as the mitogen-activated protein kinase (MAPK) family. The MAPK pathways may play an important role in the inappropriate inflammatory responses that lead to systemic inflammatory response syndrome or multiple organ dysfunction syndrome. Therefore, elucidating the activation status of the MAPK pathways may be a method to identify patients at risk for systemic inflammatory response syndrome/multiple organ dysfunction syndrome. Also, manipulating the proper pathways may improve patients' outcomes. However, the MAPK family is part of a complex interactive network, which may initiate an unpredictable reaction to the indiscriminate inhibition or activation of a single component. A major challenge is to elucidate the principles by which the network is assembled, so a more tissue- and temporal-specific approach can be used.
PMID: 11782564, UI: 21642101
J Hosp Infect 2002 Feb;50(2):110-114
Department of Microbiology, Queen Elizabeth Hospital, Birmingham, UK
Multiple-antibiotic-resistant Acinetobacter baumanii, including meropenem resistance, was first isolated from a patient in the general intensive care unit of a tertiary-referral university teaching hospital in Birmingham in December 1998. Similar strains were subsequently isolated from 12 other patients, including those on another intensive care unit within the hospital. The outbreak followed an increase in the use of meropenem in both the units. Environmental screening revealed the presence of the multiple-resistant Acinetobacter species on fomite surfaces in the intensive care unit and bed linen. The major source appeared to be the curtains surrounding patients' beds. Typing by pulsed field gel electrophoresis demonstrated that the patients' isolates and those from the environment were indistinguishable. Rigorous infection control measures including increased frequency of cleaning of the environment with hypochlorite (1000?ppm) and twice-weekly changing of curtains were implemented, along with restriction of meropenem use in the units. Isolation of the multiple-resistant Acinetobacter spp. subsequently diminished and it was not detected over a follow-up period of 18 months. To our knowledge, this is the first reported outbreak of carbapenem-resistant Acinetobacter spp. from the UK. This outbreak also highlights environmental sources, particularly dry fabrics such as curtains, as an important reservoir for dissemination of acinetobacters. Copyright 2002 The Hospital Infection Society.
PMID: 11846537
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