Rotation of antimicrobial therapy in the intensive care unit: impact on incidence of ventilator-associated pneumonia caused by antibiotic-resistant Gram-negative bacteria.

The development of antibiotic resistance is associated with high morbidity and mortality, particularly in the intensive care unit (ICU) setting. We evaluated the effect of an antibiotic rotation programme on the incidence of ventilator-associated pneumonia (VAP) caused by antibiotic-resistant Gram-negative bacteria. We conducted a 2-year before-and-after study at two medical-surgical ICUs at two different tertiary referral hospitals. We included all mechanically ventilated patients admitted for > or =48 h who developed VAP. From 1 January through 31 December 2007, a quarterly rotation of antibiotics (piperacillin/tazobactam, fluoroquinolones, carbapenems and cefepime/ceftazidime) for the empirical treatment of VAP was implemented. We analysed the incidence of VAP and the antibiotic resistance patterns of the responsible pathogens in 2006, before (P1) and, in 2007, after (P2) the introduction of the scheduled rotation programme. Overall, there were 79 VAP episodes in P1 and 44 in P2; the mean incidence of VAP was 20.96 cases per 1,000 days of mechanical ventilation (MV) during P1 and 14.97 in P2, with no significant difference between periods on segmented regression analysis. We observed a non-significant reduction of the number of both the poly-microbial (14 [17.7%] in P1 and 5 [10.6%] in P2 [p = 0.32]) and of the antibiotic-resistant Gram-negative bacteria-related VAP (42 [45.2%] in P1 and 16 [34%] in P2 [p = 0.21]). Conversely, the number of VAP caused by Pseudomonas aeruginosa passed from 8.35 per 1,000 days of MV in P1 to 2.33 per 1,000 days of MV in P2 (p = 0.02). No difference in ICU mortality and crude in-hospital mortality between P1 and P2 was noted. Moreover, no significant change of microbial flora isolated through clinical cultures was observed. We were able to conclude that, despite global microbial flora not being affected by such a programme, antibiotic therapy rotation may reduce the incidence of VAP caused by antibiotic-resistant Gram-negative bacteria in the ICU, such as Pseudomonas aeruginosa. The application of this programme may also improve antibiotic susceptibility. However, further studies are needed to confirm our results.

[Noise-induced hearing loss: are health service surveillance programs always effective?]. / Ipoacusia da rumore: i programmi di sorveglianza sanitaria sono sempre efficaci?

OBJECTIVES: To evaluate noise-induced hearing loss in a group of workers at a steel engineering works over a 20 year period (1979-1999). METHODS: A total of 2431 audiometric tests were performed in 708 workers (in 1979, 1984, 1989, 1994 and 1999). Audiometric tests were classified so that hearing loss could be assessed over time. Additionally, personal noise exposure was measured for each worker (average, 85 dB(A) in tests carried out in 1992, 1996 and 1999). RESULTS: Over 5 years of noise exposure, mean cumulative incidence of noise-induced hearing loss was 8,2%. Over 10 years ofexposure (1979-89 or 1984-94 or 1989-99), the mean incidence was 15,3%. This percentage increased to 22,9% and 25,7% when the exposure lasted 15 or 20 years respectively. CONCLUSIONS: The considerable incidence of noise-induced hearing loss within the wide group of steel workers examined greatly exceeds the expected incidence related to the occupational exposure limits. The Evidence Based Occupational Medicine suggests that our health surveillance was not effective enough.

Meticillin-resistant Staphylococcus aureus control in an intensive care unit: a 10 year analysis.

Data regarding the efficacy of programmes to control meticillin-resistant Staphylococcus aureus (MRSA) in intensive care units (ICUs) are limited. We performed an observational 'before-and-after' study to evaluate the search-and-destroy (S&D) strategy as compared with S&D and isolation (SDI), to control MRSA in a general ICU. S&D included active surveillance, contact precautions and treatment of carriers; in SDI, isolation or cohorting were added. Three phases were identified: period 1 (p1), 1996-1997, before the introduction of programme; period 2 (p2), 1998-2002, with S&D programme; period 3 (p3), 2003-2005, with SDI in a new ICU. During the 10 years of the study we observed 3978 patients; 667, 1995 and 1316 patients in p1, p2 and p3 respectively. The numbers of MRSA-infected patients were 19 in p1, 23 in p2, and 6 in p3. The infection rate was 3.5, 1.7 and 0.7 cases per 1000 patient-days in p1, p2 and p3, respectively; a significant reduction was observed between p1 vs p2 (P=0.024) and p2 vs p3 (P=0.048), although the latter was not confirmed by a segmented regression analysis. The proportion of ICU-acquired MRSA cases was 80%, 77% and 52% during p1, p2 and p3, respectively (P=0.0001 for trend). The proportion of S. aureus isolates resistant to meticillin was 51%, 32% and 23% during p1, p2 and p3, respectively (P<0.0001 for trend). S&D strategy was effective in significantly reducing MRSA infection, transmission rates and proportion of meticillin resistance in an ICU with endemic MRSA. SDI may further enhance S&D efficacy.

Blood acetone concentration in "normal people" and in exposed workers 16 h after the end of the workshift.

Acetone levels were measured by gas chromatography mass spectrometry (GC-MS) in environmental and alveolar air, blood and urine of 89 non-occupationally exposed subjects and in three groups of workers exposed to acetone or isopropanol. Acetone was detected in all samples from non-exposed subjects, with mean values of 840 micrograms/l in blood (Cb), 842 micrograms/l in urine (Cu), 715 mg/l in alveolar air (Ca) and 154 ng/l in environmental air (Ci). The ninety-fifty percentiles were 2069 micrograms/l in Cb, 2206 micrograms/l in Cu and 1675 ng/l in Ca. The blood/air partition coefficient of acetone was 597. Correlations were found in Cb, Cu and Ca. In specimens sampled at the end of the workshift from subjects occupationally exposed to acetone, a correlation was found in the blood, urine, alveolar and environmental air concentrations. The blood/air partition coefficient of acetone was 146. On average, the blood acetone levels of workers were 56 times higher than the environmental exposure level, and the concentration of acetone in alveolar air was 27% more than that found in inspiratory air. The half-life for acetone in blood was 5.8 h in the interval of 16 h between the end of the workshift and the morning after. The morning after a workshift with a mean acetone exposure of 336 micrograms/l, blood and urinary levels were 3.5 mg/l and 13 mg/l, respectively, which were still higher than those found in "normal" subjects. It can be concluded that endogenous production of acetone and environmental exposure to acetone or isopropanol do not affect the reliability of biological monitoring of exposed workers, even 16 h after low exposure.

Blood styrene concentrations in a "normal" population and in exposed workers 16 hours after the end of the workshift.

Blood styrene was measured by a gas chromatography-mass spectrometry method in 81 "normal people" and in 76 workers exposed to styrene. In the normal subjects, styrene was also tested in alveolar and environmental air. Styrene was found in nearly all (95%) blood samples. Average styrene levels in the normal subjects were 221 ng/l in blood (Cb), 3 ng/l in alveolar air (Ca) and 6 ng/l in environmental air (Ci). Styrene levels did not differ significantly between smokers and nonsmokers, 95% of values being below 512 ng/l in Cb, 7 ng/l in Ca and 15 ng/l in Ci. In workers with an average exposure to styrene of 204 micrograms/l, at the end of the workshift, mean blood styrene concentration was 1211 micrograms/l. In blood samples collected at the end of the Thursday shift, styrene levels were significantly higher (1590 micrograms/l) than those found at the end of the Monday shift (1068 micrograms/l). A similar difference was found in samples taken the morning after exposure (60 and 119 micrograms/l, respectively). Significant correlations between blood and environmental styrene were found both at the end of the shift and the morning after exposure (r = 0.61 and 0.41, respectively). In workers occupationally exposed to styrene, 16 h after the end of the workshift, blood styrene (94 micrograms/l) was significantly higher than that found in the normal subjects (0.22 microgram/l). The half-life of blood styrene was 3.9 h.