Effect of oral hygiene and 0.12% chlorhexidine gluconate oral rinse in preventing ventilator-associated pneumonia after cardiovascular surgery.

BACKGROUND: Ventilator-associated pneumonia (VAP) is a nosocomial infection of multifactorial etiology and has a negative influence on cardiovascular surgery (CVS) outcomes. OBJECTIVES: Determine the effect of toothbrushing plus 0.12% chlorhexidine gluconate oral rinse in preventing VAP after CVS. METHODS: In a quasi-experimental study, patients undergoing heart surgery were enrolled in a protocol for controlling dental biofilm by proper oral hygiene (toothbrushing) and oral rinses with 0.12% chlorhexidine gluconate (Group 1), and they were compared with a historical control group (Group 2), which included patients who underwent cardiac surgery between 2009 and 2010 and who received regular oral hygiene care. Seventy-two hours before surgery, a dentist provided instruction and supervised oral hygiene with toothbrushing and chlorhexidine oral rinses to patients in Group 1. RESULTS: Each group comprised 150 patients. A lower incidence of VAP (2.7% [95% CI 0.7-7.8] vs 8.7% [95% CI 4.9-14.7], P = .04) and a shorter hospital stay (9 ± 3 d [95% CI 8.5-9.5] vs 10 ± 4 d [95% CI 9.4-10.7], P = .01) were observed in Group 1. No significant differences in all-cause in-hospital death were observed between groups (5.3% vs 4.7%, P > .99). The risk for developing pneumonia after surgery was 3-fold higher in Group 2 (3.9, 95% CI 1.1-14.2). CONCLUSIONS: Oral hygiene and mouth rinses with chlorhexidine under supervision of a dentist proved effective in reducing the incidence of VAP.

The effects of ozone exposure and associated injury mechanisms on the central nervous system.

Ozone (O3) is a component of photochemical smog, which is a major air pollutant and demonstrates properties that are harmful to health because of the toxic properties that are inherent to its powerful oxidizing capabilities. Environmental O3 exposure is associated with many symptoms related to respiratory disorders, which include loss of lung function, exacerbation of asthma, airway damage, and lung inflammation. The effects of O3 are not restricted to the respiratory system or function - adverse effects within the central nervous system (CNS) such as decreased cognitive response, decrease in motor activity, headaches, disturbances in the sleep-wake cycle, neuronal dysfunctions, cell degeneration, and neurochemical alterations have also been described; furthermore, it has also been proposed that O3 could have epigenetic effects. O3 exposure induces the reactive chemical species in the lungs, but the short half-life of these chemical species has led some authors to attribute the injurious mechanisms observed within the lungs to inflammatory processes. However, the damage to the CNS induced by O3 exposure is not well understood. In this review, the basic mechanisms of inflammation and activation of the immune system by O3 exposure are described and the potential mechanisms of damage, which include neuroinflammation and oxidative stress, and the signs and symptoms of disturbances within the CNS caused by environmental O3 exposure are discussed.