This study demonstrates that an oxygen prescription based on continuous oximetry monitoring results in (1) a significant increase in the percentage of time that the SpO2 is between 88% and 92%, (2) a significant decrease in the amount of oxygen prescribed, (3) a slight increase in the amount of time that the SpO2 is below 88% that was not statistically significant.

Congestive heart failure is one of the few treatable causes of fulminant hepatic failure. Congestive heart failure must always be included in the differential diagnosis of fulminant hepatic failure of unknown pathogenesis.

The very interesting study by Dr. Brackenbury and colleagues (1) attempts to evaluate the effect of low-stretch mechanical ventilation on the immune properties of the intact rat lung. The authors demonstrated that ventilated animals could clear to the same extent with spontaneously breathing animals a certain quantity of Pseudomonas aeruginosa. Because the development of pneumonia relies on the balance between bacterial virulence and host immune response, the authors conclude that the effect of low-stretch mechanical ventilation on lung immune system is negligible.Depending on the traumatic characteristics of mechanical ventilation, increased alveolar-capillary permeability, surfactant alterations, neutrophil infiltration, and local inflammatory reaction have been demonstrated in animal models and in humans (2). The same findings are expected after bacterial challenge, depending on the type and size of bacterial inoculum. In the study by Dr. Brackenbury and colleagues (1), ventilated animals infected with P. aeruginosa demonstrated impaired oxygenation and compliance and increased total bronchoalveolar lavage protein compared with nonventilated infected animals. Although the ventilatory settings used in the study cannot be considered traumatic, it is difficult to exclude mechanical ventilation as a potential contributing factor of the observed alterations.One of the most striking findings of the study refers to surfactant. Infected animals seem to have an increased surfactant pool compared with noninfected, and this increase was evident both for the ventilated and the spontaneously breathing groups. Ventilated animals receiving P. aeruginosa demonstrated an increase in large aggregates that is difficult to explain because both mechanical ventilation and pneumonia are expected to cause increased conversion of large (functional surfactant) to small aggregates (nonfunctional surfactant). Another interesting finding is the increased level of surfactant protein A in infected animals. As the authors state, surfactant protein A has been found low in pneumonia with or without lung injury, and recently P. aeruginosa has been shown to secrete proteases with a specific degrading effect on surfactant proteins (3). Furthermore, messenger-RNA surfactant protein A levels were not elevated in the study, and the explanation that surfactant protein A is co-secreted with phospholipids at the initial phase of the bacterial challenge deserves further investigation because recent experimental results support that surfactant protein A has an inhibitory effect on phospholipids release in intact lung (4).In a recent article (5), we evaluated the effect of ventilator-associated pneumonia on bronchoalveolar fluid properties by performing bronchoalveolar lavage before and during ventilatorassociated pneumonia in ventilated patients without initial lung injury. Compared with mechanically ventilated controls, ventilator-associated pneumonia patients demonstrated impaired oxygenation and compliance and severely reduced surfactant pool with ext...

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