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Rationale: Patients managed at a long-term acute-care hospital (LTACH) for weaning from prolonged mechanical ventilation are at risk for profound muscle weakness and disability. Objectives: To investigate effects of prolonged ventilation on survival, muscle function, and its impact on quality of life at 6 and 12 months after LTACH discharge. Methods: This was a prospective, longitudinal study conducted in 315 patients being weaned from prolonged ventilation at an LTACH. Measurements and Main Results: At discharge, 53.7% of patients were detached from the ventilator and 1-year survival was 66.9%. On enrollment, maximum inspiratory pressure (Pi max ) was 41.3 (95% confidence interval, 39.4-43.2) cm H 2 O (53.1% predicted), whereas handgrip strength was 16.4 (95% confidence interval, 14.4-18.7) kPa (21.5% predicted). At discharge, Pi max did not change, whereas handgrip strength increased by 34.8% ( P  < 0.001). Between discharge and 6 months, handgrip strength increased 6.2 times more than did Pi max . Between discharge and 6 months, Katz activities-of-daily-living summary score improved by 64.4%; improvement in Katz summary score was related to improvement in handgrip strength ( r  = -0.51; P  < 0.001). By 12 months, physical summary score and mental summary score of 36-item Short-Form Survey returned to preillness values. When asked, 84.7% of survivors indicated willingness to undergo mechanical ventilation again. Conclusions: Among patients receiving prolonged mechanical ventilation at an LTACH, 53.7% were detached from the ventilator at discharge and 1-year survival was 66.9%. Respiratory strength was well maintained, whereas peripheral strength was severely impaired throughout hospitalization. Six months after discharge, improvement in muscle function enabled patients to perform daily activities, and 84.7% indicated willingness to undergo mechanical ventilation again.

Various studies have shown that alcohol exposure before thermal injury leads to increased morbidity and mortality. Pulmonary failure is a major complication seen in these patients. This study examines the effects of prior alcohol exposure on lung pathology after burn injury. There is a marked increase in neutrophil recruitment in the lung after thermal injury, and herein we show that this appears to be significantly elevated in animals given alcohol before burn injury. Consequently, we chose to determine whether there is a difference in pulmonary production of macrophage inflammatory protein (MIP)-2, a potent neutrophil chemoattractant, in mice subjected to a 15% total body surface area scald (or sham) injury with or without prior ethanol treatment. Lung tissue was obtained at various time points after injury and homogenates were assayed for MIP-2 by enzyme-linked immunosorbent assay. At 2 h after injury, peak levels of the chemokine were produced in both burn and burn + alcohol-treated mice. This represents a 7-fold increase above baseline. In mice exposed to burn injury alone, the level of MIP-2 returned to baseline within 8 h. In contrast, mice given alcohol before burn injury continued to show elevated levels of the chemokine at 8 h, after which MIP-2 decreased. This study may provide a basis for understanding the mechanism responsible for the increased neutrophil presence in the lung after thermal injury in individuals who have consumed alcohol. Subsequently, this may lead to the enhanced neutrophil-mediated pulmonary damage observed in these patients.