Pulmonary bacterial clearance after acute ethanol exposure and burn injury. Eva L Murdoch

ISBN: 9781109756326

Published:

NOOKstudy eTextbook

181 pages


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Pulmonary bacterial clearance after acute ethanol exposure and burn injury.  by  Eva L Murdoch

Pulmonary bacterial clearance after acute ethanol exposure and burn injury. by Eva L Murdoch
| NOOKstudy eTextbook | PDF, EPUB, FB2, DjVu, AUDIO, mp3, ZIP | 181 pages | ISBN: 9781109756326 | 6.46 Mb

Infectious complications are a major cause of mortality in trauma patients. Burn patients with prior ethanol exposure have a worse prognosis than those who sustain injury but had not been drinking. We examined pulmonary infection and lung pathologyMoreInfectious complications are a major cause of mortality in trauma patients. Burn patients with prior ethanol exposure have a worse prognosis than those who sustain injury but had not been drinking.

We examined pulmonary infection and lung pathology in mice given ethanol (1.2 g/kg) 30 minutes before being subjected to 13-15% total body surface area (TBSA) scald burn followed by intratracheal inoculation with Pseudomonas aeruginosa (2000 colony-forming units (CFUs)). Survival was monitored for up to 48 hours. Sham control groups had 100% survival after intratracheal infection regardless of ethanol exposure.

Infected burned animals had 55% survival- however, survival of infected mice exposed to ethanol and burn injury was significantly lower (27%, p<0.05). When pulmonary infection was evaluated, the lungs of sham groups were negative for bacterial colonies. In addition, at 24 hours there were no significant differences in lung CFUs from infected burned animals regardless of ethanol exposure (3.0x104).

However, pulmonary bacterial content significantly decreased (1.2x10, p<0.05) at 48 hours in mice given burn injury alone, where CFUs from the lungs of mice exposed to ethanol prior to burn did not decline (5.4x105). At the same time point, lungs from animals given ethanol and burn injury had about a 2-fold (p<0.05) increase in leukocyte infiltration and vascular congestion, as well as decreased pulmonary oxygen saturation (82.8%, p<0.05), when compared to other treatment groups.

In summary, ethanol exposure in post-burn intratracheal infection results in the inability to clear pulmonary infection marked by a prolonged pulmonary leukocyte accumulation and a decrease in pulmonary function.



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