The aim of this study was to evaluate the appearance, extent, and distribution of parenchymal changes in the lung after acute respiratory distress syndrome (ARDS) as a function of disease severity and therapeutic procedures. High-resolution computed tomography (HRCT), clinical examination, and lung function tests were performed in 15 patients, 6-10 months after ARDS. The appearance and extent of parenchymal changes were compared with the severity of ARDS, as well as with clinical and therapeutic data. Lung parenchymal changes resembling those found in the presence of pulmonary fibrosis were observed in 13 of 15 patients (87%). The changes were significantly more frequent and more pronounced in the ventral than in the dorsal portions of the lung ( p<0.01). A significant correlation was observed between the extent of lung alterations and the severity of ARDS ( p<0.01), and the duration in which patients had received mechanical ventilation either with a peak inspiratory pressure greater than 30 mmHg ( p<0.05), or with more than 70% oxygen ( p<0.01). Acute respiratory distress syndrome frequently is followed by fibrotic changes in lung parenchyma. The predominantly ventral distribution of these changes indicates that they may be caused by the ventilation regimen and the oxygen therapy rather than by the ARDS.

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Atypical pneumonia has been recognized for at least four decades as a clinical syndrome characterized by a less severe clinical course than typical bacterial pneumonia. It is caused by a variety of different organisms including Mycoplasma pneumoniae, chlamydiae, rickettsiae, viruses and Legionella pneumophila. Of the chlamydiae, TWAR-strain (Chlamydia pneumonia) is now considered the most important pathogen. Its prevalence in community-acquired pneumonia varies considerably depending on the cyclical nature of the disease, but also on the diagnostic methods applied. The first line therapy in community-acquired pneumonia is usually empirical administration of a penicillin or cephalosporin to cover the bacterial pathogens which usually cause 'typical' pneumonia, most importantly Streptococcus pneumoniae. If, however, atypical pneumonia is diagnosed by bacteriological or serological testing, or is suspected clinically or on the basis of treatment failure, the treatment of choice would be erythromycin 2-4 g or tetracyclines (doxycycline 200 mg) daily for M. pneumoniae pneumonia and C. pneumoniae (TWAR-strain) infection. For coxiella pneumonia tetracycline is preferred. Psittacosis (ornithosis) has a high mortality and must be treated with tetracyclines immediately. Legionella pneumonia is preferably treated with erythromycin 2-4 g for at least three weeks; as an alternative, tetracyclines or quinolones may be given. Quinolones are less effective in mycoplasma and chlamydial infection. The new macrolide antibiotics are promising agents in pneumonia due to M. pneumoniae, L. pneumophila and C. pneumoniae. Compared to erythromycin they have improved pharmacological properties. They have long half-lives allowing once-daily dosing and achieve high tissue and intracellular concentrations.