Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.

To appraise the effectiveness of the pneumonia case-management strategy in improving child survival, we have done a meta-analysis of six published intervention trials. The results of a seventh published study and two unpublished studies were also reviewed. The six published studies satisfied our criteria for methodological soundness. The reduction in mortality rate (control group minus intervention group) was estimated for each study, and for all the studies together. For total infant mortality, the overall reduction was 15.9 (95% confidence interval 10.6-21.1) deaths per 1000 livebirths; infant mortality due to acute lower respiratory infection was reduced by 10.7 (4.8-16.7) deaths/1000 livebirths. Mortality among children under 5 years was decreased by 36 deaths/1000 livebirths. The pooled estimates of relative risk are consistent with a 20% reduction in infant mortality and a 25% reduction in under-5 mortality. There was no clear association across the studies between the effect of the pneumonia case-management and extent of co-interventions such as immunisation and oral rehydration therapy. The consistency of findings of all the studies, despite differences in design and methods, shows that the case-management strategy has a substantial effect on infant and under-5 mortality, at least in settings with infant mortality rates of 90/1000 livebirths or more. It is important to find out the most efficient ways of implementing this strategy and integrating it into primary health care.