Clinical and autopsy studies have shown an association between pulmonary microembolism and acute
respiratory failure after
trauma or
sepsis. Prophylaxis and treatment with the aim of decreasing the
fibrin deposition in the lungs were associated with a decrease in the incidence and death rate of this syndrome. Small
fibrin degradation products (
peptides) are accumulated in the lungs and are only slowly cleared from this organ, especially during states of fibrinolysis inhibition. These
peptides may contribute to the pulmonary damage in several ways. They act by interfering with other vasoactive substances as
bradykinin,
histamine and products of the
arachidonic acid cascade. Products of the
cyclooxygenase pathways as
thromboxane A2 play a major role in early microembolism whereas
lipoxygenase products seem to be involved in delayed microembolism. Pulmonary microembolism thus seems to be one important, but certainly not the only pathogenetic factor in acute "idiopathic"
respiratory failure. Other factors such as pulmonary
contusion, aspiration of gastric contents or blood, or
oxygen toxicity, might well be contributory in some cases. Pulmonary microemboli containing
fibrin and leukocytes are probably also involved as contributory agents in some cases in the large group of acute
respiratory failure due to "known factors".