PubMed1980
We investigated morphological findings of human biopsy material taken from lung and muscle, as well as lung tissue taken from animals in hypovolatemic-traumatic shock experiments. This was an attempt to reproduce, by way of an experimental setup with animals, the morphological changes which were formely found in the biopsies. Our morphological results lead to the assumption that the posttraumatic progressive lung failure without direct lung trauma can be divided into two major phases which are of decisive importance for the clinical development. 1. Early changes: Massive leucostasis of polymorphonuclear granulocytes with partial degranulation in the lung. In additon, a swelling of the endothelium cells, fat globules and a beginning interstitial edema were observed. In none of the cases were microthrombi found. 2. The actual "shock lung or fat embolism syndrome" which can be diagnosed also clinically 24 to 72 hours after the trauma. Morphologically predominating here are the interstitial edema and the fibrosis secondary to this and which manifests itself clinically in a disturbed gas exchange. This is accompanied by serious changes in the alveolar epithelium, deposits rich in protein as well as an increased occurence of phagocytizing macrophages in the alveoli. The early morphological changes in shock lung can most likely be influenced by therapeutical measures (such as a prompt shock treatment, a balanced restoration of the loss in blood volume and an early artificial ventilation). In this way, also the feared shock lung syndrome can be avoided. In an experimental setup with animals these early changes, especially the leucostasis, can easily by reproduced. This has become possible by the experience gained from the human lung biopsies. By way of this animal experiment new methods of treatment can be tested which might lead to a clinical progress in the prophylaxis as well as in the treatment of the progressive post-traumatic lung failure.