• J P Pretorius, G Schlag, H Redl, W S Botha, D J Goosen, H Bosman, and A F van Eeden.
• Department of Surgery, H.F. Verwoerd Hospital, University of Pretoria, South Africa.
• J Trauma. 1987 Dec 1; 27 (12): 1344-53.

AbstractThe "lung in shock" syndrome is a constellation of early morphologic changes in the lung within 1 hour after polytrauma as indicated by human lung biopsies. A hypovolemic-traumatic (soft-tissue trauma together with bone fractures) baboon model with reinfusion was established to study these morphologic and associated pathophysiologic events. This model was developed in order to test the efficacy of therapeutic modalities in future studies. Nineteen baboons (eight sham, 11 shock) were anesthetized with spontaneous respiration while complete hemodynamic and blood gas monitoring was performed, along with light and electron microscopic studies of the lungs. Besides the usual shock-related hemodynamic disturbances and the metabolic acidosis, pathologic changes were found both on light and electron microscopy of the lungs but not on X-rays and measurements of blood oxygenation. In the shock group, morphologic evidence of endothelial and interstitial edema was associated with significant increases in lung weight. The fluid accumulation occurred in spite of careful control of pulmonary artery pressures during the study. More striking histologic findings were significant cellular infiltration of lung tissue, especially by leukocytes, showing evidence of degranulation. This baboon study, similar to studies undertaken in canines, shows that the hypovolemic (hemorrhagic) shock in association with trauma (fracture, soft-tissue trauma) causes ultrastructural morphologic changes that may precede potentially life-threatening functional changes in the lung.

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