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Pulmonary Trapping of Platelets and Fibrin after Musculoskeletal Trauma — A Model to Detect and Quantify Post-Traumatic Pulmonary Microembolism

Published online by Cambridge University Press:  17 February 2017

I. Jansson
Affiliation:
Department of Surgery, University Hospital, Linköping, Sweden
L. Lovén
Affiliation:
Department of Surgery, University Hospital, Linköping, Sweden
L. Rammer
Affiliation:
State Institute of Forensic Medicine, Linköping, Sweden
S. Lennquist
Affiliation:
Department of Surgery, University Hospital, Linköping, Sweden

Extract

In discussions of the pathogenesis of posttraumatic respiratory distress syndrome (adult respiratory distress syndrome, ARDS), thromboembolism or microembolism (6) is the most frequently suggested mechanism. Embolic material released from the site of injury and/or intravascularly formed aggregates of platelets and fibrin are thought to plug the pulmonary capillaries, giving rise to diffuse pulmonary damage. Pulmonary trapping of platelets and fibrin has been studied in various animal models in which intravascular aggregation was induced pharmacologically, without trauma (2). Studies in patients with ARDS are difficult to standardize, and the results therefore are often inconclusive. We have evolved an experimental model (5) by means of which changes identical to ARDS can be induced from reproducible musculoskeletal trauma in anesthetized pigs. The pigs are observed under anesthesia for three days after the trauma under standardized and carefully controlled conditions. The aim of the present study was to use this model for registration and monitoring of pulmonary trapping of platelets and fibrin in animals with ARDS following standardized trauma, without adding any pharmacologic substance that could influence platelet aggregation or fibrinolysis. Pulmonary trapping was determined by external detection of 51Cr-labeled homologous platelets and 125I-labeled human fibrinogen, intravenously administered before anesthesia and trauma.

Type
Section Two—Clinical Topics
Copyright
Copyright © World Association for Disaster and Emergency Medicine 1985

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References

1 Busch, C, Dahlgren, S, Jacobsson, S, et al. Determination of fibrin trapping in the lungs of patients developing the microembolism syndrome. Acta Chir Scand 1971; 137:599601.Google ScholarPubMed
2 Busch, C, Lindquist, O, Saldeen, T. Respiratory insufficiency in the dog induced by pulmonary microembolism and inhibition of fibrinolysis. Acta Chir Scand 1974; 140:255266.Google ScholarPubMed
3 Busch, C. Quantitative determination of pulmonary microembolism in the dog. Upsala J Med Sci 1974; 79:7283.CrossRefGoogle ScholarPubMed
4 Howell, CD, Horvath, SM, Farrand, EA. Evaluation of variability in the cardiac output of dogs. Am J Physiol 1959; 196(1):193195.CrossRefGoogle ScholarPubMed
5 Jansson, I, Eriksson, R, Liljedahl, SO, et al. Primary fracture immobilization as a method to prevent post-traumatic pulmonary changes. Acta Chir Scand 1982; 148:329338.Google ScholarPubMed
6 Saldeen, T. The Microembolism Syndrome. Stockholm: Almqvist & Almqvist International, 1979.Google Scholar