Article
Damage control orthopaedics leads to less coagulopathy than early total care in a porcine polytrauma model
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Authors
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Ümit Mert
- Department of Orthopedics, Trauma and Reconstructive Surgery, RWTH Aachen University, Aachen, Germany
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Johannes Greven
- Department of Orthopedics, Trauma and Reconstructive Surgery, RWTH Aachen University, Aachen, Germany
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Rald V. M. Groven
- Department cBITE, MERLN Institute for Technology-Inspired Regenerative Medicine, Maastricht University, Masstricht, Netherlands
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Martijn van Griensven
- Department cBITE, MERLN Institute for Technology-Inspired Regenerative Medicine, Maastricht University, Masstricht, Netherlands
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Markus Huber-Lang
- Institute of Clinical- and Experimental Trauma-Immunology, University of Ulm, Ulm, Germany
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Tom Eirik Mollnes
- Center of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway
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Elizabeth Rosado Balmayor
- Department of Orthopedics, Trauma and Reconstructive Surgery, RWTH Aachen University, Aachen, Germany
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Klemens Horst
- Department of Orthopedics, Trauma and Reconstructive Surgery, RWTH Aachen University, Aachen, Germany
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Frank Hildebrand
- Department of Orthopedics, Trauma and Reconstructive Surgery, RWTH Aachen University, Aachen, Germany
| Published: | October 23, 2023 |
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Outline
Text
Objectives: Trauma induced coagulopathy is a dreaded complication and highly associated with polytrauma and hemorrhagic shock. Fracture management and the best operative strategy are points of ongoing discussion also in regard to possible trauma induced bleeding disorders. Therefore, this study investigated the effects of two commonly used fracture treatment methods, Early Total Care (ETC) and Damage Control Orthopaedics (DCO) on coagulopathic disorders (CD) in a large animal model of multiple trauma.
Methods: Animals (sus scrofa) sustained polytrauma (PT) involving blunt chest trauma, liver laceration, bilateral femur fracture, and controlled haemorrhage. After resuscitation and stabilization of the fractures, the ventilated animals were monitored under ICU standards for 72 hours. A non-traumatized group served as control group (CG, n=6). In the two PT groups ETC (PT-ETC, n=7), and DCO (PT-DCO, n=8) strategies were performed. Venous blood samples were collected after 0/1.5/2.5/24/48 and 72 h. Plasminogen activator inhibitor-1 (PAI-1) was determined using assays from Nordic BioSite (AB, Taby, Sweden). The measurement of the thrombin-antithrombin complex (TAT) was performed with an anti-human ELISA. GraphPad Prism version 9.2.0 (San Diego, CA) was used for data visualization and statistical analysis.
Results and conclusion: Compared with CG, PT-ETC and PT-DCO presented with significantly increased concentrations of PAI-1 after 2.5 h (CG vs. PT-ETC: p=0.005, CG vs. PT-DCO: p=0.012) and 24 h (CG vs. PT-ETC: p=0.004, CG vs. PT-DCO: p=0.027). No differences were seen between CG, PT-ETC, and PT-DCO at 0, 1.5, 48 and 72 h after trauma. Interestingly, PT-ETC showed a significantly increased formation of TAT already after 1.5 h compared to CG and PT-DCO (PT-ETC vs. CG: p = 0.033, PT-ETC vs. PT-DCO: p=0.037). After 24 h, the levels of TAT were significantly higher for PT-ETC and PT-DCO than for the CG (PT-ETC vs. CG: p=0.0001, PT-ETC vs. PT-DCO: p=0.0001). However, for all other measured time points over the course of 72 h, there were no significant differences between CG, PT-ETC, and PT-DCO for the concentrations of TAT.
While signs for CD were found in both PT groups early after trauma, parameters normalized during the further clinical course. In the early phase, there was less CD in the DCO group than in the ETC group. Further research should focus on trauma severity and choice of operative strategy in regard to CD.
