Limiting Blood Loss in Orthopaedic Trauma: Strategies and Effects.

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: Declaration of Competing Interest All authors have participated in (a) conception and design, or analysis and interpretation of the data; (b) drafting the article or revising it critically for iportant intellectual content; and (c) approval of the final version. This manuscript has not been submitted to, nor is under review at, another journal or other publishing venue. The authors have no affiliation with any organization with a direct or indirect financial interest in the subject matter discussed in the manuscript 10. Ann Intensive Care. 2025 Oct 18;15(1):163. doi: 10.1186/s13613-025-01587-0. Hemostatic abnormalities after trauma resuscitation: challenges and strategies in caring for the critically injured patient. Reed CR(1), Curry N(2), Juffermans NP(#)(3), Neal MD(#)(4). Author information: (1)Division of Trauma, Acute, and Critical Care Surgery, Department of Surgery, Duke University School of Medicine, Box 2837 DUMC, Durham, NC, 27710, USA. christopher.reed@duke.edu. (2)Medical Sciences Division, Radcliffe Department of Medicine, University of Oxford, Oxford Haemophilia and Thrombosis Centre, Nuffield Orthopaedic Centre, Oxford, OX3 7LD, UK. (3)Department of Intensive Care Medicine, Laboratory of Translational Intensive Care, Erasmus Medical Center, Dr. Molewaterplein 40, Rotterdam, 3015 GD, Netherlands. (4)Trauma and Transfusion Medicine Research Center, Department of Surgery, University of Pittsburgh, Keystone Building, 3520 Fifth Avenue, Suite 500, Pittsburgh, PA, 15213, USA. (#)Contributed equally Severe polytrauma and hemorrhage is a common and life-threatening condition often leading to intensive care unit admission for those who survive their initial injury. The injury itself, hypoperfusion from hemorrhagic shock, and resuscitative efforts introduce a complex set of hemostatic derangements collectively referred to as trauma-induced coagulopathy (TIC). Although the trauma population is notoriously heterogenous, TIC can generally be divided into an "early" hypocoagulable phase and then a "late" hypercoagulable, prothrombotic phase. Existing literature on TIC focuses heavily on reversing and preventing hypocoagulation in the early, acute phase. However, intensivists commonly manage patients throughout the later post-acute resuscitation phase of TIC, during which thrombotic complications are common and may lead to major morbidity and mortality. Derangements in platelet activation, endothelial dysfunction, suppression of fibrinolysis, and crosstalk between the innate immune and coagulation systems all contribute to the prothrombotic late TIC phenotype. Deep venous thrombosis and other macrovascular thrombotic complications also commonly occur after trauma. Thrombosis prophylaxis and treatment present a challenge for patients still at high risk for bleeding. An in-depth understanding of risk factors specific to trauma patients, including iatrogenic contributions from resuscitation and hemostatic efforts in the pre-intensive care phase, can help stratify thromboembolic risk and optimize prophylaxis and surveillance efforts. We stress the importance of an individualized approach to assessment of hemorrhagic and thrombotic risks for each patient. Here, we summarize the underlying contributors to the prothrombotic phenotype in late TIC, including a description of emerging roles for HMGB1, extracellular vesicles, and endogenous inhibitors. Additionally, a general approach to thromboprophylaxis, monitoring, and anticoagulation in this patient population are discussed. Finally, we summarize relevant risk stratification systems and guidelines for clinical management of thromboembolic risk among trauma patients, and highlight limitations in these systems and guidelines as areas for future research. © 2025. The Author(s). DOI: 10.1186/s13613-025-01587-0 PMCID: PMC12534623