B-ENT

Facing coagulation disorders after acute trauma

1.

Université catholique de Louvain, CHU UCL Namur, Namur Thrombosis and Hemostasis Center (NTHC), Namur Research Institute for Life Sciences (NARILIS), Namur, Hematology Laboratory, Belgium

2.

Université catholique de Louvain, CHU UCL Namur, Department of Anesthesiology, Namur Thrombosis and Hemostasis Center (NTHC), Namur Research Institute for Life Sciences (NARILIS), Namur, Belgium

3.

Queen Astrid Military Hospital, Department of Surgery, Bruynstraat 1, 1120 Brussels, Belgium

4.

Université catholique de Louvain, CHU UCL Namur, Blood Transfusion Center, Namur, Belgium

5.

Université catholique de Louvain, CHU UCL Namur, Department of Hematology, Namur, Belgium

6.

Department of Emergency Medicine, Ghent University Hospital, De Pintelaan 185, 9000 Ghent, Belgium

7.

University of Namur, Department of Pharmacy, Namur Thrombosis and Hemostasis Center (NTHC), Namur Research Institute for Life Sciences (NARILIS), Namur, Belgium

8.

Department of Otorhinolaryngology, Ghent University, Ghent University Hospital. De Pintelaan, 185. B-9000 Ghent

B-ENT 2016; 12: Supplement 67-85
Read: 887 Downloads: 631 Published: 03 February 2020

Facing coagulation disorders after acute trauma. Problems/objectives: Trauma is the leading cause of mortality for persons between one and 44 years of age, essentially due to bleeding complications.

Methodology: We screened the PubMed, Scopus and Cochrane Library databases, using specific keywords. Only publications in English were considered.

Main results: The pathophysiology of trauma-induced coagulopathy (TIC) is complex and includes the classic “lethal triad” (i.e., haemodilution, acidosis, hypothermia) but may also include activation of protein C, endothelial and platelet dysfunction, and fibrinogen depletion. The time between trauma and treatment of the resultant massive bleeding should be as short as possible using techniques for rapid control of bleeding and avoiding aggravating factors (hypothermia, metabolic acidosis and hypocalcaemia). If given within three hours of injury, tranexamic acid (TXA) reduces all causes of mortality in trauma patients and reduces transfusion requirements. In a bleeding patient, crystalloids are preferred to colloids and the ratio of fresh frozen plasma to packed red blood cells should be at least 1:2. Damage control surgery (DCS) should be considered for patients who present with, or are at risk for developing, the “lethal triad”, multiple life-threatening injuries or shock, and in mass casualty situations. DCS can also aid in the evaluation of the extent of tissue injuries and the control of haemorrhage and infection. Finally, there is currently no evidence of the added value of laboratory assays in the management of TIC.

Conclusions: TIC appears quickly after trauma and should be anticipated and detected as soon as possible. TXA plays a central role in the management of such patients. Each institution should establish a local algorithm for the management of bleeding patients.

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EISSN 2684-4907