The Procoagulant Effect of COVID-19 on the Thrombotic Risk of Patients with Hip Fractures Due to Enhanced Clot Strength and Fibrinolysis Shutdown

Andreas G Tsantes,Panayiotis J Papagelopoulos,Argirios E Tsantes,Dimitrios V Papadopoulos,Aristeidis G Vaiopoulos,Stefanos Bonovas,Panagiotis Koulouvaris,Stavros Goumenos,Andreas F Mavrogenis,Konstantina A Tsante,Ioannis G Trikoupis,Georgios K Nikolopoulos,Daniele Piovani

doi:10.3390/jcm10153397

Abstract

Introduction: Coronavirus disease 2019 (COVID-19) in patients with hip fractures is associated with increased incidence of venous thromboembolism (VTE). The purpose of this study was to evaluate the hemostatic alterations of COVID-19 that are associated with a higher thrombotic risk using rotational thromboelastometry (ROTEM). Methods: A retrospective observational study was performed including 20 COVID-19 patients with hip fractures. To compare the coagulopathy of patients with mild COVID-19 and hip fractures with the coagulopathy associated with each of these two conditions separately, we used two previously recruited groups of patients; 198 hip fracture patients without COVID-19 and 21 COVID-19 patients without hip fractures. The demographics, clinical parameters, conventional coagulation parameters and ROTEM findings of the three groups were analyzed and compared. Results: COVID-19 hip fracture patients had higher amplitude of clot firmness at 10 min (p < 0.001), higher alpha angle (p < 0.001), higher lysis index at 60 min (p < 0.001), and shorter clot formation time (p < 0.001) than non-COVID-19 hip fracture patients, indicating increased clot strength and impaired fibrinolysis due to COVID-19. The value of lysis index at 60 min (99%) in COVID-19 patients with hip fractures was consistent with fibrinolysis shut down. Multivariable linear regression analysis further confirmed that COVID-19 resulted in increased amplitude of clot firmness at 10 min (p < 0.001), increased maximum clot firmness (p < 0.001), increased lysis index at 60 min (p < 0.001) and increased alpha angle (p < 0.001), but significantly shortened clot formation time (p < 0.001). Discussion: The higher thrombotic risk in COVID-19 patients with hip fractures is characterized by increased clot strength and fibrinolysis shutdown, as shown by ROTEM findings. Further prospective studies are warranted to evaluate the need for modification of thromboprophylaxis to balance the hemostatic derangements of COVID-19 patients with hip fractures.

Highlights

Coronavirus disease 2019 (COVID-19) in patients with hip fractures is associated with increased incidence of venous thromboembolism (VTE)
All patients tested positive for COVID-19 with real-time reversetranscriptase-polymerase chain reaction assay on admission to the hospital, while COVID-19 was considered of mild severity in all patients, and none of them needed admission to the intensive care unit due to COVID-19 related respiratory distress
Multivariable linear regression analysis demonstrated that COVID-19 was independently associated with increased amplitude of clot firmness at 10 min, maximum clot firmness, lysis index at 60 min and alpha angle in hip fracture patients, while COVID-19 significantly shortened clot formation time

Summary

Introduction

Coronavirus disease 2019 (COVID-19) in patients with hip fractures is associated with increased incidence of venous thromboembolism (VTE). Discussion: The higher thrombotic risk in COVID-19 patients with hip fractures is characterized by increased clot strength and fibrinolysis shutdown, as shown by ROTEM findings. There was a significant reduction in major orthopedic trauma due to reduced population activity, the incidence of fragility fractures such as hip fractures remained unchanged [1,2,3,4] These injuries are common in elderly people, a population highly susceptible to COVID-19. The exact impact of COVID-19 on the morbidity and mortality of these patients is not clear, it appears that the additive effect of COVID-19 leads to poor outcomes and a low survival rate [5] Both conditions have a high risk for certain adverse events such as venous thromboembolism, the overall risk for such complications is significantly increased. Viral infection-associated inflammation and endothelial dysfunction have been theorized as the leading causes of prothrombotic state, while impaired fibrinolysis has been identified as an important mechanism for COVID-19 associated coagulopathy [9,10]

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