Inflammatory and Coagulative Considerations for the Management of Orthopaedic Trauma Patients With COVID-19: A Review of the Current Evidence and Our Surgical Experience

Abstract

Mounting evidence suggests that the pathogenesis of coronavirus disease 2019 (COVID-19) involves a hyperinflammatory response predisposing patients to thromboembolic disease and acute respiratory distress. In the setting of severe blunt trauma, damaged tissues induce a local and systemic inflammatory response through similar pathways to COVID-19. As such, patients with COVID-19 sustaining orthopaedic trauma injuries may have an amplified response to the traumatic insult because of their baseline hyperinflammatory and hypercoagulable states. These patients may have compromised physiological reserve to withstand the insult of surgical intervention before reaching clinical instability. In this article, we review the current evidence regarding pathogenesis of COVID-19 and its implications on the management of orthopaedic trauma patients by discussing a case and the most recent literature. LEVEL OF EVIDENCE:: Prognostic Level V. See Instructions for Authors for a complete description of levels of evidence.

FIGURE 1.

Preoperative anteroposterior (A) and lateral (B) radiographs of the left knee demonstrating an obliquely oriented, extra-articular fracture of the distal femur.

FIGURE 2.

Preoperative anteroposterior chest radiograph demonstrating enlarged cardiomediastinal contours, low lung volumes, and bibasilar linear densities reflecting subsegmental atelectasis. No focal consolidation noted.

FIGURE 3.

Products removed from percutaneous pulmonary suction embolectomy. The yellow products are presumed intramedullary fat, and the red products are the clot burden. Image quality is suboptimal because the camera was required to be in a plastic bag due to COVID+ status.

FIGURE 4.

Diagram demonstrating different theoretical patients' biologic reserves to withstand systemic inflammation before reaching a tipping point, characterized by clinical instability.