Abstract
A variety of harmful effects can be triggered by trauma and major orthopedic surgery.
One of the key players involved in this process is thrombin. The clinical consequence
of this process has, for several decades, been considered to be formation of deep
vein thrombosis and pulmonary embolism. Controlling thrombin generation and activation
has therefore been the goal of thromboprophylaxis regimens administered to patients
suffering from trauma or undergoing major surgery. Protecting patients from venous
thromboembolism has, for many years, been the main goal of preventive strategies.
However, our knowledge of cell destruction and release of substances that may cause
organ damage has expanded in recent years. Release of molecules such as RNA and histones
from destroyed tissues may cause cell destruction and organ damage at distal sites
if released in huge amounts and disseminated systemically. This new knowledge points
toward an unmet need for therapies that prevent both vascular events and organ deterioration.
This article briefly reviews molecular mechanisms associated with the occurrence of
vascular events and cellular destruction in patients with major bone damage caused
by trauma.
Keywords
trauma - thrombosis - RNA
