Secondary injury after musculoskeletal trauma: a review and update

J Athl Train. 2002 Apr;37(2):209-17.


Objectives: To revisit the secondary injury model, to incorporate several current pathophysiologic theories into the model, and to show the need for more direct research examining the model.

Data sources: I searched MEDLINE and CINAHL from 1976 to 2001 for literature related to acute injury pathology and pathophysiology and selected classic articles and pathology, pathophysiology, and immunology texts.

Data synthesis: Acute musculoskeletal injury management is based on a pathophysiologic model, often referred to as the secondary injury model, which was originally developed more than 25 years ago. In this model, acute trauma is referred to as primary injury, whereas secondary injury refers to damage to otherwise uninjured cells that was a direct consequence of the physiologic response to primary injury. In the original model, mechanisms for secondary injury were hypothesized based on then-contemporary understandings of immunology and cellular pathology. These mechanisms were broadly categorized as either enzymatic or hypoxic. Since this time, the pathologic paradigms for cell death from trauma have evolved, and the secondary injury model requires some updating. Some controversy now exists regarding the categorization of injury as primary or secondary, specifically whether posttraumatic damage is actually secondary injury in previously uninjured tissue or delayed death of primary injured cells. Similarly, the postulated mechanisms that lead to secondary injury now appear to be considerably more complex than originally anticipated.

Conclusions/recommendations: The secondary injury model has been reconciled with our contemporary understanding of pathophysiology. Specifically, secondary hypoxic injury has been clarified to be secondary ischemic injury, and several specific mechanisms for ischemic injury have been identified. Similarly, secondary injury from mitochondrial failure and other potential mechanisms has been identified, and the role and interaction of these mechanisms in relation to total secondary injury have been expanded.