The Ohio State University, Columbus, OH.
J Athl Train. 2002 Apr;37(2):209-17.
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.
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.
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.
重新审视二次损伤模型，将当前几种病理生理学理论纳入该模型，并表明需要更多直接研究来检验该模型。
我在 1976 年至 2001 年期间在 MEDLINE 和 CINAHL 上搜索了与急性损伤病理和病理生理学相关的文献，并选择了经典文章和病理学、病理生理学和免疫学教材。
急性肌肉骨骼损伤的处理基于病理生理学模型，通常称为二次损伤模型，该模型最初是在 25 多年前开发的。在该模型中，急性创伤被称为原发性损伤，而继发性损伤是指对原本未受伤的细胞造成的损伤，这种损伤是对原发性损伤的生理反应的直接后果。在最初的模型中，继发性损伤的机制是基于当时对免疫学和细胞病理学的理解假设的。这些机制大致分为酶性或缺氧性。自那时以来，创伤后细胞死亡的病理模式已经发展，二次损伤模型需要一些更新。现在对于损伤是原发性还是继发性的分类存在一些争议，特别是在先前未受伤的组织中，创伤后损伤实际上是否是继发性损伤，或者原发性损伤细胞的延迟死亡。同样，导致继发性损伤的假设机制现在似乎比最初预期的要复杂得多。
结论/建议：二次损伤模型已经与我们对病理生理学的当代理解相协调。具体来说，继发性缺氧性损伤已被澄清为继发性缺血性损伤，并且已经确定了几种缺血性损伤的具体机制。同样，已经确定了线粒体衰竭和其他潜在机制引起的继发性损伤，并且扩大了这些机制与总继发性损伤的关系以及它们的相互作用。
