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Page 2 of 11 Kumar et al. Plast Aesthet Res 2020;7:29 I http://dx.doi.org/10.20517/2347-9264.2019.71

of the immediate environment. The extent of injury and tissue characteristics determine the extent of
biochemical damage to adjacent cells, leading to cell death and tissue dysfunction. Secondary damage
in trauma can increase patient morbidity, mortality and the cost of treatment considerably. A better
understanding and control of secondary damage is thus essential for improved outcomes in trauma
patients, which will, in turn, reduce morbidity and render management cost-efficient. In this article, we
review the existing literature and analyze possible areas where standard medical and surgical intervention
along with wound management using Limited Access Dressing (LAD) could lead to better outcomes.

METHOD
Secondary damage in trauma patients was defined. We looked up the relevant literature by using “Secondary
Damage in Trauma” and “Limited Access Dressing” on PubMed and Google search engines. Relevant
articles from molecular biology, physiology and pathophysiology were also reviewed to explain the
mechanism of secondary damage in trauma. A total of 46 relevant articles were reviewed analyzed to find
areas where standard medical and surgical intervention, along with wound management using LAD, could
lead to better outcomes.

Definition
secondary injury, in simple words “by-stander” damage, of cells result from a secondary insult with
destructive and biochemical mechanisms triggered by the mechanical destruction of tissue following
direct trauma (the primary insult). Secondary damage may develop immediately (within hours) following
the primary insult, and last from a few days up to weeks after. For instance, necrosis of peripheral tissues
[1]
surrounding the damaged tissue can develop late after crush injuries . Cells or tissue with ultra-structural
damage at the time of trauma may die within hours to a few days following trauma. It is still controversial
[2]
however, whether such cell death should be included under primary or secondary damage . Secondary
damage may also involve local or distant cells/tissues. From a biomedical point of view, it can occur due to
[1,2]
hemorrhagic shock, compartment syndrome and/or ischemic necrosis .

Mechanism of secondary damage
Secondary damage to local tissue: This was explained by Knight’s Sport Injury Model (1970) that was later
[2]
updated based on improved biochemical understanding of tissue damage.

Secondary damage to distant tissue: This mainly occurs due to systemic hypoxia following hemorrhage or
[3]
due to pro-inflammatory cytokines following systemic inflammatory response syndrome (SIRS) .

Mechanism of local secondary tissue injury
Knight’s sport injury model (1970)
Knight’s Sport Injury Model (Secondary Injury Model) was first described in the mid 70’s to account for
[2,4]
the series of events that occur following injury in athletes . This model effectively explains the possible
mechanism that is triggered due to the loss of cellular hemostasis occurring in adjacent, uninjured tissues
following primary injury and cell death.

It could be speculated that the outcomes of a primary insult/trauma is immediate cell death or permanent
ultra-structural changes that lead to death of injured cells over time. The physiological response to cell
death, in theory, could affect the functionality of uninjured cells. The physiologic stress leading to tissue
damage is called a secondary injury.

Knight hypothesized that secondary injuries are primarily caused by two mechanisms: (1) hypoxic injury
causing oncosis (cell swelling) and acidosis; and (2) enzymatic (lysosomal enzymes) injury.