When a student, intern or resident come to my clinic to do a rotation in wound care, invariably the first discussion we have is about the orderly phases of wound healing. While this seems to be a no-brainer it really should be something we as students and practitioners of wound care always have in the back of our minds. The orderly steps and chemical, structural and cellular mediators of each phase are so important not only to understand for the sake of understanding but to use as targets of treatment. A working understanding of the phases of wound healing not only helps in management of the wound by correcting the affected pathophysiology but in guiding diagnosis.
The phases of healing model we traditionally use in chronic wound management is based on the acute surgical model of wound healing. This is a useful model but it is flawed for many reasons. My first argument is that the “wound” in a multi-co-morbid patient such as those treated in a wound care center already have features of chronicity built in to them. Meaning an acute wound in a patient with significant co-morbidities at its initiation has behavior and biochemistry that makes it behave in a chronic fashion. For further discussion of the biochemistry of “acute” wounds in co-morbid patients refer to this article by Snyder, et al. Another challenge we face in the arena of chronic wounds is the wound that does not enter the healing cascade in the classic manner. The surgical model depends on a trauma/incision to activate platelets through interaction with extracellular matrix proteins, but what happens if there is not an incision or trauma to activate the cascade. A simple example of that problem is the pressure ulcer, in which the ulcer is generated by local pressure and ischemic tissue injury.
The acute surgical model of wound healing is helpful but has limitations. The next series of posts will detail each of the phases of wound healing and their importance in the cascade and progression to restoration of skin integrity.
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