It is no surprise to coworkers, colleagues and even my patients that I am a huge advocate for education and of course, the building of a strong foundation. My personal experience has been that after I had built that strong foundation—as in, understanding the skin and cells involved in each layer, wound bed preparation framework and the phases of wound healing with the key cells involved in each phase—I became more efficient, provided better services and improved positive outcomes for my patients. And once the types of wounds came along, I felt prepared and ahead of the game to accept the challenges and complexities of each wound type, and educated myself to know the differences. As a clinician driven by a passion for healing patients, I can’t help but look for ways for me to improve and further educate myself, as well as bring others on board to join me and the thousands of clinicians out there gathered to fight for a good cause.
It is simply mind blowing how meticulous and intricate our bodies were created and how it responds through adversity and of course, simple wear and tear. When our body experiences injury and our skin gets altered or wounded, it starts a cascade of events within the body that masterfully react to the situation at hand and takes care of the damage, allowing the healing process to begin. There are four phases to wound healing, though some literature talks about three as they combine the first two phases. All phases of the healing process overlap each other; as one phase is ending it also sets up and orchestrates the following phase of healing until we reach full wound closure. So allow me to break down the phases of wound healing and the cells involved so that we can continue to build that strong foundation in becoming better clinicians.
Hemostasis, the initial phase, starts immediately after injury and only lasts 5-10 minutes. Upon injury, our body's attempt to stop that leak is through vasoconstriction, which allows bleeding to slow down. As vasoconstriction occurs, platelets are released and fibrin leaks from injured vessels. Platelets go through a process of platelet aggregation and with fibrin form a clot that adheres to injured vessels. The end result of this phase is clot formation and the cessation of bleeding. As discussed before, all phases of wound healing overlap. Platelets will then release growth factors, such as platelet-derived growth factors, and key cytokines that will be participants in upcoming phases of healing.
The inflammatory phase is the second phase in the healing cascade and since the phases overlap, it initiates with injury. The inflammatory phase lasts 4-6 days and is characterized by the presence erythema, warmth, edema and pain. Our body’s objective in stopping the bleed was to create a clot, so what cells do we need in order to achieve balance and be able to clean out our wound, as due to injury, foreign objects have been introduced? Neutrophils are one of the major cells involved as they secrete chemicals to kill bacteria and are later replaced by macrophages that will assist in engulfing and digesting bacteria and any other cellular debris. The best way for me to describe this process would be to refer to macrophages as a bunch Pac-Mans eating all the debris and cleaning everything out. Macrophages produce chemoattractants and growth factors, which are needed for tissue repair. Macrophages are critical in the repair process as they play a part in releasing growth factors that increases the level of fibroblasts, all essential for the following phase.
The proliferative phase is the third phase in the healing process and lasts 6-21 days. This phase is characterized by the presence of granulation tissue and ultimately epithelialization. Fibroblasts are a key cell in this phase. Fibroblasts are responsible and lay the foundation for new extracellular matrix (ECM) for collagen and granulation tissue. In this phase, we go through proliferation, growth of new tissue, angiogenesis, collagen deposition, granular tissue formation, wound contracture and epithelial cell migration. Granulation tissue consists of macrophages, fibroblasts, immature collagen and blood vessels. Angiogenesis is the formation of new vessels that developed within the granular tissue in order to supply it with blood and nutrients. As granulation tissue develops, fibroblasts stimulate the production of collagen, which gives tissue strength and structure. Once the deficit has been filled with granulation tissue, the wound edges or margins will begin to contract until the wound bed is covered with new epithelium and resulting in the presence of a scar.
Remodeling or also known as maturation phase is the fourth and final phase in wound healing and lasts from 21 days up to 2 years. In this final and longest phase, collagen synthesis is ongoing in order to strengthen the tissue. Remodeling occurs as wound continues to contract and fibers are being reorganized. The further contraction of the wound results in scar tissue getting to about 80% the tensile strength of uninjured skin. This healed tissue will always be at higher risk for breakdown as skin tensile is no longer 100% or to that of uninjured skin. If skin were to re-injure on the same area currently at 80%, at the end of those four phases of healing, skin tensile will be between 60-70%.
Wound healing occurs by primary, secondary or tertiary intention. Wounds that heal through primary intention, such as a surgical wounds, refers to the skin being approximated with use of staples, sutures or surgical glue. These type of wounds heal faster, have a lower infection risk, have minimal tissue loss and heal with minimal scarring. Wounds left to heal by secondary intention, meaning, through granular tissue formation, wound contracture and epithelial cell migration, tend to be more of chronic etiology and because of the delay in healing, are at a greater risk for infection. Tertiary or delayed primary intention refers to surgical wounds that are left open for a few days to allow edema and infection to resolve and allow the wound to drain before closure with sutures or staples.
It is simply magical how our body reacts to injury and how well orchestrated the events are that follow. Up to this day, seeing the epithelialization of a wound remains mind boggling to me still and I get chills of excitement for the end result. As we continue our journey into this exciting world of wound management we will see the barriers that affect wound healing and fully understand and appreciate the involvement of the SWAT team (skin and wound assessment team).
I encourage you to join me in using the term wound management more and more. By educating ourselves with the skin, the phases of wound healing and the wound bed preparation framework we are not just doing wound care, we are performing wound management. We are looking at wounds at the cellular level, why wounds delay and what we must do to assist the healing cascade. So please—no more wound care—we do wound management.
Keep healing my friends!
Orchestrating wound healing: assessing and preparing the wound bed, C.T Hess, BSN, RN, CWOCN and Dr. R.S. Kirsner, MD
Scottsdale wound management guide 2nd edition: p188, M. Livingston RN, BSN, CWS, CHRN and T. Wolvos, MS, MD,
Pressure Ulcers: guidelines for prevention and management 3rd edition, ch. 4, p27-31, J. Maklebust and M. Sieggreen
About the Author
Martin Vera is a certified wound specialist with over 19 years of nursing experience, with a passion for wound management and patient-centered care.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.