The skin plays a crucial role in protecting the inner tissues of the body from external harm. Consequently, the skin undergoes a fascinating self-healing process whenever it is bruised or wounded. The process is a complex course that entails a harmonious effort from various cells, including those on the wound margin that affect the victim’s wellbeing. This healing process undergoes different phases that practitioners should strive to understand to offer the appropriate care when the patient’s body is undergoing tissue repair. While traditional scholars have identified three phases of the wound healing process, contemporary researchers pinpoint four stages, namely hemostasis, inflammatory, proliferation, and remodeling. The ensuing discussion expounds on these four stages of wound healing.
The first stage of wound healing is hemostasis, which normally occurs within minutes of the original injury. When blood vessels are injured, they have to be repaired. Vasoactive mediators facilitate the constriction to temporarily lighten the wound. Platelets are cells that carry out the task of closing the broken vessels. They facilitate healing by discharging substances that cause the blood vessels to constrict and by creating a network of cells that form a clot. Damaged tissues secrete adenosine diphosphate (ADP), which causes platelets to aggregate and agglutinate to the exposed collagen. Platelets also produce elements that trigger the production of thrombin, a substance that induces the creation of fibrin. The fibrin network fortifies the platelet clump. Finally, platelets produce growth factors, which initiate the subsequent phase of wound healing by recruiting monocytes, neutrophils, and fibroblasts, as well as stimulating the epithelial cells (Altmeyer, Hoffmann, el Gammal, & Hutchinson, 2012).
The second phase lasts up to four days after the injury. It is characterized by erythema, pain, swelling, and heat. Inflammation is the body’s natural reaction to trauma. It can easily be mistaken for infection. At this stage, the damaged tissue is subjected to an augmented bacterial encumbrance and reduced host resistance. After the process of hemostasis is complete, the vessels dilate to ensure that antibodies, growth factors, nutrients, white blood cells, and enzymes reach the site of injury. Vasodilation is mainly facilitated by leukotrienes, histamine, and kinins. The most active cells at this stage are the phagocytic cells, which ingest bacteria to provide defense against infection. This process creates the first defense against infection (Flanagan, 2013).
Cell-to-cell communication takes place through growth factors and cytokines. It creates coordination, which is vital for wound repair. Cytokines stimulate cells to move while growth factors trigger them to multiply or secrete substances such as collagen. Collagen is important in the formation of the extracellular matrix, which interacts with cells, causing epithelial migration, platelet activation, and fibroblast movement. After leaving the blood cells and adhering to the extracellular medium, monocytes break up into other elements, which release the phagocytose bacteria that form another defense against infection. Macrophages also produce extracellular substances called MMPs, which break down necrotic tissue to repair damaged cells at the site of injury. MMPs require calcium and zinc to be effective (Peate & Glencross, 2015).
Also known as the granulation or contraction phase, the proliferation stage begins about 3-4 days later after the bruise. It may last up to 21 days, although it depends on the magnitude of the wound. At this point, the phagocytic cells are done with removing dead tissues, hence allowing fibroblasts to move into the wound. These cells secrete extracellular elements that are essential for the development of fibrous tissue. The migration of fibroblasts in the wound is accelerated by macrophages and matrix, which emit particular growth factors and chemicals respectively. Unlike phagocytes, fibroblasts’ movement into the wound is normally gradual (Altmeyer et al., 2012).
Fibroblasts not only produce collagen and ground elements that are significant for tissue repair but also emit essential growth elements that are needed for regeneration. The growth factors promote the formation of new blood vessels through a process referred to as angiogenesis. This term refers to the creation of novel blood vessels. As mentioned, fibroblasts produce collagen strands that construct a tripartite-like framework for tissue repair. A granulation tissue that comprises fibroblasts, collagen, new blood vessels, macrophages, as well as matrix is eventually formed three days after the injury. As the tissue develops, other cells such as plasma are also generated from the lymphocytes. The body protects the granulation tissue from infection by supplying adequate antibodies and phagocytic cells. The tissue is also delicate and susceptible to injury because of the fragile blood cells wall. Notably, it is usually bright red because the moving blood is noticeable due to the transparent new developing tissue (Bushak, 2014).
Furthermore, epithelial tissues are also regenerated during the proliferative phase through a process known as re-epithelialization. Epithelialization is witnessed in tissues that are repaired through either primary or secondary intention. Wounds that are repaired through the primary intention start experiencing epithelial movement shortly after a bruise. In the absence of a problem, the wound is covered within two days. This observation explains why patients who have their wounds stitched are permitted to shower 48 hours later after treatment. Structurally, re-epithelialization not only occurs on the wound margins but also goes deep into hair follicles, dermis, as well as hypodermis. As such, epidermal cells have reserves in the inner parts of the skin. Consequently, the epidermis can be reconstructed from the reserves. Thus, even in situations where the epidermis is completely damaged, there is a potential for recreating a new one (Altmeyer et al., 2012).
re-epithelialization occurs between granulation tissue and a scab where the healing occurs through a primary intention. Scab refers to a layer that forms on the upper part of the wound as a residue of a blood clot that occurs after the skin suffers an injury. The layer is of great significance since it protects the healing wound from external infection until the newly formed epithelium completely seals it. Additionally, it also ensures that the epithelium and granulation tissue do not dehydrate, thus causing the cells to die and eventually tamper with the healing process. Therefore, nurses should ensure that where the healing is through a secondary intention, the wounds have moisture to protect the granulation to enhance re-epithelialization. The process is normally accomplished by dressing the wound properly to retain physiological tissue fluids. It is worth noting that the tissue fluids not only keep the wound hydrated but also possess the growth factors synthesized by macrophages and fibroblasts (Flanagan, 2013).
Bushak (2014) asserts that the process of wound repair involves the readjustment of the collagen tissue to increase its flexibility. It hinges on the continued simultaneous production and destruction of collagen. The process of eliminating extra collagen and producing a new one is enabled by collagenases and MMPs. Inhibitors of MMPs create a balance between the synthesis of new collagen and the destruction of old ones. The process begins about 21 days after the injury when stable collagen content is available in the wound. It can take a period of up to two years. For this reason, if care is not taken, the wound can be reopened within this timeframe (Hess, 2012).
During the maturation process, collagen becomes more systematized. Fibronectin slowly fades. Glycosaminoglycan and hyaluronic acid are substituted by proteoglycans. Water is regained from the wound where type I collagen gradually replaces type III collagen. These processes permit collagen fibers to assemble, thus enabling collagen networking and eventually reducing scar width. Collagen cross-links lead to improved tensile strength. The tensile strength of the skin differs with skin thickness. It measures the force needed to break an injured skin. Even after the injured skin heals, it can only obtain up to 80% of the bursting strength of skin that has not previously been wounded.
According to Altmeyer et al. (2012), nurses should be keen on observing the process and time taken for the wound to heal. Under normal cases, wounds heal in 21 days, although remodeling may stretch to a year or more. Where a wound fails to adhere to the expected trajectory, there is an assumption that it is wedged in a particular phase. The wound care nurse should then investigate the probable causes and take measures to ensure the wound heals properly.
Everyone is likely to suffer a wound that has a wavering degree of severity. Understanding the wound healing process helps clinicians and patients to work towards the proper treatment of wounds. As discussed above, wound healing is a multifaceted chain of processes that entail the organized effort of cells to help towards regenerating new tissues. The process can be categorized into four states, namely hemostasis, inflammation, proliferation, and maturation. Wound care nurses claim that the healing process undergoes a normal trajectory. Where the contrary is observed, clinicians should take measures to ensure that the wound does not become chronic.
Altmeyer, P., Hoffmann, K., el Gammal, S., & Hutchinson, J. (2012). Wound Healing and Skin Physiology. Hong Kong: Springer Science & Business Media.
Bushak, L. (2014). The 4-Stage Process of Wound Healing: Making Skin Stronger Than Before. Web.
Flanagan, M. (2013). Wound Healing and Skin Integrity: Principles and Practice. The United Kingdom, UK: John Wiley & Sons.
Hess, T. (2012). Clinical Guide to Skin and Wound Care. Philadelphia, Pennsylvania: Lippincott Williams & Wilkins.
Peate, I., & Glencross, W. (2015). Wound Care at a Glance. Massachusetts, MA: John Wiley & Sons.