Vasoconstriction occurs within a few seconds of tissue injury so blood flow from damaged blood vessels is reduced. When platelets come into contact with exposed collagen from damaged blood vessels, they release chemical messengers that stimulate a ‘clotting cascade’ (Timmons [104]). Platelets adhere to vessel walls, creating a fibrin clot that controls blood loss from compromised vessels (Doughty and Sparks [25]). Bleeding ceases when the blood vessels thrombose, usually within 5–10 minutes of injury (Hampton and Collins [43]) (Figure 18.1).

With the activation of clotting factors comes the release of histamine and associated vasodilation (Singh et al. [94]). The presence of histamine increases the permeability of the capillary walls, and plasma proteins, leucocytes, antibodies and electrolytes exude into the surrounding tissues. The wound becomes red, swollen and hot. These signs are accompanied by pain and tenderness at the wound site, last for 1–3 days and can be mistaken for wound infection (Hampton [42]) (Figure 18.2).

With haemostasis achieved, the focus then moves to preventing infection (Harper et al. [44]). Neutrophils, macrophages and then lymphocytes migrate to the wound within hours and these phagocytose debris and bacteria in the wound bed and secrete cytokines and growth factors (Stacey [99]). If the number and function of macrophages are reduced, as may occur in disease, for example diabetes (Snyder et al. [97]), healing processes are affected. Nutrients and oxygen are required to produce the aforementioned cellular activity and therefore malnourished patients and hypoxic wounds are more susceptible to infection (Singh et al. [94]). The breakdown of debris causes increased osmolarity within the area, resulting in further swelling. A chronic wound can become stuck in this phase of wound healing, resulting in prolonged healing, tendency to infection and higher levels of exudate (Martin and Nunan [66]). The phases that follow start the process of repair (Tortora and Derrickson [106]).

The fibroblasts are activated to divide and produce collagen via processes initiated by the macrophages (Timmons [104]). Newly synthesized collagen creates a ‘healing ridge’ below an intact suture line, which gives an indication of how primary wound healing is progressing. The wound surface and the oxygen tension within encourage the macrophages to instigate the process of angiogenesis – the formation of new blood vessels (Singh et al. [94]). These vessels branch and join other vessels, forming loops. The fragile capillary loops are held within a framework of collagen. This complex is known as ‘granulation tissue’ (Gray et al. [35]). The combination of angiogenesis, granulation and collagen deposition encourages the wound edges to contract (Singh et al. [94]). Then, through mitosis and migration of epithelial cells, re‐epithelialization occurs and covers the granulating wound bed, effectively restoring the bacterial barrier of the skin's surface (Doughty and Sparks [25]). Acute wounds start to granulate within 3 days, but the inflammatory and proliferative phases can overlap (Guo and DiPietro [38]) (Figure 18.3).

The mechanisms and processes within each phase of wound healing are dependent on an adequate oxygen supply at the wound bed and optimal nutrition, specifically iron, carbohydrates, protein, and vitamins A and C (Guo and DiPietro [38], Singh et al. [94]).

Maturation or remodelling of the healed wound begins at around 21 days following the initial injury and is the last phase of healing, which can last for up to 2 years (Harper et al. [44]) (Figure 18.4).

Collagen is reorganized and replaced, with the effect of emulating pre‐wounded tissue. The new collagen provides increased tensile strength, though this will not achieve more than 80% of pre‐wounded strength (Doughty and Sparks [25]).

At the end of the maturation phase, the delicate granulation tissue of the wound will have been replaced by stronger avascular scar tissue. Rationalization of the blood vessels results in thinning and fading of the scar, although it is not fully known why this varies between people (Dealey [22]).