The Royal Marsden Hospital Manual of Clinical Nursing Procedures - Lisa Dougherty [634]
Healing by tertiary intention, or delayed primary closure, occurs when a wound has been left open and is then closed primarily after a few days’ delay, usually once swelling, infection or bleeding has decreased (Giele and Cassell 2008).
Phases of wound healing
Wound healing is a cellular and biochemical process which relies essentially on an inflammatory process (Hampton and Collins 2004). These processes are dynamic, depend upon each other and overlap (Dealey 2005, Timmons 2006). It is important to support a wound-healing environment that encourages progression from one phase to the next without bacterial contamination, as this increases slough and necrosis (Hampton and Collins 2004).
The generally accepted stages of healing are:
1 haemostasis
2 inflammatory phase
3 proliferation or reconstructive phase
4 maturation or remodelling phase.
(Dealey 2005)
There are a number of internal and external factors that may influence normal wound healing and cause a delay in progress through these stages (Table 15.1). Growth factors involved throughout these phases act on individual cells to promote cell growth.
Table 15.1 Factors that delay wound healing
Haemostasis (minutes)
Vasoconstriction occurs within a few seconds of tissue injury and damaged blood vessels constrict to stem the blood flow. When platelets come into contact with exposed collagen from damaged blood vessels, they release chemical messengers that stimulate a ‘clotting cascade’ (Flanagan 2000, Hampton and Collins 2004, Timmons 2006). Platelets adhere to vessel walls and are stabilized by fibrin networks to form a clot. Bleeding ceases when the blood vessels thrombose, usually within 5–10 minutes of injury (Hampton and Collins 2004). See Figure 15.1.
Figure 15.1 Haemostasis in a wound.
Reproduced by kind permission of Wayne Naylor.
Inflammatory phase (1–5 days)
With the activation of clotting factors comes the release of histamine and vasodilation begins (Dowsett 2002, Flanagan 1996). The liberation of histamine also 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 2008). See Figure 15.2.
Figure 15.2 The inflammatory phase of wound healing.
Reproduced by kind permission of Wayne Naylor.
Polymorphonuclear leucocytes and macrophages migrate to the wound within hours and these phagocytose debris and bacteria and begin the process of repair (Hart 2002). If the number and function of macrophages are reduced, as may occur in disease, for example diabetes (Springett 2002), or due to treatment, for example chemotherapy in cancer patients (Tobias and Hochhauser 2010), healing processes are affected. Nutrients and oxygen are required to produce the cellular activity and therefore malnourished patients and hypoxic wounds are more susceptible to infection (Dealey 2005, Timmons 2006). The breakdown of debris causes an increased osmolarity within the area, resulting in further swelling. A chronic wound can get stuck in this phase of wound healing (Collier 2002, Dealey 2005, Hampton and Collins 2004) with prolonged healing, tendency to infection and high levels of exudate (Timmons 2006).
Proliferative phase (3–24 days)
Acute wounds will start to granulate within 3 days, but the inflammatory and proliferative phases can overlap, with both granulation and sloughy tissue present (Timmons 2006). See Figure 15.3.
Figure 15.3 The proliferative phase of wound healing.
Reproduced by