Whether wounds are closed by primary intention, subject to delayed primary closure or left to heal by secondary intention1, the wound healing process is a dynamic one which can be divided into three phases. It is critical to remember that wound healing is not linear and often wounds can progress both forwards and back through the phases depending upon intrinsic and extrinsic forces at work within the patient2.
The phases of wound healing are2:
- Inflammatory phase
- Proliferation phase
- Maturation phase
The inflammatory phase is the body’s natural response to injury. After initial wounding, the blood vessels in the wound bed contract and a clot is formed. Once haemostasis has been achieved, blood vessels then dilate to allow essential cells; antibodies, white blood cells, growth factors, enzymes and nutrients to reach the wounded area. This leads to a rise in exudate levels so the surrounding skin needs to be monitored for signs of maceration. It is at this stage that the characteristic signs of inflammation can be seen; erythema, heat, oedema, pain and functional disturbance. The predominant cells at work here are the phagocytic cells; ‘neutrophils and macrophages’; mounting a host response and autolysing any devitalised ‘necrotic / sloughy’ tissue.
During proliferation, the wound is ‘rebuilt’ with new granulation tissue which is comprised of collagen and extracellular matrix and into which a new network of blood vessels develop, a process known as ‘angiogenesis’. Healthy granulation tissue is dependent upon the fibroblast receiving sufficient levels of oxygen and nutrients supplied by the blood vessels. Healthy granulation tissue is granular and uneven in texture; it does not bleed easily and is pink / red in colour. The colour and condition of the granulation tissue is often an indicator of how the wound is healing. Dark granulation tissue can be indicative of poor perfusion, ischaemia and / or infection. Epithelial cells finally resurface the wound, a process known as ‘epithelialisation’.
Maturation is the final phase and occurs once the wound has closed. This phase involves remodelling of collagen from type III to type I. Cellular activity reduces and the number of blood vessels in the wounded area regress and decrease.
- Leaper DJ and Harding KG. (1998) Wounds: Biology and Management. Oxford University Press.
- Hutchinson J (1992). The Wound Programme. Centre for Medical Education: Dundee.
Caveat: The information given is a guide only and should not replace clinical judgement.