This vascular phase begins immediately there is tissue damage. Vasoconstriction occurs to minimise bleeding and assist with initiating the coagulation process. A fibrin clot forms, temporarily closing the wound. While the clot is forming, blood or serous fluid may exude from the wound as the body tries to cleanse the wound naturally.

The blood vessels around the wound dilate, causing localised erythema, oedema, heat, discomfort, throbbing and sometimes functional disturbance. Macrophages clear the wound of debris in preparation for new tissue growth. A small necrotic area forms around the wound margin where the blood supply was interrupted. Epithelial cells from the wound margin move under the base of the clot, the surrounding epithelium thickens and a thin layer of epithelial tissue forms over the wound. As the clinical signs of the inflammation phase are similar to those of infection (see below) it is important the midwife can distinguish between a wound that is healing normally and one that is infected. Provided the wound is clean, this phase lasts between 1–3 days, but is prolonged in the presence of infection or necrosis (South et al 2008).

This phase involves the growth of new tissue through three processes:

During granulation, capillaries from the surrounding vessels grow into the wound bed. At the same time, fibroblasts produce collagen fibres, providing the framework for new connective tissue formation. Collagen increases the tensile strength and structural integrity of the wound. Healthy granulation tissue has a bright red, moist, shiny appearance, a ‘pebbled’ looking base and does not bleed easily.

Once the wound is filled with connective tissue, fibroblasts collect around the edges of the wound and contract, pulling the edges together. A firmer, fibrous epithelial scar forms as the fibroblasts and collagen fibres begin to shrink, resulting in contraction of the area and obliteration of some of the capillaries. This only occurs with healthy tissue that has not been sutured.

During epithelialisation new epithelial cells grow over the wound surface to form a new outer layer, recognised by the whitish-pink, translucent appearance of the wound. The process is enhanced in a moist, clean environment.

Once epithelialisation is complete, the new tissue undergoes a time of maturation when it is ‘re-modelled’ to increase the tensile strength of the scar tissue. In lightly pigmented skin, the scar initially appears red and raised, and then with time changes to a paler, smoother, flatter appearance. Scar tissue in darkly pigmented skin has a lighter appearance initially when compared with lightly pigmented skin. Mature scar tissue is avascular and contains no sweat or sebaceous glands or hairs. This phase can take up to 2 years to complete and may be the reason why some wounds that appear to have healed suddenly break down (Keast & Orsted 1998).

This healing process also occurs around sutures. When the sutures are removed, the epithelial cells can be dislodged and may be visible on the sutures as debris.

Wound healing by secondary intention occurs with deeper, wider wounds, whose edges cannot be brought into apposition. Inflammation may be chronic, with more granulation tissue forming at the expense of collagen during proliferation. Granulation tissue gradually fills the wound with re-epithelialisation beginning at the edges. Healing by secondary intention takes longer, resulting in more scar tissue forming.

A fall or a rise (above 30°C) both cause vasoconstriction and so impair wound healing.

Infection causes increased inflammation and necrosis, which delays wound healing. Poor surgical techniques (with an increased risk of haematoma; Olsen et al 2008), poor dressing techniques, a larger number of people in theatre (Reilly 2002), inadequate or mis-timed antibiotic prophylaxis (for lower segment CS; Kaimal et al 2008) and wounds that are too dry or too wet predispose to colonisation or infection. A wound that is critically colonised has sufficient bacteria competing for oxygen and nutrients at the expense of healthy cells. It may not appear infected but will fail to heal.

An adequate intake of protein, carbohydrate, fats, vitamins A, B, C and E, copper, zinc and iron are required. Proteins supply amino acids, essential for tissue repair and regeneration. Vitamins A and B and zinc are required for epithelialisation, and vitamin C and zinc are necessary for collagen synthesis and capillary integrity. Iron is required for the synthesis of haemoglobin which combines reversibly with oxygen to transport oxygen around the body.

Good management of pain will reduce the woman’s anxiety, improve her acceptance of the wound and so reduce stress. Anxiety, isolation and altered body image all reduce wound healing (South et al 2008).

This affects all phases of wound healing due to impaired circulation and coagulation, slower inflammatory response and decreased fibroblast activity.

Medical disorders, and particularly those that impair circulation or tissue perfusion, can delay wound healing. Diabetes mellitus includes the additional risk of hyperglycaemia, this can inhibit phagocytosis and predispose to fungal and yeast infection. Malignancy and the need for chemotherapy were also shown to have an adverse influence on wound infection rates (Reilly 2002).

Anti-inflammatory drugs suppress protein synthesis, inflammation, wound contraction and epithelialisation. Corticosteroids (from stress, steroid therapy or disease) delay both the inflammatory and immune responses.

A low arterial oxygen tension may alter collagen synthesis and inhibit epithelialisation. Poor tissue perfusion may occur in the presence of hypovolaemia, anaemia, obese tissue, smoking, poor mobility and alcohol. Oxygen is necessary for fibroblast activity. Johnson et al., 2006 and Olsen et al., 2008 and the Joint Commission Perspectives on Patient Safety (JCPPS) (2008) all relate obesity with an increased risk of wound infection.

NICE (2004) suggest specific surgical techniques for caesarean section surgery. Failure to undertake these procedures increases the risk of poor healing post surgery.

Prolonged or violent vomiting, abdominal distension or laboured respirations may cause sudden tension on the wound, inhibiting the formation of collagen networks and connective tissue.

Haemostasis usually occurs within several minutes of an acute wound occurring. However, bleeding may occur if a bleeding point is not tied off, as a result of the clot or suture dislodging or infection, and may occur internally and externally. Internal bleeding can lead to haematoma formation.

Infection usually appears within 2–3 days of a traumatic injury or 4–5 days of a surgical wound. The wound site will appear red (often a spreading or tracking cellulitis), swollen and painful. There may also be weeping from the wound, usually a yellow, green or brown discharge (depending on the infecting organism); it may also be malodorous. The woman may have a pyrexia, tachycardia, a raised white cell count and a general malaise (Boyle 2006).

If an acute wound does not heal properly the layers of skin and tissue can separate, usually during the proliferation phase. Separation can be partial or complete. It occurs more commonly where there is greater strain on the wound and decreased vasoconstriction (e.g. obesity), and particularly with abdominal wounds, if a sudden strain is placed on the wound (e.g. coughing, sitting up).