WOUND HEALING AND ITS COMPLICATION
Wound healing of skin provides basically a classical example of a combination of regeneration and repair.
Healing is generally the body response to injury in an attempt to restore normal structure and function. Healing involves 2 distinct processes as following:
Wound healing can be accomplished in one of the following two ways:
- Healing by first intention (primary union)
- Healing by second intention (secondary union)
Wound Healing by First Intention (Primary Union)
This is defined as healing of wound which has the following characteristics:
i) firstly, it should be clean and uninfected;
ii) surgically incised;
iii) without much loss of cells and tissue; and
iv) lastly, edges of wound are approximated by surgical sutures
1. Initial haemorrhage.
Immediately after injury, the space between surfaces of an incised wound is basically filled with blood. So clots and seals the wound against dehydration and infection.
2. Acute inflammatory response.
This occurs basically within 24 hours. Thus along with the appearance of polymorphs from the margins of the incision. By 3rd day, polymorphs are generally replaced by macrophages.
3. Epithelial changes.
The basal cells of epidermis from either sides of incised margins start proliferating and migrating towards wound space in the form of epithelial spurs. A well-approximated wound is thus covered by a layer of epithelium in 48 hours. The migrated epidermal cells therefore separate the underlying viable dermis from the overlying necrotic material and clot. Therefore forming a scab which is cast off. The basal cells from the margins hence continue to divide. By 5th day, a multilayered new epidermis is thus formed which is differentiated into superficial and deeper layers.
By 3rd day, fibroblasts also occupies the wound area. By 5th day, new collagen fibrils start forming which are present until healing gets completed. In 4 weeks, so the scar tissue with scanty cellular and vascular elements, a few inflammatory cells, and epithelialized surface is formed.
5. Suture tracks.
Each suture track is a separate wound and incites the same phenomena as in the healing of the primary wound i.e. filling wound space with hemorrhage, inflammatory cell reaction of some cells, epithelial cell proliferation on either side and along with incision, fibroblastic proliferation, and formation of new collagen. When sutures are removed around the 7th day, much of the epithelialized suture track is avulsed and the remaining epithelial tissue in the track is absorbed.
A. The incised wound as well as the suture track on either side are filled with blood clots and there is an inflammatory response from the margins. B. Epidermal Spurs migrate along with cut margin on both side as well as around the suture track. The formation of granulation tissue also begins from below. C. Removal of suture at around 7th day results in scar tissue hence at the sites of incision.
Healing by Second Intention (Secondary Union)
This is defined as healing of a wound having the following characteristics:
i) open with a large tissue defect, generally at times infected;
ii) having extensive loss of cells and tissues; and
iii) the wound is not closed by surgical sutures but it remains to be open.
The basic events in secondary unions are similar to a primary union but differ in having a larger tissue defect which has to be bridged.
1. Initial haemorrhage.
As a result of injury, the wound space fills with blood and fibrin clot which dries.
2. Inflammatory phase.
There is generally initial acute inflammatory response that follows by the presence of macrophages which removes the debris likewise in primary union.
3. Epithelial changes.
Likewise in primary healing, the process occurs. However, the proliferating epithelial cells don’t cover surface completely until and unless granulation tissue from the base has started filling the space of wound. In this way, the pre-existing viable connective tissue hence separates from necrotic material. This clot on the surface and forms a scab generally which cast off. In time, the regenerated epidermis becomes stratified and keratinized.
4. Granulation tissue.
The main bulk of secondary healing is basically by granulations. Granulation tissue thus forms by the proliferation of fibroblasts and neovascularisation from the adjoining viable elements. The newly-formed granulation tissue is generally deep red, granular, and very fragile. With time, the scar on maturation becomes pale and white because of high collagen and decreased vascularity. Special structures of the skin e.g. hair follicles and sweat glands are not generally replacing. Unless their viable residues remain which may regenerate.
5. Wound contraction.
The contraction of a wound is therefore an important feature of secondary healing, as not seen in primary healing. Because of action of myofibroblasts present in granulation tissue, the wound contracts to 1/3 to 1/4 of its original size. Wound contraction occurs at a time when active granulation tissue is forming.
6. Presence of infection.
Bacterial contamination of an open wound delays the process of healing due to the release of bacterial toxins that provoke necrosis, suppuration, and thrombosis. Surgical removal of dead and necrosed tissue, debridement, thus helps in preventing the bacterial infection of open wounds.
A. The open wound generally fills with a blood clot and there is an inflammatory response at the junction of viable tissue. B. Epithelial spurs from the margin of wound comes in middle to cover the gap and thus separates the below viable tissue from necrotic tissue at the surface by forming a scab. C. After the contraction of the wound, a scar smaller than the original wound is left.
Complications of Wound Healing
During the course of healing, following complications can appear:
1. Infection of wound because of entry of bacteria delays the healing process.
2. Implantation (epidermal) cyst formation can also occur due to the presence of epithelial cells in wound after healing.
3. Pigmentation. Healed wounds generally have rust-like colour due to staining with haemosiderin. Some coloured particulate material left in the wound may also persist and impart colour to the healed wound.
4. Deficient scar formation. This can occur due to improper formation of granulation tissue.
5. Incisional hernia. A weak scar, especially after a laparotomy, maybe the site of bursting open of a wound (wound dehiscence) or an incisional hernia.
6. Hypertrophied scars and keloid formation. At times the scar further forms are excessive, ugly, and painful. Excessive formation of collagen in healing may result in keloid (claw-like) formation, thus seen more commonly in Blacks. Hypertrophied scars are different from keloid as they limit to the borders of the initial wound on other hand keloids have a tumor-like projection of connective tissue.
7. Excessive contraction. An exaggeration of wound contraction may result in the formation of contractures or cicatrization e.g. Dupuytren’s (palmar) contracture, plantar contracture, and lastly Peyronie’s disease.
8. Neoplasia. Rarely, a scar may be the site for the development of carcinoma later e.g. squamous cell carcinoma in Marjolin’s ulcer i.e. a scar following burns on the skin.
Extracellular Matrix— Wound Strength
The wound strengthen basically by the proliferation of fibroblasts and myofibroblasts which get structural support from the extracellular matrix (ECM). In addition to providing structural support, ECM can direct cell migration, attachment, differentiation, and organization. ECM has five main components i.e.: collagen, adhesive glycoproteins, basement membrane, elastic fibres, and proteoglycans.
Factors Influencing Healing:
Two types of factors influence the wound healing that are as following:
A. LOCAL FACTORS:
1. Infection is the important factor that acts locally and hence delays the process of healing.
2. Poor blood supply to wound slows healing e.g. injuries to face heal faster because of rich blood supply whereas injury to leg with varicose ulcers having poor blood supply heals slowly.
3. Foreign bodies including sutures interfere with healing and hence cause intense inflammatory reaction and infection.
4. Movement also delays wound healing.
5. Exposure to ionising radiation hence delays granulation tissue formation.
6. Exposure to ultraviolet light thus facilitates healing.
7. Type, size, and location of injury determines whether healing takes place by resolution or organization.
B. SYSTEMIC FACTORS:
1. Age. Wound healing is rapid in young and thus somewhat slow in age and debilitate people. Due to poor blood supply to the injured area in the latter.
2. Nutrition. Deficiency of constituents likewise protein, vitamin C (scurvy), and zinc delays the wound healing.
3. Systemic infection also delays wound healing.
4. Administration of glucocorticoids also has anti-inflammatory effect.
5. Uncontrolled diabetics are more prone to develop infections and hence delay in healing.
6. Haematologic abnormalities like defect of neutrophil functions (chemotaxis and phagocytosis), and neutropenia and bleeding disorders generally slow the process of wound healing.