Complications of wound healing pdf

Hand Abrasion – 32 minutes after injury. Hand Abrasion – 2 days 22 hours complications of wound healing pdf minutes after injury. Hand Abrasion – 17 days 11 hours 30 minutes after injury.

Hand Abrasion – 30 days 4 hours 43 minutes after injury. When the barrier is broken, a regulated sequence of biochemical events is set into motion to repair the damage. Blood clotting may be considered to be part of the inflammation stage instead of a separate stage. This activates the platelets, causing a few things to happen.

They change into an amorphous shape, more suitable for clotting, and they release chemical signals to promote clotting. Inflammation: During this phase, damaged and dead cells are cleared out, along with bacteria and other pathogens or debris. In angiogenesis, vascular endothelial cells form new blood vessels. Factors that contribute to non-healing chronic wounds are diabetes, venous or arterial disease, infection, and metabolic deficiencies of old age. Wound care encourages and speeds wound healing via cleaning and protection from reinjury or infection. Timing is important to wound healing.

Critically, the timing of wound reepithelialization can decide the outcome of the healing. If the epithelization of a wounded area is fast, the healing will result in regeneration. Wound healing is classically divided into hemostasis, inflammation, proliferation, and remodeling. Although a useful construct, this model employs considerable overlapping among individual phases. The cellular phase involves several types of cells working together to mount an inflammatory response, synthesize granulation tissue, and restore the epithelial layer. This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited.

Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors. Growth factors stimulate cells to speed their rate of division. Vasodilation is the end result of factors released by platelets and other cells. T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability. T cells also increase the activity of macrophages.

By secreting these factors, macrophages contribute to pushing the wound healing process into the next phase. They replace PMNs as the predominant cells in the wound by two days after injury. Numbers of monocytes in the wound peak one to one and a half days after the injury occurs. Once they are in the wound site, monocytes mature into macrophages. Macrophages also secrete a number of factors such as growth factors and other cytokines, especially during the third and fourth post-wounding days. These factors attract cells involved in the proliferation stage of healing to the area.

In wound healing that result in incomplete repair, scar contraction occurs, bringing varying gradations of structural imperfections, deformities and problems with flexibility. Macrophages may restrain the contraction phase. As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site. These changes indicate that the inflammatory phase is ending and the proliferative phase is underway. Because inflammation plays roles in fighting infection, clearing debris and inducing the proliferation phase, it is a necessary part of healing. Thus the reduction of inflammation is frequently a goal in therapeutic settings.

Inflammation lasts as long as there is debris in the wound. As in the other phases of wound healing, steps in the proliferative phase do not occur in a series but rather partially overlap in time. Also called neovascularization, the process of angiogenesis occurs concurrently with fibroblast proliferation when endothelial cells migrate to the area of the wound. Because the activity of fibroblasts and epithelial cells requires oxygen and nutrients, angiogenesis is imperative for other stages in wound healing, like epidermal and fibroblast migration. During the haemostatic and inflammatory phase of the wound healing process, vasodilation and permeabilisation allow leukocyte extravasation and phagocytic debridement and decontamination of the wound area.

Tissue swelling aids later angiogenesis by expanding and loosening the existing collagenous extracellular matrix. As the wound macrophages switches from inflammatory to healing mode, it begins to secrete endothelial chemotactic and growth factors to attract adjacent endothelial cells. Activated endothelial cells respond by retracting and reducing cell junctions, loosening themselves from their embedded endothelium. Characteristically the activated endothelial cells show enlarged nucleoli. The wound macrophages, mast cells and the endothelial cells themselves secrete proteases to break down existing vascular basal lamina. With the breakdown of endothelial basement membrane, detached endothelial cells from pre-existing capillaries and post-capillary venues can divide and migrate chemotactically towards the wound, laying down new vessels in the process.

Sprouted vessels can self-organise into luminal morphologies, and fusion of blind channels give rise to new capillary networks. Lastly the vessel establishes a pericyte layer. ECM to allow cell migration, proliferation and angiogenesis. When macrophages and other growth factor-producing cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors. Fibroblasts begin entering the wound site two to five days after wounding as the inflammatory phase is ending, and their numbers peak at one to two weeks post-wounding. By the end of the first week, fibroblasts are the main cells in the wound. Fibroplasia ends two to four weeks after wounding.

Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement. Oedema increases the wound histologic accessibility for later fibroplastic migration. Second, as inflammation nears completion, macrophage and mast cells release fibroblast growth and chemotactic factors to activate fibroblasts from adjacent tissue. Fibroblasts at this stage loosen themselves from surrounding cells and ECM. Phagocytes further release proteases that break down the ECM of neighbouring tissue, freeing the activated fibroblasts to proliferate and migrate towards the wound. The difference between vascular sprouting and fibroblast proliferation is that the former is enhanced by hypoxia, whilst the latter is inhibited by hypoxia.