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I cut my left foot, with 6 stitches on the outside of the sole and 4 stitches under the little toe. It has been three weeks now.
There are three stages in the healing of three kinds of wounds, including: ① the inflammatory stage of the body's response to the wound and the adjustment stage of the healing process; (2) the proliferation stage of environment and tissue regeneration; ③ Repair is the variation stage of sclerosis and scar formation.

Although the three stages of healing are intertwined, they all occur continuously, which will be discussed separately below.

(1) Inflammatory stage The inflammatory reaction stage of wound healing shows local temperature rise and redness. The role of this stage is to remove dead bacteria and cells and promote the healing process. This initial reaction started a series of interactions, which stimulated the trigger center of the body.

The damage of microcirculation in the operating area causes vasoconstriction, and the oxygenation of surrounding tissues is inhibited. Vascular contraction lasts for 5 ~ 10 minutes, and platelets and fibrin in the blood precipitate to form local blood clots to stop bleeding. As a result, hypoxia and tissue acidosis stimulated the inflammatory process.

In the initial stage of vasoconstriction, white blood cells, red blood cells and platelets contract the blood vessel wall. Platelets release local growth factors to stimulate tissue regeneration. Inflammation produces physical and chemical changes and increases vascular permeability. The injured tissue releases a sustained release state, and histamine causes vasodilation. The fluid, protein and enzyme in the normal vascular lumen leak into the extracellular space through the vascular wall, causing edema and redness. White blood cells migrate to the injured area to enhance the anti-infection ability of the wound. Two types of white blood cells, polymorphonuclear white blood cells and mononuclear white blood cells, began to enter the wound. Polymorphonuclear leukocytes began to digest the bacteria in the wound. The life span of polymorphonuclear leukocytes after digesting bacteria was very short, and they became a part of wound exudate after 2 ~ 3 days. Mononuclear leukocytes have a long life span and enter the wound together with polymorphonuclear leukocytes to play a role. Improve the function of macrophages to remove foreign bodies from wounds and release protein to stimulate the formation of fibroblasts. Together with platelet growth factor, these protein promote the growth of endothelial cells in local venules and form new blood vessels.

Epithelial formation: Epithelial formation mainly protects dehydration and prevents infection through the migration of wound epithelial cells. Epithelial cells proliferate through mitosis and begin to migrate from the wound edge to the wound center. Within 12 hours after injury, the skin lost from the wound began to form epithelium. The wound sutured after 24 hours has a firm anti-seepage function. Deep wounds need to form collagen and granulation tissue before epithelial covering migrates. Epithelial cells move forward according to their own classification until a layer of paper-like epithelium covers the wound. Similarly, if there is a hair follicle in the center of the wound, the epithelium will regrow around the hair follicle, forming pink epithelial cell islands, and the epithelial tissue islands will migrate with each other and stop mitosis after meeting with other epithelial tissues. When the wound is covered by epithelium, it can prevent fluid loss and bacterial invasion, and the new intact epithelium has a good protective effect.

Epithelium in healthy tissues grows rapidly, while chronic wounds, such as compressive ulcers. It has been found that the growth of fibroblasts and epithelial cells is delayed. Three days after trauma, the growth rate of healthy tissues was 80%. When biopsy was taken from the compression ulcer, it was found that the epithelial growth rate was lower than 70% after 14 days. Studies reported in the literature found that humid environment affected epithelial hyperplasia. The formation of wound scab increases the necessary time for epithelial formation. The best environment for epithelial migration is humidity and protecting the wound with necrotic tissue from opening. When epithelial tissue is used to prevent bacterial invasion and body fluid loss, it has a poor protective effect on re-injury, and it is very fragile, especially easy to be wiped off.

(2) The proliferative phase, also known as proliferative phase, began about 48 hours after trauma. This period is characterized by the activity of fibroblasts. Macrophages and platelets stimulate the production of fibroblasts. Five to six days after injury, when vitamin C is used, fibroblasts begin to synthesize collagen to support new tissue matrix. 2 ~ 3 weeks to produce rapid collagen synthesis.

The synthesis of collagen requires the oxidation of proline and lysine, which play an important role in the strength of collagen matrix, but there is no such reaction in the absence of vitamin C. When the wound heals without these vitamins, the binding force of the supporting matrix is weak and the tensile strength is not enough, so the risk of wound dehiscence is great.

In the best environment, collagen fibers are bound together by crosslinking. Collagen continues to dissolve and proliferate, collagenase decomposes collagen and synthesizes fibroblasts. The process change of this chain reaction increases the formation of organic tissue, the fiber becomes stronger and the matrix becomes stronger. A balance must be maintained between collagen production and collagen decomposition to avoid excessive proliferation or inappropriate production, which may lead to hypertrophic and atrophic scar formation respectively. The peak of collagen synthesis is 1 week of the wound. At this time, the tensile strength of the wound is increased by remodeling collagen fibers, and the growth of collagen is no longer increased.

The synthesis of collagen depends not only on adequate vitamin C, but also on oxygen and iron. The demand for oxygen in the cross-chain reaction of collagen molecules prompts people to adopt various methods to deliver oxygen to the wound. One of the reliable methods is to put the patient into the hyperbaric chamber, increase the pressure in the chamber and inhale 100% pure oxygen. Hemoglobin is completely saturated with oxygen, thus increasing the dissolved amount of oxygen in blood. The increase of dissolved oxygen pressure in hyperbaric oxygen chamber is more suitable for tissue needs than hemoglobin carrying. Recognizing the need for oxygen in the process of wound healing, we can use hyperbaric oxygen to treat and change the effect. After being used for treating epidermal trauma, the curative effect is remarkable. Deep tissue needs enough blood supply in the healing process, and deep wounds heal quickly if there is more blood supply.

Vasodilators cannot be used for treatment when there is enough oxygen in the wound. However, local application of vasodilators does not affect wound healing. The blood vessels in hypoxic tissue area are greatly expanded due to tissue acidosis and ischemia. Systemic application of vasodilators can actually reduce the blood volume of the wound, dilating other blood vessels and diverting the blood from the wound.