Definition of wound is a disorder that causes tearing of the tissue integrity of the vascular and extra-cellular matrix of the direct exposure of the platelet. Or can also be defined as the loss or destruction of some body tissues. This situation can be caused by sharp or blunt trauma, temperature changes, chemicals, explosions, electric shock, or animal bites. When injuries occur, some effects will appear:
A. The loss of all or part of organ function
2. Sympathetic stress response
3. Bleeding and blood clots
4. Bacterial contamination
5. Cell death
The process then occurs in the damaged tissue is healing the wound that can be divided into three phases, namely the inflammatory phase, proliferation, and remodeling of the tissue re perupaan.
2. TYPE OF WOUND
Kind of wound is often described by how to get the wound and show the degree of injury.
2.1. Based on the level of contamination
a) Clean Wounds (clean wound), the surgical wound takterinfeksi which is not a process of inflammation (inflammatory) and infections of the respiratory system, gastrointestinal, genital and urinary does not occur. Clean the wound usually results in a closed wound, if necessary put a closed drainage. The likelihood of wound infection around 1% - 5%.
b) Clean-contamined Wounds (clean-contaminated wound), a surgical wound in which the respiratory tract, gastrointestinal, genital, or urinal in controlled conditions, the contamination is not always the case, the likelihood of wound infection is 3% - 11%.
c) Contamined Wounds (Wound contamination), including open wounds, fresh, accidental wounds and surgery with major damage or contamination by aseptic technique from the gastrointestinal tract; in this category also includes the incision of acute, inflammatory nonpurulen. The possibility of wound infection 10% - 17%.
d) Dirty or Infected Wounds (gross injury or infection), the presence of microorganisms in the wound.
2.2. Based on the depth and breadth of the wound
a) Stage I: Superficial wounds ("Non-blanching Erithema): the injury that occurs in the epidermal layer of skin.
b) Stage II: Wounds "Partial Thickness": a loss of skin layers on layers of the epidermis and upper dermis. A superficial wound and the presence of clinical signs such as abrasion, blister or shallow holes.
c) Stage III: Wounds "Full Thickness": a loss of the entire skin covering damage or necrosis of subcutaneous tissue that may extend to bottom but not through the underlying network. Wound up in the epidermis, dermis and fascia but not the muscle. Injuries occur clinically as a deep hole with or without damaging the surrounding tissue.
d) Stage IV: Luka "Full Thickness" which has reached a layer of muscle, tendon and bone in the presence of destruction / damage is extensive.
Figure 1. The depth of the injury rate2.3. Based on the time of wound healing
a. Acute wounds: the wound healing period in accordance with the concept of healing that has been agreed.
Figure 2. Acute woundsb. Chronic wounds are wounds that have failed in the healing process, may be due to exogenous and endogenous factors.
Figure 3. Chronic wounds
3. MECHANISM OF INJURY
a) The wound incision (Incised Wound), occurs because the cut by a sharp instrument. Eg caused by surgery.
b) bruise (contusion Wound), occurs in a collision by a pressure and is characterized by soft tissue injury, bleeding and swelling.
c) Wound blisters (Abraded Wound), caused by skin rubbing against other objects usually with no sharp objects.
d) puncture wound (Punctured Wound), the result of the object, like a knife into the skin with a smaller diameter.
e) The wound scratch (Lacerated Wound), caused by sharp objects such as the glass or by wire.
f) penetrating wounds (Penetrating Wound), which cuts through the organs of the body usually at the beginning of the wound into a small diameter but usually at the end of the wound will be widened.
g) burns (combustio), which sores result from exposure to temperatures as hot as fire, sun, electricity, and chemicals.
4. PHASE WOUND HEALING
A healthy body has a natural ability to protect and restore itself. In the event of injury, the body will repair the wound healing mechanism comprising:
1.Hemostatis and Inflammation
3. Maturation and remodeling
Figure 4. Chart of wound healing
Estimated time for the inflammatory process 0 day s / d 6 months, the proliferation of 4 s / d 14 months, the maturation of 8 s / d is infinite. This sequence of events flowing and overlapping, and in some circumstances rotates between injury and repair. All types of injuries need to go through these biochemical events selullar and the characteristics of the healing process for the successful formation of new tissue. Increased blood flow to the damaged area, cleaning the cells and foreign bodies and the early development of the mobile part of the healing process. The healing process occurs normally without assistance, although some care ingredients can help to support the healing process. For example, protecting the wound area free of debris with the police help to improve tissue healing.
Figure 5. Logarithmic time scale
Figure 6. Phase of wound healing
Phase hemostatis and Inflammation
The process of hemostasis and inflammation, wound healing beginning with the release of chemotactic factors from the wound. Definition of injury is a disorder that causes tearing of the tissue integrity of the blood vessels and extra-cellular matrix of direct exposure to the platelet. Exposure of the platelet collagen subendotelial cause platelet aggregation, degranulation and activation of the clotting cascade. Platelet α granule release a number of active substances such as platelet-derived wound growth factor (PDGF), transforming growth factor β (TGF-β), platelet-activating factor (PAF), fibronectin, and serotonin. And to achieve the fibrin clot hemostatis scalffolding to serve as movement of inflammatory cells such as PMN, neutrophils and monocytes. Followed by cellular infiltration after injury characteristics and previously determined sequences. PMN are the first cells to infiltrate the wound with a peak between 24-48 hours. Increased vascular permeability, release of local prostaglandins, and chemotactic substances such as the emergence of complement factor, interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), TGF-β, platelet factor 4, or bacterial products that stimulate the migration neutrophils. Phagocytic function of neutrophils as the bacteria and the rest of the network. PMN as well as a source of inflammatory cytokines when utamaawal, especially TNF-α, which inco special influence on the process of angiogenesis and collagen formation. PMN also release proteases such as collagenase that plays a role in the destruction of the matrix and the wound at the time of initial wound healing. Other PMN functions to limit the infection, these cells do not play a role in collagen formation or re-obtain the power of networking, but neutrophils factors may slow the healing wound epithelialization.
Inflammatory phase lasts from the onset of injury until about - about the fifth day .. broken blood vessels in the wound will cause bleeding and the body will try to stop it by vasoconstriction, contraction of the broken end of the vessel (retraction), and reactions of hemostasis. Hemostasis occurs because platelets are out of the blood vessels cling to each other, and together with the fibrin mesh that forms clots the blood coming out of the blood vessels. Meanwhile, the inflammatory reaction.
Mast cells in the connective tissue to produce serotonin and histamine that increase capillary permeability resulting in exudation of fluid, penyebukan inflammatory cells, accompanied by local vasodilatation leading to edema and swelling. Clinical signs and symptoms of inflammation become apparent in the form of a reddish color due to dilated capillaries (rubor), warm temperatures (heat), pain (dolor), and swelling (tumor).
Cellular activity that occurs is the movement of leukocytes through the vessel wall (diapedesis) into the wound because of chemotaxis. Leukocytes release hydrolytic enzymes that help digest the bacteria and dirt wound. Lymphocytes and monocytes which then come to destroy and eat up the wound dirt and bacteria (phagocytosis). This phase is also called slow phase due to reaction of the formation of new collagen and slightly wounded by a fibrin dipertautkan only very weak.
Figure 7. Inflammatory phase
Proliferative phase is also called as a prominent fibroplasia phase is the process of fibroblast proliferation. This phase lasted from the late inflammatory phase until about - about the end of the third week. Fibroblasts derived from an undifferentiated mesenchymal cells, resulting in a mucopolysaccharide, Asama aminoglisin, and proline which is the basic ingredient of collagen fibers that will mempertautkan wound edges.
In this phase the fibers are formed and destroyed again for tuning in to the tension on the wound which tends to shrink. These properties, together with the contractile properties miofibroblast, causing traction on the edge of the wound. At the end of this phase of wound tensile strength reached 25% of normal tissue. Later, in the process of collagen fibers penyudahan strength increases due to intramolecular and inter-molecular bonds.
At this phase of fibroplasia, wound filled with inflammatory cells, fibroblasts, and collagen, forming a reddish tissue with smooth surfaces berbenjol called granulation tissue. Edge of the wound epithelium consisting of basal cells detached from their foundations and moved to fill the wound surface. The place was filled by new cells formed from the process of mitosis. The process of migration can only occur towards the lower or flat, because the epithelium could migrate toward the higher. This process is only stopped after epithelial touch each other and cover the entire surface of the wound. With the closing of the wound surface, the process of fibroplasia with the formation of granulation tissue will also stop and start the process of maturation in remodelisasi phase.
Figure 8. Proliferation phase
Collagen is the protein that most of your body, and has an important role in the success of wound healing. Formation, maturation, and remodeling of collagen is essential for improving the function and integrity of the wound. Although there are approximately 18 types of collagen were found, but with an important role of wound healing is a type I and III. Type I collagen is the major extracellular matrix component of the skin. And type III collagen is also present on the skin becomes important when the process of wound repair occurs.
In biochemical each collagen chain contains a glycine residue in every third position. Second place in the triplet filled by proline or lysine in the event of translation. Polypeptide chains are encoded from mRNA containing approximately 1000 amino acids called protokolagen. The release of endoplasmic keretikulum protokolagen hydroxylation of proline to produce dhidroksi proline and of lysine to hydroxy lysine by specific hydroksilase. Prolylhydroksilase require oxygen and iron as cofactors, α-ketoglutarate as a co-substrate and ascorbic acid (vit.C) as an electron donor. Endoplasmic reticulum in the chain by chain protokolagen diglikosilasi also galactose and glucose on specific residues hydroksilisin. Hydroxylation and glycosylation steps destructive hydrogen bonds in the chain that led to changes in the force chain steric protokolagen to assume α helical configuration. Three α chains intertwined to form a helical structure to the right superhelikal called procollagen. At the end of both, the structure of the protein has a protein called nonhelikal registration. Although initially joined with a weak ionic bond, the bond becomes stronger procollagen molecule by covalent bonding of lysine residues. In the extracellular protein nonhelikal registration terminated by the enzyme procollagen peptidase and procollagen yarn having polymerization. Then generate collagen monomers that subsequently undergo polymerization and bound by a covalent bond formation of intra-and inter-molecular.
Collagen synthesis, as well as modifications posttranslasi and highly dependent on systemic factors such as oxygen supply is sufficient, adequate nutrition (amino acids, carbohydrates) and cofactors (vitamins and elektolit) and the wound environment (the blood supply and no infection). The existence of the above factors and nutritional deficiencies can improve and optimize the synthesis of collagen formation.
In this phase, a process of maturation which consists of re-absorption of excess tissue, the contraction in accordance with the force of gravity, and finally back perupaan newly formed tissue. This phase can last for months - months and stated ends when all inflammatory signs have disappeared. Body trying to normalize all of which become abnormal because of the healing process. Edema and inflammatory cells are absorbed, the young become mature cells, new capillaries shut down and be reabsorbed, excess collagen is absorbed and the rest shrink in accordance with the existing strain. During this process scar tissue produced a pale, thin, and weak and easily moved from the bottom. Maximal contraction seen in the wound. At the end of this phase, the skin wound perupaan able to withstand the strain about - about 80% the ability of normal skin. This was achieved about - about 3-6 months after treatment.
Maturation and remodeling phase begins when the injury is characterized by fibroplasia and collagen synthesis of previous reorganization. Collagen matrix metalloproteinase that was destroyed by collagen tissue injury is the result of a balance between destruction and synthesis of collagen. Wound strength and mechanical integrity of the new injury is determined by the quality and quantity of collagen formation that had just happened. Matrix formation in wound followed a typical illustration: fibronectin and collagen type 3 matrix underlying the initial charge, glycosaminoglycans and proteoglycans that merupoakan are also important components of the matrix and collagen type I. After a few weeks after the injury rate of collagen proliferation leveled off, but the strength of the pressure continues to increase until a few months. Fibril formation and interwoven collagen fibrils resulting in reduced solubility, increased strength and resistance to enzymes degrade the collagen matrix. Bone remodeling lasts for 6 to 12 months. Mechanical strength of wounds was never such a network that does not hurt.
Figure 9. Remodelling phase
While the integrity and strength of the network is being formed, the outer defenses must also be returned. This process was first characterized by proliferation and migration of epithelial cells adjacent to the wound edge. This process begins in the first days of the formation of the wound and visible as a thickening of the epidermis at the wound edge. Lower bound on the cell loss will stick to the wound edge dermis beneath and enlarged. Basal cell repair in the zone near the wound border mitosis have a very fast and these cells appear to migrate in a way to skip other epithelial wound closed. When the wound is closed, the migration of epithelial cell loss and a flat cylindrical shape and increase mitotic activity.
Perfect Reepitelisasi think - about less than 48 hours on the incision, but can be longer depending on the width of the wound and what matters is whether there is injury of the epidermis or dermis. If only the epithelium and the superficial part of dermis are damaged, as happened at the site of STSG donor wounds or burns on the surface of the second grade, especially reepitelisasi wound repair with minimal or no fibroplasias and granulation tissue. Re-epithelialization stimuli produce a picture that is not perfect, but it seems this process is mediated by a combination of loss of inhibition, exposure to extracellular matrix components, fibronectin, and the products of cytokines by mononuclear immune cells. Especially EGF, TGF-β, basic fibroblast growth factor, PDGF and IGF-1 have shown penginisiasian epithelialization.
5. THE ROLE OF GROWTH FACTOR
Growth factors and cytokines are polypeptide products on the wound and normal tissue that stimulates cellular migration and proliferation. They are often named for the cells from which they are generated (eg, platelet-derived growth factor, PDGF) or to their original function was found (eg, fibroblast growth factor, FGF), but the name is sometimes incorrectly sense because growth factors have a wide range of functions . Growth factor may act as autocrine (which GF acts on cells that produce it), paracrine (to be released into the extra cellular environment, which acts immediately on the cell next to it). Or endocrine (which give effect to a distant place where GF is excreted and taken to the place by the blood stream effectors).
This gives effect to the polypeptide binds to the cell surface receptor, the receptor corresponding to the target cells must exist to produce biological effects. GF has a different action for each different cell types. There are different types of receptors are found such as ion channels, G-protein linked, or linked enzyme. Response generated from the sidelines is usually one or dephosporilasi between phosphorylation of second messengers through the action of phosphatase or kinase, which causes the activation or deactivation of protein in the cell nucleus sitosel or target. Phosporilasi of the core protein followed by the initiation of transcription of target genes. Signal is terminated by the internalization of the receptor ligand complex.
6. CLASSIFICATION OF HEALING
Healing of skin wounds without any outside help, as has been explained earlier, naturally. Granulation tissue filled the wound and then covered the epithelial tissue. This is called secondary healing or healing sanatio per secundam intentionem (Latin: sanatio = healing, per = through, secundus = second, the way leads to intendere =). This method usually takes quite a while and leave scars that are less good, especially if the wound is gaping wide.
Another type of healing is the primary healing or sanatio per primam intentionem, which occurs when the injury immediately commercialized drew together, usually with the help of sutures. Grated happens usually more subtle and small. However, suturing wounds can not be directly performed on a heavily contaminated wound and / or not demarcated. Ragged wounds or gunshot wounds, for example, often leave the network that can not be life difficult on first inspection is known. This situation is expected to cause infection when the wound is stitched directly.
Such a wound would be cleaned and excised (debridement) first and then left for 4-7 days. New subsequently sutured and allowed to recover the primary. This method is commonly called a delayed primary healing. If, after debridement, the wound is stitched directly, it can be expected of primary healing.
Figure 10. Classification of wound healing
addition of sterile wound dressing pressure may be required. Fluid administration and surgical intervention may be needed.
3. Dehiscence and Eviscerasi
Dehiscence and eviscerasi is the most serious complications of surgery. Wound dehiscence is the opening of partial or total layer. Eviscerasi is a discharge vessel through the incision. A number of factors including, obesity, lack of nutrition, multiple trauma, failed to converge, excessive coughing, vomiting, and dehydration, heightens the risk of wound dehiscence client experience. Wound dehiscence may occur 4-5 days after surgery before kollagen widespread in the injured area. When a wound dehiscence and eviscerasi occur immediately covered with a sterile bandage is wide, with normal saline compresses. Clients are prepared for immediate improvement in the injured area.
Keloids and hypertrophic scars result from excessive collagen fiber reaction in the wound healing process. Organized collagen fibers woven here. Keloid an excessive growth beyond the injury, before causing itching and tends to recur if surgical intervention.
Hypertrophic scarring only a prominent scar, nodular, and redness, which cause itching and sometimes - sometimes painful. Hypertrophic scar will shrink in the final phase of wound healing after about a year, while keloid not.
Keloids can be found all over the body surface. The place is a predilection for the skin, especially on the face of thoracic sternum, waist, the lower jaw, neck, face, ears, and forehead. Keloid is rather seldom seen in the central part of the face in the eyes, nostrils, or mouth.
Keloid treatment is generally not satisfactory. Intrakeloid corticosteroid injections are usually done, press the bandage, light radiation and ointments madekasol (2 times daily for 3-6 months). To prevent the occurrence of keloids, surgery should be done subtly, given a splint press and avoided the possibility of complications in wound healing process.
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