Roni Khoeroni Maruli Oloan Tua Regi Septian

Respon tubuh terhadap lukaPerbaikan untuk mengembalikan fungsi jaringan setelah terjadinya kerusakan Terjadi regenerasi dimana jaringan akan digantikan oleh komponen lain sehingga fungsinya seperti sedia kala Dapat terjadi fibrosis terjadi kelebihan dari deposisi dari kolagen di jaringan

Tissue injury

Restoration of tissue integrity

Repair process

The end result of the repair process is fibrosis and scar

Healing Process: 1. Inflamation (hemostasis occurs) 2. Proliferation (fibroplasia , granulation, contraction, dan epitelialization) 3. Remodeling : scar maturation

Hand abrasion

Approximate days since injury

17

30

Inflammation is the first stage of wound healing Immediate-- 3 days Tissue injury the lacerated vessels immediately constrict thromboplastic tissue products (predominantly from the subendothelium)

Platelets aggregate and form the initial hemostatic plug The coagulation and complement cascades are initiated

The intrinsic and extrinsic coagulation pathways activation of prothrombin to thrombin converts fibrinogen to fibrin subsequently polymerized into a stable clot The aggregated platelets degranulate, releasing potent chemoattractants for inflammatory cells, activation factors for local fibroblasts and endothelial cells,and vasoconstrictors

Platelet adhesiveness is mediated by integrin receptors such as GP2b/3a (aIIbl33 Integrin) Within minutes, the repair processes are initiated Vasoconstriction vasodilatation (secondary to the coagulation and complement cascade)

Degranulation of platelets
Histamin, Bradikinin, PGI2,PGE2--vasodilatation PDGF, TGFBnetrofil & monosit Cascade 3A & 5A--fibrin

Bradykinin is a potent vasodilator and vascular permeability factor that is generated by activation of Hageman factor in the coagulation cascade The complement cascade generates the C3a and C5a anaphylatoxins,which directly increase blood vessel permeability and attract neutrophils and monocytes to the wound

An efflux of bone marrow-derived white blood cells (first neutrophils, later monocytes) and plasma proteins enter the wound site The early neutrophil infiltrate scavenges cellular debris, foreign bodies, and bacteria Activated complement fragments aid in bacterial killing through opsonization

The primary role of the neutrophil is to sterilize the wound Accordingly, the initial neutrophil infiltrate is decreased in clean surgical wounds when compared to contaminated or infected wounds

With in 2 to 3 days, the inflammatory cell population begins to shift to one of monocyte predominance Circulating monocytes are attracted and infiltrate the wound site These elicited monocytes differentiate into macrophages and, in conjunction with resident macrophages, orchestrate the repair process.

Macrophages not only continue to phagocytose tissue and bacterial debris but also secrete multiple growth factors These peptide growth factors activate and attract local endothelial cells, fibroblasts, and keratinocytes to begin their respective repair functions

Depletion of monocytes and macrophages causes a severe alteration in wound healing, with poor debridement, delayed fibroblast proliferation, and inadequate angiogenesis

Deposition of the collagen scar matrix The activation and proliferation of local fibroblast Platelets, macrophages,other bone marrowderived cells and local ECM growth factor initiate fibroblast activation Fibroblast migrate into the wound activated increase protein synthesis cell division

Cell division and proliferation fibroblast begin synthesis and secretion ECM products

Beefy Red appearance rich bed of new cappilary networks due to endothelial division and migration Granulation dense population of blood vessels, macrofag and fibroblast, matrix of fibronectin, hyaluronic acid, collagen Has a high level of vascularity accept & support skin grafts

Contraction is the process in which the surrounding skin is pulled circumferentially toward the wound Wound contraction decreases the size of the wound without new tissue formation Wound to close and thus heal much more rapidly than by epithelialization alone the area of insensate scar is smaller

Clinically, wound contraction can lead to contracture, which distorts tissue and leads to decreased function

The process of epithelial renewal after injury. Particularly important in partial thickness injuries, but plays a role in all healing. Partial thickness wounds have epidermis and dermis damaged, with some dermis preserved. Epithelial cells involved in healing come from wound edges and sweat glands, sebaceous glands in the more central portion of wound.

In contrast in an incisional wound, cellular migration occurs over a short distance. Incisional wounds are re-epithelialized in 2448h. The sequence of events here are cellular detachment, migration, proliferation, differentiation.

First 24h, basal cell layer thickens, then elongate, detach from basement membrane and migrate to wound as a monolayer across denuded area. Generation of a provisional BM which includes fibronectin, collagens type 1 and 5. Basal cells at edge of wound divide 48-72 h after injury. Epithelial cells proliferation contributes new cells to the monolayer

Within hours after injury, morphologic changes in keratinocytes at the wound margin are evident Epidermis thickens, marginal basal cell enlarge and migrate over the wound defect Cell adhesion glycoproteins, such as tenascin and flbronectin, provide the "railroad tracks" to facilitate epithelial cell migration over the wound matrix

Following the reestablishment of the epithelial layer, keratinocytes and fibroblasts secrete laminin and type IV collagen to form the basement membrane The keratinocytes then become columnar and divide as the layering of the epidermis is established, thus re-forming a barrier to further contamination and moisture loss

Sutures in skin wounds provide tracts along which these cells can migrate Subsequent epithelial thickening and keratinization produce fibrotic reactions,cysts, or sterile abscesses centered on the suture

Collagen

Plays and impotant role in wound healing 19 types identified. Type 1(80-90%) most common, found in all tissue. The primary collagen in matrix of skin Type 3(10-20%) seen in early phases of wound healing. Type V smooth muscle, Types 2,11 cartilage, Type 4 in BM.

Synthesized by fibroblasts beginning 3-5 days after injury. Rate increases rapidly, and continues at a rapid rate for 2-4 weeks in most wounds. As more collagen is synthesized, it gradually replaces fibrin as the primary matrix in the wound.

Reorganization of previously synthesized collagen Collagenase activity is balanced against new production of collagen to produce a steady state
After 4 weeks, synthesis declines, balancing destruction by collagenase.

Normal adult ratio of 4:1 (type I to type III) collagen is restored

The number of intra and intermolecular cross-links between collagen fibers increases dramatically. A major contributor to the increase in wound strength. Remodeling continues for 12 mos, so scar revision should not be done prematurely.

Wound tensile strength increases rapidly from 1 to 8 weeks postwounding. Tensile strength increases at a slower pace However, the tensile strength of wounded skin at best only reaches approximately 80 % that of unwounded skin

The final result of tissue repair is scar, which is brittle, less elastic than normal skin, and does not contain any skin appendages such as hair follicles or sweat glands. The major benefit of repair by scar is the relatively rapid reformation of tissue integrity

Non Healing Wounds : fail to epithelialize Pressure Sores : a function of the amount of pressure,on the tissue and duration of pressure, microcirculation is compromised Lower extremity ulcers : arterial or venous insufficiency Radiation Injury : cell DNA damages and ulcer may appear

Gurjala A, Howard A. Dressing. In Kryger Z, Sisco M. Practical Plastic Surgery. Landes.Bioscience. Texas.2007

Galiano R. Wound Care. In AstonSJ, Beasley RW, Thorne CH, editor: Grabb and Smiths Plastic Surgery. 6th Edition. Lippincott-Raven. Philadelphia:2007.

Galiano R. Wound Care. In AstonSJ, Beasley RW, Thorne CH, editor: Grabb and Smiths Plastic Surgery. 6th Edition. Lippincott-Raven. Philadelphia:2007

Wound that not Heal within 3 Months

Ulkus decubitus

Infection Nutrition Oxygen and perfusion Diabetes mellitus and obesity Corticosteroids Radiation Therapy Chemotherapy Excessive Healing

Hypertropic Scar Keloid

Wound Healing: Primary Secondary

Primary intention healing occurs in closed wounds, which are wounds with the edges approximated Deep sutures are placed in collagen-rich layers such as fascia and dermis Uncomplicated wounds healing with primary intention epithelialize within 24-48 h

At this point, water barrier function has been restored, and patients can be allowed to shower or wash

Open wounds heal with the same basic processes of inflammation, proliferation, and remodeling as closed wounds The major difference is that each sequence is much longer, especially the proliferative phase. There is much more granulation tissue formation and contraction

If no infection is present and the area is of sufficient size that healing will not be complete for at least 2-3 weeks, then placement of a partial- or full-thickness skin graft should be considered

When an open wound heals, which is generally defined as complete

epithelialization, the dermal defect has been filled with collagen scar covered by

epithelium This scar has less tensile strength and is more susceptible to trauma than normal skin

Kept sterile for 24-48 h until epithelialization is complete Tensile strength : 3 wks : 20 % 6 wks : 70% max : 75-80 % Abdominal fascia : retain significant tensile strength for at least 6 weeks before absorption severely weakens the suture

heavy activity should be limited for a minimum of 6 weeks while healing of deep fascial structures occurs

Moist Desiccation causes necrosis at the base of the wound until an eschar forms, which may take several days he wound is enlarging and initiation of the healing process is delayed

Besides contributing to the inflammatory processes, bone marrow-derived cells have been shown to actively deposit collagen during repair

Subpopulations of these circulating cells, termed fibrocytes, migrate to the wound site, express collagen, and ultimately become resident antigen-presenting dendritic cells Other subpopulations, without inflammatory markers, termed mesenchymal progenitor cells, regulate the proliferation and migration of dermal and epidermal cells at the wound site

These mesenchymal progenitor cells express collagens and integrate into the resident dermal fibroblast population after repair is complete