Wound repair

wound healing concepts

1. Wound repair 1

2.  In normal skin, the   epidermis  (outermost layer) and  dermis (inner or deeper layer) exist in a steady-state equilibrium and shield from the external environment . 2 NORMAL STRUCTURE OF SKIN

3. 3 Wound is defined as “ a disruption of normal anatomic structure and function ” It is an injury to the body (as from violence, accident, or surgery) that involves breach in the contunuity of skin and usually damage to underlying tissues. Structure of oral mucous membrane

4. 4 WOUND CLASSIFICATION

5. 5 oropharynx etc According to potential risk of infection in operative wounds, they have been classified into 4 classes : CLASSIFICATION N : 1

6. 6 CLASSIFICATION: 2

7. 7 Closed wound is an injury in which no blood escapes from the body , although there may be some bleeding under the skin. Continuity of skin is maintained. Open wound is an injury that causes breach in the continuity of skin or mucous membrane and there is escape of blood from the body. OPEN AND CLOSED WOUNDS

8. 8 INCISIONS – Incisions, commonly called cuts, are wounds made by sharp cutting instruments such as knives, razors. Incisions tend to bleed freely because the blood vessels are cut cleanly and without ragged edges. There is little damage to the surrounding tissues. Of all classes of wounds, incisions are the least likely to become infected, since the free flow of blood washes out many of the microorganisms that cause infection LACERATION – They are open wounds having ragged, irregular edges and masses of torn tissue underneath. Lacerations are frequently contaminated with dirt, grease, or other material that is ground into the tissue; therefore very likely to become infected. Open wounds

9. ABRASIONS –superficial wounds produced by excoriation or removal of superficial layer of mucous membrane. Rope burns, floorburns , and skinned knees or elbows are common examples of abrasions. This kind of wound can become infected quite easily because dirt and microbes are usually embedded in the tissues. 9 PUNCTURES – Punctures are caused by objects that penetrate into the tissues while leaving a small surface opening. Wounds made by nails, needles, wire, and bullets are usually punctures. The possibility of infection is great in all puncture wounds, especially if the penetrating object has tetanus bacteria on it. To prevent anaerobic infections, primary closures are not made in the case of puncture wounds. Open w ounds

10. Gunshot wounds : ( Ballistic trauma) caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit, generally referred to as a "through-and-through. Ballistic trauma is sometimes fatal for the recipient, or causes long term negative consequences. 10 Penetrating trauma is an injury that occurs when an object pierces the skin and enters a tissue of the body, creating an open wound. Penetrating trauma can be serious because it damages internal organs and presents a risk of shock and infection. Open wounds

11. Crush injury occurs because of pressure from a heavy object onto a body part. A crush injury may also arise from squeezing of a body part between two objects. Depending upon their severity, crush injuries can be complicated by bleeding, bruising, fractured bones, poor circulation, or breakdown of muscle ( rhabdomyolysis ). Compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas 11 Closed wounds

12. 12 Contusions: more commonly known as bruises, caused by a blunt force trauma that damages tissue under the skin i.e. the subcutaneous tissue is injured but the continuity of skin is maintained. A hematoma a localized collection of extravasated blood, in an organ, space, or tissue & the mass becomes palpable to the examiner . Closed wounds

13. 13 Petechiae – small pinpoint hematomas less than 3 mm in diameter Purpura – a bruise about 1 cm in diameter, generally round in shape Ecchymosis – subcutaneous extravasation of blood in a thin layer under the skin, i.e. bruising over 1 cm in diameter. Closed wounds

14. Wound depth is another fundamental characteristics used to classify wounds. In our assessment, wound depth is recorded as partial-thickness or full-thickness. Partial-thickness They normally heal very quickly because they involve only the epidermal layer of the skin or extend through the epidermis into the dermis. The dermis remains at least partially intact to generate the new epidermis needed to close the wound. They are also less susceptible to infection because part of the body's first level of defense (the skin) is still intact.  　 Full-thickness They penetrate completely through the skin into underlying tissues. The wound may expose adipose tissue, muscle, tendon, or bone. These wounds heal by granulation and contraction, which require more body resources and more time than the healing of partial-thickness wounds. 　 14 CLASSIFICATION:3

15. 15 PHASES OF WOUND HEALING

16. 16 Wound healing   The healing wound is an overt expression of an intricate sequence of cellular and biochemical responses directed toward restoring tissue integrity and functional capacity following injury. Day 1 Day 1-4 Day 4-21 Day 21- 2yrs

17. 17 Kane’s analogy to the repair of a damaged house provides a visual understanding of and the connection to the basic physiology of wound repair

18. Hemostasis Once the source of damage to a house has been removed and before work can start, utility workers must come in and cap damaged gas or water lines. So too in wound healing damaged blood vessels must be sealed. In wound healing the platelet is the cell which acts as the utility worker sealing off the damaged blood vessels. The blood vessels themselves constrict in response to injury. . 18 Under normal conditions platelets are discoid, with a diameter of 2-4 μ m. Under the influence of ADP (adenosine diphosphate ) leaking from damaged tissues the platelets become spherical and extend long pseudopodia which adhere to subendothelium and other platelets. Upon activation platelets granules discharge their contents which encourages further platelet aggregation and fibrin formation.

19. Platelets release platelet-derived growth factor (PDGF ) and transforming growth factor beta ( TGF-b ) from their alpha granules to attract neutrophils and macrophages. They also secrete factors which interact with and stimulate the intrinsic clotting cascade through the production of thrombin, which in turn initiates the formation of fibrin from fibrinogen. The fibrin mesh strengthens the platelet aggregate into a stable hemostatic plug. Hemostasis occurs within minutes of the initial injury unless there are underlying clotting disorders. 19

20. Inflammation Phase Clinically inflammation, the second stage of wound healing presents as erythema , swelling and warmth often associated with pain, the classic “ rubor , tumor , calor , dolor ”. This stage usually lasts up to 4 days post injury. In the wound healing analogy the first job to be done once the utilities are capped is to clean up the debris. This is a job for non-skilled laborers . These non-skilled laborers in a wound are the neutrophils or PMN’s ( polymorphonucleocytes ). The inflammatory response causes the blood vessels to become leaky releasing plasma and PMN’s into the surrounding tissue. The neutrophils phagocytize debris and microorganisms and provide the first line of defense against infection. They are aided by local mast cells. As fibrin is broken down as part of this clean-up the degradation products attract the next cell involved. 20

21. The task of rebuilding a house is complex and requires someone to direct this activity or a contractor. The cell which acts as “contractor” in wound healing is the macrophage. Macrophages are able to phagocytize bacteria and provide a second line of defense . They also secrete a variety of chemotactic and growth factors such as fibroblast growth factor (FGF), epidermal growth factor (EGF), transforming growth factor beta (TGF) and interleukin-1 (IL-1) which appears to direct the next stage 21

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23. Proliferative Phase ( Proliferation, Granulation and Contraction): The granulation stage starts approximately four days after wounding and usually lasts until day 21 in acute wounds depending on the size of the wound. It is characterized clinically by the presence of pebbled red tissue in the wound base and involves replacement of dermal tissues and sometimes subdermal tissues in deeper wounds as well as contraction of the wound. In the wound healing analogy once the site has been cleared of debris, under the direction of the contractor, the framers move in to build the framework of the new house. Sub-contractors can now install new plumbing and wiring on the framework and siders and roofers can finish the exterior of the house. 23

24. 24 The “framer” cells are the fibroblasts which secrete the collagen framework on which further dermal regeneration occurs. Specialized fibroblasts are responsible for wound contraction. The “plumber” cells are the pericytes which regenerate the outer layers of capillaries and the endothelial cells which produce the lining.This process is called angiogenesis. The “roofer” and “ sider ” cells are the keratinocytes which are responsible for epithelialization . In the final stage of epithelializtion , contracture occurs as the keratinocytes differentiate to form the protective outer layer or stratum corneum . .

25. Remodeling or Maturation Phase: Once the basic structure of the house is completed interior finishing may begin. So too in wound repair the healing process involves remodeling the dermal tissues to produce greater tensile strength. The principle cell involved in this process is the fibroblast. When the levels of collagen production and degradation equalize, the maturation phase of tissue repair is said to have begun ] During maturation, type III collagen, which is prevalent during proliferation, is replaced by type I collagen. Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. Remodeling can take up to 2 years after wounding.

26. KANES ANALOGY TO WOUND REPAIR 26

27. 27 HEALING CAN BE DIVIDED INTO THREE CATEGORIES: HEALING BY PRIMARY INTENTION HEALING BY SECONDARY INTENTION HEALING BY TERTIARY INTENTION WOUND HEALING CLASSIFICATION

28. 28 This type of healing occurs when there is essentially no contamination of the wound and the edges of the wound are approximated thus closing the wound. The best example of this situation is the surgical incision where contamination of the wound is minimized and the wound is closed by suturing. Once the wound is sutured, the incision space fills with blood, which contains fibrin and blood cells and which subsequently clots. The surface of this clot becomes dehydrated and forms a scab. Within 24 hours, neutrophils appear at the edges of the incision and the epithelium at the edges of the incision begins to proliferate. It migrates under the scab and forms a thin continuous epithelial layer. By 72 hours, macrophages are usually the most numerous inflammatory cells and granulation tissue starts to develop. Collagen fibers are present but do not bridge the incision site. The epithelial cells continue to proliferate under the scab and the epidermal covering over the incision becomes thicker. By day 5, the incision space is filled with granulation tissue and collagen fibers begin to bridge the incision. The epidermis returns to its normal thickness and keratinized architecture. PRIMARY INTENTION

29. 29 Healing of a clean linear wound by primary intention

30. 30 Second intention healing differs from first intention healing in several ways. First of all the greater injury invokes a more intense inflammatory response. If conditions are less favorable , wound healing is more complicated and occurs through a protracted filling of the tissue defect with granulation and connective tissue. This process is called healing by second intention and is commonly associated with avulsive injury, local infection, or inadequate closure of the wound. Secondly, much more granulation tissue is formed. The wound is allowed to granulate Surgeon may pack the wound with a gauze or use a drainage system And thirdly, wounds that are repaired by second intention healing undergo a phenomenon known as "wound contraction" whereby specialized granulation tissue fibroblasts called myofibroblasts contract and dramatically reduce the size of the wound.

31. 31 Healing by secondary intention: there is more extensive of tissue that has gradually to be filled in and replaced by new connective tisssue .

32. ( TERTIARY INTENTION OR DELAYED PRIMARY CLOSURE) For more complex wounds, the surgeon may attempt healing by third intention through a staged procedure that combines secondary healing with delayed primary closure. The avulsive or contaminated wound is débrided and allowed to granulate and heal by second intention for 5 to 7 days. Once adequate granulation tissue has formed and the risk of infection appears minimal, the wound is sutured . The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure. The wound is purposely left open. If the wound edges are not reapproximated immediately, delayed primary wound healing transpires. This type of healing may be desired in the case of contaminated wounds. By the fourth day, phagocytosis of contaminated tissues is well underway, and the processes of epithelization , collagen deposition, and maturation are occurring . Foreign materials are walled off by macrophages that may metamorphose into epithelioid cells, which are encircled by mononuclear leukocytes, forming granulomas . Usually the wound is closed surgically at this juncture, and if the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring. 32

33. Difference between 'repair' and ‘regeneration ’.   When restitution occurs by means of tissue that is structurally and functionally indistinguishable from native tissue, regeneration has taken place. However, if tissue integrity is reestablished primarily through the formation of fibrotic scar tissue then repair has occurred. Repair predominates when injuries occur in tissues formed largely of permanent cells or when the injury results in extensive damage to stromal framework and supporting connective tissues. In these situations, the injured tissue is replaced by fibroblastic cells, usually in the form of granulation tissue, which eventually results in the formation of a scar. True tissue regeneration  or  complete regeneration , refers to the replacement of lost/damaged tissue with an ‘exact’ copy, such that both morphology and functionality are completely restored. . 33

34. 34 Based on their regenerative capabilities, the cells of the body are divided into three groups : labile cells, stable cells, and permanent cells . Labile cells proliferate normally throughout life replacing cells that are continually being destroyed. In this group are such cells as surface epithelia and the hematopoietic cells of the spleen, lymphoid organs and bone marrow. Stable cells replicate at very low levels under normal circumstances, but can be stimulated to divide rapidly in response to various stimuli. Cells in this group include the parenchymal cells of most glandular organs, vascular endothelial cells, and mesenchymal cells such as fibroblasts, smooth muscle cells, osteoblasts , and chondroblasts . Permanent cells are cells that either do not replicate in postnatal life or do so to an insignificant extent. This group includes nerve cells, skeletal muscle cells, and cardiac muscle cells.

35. Factors Affecting Wound Healing Holistic assessment of the patient is an important part of the wound care process. A number of local and systemic factors can delay or impair wound healing. These may include: Reduced Blood supply (oxygenation) - Cardiovascular disorders and Ischaemia . Oxygen is important for cell metabolism, especially energy production by means of ATP, and is critical for nearly all wound-healing processes. It prevents wounds from infection, induces angiogenesis, increases keratinocyte differentiation, migration, and re- epithelialization , enhances fibroblast proliferation and collagen synthesis, and promotes wound contraction . Chronic wounds are notably hypoxic; tissue oxygen tensions have been measured transcutaneously in chronic wounds from 5 to 20 mm Hg, in contrast to control tissue values of 30 to 50 mm Hg . 35

36. 36 Drugs - Non-steroidal anti inflammatory drugs and Corticosteroids. Systemic glucocorticoids (GC), which are frequently used as anti-inflammatory agents, are well-known to inhibit wound repair via global anti-inflammatory effects and suppression of cellular wound responses, including fibroblast proliferation and collagen synthesis. Systemic steroids cause wounds to heal with incomplete granulation tissue and reduced wound contraction . Non-steroidal anti-inflammatory drugs (NSAIDs) There are few data to suggest that short-term NSAIDs have a negative impact on healing. However, the question of whether long-term NSAIDs interfere with wound healing remains open. Most chemotherapeutic drugs are designed to inhibit cellular metabolism, rapid cell division, and angiogenesis and thus inhibit many of the pathways that are critical to appropriate wound repair. These medications inhibit DNA, RNA, or protein synthesis, resulting in decreased fibroplasia and neovascularization of wounds .

37. 37 Obesity - decreases tissue perfusion. Obese individuals frequently face wound complications, including skin wound infection, dehiscence, hematoma and seroma formation, pressure ulcers, and venous ulcers. Many of these complications may be a result of a relative hypoperfusion and ischemia that occurs in subcutaneous adipose tissue. This situation may be caused by a decreased delivery of antibiotics as well. Underlying Disease - Diabetes Mellitis and Autoimmune disorders: Several dysregulated cellular functions are involved in diabetic wounds, such as defective T-cell immunity, defects in leukocyte chemotaxis , phagocytosis , and bactericidal capacity, and dysfunctions of fibroblasts and epidermal cells. These defects are responsible for inadequate bacterial clearance and delayed or impaired repair in individuals with diabetes.

38. 38 Infection –(prolong inflammatory phase, use vital nutrients, impair epithelialisation and release toxins). prolonged inflammation also leads to an increased level of matrix metalloproteases (MMPs), a family of proteases that can degrade the ECM. P aeruginosa and Staphylococcus appear to play an important role in bacterial infection in wounds. Many chronic ulcers probably do not heal because of the presence of biofilms containing P. aeruginosa , thus shielding the bacteria from the phagocytic activity of invading polymorphonuclear neutrophils (PMNs). This mechanism may explain the failure of antibiotics as a remedy for chronic wounds .

39. 39 Age Delayed wound healing in the aged is associated with an altered inflammatory response, such as delayed T-cell infiltration into the wound area with alterations in chemokine production and reduced macrophage phagocytic capacity.review of the age-related changes in healing capacity demonstrates that every phase of healing undergoes characteristic age-related changes, including enhanced platelet aggregation, increased secretion of inflammatory mediators, delayed infiltration of macrophages and lymphocytes, impaired macrophage function, decreased secretion of growth factors, delayed re- epithelialization , delayed angiogenesis and collagen deposition, reduced collagen turnover and remodeling , and decreased wound strength. Stress The pathophysiology of stress results in the deregulation of the immune system, mediated primarily through the hypothalamic-pituitary-adrenal (HPA) and sympathetic nervous system . Stress up-regulates glucocorticoids (GCs) and reduces the levels of the pro-inflammatory cytokines IL-1β, IL-6, and TNF-α at the wound site. Stress also reduces the expression of IL-1α and IL-8 at wound sites—both chemoattractants that are necessary for the initial inflammatory phase of wound healing

40. 40 Malnutrition - inadequate supply of protein, carbohydrates, fatty acids, and trace elements essential for all phases of wound healing Substance abuse including alcohol and cigarette smoke: Alcohol abuse and smoking cause a disruption in healing time. Proper nutrition and an adequate amount of oxygen in the blood contribute to a successful recovery time. Alcohol blocks the absorption of many important nutrients in the body, and it keeps the body from using needed nutrients during healing time. Smoking may adversely affect wound healing. Nicotine causes vasoconstriction,therefore reduces blood supply to the skin and periphery. This reduces the perfusion of wounds. Smoke also contains carbon monoxide which increases the proportion of carboxyhaemoglobin in the blood. Another problem is that smokers lose more vitamin C than non-smokers. Smoke causes the breakdown and increased excretion of vitamin C from the body, resulting in a chronic shortage. As vitamin C is essential for collagen formation wound healing will be correspondingly inhibited.

41. Factors that impair wound healing, ( in an otherwise healthy individual ) Foreign material Necrotic tissue Ischemia Tension Foreign material is evrything that the hosts organisms immune system views as “non self”, Including bacteria, dirt, suture material etc Necrotic tissue : its presence serves as a barrier to ingrowth of reparative cells,the inflammatory stage is then prolonged . Also, necrotic tissue serves as niche for bacteria. It frequently includes blood that collects in a wound (hematoma), where it can serve as an excellent source of bacteria. 41

42. Ischemia: decreased blood supply to a wound interferes in wound repair in several ways; It can lead to further tissue necrosis and lessen the delivery to a wound of antibodies, wbc’s , and antibiotics which thereby increase the chances of wound infection. Wound ischemia decreses the delivery of oxygen & nutrients necessary for proper healing. Ischemia can be caused by several things, including– tight & incorrectly placed sutures, improperly designed flaps, excessive external pressure on a wound, systemic hypotension, peripheral vascular disease and anemia. 42

43. Tension : tension on a wound is the final factor that can impede wound healing. Anything tending to hold wound edges apart. If sutures are used to overcome excessive wound tension, the tissue encompassed by sutures will be strangulated, producing ischemia. If sutures are removed too early in the healing process, the wound under tension will probably reopen and then heal with excessive scar formation and wound contraction. If sutures are left in too long, in an attempt to overcome wound tension, the wound will still tend to spread open during the remodelling stage of healing, and the tract into the epithelium through which the sutures ran will epithelialize and leave a permanent disfiguring mark. 43

44. WOUND ASSESSMENT Considerations for assessment Wound Bed Granulating : healthy red tissue which is deposited during the repair process, presents as pinkish/red coloured moist tissue and comprises of newly formed collagen, elastin and capillary networks. The tissue is well vascularised and bleeds easily. Epithelializing : process by which the wound surface is covered by new epithelium, this begins when the wound has filled with granulation tissue. The tissue is pink, almost white, and only occurs on top of healthy granulation tissue 44

45. Sloughy : A layer or mass of dead tissue separated from surrounding living tissue. ( devitalized yellowish tissue). Is formed by an accumulation of dead cells. Must not be confused with, pus. Necrotic : wound containing dead tissue. It may appear hard dry and black. Dead connective tissue may appear grey. The presence of dead tissue in a wound prevents healing Hypergranulating ; granulation tissue grows above the wound margin. This occurs when the proliferative phase of healing is prolonged usually as a result of bacterial imbalance or irritant forces 45

46. Red If the wound is red (the colour of healthy granulation tissue) the wound is healthy and normal healing is under way . When a wound begins to heal, a layer of pale pink granulation tissue covers the wound bed. As this layer thickens, it becomes beefy red.  (The Royal College of Surgeons of Edinburgh [RCSE], 2005) The Red-Yellow-Black is a simple  classification , which identifies what healing phase a wound  is in. ( Cuzzell ) 1988 RYB CLASSIFICATION 46

47. If the would is yellow, beware! A yellow color in the wound bed may be a film of fibrin on the tissue. Fibrin is a sticky substance that normally acts as a glue in tissue rebuilding. However, if the wound is unhealthy or too dry, fibrin builds up into a layer that can't be rinsed off and may require debridement. Dead tissue due to ischemia or infection also may be yellow and must be debrided . 47 Yellow

48. the wound bed is black, be alarmed. A black wound bed signals necrosis (tissue death). Eschar (dead, avascular tissue) covers the wound, slowing the healing process and providing microorganisms with a site in which to proliferate. When eschar covers a wound, accurate wound depth is difficult and should be defered until eschar is removed. Black 48

49. Wound Edges Healthy wound edges present as advancing pink epithelium growing over mature granulated tissue. Colour - pink edges indicate growth of new tissue; dusky edges indicate hypoxia; and erythema indicates physiological inflammatory response or cellulitis Raised - wound edges (where the wound margin is elevated above the surrounding tissue) may indicate pressure, trauma or malignant changes Rolled -wound edges (rolled down towards the wound bed) may indicate wound stagnation or wound chronicity Contraction -    wound edges are coming together, signs of healing 49

50. Exudate An exudate is any fluid that filters from the circulatory system into lesions or areas of inflammation. Is produced by all acute and chronic wounds (to a greater or lesser extent) as part of the natural healing process. It plays an essential part in the healing process in that it: Contains nutrients, energy and growth factors for metabolising cells Contains high quantities of white blood cells Cleanses the wound Maintains a moist environment Promotes epithelialisation It is important to asses and document the type, amount and odour of exudate to identify any changes. Too much exudate leads to maceration and degradation of skin while too little can result in the wound bed drying out. It may become more viscous and odorous in infected wounds. 50

51.   Type   Colour Consistency   Significance Serous  Clear, straw coloured Thin, watery    Normal. An increase may be indicative of infection Haemoserous  Clear, pink Thin, watery   Normal   Sanguinous   Red Thin, watery    Trauma to blood vessels  Purulent  Yellow, grey, green Thick  Infection. Contains pyogenic organisms and other inflammatory cells 51

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53. Wound dehiscence  is a surgical complication in which a wound ruptures along surgical suture. Risk factors are age, diabetes, obesity, poor knotting or grabbing of stitches, and trauma to the wound after surgery. Wound dehiscence can be caused by inadequate undermining (cutting the skin away from the underlying tissues) of the wound during surgery, excessive tension on the wound edges caused by lifting or straining, or the wound being located on a highly mobile or high tension area. Individuals with Ehlers– Danlos syndrome also commonly experience wound dehiscence. Risk factors can include any of the above as well as obesity, smoking, previous scarring, surgical error, cancer and chronic use of corticosteroids 53

54. Dehiscence can be prevented through adequate undermining to reduce stress on the wound edges, avoiding heavy lifting and hematomas and speeding healing through adequate nutrition, controlled diabetes. Sterile strips may also be used to cover the sutures for up to a week. Once wound dehiscence occurs, it can be treated by allowing  granulation, revising and suturing the edges and providing prophylactic antibiotics. Exposure to the air, debridement and if indicated, frequent dressing changes may also help. HOW TO PREVENT DEHISCENCE 54

55. They often contain nerves and blood vessels. They generally develop after thermal or traumatic injury that involves the deep layers of the dermis . When a normal wound heals, the body produces new collagen fibers at a rate which balances the breakdown of old collagen. Hypertrophic scars are red and thick and may be itchy or painful. They do not extend beyond the boundary of the original wound, but may continue to thicken for up to six months. They usually improve over the one or two years, but may cause distress due to their appearance or the intensity of the itching; they can also restrict movement if they are located close to a joint. A  hypertrophic scar  is a cutaneous condition characterized by deposits of excessive amounts of collagen which gives rise to a raised scar, but not to the degree observed with  keloids . 55 SCARS: are areas of fibrous tissue that replace normal skin after injury. A scar results from the biological process of wound repair in the skin and other tissues of the body. Thus, scarring is a natural part of the healing process.

56. Langer's lines, also called cleavage lines, is a term used to define the direction within the human skin along which the skin has the least flexibility. These lines correspond to the alignment of collagen fibers within the dermis. They were first given detailed attention in 1861 by Austrian anatomist Karl Langer (1819-1887) CONCEPT OF LANGERS LINES 56 Usually, a surgical cut is carried out in the direction of Langer's lines, and incisions made parallel to Langer's lines generally heal better and produce less scarring, while perpendicular injuries will gape because they are pulled by tension. This can have important implications for surgery, particularly in cosmetic procedures where the goal may be to minimize the appearance of scarring.

57. A   keloid   is the formation that a type of scar which, depending on its maturity, is composed mainly of either type III (early) or type I (late) collagen. It is a result of an overgrowth of granulation tissue (collagen type 3) at the site of a healed skin injury which is then slowly replaced by collagen type 1. Keloids are firm, rubbery lesions or shiny, fibrous nodules, and can vary from pink to flesh-coloured or red to dark brown in colour. A keloid scar is benign and not contagious, but sometimes accompanied by severe itchiness, pain, and changes in texture. In severe cases, it can affect movement of skin. Keloids should not be confused with hypertrophic scars, which are raised scars that do not grow beyond the boundaries of the original wound. Keloids expand in claw-like growths over normal skin.  57

58. Injuries such as burns that involve damage to the dermis rarely heal without formation of a scar. Scar tissue is not identical to the tissue that it replaces and is usually more fibrous and of inferior functional quality. The scar shows an increase in the thickness of the new epithelial layer but the attachment of epidermis is poor making the surface vulnerable to further injury.  Restrictive contractures due to serious burn injuries can result in long term aesthetic and physical consequences. Skin contractures bridging or located proximal to a joint lead to joint deformities that severely restrict range of motion of the effected joint.  Skin contractures are also often accompanied by debilitating levels of chronic pain requiring a high dependency on pain medication.  SCAR CONTRACTURES 58

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