Wound repair

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In normal skin, the epidermis (outermost layer) and dermis (inner or deeper layer) exist in asteady-state equilibrium and shield from the external environment.

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NORMAL STRUCTURE OF SKIN

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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 involvesbreach in the contunuity of skin and usually damage to underlying tissues.

Structure of oral mucous membrane

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WOUND CLASSIFICATION

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oropharynx etc

According to potential risk of infection in operative wounds, they have been classified into 4 classes :

CLASSIFICATIONN:1

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CLASSIFICATION: 2

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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

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INCISIONS– Incisions, commonly called cuts, arewounds made by sharp cutting instruments such asknives, razors. Incisions tend to bleed freely becausethe blood vessels are cut cleanly and without raggededges. There is little damage to the surroundingtissues. Of all classes of wounds, incisions are theleast likely to become infected, since the free flow ofblood washes out many of the microorganisms thatcause infection

LACERATION– They are open wounds havingragged, irregular edges and masses of torntissue underneath.

Lacerations are frequently contaminated withdirt, grease, or other material that is groundinto the tissue; therefore very likely to becomeinfected.

Open

wounds

ABRASIONS–superficial wounds produced byexcoriation or removal of superficial layer ofmucous membrane. Rope burns, floorburns,and skinned knees or elbows are commonexamples of abrasions. This kind of wound canbecome infected quite easily because dirt andmicrobes are usually embedded in the tissues.

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PUNCTURES– Punctures are caused by objectsthat penetrate into the tissues while leaving asmall surface opening. Wounds made by nails,needles, wire, and bullets are usuallypunctures. The possibility of infection is greatin all puncture wounds, especially if thepenetrating object has tetanus bacteria on it.To prevent anaerobic infections, primaryclosures are not made in the case of puncturewounds.

Open

wounds

Gunshot wounds: (Ballistic trauma)caused by a bullet orsimilar projectile driving into or through the body. Theremay be two wounds, one at the site of entry and one at thesite of exit, generally referred to as a "through-and-through.Ballistic trauma is sometimes fatal for the recipient, orcauses long term negative consequences.

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Penetrating trauma is an injury that occurswhen an object pierces the skin and enters atissue of the body, creating an open wound.Penetrating trauma can be serious because itdamages internal organs and presents a riskof shock and infection.

Open

wounds

Crush injury occurs because of pressure from a heavy object onto a body part. A crushinjury may also arise from squeezing of a body part between two objects. Dependingupon their severity, crush injuries can be complicated by bleeding, bruising, fracturedbones, poor circulation, or breakdown of muscle (rhabdomyolysis).

Compression of extremities or other parts of the body that causes muscle swelling and/orneurological disturbances in the affected areas

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Closed

wounds

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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 collectionof extravasated blood, in an organ,space, or tissue & the massbecomes palpable to the examiner .

Closed

wounds

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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

Wound depth is another fundamental characteristics used to classify wounds. In ourassessment, 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 orextend through the epidermis into the dermis. The dermis remains at least partially intact togenerate the new epidermis needed to close the wound. They are also less susceptible toinfection 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. Thewound may expose adipose tissue, muscle, tendon, or bone.

These wounds heal by granulation and contraction, which require more body resources andmore time than the healing of partial-thickness wounds.

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CLASSIFICATION:3

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PHASES OF WOUND HEALING

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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

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Kane’s analogy to the repair of a damaged house provides a visualunderstanding of and the connection to the basic physiology of woundrepair

Hemostasis

Once the source of damage to a house has been removed and before workcan 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 healingthe platelet is the cell which acts as the utility worker sealing off the damagedblood vessels. The blood vessels themselves constrict in response to injury.

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Under normal conditions platelets arediscoid, with a diameter of 2-4 μm. 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.

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.

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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.

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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

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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.

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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.

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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 ofcollagen production and degradation equalize, the maturation phase of tissuerepair is said to have begun] During maturation, type III collagen, which isprevalent during proliferation, is replaced by type I collagen. Originallydisorganized collagen fibers are rearranged, cross-linked, and aligned alongtension lines.Remodeling can take up to 2 years after wounding.

KANES ANALOGY TO WOUND REPAIR

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HEALING CAN BE DIVIDED INTO THREE

CATEGORIES:

HEALING BY PRIMARY INTENTION

HEALING BY SECONDARY INTENTION

HEALING BY TERTIARY INTENTION

WOUND HEALING CLASSIFICATION

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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

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Healing of a clean linear wound by primary intention

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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 togranulateSurgeon may pack the wound with a gauze or use a drainage system

And thirdly, wounds that are repaired by second intention healing undergo aphenomenon known as "wound contraction" whereby specialized granulation tissuefibroblasts called myofibroblasts contract and dramatically reduce the size of thewound.

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

(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 granulateand 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.

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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 cellsor when the injury results in extensive damage to stromal framework and supportingconnective tissues. In these situations, the injured tissue is replaced by fibroblasticcells, usually in the form of granulation tissue, which eventually results in theformation 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.

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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 continuallybeing destroyed. In this group are such cells as surface epithelia and thehematopoietic cells of the spleen, lymphoid organs and bone marrow.

Stable cells replicate at very low levels under normal circumstances, but can bestimulated to divide rapidly in response to various stimuli. Cells in this group includethe parenchymal cells of most glandular organs, vascular endothelial cells, andmesenchymal cells such as fibroblasts, smooth muscle cells, osteoblasts, andchondroblasts.

Permanent cells are cells that either do not replicate in postnatal life or do so to aninsignificant extent. This group includes nerve cells, skeletal muscle cells, and cardiacmuscle cells.

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 measuredtranscutaneously in chronic wounds from 5 to 20 mm Hg, in contrast to control tissuevalues of 30 to 50 mm Hg .

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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 .

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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.

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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 .

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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 chemokineproduction and reduced macrophage phagocytic capacity.review of the age-related changesin healing capacity demonstrates that every phase of healing undergoes characteristic age-related changes, including enhanced platelet aggregation, increased secretion ofinflammatory mediators, delayed infiltration of macrophages and lymphocytes, impairedmacrophage 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, mediatedprimarily through the hypothalamic-pituitary-adrenal (HPA) and sympathetic nervous system. Stress up-regulates glucocorticoids (GCs) and reduces the levels of the pro-inflammatorycytokines IL-1β, IL-6, and TNF-α at the wound site. Stress also reduces the expression of IL-1αand IL-8 at wound sites—both chemoattractants that are necessary for the initialinflammatory phase of wound healing

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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 adisruption in healing time. Proper nutrition and an adequate amount of oxygen in the bloodcontribute to a successful recovery time. Alcohol blocks the absorption of many importantnutrients in the body, and it keeps the body from using needed nutrients during healingtime.

Smoking may adversely affect wound healing. Nicotine causes vasoconstriction,thereforereduces 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.

Factors that impair wound healing, ( in an otherwise healthy individual)

Foreign materialNecrotic tissueIschemiaTension

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.

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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.

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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.

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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

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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

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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

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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.

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Yellow

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

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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

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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.

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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 andother inflammatory cells

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Wound dehiscence is a surgical complication in which a wound ruptures

along surgical suture. Risk factors are age, diabetes, obesity, poor knotting or grabbing ofstitches, and trauma to the wound after surgery.

Wound dehiscence can be caused by inadequate undermining (cutting the skin awayfrom the underlying tissues) of the wound during surgery, excessive tension on thewound edges caused by lifting or straining, or the wound being located on a highlymobile or high tension area.

Individuals with Ehlers–Danlos syndrome also commonly experience wounddehiscence. Risk factors can include any of the above as well as obesity, smoking,previous scarring, surgical error, cancer and chronic use of corticosteroids

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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 andsuturing the edges and providing prophylactic antibiotics.

Exposure to the air, debridement and if indicated, frequent dressing changes may also help.

HOW TO PREVENT DEHISCENCE

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They often contain nerves and blood vessels. Theygenerally develop after thermal or traumatic injury thatinvolves the deep layers of the dermis .

When a normal wound heals, the body produces newcollagen fibers at a rate which balances the breakdownof old collagen. Hypertrophic scars are red and thickand may be itchy or painful.

They do not extend beyond the boundary of theoriginal wound, but may continue to thicken for up tosix months. They usually improve over the one or twoyears, but may cause distress due to their appearanceor the intensity of the itching; they can also restrictmovement 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.

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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.

Langer's lines, also called cleavage lines, is a term used to define the directionwithin the human skin along which the skin has the least flexibility.

These lines correspond to the alignment of collagen fibers within the dermis. Theywere first given detailed attention in 1861 by Austrian anatomist Karl Langer(1819-1887)

CONCEPT OF LANGERS LINES

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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.

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.

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Injuries such as burns that involve damage to the dermis rarely heal withoutformation of a scar. Scar tissue is not identical to the tissue that it replaces and isusually more fibrous and of inferior functional quality.

The scar shows an increase in the thickness of the new epithelial layer but theattachment of epidermis is poor making the surface vulnerable to further injury.

Restrictive contractures due to serious burn injuries can result in long term aestheticand physical consequences.Skin contractures bridging or located proximal to a joint lead to joint deformities thatseverely restrict range of motion of the effected joint.

Skin contractures are also often accompanied by debilitating levels of chronic painrequiring a high dependency on pain medication.

SCAR CONTRACTURES

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