WOUNDS, TISSUE REPAIR & SCARS

Shari Younge Lynch

BY: Shirray Bentick

Sherry

WOUND HEALING

INFLAMMATION
Reaction of the microcirculation characterized by

the movement of fluid and leukocytes from the blood to the extravascular space.

 Activation of inflammation can have distinct -

outcomes. Resolution Abscess formation Scar Persistent inflammation.

 Hemostasis, occurs first to stop blood loss.

The cells phagocytise debris, bacteria, and

damaged tissue and release factors that initiate the proliferative phase of wound healing.

 At wounds, blood comes in contact with collagen Blood platelets secrete inflammatory factors. Platelets stick to one another and to aggregate,

forming a mass. Fibrin and fibronectin cross-link forming a plug stopping blood loss. This plug forms the main structural support for the wound until collagen is deposited. Migratory cells use this plug as a matrix to crawl across, and platelets adhere to it and secrete factors. The clot is eventually lysed and replaced with granulation tissue and then later with collagen.

clotting
Platelets, are present in the highest numbers

shortly after a wound occurs. They release ECM proteins and cytokines (e.g. growth factors) Growth factors stimulate cells to speed their rate of division. Platelet proinflammatory factors :serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine. These serve to increase cell proliferation and migration to the area and to cause blood vessels to become dilated and porous.

Vasoconstriction and vasodilation

after blood vessel breach, thromboxanes and

prostaglandins are released by cell membranes. Proucing the effect of vasospasm and chemoattraction. vasoconstriction lasts 5-10 mins and is followed by vasodilation (max @ 20 min) Vasodilation is the result of histamine mainly, also causing porous vessels Edema ensues because proteins leakage to extravascular space and water follows porosity of blood vessels also facilitates leukocyte entry into the wound site .

Cellular recruitment
polymorphonuclear neutrophils (PMNs) become

predominant the first 2 days after injury . Chemoattractants are fibronectin, growth factors, neuropeptides and kinins. Action: phagocytise debris and bacteria and utilising free radicals. -wound cleansing ;proteases that break down damaged tissue. Neutrophils usually undergo apoptosis once they have completed their tasks and are engulfed and degraded by macrophages Other leukocytes to enter the area include helper T cells, which secrete cytokines to cause more T cells to divide and to increase inflammation and enhance vasodilation and vessel permeability. T cells also

 Macrophages Replace PMNs as the predominant cells after two days. Attracted by growth factors released by platelets and other

cells, Monocytes(Blood) Macrophages (tissue) clears the wound area of bacteria and debris. Macrophage function: phagocytise bacteria and damaged tissue, debrides damaged tissue by releasing proteases. secretion of growth factors and other cytokines to attract cells (fibroblasts) for proliferation . Stimulated by the low oxygen content of surroundings to produce factors that induce and speed angiogenesis and reepithelialization of the wound, create granulation tissue, and lay down a new extracellular matrix Because they secrete these factors, macrophages are vital for pushing

 Inflammation functions to: fighting infection

induce the proliferation

phase. However, inflammation can lead to tissue damage if it lasts too long. Thus the reduction of inflammation is frequently a goal in therapeutic settings. Inflammation lasts as long as there is debris in the wound. Thus the presence of dirt or other objects can extend the inflammatory phase for too long, leading to a chronic wound. As inflammation dies down, fewer inflammatory factors are secreted, existing ones are broken down, and numbers of neutrophils and macrophages are reduced at the wound site. These changes indicate that the inflammatory phase is

Mechanisms of inflammatory cell fxns

Phagocytosis

-Recognition -Internalization -Digestion

 Bactericidal activity

Oxygen species -superoxide -Hydrogen peroxide -Hypocholorous acid -Hydoxyl radicals

Non oxygen species -lysosomal hydolases Bactericidal permeability increasing protein Defensins Lactoferrin Lysozyme Bactericidal proteins of eosinophil.

Wound Healing
Wound healing is a complex and dynamic

process of restoring cellular structures and tissue layers. 3 distinct phases: the inflammatory phase, the proliferative phase, and the remodeling phase. Consist of a coordinated series of events: chemotaxis, phagocytosis, neocollagenesis, collagen degradation, and collagen remodeling. In addition, angiogenesis, epithelization, and the production of new glycosaminoglycans (GAGs) and proteoglycans are vital to the wound healing milieu.

 cytokines control the process

Facilitating as : chemoattractants or growth

factors . This process can go awry and produce an exuberance of fibroblastic proliferation with a resultant hypertrophic scar, (confined to the wound site). Further exuberance can result in keloid formation, where scar production extends beyond the area of the original insult. Conversely, insufficient healing can result in atrophic scar formation.

 Before wounds heal there are various injuries that

bring about their genesis. The mechanism of injury can either be: -Primary DIRECT OR EXTRINSIC INJURY 2) INDIRECT OR INTRINSIC INJURY 3) OVERUSE INJURY: A) ACUTE REPETITIVE FRICTION B) CHRONIC REPETITIVE MICROFATIGUE

 Secondary

SECONDARY INJURY:
1) SHORT TERM PRIMARY INJURY

MISMANAGED 2) LONG TERM DEGENERATIVE PROBLEMS ( ACL )

 And wounds may be classified as :

Hard tissue BONE FRACTURES, OSTEOCHONDRAL FRACTURES AND AVULSIONS 2) PERIOSTITIS 3) STRESS FRACTURES 4) HYALINE ARTICULAR AND EPIPHYSEAL CARTILAGE INJURIES

 SOFT TISSUE INJURIES: 1) SKIN AND DEEP FASCIA 2) MUSCLE-TENDON UNIT AND

TENDOPERIOSTEAL ATTACHMENTS 3) MUSCLE COMPARTMENTS 4) JOINTS AND THEIR ASSOCIATED STRUCTURES 5) INTEVERTEBRAL DISC

 SPECIAL TISSUE OR ORGAN INJURIES:

1) BRAIN AND PERIPHERAL NERVES

2) EYE, NOSE, SINUSES, LARYNX, TEETH 3) THORACIC, ABDOMINAL AND PELVIC

ORGANS

Dependent on the mechanism and type of injury wound can heal three ways: Primary Intention: When wound edges are directly next to one another Little tissue loss Minimal scarring occurs Most surgical wounds heal by first intention healing Wound closure is performed with sutures, staples, or adhesive at the time of initial evaluation Secondary Intention: The wound is allowed to granulate Surgeon may pack the wound with a gauze or use a drainage system Granulation- results in a broader scar Healing process can be slow due to presence of drainage from infection Wound care must be performed daily to encourage wound debris removal to allow for granulation tissue formation Tertiary Intention (Delayed primary closure): The wound is initially cleaned, debrided and observed, typically 4 or 5 days before closure. The wound is purposely left open

CLASSIFICATION AND MECHANISMS OF INJURIES

MECHANISMS OF INJURY
PRIMARY INJURY:

1) DIRECT OR EXTRINSIC INJURY

2) INDIRECT OR INTRINSIC INJURY 3) OVERUSE INJURY: A) ACUTE REPETITIVE FRICTION B) CHRONIC REPETITIVE MICROFATIGUE

MECHANISMS OF INJURY
SECONDARY INJURY:

1) SHORT TERM PRIMARY INJURY

MISMANAGED 2) LONG TERM DEGENERATIVE PROBLEMS ( ACL )

TISSUE-BASED CLASSIFICATION
SOFT TISSUE INJURIES: 1) SKIN AND DEEP FASCIA 2) MUSCLE-TENDON UNIT AND

TENDOPERIOSTEAL ATTACHMENTS 3) MUSCLE COMPARTMENTS 4) JOINTS AND THEIR ASSOCIATED STRUCTURES 5) INTEVERTEBRAL DISC

TISSUE BASED CLASSIFICATION

HARD TISSUE INJURIES: 1) BONE FRACTURES, OSTEOCHONDRAL

FRACTURES AND AVULSIONS 2) PERIOSTITIS 3) STRESS FRACTURES 4) HYALINE ARTICULAR AND EPIPHYSEAL CARTILAGE INJURIES

TISSUE BASED CLASSIFICATIONS

SPECIAL TISSUE OR ORGAN INJURIES:

1) BRAIN AND PERIPHERAL NERVES

2) EYE, NOSE, SINUSES, LARYNX, TEETH 3) THORACIC, ABDOMINAL AND PELVIC

ORGANS

PHASES OF WOUND HEALING

There are 3 main phases of Wound Healing: Inflammatory (substrate) Phase Proliferative Phase Maturation (remodeling) Phase

A. INFLAMMATORY PAHSE

a.k.a lag phase or exudative phase Main cells involved are the PMNs, platelets, and monoctyes/macrophages 1. Platelets

Present in high amounts shortly after a wound occurs Activates the clotting cascade and release ECM proteins and Cytokines, including Growth Factors, into the blood Platelets also release other proinflammatory factors like serotonin, bradykinin, prostaglandins, prostacyclins, thromboxane, and histamine, which serve a number of purposes, including to increase cell proliferation

 HEMOSTASIS When the tissue is first wounded, blood comes in

contact with collagen, triggering blood platelets to begin secreting inflammatory factors. Platelets also express glycoproteins on their cell membranes that allow them to stick to one another and to aggregate, forming a mass. Fibrin and fibronectin cross-link together and form a plug that traps proteins and particles and prevents further blood loss. This fibrin-fibronectin plug is also the main structural support for the wound until collagen is deposited. The clot is eventually lysed and replaced with granulation tissue and then later with collagen.

2. Polymorphonuclear Neutrophils Appears approximately 1hr after the injury, and remains the predominant cell for about 48hrs
They are attracted to the site by fibronectin, growth

factors, and substances such as neuropeptides and kinins.

Neutrophils phagocytise debris and bacteria They also kill bacteria by releasing free radical They also cleanse the wound by secreting proteases

that break down damaged tissue.

3. Monocytes/Macrophages Monocytes enter the wound after the PMNs, where they evolve into macrophages The macrophage's main role is to phagocytise bacteria and damaged tissue, and debride damaged tissue by releasing proteases Macrophages secrete a number of factors such as growth factors and other cytokines (especially during the third and fourth post-wounding days), these factors attract cells involved in the proliferation stage of healing to the area. Macrophages are stimulated by the low oxygen content of their surroundings to produce factors that induce and speed angiogenesis, and they also stimulate cells that re-epithelialize the wound, create granulation tissue, and lay down a new extracellular matrix.

2. PROLIFERATIVE PHASE Characterized by the production of collagen in the wound Five main processes occur in this phase:Angiogenesis, Fibroplasia and Granulation tissue formation, Collagen Deposition, Re-epitheliazation, Wound Contraction The primary cell in this phase is the Fibroblast, which produces collagen About two or three days after the wound occurs, fibroblasts begin to enter the wound site, marking the onset of the proliferative phase even before the inflammatory phase has ended

 ANGIOGENESIS In order to form new blood vessels and provide oxygen

and nutrients to the healing tissue, endothelial cells, develop pseudopodia and push through the ECM into the wound site. Through this activity, they establish new blood vessels.
Endothelial cells are attracted to the wound area by

fibronectin found on the fibrin clot and by growth factors released by other cells.
Endothelial growth and proliferation is stimulated by

hypoxia and presence of lactic acid in the wound. In a low-oxygen environment, macrophages and platelets produce angiogenic factors which attract endothelial cells chemotactically.
When macrophages and other growth factor-producing

cells are no longer in a hypoxic, lactic acid-filled environment, they stop producing angiogenic factors. Thus, when tissue is adequately perfused, migration and

 FIBROPLASIA AND GRANULATION TISSUE

FORMATION Simultaneously with angiogenesis, fibroblasts begin accumulating in the wound site. In the first two or three days after injury, fibroblasts mainly proliferate and migrate, while later, they lay down the collagen matrix in the wound site. Granulation tissue begin to appear in the wound during the inflammatory phase, (two to five days post wounding) and continues growing until the wound bed is covered. Granulation tissue consists of new blood vessels, fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, and the components of a new, provisional ECM. The provisional ECM is different in composition from the ECM in normal tissue and includes fibronectin, collagen, glycosaminoglycans, and proteoglycans.

 COLLAGEN DEPOSITION

Fibroblasts begin secreting collagen by the second or

third post-wounding day, and its deposition peaks at one to three weeks. Collagen production continues rapidly for two to four weeks, after which its destruction matches its production and so its growth levels off. Collagen deposition is important because it increases the strength of the wound; before it is laid down, the only thing holding the wound closed is the fibrin-fibronectin clot. Even as fibroblasts are producing new collagen, collagenases and other factors degrade it. Shortly after wounding, synthesis exceeds degradation so collagen levels in the wound rise, but later production and degradation become equal so there is no net collagen gain. This homeostasis signals the onset of the maturation phase.

 RE-EPITHELIALIZATION
The formation of granulation tissue in an open

wound allows the re-epithelialization phase to take place, as epithelial cells migrate across the new tissue to form a barrier between the wound and the environment. Basal keratinocytes from the wound edges and dermal appendages such as hair follicles, sweat glands and sebaceous(oil) glands are the main cells responsible for the epithelialization phase of wound healing. They advance in a sheet across the wound site and proliferate at its edges, ceasing movement when they meet in the middle.

 WOUND CONTRACTION

Around a week after the wounding takes place,

fibroblasts have differentiated into myofibroblasts and the wound begins to contract. In full thickness wounds, contraction peaks at 5 to 15 days post wounding. Myofibroblasts are attracted by fibronectin and growth factors and they move along fibronectin linked to fibrin in the provisional ECM in order to reach the wound edges. They form connections to the ECM at the wound edges, and they attach to each other and to the wound edges by desmosomes. Myofibroblasts have many adhesions, which allow them to pull the ECM when they contract, reducing the wound size.

MATURATION AND REMODELING PHASE

When the levels of collagen production and degradation

equalize, the maturation phase of tissue repair begins The maturation phase can last for a year or longer, depending on the size of the wound and whether it was initially closed or left open. During Maturation, type III collagen, which is prevalent during proliferation, is gradually degraded and the stronger type I collagen is laid down in its place. Originally disorganized collagen fibers are rearranged, cross-linked, and aligned along tension lines. As the phase progresses, the tensile strength of the wound increases, with the strength approaching 50% that of normal tissue by three months after injury and ultimately

TYPES OF WOUNDS
Rank and Wakefield Classification:
TIDY UNTIDY

TIDY WOUNDS
Inflicted by sharp instruments

Contain no devitalised
Examples:
surgical incisions cuts from glass knife wounds

Skin wounds will usually be single and clean cut. Tendons, arteries and nerves-commonly injured;

repair of these structures is usually possible .

UNTIDY WOUNDS
Result from crushing, tearing, avulsion, vascular injury or

burns,
Contain devitalised tissue
Skin wounds- often be multiple and irregular. Tendons, arteries and nerves may be exposed, and might

be injured in continuity, but will usually not be divided.

Fractures are common and may be multifragmentary.

Must not be closed primarily!

Correct MNG: conversion of untidy wound to tidy wound by

excision of devitalised tissue; can then be closed or allowed

Types of wounds
Those caused by application of physical force can be

div as foll:
BLUNT FORCE TRAUMA Abrasions Contusions lacerations SHARP FORCE TRAUMA Incised wound Stab wound NON MOTION TRAUMA Thermal Electrical Chemical Electromagnetic

Bruise, Contusion, Hematoma

Contusion/ Bruise
Blunt injury Rupture of blood vessels Leakage of blood from site of rupture into

surrounding tissues. Visible discoloration

Hematoma
Excessive bleeding

localised collection in

tissues

Bruise, Contusion, Hematoma

Bruises require no specific management, and no

treatment is of proven value. Time required for bruising to clear is extremely variable. A haematoma should be evacuated by open surgery if large or causing pressure effects (such as intracranially), or aspirated by a large-bore needle if smaller or in a cosmetically sensitive site. A haematoma will generally reabsorb without scarring.

Fat injuries
Blunt injury to the breast may result in an area of fat

necrosis that can masquerade as a breast lump. Blunt injuries to the face may result in lumpy subcutaneous collections due to haematoma in subcutaneous fat that may persist for several months. A fat fracture in the buttocks may result from a fall or sharp blow. This can result in separation of subcutaneous fat with an indentation that may not become apparent immediately due to haematoma.

Puncture wounds and bites

Puncture wound
an open injury in which foreign material and organisms are

likely to be carried deeply into the underlying tissues. standing on a nail or other sharp object. There may be little to see on the surface. Radiological examination may detect metal fragments or glass. Treatment
wound irrigation antibiotic treatment

tetanus prophylaxis
Large foreign bodies should be removed, but small particles may be

surprisingly difficult to find without a destructive dissection and are better left undisturbed.

Puncture wounds and bites

Bites
associated with a high incidence of infection, presumably from mouth

organisms. Animal bites may result in small, sharp, incised wounds or in severe tissue crushing as in horse bites. Dog bites may also be associated with a degree of tissue avulsion and often there are puncture wounds from upper and lower teeth and contusion of the intervening tissue. Human bites may be associated with avulsion of pieces of the nose or ear. An accidental type of bite injury may result from an attacker striking the victims incisor teeth with the knuckles. This is a frequent injury that presents with a puncture wound over the metacarpophalangeal (MP) joints.

TREATMENT: open surgical exploration excision of skin margins, irrigation

of the joint and antibiotic therapy.

Abrasions and friction burns

Abrasion
shearing injury of skin in which the surface is rubbed

off. most are superficial and will heal by epithelialisation, but some may result in full-thickness skin loss. may be dirt ingrained and if this dirt is not removed at the time of primary treatment permanent tattooing of the skin will result. Treatment clean with a scrubbing brush, gently brushing along the grain of the scratch lines.
Friction burn
is similar to an abrasion

but there is an element of thermal damage as well as

Laceration
Result of a blunt force overstretching the skin and

giving rise to a split which usually passes through the full thickness of the skin. Deep, bleeds B/c skin is composed of many diff tissues, some of the more resilient 1s will not be damaged by the forces that damaged the weaker 1s. These arch across the defect- bridging fibres.

Laceration
MANAGEMENT surgical inspection, cleaning and closure.

Once all of the damaged layers have been identified, each structure

must be repaired individually by the appropriate technique. Haemostasis must be ensured throughout the exploration. There are precise suture placement techniques for nerves, tendons and blood vessels. Muscles can be apposed in layers by mattress sutures and fascia, and subcutaneous fat should be opposed by interrupted absorbable sutures to allow a firm platform for skin closure in such a way that the skin margins do not invert. Prevent collections of blood or other fluids in a wound as they separate tissues and act as a nidus for infection. A corrugated or suction drain may be required. All patients sustaining open wounds should have prophylaxis against tetanus, and antibiotics should be administered where there is significant contamination, commencing generally with a broad-

Avulsions
Avulsion injuries
open injuries where there has been a severe degree of

tissue damage. occur when hands or limbs are trapped in moving machinery, such as in rollers, producing a degloving injury.
Degloving
caused by shearing forces that separate tissue planes,

rupturing their vascular interconnections and causing tissue ischaemia. frequently occurs between the subcutaneous fat and deep fascia. devascularisation of tissue and skin necrosis may become slowly apparent in the following few days.

Crush Injuries
are a further variant of blunt injury and are often

accompanied by degloving and compartment syndrome. Compartment Synd- Injury to tissues within a closed fascial compartment leads to bleeding, exudate and swelling of these tissues, and increased interstitial pressure. As the interstitial pressure rises above capillary perfusion pressure the blood supply to the viable tissues is reduced, resulting in further ischaemic tissue injury and swelling. This cycle causes a worsening compartment syndrome with muscle ischaemia and nerve ischaemia progressing to muscle necrosis, skin necrosis and limb loss. Intervention: Where compartment syndrome is suspected or confirmed fasciotomy is advised. Longitudinal incisions are made in the deep fascia and it may also be necessary to make extensive longitudinal releases in the skin.

Ulcers
Any breach in an epithelial surface. Chronic ulcers are wounds that fail to heal. Have a fibrotic margin and a bed of granulation tissue

which may include areas of slough (necrotic tissue). common in the lower third of the lower limb and foot. Number of different aetiologies, often being associated with arterial or venous insufficiency or a lack of normal skin innervation. The wound healing process is delayed by a variety of mechanisms including infection, mechanical irritation, ischaemia or other metabolic factors. Common in diabetes and rheumatoid arthritis. Treatment specific management of the underlying cause. The ulcer is managed either by dressings to allow healing by second intention or by surgical excision of granulation tissue and split-skin grafting.

Pressure Sores
Chronic wounds following tissue necrosis from

pressure. Occur over bony prominences with thin skin. Arise where there is unrelieved pressure in the soft tissues overlying bone such that the external pressure exceeds capillary perfusion pressure and ischaemic necrosis occurs. Occur in paraplegic individuals who lack the usual sensory input that tissue ischaemia is beginning and may lack the ability to move themselves and relieve this pressure. Also occur in situations where perfusion pressure is low, such as hypotension and peripheral vascular disease. Sacral and trochanteric sores occur in bed-

Pressure Sores
Treatment- identify and correct the underlying

cause (promotes healg by 2nd intention).

Incontinence should be managed appropriately and

nutritional support provided if needed. Surgical treatment can accelerate healing. The sore is excised and closed using a flap.

Types of Wound Healing

Wound healing maybe reduced

to a sequence of processes: Induction of an acute inflammatory response by the initial injury Parenchymal cell regeneration Migration and proliferation of both parenchymal and CT cells Synthesis of ECM proteins Remodeling of parenchymal elements to restore tissue function Remodeling of CT to achieve wound strength

Wound Healing
Acute Wounds
Primary intention Secondary intention Tertiary intention

 By primary intention:
Wound edges opposed
Normal healing Mininmal scar

 By secondary

intention:
Wound left open Heals by granulation,

contraction and epithelialisation Increased inflammation and proliferation Poor scar

 By tertiary intention

(delayed primary intention):

Wound initially left open Edges later opposed when

healing conditions are favourable

 Category 1
Primary wound healing or healing by first intention occurs within

hours of repairing a full-thickness surgical incision. This surgical insult results in the mortality of a minimal number of cellular constituents.

Category 2
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 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 If the "cleansing" of the wound is incomplete, chronic inflammation can ensue, resulting in prominent scarring.

 Category 3
Secondary healing or healing by secondary intention. In this type of healing, a full-thickness wound is allowed to close and heal. Secondary healing results in an inflammatory response that is more intense than

with primary wound healing. A larger quantity of granulomatous tissue is fabricated because of the need for wound closure. Secondary healing results in pronounced contraction of wounds. Fibroblastic differentiation into myofibroblasts, which resemble contractile smooth muscle, is believed to contribute to wound contraction. These myofibroblasts are maximally present in the wound from the 10th-21st days.

Category 4
Epithelization is the process by which epithelial cells migrate and

replicate via mitosis and traverse the wound. This occurs as part of the phases of wound healing In wounds that are partial thickness, involving only the epidermis and superficial dermis, epithelization is the predominant method by which healing occurs Wound contracture is not a common component of this process if only the epidermis or epidermis and superficial dermis are involved.

 Chronic Wounds
Edges are not approximated Accompanying tissue deficits

Called pressure ulcer

They usually occur in

traumatized or vascularly compromized tissues.

Factors Affecting Wound Healing

Systemic factors Age Nutrition (some indications has been found that certain foods, such as paprika, increases wound healing) Trauma Metabolic diseases (e.g. Diabetes Mellitus, uremia) Immunosuppression Connective tissue disorders (e.g. Rheumatoid arthritis) Smoking Local factors Mechanical injury Infection Edema Ischemic / necrotic tissue Topical agents Ionizing radiation Low oxygen tension Foreign bodies present in the wound

& Problems associated with wound healing

Abnormal wounds & Problems associated with wound healing

Chronic wounds

Diabetic wounds
Infection Wound dehiscence Incisions in the wrong direction Poor alignment of features Stretched scar

Abnormal wounds & Problems associated with wound healing

Contracted scar

Pigment alteration
Contour deformity Tattooing Stitch marks Hypertrophic scars Keloid scars

Chronic wounds
Wounds that have failed to proceed through the

orderly process that produces satisfactory anatomic and functional integrity or that have proceeded through the repair process without producing an adequate anatomic and functional result The majority of wounds that have not healed in 3 months are considered chronic

Chronic wounds
Repeated trauma, poor perfusion or oxygenation,

and/or excessive inflammation contribute to the causation and the perpetuation of the chronicity of wounds Unresponsiveness to normal regulatory signals also has been implicated as a predictive factor of chronic Any wound that does not heal for a prolonged period of time is prone to malignant transformation

Some complications of chronic wounds

Sinus formation Fistula Unrecognised malignancy Malignant transformation in the ulcer bed (Marjolins ulcer) Osteomyelitis Contractures and deformity in surrounding joints Systemic amyloidosis Heterotopic calcification Colonisation by multiple drug resistant pathogens, leading to antibiotic resistance Anaemia Septicaemia

Diabetic Wounds
10-15% of diabetic patients run the risk of

developing ulcers major contributors to the formation of diabetic ulcers include neuropathy, foot deformity, and ischemia loss of sensory function allows unrecognized injury to occur motor neuropathy or Charcot's foot leads to collapse or dislocation of the interphalangeal or metatarsophalangeal joints, causing pressure on areas with little protection

Infection
Continues to be a major medical problem

Affect the outcome of surgical procedures and

impact on the length of hospital stay and medical costs Surgery breaches intact epithelium allowing bacteria access to tissues and the bloodstream Antibiotic prophylaxis is most effective

Infection
The most common organisms responsible for

wound infections in order of frequency are Staphylococcus species, coagulase-negative Streptococcus, enterococci, and Escherichia coli can weaken abdominal closure or hernia repair resulting in wound dehiscence or recurrence of the hernia can lead to disfiguring, unsightly, or delayed closures

Wound dehiscence
The premature "bursting" open of a wound along

surgical suture. It is a surgical complication that results from poor wound healing. Sometimes a pink (serosanguinous) fluid may leak out.

Wrong direction
A scar which crosses tension lines will have a

greater tendency to stretch or become hypertrophic or will usually appear more conspicuous than one which follows a relaxed skin tension line

Poor alignment of feature

Where a scar crosses the junction between

distinct anatomical features, such as the vermillion of the lip, it is essential that these features are accurately realigned Mmisalignments result in conspicuous adverse scars

Stretched scar
Scars from excisional wounds on the trunk and

limbs often stretch. It has been shown that the width of a scar depends on the tension across the wound at the time of wound closure

Contracted scar
wound contraction continues in the remodeling

phase of scar maturation Where a linear scar crosses a flexor surface this shortening may result in a scar contracture which may prevent full extension of that part

Pigment alteration
The new epidermis of a scar will often not have

the same degree of pigmentation as surrounding unscarred areas. Most scars are hypopigmented, but hyperpigmentation can also occu

Contour deformity
Where wound edges are not anatomically aligned

in the vertical plane or where a bevelled cut is not repaired accurately there is a risk of contour irregularity in the healed scar.

Tattooing
Particles of grit, dirt or soot to become implanted

in the wound as it heals

Stitch marks
If skin sutures are left in place for more than 7

days then scars from the stitch marks will usually result.

Hypertrophic scars
In some circumstances scars remain in the

remodelling phase for longer than is usual. These hypertrophic scars are more cellular and more vascular than mature scars, there is increased collagen Clinically these scars are red, raised, itchy and tender. Mature to become pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic scars from keloid scars.

Keloid scars
An extreme overgrowth of scar tissue beyond the

limits of the original wound and shows no tendency to resolve.

Consequences of scar formation