WOUNDS AND WOUND HEALING

It is a breech in the integrity of a tissue or a break in the continuity of a tissue. Aetiological factors 1. Mechanical factors 2. Thermal factors like frost bite, burns; dry or moist heat 3. Chemicals 4. Radiation 5. Ischemia 6. Infective causes (ab initio) Wound classification 1. Basic classification 2. Rank and Wakefield classification 3. Based on rate of infection 4. Based on rate of healing 5. Based on depth 6. Based on involvement of other structures/ severity 7. Based on time elapsing from trauma Basic classification or based on morphology This classifies wounds as: a. Open b. Closed Open wounds They are wounds in which there is a communication with the exterior. An open wound (as in a knife cut) is a break in the skin or mucous membrane. i. ii. iii. iv. v. vi. vii. Incised wounds Abrasion Friction burn Laceration Avulsion Puncture wounds Penetrating wound

Incised wounds- which are made under sterile conditions. Most surgical wounds are incised in type and there is little tissue damage or bruising around the operation site. A cut is made into tissues of the body by a scalpel to gain access to tissues usually to repair or remove a diseased organ or allow pus to drain from an abscess or boil. There is usually no risk of foreign material.

Abrasion also called a graze- found on the skin surface caused by scrapping or rubbing. Scrapes and abrasions are superficial (on the surface) There is denudation of superficial surface and only the epithelium is affected. It is a shearing injury of the skin in which the surface is rubbed off.It heals without scarring (healing without fibrosis). Most are superficial and heal by epithelialisation but some may result in full-thickness skin loss. They may be ingrained with dirt and if this is not removed at the time of primary treatment permanent tattooing of the skin will result. The deeper skin layers are intact, and bleeding is more of a slow ooze. They are usually caused by friction or rubbing against an abrasive surface. Friction burn- is similar to an abrasion but there is an element of thermal damage as well as abrasion. Laceration- a torn irregular wound caused by stretching of skin over bony prominences. It is usually the result of contact with a sharp object although the force could be a blunt or a sharp force. The surgical equivalent of this is an incised wound. Once the cutting implement has gone deep to the dermis, there is less resistance in the subcutaneous tissues and the cut may therefore penetrate to a considerable depth. Lacerations (cuts) go through all layers of the skin and into the fat or deeper tissues. Bleeding may be more brisk or severe. Severe blows by a blunt object, falls against a hard surface, or contact with a sharp object are the most common causes of lacerations. Avulsion- caused by tearing away of body structure from its point of attachment. It usually occurs when there has been a severe degree of tissue damage. They may occur as a result of injury or be performed as part of a surgical procedure. It can be y y Complete in which tissue is completely wrenched from its attachment. Incomplete in which case tissue is still attached by a small tissue. There is torrential bleeding.

Puncture wounds- result from pointed objects such as nails and needles. The point of entry is always small but may traverse numerous tissues. Foreign materials and organisms are likely to be carried deeply into the underlying tissues. There may be little to see on the surface. Puncture wounds are generally caused by a sharp pointed object entering the skin. Most common examples are stepping on a nail, getting stuck with a needle or a tack, or being stabbed with a knife. Bleeding is usually minimal, and the wound may be barely noticeable. tissues. Such objects as nails, needles, ice picks and other pointed objects can produce puncture wounds. Even if external bleeding is slight, there may be serious internal bleeding resulting from internal damage to an organ (as in a gunshot wound). All puncture wounds require the attention of a health professional because of the danger of tetanus. Penetrating wounds Perforating wounds Human bites and animal bites can be puncture wounds, lacerations, or a combination of both. These wounds are always contaminated by saliva and require extra care.

Closed wounds: There is no communication with the exterior. A closed wound (a contusion or internal bleeding) is a bruise that damages the underlying tissue without breaking the skin (as in a black eye). i. ii. iii. iv. Contusion Haematoma Bruise Ecchymosis

Contusion - results from injury of tissues subjacent to surface epithelium usually as a result of blunt trauma. It is therefore a closed blunt injury. There is disruption of connective tissue with extravasation of blood and tissue discolouration. Haematoma- a localized collection of blood (usually clotted) caused by bleeding from a ruptured blood vessel. There is liquification within a few days after formation of the clot. It can occur anywhere in the body and vary from a minor to a potentially fatal condition. Less serious types of haematoma include those found under the nails or in tissues of the outer ear (cauliflower ear). Most disappear without treatment in a few days but if they are painful they may be drained. Serious types include extradural and subdural haematoma. Bruise- a discoloured area under the skin caused by leakage of blood from damaged capillaries. At first, the blood appears blue or black, and then the breakdown of haemoglobin turns the bruise yellow. It usually fades after one week. If they appear for no apparent reason or are severe after only a minor injury, they may be indications of a bleeding disorder. Ecchymosis- a bruise that is visible through the skin. Rank and wakefield classification This is the most useful classification from a practical point of view. They include 1. Tidy 2. Untidy Tidy wounds are inflicted by sharp objects and contain no devitalised tissue. Skin wounds will usually be single and clean cut. Tissue damage and contamination is minimal and they include: a. Surgical incisions undertaken under aseptic techniques b. Lacerations from clean glass and knife c. Abrasions Such wounds are closed immediately with expectation of quiet primary healing. Fractures are not common in tidy wounds. Untidy wounds indicate irregular skin damage with possible skin loss, external contamination and damage to underlying tissues such as blood vessels, nerves and muscles. Fractures are common and may be multifragmentary. Skin wound are multiple and irregular. It results from

a. b. c. d.

Lacerations with marginal necrosis Avulsion injuries with skin loss Crush injuries Vascular injuries or burns

If such wounds are closed immediately, healing is unlikely to occur and if it does there will be complications. At best, there may be wound dehiscence, infection and delayed healing. At worst, gas gangrene may result and death may result. The correct management of an untidy wound is wound excision. Based on risk of infection (if no antibiotics used) i. Clean wounds ii. Clean contaminated iii. Contaminated iv. Dirty wounds Clean wounds are non-traumatic wounds with no break in the surgical technique (good surgical practise has been maintained), no septic focus and no viscus opened. Such wounds are not inflammed and does not involve a site that is associated with heavy commensal flora. Closed primarily. Respiratory, gastrointestinal, biliary, and urinary tracts not entered. Closed drainage used if necessary. Less than 2% of clean wounds become infected. Example Herniorapy, lumpectomy, mastectomy, thyroidectomy, interval appendectomy. Clean contaminated wounds- are non-traumatic wounds with a minor break in technique or with contaminated entry into a viscus but with minimal spillage. It occurs at sites with a heavy commensal load. There is no sign of leakage from microbially colonised sites. Elective entry into respiratory, biliary, gastrointestinal, urinary tracts. Less than 10% of such wounds become contaminated. In gastric surgery infection rate may be up to 30% before prophylaxis. In biliary surgery, infection rate can be as high as 20% before prophylaxis. Examples, prostatectomy, cholecystectomy. Contaminated wounds-are traumatic wounds with a major break in surgical techniques with significant spillage from an open viscus. Acute inflammation is often encountered in such wounds. Penetrating traumatic wounds <4 hours. Example in emergency appendectomy. Infection rate of such wounds is between 15-20%, but may be up to 60% before prophylaxis. Dirty wounds are traumatic wounds from a dirty source, where there is delayed treatment or when significant bacterial contamination or release of pus is encountered. Purulent inflammation present. Preoperative perforation of viscera. Penetrating traumatic wounds >4 hours. Example in emergency surgery for faecal peritonitis. Wound infection rate is less than 40% but may be 60% or more before prophylaxis. It could involve incision through an abscess. Based on depth I. Superficial wounds: involving only the epidermis and dermis up to the dermal papillae

II. III. IV.

Partial-thickness wounds: involving skin loss up to the lower dermis (part of the skin remains and shafts of hair follicles and sweat glands are leftover. Full-thickness wounds: involving the skin and subcutaneous tissue. Tissue loss occurs and the skin edges are spaced out. Deep wounds: include complicated wounds (e.g. with laceration of blood vessels and nerves), wounds penetrating into natural cavities, and wounds penetrating into an organ or tissue.

Based on involvement of other structures I. Simple wounds: comprise only one organ or tissue II. Combined wounds: as seen in mixed tissue trauma Based on rate of healing I. Acute wounds: II. Chronic wounds: Based on time elapsing from trauma I. Fresh wounds: up to 8 hours from trauma II. Old wounds: after 8 hours from trauma or skin discontinuity Wound healing It is the process through which injured tissue is replaced by damaged tissue. It is the summation of a number of processes that follow injury. These include coagulation, inflammation, matrix synthesis, and deposition. These are followed by angiogenesis, fibroplasias, epithelialisation, contraction, remodelling and scar maturation. Wounds may heal by primary or secondary intention. First intention healing: this is the process of healing a clean incised wound with the edges in apposition; a properly co-apted and sutured wound. A narrow zone of granulation tissue forms and union occurs rapidly with minimal scar formation. Immediately after trauma there is a clotting cascade which involves the intrinsic and extrinsic pathways and results in the formation of thrombin and fibrin and other proteins such as fibronectin. Exposure of type IV and V collagen also disturbs the balance of platelet thromboxane A and intimal prostacyclin I2, which results in platelet aggregation. Haemostasis is promoted, and is accompanied by vessel contraction and secretion of serotonin, kinins and histamine and neural reflexes. The aggregation and activation of platelets and release of chemotactic factors are initiated and promoted by exposure of blood to fibrillar collagen of the injured tissues. The edges of the wound become sealed with platelet clot and then fibrin clot. The adjacent capillaries constrict and are plugged with clot, but within a few hours they dilate following the release of vasodilators such as serotonin, histamine, etc. The body temperature is raised usually to 37.5-38.50C. the process probably serves to raise the metabolic rate of the wound preparatory to its repair. It also brings together the materials necessary for the subsequent stages of repair i.e. plasma, fibrin, polymorphoneuclear leucocytes. The

ground substance of the connective tissue undergoes depolymerisation and granules disappear from most cells. Second intention healing: this is the process of healing a wound with separated edges. The wound gapes because of the elastic pull of the dermis on each side and/or tissue loss. The defect initially fills with blood clot which dries to forms a scab. Neutrophils and macrophages invade the wound and clear necrotic tissue and debris. Under the scab re-epithelialization begins from wound edges. The scab is gradually lifted at its edges until it falls off. In larger wounds the advancing epithelial edge can be more easily seen. Wounds heal from below upwards. Capillary loops bud and fibroblasts proliferate to form collagen-rich granulation tissue. Some fibroblasts acquire contractile properties (myofibroblasts) and cause wound to contract. This can account for the majority of closure of larger wounds, depending on surrounding skin laxity. In contrast to first intention healing, healing by second intention is slow and results in a large distorted scar. Third intention healing also called healing or delayed primary suture is done in a heavily contaminated wound. It is now common practise to delay primarily closing a heavily contaminated wound for 4 to 5 days, by which time the wound is cleaner and so an early growth of granulation tissue would have commenced. The wound is then closed secondarily. Phases of wound healing There are three phases in first intention healing: Inflammatory or lag phase (0-3 days). There is fibrinous adhesion only of the edged in this phase. Wound strength depends on the materials used for wound apposition e.g. sutures staples or glue. Wound breakdown is the result of poor technique during this phase. Acute inflammation includes a. Preparation phase (4-6 days)which is prolonged by development of bacterial infection b. Demolition phase concerned with removal of dead and dying tissues from the wound by neutrophils and monocytes which migrate into the wound. It follows the clotting, fibrinolytic and complement cascades. This is accompanied by vascular permeability and neutrophil margination and diapedesis, controlled by expression of selectins, integrins, and adhesion molecules changes (VCAM, ICAM). The influx of polymorphonuclear white cells (PMN) is followed by macrophages and lymphocytes. PMN s and macrophages release nitric oxide, oxygen free radicals, and other antimicrobials, with prostaglandins, pro-inflammatory cytokines (principally IL-1,IL-6 and TNF- ) and growth factors(PDGF, EGF, FGF, IGF-I,IGF-II, TGF and TGF )

Proliferative phase (3 days-3weeks). Wound strength progresses with the formation of granulation tissue and collagen(fibroplasias). The tensile strength of the wound increases rapidly. This is the stage of granulation tissue formation. This phase follows the acute inflammatory response, in which fibroblasts divide and mature with the formation of endothelial buds from damaged blood vessels. These buds become canalized and new capillaries grow into the dead space of the wound. They aid in bringing nutrition and oxygen to the wound and facilitate the demolition of dead tissue and removal of foreign material. The endothelial cells divide and migrate to form a new capillary network in the wound. The fibroblasts from the cells surrounding the wounds are also activated and migrate into the wound. The endothelial cells and fibroblasts use fibronectin, hyaluronic acid, laminin and other glucosaminoglycans (GAG) in the extracellular space in the wound as the scaffolding matrix. Fibroblasts now deposit collagen on the fibronectin and GAG scaffolding. Matrix degradation is blocked, synthesis of protease inhibitors is increased at the same time. Thus damage is repaired. The ground substance now shows striking metachromasia indicating depolymerisation and increasing quantities of mucopolysaccharides. Remodelling phase(3weeks-1year). There is continous reorientation and maturation of collagen fibres.in this phase collagen is formed by fibroblasts which forms scar tissue. At first, the collagen fibrils are fine and few in relation to the cells but as healing proceeds, the fibre-cell ratio increases until in the adult scar tissue only a few elongated fibroblasts are visible. Collagen is a triple helical molecule and as it cross-links, scar tissue becomes stronger and binds the wound together( but scar is never as string as unwounded tissue). In connective tissue defects, fibroblasts also aid wound closure by a process of contraction involving secreted actin and myosin fibres. During this phase there is a fine balance between breakdown of old damaged collagen by matrix metalloproteinases and tissue inhibitors. Inadequate refashioning and formation of collagen causes wound disruption or anastomotic leak, excessive production may lead to hypertrophic and keloid scars or stenosis. Maturation phase (6months -2years) is soon followed by gradual shrinkage and maturation of connective tissue in the wound. The scar, which up to this time has remained elevated and congested, over a period of weeks or months thins out and flattens and becomes progressively less conspicuous. Histologically, the blood vessels gradually disappear (Endarteritis obliterans), the number of fibroblasts in relation to collagen fibres rapidly falls so that there is progressive increase in tensile strength which is in the fasciae of the body goes on for many months. The entire process is sometimes called cicatrisation. Factors affecting wound healing They include 1. Local 2. Systemic

Local factors i. Ischaemia ii. Blood supply and location iii. Infection iv. Mechanical factors v. Foreign bodies vi. Surgical technique vii. Size and type of wound viii. Denervation ix. Haematoma Ischaemia: Tissue necrosis, resulting from local or systemic ischemia or radiation injury, impairs wound healing. Wounds in characteristically well-perfused areas, such the face and neck, may heal surprisingly well despite unfavorable circumstances. Conversely, even a minor wound involving the foot, which has a borderline blood supply, may mark the onset of a long-term, nonhealing ulcer. Hypoxia and excessive tension on the wound edges Blood supply and location -wounds in richly vascularised areas such as the face and scalp heal faster than those in poorly vascularised areas such as the foot. Sutures may be safely removed from the face and scalp by 3days. Venous ulcers also heal poorly because of impairment of local circulation. The vessels and nerves of the scalp enter the scalp from the periphery. So injury to the scalp where the scalp is torn off the bone with the peripheral attachment intact, the scalp will not only survive but also heal. The face is richly supplied with blood as the arteries anastomose freely. Hence injury to the face bleeds profusely and heals quickly. Infection-results in persistent tissue injury and inflammation. It is the single most important cause of delay in wound healing. It impairs blood flow and increases local need for oxygen in the wound. Infection potentiates collagen lysis. Bacterial contamination is a necessary condition but is not sufficient for wound infection. A susceptible host and wound environment are also required. Foreign bodies (including sutures) potentiate wound infection. Mechanical factors such as immobilization and trauma- can delay wound healing by compressing blood vessels and separating the edge of the wound. Excessive tension on wound edges: This leads to local tissue ischemia and necrosis. Foreign bodies- such as fragments of steel, glass, or even bone constitute impediments to healing. Any kind of foreign body retained in a wound will delay healing if infection is present. On the other hand a clean object such as a piece of glass may be buried in a wound which will heal without significant complication. However , local pain and tenderness may necessitate removal. Surgical technique- If wounds are not correctly apposed, a dead space soon forms which becomes filled with tissue fluid or blood and is subsequently replaced by granulation tissue. Healing is in effect by secondary intention. Rough handling of tissues and excessive trauma also delays healing not only because of increased tendency to infection but also from production of much tissue necrosis. Excessive

tension in the wound from unduly tight sutures applied in an effort to close a gaping wound has the effect of delaying the healing of the wound. The sutures strangulate and eventually cut through the skin and subcutaneous tissues. The type of suture has little effect on the rate of wound healing. Wounds sutured with catgut heal more slowly and are initially weaker than silk sutured wound but the end results are essentially the same. Size and type of wound- small injuries heal faster and with less scar formation than large excisional wounds or wounds caused by blunt trauma Denervation: Neuropathy: Sensory neuropathy involving the feet may lead to unrecognized episodes of trauma caused by ill-fitting shoes. This is compounded by motor neuropathy causing intrinsic muscle weakness and spaying of the foot on weight bearing. The result is a convex foot with a rocker-bottom appearance. Multiple fractures go unnoticed, until bone and joint deformities become marked. This is termed a Charcot foot (ie, neuropathic osteoarthropathy) and is observed most commonly in people with diabetes mellitus, affecting approximately 2% of persons with diabetes. Type of tissue Dressings or protection Hematoma Systemic factors i. Age ii. Nutritional factors iii. Metabolic status iv. Metabolic status v. Circulatory status vi. Hormones vii. Drugs viii. Radiation and cytotoxics ix. Low temperature x. Hypoxia xi. Malignant disease / neoplasms Age- oddly enough wounds heal well in old people. Delay is probably due to deficiency state, starvation or deficient blood supply. Nutritional status- has a profound effect on wound healing. Nutritional problems: Protein-calorie malnutrition and deficiencies of vitamins A, C, and zinc impair normal wound-healing mechanisms. Malnutrition, obesity and trace metal deficiency also retard wound healing. Vitamin C or ascorbic acid is a cofactor in the hydroxylation of procollagen to collagen

Zinc deficiency uncommon except in children in the middle east retards healing by preventing cellular mitosis. Excess zinc level hinders macrophage migration and phagocytosis and thus impairs wound healing. Metabolic status- can change wound healing. Diabetes mellitus is associated with delayed healing, as a consequence of the microangiopathy that is a frequent feature of this disease. Diabetes: The long-term effects of diabetes impair wound healing by diminishing sensation and arterial inflow. In addition, even acute loss of diabetic control can affect wound healing by causing diminished cardiac output, poor peripheral perfusion, and impaired polymorphonuclear leukocyte phagocytosis. Circulatory status- inadequate blood supply usually caused by arteriosclerosis or venous abnormalities such as varicose veins that retard venous drainage also impair healing. Venous insufficiency: Patients with varicose veins or nonfunctional venous valves after deep vein thrombosis develop ambulatory venous hypertension, that is, distal venous pressure remains elevated despite ambulation. This constant venous hypertension seems to cause white cell and fibrin buildup, which impairs capillary blood flow or traps growth factors. Macromolecules pass into the dermis and eventually cause the hemosiderin deposition and brawny induration in the distal leg (gaiter area) characteristic of chronic venous insufficiency. Lymphedema: Although not typically a cause of ulceration, extremity ulcers may fail to heal because of untreated lymphedema. Nocturnal leg elevation and elastic wraps or support hose are appropriate adjuncts to the treatment of recalcitrant wounds in edematous extremities. For advanced and nonresponsive lymphedema, complex decongestive physiotherapy is a useful treatment option. Hormones- such as glucocorticoids have well documented anti-inflammatory effects that influence various components of inflammation. These agents also inhibit collagen synthesis. Drugs: Steroids and antimetabolites impede proliferation of fibroblasts and collagen synthesis. Anticoagulant-induced skin necrosis is an unusual complication of anticoagulant therapy. It may occur with heparin or warfarin, though it is more common with warfarin. Warfarin-induced skin necrosis manifests as painful hemorrhagic skin lesions, usually in an area having abundant adipose tissue, such as the thighs, abdomen, or breasts. The female-to-male ratio is 4:1. This complication is often attributable to hereditary coagulation abnormalities. Warfarin (Coumadin) depletes vitamin K dependent coagulation factors, such as protein C. Therefore, during the first several days of warfarin therapy, a period of transient hypercoagulability may occur, particularly in patients with hereditary coagulation abnormalities, such as protein C deficiency or protein S deficiency, antithrombin 3 deficiency, or activated protein C resistance. Radiation and cytotoxics- the effects of radiation on tissues may be studied in acute, intermediate and chronic phases. The effect in acute phase is not only on rapidly dividing tumour cells but also on normal cells with a high turnover. The changes take the form of desquamation. The adverse effects of prolonged or excessive electromagnetic radiation vary with the wavelength. Wavelengths of electromagnetic radiation are as follows:

y y y y y y y y y

Gamma rays - Less than 0.01 nm X-rays - 0.01-10 nm Ultraviolet C - 10-280 nm Ultraviolet B - 280-320 nm Ultraviolet A - 320-400 nm Visible light - 400-760 nm Infrared - 760 nm to 1 mm Microwave - 1 mm to 30 cm Radio waves - Centimeters to meters

Gamma radiation and x-ray exposure cause a zone of stasis, in which local blood supply is impaired by coagulative necrosis due to thrombotic occlusion of smaller arteries. Gamma and x-ray radiation also spawn ionized oxygen that adversely affects DNA. The long-term result is inhibition of regeneration of skin cells from dividing basal cells. This may cause recalcitrant painful skin ulcers. The surrounding skin is atrophic, with atrophy of hair follicles and a paucity subcutaneous fat.Ultraviolet radiation exposure, particularly ultraviolet B, causes sunburn initially and subsequently conveys a continuing risk of skin malignancy (eg, basal cell carcinoma, squamous cell carcinoma, melanoma).Excessive exposure to infrared radiation, which induces repeated or persistent skin hyperthermia of 43-47C, may cause erythema ab igne. Patients with this skin condition present with telangiectasia, erythematous patches, and hyperpigmentation. Genetic disorders such as osteogenesis imperfect, Ehlers-Danlos syndrome, Marfan syndrome, epidermolysis bullosa, acrodermatitis epithotica, progeria, Werner s syndrome(progera/progressive ageing), elastoderma, cutis laxa, pseudoxanthoma elasticum Uraemia Low temperature: The relatively low tissue temperature in the distal aspects of the upper and lower extremities (a reduction of 1-1.5C [2-3F] from normal core body temperature) is responsible for slower healing of wounds at these sites. Hypoxia: Inadequate tissue oxygenation due to local vasoconstriction resulting from sympathetic overactivity may occur because of blood volume deficit, unrelieved pain, or hypothermia, especially involving the distal extent of the extremities. Malignant disease/Neoplasms: Neoplasms strongly suggest malignancy in any chronic nonhealing wound, particularly if the wound appeared to occur spontaneously. Basal cell carcinoma appears smooth, pearly, and elevated above the skin surface, whereas squamous cell cancer is often somewhat erythematous and scaly and almost always occurs on sun-exposed areas. (See image below and Image 5.) Particularly pertinent in wound care is the so-called Marjolin ulcer, a squamous cell carcinoma originating in a chronic wound, such as a burn scar or sinus tract. This implies that even a wound that is decades old is not necessarily benign. Patients with Kaposi sarcoma typically present with multifocal violaceous lower extremity lesions. Patients with cutaneous lymphoma present with a single nodule or a

group of papules from one to several centimeters in diameter, and these almost always occurs above the waist. MANAGEMENT OF WOUNDS Wound excision is the most important step in the management of any untidy wound. In order to excise a wound, adequate anaesthesia (local, regional or general) must be provided. Where possible, a bloodless field aids identification of structures. For superficial wounds the use of local anaesthetic with 1:200000 adrenaline gives good homeostasis of skin edges. In the limbs, a pneumatic tourniquet is used mainly in massive injuries attended by profuse bleeding and where amputation might be required. Blood deficit should be controlled adequately by blood transfusion. It is helpful to use a skin-marking pen to plan the skin excision and any wound extensions. Excision should proceed in a systematic fashion, dealing with each tissue layer in turn, usually starting with the superficial and moving to deeper structures. Longitudinal structures such as blood vessels, nerves and tendons are identified and exposed but left in continuity. Devitalized dermis is pink rather than white, devitalized fat is pink rather than yellow, devitalized muscle is a dark colour, has lost its usual sheen and turgor, and does not twitch when picked up with forceps. Bone fragments with no soft tissue attachment or non-vital soft tissue attachments are also discarded. The approach to radical wound excision is sometimes called pseudotumour approach, because the entire wound is excised with an appropriate margin back to healthy tissue. At the end of the wound excision, the wound should resemble an anatomical dissection. Normal bleeding should be observed in each layer. Occasionally, in very extensive wounds this very radical approach must be modified. Where radical wound excision would threaten the viability or function of the limb, it is reasonable to excise what is definitely non-viable, carry out fasciotomy as appropriate and dress the wound, with a view to returning 48hrs later for a second look and thereafter, further serial wound excisisons until a tidy wound is achieved. Gentleness in handling tissues is ideal for it reduces trauma, bruising, exudation, an hence minimizs infection thus promoting early healing. Tissue must be protected from dessication by moistening with warm packs. Sharp dissections should be preferred to blunt dissection except where safety demands otherwise. Smaller haemostats should be employed so as to reduce the amount of tissue crushed while clamping vessels. Strict asepsis should be observed routinely using gowns, caps and efficient masks for all major surgical procedures with the usual skin preparation and draping to prevent break in technique. Immobilization and elevation of the injured part are essential for they promote venous and lymphatic drainage and thus prevent congestion and pain. Prophylaxis against tetanus by active or passive immunization should be instituted and where significant wound contamination is suspected, adequate dose of broad spectrum bactericidal antibiotic should be instituted.

Wound toilet implies washing Debridement implies laying open or fasciotomy. It comes from the French unbridling or letting loose. It refers to the concept of releasing laudable pus. The use of the word is confusing whn talking about excision as it is this very excision that is designed to avoid the formation of laudable pus. The above two processes may be important in wound mamangement but do jnot describe the excision of devitalised tissue, which is the most important process. For this reason, th term wound excision is preferred. Wound closure. Most tidy wounds that do not involve loss of tissue can be closed directly. Where there is tissue loss, appropriate tissue needs to beimported. Reconstructive plastic surgical techniques can range from simple skin grafts to complex, composite, free tissue transfers. The individual components or layers of tissues should be apposed as accurately as possible to each other, epithelium to epithelium and mesothelial structures in similar fashion. This makes for minimal fibrosis and improves the resultant scar. Dead space should be avoided in the wound as this collects blood and serum suitable pabulum for bacterial growth. Dead space may be eliminated by judicious use of buried absorbable sutures and where indicated closed exterior drainage. Excessive use of buried catgut may, however predispose to infection and drains must be left in place for only as long as is necessary as they provide possible routes of wound contamination. Tension in the wound interferes with local blood flow and hence the healing process in the wound. There is a tendency to necrosis, the cutting through of sutures and wound dehiscence. Where tension is expected as a result of tissue loss, relieving excisions may be made. DEFINITION OF TERMS Granulation tissue is defined as the combination of macrophages, neovascularisation and fibroblasts which fills the dead space of wound and provides a temporary barrier. It forms the basis for healing in connective tissues. Granuloma is a collection of macrophages which form in response to chronic inflammation or infecgtion such as TB or foreign body. Organisation is the process whereby capillary loops, fibroblasts and collgen replace the initial fibrin clot. Complications of wound healing They can arise from abnormalities in any of the basic components of the repair process. These aberrations can be grouped into three categories which include    1. 2. Deficient scar formation Excessive formation of repair component Formation of contractures Infection Keloid formation

3. 4. 5. 6. 7. 8. 9. 10. 11. 12.

Hyperpigmentation Implantation cysts Neoplasia Wound dehiscence Hypertrophic scar Proud flesh or exuberant granulation Contracture Weak scars Cicatrisation Traumatic neuroma

Infection: enters via the primary wound and interferes with the healing process. Discharge is profuse, no clot forms and epithelial migration is hindered. Tissue death occurs and sloughs accumulate. Only when this is shed would adequate granulation tissue form. In effect inection converts healing by primary to healing by secondary intention. Keloid formation: is due to excessive fibroblastic activity with marked granulation tissue formation resulting in a markedly raised scar which grows beyond the boundaries of original wound and does not regress. The exact cause is unknown. Negroes or dark skinned people are predisposed to this and there may be a genetic basis. They are particularly liable to occur in the scars of burns. Age is important, the condition occurring more often in younger people. The neck is a frequent site for such lesions. Implantation cysts: are the result of epithelial elements penetrating the wound and proliferating in situ to form epidermoid cysts. Such may occur along stitch tracts. Neoplasia: the intense cellular proliferation and migration that characterizes healing tissues is reminiscent of embryonic activity or the uncontrolled growth of a neoplasm. The important difference is the factor of control. In a healing wound, the embryonic status is temporary, arresting state is soon induced presumably by contact inhibition and remodelling ensues. Wounds produced by radiant energy are particularly liable to malignant change e.g. Marjolin s ulcer of burns. Hyperpigmentation: frequently occurs at sites of chronic scars. Deposition of degraded products of haemoglobin probably contributes but the exact cause is uncertain. Cicatrisation: continued thickening and shortening of collagen may on occasion produce contractures which later embarrass function. The deformity so produced is frequently gross with untoward effects on function e.g. distortion of limbs, stricture formation in important organs- oesophagus, intestine and urethra. Contractures: an exaggeration of the normal process of contraction in the size of a wound which is an important part of the normal healing process. It results in deformities of the wound and surrounding tissues. They are particularly prone to develop in the palms, soles and anterior aspect of the thorax. They are commonly seen after serious burns and can compromise the movements of joints.

Wound closure Primary wound closure is done 5-6 hours after surgery Secondary wound closure