General Surgery Book - Wound Chapter PDF

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Damietta University

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surgery wound healing general surgery

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This document is a medical textbook chapter on wounds, focusing on causes, classifications, and treatment in general surgery. It covers topics such as acute and chronic wounds, different types of wounds (abrasions, incised wounds, etc.), factors affecting healing, and complications. The document is specifically related to the wound chapter of a general surgery textbook intended for medical students at Damietta University.

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General SURGERY GENERAL SURGERY DEPARTMENT FACAULTY OF MEDICINE – DAMIETTA UNIVERSITY Faculty of medicine – Damietta university Page |0 CONTENT Wounds........

General SURGERY GENERAL SURGERY DEPARTMENT FACAULTY OF MEDICINE – DAMIETTA UNIVERSITY Faculty of medicine – Damietta university Page |0 CONTENT Wounds............................................................................................................. 2 Cause, Hernia = Burst Wounds Page |1 Wounds Page |2 Wounds causes : Mechanicalwounds Abrasion, cut, stab wound, insect bite Introduction: or shot wound Chemicalwound skin or mucous membrane has necrotized Burns burning or frostbite DEFINITION Electricitywounds integrity Disruption of the continuity of the skin, mucous membrane or soft tissue - caused by[ [ physical, chemical or biological insult. CLASSIFICATION OF WOUNDS They are classified into:  Closed (blunt): e.g. motor car accident, falling from height. -  Open (penetrating): I - Sharp/ (Non Surgical) o Accidental e.g. gunshot, cut wounds, stabbing, bites - - - - o Surgical trauma. > - Caused by sharp instruments. They are always tidy and cleanly cut. According to intention ↑ ex : surgery  Intentional (Surgical) - results from planned treatment - & - -  Unintentional wounds (Traumatic / accidental) result from unexpected - trauma as accident, burns, shooting. - - According to extent of tissue injury: -  Superficial  Deep It can be classified according to onset into: T open -Nons > closed -  Acute wounds (goes through normal/timely healing process) -  Chronic wounds (fails to go through normal stages of healing, no timely - progress in healing) Page |3 Onset : Acute wound: go through normal healing process  Open wound o Surgical: Caused by sharp instruments. They are always tidy and cleanly cut. o Non-surgical. accidental ( gunshot, cut wounds, stabbing, bites I  Closed Wounds: with an intact epithelial cover - motor car accident - falling from height A. Open wound:  Abrasions: scraping away of the superficial layers of the skin. It is superficial injury (scratch/graze/pressure/ contact) and is due to - - - - shearing of the skin where the surface is rubbed off. -This tangential force causes loss of epidermis exposing dermal vessels and nerves leading into profuse painful oozing. -Abrasion heals by epithelialization. Any dirt or foreign body on the abrasion should be removed to avoid formation of poor tattoo like scar.  Friction burns: Forceful sheering a abrasion causing thermal injury  Penetrating (puncture) Wounds: Pressure by sharp object (pointed - - instrument) like nail or needle. The wound is deeper than longer - - increasing the risk of injury of deep important structures. External opening is small and drainage is poor encourages infection. -Deeper vital structures or organs may be injured, so should be H Q assessed; foreign body or object may be present in the depth of the CT/US ! wound. Page |4 H -Wound should be explored under general or regional anaesthesia to - ② ⑤ assess the depth and severity of the injury and sutured layer by layer after through saline wash ⑮ -  Stab wound: caused by sharp flat object such as a knife or screwdriver. These wounds are deep with possibility of deep organ injury. -Ultrasound and CT scan should be done to evaluate deeper organ ① injuries. -Under general anaesthesia wound should be explored properly. ②  Bites: caused by the teeth of animal or human. They are lacerated & contaminated wounds with increased incidence of infectionC (tetanus and6 rabies). Snake bites are poisonous.  Stings: Caused by insects, spiders and scorpions. They can be poisonous  Cut wounds: caused by sharp object with minimal blunt force. b &  Incised wound: A neat cut wound usually caused by scalpel in surgical - surgical operations - Road traffic  Lacerations: Severe violence with blunt objects e.g RTA or falling from - - & - - accident a height. - Page |5 Note box! Characters of lacerated wound: O  The wounds are severely traumatized and devascularized. 8  Irregular in shape.  Usually contaminated, so the risk of infection is high. ⑤  Inflammatory edema will develop after a few hours and will raise tension inside the wound to a high level leading to 2ry ischemia of the tissues. ④  Crushed: Extreme pressure smashing the skin and underlying tissues with marked soft tissue damage. -It is due to major wounds, war wounds, natural disaster like earthquake injuries, tourniquet injury. -It leads into compartment syndrome; muscle ischemia; loss of tissues; Lmsg gangrene; sepsis. S - Muscle will lose its viability which is identified by its colour (dark coloured with loss of shining); loss of contractility; turgid and will not bleed on cutting. --  Degloving: o Etiology:  Open degloving: e.g. ring avulsion injury with loss of finger skin  Closed degloving: e.g. rollover injury caused by passage of motor vehicle over a limb. Page |6 Note box! Character:  Skin and subcutaneous fat are stripped by avulsion from its underlying fascia, leaving underlying structures exposed.  Traction and avulsion: o Wounds caused by traction force, usually big machines which is open with marked tissue damage. o The resulting wound is like a lacerated wound with additional loss of soft tissue. o Open traction injury occurs on the surface. o Closed traction injury can occur in deeper plane like brachial plexus injury or traction bowel injury. o After initial resuscitation, definitive treatment like skin graft or nerve repair should be done.  Missile wounds o Very serious, as the bullet transmits its high kinetic energy to the tissues. o Kinetic energy of the missile is determined mainly by:  Its velocity (V).  Its weight (M) 🡲 Kinetic energy = MV2 / 2g. (g = gravity). o May be high velocity missile injuries (rifles) or low velocity ones (pistols). o Since velocity is included in the formula it proves that high velocity missiles are more dangerous than low velocity missiles. Page |7 Note box! Characters:  The edge of the inlet wound is burnt.  There may be also an exit wound.  The tunnel between the inlet and exit contains foreign materials and necrotic tissue.  There is usually associated deep organ injury The damage is due to:  Direct damage by the missile in its track.  Shock waves: damage occurs in areas far away from the missile track.  Temporary cavitation effect.  If the missile strikes a bone, the fragments of shattered bone act as 2ry missiles producing more damage.  In high velocity injuries, there’s extensive tissue damage & injury to the major blood vessels & nerves situated some distance from the tract of the missile B. Closed wound.  Contusion: o Etiology: Blunt objects cause intradermal bleeding from minor capillaries with interstitial tracking. o Character: Skin discoloration and tenderness (therefore is called Bruises or Ecchymosis). o Fate: It takes variable time for the discoloration to clear off (needs no specific treatment).  Hematoma: Collection of blood in a potential space under the skin or in deep tissues after blunt trauma. At 1st it is cystic, but it will clot within hours. Later the hematoma will liquefy. Page |8  Hematoma can occur spontaneously in coagulation disorders (haemophilia) or in individuals who are on anticoagulant drug therapy. o Clinical picture:  A tender cystic swelling.  In deep parts may be invisible (e.g. in thigh and gluteal region) o Complications:  Infection  abscess.  Fibrosis  firm mass.  Calcification  hard mass. o Treatment:  Conservative treatment as hematoma gets absorbed unless it gets complicated.  Aspiration using a large bore needle or open surgical evacuation. Abrasions Puncture wound Stab wound Page |9 Cut wound Incised wound Lacerated wound Crushed wound Degloved wound Avulsion Contusions Haematoma resolved Haematoma collection P a g e | 10 Chronic wound: These are wounds that failed to undergo the usual sequence of acute healing (haemostasias, inflammation, proliferation, and remodeling or maturation). within a reasonable time (4-6 weeks). Chronic wounds are arrested at the inflammatory & proliferative phases of wound healing, with overgrowth of granulation tissue with minimal wound contraction & collagen formation. Cause: one or a combination of factors affecting wound healing. Hypoxia initially is a potent stimulus for fibroblast activity and angiogenesis; persisting hypoxia impedes fibroblast and collagen activity and also allows bacterial invasion to make wounds chronic. Managements of chronic wounds is composed of:  Management of general factors.  Local wound management. Examples of chronic wounds are:  Leg Ulcers  Pressure Sores  Diabetic foot Note box! Chronic wounds -requires biopsy, culture study, definitive treatment like wound debridement (Vacuum Assisted Closure) therapy, skin grafting or flap. P a g e | 11 -Specific conditions like tuberculosis if present should be treated. -Malignancy if confirmed is treated by wide local excision and skin graft. -Chronic wounds are chronically infected with biofilms which interfere mainly with the inflammatory phase of healing, contributing to the non-healing. - A biofilm is a complex structure of microorganisms contained in an extracellular matrix of proteins and polysaccharides that adhere to a surface, creating a protected environment for the organisms. Chronic leg ulcer Vacuum Vacuum Assisted closure (VC) # P a g e | 12 Classification of wounds according to contamination  Carries low risk of infection 4 hours old Class IV  Ruptured or perforated organ (ex. ruptured appendix)  Tissue may appear necrotic, (dead), have a purulent (pus) drainage, and foul odor  Traumatic wound with retained devitalized tissue or foreign Body  Object or conditions surrounding injury were clean  Wound cared for within 6 hours of injury Clean  Heals by primary intention Non-  Cut that happens when loading a dishwasher Surgical  Contaminated Conditions surrounding injury not clean, or care given 6 traumatic hours after injury wounds  Heals by 2ry or 3ry intention  Injury occurs when handling feces from an animal or person P a g e | 13 Class I: Clean wound Class II: Clean-Contaminated wound Thyroidectomy Appendicectomy (no rupture) Class III: Contaminated wound Class IV: Dirty infected wound Burst Appendicitis (intra-operatively) Acute peritonitis with frank pus in peritoneal cavity due to bowel perforation Management of the wound: MANAGEMENT OF PATIENT AT ER:  Follow ATLS protocol in management of polytraumatized patient.  Local wound assessment of the type and extent of injury  Prophylaxis against tetanus (anti-tetanic serum or tetanus toxoid). P a g e | 14  Prophylactic empiric antibiotics are prescribed.  If there is bleeding from the wound, the best way is to stop it by direct local compression. Don’t apply a tourniquet except as a temporary measure before taking the patient to the theater.  Do the required investigation if needed. MANAGEMENT OF WOUND IN THE THEATER (The final goal of wound management is to obtain a good quality healing with a nice scar.)  Primary wound care: o Wound cleansing: using liberal amount of antiseptics and normal saline. o Wound debridement: where the foreign material implanted in the wound is removed and the apparently dead parts of tissues are excised. o Bleeding points are secured by electrocautery or ligatures.  Wound dressing: The ideal wound dressing should have the following properties: o Remove excess exudates. o Non-allergic. o Allow gaseous exchange. o Provide thermal o Impermeable to bacteria. insulation. o Atraumatic on removal. o Cost effective. o Comes in a wide array of sizes and shapes  Surgical wound management: Using either local, regional or general anesthesia and includes: o Direct sutures: P a g e | 15  Used in clean tidy incised wounds, which are recent (within 12 hours). o Debridement:  Used in untidy lacerated and contaminated wounds within the first 24 hours after the injury. All contused, lacerated, damaged and devitalized tissues are excised leaving only viable clean tissues. Timing of suture application: Primary sutures: Applied at the time of injury when dealing with a clean surgical wound or recent wound. Delayed primary sutures: Are applied to doubtful or contaminated wounds or in late presentation after injury. The wounds are left open after surgical excision with delayed primary suture applied 5 to 7 days later. Secondary sutures: Are used where an infected wound is left open to granulate and only when it gets clean, sutures can be applied. P a g e | 16 Reconstruction: If there is skin or tissue loss to be replaced and gaps to be bridged skin covers and different types of grafts may be needed at any stage of management. Inspect the wound & deal with every injured structure. Sutures: Suture materials are either:  Absorbable or non-absorbable  Synthetic or natural  Monofilament or multifilament Note box! The ideal suture material would be:  Strong with high tensile strength suitable for the site, type of tissues and purpose it is applied for.  Flexible and can be easily tied with a secure the knot  Excite minimal tissue reaction  Not serve as a nidus of infection (in this setting, monofilament is superior to multifilament and synthetic is superior to natural sutures) All missile injuries require exploration. In contaminated wounds:  Don’t do nerve repair.  Don’t do tendon repair.  Don’t close the deep fascia.  Don’t close the skin P a g e | 17 Wound healing: Definition  The physiological process by which the body regenerates and repairs damaged tissue leading to the restoration of its form and function. Components  Wound contraction.  Granulation tissue formation.  Epithelialization.  P a g e | 18 Stages of wound healing: These phases are not sequential but overlap. Meaning that the next phase starts before the previous phase ends: EARLY PHASE (HEMOSTASIS AND INFLAMMATORY PHASE)  This is the initial response of all tissues to injuries which takes 3-5 days.  Aim: To establish hemostasis and mobilize the immune system that will complete the healing process.  This phase is composed of a vascular response and a cellular response represented by the following: o Coagulation & Platelet plug formation:  Vasoconstriction.  Activation of intrinsic and extrinsic coagulation cascade: producing thrombin  Platelet aggregation: Platelets exposed to Types IV and V collagen of damaged vessels promoting aggregation.  Platelet activation: which activates more platelets  Formation of platelet/fibrin plug: Platelets and RBC aggregate inside a fibrin mesh to form a thrombus. It serves to:  Seal blood vessels  The resultant framework provides a scaffolding for the cells of wound healing: o Endothelial cells o Inflammatory cells o Fibroblasts P a g e | 19 o Acute Cellular Inflammation:  Characterized by redness, heat, pain and swelling.  Vasodilatation & increase in vascular permeability: Serotonin from platelets and histamine from mast cells.  Chemotaxis & Cellular response: Platelet derived growth factor (PDGF) and TGF-B from platelets  24h: Neutrophils are most abundant.  Activated neutrophils arrive immediately and scavenge necrotic debris, foreign material and bacteria.  This response may further destroy local viable tissue.  2-5 days after injury: Monocytes/Macrophages are most abundant.  Activate the release of cytokines which stimulate subsequent processes of wound healing.  Continue the neutrophil's job of phagocytosing necrotic tissue and bacteria.  5-7 days: Inflammatory cells become few:  Seal the surface of the wound.  Remove any necrotic tissue, foreign debris or bacteria. INTERMEDIATE PHASE (PROLIFERATIVE PHASE) o Begins within 48 hours of the initial injury and may continue for up to 21 days. o Mediated by cytokines. P a g e | 20 o Creates a support matrix for the new tissue that provides it with its' strength. o Oxygen, iron, vitamin C, zinc, magnesium & protein are vital for collagen synthesis. o This stage is the actual rebuilding and is influenced by the overall patient condition of the wound bed. o Epithelialization:  Epithelial cells derived from the skin surface at the wound edges and from epithelial appendages creep over the surface of the clot bridging the wound gap.  Begins within hours of injury.  Formation of an epithelial layer that seals and protects the wound from bacteria and fluid loss.  It is essential to have a moist environment to foster growth of this layer  It is a very fragile layer that can be easily destroyed with aggressive wound irrigation or cleansing of the involved area.  Closed Incisional wounds: The wound gap is very small and cellular migration occurs over less than l mm. A wound is sealed in 24-48h.  Epithelization occurs through 4 processes:  Cellular detachment: cells detach from the basement membrane in 1st 24h P a g e | 21  Cellular proliferation: starting 48-72h following migration of PMNs and macrophage differentiation.  Cellular migration: until they meet cells migrating from opposite direction then stops by contact inhibition.  Cellular differentiation. o Angiogenesis (Granulation tissue formation):  Endothelial cell migration & proliferation  The capillaries form loops which have a red/pink granular appearance – Granulation tissue grows from newly formed blood vessels, fibroblasts and collagen.  Healthy granulation tissue is the beery red in color, granular and with no offensive discharge. It is insensitive and bleeds easily on touch  Produces increased exudates from the wound bed.  Forms a flat bed and fill the wound to enable epithelialization.  Unhealthy granulation tissue is less vascular, edematous, hemorrhagic and has sloughs. o Fibroplasia (Collagen synthesis):  Fibroblasts produce collagen and ground substance (muco- polysaccharides and glycosaminoglycans).  Vitamin C acts as a co-enzyme for the hydroxylation of praline to hydroxy-proline which matures the collagen fibres. P a g e | 22  Fibroblast migration & proliferation is stimulated by many cytokines.  Arrangement of collagen at this stage is loose (Type III), fibronectin and hyaluronic acid are also formed. Note box! Collagen synthesis:  Starts 3-5 days post injury  Primarily by fibroblasts  Maximum synthesis rate is 2-4 weeks  Declines after 4 weeks  Type 3-Collagen is seen in early phases of wound healing LATE PHASE: SCAR MATURATION (REMODELING)  Capillary growing into the wound regresses.  Lysine and praline hydroxylation required for cross-linking occurs.  Type l collagen replaces type III collagen until normal ratio of 4:1 (Type I: Type III) is obtained. Collagen therefore undergoes extensive reorganization, the fibers become lined up along the stress lines of the wound. No net increase in collagen = collagen equilibrium  Scar tissue becomes softer, flat, and its color fades.  It is the final stage of normal wound healing begins around day 21 and may continue for up to 2 years. P a g e | 23  Tensile strength of wound site reaches about 60% of pre-injury strength after 6 weeks and 80-90% of pre-injury strength after 1 year but never attain its original strength Factors A ecting healing: GENERAL FACTORS  Type of patient: o Age: old patients have poor wound healing due to reduced rate of protein turnover. o Smoking:  Sympathetic action of nicotine causes vasoconstriction  Increased CO levels shift the oxygen-hemoglobin curve to the left  Carboxyhemoglobin essentially lowers the hematocrit P a g e | 24  Malnutrition: o Protein deficiency leads to diminished synthesis of collagen & ground substance. o Vitamin C deficiency leads to failure of collagen maturation. o Vitamin A deficiency leads to deficient epithelization. o Vitamin E, Calcium, Zinc, Copper & Manganese also affect wound healing.  Medications: o Steroids (effect reversed by Vit A)  Inhibit macrophages  Interferes with fibrogenesis, angiogenesis and contraction o Cancer chemotherapy & immunosuppressive drugs also inhibit wound healing.  Debilitating diseases: o As uremia, jaundice diabetes, cirrhosis, sepsis, AIDS & malignancy delay wound healing.  Hematocrit: For delivery of oxygen  Oxygen: o Prevents infection, needed for synthesis of collagen, ECM Local Factors  Type of wound (tidy Vs untidy): o Mechanism (incision Vs crushing). o Environment (dry Vs moist*, temperature, pH, infection). o Tissue loss. P a g e | 25  Vascularity: o A good blood supply (e.g. in the face & scalp leads to nice healing while in a poor blood supply (wounds below the knee) causes delayed healing.  Irradiation: o It impairs wound contraction & granulation tissue formation as it causes ischemia due to EAO.  Immobilization: It helps healing, because movement damage the blood supply of granulation tissue.  Tension: o Any increased tension in the wound will lead to ischemia & impaired healing. Sutures under tension , hematoma and infection increase tension inside the wound.  Infection: o It delays healing. Fibroblasts compete with bacteria for O2 & nutrition. o Moreover, bacteria secrete collagenolytic enzymes, which destroy collagen fibers.  Foreign bodies & necrotic tissue impair wound healing.  Adhesion of the wound to a bony surface o It prevents wound contraction (chronic venous ulcers, wounds on chin of tibia)..  Impaired venous drainage: As in post-phlebitic limbs, impairs wound healing P a g e | 26  Bad surgical technique: o Rough tissue handling, excessive cauterization, blood clots, tight sutures. tissue ischemia and subsequent necrosis extend the inflammatory phase Dry Wound Healing Moist Wound Healing  Hard to epithelialize.  Easy to epithelialize fast.  No wound nutrition.  Allows wound nutrition.  Scabs delay healing due to desiccation of  Prevents scab formation. underlying tissues.  Allows granulation through cell  Dead tissues are a good media for migration. anaerobic bacteria. Factors which favor wound infection include:  Presence of foreign bodies  Dead tissues. local factors ?  Ischemia.  Suturing under tension. P a g e | 27 Types of wound healing: 1ry intention 2ry intention 3ry intention Tidy wounds (clean) Contaminated Untidy wounds Opposed edges wounds initially left Unopposed edges Character of No complications open for 5 days, if no due to hematoma or wound Immediately closed infection closed by infection by sutures or clips delayed 1ry suturing Ugly. Extensive fibrosis Nice & neat Scar due to filling with As primary Minimal fibrosis. granulation tissue Strong scar Weak scar. Closed when the Seals in 1-2 days Much more time is wound is healthy to Heals in 1-2 weeks Needed avoid bacterial Duration contamination Note box!  After 1 week the wound has only 3% of its final strength.  After 3 weeks the wound has 20% of its final strength.  After 3 months the wound has 80% of its original strength.  The tissues never regain their original tensile strength P a g e | 28 Complications of the wound: General:  SHOCK (hypovolemic, septic, neurogenic)  Infection (specific or nonspecific)  Crush injury and crush syndrome Local:  Wound failure (wound dehiscence): It means that a wound gaps after closure. o It can be a result of any general or local factor affecting wound healing. Failure to an abdominal wound is called burst abdomen.  Stretching of the scar.  Hypertrophied scar: o In wounds with delayed healing due to infection the scar may remain in the remodeling phase longer than usual producing a more cellular and more vascular scar than mature scar. o There is increased collagen production over breakdown with collagen deposition, but the scar tissue never extends beyond the limits of the original wound. o A hypertrophic scar is itchy. It appears red, raised above the skin surface and tender. o With spontaneous maturation the scar becomes pale and flat. P a g e | 29 o The process of maturation of a hypertrophic scar can be accelerated by application of pressure to its surface by silicone gel sheets  causes ischemia of the small blood vessels leading to diminished activity of the fibroblasts & collagen synthesis.  Keloid formation: o It occurs more frequent in oriental races and Africans. o May occur in any wound after healing which could be perfect with no complication. o It is extreme overgrowth of scar tissue that grows beyond the limits of original wound and showing no spontaneous tendency to subside. o Local steroid injection may help in some cases of keloid formation. o The best result can be achieved with surgical excision and postoperative interstitial radiotherapy otherwise recurrence in inevitable.  Contracture: o This is a pathological shortening of the scar tissue resulting in deformity in scar overlying joints. o Proper positioning of the joint during healing can minimize the deformity  Surgical site infection.  Injury and ischemia.  Lymphedema/ hematoma/ seroma. P a g e | 30  Disfigurement (Ugly scar).  Chronic ulcer.  Malignant transformation (Marjolin ulcer). Hypertrophic Scars Keloid P a g e | 31 Scars formation: A scar is the inevitable consequence of wound repair. The final phase of wound repair is the process of remodeling and scar maturation. The granulation tissue in the newly healed wound is gradually replaced by relatively cellular and vascular scar tissue composed of mature collagen with scattered fibroblasts. As a result of the remodeling wound breaking strength increases until about 6 months after the injury. Ideal scar  Primary healing 1st intension  Clean incised wound Ideal scar Adverse scar 1. Primary healing 1st intension 1. Wrong direction 2. Clean incised wound 2. Stretched wound 3. No dehiscence or infection 3. Contracted wound 4. No tension 4. Tattooing 5. Langer line skin tension 5. Stitch mark 6. Opposed edges 6. Type of stitching 7. Eyelids, palms 7. Pigmented area 8. Age 8. Race 9. Sex 9. Type of stitch P a g e | 32 Note Box Abnormal wound healing: Delayed - Chronic wound (Healing > 4-6 weeks). - Chronic Ulcer Excessive Tissue Formation - Hypertrophic Scars - Keloid Additional Management of Keloid and Hypertrophic scars  Conservative management includes pharmacologic therapy, pressure, laser, and radiotherapy  Regulation of Collagen Metabolism:Intralesional Triamcinolone (Kenacort)  Radiation therapy  Compression Garments, Silastic sheets  Surgical excision P a g e | 33 GENERAL SURGERY DEPARTMENT FACAULTY OF MEDICINE – DAMIETTA UNIVERSITY GENERAL SURGERY DEPARTMENT FACAULTY OF MEDICINE – DAMIETTA UNIVERSITY

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