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1. Wound healing is a complex process involving hemostasis, inflammation, proliferation, and remodeling. During hemostasis and inflammation, platelets form clots to stop bleeding while immune cells remove debris.
2. Proliferation involves new tissue growth through cell migration, angiogenesis, collagen deposition and matrix synthesis. Remodeling strengthens the wound through collagen cross-linking and scar maturation over many months.
3. Specific tissues like skin heal through re-epithelialization while bone healing involves soft and hard callus formation over several months to achieve union. Diseases like Ehlers-Danlos syndrome involve defects in collagen formation impacting wound healing.
1. Wound healing is a complex process involving hemostasis, inflammation, proliferation, and remodeling. During hemostasis and inflammation, platelets form clots to stop bleeding while immune cells remove debris.
2. Proliferation involves new tissue growth through cell migration, angiogenesis, collagen deposition and matrix synthesis. Remodeling strengthens the wound through collagen cross-linking and scar maturation over many months.
3. Specific tissues like skin heal through re-epithelialization while bone healing involves soft and hard callus formation over several months to achieve union. Diseases like Ehlers-Danlos syndrome involve defects in collagen formation impacting wound healing.
1. Wound healing is a complex process involving hemostasis, inflammation, proliferation, and remodeling. During hemostasis and inflammation, platelets form clots to stop bleeding while immune cells remove debris.
2. Proliferation involves new tissue growth through cell migration, angiogenesis, collagen deposition and matrix synthesis. Remodeling strengthens the wound through collagen cross-linking and scar maturation over many months.
3. Specific tissues like skin heal through re-epithelialization while bone healing involves soft and hard callus formation over several months to achieve union. Diseases like Ehlers-Danlos syndrome involve defects in collagen formation impacting wound healing.
- Any breach in the surface of the body - Wound debridement via phagocytosis and contribute to - Any tissue disruption deep to the skin produced by microbial stasis via oxygen radical and nitric oxide application of energy synthesis - Injury to the body that typically involves laceration or - Most pivotal function is activation and recruitment of breaking of a membrane and damage to underlying other cells via mediators such as cytokines and growth tissues factors Wound healing - Lay a significant role in regulating angiogenesis and - Complex cellular and biochemical cascade that leads to matrix deposition and remodeling restitution to integrity and function T-Lymphocytes Phases of Wound healing - Comprise another population of inflammatory/immune - Hemostasis and inflammation cells that routinely invades the wound - Proliferation - Less numerous than macrophages - Maturation and remodeling - Numbers peak at about 1 week postinjury - Bridge the transition from inflammatory to the HEMOSTASIS AND INFLAMMATION proliferative phase of healing - Starts with disruption of blood vessels bleeding o Subendothelial collage is exposed platelet PROLIFERATIVE PHASE aggregation - Aka reparative phase - Hemostasis – 1st goal achieved in healing process - The proliferative phase is the second phase of wound - Exposure to subendothelial collagen to platelets results healing and roughly spans days 4 through 12 in platelet aggregation, degranulation, and activation of - It is during this phase that tissue continuity is re- the coagulation cascade established - Platelet α granules – release number of wound-active - Fibroblasts and endothelial cells are the last cell substances populations to infiltrate the healing wound, and the o PDGF, TGF-β, PAF, fibronectin, and serotonin strongest chemotactic factor for fibroblasts is PDGF - Fibrin clot Endothelial cells o Serves as scaffolding for the migration into the - Also proliferate extensively during this phase of healing wound of inflammatory cells (PMNs, neutrophils) - Participate in the formation of new capillaries and monocytes (angiogenesis) - Cellular infiltration after injury follows a characteristic, - Migrate from intact venules close to the wound predetermined sequence o Their migration, replication and new capillary tubule - PMNs are the first infiltrating cells to enter wound site – formation is under influence of such cytokines and peaks at 24 to 48 hours growth factors as TNF-α, TGF-β and VEGF - Increased vascular permeability, local PG release, and Matrix synthesis presence of chemotactic substances (complement - Collagen factors, IL-1, TNF- α, TGF-β, PF4, bacterial products) o The most abundant protein in the body, plays a o All stimulate neutrophil migration critical role in the successful completion of adult - Primary role of neutrophils is phagocytosis of bacteria wound healing and tissue debris - Its deposition, maturation, and subsequent remodeling - Also a major source of cytokines early during are essential to the functional integrity of the wound inflammation, especially TNF-a3 which may have - 18 types of collagen described, the main ones of interest significant influence on subsequent angiogenesis to wound repair are types I and III - PMNs also release protease such as collagenases, which - Type 1 collagen – major component of extracellular participate in matrix and ground substance degradation matrix in skin in the early phase of wound healing Proteoglycan synthesis - No role in collagen deposition or acquisition of - Major glycosaminoglycans present in wounds are mechanical wound strength Dermatan and Chondroitin Sulfate - The second of population of inflammatory cells that - Fibroblasts synthesis there compounds, increasing their invades the wound consists of macrophages, which are concentration greatly during the first 3 weeks of healing recognized as being essential to successful healing - Derived from circulating monocytes, macrophages MATURATION AND REMODELING achieve significant numbers in wound by 48-96 hours - Beings during the fibroblastic phase post-injury and remain present until wound healing is - And is characterized by reorganization of previously complete synthesized collagen - Collagen is broken down by MMPs - The net wound collagen content is the result of a balance between collagenolysis and collagen synthesis LECTURE NOTES – WOUND HEALING - Wound strength and mechanical integrity in the fresh o Results in fluid accumulation in the third wound are determined by both quantity and quality of space, increased abdominal pressure, and the newly deposited collagen tissue edema - Scar remodeling continues for many months (6-12 months) post-injury, gradually resulting in a mature, BONE avascular, and acellular scar - Hematoma formation – initial stage - The mechanical strength of the scar never achieves that - Consists of accumulation of blood at the fracture site, of the uninjured tissues which also contains devitalized soft tissue, dead bone, Epithelialization and necrotic marrow - While tissue integrity and strength are being re- - The next stage accomplishes the liquefaction and established, the external barrier must also be restored degradation of nonviable products at the fracture site - This process is cx primarily by proliferation and migration - The normal bone adjacent to the injury site can then of epithelial cells adjacent to the wound undergo revascularization, with new blood vessels - The process begins within 1 day of injury and is seen as growing into the fracture site thickening of epidermis at the wound edge - 3-4 days following injury, soft tissue forms a bridge - Marginal basal cells at the edge of the wound lose their between the fractured bone segments in the next stage firm attachment to the underlying dermis, migrate - Soft callus stage across the surface of the provisional matrix o Serves as an internal splint, preventing damage to - Fixed basal cells in a zone near the cut edge undergo a the newly laid blood vessels and achieving a series of rapid mitotic division, and these cells appear to fibrocartilaginous union migrate by moving over one another in a leapfrog o The soft callus is formed externally along the bone fashion until the defect is covered shaft and internally within the marrow cavity - The next phase consists of mineralization of the soft HEALING IN SPECIFIC TISSUES callus and conversion to bone - GI tract - Hard callus stage - Bone o This may take up to 2-3 months and leads to - Cartilage complete bony union - Tendon o This stage is followed by the remodeling phase, in - Nerve which excessive callus is reabsorbed and the marrow cavity is recanalized GASTROINTESTINAL TRACT Submucosa HERITABLE DISEASES OF CONNECTIVE TISSUE - Lies radially and circumferentially outside the lamina Ehlers-Danlos Syndrome (EDS) propria and muscularis mucosa - Group of 10 disorders that present as a defect in - Comprised of abundant collagenous and elastic fibers, collagen formation and supports neural and vascular structures - Over half of affected patients manifest genetic defects - The layer that imparts the greatest tensile strength and encoding alpha chains of collagen type V greatest suture-holding capacity - Causing it to be either quantitatively or structurally Serosa defective - Healing is essential for quickly achieving a watertight - These changes lead to “classic” EDS with phenotypic seal from the luminal side of the bowel findings that include: - The importance of serosa is underscored by the o Thin, friable skin with prominent veins significantly higher rates of anastomotic failure observed o Easy bruising clinically in segments of bowel that are extraperitoneal o Poor wound healing and lack serosa (i.e., the esophagus and rectum) o Atrophic scar formation Technical Considerations o Recurrent hernias - In order for an anastomosis to heal without o Hyperextensible joints complications it must be: - GI problems include: 1. Tension free o Bleeding 2. Have an adequate blood supply o Hiatal hernia 3. Receive adequate nutrition o Intestinal diverticula 4. Free of sepsis o Rectal prolapse - Small blood vessels are fragile, making suturing difficult - The amount of IV fluid administered perioperatively during surgery affects many aspects of recovery from colonic surgery - Large vessels may develop: - Experimental and clinical data show that anastomotic o Aneurysms healing may be adversely affected by overzealous fluid o Varicosities administration o Arteriovenous fistulas LECTURE NOTES – WOUND HEALING o Or may spontaneously rupture b) Local causes (arterial insufficiency, local - Skin Hyper-elasticity vasoconstriction, or excessive tension on - Translucent skin tissues) - Hyper-extensible joints - Steroids and chemotherapeutic drugs Marfan’s Syndrome o Large doses are chronic usage reduce collagen - Patients with Marfan’s syndrome have: synthesis and wound strength o Tall stature o The major effect of steroids is to inhibit the o Arachnodactyly inflammatory phase of wound healing (angiogenesis, - The genetic defect associated with Marfan’s syndrome is neutrophil and macrophage migration, and a mutation in the FBN1 gene, which encodes for Fibrillin fibroblast proliferation) and the release of lysosomal - Walkers sign enzymes - Steinberg sign o Steroids also inhibit epithelialization and contraction - Pectus excavatum some have carinatum and contribute to increased rates of wound infection - Ectopia lentis o All chemotherapeutic drugs adversely affect wound - Dislocation of lens healing by inhibiting cell proliferation and wound - Aortic dissection DNA and protein synthesis, all of which are critical to successful repair Osteogenesis Imperfecta - Patients with OI have: - Metabolic disorders o Brittle bones o Diabetes mellitus is the best known of the metabolic o Osteopenia disorders contributing to increased rates of wound o Low muscle mass infection and failure. o Hernias o Uncontrolled diabetes results in reduced o Ligament and joint laxity inflammation, angiogenesis, and collagen synthesis - OI is a result of a mutation in type I collagen o The large- and small-vessel disease that is the - Type I – Type IV hallmark of advanced diabetes contributes to local hypoxemia Epidermolysis Bullosa o Defects in granulocyte function, capillary ingrowth, - The disease manifestation include impairment in tissue and fibroblast adhesion within the epidermis, basement membrane, or o Obesity, insulin resistance, hyperglycemia, and dermis resulting in tissue separation and blistering with diabetic renal failure contribute significantly and minimal trauma independently to the impaired wound healing - Characteristic features of EB are blistering and ulceration observed in diabetics. - Epidermolysis bullosa is classified into four major o Uremia also has been associated with disordered subtypes wound healing o Obesity is the largest growing public health problem FACTORS AFFECTING WOUND HEALING in the United States and the world - Advance age Many studies indicate that obese patients have o Aging produces intrinsic physiologic changes that high rates of perioperative complications, with result in delayed or impaired wound healing estimates as high as 30% for wound dehiscence, o Direct correlation between older age and poor 17% for surgical site infections, 30% for wound healing outcomes incisional hernias, 19% for seromas, 13% for o The increased incidence of: hematomas, and 10% for fat necrosis a) Cardiovascular disease - Nutrition b) Metabolic diseases (diabetes mellitus) o Poor nutritional intake or lack of individual nutrients c) Malnutrition, and vitamin deficiencies significantly alters many aspects of wound healing d) Cancer o The vitamins most closely involved with wound e) Widespread use of drugs that impair wound healing are Vitamin C and Vitamin A healing o Scurvy or Vitamin C Deficiency leads to a defect in - Hypoxia, anemia, and hypoperfusion wound healing, particularly via a failure in collagen o Low oxygen tension has a profoundly deleterious synthesis and cross-linking effect on all aspects of wound healing o With zinc deficiency, there is decreased fibroblast o Optimal collagen synthesis requires oxygen as a proliferation, decreased collagen synthesis, impaired cofactor, particularly for the hydroxylation steps overall wound strength, and delayed o Major factors affecting local oxygen delivery include: epithelialization a) Hypoperfusion LECTURE NOTES – WOUND HEALING - Infections - The clinically cx picture is that of an ulcer that fails to re- o Many otherwise successful surgical operations fail epithelialize despite the presence of adequate because of the development of wound infections granulation tissue o The occurrence of infections is of major concern when implants are used, and their occurrence may Decubitus or Pressure Ulcers lead to the removal of the prosthetic material - A pressure ulcer is localized area of tissue necrosis that o Most surgical wound infections become apparent develops when soft tissue is compressed between a within 7 to 10 days postoperatively bony prominence and an external surface - Excessive pressure causes capillary collapse and impedes CLASSIFICATION OF WOUNDS the delivery of nutrients to body tissues I. ACUTE - Pressure ulcer formation is accelerated in the presence - Heal in predictable manner and time frame of friction, shear forces, and moisture - The process occurs with few, if any, complication - Other contributory factors: - The end result is a well-healed wound o Immobility, altered activity levels, altered mental status, chronic conditions, altered nutritional status Different Clinical Approaches to the Closure and Healing of o Incidence: 2.7% to 9% in acute care setting; 2.4% to Acute Wounds 23% in long-term care facilities 1) Healing with Primary intention - Close wound Staging for Pressure Ulcers 2) Healing with Secondary Intention - Stage I – skin is unbroken but inflamed; non-blanching - Heal underlying wound before closing the wound erythema 3) Tertiary Intention or Delayed Primary Closure - Stage II – Skin is broken to epidermis or dermis - Heal by secondary intention - Stage III – Ulcer extends to subcutaneous layer - And if wound is almost healed, close it - Stage IV – Ulcer extends to muscle or bone; undermining is likely II. CHRONIC WOUNDS - Wounds that have failed to proceed through the orderly Diabetic Wounds process that produces satisfactory anatomic and - The major contributors to the formation of diabetic functional integrity ulcers include: - Wounds that have proceeded through the repair process - Neuropathy (60-70%) without producing an adequate anatomic and functional o Neuropathy is both sensory and motor result Secondary to the persistently - Majority of wounds that have not healed in 3 months are elevated glucose levels considered chronic o The loss of sensory function allows unrecognized Other causes: injury to occur from ill-fitting shoes, foreign-bodies, - Repeated trauma or other trauma - Poor perfusion or oxygenation - Foot deformity - Excessive inflammation contributes to the causation and - Ischemia (15-20%) the perpetuation of the chronicity of the wound o 15-20% - combination - The motor neuropathy or Charcot’s foot Venous Stasis Ulcers - Leads to collapse or dislocation of the inter-phalangeal - Venous stasis occurs due to the incompetence of either or metatarsophalangeal joints, causing pressure on areas the superficial or deep venous systems with little protection - Chronic venous ulcers usually are due to the - There is also severe micro- and macrovascular incompetence of the deep venous system and are circulatory impairment commonly painless - Stasis ulcers tend to occur at the sites of incompetent Marjolin’s ulcer perforators, the most common being above the medial - Malignant transformation of chronic ulcers can occur in malleolus any long-standing wound - Painful – arterial occlusion - Any wound that does not heal for a prolonged period of o Associated with claudication time is prone to malignant transformation - The products of this breakdown are irritating and cause - Cancers arising de novo in chronic wounds include both pruritus and skin damage squamous and basal cell carcinomas - The resulting brownish pigmentation of skin combined with loss of subcutaneous fat produces cx changes called EXCESS HEALING Lipodermatosclerosis - Hypertrophic scar o An over-abundance of fibroplasia in the dermal healing process LECTURE NOTES – WOUND HEALING o HTSs rise above the skin level but stay within the confines of the original wound o Often regress over time o HTSs usually develop within 4 weeks after trauma - Keloid o An over-abundance of fibroplasia in the dermal healing process o Keloids rise above the skin level as well, but extend beyond the border of original wound o Rarely regress spontaneously o Keloids tend to occur 3 months to years after the initial insult o And even minor injuries can result in large lesions