- Wounding causes blood vessels to be disrupted and bleeding, initiating the healing process of hemostasis and formation of a fibrin clot. An inflammatory response then occurs, bringing neutrophils and macrophages to the wound.
- Proliferation begins after 2-3 days as fibroblasts enter the wound and begin re-epithelialization, angiogenesis to reform blood vessels, and collagen synthesis. Collagen production peaks at 5-7 days.
- Remodeling occurs over weeks as collagen is remodeled and strengthened, blood vessels mature, and the wound gains integrity through scarring. Cytokines provide communication between cells throughout the process.
This document discusses wound healing and its pathophysiology. It begins by describing the anatomy of the skin, including the epidermis and dermis layers. It then discusses the functions of intact skin, such as protection, thermoregulation, fluid balance, and vitamin D synthesis. The document classifies wounds and describes healing by primary, secondary, and tertiary intention. It explains the inflammatory, proliferative, and maturation phases of wound healing and compares fetal and adult wound healing. Finally, it discusses aberrations like hypertrophic scars and keloids.
1) The document discusses current trends in wound management, outlining the phases of wound healing and factors that affect it.
2) Key aspects of wound management covered include wound bed preparation through debridement and dressing, as well as various closure methods and the use of negative pressure wound therapy.
3) Emerging treatments like hyperbaric oxygen therapy and various wound covers including skin substitutes are also summarized.
This document provides an overview of wound healing. It begins with definitions of regeneration, repair, and the two types of wound healing: primary intention and secondary intention. For regeneration and repair, it describes the molecular events of cell growth, proliferation, and extracellular matrix formation. It then covers the stages of primary and secondary wound healing in more detail. Specialized tissue healing like fractures is also summarized. Factors influencing wound healing and complications are listed. The document contains detailed information on the cellular and molecular processes involved in wound healing.
The document provides information on wound healing and the anatomy and function of skin. It discusses the phases of wound healing (inflammation, proliferation, and maturation) and risk factors for surgical wound infection. It also covers topics like burns, pressure ulcers, scar formation, skin lesions (seborrheic keratoses, hemangiomas, verrucae, actinic keratoses), and melanoma.
This document discusses the phases and cellular processes involved in wound healing. It describes three phases - inflammatory, proliferative, and maturation. The inflammatory phase involves hemostasis, recruitment of inflammatory cells, and production of growth factors. The proliferative phase involves angiogenesis, fibroplasia, and re-epithelialization to form granulation tissue. The maturation phase involves remodeling of scar tissue and collagen. Local and systemic factors that can impact wound healing are also discussed.
The document discusses the phases of wound healing: inflammatory, proliferative, and maturation. It describes key events in each phase such as angiogenesis, granulation tissue formation, epithelialization, collagen deposition, and scar remodeling. Growth factors and cytokines that participate in wound healing are also outlined.
Wound healing is a complex process involving three overlapping phases: inflammation, proliferation, and remodeling. During the inflammatory phase, blood vessels are disrupted causing bleeding and a fibrin clot forms. Inflammatory cells are recruited to the wound to remove debris and prevent infection. In the proliferative phase, new tissue such as granulation tissue, blood vessels and epithelium form. Finally, in the remodeling phase, the wound undergoes scarring and strengthening as collagen is remodeled over several months. Factors like infection, smoking, and malnutrition can disturb the healing process, while proper wound care including debridement, dressings and management of bioburden can optimize healing.
This document discusses wound healing and its pathophysiology. It begins by describing the anatomy of the skin, including the epidermis and dermis layers. It then discusses the functions of intact skin, such as protection, thermoregulation, fluid balance, and vitamin D synthesis. The document classifies wounds and describes healing by primary, secondary, and tertiary intention. It explains the inflammatory, proliferative, and maturation phases of wound healing and compares fetal and adult wound healing. Finally, it discusses aberrations like hypertrophic scars and keloids.
1) The document discusses current trends in wound management, outlining the phases of wound healing and factors that affect it.
2) Key aspects of wound management covered include wound bed preparation through debridement and dressing, as well as various closure methods and the use of negative pressure wound therapy.
3) Emerging treatments like hyperbaric oxygen therapy and various wound covers including skin substitutes are also summarized.
This document provides an overview of wound healing. It begins with definitions of regeneration, repair, and the two types of wound healing: primary intention and secondary intention. For regeneration and repair, it describes the molecular events of cell growth, proliferation, and extracellular matrix formation. It then covers the stages of primary and secondary wound healing in more detail. Specialized tissue healing like fractures is also summarized. Factors influencing wound healing and complications are listed. The document contains detailed information on the cellular and molecular processes involved in wound healing.
The document provides information on wound healing and the anatomy and function of skin. It discusses the phases of wound healing (inflammation, proliferation, and maturation) and risk factors for surgical wound infection. It also covers topics like burns, pressure ulcers, scar formation, skin lesions (seborrheic keratoses, hemangiomas, verrucae, actinic keratoses), and melanoma.
This document discusses the phases and cellular processes involved in wound healing. It describes three phases - inflammatory, proliferative, and maturation. The inflammatory phase involves hemostasis, recruitment of inflammatory cells, and production of growth factors. The proliferative phase involves angiogenesis, fibroplasia, and re-epithelialization to form granulation tissue. The maturation phase involves remodeling of scar tissue and collagen. Local and systemic factors that can impact wound healing are also discussed.
The document discusses the phases of wound healing: inflammatory, proliferative, and maturation. It describes key events in each phase such as angiogenesis, granulation tissue formation, epithelialization, collagen deposition, and scar remodeling. Growth factors and cytokines that participate in wound healing are also outlined.
Wound healing is a complex process involving three overlapping phases: inflammation, proliferation, and remodeling. During the inflammatory phase, blood vessels are disrupted causing bleeding and a fibrin clot forms. Inflammatory cells are recruited to the wound to remove debris and prevent infection. In the proliferative phase, new tissue such as granulation tissue, blood vessels and epithelium form. Finally, in the remodeling phase, the wound undergoes scarring and strengthening as collagen is remodeled over several months. Factors like infection, smoking, and malnutrition can disturb the healing process, while proper wound care including debridement, dressings and management of bioburden can optimize healing.
This document discusses wound healing and management of both acute and chronic wounds. It begins by introducing the normal phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. It then discusses factors that can influence wound healing and describes the normal healing process in tissues like bone, nerve and tendon. The document also covers classification of wound closure, managing acute wounds, and issues related to chronic wounds like leg ulcers and pressure sores. Specific topics like bites, puncture wounds, hematomas, degloving injuries, and necrotizing soft tissue infections are also summarized. Throughout the phases and management of both acute and chronic wounds are discussed in detail in this comprehensive overview of wound healing.
The document discusses the three main phases of wound healing: inflammatory, proliferative, and remodeling. In the inflammatory phase, blood vessels constrict and immune cells are recruited to fight infection. The proliferative phase involves new tissue growth through granulation, collagen deposition, angiogenesis and epithelialization. Finally, the remodeling phase lasts for months as the scar matures and collagen is reorganized. Through these coordinated phases, the body works to close and resurface wounds.
This document discusses wound management and healing. It covers the goals of wound care including facilitating hemostasis, decreasing tissue loss, promoting healing, and minimizing scarring. The three main types of wound healing - primary, secondary, and tertiary intention - are described. Factors that affect wound healing like diabetes, infection, drugs, nutrition, tissue necrosis and hypoxia are summarized. The basics of wound evaluation, preparation, closure, and aftercare are outlined, including debridement, reducing bioburden, optimizing blood flow and oxygen supply, and using dressings appropriately.
The document discusses wounds and the wound healing process. It defines a wound as a break in the skin or tissue integrity caused by injury. Wounds are classified based on various factors like cleanliness, depth, and type. The healing process involves three phases - inflammatory, proliferative, and remodeling. The inflammatory phase prepares the wound for healing. In proliferation, new tissue is formed through granulation. Remodeling provides increased strength over months. Healing occurs through regeneration or repair, with the former restoring original tissue and the latter resulting in scar tissue. Growth factors play important roles in the complex cellular cascade of wound healing.
This document provides an overview of wound healing, including definitions of wounds, the wound healing process, and chronic wounds. It discusses the three main phases of wound healing: inflammatory, proliferative, and remodeling. Key points include that acute wounds normally heal in an orderly process, while chronic wounds fail to progress and are associated with underlying conditions. The document also covers wound classification, growth factors involved in healing, cell types proliferating during each phase, and factors that can impair the wound healing process.
Wound healing is a complex process involving three phases: inflammatory, proliferative, and remodeling. Many local and systemic factors can affect healing, such as infection, poor oxygenation, age, diabetes, smoking, nutrition, and medication use. Proper wound assessment and dressing selection based on wound type, exudate level, and surrounding skin are important for optimal healing. Various advanced dressings with properties like moisture control, antimicrobial activity, and debridement aid in wound management.
The document discusses guidelines for wound management, with the goals of quick closure, avoiding infection, and excellent cosmetic results. It outlines the "golden period" for wound repair being within 6 hours for extremities and 24 hours for face/scalp wounds. Tetanus-prone wounds are defined as being over 6 hours old, deep, contaminated, or involving dead tissue. Physical exam evaluates location, size, neurovascular status, and presence of foreign bodies. Wound preparation involves irrigation and cleaning without use of detergents or hydrogen peroxide. Closure techniques include primary, delayed primary, and secondary depending on wound characteristics. Appropriate materials include sutures, staples, tissue adhesives, or tapes depending
This document discusses wound classification and the phases of wound healing. It defines a wound and classifies wounds based on etiology, Rank and Wakefield classification, and surgical wound classification. The three phases of wound healing are described as the inflammatory phase, proliferative phase, and maturation/remodeling phase. Key cellular and vascular responses are summarized for each phase. Factors affecting wound healing include local factors like infection and ischemia, and systemic factors like nutrition, diabetes, and medications.
The document summarizes the structure and function of skin, the process of wound healing, and factors that can affect wound healing. It discusses the following key points:
- Skin is composed of several layers including the epidermis, dermis, and subcutaneous layer. Its structure varies depending on its location on the body.
- Wound healing involves regeneration of epithelial tissue and formation of connective scar tissue. It occurs through the phases of inflammation, proliferation, and remodeling.
- The three classifications of wound healing are primary intention, secondary intention, and delayed primary healing. Primary intention healing results in minimal scarring.
- The phases of wound healing involve coagulation, inflammation, proliferation, epithelialization
This document discusses different ways to classify wounds. There are several classification systems including by etiology, duration of healing, degree of contamination, and morphological characteristics. Classifying wounds is important to plan proper treatment, ensure standardized documentation, and provide prognostic information. The main types of wounds discussed are blunt trauma wounds, burn injuries, penetrating wounds, and incisional wounds. Classification helps determine whether a wound can be sutured or needs to heal by secondary intention.
The document discusses wound healing and classification. It describes the phases of wound healing as inflammatory, proliferative, and remodeling. The inflammatory phase begins immediately after wounding and lasts 2-3 days, involving vasoactive amines, growth factors, and inflammatory cells. The proliferative phase lasts from days 3 to 3 weeks, involving fibroblast activity, collagen production, angiogenesis, and re-epithelialization. The remodeling phase begins during proliferation and lasts up to 2 years, involving collagen remodeling and maturation. Healing is classified as primary intention for clean wounds or secondary intention for infected wounds. Factors like age, obesity, smoking, and malnutrition can affect wound healing.
The Reconstructive Ladder - Mussa Mensawelshbarbers
The document outlines the reconstructive ladder, which provides a systematic approach to wound reconstruction from least to most invasive options. The first rung involves dressings to promote healing by secondary intention. Primary closure and skin grafting are next options. Tissue expansion increases local skin availability. Flaps transfer tissue from a donor site and are the most complex option. The reconstructive ladder guides surgeons to initially choose the simplest method before advancing to more complex reconstruction as needed.
This document summarizes wound healing and its complications. It describes three types of wound healing: primary, secondary, and tertiary intention. The components and stages of wound healing are outlined. Factors that affect wound healing, such as age, nutrition, cortisone, and infection are discussed. Complications of wound healing include dehiscence, disfigurement, contracture, hypertrophic and keloid scarring, and infection. The document provides an overview of the wound healing process and potential problems that can arise.
This document provides information on wound management. It defines different types of wounds such as incised wounds, abrasions, punctured wounds, and burns. Wounds are classified as clean, contaminated, or infected. The stages of wound healing are hemostasis, proliferation, and remodeling. Factors that can affect healing include ischemia, infection, and patient health issues. Proper wound management includes irrigation, debridement, closure methods like sutures, and dressing. Complications to watch for are infection, scarring, and tissue necrosis.
This document provides information on wound management and wound care. It discusses the different types of wounds including acute and chronic wounds. The goals of wound care are to identify any wounds or complications, prescribe preventative measures to promote skin integrity, and treat any wounds. There are four phases of wound healing: hemostasis, inflammation, proliferation and remodeling. The three types of wound healing and closure are primary, secondary and tertiary. Various wound dressings are also described like hydrocolloid, hydrogel and alginate. The wound care market is large and growing, dominated by major players. Pricing for common wound dressings is also listed.
1. Wound healing involves regeneration, which is the restoration of original tissue through cell proliferation, or repair through proliferation of connective tissue and scarring.
2. The process of wound healing involves inflammation, granulation tissue formation, collagen deposition and remodeling. Key cell types involved are macrophages, neutrophils and fibroblasts.
3. Factors like growth factors and cytokines regulate each step of wound healing, promoting processes like angiogenesis, collagen synthesis and wound contraction. Proper wound healing restores tissue structure and function.
This document discusses wound management. It defines a wound and classifies wounds according to etiology, the Rank-Wakefield system, duration of healing, and degree of contamination. The phases of wound healing and surgical site infections are explained. Wound assessment, debridement of non-viable tissue, and various dressing types are also outlined. The goals of wound management are to create an optimal environment for healing by using techniques like debridement, dressing, and treating any underlying diseases.
The document discusses wound healing and fracture healing. It defines wounds and their classification. The main stages of wound healing are inflammation, proliferation and maturation. Wounds can heal by primary or secondary intention. Fracture healing involves an initial inflammatory response, formation of a blood clot (hematoma) and callus, and later remodeling of the bone. Key cell types involved in healing include fibroblasts, endothelial cells and macrophages. Growth factors influence various phases of the healing process.
This document discusses pathophysiology of wound healing and factors affecting it. It begins with an introduction to wound classification and the normal phases of acute wound healing. It then discusses factors that can impair wound healing and cause chronic wounds, such as diabetes, peripheral artery disease, radiation therapy, malnutrition, and infection. Recent developments to expedite healing, such as negative pressure wound therapy, are also covered. NPWT applies subatmospheric pressure to a wound which increases blood flow and stimulates cellular processes to promote granulation tissue growth and accelerate wound closure.
Lpa triggered signalling in epidermal keratinocyte migration and skin wound h...Ralph Jans
Lysophosphatidic acid (LPA) promotes epithelial cell migration during wound healing by signaling through LPA receptors. This study investigated the signaling mechanism by which LPA promotes keratinocyte migration. The study found that LPA induces calcium mobilization and NFAT/NFAT2 activation in keratinocytes through STIM1, Orai1, and lipid rafts. This signaling leads to calcineurin activation and NFAT2-dependent keratinocyte migration, promoting wound repair.
This document discusses wound healing and management of both acute and chronic wounds. It begins by introducing the normal phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. It then discusses factors that can influence wound healing and describes the normal healing process in tissues like bone, nerve and tendon. The document also covers classification of wound closure, managing acute wounds, and issues related to chronic wounds like leg ulcers and pressure sores. Specific topics like bites, puncture wounds, hematomas, degloving injuries, and necrotizing soft tissue infections are also summarized. Throughout the phases and management of both acute and chronic wounds are discussed in detail in this comprehensive overview of wound healing.
The document discusses the three main phases of wound healing: inflammatory, proliferative, and remodeling. In the inflammatory phase, blood vessels constrict and immune cells are recruited to fight infection. The proliferative phase involves new tissue growth through granulation, collagen deposition, angiogenesis and epithelialization. Finally, the remodeling phase lasts for months as the scar matures and collagen is reorganized. Through these coordinated phases, the body works to close and resurface wounds.
This document discusses wound management and healing. It covers the goals of wound care including facilitating hemostasis, decreasing tissue loss, promoting healing, and minimizing scarring. The three main types of wound healing - primary, secondary, and tertiary intention - are described. Factors that affect wound healing like diabetes, infection, drugs, nutrition, tissue necrosis and hypoxia are summarized. The basics of wound evaluation, preparation, closure, and aftercare are outlined, including debridement, reducing bioburden, optimizing blood flow and oxygen supply, and using dressings appropriately.
The document discusses wounds and the wound healing process. It defines a wound as a break in the skin or tissue integrity caused by injury. Wounds are classified based on various factors like cleanliness, depth, and type. The healing process involves three phases - inflammatory, proliferative, and remodeling. The inflammatory phase prepares the wound for healing. In proliferation, new tissue is formed through granulation. Remodeling provides increased strength over months. Healing occurs through regeneration or repair, with the former restoring original tissue and the latter resulting in scar tissue. Growth factors play important roles in the complex cellular cascade of wound healing.
This document provides an overview of wound healing, including definitions of wounds, the wound healing process, and chronic wounds. It discusses the three main phases of wound healing: inflammatory, proliferative, and remodeling. Key points include that acute wounds normally heal in an orderly process, while chronic wounds fail to progress and are associated with underlying conditions. The document also covers wound classification, growth factors involved in healing, cell types proliferating during each phase, and factors that can impair the wound healing process.
Wound healing is a complex process involving three phases: inflammatory, proliferative, and remodeling. Many local and systemic factors can affect healing, such as infection, poor oxygenation, age, diabetes, smoking, nutrition, and medication use. Proper wound assessment and dressing selection based on wound type, exudate level, and surrounding skin are important for optimal healing. Various advanced dressings with properties like moisture control, antimicrobial activity, and debridement aid in wound management.
The document discusses guidelines for wound management, with the goals of quick closure, avoiding infection, and excellent cosmetic results. It outlines the "golden period" for wound repair being within 6 hours for extremities and 24 hours for face/scalp wounds. Tetanus-prone wounds are defined as being over 6 hours old, deep, contaminated, or involving dead tissue. Physical exam evaluates location, size, neurovascular status, and presence of foreign bodies. Wound preparation involves irrigation and cleaning without use of detergents or hydrogen peroxide. Closure techniques include primary, delayed primary, and secondary depending on wound characteristics. Appropriate materials include sutures, staples, tissue adhesives, or tapes depending
This document discusses wound classification and the phases of wound healing. It defines a wound and classifies wounds based on etiology, Rank and Wakefield classification, and surgical wound classification. The three phases of wound healing are described as the inflammatory phase, proliferative phase, and maturation/remodeling phase. Key cellular and vascular responses are summarized for each phase. Factors affecting wound healing include local factors like infection and ischemia, and systemic factors like nutrition, diabetes, and medications.
The document summarizes the structure and function of skin, the process of wound healing, and factors that can affect wound healing. It discusses the following key points:
- Skin is composed of several layers including the epidermis, dermis, and subcutaneous layer. Its structure varies depending on its location on the body.
- Wound healing involves regeneration of epithelial tissue and formation of connective scar tissue. It occurs through the phases of inflammation, proliferation, and remodeling.
- The three classifications of wound healing are primary intention, secondary intention, and delayed primary healing. Primary intention healing results in minimal scarring.
- The phases of wound healing involve coagulation, inflammation, proliferation, epithelialization
This document discusses different ways to classify wounds. There are several classification systems including by etiology, duration of healing, degree of contamination, and morphological characteristics. Classifying wounds is important to plan proper treatment, ensure standardized documentation, and provide prognostic information. The main types of wounds discussed are blunt trauma wounds, burn injuries, penetrating wounds, and incisional wounds. Classification helps determine whether a wound can be sutured or needs to heal by secondary intention.
The document discusses wound healing and classification. It describes the phases of wound healing as inflammatory, proliferative, and remodeling. The inflammatory phase begins immediately after wounding and lasts 2-3 days, involving vasoactive amines, growth factors, and inflammatory cells. The proliferative phase lasts from days 3 to 3 weeks, involving fibroblast activity, collagen production, angiogenesis, and re-epithelialization. The remodeling phase begins during proliferation and lasts up to 2 years, involving collagen remodeling and maturation. Healing is classified as primary intention for clean wounds or secondary intention for infected wounds. Factors like age, obesity, smoking, and malnutrition can affect wound healing.
The Reconstructive Ladder - Mussa Mensawelshbarbers
The document outlines the reconstructive ladder, which provides a systematic approach to wound reconstruction from least to most invasive options. The first rung involves dressings to promote healing by secondary intention. Primary closure and skin grafting are next options. Tissue expansion increases local skin availability. Flaps transfer tissue from a donor site and are the most complex option. The reconstructive ladder guides surgeons to initially choose the simplest method before advancing to more complex reconstruction as needed.
This document summarizes wound healing and its complications. It describes three types of wound healing: primary, secondary, and tertiary intention. The components and stages of wound healing are outlined. Factors that affect wound healing, such as age, nutrition, cortisone, and infection are discussed. Complications of wound healing include dehiscence, disfigurement, contracture, hypertrophic and keloid scarring, and infection. The document provides an overview of the wound healing process and potential problems that can arise.
This document provides information on wound management. It defines different types of wounds such as incised wounds, abrasions, punctured wounds, and burns. Wounds are classified as clean, contaminated, or infected. The stages of wound healing are hemostasis, proliferation, and remodeling. Factors that can affect healing include ischemia, infection, and patient health issues. Proper wound management includes irrigation, debridement, closure methods like sutures, and dressing. Complications to watch for are infection, scarring, and tissue necrosis.
This document provides information on wound management and wound care. It discusses the different types of wounds including acute and chronic wounds. The goals of wound care are to identify any wounds or complications, prescribe preventative measures to promote skin integrity, and treat any wounds. There are four phases of wound healing: hemostasis, inflammation, proliferation and remodeling. The three types of wound healing and closure are primary, secondary and tertiary. Various wound dressings are also described like hydrocolloid, hydrogel and alginate. The wound care market is large and growing, dominated by major players. Pricing for common wound dressings is also listed.
1. Wound healing involves regeneration, which is the restoration of original tissue through cell proliferation, or repair through proliferation of connective tissue and scarring.
2. The process of wound healing involves inflammation, granulation tissue formation, collagen deposition and remodeling. Key cell types involved are macrophages, neutrophils and fibroblasts.
3. Factors like growth factors and cytokines regulate each step of wound healing, promoting processes like angiogenesis, collagen synthesis and wound contraction. Proper wound healing restores tissue structure and function.
This document discusses wound management. It defines a wound and classifies wounds according to etiology, the Rank-Wakefield system, duration of healing, and degree of contamination. The phases of wound healing and surgical site infections are explained. Wound assessment, debridement of non-viable tissue, and various dressing types are also outlined. The goals of wound management are to create an optimal environment for healing by using techniques like debridement, dressing, and treating any underlying diseases.
The document discusses wound healing and fracture healing. It defines wounds and their classification. The main stages of wound healing are inflammation, proliferation and maturation. Wounds can heal by primary or secondary intention. Fracture healing involves an initial inflammatory response, formation of a blood clot (hematoma) and callus, and later remodeling of the bone. Key cell types involved in healing include fibroblasts, endothelial cells and macrophages. Growth factors influence various phases of the healing process.
This document discusses pathophysiology of wound healing and factors affecting it. It begins with an introduction to wound classification and the normal phases of acute wound healing. It then discusses factors that can impair wound healing and cause chronic wounds, such as diabetes, peripheral artery disease, radiation therapy, malnutrition, and infection. Recent developments to expedite healing, such as negative pressure wound therapy, are also covered. NPWT applies subatmospheric pressure to a wound which increases blood flow and stimulates cellular processes to promote granulation tissue growth and accelerate wound closure.
Lpa triggered signalling in epidermal keratinocyte migration and skin wound h...Ralph Jans
Lysophosphatidic acid (LPA) promotes epithelial cell migration during wound healing by signaling through LPA receptors. This study investigated the signaling mechanism by which LPA promotes keratinocyte migration. The study found that LPA induces calcium mobilization and NFAT/NFAT2 activation in keratinocytes through STIM1, Orai1, and lipid rafts. This signaling leads to calcineurin activation and NFAT2-dependent keratinocyte migration, promoting wound repair.
This document provides an overview of skin anatomy, wound classification, and wound management. It discusses the objectives of understanding wound care, outlines different topics to be covered including wound healing process and complications. The document defines wounds and classifies them by mechanism of injury, depth and degree of contamination. It describes the three phases of wound healing and different types of healing. Key steps of wound assessment and factors affecting healing are highlighted. Common wound dressings and their properties/indications are also summarized.
This document discusses wound management and provides guidance on creating wound care plans. It begins with an overview of acute versus chronic wounds and the factors that can impede wound healing. The main types of wounds are then described - necrotic, sloughy, granulating, and epithelialized wounds. Key elements of a wound care plan are outlined, including cleaning the wound, possible debridement, exudate management, promoting healing, treating infections, and minimizing discomfort. The goal of wound care plans should be patient-centered and holistic to address the wound as well as the person's overall health needs.
This document provides information on wound healing and care. It begins with the anatomy and functions of healthy skin. The three layers of skin - epidermis, dermis and subcutaneous tissue - are described. The four phases of wound healing are explained: inflammatory, proliferative, maturation and remodeling. Types of wounds and factors influencing healing are defined. Proper wound observation, cleaning, dressing and drainage are outlined as important for promoting healing.
Wound healing involves three main phases - inflammation, proliferation, and maturation. During inflammation, hemostasis occurs within the first few hours followed by an inflammatory response involving neutrophils and macrophages over the next few days. Proliferation begins around 4-14 days as new tissue is formed through granulation, re-epithelialization, angiogenesis and collagen deposition by fibroblasts. Maturation occurs over weeks to months as remodeling and scar contraction takes place. Abnormal wound healing can result in excessive scarring like hypertrophic scars and keloids. Treatment depends on the type of abnormality but may involve pressure, silicone sheeting, steroid injections, excision and radiation. Contractures can also form from scars limiting
Wound healing involves three phases: inflammatory, proliferative, and maturational. Primary healing occurs when wound edges are in direct contact while secondary healing involves granulation tissue formation. Many factors can affect wound healing including infection, nutrition, steroids, ischemia, and diabetes. Growth factors are important for different stages of healing. Stem cells can help regenerate damaged tissue. Aberrations like keloids and hypertrophic scarring exist. New treatments include skin substitutes, dressings, growth factors, and therapies like hyperbaric oxygen and offloading casts.
The primary goal of wound care is facilitating the natural healing processes rather than technical repair alone. Wound healing involves inflammatory, proliferative, and remodeling phases. Wound preparation includes anesthesia, hemostasis, debridement, cleaning, and closure or dressing. Factors like infection, nutrition, tissue ischemia, and tension can impair healing. Proper wound evaluation and management are essential for optimal healing outcomes.
Digitoxin was found to increase resistance of lung cancer cell layers at 20 nM concentrations by stimulating tight junction formation between cells rather than affecting cell growth, adhesion, or membrane properties. Digitoxin increased localization of the tight junction protein ZO-1 at cell edges over time and inhibited cell proliferation and expression of the cell cycle regulator CDK4 at 20 nM. Stimulation of tight junctions by digitoxin correlated with its antiproliferative effects on lung cancer cells.
EWMA 2014 - EP454 EXPERIENCES WITH USING A COLLAGEN WOUND MATRIX* ON RECALCIT...EWMA
The document describes a case series that evaluated the use of a collagen wound matrix on various recalcitrant complex chronic wounds. The study found that 4 patients experienced a decrease in wound size and increase in healthy tissue, with one patient healing completely and another almost healing. In 3 patients, infection developed and treatment was stopped to resolve the infection. The collagen wound matrix showed potential to increase tissue formation and encourage wound closure in patients without infection.
This document summarizes a study on the natural history and spontaneous resolution of keloid scars. The study followed 34 patients with 126 keloid scars over several years. It found that some keloid scars can resolve spontaneously, especially early in the disease course. Resolution often occurred within the first 5 years. The study provides useful prognostic information for patients and a baseline for future research on keloid scar treatment. However, questions remain about what causes some keloids to resolve spontaneously while others do not.
Prevention of tooth loss and dental pain for reducing the global burden of or...fdiworlddental
ORAL HEALTH FOR AN AGEING POPULATION FORUM
Prevention of tooth loss and dental pain for reducing the global burden of oral disease
Susan Hyde
FDI World Dental Congress 2016 Poznań
Tissue repair involves cell proliferation, differentiation, and apoptosis to regenerate or replace injured tissue through two main processes: regeneration of the same cell type or formation of fibrous scar tissue. The capacity for regeneration varies between tissues. Wound healing involves inflammation, proliferation of fibroblasts and new blood vessels, and remodeling. Bone healing occurs through formation of a fracture hematoma, fibrocartilaginous callus, bony callus, and remodeling. Factors like infection, poor blood supply, or inadequate immobilization can delay or prevent proper tissue repair.
This document discusses wound colonization, contamination, and infection. It defines each term and distinguishes colonization from contamination. Colonization refers to the harmless existence of bacteria in a wound with no host reaction, while contamination is the introduction of microorganisms or foreign material into the wound. Infection involves bacterial invasion and multiplication causing local or systemic effects. The document emphasizes acknowledging colonization as normal, preventing contamination, and treating infection. It also discusses wound bed preparation techniques like cleansing, debridement, and the wound field concept of distinguishing clean from dirty areas during dressing.
1. The document discusses gastrointestinal anastomosis healing, comparing compression anastomoses to sutured/stapled techniques.
2. It describes the three phases of acute wound healing - inflammation, proliferation, and remodeling - and how complications can arise if the phases are prolonged or abnormal.
3. Studies comparing the ColonRing compression device to circular staplers found the ColonRing anastomoses had higher burst pressures, less scarring and narrowing, and more stable tissue regeneration over time.
This document discusses keloids, which are non-cancerous growths that form scar tissue beyond the boundaries of the original skin injury or wound. Keloids most commonly affect individuals with darker skin and tend to run in families. While the exact causes are unknown, keloids result from an overactive inflammatory response and abnormal collagen deposition during wound healing. Common symptoms include pain, itching, and restriction of motion, as well as cosmetic concerns. Treatment involves surgical excision followed by radiation therapy within 72 hours, as this combination has shown success with a low recurrence rate. The Oncology and Cancer Center at Nairobi Hospital administers keloid treatment using radiation doses measured in Grays over one to three sessions, starting
This document provides an overview of chronic wound management and discusses the multidisciplinary approach needed. It notes that chronic wounds that do not heal within 3 months are considered chronic and cause patients severe stress. The document then provides statistics on chronic wound prevalence in the US and costs associated with wound care. It also discusses the growth in obesity and diabetes and their relationship to chronic wounds. Common chronic wound types and classification systems are summarized. Treatment approaches like compression therapy, VAC therapy, and the importance of evidence-based medicine are also highlighted at a high level.
The document discusses various topics related to eyelid and facial reconstruction:
- It describes the different layers of the eyelid and techniques for repairing full-thickness eyelid lacerations.
- Entropion, ectropion, canalicular injuries, and dacryocystorhinostomy procedures are summarized.
- Facial nerve anatomy and various modalities for facial reanimation including nerve grafts, muscle transfers, and static procedures are outlined.
- Techniques for managing eyelid dysfunction in facial paralysis cases such as tarsorrhaphy and gold weights are also mentioned.
This document describes the anatomy and reconstruction of the eyelids. It discusses:
1. The layers and structures of the eyelid including the skin, orbicularis oculi muscle, tarsal plates, levator palpebrae superioris muscle, and conjunctiva.
2. Embryology, blood supply, innervation, and cross section of the eyelid.
3. Specific structures like the orbital septum, tarsal plates, pre-aponeurotic fat, and lacrimal system.
4. Goals and requirements of eyelid reconstruction including reestablishing function, protection, cosmesis as well as anterior and posterior lamellae reconstruction techniques.
Periodontal wound healing involves four overlapping phases - exudative, resorptive, proliferative, and regenerative. The proliferative phase includes re-epithelialization, fibroplasia, granulation tissue formation, collagen deposition, angiogenesis, and wound contraction. Growth factors play an important role in regulating periodontal wound healing. Healing after periodontal procedures like scaling and root planing, curettage, ultrasonic curettage, and gingivectomy depends on the extent of tissue disruption and follows a timeline of inflammatory response, epithelial migration, granulation tissue formation, collagen deposition and remodeling.
The document summarizes the key stages of wound healing:
1. Hemostasis, where damaged blood vessels constrict to stop bleeding and a clot forms via platelet activation and coagulation pathways.
2. Inflammation, where neutrophils and macrophages are recruited to the wound to remove debris and fight infection over the first few days.
3. Proliferation, the longest phase, involves new blood vessel growth (angiogenesis), fibroblast migration and collagen deposition to form granulation tissue, re-epithelialization of the wound edges, and wound contraction over weeks.
4. Remodeling lasts up to 2 years as scar tissue matures and strengthens.
1. The document discusses the process of wound healing, which involves regeneration and repair through distinct phases - inflammatory, proliferative, and maturation.
2. During the inflammatory phase, platelets form clots to stop bleeding while macrophages and leukocytes remove debris. Growth factors are released to stimulate healing.
3. In the proliferative phase, new tissue is formed through granulation, angiogenesis, collagen deposition, epithelialization, and contraction.
4. Finally, in the maturation phase scar tissue is remodeled and strengthened over time through collagen remodeling.
The document discusses wound healing and provides definitions, a brief history, and an overview of the key concepts. It defines a wound and healing, outlines the types of wounds and the phases of healing. The document describes the processes of regeneration and repair, including granulation tissue formation and wound contraction. It discusses healing of specialized tissues like fractures. Overall, the document provides a comprehensive overview of wound healing.
This document provides information on wounds and wound healing. It defines a wound and classifies wounds based on etiology and surgical classification. It describes the stages of wound healing including inflammation, proliferation, and maturation. It discusses the vascular and cellular responses during inflammation and the roles of platelets, neutrophils, and macrophages. It also explains granulation tissue formation, epithelialization, wound contraction, and the extracellular matrix and growth factors involved in healing. Factors that can affect normal wound healing as well as abnormal healing processes like keloids and hypertrophic scars are also summarized.
Healing is the body's response to injury and involves regeneration and repair. Regeneration involves proliferation of original cells to reconstitute tissue, while repair forms scar tissue. The healing process involves inflammation, granulation tissue formation, epithelialization, and scar maturation. Local factors like infection and poor blood supply as well as general factors like smoking and malnutrition can affect wound healing. Complications include infection, scarring, and hernia formation.
Healing is the body's response to injury and involves regeneration and repair. Regeneration involves proliferation of original cells to reconstitute tissue, while repair forms scar tissue. The healing process consists of inflammation, granulation tissue formation, epithelialization, and scar maturation. Local factors like infection and poor blood supply as well as general factors like smoking and malnutrition can affect wound healing. Complications include infection, scarring, and hernia formation.
This document provides an overview of wound healing. It defines wounds and classifies them based on several factors. The stages and phases of wound healing are described, including inflammation, proliferation, and maturation. During inflammation, a clot forms and neutrophils and macrophages work to clean the wound. Proliferation involves granulation tissue formation through fibroblasts and angiogenesis. Epithelialization then occurs to close the wound. Factors affecting healing and complications are also mentioned.
healing regeneration and repair mechanism.pptxGopikaMenon26
This document provides an overview of healing, regeneration, and repair mechanisms in the body. It discusses the processes of regeneration and repair, the phases of wound healing including hemostasis, inflammation, granulation tissue formation, and maturation. It also covers healing of different tissue types like skin wounds (primary and secondary healing) and bone fractures (primary and secondary healing). Local factors like infection and systemic factors like diabetes that can influence the healing process are also summarized.
Chronic inflammation is characterized by prolonged inflammation lasting weeks or months, where inflammation, tissue injury, and repair occur simultaneously. It is caused by persistent infections, immune-mediated diseases, or toxic agents. Chronic inflammation involves infiltration of mononuclear cells like macrophages and lymphocytes, ongoing tissue destruction, and attempts at repair through fibrosis and angiogenesis. Macrophages play a key role by secreting cytokines and growth factors that mediate both inflammatory tissue injury and repair.
Wound healing and sterilization for MBBS students vaibhav trivedi
The document discusses wound healing and the factors that affect it. It begins by defining wounds and classifying them as open or closed. It then describes the phases of wound healing - inflammation, proliferation, and maturation/remodeling. Key events in each phase like hemostasis, granulation tissue formation, collagen deposition, and wound contraction are explained. Finally, it lists and describes various internal and external factors that can positively or negatively influence the wound healing process, such as nutrition, infection, hypoxia, steroids, and radiation.
This document discusses the process of healing through regeneration and repair. It describes the key stages and phases of wound healing, including inflammation, granulation tissue formation, epithelialization, and scar formation. Factors that can affect healing, both locally such as infection or poor blood supply, and generally such as age, obesity, or malnutrition are also outlined. Complications from improper or delayed healing include infection, cysts, scarring issues, and hernias.
5.1 Wounds, normal wound healing and factors affecting healing (2).pptxPreetinderBrar2
Wound healing normally occurs in three phases: inflammatory, proliferative, and remodeling. The inflammatory phase begins immediately after injury and lasts 2-3 days. The proliferative phase lasts from days 3 to 3 weeks and involves fibroblast activity, angiogenesis, and re-epithelialization. During the remodeling phase, collagen matures over 12 weeks to regain 80% of skin strength. Abnormal healing can result from factors like infection, poor blood supply, or malnutrition. The goal is primary intention healing with minimal scarring.
This document summarizes the wound healing process in 3 phases: inflammatory, proliferative, and remodeling. It describes the cellular and biochemical events in each phase including platelet activation, neutrophil and macrophage recruitment, angiogenesis, fibroplasia, and collagen deposition. Factors that can influence healing such as wound type, age, medications, disease states, and wound care are also discussed. The goals of wound management and ideal properties of wound dressings are provided.
Wound healing is a complex process involving inflammation, proliferation, and remodeling phases. Factors like wound classification, location, contamination and patient health can influence healing. Proper wound care includes cleaning, debridement, dressing, and preventing infection through aseptic techniques, sterilization, disinfection and antibiotics when needed. Following guidelines helps reduce surgical site infections and promotes optimal wound repair.
1) The document discusses tissue healing, inflammation response, scar formation and skin regeneration. It describes the stages of wound healing including inflammation, proliferation and remodeling.
2) The inflammatory phase involves edema, fibrin deposition and neutrophil infiltration. The proliferative phase includes neovascularization and fibroplastification leading to collagen deposition and epithelialization.
3) During remodeling, the scar changes its structure and strength. Hypertrophic and keloid scars can form if remodeling is altered. The document lists various growth factors involved in wound healing.
Wound healing involves three overlapping phases: inflammatory, proliferative, and maturation/remodeling. The inflammatory phase begins immediately after injury and involves hemostasis and recruitment of neutrophils and macrophages to remove debris. The proliferative phase spans days 4-12, when new tissue is formed through angiogenesis, collagen deposition, and re-epithelialization. During the maturation/remodeling phase, the wound gains strength over months as collagen is reorganized and the scar matures. Healing occurs through primary, secondary, or tertiary intention depending on wound characteristics.
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This document discusses chronic disease management in respiratory patients. It notes that chronic respiratory diseases are a leading cause of disability in Thailand. Effective chronic disease management programs can help improve outcomes for patients with conditions like COPD. Key elements of chronic respiratory disease management include education for patients and caregivers, care coordination, self-management support, and addressing exacerbation risks. The chronic care model emphasizes productive interactions between activated patients and prepared healthcare teams. Holistic care requires understanding patients' overall needs and promoting independent self-care. Primary care clusters and district health boards can help coordinate services for chronic respiratory conditions in a value-based, patient-centric way.
โรคเรื้อรังเกี่ยวกับระบบทางเดินหายใจ นับว่าเป็นปัญหาสาธารณสุขที่กระทบต่อคุณภาพชีวิตประชาชนมากเป็นอันดับต้นๆ การพัฒนาระบบการดูแลที่เรียกว่า chronic care model นับว่าจะช่วยทั้ง health and well being คนไข้ ครอบครัว และช่วยทางด้าน equity efficiency ระบบบริการสาธารณสุขด้วย
การจัดการกับเรื่องราวให้มีการพัฒนาอย่างยั่งยืน sustainable development goal ให้เกิด health and well being ตาม SDG 3 สำหรับสังคมผู้สูงอายุนั้น ต้องการการร่วมมือบูรณาการและผลักดันอย่างยิ่ง ทั้งนโยบายประชากร นโยบายทางการเงิน การจัดสวัสดิการ การจัดการสุขภาพ การจัดการสิ่งแวดล้อมและความปลอดภัย
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Healthy Eating Habits:
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Encourages consistency, variety in exercises, setting realistic goals, and finding enjoyable activities to maintain motivation.
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This particular slides consist of- what is hypotension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
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Here is the summary of hypotension:
Hypotension, or low blood pressure, is when the pressure of blood circulating in the body is lower than normal or expected. It's only a problem if it negatively impacts the body and causes symptoms. Normal blood pressure is usually between 90/60 mmHg and 120/80 mmHg, but pressures below 90/60 are generally considered hypotensive.
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Empowering ACOs: Leveraging Quality Management Tools for MIPS and BeyondHealth Catalyst
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Hypertension and it's role of physiotherapy in it.Vishal kr Thakur
This particular slides consist of- what is hypertension,what are it's causes and it's effect on body, risk factors, symptoms,complications, diagnosis and role of physiotherapy in it.
This slide is very helpful for physiotherapy students and also for other medical and healthcare students.
Here is summary of hypertension -
Hypertension, also known as high blood pressure, is a serious medical condition that occurs when blood pressure in the body's arteries is consistently too high. Blood pressure is the force of blood pushing against the walls of blood vessels as the heart pumps it. Hypertension can increase the risk of heart disease, brain disease, kidney disease, and premature death.
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2. INTRODUCTION
Wound healing is a vague term that often confuses
and diverts the clinician from focusing on a specific
diagnosis.
Over the ages, many agents have been placed on
wounds to improve healing.
3. To date nothing has been identified that
can accelerate healing in a normal
individual.
• Over the ages, many agents have been
placed on wounds to improve healing.
• Many hinder the healing process.
• A surgeon’s goal in wound management
is to create an environment where the
healing process can proceed optimally.
4. Normal Wound-healing Process
Phase Cellular and Bio-physiologic Events
Hemostasis 1.vascular constriction
2.platelet aggregation, degranulation, and fibrin
formation (thrombus)
Inflammation 1.neutrophil infiltration
2.monocyte infiltration and differentiation to
macrophage
3.lymphocyte infiltration
Proliferation 1.re-epithelialization
2.angiogenesis
3.collagen synthesis
4.ECM formation
Remodeling 1.collagen remodeling
2.vascular maturation and regression
ECM, extracellular matrix.
ที่มา J Dent Res. Mar 2010; 89(3): 219–229.
5. Wound Healing Events
Approximate times of the different phases of wound healing, with
faded intervals marking substantial variation, depending mainly on
wound size and healing conditions, but image does not include
major impairments that cause chronic wounds.
6. Wounding
• Blood vessels are disrupted, resulting in
bleeding. Hemostasis is the first goal achieved
in the healing process.
• Cellular damage occurs, this initiates an
inflammatory response.
• The inflammatory response triggers events that
have implications for the entire healing
process.
• Step one then is hemostasis, resulting in Fibrin.
7. Wound Healing
1. Vascular and inflammatory
phase
2. Re epithelization
3. Granulation tissue formation
4. Fibroplasia and matrix
formation
5. Wound contraction
6. Neo vascularization
7. Matrix and collagen
remodelling
10. Steps
i. diapedesis
ii. hemostatic clot – formed by
plateletes
iii. fibrin clot formation –
formed by fibroblasts
Plateletes – 1st cells to produce
essential cytokines which
modulates most of the
subsequent steps in wound
healing
11. Early Events
The early phase, which begins
immediately following skin
injury, involves cascading
molecular and cellular
events leading to
hemostasis and formation
of an early, makeshift
extracellular matrix—
providing structural support
for cellular attachment and
subsequent cellular
proliferation.
12. Hemostasis : Vascular
• Initial vasoconstriction (5-10
min) then vasodilation
(persistent)
• Exposure of sub endothelial
von Willebrand / factor VII,
and fibrillar collagen –
platelet plug
• Hageman factor (XII) –
initiation of clotting cascade
and fibrin clot formation
13. Hemostasis : Fibrin
• Fibrin and fibronectin form a lattice
that provides scaffold for migration
of inflammatory, endothelial, and
mesenchymal cells.
• Fibronectin is produced by
fibroblasts, has a dozen or so
binding sites.
• Binds cytokines
• Its breakdown products stimulate
angiogenesis.
14. Hemostasis : Clotting Cascade
Intrinsic Pathway
Surface Contact
F XI F XIa
F IX F IXa
Platelet Factor 3
Factor F X
Collagen
FXII activator
F XII F XIIa
Ca2+
Ca2+
Extrinsic Pathway
Tissue/Cell Defect
F VIIa F VII
Ca2+
F III (Tissue
Thromboplastin)
Ca2+ Factor F X
Ca2+
Fibrin Fibrinogen
monomers
Fibrin
polymers
Crosslinked
Fibrin Meshwork
F XIIIa F XIII
F Va F V
F VIII F VIIIa
Prothrombin I
Factor F Xa
Ca2+ Thrombin
15. Inflammation : Signs
• Erythema
• Edema
• Pain
• Heat
Inflammation – migration of leukocytes into the wound. 1st 24
hours, polymorphonucleocytes followed by macrophages.
16. Inflammation : Physiological Changes
• Immediately after injury, intense
vasoconstriction leads to blanching, a process
mediated by epinephrine, NE, and
prostaglandins released by injured cells.
• Vasoconstriction reversed after 10 min, by
vasodilatation.
• Now redness and warmth.
• Vasodilatation mediated by histamine, linins,
prostaglandins.
17. • Platelets
– derived growth factor (PDGF), proteases and
vasoactive substances such as serotonin and
histamine
• Polymorphonuclear leukocytes
• Macrophages (replace PMNs after 5 days)
• Fibroblasts (recruited by chemotactic factors
released by the above cells)
18. Inflammation : Physiological Changes
• As microvenules dilate, gaps form between the
endothelial cells , resulting in vascular
permeability. Plasma leaks out into
extravascular space.
• Leukocytes now migrate into the wound by
diapedesis, adhere to endothelial cells, to
wounded tissues.
• Alteration in pH from breakdown products of
tissue and bacteria, along with swelling causes
the pain.
19. Inflammation : Physiological Changes
• Neutrophils, macrophages and lymphocytes come
into wound.
• Neutrophils first on scene, engulf and clean up.
Macrophages then eat them or they die releasing O2
radicals and destructive enzymes into wound.
• Monocytes migrate into extravascular space and turn
into macrophages.
• Macrophages very important in normal wound
healing.
20. Inflammation : Physiological Changes
• Macrophages eat bacteria, dead tissue, secrete
matrix metallo proteinases that break down
damaged matrix.
• Macrophages source of cytokines that stimulate
fibroblast proliferation, collagen production.
• Lymphocytes produce factors like FGF, EGF, IL-2.
• At 48-72 hrs, macrophages outnumber neuts.
• By days 5-7 few remain.
22. Intermediate Events
As in the other phases of wound healing, steps in
the proliferative phase do not occur in a series but
rather partially overlap in time.
•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.
23. Proliferation
• Mesenchymal cell
chemotaxis
• Mesenchymal cell
proliferation
• Angiogenesis
• Epithelialization
Fibroplasia – increases wound strength, hence tissue integrity is
restored. Within 10 hours after injury, there is increased wound
collagen synthesis. Within 5-7 days, collagen has peaked and will
decline gradually.
24. Proliferation
• Fibroblasts are the major mesenchymal cells
involved in wound healing, although smooth
muscle cells are also involved.
• Normally reside in dermis, damaged by
wounding.
• Macrophage products are chemotactic for
fibroblasts. PDGF, EGF, TGF, IL-1, lymphocytes
are as well.
25. Proliferation
Angiogenesis reconstructs vasculature in areas damaged by
wounding, stimulated by high lactate levels, acidic pH, decreased O2
tension in tissues.
• Cytokines directly stimulate the endothelial cell
migration and proliferation required for angiogenesis.
Many are produced by Macs.
• Fibroblast growth factor : FGF-1 is most potent
angiogenic stimulant identified. Heparin important as
cofactor, Transforming growth factor : TGF-alpha, beta,
prostaglandins also stimulate.
26. 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.
They advance in a sheet across the
wound site and proliferate at its
edges, ceasing movement when
they meet in the middle.
27. Epithelialization
• The process of epithelial renewal
after injury.
• Particularly important in partial
thickness injuries, but plays a role
in all healing.
• Partial thickness wounds have
epidermis and dermis damaged,
with some dermis preserved.
• Epithelial cells involved in healing
come from wound edges and
sweat glands, sebaceous glands in
the more central portion of
wound.
28. Re epithelization
• Migration (wound edges, hair follicles,
adnexa)
• Proliferation (48-72 hours)
• Sutured wounds have a layer of keratinocytes
within 24-48 hours
29. Skin Anatomy
• Epidermis is composed of multiple layers of
epithelial cells superficial to the dermis.
• The first layer above the dermis is the basal
layer, which is composed of basaloid cells.
• The cells become more elongated as you go
to superficial stratum corneum.
• Stratum corneum is mostly keratin and dead
tissue.
31. Clean incision wound
Epithelialization
• In contrast in an incisional wound, cellular
migration occurs over a short distance.
• Incisional wounds are re-epithelialized in 24-
48h.
• The sequence of events here are cellular
detachment, migration, proliferation,
differentiation.
32. Epithelialization
• First 24h, basal cell layer thickens, then elongate,
detach from basement membrane (BM) and migrate
to wound as a monolayer across denuded area.
• Generation of a provisional BM which includes
fibronectin, collagens type 1 and 5.
• Basal cells at edge of wound divide 48-72 h after
injury.
• Epithelial cells proliferation contributes new cells to
the monolayer. Contact inhibition when edges come
together.
34. Late Wound Healing Events
RE MODELING
Cytokines –provides communication for cell to cell interaction.
Roles include:
1. Regulation of Fibrosis
2. Healing of wounds and skin grafts.
3. Vascularization
4. Bone and Tendon Strengthening
5. Control of Malignancy
35. Collagen
• Synthesized by fibroblasts beginning 3-5 days after
injury.
• Rate increases rapidly, and continues at a rapid rate
for 2-4 weeks in most wounds.
• As more collagen is synthesized, it gradually replaces
fibrin as the primary matrix in the wound.
• After 4 weeks, synthesis declines, balancing
destruction by collagenase.
36.
37. Keratinocytes
• Fibronectin
– Cross links to fibrin – matrix/scaffold for keratinocyte adhesion and
migration
– Functions as an early component of the extracellular matrix.
– Binds to collagen and interacts with matrix glycosaminoglycans.
– Has chemotactic properties for macrophages, fibroblasts and endothelial
and epidermal cells.
– Promotes opsonization and phagocytosis.
– Forms a component of the fibronexus.
– Forms scaffolding for collagen deposition
• Collagenases and neutral proteases – debridement
• Plasminogen activator – clot dissolution
• Type V collagen
• Requires moisture for epithelial migration
38. Granulation
• Highly vascular network of
glycoproteins, collagen and
glycosaminoglycans
• Fibroblasts
– collagen
– Elastin
– Fibronectin
– Sulfated and non-sulfated
Glycosaminoglycans
– Proteases
• Inflammatory cells
39. Fibroplasia
• Fibroblasts
• Mainly Type III collagen first
• Replaced by type I and II collagen
• Hydroxylation of proline and lysine
– Iron, copper, vitamin C
– Cross linkage
40. Collagen
• Synthesized by fibroblasts beginning 3-5 days after
injury.
• Rate increases rapidly, and continues at a rapid rate
for 2-4 weeks in most wounds.
• As more collagen is synthesized, it gradually replaces
fibrin as the primary matrix in the wound.
• After 4 weeks, synthesis declines, balancing
destruction by collagenase.
41.
42. Collagen
• Age, tension, pressure and stress affect rate of
collagen synthesis.
• TGF-b stimulates it, glucocorticoids inhibit it.
• 28 types identified. Type 1(80-90%) most common,
found in all tissue. The primary collagen in a healed
wound.
• Type 3(10-20%) seen in early phases of wound
healing. Type V smooth muscle, Types 2,11 cartilage,
Type 4 in BM.
43. Collagen
• Three polypeptide chains, right handed
helix.
• Most polypeptide chains used in collagen
assembly are alpha chains.
44.
45. Collagen
• Every third AA residue is Glycine.
• Another critical component is hydroxylation of lysine
and proline within the chains. Hydroxyproline is
necessary for this. Requires Vit C, ferrous iron, and
alpha ketoglutarate as co-enzymes.
• Steroids suppress much of this, resulting in
underhydroxylated collagen, which is incapable of
making strong cross-links leading to easy breakdown.
46. Wound Contraction
• Contraction is a key phase of wound healing. If
contraction continues for too long, it can lead to
disfigurement and loss of function.
• Fibroblasts, stimulated by growth factors,
differentiate into myofibroblasts. Myofibroblasts,
which are similar to smooth muscle cells, are
responsible for contraction. Myofibroblasts
contain the same kind of actin as that found
in smooth muscle cells.
47. Contraction
• Myofibroblasts
• Fibronexus (Singer)
– Connections between intracellular actin
microfilaments and extracellular
collagen, fibronectin, and between
myofibroblasts
– Transmits force along entire network
– Centripetal contraction
48. Wound Contraction
• Begins approximately 4-5 days after wounding.
• Represents centripetal movement of the
wound edge towards the center of the wound.
• Maximal contraction occurs for 12-15 days,
although it will continue longer if wound
remains open.
49. Wound Contraction
• The wound edges move toward
each other at an average rate of
0.6 to .75 mm/day.
• Wound contraction depends on
laxity of tissues, so a buttocks
wound will contract faster than
a wound on the scalp or
pretibial area.
• Wound shape also a factor,
square is faster than circular.
50. Wound Contraction
• Contraction of a wound across a joint can
cause contracture.
• Appears in 2nd degree burns or skin loss
51. Wound Contraction
• Can be limited by skin grafts, full better than
split thickness.
• The earlier the graft the less contraction.
• Splints temporarily slow contraction.
54. Wound Remodeling
• Increased tensile strength
• Decreased bulk, and
erythema
• Replacement of fibronectin
by collagen
• Dehydration
– Promotes further crosslinkage
of collagen
– Reorientation of collagen to
parallel skin collagen.
55. Remodeling
• After 21 days, net accumulation of collagen
becomes stable. Bursting strength is only 15%
of normal at this point. Remodeling
dramatically increases this.
• 3-6 weeks after wounding greatest rate of
increase, so at 6 weeks you are at 80% to 90%
of eventual strength and at 6mos 90% of skin
breaking strength.
56. Remodeling
• The number of intra and intermolecular cross-links
between collagen fibers increases dramatically.
• A major contributor to the increase in wound
breaking strength.
• Quantity of Type 3 collagen decreases replaced by
Type 1 collagen
• Remodeling continues for 12 mos, so scar revision
should not be done prematurely.
58. Healing at Different Part of Body
Skin graft
• donor site
• Split (partial) thickness skin graft
• Full thickness skin graft
Skin Flap
• Local flap
• Distance flap
Contraction : the process whereby there is
spontaneous closure of full thickness skin
wounds
59. Healing at Different Part of Body
• Tendon – composed mainly of type I
collagen with significant amounts of
proteoglycan. After disruption tendon and
sheath have to be sutured.
– Connective Tissue Matrix Deposition : the process
whereby fibroblasts are recruited to the site of
injury and produce a new connective tissue
matrix. The cross-linked collagen provides the
strength and integrity to all tissue.
60. Healing at Different Part of Body
Bone
• Soft callus formation
• Mineralized as cartilage
• Replaced by osteoid or bone – beginning of
remodeling
61. Healing at Different Part of Body
Gastrointestinal Tract : Bowel anastomotic
strength develops more rapidly than that of the
skin.
Major complications of intestinal anastomoses are
a. leak
b. disruption
The submucosa provide the major strength in
anastmotic closure because it contains the majority
of the fibrous connective tissue.
Contraction : constriction of tubular organs such as
the CBD or esophagus.
63. Factors Affecting Wound Healing
Local Factors Systemic Factors
•Oxygenation
•Infection
•Foreign body
•Venous
sufficiency
•Age and gender
•Sex hormones
•Stress
•Ischemia
•Diseases: diabetes, keloids, fibrosis, hereditary
healing disorders, jaundice, uremia
•Obesity
•Medications: glucocorticoid steroids, non-steroidal
anti-inflammatory drugs, chemotherapy
•Alcoholism and smoking
•Immunocompromised conditions: cancer,
radiation therapy, AIDS
•Nutrition
64. รายละเอียดของ Local Factors
• Infection versus contamination
• Infection is when number or virulence of
bacteria exceed the ability of local defenses to
control them.
• 100,000 organisms per gram of tissue.
• Foreign bodies, hematomas promote infection,
impaired circulation, radiation.
66. รายละเอียดของ Systemic Factors
• Radiation damages the DNA of cells in exposed areas.
• Fibroblasts that migrate into radiated tissues are
abnormal.
• Collagen is synthesized to an abnormal degree in
irradiated tissue causing fibrosis.
• Blood vessels become occluded.
• Damage to hair and sweat glands
• Vitamin A has been used to counteract this.
67. รายละเอียดของ Systemic Factors
• Malnutrition
• Cancer
• Old Age
• Diabetes- impaired neutrophil chemotaxis,
phagocytosis.
• Steroids and immunosuppression suppresses
macrophage migration, fibroblast proliferation,
collagen accumulation, and angiogenesis.
Reversed by Vitamin A 25,000u per day.
69. เมื่อแผลไม่หายหรือหายช้า
Consider the negative effects of
6. GI problems that cause malnutrition and
vitamin deficiencies
7. Obesity
8. Peripheral vascular pathology (eg,
atherosclerotic disease, chronic venous
insufficiency, lymphedema)
72. Hypertrophic Scars and Keloids
• Excessive healing results in a
raised, thickened scar, with
both functional and cosmetic
complications.
• If it stays within margins of
wound it is hypertrophic.
Keloids extend beyond the
confines of the original injury.
• Dark skinned, ages of 2-40.
Wound in the presternal or
deltoid area, wounds that
cross langerhans lines.
74. Plasminogen activator inhibitor
• Found to be elevated in
Keloid scars
• PAI-1 -/- “knockout” mice
show accelerated wound
healing after cutaneous
injury
• PAI-1 seems to regulate
fibrinolytic and proteolytic
activity during the
replacement of fibrin by
collagen.
• PAI-1 is upregulated in
cultured fibroblasts in a
hypoxic environment
75. Metalloproteinases & Tissue Inhibitor of
Metalloproteinases
• Regulatory role in fibroblasia and scarring
– Found in high concentrations in fetal wounds
– MMP/TIMP is higher in “scarless” fetal wounds
– TGF-beta decreased the MMP/TIMP ratio by
increasing TIMP
– May promote more rapid epithelization
76. TGF Beta-1
• Higher concentrations and
exaggerated response in
keloid fibroblasts
• When added to fetal
wounds – thicker scars
made.
77.
78. Hypertrophic Scars and Keloids
• Excessive healing results in a
raised, thickened scar, with both
functional and cosmetic
complications.
• If it stays within margins of wound
it is hypertrophic. Keloids extend
beyond the confines of the
original injury.
• Dark skinned, ages of 2-40.
Wound in the presternal or
deltoid area, wounds that cross
langerhans lines.
79. Hypertrophic Scars and Keloids
• Keloids more familial
• Hypertrophic scars
develop soon after
injury, keloids up to a
year later.
Hypertrophic scars more likely to
cause contracture over joint
surface.
80. Hypertrophic Scars and Keloids
Keloids Treatment
i. Triamcinolone
ii. Excision – high recurrence rate
83. Types of Wound Closure
Primary intention
1. Primary Closure
approximate disrupted tissues by sutures,
staples, or tapes. With time there will be
a. synthesis
b. deposition
c. cross-linking of collagen to
provide the tissue with strength.
84. Types of Wound Closure
Secondary intention
2. Delayed Primary Closure – also called
tertiary closure.
Wound closure is delayed for several days to
prevent wound infection where there is:
a. bacterial contamination
b. foreign bodies
c. extensive tissue trauma
* Cleaning of the wound is done daily using NSS
85. Primary intention
Examples: well-repaired lacerations, well reduced bone fractures,
healing after flap surgery
• involves epidermis and dermis
without total penetration of dermis
healing by process of epithelialization
• When wound edges are brought
together so that they are adjacent to
each other (re-approximated)
86. Primary intention
Examples: well-repaired lacerations, well reduced bone fractures,
healing after flap surgery
• Minimizes scarring
• Most surgical wounds heal by
primary intention healing
• Wound closure is performed with
sutures (stitches), staples, or
adhesive tape
87. Secondary intention
Examples: gingivectomy, gingivoplasty, tooth extraction sockets,
poorly reduced fractures.
• 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
88. Secondary intention
Examples: hepatectomy, loss skin open wound, burn
• 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
89. Types of Wound Closure
Delayed primary closure or secondary suture
3. Spontaneous Closure
- wound closes by contraction of the
wound edges.
90. Tertiary intention
(Delayed primary closure or secondary suture)
Examples: healing of wounds by use of tissue grafts.
• The wound is initially cleaned, debrided and
observed, typically 4 or 5 days before closure.
• The wound is purposely left open
91. Tertiary intention
• If the wound edges are not re approximated
immediately, delayed primary wound healing
transpires.
• This type of healing may be desired in the case of
contaminated wounds. By the fourth day, phagocytosis
of contaminated tissues is well underway, and the
processes of epithelization, collagen deposition, and
maturation are occurring.
92. Tertiary intention
• Foreign materials are walled off by macrophages that
may metamorphose into epithelioid cells, which are
encircled by mononuclear leukocytes, forming
granulomas.
• Usually the wound is closed surgically at this
juncture, and if the "cleansing" of the wound is
incomplete, chronic inflammation can ensue,
resulting in prominent scarring.
94. Basic Elements of Wound Care
• Cleanse Debris from the Wound
• Possible Debridement
• Absorb Excess Exudate
• Promote Granulation and Epithelialization
When Appropriate
• Possibly Treat Infections
• Minimize Discomfort
95. Prevention
• Inspect skin
• Moisture control
• Proper positioning and transfer techniques
• Nutrition
• Avoid pressure on heels and bony prominences
• Use of positioning devices
96. Risk Assessment
• Nutritional status
• Alteration in sensation
• Co-morbid conditions
• Medications that delay healing
• Decreased blood flow
97. Assessment & Monitor
• Location
• Stage and Size
• Periwound
• Undermining
• Tunneling
• Exudate
• Color of wound bed
• Necrotic Tissue
• Granulation Tissue
• Effectiveness of
Treatment
99. Wet or Dry Dressings
• Causes Injury to New Tissue Growth
• Is Painful
• Predisposes Wound to Infection
• Becomes a Foreign Body
• Delays Healing Time
100. Frequency
• Goal is to minimize the
frequency of dressing
change
• Daily dressing changes
increase chances of
infection and disrupts the
healing of tissue
Decrease Frequency
of Dressing Changes
101. General treatment of non healing wounds
• Successful treatment of difficult wounds
requires assessment of the entire patient and
not just the wound.
• Systemic problems often impair wound
healing; conversely, non healing wounds may
herald systemic pathology.
102. Successful treatment of wounds
• Characterize the wound
– chemotherapeutic drugs inhibit wound healing
• Ensure adequate oxygenation
• Ensure adequate nutrition
– (malnutrition affects wound healing by inhibiting
the immune response (opsonization)
– Address protein-calorie malnutrition and
deficiencies of vitamins and minerals e.g. Vitamin
C, E, Zinc)
103. Successful treatment of wounds
• Treat infection
– Bowel anastomotic strength develops more
rapidly than that of the skin. The submucosa
provide the major strength in anastmotic closure
because it contains the majority of the fibrous
connective tissue.
• Remove foreign bodies
• Irrigate, Provide a moist (not wet) wound bed
106. The Ideal Suture Material
• Can be used in any tissue
• Easy to handle
• Good knot security
• Minimal tissue reaction
107. The Ideal Suture Material
• Unfriendly to bacteria
• Strong yet small
• Won’t tear through tissues
• Cheap
108. What’s It Used for?
• To bring tissue edges together and speed
wound healing (=tissue apposition)
• Orthopedic surgery to help stabilize joints
– Repair ligaments
• Ligate vessels or tissues
109. Types of Needles
• Eyed needles
– More Traumatic
– Only thread through
once
– Suture on a reel
– Tends to unthread
itself easily
110. Types of Needles
• Swaged-on needles
– Much less traumatic
– More expensive suture
material
– Sterile
118. Non-absorbable Suture
• Primarily Skin
– Needs to be removed later
• Stainless steel = exception
– Can be used internally
• Ligature
• Orthopedics
– Can be left in place for long periods
119.
120. Reading the Suture Label
Size
Needle
• Company
Order Code
Name
Also:
LENGTH
NEEDLE
SYMBOL
COLOR
Absorbable
or Non
121. Choosing
Absorbable Vs. Nonabsorbable
• How long you need it to
work
• Do you want to see the
animal again for suture
removal
122. Monofilament Vs. Multifilament
• memory easy to handle
• less tissue drag more tissue drag
• doesn’t wick wicks/ bacteria
• poor knot security good knot security
• - tissue reaction +tissue reaction
123. Natural Vs. Synthetic
• Natural:
– Gut
– Chromic Gut
– Silk
– Collagen
• All are absorbable
124. Gut/ Chromic Gut
• Made of submucosa of
small intestines
• Multifilament / Mono
filament
• Breaks down by
phagocytosis:
inflammatory reaction
common
125. Gut/ Chromic Gut
• Chromic: tanned, lasts
longer, less reactive
• Easy handling
• Plain: 3-5 days
• Chromic: 10-15 days
• Bacteria love this stuff!
126. Collagen and Silk
• Natural sutures
• VERY reactive,
absorbable
• Collagen : Ophthalmic
surgery only
127. Synthetic
Vicryl (Polyglactin 910)
• Braided, synthetic, absorbable
• Stronger than gut: retains strength 3 weeks
• Broken down by enzymes, not phagocytosis
• Break-down products inhibit bacterial growth
– Can use in contaminated wounds, unlike other
multifilaments
128. Synthetic
Dexon and PGA
• Polymer of glycolic acids
• Braided, synthetic, absorbable
• Broken down by enzymes
• Both PGA and dexon have increased tissue
drag, good knot security
• Both are stronger than gut
129. Synthetic
PDS (polydioxine)
• Monofilament (less drag,
worse knot security – lots
of “memory”)
• Synthetic, absorbable
• Very good tensile strength
(better than gut, vicryl,
dexon) which lasts months
• Absorbed completely by
182 days
130. Synthetic
Maxon (polyglyconate)
• Monofilament- memory
• Synthetic Absorbable
• Very little tissue drag
• Poor knot security
• Very strong
132. NYLON
• Synthetic
• Mono or Multifilament
• Memory
• Very little tissue
reaction
• Poor knot security
133. Polypropylene
• Prolene, Surgilene
• Monofilament, Synthetic
• Won’t lose tensile strength over time
• Good knot security
• Very little tissue reaction
134. Stainless Steel
• Monofilament
• Strongest !
• Great knot security
• Difficult handling
• Can cut through tissues
• Very little tissue reaction, won’t harbor
bacteria
135. Suture Sizes
• Sized #5-4-3-2-1-0-00-000-
0000…30-0
BIGGER
>>>>>>>>>>>>>>>>SMALLER
• 00 = 2-0, “two ought”
• SA : 0 through 3-0 (Optho
5-0 >>7-0)
• LA : 0 through 3
137. Skin Staples
• Very common in human medicine
• Expensive
• Very easy
• Very secure
• Very little tissue reaction
• Removal =
– Special tool required
138. Staples
• Rapid closure of wound
• Easy to apply
• Evert tissue when placed
properly
139. Tissue Adhesive
• Nexaband, Vetbond,
and others
• Little strength
• Should not be placed
between skin layers or
inside body
140. Steri-strips
• Sterile adhesive tapes
• Available in different
widths
• Frequently used with
subcuticular sutures
• Used following staple or
suture removal
• Can be used for delayed
closure
143. Knot Strength
• Generally 4 “throws” for >90% knot security
(nylon may need 5)
– Less “throws” = more likely to untie itself
• Stainless steel = exception again
– 2 “throws” = 99% knot security
144. Two-Hand Square Knot
• Easiest and most
reliable
• Used to tie most
suture materials
145. Instrument Tie
• Useful when one or
both ends of suture
material are short
• Commonly used
technique for
laceration repair
149. Simple Sutures
Simple interrupted stitch
– Single stitches, individually
knotted (keep all knots on
one side of wound)
– Used for uncomplicated
laceration repair and wound
closure
153. Mattress Sutures
• Horizontal mattress stitch
– Provides added strength in
fascial closure; also used in
calloused skin (e.g. palms and
soles)
– Two-step stitch:
• Simple stitch made
• Needle reversed and 2nd
simple stitch made adjacent
to first (same size bite as first
stitch)
154. Mattress Sutures
Vertical mattress stitch
– Affords precise
approximation of skin edges
with eversion
– Two-step stitch:
• Simple stitch made – “far, far”
relative to wound edge (large
bite)
• Needle reversed and 2nd
simple stitch made inside first
– “near, near” (small bite)
155.
156. Subcuticular Sutures
• Usually a running stitch,
but can be interrupted
• Intradermal horizontal
bites
• Allow suture to remain
for a longer period of
time without
development of
crosshatch scarring
PDGF platelet derived growth factor – D induce macrophage recruitment, increase interstitial pressure ,and blood vessel maturation during angiogenesis.
EGF epidermal growth factor mediate monocyte chemotaxis and macropage proliferation to sub endothelial space.
TGF transforming growth factor β enhance macrophage ability to produce IL 10
FGF 1 fibroblast growth factor family member possess broad mitogenic and cell survival activities, and are involve in a variety of biological processes including embryogenic development , cell growth, morphogenesis, tissue repair, tumor growth and invasion.
Collagen is a group of naturally occurring protein found in animals, especially in the fresh and connective tissues of mammals. It is making up about 25% - 35% of the whole body protein content. Collagen , in the form elongated fibril , is mostly found infibrous tissue. The fibroblast is the most common cell which create collagen.
Over 90% of collagen is of type 1.So far 28 type of collagen have been identified and described. Type 1 skin , tendon, vascular ligature, organs, bone. 2 cartilage.3 reticulate 4 base of cell basement membrane. 5 cell surface and placenta.
opsonization and phagocytosis a process call antibodies dependent cellular cytotoxicity