Download Free Medical Wound Healing PowerPoint Presentation

Wound Healing PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Skin Inflammation, which is titled "Wound Healing", to know about the anatomy of skin, function of integument, and classification of wounds, etc.

Tags : Skin Inflammation, Wound Healing, anatomy of skin, function of integument, classification of wounds

Published on : Jul 05, 2021 | Views : 3233 | Downloads : 10

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

WOUND HEALING
Slide 2-

Anatomy of Skin Epidermis: composed of several thin layers: stratum basale, stratum spinosum, stratum granulosum, stratum lucidum, stratum corneum the several thin layers of the epidermis contain the following: a) melanocytes, which produce melanin, a pigment that gives skin its color and protects it from the damaging effects of ultraviolet radiation. b) keratinocytes, which produce keratin, a water Repellent protein that gives the epidermis its tough, Protective quality.
Slide 3-

Anatomy of Skin Dermis: composed of a thick layer of skin that contains collagen and elastic fibers, nerve fibers, blood vessels, sweat and sebaceous glands, and hair follicles. Subcutaneous Tissue: composed of a fatty layer of skin that contains blood vessels, nerves, lymph, and loose connective tissue filled with fat cells
Slide 4-

ppt slide no 4 content not found
Slide 5-

Function of Integument Protection: intact skin prevents invasion of the body by bacteria Thermoregulation: intact skin facilitates heat loss and cools the body when necessary through the following processes: production of perspiration which assists in cooling the body through evaporation production of vasodilatation which assists in facilitating heat loss from the body through radiation and conduction production of vasoconstriction which assists in preventing heat loss from the body through radiation and conduction
Slide 6-

Function of Integument Fluid and Electrolyte Balance: intact skin prevents the escape of water and electrolytes from the body Vitamin D Synthesis Sensation Psychosocial
Slide 7-

Classification of Wounds 1) Clean Wound: Operative incisional wounds that follow nonpenetrating (blunt) trauma. 2) Clean/Contaminated Wound: uninfected wounds in which no inflammation is encountered but the respiratory, gastrointestinal, genital, and/or urinary tract have been entered. 3) Contaminated Wound: open, traumatic wounds or surgical wounds involving a major break in sterile technique that show evidence of inflammation. 4) Infected Wound: old, traumatic wounds containing dead tissue and wounds with evidence of a clinical infection (e.g., purulent drainage).
Slide 8-

Classification of Wounds Closure Healing by Primary Intention: All Layers are closed. The incision that heals by first intention does so in a minimum amount of time, with no separation of the wound edges, and with minimal scar formation. Healing by Secondary Intention: Deep layers are closed but superficial layers are left to heal from the inside out. Healing by second is appropriate in cases of infection, excessive trauma, tissue loss, or imprecise approximation of tissue. Healing by Tertiary Intention: Also referred to as delayed primary closure.
Slide 9-

Wound Healing Inflammation occurs when the damaged endothelial cells release cytokines that increase expression of integrands in circulating lymphocytes. Histamine, serotonin, and kinins cause vessel contraction (thromboxane), decrease in blood loss, and act as chemotactic factors for neutrophils, the most abundant cells in the initial 24 hour period.
Slide 10-

Wound Healing Proliferative phase occurs next, after the neutrophils have removed cellular debris and release further cytokines acting as attracting agents for macrophages. Fibroblasts now migrate into the wound, and secrete collagen type III. Angiogenesis occurs by 48 hours. The secretion of collagen, macrophage remodeling and secretion, and angiogenesis continues for up to 3 weeks. The greatest increase in wound strength occurs during this phase.
Slide 11-

Wound Healing Maturation phase is the final phase and starts from the 3rd week and continues for up to 9-12 months. This is where collagen III is converted to collagen I, and the tensile strength continues to increase up to 80% of normal tissue.
Slide 12-

Surgical Wound Infection Incisional infections identified by purulent or culture positive drainage is isolated from any structure above the fascia in proximity to the initial wound Deep infections are characterized by purulent drainage from subfascial drains, wound dehiscence, or abscess formation and involve adjacent sites manipulated during surgery. Wound Dehiscence Breakdown of the surgical wound
Slide 13-

Risk Factors for SWI Patient-related factors: Age > 60, sex (female), weight (obesity) Presence of remote infections Underlying disease states Diabetes, Congestive heart failure (CHF) Liver disease, renal failure Duration of preoperative stay hospitalization > 72 hours, ICU stay Immuno-suppression ASA (American Society of Anesthesiologists) physical status (3,4, or 5)
Slide 14-

Risk Factors for SWI Surgery-related factors: Type of procedure, site of surgery, emergent surgery Duration of surgery (>60- 120 min) Previous surgery Timing of antibiotic administration Placement of foreign body Hip/knee replacement, heart valve insertion, shunt insertion Hypotension, hypoxia, dehydration, hypothermia
Slide 15-

Risk Factors for SWI Surgery related factors: Patient preparation Shaving the operating site Preparation of operating site Draping the patient Surgeon preparation Hand washing Skin antiseptics Gloving
Slide 16-

Risk Factors for SWI Wound-related factors: Magnitude of tissue trauma and devitalization Blood loss, hematoma Wound classification Potential bacterial contamination Presence of drains, packs, drapes Ischemia Wound leakage
Slide 17-

Antibiotic Use Characteristics of an optimal antibiotic for surgical prophylaxis: Effective against suspected pathogens Does not induce bacterial resistance Effective tissue penetration Minimal toxicity Minimal side effects Long half-life Cost effective
Slide 18-

Antibiotic Use Appropriate antibiotic use for prevention of SWI includes the following: Appropriate timing of administered agents and repeated dosing based on length of procedure and antibiotic half-life Consider redosing if procedure > 4 hours Appropriate selection based on procedure performed Appropriate duration to avoid infection and decrease potential for development of resistance
Slide 19-

Antibiotic Use Nose S. aureus, pneumococcus, meningococcus Skin S. aureus, S. epidermidis Mouth/pharynx Streptococci, pneumococcus, e.coli, bacteroides, fusobacterium, peptostreptococcus Urinary tract E.coli, proteus, klebsiella, enterobacter
Slide 20-

Antibiotic Use Colon E. coli, klebsiella, enterobacter, bacteroides spp, peptostreptococci , clostridia Biliary tract E. coli, klebsiella, proteus, clostridia Vagina Streptococci, staphylococci, E. coli, Peptostreptococci, bacteroides spp. Upper respiratory tract Pneumococcus, H. influenzae
Slide 21-

Antibiotic Use Identify wound infection risk based on patient’s surgical procedure: Clean: Cefazolin Clean/contaminated: Cefazolin vs broad spectrum (Cefoxitin or Cefotetan) Contaminated: Broad spectrum (Cefoxitin or Cefotetan) Dirty: Therapeutic antibiotics
Slide 22-

Fetal Wound Healing Fetal wound healing proceeds without fibrosis or scar formation in contrast to adult wound healing. The mechanisms responsible for this remarkable process are mediated in part through a fetal wound extracellular matrix rich in hyaluronic acid (HA). Proposed contributing factors to scarless healing in fetal wounds are the presence of fewer neutrophils and more monocytes during the inflammatory period, different concentrations of cytokines, and a greater proportion of type III collagen in contrast to adult wounds.
Slide 23-

Fetal Wound Healing Transforming growth factor-b (TGF- β, specifically, low levels of TGF-β1 and TGF- β2 and high levels of TGF- β3—probably has a central role in scar formation, and studies of its role are ongoing. Low levels of platelet-derived growth factor (PDGF), a greater amount of epidermal growth factor (a mitogen for epithelialization), a faster rate of wound healing, and a greater amount of hyaluronic acid in the extracellular matrix has been documented and suggests a more efficient process of wound healing in fetal models.
Slide 24-

Diabetic foot ulcers
Slide 25-

Staging of Pressure Ulcers Stage I: redness and warmth Stage II: shallow ulcer with distinct edges Stage III: full-thickness loss of skin Stage IV: involvement of fascia, connective tissue, muscle and bone Stage V: area covered with black eschar (aka scab)
Slide 26-

Stage I
Slide 27-

Stage II
Slide 28-

Stage III
Slide 29-

Stage IV
Slide 30-

Hypertrophic Scars and Keloids The natural response to injury involves several stages of wound healing, migration of macrophages, neutrophils, and fibroblasts and the release of cytokines and collagen in an array to promote wound healing and maturation. Hypertrophy and keloid formation are an overactive response to the natural process of wound healing.
Slide 31-

Hypertrophic Scars These lesions are raised and thickened. This process does not extend beyond the boundary of the incision/scar. This process is exacerbated by tension lines on the area of surgery: incisions over the knee and elbow have a higher incidence of hypertrophic reaction.
Slide 32-

Hypertrophic Scars NOTE: hypertrophic scars and keloids are indistinguishable by plain H&E staining. Treatment: nearly all hypertrophic scars undergo a degree of spontaneous resolvement. If still present after six months, surgical excision is indicated. Pressure applied early to a lesion is also of benefit. Intractable lesions can be injected with triamcinolone.
Slide 33-

Keloids Raised and thickened. This process extends beyond the boundary of the incision. Continues weeks to months past the initial insult. Higher incidence in African Americans. May have different incidences in different parts of the same person; may not develop a keloid on the arm, yet has a keloid after earring insertion.
Slide 34-

ppt slide no 34 content not found
Slide 35-

Keloids NOTE: hypertrophic and keloids are indistinguishable by plain H&E staining. Treatment: Pressure applied early may decrease the extent of keloid formation. Injection of triamcinolone, or corticosteroid injection may be helpful. Excision with intramarginal borders is reserved for intractable keloids, and used in conjunction with the above.
Slide 36-

Burns Are divided by depth of injury. Classically, and in some institutions the burn is organized by “degree:’ First-degree: involve the epidermis and demonstrates erythema and minor microscopic changes. Pain is major complaint. No scar is left. Healing is complete in up to 10 days. Second-degree burns: involves all the epidermis and part of the dermis. Superficial second-degree burns are characterized by blister formation while deeper burns have a more reddish or non-viable whitish appearance.
Slide 37-

Burns Third-degree: these full thickness burns are characteristically white, non-viable. They may demonstrate darkened brown or black adipose tissue. Skin is non-sensate, and leathery. Muscle injury may also occur.
Slide 38-

ppt slide no 38 content not found
Slide 39-

Burns The most important assessment of volume status and adequate volume administration is monitoring of the urine output. Burn Resuscitation: (Parkland Formula) 4x % Burn x Weight in kg for 24 hours, Lactated Ringer’s. Give the first half in first 8 hours and the next half in the next 16 hours. Urine output is normally 0.5ml/kg, but for burns and trauma patients is at least 1-1.5 ml/kg/hour. Initial treatment of the actual burn is first debridement of the denuded skin with moist gauze. This additionally aids in estimating volume of burn. Coverage with topical antibacterial agents is necessary.
Slide 40-

Burns Silver sulfadiazine: wide spectrum, moderate eschar penetration. May cause leucopenia Silver nitrate: mild spectrum, non-painful. Does not penetrate eschar, causes staining. Sodium, calcium, and potassium wasting. Mafenide: wide spectrum penetrates eschar. Painful. Causes metabolic acidosis. Initial coverage can include culture skin and skin substitutes. Split thickness skin grafts for burns of small percentage (<25%) can be utilized.
Slide 41-

Seborrheic Keratoses These lesions are superficial, non-invasive tumors that originate in the epidermis. Typically appear in older people as multiple slightly elevated yellowish, brown or brownish-plaque rounded plaques, and are found typically on the shoulders, trunk, scalp, and face. Treatment is by shave excision.
Slide 42-

Seborrheic Keratoses
Slide 43-

Involuting Hemangiomas Most common tumors that occur in childhood, 95% of all hemangiomas that are seen in childhood. Typically present at birth or during 2-3 weeks of life, grow at a rapid rate for 4-6 months, then involution begins and is complete by 5-7 years of age.
Slide 44-

Involuting Hemangiomas
Slide 45-

Involuting Hemangiomas These types include strawberry nevus, nevus vasculosus, capillary hemangioma, and cavernous hemangioma. Treatment is not usually indicated. Only indicated if the lesions impair vision (eyelid), a condition that can lead to amblyopia.
Slide 46-

Noninvoluting Hemangioma Most of these lesions are present at birth. They grow in proportion to the growth of the infant, and persist into adulthood. Unlike involuting, these are not true neoplasms, but malformations of arterial and/or veins
Slide 47-

Non-involuting Hemangiomas These lesions malformations include: Port wine stains: most common, mainly occur on face or neck. Best to observe, or laser surgery. Cavernous Hemangioma: more common on head and neck. Observation or injection of sclerosing agents.
Slide 48-

Non-involuting Hemangiomas Port Wine Stain Cavernous Hemangioma
Slide 49-

Verrucae Also known as common warts, these lesions are seen in childhood and in young adults, typically on fingers and hands. These lesions appear as round or dome-shaped elevated masses with rough surfaces with multiple villi like keratinized projections. They may range from brown to gray to skin colored.
Slide 50-

Verrucae The etiology is by human papillomaviruses (over 50 different types exist). Types 1, 2, 4, and 7 typically cause verrucae. Treatment: is by electrodessication or liquid nitrogen. Surgical excision is not recommended. Most treatment can be delayed by several months because these lesions may spontaneously resolve. Duct tape is listed in many current journals as most non-invasive method of treatment.
Slide 51-

Actinic Keratoses Actinic keratoses are the most common precancerous skin lesions. Most commonly appear as single or multiple, slightly elevated, scaly or warty lesions that are red to yellow, brown or black. Occur most frequently on the face and backs of hands in fair-skinned Caucasians. Approximately 15-20% become malignant, invade the dermis as squamous cell carcinomas. Treatment: curettement and electrodessication or 5-FU.
Slide 52-

Actinic Keratoses
Slide 53-

Melanoma Melanocytes are cells of neural crest origin that migrate during fetal development to multiple sites in the body, principally the skin. These cells are exposed to carcinogenic stimuli that result in malignant transformation to become melanoma. Melanoma accounts for only 4% to 5% of all skin cancers but causes the majority of deaths from skin malignancies. It is the eighth most common cancer in the United States, and the incidence is rising faster than any other type of cancer.
Slide 54-

Epidemiology and Etiology The incidence and outcome of melanoma are related to multiple factors. Melanoma is principally a disease of whites, particularly those of Celtic ancestry. It is estimated that melanoma occurs 20 times more often in whites than in blacks. The median age of diagnosis is in the range of 45 to 55 years. There is a significant incidence in the 3rd and 4th decades of life.
Slide 55-

Epidemiology and Etiology It is well established that exposure to sunlight increases the risk of developing melanoma in susceptible populations. This is specifically attributed to solar ultraviolet (UVA/UVB) radiation. Additional factors that increase the risk for development of melanoma include fair skin, dysplastic nevus (DN) syndrome, xeroderma pigmentosum, a history of non-melanoma skin cancer (NMSC), and a family history of melanoma.
Slide 56-

Precursor Lesions and Risk Factors Congenital nevi, DNs, Spitz nevi, and familial patterns all raise the risk of developing melanoma. Individuals with congenital nevi have an increased risk that is proportional to the size and number of nevi. Giant congenital nevi are rare (1 in 20,000 newborns) and carry an increased risk for development of melanoma within the nevi
Slide 57-

ppt slide no 57 content not found
Slide 58-

Melanoma Screening: Any new pigmented nevus should be suspected. Approximately one third arise from pigmented nevi. Junctional nevi: small, circumscribed and are light brown to black. Rarely have hair. Appear on all parts of the body, and mucous membranes, genitalia, palms, and soles. Located on the epidermis and dermal-epidermal junction.
Slide 59-

Melanoma Intradermal nevi: small spots to large extensive areas, variable shape. Often black or brown and slightly elevated, and confined to the dermis. Compound nevi: combination junctional and intradermal.
Slide 60-

Melanoma Blue nevi: flat or dome-shaped, bluish-black usually on hands arms, or face. May resemble nodular melanoma. Dysplastic nevi: are larger, up to 5-12 mm, have macular and popular features, varied in color with pink base, and have indistinct, irregular edges. PRECURSOR OF MELANOMA. Congenital nevi: occur in approximately 1% of newborns. PRECURSOR OF MELANOMA.
Slide 61-

Melanoma Symptoms: features that are suggestive of melanoma are the following Irregular areas of differentiating color (black to brown to tan with focal discoloration) Rapid enlargement Irregular edges Erosion, bleeding or crust formation Pruritis Location: lesions on back and lower extremities require close motoring.
Slide 62-

Melanoma Several different tumor types exist: Superficial spreading: Most common type. Typically appears on back, and may be black, gray blue or pinkish in color. Nodular: may develop from a preexisting nevi, and rapidly becomes palpable. May also ulcerate, and is worse prognosis. Lentigo maligna: usually occurs in older patients. Seen most often as a large melanotic freckle (Hutchinson’s freckle) on the temple or malar region. Grows very slowly, and is the largest of the malignant melanomas. Acral Lentiginous: Confined to the subunual areas and glabrous skin of the palms and soles. Most common in black population.
Slide 63-

Lentigo maligna melanoma Superficial spreading melanoma
Slide 64-

Lentigo Maligna
Slide 65-

Acral Lentiginous
Slide 66-

Acral lentiginous melanoma Nodular melanoma
Slide 67-

Breslow’s Depth (old)
Slide 68-

AJCC Classification Primary Tumor (T) Regional LN (N) TX Can not be assessed NX can not be assessed T0 No evidence of Tumor N0 No regional LN Mets Tis Melanoma in situ N1 Mets into 1 LN T1 Melanoma < 1mm N1a Microscopic Mets with or without ulceration N1b Macroscopic Mets T1a Melanoma < 1mm, level II N2 Mets in 2 or 3 regional LN or level III, No ulceration N2a Microscopic Mets T1b Melanoma <1 mm, level IV or N2b Macroscopic Mets level V with ulceration N2c Satellite or in-transit Mets T2 Melanoma 1.02-2.0mm, N3 Metastasis in 4 or more LN with or without ulceration T2a Melanoma 1.01-2.0mm, No ulceration Distant Metastasis (M) T2b Melanoma 1.02-2.0 mm Mx cannot be assessed with ulceration M0 No distant Mets T3 Melanoma 2.01-4.0mm M1a-c Distant Mets T4 Melanoma > 4.0mm
Slide 69-

Recommended Margins for Surgical Resection Tumor Thickness (mm) Margin Radius (cm) In Situ 0.5 <1.0 1.0 1-2 2.0 >2.0 >2.0
Slide 70-

Surgical Management of Melanoma Stage 0 in situ Excision: 1cm margins Stage I < 1mm thick Stage I-II 1-4 mm thick Excision: 0.5 cm margins Stage III N0 >4mm >thick CXR (optional) LDH (optional) Evaluation for lymphatic mapping and SNL Bx Excision: 2cm Margins without mapping Excision: 2cm margins and mapping and SNL Bx Node negative Node positive: Completion LN dissection
Slide 71-

Squamous Cell Carcinoma Second most common cancer of the skin, and the most common skin cancer in darkly pigmented racial groups Most common etiological factor is ultraviolet light. Most common sites are ears, cheeks, lower lip, areas of burns (Marjolin ulcer) and scars, chronic ulcers, and areas exposed to radiation. Human papillomaviruses, especially types 5, 8, and 14 are also indicated.
Slide 72-

Squamous Cell Carcinoma
Slide 73-

Squamous Cell Carcinoma Most of these lesions arise from actinic keratoses. Natural history ranges from slow growth lesions (typical of lesions arising from actinic keratoses) or rapid, early metastatic lesions.
Slide 74-

Squamous Cell Carcinoma Histiologically the lesions are seen to extend down into the dermis as broad rounded masses or slender strands with keratinization and layers of intercellular bridges. Treatment: total surgical excision versus irradiation. Lymph node dissection is not necessary except in aggressive cancers of the anal and genitalia areas.
Slide 75-

Basal Cell Carcinoma Most common skin cancer. Lesions usually appear on face. More common in men versus women. Etiology is exposure to ultraviolet rays; geographic areas where sun is plentiful and increased incidence in fair-skinned individuals. Growth rate is very slow, locally invasive and may spread to local tissues or penetrate to the bones of the face and the skull. Metastasis is rare.
Slide 76-

Basal Cell Carcinoma Typical appearance is small, translucent or shiny “pearly” elevated nodules with telangiectatic vessels present. Superficial ulceration may also be present. Treatment includes: Curettage and electrodessication with ~ 3 mm free margin Surgical excision with 3-5 mm free margin X-ray therapy for difficult to reconstruct areas (eyelids, tear ducts, nasal tip)
Slide 77-

Basal Cell Carcinoma
Slide 78-

ppt slide no 78 content not found
Slide 79-

Hippocratic Oath “Primum Non Nocere” (First Do Not Harm)
Slide 80-

Questions?