Anatomy of Skin Epidermis:––composed of several thin layers:stratum basale, stratum spinosum, stratumgranulosum, stratum lucidum, stratum corneumthe several thin layers of the epidermis contain thefollowing:a) melanocytes, which produce melanin, a pigment thatgives skin its color and protects it from the damagingeffects of ultraviolet radiation.b) keratinocytes, which produce keratin, a waterRepellent protein that gives the epidermis its tough,Protective quality.
Anatomy of Skin Dermis:– composed of a thick layer of skin that contains collagenand elastic fibers, nerve fibers, blood vessels, sweatand sebaceous glands, and hair follicles.Subcutaneous Tissue:–composed of a fatty layer of skin that contains bloodvessels, nerves, lymph, and loose connective tissuefilled with fat cells
Function of Integument Protection:– intact skin prevents invasion of the body by bacteriaThermoregulation: intact skin facilitates heat loss and cools thebody when necessary through the followingprocesses:–––production of perspiration which assists in cooling thebody through evaporationproduction of vasodilatation which assists in facilitatingheat loss from the body through radiation andconductionproduction of vasoconstriction which assists inpreventing heat loss from the body through radiationand conduction
Function of Integument Fluid and Electrolyte Balance:– intact skin prevents the escape of water andelectrolytes from the bodyVitamin D SynthesisSensationPsychosocial
Classification of Wounds 1) Clean Wound:– 2) Clean/Contaminated Wound:– uninfected wounds in which no inflammation isencountered but the respiratory, gastrointestinal,genital, and/or urinary tract have been entered.3) Contaminated Wound:– Operative incisional wounds that follow nonpenetrating(blunt) trauma.open, traumatic wounds or surgical wounds involving amajor break in sterile technique that show evidence ofinflammation.4) Infected Wound:–old, traumatic wounds containing dead tissue andwounds with evidence of a clinical infection (e.g.,purulent drainage).
Classification of Wounds Closure Healing by Primary Intention:– Healing by Secondary Intention:– All Layers are closed. The incision that heals by firstintention does so in a minimum amount of time, with noseparation of the wound edges, and with minimal scarformation.Deep layers are closed but superficial layers are left toheal from the inside out. Healing by second isappropriate in cases of infection, excessive trauma,tissue loss, or imprecise approximation of tissue.Healing by Tertiary Intention:–Also referred to as delayed primary closure.
Wound Healing– Inflammation occurs when the damagedendothelial cells release cytokines thatincrease expression of integrands incirculating lymphocytes.– Histamine, serotonin, and kinins cause vesselcontraction (thromboxane), decrease in bloodloss, and act as chemotactic factors forneutrophils, the most abundant cells in theinitial 24 hour period.
Wound Healing– Proliferative phase occurs next, after theneutrophils have removed cellular debris andrelease further cytokines acting as attractingagents for macrophages.– Fibroblasts now migrate into the wound, andsecrete collagen type III.– Angiogenesis occurs by 48 hours.– The secretion of collagen, macrophageremodeling and secretion, and angiogenesiscontinues for up to 3 weeks.– The greatest increase in wound strength occursduring this phase.
Wound Healing– Maturation phase is the final phase andstarts from the 3rd week and continues for upto 9-12 months.– This is where collagen III is converted tocollagen I, and the tensile strength continuesto increase up to 80% of normal tissue.
Surgical Wound Infection– Incisional infections identified by purulent orculture positive drainage is isolated from anystructure above the fascia in proximity to the initialwound– Deep infections are characterized by purulentdrainage from subfascial drains, wounddehiscence, or abscess formation and involveadjacent sites manipulated during surgery.– Wound Dehiscence– Breakdown of the surgical wound
Risk Factors for SWI– Patient-related factors:––––––––––Age 60, sex (female), weight (obesity)Presence of remote infectionsUnderlying disease statesDiabetes, Congestive heart failure (CHF)Liver disease, renal failureDuration of preoperative stay hospitalization 72 hours, ICU stayImmuno-suppressionASA (American Society of Anesthesiologists)physical status (3,4, or 5)
Risk Factors for SWISurgery-related factors:– Type of procedure, site of surgery, emergentsurgery– Duration of surgery ( 60- 120 min)– Previous surgery– Timing of antibiotic administration– Placement of foreign body– Hip/knee replacement, heart valve insertion, shuntinsertion– Hypotension, hypoxia, dehydration, hypothermia
Risk Factors for SWISurgery related factors:– Patient preparation– Shaving the operating site– Preparation of operating site– Draping the patient– Surgeon preparation– Hand washing– Skin antiseptics– Gloving
Risk Factors for SWIWound-related factors:– Magnitude of tissue trauma and devitalization– Blood loss, hematoma– Wound classification– Potential bacterial contamination– Presence of drains, packs, drapes– Ischemia– Wound leakage
Antibiotic UseCharacteristics of an optimal antibiotic forsurgical prophylaxis:–––––––Effective against suspected pathogensDoes not induce bacterial resistanceEffective tissue penetrationMinimal toxicityMinimal side effectsLong half-lifeCost effective
Antibiotic UseAppropriate antibiotic use for prevention ofSWI includes the following:– Appropriate timing of administered agentsand repeated dosing based on length ofprocedure and antibiotic half-life Consider redosingif procedure 4 hours– Appropriate selection based on procedureperformed– Appropriate duration to avoid infection anddecrease potential for development of resistance
Antibiotic Use– NoseS. aureus, pneumococcus, meningococcus– SkinS. aureus, S. epidermidis– Mouth/pharynxStreptococci, pneumococcus, e.coli, bacteroides,fusobacterium, peptostreptococcus– Urinary tractE.coli, proteus, klebsiella, enterobacter
Antibiotic Use– ColonE. coli, klebsiella, enterobacter, bacteroides spp,peptostreptococci , clostridia– Biliary tractE. coli, klebsiella, proteus, clostridia– VaginaStreptococci, staphylococci, E. coli, Peptostreptococci,bacteroides spp.– Upper respiratory tractPneumococcus, H. influenzae
Antibiotic UseIdentify wound infection risk based onpatient’s surgical procedure:– Clean: Cefazolin– Clean/contaminated: Cefazolin vs broadspectrum (Cefoxitin or Cefotetan)– Contaminated: Broad spectrum (Cefoxitin orCefotetan)– Dirty: Therapeutic antibiotics
Fetal Wound Healing– Fetal wound healing proceeds without fibrosis or scarformation in contrast to adult wound healing. Themechanisms responsible for this remarkable processare mediated in part through a fetal woundextracellular matrix rich in hyaluronic acid (HA).– Proposed contributing factors to scarless healing infetal wounds are the presence of fewer neutrophilsand more monocytes during the inflammatory period,different concentrations of cytokines, and a greaterproportion of type III collagen in contrast to adultwounds.
Fetal Wound Healing– Transforming growth factor-b (TGF- β, specifically,low levels of TGF-β1 and TGF- β2 and high levels ofTGF- β3—probably has a central role in scarformation, and studies of its role are ongoing.– Low levels of platelet-derived growth factor (PDGF), agreater amount of epidermal growth factor (a mitogenfor epithelialization), a faster rate of wound healing,and a greater amount of hyaluronic acid in theextracellular matrix has been documented andsuggests a more efficient process of wound healing infetal models.
Diabetic foot ulcers
Staging of Pressure Ulcers Stage I: redness and warmthStage II: shallow ulcer with distinct edgesStage III: full-thickness loss of skinStage IV: involvement of fascia,connective tissue, muscle and bone Stage V: area covered with black eschar(aka scab)
Hypertrophic Scars and Keloids The natural response to injury involves several stages ofwound healing, migration of macrophages, neutrophils,and fibroblasts and the release of cytokines and collagenin an array to promote wound healing and maturation. Hypertrophy and keloid formation are an overactiveresponse to the natural process of wound healing.
Hypertrophic Scars These lesions are raised and thickened. This process does not extend beyond the boundary ofthe incision/scar. This process is exacerbated by tension lines on the areaof surgery: incisions over the knee and elbow have ahigher incidence of hypertrophic reaction.
Hypertrophic Scars NOTE: hypertrophic scars and keloids areindistinguishable by plain H&E staining. Treatment: nearly all hypertrophic scars undergo adegree of spontaneous resolvement. If still present after six months, surgical excision isindicated. Pressure applied early to a lesion is also of benefit. Intractable lesions can be injected with triamcinolone.
Keloids Raised and thickened. This process extends beyond theboundary of the incision.– Continues weeks to months past the initial insult. Higher incidence in African Americans. May have different incidences in different parts of thesame person;– may not develop a keloid on the arm, yet has a keloid afterearring insertion.
Keloids NOTE: hypertrophic and keloids are indistinguishable byplain H&E staining. Treatment: Pressure applied early may decrease theextent of keloid formation. Injection of triamcinolone, or corticosteroid injection maybe helpful. Excision with intramarginal borders is reserved forintractable keloids, and used in conjunction with theabove.
Burns Are divided by depth of injury. Classically, and in someinstitutions the burn is organized by “degree:’ First-degree: involve the epidermis and demonstrateserythema and minor microscopic changes. Pain is majorcomplaint. No scar is left. Healing is complete in up to10 days. Second-degree burns: involves all the epidermis andpart of the dermis. Superficial second-degree burns arecharacterized by blister formation while deeper burnshave a more reddish or non-viable whitish appearance.
Burns– Third-degree: these full thickness burns arecharacteristically white, non-viable.– They may demonstrate darkened brown orblack adipose tissue.– Skin is non-sensate, and leathery.– Muscle injury may also occur.
Burns The most important assessment of volume status and adequatevolume administration is monitoring of the urine output. Burn Resuscitation: (Parkland Formula) 4x % Burn x Weight in kgfor 24 hours, Lactated Ringer’s. Give the first half in first 8 hours andthe next half in the next 16 hours. Urine output is normally 0.5ml/kg, but for burns and trauma patientsis at least 1-1.5 ml/kg/hour. Initial treatment of the actual burn is first debridement of thedenuded skin with moist gauze. This additionally aids in estimating volume of burn. Coverage with topical antibacterial agents is necessary.
Burns Silver sulfadiazine: wide spectrum, moderate escharpenetration. May cause leucopenia Silver nitrate: mild spectrum, non-painful. Does notpenetrate eschar, causes staining. Sodium, calcium,and potassium wasting. Mafenide: wide spectrum penetrates eschar. Painful.Causes metabolic acidosis. Initial coverage can include culture skin and skinsubstitutes. Split thickness skin grafts for burns of smallpercentage ( 25%) can be utilized.
Seborrheic Keratoses These lesions are superficial, non-invasive tumors thatoriginate in the epidermis. Typically appear in older people as multiple slightlyelevated yellowish, brown or brownish-plaque roundedplaques, and are found typically on the shoulders, trunk,scalp, and face. Treatment is by shave excision.
Involuting Hemangiomas Most common tumors that occur inchildhood, 95% of all hemangiomas thatare seen in childhood. Typically present at birth or during 2-3weeks of life, grow at a rapid rate for 4-6months, then involution begins and iscomplete by 5-7 years of age.
Involuting Hemangiomas These types include strawberry nevus, nevusvasculosus, capillary hemangioma, andcavernous hemangioma. Treatment is not usually indicated.– Only indicated if the lesions impair vision (eyelid), acondition that can lead to amblyopia.
Noninvoluting Hemangioma Most of these lesions are present at birth. They grow in proportion to the growth of theinfant, and persist into adulthood. Unlike involuting, these are not true neoplasms,but malformations of arterial and/or veins
Non-involuting Hemangiomas These lesions malformations include:– Port wine stains: most common, mainly occuron face or neck. Best to observe, or lasersurgery.– Cavernous Hemangioma: more common onhead and neck. Observation or injection ofsclerosing agents.
Non-involuting HemangiomasPort Wine StainCavernous Hemangioma
Verrucae Also known as common warts, these lesions areseen in childhood and in young adults, typicallyon fingers and hands. These lesions appear as round or dome-shapedelevated masses with rough surfaces withmultiple villi like keratinized projections. They may range from brown to gray to skincolored.
Verrucae The etiology is by human papillomaviruses (over 50different types exist). Types 1, 2, 4, and 7 typicallycause verrucae. Treatment: is by electrodessication or liquid nitrogen. Surgical excision is not recommended. Most treatment can be delayed by several monthsbecause these lesions may spontaneously resolve. Duct tape is listed in many current journals as most noninvasive method of treatment.
Actinic Keratoses Actinic keratoses are the most common precancerousskin lesions. Most commonly appear as single or multiple, slightlyelevated, scaly or warty lesions that are red to yellow,brown or black. Occur most frequently on the face and backs of hands infair-skinned Caucasians. Approximately 15-20% become malignant, invade thedermis as squamous cell carcinomas. Treatment: curettement and electrodessication or 5-FU.
Melanoma Melanocytes are cells of neural crest origin thatmigrate during fetal development to multiple sitesin the body, principally the skin. These cells are exposed to carcinogenic stimulithat result in malignant transformation to becomemelanoma. Melanoma accounts for only 4% to 5% of all skincancers but causes the majority of deaths fromskin malignancies. It is the eighth most commoncancer in the United States, and the incidence isrising faster than any other type of cancer.
Epidemiology and Etiology The incidence and outcome of melanoma arerelated to multiple factors. Melanoma is principallya disease of whites, particularly those of Celticancestry. It is estimated that melanoma occurs 20times more often in whites than in blacks. The median age of diagnosis is in the range of 45to 55 years. There is a significant incidence in the3rd and 4th decades of life.
Epidemiology and Etiology It is well established that exposure to sunlightincreases the risk of developing melanoma insusceptible populations. This is specificallyattributed to solar ultraviolet (UVA/UVB) radiation. Additional factors that increase the risk fordevelopment of melanoma include fair skin,dysplastic nevus (DN) syndrome, xerodermapigmentosum, a history of non-melanoma skincancer (NMSC), and a family history ofmelanoma.
Precursor Lesions and Risk Factors Congenital nevi, DNs, Spitz nevi, and familialpatterns all raise the risk of developingmelanoma. Individuals with congenital nevi havean increased risk that is proportional to the sizeand number of nevi. Giant congenital nevi are rare (1 in 20,000newborns) and carry an increased risk fordevelopment of melanoma within the nevi
Melanoma Screening: Any new pigmented nevus should besuspected. Approximately one third arise from pigmented nevi. Junctional nevi: small, circumscribed and arelight brown to black.– Rarely have hair.– Appear on all parts of the body, and mucousmembranes, genitalia, palms, and soles.– Located on the epidermis and dermal-epidermaljunction.
Melanoma– Intradermal nevi: small spots to largeextensive areas, variable shape. Often blackor brown and slightly elevated, and confinedto the dermis.– Compound nevi: combination junctional andintradermal.
Melanoma– Blue nevi: flat or dome-shaped, bluish-black usuallyon hands arms, or face. May resemble nodularmelanoma.– Dysplastic nevi: are larger, up to 5-12 mm, havemacular and popular features, varied in color withpink base, and have indistinct, irregular edges.PRECURSOR OF MELANOMA.– Congenital nevi: occur in approximately 1% ofnewborns. PRECURSOR OF MELANOMA.
Melanoma Symptoms: features that are suggestive of melanomaare the following– Irregular areas of differentiating color (black to brownto tan with focal discoloration)– Rapid enlargement– Irregular edges– Erosion, bleeding or crust formation– Pruritis– Location: lesions on back and lower extremitiesrequire close motoring.
Melanoma Several different tumor types exist:– Superficial spreading: Most common type. Typicallyappears on back, and may be black, gray blue or pinkish incolor.– Nodular: may develop from a preexisting nevi, and rapidlybecomes palpable. May also ulcerate, and is worseprognosis.– Lentigo maligna: usually occurs in older patients. Seenmost often as a large melanotic freckle (Hutchinson’sfreckle) on the temple or malar region. Grows very slowly,and is the largest of the malignant melanomas.– Acral Lentiginous: Confined to the subunual areas andglabrous skin of the palms and soles. Most common inblack population.
Superficial spreadingmelanomaLentigo malignamelanoma
Acral lentiginousmelanomaNodular melanoma
Breslow’s Depth (old)Thickness (mm) 0.750.76-1.51.51-2.252.26-3 3Recurrence or metastasis at5 years0%33%32%69%84%
AJCC ClassificationPrimary Tumor (T)TXCan not be assessedT0No evidence of TumorTisMelanoma in situT1Melanoma 1mmwith or without ulcerationT1aMelanoma 1mm, level IIor level III, No ulcerationT1bMelanoma 1 mm, level IV orlevel V with ulcerationT2Melanoma 1.02-2.0mm,with or without ulcerationT2aMelanoma 1.01-2.0mm,No ulcerationT2bMelanoma 1.02-2.0 mmwith ulcerationT3Melanoma 2.01-4.0mmT4Melanoma 4.0mmRegional LN (N)NXcan not be assessedN0No regional LN MetsN1Mets into 1 LNN1aMicroscopic MetsN1bMacroscopic MetsN2Mets in 2 or 3 regional LNN2aMicroscopic MetsN2bMacroscopic MetsN2cSatellite or in-transit MetsN3Metastasis in 4 or more LNDistant Metastasis (M)Mxcannot be assessedM0No distant MetsM1a-c Distant Mets
Recommended Margins for SurgicalResectionTumor Thickness (mm)Margin Radius (cm)In Situ0.5 1.01.01-22.0 2.0 2.0
Surgical Management of MelanomaStage 0in situExcision:0.5 cm marginsStage I 1mm thickExcision: 1cmmarginsStage I-II1-4 mmthickStage IIIN0 4mm thickExcision: 2cmMargins for lymphaticmapping andSNL BxExcision: 2cmmargins andmapping andSNL BxNodenegativeNode positive:Completion LNdissection
Squamous Cell Carcinoma Second most common cancer of the skin, andthe most common skin cancer in darklypigmented racial groups Most common etiological factor is ultravioletlight. Most common sites are ears, cheeks,lower lip, areas of burns (Marjolin ulcer) andscars, chronic ulcers, and areas exposed toradiation. Human papillomaviruses, especiallytypes 5, 8, and 14 are also indicated.
Squamous Cell Carcinoma
Squamous Cell Carcinoma Most of these lesions arise from actinickeratoses. Natural history ranges from slow growth lesions(typical of lesions arising from actinic keratoses)or rapid, early metastatic lesions.
Squamous Cell Carcinoma Histiologically the lesions are seen to extend down intothe dermis as broad rounded masses or slender strandswith keratinization and layers of intercellular bridges. Treatment: total surgical excision versus irradiation. Lymph node dissection is not necessary except inaggressive cancers of the anal and genitalia areas.
Basal Cell Carcinoma Most common skin cancer. Lesions usually appear on face. More common in menversus women. Etiology is exposure to ultraviolet rays; geographic areaswhere sun is plentiful and increased incidence in fairskinned individuals. Growth rate is very slow, locally invasive and mayspread to local tissues or penetrate to the bones of theface and the skull. Metastasis is rare.
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 freemargin– Surgical excision with 3-5 mm free margin– X-ray therapy for difficult to reconstruct areas (eyelids,tear ducts, nasal tip)
Basal Cell Carcinoma
Hippocratic Oath“Primum Non Nocere”(First Do Not Harm)
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.File Size: 1MBPage Count: 80Explore furtherPPT – Wounds and Wound Healing PowerPoint presentation .www.powershow.comPhases of the wound healing process - EMAPcdn.ps.emap.comWound Healing - Primary Intention - Secondary Intention .teachmesurgery.comWound healing - SlideSharewww.slideshare.netWound Care: The Basics - University of Virginia School of .med.virginia.eduRecommended to you b
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Wound Healing and General Wound Management Wound Healing Wound healing proceeds in several phases. The wound surface is initially covered with a brin net, and after 24 hours the epi-dermis begins to close over the wound. Wounds that are surgi-cally closed have already achieved epithelial coverage, prevent-ing the in ltration of pathogens.
health care personnel about the physiology of wound healing and to review key concepts and practices for providing wound care in the perioperative setting. OBJECTIVES After viewing the video and completing the study guide, the learner will be able to: 1. Define wound healing. 2. List types of wound closure. 3. Describe the physiology of wound .
Wound Healing for the Plastic Surgery Nurse: Wound Healing 101 Valentina S. Lucas, PhD, APRN-BC VCUHS Plastic and Reconstructive Surgery VCUHS Wound Healing Center. Course Objectives . Exudate Management Wound Edges BED
board-certified wound care nurse from 8am–5pm Central Standard Time Monday–Friday. 1-888-701-SKIN (7546) » The NE1 Wound Assessment Tool This proprietary wound assessment tool is designed to dramatically increase accuracy, consistency and transparency in wound assessment. » WoundRounds Wound Management System This unique wound management
Wound edges open Not healing Wound with 25% avascular tissue (eschar and/or slough) OR Signs/symptoms of infection OR Clean but nongranulating wound bed OR Closed/hyperkeratotic wound edges OR Persistent failure to improve despite appro-priate comprehensive wound management Note. Data from WOCN (2009).
Wound Classification Guides Treatment & Management Etiology Provides an algorithm or strategy for the global management of the patient, with the ultimate goal of achieving wound healing Appearance Generally guides the wound care management regarding the use of topicals and dressings Wound Classif
One of the authors of this presentation is member of one of the user groups with access to TARGET2 data in accordance with Article 1(2) of Decision ECB/2010/9 of 29 July 2010 on access to and use of certain TARGET2 data.