healing and wound care surgery 2

Upload: aaron-christian-earl-villoso

Post on 07-Apr-2018

218 views

Category:

Documents


0 download

TRANSCRIPT

  • 8/6/2019 Healing and Wound Care Surgery 2

    1/12

    11

    Types of woundsWounding: disruption of tissue integrity

    Insect bite:

    Laceration:

    Scalp avulsion:

    Electrical burn: probably willsustain digital amputation

    Burn

    Foreign body reaction: fromsilicone injection. Picture thatfollows shows revisional surgery.

    Subject: SURGERYTopic: Healing and Wound careLecturer: Dr. MarquinaDate of Lecture: June 22, 2011Transcriptionist: MopsterPages: 11 S

    Y

    2011-2

    012

  • 8/6/2019 Healing and Wound Care Surgery 2

    2/12

    11

    General Objectives

    At the end of the lecture, the studentsshould be able to discuss the basicconcepts of wound healing, as well as, thefundamental principles of woundmanagement.

    Specific Objectives

    At the end of the lecture, thestudents should be able to:o To discuss the bodys response

    to injury and the sequence ofevents that follow during thecourse of normal woundhealing,

    o To define the effects of local

    and systemic factors on woundhealing

    o To describe the steps in the

    proper evaluation, care, andtreatment of the different typesof wounds

    Course Outline

    I. Historical backgroundII. Biology of normal wound healingA. Phases of wound healing

    1. Inflammatory phase2. Proliferative phase3. Maturation and

    remodeling phaseB. EpithelializationC. Wound ContractionD. Fetal wound healing

    III. Factors affecting wound healingIV. Excessive healing/abnormal scars

    V. Wound care and managementA. Classification of woundB. Types of wound closureC. Local wound careD. Dressings

    Historical Background

    Ancient timeso 2000 BC Sumerians

    Incantations: probably inthe belief that the woundswere caused by evil spirits orthe gods.

    Application of poultice likematerials

    o 1650 BC: Egyptian papyrusdocuments

    Infected vs. non infectedwounds

    Used concoctions containing

    Honey (antibacterialproperties

    Lint (absorbentproperties)

    Grease (barrier) fortreating wounds

    o 2nd-3rd century AD

    Greeks

    Acute vs. chronic wounds

    Practiced gentle tissuehandling, foreign bodyremoval, suturing skinedges, and protecting thewound with cleanmaterials

    Galen, a doctor to Romangladiators

    Emphasized theimportance of a moistwound environment to

    ensure adequate healingo Present

    Mid 1500: Ambroise Pare(French army doctor)

    Rediscovered the value ofgentle methods of woundcare

    Wounds healed rapidlywhen milder measureswere used.

    1728 - 1793: John Hunter

    Injury alone has in all

    cases a tendency toproduce the depositionand the means toproduce a cure

    1818-1865: Ignaz PhilippSemmelweiss (Hungarianobstetrician)

    Introduced washing ofhands with soap andhypochlorite to decreasepuerperal infection.During those times, thestudents, sometimescoming from anatomydissections assisted withdeliveries, whichprobably led to manyinfections.

    1822-1895: Louis Pasteur.

  • 8/6/2019 Healing and Wound Care Surgery 2

    3/12

    11

    Concept of germsentering the wound fromthe environment.

    Used phenol to disinfectinstruments and ORwhich resulted in amarkedly reducedmortality rate

    1876: Robert Johnson. Antiseptic dressing

    (cotton gauzeimpregnated withiodoform)

    1929: Howe, et al

    3 classic phases of woundhealing

    1962: Winter.

    Proved scientifically thatepithelialization rateincreased by 50% in a

    moist woundenvironment

    Recent advances in research have notchanged our knowledge of the events ofwound healing but rather have addednew information on the methods by whichwound healing responses are controlled:

    Inflammatory cytokines

    Growth factors

    Bioengineered tissues: for woundcoverage

    Biology of Normal Wound Healing

    Phases of Wound Healing1. Inflammatory (hemostasis and

    inflammation)2. Proliferative (Fibroblastic phase)3. Maturation and Remodeling

    There is overlap of the stages

    Time Sequence of Classical WoundHealing

    Note the overlap of the differentstages

    Inflammatory Phase (Hemostasis andInflammation)

    Inflammationo Vascular and cellular response

    o Serves to clean the wound ofdevitalized tissue and foreignmaterial

    Stimulus to inflammationo Physical injuryo Antigen antibody reactiono Infection

    After the injury, initial changes are

    vascular.o Within 5-10 minutes,

    vasoconstriction occurs to slowblood flow

    o Followed by active vasodilation

    and increased permeabilityo Platelets, erythrocytes,

    leukocytes line the vessel wallsand serum gains entry into thewound

    Wounding disrupts tissue

    integrityDivision of blood

    vesselsDirect exposure of extracellularmatrix (collagen) to plateletsPlateletaggregation and

    degranulationActivation of coagulationcascade

    Platelet activation results in:

    Release of wound activesubstanceso Platelet derived growth factor

    (PDGF)o Transforming growth factor

    (TGF)o Platelet activating factoro Fibronectino Serotonino Promote migration and

    adhesion of neutrophils,monocytes, fibroblasts, andendothelial cells into the wound

  • 8/6/2019 Healing and Wound Care Surgery 2

    4/12

    11

    Activation of coagulation cascade

    Culminates in the formation offibrin clot which serves asscaffolding for the migration ofPMNs, monocytes, and fibroblastsinto the wound

    Cellular infiltration follows acharacteristic pattern:

    Note: platelets come first, last toarrive are the fibroblasts andcapillaries.

    Polymorphonuclear cells (PMNs)

    Neutrophilso 1st infiltrating cellso Peak at 24-48 hours post

    woundingo Phagocytosis of bacteria and

    tissue debris (main task is toclean wound)

    o Releases collagenases Matrix and ground substance

    degradationo Do not appear to play a role

    in collagen deposition oracquisition of mechanicalwound strength

    Simpson and Ross inducedneutropenia in guinea pigs,

    and noted that in theabsence of gross infection,wound repair proceededidentically to that of normalanimals

    Macrophages

    From monocytes

    Peak at 48-96 hours post wounding Wound debridemnt via

    phagocytosis

    Contribute to microbial stasis byoxygen radial and nitric oxidesynthesis

    Release cytokines and growthfactors that regulate fibroblastproliferation, matrix synthesis, andangiogenesis

    Activated by:o IL-1

    o TNFo TGFo VEGF (Vascular Endothelial

    Growth Factor)o Insulin like Growth Factoro Epithelial Growth Factoro Lactate

    Leibovich and Ross

    Complete disappearance ofmacrophage from the wound byadministration of systemhydrocortisone and subcutaneousantimacrophage serum

    Documented impairment ofphagocytosis, qualitative as well asquantitative decrease infibrinogenesis

    T-Lymphocytes

    Peak at 1 week post injuryo Produce lymphokineso Found to both inhibit and

    stimulate fibroblast recruitmentand proliferation

    Peterson, et al, have shown that:o Depletion of T lymphocytes

    within 1 week after woundingresults in impaired collagensynthesis and deposition, anddecreased breaking strength ofthe wound

    Proliferative Phase

    Begins around 4th day and lasts 2-4

    weeks post injury Fibroblasts (matrix synthesis) and

    endothelial cells (angiogenesis):most important cells at this stage.

    Culminates in the re-establishmentof tissue continuity

    Fibroblastso Activated by cytokines and GFs

    released by macrophages

  • 8/6/2019 Healing and Wound Care Surgery 2

    5/12

    11

    o Move along a framework offibrin fibers established duringthe initial hemostasis

    o Responsible for matrix synthesis(glycosaminoglycans andfibrillar collagen)

    Endothelial cellso Participate in angiognenesiso

    Migrate and replicate form newcapillary tubules underinfluence of TNF, TGF, VEGF

    Matrix synthesiso GAGS

    Ground substance that playsa role in the subsequentaggregation of collagenfibers

    An amorphous gel made upof a repeating disaccharideunits attached to a protein

    core Chondroitin 4 sulfate

    Dermatan sulfate

    Heparan sulfate

    Hyaluronic acido Collagen

    Most abundant protein in thehuman body

    18 types; 5 types are foundin human body

    Type I (skin, tendon, and

    bone) is 90% of all collagen Normal skin contains Type I

    and III collagen in ratio of 4:1

    Type and distribution ofcollagen (see below):

    Collagen synthesiso Occurs intracellularly and

    extracellularlyo Glycine Proline - Lysineo Protocollagen is translated from

    mRNAo Hydroxylation

    ProlineHydroxyproline

    LysineHydroxylysine

    o Prolyl hydroxylase requiresoxygen and iron as cofactors , ketoglutarate as cosubstrate,ascorbic acid (vitamin C) as anelectron donor

    o Protocollagen is alsoglycosylated and assumes an -helical configuration

    o 3 -helical chains form a righthanded superhelical structurecalled procollagen

    o Excreted extracellularly,procollagen undergo polymerand cross - linking formingcollagen filaments

    o ProtocollagenProcollagenCol

    lagen filamentsCollagen

    fibrilsCollagen fibers

    Tensile Strength Tensile strength of the wound

    o Measurement of its loadcapacity per unit area

    o Constant

    Breaking strength of the woundo The force required to break it

    regardless of its dimension

  • 8/6/2019 Healing and Wound Care Surgery 2

    6/12

    11

    o Dependent of the thickness oftissues

    o Collagen fibers are largelyresponsible for tensile strengthof wounds

    o All wounds gain strength atapproximately the same rateduring first 14-21 days

    o

    In the skin, peak tensilestrength is achieved atapproximately 60 days afterinjury

    o Tensile strength of a wound

    reaches only about 80% of theoriginal unwounded skin

    Maturation and Remodeling Phase

    Begins approximately 3 weeks postinjury

    Collagen synthesis and degradation

    are accelerated no net increasein the wound collagen content

    Reorganization of previouslysynthesized collageno More stable and permanent

    cross links are establishedo Gain in tensile strength

    Normal Type I: Type III collagenratio of 4:1 is achieved

    Remodeling continues for 6 12months post - injury

    Initially indurated, raised andpruritic scar becomes a maturescaro Large number of new capillaries

    growing into wound regress anddisappear

    o Water content of tissue returnto normal

    o Avascular and acellular scar

    Epithelialization

    Proliferation and migration of

    epithelial cells adjacent to thewound

    Begins within 1 day of injury

    Seen as thickening of theepidermis at the wound edge

    Reepithelialization is complete inless than 48 hours in the case ofapproximated incised wound

    In split thickness graft donor orsuperficial partial thickness burns,healing consists primarily of re epithelialization with minimal or no

    fibroplasias and granulation tissueformation

    Process:o Mobilization

    Epithelial cells immediatelyadjacent to wound enlarge,flatten and detach fromneighboring cells and thebasement membrane

    o Migration

    Loss of contact inhibition, socell moves away from itsoriginal neighboring cells.

    Cells flow away from theadjoin cells until they meetcells from the opposite sideof the wound

    o

    Mitosis Fixed basal cells divide to

    replace the migrating cellswhile the migrating cells, inturn, also divide and multiply

    o Cellular differentiation

    Upon reepithelialization, theorderly progression from thebasal mitotic cells throughlayers of differentiatedkeratinocytes to stratumcorneum is again established

    Wound Contraction

    Part of the repair process thatcloses a gap in soft tissue

    The area of the wound is decreasedby this action (healing bysecondary intention)

    In contrast to contracture which is:o Undesirable effect of wound

    healingo Shortening of the scar that may

    result in deformitieso May be due to contraction,

    fibrosis, or other tissue damage

    Myofibroblastso Cells postulated to be

    responsible for woundcontraction (still controversial)

    o Cytoskeletal structure (

    smooth muscle actin)o Well formed intercellular

    attachments such asdesmosomes and macula

    adherens

    Fetal Wound Healing

    Lack of scar formation

    More of a regenerative processwith minimal or no scar formation

    Transition woundo Occurs at the beginning of the

    3rd trimestero Scarless healing but there is a

    loss of ability to generateappendages

    Difference between adult and fetalwound healing

    Wound environmento Fetus is bathed in sterile and

    temperature stable fluidenvironment

  • 8/6/2019 Healing and Wound Care Surgery 2

    7/12

  • 8/6/2019 Healing and Wound Care Surgery 2

    8/12

    11

    o Constituent of several enzymesessential for normal woundhealing

    o Low serum levels impairepithelial and fibroblasticproliferation

    o Studies have shown that zinc

    enhances wound healing only

    when there is a pre existingzinc deficiency state

    Diabetes mellituso Results in reduced

    inflammation, angiogenesis,and collagen synthesis

    o Large and small vessel diseasescontributes to local hypoxemia

    o Careful preoperative correctionof blood sugar levels improvesoutcome of wounds in pts.

    o Insulin restores collagen

    synthesis and granulation tissueformation to normal levels

    Excessive Wound Healing/AbnormalScars

    Widespread scars

    Hypertrophic scars

    KeloidsA preferred scar is one that has maturedrapidly without contracture or increase inwidth, and without forming more collagenthan necessary for its strength.

    Wide spread scar

    Typically flat, wide, and oftendepressed

    Consequence of continued tensionin the dermis (covered byepidermis instead) and mobility ofthe wound

    Hypertrophic scar

    Elevated above skin surface butlimited to the initial boundaries ofthe injury

    Tend to regress spontaneously

    Responsive to treatment

    Keloids

    Extend beyond the border of theoriginal wound

    Lack regression

    Commonly in presternal, deltoids,back, and earlobes

    Resistant to treatment, often worseafter surgery

    Familiar predilection

    Young age and dark skin color

    Treatment modalities

    Intralesional corticosteroindinjection

    Silicone sheet/gel: shown to havesome positive effect on scarremodeling

    Irradiation and pressure

    Surgery (high recurrence rate)

    Wound Care and ManagementClassification

    Acute woundso Lacerations, tissue avulsions,

    surgical woundo Heal in a predictable manner

    and time tableo Result in a well healed wound

    with few or no complications

    Chronic woundso Wounds that have not healed in

    3 monthso Risk factors include repeated

    trauma, poor tissue perfusion,excessive inflammation

    Ischemic arterial ulcers

    Due to lack of bloodsupply

    Symptoms of peripheralvascular disease like rest

  • 8/6/2019 Healing and Wound Care Surgery 2

    9/12

    11

    pain, intermittentclaudication, and colorchanges

    On examination,diminished or absentpulses and poorformation of granulationtissue

    Management isrevascularization oftissue and wound care

    Venous stasis ulcers

    Due to venous stasis andhydrostatic back pressure

    Distention of dermal capsresult in leaking offibrinogen and theformation of perivascularfibrin cuffs that impedeoxygen delivery to tissue

    Lipodermatosclerosis

    Management iscompression and woundcare

    Diabetic wounds

    Neuropathy, footdeformity, and ischemia

    Unrecognized injury from

    ill fitting shoes, foreignbody, and trauma

    Severe micro- andmacrovascularimpairment

    Mangement includesadequate control of bloodglucose, control ofinfection by debridementand antibiotic

    Decubitus/Pressure Ulcer

    When soft tissue iscompressed betweenbony prominence andexternal surface

    Excessive pressurecauses capillary collapseand impedes the deliveryof nutrients to tissues

    Risk factors includeimmobility, chronicconditions, alteredmental status

    Pressure ulcer at thetrochanteric area

    Stages of Pressure Ulcer FormationI. Non blanching erythema of intact

    skinII. Partial thickness kin lossIII. Full thickness skin loss but not thru

    fasciaIV. Full thickness skin loss with

    involvement of muscle and

    boneMarjolins Ulcers:

    Malignant transformation of long standing chronic ulcer

    Squamous or basal carcinomas

    Types of Wound Closure

    Primary intention or primaryclosureo Wound edges are immediately

    approximated using sutures,staples, or tapeo Delayed primary closure: in

    contaminated wounds, woundedges are approximated after adelay of several days

    Secondary Intention orSecondary Closureo Due to bacterial contamination

    and tissue loss, the wound is

  • 8/6/2019 Healing and Wound Care Surgery 2

    10/12

    11

    left open to heal by granulationtissue formation and contraction

    Tertiary Closureo Wound is closed by bringing

    tissues from elsewhere in theform of graft or flap

    See below: scar formation for thedifferent types of closure.

    Local Wound Care

    Obtain a history of eventssurrounding injury

    Examine the wound to assess itsdepth and configuration, extent ofnon-viable tissues as well as thepresence of FB and contaminants

    Irrigation and debridement of theedges of the wound under localanesthesiao High pressure (70 PSI) irrigation

    with normal salineo Gentle handling of tissues

    o Marginally viable flap of skinand tissues should be resectedor revascularized before woundrepair

    o Use of povidone iodine,hydrogen peroxide impairwound healing

    Antibiotic administrationo Must appropriate for organism

    o Must be given at proper time, inproper dose, via proper route

    Eg, elective surgery,contaminated, traumaticwounds

    Tetanus prophylaxis

    Planning the type and timing ofwound repair

    Dressing

    Mimics the barrier role ofepithelium

    Primary dressing vs. secondarydressingo Primary dressing

    Placed directly on the wound

    Absorption of secretions,prevent dessication,infection and adhesion ofsecondary dressings

    o Secondary dressing Placed over the primary

    dressing

    Provide compression andocclusion and form a barrier

    Absorbent dressingo Cotton, wool, and spongeo Should absorb without getting

    soaked through, as this wouldpermit entrance of bacteriafrom the outside

    Non adherent dressingso Impregnated with paraffin,

    petroleum jelly, water solublejelly

    o Used as primary dressing

    Medicated dressingso Used as a drug delivery systemo May contain benzoyl peroxide,

    zinc oxide, neomycin,bacitracin, and chlorhexidine

    o Shown to increase

    epithelializaton by 28%

    Skin Replacements

    Conventional skin graftso Split or partial thickness

    skin grafts

    Epidermis and part of dermis

    Donor site heals byepithelialization

    Lower rate of primarycontraction (contractionafter harvesting) but higherrate of secondary

    contraction (contracture) Contraction:centripetal

    movement of the wholethickness of surrounding skinreducing scar

    Contracture: the physicalconstriction or limitation offunction as the result ofContraction (scars acrossjoints, mouth, eyelid)

  • 8/6/2019 Healing and Wound Care Surgery 2

    11/12

    11

    o Full thickness skin grafts

    Entire epidermis and dermis

    Higher rate of contraction

    (contraction afterharvesting) but lower rate ofsecondary contraction(contracture

    Best coverage of lesion onthe face and over jts.

    Donor site should be closedprimarily, but size is limited

    Sources of Grafts

    Autograft: from same individual

    Isograft: from a twin Allograft/homograft: from the

    same species. Eg, from non identical donor or cadaver

    Xenograft/heterograft: fromanother species. Eg, porcine

    Skin substitutes

    Provide coverage for extensivewounds with limited availability ofautografts

    Product of tissue engineering;novel materials are combined withliving cells

    Disadvantages include limitedsurvival, high cost, and the needfor multiple applications

    Types:o Cultured epithelial

    autografts

    Keratinocytes harvestedfrom a biopsy of patientsskin are cultured withfibroblasts and growthfactors, and grown intosheets.

    o Cultured allogenic

    keratinocyte graft

    From cadavers andunrelated donors

    o Cultured bilayer skinequivalent

    Acellular (collagen orsynthetic materials)elements that act asscaffolding for cell growthand migration and cellularelements to reestablish losttissue.

    Eg, Biobrane

    Important points1. Regardless of the cause of injury,the body responds in a predictablesequence of events

    2. An understanding of the biology ofnormal wound healing guides thephysician in the care of wounds.

    3. Several local and systemic factorsaffect wound healing; controllingthese factors will ensure that thenormal processes of wound healingshall proceed efficiently

    4. In the care of wounds, thephysician must remember thebasic surgical principles: gentlehandling of tissues, maintenance ofaseptic technique, ensuring tissueviability, and avoidance of tension.

  • 8/6/2019 Healing and Wound Care Surgery 2

    12/12

    End of transcriptionIn all these things we have complete

    victory through him who loved us.

    Romans 8:37-39