2 1 0 2 1 1 0 2
Subject: SURGERY Topic: Healing and Wound care Lecturer: Dr. Marquina Date of Lecture: June 22, 2011 Transcriptionist: Transcriptionist: Mopster Pages: 11
Y S
Types of wounds of tissue integrity Wounding: disruption of tissue I nsect nsect bite: y
y
y
y
Lacer ation: y
Burn
y
oreign body reaction: F oreign
alp av ul sion: sion: Sc alp
lectric e ctric al al burn: E l
from silicone injection. Picture that follows shows revisional surgery.
probably will sustain digital
amputation
1
o
o
General Objectives of the lecture, the students should be At the end of the able to discuss the basic concepts of wound healing, as well as, the fundamental principles of wound management. Specific Objectives At the end of the of the lecture, the students should be able to: o To discuss the bodys response to injury and the sequence of events of events that follow during the course of normal of normal wound healing, o To define the effects of local of local and systemic factors on wound healing o To describe the steps in the proper evaluation, care, and treatment of the of the different types of wounds y
Course Outline I. Historical background Biology of normal of normal wound healing II. A. Phases of wound healing 1. Inflammatory phase 2. Proliferative phase 3. Maturation and remodeling phase B. Epithelialization C. Wound Contraction D. Fetal wound healing Factors affecting wound healing III. Excessive healing/abnormal scars IV. Wound care and management V. A. Classification of wound B. Types of wound closure C. Local wound care D. Dressings Historical Background y
Ancient o
times 2000 BC Sumerians Incantations: probably in the belief that the wounds were caused by evil spirits or the gods.
o
Application
of poultice of poultice like
materials 1650 BC: Egyptian papyrus documents Infected vs. non infected wounds Used concoctions containing Honey (antibacterial properties Lint (absorbent properties) Grease (barrier) for treating wounds nd rd 2 -3 century AD Greeks Acute vs. chronic wounds Practiced gentle tissue handling, foreign body removal, suturing skin edges, and protecting the wound with clean materials Galen, a doctor to Roman gladiators Emphasized the importance of a moist wound environment to ensure adequate healing Present Mid 1500: Ambroise Pare (French army doctor) Rediscovered the value of gentle methods of wound care Wounds healed rapidly when milder measures were used. 1728 - 1793: John Hunter Injury alone has in all cases a tendency to produce the deposition and the means to produce a cure 1818-1865: Ignaz Philipp Semmelweiss (Hungarian obstetrician) of hands Introduced washing of hands with soap and hypochlorite to decrease puerperal infection. During those times, the students, sometimes coming from anatomy dissections assisted with deliveries, which probably led to many infections. 1822-1895: Louis Pasteur. Concept of germs of germs entering the wound from the environment. Used phenol to disinfect instruments and OR which resulted in a markedly reduced mortality rate 1876: Robert Johnson. Antiseptic dressing (cotton gauze impregnated with iodoform) 1929: Howe, et al 3 classic phases of wound healing 1962: Winter. Proved scientifically that epithelialization rate increased
2
by 50% in a moist wound environment Recent advances in research have not changed our knowledge of the of the events of wound healing but rather have added new information on the methods by which wound healing responses are controlled: Inflammatory cytokines Growth factors Bioengineered tissues: for wound coverage y y y
Biology of Normal Wound Healing Phases of Wound Healing 1. Inflammatory (hemostasis and inflammation) 2. Proliferative (Fibroblastic phase) 3. Maturation and Remodeling There is overlap of the of the stages Time Sequence of Classical Wound Healing of the different stages Note the overlap of the y
Platelet activation results in: Release of wound active substances o Platelet derived growth factor (PDGF) Transforming growth factor (TGF) o o Platelet activating factor Fibronectin o o Serotonin o Promote migration and adhesion of neutrophils, monocytes, fibroblasts, and endothelial cells into the wound y
Inflammatory Phase (Hemostasis and Inflammation) Inflammation o Vascular and cellular response o Serves to clean the wound of devitalized tissue and foreign material Stimulus to inflammation o Physical injury Antigen antibody reaction o o Infection After the injury, initial changes are vascular. o Within 5-10 minutes, vasoconstriction occurs to slow blood flow Followed by active vasodilation and o increased permeability o Platelets, erythrocytes, leukocytes line the vessel walls and serum gains entry into the wound Wounding disrupts tissue integrityDivision of blood vesselsDirect exposure of extracellular of extracellular matrix (collagen) to plateletsPlatelet aggregation and degranulationActivation of coagulation of coagulation cascade y
Activation of coagulation cascade of fibrin clot Culminates in the formation of fibrin which serves as scaffolding for the migration of PMNs, monocytes, and fibroblasts into the wound y
y
y
3
Cellular infiltration follows a characteristic pattern: Note: platelets come first, last to arrive are the fibroblasts and capillaries.
y
y
y
Peak at 1 week post injury o Produce lymphokines Found to both inhibit and stimulate o fibroblast recruitment and proliferation Peterson, et al, have shown that: o Depletion of T lymphocytes within 1 week after wounding results in impaired collagen synthesis and deposition, and decreased breaking strength of the of the wound
Proliferative Phase th Begins around 4 day and lasts 2-4 weeks post injury Fibroblasts (matrix synthesis) and endothelial cells (angiogenesis): most important cells at this stage. of tissue Culminates in the re-establishment of tissue continuity Fibroblasts Activated by cytokines and GFs released o by macrophages Move along a framework of fibrin of fibrin fibers o established during the initial hemostasis o Responsible for matrix synthesis (glycosaminoglycans and fibrillar collagen) Endothelial cells o Participate in angiognenesis Migrate and replicate form new o capillary tubules under influence of TNF, TGF, VEGF Matrix synthesis o GAGS Ground substance that plays a role in the subsequent aggregation of collagen fibers An amorphous gel made up of a of a repeating disaccharide units attached to a protein core Chondroitin 4 sulfate Dermatan sulfate Heparan sulfate Hyaluronic acid o Collagen Most abundant protein in the human body 18 types; 5 types are found in human body Type I (skin, tendon, and bone) is of all collagen 90% of all Normal skin contains Type I and III collagen in ratio of 4:1 Type and distribution of collagen of collagen (see below): y
y
Polymorphonuclear cells (PMNs) Neutrophils st o 1 infiltrating cells o Peak at 24-48 hours post wounding of bacteria and tissue o Phagocytosis of bacteria debris (main task is to clean wound) o Releases collagenases Matrix and ground substance degradation o Do not appear to play a rol e in collagen de position or acquisition of mechanic al al wound strength Simpson and Ross induced neutropenia in guinea pigs, and noted that in the absence of gross of gross infection, wound repair proceeded identically to that of normal of normal animals y
y
y
y
y
Macrophages From monocytes Peak at 48-96 hours post wounding Wound debridemnt via phagocytosis Contribute to microbial stasis by oxygen radial and nitric oxide synthesis Release cytokines and growth factors that regulate fibroblast proliferation, matrix synthesis, and angiogenesis Activated by: o IL-1 o TNF o TGF o VEGF (Vascular Endothelial Growth Factor) o Insulin like Growth Factor Epithelial Growth Factor o Lactate o y y y y
y
y
Leibovich y
y
and Ross of macrophage Complete disappearance of macrophage from the wound by administration of system hydrocortisone and subcutaneous antimacrophage serum of phagocytosis, Documented impairment of phagocytosis, qualitative as well as quantitative decrease in fibrinogenesis
T-Lymphocytes
4
y
Collagen synthesis o Occurs intracellularly and extracellularly o Glycine Proline - Lysine o Protocollagen is translated from mRNA o Hydroxylation ProlineHydroxyproline LysineHydroxylysine o Prolyl hydroxylase requires oxygen and iron as cofactors , ketoglutarate as cosubstrate, ascorbic acid (vitamin C) as an electron donor o Protocollagen is also glycosylated and assumes an -helical configuration o 3 -helical chains form a right handed superhelical structure called procollagen Excreted extracellularly, procollagen o undergo polymer and cross - linking forming collagen filaments o ProtocollagenProcollagenCollagen filamentsCollagen fibrilsCollagen fibers
Tensile Strength of the wound Tensile strength of the o Measurement of its of its load capacity per unit area o Constant Breaking strength of the of the wound o The force required to break it regardless of its of its dimension of the thickness of tissues of tissues o Dependent of the o Collagen fibers are largely responsible for tensile strength of wounds o All wounds gain strength at approximately the same rate during first 14-21 days o In the skin, peak tensile strength is achieved at approximately 60 days after injury Tensile strength of a of a wound reaches o only about 80% of the of the original unwounded skin y
y
Maturation and Remodeling Phase Begins approximately 3 weeks post injury Collagen synthesis and degradation are accelerated no net increase in the wound collagen content y y
5
y
y
y
y
of previously synthesized Reorganization of previously collagen More stable and permanent cross links o are established Gain in tensile strength o Normal Type I: Type III collagen ratio of 4:1 is achieved Remodeling continues for 6 12 months post - injury Initially indurated, raised and pruritic scar becomes a mature scar Large number of ne of new capillaries o growing into wound regress and disappear Water content of tissue of tissue return to o normal Avascular and acellular scar o
Epithelialization of epithelial Proliferation and migration of epithelial cells adjacent to the wound Begins within 1 day of injury of injury of the epidermis at the Seen as thickening of the wound edge Reepithelialization is complete in less than of approximated 48 hours in the case of approximated incised wound In split thickness graft donor or superficial partial thickness burns, healing consists primarily of re of re epithelialization with minimal or no fibroplasias and granulation tissue formation Process: o Mobilization Epithelial cells immediately adjacent to wound enlarge, flatten and detach from neighboring cells and the basement membrane Migration o Loss of contact of contact inhibition, so cell moves away from its original neighboring cells. Cells flow away from the adjoin cells until they meet cells from the opposite side of the of the wound Mitosis o Fixed basal cells divide to replace the migrating cells while the migrating cells, in turn, also divide and multiply o Cellular differentiation Upon reepithelialization, the orderly progression from the basal mitotic cells through layers of differentiated keratinocytes to stratum corneum is again established y
y y
y
y
y
Wound Contraction of the repair process that closes a gap Part of the in soft tissue y
y
y
y
The
area of the of the wound is decreased by this action (healing by secondary intention) In contrast to contracture which is: o Undesirable effect of wound healing of the scar that may result in o Shortening of the deformities o May be due to contraction, fibrosis, or other tissue damage Myofibroblasts o Cells postulated to be responsible for wound contraction (still controversial) o Cytoskeletal structure ( smooth muscle actin) Well formed intercellular attachments o such as desmosomes and macula adherens
Fetal Wound Healing Lack of scar of scar formation More of a of a regenerative process with minimal or no scar formation Transition wound rd of the 3 o Occurs at the beginning of the trimester o Scarless healing but there is a loss of ability to generate appendages y y
y
Difference between adult and fetal wound healing Wound environment Fetus is bathed in sterile and o temperature stable fluid environment o However scarless healing can occur outside the amniotic fluid environment Inflammation o Reduced fetal inflammation due to the immaturity of the of the immune system Less PMNs and macrophages o Growth Factors o Absence of TGF Studies have shown that neutralizing TGF using antibiotics reduce scar formation in adult wounds o Wound matrix Fetal fibroblasts produce more collagen Excessive and sustained hyaluronic acid production in the fetus which may aid in the orderly organization of collagen of collagen y
y
y
Factors Affecting Wound Healing Oxygen o Fibroblasts are oxygen sensitive o Collagen synthesis occurs at PO2 is >40mm Hg Fibroblast and collagen production can o be stimulated by maintaining the of hyperoxia wound in a state of hyperoxia Hematocrit Mild to moderate normovolemic o anemia does not adversely affect y
y
6
y
y
y
y
y
y
y
y
collagen synthesis, unless the hematocrit falls below 15% Infection 5 Threshold >10 microorganisms/gm of o tissue or lower for hemolytic streptococcus o Decrease leukocyte chemotaxis and migration, phagocytosis, and intercellular killing o Impairs angiongenesis and epithelialization o Promotes collagenolytic activity resulting in decreased wound strength and contraction Radiation therapy of small vessels o Stasis and occlusion of small of ionizing o Direct adverse effect of ionizing radiation on fibroblast proliferation o Decreased in wound tensile strength and total collagen deposition o Recommendation is thorough debridement and coverage with a well vascularized flap Chemotherapy Generally decrease fibroblast o proliferation and wound contraction Smoking Nicotine: produce vasoconstriction and o limit capillary blood flow necessary for distal perfusion o Carbon monoxide: Forms carboxyhemoglobin; shifts oxygen hemoglobin curve to left Age o Tensile strength and closure rates decrease with age o The phases of healing of healing are protracted as one gets older Nutrition o Protein energy malnutrition impairs fibroplasias and diminish collagen deposition Malnutrition correlates with high rates o of wound complication o Nutritional intervention (parenteral or enteral), can reverse the effect of malnutrition or postoperative starvation on healing Steroids o Inhibit wound macrophages o Interferes with fibrogenesis, angiogenesis, and wound contraction Vitamin A o Stimulates collagen deposition and reepithelialization o Contributes to increased breaking strength of wounds o Vitamin A deficiency retards wound repair o Vitamin A restores monocytic inflammation that has been replaced by anti inflammatory steroids
Daily oral dose of 25,000 IU Topical application of 200,000 IU every 8 hours Vitamin C Essesntial cofactor in synthesis of o collagen o Scurvy or Vitamin C deficiciency Failure of collagen of collagen synthesis and cross linking Formation of defective of defective capillaries leading to local hemorrhages Muscle weakness, joint eakness, joint and muscle aches, rashes on legs, and bleeding gums o Excessive concentrations do not promote supranormal healing Zinc of several enzymes o Constituent of several essential for normal wound healing Low serum levels impair epithelial and o fibroblastic proliferation o Studies have shown that zinc enhances wound healing only when there is a pre existing zinc deficiency state Diabetes mellitus o Results in reduced inflammation, angiogenesis, and collagen synthesis Large and small vessel diseases o contributes to local hypoxemia o Careful preoperative correction of blood sugar levels improves outcome of wounds in pts. o Insulin restores collagen synthesis and granulation tissue formation to normal levels
y
y
y
Excessive Excessive Wound Wo und Healing/Abnormal Scars Widespread scars Hypertrophic scars Keloids A preferred scar is one that has matured rapidly without contracture or increase in width, and without forming more collagen than necessary for its strength. y y y
Wide spread scar Typically flat, wide, and often depressed of continued tension in the Consequence of continued dermis (covered by epidermis instead) and mobility of the of the wound y y
7
Wound Care and Management lassific ation C la Acute wounds Lacerations, tissue avulsions, surgical o wound o Heal in a predictable manner and time table o Result in a well healed wound with few or no complications hronic wounds C hronic Wounds that have not healed in 3 o months o Risk factors include repeated trauma, poor tissue perfusion, excessive inflammation I schemic schemic arteri al al ul cers cers of blood supply Due to lack of blood of peripheral Symptoms of peripheral vascular disease like rest pain, intermittent claudication, and color changes On examination, diminished or absent pulses and poor formation of granulation of granulation tissue Management is revascularization of tissue of tissue and wound care enous st asis ul cers cers V enous Due to venous stasis and hydrostatic back pressure of dermal caps result Distention of dermal in leaking of fibrinogen of fibrinogen and the formation of perivascular of perivascular fibrin cuffs that impede oxygen delivery to tissue Lipodermatosclerosis y
y
Hypertrophic scar y
y y
Elevated above skin surface but limited to the initial boundaries of the of the injury Tend to regress spontaneously Responsive to treatment
Keloids y
y y
y
y y
Extend beyond the border of the of the original wound Lack regression Commonly in presternal, deltoids, back, and earlobes Resistant to treatment, often worse after surgery Familiar predilection Young age and dark skin color
Management is compression and wound care Di abetic wounds Neuropathy, foot deformity, and ischemia Unrecognized injury from ill fitting shoes, foreign body, and trauma Severe micro- and macrovascular impairment Mangement includes adequate control of blood of blood glucose,
Treatment modalities Intralesional corticosteroind injection Silicone sheet/gel: shown to have some positive effect on scar remodeling Irradiation and pressure Surgery (high recurrence rate) y y
y y
8
control of infection of infection by debridement and antibiotic
y
y
lcer Decubitus/Pressure U l c er
When soft tissue is compressed between bony prominence and external surface Excessive pressure causes capillary collapse and impedes the delivery of nutrients of nutrients to tissues Risk factors include immobility, chronic conditions, altered mental status Pressure ulcer at the trochanteric area
Stages of Pressure Ulcer Formation of intact skin I. Non blanching erythema of intact II. Partial thickness kin loss Full thickness skin loss but not thru III. fascia Full thickness skin loss with involvement IV. of muscle of muscle and bone ins U l lcers: c ers: Marjol ins Malignant transformation of long of long standing chronic ulcer Squamous or basal carcinomas
y
Local y
y
y
y
y
y
Types of Wound Closure Primary intention or p primary c l losure o sure o Wound edges are immediately approximated using sutures, staples, or tape
c l losure: o sure: in contaminated wounds, wound edges are approximated after a delay of several days ntention or Second ary C l l osure osure Second ary I ntention o Due to bacterial contamination and tissue loss, the wound is left open to heal by granulation tissue formation and contraction erti ary C l losure o sure T erti Wound is closed by bringing tissues o from elsewhere in the form of graft of graft or flap See below: scar formation for the different types of closure. of closure. o
y
y y
primary Delayed p
Wound Care of events surrounding Obtain a history of events injury Examine the wound to assess its depth and configuration, extent of non-viable of non-viable tissues as well as the presence of FB of FB and contaminants of the edges of Irrigation and debridement of the the wound under local anesthesia o High pressure (70 PSI) irrigation with normal saline Gentle handling of tissues of tissues o Marginally viable flap of skin of skin and tissues o should be resected or revascularized before wound repair Use of povidone of povidone iodine, hydrogen o peroxide impair wound healing Antibiotic administration Must appropriate for organism o o Must be given at proper time, in proper dose, via proper route Eg, elective surgery, contaminated, traumatic wounds Tetanus prophylaxis Planning the type and timing of wound repair 9
o
Dressing Mimics the barrier role of epithelium of epithelium Primary dressing vs. secondary dressing o Primary dressing Placed directly on the wound Absorption of secretions, of secretions, prevent dessication, infection and adhesion of secondary of secondary dressings o Secondary dressing Placed over the primary dressing Provide compression and occlusion and form a barrier Absorbent dressing o Cotton, wool, and sponge o Should absorb without getting soaked through, as this would permit entrance of bacteria of bacteria from the outside Non adherent dressings o Impregnated with paraffin, petroleum jelly, water soluble jelly soluble jelly o Used as primary dressing Medicated dressings Used as a drug delivery system o May contain benzoyl peroxide, zinc o oxide, neomycin, bacitracin, and chlorhexidine o Shown to increase epithelializaton by 28% y y
Full thickness skin grafts Entire epidermis and dermis of contraction Higher rate of contraction (contraction after harvesting) but lower rate of secondary of secondary contraction (contracture Best coverage of lesion of lesion on the face and over jts. over jts. Donor site should be closed primarily, but size is limited
y
y
y
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: from another species. Eg, porcine y y y
y
Skin Replacements onv ention entional skin gr a fts C on it or pa parti al al thickness skin gr a fts o S pl it Epidermis and part of dermis of dermis Donor site heals by epithelialization Lower rate of primary of primary contraction (contraction after harvesting) but higher rate of secondary of secondary contraction (contracture) ontr action: centripetal movement C ontr of the of the whole thickness of surrounding skin reducing scar ontr acture: the physical C ontr constriction or limitation of function as the result of Contraction across joints, mouth, eyelid) (scars across joints, y
Skin substitutes Provide coverage for extensive wounds with limited availability of autografts of autografts of tissue engineering; novel Product of tissue materials are combined with living cells Disadvantages include limited survival, high cost, and the need for multiple applications Types: o tured e pithel i ial a a l autogr a fts C ul tured Keratinocytes harvested from a biopsy of patients of patients skin are cultured with fibroblasts and growth factors, and grown into sheets. tured all ogenic ogenic ker atinocyte gr a ft o C ul tured From cadavers and unrelated donors tured bi la layer skin equi val val ent ent o C ul tured Acellular (collagen or synthetic materials) elements that act as scaffolding for cell growth and migration and cellular elements to reestablish lost tissue. Eg, Biobrane y
y
y
y
10
Important points of the cause of injury, of injury, the body 1. Regardless of the responds in a predictable sequence of events of the biology of normal of normal 2. An understanding of the wound healing guides the physician in the care of wounds. 3. Several local and systemic factors affect wound healing; controlling these factors will ensure that the normal processes of wound healing shall proceed efficiently 4. In the care of wounds, the physician must remember the basic surgical principles: gentle handling of tissues, of tissues, maintenance of aseptic technique, ensuring tissue viability, and avoidance of tension. of tension.
End of transcription of transcription In all these things we have complete victory through him who loved us. Romans 8:37-39
11
