20 vol. 23, no. 1 january 2001 v ce refereed peer review ... · are large, have extensive tissue...

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20 Vol. 23, No. 1 January 2001 Article #2 (1.5 contact hours) Refereed Peer Review FOCAL POINT KEY FACTS Because contraction is a major component of the healing process for open wounds, practitioners should know which factors enhance or inhibit contraction. Wound Contraction: Basic and Clinical Factors Auburn University Johnson & Johnson Steven F. Swaim, DVM, MS Skillman, New Jersey Sherri H. Hinkle, BS, LVT Dino M. Bradley, DVM, MS, PhD ABSTRACT: Wound contraction, the centripetal or concentric reduction in size of an open wound, is essential to second-intention healing. Wound contraction is caused by movement of fibroblasts in granulation tissue collagen and pulling forces of granulation tissue myofibrob- lasts on the skin edges. Contraction can result in complete and normal wound closure; howev- er, abnormalities may cause incomplete and abnormal healing. Numerous factors affect wound contraction, including the amount of skin surrounding the wound; pressure on the wound; and medications, dressings, and surgical procedures that enhance or inhibit wound contraction. Other factors that can affect wound contraction are movement, exposed bone, in- fection, radiation therapy, and wound shape. Wound contraction is a major component of second-intention wound heal- ing, and the center for contraction is granulation tissue. This article reviews sec- ond-intention wound healing, granulation tissue components and their entry into wounds, and basic clinical information about wound contraction. SECOND-INTENTION WOUND HEALING Second-intention wound healing is the healing of an open wound by contrac- tion and epithelialization. 1 This method is generally used to treat wounds that are large, have extensive tissue damage, and are contaminated or infected. Prima- ry closure, delayed primary closure, or secondary closure of these wounds is not advisable. 1,2 In many cases, this practical and economical method can be used to attain wound closure as long as adequate wound care is provided. 1 This healing method allows progressive, gradual debridement to ensure that only devitalized tissue is removed. It also provides optimal wound drainage. 2 GRANULATION TISSUE The basic components of granulation tissue are fibroblasts, macrophages, cap- illaries, and collagen. 2,3 Fibroblasts in wounds originate from undifferentiated mesenchymal cells in adjacent connective tissue, primarily from the adventitia of small blood vessels. Under the influence of cytokines released by platelets and macrophages, they usually appear about the third or fourth day after injury and CE V Wound contraction is caused by a combination of movement of fibroblasts in collagen and the pulling forces of myofibroblasts on the skin edges, p. 22. Appropriate splinting and bandaging can eliminate pressure over wounds in certain areas and are necessary for wound contraction, p. 24. Drugs can be used to either stimulate or inhibit wound contraction, p. 26. Immobilization of wounds over flexion surfaces and in areas in which movement causes shearing and tension helps prevent wound contracture and impaired wound contraction, respectively, p. 29. Topical medications and dressings have been described to stimulate the growth of granulation tissue coverage over exposed bone and thus enhance wound contraction, p. 30.

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Page 1: 20 Vol. 23, No. 1 January 2001 V CE Refereed Peer Review ... · are large, have extensive tissue damage, and are contaminated or infected. Prima-ry closure, delayed primary closure,

20 Vol. 23, No. 1 January 2001

Article #2 (1.5 contact hours)Refereed Peer Review

FOCAL POINT

KEY FACTS

HBecause contraction is a majorcomponent of the healingprocess for open wounds,practitioners should knowwhich factors enhance orinhibit contraction.

Wound Contraction:Basic andClinical FactorsAuburn University Johnson & Johnson

Steven F. Swaim, DVM, MS Skillman, New Jersey

Sherri H. Hinkle, BS, LVT Dino M. Bradley, DVM, MS, PhD

ABSTRACT: Wound contraction, the centripetal or concentric reduction in size of an openwound, is essential to second-intention healing. Wound contraction is caused by movement offibroblasts in granulation tissue collagen and pulling forces of granulation tissue myofibrob-lasts on the skin edges. Contraction can result in complete and normal wound closure; howev-er, abnormalities may cause incomplete and abnormal healing. Numerous factors affectwound contraction, including the amount of skin surrounding the wound; pressure on thewound; and medications, dressings, and surgical procedures that enhance or inhibit woundcontraction. Other factors that can affect wound contraction are movement, exposed bone, in-fection, radiation therapy, and wound shape.

Wound contraction is a major component of second-intention wound heal-ing, and the center for contraction is granulation tissue. This article reviews sec-ond-intention wound healing, granulation tissue components and their entryinto wounds, and basic clinical information about wound contraction.

SECOND-INTENTION WOUND HEALINGSecond-intention wound healing is the healing of an open wound by contrac-

tion and epithelialization.1 This method is generally used to treat wounds thatare large, have extensive tissue damage, and are contaminated or infected. Prima-ry closure, delayed primary closure, or secondary closure of these wounds is notadvisable.1,2 In many cases, this practical and economical method can be used toattain wound closure as long as adequate wound care is provided.1 This healingmethod allows progressive, gradual debridement to ensure that only devitalizedtissue is removed. It also provides optimal wound drainage.2

GRANULATION TISSUEThe basic components of granulation tissue are fibroblasts, macrophages, cap-

illaries, and collagen.2,3 Fibroblasts in wounds originate from undifferentiatedmesenchymal cells in adjacent connective tissue, primarily from the adventitia ofsmall blood vessels. Under the influence of cytokines released by platelets andmacrophages, they usually appear about the third or fourth day after injury and

CE

VV

n Wound contraction is caused bya combination of movement offibroblasts in collagen and thepulling forces of myofibroblastson the skin edges, p. 22.

n Appropriate splinting andbandaging can eliminate pressureover wounds in certain areas andare necessary for woundcontraction, p. 24.

n Drugs can be used to eitherstimulate or inhibit woundcontraction, p. 26.

n Immobilization of wounds overflexion surfaces and in areasin which movement causesshearing and tension helpsprevent wound contracture andimpaired wound contraction,respectively, p. 29.

n Topical medications anddressings have been described tostimulate the growth ofgranulation tissue coverage overexposed bone and thus enhancewound contraction, p. 30.

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advance into a wound by using thefibrin of the clot as a scaffold alongwhich to grow. The fibroblasts havecytoplasmic extensions along theirleading edge called lamellipodia, whichadhere to the underlying scaffold of fi-bronectin-coated fibrin and collagen.By chemotaxis, haptotaxis, and con-tact guidance, the fibroblasts advanceinto the wound.2–4 Macrophages phago-cytize necrotic tissue and debris. In ad-dition, these cells are multipotentialand release a large number of cyto-kines that direct the repair stage ofhealing. Macrophages remain active un-til the repair stage ceases.2

The capillaries of granulation tissueoriginate from the capillaries in thewound. Three days after injury, vascu-lar buds form from preexisting vessels(primarily venules) in the wound.Macrophage- and platelet-derived cy-tokines and growth factors stimulatethis neovascularization. The endothelialcells of these vessels are activated andbegin to produce enzymes that breakdown the vascular basal membrane. En-dothelial cells then migrate through the resulting gapand form tubular structures that grow in the direction ofthe wound. These structures connect with other suchstructures, leading to vascular loop formation.4–6 Bloodflow then begins in the looplike structures. Vessels devel-op and differentiate, but loops with no blood flowregress.2,4–6 The new vasculature grows into the woundimmediately behind the fibroblasts at a rate of 0.4 to 1.0mm/day. The endothelial cells produce a plasminogenactivation, resulting in fibrinolysis and breakdown of theoriginal fibrin network in the wound. The fibrin is re-placed by collagen.2

The fibroblasts de-posit new collagen afterthey first secrete fi-bronectin and proteo-glycans, which consti-tute an amorphousmilieu of ground sub-stance in the wound.This process is neces-sary before collagendeposition and peaksat 3 to 5 days after in-jury. At 4 to 5 days,tropocollagen molecules

are extruded from the fibroblasts afterthe amino acids (i.e., proline and ly-sine) in the amino acid chains of thecollagen have been hydroxylated.These molecules aggregate to form im-mature collagen fibrils near the fibrob-last. Molecular bonding of the fibrilsresults in collagen fibers. The earlytype III collagen in wounds is quicklyreplaced by more mature type I colla-gen. As inter- and intramolecularbonding of collagen molecules contin-ues, wound strength increases; and asthe collagen content of the wound in-creases, the ground substance and fi-broblast content decrease.2

The new tissue that is formed con-stitutes granulation tissue (Figure 1). Ithas a bright red granular appearanceand begins to appear in a wound 3 to6 days after injury. In small wounds itis present under a scab, whereas inlarge open wounds its formation is vis-ible. The granular appearance of thetissue comes from the capillary loopsor knuckles. Each granule is composedof a raised capillary loop capped pri-

marily by fibroblasts and macrophages. Anastomosisbetween these new vessels and preexisting vessels withinthe wound tissue is considerable.2,3 Granulation tissuefills in wound depressions, serves as a barrier against in-vasion of underlying tissue by surface microorganisms,1

and is the seat of wound contraction.

WOUND CONTRACTIONClinical Basics

Wound contraction is the centripetal or concentric re-duction in size of an open wound (Figure 2). The full-

Compendium January 2001 Small Animal/Exotics 21

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Figure 1—The basic components ofgranulation tissue are fibroblasts, mac-rophages, capillary loops, and collagen.

Figure 2A Figure 2B

Figure 2—(A) An open wound in the repair stage of healing with a healthy bed of granulation tissue.(B) A few days later, the edges have moved closer together as the wound contracts.

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thickness skin that surrounds the wound is advanced in-ward by its margins so that the area to be covered by ep-ithelium is reduced or eliminated. No new skin is formedin the process, which is independent of epithelial-ization.2,5,7,8 In dogs, visible contraction usually begins 5to 9 days after wound infliction.2 In areas in which skin isloosely attached to underlying structures, wound contrac-tion can result in complete wound closure, even withlarge wounds.1,2 The rate of wound contraction varies de-pending on the wound location. In horses, a 400-mm2

skin defect in the flank area has been reported to contractat 0.8 to 1 mm/day, whereas similar lower-limb woundscontracted at 0.2 mm/day.7 One report4 states that con-traction begins approximately 1 week after injury andprogresses at a fairly constant rate of 0.6 to 0.8 mm/day.

Wound contraction stops when contact inhibition oc-curs as like-tissue cells from the sides of the wound comein contact with each other or when tension from the sur-rounding skin equals or exceeds the force of con-traction.2,3,7 Restrictive fibrosis can also mechanically im-pair skin advancement.1 Although skin surrounding awound may be lax, contraction may stop before woundedges meet because of poor granulation tissue quality.3

The presence of exuberant granulation tissue in a woundhas been found to impede contraction in horses.7

To assess wound contraction results, the skin aroundthe wound can be manually pushed or gentle tractioncan be applied with nontraumatic forceps to determineits degree of laxity.1,2 Skin tension is best evaluated be-

fore the wound has entered the inflammatory stage ofhealing when edema and enlargement of the underlyingtissue occur because these changes impair skin maneu-vering over the wound, especially on the limbs.2 If skinadjacent to the wound is lax enough, unimpededwound contraction can be expected. If a wound re-mains partially open when this maneuver is performed,this area may close by epithelial cell migration oncecontraction is complete.1 Any deformity (e.g., jointflexion or distortion of the surrounding tissue causedby manipulating the skin edges into apposition) will re-main if the wound is allowed to heal by contraction. Insuch cases, skin grafts or flaps are indicated for woundrepair9 (Table I).

Cause of ContractionUntil recently, wound contraction has been attribut-

ed to the contraction of myofibroblasts. Today, fibro-blasts are believed to play a major role in wound con-traction. Fibroblasts move into a defect early,proliferate, and lay down collagen. As fibroblasts movewithin the surrounding collagen,10,11 they reorganize itby cell membrane tractional forces,2,10–14 thus consoli-dating the tissue into a smaller unit and pulling theskin with it.10,11 This process could be likened to thetread on a toy tank or caterpillar tractor as it moves onloose carpet. The tread simulates the moving fibroblastcell membrane, and the carpet simulates the collagen-containing wound matrix. In effect, the collagen is being

22 Small Animal/Exotics Compendium January 2001

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TABLE IIndications for Skin Grafts and Flapsa

Wound Type Reconstructive Procedure

Indolent pocket woundFollowing revision of involved tissue Possible use of omental flapFollowing excision of overlying nonhealing skin Skin flap or full-thickness mesh graft

Large open wound over a joint flexion surface in which Skin flap or full-thickness mesh graftcontraction would cause contracture deformity

Wound in which contraction will result in contractural Skin flap or full-thickness mesh graftdeformity of adjacent tissue or structures (e.g., eyelids,anus)

Limb wound in which contraction will not heal the wound Full-thickness mesh or strip graftand delicate epithelium will cover the area

Nonhealing axillary wound in cats Rotation flap or omental flap followed by closure

Irradiated wound tissue with a compromised blood supply Skin flap or full-thickness mesh graft afterdebridement to vascularized tissue or placement of a muscle flap

aSee Pavletic1 and Swaim and Henderson2 for detailed information on performing skin grafts and flaps in dogs and cats.

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gradually moved to the wound’scenter as the fibroblasts migrate2

(Figure 3). A recent study15 ofopen wounds on rats showed thatcontraction was caused by fibrob-lasts; therefore, myofibroblastswere not needed for contraction.

Because myofibroblasts are pres-ent in wounds, the question arisesas to their function. It has been the-orized that fibroblasts may developmuscle characteristics in responseto demand.15 Development of thesecells is an attempt by the fibroblaststo resist the outward tension on thewound edges2,10 (Figure 3). This ac-tivity appears to predominate laterin wound contraction.2,5 Thus fi-broblasts and collagen play majorroles in wound contraction becauseof their interaction.

CLINICAL FACTORSAFFECTING WOUNDCONTRACTIONAmount of Surrounding Skin

The amount of skin and its at-tachment to underlying tissue affectwound contraction. During second-intention healing, anabundance of skin that has loose connective tissue attach-ments to underlying tissue allows for closure of even largewounds (Figure 4). On dogs and cats, skin is loose andabundant on most of the body, particularly on the neckand trunk. Skin is less abundant on the limbs, tail, andhead. With dogs in particular, the quantity and elasticityof skin differ among breeds. In addition, an animal’sphysical condition has a bearing on the amount of looseskin that is present. Forexample, the trunk of athin animal has moreloose skin than doesthat of an obese dog.2

As wounds contract,the surrounding skin isstretched, thinned, andplaced under tension;but this state does notpersist. Gradually, newcollagen is laid downin the dermis, tensionis relieved, and the der-mis regains thickness.In addition, new ep-

ithelial cells are produced in areasunder tension until the skin attainsfull thickness. This procedure iscalled intussusceptive growth.1,16

Insufficient skin surrounding awound can present problems forcontraction in second-intentionhealing. In some areas, the skinwill contract as far as possible andthe remaining wound area will healwith a thin delicate epithelium.These wounds often occur on thelimbs and frequently require a skingraft to provide durable tissue2

(Table I).In indolent pocket wounds, suffi-

cient skin surrounding a woundand healthy granulation tissue arepresent; however, wound contrac-tion does not occur. Granulationtissue is present on the dermal sur-face of skin around the wound andon the underlying muscle fascia; butthe two surfaces, which are not at-tached, form a granulation-tissue–lined pocket. Because the dermalsurface tissue fails to bond with theunderlying granulation tissue, the

skin does not adhere to the wound margins. Thus woundcontraction forces cannot advance the skin; however, asgranulation tissue on the dermal surface of the skin causescontraction, the skin margins begin to arc or curl under(Figure 5). Epithelial cells from the skin migrate beneathits margin onto the dermal surface. As the granulation tis-sue matures and collagen deposition increases, circulationdecreases and the pocket supports bacterial growth.1 Clo-sure of indolent pocket wounds requires infection control,

Compendium January 2001 Small Animal/Exotics 23

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Figure 3—Theory of the cause of wound con-traction. (1) Fibroblast activity occurs in earlycontraction; cell membrane tractional forcesconsolidate collagen in the wound center,pulling skin inward. (2) This is similar to thetread movement of a toy caterpillar tractor as itbunches up loose carpet. (3) Myofibroblast ac-tivity occurs in later contraction; myofibroblastsattach to the wound edge and exert tension toresist the outward skin tension.

Figure 4A Figure 4B

Figure 4—(A) Large open wound on the trunk of a cat. (B) The wound is almost healed by contrac-tion. (From Swaim SF, Henderson RA: Small Animal Wound Management, ed 2. Baltimore, Williams& Wilkins, 1997, p 28; with permission.)

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excision of the scarred and oftencurled-under skin edge, and carefulincision of the granulation tissue onthe dermal surface of the skin. Thisprocess is necessary to preserve cuta-neous circulation while allowing theskin to straighten and advance overthe wound for closure.1 In cases inwhich wounds do not lend them-selves to closure in this manner, theuse of skin flaps or grafts may beconsidered (Table I). Another op-tion would be to use omental flapsto bring vascularized tissue into thearea before closure.17–19

PressureExternal pressure on a wound

can affect wound contraction. Ban-dage pressure can splint the woundedges, pushing them centrifugally.Planimetric studies20–23 have shownthat open wounds actually increasein size during the first 7 days com-pared with the size of the freshlycreated wound. This increase hasbeen attributed to the pressure of the bandages used in treat-ment.20–23 After granulation tissueforms in the wound, the contrac-tile properties of fibroblasts andmyofibroblasts can overcome thebandage pressure and wound con-traction can proceed. Rigid castimmobilization of open woundsover areas of potentially maximalmovement (i.e., flexion surface ofthe tarsus) inhibits wound con-traction. This inhibition has beenattributed to the passive pressureof the cast against the wound.9 Al-though rigid immobilization ofthese wounds in extension couldhelp prevent wound contracturedeformities, cast pressure againstthe wound may impede healing.Thus immobilization should beprovided by some means that does not place pressureon the wound (e.g., a rigid splint on the side of thelimb opposite the wound; Figure 6).

Bandage pressure on a wound over a bony prominencecan interfere with wound contraction. Placing additionalpadding in a bandage to help prevent pressure over an

open wound over a bony promi-nence can further deter woundcontraction. Additional padding insuch an area increases pressurewhen the outer layers of the ban-dage are applied, especially an elas-tic bandage material.2 This pressurecounteracts the action of the fi-broblasts and myofibroblasts thatare trying to cause wound contrac-tion. Therefore, it is better to keeppressure off the area by redistribut-ing it around the wound. Alleviat-ing pressure can be accomplishedby using a modified minor donutpad in the bandage. The pad canbe made by folding over several lay-ers of soft cast padding (SpecialistCast Padding, Johnson & Johnson,Raynham, MA)a and cutting a holein the center of the pad to accom-modate the bony prominence2

(Figure 7).Wounds on paw pads can cause

wound enlargement. Most pad lac-erations would be sutured; withlarge pad wounds that do not lendthemselves to suturing, however,open wound management is indi-cated. As pressure is placed on thepads when the animal bears weight,the tissue performs its normalshock-absorbing function andspreads out, causing the edges of thewound to be pushed apart. With anopen wound, enlargement can re-sult before granulation tissue forms,thereby counteracting wound con-traction.3,24,25 Open paw padwounds should be bandaged and asplint applied to the paw to mini-mize pressure on the pads thatwould interfere with wound con-traction. A localized crutch can beapplied to the paw. After applying abandage to a paw, two metalsplints—one on the palmar/plantar

surface and one on the dorsal surface—should be taped to

24 Small Animal/Exotics Compendium January 2001

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Figure 5—Indolent pocket wound. (A) Thepocket of the wound is lined with smooth gran-ulation tissue (stippled cross-section of tissue).(B) The skin margin curls under as granulationtissue on the dermal side of the skin contracts.

Figure 6—(A) Passive pressure from a cast overan area of potential maximal movement (tarsalflexion surface) inhibits wound contraction(small arrows). (B) Splint immobilization on theextensor surface with a light bandage on theflexion surface and around the splint helps pre-vent passive pressure.

Figure 7—(A) Bandage pressure on a woundover a bony prominence (calcaneal process) in-hibits wound contraction (small arrows). (B) Amodified minor donut bandage over the bonyprominence helps prevent the pressure.

aThe products and preparations mentioned in this article forwound prevention and treatment are those described in refer-enced articles. Other common products/preparations may nothave the same mode of action or give the described results ofthe referenced products/preparations.

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the outer bandage surface. The cupsof the metal splints should face eachother and extend beyond the distalend of the bandage about 1 inch.This clam shell bandage/ splintplaces the paw in a toe-dancing pos-ture so weight is not borne on thepads.26 The splint allows fasterwound contraction (Figure 8). Incases of sutured wounds, the splinthelps keep the sutures from tearingthrough the skin, which may occurwhen animals—especially largedogs—bear weight on the pad.

Medications, Dressings, Irradiation, and Surgical Procedures

When treating second-intention wound healing, prac-titioners should know which medications, dressings, ir-radiation, and surgical procedures enhance wound con-traction and which slow wound contraction. In somecases, it is desirable to enhance contraction whereas inothers contraction should be inhibited (Table II).

Wound Contraction Stimulants/EnhancersNew medications and dressings have become avail-

able or can be prepared (i.e.,equine amnion) that stimulatewound healing. Part of the actionof these products is to enhancegranulation tissue formation andthus wound contraction.

Acemannan is a polydispersedβ-(1,4) acetylated mannan, avail-able in a topical hydrogel (Car-ravet Wound Dressing®, Carring-ton Laboratories, Irving, TX) thatstimulates macrophages to secreteinterleukin-1 and tumor necrosisfactor–α. These secretions enhance

fibroblast proliferation and angiogenesis (capillaries) inwounds.27 These structures are the components of granu-lation tissue. This medication has been found to stimu-late the healing of paw pad wounds by wound contrac-tion and epithelialization when applied as a topical gel24

or injected intralesionally.25 In addition, daily applicationof freeze-dried acemannan (Carra™ Sorb M, CarringtonLaboratories) has been shown to stimulate granulationtissue formation over exposed bone, which in turn resultsin enhanced wound contraction.28 This factor is impor-tant in treating distal limb degloving wounds.

A glycyl-L-histadyl-L-lysine tripeptide copper complextopical medication is a chemoattractant for mast cells andmonocytes/macrophages. Topical tripeptide (Iamin-VetSkin Care Gel®, Procyte Corp., Redmond, WA) andtetrapeptide-copper–complex medications have advancedopen wound healing to include the contraction portionof healing in dogs as compared with untreated controlsand placebo-treated wounds, especially during the first 7days of treatment.21 Both acemannan and tripeptide cop-per complex are active in stimulating granulation tissueformation and thus wound contraction.27

Occlusive hydrogel dressings have been reported tohave varying effects on granulation tissue formationand wound contraction. One dressing (Curity Confor-ma Gel®, Kendall Canada, Petersborough, Ontario,Canada) used on dog limb wounds caused exuberantgranulation tissue; despite this, it stimulated woundcontraction on the limbs.29 Conversely, wound contrac-tion was delayed when a hydrogel dressing (BioDres®,DVM Pharmaceuticals, Miami, FL) was used on trun-cal wounds in another canine study.30 Occlusive dress-ings retain bacteria that are on the wound surface;therefore, bacteria cannot be absorbed into outer ban-dage layers and away from the wound. It would be sus-pected that such an environment would promote thedevelopment of wound infection; evidence suggests,however, that this is not the case31 and that occlusionmay reduce the incidence of wound infection.32 In ad-

26 Small Animal/Exotics Compendium January 2001

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Figure 8—(A) Pressure on a paw pad woundpushes wound edges apart (arrows). (B) A clamshell bandage/splint places the paw in a verticaltoe-dancing posture so weight is not borne onthe pads.

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dition, occlusive bandages have been recommended forwounds in the repair stage of healing with a healthybed of granulation tissue. Such tissue is a barrier againstsystemic infection.2 Topical placement of equine am-nion on open wounds has been found to enhancewound contraction of trunk wounds on dogs.30

The effect of pulsed electromagnetic field radiationon open wound healing has been evaluated.22 This ther-apy indicated that early wound contraction occurred intreated wounds. Five days after surgery, untreated con-

trol wounds had enlarged, indicating bandage pressurehad pushed the edges apart; treated wounds had de-creased in size, indicating early formation of contractileelements (i.e., granulation tissue) in wounds.22

An adjustable horizontal mattress suture has been de-scribed for placing gradual tension on wound edges aftergranulation tissue has formed and contraction has be-gun, thus enhancing contraction. The technique hasbeen used primarily on distal limb wounds with place-ment of a continuous intradermal monofilament suture

Compendium January 2001 Small Animal/Exotics 27

H Y D R O G E L D R E S S I N G S n E Q U I N E A M N I O N n H O R I Z O N T A L M A T T R E S S S U T U R E

TABLE IIMedications, Dressings, Irradiation, and Surgical Procedures that Affect Wound Contraction

Wound contraction stimulants/enhancers

Medication, Dressing, Irradiation, or Procedure Recommended Use a

AcemannanTopical hydrogel Wounds under a bandage; use with a topical antibacterial

Injectable Intralesional injection; days 0, 3, and 6 in wounds in whichbandage loss would result in topical medication being worn orlicked off (e.g., paw pad wounds)

Freeze-dried gel Wounds with exposed bone under a bandage; use incombination with a topical antibacterial

Tripeptide copper complex gel Wounds under a bandage; use in combination with a topicalantibacterial

Occlusive hydrogel dressings Limb wounds in the repair stage of healing

Equine amnion Trunk wounds

Pulsed electromagnetic field radiation Wounds in which enhanced contraction is indicated

Adjustable horizontal mattress suture Distal limb wounds on dogs; use in combination with topicalhydrogel, freeze-dried gel, or tripeptide copper complex gel

Skin stretchers Large wounds on dogs; use in combination with topicalhydrogel, freeze-dried gel, or tripeptide copper complex gel

Wound contraction inhibitors

Medication, Dressing, or Procedure Recommended Use and Effect of Usage

Corticosteroids Topically on wounds around body orifices to help preventcontracture constriction

Silver sulfadiazine Topical antibacterial that may prolong contraction

Mafenide acetate Topical antibacterial that may prolong contraction

Hydrocolloid dressings Occlusive wound dressing that may prolong contraction

Porcine small intestine submucosa Topical wound dressing that may prolong contraction

Thick skin grafts and flaps Early placement in wound management on large wounds overjoint flexion surfaces or wounds in which open healing willresult in surrounding tissue distortion

aRecommendations are based on our general experience.

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in the skin edges. At the ends of the suture, an arrange-ment of a button and a removable fishing weight shouldbe used to hold tension on the suture after its daily tight-ening. The attachment of the skin edge to the granula-tion tissue should not be disturbed; thus wound contrac-tion is not disturbed but enhanced by suture tension.2,33

A skin stretching device can be used to stretch skinsurrounding a wound during the course of open woundmanagement,1 thus making skin available for the con-traction process. This device consists of self-adherentskin pads, which are affixed to the skin around thewound, and elastic cables, which are used to connectthe skin pads.

Wound Contraction InhibitorsCorticosteroids, which primarily affect the inflamma-

tory stage, retard wound healing. This slowing is car-ried into the early repair stage of healing with a signifi-cant delay in angiogenesis, fibroblastic proliferation,and the synthesis of proteoglycans and collagen.34 Thuscorticosteroids impair the epithelialization, woundstrength, and closure of open wounds.34,35 Epithelializa-tion and contraction are both inhibited by glucocorti-coids at any time during healing.36 This factor shouldbe considered when an animal that is being treated foran open wound must be given corticosteroids. Beer andcolleagues37 have shown that higher glucocorticoid con-centrations inhibit the later repair stage functions ofhealing. The use of corticosteroids for inhibition ofgranulation tissue formation and wound contractionand contracture can be beneficial. For instance, topicalsteroids could also be used to treat open woundsaround orifices in which contraction and/or contrac-ture could result in orifice stenosis.

Silver sulfadiazine, a topical antibacterial, is com-monly used to treat open wounds, especially burns. Al-though this medication enhances epithelialization inthe open wound healing process, it has been shown tohave a negative effect on fibroblasts and thus impedeswound contraction.2,38 The topical burn therapy maf-enide acetate has been shown to have the same effect.38

Once wound infection is controlled, the effect of thesedrugs on wound contraction and epithelialization is oflittle concern if graft or flap reconstruction is to beused. However, if open wound healing is to be em-ployed, the contraction of such wounds may be pro-longed, and the delicate epithelium may need protec-tion during the healing process.

Factors associated with antineoplastic drugs that mayhave a negative effect on wound healing/contraction arereduced mesenchymal cell proliferation, thrombocy-topenia and leukopenia with reduced quantities ofplatelets and inflammatory cell–derived growth factors,

and susceptibility to infection caused by leukopenia.35

The anorexia, negative nitrogen balance, and weightloss associated with these drugs negatively affect heal-ing. Some chemotherapeutic agents damage the gas-trointestinal tract and interfere with nutrient absorp-tion, thus decreasing the substrate available for collagensynthesis.39 These factors should be considered whentreating open wounds in the presence of chemothera-peutic agents.

Radiation therapy used in the treatment of neoplasiacan impair wound healing, resulting in chronicwounds. This therapy causes a progressive obliterativeendarteritis of wound microvasculature, which resultsin tissue ischemia. In addition, it directly affects fibro-blast proliferation, causing permanent damage.39 Ab-normal microvasculature and fibroblasts would equateto poor granulation tissue and impaired wound con-traction. In addition, decreased blood supply and fibro-sis may limit the delivery of platelets and inflammatorycells to the wound. Factors available to stimulatechemotaxis, mitogenesis, and collagen synthesis are,therefore, decreased. Thus irradiated open wounds aredifficult to heal by second intention because of im-paired angiogenesis, wound contraction, fibroplasia,and epithelialization.1 The lack of inflammatory cellsmay also permit bacteria to proliferate more readily,39

also impairing wound healing. If acute or chronic ulcers result from radiation thera-

py, staged debridement should be performed over alonger period than occurs with other types of woundsbecause necrosis and persistent infection may progress.Only visible necrotic tissue should be debrided. Debrid-ing to bleeding edges is unreliable because of ongoingprogressive endarteritis. Overly aggressive debridementmay result in removal of normal tissue.2 Because openwound healing with contraction will not be optimal inirradiated tissue, skin grafts or flaps should be consid-ered for proper healing (Table I). Flaps take their bloodsupply with them. However, if a graft is to be used, thewound must be debrided back to healthy vascular tissueto help ensure graft revascularization.1,2 The use of skinflaps should be the first choice for reconstruction.

In addition, muscle flaps have been described1 andcould be used to take the blood supply to a chronic ra-diation wound if the wound is located such that one ofthe muscle flaps can be used on it. Skin grafts could beplaced on muscle flaps. New medications that stimulatewound healing should be considered to help establish ahealthy bed of granulation tissue to support a graft (seeWound Contraction Stimulants/Enhancers section).

Wound contraction can be minimized or preventedby replacing skin immediately with thick skin grafts orflaps. Skin grafts or flaps can inhibit contraction more

28 Small Animal/Exotics Compendium January 2001

T O P I C A L A N T I B A C T E R I A L n A N T I N E O P L A S T I C D R U G S n R A D I A T I O N T H E R A P Y n D E B R I D E M E N T

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effectively than can split-thickness grafts, especially ifthey are applied before contraction has started.10 Whentreating large open wounds over flexion surfaces, skingrafts or flaps should be considered to prevent woundcontracture deformities9 (Table I). If joint flexion isnecessary for apposition of wound edges, wound mo-bility will likely result in deformity because the joint ispulled into flexion as contraction takes place.9 Thus askin graft or flap is indicated.

Hydrocolloid dressings are water-impermeable with a

polyurethane outer cov-ering separated from thewound by a hydrocol-loid material. The hy-drocolloid adheres to theskin around the woundand is dissolved over thewound itself.40 A caninestudy41 found that hy-drocolloid dressings(DuoDerm®, ConvaTec,Princeton, NJ and Der-maheal™, E.R. Squibb& Sons, Princeton, NJ)tended to enhancewound epithelialization

but slowed wound contraction. This effect was attribut-ed to the strong adherent nature of the dressing: It ad-hered to the skin around the wound, splinting it suchthat contractile forces of the granulation tissue could noteffectively contract the wound.41 This type of wounddressing may not be desirable on wounds in which con-traction with open wound healing is preferred.

One study42 on rodents showed that using porcinesmall intestinal submucosa as a dressing for openwounds slowed wound contraction.

Compendium January 2001 Small Animal/Exotics 29

Figure 9A Figure 9B

Figure 9—Contracture deformity of the carpus (A) and coxofemoral area (B) caused by wound con-traction on the joints’ flexion surface. (Part B From Swaim SF, Henderson RA: Small AnimalWound Management, ed 2. Baltimore, Williams & Wilkins, 1997, p 28; with permission.)

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MovementWound movement can affect

wound contraction. Extensivewounds over flexion surfaces ofjoints that heal by second intentionare subject to excess scarring, jointdeformity, and impaired mobilitybecause wound contraction resultsin wound contracture1–3,5,8 (Figure9). This occurrence can be ex-plained by a combination of twophenomena. A buckling phe-nomenon has been described inwhich the tissue of a flexion surfacewound is folded together or buckledwith the predominant flexion kinet-ics of the joint. As these fibers foldon one another, the inter- and in-tramolecular bonding of the fibersoccurs as the tissue gluing phe-nomenon9,43 (Figure 10).

With the tissue gluing phenomenon, contraction occurs,and collagen fibers become shorter in the wound and fusedinto a contracted mass by mucopolysaccharides of thewound’s ground substance.9,44 Immobilizing a large woundover a flexion surface in extension may help prevent suchcontracture deformities. A splint can help to keep the tissuestretched mechanically during the active phase of woundcontraction.10 A skin flap or graft should also be consideredfor such wounds (Table I). Thus immobilization helps pre-vent wound contracture mechanically as well as providingthe immobility for a graft or flap to heal in place. When agraft is healing, immobility allows vascular connections tobe made between the graft and its bed.

The desired result of wound healing is for one side ofthe wound to heal to the opposite side. Thus wound im-mobilization is needed for proper tissue bonding to occur.Immobilization can play a major role in wound healingin areas of considerable movement, especially if they areto heal as open wounds. Movement interferes withwound contraction. An example of movement interferingwith open wound contraction is a wound over the exten-sor surface of a joint (e.g., carpus or stifle) where jointflexion pulls wound edges apart (Figure 11A). Meticuloussuturing, followed by casting or splinting to prevent jointflexion, is necessary for proper healing.2

Another area in which movement presents a problemis the axillary region of cats. The wound usually resultsfrom the cat manipulating one forelimb up through itscollar, and the limb remains in this position for an ex-tended time. Thus the collar exerts pressure in the axil-lary region and cuts into the tissue. After the collar isremoved, open wound healing with wound contraction

is often impeded because of thetension and shearing forces ofmovement as one side of thewound moves against the other asthe cat walks (Figure 11B). Insuch cases, meticulous suture im-mobilization of deep wound tis-sue, use of an intradermal or sub-cutaneous suture, and finallytension-apposition sutures in theskin may allow healing. Immobi-lization of the limb in a Velpeauflexion bandage is also indicated.In some cases, a rotation flapfrom the adjacent thoracic skincan be used for wound closure2

(Table I). Omental flaps may alsobe used to provide vascular tissuein the area before closure, thusenhancing healing.18,19

Exposed BoneExposed bone in wounds is common. In small animals,

bone is often exposed in distal limb degloving woundsthat result from automobile trauma. Exposed bone in awound has an indirect influence on healing by inhibitingwound contraction and epithelialization.45,46 Wounds withexposed bone that are to be allowed to heal by second in-tention require a bed of granulation tissue for healing toprogress.2,45 Granulation tissue forms from the vascularizedsoft tissue at the periphery of a wound and gradually ad-vances over the bone.

Means of enhancing granulation tissue coverage overbone are beneficial to the contraction aspect of second-intention healing. Topical medications and dressingshave been described for this purpose. Another tech-nique that stimulates granulation tissue to form overexposed bone entails drilling small holes in the bone(forage) to the level of the marrow cavity to allow clotformation over the bone. The clot, which is well at-tached at the drill holes, serves as a matrix for the fi-broblast ingrowth and neovascularization of granula-tion tissue.1,2,47

EscharsEschars are composed of full-thickness degenerated skin

overlying a wound, usually a burn (Figure 12). An escharmay serve as a biologic bandage to protect the wound.However, the eschar may harbor bacteria beneath it, andits edge may splint the wound edge by its attachment.Therefore, wound contraction by underlying granulationtissue is impeded. The eschar should be removed as soonas the animal is stable enough for anesthesia.1,2,10 Allowing

30 Small Animal/Exotics Compendium January 2001

J O I N T S U R F A C E n B U C K L I N G P H E N O M E N O N n O M E N T A L F L A P S

Figure 10—Buckling and tissue gluing phenome-na resulting in a flexion contracture deformity.(A) Exaggerated diagram of a collagen fiber inan open wound on the flexion surface of a ra-diohumeral joint. (B) Joint flexion folds thefiber together or buckles it. Inter-and intra-molecular bonding glues the fiber together toshorten it, resulting in impaired joint mobility.

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with thorough woundlavage.48 Staged debridement(as needed), lavage, and pro-tective bandaging should bedone daily. Culture and sen-sitivity evaluation of thewound may be necessary.Topical and systemic antibi-otics are indicated.

Wound ShapeAs wounds contract, the

edges move toward the cen-ter and the shape of the re-sulting scars depends on theoriginal wound shape. Skinelasticity and mobility arenot the same in all direc-tions, thus skin will notmove to the same extent orat the same rate. The amountof movement will depend onskin availability on differentsides of the wound. On someareas of an animal (e.g., thetrunk), skin may be freelyavailable on all sides of thewound. In other areas (e.g.,the limbs), skin will be rela-tively sparse on all sides; andin some places it may onlybe available on certain sidesof the wound but not onothers (e.g., a wound adja-cent to a body structure suchas an eye or anus).

When skin is equally avail-able on all sides of a wound,triangular, rectangular, andsquare wounds heal cen-tripetally, with the cornersmoving less than the sides as the sides move centrally.The results are a three-armed

stellate scar, a double-V–shaped scar with the points ofthe V’s pointing toward each other and connected by athin line, and a four-armed stellate scar, respectively.Circular wounds also heal centripetally; however, asthe wound edge approaches the center of the wound,the skin will start to mechanically interfere with itsown movement. The result is a crumpled, unpre-dictable healing pattern with a slower healing rate2,7

(Figure 13).

Compendium January 2001 Small Animal/Exotics 31

S K I N A V A I L A B I L I T Y n C I R C U L A R W O U N D S n H E A L I N G P A T T E R N S

Figure 11—Wound management and dis-ruption. (A) A wound over the carpal ex-tension surface disrupts from tension withjoint flexion (curved arrows). (B) A woundin the axillary region disrupts from tensionand shearing forces (small arrows) as thelimb moves (large arrows). (From SwaimSF, Henderson RA: Small Animal WoundManagement, ed 2. Baltimore, Williams &Wilkins, 1997, p 145; with permission.)

Figure 12—Eschar over a wound. The area wherethe eschar attaches to the edge of the wound cansplint the edge and impede wound contraction(arrowheads).

the wound to heal as an open woundwould enable contraction to take placequickly.

InfectionInfection can inhibit wound healing to

include the contraction of openwounds. The presence of bacterial colla-genases, decreased wound pH and oxy-gen tension, interference with blood supply, and me-chanical interference by exudate are factors contributingto the lack of healing.48 With infection, the inflammato-ry stage of healing is prolonged and the healing processis retarded. The epithelialization, contraction, and colla-gen deposition do not occur or occur in a limited fash-ion, and healing does not take place until infection isunder control.35 When infection occurs, debridement ofdebris and necrotic tissue should be performed along

Figure 13—Healing process of various-shapedwounds by wound contraction: (A) triangular,(B) rectangular, (C) square, and (D) circular.(From Swaim SF, Henderson RA: Small AnimalWound Management, ed 2. Baltimore, Williams& Wilkins, 1997, p 7; with permission.)

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About the AuthorsDr. Swaim is affiliated with the Department of Clinical Sci-ences and the Wound Healing/Reconstructive SurgeryProgram of the Scott-Ritchey Research Center, Collegeof Veterinary Medicine, Auburn University, Alabama. Mrs.Hinkle is also associated with the Wound Healing/Recon-structive Surgery Program of the Scott-Ritchey ResearchCenter. Dr. Bradley is associated with the Wound HealingTechnology Resource Center, Johnson & Johnson, Skill-man, New Jersey.

REFERENCES1. Pavletic MM: Basic principles of wound healing, in Atlas of

Small Animal Reconstructive Surgery, ed 2. Philadelphia, WBSaunders Co, 1999, pp 11–63.

2. Swaim SF, Henderson RA: Small Animal Wound Manage-ment, ed 2. Baltimore, Williams & Wilkins, 1997, pp. 1–51,87–190, 295–370.

3. Lee AH, Swaim SF: Granulation tissue: How to take advan-tage of it in management of open wounds. Compend ContinEduc Pract Vet 10(2):163–171, 1988.

4. Fowler D: Principles of wound healing, in Harari J (ed): Sur-gical Complications and Wound Healing in the Small AnimalPractice. Philadelphia, WB Saunders Co, 1993, pp 1–31.

5. Asmussen PD, Söllner B: Wound Care: Principles of Healing.Stuttgart, Germany, Druckerei Kohlhammer, 1993, pp.24–50.

6. Whalen CF, Zetter BR: Angiogenesis, in Cohen IK, Diegel-mann RF, Lindblad WJ (eds): Wound Healing: Biochemicaland Clinical Aspects. Philadelphia, WB Saunders Co, 1992,pp 77–95.

7. Stashak TS: Equine Wound Management. Philadelphia, Lea &Febiger, 1991, pp. 1–18.

8. Mast BA: The skin, in Cohen IK, Diegelmann RF, LindbladWJ (eds): Wound Healing: Biochemical and Clinical Aspects.Philadelphia, WB Saunders Co, 1992, pp 344–355.

9. Swaim SF, Lee AH, Henderson RA: Mobility versus immo-bility in the healing of open wounds. JAAHA 25:91–96,1989.

10. Rudolph R, Vande Berg J, Ehrlich HP: Wound contractionand scar contracture, in Cohen IK, Diegelmann RF, Lind-blad WJ (eds): Wound Healing: Biochemical and Clinical As-pects. Philadelphia, WB Saunders Co, 1992, pp 96–114.

11. Berry DP, Harding KG, Stanton MR, et al: Human woundcontraction: Collagen organization, fibroblasts and myofi-broblasts. Plast Reconstr Surg 102:124–131, 1998.

12. Ehrlich HP: Wound closure: Evidence of cooperation be-tween fibroblasts and collagen matrix. Eye 2:149–157, 1988.

13. Stopak D, Harris AK: Connective tissue morphogenesis by fi-broblast traction. I. Tissue culture observations. Dev Biol90:383–398, 1982.

14. Ehrlich HP, Rajaratnam JB: Cell locomotion forces versuscell contraction forces for collagen lattice contraction: an invitro model of wound contraction. Tissue Cell 22:407–417,1990.

15. Ehrlich HP, Keefer KA, Myers RL, et al: Vanadate and theabsence of myofibroblasts in wound contraction. Arch Surg134:494–501, 1999.

16. Billingham RE, Medawar PB: Contracture and intussuscep-

tive growth in healing of extensive wounds in mammalianskin. J Anat 89:114–123, 1955.

17. Ross WE, Pardo AD: Evaluation of an omental pedicle ex-tension technique in the dog. Vet Surg 22:37–43, 1993.

18. Brockman DJ, Pardo AD, Conzemius MG, et al: Omentumenhanced reconstruction of chronic nonhealing wounds incats: Techniques and clinical use. Vet Surg 25:99–104, 1996.

19. Bright RM: Surgical management of nonhealing wounds incats. Sci Proc Amer Anim Hosp Assoc Ann Mtg, 248–251,1998.

20. Lee AH, Swaim SF, Yang ST, et al: Effects of gentamicin so-lution and cream on the healing of open wounds. Am J VetRes 45:1487–1492, 1984.

21. Swaim SF, Bradley DM, Spano JS, et al: Evaluation of multi-peptide-copper complex medications on open wound healingin dogs. JAAHA 29:519–525, 1993.

22. Scardino MS, Swaim SF, Sartin EA, et al: Evaluation of treat-ment with a pulsed electromagnetic field on wound healing,clinicopathologic variables, and central nervous system activi-ty in dogs. Am J Vet Res 59:1177–1181, 1998.

23. Scardino MS, Swaim SF, Sartin EA, et al: The effects ofomega-3 fatty acid diet enrichment on wound healing. VetDermatol 10:283–290, 1999.

24. Swaim SF, Riddell KP, McGuire JA: Effects of topical medi-cations on the healing of open pad wounds in dogs. JAAHA28:499–502, 1992.

25. Swaim SF, Vaughn DM, Kincaid SA, et al: Effects of locallyinjected medications on healing of pad wounds in dogs. Am JVet Res 57:394–399, 1996.

26. Swaim SF: Bandaging and splinting techniques, in Bistner SI,Ford RB, Raffe MR (eds): Handbook of Veterinary Proceduresand Emergency Treatment, ed 7. Philadelphia, WB SaundersCo, 2000, pp 549–571.

27. Swaim SF, Gillette RL: An update on wound medicationsand dressings. Compend Contin Educ Pract Vet 20(10):1133–1145, 1998.

28. Bradley DM: The Effects of Topically Applied Acemannan onthe Healing of Wounds with Exposed Bones. PhD Dissertation,Auburn University, Alabama, 1998.

29. Morgan PW, Binnington AG, Miller CW, et al: The effectof occlusive and semiocclusive dressings on the healing ofacute full-thickness skin wounds on the forelimbs of dogs.Vet Surg 23:494–502, 1994.

30. Ramsey DT, Pope ER, Wagner-Mann C, et al: Effects ofthree occlusive dressing materials on the healing of full-thickness skin wounds in dogs. Am J Vet Res 56:941–949,1995.

31. Gilchrist B, Hutchinson JJ: Does occlusion lead to infec-tion? Nurs Times 86:70–71, 1990.

32. Hutchinson JJ, Lawrence JC: Wound infection under occlu-sive dressings. J Hosp Infect 17:83–94, 1991.

33. Scardino MS, Swaim SF, Henderson RA, et al: Enhancingwound closure on the limbs. Compend Contin Educ PractVet 18(8):919–951, 1996.

34. Levenson SM, Demetriou AA: Metabolic factors, in CohenIK, Diegelmann RF, Lindblad WJ (eds): Wound Healing:Biochemical and Clinical Aspects. Philadelphia, WB SaundersCo, 1992, pp 248–273.

35. Lawrence WT: Clinical management of nonhealing wounds,in Cohen IK, Diegelmann RF, Lindblad WJ (eds): WoundHealing: Biochemical and Clinical Aspects. Philadelphia, WBSaunders Co, 1992, pp 541–561.

36. Stephens FO, Dunphy E, Hunt TK: Effect of delayed ad-ministration of corticosteroids on wound contraction. Ann

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Surg 173:214–218, 1971.37. Beer HD, Fassler R, Werner S: Glucocorticoid-regulated

gene expression during cutaneous wound repair. VitamHorm 59:217–239, 2000.

38. Leitch IO, Kucukcelebi A, Robson MC: Inhibition ofwound contraction by topical antimicrobials. Aust N Z JSurg 63:289–293, 1993.

39. Laing EJ: The effects of chemotherapy and radiation onwound healing, in Harari J (ed): Surgical Complications inWound Healing in the Small Animal Practice, Philadelphia,WB Saunders Co, 1993, pp 125–141.

40. Haimowitz JE, Margolis DJ: Moist wound healing, in Kras-ner D, Kane D (eds): Chronic Wound Care: A Clinical SourceBook For Health Care Professionals, ed 2. Wayne, PA, HealthManagement Publications, 1997, pp. 49–56.

41. Lee AH, Swaim SF, Yang ST, et al: The effects of petrola-tum, polyethylene glycol, nitrofurazone, and a hydroactivedressing on open wound healing. JAAHA 22:443–451,1986.

42. Prevel CD, Eppley BL, Summerlin DJ, et al: Small intestinalsubmucosa: Utilization as a wound dressing in full-thicknessrodent wounds. Ann Plast Surg 35:381–388, 1995.

43. Brody GS, Peng STJ, Landel RF: The etiology of hyper-trophic scar contracture: another review. Plast Reconstr Surg67:673–684, 1981.

44. Baur PS, Barratt G, Linares HA, et al: Wound contractions,scar contractures, and myofibroblasts: A classical case study.J Trauma 18:8–22, 1978.

45. Bradley DM, Swaim SF, Stuart SW: An animal model forresearch on wound healing over exposed bone. Vet CompOrthop Traumatol 11:131–135, 1998.

46. Hurwitz DJ: Osseous interference of soft tissue healing. SurgClin North Amer 64:699–704, 1984.

47. Swaim SF, Pope ER: Early management of limb deglovinginjuries. Semin Vet Med Surg (Small Anim) 3:274–281,1988.

48. Mason LK: Treatment of contaminated wounds, includingwounds of the abdomen and thorax, in Harari J (ed): Surgi-cal Complications in Wound Healing in the Small AnimalPractice, Philadelphia, WB Saunders Co, 1993, pp 33–62.

1. The four components of granulation tissue area. lymphocytes, eosinophils, capillary loops, and colla-

gen.b. fibroblasts, macrophages, capillary loops, and colla-

gen.c. fibroblasts, neutrophils, capillary buds, and ground

substance.d. basophils, eosinophils, arterioles, and tropocolla-

gen.e. dermacytes, macrophages, venules, and ground sub-

stance.

2. Which of the following is not associated with fibro-blasts?a. ground substance productionb. collagen productionc. wound contractiond. fibrin dissolutione. myofibroblasts formation

3. Which of the following statements regarding woundcontraction is true?a. Contraction is the centripetal or concentric reduc-

tion in size of an open wound.b. New dermis and epidermis are formed as wound

contraction takes place.c. Placement of a skin graft or flap has no effect on

wound contraction.d. Skin tension around a wound is best evaluated after

the wound has entered the inflammatory stage ofhealing.

e. Wound contraction is dependent on wound epithe-lialization.

4. The function of fibroblasts in wound contraction is toa. destroy the fibrin clot to allow the myofibroblasts

to cause wound contraction.b. provide preliminary contact guidance for myofi-

broblasts to enter a wound to cause wound contrac-tion.

c. have cell membrane movement within surroundingcollagen and consolidate tissue into a smaller unit.

d. enhance angiogenesis and provide a blood supplyfor new collagen.

e. provide a base for epithelialization.

5. Which statement regarding indolent pocket wounds isfalse?a. The skin edge of the pocket everts.b. Circulation in the pocket decreases.c. Wound contraction is slowed.d. Skin margins begin to curl under.e. The pocket supports bacterial growth.

6. When bandaging an open wound over a bony promi-nence, the best way to prevent pressure is toa. apply additional padding over the wound.b. immobilize the wound area with a splint or cast.c. place a modified minor donut bandage over the

area.d. use an occlusive hydrogel dressing to cushion the

wound.e. use a polyurethane sponge dressing over the wound.

7. ____________ is not a wound contraction stimulant/enhancer.a. Acemannanb. A semiocclusive adherent dressingc. An occlusive hydrogel dressingd. Equine amnion

Compendium January 2001 Small Animal/Exotics 33

CEARTICLE #2 CE TEST

The article you have read qualifies for 1.5 con-tact hours of Continuing Education Credit fromthe Auburn University College of VeterinaryMedicine. Choose only the one best answer to eachof the following questions; then mark your an-swers on the test form inserted in Compendium.

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e. Glycyl-L-histadyl-L-lysine tripeptide copper com-plex

8. Silver sulfadiazine topical medicationa. has antibacterial properties.b. slows wound epithelialization.c. impedes wound contraction.d. a and be. a and c

9. Wound contracture deformities occur in woundsa. over flexion surfaces of joints.b. that have excess epithelialization.c. over extension surfaces of joints.d. with irregular edges.e. over areas of little movement.

10. Eschars inhibit wound contraction bya. producing collagenases that dissolve collagen.b. allowing subeschar epithelialization.c. enhancing granulation tissue maturation.d. splinting the wound edges.e. allowing wound movement.

34 Small Animal/Exotics Compendium January 2001