wound healing lecture 2

8/18/2019 Wound Healing Lecture 2

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WOUND HEALING


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Anatomy of Skin

• Epidermis: – composed of several thin layers:stratum basale, stratum spinosum, stratum

granulosum, stratum lucidum, stratum corneum

– the several thin layers of the epidermis contain the

following:

a) melanocytes, which produce melanin, a pigment that

gives skin its color and protects it from the damaging

effects of ultraviolet radiation.

b) keratinocytes, which produce keratin, a water Repellent protein that gives the epidermis its tough,

Protective uality.


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Anatomy of Skin

• Dermis: – composed of a thick layer of skin that contains collagenand elastic fibers, nerve fibers, blood vessels, sweat

and sebaceous glands, and hair follicles.

• Subcutaneous issue: – composed of a fatty layer of skin that contains blood

vessels, nerves, lymph, and loose connective tissue

filled with fat cells


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!unction of Inte"ument

• #rotection: – intact skin prevents invasion of the body by bacteria• $ermore"u%ation:

• intact skin facilitates heat loss and cools the

body when necessary through the followingprocesses:

– production of perspiration which assists in cooling the

body through evaporation

– production of vasodilatation which assists in facilitatingheat loss from the body through radiation and

conduction

– production of vasoconstriction which assists in

preventing heat loss from the body through radiation

and conduction


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!unction of Inte"ument

• !%uid and E%ectro%yte &a%ance: – intact skin prevents the escape of water andelectrolytes from the body

• 'itamin D Synt$esis

• Sensation• #syc$osocia%


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(%assification of Wounds

• !) (%ean Wound: – "perative incisional wounds that follow nonpenetrating#blunt) trauma.

• $) (%ean)(ontaminated Wound: – uninfected wounds in which no inflammation is

encountered but the respiratory, gastrointestinal,genital, and%or urinary tract have been entered.

• &) (ontaminated Wound: – open, traumatic wounds or surgical wounds involving a

ma'or break in sterile techniue that show evidence ofinflammation.

• () Infected Wound: – old, traumatic wounds containing dead tissue and

wounds with evidence of a clinical infection #e.g.,

purulent drainage).


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(%assification of Wounds (%osure

• Hea%in" by #rimary Intention: – ll *ayers are closed. +he incision that heals by firstintention does so in a minimum amount of time, with no

separation of the wound edges, and with minimal scar

formation.

• Hea%in" by Secondary Intention: – eep layers are closed but superficial layers are left to

heal from the inside out. -ealing by second is

appropriate in cases of infection, ecessive trauma,

tissue loss, or imprecise approimation of tissue.

• Hea%in" by ertiary Intention: – lso referred to as delayed primary closure.


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Wound Hea%in"

– Inf%ammation occurs when the damagedendothelial cells release cytokines thatincrease epression of integrands in

circulating lymphocytes.

– -istamine, serotonin, and kinins cause vesselcontraction #thromboane), decrease in blood

loss, and act as chemotactic factors forneutrophils, the most abundant cells in theinitial $( hour period.


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Wound Hea%in"

– #ro%iferati*e p$ase occurs net, after theneutrophils have removed cellular debris andrelease further cytokines acting as attractingagents for macrophages.

– /ibroblasts now migrate into the wound, andsecrete collagen type 000.

– ngiogenesis occurs by (1 hours.

– +he secretion of collagen, macrophage

remodeling and secretion, and angiogenesiscontinues for up to & weeks.

– +he greatest increase in wound strength occursduring this phase.


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Wound Hea%in"

– +aturation p$ase is the final phase and

starts from the &rd week and continues for up

to 23!$ months.

– +his is where collagen 000 is converted to

collagen 0, and the tensile strength continues

to increase up to 145 of normal tissue.


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Sur"ica% Wound Infection

– Incisiona% infections identified by puru%ent or

cu%ture positi*e draina"e is iso%ated from any

structure abo*e t$e fascia in pro,imity to t$e initia%

-ound – Deep infections are c$aracteri.ed by puru%ent

draina"e from subfascia% drains/ -ound

de$iscence/ or abscess formation and in*o%*e

ad0acent sites manipu%ated durin" sur"ery1

– Wound De$iscence

– &reakdo-n of t$e sur"ica% -ound


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2isk !actors for SWI

– #atient3re%ated factors: – ge 6 74, se #female), weight #obesity)

– Presence of remote infections

– 8nderlying disease states – iabetes, 9ongestive heart failure #9-/)

– *iver disease, renal failure

– uration of preoperative stay hospitaliation

–6 ;$ hours, 098 stay – 0mmuno3suppression

–


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Sur"ery3re%ated factors:

– +ype of procedure, site of surgery, emergent

surgery

– uration of surgery #6743 !$4 min) – Previous surgery

– +iming of antibiotic administration

– Placement of foreign body

– -ip%knee replacement, heart valve insertion, shunt

insertion

– -ypotension, hypoia, dehydration, hypothermia


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Sur"ery re%ated factors:

– Patient preparation

–


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Wound3re%ated factors:

– ?agnitude of tissue trauma and devitaliation

– @lood loss, hematoma

– Aound classification

– Potential bacterial contamination

– Presence of drains, packs, drapes

– 0schemia

– Aound leakage


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Antibiotic Use

($aracteristics of an optima% antibiotic for

sur"ica% prop$y%a,is:

– Bffective against suspected pathogens

– oes not induce bacterial resistance

– Bffective tissue penetration

– ?inimal toicity

– ?inimal side effects

– *ong half3life

– 9ost effective


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Antibiotic Use

Appropriate antibiotic use for pre*ention of

SWI inc%udes t$e fo%%o-in": – ppropriate timing of administered agents

and repeated dosing based on length of procedure and antibiotic half3life 9onsider redosing

if procedure 6 ( hours

– ppropriate selection based on procedure

performed – ppropriate duration to avoid infection and

decrease potential for development of resistance


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Antibiotic Use

– Nose


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Antibiotic Use

– (o%on

B. coli, klebsiella, enterobacter, bacteroides spp,

peptostreptococci , clostridia

– &i%iary tractB. coli, klebsiella, proteus, clostridia

– 'a"ina


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Antibiotic Use

Identify -ound infection risk based on

patient4s sur"ica% procedure:

– (%ean: 9efaolin

– (%ean)contaminated: 9efaolin vs broad

spectrum #9efoitin or 9efotetan)

– (ontaminated: @road spectrum #9efoitin or

9efotetan) – Dirty: +herapeutic antibiotics


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!eta% Wound Hea%in"

– /etal wound healing proceeds without fibrosis or scar

formation in contrast to adult wound healing. +he

mechanisms responsible for this remarkable process

are mediated in part through a fetal wound

etracellular matri rich in hyaluronic acid #-).

– Proposed contributing factors to scarless healing in

fetal wounds are the presence of fewer neutrophils

and more monocytes during the inflammatory period,

different concentrations of cytokines, and a greaterproportion of type 000 collagen in contrast to adult

wounds.


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!eta% Wound Hea%in"

– +ransforming growth factor3b #+>/3 C, specifically,

low levels of +>/3C! and +>/3 C$ and high levels of

+>/3 C&Dprobably has a central role in scar

formation, and studies of its role are ongoing.

– *ow levels of platelet3derived growth factor #P>/), a

greater amount of epidermal growth factor #a mitogen

for epithelialiation), a faster rate of wound healing,

and a greater amount of hyaluronic acid in the

etracellular matri has been documented andsuggests a more efficient process of wound healing in

fetal models.


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Diabetic foot u%cers


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Sta"in" of #ressure U%cers

•


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Sta"e III


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-ypertrophic


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-ypertrophic


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-ypertrophic


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Feloids

• Raised and thickened. +his process etends beyond theboundary of the incision. – (ontinues -eeks to mont$s past t$e initia% insu%t1

• -igher incidence in frican mericans.

• ?ay have different incidences in different parts of thesame personI

– may not develop a keloid on the arm, yet has a keloid afterearring insertion.


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Feloids

• G"+B: hypertrophic and keloids are indistinguishable byplain -HB staining.

• +reatment: Pressure applied early may decrease the

etent of keloid formation.

• 0n'ection of triamcinolone, or corticosteroid in'ection maybe helpful.

• Bcision with intramarginal borders is reserved forintractable keloids, and used in con'unction with theabove.


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@urns

• re divided by depth of in'ury. 9lassically, and in someinstitutions the burn is organied by Jdegree:K

• !irst3de"ree: involve the epidermis and demonstrates

erythema and minor microscopic changes. Pain is ma'orcomplaint. Go scar is left. -ealing is complete in up to!4 days.

• Second3de"ree burns: involves all the epidermis andpart of the dermis.


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@urns

– $ird3de"ree: these full thickness burns arecharacteristically white, non3viable.

– +hey may demonstrate darkened brown orblack adipose tissue.

–


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@urns

• +he most important assessment of volume status and adeuatevolume administration is monitoring of the urine output.

• &urn 2esuscitation: ##ark%and !ormu%a) ( 5 @urn Aeight in kgfor $( hours, *actated RingerKs. >ive the first half in first 1 hours andthe net half in the net !7 hours.

• 8rine output is normally 4.=ml%kg, but for burns and trauma patients isat least !3!.= ml%kg%hour.

• 0nitial treatment of the actual burn is first debridement of the denudedskin with moist gaue.

• +his additionally aids in estimating volume of burn.

• 9overage with topical antibacterial agents is necessary.


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@urns

•


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0nvoluting -emangiomas

• ?ost common tumors that occur in

childhood, 2=5 of all hemangiomas that

are seen in childhood.

• +ypically present at birth or during $3&

weeks of life, grow at a rapid rate for (37

months, then involution begins and is

complete by =3; years of age.


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• +hese types include strawberry nevus, nevus

vasculosus, capillary hemangioma, and

cavernous hemangioma.

• +reatment is not usually indicated.

– "nly indicated if the lesions impair vision #eyelid), acondition that can lead to amblyopia.


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Goninvoluting -emangioma

• ?ost of these lesions are present at birth.

• +hey grow in proportion to the growth of the

infant, and persist into adulthood.

• 8nlike involuting, these are not true neoplasms,

but malformations of arterial and%or veins


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Gon3involuting -emangiomas

• +hese lesions malformations include:

– Port wine stains: most common, mainly occur

on face or neck. @est to observe, or lasersurgery.

– 9avernous -emangioma: more common on

head and neck. "bservation or in'ection ofsclerosing agents.


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Gon3involuting -emangiomas

Port Aine


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Eerrucae

• lso known as common warts, these lesions areseen in childhood and in young adults, typicallyon fingers and hands.

• +hese lesions appear as round or dome3shapedelevated masses with rough surfaces withmultiple villi like keratinied pro'ections.

• +hey may range from brown to gray to skincolored.


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Eerrucae

• +he etiology is by human papillomaviruses #over =4different types eist). +ypes !, $, (, and ; typically causeverrucae.

• reatment: is by electrodessication or liuid nitrogen.

•


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ctinic Feratoses

• ctinic keratoses are the most common precancerous skinlesions.

• ?ost commonly appear as single or multiple, slightly

elevated, scaly or warty lesions that are red to yellow,brown or black.

• "ccur most freuently on the face and backs of hands infair3skinned 9aucasians.

• pproimately !=3$45 become malignant, invade thedermis as suamous cell carcinomas.

• +reatment: curettement and electrodessication or =3/8.


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ctinic Feratoses


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+e%anoma

• ?elanocytes are cells of neural crest origin thatmigrate during fetal development to multiple sitesin the body, principally the skin.

• +hese cells are eposed to carcinogenic stimulithat result in malignant transformation to becomemelanoma.

• ?elanoma accounts for only (5 to =5 of all skin

cancers but causes the ma'ority of deaths fromskin malignancies. 0t is the eighth most commoncancer in the 8nited


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Epidemio%o"y and Etio%o"y

• +he incidence and outcome of melanoma are

related to multiple factors. ?elanoma is principally

a disease of whites, particularly those of 9eltic

ancestry. 0t is estimated that melanoma occurs $4times more often in whites than in blacks.

• +he median age of diagnosis is in the range of (=

to == years. +here is a significant incidence in the&rd and (th decades of life.


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Epidemio%o"y and Etio%o"y

• 0t is well established that eposure to sunlight

increases the risk of developing melanoma in

susceptible populations. +his is specifically

attributed to solar ultraviolet #8E%8E@) radiation.• dditional factors that increase the risk for

development of melanoma include fair skin,

dysplastic nevus #G) syndrome, eroderma

pigmentosum, a history of non3melanoma skincancer #G?


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#recursor Lesions and 2isk !actors

• 9ongenital nevi, Gs, iant congenital nevi are rare #! in $4,444

newborns) and carry an increased risk for

development of melanoma within the nevi


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?elanoma

•


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?elanoma

– Intraderma% ne*i: small spots to large

etensive areas, variable shape. "ften black

or brown and slightly elevated, and confined

to the dermis.

– (ompound ne*i: combination 'unctional and

intradermal.


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?elanoma

– &%ue ne*i: flat or dome3shaped, bluish3black usually

on hands arms, or face. ?ay resemble nodular

melanoma.

– Dysp%astic ne*i: are larger, up to =3!$ mm, have

macular and popular features, varied in color with pink

base, and have indistinct, irregular edges.

PRB98R


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?elanoma

• Symptoms: features that are suggestive of melanomaare the following

– 0rregular areas of differentiating color #black to brown

to tan with focal discoloration) – Rapid enlargement

– 0rregular edges

– Brosion, bleeding or crust formation

– Pruritis – *ocation: lesions on back and lower etremities

reuire close motoring.


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?elanoma

•


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me%anomaSuperficia% spreadin"

me%anoma


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Lenti"o +a%i"na


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Acra% Lenti"inous

Acra% %enti"inous

% Nodu%ar me%anoma


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me%anoma Nodu%ar me%anoma


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@reslowKs epth #old)

Thickness (mm) Recurrence or metastasis at

5 years


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M99 9lassification

Primary Tumor (T) Regional LN (N) TX Can not be assessed NX can not be assessed T0 No evidence of Tumor N0 No regional LN Mets Tis Melanoma in situ N1 Mets into 1 LN T1 Melanoma < 1mm N1a Microscopic Mets

with or without ulceration N1b Macroscopic Mets T1a Melanoma < 1mm, level N! Mets in ! or " regional LN

or level , No ulceration N!a Microscopic Mets T1b Melanoma


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Recommended ?argins for


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E*a%uation

for %ymp$atic

mappin" andSNL &,

E,cision: ?cm

+ar"ins -it$out

mappin"

E,cision: ?cm

mar"ins andmappin" and

SNL &,

Node

ne"ati*e

Node positi*e:

(omp%etion LN

dissection


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@asal 9ell 9arcinoma

• ?ost common skin cancer.

• *esions usually appear on face. ?ore common in menversus women.

• Btiology is eposure to ultraviolet raysI geographic areaswhere sun is plentiful and increased incidence in fair3skinned individuals.

• >rowth rate is very slow, locally invasive and may spreadto local tissues or penetrate to the bones of the face andthe skull. ?etastasis is rare.


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• +ypical appearance is small, translucent or shiny JpearlyNelevated nodules with telangiectatic vessels present.

•


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Hippocratic Oat$

“Primum Non Nocere”

(First Do Not Harm)


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@uestions

wound healing lecture 2

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