Activate Windows

Go to Settings to activate Windows.

PL9 Plastic Surgery Toronto Notes 2023

PHASE I [ PROCESS

1. Inflammatory Phase (Reactive) (Days1-6)

• Limits damage, preventsfurther injury

• Debris and organisms cleared via inflammatory response:

•Neutrophils(24-46 h)

•Macrophages:critical to wound healing by

orchestrating growth factorsfor collagen production

(48-96 h )

•Lymphocytes: role poorly defined (5-7 d)

1. Hemostasis- vasoconstriction + platelet plug

2.Chemotaxis-migration of macrophages and PMN

2. Proliferative Phase (Regenerative) (Oay 4- Week 3)

• Fibroblasts attracted and activated by macrophage

growth factors

• Reparative process:re-epithetialization. matrix synthesis,

angiogenesis(relievesischemia)

• Tensile strength beginsto increase at 4-5d

1. Collagen synthesis(mainly type III)

2.Angiogenesis

3. Epithehaluation

3 Remodeling Phase (Maturation) (Week 3-Year 1)

• Increasing collagen organization and stronger crosslinks

• Type I collagen replaces Type III until normal 4:1

ratio achieved

• Peak tensile strength at 60 d -80% of pre-injury strength

1. Contraction

2.Scarring

3.Remodeling of scar

Figure 13. Stages of wound healing

TYPES OF WOUND HEALING

Primary (1°) Healing (First Intention)

• definition: wound closure by direct approximation of edges within hours of wound creation (i.e. with

sutures,staples,skin graft, etc.)

• indication:recent (6-8 h,longer with facial wounds) wounds

• contraindications:animal/human bites, crush injuries,infection,long time lapse since injury'(>6-8

h),retained foreign body

Secondary (2°) Healing/Spontaneous Healing (Second Intention)

• definition: wound left open to healspontaneously (epithelialization occurs at 1 mm/d from wound

margins in concentric pattern, contraction (myofibroblasts), and granulation)- maintained in

inflammatory phase until wound closed;requires dressing changes

• indication: when 1° closure not possible or indicated (see Primary Healing)

Myofibroblasts are the cells responsible

for wound contraction

Tertiary (3°) Healing/Delayed Primary Healing (Third Intention)

• definition: intentionally interrupt healing process (e.g.with packing,sharp debridement), then

wound can be closed primarily at 4-10 d post-injury after granulation tissue has formed and there is

<105 bacteria/g of tissue

• indication: contaminated (high bacterial count),long time lapse since initial injury,severe crush

component with significant tissue devitalization, closure of fasciotomv wounds

• prolongation of inflammatory phase decreases bacterial count and lessens chance of infection after

closure

ABNORMAL HEALING

Hypertrophic Scar

• definition:scar remains within boundaries of original scar

• red, raised, widened, frequently pruritic

• common sites: back,shoulder,sternum

• treatment:scar massage, pressure garments,silicone gel sheeting,corticosteroid injection,surgical

excision if other options fail (however, may still recur)

Keloid Scar

• definition:scar grows outside boundaries of original scar

• red, raised, widened,frequently pruritic

• caused by:

• genetic factors (highest rates in Black, and Asian individuals)

• excess tension on wound or delayed closure (as in burn wounds)

• common sites: central chest, back,shoulders,deltoid, ear,angle of mandible

• treatment: multimodal therapy including: pressure garments,silicone gel sheeting, corticosteroid

injection, fractional carbon dioxide ablative laser,surgical excision if radiation to be performed within

the next 48 hours(however, this istypically very unsuccessful and there is often recurrence)

L J

+

Activate Windows

Go to Settings to activate Windows.

PL10 Plastic Surgery Toronto Notes 2023

Spread Scar

• characterized by having exactly the same order of collagen fibres as normal scars

• clinically, a typical spread scar is flat, wide, and often depressed

• treatment:surgical excision and closure

Chronic Wound

• wound fails to achieve primary wound healing within 4-6 wk

• common chronic wounds include:diabetic,pressure,and venousstasis ulcers

• treatment: need to address underlying cause of chronicity (i.e.infection, ischemia, metabolic

conditions, immunosuppression, radiation)

• Marjolin’

s ulcer:squamous cell carcinoma arising in a chronic wound secondary to genetic changes

caused by chronic inflammation.All chronic woundsshould be biopsied to rule out Marjolin’

s ulcer

Infected Wounds

Definitions

• the presence of bacteria within a wound may be divided into 4 categories:

contamination: the presence of non-replicating microorganisms within a wound

colonization:the presence of replicating microorganisms within a wound

critical colonization: increasing bacterial burden; have delayed healing

infection: the presence of >105 microorganismsin a wound without intact epithelium orsmall

amounts of a very virulent organism (e.g.GBS); have delayed healing and exhibit classic signs of

infection

signs of infection:redness,swelling,pain, clinically unwell

Management of Acute Contaminated Wounds (<24 h)

• cleanse and irrigate open wound with at least 150 cc of physiologic solution ( NS or RL) using sufficient

pressure (4 to 15 PSI)

• evaluate for injury to underlying structures (vessels, nerves, tendons, and bone)

• control active bleeding, irrigation, and debridement

• debridement: removal of foreign material, devitalized tissue, and old blood (always take a swab if you

suspect infection)

surgical debridement: blade and irrigation if indicated

• tetanus prophylaxis

• re-evaluate in 24-48 h to remove more dead tissue

if evidence of infection (i.e. erythema, warmth, pain, discharge), open infected portion of wound

by removing sutures,swab sample for culture and sensitivity, irrigate wound, and allow healing

by secondary intention via dressing use

risk factors for infection include:wound >8h,severely contaminated, immunocompromised,

involvement of deeperstructures (e.g.joints,fractures)

use systemic antibiotics if wound cultures are positive and there are signs of infection;tailor

antibiotics as cultures return

Risk Factorsfor Infection

• Virulence of the infecting

microorganism

• Amount of bacteria present

• Host resistance

• Immunocompromised host

Wound Exudate Characteristics

• Serous drainage (plasma):thin:dear

or light yellowish

• Sanguineous drainage (fresh blood):

bright red

. Serosanguincous drainage (mix ol

blood and serousfluid):thin and

watery: pale red to pink

• Purulent drainage (infection):thick

and opaque; white, yellow,or pale

green

Management of Late Contaminated Wounds (>24 h)

• tetanus prophylaxis

• irrigation and debridement

• systemic antibiotics if there are clinical signs of infection

• closure:final closure via secondary intention (most common), delayed wound closure (3° closure),

skin graft, or flap

Table 9. Risks for Tetanus Infection

Wound Characteristics Tetanus-Prone Not Tetanus-Prone

Time Since Injury

Depth of Injury

Mechanism of Injury

>< h <6 h

<1cm

Sharp cut(e.g.dean knife,dean glass)

>1cm

Crush, burn,gunshot,frostbite,puncture

through dothing.farming injury

Devitalized Tissue Present

Contamination (e.g.soil,dirt,saliva, grass) Yes

Retained Foreign Body

Not present

No

Yes No

+

Activate Windows

Go to Settings to activate Windows;

PL11 Plastic Surgery Toronto Notes 2023

Totnnus Prophylaxis in Routino Wound Mnnngoniont

,

ASSESS WOUND

1

1

( A clean, minor wound ] All other wounds (contaminated with dirt, feces, saliva,

soil;puncture wounds; avulsions; wounds resulting from

flying or crushing objects, animal bites, burns,frostbite)

'

t

*Has patient completed a primary

tetanus diphtheria series?

1

’

Has patient completed a primary

tetanus diphtheria series?

1

’

NO: YES NO/ YES UNKNOWN \ r UNKNOWN

Administer vaccine today ’"

'

l Was the most

Instruct patient to complete

series pel age-appropriate

vaccine schedule

r A

Administer vaccine

and tetanus

immune gobulin

(TIG) nowrA

**’

Was the most

recent dose

within the past

5 years?

recent dose

within the past

I I 10 years?

NO YES NO YES

T I I

Administer vaccine today fVaccine not needed today

~

) (Administer vaccine todayl

*l [Vaccine not needed today

Patient should receive

next dose at 10 year

J

^

interval after last dose

Patient should receive next

dose per age-appropriate

schedule

Patient should receive next

dose at 10 year interval

[after last dose

Patient should receive next

dose per age-appropriate

I [schedule

’ A primary series consists of a minimum of 3 doses of tetanus and

diphtheria containing vaccine IDTaFVDTP/Tdap/DT/Tdl

> Age appropriate vaccine:

•0T.il

* for infants and children6 weeks up to 7 years of age (or

0T pediatric if pertussis vaccine is contraindicated),

•Tetanus diphthoria lTd) toxoid for persons 7 9 years of age;and have recurved a Tdap previously. If TT is administered, an

>63 years of age; adsorbed TT product is preferred to fluid TT fall OTaP/DTP/T

•Tdap for persons 10 64 years of ago if using Adacel

’

** ’

or > 10 dap

'

0T/Td products contain adsorbed tetanus loxoidl

yoars of age if using Boostnx

'"’

,unless the person has 'Give TIC 250UIM for all ogos.It can and should bo given

received a prior dose of Tdap' simultaneously with the tetanus containing vaccine

> No vaccine or TIG is recommended for infants <6 weeks of age for infants <6 weeks of age. TIG (without vaccine)is recommended

with clean,minor wounds (and no vaccine is licensed for infants for 'dirty'wounds (wounds other than clean,minor)

<6 weeks of agel Persons who are HIV positive should receive TIG regardless of

tetanus immunization history

•Tdap* is preferred for persons 10 64 years of age if using Adacel

or >10 years of ago if using BaostrixTMwho have never received

Tdap

Td is preferred to tetanus toxoid (TTI for persons 7 9 years of age,

or >65 years of ago if only Adacol,M,

is available,or those who

’

Tdap vaccines:

•Adacel (Sanofil is licensed for persons 10 64 years of age

•Boosuix"1

’(GSK) is licensed for persons >10 years of age

’Brand names are used for the purpose of clarifying product characteristics and are notin any way an endorsement of either product

Figure 14. Tetanus immunization recommendations

BITES

• see Emergency Medicine, ER47

Dog and Cat Bites

• pathogens: Pasteurella mullocida,Staphylococcus aureus, Streptococcus viridans, Moraxclla species,

and Corynebactcrium species

• investigations

radiographs prior to therapy to rule out foreign body (e.g. tooth) or fracture

culture for aerobic and anaerobic organisms. Gram stain

• treatment:Clavulin* (amoxicillin + clavulanic acid) 500 mg PO q8 h started immediately

consider rabies prophylaxis if animal has symptoms of rabies or unknown animal

± rabies lg (20 IU/kg around wound, or IM) and 1 of the 3 types of rabies vaccines (1.0 mL IM

in deltoid, repeat on days 3, 7, 14, 28)

• irrigation with debridement

• healing by secondary intention is mainstay of treatment

• only consider primary closure for bite wounds on the face if large and done in OR; otherwise primary

closure is contraindicated

• contact Public Health if animal status unknown

Human Bites

• pathogens:Staphylococcus aureus > GAS> tikenella corrodens > Bacteroides

• serious condition, as mouth has 10 fmicroorganisms/mL, which can get trapped in joint space when

the overlying skin forms and air-tight covering ideal for anaerobic growth (e.g. fight bite injury when

fist unclenches) - can lead to septic arthritis

• investigations

radiographs prior to therapy to rule out foreign body (e.g.tooth) or fracture

culture for aerobic and anaerobic organisms, Gram stain

r i

l L

+

Activate Windows

Go to Settings to activate Windows.

PL12 Plastic Surgery Toronto Notes >023

• treatment

• if joint infected, urgentsurgical exploration of joint, drainage, and debridement of infected tissue

• otherwise,can be managed with I & D and antibiotic treatment in ER

• if due toMSSA.Cefazolin 2 g IV q8h or (if penicillin allergy or MRSA) vancomycin 15 mg/kg IV

ql2h + secondary closure

splint

Dressings

• dressing selection depends on the wound characteristics, goal of dressing,and surgeon preference

asthe wound progressesthrough healing, it will require different types of dressings;therefore,

routine inspection is recommended

principles of dressing clean vs.infected wounds

- clean wounds can be dressed with non-adherent dressing (which is non-adhering to

epithelialising tissue);requires secondary dressing

- infected wounds may need debridement, antibiotics,and antimicrobial dressings (i.e.

iodinegauze and silver-containing dressings)

moist vs.dry wounds

- purpose of dressingsshould be to promote moist wound healing i.e.moistening dry

wounds or drying (removing excess exudate/blood) wet wounds

wide-based vs.cavitary/tunneling wounds

- cavitary or tunneling wounds (i.e. through a fascial layer) can be packed with loose,

large, and radiopaque packing materials

negative pressure wound therapy uses wound dressings that apply subatmospheric pressure

to the wound site to promote blood (low to the region and enhance the healing process, (he

resultant pressure gradient promotes fluid transport from the wound bed and interstitial

space to reduce wound edema

indications:diabetic foot ulcers, reconstructive surgery, and following debridement of acute

or chronic wounds

contraindications:wounds with exposed vitalstructures(i.e.organs,blood vessels, vascular

grafts) and malignant tissue

Table 10. Wound Dressings and Their Use

Dressing Type Example Use

Low adherentdressings Jelonet.tullegras.mepilex,mepitel

Semipermeable films llefilm.legaderm,Siodusive

CombiDESH.Tegasorb.Aquace!

Flat and shallow wounds with low exudates

Wounds in difficult anatomicsites(ex:oxer joints)

Hydrocolloid sheets:flat,shallow wounds with low exudate:difficult

areas(elbow,heel,etc.)

Hydrocolloids

Hydrofibre:flat wounds,cavities,sinuses;medium - high exudate

wounds

Antimicrobial Acticoat,Avance. lodosorb locally infected wounds

Reconstruction

RECONSTRUCTION LADDER Reconstruction Ladder

Vascularized composite

Definition *—allotransplantation

•an approach to wound management with successively more complex methods of treatment

•surgeonsshould start with the least complex method and progressively increase in complexity as

appropriate

«

—Free flap

flap

a

—Random pattern flap

SKIN GRAFTS

*

—tissue expansion

Definition

•tissue composed of epidermis and varying degrees of dermis, that does not carry its own blood supply.

Survival requiresthe generation of new’

blood vessels from the recipientsite bed

Donor Site Selection

•must considersize, hair pattern, texture, thickness of skin, and colour (facial grafts best if taken from

“blush zones"

- harvest sites above clavicle where colour match for full thickness grafts is optimized

(e.g. pre/post auricular or neck))

•partial thickness grafts usually taken from inconspicuous areas (e.g. buttocks,lateral thighs, etc.)

«

—Full thicknessgraft

« Split thicknessgraft

„ Delayed closure

4

—Primary closure

Healing by secondary

* intention

(DTirtany Ni 2T4 2022

Figure15. Reconstructive ladder - in

order of increasing complexity +

Activate Windows

Go to Settings to activate Wirvrio

PL13 Plastic Surgery Toronto Notes 2023

Partial Thickness Skin Graft Survival

• initial stabilization of graft provided by fibrin network between recipient site and graft

• 3 phases ofskin graft "

take"

1. plasmatic imbibition: diffusion of nutrition from recipient site (first 48 h)

2. inosculation:growth of vessels from bed and graft toward each other (d 2-3)

3. neovascular ingrowth:growth of new vessels which vascularize graft (d 3-5)

• requirementsfor graft survival

• well-vascularized bed (recipient site).Examples of unsuitable beds include heavily irradiated

wounds and infected wounds

coagulation begins assoon as graft is placed on bed

• good contact between graft and recipient bed..Staples,sutures,splinting,and pressure dressings

are used to prevent movement/shearing of graft and hematoma orseroma formation

• low bacterial count at recipient site (<105/cm 3, to prevent infection)

• common reasonsfor graft loss:hematoma/seroma, infection, mechanical force (e.g.shearing,

pressure), radiotherapy

Classification of Skin Grafts

1.by species

autograft:from same individual

• allograft (homograft):from same species, different individual

xenograft ( heterograft):from different species (e.g. porcine)

2. bv thickness:see Table II

Table 11. Skin Grafts

Split Thickness Skin Graft Full Thickness Skin Graft

Definition

Donor Site

Healing of Donor Site

Epidermis and part of dermis

Mote sites

Re-eprtlrelialitalion via dermal appendages in wound

edges

-10 d (faster on scalp)

More reliable and better survival:shorter nutrient

diffusion distance

LessT contraction,greater 2' contraction (less with

thicker graft)

Poor

lakes well inless favourable conditions

Can cover a larger area

Canbe meshed for greater area

A:!ows for extravasation of bloodi'serum

large number of donor sites

Contracts significantly,abnormal pigmentation,high

susceptibility to Irauma. donor site scar,requires well

vascutariced bed

large areas of skin,granulating tissue beds

tpidermis and allof dermis

Donor sites limited by the ability to use primary closure

Primary closure

Re-Harvesting

Graft Take

N.' A

lower rate of survival(thicker,slower

revascularization)

Contraction* Greater Tcontracbon.less 2° contraction

Aesthetic Good

Resists contraction,better colour match

May use on face and fingers

Advantages

Disadvantages Requires well vascularized bed

Uses Face (colour match),site where thick skm or decreased

contracture isdesired(e.g.finger)

•r contraction: vrtredule reduction m size upon harvesting:2' contraction:reduction In size once graft ptaced on wound bed and healing has

occurred

Meshed Grafts

• split thickness grafts can be meshed after harvest by a mesher to a variety of ratios

• advantages

prevents accumulation of fluids (e.g. hematoma,seroma)

covers a larger area

best for contaminated recipient site

• disadvantages

poor cosmesis ( “alligator hide"

appearance)

has greatersecondary contraction than full thickness grafts (see Table 1!)

+

Activate Windows

GoTaSettiTTgsTtTaCtivaTe'

Wincows;

PLU Plastic Surgery Toronto Notes 2023

OTHER GRAFTS

Table 12.Various Tissue Grafts

Graft Type Use Preferred Donor Site

Bone (Vascularized or Hon-Vascularized)

Cartilage

Tendon

Cranial,rib,iliac,fibula,scapula

Ear, nasalseptum, costal cartilage

Palmaris longus, plantaris(present in 85% ol

population)

Conduit lor regeneration across nerve gap Sural, antebrachialcutancous, medial brachial

cutaneous

Forearm or tool vesselsfor small vessels,

saphenous vein for larger vessels; veins are

typically used lor any vessel graft

Contour restoration (tfatfor bulk); not used Groin, abdomen,thigh

often

Contour restoration

Repair rigid defects

Restore contour of ear and nose

Repair or replace a damaged tendon

Nerve

Vessel Bridge vascular gaps

Dermis

Fat Abdomen, thighs, buttocks

FLAPS

• definition: tissue of varying composition (muscle alone,skin and subcutaneous tissue, bone alone

with vascular supply, etc.), that has a known blood supply (random, pedided, or named); not

dependent on neovascularization, unlike a graft

• may consist of:skin,subcutaneous tissue, fascia, muscle, tendon, bone, other tissue (e.g.omentum)

• classification: based on tissue composition, blood supply to skin (random, axial),location of the

donor site (local, regional, distant), etc.

• indicationsfor flaps

» replaces tissue loss due to trauma orsurgery (reconstruction)

providesskin and soft tissue coverage through which surgery'

can be carried out later

• complications:flap loss due to hematoma,seroma, infection, poor flap design, extrinsic compression

(dressing too tight) or vascular failure/thrombosis,fat necrosis (in free and pedicled flaps)

Random Pattern Flaps

• blood supply by dermal and subdermal plexus to skin and subdermal tissue with random vascular

supply

• limited length:width ratio to ensure adequate blood supply

• flap choice is often a combination of available tissue, type of tissue needed, location of reconstruction

site with respect to donorsite, blood supply, ability to close the donor site, and surgeon preference

• types

rotation:semicircular tissue rotated around a pivot point for defect closure;commonly used on

sacral pressure sores,scalp, and cheek defects (height of triangular defect:radius of flap curve

should be 0.5-l:l)

transposition: tissue is transposed (i.e. lifted up from its native location and brought into the

defect) around a pivot point from one location to another;commonly used on certain areas of the

face using adjacent areas of excess skin laxity

/. plasty: two triangular flaps are designed around a scar to reorient a scar, lengthen the line of a

scar, or to break up a scar

• advancement flaps ( V-Y, Y-V ):defect is closed with unidirectional tissue advancement

single/ bipedicle V-Y flaps:wounds with lax surrounding tissue; the pedicle flap is attached

to the donorsite via a pedicle containing the blood supply

****** ..*•*

?

is

Rotation Flap Z-plasty

b T T

Rhomboid Transposition Flap (Limberg) Single Pedicle Advancement Flap

I

r "l \

T.

1

/

e « |

V-Y Advancement Flap +

Figure16. Wound care flaps -random pattern

Activate Windows

Go ToSettingsToacTivate Windows,

PL15 Plastic Surgery Toronto Notes 2023

Axial Pattern Flaps (Arterialized)

• flap contains a well-defined artery and vein

• allows greater length:width ratio (5-6:1)

• types

peninsular flap:skin and vessel intact in pedicle

island flap: vessel remains intact, but is skeletonized such that the pedicle is better defined

free flap:segment of tissue with named blood supply (artery and vein) that can be harvested

with that blood supply and re-anastomosed in a different anatomical location by microsurgical

techniques

• can be sub-classified according to categoriessuch astissue type, blood supply type,and calibre of

vessels

e.g. myogenic, myocutaneous,fasciocutaneous

Peninsular Axial Pattern Hap

\ Direct cutaneous artery & vein

Island Axial Pattern Hap

Free Hap

Free Flaps

• transplanting expendable donor tissue from one part of the body to another by isolating and dividing

a dominant artery and vein to a flap, and performing a microsurgical anastomosis between these and

the vessels in the recipient wound

• types: muscle and skin (common), bone, jejunum,omentum,fascia,or any combination of tissue

where a common blood supply can be harvested to provide vascularsupply to all the tissue types

• e.g.radial forearm,scapular,latissimus dorsi

EMona Li 2020

Figure 17. Axial/arterial pattern flaps

Table 13. Characteristics of HealthyFree Flap

Characteristic Normal Arterial Insufficiency Venous Insufficiency

Colour’

Temperature

Arterial Pulse (Doppler)

Turgor

Pink Pale Purple or blue

Warm Cool Warm or cool

t

Soft, but with some firmness Decreased tissue firmness Increased (tissue femness with

tissue stiffness)

Capillary Refill 2-5s >5s *2s

'Variation depending on patient'

sskin colour

Vascularized Composite Allotransplantation (i.e. composite tissue allotransplantation)

• considered free flaps because it is a functional and vascularized construct;vessels are anastomosed, as

well as the nerves

• similar to solid organ transplantation, although VCA involves the transplantation of a composite of

tissue (skin,fat, muscle, nerve,and vessels) from one individual to another,after matching sex and

blood ± HLA type

• skin is highly immunogenic,containing effector Tcells and antigen presenting cells which can mount

a proinflammatory state and contribute to allograft rejection;regulatoryT cells(Tregs) can modulate

effector T cell inflammation through inhibitory cytokines(e.g.TGF-jJ,1L-10)

• patients require immunosuppression therapy

induced with antithymocyte globulin and basiliximab (anti-T cell antibodies)

maintained with tacrolimus, mycophenolate mofetil, and prednisone

• acute rejection appearsto affect the skin first treatment consists of increased oral or IV steroids,

mono/polyclonal antibodies, and topical immunosuppressants

Soft Tissue Infections

Erysipelas

Definition

• acute skin infection of the upper dermis and superficial lymphatics(more superficial than cellulitis)

Etiology

• typically caused by GAS

Clinical Features

• intense erythema, induration, and sharply demarcated borders (differentiates it from otherskin

infections)

Treatment

• penicillin or first-generation cephalosporin (e.g.cefazolin or cephalexin)

+

Activate Windows

PL16 Plastic Surgery Toronto Notes 2023

Cellulitis

Definition

• non-suppurative infection ofskin and subcutaneous tissues

Etiology

• skin flora are most common organisms:Staphylococcus aureus, GAS

• immunocompromised: Gram-negative rods and fungi

Clinical Features

• source of infection

trauma, recentsurgery

PVD, DM - xerotic skin in feet/toes

foreign bodies(IV, orthopaedic pins)

• systemic symptoms (fever, chills, malaise)

• pain,tenderness, edema, erythema with poorly defined margins, regional lymphadenopathy

• can lead to ascending lymphangitis(common in GAS; visible red streaking in skin proximal to area of

cellulitis)

Investigations

• CBC, blood cultures

• culture a collection/aspirate from wound if open wound

Treatment

antibiotics:first line - cephalexin 500 mg PO q6 h or cloxacillin 500 mg PO q6 h x 7 d;if complicated

(e.g. lymphangitis, DM,severe infection,oral antibiotic therapy failure), consider IV cefazolin 1-2 g q8

h or IV cloxacillin, IV penicillin.All patientsshould have reassessment in 48 h for resolution if on an

oral antibiotic

• outline area of erythema to monitorsuccess of treatment

immobilize upper and lower extremities;consider non-weight bearing forlower extremities

Necrotizing Fasciitis

Definition

• rapidly spreading, very painful infection of the fascia with necrosis ofsurrounding tissues

• some bacteria create gas that can be felt as crepitus and can be seen on x-rays (subcutaneous

emphysema)

• infection spreads rapidly along deep fascial plane and islimb-and life-threatening

Etiology

• Type1:polymicrobial (more common in immunocompromised)

• Type 11:monomicrobial, usually GAS (more common in healthy patients)

Risk Factors

• immunocompromised, DM,obesity,IV drug use, age >50 yr, peripheral vascular disease, and

malnutrition

Clinical Features

• pain out of proportion to clinical findings and beyond border of erythema

• edema, tenderness, ± crepitus (subcutaneous gas from anaerobes), ± sepsis-typ

nausea,fever,diarrhea, dizziness, malaise)

• overlying skin changes including blistering and ecchymoses

• patients may look deceptively well at first, but have some physiological abnormalities on initial labs

and may rapidly become very sick/toxic

• late findings:

skin turns dusky blue and black (secondary to thrombosis and necrosis)

induration, formation of bullae

cutaneous gangrene,subcutaneous emphysema

e symptoms (e.g.

Investigations

• a clinical diagnosis

• CT scan only ifsuspect it is not necrotizing fasciitis (looking for abscess, gas collection, myonecrosis

and possible source of infection)

• severely elevated CK: usually means myonecrosis(late sign)

• bedside incision, exploration, and incisional biopsy when ruling out conditions, clinical feature is not

supportive,or difficult exam

• during incisional biopsy, often see "dishwater pus" (GAS) and a hemostat easily passed along fascial

plane (fascial biopsy to rule out in equivocal situations)

n V

LJ

+

Activate Windows

Go to Settingsto activate Windows.

PLI 7 Plastic Surgery Toronto Notes 2023

Treatment

• vigorous resuscitation (ABCs)

• urgent surgical debridement: remove all necrotic tissue, copious irrigation with plansfor repeat

surgery in 24-48 h

• IV antibiotics: as appropriate for clinical scenario; consider penicillin 4 million 1U IV q4 h and

clindamycin 900 mg IV q6 h until final cultures available (the combination can be synergistic if GAS)

or vancomycin and clindamycin

• postoperative ICC admission and infectious disease consult after urgent surgical debridement by

plastic surgery

Ulcers IV I®,

Lower Limb Ulcers

Traumatic Ulcers (Acute)

• failure of wound to heal, usually due to compromised blood supply and unstable scar,secondary to

pressure or bacterial colonization/infection

• usually over bony prominence ± edema ± pigmentation changes ± pain

• treatment, in consultation with vascular surgery

any debridement of ulcer and compromised tissues must be preceded by ABIs and vascular

Doppler

ulcers or compromised tissuesleft to heal by secondary intention with dressings may need

reconstruction with local or distant flap in select cases;vascularstatus of limb must be assessed

clinically and via vascularstudies(i.e. AB1, duplex Doppler)

Table 14. Venous vs. Arterial vs. Diabetic Ulcers

Characteristic Venous (70% of vascular

ulcers)

Arterial Diabetic

Cause 2

*

to small and/or large vessel disease (be

aware of risk factors)

Peripheral neuropathy:decreased

sensation

Atherosclerosis:microvascular

disease

Valvular incompetence

Venous HTN In patients with DM.ABI can be falsely

normal due to incompressible arteries

secondary to plaques/calcification

History Dependent edema, trauma

Rapid onset t thrombophlebitis,

varicosities

Medial malleolus (‘Gaiter'

locations)

Vellow exudates

Granulation tissue

Varicose veins

Brown discolouration of surrounding

Arteriosclerosis, claudication

Usually >45 yr

Slow progression

Distal locations(e.g.lower limb,feel)

DM

Peripheral neuropathy

Irauma/prcssure

Pressure point distribution (more

likely metatarsal heads)

Necrotic base

Common

Distribution

Appearance Pale/white, necrotic base t dry eschar

covering

skin

Wound Margins Irregular Even ("punched out") Irregular or "punched out" or

deep

Superficial/deep

Thin,dry skin ± hyperkeratotic

border

Hypersensitive/ischemic

Decreased pulses likely (lake

caution in calcified vessels)

ABI is inaccurately high (due

to PVD )

Usually associated with arterial

disease (microvascular/

macrovascular disease)

Painless (if neuropathy)

Decreased with dependency, increased with No claudication or rest pain

leg elevation and exercise (claudication) Associated paresthesia.

Rest pain

Deep

Venousstasis discolouration (brown) Thin,shiny, dry skin; hairless, cool

Depth Superficial

Surrounding Skin

Pulses Normal distal pulses Decreased or no distal pulses

ABI '0.9

Doppler: abnormal venous system

ABI «0.9

Pallor on elevation, rubor on dependency

Delayed venous filling

Vascular Exam

Pain Moderately painful

Increased with leg dependency,

decreased with elevation

No rest pain

Extremely painful

anesthesia

Control DM

Carelul wound care

Fool care

Treatment Rest, leg elevation

Compression at 30 mmHg (stockings Moist wound dressing •topical and/or

or elastic bandages) (Ensure ABI is systemic antibiotics if infected

safe for compression)

Moist wound dressings

t topical,systemic antibioticsif

infected

wound dressings

Rest, no elevalion. no compression

r T Modify risk factors (smoking, diet,exercise. Orthotics, off loading

Early intervention for infections

(topical and/or systemic

antibiotics if infected)

Vascular surgical consultation

L J

etc.)

Vascular surgical consultation (angioplasty

or bypass)

Treat underlying conditions (DM. proximal

arterial occlusion, etc.) +

Activate Windows

Go to Settings To activate Windows.

PL1S Plastic Surgery Toronto Notes 2023

Pressure Ulcers

Common Sites

• over bony prominences;95% on lower body

Stages of Development

1. hyperemia: disappears 1 h after pressure removed

2. ischemia: follows 2-6 h of pressure

3. necrosis:follows >6 h of pressure

4. ulcer: necrotic area breaks down

Classification (National Pressure Ulcer Advisory Panel 2014)

• Stage I: non-blanchable erythema present > l h after pressure relief, skin intact

• Stage II: partial-thickness skin loss

• Stage 111:full-thickness skin loss into subcutaneous tissue

• Stage IV: full-thickness skin loss into muscle, bone, tendon, or joint

if an eschar is present, must fully debride before staging possible

• Stage X: unstageable

A Nutritionalformal!

(niiched with Arginine,

tint, and Antioiidantsfor the Healing ol Pressure

Ukers:ARandomired Trial

Ann Intern Med 2015:162(3|:167-174

Purpose: to deter- -e whethersupplementation

with arginine,nut.and antioidants within a

high-calorie,high-protein formula improves pressure

ulcer healing.

Methods:200 adrift patientsfrom long -term care

and home care sertieswith stage II.Ill, aid IV

pressure ulcers received either an energy-dense,

protein-rich oral formula enriched with arginine, line,

and antioedantsoran egualrolumeol an isocaloric.

isonitrogenousfocmnlaforSwk.

Results: Supplementation with '.he enriched firinula

resulted nr a greater reduction in pressure ulcer area.

A more Ireguenl reduction in area ol <0% oi greater at

8 wk was also seen.

Conclusion : (mong malnourished patients with

pressure ulcers.8wk of supplementation with an oral

nutritional formula ennehed with arginine, zinc, and

antioxidants imprests pressure ulcer healing.

Prevention

• clean and dry skin,frequently reposition,special beds or pressure reliefsurface, proper nutrition,

activity, early identification of individuals at risk (e.g. immobility, incontinence, paraplegia,

immunocompromised, DM, etc.), treatment of underlying medical conditions

Treatment

• treatment plan individualized to patient

• 4 main principles:

preventative measures (pressure relief, assess for pressure points e.g. wheelchairs; manage

continence issues, divert contaminants e.g. urine and feces, ensure appropriate nutrition )

• treatment of underlying medical issues including nutrition

• moisture reduction and pressure relief

wound bed preparation and treatment

• systemic antibioticsfor infections

• assess for possible reconstruction

Complications

• cellulitis, osteomyelitis,sepsis, gangrene

Burns

Burn Injuries

Causal Conditions

• thermal (flame contact,scald)

• chemical

• radiation (U V, medical/therapeutic)

• electrical Epidermis

Dermis:

( Nerves

Vessels

Most Common Etiologies

• children:scald burns

• adults: Ha me burns

Zone ol hyperemia

F7T71 Zone of stasis

HZone of coagulation

Blood vessels and most nerves

are found in the dermis ©

^

£

Table 15. Skin Function and Burn Injury i

"

I

Skin Function Consequence of Burn Injury Intervention Required —

Thermoregulation

Control of Fluid loss

Prone to lose body heat

Loss ot large amounts of water and protein

from the skin and other body tissues

Must keep patient covered and warm

Adequate fluid resuscitation isimperative

Figure 18. Zones of thermal injury Antimicrobial dressings(systemic antibiotics if

signs of specific infection present)

Tetanus prophylaxis if not already

administered

Mechanical Barrier to Bacterial Invasion and High -risk of infection

Immunological Organ

ri

c.J

+

Activate Windows

Go to Settings to activate Windows.

PL19 Plastic Surgery Toronto Notes 2023

Pathophysiology of Burn Wounds

• amount of tissue destruction is based on temperature, time of exposure, and specific heat of the

causative agent

• zone of hyperemia: vasodilation from inflammation; entirely viable, cells recover within 7 d;

contributes to systemic consequences seen with major burns

• zone of stasis (edema):decreased perfusion;microvascular sludging and thrombosis of vessels results

in progressive tissue necrosis -> cellular death in 24-48 h without proper treatment

• factors favouring cell survival:moist,aseptic environment, rich blood supply

zone where appropriate early intervention has most profound effect in minimizing injury

• zone of coagulation (ischemia): no blood flow to tissue -» irreversible cell damage -> cellular death/

necrosis

Diagnosis and Prognosis Prognosis best determined by bum

size (TBSA), age of patient, presence/

absence of inhalation injury

• burn size

% of TBSA burned:rule of 9sfor 2" and 3° burns only (children <10 yr use Lund-Browder chart)

• for patchy burns,surface area covered by patient'

s palm (fingers adducted) represents

approximately 1% of TBSA

• age: more complications if <3 yr or >60 yr

• depth: difficult to assess initially - history of ctiologic agent and time of exposure helpful (see Table

15, PL18 )

• location: face and neck, hands, feet, perineum arc critical areas requiring special care of a burn unit

(see Indicationsfor Transfer to Burn Centre, PL20)

• inhalation injury: can severely compromise respiratory system, affect fluid requirement estimation

(underestimate), mortality secondary to ARDS

• associated injuries(e.g. fractures)

• comorbid factors can exacerbate extent of injury (e.g. concurrent disability, alcoholism,seizure

disorders,chronic renal failure, other trauma)

Circumferential burns can restrict

respiratory excursion and/or blood flow

to octremities and require cscharotomy

TBSA does not include areas with 1"

bums

Anterior Posterior 4

'

.- 4

'

.

1

/ \

18% 18%

y v

4m -4m 4W%- 416%

9%

I l

Figure19. Rule of 9sfor TBSA

+

Activate Windows

Go to Settings to activate Windows.

PL20 Plastic Surgery Toronto Notes 2023

O

CSJ

5

Area Age 0 Age 1 Age 5 Age 10 Age 15 Adult

A = Vi head area 9 V48 V46 V45 V4454354

B =14 thigh area 2543 Vi 4 Vi 454454434

C = 54 leg area 25425433354354

.1

1

e

Figure 20. Lund-Browder diagram

Table 16. Burn Depth (1st, 2nd,3rd degree)

Nomenclature Traditional Nomendature Depth Clinical Features

Erythema/Superficial First degree

Superficial-Partial Second degree

Thickness

Deep-Partial Thickness Second degree

Epidermis

Into superficial

( papillary) dermis

Into deep (reticular)

dermis

Painful,sensation intact, erythema,blanchable

Painful sensation intact erythema, blisters with clear

fluid,blanchable.hair follicles present

Insensate,difficult to distinguish from full thickness,

does not blanch,some hair folliclesstill attached,softer

than full thickness burn

Injury to underlying tissue structures(e.g. muscle, bone)

Insensate (nerve endings destroyed), hard leathery

Injury to underiymg eschar that is black,grey,white, or cherry red in colour;

tissue structures hairs do notstay attached, may see thrombosed veins

|e.g.muscle,bone)

Full Thickness Third degree Through epidermis

and dermis

Fourth degree

Indications for Transfer to Burn Centre

American Burn Association Criteria

• patients with partial or full-thickness burns that involve the hands, feet,genitalia,face, eyes, ears,

and/or major joints or perineum

• electrical burns including lightning (internal injury underestimated by TBSA),and chemical burns

• inhalation injury (high risk of mortality and may lead to respirator)- distress)

• burn injuries in patients with medical comorbidities which could complicate management and

recovery

• any patients with simultaneous trauma and burns should he stabilized for trauma first, then triaged

appropriately to burn centre

• any patients with burn injury who will require special emotional,social, and rehabilitation

intervention

• children with burns in a hospital not equipped with paediatric care specialists ri

L J

+

Activate Windows

Go to Settings to activate Windows.

PL21 Plastic Surgery Toronto Notes 2023

Acute Care of Burn Patients

•adhere to ATLS protocol

•resuscitation using Parkland formula to treat fluid losssecondary to injury and cardiac output.

Parkland formula is a starting estimate and patients may require more volume.Other formulas exist,

but the Parkland formula is predominantly used in North America (see Table 17)

•extra fluid administration required if:

• burn >80% T

'

BSA

• 4" burns

• associated traumatic injury

• electrical burn

inhalation injury

delayed start of resuscitation

• paediatric burns

•monitor resuscitation

urine output is best measure: maintain at >0.5 cc/kg/h (adults) and 1.0 cc/kg/h in children <12 yr

maintain a clearsensorium,HR <120/min,MAP >70 mmHg

•burn-specific care

• escharotomy in circumferential extremity burns, including digits

prevent and/or treat burn shock: 2 large bore lVsfor fluid resuscitation

• insert l

'

oley catheter to monitor urine output

• identify and treat immediate life-threatening conditions (e.g. inhalation injury,CO poisoning)

• determine TBSA affected first, since depth is difficult to determine initially (easier to determine

after 24 h)

•tetanus prophylaxis if needed

• all patients with burns >10% TBSA, or deeper than superficial-partial thickness, need 0.5 cc

tetanustoxoid

also give 250 U of tetanuslg if prior immunization is absent/unclear, or the last booster >10 yr

ago

•baseline laboratory studies(Hb, U/A, BUN,CXR, electrolytes, Cr, glucose,CK, ECG,cross-match if

traumatic injury, ABG, carboxyhemoglobin )

•cleanse, debride, and treat the burn injury (antimicrobial dressings)

•early excision and grafting are standard of care and important for outcome

Respiratory Problems

•3 major causes

• burn eschar encircling chest

distress may be apparent immediately

perform escharotomy to relieve constriction

• CO poisoning

may present immediately or later

treat with 100% 02 by facemask (decreases half-life of carboxyhemoglobin from 210 to 59

min) until carboxyhemoglobin <10%

smoke inhalation leading to pulmonary injury

chemical injury to alveolar basement membrane and pulmonary edema (insidious onset)

risk of pulmonary insufficiency (up to 48 h ) and pulmonary edema (48-72 h)

» watch for secondary bronchopneumonia (3-25 d) leading to progressive pulmonary

insufficiency

intubate patient with any signs of inhalation injuries

Burn Wound Healing

Inhalation Injuries101

Indicators of Inhalation Injury

• Injury in a closed space

• Facial burn

- Singed nasal hair/eyebrows

• Soot around nares/oral cavity

• Hoarseness

• Conjunctivitis

• Tachypnea

• Carbon particlesin sputum

• Elevated blood CO levels(i.e.

brighter red)

• Suspected inhalation injury requires

immediate intubation due to

impending airway edema:failure to

diagnose inhalation injury can result

In airway swelling and obstruction,

which, if untreated, can lead to death

• Neither CXR or ABG can be used to

rule out inhalation injury

• Direct bronchoscopy now used for

diagnosis

• Signs of CO poisoning (headache,

confusion,coma,arrhythmias)

Table 17. Bum Shock Resuscitation (Parkland Formula)

Parkland Formula

Hour 0-24 4 cc s mass in kg x % TBSA with1/2of total in first 8 h from time of injury and1/2 of total in next 16h from

time of injury

0.35-0.S cc plasma x mass inkg x % IBS

*

DSW atrate tomaintain normal serum sodium

Hour 24- 30

•Hour 30

'Remember to add maintenance fluid to resuscitation

ri

L J

+

Activate Windows

GotoSetttngrtcractivateWrndows.

PL22 Plastic Surgery Toronto Notes 2023

Table 18. Burn Wound Healing

Depth Healing

No scarring:complete healing

Second Degree (superficialpartial) Spontaneously re epilhelialize in 714 d from retained epidermal structures

Residual skin discolouration

Hypertrophic scarring uncommon:grafting rarely required

Deep Second Degree (deep partial) Re-epithelialize in14-35 d from retained epidermal structures

Hypertrophic scarring frequent

Crafting recommended to expedite healing

Third Degree (full thickness) Re epithelialize from the wound edge

Grafting/ flap necessary to replace dermal integrity and limit hypertrophic scarring

Often results in amputations

If notrequiring amputation,needs flap lor coverageafter debridement (does not re- epithetiatize. cannot

grail)

First Degree

Fourth Degree

Treatment

• three stages

1.assessment: depth determined

2.management: specific to depth ofburn and associated injuries

3.rehabilitation

• first degree

• treatment aimed at comfort

• topical creams (pain control, keep skin moist) ± aloe

• oral NSAlDs (pain control)

• superficial second degree/partial thickness

daily dressing changes with topical antimicrobials (such as Polysporin*);leave blisters intact

unless impaired or over joint and inhibiting motion

• deep second degree/deep partial thickness and third degree/full thickness

• prevent infection and sepsis (significant complication and cause of death in patients with burns)

most common organisms:.S', aureus, P. aeruginosa, ami albicans

- day 1*3 (rare): Gram-positive

- day 3-5: Gram-negative ( Proteus, Klebsiella)

* topical antimicrobials: treat colonized wounds (from skin flora,gut flora, or caregiver)

• remove dead tissue

• surgically debride necrotic tissue, excise to viable (bleeding) tissue

Risk Factors for Infection of Burn

Wounds

Patient Related

Extent >30% TBSA

• Depth:full thickness and deep partial

thickness

• Patient age (higher risk with very

young and very old)

• Comorbidities

• Wound dryness

• Wound temperature

• Secondary impairment of blood flow

to wound

• Acidosis

Microbial Factors

• Density >105 organisms per gram

of tissue

• Motility

• Virulence and metabolic products

(endotoxin,exotoxin,permeability

factors, other factors)

• Antimicrobial resistance Table 19. Antimicrobial Dressings for Burns

Antibiotic Pain with Application Penetration Adverse Effects

Silver Nitrate (0.5% solution) None May cause methemoglobinemia, stains (black) ,

leeches sodium from wounds

May stain,producing a pseudoeschar or facial

discolouration (bluish-gray discolouration:raised

liver enzymes

Slowed healing,leukopenia,mild inhibition of

epithelialisation;pseudoeschar must be washed

off prior to each application

Well,penetrates eschar: Mild inhibition of epithelialization.may cause

only used on ears metabolic acidosis with wide application

Minimal

Nanocrystallinc Silver-Coated None or transient

Dressing (Acticoat )

Medium,does not

penetrate eschar

Silver Sulfadiazine (cream)

(Ftamazine !

.Silvadene )

Minimal Medium,penetrates

eschar

Sulfamylon Moderate

• early excision and grafting is the mainstay of treatment for deep/full thickness burns

• initial dressing should decrease bacterial proliferation

Other Considerations in Burn Management

Altered Hemodynamics (X CO,t SVR)

Vascular Permeability and Edema 4

>