10
Pathophysiology and Current Management of Burn Injury Leslie DeSanti, BS, RN & Burn Research Nurse & Burn Center & Brigham and Women_s Hospital & Boston, MA The author has disclosed that she has no significant relationships or financial interests in any commercial companies that pertain to this education activity. Wolters Kluwer Health has identified and resolved all faculty conflicts of interest regarding this educational activity. PURPOSE To provide the physician and registered professional nurse with an overview of the pathophysiology and current management of burn injuries. TARGET AUDIENCE This continuing education activity is intended for physicians and nurses with an interest in learning about evidence-based prevention and management of burn wounds. OBJECTIVES After reading the article and taking the test, the participant should be able to: 1. Explain the pathophysiology of skin function. 2. Describe the different types of burn injuries. 3. Identify the treatment strategies for burn injuries. ADV SKIN WOUND CARE 2005;18:323-32; quiz 333-4. T remendous advances have been made in the manage- ment of burn injury in the past decade. Mortality and morbidity have been markedly reduced due to overall major improvements in critical care, metabolic support, infec- tion control, and wound management. 1-8 As with any wound, many systemic factors impact burn wound healing, including metabolic response to injury, nutri- tional status, presence of systemic infection, and other systemic insults such as pain and stress. Fortunately, the advances in burn wound care have focused on addressing these factors. Aggressive surgical management of deep burns, improvement of the wound healing environment with use of silver release dressings, better pain control in partial-thickness burns, im- proved healing of partial-thickness burns with temporary skin substitutes, improved functional and cosmetic outcomes of massive burns with use of adjuvant therapies, and optimum C M E CATEGORY 1 1 Credit ce ce ANCC/AACN 3.5 Contact Hours JULY/AUGUST 2005 e x tra C L I N I C A L M A N A G E M E N T ADVANCES IN SKIN & WOUND CARE & JULY/AUGUST 2005 323 WWW.WOUNDCAREJOURNAL.COM Copyr ight © Lippincott Williams & Wilkins. Unauthor iz ed reproduction of this article is prohibited.

JULY/AUGUST 2005 e C LI N I CAL MANAG E M E NT tra of major burns in burn centers are among the advances in burn care.1-8 A burn is defined as damage to the skin caused by excessive

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Pathophysiology andCurrent Management ofBurn Injury

Leslie DeSanti, BS, RN & Burn Research Nurse & Burn Center & Brigham and Women_s Hospital & Boston, MA

The author has disclosed that she has no significant relationships or financial interests in any commercial companies that pertain to this education activity.

Wolters Kluwer Health has identified and resolved all faculty conflicts of interest regarding this educational activity.

PURPOSE

To provide the physician and registered professional nurse with an overview of the pathophysiology and current

management of burn injuries.

TARGET AUDIENCE

This continuing education activity is intended for physicians and nurses with an interest in learning about

evidence-based prevention and management of burn wounds.

OBJECTIVES

After reading the article and taking the test, the participant should be able to:

1. Explain the pathophysiology of skin function.

2. Describe the different types of burn injuries.

3. Identify the treatment strategies for burn injuries.

ADV SKIN WOUND CARE 2005;18:323-32; quiz 333-4.

Tremendous advances have been made in the manage-

ment of burn injury in the past decade. Mortality and

morbidity have been markedly reduced due to overall

major improvements in critical care, metabolic support, infec-

tion control, and wound management.1-8

As with any wound, many systemic factors impact burn

wound healing, including metabolic response to injury, nutri-

tional status, presence of systemic infection, and other systemic

insults such as pain and stress. Fortunately, the advances in

burn wound care have focused on addressing these factors.

Aggressive surgical management of deep burns, improvement

of the wound healing environment with use of silver release

dressings, better pain control in partial-thickness burns, im-

proved healing of partial-thickness burns with temporary skin

substitutes, improved functional and cosmetic outcomes of

massive burns with use of adjuvant therapies, and optimum

C M ECATEGORY 1

1 Credit

ceceANCC/AACN

3.5 Contact Hours

JULY/AUGUST 2005

extraC L I N I C A L M A N A G E M E N T

ADVANCES IN SKIN & WOUND CARE & JULY/AUGUST 2005323WWW.WOUNDCAREJOURNAL.COM

Copyr ight © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

management of major burns in burn centers are among the

advances in burn care.1-8

A burn is defined as damage to the skin caused by excessive

heat or caustic chemicals. The most common burn injuries

result from exposure to heat and chemicals. Full-thickness

burns usually develop, causing immediate cell death andmatrix

destruction, with the most severe damage on the wound

surface.8 -10 Additional heat and inflammation induce tissue

injury beneath the nonviable surface, which can either progress

over time to healing or can deteriorate to further necrosis,

depending on the approach to treatment.

Managing a burn wound is challenging because treatment

must be continuously adapted to the changing wound biology,

dictated by the burn injury process, the host_s response to

injury, and the wound environment.6-8 Flexibility in adapting

care to the changing wound is essential.

SKIN FUNCTIONUnderstanding a burn injury requires recognition of the

anatomy and physiology of the skin. The skin is a bilayer

organ (Figure 1) with many protective functions essential for

survival11 (Table 1). The outer epidermal layer provides critical

barrier functions and is composed of an outer layer of dead

cells and keratin, which present a barrier to bacterial and

environmental toxins. The basal epidermal cells supply the

source of new epidermal cells. The undulating surface of the

epidermis, called rete pegs, increases adherence of the epi-

dermis to the dermis via the basement membrane.

The inner dermal layer has a number of essential functions,

including continued restoration of the epidermis. The dermis

is divided into the papillary dermis and the reticular dermis.

The former is extremely bioactive; the latter, less bioactive.

This difference in bioactivity within the dermis is the reason

that superficial partial-thickness burns generally heal faster

than deeper partial-thickness burns; the papillary component

is lost in the deeper burns.

Loss of the normal skin barrier function causes the common

complications of burn injury. These include infection, loss of

body heat, increased evaporative water loss, and change in key

interactive functions such as touch and appearance (Table 2).

BURN SEVERITYBurn severity can be determined by burn depth, size, location,

and patient age.8-10,12,13 Burn size is defined by the percentage

of total body surface area (TBSA) that is burned. The Rule of

Nines is a commonly used tool; it divides the surface area of

the body into segments of 9% (Figure 2). Age is a major

determining factor in a patient_s prognosis. Infants and the

older adults have a higher mortality rate than older children

and young and middle-aged adults.

Table 1.

SKIN FUNCTIONS

Epidermis

& Protection from desiccation

& Protection from bacterial entry

& Protection from toxins

& Fluid balance; prevents excess evaporative loss

& Neurosensory

& Social-interactive

Dermis

& Protection from trauma (due to elasticity and durability

properties of the dermis)

& Fluid balance through regulation of skin blood flow

& Thermoregulation through control of skin blood flow

& Growth factors for epidermal replication and dermal repair

Figure 1.

ANATOMY OF NORMAL SKIN

Table 2.

COMPLICATIONS OF BURN-INDUCED SKIN

BARRIER LOSS

& Increased heat loss (hypothermia)

& Increased infection risk

& Wound desiccation

& Increased evaporative water loss

& Loss of sensation or hyperalgesia

& Loss of skin elasticity

ADVANCES IN SKIN & WOUND CARE & VOL. 18 NO. 6 324 WWW.WOUNDCAREJOURNAL.COM

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The depth of heat injury depends on the degree of heat

exposure and depth of heat penetration. Wet heat (scald)

travels more rapidly into tissue than dry heat (flame) because

water conducts heat 100 times greater than air. In addition,

skin thickness is critical; the thinner the skin, the deeper the

burn will be due to less residual dermis. Children and older

adults have thin skin and, therefore, are at risk for deeper

injury than younger adults from the same heat exposure.

Burn depth is defined by how much of the skin_s 2 layers are

destroyed by the heat source, and it is the primary factor that

dictates wound management. In the past, burn wounds were

categorized by degrees, namely, first through fourth degrees.

However, it is more accurate to refer to burn wound depth by

the anatomic thickness of the skin involved, as follows:

& A superficial burn is confined to the outer epidermal layer.

& A partial-thickness burn involves the epidermal layer and

part of the inner dermis.

& A full-thickness burn involves destruction of both layers.

& A subdermal burn involves destruction of both layers and

extends to the tissue below, including fat, tendons, muscle,

and bone.

Burnwounds are dynamic and can evolve into deeper injuries

over time, depending on the initial injury and subsequent

environmental insults. Burn wounds are composed of an

outer layer of nonviable tissue, known as the zone of necrosis.

This involves both layers of skin in a full-thickness burn. In a

partial-thickness burn, the viable tissue beneath the layer of

necrosis is still injuredVknown as the zone of injuryV and can

become nonviable over time, depending on the degree of injury

and subsequent insults, such as infection. This process is known

as wound conversion.

Several significant differences exist between management

of a burn wound and management of a nonburn wound. First,

infection is of greater concern with a deep burn due to its

impaired blood flow and, in part, historic patterns of care.

Topical antimicrobials are routinely used from the onset, com-

pared with more selective use in nonburn wounds.14-17 Sec-

ond, deep burn wounds are typically surgically excised and

closed with a skin graft or skin substitute early in their course.

By comparison, healing by secondary intention is more com-

mon in nonburn wounds.2,18 Third, less attention is paid to

moist wound healing in a burn wound, although desiccation

is prevented by the use of temporary skin substitutes in

superficial burns and use of moist dressings over excised or

grafted burns. Hydrocolloids and alginates are less commonly

used on burn wounds.19-22

BURN WOUND MANAGEMENT

Superficial burnA superficial burn is confined to the epidermis and is not

considered to be a significant burn. No barrier functions are

Figure 2.

RULE OF NINES

Figure 3.

SUPERFICIAL PARTIAL-THICKNESS BURN

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altered. The most common form of superficial burn is caused

by ultraviolet radiation from the sun (sunburn). It generally

heals by itself in less than a week without scarring. Skin

moisturizers can be used to treat a superficial burn.

Partial-thickness burnA partial-thickness burn involves the destruction of the

epidermal layer and portions of the dermis; it does not extend

through both layers. There are 2 depths of partial-thickness

burnsVsuperficial partial-thickness and deep partial-thick-

nessVand each corresponds with a predictable healing time,

treatment modality, and outcome.

& A superficial partial-thickness burn involves destruction

of the entire epidermis and no more than the upper third of

the dermis (Figure 3). The microvessels perfusing this area are

injured, leading to leakage of large amounts of plasma. This

lifts off the heat-destroyed epidermis and causes a blister to

form (Figure 4). The resulting wound is pink, wet, and painful.

These are the most painful burns because the nerve endings

of the skin are exposed to air. Remaining blood flow is ade-

quate and the infection risk is low. Despite loss of the entire

epidermis, the zone of injury is relatively small and conver-

sion is uncommon except with extremes of age or presence of

chronic illness. Rapid healing occurs in 1 to 2 weeks. Scarring

is uncommon unless the wound is grossly contaminated.

Treatment begins with cleansing and debridement of loose

epidermis and remaining large blisters from the wound

surface. Large blisters should remain intact for no more than

2 days, as the infection risk is increased. A topical antibiotic is

not required. Areas such as the face and ears are treated open,

without a dressing; an ointment such as bacitracin is generally

used to maintain wound moisture and control the predomi-

nantly Gram-positive bacteria on the face. Open areas are

gently cleansed daily with a dilute chlorhexidine solution to

remove crust and surface exudate. Areas such as the hands,

upper and lower extremities, and trunk can be treated with

petrolatum-impregnated gauze. A petrolatum-impregnated

gauze is covered with several layers of dry absorbent gauze. If

the petrolatum-impregnated gauze appears well adhered to a

superficial partial-thickness burn wound with no underlying

exudate, the gauze does not need to be changed. If some

exudate is present, the dressing should be removed, the

wound gently cleansed, and the dressing reapplied. Silver

sulfadiazine cream is not recommended for treatment of a

superficial partial-thickness burn because the cream retards

healing. An antibiotic ointment is a better choice. Exceptions

include a dirty wound that has not been cleansed of initial

debris or a perineal or buttock wound, for which a silver-

based topical antibiotic is typically required (Table 3).

A superficial partial-thickness burn can also be managed

with a temporary skin substitute, which protects the wound

surface and provides moist wound healing (Figure 5). The outer

layer of gauze needs to be changed when it becomes saturated

with plasma from the wound surface. When the wound no

longer oozes, the skin substitute can be left open to heal.

Figure 4.

SUPERFICIAL PARTIAL-THICKNESS BURN

CAUSING BLISTERS

Photo

usedwithperm

issionfrom

RobertDemling,MD

Table 3.

ADVANTAGES OF SILVER DRESSINGS

& Release pure silver that is nontoxic to tissue

& Release silver over days in antimicrobial quantities

& Decrease mechanical trauma to the wound with no need for

frequent dressing changes

& Maintain moist wound healing

Figure 5.

SKIN SUBSTITUTE COVERING A SUPERFICIAL

PARTIAL-THICKNESS BURN

Photo

usedwithperm

issionfrom

RobertDemling,MD

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& A deep partial-thickness burn involves destruction of

most of the dermal layer, with few viable epidermal cells

remaining (Figure 6). Reepithelialization is slow, sometimes

taking months. Blisters do not generally form because the

dead tissue layer is thick and adheres to the underlying viable

dermis (eschar). The wound appears white and dry. Blood

flow is compromised, making the wound vulnerable to in-

fection and conversion to a full-thickness injury. The wound

is often a mixed partial- and full-thickness injury. Direct con-

tact with a flame source is a common cause; most chemical

burns are also deep partial-thickness injuries. Pain is reduced

because the nerve endings have been destroyed. It is difficult

to distinguish between a deep partial-thickness and a full-

thickness burn wound by visualization; however, the presence

of sensation to touch indicates that the burn is a deep partial-

thickness injury.

Deep partial-thickness burn wounds heal in 4 to 10 weeks

(sometimes longer). Wound breakdown is common because

the new epidermis is thin and not well adhered to the dermis

due to the lack of rete pegs.

The focus of treatment includes removing eschar and

using topical antibiotics during the debridement process or

until surgical wound closure occurs. Excision and grafting is

the preferred treatment because dense scarring is seen when

these wounds are allowed to heal through primary

intention.

The predominant antimicrobial used in deep partial-thick-

ness burn wounds is an agent containing silver, either in the

form of a cream or silver-impregnated membrane used as a

dressing on the wound surface. The cream must be removed

and reapplied at least once a day. Silver dressings continuously

release silver over several days, minimizing the need for

frequent dressing changes. These dressings need to be kept

moist to activate release of the silver; the wound fluid from the

burn injury is often sufficient. Moist wound healing is preserved

under the silver membrane. A dry gauze dressing is used over

the silver cream or dressing.

Full-thickness burnA full-thickness burn results in complete destruction of the

epidermis and dermis, leaving no residual epidermal cells

to repopulate (Figure 7). Initially, the dead avascular burn

tissue (eschar) appears waxy white in color. If the burn

produces char or extends into the adipose layer due to

prolonged contact with a flame source, a leathery brown or

black appearance can be seen, along with surface coagula-

tion veins. Direct exposure to a flame source is the usual

cause of a full-thickness burn injury; however, contact with

hot liquids, such as grease, tar, or caustic chemicals, will

also produce a full-thickness burn. Similar to a deep partial-

thickness burn, a full-thickness burn is also painless. One

Figure 6.

DEEP PARTIAL-THICKNESS BURN

Figure 7.

FULL-THICKNESS BURN

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major difficulty is distinguishing a deep partial-thickness

burn from a full-thickness burn; however, treatment is sim-

ilar for both.

Treatment of a full-thickness burn wound includes early

surgical debridement and wound closure with a skin graft or

permanent skin substitute. Before the planned surgery, the

wound is treated with a silver-based antibiotic cream or

dressing, using a closed dressing technique.

Subdermal burnA subdermal burn entails complete destruction of the epi-

dermis and dermis, with extension into underlying tissue, such

as connective tissue, muscle, and bone. The wound appears

charred, dry, and brown or white without sensation; typi-

cally,the affected digit or extremity has limited or no move-

ment. Treatment often requires amputation of the involved

area.

BURNS REQUIRING SPECIAL CAREBurns to the face, eyes, ears, hands, feet, and perineum have a

greater risk of complications and potential functional and

cosmetic disabilities. These burns should be managed in a

burn care facility.23,24

FaceBurns to the face are at high risk for cosmetic and functional

disability. For superficial burns, gentle and frequent cleansing

to remove all devitalized tissue is followed by application of an

antibiotic ointment such as bacitracin 2 to 3 times a day to pre-

vent desiccation and control residual Gram-positive organisms.

The face is treated open. Temporary skin substitutes can be

useful because they help protect the wound and eliminate

pain.25

Deeper facial burns require a more aggressive approach to

help prevent infection, including the use of silver products and

frequent debridement of loose necrotic tissue. Surgical

management is typically needed.

EarsSuperficial ear burns are managed similarly to facial burn

injuries; however, external pressure should not be applied to

the injured helix. The cartilage in this area is already poorly

vascularized and any compressionwill potentiate further injury.

Pressure control includes removing pillows or pressure while

sleeping. Deeper burns need more potent topical therapy,

usually with a silver or mafenide cream. Chondritis, or cartilage

infection, is a major complication and leads to loss of cartilage

and permanent deformity. Systemic antibiotics are required.

Hands and feetBurns to the hands and feet can cause functional disability.

Superficial burns are managed with a petrolatum-impreg-

nated gauze or skin substitute. Skin substitutes help provide

wound protection and pain control, especially in wounds on

the feet. Deeper burns require therapy with silver-based

products. When the hands and feet are injured, each digit

should be individually wrapped to minimize functional

disability, such as web space contractures, and to allow for

continued movement and aggressive physical therapy.

PerineumA perineal burn is at high risk for developing infection and

requires thorough cleansing and reapplication of topical

agents after urination or defecation.

Major burnsMajor burns can lead to significant morbidity or mortality;

treating them requires expertise in burn care. They are defined

as follows:

& partial-thickness burns greater than 10% of TBSA

& burns that involve the face, hands, feet, genitalia, perineum,

or major joints

& full-thickness burns in any age group, over 1% of body

surface

& electrical burns, including lightning injury

& chemical burns

& inhalation injury

& a child with any of the above burn injuries

& burn injury in patients with preexisting medical disorders

that could complicate management

& any burned child, if the hospital initially receiving the patient

does not have qualified personnel or equipment for children.

Patients with major burns are usually admitted to the

hospital and should be treated in a burn center.23,24

BURN WOUND INFECTIONMost burns are at risk for infection. Burn wound infection is

defined as bacterial invasion into viable tissue beneath the

burn eschar.16,17,26,27 Because all burns are colonized with

bacteria, a positive swab culture does not mean infection is

Table 4.

LOCAL SIGNS OF BURN WOUND INFECTION

& Black or brown focal areas of discoloration

& Enhanced sloughing of burned tissue

& Partial-thickness wound converting to full-thickness wound

& Increasing edema around the wound edges

& Softening of focal subeschar

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present. Infection is diagnosed by quantitative culturing of a

small full-thickness biopsy of the burn wound, including some

viable tissue. A bacterial count exceeding 105 organisms per

gram of tissue indicates infection because this amount of

bacteria typically overwhelms local immune defenses. Infec-

tion can also be diagnosed clinically, although this method is

less reliable.

Table 4 describes some of the local signs of burn wound

infection. Although systemic signs of increased fever and other

signs of sepsis provide valuable information when evaluating

for infection, fever and elevated white count are commonly

seen in burn patients without infection because of the

inflammatory response to burn tissue.

Systemic antibiotics plus topical antibiotics specific to the

cultured organisms are used to treat burn wound infection.

Eschar is also debrided to help remove the source of infection

while providing better access to the remaining infected viable

tissue for topical antibiotics. The topical antibiotic mafenide

(Sulfamylon) is often used either as a solution or cream to

treat burn wound infections because it has better tissue

penetration than available silver products. Silver-based agents

can be used after debridement has removed most of the in-

fected tissue.

ADVANCED PRODUCTS FOR BURN CARE

Silver-release productsSilver has been used for centuries to prevent and treat a variety

of diseases, most notably infections. Silver has extremely potent

antimicrobial properties, with levels in solutions exceeding 10

parts per million. Silver ions appear to kill microorganisms

instantly by blocking their respiratory enzyme system (energy

production) and altering microbe deoxyribonucleic acid (DNA)

and the cell wall; they have no toxic effect on human cells in

vivo. However, the available delivery systemsVoften in the

form of a saltVhave been limiting factors to successful biologic

use of this noble metal in burn wound care.

Silver nitrate and silver sulfadiazine have been used to

deliver antimicrobial silver for the past 40 years. However,

they impair fibroblast and epithelial proliferation, which

impairs healing.28-30

Silver itself is considered to be nontoxic to human cells

in vivo. The only reported complication is the cosmetic

abnormality argyria, which is caused by precipitation of silver

salts in the skin and results in a bluish gray discoloration.

Clinical evaluations have found no tissue toxicity. The major

complications attributed to silver compounds are due to the

Table 5.

TEMPORARY SKIN SUBSTITUTES

Product Origin ofTissue

Layers Category Uses

Human

(allograft)

Human

cadaver

Epidermis and dermis Split thickness & Temporary

coverage for large

excised wounds

Pig skin

(xenograft)

Porcine

dermis

Dermis Dermis & Temporary

coverage for

partial-thickness

and excised burns

Biobrane Synthetic with

added

denatured

bovine

collagen

Bilayer product: outer

silicone layer; inner nylon

mesh with collagen

Synthetic epidermis

and dermis

& Superficial partial-

thickness burns

& Temporary

coverage for

excised burns

TransCyte Allogenic

dermis

Bilayer product: outer

silicone layer; inner nylon

seeded with neonatal

fibroblasts

Bioactive dermal

matrix components on

synthetic dermis and

epidermis

& Superficial partial-

thickness to mid-

partial-thickness

burns

& Temporary

coverage for

excised burns

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complex, or anionVnamely, nitrate and sulfadiazineVand not

the silver itself.

Pure silver present in current silver dressings has been shown

not only to have potent antimicrobial activity, but also to lack

toxicity to wound cells. Some data also indicate prohealing and

anti-inflammatory properties of pure silver, including blocking

excess matrix metalloproteinase (MMP) activity.31-34

Current silver dressings release pure silver ions in anti-

microbial concentrations from a membrane surface over a

period of days. Sustained release of silver is important in

reducing bacterial burden. Silver nitratemust be applied every 2

hours to be effective, and the cream base in silver sulfadiazine

reacts with serous exudate to form a pseudo-eschar that must

be removed before the cream can be reapplied. Current silver

dressings can be left in place for up to 7 days. The wound does

not have to bemanipulated during this period, which decreases

trauma to new epithelial growth and reduces the wound_s

bacterial burden. A thin moisture layer beneath the silver

dressing also maintains a moist healing environment. The

available hyperosmolar creams, which have a short period of

silver activity, can also cause surface desiccation.

Skin substitutesMajor advances in patient care have resulted in a marked

decrease in morbidity and mortality, especially with massive

burns. In addition to survival, the current focus of burn wound

care is on improving long-term function and appearance of

the healed or replaced skin cover and the quality of life.35-50

The issue of quality of life has generated a significant interest

in the use of skin substitutes to improve wound healing,

control pain, create more rapid closure, improve functional

and cosmetic outcome, and, in the case of massive burns, in-

crease survival.

To more effectively address these issues, the new genera-

tion of skin substitutes is typically biologically active. The

bioactivity can modulate the burn wound instead of only

providing coverage. The new products have not displaced the

more inert standard burn wound dressings. Instead, they are

used in conjunction with these products and have specific

indications. Skin substitutes can be classified as temporary

wound coverings used to decrease pain and augment healing

or permanent skin substitutes used to add or replace the

remaining skin components.

& Temporary skin substitutes are used to help heal partial-

thickness burns or donor sites and close clean excised wounds

until skin is available for grafting (Table 5). There are typically

no living cells present in temporary skin substitutes.

Temporary skin substitutes typically feature a bilayer

structure consisting of an outer epidermal analog and a more

biologically active inner dermal analog. The purpose of a

temporary skin substitute is twofold. The first objective is to

close the wound, thereby protecting it from environmental

insults. The second objective is to provide an optimal wound

healing environment by adding dermal factors that activate

Table 6.

PERMANENT SKIN SUBSTITUTES

Product Origin ofTissue

Layers Category Uses

Apligraf

(Graftskin)

Allogenic

composite

Collagen matrix seeded with human

neonatal keratinocytes and fibroblasts

Composite:

epidermis

and dermis

& Chronic wounds; often used with

thin split-thickness skin graft

& Excised deep burns

Epicel Autogenous

keratinocytes

Cultured autologous keratinocytes Epidermis

only

& Deep partial- and full-thickness

burns (> 30% TBSA)

AlloDerm Allogenic

dermis

Acellular dermis (processed allograft) Dermis only & Deep partial-thickness burns

& Soft tissue replacement

& Tissue patches

Integra Synthetic Silicone outer layer on a collagen GAG

dermal matrix

Biosynthetic

dermis

& Full-thickness excised burn;

definitive closure requires thin

skin graft

Table 7.

EFFECTS OF TOPICAL NEGATIVE PRESSURE

& Enhances dermal perfusion, increasing blood flow

& Decreases edema formation

& Controls exudate, including removal of toxic products of

inflammation

& Decreases bacterial colonization

& Secures skin grafts and permanent skin substitutes to the

wound

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and stimulate wound healing. Biologically active dermal

components are typically naturally provided to the inner

layer, which is then applied to the remaining dermis in a

partial-thickness burn or an excised wound.

& Permanent skin substitutes are used to replace lost skin by

providing an epidermis, dermis, or both. They offer a higher

quality of skin than a thin skin graft (Table 6). Most perma-

nent skin substitutes contain viable skin cells as well as

components of the dermal matrix.

The purpose of a permanent skin substitute is to restore

full-thickness skin loss and improve the quality of the skin

that has been replaced after a severe burn. Permanent skin

replacement is a more complex process than the use of a

temporary skin replacement product.35-50

Two approaches are available to develop a permanent skin

substitute. The first is the use of a bilayer skin substitute, with

the inner layer being incorporated into the wound as a neo-

dermis, rather than removed like a temporary product. The

outer layer is either a synthetic to be replaced by autograft

(epidermis) or actual human epithelial cells. The epithelial

cells, which will form the epidermal barrier, are often not

sufficiently developed at placement to immediately act in this

capacity.

The second approach is to provide either an epidermal or

dermal analog or a 1-layer tissue. These products are technically

not permanent skin substitutes on initial placement because

there is no bilayer structure, although they are often described

as such.

One disadvantage of skin substitutes is the absence of active

antimicrobial activity; however, early effective wound closure

decreases the risk of bacterial growth.

Topical negative pressure therapyThe use of topical negative pressure (TNP) in the form of

vacuum-assisted closure (VAC) is a recognized treatment for

wounds.36-45 Some of the effects of TNP therapy using VAC

are listed in Table 7.

Because of its beneficial effects, TNP therapy has been

introduced to various aspects of burn wound management

with positive results. For example, TNP therapy has been

used for the initial management of high-risk burns, such as

moderately deep hand burns, to decrease edema and

improve outcomes. Wound conversion appears less likely

when TNP is used in these cases because it removes edema

and improves dermal blood flow. TNP therapy has also

been found to improve management of difficult burns,

especially those on the perineum and buttocks. Increased

healing of donor sites and improved skin graft take have

also been reported.

SUMMARYMultiple factors affect burn severity and outcome. Burn depth,

percentage of TBSA, age, chronic illness, overall heath status,

part of the body burned, and presence of smoke inhalation

injury contribute to the rate of burn survival.

Management of a burn wound has made remarkable

progress over the last 10 years. Statistics indicate that burn

survival has markedly improved in recent years, provided

that optimum care is available from the injury scene to

discharge. These outcomes, in part, parallel the advances made

in wound healing and general wound management. Improve-

ments in technology, infection control, and skin substitutes

have also contributed to the improvements made in burn

wound care.

Although significant differences remain in the pathophy-

siology and treatment of burn wounds compared with

nonburn wounds, the focus of wound care remains the same:

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