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ACUTE BURNSJohn L Hunt MD

EPIDEMIOLOGY

In 1991 there were an estimated 5500 fire- andburn-related deaths in the United States. An addi-tional 750 deaths were either partially or totallycaused by burns. Of these approximately 87% wereunintentional, 11% were the result of assault orsuicide, and 3% were secondary to hot liquid sub-stances or objects, the latter including chemicalinjuries. Between 1971 and 1991, deaths attribut-able to flames and hot liquids dropped an estimated40% while deaths from smoke inhalation decreasedonly 12%. Burn deaths have probably declinedrapidly as a result of successful prevention strategiesand improved burn care. It must be noted, how-ever, that the gathering of statistical data on burns,including mortality, is most assuredly incomplete.1

In 1993 the LA50 (defined as burn size lethal to50% of patients) in most burn units approached75% total body surface area (TBSA) burn.2,3 Thiswas ascribed to a number of factors such as earlyexcision and skin grafting; improved ICU care, ven-tilation, and nutrition; antibiotics; and, as always,the “team approach” in dedicated burn units.Infection continues to be the leading cause of mor-bidity and mortality in patients with thermal injury.The lung is now the primary source of infection,while burn wound sepsis has virtually disappeared.4

Saffle and colleagues5 reviewed 6417 patientswith a mean burn size of 14.1% who were treatedin 28 burn centers in the United States between1991 and 1993 and noted that 95.9% survived. Foryoung adults in this group, the LA50 was 81% TBSA.Deaths associated with inhalation injury amountedto 29.4%. The mean length of hospital stay (LOS)

was 13.5 days, and average total charges per staywere $39,533.

The American Burn Association has embarkedon a registry project to determine the “real” out-come data on LOS and charges stemming from burninjuries. Data gathered through this registry willinclude diagnosis, morbidity, treatment methods,survival and mortality figures, and rehabilitation.

THE BURN WOUND

There are three zones of burn.6 The central areais called the zone of coagulation and is composedof nonviable tissue. Surrounding this central area isthe zone of stasis. Initially blood flow is presenthere, but over the subsequent 24 hours hypo-perfusion and ischemia prevail and part of this areacombines with the zone of coagulation. Surround-ing the zone of stasis is the outer zone of hyper-emia, which contains viable tissue.

Along with the extent of burn and age of thepatient, the depth of the burn wound is a primarydeterminant of mortality following thermal injury.Wound depth is also a major determinant of apatient’s long term appearance and function after aburn. At this time the most accurate way to deter-mine depth of burn is clinical assessment based onexperience. The changing perfusion in the zone ofstasis and the fact that burn depth is not uniformeverywhere make it difficult for the physician toaccurately determine the depth of burn for the first24 to 48 hours after injury. Immersion scalds invery young children are particularly difficult to assessfor depth. A number of techniques such as burnbiopsy, vital dyes, fluorescein, and laser Dopplerflowmeter have been tried in an attempt to aidclinical observation, but none has been completelysuccessful.7

BURNS:ACUTE BURNS, BURN SURGERY,

AND POSTBURN RECONSTRUCTION

John L Hunt MD, Gary F Purdue MD, and Ross I S Zbar MD

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Thanks largely to the prevalence of topical anti-microbial agents, burn wound sepsis in most burnunits in this country is of minor clinical importance.Topical antimicrobials, however, by decreasing thebacterial concentration of the burn wound, haveresulted in prolonged separation of the eschar. As aresult, surgical excision with skin grafting of notonly full-thickness but also partial-thickness burns isaggressively followed.

BURN CLASSIFICATION

Partial-Thickness Burns

Minor burns, those that are superficial and donot exceed 10% to 15% of total body surface area,generally do not require hospitalization. Largerburns than these may be treated on an outpatientbasis, but only in unique circumstances.8 Survivalafter this type of burn is not an issue and scarring isnot a problem.

A partial-thickness burn will reepithelialize spon-taneously over a period of time that varies withdepth of the burn. Superficial partial-thickness burnscan be treated in a variety of ways. Most authorsrecommend application of a topical antimicrobialagent. Once the wound has been cleaned anddebrided, it may be “closed” with pig skin orBiobrane to help relieve pain and simplify woundcare.9 The dressing is left on the burn wound untilthe wound begins to spontaneously reepithelialize,at which time the dressing membranes separatefrom the underlying epidermis and are peeled orcut off. Very deep burns that are allowed to healspontaneously scar severely, so that most surgeonsrecommend surgery for coverage once the depth isascertained. Children with scalding wounds whoare under 1 year of age must be examined daily,and if by 14 days there is no gross evidence ofreepithelization, surgical excision should be con-sidered.

Full-Thickness Burns

Full-thickness burns may extend into fat, fascia,muscle, and even bone, and all must be excisedand skin grafted. If only the dermis or superficial fatis involved, tangential excision into fat is recom-

mended. Early wound closure has obvious ben-efits, but factors contributing to surgical morbidity,especially age and burn location, should be consid-ered in the decision.10 Only isolated reports haveshown that mortality decreases with early (first 24hours) total excision of full-thickness burns in patientswith massive injuries.11

BURN TRIAGE

The American Burn Association has identifiedburns that should be treated in a specialized cen-ter. This category includes the following injuries:

• 2nd and 3rd degree burns >10% TBSA in patientsunder 10 or over 50 years of age

• 2nd and 3rd degree burns >20% TBSA in otherage groups

• 3rd degree burns >5% TBSA in any age group

• 2nd and 3rd degree burns involving the face,hands, feet, genitalia, perineum, or major joints

• electric burns, including lightning injury

• chemical burns with serious threat of functionalor cosmetic impairment

• inhalation injuries

• lesser burns in patients with preexisting medicalproblems that could complicate management

• combined mechanical and thermal injury inwhich the burn wound poses the greater risk

If an adult burn victim is within 20 minutes of ahospital, there is no need to start an intravenousdrip on site which may delay transport. For theyoung pediatric patient, it is best to “scoop andrun” if transport time is under 1 hour.

On admission to the hospital, the burn victim istreated as any trauma patient, ie, is evaluated forAirway, Breathing, and Circulation. Burn patientsgenerally have normal vital signs (if there is no otherassociated trauma) and are able to communicatewith the examiner. At the hospital two large-boreperipheral catheters are inserted, preferably throughunburned skin. This avoids the complications thatmay ensue with central lines, such as pneumotho-rax (subclavian a), inadvertent arterial injury (femo-ral a), and venous thrombosis.

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BURN RESUSCITATION

Burn Shock

The successful management of burn shock is criti-cal to a patient’s survival. Burn shock is both hypo-volemic and cellular in nature, and is characterizedby specific hemodynamic changes includingdecreased cardiac output and plasma volume,increased extracellular fluid, and oliguria.

Fluid Replacement

Both the depth and extent of burn determinethe volume of fluid needed for resuscitation. The“rule of nines” is a simple and relatively accurateway to estimate the percentage of total body sur-face area burn in patients over 15 years of age(Fig 1).

Head and neck 9%Anterior trunk 18%Posterior trunk 18%Left arm 9%Right arm 9%Left leg 18%Right leg 18%Genitalia and perineum 1%

Fig 1. The “Rule of Nines” for estimating percent of total bodysurface area burn (%TBSA) in adults.

The goal of therapy is to replace the fluid seques-tered as a result of the injury. Ideally one shouldadminister the least amount of fluid necessary tomaintain adequate organ perfusion. The best guideto adequacy of resuscitation in the first 24 to 48hours is the hourly urine output. The volume infusedshould be continually titrated to avoid bothunderresuscitation and overresuscitation.

The main ingredient of any resuscitation fluid issalt replacement. Crystalloid in the form of lactatedRinger’s solution at a concentration of 130 mEq/L isthe most popular and easily used resuscitation fluid.Warden12 discusses several formulas used to resus-citate burn patients. The one generally recom-mended is the Parkland formula, which calls forlactated Ringer’s, 4 mL/kg/% burn in the first 24hours. Colloid is usually unnecessary in the first 24hours, as protein leaks from the capillaries into theextravascular space. (Of note: Capillaries inunburned tissue continue to sieve protein andaccount for edema in areas outside the injury.) Aurine output of 0.5 mL/kg/h indicates adequate tis-sue perfusion so long as there is no glycosuria.

During the second 24 hours, a 5% albumin solu-tion is administered in a volume of 0.1 mL/kg/%burn. The fluid is infused over a period of 2 to 3hours. Up to 1 in 5 adult burn patients will requiremore or less fluid than calculated.

In some situations it may be appropriate to moni-tor the central venous pressure of burn patientswith a Swan-Ganz catheter. These circumstancesinclude failure to resuscitate according to the pre-scribed urine output; extremes of age, particularlythe elderly; preexisting cardiac disease if the patientis symptomatic—eg, angina—or there is evidenceof pump failure; and patients with severe inhala-tion injury or pulmonary insufficiency where highpositive end expiratory pressure is required.13

Resuscitation in Children

Because of differences in proportion of bodyparts between children and adults and larger sur-face area per unit weight in children, the Berkowchart is used for calculating % TBSA in pediatricburn patients (Table 1).

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TABLE 1The Berkow Formula for Calculating % TBSA

in Children and AdolescentsAREA 1 YR 1-4 YRS 5-9 YRS 10-14

YRS 15 YRS

Head 19 17 13 11 9Neck 2 2 2 2 2

Ant. Trunk 13 13 13 13 13

Post. Trunk 13 13 13 13 13

R. Buttock 2½ 2½ 2½ 2½ 2½

L. Buttock 2½ 2½ 2½ 2½ 2½

Genitalia 1 1 1 1 1

R.U. Arm 4 4 4 4 4

L.U. Arm 4 4 4 4 4

R.L. Arm 3 3 3 3 3

L.L. Arm 3 3 3 3 3

R. Hand 2½ 2½ 2½ 2½ 2½

L. Hand 2½ 2½ 2½ 2½ 2½

R. Thigh 5½ 6½ 8 8½ 9

L. Thigh 5½ 6½ 8 8½ 9

R. Leg 5 5 5½ 6 6½

L. Leg 5 5 5½ 6 6½

R. Foot 3½ 3½ 3½ 3½ 3½

L. Foot 3½ 3½ 3½ 3½ 3½

The Parkland formula must be modified in pedi-atric patients by adding maintenance fluid to theresuscitation volume, 1500 mL/m2. A urine outputof 1 mL/kg/h is considered evidence of adequateresuscitation in children.

During the second 24 hours, a solution of either0.25% or 0.45% sodium chloride is given as fluidreplacement because of the small intravascular vol-ume of children. If only 5% dextrose and water isused and the infusion rate is too rapid, hyponatre-mia and seizures may occur.

Young children under 3 years of age, and espe-cially infants younger than 6 months, have a limitedamount of glycogen stored in the liver, which maybe rapidly depleted under conditions of burn stress.Blood glucose in young children should be mea-sured every hour for the first 24 hours postburnbecause of the high risk of hypoglycemia.

BURN EDEMA

Significant fluid shifts occur from the intravascu-lar to the extravascular space soon after a burn.This altered state persists for the first 24 hourspostinjury. The rate and amount of edema forma-tion depends on burn depth and size. In smallburns edema peaks early, while in large burnsedema development continues for 18 to 24 hours.When the burn exceeds 35% to 40% TBSA, edemaalso occurs in unburned tissue.

Early increased vascular permeability is in partrelated to histamine, but many of the local effectsare similar to a reperfusion injury.14 The reestab-lishment of blood flow to ischemic areas triggers asequence of events that produce irreversible dam-age. The mechanism accounting for this increasedvascular permeability is likely related to polymor-phonuclear leukocytes (PMN) and their adhesionto the endothelium. PMN have been identified ascontributing to the microvascular occlusion seenboth systemically and locally following burn injury.The adherence of PMN to vascular endothelial cellsurfaces creates a microenvironment in which PMN-derived proteases and toxic oxygen radicals,hydrogen peroxide and hydroxyl radicals arereleased by both endothelial cells and PMN. Theseradicals trigger peroxidation of lipids in cell mem-branes and resultant cell lysis, to the detriment ofvessel lining. Intercellular gap formation, whichincreases the microvascular permeability, results inedema and thrombosis.15

Fluid is lost through a “capillary leak” in the burnwound and underlying tissue. The pathophysiologyof the loss of capillary integrity is complex and onlypartially understood.16 Local vascular damage is thedirect result of heat applied to the tissues, but moreprofound vascular effects are related to both sys-temic and local factors. Endothelial cells swell, formgaps, and allow extravasation of fluid into the perivas-cular space. The altered cell transmembranepotential causes sodium to be drawn into cells, whichconsequently swell. At the same time significanthypoproteinemia causes a decrease in capillaryhydrostatic pressure and plasma oncotic pressure,with a corresponding increase in interstitial oncoticpressure.

Any injury—and burns are no exception—elicitsa massive systemic inflammatory response “in whichcytokines and other metabolic products of activatedleukocytes can act either beneficially to provide forenhanced host resistance or deleteriously to depressthe function of remote organs.”17 Local tissuetrauma, ie, the burn, activates the release of anarray of systemic mediators such as complement,arachidonic acid, and cytokines, particularly IL-1and TNF. A number of local mediators, includingoxidants and arachidonic acid metabolites, appear

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to be involved in burn edema.18 These localmediators of inflammation also influence the pro-duction of systemic mediators, with resultantincreases in substances such as PGE2. Hyperme-tabolism develops along with muscle catabolism, allcommon to the large cutaneous burn victim.

Experimental administration of catalase andsuperoxide dismutase, two antioxidant enzymes, isassociated with less edema and decreased fluidrequirements in burns.19 Vitamin C and plateletactivating factor (PAF) show similar effects.20,21

Therapeutic manipulation of monoclonal antibod-ies against neutrophil membrane glycoprotein CD-18 (important in neutrophil adhesion to microvas-cular endothelium) is being evaluated in clinicaltrials.22

INHALATION INJURY

Approximately 10% to 20% of all hospitalizedburn patients have sustained an associated inhala-tion injury. The consequences of such injury arenot only to increase fluid requirements during re-suscitation,23 but also to increase mortality signifi-cantly.24,25 An inhalation injury can damage all lev-els of the respiratory tract, from the oropharynx—evidenced by airway edema and occlusion—to thelung, where it manifests as alveolar derangementwith associated acute respiratory distress and bron-chopneumonia. The majority of patients with mas-sive burns will survive the resuscitation period (thefirst 72 hours postburn) only to succumb to pulmo-nary sepsis. It must be emphasized again that greaterthan predicted fluid requirements are the rule ratherthan the exception in patients with inhalation inju-ries.

Any patient who has had smoke exposure is sus-pected of having inhalation injury. A history andphysical examination, coupled with laboratory testsand bronchoscopy, aid in identifying those patientsat risk for developing pulmonary problems. Thetypical clinical profile is that of a patient who wasburned in a closed space and who inhaled smoke,has a facial burn, singed nasal hairs, erythema, andcarbonaceous material in the back of the throat.Bronchoscopic findings are those of erythema andsooty deposits in the airway.26 In addition, the

carboxyhemoglobin level may be elevated (>15%)and hypoxemia may or may not be present.

The treatment of a patient with inhalation injuryis supportive.27-29 The upper airway must be pro-tected. Prophylactic intubation is indicated whenthere is a question of upper airway edema andswelling.30 Either nasotracheal or endotrachealintubation is preferable to early tracheostomy.31

Once an airway is made secure, ventilation shouldbe gently maintained using a volume ventilator.Prophylactic antibiotics and steroids are not indi-cated.

BURN SURGERYGary F Purdue, MD

ESCHAROTOMY AND FASCIOTOMY

The circumferentially burned extremity is at riskof becoming vascularly compromised. During thefirst 24 to 48 hours postburn, continual evaluationof the status of peripheral circulation is mandatory.The Doppler flowmeter is the only reliable meansof doing this, as the physical signs of arterial insuffi-ciency are obscured either by overlying burn ortissue edema.1

Numbness and tingling of the limb are the earli-est signs of ischemia. Arterial flow in the upperextremity must be assessed in the superficial pal-mar arch of the hand as well as in the ulnar andradial arteries. The development of an “intrinsicminus” hand is an indication for decompression ofthe deep muscle compartment of the hand.Decompression of this compartment involves mak-ing three radial incisions in the dorsum of thehand then bluntly dissecting deep into the handwith a hemostat. Both medial and lateral incisionsare required for decompression of the arm andleg.

Occasionally chest escharotomies are requiredto permit appropriate ventilatory expansion. Fig-ure 2 illustrates the preferred escharotomy sites.

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Fig 2. Preferred sites for escharotomy. (Reprinted with permissionfrom Moylan JA Jr, Inge WW Jr, Pruitt BA Jr: Circulatory changesfollowing circumferential extremity burns evaluated by the ultra-sonic flowmeter. An analysis of 60 thermally injured limbs. JTrauma 11:763, 1971.)

EXCISION AND GRAFTING

The surgical principles of burn care are• preservation of life

• prevention and control of infection

• conservation of all viable tissue

• maintenance of function

• timely closure of the burn wound

Early burn wound closure is instrumental in fulfillingthe first four principles.

Since Janzekovic’s classic paper in 1970,2 a num-ber of articles have been published both for andagainst early excision of partial and 3rd degree burns.In the last decade, however, most burn surgeonshave largely abandoned the conservative, non-excisional approach to burn injury management infavor of early excision and grafting. The only caveatto this practice is that a wound must not be excisedunless it can be immediately closed. Sheridan andcolleagues3 review the technique and outcome ofprompt excision and closure of burn wounds.

Does early excision of large burns have any effecton morbidity and mortality? A report by Cryer andothers4 notes markedly improved survival of patients

41 to 60 years of age who have burns over 20% to65% TBSA and are treated with early excision andgrafting. Early wound closure may decrease overallmortality5 but does not change the morbidity pat-tern or cause of death of patients who die morethan 3 days postburn.6

A retrospective study from the Shriners BurnsInstitute7 in Galveston failed to confirm the benefitof massive burn wound excision. Pediatric patientswhose burns were <50% TBSA showed no signifi-cant change in length of stay, blood requirementsor mortality. Patients with burns >50% TBSA (with-out inhalation injury) had decreased mortality whentheir burn wounds were excised early.7 Monafoand Bessey8 showed that the importance of surgicaltherapy of burns became more difficult to identifyas the size of the burn injury increased beyond20% TBSA.

Herndon and Parks9 compared two methods ofburn treatment: serial debridement and autograftingversus early massive excision and coverage withcadaver skin. The latter protocol consisted of woundexcision to fascia in the first 3 days postburn fol-lowed by immediate coverage with meshedautograft overlaid by ABO-matched fresh or frozenallograft. The authors found no difference in patientsurvival with either treatment. The only tangibleimprovement of early excision and allograft place-ment over conventional treatment was a decreasein hospital stay and interval to final wound cover-age. Differences in the number of procedures,operating room time and blood loss between thetwo groups were not statistically significant.9

Tangential or full-thickness excision into fat or tofascia should be performed with the Humby knifeunder tourniquet control to prevent massive bloodloss.10 Full-thickness excision to fascia is ideal forminimizing blood loss in areas such as the back andchest, but is cosmetically unsightly.6 The cosmeticdeformity created by excision to fascia is of suchmagnitude that tangential excision into fat is prefer-able in these cases. When operating on preadoles-cent females, the nipple and underlying breast tis-sue should be preserved whenever possible. Theearly excision of deep hand burns provides excel-lent functional results.11

The decision to undertake early eschar excisionin patients with inhalation injuries presents a clini-cal dilemma. Early excision is probably warrantedin burn patients who have inhalation injury or

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chronic obstructive pulmonary disease12 if the fol-lowing conditions are met:• pulmonary function can be maintained

• the patient is hemodynamically stable

• operating room and body temperatures are keptabove 37 °C

• anesthesia time is limited to 2 hours

• no more than 25% of TBSA is excised at onetime

BURN WOUND CLOSURE

In the interim between admission to the burncenter and grafting session(s) under anesthesia,patients benefit from having their burn woundsclosed for relief of pain and to avert infection. Inthe absence of sufficient autograft, the standard forwound closure after massive burn excision iscadaver allograft.

Numerous physiologic dressings have beendeveloped13-15 to temporarily cover the burn wounduntil definitive closure can be managed. Theadvantages and disadvantages of some of the mostpopular artificial coverings in use today are listed inTable 2.

TABLE 2Temporary Wound Dressings

Material Source Advantages Disadvantages

Allograft cadaver effective,vascularizes

expensive, maynot be available

Xenograft pig comes in largesizes, can beappliedrapidly

biodegradable,will notincorporate inwound

Amnion deliveryroom

inexpensive,widelyavailable

must bechanged every2-4 d, subjectto high waterfluxes

Biobrane© nylon &silicon

elastic,uniform,transparent

variablyadherent

The use of artificial skin and cultured epidermalautografts has been reviewed in a recent issue ofSelected Readings in Plastic Surgery (Vol 9, No 1)16

and will not be discussed further here. Dermalsubstitutes combine the recipient site advantagesof thick grafts with the donor site advantages of thingrafts,17 and are currently under investigation.

INFECTION

Before the advent of effective topical antimicro-bials, partial-thickness burns frequently becameinfected and converted to full-thickness injuries.Twenty-five years ago silver nitrate, mafenideacetate, and silver sulfadiazine were introducedand changed the epidemiology of burn wound sep-sis. Table 3 lists the attributes and limitations of thethree most commonly prescribed agents for the topi-cal control of infection in burn patients.18

The use of prophylactic antibiotics such as peni-cillin offers no protection against the developmentof either cellulitis or burn wound sepsis, but doespromote the selection of antibiotic-resistant bacte-ria.19 The importance of environment in the spreadof infection cannot be overemphasized. McManusand associates20 report a profound decrease in gramnegative bacteremia when burn patients weremoved from open wards to single-bed isolationenvironments where no cross infection or coloni-zation by endemic resistant bacteria occurred.

Burn wound sepsis is defined as >105 organismsper gram of tissue. Bacteremia is not synonymouswith burn wound sepsis, and many “clinically sep-tic” patients never have evidence of bacteremia.21

Serial blood cultures are often negative in the pres-ence of burn wound sepsis, and positive burn woundcultures are generally not recovered until 5 to 10days after proven heavy bacterial wound infection.

Group D streptococci (Enterococcus sp) areimportant pathogens in the severely burned patient.Secondary enterococcal bacteremia has been asso-ciated with 50% mortality.22 Once blood culturesare positive, therapeutic intervention appears tohave little effect on mortality.

Fungi and yeasts are often late colonizers andinvaders of the burn wound. Pensler23 reviewedthe clinical course of 72 patients with fungal sepsisand noted mortality of 32%. Changes in topicalantimicrobial therapy did not influence survival;rather, once histologic invasion was identified, thepatients were taken to the operating room for sur-gical debridement. The author states that broadspectrum antibiotics, a common denominator in allhospitalized patients, should not be used withoutspecific indications in burns.

Infection is the leading cause of death in burnpatients. Susceptibility to infection increases withthe extent of burn injury, especially when >30%TBSA. Other risk factors include24

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• 3rd degree or deep 2nd degree burns

• patient age under 16 or over 60 years

• preexisting disease (diabetes mellitus, cardio-pulmonary insufficiency, malnutrition)

• a hot, moist wound environment

• impaired blood supply (shock, thick avasculareschar)

• low wound pHMerrell25 showed a significant decrease in

postburn septic mortality to 0.7% by successfullymanaging septic complications of the burn patient.During the past 10 years, the primary cause of deathhas shifted from invasive burn wound infection tobronchopneumonia.26 Robson,27 Luterman and oth-ers,28 and Pruitt and McManus26 provide excellentoverviews of burn sepsis and its control.

INFLICTED BURNS IN CHILDREN

Approximately 10% of burned children admittedto hospitals have purposely inflicted injuries, pri-marily tap water immersion scald burns. Theseinjuries can often be recognized by their patternsand distribution.29 Physicians involved in pediatricburn care are urged to familiarize themselves withthe typical signs of these inflicted injuries so that

they may recognize them and intervene appropri-ately.

IMMUNOLOGIC FUNCTION

Virtually every aspect of the immune system isdisturbed by the burn injury. Humoral as well ascell-mediated immunity is impaired and manifestsas depressed levels of immunoglobulin, reducedactivation of complement to form membrane-attacking complexes,30 and diminished stimulationof lymphocyte proliferation and response. Thera-peutic interventions to enhance the immune stateare still experimental. “The redundancies of thecell populations and the cytokines and other me-tabolites produced by the cells predictably limit theeffectiveness of any single agent and make clinicalevaluation of such agents difficult.”31

METABOLISM AND NUTRITION

All large burns are associated with hypermetabo-lism. The metabolic rate can exceed 200% of nor-mal in extremely large or septic burns.32 Thisincrease in metabolic rate is proportional to burnsize up to approximately 60% TBSA, leveling offthereafter. Decrease in wound size either by

TABLE 3Commonly Used Topical Antimicrobial Burn Wound Agents

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spontaneous reepithelialization or by excision andgrafting does not appear to change energy expen-diture in a predictable manner.33,34 An excellentoverview of nutritional support in the burn patientis presented by Waymack and Herndon.35

Formulas recommended for calculating the meta-bolic requirements of hospitalized patients do notapply to burn patients whose clinical status is inconstant flux. Although a number of formulas havebeen devised for estimating nutritional require-ments in burn patients, it is possible to quantifyactual energy expenditure by indirect calorimetryusing a portable unit.36,37 Indirect calorimetry helpsidentify patients who receive either too much ortoo little nutrition and allows for prompt correction.The measured energy expenditure (MEE) at restreveals that a mean nutritional intake 1.4X the esti-mated energy expenditure (EEE) is associated withsatisfactory maintenance of body weight in themajority of patients. Using measured energy ex-penditures,38

EEE(v) = 1925 - 10(A) + 5(W) + 281(S) + 292(T) + 851(B)

EEE(s) = 629 - 11(A) + 25(W) - 609 (O)where EEE = estimated energy expenditure (kcal/day); v = ventilatory dependency; s = spontane-ously breathing; A = age (yr); W = body weight(kg); S = sex (male 1, female 2); T = 1 for diagnosisof trauma; B = 1 for burn; and O = obesity (1 ifpresent, 0 if absent).

Pediatric burn patients have very different energyrequirements from those of adults, and their dietsshould be adjusted accordingly.39 Bell and others40

found that most burned children maintained 90%of their premorbid body weight when given caloricintakes of basal metabolic rate X2 (Wolfe’s formula41)in conjunction with a generous protein intake andaggressive early excision and grafting procedures.

The daily protein requirement can be met with1–2 g/kg body weight/d for adults and 2–3 g/kgbody weight/d for infants.42 Fat emulsions are bestlimited to 4 g/kg body weight/d because of theinability of the liver to clear fat more rapidly. Dietsthat have a nonprotein kcal:nitrogen ratio of 100:1promote a positive energy balance.43

Excessive glucose administration is detrimentalto burn patients. Unlike normal persons, burnpatients appear to have an upper limit of glucoseutilization of approximately 6.2 mg/kg/min, whichrepresents about 60% to 70% of a burn patient’s

caloric requirements. Excessive glucose is con-verted to fat, while excessive carbon dioxide andwater production may cause fluid overload orinability to wean the patient from mechanical ven-tilation.

When possible, the gastrointestinal tract shouldbe used to provide the needed nutrition becausespontaneous food intake appears to be close to pre-injury level. Enteral tube feeding is frequently nec-essary in burn patients.

TOXIC EPIDERMAL NECROLYSIS

Toxic epidermal necrolysis (TEN) is character-ized by epidermal sloughing, usually in conjunctionwith mucosal inflammation and ulceration. Theepidermis separates at the epidermis-dermis junc-tion, and the extent of slough varies from minimalto 100% TBSA. The precipitating event is uncer-tain, but TEN may follow nonspecific infections ordrug administration. Commonly implicated drugsinclude phenobarbital, diphenylhydantoin, sulfona-mides, various antibiotics, and nonsteroidal antiin-flammatory agents.

While spontaneous reepithelization does occurfollowing an episode of toxic epidermal necrolysis,the reepithelialization process is very slow, so thatpatients whose epidermal slough is greater than10% TBSA are best treated in a burn center.

The management of TEN wounds is very similarto that of burn wounds. Appropriate fluid resuscita-tion, nutritional support, and prevention of infec-tion are the goals of therapy. Early wound debride-ment and coverage with a biologic dressing (al-lograft, xenograft or Biobrane) give excellentresults.44,45 Corticosteroids are not recommendedbecause of the increased risk of infection.46

ELECTRICAL INJURY

An electrical injury occurs when electricity isconverted into heat as it travels through tissue.47

Acute electrical injuries constitute the primary rea-son for hospitalization in about 2% of admissions toa burn center. Approximately 15% of these patientshave associated multiple trauma. Although the meancutaneous injury is only 10% to 15% TBSA,48 thecutaneous injury usually does not reflect the pres-ence of deep tissue damage. Muscle damage shouldbe suspected if the urine is grossly pigmented (light

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pink to deep brown). Damaged muscle is mostcommonly found directly underneath or adjacentto contact points, but the exact location and extentof the muscle damage can be ascertained with atechnetium-99m stannous pyrophosphate musclescan.49

The fluid replacement needed for resuscitation iscalculated from the size of the cutaneous injury plusan undetermined additional amount when muscledamage is present. If gross urinary pigment is present,2 ampules of sodium bicarbonate and 2 ampules ofmannitol are initially given in addition to intravenousRinger’s lactate. Further use of diuretics is contrain-dicated. Urine output should be maintained be-tween 100 and 125 mL/h until it is seen to clear.

Acute electrical injuries may precipitate cardiacarrhythmia, which is nearly always diagnosed beforeor during admission. Routine cardiac monitoring isnot necessary unless the patient suffered cardiacarrest at the scene of the accident, has an abnormalelectrocardiogram, or arrhythmia was documentedduring transport.50 Vigorous resuscitation, continu-ous hemodynamic and metabolic support, and earlyaggressive surgical intervention limit mortality inpatients with electrical injuries to the heart.51

Muscle injury is often associated with the devel-opment of increased compartmental pressures anddecreased peripheral perfusion, and therefore thestatus of the soft-tissue compartments should be con-tinually evaluated for the first 24 hours postinjury.Fasciotomy is selectively performed on the basis ofclinical symptoms and should be done in the oper-ating room with the patient under general anesthe-sia.52 Regional anesthesia should be avoided. Ini-tial operative debridement is carried out 24 to 48hours after injury. Exposed neurovascular bundles,tendons, and bone must be covered early witheither remote or local muscle flaps. Mafenideacetate (Sulfamylon®) is the antimicrobial agent ofchoice for the contact points and areas of deepinjury by virtue of its excellent tissue penetrationand anti-gram-negative bacterial action.

CHEMICAL BURNS

Chemical burns can be roughly classified as thoseinvolving alkalis, acids, or special chemicals. Alka-line substances such as sodium and potassiumhydroxides and cements are the most commoncauses of chemical burn.53 Chemical agents usually

injure the skin by direct chemical reaction ratherthan by production of heat, but inadequate irriga-tion or neutralization may cause a thermal burn tocompound the original chemical injury.

The severity of a chemical burn is often underes-timated on first examination. Immediate treatmentconsists of lavaging the area with copious volumesof tap water. In addition, several injuries requirespecial care, as follows.53,54

Hydrofluoric acid burns are initially treated witha paste made of 35 mL of 10% calcium gluconatein 150 gm of K-Y Jelly®. This paste is applied overthe affected area and changed every hour asneeded. More severe injuries may require subcu-taneous injection of calcium gluconate into the pain-ful area.

Phenol is not soluble in water and is readilyabsorbed through intact skin. Topical applicationof polyethylene glycol or vegetable oil is beneficialin these injuries.

Phosphorus burns are treated by keeping theareas copiously irrigated and continuously wet withwater, followed as soon as possible by surgicaldebridement of any extraneous particles.

Cement burns are rinsed with water until thesoapy feeling has disappeared and then the area isdried thoroughly.

Tar burns, while not true chemical burns, respondwell to application of bacitracin or neomycin oint-ment for 12 hours, at which time the ointment iswashed off and silver sulfadiazine is applied.

POSTBURN RECONSTRUCTIONRoss I S Zbar MD

HYPERTROPHIC SCAR AND CONTRACTURE

The goal of all secondary burn reconstruction istwofold: to restore function and appearance. Afterinitial wound closure, surgical intervention proceedsonly when the recovery process has plateaued. Ini-tial treatment, prior to postburn secondary recon-struction, includes mobilization therapy with pas-sive and active range of motion. Additionally, splints

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and compression garments may be required. Patientcooperation is essential

Despite active intervention, two pathologic pro-cesses cause limitation of motion: hypertrophicscar formation and joint contracture. Hypertrophicscar formation begins 3 weeks after wound closureand is most exuberant by the second and thirdmonth, after which the scar slowly regresses overthe next 12 to 24 months. Hypertrophic scar for-mation is especially common in burns that areallowed to granulate spontaneously for longer than3 weeks. Deitch and colleagues1 demonstratedthat the best indicator of hypertrophic scar forma-tion is the time required for healing. When woundsheal in less than 3 weeks, 33% result in hyper-trophic scars, whereas of wounds that require morethan 21 days to heal, 78% form hypertrophic scars.Grafting of wounds after 14 days of granulation alsoproduces poor results.

Young patients and dark-skinned patients are atincreased risk of developing hypertrophic scar.Although the exact etiology of hypertrophic scarremains elusive, it is likely related to cell stimula-tion stemming from traumatic injury. Extensive orchronic injuries trigger a high degree of inflam-mation and cytokine release. These polypeptidegrowth factors generate a pathologic cellularresponse that presumably results in a hypertrophicscar in genetically susceptible individuals. Thedepth of injury also plays a role in the magnitudeof the cellular response.

Wound contracture is an additional problem. Thepathologic process involves contraction of tissue bymyofibroblasts until the limits of motion are reached.Wound contracture occurs during scar remodelingas collagen undergoes reorganization. The result-ing distortion may be either extrinsic or intrinsic.Extrinsic contracture results from contracture ofan adjacent body part—eg, ectropion from a burnof the cheek—whereas intrinsic contractureresults from direct contracture of the region—eg,shortening of the lower lid from a burn of the liditself. A burn deformity may involve either or bothof these processes (Fig 1).

Proper burn reconstruction requires identifi-cation of the type of contracture and surgicalintervention. Extrinsic contracture requiresrelease whereas intrinsic contracture requiresreconstruction.

Fig1. Intrinsic (left) and extrinsic (right) scar contracture after afacial burn, both causing lid ectropion.

Nonsurgical Prevention

Several nonsurgical methods have been pro-posed to limit hypertrophic scars and contracture,as described below.

Constant external pressure on the wound pro-duces softer and thinner scars. Collagen fibrils thatare haphazardly deposited by fibroblasts in thewound are gradually reoriented and aligned throughmechanical traction until the fibers are parallel tothe forces of stress.2,3 The pressure is applied bymeans of splints, bandages, and elastic garments onthe healed burn wound. Pressures in the order of25 mmHg are required to inhibit hypertrophic scar-ring. To be successful, the pressure must be main-tained during the entire process of scar matura-tion—up to 2 years. Ideally the elastic garments arecustom-fitted to the individual (Fig 2) and appliedjust after the wound is healed.4 The garments lastbetween 1 and 3 months and should be replacedbefore they lose their effectiveness.

Intralesion injection of triamcinolone can limithypertrophic scar formation in certain cases.5 Sili-cone gel is also potentially beneficial, although itsprecise mode of action remains unclear.6,7

Surgical Prevention

Timely surgical intervention also may help pre-vent subsequent hypertrophic scar and burn con-tracture. Janzekovic8 noted better esthetic and func-

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tional outcome of burn scars with early excisionand grafting than with conservative management.Jonsson and Dalsgaard9 note faster healing andless scarring when early tangential excision andgrafting is used in the face. Selection criteria forearly excision of burns of the face include woundsexpected to take more than 3 weeks to granulatespontaneously; surgery that is not life threaten-ing; and available operative facilities and ancil-lary support. Only deep dermal and subdermalburns are excised. Split-thickness skin grafts mustbe 0.012- to 0.014-inch thick. The authors be-lieve that conservative management can lead tonecrosis of the dermis from infection or desicca-tion, eventually yielding a hypertrophic scar,whereas early excision and grafting improves theoutcome.

An excellent study by Fraulin and colleagues10

demonstrates that early tangential excision and graft-ing of the face results in better scars compared withprolonged spontaneous granulation.

Skin grafts inhibit the proliferation of myofibro-blasts11–13 in the wound bed and hinder woundcontraction. Full-thickness grafts are superior tosplit-thickness grafts in preventing wound contrac-tion regardless of the absolute thickness of the graft.The key factor is the total percentage of dermisgrafted: The more dermis there is in the skin graft,the greater the subsequent myofibroblast inhibitionthere is in the wound bed.12

PRINCIPLES OF BURN RECONSTRUCTION

Like all reconstruction in plastic surgery, a masterplan should be outlined to establish the sequenceof surgical procedures. Additionally the surgeonand patient must be aware that at times a variety ofprocedures may solve a particular reconstructivedilemma, and that each procedure has its inherentrisks and benefits. Lastly the surgeon must be famil-iar with the reconstructive ladder of increasing sur-gical complexity of procedures to solve a particularproblem.4,14

Feldman15 lists basic tenets of burn reconstruc-tion:• Analyze the deformity and note distorted and

absent tissue.• Generate a long-range plan for reconstruction

that establishes priorities and addresses bothfunctional and esthetic concerns.

• Delay reconstruction until the scars and graftshave matured. Use splints and elastic garmentsto minimize scar hypertrophy.

• Release extrinsic contracture before intrinsiccontracture.

• Orient scars parallel to relaxed skin tension lines.• Identify and ration potential donor site skin.• Resurface according to regional esthetic units.

If possible, adjacent units should be coveredwith a single large graft to avoid seams betweenterritories.

• Match donor skin according to thickness, color,and texture. Thicker skin grafts produce lesspostoperative contracture.

• Protect new scars and grafts from ultravioletradiation to decrease the chance of hyperpig-mentation.

RECONSTRUCTIVE LADDER

After burn scar excision, several options are avail-able to the surgeon to close the resulting defect.

Direct closure is the simplest form of scar revi-sion. The releasing incision should be oriented sothat the new scar falls within the lines of minimalskin tension. Tension on the wound closure isunacceptable.

Adjacent tissue transfer is another techniquethat closes a defect. The Z-plasty is particularlyhelpful in burn surgery because there is an overall

Fig 2. Elastic compression garment. (Reprinted with permissionfrom Robson MC, Barnett RA, Leitch IOW, Hayward PG: Preven-tion and treatment of postburn scars and contracture. World J Surg16:87, 1992.)

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gain in length along the scar after the skin flaps arerotated. Understanding the geometry of the Z-plasty is paramount. The limbs must be of equallength with identical angles. Rohrich and Zbar16

review the Z-plasty and its myriad uses.Skin grafts provide skin when local tissue is

simply inadequate. Full thickness skin grafts (FTSG)are preferred because they prevent future tissuecontracture by virtue of the inhibitory propertiesof the transferred dermis. Split thickness skingrafts (STSG) are commonly used for large-sur-face defects, but STSG tend to shrink consider-ably, leading to secondary burn wound contrac-ture. If graft meshing of STSG is necessary, theskin must not be spread out too widely to preventruggae-type granulation and hypertrophic scar-ring. All grafts, unfortunately, can hyperpigmentover time.

The donor site is important too. The donor siteskin should be of similar texture and color to that ofthe recipient site; hair-bearing skin should be trans-ferred only when appropriate or unavoidable.Grafted skin should be transferred in sheets andused to replace entire esthetic units, as Gonzalez-Ulloa recommends (Fig 3).17

Fig 3. Regional esthetic units of the face. (Modified fromGonzalez-Ulloa M: Restoration of the face covering by means ofselected skin in regional aesthetic units. Br J Plast Surg 9:212,1956.)

The use of cultured epithelial autografts (CEA)is routine in acute burn patients. Preliminary stud-ies indicate its success also in postburn reconstruc-tion, particularly when resurfacing burn scars inwhich autologous dermal elements are present.18

Drawbacks of CEA are high cost and the delicate,time-consuming application.

Flaps are necessary when the burn wound showsbare bone, tendon, or cartilage, or when irradiatedtissue is present. Flaps are useful for limb salvage,in coverage of unstable scars or a mobile joint, andin cases of recurrent contracture after previous Z-plasty. In addition, most surgeons opt for flap trans-fer when large amounts of tissue are required.

The flaps used in burn reconstruction may bepedicled or freely vascularized, musculocutaneousor fasciocutaneous. Free flaps provide a means forsingle stage reconstruction with rapid transfer oftissue, early wound closure, early mobilization, anddecreased hospitalization. Free flaps also allow forbetter esthetic contouring than pedicled flaps.19

Grotting and Walkinshaw20 state that free flaps areindicated in burn patients who have exposed bone,cartilage, or tendon, particularly of the extremity,and in whom ordinary means cannot be used toexpediently close the wound. Age is not a con-traindication to free-flap use.

Platt and associates21 report that of 604 patientswho required surgical intervention for burns from1989 to 1993, only 1.5% needed free-tissue trans-fer. The rate of flap loss in these patients was higherthan the average in a non-burn population. Theauthors believe that incomplete debridement andpoor recipient site vessels led to the higher rate offailure in burn patients. On the other hand,Abramson and colleagues22 performed 45 free-tissuetransfers in 35 burn patients during a similar period(1987–1994) and report 96% flap survival.

Tissue expansion is another technique thatfacilitates burn reconstruction. By expanding theskin peripheral to the scar, sufficient skin of idealcolor, texture, thickness, and sensation can beobtained while minimizing the donor defect.23–27

The foremost disadvantage of tissue expansion isthe necessity to have at least two surgical proce-dures. Additionally, although the technique isstraightforward, there is a risk of complicationsincluding exposure or extrusion of the tissueexpander, neurapraxia, pain, and infection.

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A recent study from Bellevue Hospital in NewYork City by Youm and associates28 illustrates theproblems of tissue expansion in a public hospital.Complications occurred in 22 of 34 expanders(65%). Major complications resulted in prematureremoval in 13 of 34 expanders (38%). Major com-plications included deep infection (32%); exposure(21%); and deflation (3%). Minor complicationsconsisted of dehiscence of the surgical wound, cel-lulitis, and drainage, and occurred in 9 of 34expanders (27%). The authors note that risk factorsfor major complications of tissue expansion in thissetting are pediatric patients and placement of mul-tiple expanders.

Another study from Children’s Medical Centerin Dallas29 confirms this observation. Friedman andcolleagues29 demonstrate an increased risk of fail-ure when placing tissue expanders in children lessthan 7 years old. Other risk factors uncovered bythis study include the use of internal ports with thetissue expanders and a history of at least two priorexpansions.

Neale and associates30 outline some basic prin-ciples of tissue expansion in the head and neck, asfollows:• Use caution when advancing expanded skin

beyond the border of the mandible.• Avoid creating vertical linear scars.

• Do not expand unburned regions of the face orneck.

• Advance expanded skin caudally rather thancephalically when possible to decrease the pos-sibility of iatrogenic ectropion.

• Remember that other techniques may be moreappropriate.

• Advance flaps with the head and neck in exten-sion to minimize postoperative tension.

• Exercise prudent patient selection.Despite these precautions, the authors still expe-

rienced approximately 30% complications in theirseries.30

Contrary to popular belief, the use of tissueexpansion in pediatric burn patients is not associ-ated with more complications than tissue expan-sion in pediatric patients with other diagnoses.31

A novel concept is the use of pretransfer tissueexpansion followed by microvascular free-tissuetransfer. This combination increases the versatility

of both techniques. Not only is a large amount ofvascularized tissue available for the burn scar defect,but donor site closure is possible with pretransferexpansion. Entire esthetic units can be replacedwith this technique. Additional advantages ofpretransfer tissue expansion include enhanced flapvascularity due to neovascularization at the papil-lary dermal level; a surgical delay effect created byplacing the tissue expander; potential increase insize of the pedicle vessel, which facilitates free trans-fer; and resultant fat atrophy accompanying tissueexpansion, which creates a thinner and more pli-able cutaneous flap.32 Recognized drawbacks ofpretransfer tissue expansion are the potential oblit-eration of surgical planes by the expander andedema around the flap pedicle making dissectionmore difficult.

Spence33 describes using tissue expansion at FTSGdonor sites prior to harvest to supply large amountsof skin from a donor site that can be closed prima-rily. The transferred skin behaves like a regularFTSG.

BURNS OF THE SCALP

Burn alopecia differs from hereditary hair loss inthat the scalp is tight, thin, and poorly vascularizedsecondary to burn cicatrix. Despite these obstacles,there are recent reports of successful hairmicrografting in burn patients directly into scar.34,35

If burn scar excision is required and the resultingdefect is small, it may be closed using classic rota-tional flaps as described by Juri36 and Orticochea.37

A common problem with these techniques isimproper hair follicle orientation.

Tissue expansion is an ideal method of recon-struction in large areas of burn alopecia encom-passing up to 50% of the scalp. The transferred hairis of similar texture and color and the scars areeasily camouflaged. Negatives of tissue expansioninclude prolonged treatment duration, temporaryexternal disfigurement from the expanders, andmultiple surgical procedures.38,39

Larger burns may require free-tissue transfer forappropriate coverage, especially when there is cal-varial or dural involvement. Classic choices includethe parascapular flap, the radial forearm free flap,and the latissimus dorsi flap.40–42 When osteomy-elitis of the calvarium is present, a free muscle trans-

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fer is superior to a fasciocutaneous transfer becauseof the recognized scavenger effect of muscle.

BURNS OF THE FACE

Forehead

For small burns of the forehead, primary excisionwith direct approximation or transfer of adjacenttissue is best. For larger burns of no more than 50%of the forehead, tissue expansion is a reasonableoption. When more than 50% of the forehead isinvolved in the burn, resurfacing of the entireesthetic unit with a thick STSG or FTSG leads to agood reconstructive result. The forehead estheticunit extends from eyebrows to hairline and to theouter canthi bilaterally. Care must be taken to pre-serve the temporal branch of the facial nerve dur-ing dissection.

When exposed bone is present, free-tissue trans-fer or Millard’s crane principle is required.43 Thecrane principle calls for a scalp flap to be rotatedinto the defect and allowed to mature for 2-3 weeks,at which time it is returned to its native position atthe donor site while leaving soft-tissue over thepreviously exposed calvarium. The soft-tissue isallowed to granulate for 5-7 days, and a graft maythen be placed over it.

Eyebrow

Eyebrow reconstruction is accomplished witheither strip grafts or micrografts.34,35 Recentadvances in hair transplantation and micrograftinghave improved graft survival despite the poor qual-ity of the recipient bed. The surgeon must respectthe esthetic landmarks of the eyebrow as describedby Ellenbogen (Fig 4).44

Vascularized island pedicle flaps from the tem-poral scalp45 are based on the anterior branch ofthe superficial temporal artery and carry an overly-ing island of scalp hair that is tunneled subcutane-ously to the brow area (Fig 5).46 Follicular misalign-ment is the greatest drawback of this technique.

Tattooing a hairline has been suggested by someas an alternative to hair-bearing surgical flaps.47 Thistechnique has esthetic limitations as a two-dimen-sional structure attempts to mimic a three-dimen-sional requirement.

Fig 4. Spatial relationships of the ideal eyebrow. (Data fromWestmore; reprinted with permission from Ellenbogen R:Transcoronal eyebrow lift with concomitant upper blepharoplasty.Plast Reconstr Surg 71:490, 1983.)

Fig 5. Eyebrow reconstruction with a scalp flap based on thesuperficial temporal vessels. (Reprinted with permission fromAchauer BM: Burn Reconstruction. New York, Thieme, 1990,p 49.)

Eyelid

The eyelids should have high priority in thereconstructive plan in order to preserve vision. Cor-neal exposure is a dreaded complication from burnand must be prevented; globe protection is of para-mount importance. Lubricating drops and oint-ment must be used if necessary. Generally, tarsor-rhaphy is inadequate in these situations because ofthe lack of sufficient unburned tissue.

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Ectropion is the most common cause of eyelidproblems in burn patients. The surgeon must dif-ferentiate between internal and external contrac-ture to be able to treat it successfully. If the con-tracture is external, releasing incisions are required.These incisions are placed just 1–2 mm away fromthe ciliary margin, taking care not to violate thesupratarsal fold while working in the upper eyelid.Skin deficiencies of the upper eyelid may bereplaced with a FTSG harvested from the contralat-eral upper eyelid. A FTSG harvested from theretroauricular region works well to replace lowereyelid skin.

A variety of adjacent tissue transfers may also beused to replace missing skin of the eyelid afterexternal contracture release. A modified Tripierflap keeps the donor upper eyelid skin and orbicu-laris oculi muscle pedicled to the lateral canthalregion, and can be used to resurface the lowereyelid.48 A Fricke flap, which uses pedicled fore-head skin in a similar manner, is also useful whenreplacing skin in the upper eyelid (Fig 6).49

Fig 6. Local flaps for eyelid reconstruction. A, bipedicled Tripierflap; b, Fricke flap; c, midline forehead or glabellar flap; d,medial and lateral skin-muscle flaps; e, nasolabial flap, superi-orly based; cheek flap. (Reprinted with permission from CarrawayJ: Reconstruction of the eyelids and correction of ptosis of the eyelid.In: Aston SJ, Beasley RW, Thorne CHM (eds), Grabb and Smith’sPlastic Surgery, 5th ed. Philadelphia, Lippincott-Raven, 1997.Ch 45, p 529-544.

Regional resurfacing uses separate skin grafts foreach esthetic subunit around the eye (Fig 7).15

Fig 7. Resurfacing the esthetic unit of the eyelids with skin grafts.At the lateral canthus the graft edges should extend up and out,never downwards. (After Feldman JJ: Reconstruction of theburned face in children. In Serafin D, Georgiade NG (eds),Pediatric Plastic Surgery. St Louis, Mosby, 1984, Vol 1, Ch 32,pp 612 and 614.)

Intrinsic contractures require entire eyelidreconstruction. For burns of the upper eyelid, andonly if the ipsilateral lower eyelid skin is of goodquality, either a Cutler-Beard50 or Hughes flap51 isan excellent alternative. For burns of the lowereyelid, Mustardé cheek advancement flaps are suit-able provided that unburned skin is available in thedonor area.52 In the event that complex burns havedestroyed all local tissue, reconstruction withtemporoparietalis fascia pedicled or free flap maybe required.

Nose

Postburn scar contracture of the nose producesthe typical facies of foreshortened nose with elevatedtip and everted nostrils. Lesser burn scars can beexcised within an esthetic unit and the resultingdefect covered with FTSG. Unfortunately, this isthe rarer presentation, and most postburn nasal con-tracture is severe and involves the underlying skel-etal support.

The reconstruction must address all involved lay-ers of the nose: the mucosa, the cartilage, and theskin envelope. Since neighboring skin of the faceis generally involved in the burn, adjacent tissuetransfers are often impossible. Alternatives fromdistant donor sites include the Washio retroauricular

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flap53 and radial forearm free flap.54 For small defectsof the ala rim, composite grafts from the ear workwell (Fig 8).4

Fig 8. Reconstruction of nasal alae with composite grafts fromthe helix of the ear. (Reprinted with permission from Robson MC,Barnett RA, Leitch IOW, Hayward PG: Prevention and treatmentof postburn scars and contracture. World J Surg 16:87, 1992.)

Ear

The biggest concern regarding burns of the ear issuppurative chondritis caused by Pseudomonas.Prevention is far preferable to treatment of theinfection, and is accomplished by controlling thelocal bacterial environment with topical antibiotics.Sulfamylon is the agent of choice because of itsdeep eschar penetration.55 Protective ear cups arealso helpful in preventing infection. Symptoms ofimpending chondritis include severe ear pain,erythema, warmth, and edema. Once the diagno-sis of chondritis is made, incision and drainage ismandatory and all necrotic tissue must be debrided.

For small helical defects, scar excision andreconstruction with an Antia-Buch advancement56

is adequate. For larger helical rim defects, a Davisconchal transposition flap57 is useful. This tech-nique consists of elevating a composite flap of skinand cartilage from the concha, with its pedicle atthe crus helix, and transferring it to the upper thirdof the ear (Fig 9). The donor site is closed with askin graft.

More extensive reconstruction demands the useof a temporoparietal fascial flap covering a cartilageframework, as described by Brent and Byrd.58

Fig 9. Ear reconstruction with a conchal transposition flap. Theconcha is mobilized on an anterior pedicle and transposedsuperiorly to restore the upper third of the ear. The donor siteis covered with a split-thickness skin graft. (Reprinted withpermission from Donelan MB: Conchal transposition flap forpostburn ear deformities. Plast Reconstr Surg 83:641, 1989.)

Cheek

Postburn contracture of the cheek is best recon-structed with a large full-thickness graft, skin flap, orby tissue expansion. The entire esthetic unit shouldbe replaced to prevent a quilt-like appearance post-operatively. Care is taken to avoid traction on thelower lid that might cause ectropion afterwards.Compression garments help decrease the likelihoodof hypertrophic scar.

Perioral Region

Functional disabilities of the mouth resulting fromlip ectropion include drooling, oral incontinence,constriction, feeding difficulty, and poor hygiene.Usually the lower lip is released first becausecontractures here are more disabling and contrib-ute to extrinsic contractures of the upper lip.

Oral Commissure

True commissure burns are commonly seen whenyoung children chew on electrical cords. Recentadvances in oral splinting59,60 have contributed toimproved outcomes when the wound is managedconservatively. Appliances are typically worn for 6to 12 months. Younger children tend to fare poorlybecause treatment depends on the patient’s coop-eration. Patients and their families must be informedof the risk of subsequent labial artery bleeding,which may occur 7 to 10 days after the injury as theeschar dries.

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When surgical reconstruction is required, theGillies-Millard commissure repair61 or a V-Yadvancement is indicated. Other methods havebeen described that use mucosal transposition flapsor tongue flaps.62–64

Upper Lip

Burn ectropion of the upper lip is released byincising both nasolabial folds and the base of thenose to let the lip fall back into its native position.As described by Gonzalez-Ulloa,17 the regionalesthetic unit of the upper lip extends from thenasolabial folds to the vermilion margin, to thenasal sill and columellar base, including the twonasojugal triangles. Within this unit are three sub-units: the two lateral lip elements and the phil-trum (Fig 10).15 Resurfacing must respect thesesubunits.

The columella can be lengthened with forkedflaps from the upper lip as in bilateral cleft lip repair.65

Fig 10. The regional esthetic subunits of the upper lip: two lateraland the central philtrum. (Reprinted with permission fromFeldman JJ: Secondary repair of the burned upper lip. PerspectPlast Surg 1(2):31, 1987.)

A composite strip graft from the scalp66 or a scalpflap based on the superficial temporal artery,67,68

either pedicled or free, can be used to restore themustache.

Several authors34,35 recently described microplughair transplantation for burn patients with alopecia.Proper orientation of hair follicles is crucial to thesuccess of this technique.

Lower Lip/Chin

The lower lip and chin respond well to estheticunit replacement. A sufficient quantity of soft-tissueshould remain on the pogonion for prominence ofthe chin and a sufficient amount of scar should becarved from the labiomental crease to mark thisbreak. Unless associated contractures of the neckare also released, recurrence of lower lip ectropioncan be expected.

BURNS OF THE NECK

The skin of the neck is prone to flexion contrac-ture, and burn scars here tend to produce signifi-cant extrinsic contracture of the lower face andmechanical disability. Mentosternal synechiae arenot uncommon, and in children can lead to micro-gnathia.69,70 At times the mentosternal synechia isso severe that neck extension for endotrachealintubation is impossible. In these cases the neckscar should be released first under local anesthesiawith intravenous sedation before attempting induc-tion of general anesthesia.

A wide, isolated burn scar can be released by asingle or multiple Z-plasties. Excision of all burnscar, including the platysma if appropriate, is man-datory. When incising platysma muscle, care mustbe taken not to injure the marginal mandibularbranch of the facial nerve.

Large burn scars may require grafting or combina-tion of grafts and local flaps (Fig 11).15 Either a thickSTSG or a FTSG is applied to limit secondary con-tracture and recurrence of the deformity. Skin graftsare hidden under the jaw shadow or low on theneck when possible. Vertical scars are to be avoided.

When skin adjacent to the burn is available, tis-sue expansion is an option. Multiple expanders arebest placed subcutaneously in the lateral neck orinfraclavicular region.

Postoperatively the patient is fitted with a necksplint or compression garment to simultaneouslyextend the neck and mold its contour. Splinting ofthis nature is maintained for at least 6 months.Because both extension and pressure are impor-tant to the eventual functional and esthetic out-come, the splint may need frequent readjustment.

In the event of massive burn scars of the neck,contour is best restored with sheet grafts or largedeltopectoral advancement flaps. Excellent results

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have also been obtained with free flaps.71,72 Unfor-tunately free flaps require multiple defatting proce-dures.22

Fig 11. Neck release and resurfacing with a combination of localflaps and skin grafts. (After Feldman JJ: Reconstruction of theburned face in children. In: Serafin D, Georgiade NG (eds),Pediatric Plastic Surgery. St Louis, Mosby, 1984, vol 1, ch 32,p 578.)

BURNS OF THE BREAST

Burns of the anterior chest wall in prepubescentgirls can cause significant deformity and hampersubsequent breast development, partly from theburn itself and partly from its treatment. When thenipple-areola complex (NAC) is directly burned,progenitor cells of the breast bud may be destroyed,but as long as the NAC is intact, breast tissue is likelyto be undamaged, as the progenitor cells lie deep.Later, contracture of the skin envelope of the breastmay impede normal breast development. Lastly,excessive debridement during acute burn care canaggravate the breast deformity.

The ideal time to reconstruct a young girl’s breastis before the burn scar has constricted breast devel-opment. Neale and colleagues73 describe the pro-tocol of breast reconstruction in female burn patients.The breast mound should be fully released beforegrowth is restricted. The breasts should be outlinedbilaterally to plan a symmetric release, using any

palpable mammary structures as landmarks for therelease. Once the scar is released and the breast issculpted, skin grafts are used to cover the defect.An inframammary incision will release mostcontractures, although superior and lateral incisionsare sometimes indicated too.74

For the postadolescent female with a subsequentburn of the breast, treatment follows a reconstruc-tive algorithm based on the severity of the defect.75

1. If breast parenchyma is intact but asymmetric,local scar release is required. Maneuvers toobtain symmetry in cases of extrinsic contrac-ture of the skin envelope include scar excision,Z-plasty, STSG, and FTSG.

2. If the breast parenchyma is burned, glandularvolume becomes an issue. In these cases thereconstructive plan is similar to that of apostmastectomy defect, with the added compli-cation that surrounding tissue is constricted andscarred from the burn, somewhat similar to apostradiation breast reconstruction. Tissueexpansion and prosthesis placement, both withand without muscle coverage, can be consid-ered, although the esthetic outcome is inferiorbecause of poor surrounding skin quality. Breastreconstruction with a transverse rectus abdominismuscle (TRAM) flap is possible in burns having asignificant volume discrepancy. Contralateralbreast reduction should be considered for sym-metry.

3. For adult women who were burned as childrenand failed to get adequate release of the breastscars during puberty, significant tissue expan-sion is often required. In these cases mammarydevelopment is likely to be impaired and a greatdeal of volume is needed. Because the sur-rounding skin is typically contracted and of poorquality, expansion is plagued by problems suchas skin ulceration, prothesis exposure, necrosisof expanded skin, and prolonged course ofexpansion.75–77 Ozgur and associates75 report14% exposure rate of expanders in this setting,and recommend liberal use of the latissimus dorsimuscle flap for coverage in these cases.Moreover, Garner and Smith74 stress the impor-

tance of covering the tissue expanders with muscleso as to essentially encase the expanders with pad-ding to keep them from eroding through the thin,damaged skin (Fig 12).74

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This situation is not unlike that of the irradiatedpostmastectomy defect: poor-quality skin with apoor vascular supply. As in mastectomy, recon-struction with autogenous tissue is preferable whenthe patient is a good candidate for TRAM flap cov-erage.

Slator and colleagues78 opt for tissue expansionfirst, then release of contractures over the expanderand reconstruct with thick STSG. The expander isleft in place for several months to serve as a stentand counteract the contraction forces beforeinserting a permanent prosthesis. Neale andKurtzman79 strongly disagree with this protocol,arguing that improved symmetry can only beobtained if the contracture is excised prior to tissueexpansion. They support excisional scar releasefollowing subunit principles where possible to pre-vent a patchwork appearance (Fig 13).79

An inframammary fold incision perpendicular tothe chest wall creates a natural cleavage plane andallows for breast sculpting. Neale and Kurtzmanargue that if tissue expansion is still required, scartissue has been removed already and expansion iseasier.

Delayed nipple reconstruction is advisable. Thetechnique is similar to that used in postmastectomynipple reconstruction, with the added complica-

tion that the chest wall vascularity may be impaired.Medical tattooing of nipple and areola is a usefuladjunct to the reconstruction.

BURNS OF THE UPPER EXTREMITY

Successful treatment of upper extremity burnsrequires an aggressive physical therapy programcombined with surgical reconstruction when nec-essary. Physical therapy is mandatory before com-mencing any postburn reconstruction. Therapy notonly helps to decrease skin and joint contracturepreoperatively, but is a useful predictor of patientinvolvement in the treatment postoperatively. Evenin the face of a technically perfect procedure, allpatients will experience postoperative contractureif physical therapy and joint splinting are not pur-sued appropriately. Elastic garments are also help-ful during the recovery period.

Upper extremity contractures are best releasedin a proximal-to-distal direction, from axilla to fin-gers.

Axilla

Adduction contracture of the axilla is prevent-able through early splinting and range of motion

Fig 12. Excision of burn scar and grafting ofdeficit with thick (0.020 inch) STSG. (Reprintedwith permission from Garner WL, Smith DJ:Reconstruction of burns of the trunk and breast.Clin Plast Surg 19(3):683, 1992.)

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exercises, yet remains a frequent problem in burnsof the upper chest wall and arm. Kurtzman andStern80 describe three types of axillary contracture,as follows:Type 1 contractures involve either the anterior (1A)

or posterior (1B) axillary fold;

Fig 13. Deep inframammary incisional release of breast burnperpendicular to the chest wall. Release allows the breastcontour to improve and creates a distinct inframammary crease.(Reprinted with permission from Neale HW, Kurtzman LC: Dis-cussion of “Postburn breast reconstruction: tissue expansion priorto contracture release”, by Slator RC, Wilson GR, Sharpe DT. PlastReconstr Surg 90:672, 1992.

Type 2 contractures involve both the anterior andposterior axillary folds; and

Type 3 contractures involve both axillary folds andthe axillary dome.Type 1 and 2 injuries can be managed by

sequential release and resurfacing with either thickSTSG or FTSG. Type 3 injuries require copiousamounts of skin for resurfacing and are bestreconstructed with well-vascularized, flexible, non-contracting flaps. A pedicled parascapular fascio-cutaneous flap will do the job well and can beeasily rotated into the axilla. The surgeon shouldavoid displacing the axillary hair and sweat glandsduring axillary reconstruction. Release of the axil-lary scar must be deep enough to penetratethrough the burn scar to the normal tissue under-neath. Postoperative physical therapy and splint-ing are essential to prevent recurrence of the con-tracture.

Roberts and Dickson81 use fasciocutaneous flapsto resurface the axilla. Pitfalls of the techniqueinclude rotating the flaps through more than 90°and failing to undermine the flap adequately toallow easy rotation. Good donor sites of fascio-cutaneous tissue include the parascapular and latis-simus dorsi territories.82,83 These flaps are thin butsturdy, pliable, and reach the anterior axillary foldon their pedicles.

Elbow

If no bone, cartilage, nerve, or vessel is exposed,the best method for resurfacing a burn scar of theelbow is with a thick STSG. When vascularizedtissue is required, a fasciocutaneous flap such as areverse radial forearm84 or reverse ulnar flap85 isindicated so long as adequate perfusion to thedistal extremity is assured.86 Local, random fascio-cutaneous flaps have been described based paral-lel to the longitudinal axis of the perifascial circu-lation (Fig 14).86 In the event no local or regionalfasciocutaneous tissue of suitable quality is avail-able, free-flap transfer may be contemplated.Muscle-containing flaps are generally too bulky touse in joints, and may interfere with elbow flex-ion.

Heterotopic ossification of the elbow is a recog-nized complication of upper extremity burn thatproduces an immobile joint. Treatment consists ofsurgical excision.

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Fig 14. Cubital angiosomes and their source vessels. (Reprintedwith permission from Hallock GG: Local random fasciocutaneousflaps for repair of the burned elbow. J Burn Care Rehabil 12:16,1991.)

Hand

From a functional point of view, burns of thehand are devastating. It is far easier to prevent thanto treat burn contractures of the hand. Aggressiveand early tangential excision of the burned hand,combined with splinting and mobilization therapy,leads to improved long term results (Fig 15).87,88

Fig 15. Elastomer inserts placed under compression garmentshelp reduce post burn contracture. (Reprinted with permissionfrom Dado DV, Angelats J: Management of burns of the hands inchildren. Hand Clin 6:711, 1990.)

Recovery depends upon the depth of injury,adequacy of acute care given, and choice ofreconstruction.89 Permanent joint stiffness resultsfrom prolonged extremity edema with accompany-ing immobility, and must be avoided. Some authorssupport radical debridement with early free-flapcoverage90 in the belief that rapid removal of dam-aged tissue decreases overall inflammation and pro-duces a better functional outcome. The problemwith this approach is how to identify damagedmuscle at risk of necrosis. Schiller and colleagues91

report using laser Doppler imaging to predict whichwounds will be slow to heal.

The most common secondary deformity of theburned hand is postburn syndactyly. Many proce-dures have been devised to address this problem;none is completely successful. Alexander and asso-ciates92 compare the various operations used totreat burn syndactyly, including excision, Z-plasty,rotational flaps, VY-plasties, and skin grafts (Figs 16& 17).92 No single procedure worked in all cases,and the authors describe a VM-plasty with postop-erative splinting as an alternative.

A shortage of skin at the flexion creases manifestsas contracture bands. Before the scar is released,the joint is manipulated to check for mobility. If thejoint is supple, the scar bands are released withsimple or multiple Z-plasties. Occasionally a K-wire is required to help keep the digits in properposition. For the thenar web space, a four flap Z-plasty is appropriate (Fig 18).16

Skin grafts are required to treat patients withsevere skin shortage of the hand after a burn. Clini-cians are divided regarding the merits of FTSG ver-sus thick STSG versus tissue-expanded FTSG donorsites.93 For cases requiring bone, cartilage, tendon,nerve, or vessel coverage, a pedicled or freefasciocutaneous flap is indicated (Fig 19).16

When the joint is fixed and immobile because ofadhesion of deeper tissues, simple scar release isinadequate for correction. These cases requirejoint capsulectomy, with or without release of thescarred tendons,94,95 followed by early postopera-tive range of motion exercises and aggressive physi-cal therapy.

BURNS OF THE PERINEUM

Operative procedures for perineal reconstruc-tion range from contracture release to complete

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external genital reconstruction. As in other burnsites, the etiology of the distortion must be ana-lyzed. Extrinsic contracture can be corrected withscar release and resurfacing. Meshed STSG aremore pliable than standard sheet grafts and adaptbetter to the contour of the perineal region, but

tend to contract more with time. Sheet grafts, ifbolstered properly, give a good esthetic result. Iso-lated scar bands may be released by Z-plasty.74,96

Surgical reconstruction of the external genitaliais a complex and sophisticated undertaking. Ofparticular importance is the creation of a neourethra.

Fig 16 and 17. Various methods described to treat postburn syndactyly. (Reprinted with permission from Alexander JW, MacMillanBG, Martel L: Correction of postburn syndactyly: an analysis of children with introduction of the VM-plasty and postoperative pressureinserts. Plast Reconstr Surg 70:345, 1982.)

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Fig 19. (Above) The four-flap Z-plasty is used to change thecontour of a web of the left adductor space. (Below) Executionof this maneuver effaces the web. (Reprinted with permissionfrom Rohrich RJ, Zbar RIS: A simplified algorithm for the use of Z-plasty. Plast Reconstr Surg 103:1513, 1999.)

In male patients the available techniques includemultistaged, tubed pedicle flaps,97 axial musculocu-taneous flaps, and free flaps.98,99 A penile prosthesisto allow erectile function is also an option. Thereader is referred to Selected Readings in Plastic

Surgery volume 8, number 40,100 for a discussion ofgenital reconstruction in either sex.

BURNS OF THE LOWER EXTREMITY

Adequate care of lower extremity burns in theacute setting makes postburn reconstruction signifi-cantly easier. Early recognition of compartment syn-drome can prevent limb loss. As in the upperextremity, many problems with joint contracture canbe averted by early wound grafting and aggressivephysical therapy, to include both range of motionexercises as well as compression garments and splints.

When scar release is required, narrow bands aredivided and lengthened with Z-plasty. Largerpostburn contractures may require skin grafts tocover denuded areas after the scar is released. Long-term postoperative splinting, particularly at night, isnecessary to prevent recurrence of contracture.Exposed vital structures—such as nerves, vessels,bone, cartilage, and tendons—should be protectedand covered with flap tissue, either pedicled ortransferred by microvascular anastomosis.101

Chronic lymphedema is best managed by elasticcompression garments.

Marjolin’s Ulcer

Chronic, non-healing burn scars must be evalu-ated carefully for the presence of squamous cellcarcinoma. For a discussion of the epidemiologyand management of Marjolin’s ulcer, the reader isreferred to Selected Readings in Plastic Surgery vol-ume 9, number 5.102

Fig 18. Use of the Z-plasty maneuver to lengthen a scar contracture of the volar surface of the right index finger proximal interphalangealjoint. (Reprinted with permission from Rohrich RJ, Zbar RIS: A simplified algorithm for the use of Z-plasty. Plast Reconstr Surg 103:1513,1999.)

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POSTBURN RECONSTRUTION INDEVELOPING NATIONS

The great majority of burn injuries occur indeveloping countries, where many people still useopen fires for cooking and heat. Children espe-cially are commonly injured as they stumble intofires. Additionally, in some regions of India,Bangladesh, Nepal, and Sri Lanka, women are vic-tims of deliberate fire or chemical (caustic) burningin arguments over family dowries. Due to the pau-city of medical resources, adequate acute burn careis simply not available in many of these tragic cases;at other times local beliefs concerning burn careadd to the delay in treatment.103 The upshot of

Acute Burns

1. Brigham PA, McLoughlin E: Burn incidence and medicalcare use in the United States: estimates, trends, and datasources. J Burn Care Rehabil 13:573, 1992.

2. Cryer HG et al: Effects of early tangential excision andgrafting on survival after burn injury. Surg Gynecol Obstet173:449, 1991.

3. Deitch E: A policy of early excision and grafting in elderlyburn patients shortens the hospital stay and improvessurvival. Burns 12:109, 1985.

4. Luterman A, Dacso CC, Curreri PW: Infections in burnpatients. Am J Med 81:45, 1986.

5. Saffle JR, Davis B, Williams P, The American Burn Associa-tion Registry Participant Group: Recent outcomes in thetreatment of burn injury in the United States: a report fromthe American Burn Association Patient Registry. J BurnCare Rehabil 16:219, 1995.

6. Arturson MG: The pathophysiology of severe thermalinjury. J Burn Care Rehabil 6:129, 1985.

7. Heimbach D, Engrav L, Grube B, Marvin J: Burn depth:a review. World J Surg 16:10, 1992.

8. Warden GD, Kravitz M, Schnebly A: The outpatientmanagement of moderate and major thermal injuries. JBurn Care Rehabil 2:159, 1981.

9. Gerding RL et al: Outpatient management of partial-thickness burns: Biobrane® versus 1% silver sulfadiazine.Ann Emerg Med 19:121, 1990.

10. Hunt JL, Purdue GF: The elderly burn patient. Am J Surg164:472, 1992.

11. Herndon DN et al: A comparison of conservative versusearly excision. Ann Surg 209:547, 1989.

12. Warden GD: Burn shock resuscitation. World J Surg16:16, 1992.

13. Morehouse JD, Finkelstein JL, Marano MA, et al: Resus-citation of the thermally injured patient. Crit Care Clin8(2):355, 1992.

14. Zimmerman BJ, Granger DN: Reperfusion injury. SurgClin North Am 72:65, 1992.

15. Mileski W, Borgstrom D, Lightfoot E, et al: Inhibition ofleukocyte-endothelial adherence following thermal in-jury. J Surg Res 52:334, 1992.

16. Dziewulski P: Burn wound healing: James Ellsworth Laingmemorial essay for 1991. Burns 18:466, 1992.

17. Cioffi WG, Burleson DG, Pruitt BA Jr: Leukocyte responsesto injury. Arch Surg 128:1260, 1993.

18. Youn YK, LaLonde C, Demling R: The role of mediatorsin the response to thermal injury. World J Surg 16:30,1992.

19. Thomson PD et al: Superoxide dismutase prevents lipidperoxidation in burned patients. Burns 16:406, 1990.

20. Ono I et al: Effects of platelet activating factor antagoniston oedema formation following burns. Burns 19:202,1993.

21. Mileski W et al: Inhibition of leukocyte (WBC) adherencein a rabbit model of major thermal injury. Presented at theAnnual Meeting of the American Burn Association, Cincin-nati, Ohio, 1993.

22. Tanaka H et al: How long do we need to give antioxidanttherapy during resuscitation when its administration isdelayed for two hours? J Burn Care Rehabil 13:567, 1992.

23. Navar PD, Saffle JR, Warder GD: Effect of inhalation injuryon fluid resuscitation requirements after thermal injury.Am J Surg 150:716, 1985.

24. Thompson PB et al: Effect on mortality of inhalationinjury. J Trauma 26:163, 1986.

25. Sobel JB, Goldfarb IW, Slater H, Hammell EJ: Inhalationinjury: a decade without progress. J Burn Care Rehabil13:573, 1992.

26. Hunt JL, Agee RN, Pruitt BA Jr: Fiberoptic bronchoscopyin acute inhalation injury. J Trauma 15:641, 1975.

27. Herndon DN et al: Respiratory injury. Part I: Incidence,mortality, pathogenesis, and treatment of pulmonary in-jury. J Burn Care Rehabil 7:184, 1986.

BIBLIOGRAPHY

these circumstances is that many burn wounds healby secondary intention, and therefore many burnsurvivors develop massive contractures as theirwounds are allowed to granulate. Scar hypertrophyand synechiae are the rule rather than the excep-tion in the developing world. The typical injuriesare severe finger-in-palm-on-forearm deformities,mentosternal synechia, and even sternum-to-thighdeformities that prevent walking.

Because physical therapy and splinting is such anintegral part of successful postburn reconstruction,until this modality is available to all burn patients,many reconstructions in the developing world willunfortunately fail due to contracture recurrence.

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28. Herndon DN et al: Inhalation injury in burned patients:Effects and treatment. Burns 14:349, 1988.

29. Herndon DN, Thompson PB, Trayber DL: Pulmonaryinjury in burn patients. Crit Care Clin 1:79, 1988.

30. Lund T et al: Upper airway sequelae in burn patientsrequiring endotracheal intubation or tracheostomy. AnnSurg 201:374, 1985.

31. Hunt JL, Purdue GF, Gunning T: Is tracheostomy war-ranted in the burn patient? Indications and complica-tions. J Burn Care Rehabil 7:492, 1986.

Burn Surgery

1. Moylan JA Jr, Inge WW Jr, Pruitt BA Jr: Circulatory changesfollowing circumferential extremity burns evaluated bythe ultrasonic flowmeter: An analysis of 60 thermallyinjured limbs. J Trauma 11:763, 1971.

2. Janzekovic Z: A new concept in the early excision andimmediate grafting of burns. J Trauma 19:1103, 1970.

3. Sheridan RL, Tompkins RG, Burke JF: Management ofburn wounds with prompt excision and immediate clo-sure. J Intensive Care Med 9:6, 1994.

4. Cryer HG et al: Effects of early tangential excision andgrafting on survival after burn injury. Surg Gynecol Obstet173:449, 1991.

5. Peck MD, Heimbach DM: Does early excision of burnwounds change the mortality? J Burn Care Rehabil 10:7,1989.

6. Foy HM, Pavlin E, Heimbach DM: Excision and graftingof large burns: Operation length not related to increasedmorbidity. J Trauma 26:51, 1986.

7. Thompson P et al: Effective early excision on patients withmajor thermal injury. J Trauma 27:205, 1987.

8. Monafo WW, Bessey PQ: Benefits and limitations of burnwound excision. World J Surg 16:37, 1992.

9. Herndon DN, Parks DH: Comparison of serial debride-ment and autografting and early massive excision withcadaver skin overlay in the treatment of large burns inchildren. J Trauma 26:149, 1986.

10. Rosenberg JL, Zawacki BE: Reduction of blood loss usingtourniquets and “compression” dressings in excising limbburns. J Trauma 26:47, 1986.

11. Frist W, Ackroyd F, Burke J, Bondoc C: Long-termfunctional results of selective treatment of hand burns. AmJ Surg 149:516, 1985.

12. Demling RH: Effect of early burn excision and grafting onpulmonary function. J Trauma 24:830, 1984.

13. Gallico GG III: Biologic skin substitutes. Clin Plast Surg17(3):519, 1990.

14. Atnip RG, Burke JF: Skin coverage. Curr Probl Surg 20, No10, Oct 1983.

15. Pruitt BA Jr, Levine NS: Characteristics and uses of biologicdressings and skin substitutes. Arch Surg 119:312, 1984.

16. Kelton PL: Skin grafts. Selected Read Plast Surg 9(1), 1999.17. Zawacki BE: Temporary wound closure after burn exci-

sion. J Burn Care Rehabil 7:138, 1986.18. Pruitt BA Jr: The burn patient: II. Later care and

complications of thermal injury. Curr Problem Surg 16, No5, May 1979.

19. Mason AD Jr, McManus AT, Pruitt BA Jr: Association ofburn mortality and bacteremia. A 25-year review. ArchSurg 121:1027, 1986.

20. McManus AT, Mason AD Jr, McManus WF, Pruitt BA Jr: Adecade of reduced gram-negative infections and mortalityassociated with improved isolation of burned patients.Arch Surg 129:1306, 1994.

21. Marvin JA et al: Usefulness of blood cultures in confirmingseptic complications in burn patients: Evaluation of a newculture method. J Trauma 15:657, 1975.

22. Jones WG et al: Enterococcal burn sepsis. A highly lethalcomplication in severely burned patients. Arch Surg121:649, 1986.

23. Pensler JR et al: Fungal sepsis: An increasing problem inmajor thermal injuries. J Burn Care Rehabil 7:488, 1986.

24. Pruitt BA Jr: The diagnosis and treatment of infection in theburn patient. Burns 11:79, 1984.

25. Merrell SW et al: The declining incidence of fatal sepsisfollowing thermal injury. J Trauma 29:1362, 1989.

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27. Robson MC: Burn sepsis. Crit Care Clin 4:281, 1988.28. Luterman A, Dacso CC, Curreri PW: Infections in burn

patients. Am J Med 81:45, 1986.29. Purdue GF, Hunt JL, Prescott PR: Child abuse by burn-

ing—an index of suspicion. J Trauma 28:221, 1988.30. Heideman M, Begtsson A: The immunologic response to

thermal injury. World J Surg 16:53, 1992.31. Cioffi WG, Burleson DG, Pruitt BA Jr: Leukocyte responses

to injury. Arch Surg 128:1260, 1993.32. Wilmore DW et al: Stress in surgical patients as a neuro-

physiologic reflex response. Surg Gynecol Obstet 142:257,1976.

33. Ireton CS et al: Do changes in burn size affect measuredenergy expenditures? J Burn Care Rehabil 6:419, 1985.

34. Rutan TC et al: Metabolic rate alterations in early excisionand grafting versus conservative treatment. J Trauma26:140, 1986.

35. Waymack JP, Herndon DN: Nutritional support of theburned patient. World J Surg 16:80, 1992.

36. Ireton-Jones CS et al: Equations for the estimation ofenergy expenditures in patients with burns with specialreference to ventilatory status. J Burn Care Rehabil 13:330,1992.

37. Ireton CS et al: Evaluation of energy expenditures in burnpatients. J Am Diet Assoc 86:331, 1986.

38. Saffle JR et al: Use of indirect calorimetry in the nutritionalmanagement of burned patients. J Trauma 25:32, 1985.

39. O’Neil CE, Hutsler D, Hildreth MA: Basic nutritionalguidelines for pediatric burn patients. J Burn Care Rehabil10:278, 1989.

40. Bell SJ, Molnar JA, Krasker WS, et al: Weight maintenancein pediatric burned patients. J Am Diet Assoc 2:207, 1986.

41. Wolfe RR: Caloric requirements of the burned patient. JTrauma 21:712, 1981.

42. Alexander JW et al: Beneficial effects of aggressive proteinfeeding in severely burned children. Ann Surg 192:505,1980.

43. Matsuda T et al: The importance of burn wound size indetermining the optimal calorie:nitrogen ratio. Surgery94:562, 1983.

44. Heimbach DM et al: Toxic epidermal necrolysis: A stepforward in treatment. JAMA 257:2171, 1987.

45. Souder LL: Biobrane dressing used in the treatment oftoxic epidermal necrolysis: A case report. J Burn CareRehabil 11:237, 1990.

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46. Halebain P et al: Improved burn center survival of patientswith toxic epidermal necrolysis managed without cortico-steroids. Ann Surg 204:503, 1986.

47. Hunt JL et al: The pathophysiology of acute electricinjuries. J Trauma 16:335, 1976.

48. Hunt JL, Sato RM, Baxter CR: Acute electric burns. Currentdiagnostic and therapeutic approaches to management.Arch Surg 115:434, 1980.

49. Hunt JL et al: The use of technetium-99m stannouspyrophosphate scintigraphy to identify muscle damage inacute electric burns. J Trauma 19:409, 1979.

50. Purdue GF, Hunt JL: Electrocardiographic monitoringafter electrical injury: Necessity or luxury. J Trauma26:166, 1986.

51. Hanumadass ML et al: Acute electrical burns: A 10-yearclinical experience. Burns 12:427, 1986.

52. Mann R, Gibran N, Engrav L, Heimbach D: Is immediatedecompression of high voltage electrical injuries to theupper extremity always necessary? J Trauma 40:584,1996.

53. Sykes RA, Mani MM, Hiebert JM: Chemical burns:retrospective review. J Burn Care Rehabil 7:343, 1986.

54. Saydjari R et al: Chemical burns. J Burn Care Rehabil7:404, 1986.

Burn Reconstruction

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2. Kischer CS: Collagen and mucopolysaccharides in thehypertrophic scar. Connect Tiss Rev 2:205,1974.

3. Larson DL, Abston S, Evans EB, et al: Techniques fordecreasing scar formation and contractures in the burnpatient. J Trauma 11:807,1971.

4. Robson MC, Barnett RA, Leitch IOW, Hayward PG:Prevention and treatment of postburn scars and contrac-ture. World J Surg 16:87, 1992.

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7. Ahn ST, Monafo WW, Mustoe TA: Topical silicone gel:a new treatment for hypertrophic scars. Surgery 106:781,1989.

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9. Jonsson CE, Dalsgaard CJ: Early excision and skin graftingof selected burns of the face and neck. Plast Reconstr Surg88:83, 1991.

10. Fraulin FOG, Illmayer SJ, Tredget EE: Assessment ofcosmetic and functional results of conservative versussurgical management of facial burns. J Burn Care Rehabil17:19, 1996.

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12. Rudolph R, et al: The lifecycle of the myofibroblast. SurgGynecol Obstet 145:389, 1977.

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16. Rohrich RJ, Zbar RIS: A simplified algorithm for the use ofZ-plasty. Plast Reconstr Surg 103:1513, 1999.

17. Gonzalez-Ulloa M: Restoration of the face covering bymeans of selected skin in regional aesthetic units. Br J PlastSurg 9:212, 1956.

18. Gobet R, Raghunath M, Altermatt S, et al: Efficacy ofcultured epithelial autografts in pediatric burns and re-constructive surgery. Surgery 121:654, 1997.

19. Shen T, Sun Y, Cao D, Wang N: The use of free flaps in burnpatients: experiences with 70 flaps in 65 patients. PlastReconstr Surg 81:352, 1988.

20. Grotting J, Walkinshaw M: The early use of free flaps inburns. Ann Plast Surg 15:127, 1985.

21. Platt AJ, McKiernan MV, McLean NR: Free tissue transferin the management of burns. Burns 22:474, 1996.

22. Abramson DL, Pribaz JJ, Orgill DP: The use of free tissuetransfer in burn reconstruction. J Burn Care Rehabil17:402, 1996.

23. Chun JT, Rohrich RJ: Versatility of tissue expansion in headand neck burn reconstruction. Ann Plast Surg 41:11,1998.

24. Still J, Craft-Coffman B, Law E: Use of pedicled flaps andtissue expanders to reconstruct burn scars of the skin of theanterior abdomen and chest. Ann Plast Surg 40:226,1998.

25. Yamamoto Y, Yokoyama T, Minakawa H, Sugihara T: Useof the expanded skin flap in esthetic reconstruction ofpostburn deformity. J Burn Care Rehabil 17:397, 1996.

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28. Youm T, Margiotta M, Kasabian A, Karp N: Complicationsof tissue expansion in a public hospital. Ann Plast Surg42:396, 1999.

29. Friedman RM, Ingram AE, Rohrich RJ, et al: Risk factors forcomplications in pediatric tissue expansion. Plast ReconstrSurg 98:1242, 1996.

30. Neale HW, Kurtzman LC, Goh KBC, et al: Tissue expand-ers in the lower face and anterior neck in pediatric burnpatients: limitations and pitfalls. Plast Reconstr Surg91:624, 1993.

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36. Juri J: Use of parietooccipital flaps in the surgical treatmentof baldness. Plast Reconstr Surg 55:456, 1975.

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40. Norkus T, Klebanovas J, Viksraitis S, et al: Deep electricalburns of the calvarium: early or delayed reconstruction?Burns 24:569, 1998.

41. Chui DTW, Sherman JE, Edgerton BW: Coverage of thecalvarium with a free parascapular flap. Ann Plast Surg12:60, 1984.

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44. Ellenbogen R: Transcoronal eyebrow lift with concomittentupper blepharoplasty. Plast Reconstr Surg 71:490,1983.

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47. Coessens B, Van Geertruyden J, DeMey A: Surgicaltattooing as an aesthetic improvement in facial reconstruc-tion with free radial forearm flap. J Reconstr Microsurg9:331, 1995.

48. Tripier L: Musculocutaneous flap in the form of a bridge,applied to the reconstruction of the eyelids. Compt RendAcad Sc (Paris) 109:620, 1889.

49. Carraway J: Reconstruction of the eyelids and correctionof ptosis of the eyelid. In: Aston SJ, Beasley RW, ThorneCHM (eds), Grabb and Smith’s Plastic Surgery, 5th ed.Philadelphia, Lippincott-Raven, 1997. Ch 45, p 529-544.

50. Cole JG: Reconstruction of large defects of the uppereyelid. Am J Ophthalmol 64:376, 1967.

51. Rohrich RJ. Zbar RIS: The evolution of the Hughestarsoconjunctival flap for lower eyelid reconstruction.Plast Reconstr Surg 104:518, 1999.

52. Mustarde JC: Reconstruction of eyelids. Ann Plast Surg11:149, 1983.

53. Washio H: Retroauricular temporal flap. Plast ReconstrSurg 43:162, 1969.

54. Stamatopoulos C, et al: Use of free flaps in the aestheticreconstruction of face and neck deformities. Microsurgery13:188, 1992.

55. Purdue GF, Hunt HL: Chondritis of the burned ear: apreventable complication. Am J Surg 152:257, 1986.

56. Antia NH, Buch VI: Chondrocutaneous advancementflap for the marginal defect of the ear. Plast Reconstr Surg39:472, 1967.

57. Donelan MB: Conchal transposition flap for postburn eardeformities. Plast Reconstr Surg 83:641, 1989.

58. Brent B, Byrd HS: Secondary ear reconstruction withcartilage grafts covered by axial, random, and free flapsof temporoparietal fascia. Plast Reconstr Surg 72:141,1983.

59. Silverglade D, Zacher JB, Ruberg RL: Improved splintingof oral commissure burns: Results in 21 consecutivepatients. Ann Plast Surg 9:316, 1982.

60. Canady JW, Thompson SA, Bardach J: Oral commissureburns in children. Plast Reconstr Surg 97:738, 1996.

61. Gillies HD, Millard DR Jr: Principles and Art of PlasticSurgery. Boston, Little Brown, 1957.

62. Pensler JM, Rosenthal A: Reconstruction of the oralcommissure after an electrical burn. J Burn Care Rehabil11:50, 1990.

63. Ortiz-Monasterio F, Factor R: Early definitive treatment ofelectrical burns of the mouth. Plast Reconstr Surg 65:169,1980.

64. Donelan MB: Reconstruction of electrical burns of theoral commissure with a ventral tongue flap. Plast ReconstrSurg 95:1155, 1995.

65. Millard DR Jr: Columella lengthening by a forked flap.Plast Reconstr Surg 22:454, 1958.

66. Vallis CP: Hair transplantation to the upper lip to createa moustache. Plast Reconstr Surg 54:606, 1974.

67. Marks MW, et al: The temporal island scalp flap formanagement of facial burn scars. Plast Reconstr Surg82:257, 1988.

68. Lyons GB, et al: Upper lip reconstruction: use of the freesuperficial temporal artery hair-bearing flap. Br J Plast Surg42:333, 1989.

69. Herndon DN, et al: Treatment of burns in children.Pediatr Clin North Am 32:1311, 1985.

70. Almaguer E, Dillon BT, Parry SW: Facial resurfacing atShriners Burns Institute: a 16-year experience in youngburned patients. J Trauma 25:1081, 1985.

71. Economides NG, Ferrell TH: Neck resurfacing with freeTRAM flap. Microsurgery 13:240, 1992.

72. Angrigiani C: Aesthetic microsurgical reconstruction ofanterior neck burn deformities. Plast Reconstr Surg 93:507,1994.

73. Neale HW, et al: Breast reconstruction in the burnedadolescent female: an 11-year, 157-patient experience.Plast Reconstr Surg 70:718, 1982.

74. Garner WL, Smith DJ: Reconstruction of burns of the trunkand breast. Clin Plast Surg 19(3):683, 1992.

75. Ozgur F, et al: Reconstruction of postburn breast defor-mities. Burns 18:504, 1992.

76. Marks MW, Argenta LC, Thornton JW: Burn manage-ment: the role of tissue expansion. Clin Plast Surg 14:543,1987.

77. Cohen M, Marshall, Schafer MA: Tissue expansion for thereconstruction of burn defects. J Trauma 28:158, 1988.

78. Slator RC, Wilson GR, Sharpe DT: Postburn breastreconstruction: tissue expansion prior to contracturerelease. Plast Reconstr Surg 90:668, 1992.

79. Neale HW, Kurtzman LC: Discussion of “Postburn breastreconstruction: tissue expansion prior to contracturerelease”, by Slator RC, Wilson GR, Sharpe DT. PlastReconstr Surg 90:672, 1992.

80. Kurtzman LC, Stern PJ: Upper extremity burn contractures.Hand Clin 6(2):261, 1990.

81. Roberts AHN, Dickson WA: Fasciocutaneous flaps forburn reconstruction: a report of 57 flaps. Br J Plast Surg41:150, 1988.

82. Achauer BM, Spenler CW, Gold ME: Reconstruction ofaxillary burn contractures with the latissimus dorsifasciocutaneous flap. J Trauma 28:211, 1988.

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83. Tolhurst DE, Haeseker B: Fasciocutaneous flaps in theaxillary region. Br J Plast Surg 35:430, 1982.

84. Salinas Velasco VM, Garcia-Morato V, Fregenal Garcia FJ:Burn of the elbow: the role of the radial forearm island flap.Burns 18:71, 1992.

85. Lovie MJ, Duncan GM, Glasson DW: The ulnar arteryforearm free flap. Br J Plast Surg 37:486, 1984.

86. Hallock GG: Local random fasciocutaneous flaps for repairof the burned elbow. J Burn Care Rehabil 12:26, 1991.

87. Hunt JL, Sato R, Baxter CR: Early tangential excision andimmediate mesh autografting of deep dermal hand burns.Ann Surg 189:147, 1979.

88. Quan PE, Bieringer R, Alston DW, Curreri PW: Control ofscar tissue in the finger web spaces by use of gradedpressure inserts. J Burn Care Rehabil 2:27, 1981.

89. Falcone PA, Edstrom LE: Decision making in the acutethermal hand burn: an algorithm for treatment. Hand Clin6(2):233, 1990.

90. Chick LR, Lister GD, Sower L: Early free flap coverage ofelectrical and thermal burns. Plast Reconstr Surg 89:1013,1992.

91. Schiller WR, Garren RL, Bay RC, et al: Laser Dopplerevaluation of burned hands predicts need for surgicalgrafting. J Trauma 43:35, 1997.

92. Alexander JW, MacMillan BG, Martel L: Correction ofpostburn syndactyly: an analysis of children with intro-duction of the VM-plasty and postoperative pressureinserts. Plast Reconstr Surg 70:345, 1982.

93. Dado DV, Angelats J: Management of burns of the handsin children. Hand Clin 6:711, 1990.

94. Graham TJ, Stern PJ, True MS: Classification andtreatment of postburn metacarpophalangeal joint ex-tension contractures in children. J Hand Surg 15A:450,1990.

95. Alexander JW, et al: Surgical correction of postburnflexion contractures of the fingers in children. PlastReconstr Surg 68:218, 1981.

96. Michielsen D, Van Hee R, Neetens C, et al: Burns to thegenitalia and the perineum. J Urol 159:418, 1998.

97. Gilles H, Harrison RJ: Congenital absence of the penis. BrJ Plast Surg 1:8, 1948.

98. Gottlieb LJ, Saunders JN: Perineal Burns. In: Achauer B(ed), Burn Reconstruction. New York, Thieme, 1991, p165-183.

99. Hester JR, Hill HL, Jurkiewicz MJ: One stage reconstructionof the penis. Br J Plast Surg 31:279, 1978.

100. Kelton PL Jr: Genitourinary Reconstruction. SelectedRead Plast Surg 8(40), 1999.

101. Mani MM, Chhatre M: Reconstruction of the burnedlower extremity. Clin Plast Surg 19(3):693, 1992.

102. Zbar RIS, Cottel WI: Skin Tumors I: Nonmelanoma SkinTumors. Selected Read Plast Surg 9(5), 2000.

103. Manktelow A: Burn injury and management in Liberia.Burns 16:432, 1990.

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RECOMMENDED READING

Arturson MG: The pathophysiology of severe thermal injury. J Burn Care Rehabil 6:129, 1985.

Demling RH: Fluid and electrolyte management. Crit Care Clin 1(1):27, 1985.

Horton JW, White DJ, Baxter CR: Hypertonic saline dextran resuscitation of thermal injury. Ann Surg211:301, 1990.

Cryer HG, Anigian GM, Miller FB, et al: Effects of early tangential excision and grafting on survival afterburn injury. Surg Gynecol Obstet 173:449, 1991.

Hunt JL, Sato RM, Baxter CR: Acute electric burns. Current diagnostic and therapeutic approaches tomanagement. Arch Surg 115:434, 1980.

Sykes RA, Mani MM, Hiebert JM: Chemical burns: retrospective review. J Burn Care Rehabil 7:343,1986.

Ketchum LD, Cohen IK, Masters FW: Hypertrophic scars and keloids. Plast Reconstr Surg 53:140, 1974.

Fraulin FOG, Illmayer SJ, Tredget EE: Assessment of cosmetic and functional results of conservative versussurgical management of facial burns. J Burn Care Rehabil 17:19, 1996.

Robson MC, Barnett RA, Leitch IOW, Hayward PG: Prevention and treatment of postburn scars andcontracture. World J Surg 16:87, 1992.

Feldman JJ: Reconstruction of the burned face in children. In: Serafin D, Georgiade NG (eds): PediatricPlastic Surgery. St Louis, Mosby, 1984, vol 1, ch 32.

Rohrich RJ, Zbar RIS: A simplified algorithm for the use of Z-plasty. Plast Reconstr Surg 103:1513, 1999.

Neale HW, Kurtzman LC, Goh KBC, et al: Tissue expanders in the lower face and anterior neck inpediatric burn patients: limitations and pitfalls. Plast Reconstr Surg 91:624, 1993.

Platt AJ, McKiernan MV, McLean NR: Free tissue transfer in the management of burns. Burns 22:474,1996.

Moreno-Arias GA, Campos-Fresneda A: Hair grafting in postburn alopecia. Dermatol Surg 25:412, 1999.

Purdue GF, Hunt HL: Chondritis of the burned ear: a preventable complication. Am J Surg 152:257,1986.

Brent B, Byrd HS: Secondary ear reconstruction with cartilage grafts covered by axial, random, and freeflaps of temporoparietal fascia. Plast Reconstr Surg 72:141, 1983.

Canady JW, Thompson SA, Bardach J: Oral commissure burns in children. Plast Reconstr Surg 97:738,1996.

Marks MW, Friedman RJ, Thornton JW, Argenta LC: The temporal island scalp flap for management offacial burn scars. Plast Reconstr Surg 82:257, 1988.

Economides NG, Ferrell TH: Neck resurfacing with free TRAM flap. Microsurgery 13:240, 1992.

Garner WL, Smith DJ: Reconstruction of burns of the trunk and breast. Clin Plast Surg 19(3):683, 1992.