Burns

Robert L. Sheridan, MD, FAAP

T he natural history of seriousburns is characterized by burnshock, which is usually lethalto those with large burns dur-

ing the first few postinjury days, burnwound sepsis, which commonly killsthose who survive burn shock during thefirst few postinjury weeks, and postburndeformity in those who survive to healtheir wounds by contraction and epithe-lialization. Each of these issues has beensystematically addressed in recent yearswith varying but substantial success.

Burn shock has been a focus of study for50 yrs. Stimulated by care of victims of the1930 Rialto Concert Hall (1) and 1942 Co-conut Grove (2) fires, various resuscitationformulas based on body weight and burnsize were promulgated (3, 4). Recognitionof the need to individualize resuscitationhas resulted in burn shock being now aninfrequent cause of death.

Control of burn wound sepsis had towait until surgical, critical care, and bloodbanking techniques evolved to the degreethat early identification, excision, and bio-logical closure of deep wounds could besafely practiced. This was first systemati-cally described in the 1970s in patients withsmall wounds, truncating hospital stays (5).In the 1980s and 1990s, with critical careand blood bank support, early surgery wassubsequently used to address increasinglylarger wounds, demonstrating markedly

truncated hospital stays and enhanced sur-vival in patients with large wounds, withburns over 30% of the body surface beingcommonly fatal before this (6, 7).

Postburn deformity remains a difficultclinical problem. Early wound excisionand closure seems to reduce deformity byeliminating the degree of contractionotherwise required for spontaneous clo-sure of deep wounds, but optimal func-tion is only realized in many patientsthrough a series of reconstructive opera-tions in the months and years after initialrecovery. The absence of an animal modelof hypertrophic scarring has contributedto the paucity of clinical tools for modi-fication of this inevitable process.

LONG-TERM OUTCOMES

Available data suggest that most sur-vivors of serious childhood burns have asatisfying quality of life (8, 9). A recentreport of 15-yr outcomes of children sur-viving massive burns confirmed this anddemonstrated the importance of long-term involvement with an experiencedmultidisciplinary team (10).

EPIDEMIOLOGY

In America each year, approximately 2million people are burned, 80,000 arehospitalized, and 6,500 die (11). Approx-imately 70% of pediatric burns are causedby hot liquid, whereas flame injuriesmore often cause burns in working-ageadults (12). Younger children are athigher risk for burn injury (13), and up to20% of injuries in this age group involveabuse or neglect (14). Large-scale burnprevention efforts have met with mixed

success (15). Legislation seems more ef-fective than education, with legislationon hot water heater temperature (16) andmandatory installation of smoke detec-tors being models. On the horizon is leg-islation involving fire-safe cigarettes andclothing flammability standards.

ORGANIZATION OF BURNCARE

Data exist linking volume with out-come in several complex surgical areas,including burn care (10, 17) and traumacare (18). It has been recognized thatburn care requires expertise, personnel,and equipment that are not cost effec-tively maintained in low-volume pro-grams. These issues have led to the for-mation of the burn center verificationprogram, a combined effort of the Amer-ican Burn Association and American Col-lege of Surgeons. Patients with seriousburns are increasingly sent to regionalprograms for comprehensive care (Table1, American Burn Association Burn Cen-ter transfer criteria).

BURN INJURY PHYSIOLOGY

A local response to burning involvesnot only direct tissue coagulation butalso microvascular reactions in the sur-rounding dermis that may result in ex-tension of injury (19). The systemic re-sponse to burning is driven by the loss ofthe skin barrier and release of vasoactivemediators from the wound and from sub-sequent infection. When burn size ex-ceeds about 20% of the body surface, in-terstitial edema develops in distantorgans and soft tissues secondary to a

From the Burn Surgery Service, Shriners BurnsHospital, Sumner Redstone Burn Center, Massachu-setts General Hospital, Harvard Medical School, Bos-ton, MA.

Copyright © 2002 by Lippincott Williams & Wilkins

DOI: 10.1097/01.CCM.0000034128.77577.30

During the past 20 yrs, as burn care has evolved as a specialtyof surgery, survival and outcome quality have soared. Publicexpectations for survival and long-term outcomes are at previ-ously unprecedented levels. These changes are the result of anumber of advances in aspects of burn care that have occurred inparallel and have fostered increasing regionalization of this re-source-intensive activity into fewer specialized centers. These are

complex hospitalizations and can be divided into four phases:initial evaluation and resuscitation, initial wound excision andbiological closure, definitive wound closure, and rehabilitationand reconstruction. (Crit Care Med 2002; 30[Suppl.]:S500–S514)

KEY WORDS: burn wound; sepsis; postburn deformity; fluid re-suscitation; inhalation injury

S500 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

combination of wound-released media-tors (20) and hypoproteinemia (21).

After successful resuscitation, a hyper-metabolic response occurs with near dou-bling of cardiac output and resting energyexpenditure (22). Enhanced gluconeogene-sis, insulin resistance, and increased pro-tein catabolism accompany this and havemajor implications for the care of burnpatients. The etiology of this physiology isnot well understood but is assumed to in-volve a combination of factors including achange in hypothalamic function and in-creased glucagon, cortisol and catechol-amine secretion (20), gastrointestinal bar-rier dysfunction and translocation (23),bacterial growth in the burn wound (24),and heat loss across the wound (25).

Elimination of hypermetabolism is ofunknown value. �-Adrenergic blockade(26, 27), �-adrenergic supplementation(28), nonsteroidal anti-inflammatoryagents (29), recombinant growth hor-mone (30, 31), and insulin-like growthfactor-1 (32) are all under active investi-gation. The goal is to eliminate unfavor-able aspects of the hypermetabolic re-sponse, particularly muscle catabolism,without inadvertently harming the pa-tient. Currently, data seem inadequate tosupport the routine use of such therapiesoutside clinical trials.

PREHOSPITAL CARE ANDTRANSPORT

Important issues to consider whentransporting children with serious burnsinclude control of the airway, appropriatevenous access, placement of bladder andnasogastric catheters, maintenance ofbody temperature, fluid administration iftransport time will be �1 hr, documen-tation of the events of the injury, notifi-

cation of family members, identificationof the child’s legal custodian, and docu-mentation of administered medicationsand fluids.

Hypothermia is a particular problemduring transport. Transporting vehiclesand receiving areas should be heated be-fore patient arrival. Initial dressingshould be dry rather than wetted. Imme-diate cooling of small wounds may helplimit burn depth without causing sys-temic hypothermia, but by the timeemergency response personnel have ar-rived, this window of opportunity is usu-ally gone.

Delaying transport that is anticipatedto be �1 hr to achieve venous access forfluid administration is probably not jus-tified in most cases. In those circum-stances in which longer transport timesare anticipated, venous access should beobtained unless inordinate delay results.

PRIMARY SURVEY

All seriously burned children shouldbe evaluated initially as multiple traumapatients, following the guidelines of theAmerican College of Surgeons Commit-tee on Trauma and the Advanced TraumaLife Support Course (33). A similarcourse, directed at the unique needs ofthe burned patient, is available from theAmerican Burn Association. There is sig-nificant morbidity to missed injuries.Liberal use of computerized tomographicscanning of the head, chest, and abdomenis justified if the mechanism of injury isconsistent with head or abdominal in-jury.

Airway security is the first priority is-sue during the initial evaluation. Usually,a few minutes exist in which to call forexperienced help, which is advisable as

these edematous airways can be difficultto intubate (Fig. 1). It is essential to se-cure the endotracheal tube well, as rein-tubation will become increasingly diffi-cult as edema advances. Hot liquidaspiration can present much like epiglot-titis, resulting in a need for urgent intu-bation (34) (Fig. 2).

Adequate reliable vascular access is re-quired to support resuscitation needs. Pe-ripheral vascular access can be difficult tosecure in hypovolemic burn patients, es-pecially young children, in whom in-traosseous access may be useful to beginresuscitation. Central access is generallyrequired in children with large injuries.

Figure 1. It is essential to secure the endotra-cheal tube well, as reintubation will become in-creasingly difficult as edema advances.

Table 1. American Burn Association Burn Center transfer criteria

Second and third degree burns on �10% of total body surface area (TBSA) in patients under 10 or over 50 yrs of ageSecond and third degree burns on �20% of TBSA in other age groupsSecond and third degree burns that involve the face, hands, feet, genitalia, perineum, and major jointsThird degree burns on �5% of TBSA in any age groupElectrical burns including lightning injuryChemical burnsInhalation injuryBurn injury in patients with pre-existing medical disorders that could complicate management, prolong recovery, or affect mortalityAny patients with burns and concomitant trauma (such as fractures) in which the burn injury poses the greatest risk of morbidity or mortality; in

such cases, if the trauma poses the greater immediate risk, the patient may be treated initially in a trauma center until stable before beingtransferred to a burn center; physician judgment will be necessary in such situations and should be in concert with the regional medical controlplan and triage protocols

Hospitals without qualified personnel or equipment for the care of children should transfer children with burns to a burn center with thesecapabilities

Burn injury in patients who will require special social/emotional and/or long-term rehabilitative support, including cases involving suspected childabuse and substance abuse

S501Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

BURN-SPECIFIC SECONDARYSURVEY

A burn-specific secondary survey com-plements the trauma secondary survey. Itdetails burn-specific issues by systems:neurologic, otolaryngologic, chest, car-diac, abdomen, genitourinary, extremityissues, radiographs, and laboratory stud-ies. This burn-specific secondary surveyoften occurs in the intensive care or burnunit.

Neurologic priorities are to excludeintracranial trauma, to asses for signifi-cant anoxic or carbon monoxide (CO) in-jury, and to address pain and anxiety.Intracranial trauma is excluded by his-tory, supplemented by liberal use of com-puterized axial tomographic scanning.Patients with large injuries usually be-come obtunded from fluid shifts andmedication over the days after injury, andits good to know that this change doesnot represent missed intracranial injury.

A depressed level of consciousness canalso be due to drugs, alcohol, pain med-ications, hypoxia, and hypotension, butCO intoxication should be consideredgiven appropriate injury mechanisms. CObinds to heme containing enzymes, in-cluding hemoglobin and mitochondrialcytochromes, interfering with their func-tion (35). Significant CO poisoning mayalso cause lipid peroxidation in sensitiveareas of the central nervous system (36).Breathing 100% oxygen will clear theblood of carboxyhemoglobin (half-life, 2.5hrs on room air and 40 mins on 100%oxygen). However, CO also binds to mi-tochondrial cytochromes and thereby in-terferes with oxygen utilization. Patientswith serious CO poisoning are at risk fordelayed neurologic sequale such as ataxiaand choreiform movement disorders. Theability of hyperbaric oxygen treatment toreduce the risk of these sequelae is notentirely clear (37), but if it can be safely

administered, it is reasonably consideredin those with carboxyhemoglobin levelsof �30% or with overt neurologic dys-function not otherwise explained (36).Hemodynamic instability, wheezing orair trapping, and the need to effect trans-ports inconsistent with good generalburn care are contraindications (38).

Immediate eye and otolaryngologic is-sues include evaluation of the cornea andthe external ear. If one waits until facialand ocular adnexal edema is advanced, itcan be difficult to evaluate the globes.The eye evaluation should include fluo-rescein staining to detect more subtleinjury. Burns of the external ear shouldbe identified and treated with topicalmafenide acetate to reduce the preva-lence of suppurative chondritis (39).

The focus on the initial evaluation ofthe chest is ensuring adequate ventila-tion, which is usually compromised bydecreased chest wall compliance second-ary to circumferential eschar and bybronchospasm secondary to aerosolizedirritants. Torso escharotomy is done us-ing coagulating electrocautery to makeaxial incisions along the flanks that areconnected across the midline (Fig. 3).Bronchospasm is managed with aerosol-ized bronchodilators and ventilationstrategies, minimizing the breath stack-ing and dynamic hyperinflation that can

accompany increases in small airway re-sistance.

Initial evaluation of the abdomen isdone to exclude associated injuries, toensure torso compliance, and to reducethe prevalence of gastroduodenal ulcer-ation and gastric dilation. Occult abdom-inal injury can explain excessive resusci-tative fluid requirements or aparadoxically falling hemocrit during theearly resuscitative phase and should beeliminated with liberal imaging givensuspicious injury mechanisms. On occa-sion, circumferential torso eschar ormassive accumulation of transudative in-traperitoneal fluid or bowel edema cancause an abdominal compartment syn-drome, with decreasing urine output anddifficulty with ventilation. This is gener-ally well managed with generous escha-rotomy and control of fluid resuscitation.In rare children with massive visceraledema, abdominal decompression may benecessary (40). In other children (equallyrare), drainage of peritoneal fluid is ade-quate to effect abdominal decompression.Gastroduodenal ulceration can developduring burn resuscitation because of re-duced splanchnic flow (41), and prophy-laxis (generally histamine receptor antag-onists) is indicated. Air swallowing andgastric dilation frequently occurs (Fig. 4)and is managed with nasogastric decom-pression.

Genitourinary considerations in thesecondary survey include ensuring the

Figure 2. Hot liquid aspiration, suggested by ex-amination in this child, can present like epiglot-titis.

Figure 3. Torso escharotomy is done using coag-ulating electrocautery to make axial incisionsalong the flanks that are connected across themidline.

Figure 4. Chest radiographs should be examinedfor chest injury, proper position of resuscitativecannulas, and acute gastric dilation.

S502 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

foreskin in reduced over the bladder cath-eter after insertion to prevent the devel-opment of paraphimosis as soft-tissueedema progresses. Occasionally, it is nec-essary to section a deeply burned foreskinto allow access to the meatus to facilitateinsertion of a bladder catheter.

Excluding associated nonburn injuriesbased on mechanism and monitoring pe-ripheral perfusion in extremities at risk ofischemia is the important aspect of theextremity secondary survey. Extremityperfusion can be compromised by pro-gressive soft-tissue edema within non-elastic compartments or beneath overly-ing eschar. Early identification ofextremities at risk and serial examinationare essential. Extremities at risk shouldbe dressed to facilitate frequent examina-tion and be regularly accessed for tem-perature, pliability, voluntary motion,pain with passive motion, named vesselpulsations, and low-pressure flow usingcapillary refill and Doppler signals in thedigital vessels and digital pulp. Serialclinical examination will reliably deter-mine the need for escharotomy or fas-ciotomy in most situations while elimi-nating any risk of seeding compartmentsby passing pressure monitoring cathetersthrough contaminated wounds (42). Ex-tremity escharotomies can be performedat the bedside using the coagulating elec-trocautery to minimize blood loss. Axiallyoriented medial and lateral incisionsshould be designed to completely sectionthe deep eschar while avoiding injury tounderlying superficial structures. Thosesuperficial structures most at risk duringescharotomy are the brachial artery inthe upper arm, ulnar nerve at the elbow,superficial peroneal nerve at the knee,and the neurovascular bundles and exten-sors of the digits (Fig. 5). Fasciotomiesshould generally be done in the operatingroom.

Radiographic evaluation during theburn-specific secondary survey are lim-ited to those needed to exclude otherinjuries, based on mechanism, and todocument position of central venouscatheters and endotracheal tubes. Spinefractures have been reported in associa-tion with high-voltage injury, either fromfall or tetanic contraction of paraverte-bral muscles. Laboratory studies neces-sary to the initial evaluation are generallylimited to routine chemistries, hemocrit,carboxyhemoglobin level in those injuredin structural fires, and urine myoglobinin those with a history of electrical injuryor pigmented urine.

Finally, the possibility of abuse shouldbe considered in every child. Suspiciousinjuries must be filed with the appropri-ate state agency. Important data thatshould be obtained during the initialevaluation include tap water tempera-ture, duration of contact, caretakers in-volved, documentation of conflicting re-ports from involved caretakers, delay inseeking treatment, and prior injuries. Im-portant points of examination includeuniformity of burn depth, absence ofsplash marks, sharply defined woundmargins, porcelain-contact sparing,flexor sparing, stocking or glove patterns,dorsal location of contact burns of thehand, and localized very deep contactburns (Fig. 6) (43). These children shouldbe admitted to the hospital for evaluationeven if the injury itself is of little physi-ologic significance. Screening long boneseries and computerized axial tomo-graphic scanning of the head for occultinjuries should be considered.

FLUID RESUSCITATION

In the hours after a serious burn,there is a systemic capillary leak thatincreases with injury size, delay in initi-ation of resuscitation, and the presence ofinhalation injury. It typically “seals” after18–24 hrs if resuscitation has been suc-cessful. Its thought that an initial releaseof vasoactive substances from the injuredtissue and subsequent generation ofhighly reactive oxygen species after per-fusion of marginally perfused or previ-ously ischemic tissues drives the patho-

physiology (44). The ability to block thesemediators or otherwise modify thispathophysiology is not currently possible,although it remains a research focus (45,46).

There is no formula that will accu-rately predict the volume requirements ofindividual patients. The inherent inaccu-racy of formulas requires continuous re-

Figure 5. Limb escharotomies can be performedat the bedside using the coagulating electrocau-tery to minimize blood loss. Axially oriented me-dial and lateral incisions should be designed tocompletely section the deep eschar while avoid-ing injury to underlying superficial structures.Those superficial structures most at risk duringescharotomy are the brachial artery in the upperarm, ulnar nerve at the elbow, superficial pero-neal nerve at the knee, and the neurovascularbundles and extensors of the digits.

Figure 6. The possibility of abuse is suggested byuniform burn depth, absence of splash marks,sharply defined wound margins, porcelain con-tact sparing, flexor sparing, stocking or glovepatterns, dorsal location of contact burns of thehand, and localized, very deep contact burns.

S503Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

evaluation adjustment of infusions basedon resuscitation targets (Table 2). Themodified Brooke or Parkland formulasare reasonable consensus formulas andare used to determine the initial volumeinfusion. One half of the total calculated24-hr volume is administered the duringthe first eight postinjury hours. Shouldthe resuscitation be delayed, this volumeis administered so that infusion is com-pleted by the end of the eighth postinjuryhour. The importance of assessing resus-citation end points and appropriately in-creasing or decreasing the infusionshourly cannot be overemphasized. Theseconsensus formulas are detailed in Table3.

Most formulas recommend that allcrystalloid be isotonic during the first 24hrs, generally lactated Ringer’s solution.Hypertonic saline (47) has been recom-mended for resuscitation, but it haslargely been abandoned because it istechnically challenging and may compro-mise outcome (48). A slightly hypertonicsolution made by adding sodium bicar-bonate to lactated Ringer’s solution hassome utility in resuscitation of childrenwith very large injuries (49). A frequentquestion that arises is the minimum burnsize at which a formal fluid resuscitationis required. As a general rule, burns of

�15% of the body surface are not asso-ciated with an extensive capillary leak,and children with burns in this size rangecan be managed with fluid administeredat 150% of a calculated maintenance rate,with close observation of the status oftheir hydration. Those who are able andwilling to take fluid by mouth may begiven fluid by mouth with additional fluidgiven intravenously at a maintenancerate. The gluconeogenetic capacity ofolder children and adolescents is suchthat no glucose-containing solutions areusually required during resuscitation. Insmaller children, particularly those of�20 kg, hypoglycemia is a threat, andRinger’s lactate with 5% dextrose shouldbe administered at a maintenance rate.

Most resuscitation formulas recom-mend the administration of colloid whencapillary integrity returns, generally by24 hrs, as colloid is more likely to remainin the intravascular compartment at thattime. In some circumstances, earlier useof colloid seems to improve hemodynam-ics and decrease volume needs. Most cli-nicians use 5% albumin in isotonic crys-talloid; however, fresh frozen plasma isadvocated by others, although this seemsbetter used to correct coagulopathy toavoid disease transmission. Colloid isgenerally administered by continuous in-

fusion at a dose graded by burn size (Ta-ble 3). It is ideal to begin enteral feedingsat about this time, except in patients withmassive injuries or in those who are un-der-resuscitated and are less likely to tol-erate tube feedings because of ileus sec-ondary to splanchnic underperfusion.

It is a frequent observation that inha-lation injury, delay in resuscitation, andunusually deep burns result in a higherfluid requirement. It has also been a com-mon belief that young children requirehigher resuscitation volumes per bodymass than older children and adults (50).However, to a certain extent this obser-vation may be an artifact of setting an endpoint for urine output of 2 mL·kg�1·hr�1.In infants, whose renal concentratingabilities are immature, this is probablyappropriate. However, in toddlers andolder children, whose renal concentrat-ing abilities are more mature, this mayresult in an excessive volume administra-tion.

Sometimes resuscitation does not gowell. If total resuscitation needs are esti-mated to exceed 6 mL/kg of the percent-age of total body surface area burned per24 hrs, it is often prudent to obtain moreinformation regarding the status of theintravascular volume. This can be donewith a directed physical examination,supported by measurement of central ve-nous pressures or placement of a pulmo-nary artery catheter. If intravascular vol-ume is felt to be adequate, dopamine,infused at “renal dose” (5 �g·kg�1·min�1),will sometimes improve renal perfusionenough to increase urine output withoutfurther increases in fluid administration.Early administration of colloid will some-

Table 2. Burn resuscitation end points

Sensorium: arousable and comfortableDigital temperature: warm peripherallySystolic blood pressure: for infants, 60 mm Hg systolic; for older children, 70–90 plus 2 � age in

yrs mm Hg; for adults, mean arterial pressure over 60 mm HgPulse: 80–180 per min (age dependent)Urine output: 0.5–1 mL � kg�1 � hr�1 (glucose negative)Base deficit: �2

Table 3. Consensus resuscitation formula

First 24 hrsAdults and children �20 kg

Ringers lactate: 2–4 mL/kg/%burn/24 hrs (first half in first 8 hrs)Colloid: none

Children �20 kgRingers lactate: 2–3 mL/kg/%burn/24 hrs (first half in first 8 hrs)Ringers lactate with 5% dextrose: maintenance rate (approximately 4 mL/kg/hr for the first 10 kg, 2 mL/kg/hr for the next 10 kg, and 1 mL/kg/hr

for weight �20 kg)Colloid: none

Second 24 hrsAll patients

Crystalloid: to maintain urine output; if silver nitrate is used, sodium leeching will mandate continued isotonic crystalloid; if other topical isused, free water requirement is significant; serum sodium should be monitored closely; nutritional support should begin, ideally by the enteralroute

Colloid: (5% albumin in Ringers lactate)0–30% burn: none30–50% burn: 0.3 mL/kg/%burn/24 hrs50–70% burn: 0.4 mL/kg/%burn/24 hrs70–100% burn: 0.5 mL/kg/%burn/24 hrs

S504 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

times help. Occasionally, children with verylarge injuries demonstrate some degree ofmyocardial dysfunction (51), and a thera-peutic trial of �-adrenergic agents mayprove useful.

Pigmented urine is commonly seen inthe setting of high-voltage or very deepthermal injury. To avoid renal tubularinjury, pigment should be clearedpromptly. This can usually be done in 2–3hrs by administration of additional crys-talloid to the end point of a urine outputof 2 mL·kg�1·hr�1. Judicious administra-tion of bicarbonate may facilitate clear-ance of myoglobin by preventing its entryinto the tubular cells. In rare circum-stances, mannitol is a reasonable adjunct,but its use obscures urine output as anindicator of circulating volume, and cen-tral venous pressures should be moni-tored.

After 18 –24 hrs, capillary integritygenerally returns if resuscitation hasbeen successful. At this point, fluid re-quirements abruptly decrease, and it isimportant to decrease fluid administra-tion appropriately after resuscitation endpoints. Over administration of fluid dur-ing this time is associated with potentialmorbidity.

After the capillary leak seals and fluidinfusions are reduced, wound manage-ment has an increasing influence on theamount of fluid and type of electrolytereplacement required. Wounds treatedwith nonaqueous topicals (such as silversulfadiazine) generate a free-water re-quirement, generally provided as 5% dex-trose in water or free water added toenteral feedings. Extreme hypernatremiacan be associated with adverse centralnervous system effects, including intra-cranial bleeding. Wounds treated withaqueous topical agents (such as 5% silvernitrate solution) are associated with elec-trolyte leeching and secondary hypona-tremia that requires isotonic crystalloidand additional salt in enteral feedings.

Cerebral edema and seizures can occurwith severe hyponatremia (52, 53). Overlyrapid correction of hyponatremia may re-sult in central pontine demyelinating le-sions (54). There is serious morbidity as-sociated with poor control of serumsodium at this time, and it should bemonitored and kept in the physiologicrange. Serum ionized calcium and mag-nesium should be monitored as supple-mentation is commonly required duringthis period.

TOPICAL WOUND CARE

Topical agents are applied to controlpain, decrease vapor loss, prevent desic-cation, and slow bacterial growth. Thereare an increasing number of optionsavailable. Silver sulfadiazine is a whiteopaque cream that is painless on applica-tion, has fair to poor eschar penetration,has no metabolic side effects, and has abroad antibacterial spectrum. Mafenideacetate, although painful on applicationand a carbonic anhydrase inhibitor, hasexcellent eschar penetration and a broadantibacterial spectrum. Silver is an ex-tremely effective topical agent and is gen-erally applied as aqueous 0.5% silver ni-trate. Applied in this fashion, silver ispainless on application but has poor es-char penetration and leeches electrolytes.It is popular because it has a broad spec-trum of activity (including fungi) and canbe used on adjacent wounds, grafts, anddonor sites. Silver-impregnated dress-ings, such as Acticoat (Westhaim Bio-medical Inc, Voorhees, NJ), are also use-ful in selected wounds. Debridingenzymes have been applied to wounds inan effort to soften or remove eschar (55,56). New formulations of debriding en-zymes that are deactivated by circulatingproteases are available and are designedto liquefy necrotic tissue while avoidinginjury to healthy tissue (57). These sub-stances may facilitate wound-depth eval-

uation and blood conserving removal ofeschar. At present, the role of these sub-stances is limited.

Burns are tetanus-prone wounds, andproper documentation of tetanus im-mune status is important. If in doubt,active immunization should be adminis-tered. In those who are not immunized orwho have incomplete or questionable tet-anus immune status, passive immuniza-tion is advisable. This is particularly trueif burns are extensive, deep, or heavilycontaminated.

INITIAL WOUND EXCISION ANDCLOSURE

Early identification, excision, and clo-sure of full-thickness wounds change thenatural history of burn injury and are atthe heart of recent progress in burn care.The objective of this phase of care is toremove the bulk of the full-thickness in-jury and to achieve biological closure.When performed before the developmentof wound colonization and infection, itcircumvents the development of woundsepsis and systemic inflammation. Theseoperations have a reputation of beingbloody and physiologically stressful.However, these negatives can be mini-mized if operations are planned and exe-cuted properly.

An early estimate of burn size anddepth is useful for planning (Table 4).Burn diagrams are commonly central tosubsequent litigation, and if, as is so oftenthe case, they are rough working dia-grams, it is ideal to so note this on thediagram so that inaccuracies are not thefocus of later confusion. Burn extent isbest estimated using a chart based on theLund-Browder diagram that compensatesfor the changes in body proportions withgrowth (Fig. 6). An alternative in adults isthe “rule of nines.” However, this is notaccurate in children because their bodyproportions are different from those ofadults. For areas of irregular or noncon-fluent area burns, the palmar surface ofthe child’s hand can be used, as the areaof the palm only, not including the digits,has been shown to represent 0.5% of thebody surface over a wide range of ages(58). Burns are classified as first, second,third, or fourth degree (Table 4). As ageneral rule, burns are usually underes-timated in depth on initial examination.Circumferential, or near circumferential,components should be noted becausethey represent areas where special mon-itoring, and sometimes escharotomy, is

Table 4. Initial evaluation of burn wounds

ExtentLund-Browder chart: an age-specific chart that accounts for the changing body proportions with

age; preferred in childrenRule of nines: assumes adult body proportions; head and neck, 9%; anterior chest, 9%; posterior

chest, 9%; anterior abdomen, 9%; posterior abdomen (including buttocks), 9%; each upperextremity, 9%; each thigh, 9%; each leg and foot, 9%; genitals, 1%

Palmar surface of hand: Palmar surface of hand (without the fingers), approximately 0.5%Depth

First degree: red, dry, and painfulSecond degree: red, wet, and very painfulThird degree: leathery in consistency, dry, insensate, and waxyFourth degree: involves underlying subcutaneous tissue, tendon, or bone

S505Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

needed. Accurate knowledge of the prob-ability a wound will heal (different fromthe easier to measure burn depth) is cen-tral to operative planning. Examinationby an experienced burn surgeon remainsthe most reliable method, despite themany devices developed to measure burndepth or burn blood flow (59, 60). Thechanges in wound appearance over thefirst few days after injury make serialexamination a particularly useful tool insurgical planning.

Overall wound size is the most impor-tant factor in determining the need forearly operation, as this correlates withthe physiologic threat represented by theinjury. Patients with small burns rarelydevelop overwhelming wound sepsis, andsuch children may have the luxury oftime to allow the wound to fully evolve toa point that it is easy to determine burndepth on physical examination. An initialnonoperative approach to such wounds iswidely practiced and is associated withminimizing the need for operation (61).At the end of the first postburn week, itusually is quite clear which areas, if any,need to be excised and grafted, and this isthen done. In this way, all grafts, donorsites, and second-degree burns are fullyhealed by 3 wks, and the child can re-sume normal activities.

Patients with larger injuries generallydo better if their wound is addressed sur-gically early, the full-thickness compo-nent being identified, excised, and closedduring the first postburn week. When thewounds are �40%, this may requirestaged procedures. If the wounds involve�50% of the body surface, it is oftenimpossible to achieve immediate au-tograft closure. When autograft is ex-hausted, temporary biological closure isachieved with human allograft or othertemporary wound closure material.Wounds are later resurfaced with au-tograft when donor sites have healed.

Techniques of burn-wound excisionhave evolved substantially over the pastdecade. Most children can be managedwith layered excisions that optimize laterappearance and function. Sheet grafts areused whenever reasonable. Published es-timates of the amount of bleeding asso-ciated with these operations are in therange of 3.5–5% of the blood volume forevery 1% of the body surface excised (62,63). Blood loss during excision should beminimized through the use of extremitytourniquets, dilute epinephrine injection,and a brisk operation pace (64). Intraop-

erative hypothermia should be antici-pated and prevented.

SKIN SUBSTITUTES

Temporary skin substitutes, or biolog-ical dressings, provide transient physio-logic wound closure, which implies pro-tection from mechanical trauma, a vaporbarrier similar to skin, and a physicalbarrier to bacteria (65). Split-thicknesshuman allograft is procured from organand tissue donors and remains the stan-dard by which other temporary skin cov-ers are judged. These membranes con-tribute to moist wound environment witha low bacterial density that is consistentwith optimal wound healing. There mem-branes are typically used in one of foursettings: as a dressing on donor sites tofacilitate pain control and epithelializa-tion from skin appendages, as a dressingon clean superficial wounds to a similarend, to provide temporary physiologicclosure of deep dermal and full-thicknesswounds after excision while awaiting au-tografting or healing of underlying widelymeshed autografts, and as a “test” graft inquestionable wound beds. There are anincreasing variety of such materials avail-able, with none clearly superior. It is im-portant to monitor for submembrane in-fection if these materials are used.

An inexpensive, reliable, and durablepermanent skin substitute would pro-foundly change burn care. Although nosuch substitute exists presently, a num-ber of devices have been recently devel-oped that contribute to permanent cov-erage of burn wounds. They can beclassified as epidermal substitutes, der-mal substitutes, and composite substi-tutes. Autologous epithelial cells grownfrom a single full-thickness skin biopsyhave been available for nearly two de-cades and are useful in children with verylarge wounds (66), although they provideimperfect cover (67), which may be im-proved by combination with a vascular-ized remnant of allogenic dermis (68).Dermal analogs have been made availablefor clinical use in recent years. Integra(Integra Life Sciences, Plainboro, NJ) wasrecently approved by the United StatesFood and Drug administration for use inlife-threatening burns (69). The innerlayer of this material is a 2-mm-thickcombination of fibers of collagen isolatedfrom bovine tissue and the glycosamino-glycan chondroitin-6-sulfate that has a70–200 �m pore size that facilitates fi-

brovascular ingrowth from the host andthen undergoes biodegradation. Theouter layer is 0.009-inch polysiloxanepolymer with vapor transmission charac-teristics that simulate normal epithe-lium. Post-marketing trials are inprogress at this time. Allogenic dermisdesigned to be combined with a thin ep-ithelial autograft (AlloDerm, LifeCellCorporation, The Woodlands, TX) is man-ufactured from split-thickness skin allo-grafts procured from properly screenedcadaver donors. Clinical experience withthis material in acute and reconstructiveburn wounds is still early but has beenfavorably reported (70, 71). The truly suc-cessful permanent skin substitute willprobably be a laboratory-derived autolo-gous composite. Exciting work is under-way in many centers, but the solution isnot yet on the horizon.

INHALATION INJURY

The diagnosis of inhalation injury isprimarily clinical, based on a history ofclosed-space exposure, facial burns,singed nasal hairs, and carbonaceous de-bris in the mouth and pharynx or sputum(Fig. 7). Chest radiographs are routinelynormal until complications (usually in-fection) have developed. If fiberopticbronchoscopy reveals carbonaceous de-bris, ulceration, or erythema (72), it sup-ports the diagnosis, but a normal studydoes not exclude it. Technetium scanninghas also been used to confirm the diag-nosis of inhalation injury (73, 74). Notechnique will reliably stratify injury se-verity or predict subsequent clinicalcourse.

The clinical consequences of inhala-tion injury include upper airway edemafrom direct thermal injury exacerbated bysystemic capillary leak, bronchospasm

Figure 7. The diagnosis of inhalation injury is basedon a history of closed-space exposure, facial burns,singed nasal hairs, and carbonaceous debris in themouth and pharynx or in the sputum.

S506 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

from aerosolized irritants, small airwayocclusion from sloughed endobronchialdebris and loss of the ciliary clearancemechanism, increased dead space and in-trapulmonary shunting from alveolarflooding, decreased lung and chest wallcompliance from interstitial and alveolaredema and swelling or burn of the chestwall, and infection of the denuded tra-cheobronchial tree (tracheobronchitis) orpulmonary parenchyma (pneumonia).

Management is supportive only. Upperairway edema usually resolves in 2 to 3days and can be facilitated by elevation ofthe head of the bed and avoidance ofexcessive fluid administration. Bronchos-pasm generally responds to inhaled�-agonists. If mechanical ventilation isrequired, air trapping should be antici-pated and managed by ensuring adequateexpiratory times and being alert for dy-namic hyperinflation (75). Inflating pres-sures to �40 cm H2O should be avoided,unless there is severely impaired chestwall compliance, implying that the inflat-ing pressures are not transpleural. Chil-dren with even severe inhalation injurytypically have normal gas exchange andcompliance for 48–72 hrs after injury.During this period, it is ideal to effectinterhospital transfers or needed opera-tions, as deteriorating gas exchange maycomplicate both.

In the days after inhalation injury, en-dobronchial debris collect, alveolar seg-ments flood, compliance suffers, infectionoccurs, and gas exchange deteriorates. Thisis managed with vigorous pulmonary toiletand ventilator support designed to preventsecondary lung injury by capping inflatingpressures at 40 cm H2O and concentrationsof oxygen at 60% if possible. Both havebeen demonstrated to cause pulmonary in-jury (76, 77). The end points of oxygenationand ventilation should be reset to physio-logically acceptable ventilation (any PaCO2

with a pH of �7.2) and oxygenation (anyPaO2 consistent with an SaO2 of �90%).This approach, permissive hypercapnia, isassociated with excellent outcomes (78,79). If the reset physiologic end points can-not be achieved without violating pressureand oxygen caps for significant lengths oftime, innovative methods of support suchas inhaled nitric oxide (80), high-frequencypercussive ventilation (81), or extracorpo-real life support (82) should be considered,or these caps will be transiently violated.

Pneumonia or tracheobronchitis oc-curs in about 30% of these children sec-ondary to loss of the ciliary clearancemechanism, small-airway occlusion, alve-

olar flooding, and endotracheal intuba-tion (83). Signs of pulmonary infectioninclude fever and purulent endobronchialsecretions. Radiographic infiltrates or lo-bar consolidation suggest pneumonia. Inthe absence of radiographic changes, adiagnosis of tracheobronchitis is made.Neither bronchoalveolar lavage nor pro-tected specimen brush specimens areroutinely required for diagnosis and man-agement (84). Antibiotic therapy is di-rected by sputum Gram-negative stain,and cultures and should not be prolongedbeyond a 7–10 day therapeutic course.Vigorous pulmonary toilet, with toiletbronchoscopy in selected patients, is avery important component of therapy.

The role of tracheostomy in the man-agement of inhalation injury is contro-versial. It can be very useful, particularlyif prolonged intubation or difficult wean-ing is anticipated (85) or if unusuallythick secretions are unmanageablethrough an endotracheal tube. Tracheos-tomy in children is associated with ahigher prevalence of serious structuralproblems requiring prolonged cannula-tion and reconstruction and is ideallyavoided when possible (86). Althoughthere are data suggesting modest long-term exercise intolerance (87), most in-halation injury survivors do extremelywell, with clinically normal long-termpulmonary function.

UNIQUE ASPECTS OFPEDIATRIC BURN CRITICALCARE

Although most issues that arise incritically ill burned children are not dif-ferent from children with other primarydiagnoses, there are a few unique prob-lems that merit discussion. These will beaddressed briefly by systems.

Neurologic issues include occult inju-ries, seizures, neuropathies, and paincontrol. Children with large burns, al-though often alert in the first hours afterinjury, predictably become obtunded overthe ensuing hours and days secondary tofluid shifts, pain medication, sleep depri-vation, and exhaustion. Occult head in-jury should be excluded by early comput-erized axial tomographic scanning, if themechanism of the accident is consistent.Cerebral edema and seizures are associ-ated with rapid development of hypona-tremia, especially in small children.Overly rapid correction of hyponatremiais associated with demyelinization in thecentral nervous system. This problems

are ideally avoided by close attention toserum electrolytes (52–54). Peripheralneuropathies occur in about 5% of seri-ous burns (88, 89) secondary to directthermal injury or metabolic derange-ments. Some may be avoided by tightcontrol of electrolyte disturbances,prompt decompression of ischemic ex-tremities, attention to the fitting ofsplints, and careful intraoperative posi-tioning. Adequate management of painand anxiety is as essential as it is difficult(90). A unit-specific guideline is useful.One such guideline divides patients intofour types: mechanically ventilated acute,spontaneously breathing acute, acute re-habilitation, and reconstructive. It ad-dresses background pain, proceduralpain, and transition issues for each pa-tient group by using a limited formularyand dose ranging (91).

Hemodynamic issues that arise afterresuscitation are predictable. A hyperdy-namic state occurs, characterized by ahigh cardiac output and low peripheralresistance. This physiology is effected bywound colonization, translocation of bac-teria and their byproducts from the gut(92), and the neurohormonal changes as-sociated with the open wound (20). It canbe difficult to know the status of intra-vascular volume and perfusion duringthis time, particularly during episodes ofsepsis, which are often preceded by anincrease in capillary leak and subtle in-creased fluid needs. This is best judged bycareful serial physical examinations, withconsideration of intravascular pressuresand selected laboratory data. Findings ofparticular importance include soft-tissueedema, hepatic size, central venous pres-sure, urine output, serum osmolality, andserum sodium concentration. It is impor-tant to have clearly in mind age-appro-priate fluid administration targets and toinclude all catheter flushes and medica-tions into fluid calculations to avoid in-advertent volume overload. In most situ-ations, hypoperfusion is related toinadequate preload, improved by admin-istration of additional volume, or inade-quate afterload, improved by cautious in-fusion of �-adrenergic agents. In thoseexceptional circumstances in which theseagents need to be used, simultaneous in-fusion of renal dose dopamine may pro-tect the splanchnic bed from the adverseeffects of excessive vascular tone.

Serum electrolyte concentrations arestrongly influenced by transeschar flux ofwater and small molecules. If nonaque-ous topical medications are applied to

S507Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

wounds, particularly in a dry environ-ment or high air loss beds, free water lossbecomes a prominent influence on serumelectrolyte concentrations. If aqueoustopicals are used, such as 0.5% silvernitrate, transeschar leeching of sodium(approximately 350 and 25 mEq·m�2·24hrs�1) requires continued administrationof isotonic crystalloid (93, 94). Rapidswings in serum electrolytes are associ-ated with significant morbidity, so dili-gent electrolyte monitoring and replace-ment is a critical component of care. Aspatients are fed, glucose enters the cellsand is phosphorylated. This may in partexplain the frequent occurrence of hy-pophosphatemia in those with serious in-juries. When looked for, hypomag-nesemia is quite common as well (95).Both are associated with surprising mor-bidity if not corrected with enteral orparenteral supplements.

The physiology of injury includes areduction of hepatic albumin synthesis atthe transcriptional level in favor of acutephase protein production (96). This re-duced synthesis combined with enhancedalbumin loss through open wounds re-sults in predictable hypoalbuminemia.How low one should allow serum albu-min to fall has been an area of contro-versy for many years (97). It has been ourpractice to tolerate levels of �1.0 g/dL aslong as there is no significant enteralfeeding intolerance (98) or pulmonarydysfunction (99), as these two problemsmay potentially be exacerbated by hy-poalbuminemia. If serum albumin is�1.0 g/dL, or 1.5 g/dL in the presence ofenteral feeding intolerance or pulmonarydysfunction, supplemental infusion of1–2 g·kg�1·day�1 to a target value of 2.0g/dL is probably warranted (100).

Chronic central vascular access is es-sential to the successful management ofserious burns. The importance of carefultechnique cannot be overemphasized iflife- and limb-threatening complications,reported to occur in 4% of insertion at-tempts, are to be minimized. Centralveins are limited and will clot if cannu-lated with large catheters. The prevalenceof thrombosis of these valuable sites maybe reduced by using the smallest diame-ter catheter that will reasonably meet thepatient’s needs. Rotation of catheters, inan effort to diminish the prevalence ofcatheter sepsis, remains an area of signif-icant controversy, with little data to sup-port individual practices. Unit policiesvary from replacement at a new site every48 hrs to replacement only for clear evi-

dence of catheter sepsis or malfunction insome pediatric units. Although data arenot conclusive, we are convinced that atleast weekly rotation of catheters is areasonable compromise that minimizesboth catheter-related sepsis and the me-chanical complications associated withcatheter insertion (101, 102). Arterialcatheters are not routinely required, butare useful in the patients with respiratoryfailure who requires frequent arterialblood gas monitoring or in hemodynam-ically labile patients who require minute-to-minute blood pressure monitoring.Those intubated primarily for airway pro-tection can be very well managed with apulse oximeter to monitor arterial oxygensaturation and an extremity sphygmoma-nometer. Probably because of the rela-tively high flow rates around arterialcatheters, they are less likely to becomeinfected and are not routinely rotated, asare central venous catheters, unless thesite becomes inflamed or there is somereason to suspect infection (19). Appro-priate sites are the dorsalis pedis artery,the femoral artery, and the radial artery.It is extremely important to use carefultechnique when inserting femoral arte-rial catheters to avoid limb-threateningischemia. Brachial and axillary arterialcatheters should be used with extremecaution because of the risk of ischemia tothe hand and the risk of cerebral embo-lization with vigorous flushing in smallchildren.

Support of the hypermetabolic re-sponse is characterized by fever, in-creased metabolic rate, increased minuteventilation, increased cardiac output, de-creased afterload, increased gluconeo-genesis that is resistant to glucose infu-sion, and increased skeletal and visceralmuscle catabolism (103, 104). Patientsremain hypermetabolic until wound clo-sure is complete and for a variable periodthereafter. Accurate support of this phys-iology is essential. Overfeeding is associ-ated with hepatic steatosis, leading to he-patic dysfunction and increased CO2

production exacerbating respiratory in-sufficiency. Underfeeding results in ina-nition and poor wound healing. Patientsmanaged with prompt wound excisionand biological closure have a reduced en-ergy expenditure compared with historiccontrols (105), and multiple studies havedemonstrated that standard formulas donot accurately predict energy require-ments in individuals. For these reasons,expired gas indirect calorimetry is com-monly used to monitor nutritional sup-

port. Total energy expenditure can beroughly estimated by using expired gasindirect calorimetry to determine a rest-ing energy expenditure and then multi-plying resting energy expenditure by afactor of 1.3 to 1.7 (106). Protein admin-istration of 2.5 to 3.0 g·kg�1·day�1 willadequately support the needs of burn pa-tients (107). The route of nutritional sup-port is ideally enteral tube feeding begin-ning during resuscitation. Not only doesthis provide immediate protein and calo-rie needs, but enteral feedings may bettersupport the gut barrier, possibly decreas-ing the prevalence of bacterial transloca-tion (108). Some children, particularlythose with very large burns during theearly resuscitation period or those withintervening sepsis, will not tolerate en-teral feedings at goal rates, and supple-mental parenteral nutrition, in additionto enteral feedings at low rates, is justi-fied to ensure delivery of all needed nu-trients. The use of anabolic agents is anarea of active investigation. Recombinanthuman growth hormone in daily subcu-taneous doses has been reported to accel-erate donor site healing and restore ear-lier positive nitrogen balance (109, 110).The use of recombinant human growthhormone and other anabolic agents suchas �-agonists (28, 111), �-antagonists(111), and anabolic steroids (112) in se-riously burned children remains an im-portant area of ongoing investigation.Available data do not seem sufficient tosupport their routine use.

Seriously burned children have a de-gree of global immunosuppression andhave violated epithelial barriers and mul-tiple invasive devices. Consequently, theyare prone to a host of septic complica-tions until all of their wounds are closed.Constant vigilance is required to allowearly detection and treatment of thesecomplications (113–116). Infection con-trol measures should be rigorously fol-lowed to prevent cross-infection with re-sistant organisms (117). In burn patients,the sequence of multiple organ failure iscommonly increasing obtundation, pro-gressive intrapulmonary shunting, andhypoxia, ileus, nonoliguric renal failure,rising cholestatic chemistries, thrombo-cytopenia, anuria, vasomotor failure, anddeath (118). Treatment involves supportof failing organs and a thorough searchfor occult infection. Certainly, woundsepsis is an obvious potential source.However, this should be rarely seen ifdeep wounds are promptly excised andclosed. When an underlying infectious fo-

S508 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

cus can be identified and addressed, or-gan functions improve. Vigilant bedsidecare and effective surgery remain themost effective immunomodulators.

DEFINITIVE WOUND CLOSURE

In this phase of care, allograft andother temporary wound closures are re-placed with permanent covers, and smallbut complex wounds are addressed. Bythis time, the patient should have bulkphysiologic wound closure and is gener-ally in a stable systemic state. The firstobjective is to achieve bulk wound clo-sure with definitive covers, generally re-harvested autograft. When this has beenachieved, attention is turned to small,complex wounds, particularly the headand neck, hands, feet, and genitalia.These are areas of small physiologic size,but great functional and aesthetic impor-tance. A studied and careful approach tothese wounds is essential.

The face should be rendered func-tional, with good coverage of the globesand competence of the mouth and accessto the airway (Fig. 8). Portions of the facethat need to be grafted should be resur-faced with thick split-thickness grafts ofoptimal color match in cosmetic units aslong as this does not require the sacrificeof significant areas of healed burn or un-burned skin. It is important to be watch-ful for the occurrence of globe exposure,caused by retraction of burned periorbitaltissues. This should be addressedpromptly when it occurs, initiallythrough intensive ocular lubrication andthen with early lid release if keratitis de-velops in the face of ocular lubrication.Not to do so will risk loss of the globethrough corneal ulceration and infection(Fig. 9).

Serious hand burns should be a focusof attention from the onset of resuscita-tion, or ultimate function will be com-promised (119). During the first 72 hrs,the team must ensure that hand perfu-sion is not compromised by near circum-ferential eschar or elevated compartmentpressures. If consistent with critical careneeds, the hands are ideally takenthrough a full range of motion twice dailyand at other times splinted in a positionof function, with the metatarsophalan-geal joints at 70 to 90 degrees, the inter-phalangeal joints in extension, the firstweb space open, and the wrist at 20 de-grees of extension. Hands should be ele-vated to minimize edema and rangedtwice daily. Deep dermal and full-thick-

ness burns should undergo prompt exci-sion and sheet autograft closure. At 7days after surgery, passive and, if consis-tent with patient condition, active handtherapy should begin. Even very destruc-tive hand burns should be managed withan expectation of a functional result con-sistent with activities of daily living. Thekey features of this focus are surgicalefforts to maintain normal flexion at themetacarpophalangeal joints and toachieve opposition between the remnantof the thumb and one or more digits(119, 120)

SPECIAL SITUATIONS

A number of special situations that canbe expected as burn center referrals aredetailed in Table 5) (121). These includehigh-voltage electrical injuries, chemicalburns, burns from tar and other thermo-plastic road materials, cold injuries, toxicepidermal necrolysis, purpura fulminans,soft-tissue injuries and infections, and in-juries caused by abuse or neglect.

Exposures to �1000 V are consideredhigh voltage. It is uncommon for com-partment syndromes, loss of conscious-ness, or myoglobinuria to be seen in pa-tients exposed to �500 V. Childrensustaining good electrical contact withmidrange voltage sources (200–1000 V)can sustain quite destructive local inju-ries. Locally destructive injuries are man-

aged with early excision and closure. Flapclosure is often an attractive option inthose patients with very destructive inju-ries of limited extent (122). An exceptionto this approach is in the child with acommissure burn (Fig. 10). Such chil-dren are best managed conservatively,awaiting eschar separation and spontane-ous healing and delaying reconstruction,as they will often heal surprisingly well.Parents should be advised to be alert forbleeding that can occur with separationof the eschar. If it occurs, bleeding iscontrolled with pressure en route to thehospital (123). High-voltage injuries arecommonly associated with other prob-lems, including loss of consciousness,falls, fractures, myoglobinuria, compart-ment syndromes, and arrhythmias. Thesepatients should initially be approached asa polytrauma patient. After appropriateairway and vascular access have beenachieved, a systematic secondary surveyshould be done, with a directed effort tolook for visceral injuries, long bone and

Figure 8. A deeply burned face should be addressedin a studied manner, using thick-sheet autograftplaced in cosmetic units when possible.

Figure 9. It is important to be watchful for theoccurrence of globe exposure caused by retrac-tion of burned periorbital tissues. This should beaddressed promptly when it occurs, initiallythrough intensive ocular lubrication and thenwith early lid release if keratitis develops in theface of ocular lubrication. Not to do so will riskloss of the globe through corneal ulceration andinfection.

Figure 10. Commissure burns are best managedconservatively. Parents should be advised to bealert of bleeding that can occur with separation ofthe eschar.

S509Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

spine fractures, myoglobinuria, and com-partment syndromes.

Treatment of chemical exposuresshould begin with immediate removal ofclothing, including jewelry and shoes,and dusting off of any powders. Emer-gency personnel need to protect them-selves from injury. Copious irrigationwith tap water should then be done for atleast 30 mins. Alkaline substances, lesssoluble in water, often take longer toclear; the adequacy of irrigation can betested by rubbing gloved fingers togetherafter contact is made with the wound.Litmus paper can also be used to verifythe completeness of irrigation of acid oralkali wounds, ceasing irrigation when aneutral pH is documented. Consultationwith a poison control center should beconsidered when evaluating anyone witha chemical burn, as there may be associ-ated systemic toxicities in addition to thewound. Adequate ocular irrigation can befacilitated by topical ocular anesthetics.With larger injuries, fluid resuscitationmay be required, and some agents will

generate an irritating fume that can re-sult in airway compromise.

Toxic epidermal necrolysis is a sys-temic inflammatory process seeminglytriggered by a medication or viral syn-drome that results in a separation at thedermal-epidermal junction (124). Thereis both a cutaneous wound involving theskin to a variable degree and a visceralwound with variable degrees of mucosaland conjunctival involvement (Fig. 11).Often, the latter is more difficult to man-age. The pain of the oral ulcerations canbe so intense that airway protection withendotracheal intubation is required.Principle components of therapy includeairway protection as needed, wound carethat prevents desiccation and superinfec-tion, nutritional support (generally en-terally), close monitoring for septic com-plications with specific treatment, andvigilant eye care (125). Although residualskin and nail deformities are common(126), when properly managed, these pa-tients can be expected to heal theirwounds and do extremely well long term,

unless they have complicating comorbidconditions.

REHABILITATION ANDRECONSTRUCTION

This final phase of burn care has as-sumed a rapidly increasing importance assurvival has improved and public expec-tations have increased. Until the recentpast, survival was the principal measure

Figure 11. Toxic epidermal necrolysis results inboth a cutaneous and a visceral wound. Often, thelatter is the more difficult to manage.

Table 5. Special situations

Electrical injuryMonitor cardiac rhythm in high (�1000 volt) or intermediate (greater than 220 V) voltage exposures for 24–72 hrsLow and intermediate voltage exposures can cause locally destructive injuries, but uncommonly result in systemic sequelaeAfter high-voltage exposures, delayed neurologic and occular sequelae can occur, so a carefully documented neurologic and occular examination is

an important part of the initial assessmentInjured extremities should be serially evaluated for intracompartmental edema and promptly decompressed when it developsBladder catheters should be placed in all patients with high-voltage exposure to document the presence or absence of pigmenturia; this is treated

adequately with volume loading in most patientsChemical

Irrigate wounds with tap water for at least 30 mins; irrigate the globe with isotonic crystalloid solutionExposures to concentrated or anhydrous hydrofluoric acid may be complicated by life-threatening hypocalcemia; such patients should have serum

calcium closely monitored and supplemented; subeschar injection of 10% calcium gluconate solution is appropriate after exposure to highlyconcentrated or anhydrous solutions

TarTar should be initially cooled with tap water irrigation and later removed with a lipophyllic solvent

Toxic epidermal necrolysisDiffuse epidermal slough at the dermal-epidermal junction, usually associated with progression of a drug eruptionThe degree of mucous membrane and conjunctival involvement variesDifferentiation from staphylococcal scalded skin syndrome can usually be made on clinical groundsTreatment involves prevention of wound desiccation and superinfection with topical antimicrobials with xenografting of clean confluent areasOphthalmologic care is criticalThose with severe oropharyngeal involvement may require intubation for airway protection with enteral tube feeding

Purpura fulminansTypically a complication of meningococcal sepsisLikely secondary to transient protein C deficiency; therefore, fresh frozen plasma should be considered as a resuscitative colloidFrequently accompanied by organ failuresTreatment involves management of organ failures and excision and grafting of wounds to prevent inevitable wound sepsisCan be associated with adrenal necrosisLong-term morbidity secondary to major amputation and epiphyseal arrest is common

Staphylococcal scalded skin syndromeReaction to a staphylococcal exotoxin that causes a separation in the granular layer of the epidermis, most commonly seen in young childrenThis superficial wound generally heals quickly if superinfection and desiccation is preventedMucous membrane and conjunctival involvement are not seenA detailed search for a focus of staphylococcal infection is warranted

Soft-tissue infectionsSerious morbidity associated with delay in diagnosis and managementEssential first steps are suspicion, exploration of suspicious soft tissues, and aggressive excision of nonviable or infected tissue

S510 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

of success in burn care. Now that themajority of those suffering even seriousinjuries are surviving, the bar is higherand the quality of function and appear-ance is the new standard of success. Todeliver a high-quality functional and cos-metic result absolutely requires the in-tensive involvement of interested andknowledgeable physical and occupationalburn therapists who are involved throughthe entire spectrum of care, from theintensive care unit through the outpa-tient clinic. The field of burn therapy israpidly evolving and has become highlyspecialized (127).

In the critical care setting, there arethree priorities for the therapist: ranging,splinting and antideformity positioning,and establishing initial contact with thepatient and his or her family. If a bodypart is left immobile for a protracted pe-riod of time, capsular contraction andshortening of tendon and muscle groupsthat cross the joints occur. Even in youngchildren, if extremities are left immobile,this will occur over the course of days. Itis therefore important that this be pre-vented by passive ranging. This is ideallydone twice daily, with the therapist tak-ing all joints through a passive of range ofmotion. The therapist needs to be sensi-tive to the wounds, the status of extrem-ity perfusion, the state of pain and anxi-ety, and essential airway and vascularaccess devices. Within the bounds ofsafety, it is appropriate to medicate pa-tients so they can tolerate any discomfortand anxiety associated with ranging. Itwill not be effective if it is painful andfrightening. Ideally, ranging can be timedto coincide with medications adminis-tered for dressing changes and woundcare.

The burn therapist should be knowl-edgeable about airway and vascular ac-cess devices used in the intensive care

unit. There is substantial morbidity, andeven mortality, associated with unex-pected loss of these devices. Therefore,before initiating ranging, therapistsshould communicate with the intensivecare unit team regarding the location andsecurity of endotracheal tubes, nasogas-tric tubes, central venous catheters, arte-rial catheters, and other monitoring de-vices. Routine in-servicing of therapistswill facilitate adherence to necessary pre-cautions. The presence of such a device isclearly not a contraindication to full pas-sive ranging. However, the activityshould be done with the security of thesedevices in mind.

Antideformity positioning and splint-ing during the phase of critical illnesswill prevent the occurrence of some verycommon contractures. The commoncontractures seen to develop in the crit-ically ill tend to be associated with theflexed position of comfort, except inthe hands, and include the flexed neck,the adducted axilla or shoulder, the flexedelbow, the flexed hip, the flexed knee, andthe extended ankle deformities.

As the seriously burned patient is ex-tubated and weaned from the critical careenvironment, the demands placed on theburn therapists increases. In many waysit becomes more difficult for the therapistto provide the needed care. Children areaware of what has happened to them,have been sensitized to uncomfortableprocedures, and may become fearful ofthe therapist. There are several key com-ponents to therapy during this period,including continued passive ranging, in-creasing active ranging and strengthen-ing, minimizing edema, activities of dailyliving, and preparation for work or playand school.

Important aspects of acute rehabilita-tion after discharge include ongoing andprogressive ranging and strengthening,ongoing evaluation of evolving problemareas, specific postoperative therapy afterreconstructive operations, and scar man-agement. It is quite common to see someloss of range and strength between thedischarge and the first clinic visit. This isparticularly true if there is an inadequateoutpatient rehabilitation plan or if therehabilitation therapy is turned over to atherapist inexperienced with burns. Ifsubstantial range and strength has beenlost due to inadequate therapy, readmis-sion for focused rehabilitation efforts isappropriate.

Scar management is an essential as-pect of outpatient burn therapy. The

most virulent hypertrophic scarring isseen in very deep dermal burns that healspontaneously in �3 wks. This is partic-ularly true in those areas of highly elasticskin, such as the submental triangle andanterior neck, and in areas where jointmotion results in tension across burnscars (128). Initial wound hyperemia typ-ically begins to resolve about 9 wks afterinjury. In those wounds destined to be-come hypertrophic, there is a marked in-crease in neovessel formation, resultingin increasing erythema after this period(129, 130). Ideally, therapies to minimizehypertrophic scarring are begun as soonas burns are well healed, ideally by thetime posthealing wound erythema beginsto increase.

There are no completely effective toolsto control hypertrophic scar. Availablemethods include scar massage (131),compression garments (132), topical sil-icone (133), steroid injections, and sur-gery. Serial casting (134) has a limitedrole in management of established scarsthat limit joint motion. Properly done,scar massage is perhaps the most effec-tive and can be done by patients andfamily members. This consists of firm,slow massage and stretching of evolvinghypertrophic areas after application ofbland skin emollients, and it is ideallydone several times each day.

An acute reconstructive plan for thosewith serious burns should be made col-laboratively with the patient and the pa-tient’s family, the patient’s therapists,and the surgical team. Although oneshould not rush in to these procedures,the concept of waiting until all scars havecompletely matured for two or moreyears before embarking on any recon-structive operations will interfere undulywith function and development. A bal-ance must be drawn between the repeattrauma of surgery and the patient’s func-tional and cosmetic needs.

CONCLUSION

Ideally, the objective is to have thechild return to his or her family, school-mates, and community as if the injuryhad never occurred. Having this goalmeans respecting school schedules for re-constructive operations and giving prior-ity to operations that are important fordevelopment or favorite activities. Formany, the child’s burn represents anenormous stress affecting all members ofthe extended family. Many children willbenefit from transient psychotherapy and

S uccessful burn

care requires the

focused efforts of a

team of experienced people

committed to the entire con-

tinuum of acute burn care

and recovery.

S511Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

pharmacotherapy to help deal with thetrauma they’ve sustained. Posttraumaticstress disorder is common (135, 136).Signs and symptoms include hyper-alertness, nightmares, and chronic fear-fulness. The burn inpatient and outpa-tient teams should have sensitivity to thiscommon problem and have a strategy toaddress it. Not doing so may protractrecovery. Extended family members,teachers, coaches, playmates, daycarecenter staff members, and relatives allcan have an impact on recovery. Burncare has evolved greatly over recent de-cades. An intensive care unit with theobjective of patient survival simply can-not generate the quality outcomes thatare now possible. Successful burn carerequires the focused efforts of a team ofexperienced people committed to the en-tire continuum of acute burn care andrecovery.

REFERENCES

1. Underhill FP: The significance of anhydre-mia in extensive superficial burns. JAMA1930; 95:852–857

2. Saffle JR: The fire at Boston’s CocoanutGrove nightclub. Am J Surg 1993; 1942:166:581–591

3. Moore FD: The body-weight burn budget:Basic fluid therapy for the early burn. SurgClin North Am 1970; 50:1249–1265

4. Artz CP, Moncrief JA: The burn problem. In:The Treatment of Burns. Artz CP, MoncriefJA (Eds). Philadelphia, WB Saunders, 1969,pp 1–22

5. Janzekovic Z: A new concept in the earlyexcision and immediate grafting of burns.J Trauma 1970; 10:1103–1108

6. Burke JF, Quinby WC Jr, Bondoc CC: Pri-mary excision and prompt grafting as rou-tine therapy for the treatment of thermalburns in children. Surg Clin North Am1976; 56:477–494

7. Herndon DN, Gore D, Cole M, et al: Deter-minants of mortality in pediatric patientswith greater than 70% full-thickness totalbody surface area thermal injury treated byearly total excision and grafting. J Trauma1987; 27:208–212

8. Blakeney P, Herndon DN, Desai MH, et al:Long-term psychosocial adjustment follow-ing burn injury. J Burn Care Rehabil 1988;9:661–665

9. Herndon DN, LeMaster J, Beard S, et al: Thequality of life after major thermal injury inchildren: An analysis of 12 survivors withgreater than or equal to 80% total body,70% third-degree burns. J Trauma 1986;26:609–619

10. Moon RE: Treatment of diving emergencies.Crit Care Clin 1999; 15:429–456

11. Brigham PA, McLoughlin E: Burn incidenceand medical care use in the United States:

Estimates, trends, and data sources. J BurnCare Rehabil 1996; 17:95–107

12. Rossignol AM, Boyle CM, Locke JA, et al:Hospitalized burn injuries in Massachu-setts: An assessment of incidence and prod-uct involvement. Am J Public Health 1986;76:1341–1343

13. Tucker P: The burn victim: A review ofpsychosocial issues. Aust N Z J Psychiatry1986; 20:413–420

14. Sheridan RL, Ryan CM, Petras LM, et al:Burns in children younger than two years ofage: An experience with 200 consecutiveadmissions. Pediatrics 1997; 100:721–723

15. Sheridan RL, Hoey ME, Daley WM, et al:Childhood burns in camping and outdoorcooking accidents: A focus for prevention.J Burn Care Rehabil 1997; 18:369–371

16. Erdmann TC, Feldman KW, Rivara FP, et al:Tap water burn prevention: The effect oflegislation. Pediatrics 1991; 88:572–577

17. Moon RE, DeLong E: Hyperbaric oxygen forcarbon monoxide poisoning. Med J Aust1999; 170:197–199

18. Kesecioglu J, Telci L, Esen F, et al: Respi-ratory and haemodynamic effects of con-ventional volume controlled PEEP ventila-tion, pressure regulated volume controlledventilation and low frequency positive pres-sure ventilation with extracorporeal carbondioxide removal in pigs with acute ARDS.Acta Anaesthesiol Scand 1994; 38:879–884

19. Aggarwal SJ, Diller KR, Blake GK, et al:Burn-induced alterations in vasoactivefunction of the peripheral cutaneous micro-circulation. J Burn Care Rehabil 1994; 15:1–12

20. Youn YK, LaLonde C, Demling R: The roleof mediators in the response to thermalinjury. World J Surg 1992; 16:30–36

21. Demling RH, Niehaus G, Perea A, et al:Effect of burn-induced hypoproteinemia onpulmonary transvascular fluid filtrationrate. Surgery 1979; 85:339–343

22. Wilmore DW, Aulick LH, Pruitt BA Jr: Me-tabolism during the hypermetabolic phaseof thermal injury. Adv Surg 1978; 12:193–225

23. Deitch EA: Multiple organ failure. Adv Surg1993; 26:333–356

24. Sasaki TM, Welch GW, Herndon DN, et al:Burn wound manipulation-induced bacte-remia. J Trauma 1979; 19:46–48

25. Wilmore DW, Mason AD Jr, Johnson DW, etal: Effect of ambient temperature on heatproduction and heat loss in burn patients.J Appl Physiol 1975; 38:593–597

26. Aarsland A, Chinkes D, Wolfe RR, et al:Beta-blockade lowers peripheral lipolysis inburn patients receiving growth hormone:Rate of hepatic very low density lipoproteintriglyceride secretion remains unchanged.Ann Surg 1996; 223:777–787; discussion,787–789

27. Baron PW, Barrow RE, Pierre EJ, et al:Prolonged use of propranolol safely de-creases cardiac work in burned children.J Burn Care Rehabil 1997; 18:223–227

28. Hollyoak MA, Muller MJ, Meyers NA, et al:Beneficial wound healing and metabolic ef-fects of clenbuterol in burned and non-burned rats. J Burn Care Rehabil 1995;16:233–240

29. Dong YL, Fleming RY, Yan TZ, et al: Effectof ibuprofen on the inflammatory responseto surgical wounds. J Trauma 1993; 35:340–343

30. Takagi K, Suzuki F, Barrow RE, et al:Growth hormone improves immune func-tion and survival in burned mice infectedwith herpes simplex virus type 1. J Surg Res1997; 69:166–170

31. Herndon DN, Hawkins HK, Nguyen TT, etal: Characterization of growth hormone en-hanced donor site healing in patients withlarge cutaneous burns. Ann Surg 1995; 221:649–56

32. Wolf SE, Barrow RE, Herndon DN: Growthhormone and IGF-I therapy in the hyper-catabolic patient. Baillieres Clin EndocrinolMetab 1996; 10:447–463

33. American College of Surgeons Committeeon Trauma: Resources of Optimal Care ofthe Injured Patient. Chicago, American Col-lege of Surgeons, 1993

34. Sheridan RL: Recognition and managementof hot liquid aspiration in children. AnnEmerg Med 1996; 27:89–91

35. Weiss LD, Van Meter KW: The applicationsof hyperbaric oxygen therapy in emergencymedicine. Am J Emerg Med 1992; 10:558–568

36. Tibbles PM, Edelsberg JS: Hyperbaric-oxygen therapy. N Engl J Med 1996; 334:1642–1648

37. Weaver LK, Hopkins RO, Larson-Lohr V:Neuropsychologic and functional recoveryfrom severe carbon monoxide poisoningwithout hyperbaric oxygen therapy. AnnEmerg Med 1996; 27:736–740

38. Langan EM III, Miller RS, Casey WJ III, etal: Prophylactic inferior vena cava filters intrauma patients at high risk: Follow-up ex-amination and risk/benefit assessment.J Vasc Surg 1999; 30:484–488

39. Mills DC, Roberts LW, Mason AD Jr, et al:Suppurative chondritis: Its incidence, pre-vention, and treatment in burn patients.Plast Reconstr Surg 1988; 82:267–276

40. Greenhalgh DG, Warden GD: The impor-tance of intra-abdominal pressure measure-ments in burned children. J Trauma 1994;36:685–690

41. Bruck HM, Pruitt BA Jr: Curling’s ulcer inchildren: A 12-year review of 63 cases.J Trauma 1972; 12:490–496

42. Sheridan RL, Tompkins RG, McManus WF,et al: Intracompartmental sepsis in burnpatients. J Trauma 1994; 36:301–305

43. Hummel RP, Greenhalgh DG, Barthel PP,et al: Outcome and socioeconomic aspectsof suspected child abuse scald burns. J BurnCare Rehabil 1993; 14:121–126

44. Heggers JP, Loy GL, Robson MC, et al: His-tological demonstration of prostaglandins

S512 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

and thromboxanes in burned tissue. J SurgRes 1980; 28:110–117

45. Tanaka H, Matsuda H, Shimazaki S, et al:Reduced resuscitation fluid volume for sec-ond-degree burns with delayed initiation ofascorbic acid therapy. Arch Surg 1997; 132:158–161

46. LaLonde C, Nayak U, Hennigan J, et al:Antioxidants prevent the cellular deficitproduced in response to burn injury. J BurnCare Rehabil 1996; 17:379–383

47. Monafo WW, Halverson JD, Schechtman K:The role of concentrated sodium solutionsin the resuscitation of patients with severeburns. Surgery 1984; 95:129–135

48. Huang PP, Stucky FS, Dimick AR, et al:Hypertonic sodium resuscitation is associ-ated with renal failure and death. Ann Surg1995; 221:543–54; discussion, 554–557

49. Warden GD: Burn shock resuscitation.World J Surg 1992; 16(1):16–23

50. Graves TA, Cioffi WG, McManus WF, MasonAD, Jr, Pruitt BA, Jr: Fluid resuscitation ofinfants and children with massive thermalinjury. J Trauma 1988; 28:1656–1659

51. Reynolds EM, Ryan DP, Sheridan RL, et al:Left ventricular failure complicating severepediatric burn injuries. Journal of PediatricSurgery 1995; 30:264–9

52. McManus WF, Hunt JL, Pruitt BA, Jr: Post-burn convulsive disorders in children.J Trauma 1974; 14:396–401

53. Hughes JR, Cayaffa JJ, Pruitt BA Jr, et alSeizures following burns of the skin. DisNerv Syst 1973; 34:347–353

54. Cohen BJ, Jordan MH, Chapin SD, et al:Pontine myelinolysis after correction of hy-ponatremia during burn resuscitation.J Burn Care Rehabil 1991; 12:153–156

55. Levine N, Seifter E, Levenson SM: Enzy-matic debridement of burns. SurgicalForum 1971; 22:57–58

56. Makepeace AR: Enzymatic debridement ofburns: a review. Burns, Including ThermalInjury 1983; 9:153–157

57. Rowan AD, Christopher CW, Kelley SF, etal: Debridement of experimental full-thickness skin burns of rats with enzymefractions derived from pineapple stem.Burns 1990; 16:243–246

58. Sheridan RL, Petras L, Basha G, et al:Planimetry study of the percent of bodysurface represented by the hand and palm:sizing irregular burns is more accuratelydone with the palm. J Burn Care Rehabil1995; 16:605–606

59. Heimbach D, Engrav L, Grube B, et al: Burndepth: A review. World J Surg 1992; 16:10–15

60. Sheridan RL, Schomaker KT, Lucchina LC,et al: Burn depth estimation by use of in-docyanine green fluorescence: initial hu-man trial. J Burn Care Rehabil 1995; 16:602–604

61. Desai MH, Rutan RL, Herndon DN: Conser-vative treatment of scald burns is superiorto early excision. J Burn Care Rehabil 1991;12:482–484

62. Budny PG, Regan PJ, Roberts AH: The esti-mation of blood loss during burns surgery.Burns 1993; 19:134–137

63. Housinger TA, Lang D, Warden GD: A pro-spective study of blood loss with excisionaltherapy in pediatric burn patients.J Trauma 1993; 34:262–263

64. Sheridan RL, Szyfelbein SK: Staged highdose epinephrine clysis in pediatric burnexcisions: Proceedings of the AmericanBurn Association. J Burn Care Rehabil1998; 19:S199

65. Sheridan RL, Tompkins RG: Skin substi-tutes in burns. Burns 1999; 25:97–103

66. Green H: Cultured cells for the treatment ofdisease. Sci Am 1991; 265:96–102

67. Sheridan RL, Tompkins RG: Cultured au-tologous epithelium in patients with burnsof ninety percent or more of the body sur-face. J Trauma 1995; 38:48–50

68. Langdon RC, Cuono CB, Birchall N, et al:Reconstitution of structure and cell func-tion in human skin grafts derived fromcryopreserved allogeneic dermis and autol-ogous cultured keratinocytes. J Invest Der-matol 1988; 91:478–485

69. Tompkins RG, Burke JF: Progress in burntreatment and the use of artificial skin.World J Surg 1990; 14:819–824

70. Sheridan RL, Choucair RJ: Acellular allo-graft dermis does not hinder initial engraft-ment in burn resurfacing and reconstruc-tion. J Burn Care Rehabil 1997; 18:496–499

71. Sheridan RL, Choucair RJ: Acellular allo-dermis in burn surgery: 1-year results of apilot trial. Abstr. J Burn Care Rehabil 1998;19:528–530

72. Hunt JL, Agee RN, Pruitt BA Jr: Fiberopticbronchoscopy in acute inhalation injury.J Trauma 1975; 15:641–649

73. Lin WY, Kao CH, Wang SJ: Detection ofacute inhalation injury in fire victims bymeans of technetium-99m DTPA radioaero-sol inhalation lung scintigraphy. Eur J NuclMed 1997; 24:125–129

74. Lull RJ, Anderson JH, Telepak RJ, et al:Radionuclide imaging in the assessment oflung injury. Semin Nucl Med 1980; 10:302–310

75. Parker JC, Hernandez LA, Peevy KJ: Mech-anisms of ventilator-induced lung injury.Crit Care Med 1993; 21:131–143

76. Slutsky AS: Mechanical ventilation: Ameri-can College of Chest Physicians’ ConsensusConference. Chest 1993; 104:1833–1859

77. Shapiro BA, Cane RD, Harrison RA, et al:Changes in intrapulmonary shunting withadministration of 100 percent oxygen.Chest 1980; 77:138–141

78. Sheridan RL, Kacmarek RM, McEttrick MM,et al: Permissive hypercapnia as a ventila-tory strategy in burned children: Effect onbarotrauma, pneumonia, and mortality.J Trauma 1995; 39:854–859

79. Hickling KG, Walsh J, Henderson S, et al:Low mortality rate in adult respiratory dis-tress syndrome using low-volume, pres-

sure-limited ventilation with permissive hy-percapnia: A prospective study. Crit CareMed 1994; 22:1568–1578

80. Sheridan RL, Hurford WE, Kacmarek RM,et al: Inhaled nitric oxide in burn patientswith respiratory failure. J Trauma 1997;42:629–634

81. Rodeberg DA, Housinger TA, GreenhalghDG, et al: Improved ventilatory function inburn patients using volumetric diffusiverespiration. J Am Coll Surg 1994; 179:518–522

82. Goretsky MJ, Greenhalgh DG, Warden GD,et al: The use of extracorporeal life supportin pediatric burn patients with respiratoryfailure. J Ped Surg 1995; 30:620–623

83. Fitzpatrick JC, Cioffi WG Jr, Cheu HW, et al:Predicting ventilation failure in childrenwith inhalation injury. J Ped Surg 1994;29:1122–1126

84. Niederman MS, Torres A, Summer W: Inva-sive diagnostic testing is not needed rou-tinely to manage suspected ventilator-associated pneumonia. Am J Respir CritCare Med 1994; 150:565–569

85. Sellers BJ, Davis BL, Larkin PW, et al: Earlyprediction of prolonged ventilator depen-dence in thermally injured patients.J Trauma 1997; 43:899–903

86. Calhoun KH, Deskin RW, Garza C, et al:Long-term airway sequelae in a pediatricburn population. Laryngoscope 1988; 98:721–725

87. Desai MH, Mlcak RP, Robinson E, et al:Does inhalation injury limit exercise endur-ance in children convalescing from thermalinjury? J Burn Care Rehabil 1993; 14:12–16

88. Marquez S, Turley JJ, Peters WJ: Neuropa-thy in burn patients. Brain 1993; 116:471–483

89. Dagum AB, Peters WJ, Neligan PC, et al:Severe multiple mononeuropathy in pa-tients with major thermal burns. J BurnCare Rehabil 1993; 14:440–445

90. Stoddard FM, Martyn JJ, Sheridan RL: Psy-chiatric issues in pain of burn injury: Con-trolling pain and improving outcomes. CurrRev Pain 1997; 1:130–136

91. Sheridan RL, McEttrick M, Bacha G, et al:Midazolam infusion in pediatric patientswith burns who are undergoing mechanicalventilation. J Burn Care Rehabil 1994; 15:515–518

92. Deitch EA: The role of intestinal barrierfailure and bacterial translocation in thedevelopment of systemic infection and mul-tiple organ failure. Arch Surg 1990; 125:403–404

93. Bondoc CC, Morris PJ, Wee T, et al: Meta-bolic effects of 0.5 per cent silver nitratetherapy for extensive burns in children.Surg Forum 1966; 17:475–477

94. Burke JF, Bondoc CC, Morris PJ: Metaboliceffects of topical silver nitrate therapy inburns covering more than fifteen percent ofthe body surface. Ann NY Acad Sci 1968;150:674–680

S513Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)

95. Zaloga GP: Interpretation of the serummagnesium level. Chest 1989; 95:257–258

96. Wu JZ, Ogle CK, Fischer JE, et al: ThemRNA expression and in vitro production ofcytokines and other proteins by hepatocytesand Kupffer cells following thermal injury.Shock 1995; 3:268–273

97. Greenhalgh DG, Housinger TA, Kagan RJ,et al: Maintenance of serum albumin levelsin pediatric burn patients: A prospective,randomized trial. J Trauma 1995; 39:67–73

98. Guenter PA, Settle RG, Perlmutter S, et al:Tube feeding-related diarrhea in acutely Illpatients. JPEN J Parenter Enteral Nutr1991; 15:277–280

99. Sapijaszko MJ, Brant R, Sandham D, et al:Nonrespiratory predictor of mechanicalventilation dependency in intensive careunit patients. Crit Care Med 1996; 24:601–607

100. Sheridan RL, Prelack K, Cunningham JJ:Physiologic hypoalbuminemia is well toler-ated by severely burned children. J Trauma1997; 43:448–452

101. Sheridan RL, Weber JM, Peterson HF, et al:Central venous catheter sepsis with weeklycatheter change in paediatric burn patients:An analysis of 221 catheters. Burns 1995;21:127–129

102. Goldstein AM, Weber JM, Sheridan RL:Femoral venous access is safe in burnedchildren: An analysis of 224 catheters.J Pediatr 1997; 130:442–446

103. Strome DR, Aulick LH, Mason AD Jr, et al:Thermoregulatory and nonthermoregula-tory heat production in burned rat. J ApplPhysiol 1986; 61:688–693

104. Souba WW: Cytokine control of nutritionand metabolism in critical illness. CurrProbl Surg 1994; 31:577–643

105. Carlson DE, Cioffi WG Jr, Mason AD Jr, etal: Resting energy expenditure in patientswith thermal injuries. Surg Gynecol Obstet1992; 174:270–276

106. Saffle JR, Medina E, Raymond J, et al: Use ofindirect calorimetry in the nutritional man-agement of burned patients. J Trauma1985; 25:32–39

107. Prelack K, Cunningham JJ, Sheridan RL, etal: Energy and protein provisions for ther-mally injured children revisited: An out-come-based approach for determining re-quirements. J Burn Care Rehabil 1997; 18:177–181

108. Mainous MR, Block EF, Deitch EA: Nutri-tional support of the gut: How and why.New Horiz 1994; 2:193–201

109. Gilpin DA, Barrow RE, Rutan RL, et al:Recombinant human growth hormone ac-celerates wound healing in children with

large cutaneous burns. Ann Surg 1994; 220:19–24

110. Meyer NA, Muller MJ, Herndon DN: Nutri-ent support of the healing wound. NewHoriz 1994; 2:202–214

111. Martineau L, Little RA, Rothwell NJ, et al:Clenbuterol, a beta 2-adrenergic agonist,reverses muscle wasting due to scald injuryin the rat: The acute-phase response of cul-tured rat hepatocytes. System characteriza-tion and the effect of human cytokines.Burns 1984; 224:505–514

112. Mendenhall CL, Moritz TE, Roselle GA, etal: A study of oral nutritional support withoxandrolone in malnourished patients withalcoholic hepatitis: Results of a Departmentof Veterans Affairs cooperative study Inves-tigations on the influence of Clenbuteroland recombinant porcine somatotropin onnitrogen and energy metabolism in growingpigs. Hepatology 1993; 45:1–11

113. Weber JM, Sheridan RL, Pasternack MS, etal: Nosocomial infections in pediatric pa-tients with burns. Am J Infect Control 1997;25:195–201

114. Sheridan RL, Weber JM, Tompkins RG:Candidemia in pediatric burn patient.J Burn Care Rehabil 1995; 16:440–443

115. Sheridan RL, Ryan CM, Tompkins RG:Acute adrenal insufficiency in the burn in-tensive care unit. Burns 1993; 19:63–66

116. Sheridan RL, Ryan CM, Pasternack MS, etal: Flavobacterial sepsis in massively burnedpediatric patients. Clin Infect Dis 1993; 17:185–187

117. Sheridan RL, Weber J, Benjamin J, et al:Control of methicillin-resistant Staphylo-coccus aureus in a pediatric burn unit. Am JInfect Control 1994; 22:340–345

118. Goodwin CW: Multiple organ failure: Clini-cal overview of the syndrome. J Trauma1990; 30:S163–S165

119. Sheridan RL, Hurley J, Smith MA, et al: Theacutely burned hand: Management and out-come based on a ten-year experience with1047 acute hand burns. J Trauma 1995;38:406–411

120. Sheridan RL, Baryza MJ, Pessina MA, et al:Acute hand burns in children: Managementand long-term outcome based on a 10-yearexperience with 698 injured hands. AnnSurg 1999; 229:558–564

121. Sheridan RL, Gagnon SW, Tompkins RG:The burn unit as a resource for the man-agement of acute nonburn conditions inchildren. J Burn Care Rehabil 1995; 16:62–64

122. Rabban JT, Blair JA, Rosen CL, et al: Mech-anisms of pediatric electrical injury: Newimplications for product safety and injury

prevention. Arch Pediatr Adolesc Med 1997;151:696–700

123. Donelan MB: Reconstruction of electricalburns of the oral commissure with a ventraltongue flap. Plast Reconstr Surg 1995; 95:1155–1164

124. Moon RE, Hart BB: Operational use andpatient monitoring in a multiplace hyper-baric chamber. Respir Care Clin North Am1999; 5:21–49

125. Heimbach DM, Engrav LH, Marvin JA, et al:Toxic epidermal necrolysis: A step forwardin treatment [published erratum appears inJAMA 1987; 258:1894]. JAMA 1987; 257:2171–2175

126. Sheridan RL, Schulz JT, Ryan CM, et al:Long-term consequences of toxic epidermalnecrolysis in children. Pediatrics 2002; 109:74–78

127. Salisbury R: Burn rehabilitation: Our unan-swered challenge: The 1992 presidential ad-dress to the American Burn Association.J Burn Care Rehabil 1992; 13:495–505

128. Deitch EA, Wheelahan TM, Rose MP, et al:Hypertrophic burn scars: Analysis of vari-ables. J Trauma 1983; 23:895–898

129. Kischer CW: The microvessels is hyper-trophic scars, keloids and related lesions.J Submicrosc Cytol Path 1992; 24:281–296

130. Sheridan RL, MacMillan K, Donelan M, etal: Tunable dye laser neovessel ablation asan adjunct to the management of hypertro-phic scarring in burned children: Pilot trialto establish safety. J Burn Care Rehabil1997; 18:317–320

131. Carr-Collins JA: Pressure techniques for theprevention of hypertrophic scar. Clin PlastSurg 1992; 19:733–743

132. Clark JA, Cheng JC, Leung KS, et al: Me-chanical characterisation of human post-burn hypertrophic skin during pressuretherapy. J Biomech 1987; 20:397–406

133. Ahn ST, Monafo WW, Mustoe TA: Topicalsilicone gel for the prevention and treat-ment of hypertrophic scar. Arch Surg 1991;126:499–504

134. Ridgway CL, Daugherty MB, Warden GD:Serial casting as a technique to correctburn scar contractures: A case report.J Burn Care Rehabil 1991; 12:67–72

135. Stoddard FJ, Stroud L, Murphy JM: Depres-sion in children after recovery from severeburns. J Burn Care Rehabil 1992; 13:340–347

136. Rizzone LP, Stoddard FJ, Murphy JM, et al:Posttraumatic stress disorder in mothers ofchildren and adolescents with burns. J BurnCare Rehabil 1994; 15:158–163

S514 Crit Care Med 2002 Vol. 30, No. 11 (Suppl.)