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Acute Burns
Chia Chi Kao, M.D., and Warren L. Garner, M.D.
Los Angeles, Calif., and Ann Arbor, Mich.

Learning Objectives: After studying this article, the participant should be able to: 1. Describe the pathophysiology of burn
injury. 2. Calculate burn size and resuscitation requirements and predict survival. 3. Treat inhalation injury. 4. Describe
preoperative selection, intraoperative procedures, and postoperative protocols for patients who require surgical care for
their burn injuries. 5. Know the survival and functional outcomes of burn injury.

Burn injuries are complex cutaneous traumas cared for and the predominant mechanism is accidental
by many plastic surgeons. Care is stratified by burn size, scalding. In teenagers and young adults, burn
depth, and associated injuries. Advances in surgical tech-
nique, wound care, and bioengineered skin have resulted injury most often results from accidents with
in excellent outcomes for most burn survivors. Moderate flammable liquids. Work-related accidents are
burn injuries can be treated effectively by an interested a common cause. Overall, the most likely adult
and experienced plastic surgeon. (Plast. Reconstr. Surg. burn victims are men between 17 and 30 years
105: 2482, 2000.) of age. In adults, many burn injuries result
from alcohol or drug abuse or preexisting psy-
chiatric illness. Structural fire accounts for less
Burn injuries are extremely complex, and than 5 percent of all burn admissions, but it is
optimal treatment requires an understanding responsible for more than 12 percent of burn-
of nutrition, immunology, psychological issues, related deaths.2
and the physiology of and the metabolic inter- During the past two decades, fire-related
actions among all of the major organ systems. deaths have declined. This is due to improved
In addition, the pathophysiology proceeds in a fire-fighting techniques and emergency medi-
time-dependent manner. Therefore, a proper cal services. Educational programs teaching
and timely intervention and control of the children to combat flaming cloth (stop, drop,
pathogenic mechanisms involved in thermal and roll) and lowering the thermostat on water
injury are the keys to a successful clinical out- heating units have made a significant impact.
come. The purpose of this discussion is to re- The use of home smoke detectors has dramat-
view the pathophysiology of burn injury and to ically reduced the severity of burn injuries, re-
relate it to clinical manifestation and current sulting in an estimated 80 percent reduction in
mode of surgical therapy, with highlights mortality and a 74 percent decrease in injuries
on modern dressings and wound care. from residential fires.3
An estimated two million people require ANATOMY AND FUNCTIONS OF THE SKIN
medical attention yearly for burn injury in the Skin is the largest organ in the human body.
United States. In 1991, 5053 burn-related It consists of two layers, the epidermis and the
deaths occurred.1 About a quarter of these peo- dermis. The outermost epidermal layer is the
ple had major burn injuries that required treat- stratum corneum. It is continually sloughed off
ment in a burn center. The epidemiology of and regenerated by keratinocytes, and it serves
burn injuries has remained fundamentally un- as a protective barrier to the environment. The
changed in recent years. Infants and children dermis is composed primarily of fibrous con-
between 1 and 5 years of age are at a high risk, nective tissue. Embedded within the dermis are
From the Division of Plastic and Reconstructive Surgery at the University of Southern California. Received for publication April 5, 1999; revised
December 6, 1999.
Vol. 101, No. 7 / ACUTE BURNS 2483
blood vessels, cutaneous nerves, skin append- blood flow in the zone of stasis would decrease
ages, hair follicles, and sebaceous and sweat and result in increased tissue loss. In general,
glands. Because these skin appendages are the amount of tissue destruction is related to
lined with epidermal cells, they are a source of the temperature and duration of exposure.
regenerating epidermal cells after thermal in- Scalding burns from boiling water, for exam-
jury. The important functions of the skin are ple, are usually less severe than grease or flame
illustrated in Table I. burns. A careful determination of the mecha-
When the skin is burned, these functions are nism of injury can have useful predictive value
lost. The loss of the stratum corneum allows in the evaluation of indeterminate injuries.
the invasion of microorganisms, and the Lang- Several inflammatory mediators that can po-
erhans’ cells, which mediate local immune re- tentiate tissue ischemia in the zone of stasis
sponse, are also gone. In severely burned pa- have been identified in acute burn wounds.
tients, the systemic immune response is Vasoactive mediators such as prostaglandins,
suppressed, which renders the patient highly histamine, and bradykinin can produce edema
susceptible to serious infections. Thus, topical by altering endothelial cell and basement
antimicrobial dressings are essential in control- membrane function to increase permeability.
ling wound surface pathogens. The loss of the Robson et al.5 discovered various prostaglan-
epidermal barrier causes increased fluid losses din derivatives in burn wounds; they suggested
until the wound is completely reepithelialized, an imbalance in vasoconstrictive and vasodila-
not just during the initial resuscitation period. tory prostanoids could lead to progressive tis-
Deep thermal injuries that destroy the dermis sue loss in the zone of stasis. The activation of
and subcutaneous tissue often heal with signif- the complement and coagulation systems re-
icant wound contractures and impaired mobil- sults in thrombosis within the microvasculature
ity, especially across joint surfaces.
and the release of histamine and bradykinin,
PATHOPHYSIOLOGY OF BURN INJURY which increases capillary leak and tissue ede-
ma.6 An increased level of oxygen free radicals,
Local Tissue Response such as xanthine oxidase, in acute burn
The final extent of tissue injury after thermal wounds plays a major role in the formation of
trauma is due to several factors. Most tissue is burn edema. Pretreatment with xanthine oxi-
lost as the direct result of heat coagulation of dase inhibitors markedly attenuates edema for-
the protein within the tissue. However, the mation.7
release of local mediators and changes in Recently, new investigations into inflamma-
blood flow, tissue edema, and infection can tory cytokines and the mechanisms involved in
lead to the further progression of injury and neutrophil adherence have increased our un-
cell death. Jackson4 first described these initial derstanding of the events that lead to progres-
events in 1947. The area of irreversible tissue sive tissue loss during these first hours after
destruction was termed a zone of coagulation. burn injury. First, the release of inflammatory
Surrounding this is a zone of decreased perfu- cytokines, such as tumor necrosis factor-␣ and
sion called a zone of stasis; this is followed by a interleukins 1 and 8, increases chemotaxis into
zone of hyperemia. These latter zones were the wound and causes the upregulation of cell
considered to be “at risk” but, with optimal surface adherence receptors (integrins) on
resuscitation and care, they can recover and both neutrophils and endothelial cells.8 The
heal. Without proper intervention, marginal neutrophils then adhere to the “sticky” capil-
lary endothelium and migrate into the injured
tissue.9 These wound neutrophils, primed by
Function of Skin
cytokines, are more likely to degranulate, thus
releasing proteases and toxic oxygen byprod-
Protection From chemicals, microorganisms, and ucts. Experimental studies using antibodies di-
minor trauma
Barrier Against water loss rected against various integrins on endothelial
Sensation Mediates touch, position, pressure, cell and neutrophil surfaces blocked neutro-
temperature, and pain
Immunological Using Langerhans’ cells and local
phil adherence and prevented the subsequent
defense cytokine networks cascade of events that leads to cellular injury
Vitamin D synthesis Occurs in response to sun exposure and progressive tissue necrosis.10,11 It must be
Ultraviolet protection With melanocytes
noted, however, that clinically useful treat-
ments to prevent this process in patients are teric blood flow. Enteral nutrition in general
not yet available. and glutamine in particular have a tropic effect
on the enterocytes that preserve mucosal integ-
Systemic Response rity.
In general, when burned areas exceed 30
percent of the total body surface area (TBSA), Immune Consequences
the release of cytokines and other mediators In the face of massive tissue injury, necrotic
into the systemic circulation results in a sys- tissue, and bacterial translocation, infection is
temic inflammatory response. Hypovolemia is the major cause of death in patients who sur-
the immediate consequence of fluid loss; this vive beyond the initial resuscitation period.
then results in decreased perfusion and oxygen Specific deficits in neutrophil chemotaxis,
delivery. In patients with large burns, the re- phagocytosis, and intracellular bacterial killing
lease of catecholamines, vasopressin, and an- have all been documented in patients with se-
giotensin causes peripheral and splanchnic vere thermal injury.14,15 Cell-mediated immu-
bed vasoconstriction, which can result in com- nity, as measured by skin testing, is often im-
promised end-organ perfusion. Myocardial paired. This deficiency is related to both
contractility may be suppressed by the release decreased lymphocyte activation and the sup-
of the inflammatory cytokine tumor necrosis pressive mediators present in the serum of
factor-␣.12 Hemolysis is a predictable clinical burned patients. Other studies have shown a
feature, especially after deep third-degree decrease in immunoglobulin synthesis as well.
burns, and patients may require a blood trans-
fusion. A deterioration in pulmonary function QUANTIFYING BURN SEVERITY
can occur in severely burned patients indepen-
dent of inhalational injury. This is due to the Burn Depth
bronchoconstriction caused by humoral fac- Survival after a burn injury is related to burn
tors, such as histamine, serotonin, and throm- size and depth, age, presence of inhalation
boxane A2, and a decrease in lung and chest injury, and patient comorbidity. First-degree
wall compliance. Increased evaporative water burns involve only the superficial epidermis.
loss is associated with an obligatory concurrent The skin is red, dry, and hypersensitive. The
heat loss exacerbated by the loss of protective epidermal barrier remains intact. Therefore,
vasoconstriction, which can result in hypother- the metabolic response and risk of infection
mia. are minimal. No treatment is necessary except
analgesia. In second-degree burns, the epider-
Bacterial Translocation mis is destroyed and part of the dermis is in-
Severe thermal injury induces a hypermeta- jured. Dermal involvement can either be super-
bolic state that is characterized by a profound ficial or deep. The skin is edematous, red, wet,
increase in resting energy expenditure and re- and painful, and blistering may occur. Healing
sulting in glycolysis and gluconeogenesis via occurs by epidermal proliferation and migra-
the breakdown of muscle (Cori cycle). Thus, tion from epidermal cells lining the skin ap-
nutritional support is paramount, especially via pendages. Superficial second-degree burn
the enteral route, to prevent intestinal villous wounds usually re-epithelialize 7 to 10 days
atrophy. Deitch et al.13 described a syndrome after the injury, and the risk of hypertrophic
of decreased bowel mucosal integrity, capillary scarring is small. Deep second-degree burns
leak, and decreased mesenteric blood flow, may take 21 days to completely heal. The risk
which can result in bacterial translocation into of hypertrophic scar formation is great. Be-
the portal circulation. These bacteria and their cause the epidermal barrier is lost, treatment
byproducts can significantly alter hepatocyte with topical antimicrobial dressings is neces-
function, spread systemically to induce sys- sary to prevent infection during the healing
temic sepsis, and act as a source of pathogens process. In third-degree (full-thickness) burns,
for infections of the blood, lungs, wound, or the tissue is pale, contracted, insensate, and
bladder. Substantial evidence indicates that leathery. Fourth-degree burns are deeper inju-
these events are linked to the development of ries involving the underlying muscle, bone, or
multisystem organ failure syndrome. The pre- other tissues (Table II).
vention of these events is relatively straightfor- A time-honored method of approximating
ward. Adequate resuscitation ensures mesen- burn size is the rule of nines. Simply put, the
Vol. 101, No. 7 / ACUTE BURNS 2485
Signs and Symptoms of Burn Injury

Degree Common Causes Color Sensitivity Appearance Treatment Risk of Poor Scarring

First Flash, sunburn Pink Painful Intact epithelium Symptomatic None

Second (superficial) Hot water Pink Very painful Wet ATB vs dressing Little
Second (deep) Hot soup Pink Painful Wet ATB, possible Depends on healing
Third Flame, grease White, brown Little pain Dry Surgery High

body is divided into regions and each region is Physical stigmata include facial burns, singed
described as a multiple of nine. The values are nasal hair, and soot in the pharynx. A new
as follows: each arm and the head, 9 percent; onset of hoarseness may indicate vocal cord
legs, 18 percent each; and torso, 36 percent. swelling, and a bronchoscopy can help to make
The relative amount of each area is multiplied a definitive diagnosis of inhalational injury.
by its body percentage, and the results are Carbon monoxide is a colorless, odorless gas
summed. It is sometimes useful to use the fact that binds to hemoglobin 200 times more av-
that the patient’s palm is 1 percent of their idly than oxygen, thereby limiting the ability of
TBSA. It is important to note that first-degree the hemoglobin to transport oxygen. The tox-
burns are not included in the estimation of icity of CO is directly related to the percentage
burn size. In general, a direct but inverse rela- of hemoglobin it saturates (Table IV).
tionship exists between age and survival for any Treatment for carbon monoxide intoxica-
size burn. Thus, while the mortality of a 40 tion is based on the ability of increased con-
percent TBSA burn in a 20-year-old patient is 8 centrations of oxygen to increase the rate at
percent, the mortality of the same injury in which CO is diffused. A concentration of 100%
someone older than 70 is 94 percent. Children oxygen increases the rate of CO diffusion from
younger than l also survive large burns at a hemoglobin from 4 hours to 45 minutes. Al-
decreased rate, although the reasons for this though hyperbaric oxygen is useful in treating
are not clear. For older patients, these effects patients with isolated CO intoxication, its use
are the result of preexisting medical ailments, complicates the care of patients with skin inju-
including cardiac, pulmonary, renal, and/or ries. Patients should only be referred to a hy-
hepatic dysfunction. perbaric facility if the institution also has a
burn center.
Inhalational Injury Upper airway swelling is a very dangerous
Inhalation injury has a significant impact on sequelae of inhalation injury because swelling
the survivability of a burn injury.16,17 It has can quickly progress to total airway obstruc-
three components: carbon monoxide intoxica- tion. This process begins several hours after
tion, upper airway swelling, and acute respira- injury and lasts for 2 to 4 days as tissue edema
tory failure. These components may occur wanes. The diagnosis is made by a direct visu-
alone or in combination, and they may vary in alization of the upper airway. If swelling, ery-
severity from inconsequential to life-threaten- thema, or soot is present, the patient should be
ing. Inhalation injury is usually evident by a intubated. The airway should be visualized
characteristic history and physical examination again at 48 hours and daily thereafter to assess
(Table III). Patients are usually injured in an airway edema. Extubation is safe when soft-
enclosed space, such as a house or car. They TABLE IV
may be coughing up carbonaceous sputum. Signs and Symptoms of Carbon Monoxide Intoxication

Signs of Inhalational Injury Percentage of CO in
Hemoglobin Symptoms
0–10 None
Burned in closed space 10–20 Headache, confusion
Burned in motor vehicle accident 20–40 Disorientation, fatigue, nausea, and
Facial burns visual changes
Singed nasal hairs 40–60 Hallucination, combativeness, coma,
Carbonaceous sputum and shock
Carbonaceous particles in larynx ⬎60 Mortality ⬎50%
tissue swelling has waned. If the patient can fective in helping to restore renal and splanch-
breathe or talk with the endotracheal tube oc- nic blood flow. The Parkland formula overes-
cluded and the cuff deflated, airway swelling timates the fluid needs for some adults with
has usually subsided. moderate-sized burns (15 to 40 percent TBSA)
Acute respiratory failure can occur hours to who do not have inhalation injuries. There-
days after a burn injury. This process is a type fore, practitioners should be reminded that the
of chemical pneumonitis caused by the toxic resuscitation formula is only a guide. Fluid re-
products of combustion. Patients should be suscitation should be adjusted on the basis of
treated using PEEP, low FIO2, frequent suc- the patient’s clinical response. The goal is ad-
tioning, and other supportive measures. equate oxygen delivery and end-organ perfu-
sion. In general, a urine output greater than 30
Fluid Resuscitation and Maintenance of to 50 cc/hour (0.5 to 1 cc/kg/hour in chil-
Hemodynamic Stability dren) indicates adequate resuscitation. When
All patients with a major burn injury should patients do not respond to fluid resuscitation
undergo a formal fluid resuscitation. Patients as expected, when there is preexisting or burn-
with injuries smaller than 20 percent TBSA can induced cardiac dysfunction, when the patient
be treated with liberalized oral and intravenous is elderly, or if serious pulmonary injury com-
fluids. The Parkland formula and its variations plicates treatment, invasive monitoring includ-
have become the standard method for resusci- ing pulmonary artery catheters is strongly rec-
tating those who are burn-injured.18 This ommended.
method is simple: during the initial 24 hours A variety of alternate resuscitation fluids and
after injury, the patient receives 4 cc/kg/ associated agents have been proposed. These
percent TBSA burn of Ringer’s lactate. Half of include hypertonic saline (3% NaCl), hyper-
this total is given in first 8 hours after injury, tonic saline dextran (7.5% NaCl in 6% dextran
and the remainder is given in the subsequent 70), and deferoxamine and ascorbic acid as
16 hours. At 24 hours after injury, begin giving free-radical scavengers. Although the use of
the patient 0.5 cc/kg/percent TBSA of 5% each of these is supported by experimental
albumin in Ringer’s lactate over the next 8 evidence, no clinical evidence in burned pa-
hours. tients supports their widespread use. In fact,
For example, a 100-kg man with a 65 percent one comparative trial found the incidence of
TBSA burn who arrives 4 hours after injury renal failure was increased four-fold and mor-
should be treated in the following manner. His tality by two-fold with hypertonic saline resus-
overall fluid requirement is 26,000 cc (4 cc ⫻ citation.19
100 kg ⫻ 65 percent TBSA) or 26 liters. He When survival from a burn injury is unprec-
should be given half of this amount in the first edented, strong consideration should be given
8 hours, 4 of which have already passed. Thus, to not beginning fluid resuscitation. Elderly
he should be given 13 liters of Ringer’s lactate patients with large burns will not survive. If
in the next 4 hours (3250 cc/hour). The re- resuscitated, they will survive for days to weeks
maining 13 liters should be given over the next before eventually dying of sepsis and organ
16 hours (800 cc/hour). Fluid administration failure. Many of these patients are alert and
should be adjusted to maintain a urine output communicative very early after the injury. In
of 30 to 50 cc/hour. At 24 hours after injury, general, these patients and their families ap-
give the patient 400 cc/hour Ringer’s lactate preciate frank discussions about the possibility
with 5% albumin for 8 hours. or impossibility of survival. When resuscitation
During this period of endothelial leak and is not performed, the patient should be kept
fluid administration, significant amounts of in- warm, pain-free, and with their family.
travascular protein are lost. Some authors favor
the administration of 5% albumin at 0.5 cc/ Escharotomy
kg/percent TBSA to maintain dynamic forces In large burns with generalized edema, cir-
between the intravascular and extracellular cumferential burn eschar of the extremities
spaces. This is usually initiated 24 hours after can prevent swelling of the underlying tissue.
injury when endothelial integrity is restored, The result is elevated tissue pressures and im-
and it is discontinued when the initial resusci- pairment of tissue perfusion. Inflexible eschar
tation period is over. In addition, a low-dose and underlying tissue edema can also prevent
dopamine infusion (3 to 5 ␮g/kg/min) is ef- chest wall motion and, thus, limit ventilation.
Vol. 101, No. 7 / ACUTE BURNS 2487
The surgical division of these constricting es- BURN WOUND MANAGEMENT
chars (escharotomies) is performed to main- The initial treatment of a burn wound in-
tain the blood flow to the distal extremities. volves removing all necrotic tissue, ruptured
Because the eschar itself is insensate, this pro- blisters, and debris. The senior author thinks
cedure can be performed in most patients at that the removal of blisters simplifies care and
the bedside using sedation and analgesics. may be beneficial, although all practitioners do
Both sharp division and electrocautery are ef- not recommend this protocol. Only blisters
fective. Escharotomies should be performed smaller than 1 cm in diameter or those on the
on the midlateral or medial aspects of limbs soles of feet are left intact. The wound is
and digits to prevent joint exposure. The es- washed with soap and tap water and then cov-
char should be divided completely down to the ered with a topical antimicrobial dressing. Top-
viable underlying tissue, and it should be di- ical antibiotics are used to decrease microbial
vided down its entire length to fully release the growth and to prevent invasive infection. Pro-
obstruction. In addition to escharotomies, fas- phylactic systemic antibiotics do not have a role
ciotomies may be needed in patients with large in the prevention of wound sepsis. Antibiotics
burns and generalized massive tissue edema. are indicated when cellulitis exists in the sur-
rounding unburned tissue.
The wound should then undergo daily dress-
NUTRITIONAL SUPPORT ings that repeat this process until healing or
Burn injuries induce an inflammatory and surgical intervention has occurred. In the past,
cytokine response that results in a marked in- most practitioners performed twice-daily dress-
crease in metabolic rate. Basal energy expen- ings. Recently, many patients have been
diture is increased three-fold above normal. dressed daily with a significant decrease in cost,
Early and aggressive nutritional support via the nursing time, and pain. This strategy is ideal
enteral route is critical in preventing bacterial for children with superficial scald burns. Pa-
translocation from the gut and systemic sepsis. tients with larger wounds, wounds that are or
Nutritional support is begun within 18 hours of have been infected, or those with excessive
admission through a Dobbhoff feeding tube. amounts of exudate benefit from twice-daily
Although gastric feedings are safe in most pa- dressings. During these dressings, the wound
tients, placing the tip more distally prevents should be gently washed with pathogen-free
the aspiration of food during anesthesia and tap water and mild soap. The previously ap-
allows the patient to be fed continuously, with- plied topical antibiotic should be completely
out holding feeds before and during repetitive removed. Fibrinous exudate and loosely adher-
ent eschar should be removed with a wet wash-
debridement and grafting sessions. Metoclo-
cloth or forceps. Extensive bedside debride-
pramide or erythromycin can be used to help
ments are very painful and are not indicated.
propel the tip of the tube past the pylorus.
In most cases, the wound should then be cov-
It is possible to estimate the patient’s caloric
ered with antibiotic cream and gauze.
requirements using either the Curreri formula
(25 kcal/kg ⫹ 40 kcal/percent TBSA) or twice
the Harris-Benedict estimate.20 Because these Topical Antimicrobials and Other Treatments
estimates can be very inaccurate, most practi- Most partial-thickness burns less than 10 per-
tioners measure the resting energy expendi- cent TBSA can be simply and safely cared for
ture by indirect calorimetry and then provide with a once-daily antibiotic dressing. For most
20 percent more calories than this number patients, the agent of choice is silver sulfadia-
indicates. The resting energy expenditure zine (Silvadene). This agent has a broad spec-
should be measured on admission and weekly trum of activity and few complications. When a
thereafter. Clinical measurements of protein sulfa allergy complicates care, alternative
requirements for these patients suggest that agents include Polysporin, bacitracin, and Bac-
they require a nonprotein kilocalorie-to- troban. These agents are relatively inexpensive
nitrogen ratio of 100:1 and at least 2 g of but have a tendency to induce allergies.
protein/kg/day. In most cases, we document Mafenide (Sulfamylon) is an alternate agent
the effectiveness of nutritional support by mea- that has significant complications but pene-
suring the prealbumin level. trates burn eschar. This makes it ideal for treat-
ing undebrided, infected wounds. It is also the INDICATIONS FOR SURGERY
treatment of choice for serious burns of the Surgery is indicated for full-thickness inju-
ears to help prevent infectious chondritis. ries or when the wound is unlikely to heal
However, it should be used with caution be- within 3 weeks. After this time period, the risk
cause of its tendency to induce metabolic aci- of hypertrophic scar and contracture forma-
dosis. Acticoat takes advantage of the proven tion increase and outweigh the morbidity and
antimicrobial properties of the silver ion by costs of surgery. When the depth of injury is
coating the dressing material with a thin, solu- indeterminate, a close observation of wound
ble silver film. The dressing seems to maintain healing for 7 to 10 days before initiating surgi-
antibacterial levels of silver ions in the wound cal intervention is reasonable. However, in ar-
for up to 5 days. The Acticoat dressing reduces eas harboring a dense cross-section of dermal
infection rates and has the additional benefit appendages, such as the face, scalp, and ears,
of decreased pain and expense because daily an observational period of up to 3 weeks is
dressings do not seem to be necessary.21 Al- reasonable until the healing potential of the
though initially promising, additional studies wound has a chance to declare itself.
are needed to determine the final role of this
product in burn wound treatment.
Surgical Debridement
An alternate method of managing wounds is
with an occlusive dressing. When superficial Tangential excision is the debridement of
second-degree burns are clean and less than 24 graduated amounts of necrotic tissue until via-
hours old, an occlusive dressing can be ap- ble tissue is reached. This usually can be deter-
plied. These products maintain a moist wound mined by punctate hemorrhage in the wound
environment, which speeds healing and de- bed. The advantages of this technique are an
creases the frequency and pain of daily wound accurate removal of nonviable tissue and the
care. There are several new types of occlusive preservation of as much subcutaneous tissue as
dressings commercially available. Biobrane is a possible. The disadvantage is blood loss. Sev-
biosynthetic wound dressing constructed of a eral methods of reducing operative blood loss
silicon film with a nylon fabric partially imbed- exist. One is the use of tumescent fluid solu-
ded in the film. The fabric presents to the tion. The burn areas to be excised are infil-
wound bed a complex, three-dimensional trated with a 1:1,000,000 dilution of injectable
structure of trifilament threads to which colla- epinephrine solution. Ten minutes are allowed
for the vasoconstrictive effect to take place be-
gen has been chemically bound. Blood/sera
fore excision is begun. Extremity burns should
clot in the nylon matrix, thereby firmly adher-
be excised with the use of tourniquets. Topical
ing the dressing to the wound until epithelial-
thrombin and Neo-Synephrine can be placed
ization occurs. The dressing is carefully
on the wound to obtain hemostasis before the
trimmed as it falls off on an outpatient basis. application of the skin graft. In cases of very
Transcyte is produced by culturing human der- deep burns or massive burn injuries, excision
mal fibroblasts onto a biosynthetic material to the fascia is an alternative. In these cases, the
consisting of an ultrathin, semipermeable viability of the subcutaneous fat is question-
membrane bonded to nylon mesh. The nylon able. Fascial excision can be performed with
mesh forms a three-dimensional scaffold for electrocautery to decrease blood loss. The dis-
growth of the dermal tissue, and the mem- advantages of this procedure include contour
brane forms a synthetic (nonimmunogenic) irregularities and decreased mobility. What-
epidermis. As the fibroblasts proliferate in the ever the method of debridement, it is essential
nylon mesh, they secrete structural proteins that it be continued until only viable tissue
and growth factors, thereby generating a three- remains.
dimensional human dermal matrix. In general, The second phase of surgical treatment is
occlusive dressings are an excellent alternative wound closure. Some small burns can be ex-
for small, superficial, or previously debrided cised and closed primarily. This obviates donor
wounds. In general, when a patient’s wounds site morbidity and gives an excellent result, but
are not healing at a rate sufficient to expect it is seldom possible. The gold standard of
closure within 3 weeks, operative intervention wound coverage is autologous split-thickness
should be considered. skin grafting. Grafts are typically taken from
Vol. 101, No. 7 / ACUTE BURNS 2489
TABLE V able through skin banks throughout the
Recommended Donor Graft Thickness According to Age United States. Porcine xenografts were used in
and Site the past, but are now seldom available. The
allograft “takes” like a skin graft and is then
Depth (1⁄1000 inch) rejected via cell-mediated immunity 10 to 14
Age 8 10 12 days later. In patients with massive burns who
Neonate to 2 Thigh, buttocks Trunk, scalp
are immunosuppressed, the allograft may re-
years main intact for weeks. This strategy is valuable
2–10 years Thigh, buttock, Scalp for maintaining wound bed integrity until do-
Teens and Thigh, buttocks,
nor sites have healed and are ready for rehar-
adult scalp, trunk vesting. Transcyte (the biological dressing de-
Elderly Thigh, buttocks Scalp, trunk scribed above) is a bioengineered alternative.
Integra Artificial Skin is another bioengi-

8 1000to 12⁄1000 of an inch, depending on donor neered dermal substitute. It consists of a bi-
location and patient age (Table V). layer membrane system for skin replacement.
Several important surgical decisions must be The dermal replacement layer is made of a
made about the graft and donor site. The thin- porous matrix of fibers of cross-linked bovine
ner the graft, the higher the rate of take but tendon collagen and a glycosaminoglycan
the more the wound undergoes secondary con- (chondroitin-6-sulfate) that is manufactured
tracture. Meshed grafts have a better take rate with a controlled porosity and defined degra-
and achieve closure effectively. However, the dation rate. The temporary epidermal substi-
resulting “cobblestone” appearance is un- tute layer is made of synthetic polysiloxane
sightly and very difficult to reconstruct. In pa- polymer (silicone) and functions to control
tients with small to moderate-sized burns, in moisture loss from the wound. The collagen
children, and in those individuals for whom dermal replacement layer serves as a matrix for
the aesthetic result is a concern, strong consid- the infiltration of fibroblasts, macrophages,
eration should be given to sheet grafting. lymphocytes, and capillaries derived from the
Meshed grafting better treats patients with ma- wound bed. As healing progresses, an endoge-
jor burns or others with insufficient donor sites nous collagen matrix is deposited by fibro-
and wounds that have previously failed graft- blasts; simultaneously, the dermal layer of In-
ing. In the elderly patient, the increased met- tegra Artificial Skin is degraded. Upon
abolic demands of a large donor site and a lack adequate vascularization of the dermal layer
of concern about aesthetic outcome make and the availability of donor autograft tissue,
mesh grafting a better option. Various meth- the temporary silicone layer is removed and a
ods of dressing donor sites can be used. The thin, meshed layer of epidermal autograft is
senior author most often uses an occlusive placed over the “neodermis.” Cells from the
dressing because it decreases pain and simpli- epidermal autograft grow and form a conflu-
fies the need for future wound care. ent stratum corneum, thereby closing the
wound and reconstituting a functional dermis
Alternatives to Autografts and epidermis. The advantages of this product
In many situations, the surgeon should con- are that it simultaneously provides temporary
sider closing the wound with a biological dress- wound coverage, improves the success of epi-
ing. These situations include patients with dermal cell grafting, and allows the use of thin-
large, partial-thickness burns, the existence of ner autografts, which speeds donor site heal-
insufficient autograft to close the wound after ing. 22 These products may decrease
debridement, and after the debridement of contracture formation and improve appear-
chronically open, infected wounds. The advan- ance. However, all are sensitive to infection
tages of a biological dressing in these situations and are expensive. The ultimate cost-benefit of
include decreased pain, the prevention of in- these products is as yet uncertain.
fection and water loss, and faster epithelializa- Cultured epidermal autografts and allografts
tion. are another strategy of skin replacement for
Previously, the most commonly used dress- burn wounds. The results of this treatment and
ing was a human cadaver allograft. Although the role of this technique in the care of burn
somewhat limited in availability, many organ patients have been controversial. Points of uni-
donors also donate skin. This product is avail- versal agreement are the following. These
grafts are extremely fragile and are sensitive to first 48 hours. Even dislodged or misplaced
infection, antimicrobial agents, shear, and skin grafts can be successfully repositioned in
dressing change. The limited data that exist the first 2 days after placement. Early graft
suggest that they do not increase survival or infection can sometimes be effectively treated
decrease costs.23 It takes 3 to 4 weeks to grow by the application of topical antimicrobials,
sufficient cells from a tissue biopsy to resurface such as Sulfamylon. We prefer to individualize
a burn wound of significant size. During this the surveillance plan on the basis of clinical
time, many wounds become infected, which needs. Sheet-grafted areas that can be easily
prolongs the time period before the grafts can redressed, such as in the upper extremity, are
be used to close the wound. After successful inspected at 24 to 48 hours. Hematomas/
engraftment, the resulting epidermis remains seromas present under the sheet graft can be
very fragile and frequently blisters. This seems “rolled out” with cotton swabs, and the dress-
to be due to the slow development of anchor- ing is then not changed for an additional 2
ing complexes, which occurs, in part, because days. Wounds at risk for infection are inspected
some of the components of this structure are at 3 days, and a daily Silvadene or Sulfamylon
synthesized by dermal fibroblasts. This partially dressing is used to treat signs of infection. Most
explains why the results of epidermal grafting other graft sites are changed at day 4. Areas
are much better when the cells are used as a that are hard to protect from mechanical
composite graft. At present, most practitioners forces, such as when the patient has both an-
believe that cultured epidermal autografts and terior and posterior surface burns on the but-
allografts are of uncertain value for the major- tocks, are sometimes kept dressed for longer
ity of burn patients and that they should be periods of time.
reserved for the treatment of massive burn in- When graft take is stable (usually 4 days after
juries. Anecdotally, these grafts seem to de- surgery), therapy is begun. The goals of ther-
crease the incidence of hypertrophic scarring, apy are listed in Table VI.
but they are associated with significant contrac- In general, active and passive range of mo-
tion problems. Many surgeons now use these tion exercises are used to retain motion. Splint-
types of grafts in conjunction with a bioengi- ing is used to retain position when the patient
neered dermis or allograft from which the epi- is not moving. The positioning guidelines are
dermis is removed. the same as those for the time immediately
after surgery. Because burn injury stimulates
POSTOPERATIVE CARE intense wound contraction, the early and ag-
A well-placed skin graft can be lost during gressive use of these modalities is essential to
the immediate postoperative period for several maintain function. When the grafts are secure,
reasons. They include shear/motion, hemato- most patients are measured for pressure gar-
ma/seroma formation, and infection. Graft ments.
protection and close surveillance are key dur-
ing this critical time period to ensure graft Scar Management
take. Skin-grafted areas should be immobilized One of the most devastating sequelae a burn
postoperatively to avoid shear forces. For ex- survivor has to face is the formation of hyper-
tremities, splinting is an excellent method of trophic scars. These scars can seriously impede
immobilization. The splints should be de- the aesthetic, functional, and psychological re-
signed to place joints at maximal stretch. Spe-
cific recommendations for positions include TABLE VI
the following: axilla, 90 degrees horizontal with Goals of Therapy
bedside troughs or an airplane splint; elbow,
fully extended; wrist, slightly extended (10 de- Correct, prevent, or minimize deformity
grees); metatarsophalangeal joints of the fin- Protect weak muscles from overstretching
Provide a functional position
gers, flexed; interphalangeal joints, fully ex- Aid in maintaining range of motion
tended; thumb, in 40 to 50 degrees of Protect exposed tendons and joints
abduction with interphalangeal joint ex- Provide immobilization across joints after grafting
Minimize scarring with pressure garment therapy
tended. Develop functional skills to facilitate:
The timing of the first dressing change is Independence in daily living activities
controversial. Hematomas and seromas will not Community reentry through group activities, patient and
family education, and community-based activities
likely affect engraftment if drained within the
Vol. 101, No. 7 / ACUTE BURNS 2491
covery from an already devastating injury. preinjury employment are the best predictors
Their pathophysiology is not completely un- of eventual return to work status.
derstood, but the formation of a hypertrophic On average, burn patients with a mean TBSA
scar may be associated with elevated levels of of 5 percent returned to work within 1 month,
transforming growth factor in the scar.24,25 Hy- patients with a mean TBSA of 10 percent re-
pertrophic scarring is more common in chil- turned to work within 1 to 6 months, patients
dren, people of color, and in areas of stretch or with mean TBSA of 20 percent returned to
motion. Pressure garments customized to exert work within 6 months to a year, and patients
25 mm of pressure are used to decrease the with a mean TBSA of 35 percent returned to
intensity of scar formation, but a recent study work more than a year later. Interdisciplinary
questions the efficacy of this process.26 The involvement, such as counseling, group ther-
mechanism of action is thought to be due to a apy, and occupational and physical therapy, is
combination of pressure-induced remodeling very important in maximizing a patient’s clini-
and hypoxia-induced tissue atrophy. Silicone cal outcome. Interventions designed to aid ad-
sheets in direct contact with the scars can im- justment, work hardening, and other rehabili-
prove their appearance and reduce redness tation services and marital/family therapy are
and itching.27 They can be used in conjunction also important.
with pressure garments. Finally, corticosteroid Warren L. Garner, M.D.
injections can also improve the appearance of University Southern California
hypertrophic scars and reduce itching. How- Section of Plastic and Reconstructive Surgery
ever, injections can be painful and can only be 1450 San Pablo Street
used in limited areas. Suite 2000
Los Angeles, Calif. 90033
Over the past 25 years, survival rates from
burn injury have dramatically improved. In 1. National Center for Health Statistics. Fire/Burn Deaths
and Rates per 100,000. Mortality Data Tapes, E890-
1971, 50 percent of the patients admitted with 899, E923-925. Division of Unintentional Injury Pre-
burns larger than 40 percent of the TBSA died. vention, National Center for Injury Prevention and
In contrast, in 1990, 50 percent of the patients Control, Centers for Disease Control and Prevention,
admitted with a burn covering more than 50 Atlanta, Ga., 1991.
percent of the TBSA routinely survived.28 Sur- 2. Feck, G. A., Baptiste, M. S., and Tate, C. L., Jr. Burn
injuries: Epidemiology and prevention. Accid. Anal.
vival rates have increased by almost 1 percent Prev. 11: 129, 1979.
every year due to improvements in resuscita- 3. Mallonee, S., Istre, G. R., Rosenberg, M., et al. Surveil-
tion, the treatment of inhalation injuries, and lance and prevention of residential-fire injuries.
other advances in critical care. Empirical data N. Engl. J. Med. 335: 27, 1996.
regarding the long-term sequelae of burn inju- 4. Jackson, D. M. The diagnosis of the depth of burning.
Br. J. Surg. 40: 588, 1953.
ries indicate that many burn patients do 5. Robson, M. C., Del Beccaro, E. J., and Heggers, J. P. The
achieve a satisfactory quality of life and that effect of prostaglandins on the dermal microcircula-
they seem to be well-adjusted individuals. A tion after burning, and the inhibition of the effect by
rough indicator of an individual’s psychologi- specific pharmacological agents. Plast. Reconstr. Surg.
cal rehabilitation after a burn injury is re- 63: 781, 1979.
6. Demling, R. H., and LaLonde, C. Early postburn lipid
flected by employment status. Patients who re- peroxidation: Effect of ibuprofen and allopurinol.
turn to work after a burn injury have higher Surgery 107: 85, 1990.
self-esteem, less behavioral avoidance, and 7. Friedl, H. P., Till, G. O., and Ward, P. A. Roles of his-
greater attention to goals. A 1995 study showed tamine, complement and xanthine oxidase in thermal
that the most significant predictors of return to injury of skin. Am. J. Pathol. 135: 203, 1989.
8. Garner, W. L., Rodriguez, J. L., Miller, C., Remick, D., and
work are hand involvement, grafting, and size Smith, D. J., Jr. Acute skin injury releases neutrophil
of burn29; a 1989 study showed that the most chemoattractants. Surgery 116: 42, 1994.
significant variables influencing return to work 9. Mileski, W., Borgstrom, D., Lightfoot, E., et al. Inhibi-
after injury are the degree of burns, hand tion of leukocyte-endothelial adherence following
burns, age (those younger than 45 have a thermal injury. J. Surg. Res. 52: 334, 1992.
10. Nwariaku, F., Sikes, P. J., Lightfoot, E., Jr., et al. Inhi-
higher return to work rate), and the type of bition of selectin- and integrin-mediated inflamma-
work done before injury. The length of time a tory response after burn injury. J. Surg. Res. 63: 355,
patient is off work, their burn size, and their 1996.
11. Bucky, L. P., Vedder, N. B., Hong, H. Z., et al. Reduc- Burrell, R. A matched pair, randomized study eval-
tion of burn injury by inhibiting CD18-mediated leu- uating the efficacy and safety of Acticoat silver-coated
kocyte adherence in rabbits. Plast. Reconstr. Surg. 93: dressing for the treatment of burn wounds. J. Burn
1473, 1994. Care Rehabil. 19: 531, 1998.
12. DeMeules, J. E., Pigula, F. A., Mueller, M., et al. Tumor 22. Sheridan, R. L., Hegarty, M., Tompkins, R. G., and Burke,
necrosis factor and cardiac function. J. Trauma 32: J. F. Artificial skin in massive burns: Results to ten
686, 1992. years. Eur J. Plast. Surg. 17: 91, 1994.
13. Deitch, E. A., Rutan, R., Waymack, J. P., et al. Trauma, 23. Rue, L. W., Cioffi, W. G., McManus, W. F., and Pruitt,
shock, and gut translocation. New Horiz. 4: 289, 1996. B. A., Jr. Wound closure and outcome in extensively
14. Nelson, R. D., Hasslen, S. R., Ahrenholz, D. H., et al. burned patients treated with cultured autologous ker-
Mechanisms of loss of human neutrophil chemotaxis atinocytes. J. Trauma 34: 662, 1993.
following thermal injury. J. Burn Care Rehabil. 8: 496, 24. Garner, W. L., Rittenberg, T., Ehrlich, H. P., et al. Hy-
1987. pertrophic scar fibroblasts accelerate collagen gel con-
15. Warden, G. D., Jr., Mason, A. D., and Pruitt, B. A., Jr. traction. Wound Repair Regen. 3: 185, 1995.
Evaluation of leukocyte chemotaxis in vitro in ther- 25. Ghahary, A., Shen, Y. J., Scott, P. G., and Tredget, E. E.
mally injured patients. J. Clin. Invest. 54: 1001, 1974. Immunolocalization of TGF-beta 1 in human hyper-
16. Smith, D. L., Cairns, B. A., Ramadan, F., et al. Effect of trophic scar and normal dermal tissues. Cytokine 7: 184,
inhalation injury, burn size, and age on mortality: A 1995.
study of 1447 consecutive burn patients. J. Trauma 37: 26. Chang, P., Laubenthal, K. N., Lewis, R. W., Jr., Rosen-
655, 1994. quist, M. D., Lindley-Smith, P., and Kealey, G. P. Pro-
17. Tredget, E. E., Shankowsky, H. A., Taerum, T. V., et al. spective, randomized study of the efficacy of pressure
The role of inhalation injury in burn trauma: A Ca- garment therapy in patients with burns. J. Burn Care
nadian experience. Ann. Surg. 212: 720, 1990. Rehabil. 16: 473, 1995.
18. Baxter, C. R. Fluid volume and electrocyte changes in 27. Ahn, S. T., Monafo, W. W., and Mustoe, T. A. Topical
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19. Huang, P. P., Stucky, F. S., Dimick, A. R., et al. Hyper- 28. Saffle, J. R., Davis, B., and Williams, P. Recent outcomes
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20. Pasulka, P. S., and Wachtel, T. L. Nutritional consider- Registry. J. Burn Care Rehabil. 16: 219, 1995.
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109, 1987. lating to return to work after burn injury. J. Burn Care
21. Tredget, E. E., Shankowsky, H. A., Groeneveld, A., and Rehabil. 16: 445, 1995.

Self-Assessment Examination follows on

page 2493.
Self-Assessment Examination

Acute Burns
by Chia Chi Kao, M.D., and Warren L. Garner, M.D.

A) 2700 cc
B) 5400 cc
C) 5980 cc
D) 7560 cc
E) 10,800 cc


A) D5 Ringer’s lactate
B) 3% NaCl
C) Ringer’s lactate
D) 5% albumin in D5 0.45% normal saline
E) D5 0.45% normal saline


A) Within 6 weeks
B) Within 3 months
C) Within 6 months to 1 year
D) After 1 year or more
E) Never


A) Tracheal intubation
B) Transfer to a hyperbaric oxygen chamber
C) 100% oxygen
D) Positive end-expiratory pressure
E) Optimizing cardiac function with invasive monitoring


A) Metatarsophalangeal joints straight, proximal interphalangeal joints flexed, distal interphalangeal joints straight
B) Metatarsophalangeal joints flexed, proximal interphalangeal joints flexed, distal interphalangeal joints straight
C) Metatarsophalangeal joints straight, interphalangeal joints straight
D) Metatarsophalangeal joints flexed, interphalangeal joints straight
E) Metatarsophalangeal joints flexed, proximal interphalangeal joints straight, distal interphalangeal joints flexed

A) Moist gauze
B) Silver sulfadiazine
C) Mafenide
D) Radical debridement
E) Integra

To complete the examination for CME credit, turn to page 2645 for instructions and the response form.