Bongard Frederic , Darryl Sue. Diagnosis and Treatment Critical Care

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production by peripheral blood lymphocytes. Septic compli-

cations result in a further decrement in IL-2 production.

Serum IgG levels are decreased following burn injury and

gradually return to normal over 2–4 weeks as the patient

recovers. Restoration of IgG levels to normal by exogenous

administration has not been shown to affect morbidity or

mortality. Many investigators, using a number of experimen-

tal approaches, have demonstrated immunosuppressive fac-

tors present in the serum of thermally injured patients.

Similar immunosuppressive properties have been detected in

burn blister fluid. Immunosuppressive polypeptides have

been the most commonly invoked agents; however, other fac-

tors, including complement degradation products,

immunoglobulin fragments, prostaglandins, and endocrine

secretions, occur in the serum following thermal injury.

Alterations in granulocyte chemotaxis, degranulation,

adherence, oxygen free-radical production, and complement

receptor expression have been observed following thermal

injury. Granulocytes from burned patients exhibit an

increase in cytosolic oxidase activity, suggesting in vivo acti-

vation. They also exhibit greater than normal oxidase activ-

ity after in vitro stimulation. This increase suggests that

neutrophils from burned patients have an increased oxida-

tive burst potential that, if activated, could cause increased

tissue and organ injury. A marked and sustained increase in

neutrophil expression of the complement opsonin receptors

CRT and CR3 has been described following burn injury. The

increase in receptor expression correlated with decreased

chemotaxis in response to zymosan-activated serum, sug-

gesting that C5A was responsible for inducing systemic neu-

trophil activation. Recent investigations have demonstrated

significant elevation of F-actin content and decreased ability

to polymerize and depolymerize F-actin in the granulocytes

of burn patients when compared with controls. These alter-

ations may be partly responsible for the observed changes in

chemotaxis and migration following thermal injury.

Almost every aspect of immunoregulation is affected fol-

lowing burn injury. At present, no effective immunomodula-

tory treatment has been identified; however, the development

of new immunomodulatory drugs and recombinant lym-

phokines and their antagonists may prove beneficial in cor-

recting immune dysfunction following burn injury.

Aulick LH et al: Influence of the burn wound on peripheral circu-

lation in thermally injured patients. Am J Physiol

1977;233:H520. [PMID: 910969]

Bowen BD et al: Microvascular exchange during burn injury: III.

Implications of the model. Circ Shock 1989;28:221–33. [PMID:

2766478]

Burleson DG et al: Flow cytometric measurement of rat lympho-

cyte subpopulations after burn injury and burn injury with

infection. Arch Surg 1987;122:216–20. [PMID: 3813870]

Cioffi WG et al: Dissociation of blood volume and flow in regula-

tion of salt and water balance in burn patients. Ann Surg

1991;214:213–8. [PMID: 1656902]

Cioffi WG et al: Granulocyte oxidative activity after thermal injury.

Surgery 1992;112:860–5.

Demling RH et al: Early lung dysfunction after major burns: Role

of edema and vasoactive mediators. J Trauma 1985;25:959–66.

[PMID: 2413227]

Demling RH, Kramer G, Harms B: Role of thermal injury-induced

hypoproteinemia on fluid flux and protein permeability in

burned and non-burned tissue. Surgery 1984;95:136–44.

Ferrara JJ et al: The suppressive effect of subeschar tissue fluid

upon in vitro cell-mediated immunologic function. J Burn Care

Rehabil 1988;9:584–8. [PMID: 3220864]

Fleming RY et al: The effect of erythropoietin in normal healthy

volunteers and pediatric patients with burn injuries. Surgery

1992;112:424–31.

Fukuzuka K et al: Glucocorticoid-induced, caspase-dependent

organ apoptosis early after burn injury. Am J Physiol Regul

Integr Comp Physiol 2000;278:R1005–18. [PMID: 10749790]

Gadd MA et al: Defective T-cell surface antigen expression after

mitogen stimulation: An index of lymphocyte dysfunction after

controlled murine injury. Ann Surg 1989;209:112–18. [PMID:

2783362]

Harms BA et al: Microvascular fluid and protein flux in pulmonary

and systemic circulations after thermal injury. Microvasc Res

1982;23:77–86. [PMID: 7099009]

Jones WG II et al: Differential pathophysiology of bacterial translo-

cation after thermal injury and sepsis. Ann Surg 1991;214:

24–30. [PMID: 2064468]

LeVoyer T et al: Alterations in intestinal permeability after thermal

injury. Arch Surg 1992;127:26–9. [PMID: 1734847]

Lund T, Reed RK: Microvascular fluid exchange following thermal

skin injury in the rat: Changes in extravascular colloid osmotic

pressure, albumin mass, and water content. Circ Shock

1986;20:91–104. [PMID: 3779907]

Ozkan AN, Hoyt DB, Ninnemann JL: Generation and activity of

suppressor peptides following traumatic injury. J Burn Care

Rehabil 1987;8:527–30. [PMID: 3325512]

Pruitt BA Jr, Goodwin CW, Mason AD Jr: Epidemiological, demo-

graphic, and outcome characteristics of burn injury. In

Herndon DN (ed), Total Burn Care, 2nd ed. Philadelphia:

Saunders, 2002.

Pruitt BA Jr, Mason AD Jr, Moncrief JA: Hemodynamic changes in

the early postburn patient: The influence of fluid administra-

tion and of a vasodilator (hydralazine). J Trauma 1971;11:

36–46. [PMID: 5099912]

Pruitt BA Jr: The universal trauma model. Bull Am Coll Surg

1985;70:2.

Solomkin JS: Neutrophil disorders in burn injury: Complement,

cytokines, and organ injury. J Trauma 1990;30:S80–85. [PMID:

2254997]

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thermal injury of rat skin. J Trauma 1983;23:269–77. [PMID:

6842628]

INITIAL CARE OF THE BURN PATIENT

Prehospital Treatment

The primary concern at the accident scene is to stop the

burning process. Burning and smoldering clothing should be

extinguished. Patients with electrical injury should be sepa-

rated from points of electric contact, taking all necessary care

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to avoid injuring oneself. If the burn was caused by a chemi-

cal agent, all contaminated clothing should be removed and

copious water lavage initiated.

As with all trauma patients, the primary concern during

initial assessment is maintenance of cardiopulmonary func-

tion. Airway patency and adequacy of ventilation must be

maintained and supplemental oxygen administered as neces-

sary. In the absence of associated mechanical trauma or need

for cardiopulmonary resuscitation, placement of an intra-

venous cannula is not necessary if transport to a treatment

facility can be accomplished in less than 45 minutes. The

application of ice or cold water soaks will relieve pain in areas

of second-degree burn. If the cold therapy is initiated within

10 minutes of burning, tissue heat content is also reduced,

and the depth of thermal injury may be lessened. If cold ther-

apy is used, care must be taken to avoid causing hypother-

mia. Cold soaks or ice should only be used on patients with

burns of less than 10% of the body surface and only for the

time required to produce analgesia. After the ice or cold soak

is removed, the patient should be covered with a clean sheet

and blanket to conserve body heat and minimize contamina-

tion of the burn wounds during transport to the hospital.



Emergency Management

On arrival at the hospital, the patency of the airway and ade-

quacy of breathing should be reassessed and endotracheal

intubation performed if necessary. Intravenous fluid resusci-

tation is initiated by infusing a physiologic salt solution, for

example, lactated Ringer’s solution, through a large-bore

intravenous cannula. The order of preference for the site of

intravenous cannulation is a peripheral vein underlying

unburned skin, a peripheral vein underlying burned skin,

and lastly, a central vein.

A history should be obtained, paying special attention to

the circumstances of the injury, the presence of preexisting

disease, allergies and medications, and the use of illicit drugs

or alcohol prior to injury. A complete physical examination

should be performed and associated injuries identified.

Baseline laboratory data should include an arterial blood gas

and pH analysis, serum electrolytes, urea nitrogen, creati-

nine, and glucose, and a complete blood count. If available,

continuous transcutaneous pulse oximetry determination of

oxygen saturation should be initiated in patients with sus-

pected inhalation injury or extensive burns.

Since all currently used resuscitation formulas are based on

body weight and the percentage of total body surface area

burned (TBSB), the patient should be weighed and the depth

and extent of burn estimated. The extent of body surface area

burned can be estimated easily using the “rule of nines,” which

recognizes that specific anatomic regions represent 9% or 18%

of the total body surface area (Figure 35–1). Since the area of

one surface of the patient’s hand (palm and digits) represents

1% of that person’s total body surface, one can use that rela-

tionship in estimating the extent of irregularly distributed

burns. Infants and children have a different body surface area

distribution, with relatively larger heads and smaller lower

extremities. When estimating the body surface burn area for

children under age 10, the Lund and Browder burn diagram

(Figure 35–2) or other similar diagram should be used to deter-

mine the body surface area burned with greater precision.

The depth of burn is classified as partial- or full-thickness

with respect to the extent of dermal destruction by coagula-

tion necrosis (Figure 35–3). First- and second-degree burns

are considered partial-thickness injuries and third-degree

burns full-thickness injuries. Superficial partial-thickness

burns heal spontaneously by epithelial migration from pre-

served dermal appendages. Full-thickness injuries have com-

plete destruction of all epithelial elements and require skin

grafting for wound closure. Deep partial-thickness burns

may heal over a long period of time, but grafting is frequently

performed to decrease time to wound closure, reduce scar

formation, improve functional outcome, and shorten the

hospital stay. The clinical criteria in Table 35–2 permit initial

differentiation among the different depths of burn injury.

Only the total percentage of skin surface area involved in

second- and third-degree burns is calculated or estimated for

resuscitation purposes. First-degree burns do not cause sig-

nificant edema formation or metabolic alteration and are not

considered in the calculation of burn size for estimation of

resuscitation requirements. Differentiation between second-

and third-degree burns is more important in the later post-

burn course because it has implications for the duration of

hypermetabolism, the need for autograft closure of the burn

wound, and the anticipated functional result.

ADULT

“Rule of Nines”



Figure 35–1. Rule of nines showing distribution of

body surface area (BSA) by anatomic parts in the adult.

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729

The presence of associated mechanical trauma may affect

the resuscitation requirements of the thermally injured

patient. Soft tissue trauma and bleeding from any injury will

increase the fluid required to establish adequate urine out-

put. The presence of thermal injury should not delay or alter

the evaluation and subsequent treatment, including opera-

tive intervention, of mechanical trauma. An indwelling

urethral catheter should be inserted in all patients requiring

intravenous fluid therapy, and the urinary output should be

measured and recorded hourly. Vital signs and the patient’s

general condition should be monitored and recorded fre-

quently on a flowsheet. The rectal temperature should be

measured hourly, providing a guide for maintenance of core

temperature. In patients with high-voltage electrical injury,



Figure 35–2. The use of a burn diagram permits a more exact estimation of the extent of burn. Note that the sur-

face areas of the head and lower extremities change significantly with age.

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CHAPTER 35

730

electrocardiographic monitoring should be initiated in the

emergency department.

The tetanus immunization status of the patient should be

determined in the emergency department. The burn patient

who has been immunized against tetanus previously should

be given a booster dose of tetanus toxoid if the last dose was

administered more than 5 years previously. Patients with no

history of active immunization should receive tetanus

immune globulin in addition to an initial dose of tetanus

toxoid. Active immunization is completed subsequently

according to the routine dosage schedule.

PRINCIPLES OF BURN TREATMENT



Fluid Resuscitation

Fluid resuscitation should be started as soon as possible fol-

lowing thermal injury. Generally, burns involving more than

25% of the body surface area require intravenous fluid resus-

citation because ileus precludes oral resuscitation. Patients

with smaller burns in whom ileus does not develop should

have liberal access to electrolyte-containing fluids such as

fruit juices or milk, but excessive intake of electrolyte-free

water should be avoided to prevent hyponatremia. Many for-

mulas have been proposed for calculation of intravenous

fluid resuscitation of thermally injured patients (Table 35–3).

The central theme is that the volume of fluid required

depends on the patient’s weight and the extent of burn. Most

often it is recommended that half the calculated requirement

be infused over the first 8 hours following injury, that is, at

the time of maximal vascular permeability; the remainder of

the first 24-hour resuscitation volume is delivered over

the next 16 hours. Certain subgroups of patients require a

significantly greater resuscitation volume than that estimated

by the formulas. A delay in starting fluid resuscitation,

inhalation injury, and ethanol intoxication frequently are

associated with greater than predicted fluid requirements.

Patients with high-voltage electrical injuries frequently

require more resuscitation fluid than that predicted based on

the extent of cutaneous injury. One must recognize that any

resuscitation formula serves only to guide the initiation of

fluid therapy. The actual amount of resuscitation fluid is tai-

lored to each patient’s physiologic responses, with frequent

reassessment and adjustment of infusion rates as needed to

preserve vital organ perfusion.

The various burn formulas in Table 35–3 differ consider-

ably with respect to the volume and composition of the

resuscitation fluids; however, each formula has been found to

be clinically effective. The general use of burn formulas has

decreased the frequency of burn-induced hypovolemic shock

and organ dysfunction, which were secondary to inadequate



Figure 35–3. Diagram of the skin and subcutaneous

tissues demonstrating the depth of burn and relationship

to the location of the cutaneous adnexa. First- and sec-

ond-degree burns are considered partial-thickness.

Preservation of the hair follicles and sweat glands per-

mits spontaneous healing by epithelial cell migration.

Full-thickness (third-degree) burns will not reepithelialize

and require skin grafting for closure.

First-Degree Second-Degree Third-Degree

Cause Exposure to sunlight, very brief expo-

sure to hot liquid, flash, flame, or

chemical agent.

Limited exposure to hot liquid, flash,

flame, or chemical agent.

Prolonged exposure to flame, hot object, or chem-

ical agent. Contact with high-voltage electricity.

Color Red Pink or mottled red Pearly white, charred, translucent, or parchment-

like. Thrombosed vessels may be visible.

Surface Dry or very small blisters Bullae or moist, weeping surface Dry and inelastic

Sensation Painful Painful Insensate surface

Table 35–2. Characteristics of first-, second-, and third-degree burns.

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resuscitation. Failure to reevaluate the patient’s response to

resuscitation frequently on a scheduled basis may lead to

over- or underresuscitation. This is frequently observed

when the volume of fluid administered is based solely on the

initial estimate. With overzealous administration of intra-

venous fluids, pulmonary, cerebral, and excessive burn

wound edema may result. These complications are most evi-

dent from the third to sixth postburn days, when vascular

permeability has returned to “normal,” vascular resistance

has decreased, and burn wound edema is being resorbed.

Laboratory and clinical studies evaluating transcapillary

fluid movement and the physiologic response to resuscita-

tion have failed to demonstrate a benefit from the use of col-

loid-containing solutions during the first 24 hours of

resuscitation. Extravascular lung water has been shown to

remain essentially unchanged during the first postburn week

in patients who received only crystalloid-containing fluids in

the first 24 hours following injury. However, extravascular

lung water increased progressively in patients who received

colloid-containing fluids as part of the initial resuscitation.

During the latter half of the first week following injury, cap-

illary permeability normalizes and fluid requirements

decrease. As this occurs, the use of colloid-containing fluids

repletes the intravascular volume deficit more efficiently and

with a lesser volume than with crystalloid fluids alone.

The use of hypertonic saline has been proposed as a

means of reducing resuscitation fluid volume requirements.

Although the initial volume of fluid administered when

using hypertonic fluid is clearly less, the proposed benefits of

a decreased need for escharotomy, decreased incidence and

duration of ileus, and decreased fractional sodium retention

have not been found in all studies. Potential problems with

hypertonic saline resuscitation include hypernatremia,

which, if of sufficient magnitude to require infusion of hypo-

tonic fluid, negates the potential benefits of this resuscitation

strategy. The cellular dehydration induced by hypertonic

saline infusion of sufficient magnitude (15%) may cause cel-

lular and organ dysfunction necessitating correction with

hypotonic fluid administration. Subsequent evaporative

water loss from the burn wound may worsen the expected

hypernatremia from hypertonic saline resuscitation, requir-

ing additional hypotonic fluid infusion. Occasionally, some

patients with markedly reduced cardiac reserve may benefit

from resuscitation protocols employing hypertonic saline;

however, isotonic fluid resuscitation formulas provide ade-

quate resuscitation in most patients. Caution should be

Formula Electrolyte-Containing Solution Colloid-Containing Solution 5% Glucose in Water

First 24 Hours Postburn

Parkland Lactated Ringer’s, 4 mL/kg per % burn.

Hypertonic sodium

resuscitation

Volume of fluid containing 250 meq of

sodium/L to maintain hourly urinary

output of 30 mL.

Modified Brooke Lactated Ringer’s, 2 mL/kg per % burn.

Consensus

∗

Lactated Ringer’s, 2–4 mL/kg per %

burn.

Second 24 Hours Postburn

Parkland 20–60% of calculated plasma volume. As necessary to maintain urinary

output.

Hypertonic sodium

resuscitation

33% isotonic salt solution up to

3500 mL limit.

Modified Brooke

0.3–0.5 mL/kg per % burn

†

As necessary to maintain urinary

output.

Consensus

∗

0.3–0.5 mL/kg per % burn

†

As necessary to maintain urinary

output.

∗

American Burn Association: Advanced Burn Life Support Course.

†

Administered as a plasma equivalent (eg, 5% albumin in 0.9% sodium chloride solution.)

Table 35–3. Commonly used resuscitation formulas.

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observed when implementing hypertonic saline resuscitation

because increases in early acute renal failure and mortality

have been reported.

Adjuvant administration of high-dose ascorbic acid dur-

ing the first 24 hours after thermal injury has been shown to

reduce the resuscitation fluid volume required significantly

during this period in burn patients. Wound edema and body

weight gain also were decreased. Infusion of ascorbic acid has

been shown to attenuate postburn lipid peroxidation as a

known antioxidant. It is uncertain as to the exact mechanism

by which vitamin C seems to confer these benefits during

burn resuscitation. Additional study of this treatment should

be performed.

The modified Brooke formula (see Table 35–3), which is

recommended by the authors, employs a physiologic salt

solution during the first 24 hours without the addition of

colloid or electrolyte-free crystalloid solutions. Lactated

Ringer’s is the preferred solution because of its more nearly

physiologic concentration of chloride ions than normal

saline. Fluid needs are estimated as 3 mL (children) or 2 mL

(adults) per kilogram body weight per percent TBSA of lac-

tated Ringer’s solution. Children have a greater body surface

area per unit of body mass and require more resuscitation

fluid than adults. One-half the calculated estimate is admin-

istered in the first 8 hours and the second half over the sub-

sequent 16 hours postburn. If initiation of fluid resuscitation

is delayed, that amount of fluid calculated to be administered

in the first 8 hours should be infused at a rate such that half

the estimated 24-hour fluid requirement will be delivered by

8 hours postburn.

In the second 24 hours following burn injury, 5% albumin

solution in physiologic saline is administered in an amount

proportional to body weight and the extent of burn to aid in

correction of the plasma volume deficit (Table 35–4). During

the second 24 hours, lactated Ringer’s infusion is stopped,

and 5% dextrose and water is delivered to maintain adequate

urine output.

Monitoring Resuscitation

The objective of fluid resuscitation following thermal injury

is maintenance of organ perfusion and function. The ade-

quacy of resuscitation may be assessed by the hemodynamic

response, the status of mental function, indicating the ade-

quacy of cerebral perfusion, and the volume of urine output,

indicating effective renal perfusion.

Patient disorientation, anxiety, and restlessness may be

early signs of hypovolemia or hypoxemia that require imme-

diate assessment and correction. Sphygmomanometric mon-

itoring of blood pressure in patients with extensive burns can

be misleading. In a burned limb—or in an unburned

extremity in which massive edema develops—Korotkoff

sounds may be progressively attenuated, falsely implying

hypoperfusion. Blood pressure measurements, even when

obtained by use of an indwelling peripheral arterial cannula,

may not reflect true hydration status because markedly ele-

vated circulating levels of catecholamines and other vasoac-

tive materials may cause severe vasospasm. A resting

tachycardia between 100 and 120 beats/min is common fol-

lowing thermal injury. Rates above this level may reflect

inadequate pain control or inadequate fluid resuscitation. A

more objective indication of the adequacy of resuscitation is

the rate of production of urine, which reflects the adequacy

of renal perfusion. In the absence of osmotically driven

diuresis, a urinary output of 30–50 mL/h indicates adequate

resuscitation in most adult patients, and 1 mL/kg per hour

indicates adequate resuscitation in patients weighing less

than 30 kg.

Routine use of flow-directed pulmonary artery catheters

during burn resuscitation is unnecessary. Even with extensive

injury, healthy young adults usually respond to fluid resusci-

tation in a predictable manner. The previously discussed

indicators of adequacy of resuscitation may be used to guide

fluid infusion rates. Fluid infusion rates should be adjusted if

the hourly urine output is below or above the desired urinary

output by more than 33% for 2 consecutive hours. Only

patients who do not respond to fluid resuscitation as

expected—or whose fluid administration in the first 6 hours

exceeds that volume which will result in a 6 mL/kg per

percent burn resuscitation—should be monitored with a

flow-directed pulmonary artery catheter. If the pulmonary

artery occlusion pressure or measurements of right ventricu-

lar end-diastolic volume indicate an adequate intravascular

volume, this type of patient may benefit from the use of a

cardiac inotropic agent to augment cardiac output.

Occasionally, patients manifest a diminished cardiac out-

put with a markedly elevated systemic vascular resistance

when pulmonary artery wedge pressures indicate adequate

fluid resuscitation. In these patients, administration of a

short-acting afterload-reducing agent may result in a

decrease in the systemic vascular resistance and an increase

in the hourly urinary output. Administration of small doses

of hydralazine (0.5 mg/kg) has been shown to be effective

when used in this manner. In animal models of burn injury,

sodium nitroprusside and verapamil administered during

the resuscitation period reduced peripheral vascular resist-

ance and increased cardiac output. This therapy should be

administered cautiously and only to patients who have

received adequate fluid loading. If used inappropriately, the

resulting vasodilation will exacerbate the hypovolemia and

further depress cardiac output and organ perfusion.

Table 35–4. Estimation of colloid replacement during

second 24 hours postburn.

30–50% burn: 0.3 mL/kg body weight per % burn

50–70% burn: 0.4 mL/kg body weight per % burn

>70% burn: 0.5 mL/kg body weight per % burn

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Excessive fluid administration during resuscitation may

result in pulmonary edema, increased need for escharotomy,

and even the need for fasciotomy in unburned limbs.

Recently, the occurrence of intraabdominal compartment

syndrome has been recognized as a complication of excessive

fluid resuscitation. An increase in intraabdominal pressure to

greater than 25 mm Hg may impair venous return and

decrease cardiac output. This is often associated with elevated

peak and mean airway pressures and high pulmonary artery

wedge and central venous pressures. It is prudent to monitor

intraabdominal pressure routinely using an indwelling blad-

der catheter in patients with extensive burns who receive fluid

volumes of more than 25% of preburn total body weight dur-

ing the resuscitation phase. More important, strict attention

to the rate of fluid administration and reduction of excessive

resuscitation fluid volumes should be emphasized.

Continuous monitoring of arterial blood pressure with

indwelling arterial cannulas is not required in uncomplicated

burn resuscitations. In patients with inhalation injury or

those who do not respond as expected to fluid resuscitation,

frequent monitoring of arterial blood gases should be per-

formed, and a distal extremity artery should be cannulated to

decrease the risk of complications associated with repetitive

arterial puncture. Femoral arterial cannulation also has a low

complication rate and may be employed if distal arterial can-

nulation is not possible.

Other measures of perfusion such as serum lactate, base

deficit, and intramucosal pH, commonly followed during

resuscitation of various shock states, may be difficult to

interpret when used to monitor burn resuscitation. An eleva-

tion of plasma lactate concentration is observed frequently in

severely burned patients and may in part reflect increased

circulating levels of catecholamines. Glucose administration

increases the rate of glucose oxidation with a subsequent

increase in plasma lactate and pyruvate concentrations fol-

lowing thermal injury. Thus caution must be used in inter-

preting elevated serum lactate levels as related to the

adequacy of burn resuscitation and systemic oxygen delivery.

Similarly, measurement of the arterial base deficit during

burn resuscitation often will yield values as low as –6 even

though other measures of resuscitation, such as urinary out-

put, are at normal levels. This may reflect a relative deficit in

systemic oxygen delivery; however, the excessive fluid admin-

istration required to reverse the base deficit will result in

complications of overresuscitation. Measurement of gastric

intramucosal P

changes using a gastric tonometer may be

used to detect intestinal ischemia during burn resuscitation.

Patients with significant gastric acidosis have a mortality rate

twice that of patients without acidosis. The deaths in this

group were predominantly from multiple-organ dysfunction

occurring several weeks after injury. This suggests that intes-

tinal ischemia still may occur in some patients despite appar-

ently adequate fluid resuscitation after thermal injury,

inflicting persistent deleterious effects on distant organ func-

tion. Conversely, Venkatesh and colleagues have reported

depression of gastric mucosal pH in the presence of “nor-

mal” indices of systemic circulation and attributed this dis-

parity to selective GI vasoconstriction and the development

of tissue edema.

At the beginning of the second postburn day, when col-

loid replacement is initiated and infusion of lactated Ringer’s

solution is discontinued, the volume of 5% dextrose in water

infused per hour should be equal to 25–50% of the preced-

ing hour’s volume of lactated Ringer’s solution. If the urinary

output remains greater than 30 mL/h, that infusion rate

should be maintained for the next 3 hours, at which time the

rate of infusion of 5% dextrose in water should be further

reduced in a similar manner.

Pulmonary function must be reassessed continually

throughout the resuscitative phase. Tachypnea may indicate

metabolic acidosis from underresuscitation, hypoxemia, or

restriction of chest wall motion owing to circumferential

burns or massive edema. Evaluation must include ausculta-

tion, chest x-rays, and arterial blood gas analyses if a signifi-

cant tachypnea occurs. Thermally injured patients in the ICU

should be monitored with a pulse oximeter. In most patients,

hemoglobin saturation by arterial blood gas analysis matches

that obtained by pulse oximetry; however, patients with

severely burned digits may be difficult to monitor using this

method. In addition, a decrease in intensity of the pulsed sig-

nal detected in an extremity monitored by pulse oximetry

may reflect inadequate distal perfusion from underresuscita-

tion, constricting circumferential burn wounds, or arterial

spasm owing to high levels of circulating catecholamines.

Low oxygen saturation, as measured by pulse oximetry, also

may indicate circulating levels of carboxyhemoglobin or

methemoglobin as a consequence of the inhalation of carbon

monoxide or cyanide, respectively.

In thermally injured patients requiring endotracheal

intubation and mechanical ventilation, end-tidal CO

moni-

toring should be used to detect early changes in ventilation

owing to inhalation injury or restriction of chest wall

motion. This method of monitoring is particularly useful in

pressure-controlled modes of mechanical ventilation. Chest

radiographs should be obtained at least daily during resusci-

tation and the period of edema absorption. Subsequent x-

rays are ordered as clinically indicated.

Serum chemistry profiles, complete blood count, arterial

blood gases, and other baseline blood studies are obtained on

admission, with further tests depending on the clinical situa-

tion. The patient’s weight should be measured on admission

and followed daily as an indicator of fluid balance.

Evaporative water loss from the wound typically peaks on

the third postburn day and persists until the burn wound is

healed or grafted. Insensible water losses may be estimated

according to the following formula:

Insensible water loss (mL/h) = (25% + % BSA

burned) × total BSA (m

)

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734

This formula, like the initial resuscitation formulas, is

only an estimate, and replacement of evaporative water loss

should be guided by assessing the adequacy of hydration by

monitoring the patient’s weight, serum osmolality, and

serum sodium concentrations. Following elimination of the

resuscitation-related salt and water load, salt-containing flu-

ids should be administered in the amount needed to main-

tain a normal serum sodium concentration.

Goodwin CW et al: Randomized trial of efficacy of crystalloid and

colloid resuscitation on hemodynamic response and lung water

following thermal injury. Ann Surg 1983;197:520–31. [PMID:

6342554]

Gore DC et al: Influence of glucose kinetics on plasma lactate con-

centrations and energy expenditure in severely burned patients.

J Trauma Inj Infect Crit Care 2000;49:673–8.

Gunn ML et al: Prospective randomized trial of hypertonic sodium

lactate versus lactated Ringer’s solution for burn shock resusci-

tation. J Trauma 1989;29:1261–7. [PMID: 2671402]

Huang PP et al: Hypertonic sodium resuscitation is associated with

renal failure and death. Ann Surg 1995;221:543–54. [PMID:

7748036]

Ivy ME et al: Intra-abdominal hypertension and abdominal com-

partment syndrome in burn patients. J Trauma Inj Infect Crit

Care 2000;49:387–91.

Lorente JA et al: Systemic hemodynamics, gastric intramucosal

changes and outcome in critically ill burn patients. Crit

Care Med 2000;28:1728–35. [PMID: 10890610]

Onarheim H et al: Effectiveness of hypertonic saline–dextran 70

for initial fluid resuscitation of major burns. J Trauma

1990;30:597–603.

Pruitt BA Jr, Mason AD Jr, Moncrief JA: Hemodynamic changes in

the early postburn patient: The influence of fluid administra-

tion and of a vasodilator (hydralazine). J Trauma 1971;11:

36–46. [PMID: 5099912]

Pruitt BA Jr: Discussion of Caldwell FT and Bowser BH: Critical

evaluation of hypertonic and hypotonic solutions to resuscitate

severely burned children: A prospective study. Ann Surg

1979;189:551–2.

Tanaka H et al: Reduction of resuscitation fluid volumes in severely

burned patients using ascorbic acid administration: A random-

ized, prospective study. Arch Surg 2000;135:326–31. [PMID:

10722036]

Venkatesh B et al: Monitoring tissue oxygenation during resuscita-

tion of major burns. J Trauma 2001;50:485–94.



Escharotomy & Fasciotomy

Edema formation beneath the inelastic eschar of circumfer-

ential full-thickness burns of the extremities may impair the

circulation to the distal and underlying tissues. To prevent

secondary ischemic necrosis of those tissues, an escharotomy

may be necessary to reduce the elevated tissue pressure. To

identify the need for escharotomy, the adequacy of circula-

tion must be assessed at no less than hourly intervals. The

most reliable determination is made with a Doppler flowme-

ter to detect pulsatile blood flow in the palmar arch, digital

vessels in the upper limbs, and pedal vessels in the lower

limbs. Absence or progressive decrease of pulsatile flow on

sequential examination is an indication for escharotomy.

Clinical indicators of impaired extremity perfusion, includ-

ing distal cyanosis, impaired capillary refilling, neurologic

deficits, and deep tissue pain, are less precise in determining

true impairment of blood flow and should be used only as

indications for escharotomy when a Doppler flowmeter is

unavailable. Fascial compartment pressure monitoring also

has been described following thermal injury. Fascial com-

partment pressures often exceed 30 mm Hg following cir-

cumferential extremity burns, and escharotomy based on

compartment pressures has been proposed. A greater sensi-

tivity of direct compartment pressure measurements in

detecting critically low-flow states and preserving threatened

tissues has not been confirmed by direct comparison with

Doppler flowmeter assessments. This technique is associated

with a risk of infection arising in the pressure cannula tract,

but the magnitude of the risk is undefined.

The escharotomy procedure may be performed in the

ICU without the use of general or local anesthesia. Since only

insensate, full-thickness burn is incised, the use of anesthetic

agents is unnecessary. The first escharotomy incision is

placed in the midlateral line of the involved extremity. If this

does not improve distal blood flow, a second escharotomy

incision is made in the mid-medial line of that limb

(Figure 35–4). The escharotomy incision should be per-

formed along the entire length of the full-thickness burn to



Figure 35–4. The dashed lines show the preferred

sites for escharotomy incisions. The solid segments of

the lines demonstrate the importance of extending the

incisions across joints with full-thickness burns.



BURNS

735

ensure adequate release of vascular and neural compression.

The incision must cross involved joints because the relative

lack of subcutaneous tissue in these areas permits ready com-

pression of vessels and nerves. The escharotomy incision

should only penetrate the eschar and immediately subjacent

thin connective tissue to permit expansion of the edematous

subcutis. When performed at this level, loss of blood from

the escharotomy incision is minimal and readily controlled

by electrocoagulation or application of pressure. When inci-

sions are carried into the subcutaneous tissues, excessive

bleeding often occurs. The consumptive coagulopathy that

may occur in the early postburn period may contribute to

excessive blood loss when escharotomy incisions are made

too deep.

Fasciotomy is rarely required to restore circulation in a

thermally injured limb. However, in patients with high-

voltage electrical injury, fasciotomy is often necessary.

Patients with very deep burns involving fascia and muscle or

patients with associated traumatic injuries may require

fasciotomies to restore adequate limb circulation.

Escharotomies also may be required in patients with cir-

cumferential truncal burns to relieve restriction of chest wall

movement by the unyielding eschar and restore more effec-

tive ventilation. The escharotomy incision is made in the

anterior axillary line in the area of full-thickness burn. An

incision along the lower margin of the rib cage may be nec-

essary in patients with deep burns extending onto the upper

abdominal wall (see Figure 35–4). Patients may become rest-

less, agitated, and tachypneic despite having an adequate air-

way, indicating the need for chest escharotomy. In

mechanically ventilated patients, the need for escharotomy is

manifested by a progressive increase in peak inspiratory pres-

sure, decreased tidal volumes in pressure-controlled ventila-

tion, and an increase in the end-tidal CO

fraction. Once

chest escharotomy is performed, these changes promptly

revert toward normal.

Saffle JR, Zeluff GR, Warden GD: Intramuscular pressure in the

burned arm: Measurement and response to escharotomy. Am J

Surg 1980;140:825–31. [PMID: 7457708]

CARE OF THE BURN WOUND



Debridement

Only after respiratory and hemodynamic stability have been

achieved should care of the burn wound be addressed.

During transport of the patient from the accident scene or

from the initial care facility to a burn center, the burns

should be covered with clean sheets or blankets and no

attempt made to debride or dress them. In the absence of

gross contamination, burn wounds may be managed safely

without topical antimicrobial agents for the first 24–48

hours. When the patient arrives at the definitive care facility,

general anesthesia is not necessary for initial burn wound

debridement; intravenous analgesia is sufficient for pain

control during this procedure. The burns are gently cleansed

with a surgical soap solution, and nonviable epidermis is

debrided. Bullae are excised, and body hair is shaved from

the area of thermal injury beyond the margin of normal skin.

The patient is placed in a clean bed, and bulky dressings may

be placed beneath the burned parts to absorb the serous exu-

date. These dressings should be changed as they become sat-

urated. Patients should be turned frequently to prevent

maceration of burned and unburned skin.



Topical Antimicrobial Therapy

The development and clinical use of effective topical antimi-

crobial agents has decreased the incidence of invasive burn

wound infection and subsequent sepsis significantly. This has

been associated with improved survival of burn patients and

nearly eliminated invasive bacterial burn wound infection as

a cause of death. Mafenide (Sulfamylon), silver sulfadiazine

(Silvadene), and silver nitrate are the three topical antimicro-

bial agents employed most commonly for burn wound care.

Each agent has specific advantages and limitations with

which the physician must be familiar to ensure optimal ben-

efit and patient safety. Mafenide acetate and silver sulfadi-

azine are available as topical creams to be applied directly to

the burn wound. Silver nitrate is applied as a 0.5% solution

in occlusive dressings.

Mafenide burn cream is an 8.5% by weight suspension of

mafenide acetate in a water-soluble base. Mafenide is very

water-soluble and diffuses freely into the eschar. Mafenide is

the preferred agent if the patient has heavily contaminated

burn wounds or has had burn wound care delayed by several

days. Mafenide has the added advantage of being highly

effective against gram-negative organisms. The limitations of

mafenide burn cream include hypersensitivity reactions in

7% of patients, pain or discomfort of 20–30 minutes’ dura-

tion when applied to partial-thickness burns, and carbonic

anhydrase inhibition. The latter may produce an early bicar-

bonate diuresis and increase postburn hyperventilation.

This metabolic acidosis may develop into significant

acidemia if respiratory complications occur and the com-

pensatory hyperventilation is impaired. Carbonic anhydrase

inhibition rarely persists for more than 7–10 days, and the

severity of acidosis can be minimized if mafenide is applied

once per day followed by an application of silver sulfadiazine

cream 12 hours later.

Silver sulfadiazine burn cream is a 1% suspension of sil-

ver sulfadiazine in a water-miscible base. Unlike mafenide

acetate, silver sulfadiazine has limited solubility in water and

thus limited penetration into the eschar. The agent is most

effective when applied to burns immediately after injury to

minimize bacterial proliferation on the wound’s surface. This

agent has the advantage of being painless on application and

has no effect on serum electrolytes or acid-base balance.

Silver sulfadiazine burn cream may induce neutropenia,

which usually subsides after discontinuation of the agent.



CHAPTER 35

736

Hypersensitivity is uncommon and is manifested by an ery-

thematous maculopapular rash on unburned skin. The sulfa-

diazine component of silver sulfadiazine is ineffective against

certain strains of Pseudomonas and virtually all Enterobacter

species; however, the sensitivity of microorganisms coloniz-

ing burn wounds to the silver ion of this compound main-

tains its effectiveness as a topical antimicrobial agent.

Either cream is applied in an

-inch layer to the entire

burn wound in an aseptic manner following initial debride-

ment and is reapplied at 12-hour intervals to ensure contin-

uous topical chemotherapy. Once each day, all the topical

agent should be cleansed from the patient using a surgical

detergent or disinfectant solution and the wounds inspected

by the attending physician.

Silver nitrate solution (0.5%) delivered in multilayered

occlusive gauze dressings may provide an effective antimicro-

bial barrier to the burn wound surface. This agent is employed

most commonly when a history of allergy to sulfonamide

drugs is elicited or when the patient develops a hypersensitiv-

ity reaction to one of the burn creams. The dressings are

changed two or three times daily and moistened every 2 hours

to prevent evaporation from increasing the silver nitrate con-

centration to cytotoxic levels within the dressings. Transeschar

leaching of sodium, potassium, chloride, and calcium should

be anticipated and replaced appropriately. Because silver

nitrate precipitates on contact with the proteinaceous exudate

of the burn wound and does not penetrate the eschar, it is not

effective for treatment of burn wound infection or for prophy-

lactic treatment of heavily contaminated wounds. A common

use of silver nitrate is for topical antimicrobial prophylaxis in

patients with toxic epidermal necrolysis syndrome, a disorder

caused by idiosyncratic drug reactions resulting in significant

epidermal sloughing. Hypersensitivity to silver nitrate has not

been described.

Acticoat is a new burn wound dressing. It consists of a

urethane film onto which nanocrystalline elemental silver is

deposited. When moistened, application of this dressing to

the wound results in a sustained release of elemental silver,

which is bactericidal and fungicidal. The mechanism of

action is probably much like that of silver nitrate dressings;

however, Acticoat does not cause transeschar leaching of

electrolytes. The silver does not penetrate the eschar, limiting

its use on infected or heavily contaminated wounds.

Transient mild pain may be noted occasionally after applica-

tion. The use of Acticoat is currently limited to partial-thick-

ness burns.

Aquacel Ag hydrofiber (ConvaTec, a Bristol-Myers Squibb

Company, Skillman, NJ) is another dressing containing ele-

mental silver, although at a much lower concentration. When

compared with silver sulfadiazine on partial-thickness burns,

this dressing was associated with an increased rate of reep-

ithelization and was a slightly more cost-effective. This study

was limited owing to sample size; however, the replacement

of burn cream pharmaceuticals with silver-containing bar-

rier dressings is occurring in certain settings, namely, those

of superficial burns.

All these agents are effective in the prevention of inva-

sive burn wound infection. However, because of their lack

of eschar penetration, silver nitrate soaks and silver sulfa-

diazine burn cream are most effective in the treatment of

full-thickness burns when applied immediately following

burn injury.



Burn Wound Infection (See Figure 35–5)

ESSENTIALS OF DIAGNOSIS



Hypo- or hyperthermia.



Tachycardia and tachypnea.



Glucose intolerance.



Disorientation.



Ileus.



Change in appearance of the burn wound.

General Considerations

Inherent characteristics of the microorganisms and the burn

wound they colonize influence the rate of microbial penetra-

tion of and proliferation in the eschar. The moist, protein-

rich, avascular eschar serves as an excellent culture medium

from which white blood cells and systemically administered

antibiotics are excluded. The density of bacterial coloniza-

tion of the eschar influences the likelihood of burn wound

infection. Bacterial invasion is uncommon unless the num-

ber of microorganisms exceeds 10

per gram of tissue.

Bacterial strain–specific factors such as enzyme production



Figure 35–5. The frequency of infection by site

expressed as a percentage of all infections complicating

thermal injury.