Professional Documents
Culture Documents
Anes Mnge Burn 1212 p430 439 PDF
Anes Mnge Burn 1212 p430 439 PDF
Burn Injury
Burn injury is a leading cause of life-threatening trauma because of dramatic pathophysiologic changes that
worldwide, affecting more than 450,000 Americans compromise hemodynamic stability and alter patient
each year, and is associated with an average mortality response to many anesthetic agents.
rate of 0.8%. Patients with an increased risk of death The following article reviews the literature related
from burn injuries include elderly patients and patients to the pathophysiology and clinical management of
with large burns or inhalation injury. Providing optimal major burn injuries and highlights the key concepts
care for patients with major burn injuries requires the relevant to the delivery of safe and efficacious anes-
coordinated effort of multidisciplinary teams in which thesia for these patients.
anesthesia providers play a critical role. Anesthetic
management for burn surgery can be technically chal-
lenging because of difficult airway management and Keywords: Burn management, burn shock, burn sur-
vascular access, as well as cognitively demanding gery, inhalation injury, major burn surgery.
B
urns are among the most devastating injuries derangements due to massive destruction of tissues that
encountered in medicine and are a leading affect virtually all organ systems and alter patient re-
cause of life-threatening trauma worldwide.1,2 sponse to anesthetic agents. Providing safe and effective
According to the Centers for Disease Control anesthesia for burn surgery requires a fundamental un-
and Prevention, someone in the United States derstanding of the pathophysiological consequences of
dies in a fire every 175 minutes and is injured every 31 major burn injury as well as a familiarity with aspects of
minutes.3 Groups with an increased risk for fire-related assessment, resuscitation, and pharmacotherapy that are
injury and death include children under 5 and adults unique to this patient population.
more than 65 years of age, poorer Americans, and those
living in rural areas or in substandard housing. Pathophysiology of Major Burn Injury: A
The American Burn Association estimates that more Brief Review for Anesthesia Providers
than 450,000 burn-injured patients seek medical treat- Burn Injury. Major burns cause massive tissue de-
ment in the United States each year, resulting in 45,000 struction and activation of an inflammatory response that
hospitalizations and 4,000 deaths.4,5 The risk of death leads to dramatic systemwide physiologic derangements.12
from burn injury increases with advancing age, increas- Burn injury pathophysiology evolves in 2 distinct phases,
ing burn size, and the presence of inhalation injury. Up a burn shock phase followed by a hypermetabolic phase,
to 30% of burn injuries sustained each year are consid- both of which have an impact on anesthetic management
ered major burn injuries, characterized by burns to over by altering patient hemodynamics (Table 3).8-11
20% of total body surface area (TBSA) in adults, more Acute burn injury results in an area of necrosis sur-
than 10% TBSA in children and elderly patients, or full- rounded by ischemic tissues that may potentially become
thickness burns to >5% TBSA (Tables 1 and 2).5-8 Burns viable if adequate perfusion is restored.12 Within minutes
involving the face, airway, or genitalia are also classified to hours of injury, burned tissues release inflammatory
as major burn injuries regardless of the percentage of and vasoactive mediators including histamine, prosta-
TBSA affected.6 glandins, kinins, thromboxane, and nitric oxide that
Dramatic improvement in patient outcomes over the increase capillary permeability and cause localized burn
past 3 decades has been attributed to advancements in wound edema.12,13 Subsequent reperfusion of ischemic
the understanding of major burn injury pathophysiol- tissues produces reactive oxygen species, toxic cell me-
ogy, improved burn shock management, early aggressive tabolites that cause further cellular membrane dysfunc-
surgical intervention, and the development of specialized tion and propagation of the immune response.
burn treatment centers.8,9 Yet providing optimal care to Burn Shock. In addition to the local effects of burn
patients with major burn injuries remains challenging.8-11 injury, major burns cause the release of circulating me-
Anesthetic management is complicated by physiologic diators such as tumor necrosis factor and interleukins
that result in a systemic inflammatory response syn- sion ensues. Failure to adequately replace intravascular
drome.12-14 Within 6 to 8 hours of injury, increased mi- volume can lead to significant organ injury from systemic
crovascular permeability, vasodilatation, vascular stasis, inflammatory responses and multiorgan dysfunction. In
decreased cardiac contractility, and reduced cardiac the event that fluid resuscitation is successful, a pro-
output result in massive edema formation in both injured nounced hypermetabolic response develops over several
and noninjured tissues. A massive leak of fluid and elec- days to weeks.13-16
trolytes from the intravascular space into the interstitial Hypermetabolic Phase. The hypermetabolic response
space, combined with fluid losses through drainage and to burns is more severe and sustained than any other
evaporation from burn wounds, further impairs tissue form of trauma.15 A massive surge in catecholamines and
perfusion. Rapid and effective intravascular volume re- corticosteroids, 10 to 50 times greater than nonburned
placement is critical to the prevention of burn shock, a plasma levels, drives the hypermetabolic response causing
combination of distributive, hypovolemic, and cardio- increased myocardial oxygen consumption and cardiac
genic shock, in which plasma volume is insufficient to work. Persistent tachycardia, systemic hypertension, in-
maintain preload or cardiac output and tissue hypoperfu- creased muscle protein degradation, insulin resistance,
Table 3. Pathophysiologic Changes During Early and Late Phases of Major Burn Injury
Abbreviations: , decreased; , increased; SVR, systemic vascular resistance; HTN, hypertension.
(Adapted from MacLennon et al8 and Fuzaylov and Fidkowski.11)
elevated core temperature, and liver dysfunction are char- monary status, and the distribution and severity of burn
acteristic of this hyperdynamic phase of burn injury.15,16 wounds.9 The patients current physiologic status should
Cardiac output and heart rate increase up to 150% above be thoroughly evaluated by considering vasopressor re-
nonburned patient values and may remain elevated for up quirements, ventilator settings, pulmonary compliance,
to 2 years postburn.15 Hyperventilation occurs during the adequacy of resuscitation (ie, volume status and urine
hypermetabolic phase and persists until wound closure. output), and derangements in laboratory study values,
Elevated metabolic rates also compensate for the large particularly acid-base disturbances. Table 4 provides a suc-
amounts of heat and water (up to 4,000 mL per m2 burn cinct list of preoperative concerns to guide the preopera-
area per day) lost through disrupted tissues.15 Proteins tive evaluation of patients with major burn injuries.
and amino acids are mobilized to meet immense metabol- Burn wound severity is quantified according to TBSA
ic demands and energy requirements, resulting in signifi- burned (see Table 1) and wound depth (see Table 2) and
cant loss of lean body mass that further impairs immune is used in the initial management period to direct fluid re-
function and wound healing.15-17 suscitation and surgical intervention.6 The TBSA burned is
The severity of the hyperdynamic, hypercatabolic typically estimated by head-to-toe visualization of wounds
response is related to TBSA burned and the duration of and subsequent calculation according to the rule-of-nines
time patients are exposed to elevated levels of catechol- method for adults (Figure 1) and the Lund-Browder age/
amines and stress hormones.17 Left untreated, hyperme- growth-adjusted chart for children (Figure 2).18
tabolism leads to physiologic exhaustion and death.15 Airway Assessment. Immediate airway assessment
Strategies used to ameliorate the hypermetabolic re- is always the first priority because of the potential for
sponse include early surgical intervention, maintenance massive airway edema that can result in acute obstruc-
of a warm environment, nutritional support to replenish tion and death.19 The key features of airway assessment
catabolic losses, and pharmacological agents such as in major burn injury patients include preexisting airway
insulin and b-antagonists.15-17 Early excision and grafting abnormality, current airway injury (ie, inhalation injury),
of burn eschar attenuates the hypermetabolic response by and signs of airway obstruction. Inhalation injury is the
preventing further net protein loss, catabolism, and the most frequent cause of death in burn patients in the
development of sepsis.17 Warming the environment to a United States, occurring in 10% to 25% of burn injured
neutral temperature (28-33C) has been shown to reduce patients and increasing mortality by up to 25%.5 Clinical
the magnitude of the hypermetabolic response.15-17 manifestations of an inhalation injury may be delayed up
to several hours postexposure, but a history of entrap-
Anesthesia for Burn Surgery ment in a closed space, facial burns, symptoms of respira-
Preoperative assessment of patients with major burn inju- tory distress, and the presence of carbonaceous sputum
ries should include routine features of preoperative evalu- increase the likelihood that an inhalation injury has oc-
ation with particular attention to airway management, pul- curred.19,20 Because of the significant impact that inhala-
of renal clearance. During the subsequent hypermeta- down-regulation of receptor affinity.10 Because ketamine
bolic phase, high blood flow to the liver and kidneys, increases cerebral blood flow and systemic blood pres-
decreased plasma albumin, and an increased level of -1- sure, it should be avoided in patients with closed head or
acid-glycoprotein result in altered protein binding and penetrating eye injuries. Unpleasant emergence delirium
increased renal clearance. Anesthetic requirements are associated with ketamine may be mitigated by adminis-
generally increased including minimum alveolar concen- tration of benzodiazepines or dexmetetomidine.10,33
tration for volatile anesthetics, and the duration of action Intubation. All patients with face, neck, and upper
is decreased requiring frequent redosing of agents. chest burns are considered potential difficult airways
Induction. Balanced general anesthesia consisting of due to facial and airway edema that may distort the
an opioid, muscle relaxant, and volatile agent is the most normal anatomy and/or limit neck and mandibular mo-
common anesthetic technique used for burn excision and bility.8-11,21 Mask ventilation after anesthetic induction
grafting.8,10 Propofol and thiopental have been used suc- may be challenging and intubation by direct laryngos-
cessfully for induction, though they should be carefully ti- copy may be virtually impossible. Fiberoptic intubation
trated to minimize dose dependent cardiac and respiratory in the awake and spontaneously breathing adult patient
depression.10,11 Etomidate is an effective induction agent may be the safest and most efficacious option for patients
because of its stable hemodynamic profile and is consid- with a suspected difficult airway and can be facilitated
ered a good choice for burned patients who may not toler- with topical anesthesia and sedation.21 Pediatric patients
ate changes in heart rate or cardiac output. However, the require deep sedation for fiberoptic intubation, which
use of etomidate in septic patients is controversial because can be facilitated by inhalation induction with a volatile
of adrenocorticol supression following a single bolus dose anesthetic or intravenous ketamine, 1 to 2 mg/kg.11
and likewise may not be the best choice of induction agent Cuffed endotracheal tubes (ETTs) are the standard of
for immunocompromised burn patients.32 care for burn-injured adults and recent evidence suggests
Ketamine offers many advantages for induction and they may also be advantageous in infants and children
maintenance of anesthesia for burn-injured patients and undergoing burn surgery.11,35 In a recent retrospective
is routinely used for burn-related procedures.8,10,11,33 review of pediatric patient outcomes following intubation
Ketamine may be particularly useful for the induction for burn surgery at a Washington burn center, Dorsey et
of hypovolemic patients due to sympathomimetic effects al35 found modern low-pressure, high-volume cuffed ETTs
that cause dose-dependent increases in arterial blood were not associated with increased incidence of postextu-
pressure and heart rate.34 Increased systemic vascular bation stridor but were instead associated with reduced
resistance may be advantageous during burn surgery, as it rates of clinically significant air leak and immediate reintu-
reduces heat and blood loss from burned skin compared bation when compared with uncuffed ETTs. Cuffed ETTs
with vasodilation caused by virtually all other anesthetic may be particularly useful in pediatric patients with major
agents. Ketamine offers additional benefits of airway burn injuries who require high ventilatory pressures due
reflex preservation, dissociative anesthesia, and potent to decreased lung compliance associated with inhalation
analgesia. Minimal increases in heart rate observed after injury and/or large volume fluid resuscitation.
ketamine is administered to hypermetabolic patients may Maintenance. Volatile anesthetics are routinely
result from preexisting elevated levels of catecholamines used during maintenance of adult patients and for
that result in a decrease in the number of receptors and a induction and maintenance of pediatric patients.8-11