Avances Anestesia 2013

Advances in Anesthesia 31 (2013) 137–161
ADVANCES IN ANESTHESIA
Advances in Perioperative and Critical

Care of the Burn Patient
Anesthesia Management of Major Thermal Burn
Injuries in Adults
Heather E. Kaiser, MD, MPHa,*, Cindy Meerim Kim, MDb,

Sam R. Sharar, MDc, Hernando P. Olivar, MDc
a
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Hospital, 1800
Orleans Street, Bloomberg Children’s Center Room 6220, Baltimore, MD 21287, USA; bDepart-
ment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, 55 Fruit
Street, Gray-Bigelow 444, Boston, MA 02114-2696, USA; cDepartment of Anesthesiology & Pain
Medicine, Harborview Medical Center, University of Washington, 325 9th Avenue, Box 359724,
Seattle, WA 98104, USA
Keywords
Burn injury Trauma anesthesia Smoke-inhalation injury
Pathophysiology of burn injury Anesthetic management of burns
Key points
Patients with burn injury can and will present to any hospital.
Many of those hospitalized for burn injury will require surgical treatment of their
injuries.
Patients undergoing surgical treatment for major thermal burn injury often exhibit
preexisting medical issues and/or burn-related pathophysiology that must be
considered in the anesthetic plan.
Performing a focused preoperative assessment of a patient with burn injury is
paramount, particularly with respect to airway abnormalities, gas exchange,
and hemodynamic status.
Smoke-inhalation injury largely influences the clinical course of patients with
major burn injury.
Recognizing and managing intraoperative blood loss and volume replacement is
critical.
Continued
No financial disclosures or conflict of interest are declared by any author.
*Corresponding author. E-mail address: hkaiser6@jhmi.edu
0737-6146/13/$ – see front matter

http://dx.doi.org/10.1016/j.aan.2013.08.007 Ó 2013 Elsevier Inc. All rights reserved.
138 KAISER, KIM, SHARAR, ET AL
Continued
Postoperative management of pain is challenging and must be anticipated during
the intraoperative period.
Further research into both smoke-inhalation injury and major burn injury is
necessary to improve perioperative management by anesthesiologists and other
medical providers.
INTRODUCTION
In 2012 approximately 450,000 people with burn injury sought medical treat-
ment in the United States [1]. Of these, 40,000 people required hospitalization
and, presumably, many of these patients underwent surgical treatment of their
injuries [1]. Given the high incidence of burn injury managed at both desig-
nated burn centers and other hospitals, the authors have sought to review
the literature on major thermal burn injury as it pertains to anesthesia manage-
ment. Information in this article may be extrapolated to include adult patients
with a lesser severity of burn classification.
PREOPERATIVE PERIOD
The early treatment of patients with burn injury begins at the injury scene and
continues on arrival to the emergency department with a complete trauma
assessment based on the Advanced Trauma Life Support (ATLS) guidelines
[2]. Once life-threatening ATLS priorities have been addressed, a secondary
survey of the burn injuries should ensue. After hospital admission, burn-
injured patients can undergo a wide range of surgical procedures at various
phases of the burn care continuum, including the postdischarge rehabilitation
phase. Unique physiologic conditions at these various phases of burn care pre-
sent a variety of anesthetic challenges and require comprehensive preanesthetic
assessment.
Patient history and physical assessment

Burn injury is classified by the percentage of total body surface area (TBSA)
burned based on the Lund-Browder chart, the depth of the burn, and
whether an inhalation injury has occurred (Box 1, Fig. 1) [2,3]. As defined
by the American Burn Association (ABA), major burn injury is a partial-
thickness burn greater than 25% TBSA in adults or greater than 20%
TBSA in children younger than 10 years or adults older than 40 years [4].
Major burn injury is also defined as full-thickness burns involving more
than 10% TBSA [4]. Major burn injuries also occur when the patient has
sustained a high-voltage burn; a known smoke-inhalation injury; burns to
the face, eyes, ears, hands, feet, or perineum that are likely to result in func-
tion or cosmetic impairment; or concomitant traumatic injury [4]. Specific
criteria for referral to a designated burn center are given by the American
Burn Association [5].
ANESTHESIA MANAGEMENT OF BURN PATIENTS 139
Box 1: Depth of burn injury

First-degree burn
Superficial burns
Limited to the epidermis
Erythema and swelling
Second-degree burn
Partial-thickness burns
Involves the epidermis and dermis
Blister formation
Third-degree burn
Appears white or poorly vascularized
Full-thickness burns
Involves epidermis, dermis, and subcutaneous tissue
Appears dry and leathery
Fourth-degree burn
Full-thickness burns extending to muscle and bone
Airway and pulmonary system

Airway and ventilatory management of patients with burn injury is of utmost
importance. Indications for immediate tracheal intubation of burn-injured pa-
tients are listed in Box 2. Whether or not intubation occurs immediately after
injury, frequent reevaluation of the airway and respiratory status is critical
because of the dynamic evolution of maximal airway edema and complications
that may develop as a result of superimposed smoke inhalation. Both of these
situations may impair ventilation and oxygenation [6].
Airway obstruction and symptoms of smoke-inhalation injury may not yet
be evident on initial assessment; however, they can occur on a rapid and
unpredictable time course after the initial injury [7,8]. Impending airway
obstruction frequently occurs in the presence of moderate to severe facial
burns, full-thickness nasolabial burns, or oropharyngeal burns. Stridor, hoarse-
ness, and dysphagia are classic signs of impending airway obstruction [3].
Owing to the likelihood of worsening airway edema in the 24 hours after
injury, the clinical axiom is to have a low threshold for early tracheal intuba-
tion, before increasing edema of upper airway structures makes the procedure
more difficult.
Smoke-inhalation injury has a direct impact on the anesthetic management of
burn-injured patients. Smoke inhalation is suspected if the injury has been
sustained from fire in a closed space. Singeing of facial or nasal hair, evidence
of oropharyngeal carbonaceous deposits, and carboxyhemoglobin (COHb)
levels greater than 10% are highly predictive of subsequent positive broncho-
scopic confirmation of inhalation injury [9]. In studies comparing isolated
Fig. 1. The Lund-Browder chart classifies burn injury by the percentage of total body surface
area.
burn injury with burn injury with concomitant smoke inhalation, the latter
combination is associated with increased fluid-resuscitation requirements, pul-
monary complications, and mortality [10–13]. Moreover, in one study the inci-
dence of respiratory failure increased from 5% to 73% in burn-injured patients
with concomitant smoke inhalation injury [14]. Thus, inhalation injury signifi-
cantly influences the clinical course of patients with major burn injury.
Box 2: Indications for immediate tracheal intubation of patients

with major burn injury
Total body surface area burns of greater than 40%
Signs of impending airway obstruction
Evidence of smoke-inhalation injury
Prolonged transport time
Data from Dunham CM, Barraco RD, Clark DE, et al. Guidelines for emergency tracheal intuba-
tion immediately after traumatic injury. J Trauma 2003;55(1):162–79.
Furthermore, mortality rates of patients with smoke inhalation injury have

largely remained unchanged in the past 20 years in the United States [15]. Smoke
inhalation may cause injury by 3 different mechanisms: direct thermal injury,
chemical irritation/inflammation, and systemic toxicity [7]. Upper airway injury
is typically caused by direct thermal insult, whereas tracheobronchial injury is
usually caused by inflammatory responses to chemicals in smoke [7]. The inflam-
matory process may induce bronchospasm, impairment of ciliary function, distal
airway obstruction from viscous secretions, and atelectasis [7,8,16]. Increases in
transvascular fluid flux and bronchial blood flow may promote edema in the
tracheobronchial system [7,17]. Smoke-induced bronchial epithelial necrosis re-
sults in a profuse transudate that can consolidate over time and cause obstruction
of the lower airways [7]. These pathophysiologic changes cause hypoventilation
and loss of hypoxic pulmonary vasoconstriction, with increased pulmonary
shunting and ventilation-perfusion mismatch (Fig. 2) [7,8].
Systemic effects of carbon monoxide (CO) and cyanide toxicity are frequent
complications of smoke inhalation. CO has 250 times more affinity for hemo-
globin than oxygen, forming COHb and reduced hemoglobin oxygen-carrying
capacity, while simultaneously shifting the oxygen dissociation curve to the left
[3]. Symptoms of CO toxicity include headache, nausea, and confusion [8].
Severe neurologic dysfunction and coma may occur with COHb levels greater
Fig. 2. Pathophysiologic response to smoke inhalation.

than 40% [18]. Cardiac dysrhythmias and brain injury may become prominent
at levels greater than 55% [18]. A COHb level greater than 90% may lead to
immediate cardiac arrest (Fig. 3) [7]. In the presence of COHb, conventional
pulse oximeters are inaccurate and provide falsely elevated oxygen saturation
readings. Thus, a CO-oximeter is necessary to obtain accurate measurements
of arterial oxygen saturation [3].
Cyanide toxicity interferes with the intracellular cytochrome cascade, and
disrupts mitochondrial oxygen consumption and aerobic energy production,
resulting in lactic acidosis. At a cyanide concentration of 50 parts per million
(ppm), the patients may present with headache, dizziness, tachycardia, and
tachypnea [19]. Above 100 ppm, lethargy, seizures, and respiratory failure
may ensue [19]. An anion gap metabolic acidosis that fails to improve with
oxygen administration should be concerning for cyanide toxicity [3]. Plasma
lactate levels will correlate with cyanide levels and mixed venous oxygen satu-
ration will appear elevated [3].
In addition to direct inhalation injury, the burn-induced systemic inflamma-
tory process can lead to pulmonary hypertension and disruption of the pul-
monary vascular endothelial barrier. In combination with burn-induced
hypoproteinemia and decreased plasma oncotic pressure, this increases extravas-
cular lung water and impairs gas exchange [3,6]. Moreover, decreased lung and
chest-wall compliance may develop in the first 24 to 36 hours after the burn
injury, particularly in patients with circumferential thorax burns that create a
restrictive lung defect (and may necessitate emergent escharotomy) [3,6].
Cardiovascular system
Important cardiovascular changes occur in the presence of major burn injury.
Patients with major burn injury are initially hypovolemic, owing to extensive
Fig. 3. Effects of carbon monoxide toxicity.

plasma loss into burned tissues and increased systemic vascular permeability
[20,21]; thus, fluid resuscitation is one of the pillars of treatment of this patient
population [22,23]. Baxter and Shires [24] developed the well-known Parkland
Formula (PF) for initial postburn fluid resuscitation with isotonic crystalloid
based on body weight and burn size (4 mL/kg/%TBSA burn). One-half of
the calculated volume should be infused during the first 8 hours, followed
by one-half in the subsequent 16 hours. After this initial crystalloid resuscita-
tion, the PF recommends maintenance volumes of isotonic crystalloid and
the addition of colloid boluses in the second 24 hours, as needed, to meet treat-
ment end points such as urine output of at least 0.5 to 1 mL/kg/h.
However, studies addressing hemodynamic monitoring have suggested
that urine output, blood pressure, heart rate, and laboratory examination
may provide insufficient information to guide adequate resuscitation in
patients with major burns [3,25–27]. Although the best end points of resusci-
tation in major burn injury have not been conclusively determined, the
current recommendation is that urinary output be maintained between
30 mL/h and 50 mL/h, or 0.5 mL/kg/h [26,28]. In 2001, the ABA introduced
a guideline that invasive hemodynamic monitoring should be restricted to
patients with burn injury who have refractory shock or limited cardiopulmo-
nary reserve [2].
Growing evidence suggests that burn patients often receive far more fluid-
resuscitation volumes than calculated by the PF [29–32]. This phenomenon
of resuscitation volume that exceeds the PF has been termed fluid creep [33].
Fluid creep is associated with complications such as pulmonary edema and
abdominal compartment syndrome. Thus, although providers frequently use
the PF for burn resuscitation, alternative resuscitation formulas and adjunctive
techniques (eg, hemofiltration) are emerging, which are described elsewhere in
detail [34–36].
In addition to hypovolemia caused by increased permeability of the microcir-
culation [3,27,28], the first 24 to 48 hours after burn injury are characterized by a
reduced cardiac output as low as 60% of the normal resting value [6]. This reduc-
tion in the cardiac output has been attributed to systemic humoral factors, dimi-
nution in catecholamine response, and decreased contractility from reduced
coronary blood flow [3]. Concomitantly, systemic vascular resistance increases.
After 48 hours the recovery phase commences, and cardiovascular changes
evolve into a hyperdynamic state with increased cardiac output, tachycardia,
and decreased systemic vascular resistance, all of which must be accounted for
during subsequent intraoperative anesthetic management, because operative
burn care typically occurs during this phase.
INTRAOPERATIVE PERIOD
Airway management
If the patient is not already tracheally intubated before arrival in the operating
room, the method for tracheal intubation should be determined according to
clinical judgment. Patients with major burn injuries frequently present to the
operating room with a combination of respiratory and anatomic characteristics

that accentuate the risk for hypoxemia during induction and tracheal intuba-
tion. These characteristics vary depending on the stage of the burn injury.
During the acute postinjury phase oxygen demand is elevated, and generalized
edema involving the face and upper airway is often present. During the recov-
ery and reconstructive phases, postburn face and neck contractures represent
the most common challenges during airway management.
In patients with burns to the face, the presence of burn dressings can make
bag-mask ventilation challenging because of difficulty in achieving a good seal
around the mask, such that 2-person mask ventilation may be needed. If this
proves to be ineffective, removal of the dressings is imperative. Neck mobility
and mouth opening may be impaired by pain, edema, and burn injuries, and in
later stages of care by wound contractures. Thus, one key assessment that the
anesthesiologist should make before managing the airway of a burn victim is to
determine the patency and soft-tissue compliance of the airway. Palpation of
the neck and submandibular space may reveal tightness that will limit displace-
ment of the tongue and soft tissues into the submandibular area, making laryn-
goscopy challenging. Both tongue edema and pharyngeal edema are frequent
findings in patients with major burns. A tongue depressor or laryngoscope
can be helpful in assessing tongue mobility and in visualizing the pharynx. If
patency of the hypopharynx is in question, a flexible fiberoptic scope can be
gently advanced to assess the epiglottis and surrounding tissues.
If the preoperative examination reveals concern for upper airway patency,
mobility, or mask ventilation, and the patient is cooperative, an awake fiberoptic
tracheal intubation is warranted. If the patient is uncooperative, a gentle intrave-
nous or inhalational induction preserving spontaneous ventilation (with or
without bag-mask assistance) may permit the advancement of the fiberoptic
scope. If the examination reveals less concerning airway anatomy, a gentle post-
induction test of mask ventilation is nonetheless indicated before injection of a
neuromuscular blocker. In these scenarios, a video laryngoscope can also be
used not only as an intubating tool but also as a diagnostic tool, permitting assess-
ment of hypopharyngeal and glottic anatomy. A potential algorithm that sum-
marizes these issues is shown in Fig. 4.
For patients with fresh facial burns or those undergoing debridement and
skin grafting in the region of the nasal or oral cavity, securing the endotracheal
tube or supraglottic device with adhesive tape may not prove feasible or ideal.
Placement of a nasogastric tube through the nostril into the oropharynx and
retrieved from the mouth can form a taut loop around the hard palate, to
which an oral endotracheal tube can be secured [37]. Other techniques to
secure endotracheal tubes in patients with facial burns include attachment
with interdental wires or a surgical suture to the teeth [38,39], and use of cir-
cummandibular, transcartilagenous septal, or nasomaxillary sutures [40,41].
After securing the endotracheal tube, suspending the ventilatory circuit from
the ceiling maintains a sterile field and provides adequate surgical exposure
for facial debridement.
Fig. 4. Recommended algorithm for airway management of burn patients.
Tracheostomy
Severely burned patients may require tracheostomies for long-term mechanical
ventilation because of the potential complications of prolonged endotracheal
tube placement [42,43]. In a retrospective review by Aggarwal and colleagues
[43], the indications for early tracheostomy (defined as <10 days after admission)
included the presence of facial burns or injuries, and expected prolonged
mechanical ventilation as determined by factors such as presence of inhalation
injury, advanced age, chronic pulmonary disease, other significant comorbid-
ities, and large burn size. The indications for tracheostomy placement more
than 10 days after admission included failure to wean, failed extubation, or ex-
pected prolonged mechanical ventilation (Box 3) [43]. A randomized controlled
trial by Saffle and colleagues [44], by contrast, showed that early tracheostomy
does not improve outcome in burn patients. Regardless, the decision to place a
tracheostomy should involve weighing the benefits of placement based on clin-
ical judgment with the risks of long-term morbidity including tracheal stenosis
and tracheoesophageal fistula, which has been found to occur in nearly one-
third of patients requiring tracheostomy [45].
Ventilation strategies
Intraoperative ventilation of patients with burns and/or inhalation injury can be
difficult because of increased airway reactivity, retained secretions, acute lung
injury, and adult respiratory distress syndrome (ARDS), with the latter occur-
ring in as many as 54% of mechanically ventilated patients with burn injury
[7,46]. Both hyperinflation and collapse of aerated lung regions have been
proposed to cause barotrauma by overextension and shearing forces, respec-
tively [47]. Conventional mechanical ventilation involves maintaining airway
plateau pressure at lower than 35 cm H2O while using sufficient positive
Box 3: Indications for tracheostomy

Presence of facial burns or injuries
Expected prolonged mechanical ventilation
Inhalational injury
Advanced age
Chronic pulmonary disease
Significant comorbidities
Large burn size
Indications for tracheotomy placement more than 10 days after admission
Failure to wean
Failed extubation
Expected prolonged mechanical ventilation
end-expiratory pressure to maintain alveolar and airway patency [47]. At pre-

sent, standard of care utilizes low tidal volume ventilation with associated
permissive hypercapnia as described by the ARDS Network Study [48], despite
this study having excluded patients with burns of more than 30% TBSA [7]. In
severe cases, special ventilatory strategies can be implemented to provide
adequate oxygenation and ventilation, while preventing further respiratory
compromise resulting from barotrauma caused by increased alveolar distention
and shearing forces [47,48].
Bronchospasm is frequently present in burn-injured patients, and aggressive
bronchodilator therapy with b2-agonists is warranted. Albuterol has been asso-
ciated with improvement in the PaO2/FiO2 ratio (ratio of partial pressure of arte-
rial oxygen and fraction of inspired oxygen) and a reduction in pulmonary
edema, pulmonary vascular permeability, and airway pressures [49,50].
Another useful strategy to prevent respiratory dysfunction during the intrao-
perative period is to minimize retained secretions and cellular debris by atten-
tion to body positioning and frequent suctioning [47].
As mentioned earlier, the fluid-creep phenomenon associated with burn
resuscitation can put severely burned patients at risk for intra-abdominal
hypertension [51]. Intra-abdominal hypertension and abdominal compartment
syndrome alter respiratory mechanics (restrictive lung defect) and prevent
adequate ventilation [52,53]. Additional restrictive lung defects can be imposed
if the patient is positioned prone for surgical debridement of posterior body
burns or donor skin harvesting. Thus, measurement of intra-abdominal pressure
(eg, transducing urinary catheter) can help guide safe prone positioning in such
patients.
Monitoring
Standard intraoperative monitoring is often challenging in patients with major
burn injury (Table 1). Electrocardiogram adhesive lead placement may be
Table 1
Intraoperative monitoring challenges in patients with major burn injury
Possible challenges
Monitor of burn injury Possible solutions
Electrocardiography (ECG) ECG electrodes may not Consider needle electrodes
adhere or stapling of electrodes
Noninvasive blood Edema or extensive burns in Consider alternative location,
pressure monitor the extremities may limit use dressing or gauze
use of cuff under cuff
Consider invasive monitoring
Invasive blood Hypothermia, hypovolemia, Consider alternative location,
pressure monitor initial decreased cardiac trend values, confirm with
output, vasoconstriction noninvasive blood pressure
Pulse oximetry Extensive burn injury may Consider alternative location,
limit placement trend values, assess partial
Carboxyhemoglobin will pressure of oxygen by
falsely elevate oxygen arterial blood gas
saturation reading
problematic in those with extensive burns, particularly on the torso and upper
extremities. Needle electrodes or surgically stapling the electrodes may be
necessary [3]. Significant edema or widespread extremity burns may preclude
placement of noninvasive blood pressure cuffs, and peripheral vasospasm dur-
ing a high catecholamine state may alter arterial-line pressure waveforms [28].
Similarly, pulse oximetry may be unreliable in clinical scenarios of hypother-
mia, hypovolemia, and the early postburn stage of decreased cardiac output
and vasoconstriction [54]. In combination with limited anatomic locations to
apply the pulse oximeter probe in patients with extensive extremity burns,
this can make monitoring of arterial oxygen saturation challenging. Moreover,
conventional pulse oximetry is inaccurate (ie, falsely elevated readings) in the
presence of COHb, as already noted.
A review by Lavrentieva and Palmieri [25] examined arterial pressure wave-
form analysis techniques in burn-injured patients. Although arterial pressure
waveform analysis did not affect outcomes in critically ill patients with burn in-
juries, the technique is less invasive and less costly than pulmonary artery cath-
eter placement, and may play a valuable role in these patients. However, no
large, prospective randomized trials have assessed this technique to validate
the findings of these smaller studies.
Esophageal echo-Doppler is also a potential choice for short-term hemody-
namic monitoring in burn-injured patients [26]. Monitoring of myocardial
contractility trends may provide better insight into resuscitation adequacy than
either fluid status or preload, based on reports that the early hypodynamic stage
of burn injury may be, in larger part, due to myocardial depression rather than
hypovolemia [26]. Indeed, underresuscitation and compromised cardiac perfor-
mance both contribute to hemodynamic instability immediately following burn
injury [55]. Similarly, a retrospective review by Etherington and colleagues [55]
of transesophageal echocardiography (TEE) at a regional burn center over a 5-

year period reported that TEE was used most commonly to determine the cause
of unexplained hypotension. TEE was found to provide valuable real-time infor-
mation regarding ventricular filling, contractility, and valvular competence, with
no attendant major complications. However, no randomized controlled trials
exist to assess the utility of echocardiography in determining end points of resus-
citation in the management of burn-injured patients.
Intraoperative maintenance of body temperature is critical, yet challenging,
in patients with major burns, who can lose up to 1 C every 15 minutes if
proper warming techniques are not used. Heat loss results from a combination
of increased vascular permeability with fluid extravasation, loss of heat at
the site of burn injury, and generous administration of intravenous fluid
[56]. Basal metabolic rate in burned patients is significantly elevated and
increases further in proportion to burn size as ambient temperature decreases
[57]. Many detrimental perioperative complications are associated with hypo-
thermia; specific to burn injury, however, decreased body temperature during
burn excisions may increase blood loss and worsen morbidity and mortality
[56]. For example, a decrease in intraoperative body temperature as small as
1 C in patients undergoing burn excision is associated with a significant in-
crease in postoperative acute lung injury [56]. Therefore, efforts to minimize
intraoperative heat loss should include increasing the temperature in the oper-
ating room to higher than 25 C, using convective warming devices and
warmed intravenous fluids, minimizing skin surface exposure, and encircling
nonoperative extremities in impervious plastic wrap to prevent evaporative
heat loss.
Pharmacology
Major burn injury can lead to changes in medication pharmacokinetics and
pharmacodynamics that may vary depending on the burn severity and the
time elapsed after burn injury [58–65]. Burn injury results in plasma protein
loss through injured skin and increased free-fraction concentration of protein-
bound drugs. Volume resuscitation results in further plasma protein dilution
and increases the volume of distribution (Box 4) [3,58]. Clinical effects of these
altered pharmacokinetics include a reduction in the therapeutic index of drugs
with high protein binding, and altered effectiveness of regular doses of anal-
gesic drugs attributable to an increase in volume of distribution [3]. In addition,
pharmacodynamic modification at the drug-receptor interaction level also plays
a significant role after burn injury [3]. Several commonly used and representa-
tive medications are discussed in detail here.
Hypnotics
Propofol clearance and volume of distribution are increased in patients with
major burns during the hyperdynamic phase of burn injury [58,59]. Specif-
ically, propofol pharmacokinetics are determined by the interplay between
(1) increased cardiac output, hepatic clearance, and renal clearance; (2)
decreased binding of serum protein; and (3) pulmonary dysfunction [59,65].
Box 4: Pathophysiologic changes of burn injury that may alter drug

pharmacokinetics
Plasma protein dilution
Fluctuations in intravascular volume
Proliferation of extrajunctional acetylcholine receptors
Decreased pseudocholinesterase
Changes in cardiac output; increased cardiac output in hyperdynamic state
Changes in cerebral blood flow; increased cerebral blood flow in hyperdynamic
state
Changes in hepatic function
Changes in renal function; increased glomerular filtration rate in hyperdynamic
state
Increased cardiac output increases cerebral blood flow, which typically in-
creases anesthetic depth, but this may be less recognizable with propofol given
that the drug itself may reduce cerebral blood flow by up to 50% [65]. Despite a
burn-induced hepatic ischemic-reperfusion injury, hepatic clearance continues
to account for the majority of total propofol clearance [65]. Decreased plasma
proteins increase the free propofol fraction, particularly during prolonged
administration, such that both hepatic and renal clearance can be elevated
[65]. Smoke-inhalation injury may alter pulmonary blood flow and reduce
the known propofol uptake and elimination that takes place in the lungs
[65]. These pharmacokinetic changes, in addition to pharmacodynamic alter-
ations at the level of the receptor possibly causing increased drug resistance,
contribute to a decreased hypnotic effect of propofol [59,65]. Therefore, in
comparison with nonburned surgical patients, those with major burn injuries
may require larger bolus doses or increased infusion rates of propofol to attain
or maintain therapeutic plasma drug concentrations [58,59].
Neuromuscular blocking drugs
Succinylcholine can be safely used immediately after acute burn injuries for
tracheal intubation; however, its use at a time point greater than 24 hours
after burn injury is contraindicated, owing to the risk of acute hyperkalemia
and life-threatening dysrhythmias. However, the length of time a hyperkalemic
response may manifest after burn injury is unclear [3]. Acute hyperkalemia
after use of a depolarizing neuromuscular blocking drug (NMBD) is thought
to result from the proliferation of extrajunctional acetylcholine receptors, in
numbers proportionate to the magnitude of burn injury [3]. Related to this,
plasma pseudocholinesterase is decreased in burn injury by as much as 50%,
and may contribute to increased sensitivity to, or prolonged effects of, succinyl-
choline [60].
Conversely, resistance to nondepolarizing NMBDs is well described after
major burn injury [60,62,64]. Resistance to nondepolarizing NMBDs may
take several days to manifest, is typically only observed if the burn injury is
greater than 20% TBSA, and may persist up to 18 months after burn wounds
have healed [62,64]. The decreased effectiveness of nondepolarizing NMBDs
after burn injury is thought to be multifactorial, with both delayed onset time
and decreased duration of action reported. As with succinylcholine, the burn-
induced upregulation of acetylcholine receptors, including immature, fetal-
type acetylcholine receptors, at the neuromuscular junction has been implicated
in the pharmacodynamics changes of nondepolarizing NMBDs in patients with
burns [62,64,66,67]. Other reasons for such resistance include enhanced renal
elimination caused by increased glomerular filtration, and alterations in the
medication profile of these agents by circulating factors seen in burn injury,
including prostaglandins and a1-acid glycoprotein [64]. An increased rocuro-
nium dose of 1.2 to 1.5 mg/kg for rapid-sequence induction has been recommen-
ded to counteract these effects in patients with major burn injury [62].
In contrast to the other nondepolarizing NMBDs, atracurium and cisatracu-
rium are broken down by organ-independent pathways (eg, Hofmann elimina-
tion). However, resistance to these drugs still occurs because of their similar
pharmacodynamic mechanisms. For example, the increased atracurium dose
required for 50% maximal depression in twitch in burn-injured patients cannot
be explained by pharmacokinetics or alterations in plasma protein binding alone
[68]. As for cisatracurium, no research has specifically addressed the effect of
burn injury on its duration of action. However, it can be inferred that cisatracu-
rium may, too, have an altered pharmacodynamic profile, and dosing should be
adjusted accordingly.
Given the increased resistance to nondepolarizing NMBDs and the decreased
levels of pseudocholinesterase, mivacurium should be used cautiously, as it will
have a slower onset and increased duration of action in burn-injured patients
[60]. The decrease in pseudocholinesterase does not offset the decreased affinity
of the acetylcholine receptors for NMBDs, and the onset of action remains pro-
longed [60].
Opioids
Opioid requirements are increased in burn-injured patients for several reasons
that have not been fully elucidated [59]. A decreased volume of distribution
and clearance of morphine has been reported, with an expected increase in
elimination half-life [69]. Similarly, burn injury affects fentanyl pharmacoki-
netics via an expanded volume of distribution rather than increased clearance
or metabolism [61]. However, a separate study found no significant difference
in morphine pharmacokinetics between adults with and without burn injury
[70]. Nevertheless, pharmacokinetic findings cannot completely explain the
increased resistance to opioids among burn patients, suggesting that other
parameters, such as intrinsic pharmacodynamic opioid-receptor alterations,
may be the primary cause [61,69,71,72]. Opioid tolerance is an important factor
that makes pain management challenging throughout all phases of burn care,
and is characterized by increasingly poor response to standard doses of
analgesics. Opioid tolerance may be apparent after as little as 2 weeks of unin-

terrupted opioid use, or in patients with preexisting recreational opioid abuse.
It is not uncommon for burn-injured patients to manifest opioid tolerance
requiring dosing that far exceeds common textbook recommendations.
Intraoperative fluid administration

Standard intraoperative fluid administration is adjusted for the magnitude of
burn excision (large excisions incur more blood loss), the depth of burn
(partial-thickness burn excisions involve more blood loss than full-thickness
burn excisions), the specific hemostatic techniques used (eg, topical epineph-
rine), and the surgeon’s possible use of tumescent fluid administration. Fluid
repletion must be carefully optimized so as to not underresuscitate or overre-
suscitate, both of which may lead to further complications in the postoperative
period.
Maintaining hemostasis
Excessive blood loss during burn excision is a major complication of surgical
burn care. Budny and colleagues [73] estimated that the mean intraoperative
blood loss in an adult patient undergoing excision and grafting of burn wounds
could be as high as 117 mL/%TBSA burn wound excised. Multiple techniques
have been used to minimize intraoperative bleeding, such as application of
topical thrombin, use of compressive devices (tourniquets), staged procedures,
and topical or subcutaneous injection of vasoconstrictors (epinephrine, vaso-
pressin analogues, or phenylephrine) [74–78]. Tourniquet use during burn-
wound excision and grafting has also been shown to reduce the rate and
amount of intraoperative blood loss [3,79]. Systemic effects of topically applied
or subcutaneously injected vasoconstrictors during burn excision can be signif-
icant (eg, increased blood pressure, heart rate, or serum glucose), yet unpredict-
able. Intravenous tryglycidyl-lysine vasopressin during burn-wound excision is
reported to result in decreased blood loss because of its selective action in
reducing dermal blood flow; however, no cardiovascular parameters have
been analyzed [75]. Mitchell and colleagues [80] demonstrated decreased blood
loss in skin donor sites infiltrated with subcutaneous phenylephrine (5 lg/mL).
Systemic effects of phenylephrine were not appreciated, but the study was not
powered to expose such differences.
Topical epinephrine is the most commonly used technique for limiting blood
loss during both burn excision and donor skin harvests. A comparison of topical
epinephrine use during skin grafting in burned and nonburned patients reported
increased levels of serum epinephrine and lactate, a higher lactate/pyruvate
ratio, and higher heart rates in burn-injured patients [81]. Similarly, McQuitty
and colleagues [82] demonstrated increased levels of plasma epinephrine
when topical or subcutaneous epinephrine was used for surgical hemostasis.
However, the results of these studies are contrary to others reporting no differ-
ence in catecholamine levels or hemodynamic parameters in burn-injured pa-
tients receiving topical or subcutaneous epinephrine solutions [83,84]. Further
studies are necessary to better define practices aimed at decreasing intraopera-

tive blood loss during excision and grafting of thermal injuries.
Transfusion guidelines
With advancements in fluid resuscitation and implementation of early excision
and grafting, burn surgery has seen improved survival in the past 30 years [78].
Despite the efforts to decrease hemorrhage intraoperatively, burn excision may
still be accompanied by significant blood loss. Traditionally the erythrocyte
transfusion trigger has occurred when hemoglobin has decreased to less than
10 g/dL. However, with publication of the Transfusion Requirements in Crit-
ical Care (TRICC) trial and the American Society of Anesthesiologists transfu-
sion guidelines, intensivists and anesthesiologists have since recognized the
potential benefits of a more restrictive transfusion threshold (w7 g/dL) [85–
87], although this more restrictive policy has yet to be uniformly implemented,
with transfusions still occurring at a mean hemoglobin level of 8.6 1.7 g/dL
in intensive care units across the United States [88]. A recent survey of United
States burn centers reported that the hemoglobin transfusion threshold for pa-
tients with greater than 20% TBSA burns also remained high, at 8.1 g/dL, and
that more transfusions were associated with both higher mortality and infec-
tious complications [89].
Despite its obvious risks, the concept of an objective transfusion trigger for
burn-injured patients in the operating room is challenging, given (1) their un-
predictable hemodynamics owing to intensely painful surgical stimulation,
hyperdynamic cardiovascular physiology, and common intraoperative use of
topical vasoconstrictors; and (2) the inability of clinicians to accurately assess
intraoperative blood loss. In clinical practice, serial hemoglobin measurement
in euvolemic patients is the tool most commonly used to determine the need
for intraoperative transfusion.
Despite extensive research, no consensus exists regarding the appropriate
use of blood products for patients with major burn injury. One recent study
explored this issue, analyzing data from 2 3-year periods, before and after im-
plementation of an institutional blood-conserving protocol that included early
excision and donor harvesting with use of epinephrine- and thrombin-soaked
gauze followed by 10 to 14 minutes of pressure, electrocautery, and tourniquets
to minimize blood loss [90]. Use of this protocol was successful in reducing
transfusion requirements from 1 in every 3 patients with burn injury to 1 in
every 25, and demonstrates one valuable approach to minimizing intraopera-
tive blood loss using routinely available techniques.
Various innovative methods of reducing blood loss and assessing transfusion
requirements in burn-injured patients have been reported. One such approach
uses perioperative hemodilutional autologous blood transfusion (HABT). Imai
and colleagues [91] demonstrated that patients with less than 20% TBSA burns
who received HABT had reduced allogenic transfusion requirements.
Although total blood volume loss was unchanged, HABT significantly reduced
the actual loss of red blood cells, coagulation factors, and platelets. Activated
recombinant factor VII (rFVIIa) has also been used to minimize blood loss in
burn-injured patients. In a single-center pilot study, Johansson and colleagues
[92] showed that 2 empiric doses of 40 lg/kg recombinant rFVIIa (at incision
and 90 minutes later) decreased the total number of blood products transfused
in burn patients undergoing excision and skin grafting by 59%. Confirmation
of these and other novel techniques is necessary, however, before widespread
clinical adoption is possible.
Regardless of the advancements in intraoperative burn management,
emphasis on the individual patient and accurate clinical judgment remains a
vital component. Clinical judgment and the acuity of blood loss play a pivotal
role in transfusion of burn patients, with clinical assessment using markers of
hypoxemia, perfusion (base deficit, serum lactate), erythrocyte mass, and coag-
ulation as key assessment tools. As Curinga and colleagues [93] concluded in
their review of burn and transfusion, the quest for a universal transfusion
trigger should be abandoned, and instead such decisions should be tailored
to the individual needs of each patient.
Local and regional anesthesia

The use of local anesthesia, such as topical anesthetic creams or localized infil-
tration, is common in patients with burn injury. Local anesthetic creams allow
nerve endings in the superficial layers of skin to be anesthetized; however, the
time to peak effect may be on the order of hours, and the duration of action
may be inadequate for both postoperative pain and initial dressing changes
[94]. Furthermore, the amount of cream that can be safely used is ambiguous,
given the concern for local anesthetic toxicity with unpredictable drug absorp-
tion from open wounds [94]. For smaller burn injuries, however, this may be a
helpful adjunctive technique.
An alternative approach to local anesthesia is tumescent infiltration of lido-
caine and epinephrine into subcutaneous tissue. This approach has gained
widespread popularity in plastic surgery, in particular for liposuction and
hair transplant. By creating swelling and firmness of the surgical area, donor
harvests and burn excisions can also be more easily performed following
such infiltration. In addition, large areas of body surface can be anesthetized
with less surgical bleeding, and postoperative analgesia achieved. Although
subcutaneous injection of dilute epinephrine or lidocaine has been variably
adopted for burn escharectomy, debridement, excision, and grafting, studies
reporting this tumescent technique are limited. However, high-dose lidocaine
(up to 7 mg/kg) with epinephrine is reported to result in minimal blood loss,
excellent postoperative analgesia for up to 8 hours, and easier surgical dissec-
tion [95].
The use of regional anesthesia is typically limited to smaller burns on iso-
lated extremities, where the burn injury does not involve the site of needle
placement. Peripheral nerve blocks may achieve sufficient surgical anesthesia,
but placement must take into consideration that skin donor sites and burn-
injury sites are often in different anatomic locations, particularly because
patients often have more intense postoperative pain from the split-thickness
skin donor site than from the grafted burn wound. The use of regional anes-
thesia can provide intraoperative anesthesia, improve postoperative analgesia,
and promote rehabilitation. For example, a study by Gupta and colleagues
[94] assessed peripheral nerve blocks of the lower extremity for graft sites in
50 patients with 1% to 15% TBSA burns, reporting that patients had sufficient
analgesia during the procedure, with no patients requesting that the procedure
be aborted secondary to pain. Similar results were reported for ultrasound-
guided lateral femoral cutaneous nerve blocks during skin harvesting from
the lateral thigh to avoid general anesthesia [96]. First described by Dalens
and colleagues [97], the fascia iliaca compartment block is a modification of
the 3-in-1 femoral block [98], and has been reported in conjunction with general
anesthesia to reduce pain at split-skin donor sites of the thigh [99]. Patients who
received both a ropivacaine bolus and infusion during the operation demon-
strated significantly reduced postoperative morphine consumption [99]. Critics
of the fascia iliaca compartment block, however, state that the block requires
large anesthetic volumes and may initially limit rehabilitation because of motor
weakness [96]. Epidural or spinal anesthesia may also be used for operative
burn care, although extensive surgical debridement with risk for significant
blood loss and attendant hypovolemia is a relative contraindication for these
techniques [3].
In summary, although some studies have shown some potential benefit of
regional anesthesia in patients with burn injury, regional anesthesia often
cannot be used, at least as the sole anesthetic, given the distribution of burn
injury, the need for donor skin harvests at distant sites, or other associated in-
juries that the patient may have sustained. However, regional anesthesia may
prove advantageous in targeting specific aspects of burn-injury management,
such as intraoperative care of small and/or localized burns.
POSTOPERATIVE PERIOD
In the immediate postoperative period, clinical judgment should determine the
most appropriate time for tracheal extubation, particularly if the patient has
received large intraoperative fluid volumes, has had preexisting airway abnor-
malities, or has received excessively high intraoperative doses of opioids. Post-
operative mechanical ventilation is generally indicated in patients with
preoperative mechanical ventilation, as well as those undergoing delicate sheet
grafting to the face/neck, in an effort to minimize motion and graft disruption
in the initial postoperative days. Because of the frequent presence of unpre-
dictable opioid tolerance, when postoperative extubation is planned, opioid
dosing should ideally be titrated and individualized before emergence using
spontaneous ventilation, targeting a respiratory rate of 10 to 20 breaths per
minute and a normal expired carbon dioxide concentration. However, owing
to the intense pain associated with these procedures, additional opioids and/
or low-dose ketamine may be necessary in the postanesthesia care unit. Pain
management and procedural sedation remain key treatment priorities
throughout the remainder of the postoperative period, with care strategies

detailed elsewhere for burn-injured adults and children [100,101].
SUMMARY
Hospitalized burn-injured patients frequently require surgical treatment, yet
pose a myriad of pathophysiologic challenges to acute and intraoperative
care, whether treated at a community hospital or a specialized burn center.
Optimal perioperative care requires a comprehensive preoperative assess-
ment and attention to risk factors (eg, burn shock and resuscitation, diffi-
cult airway anatomy, inhalation injury) that predispose these patients to
increased morbidity and mortality. Anticipation of these issues, as well as
altered pharmacokinetics and pharmacodynamics, will help ensure safe and
effective perioperative management of patients with burn injury, including
guidance to surgical and nursing colleagues regarding challenges in pain
management.
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Advances in Anesthesia 31 (2013) 137–161

Advances in Perioperative and Critical

Heather E. Kaiser, MD, MPHa,*, Cindy Meerim Kim, MDb,

No financial disclosures or conflict of interest are declared by any author.

*Corresponding author. E-mail address: hkaiser6@jhmi.edu

0737-6146/13/$ – see front matter

Patient history and physical assessment

Box 1: Depth of burn injury

Airway and pulmonary system

Box 2: Indications for immediate tracheal intubation of patients

Furthermore, mortality rates of patients with smoke inhalation injury have

Fig. 2. Pathophysiologic response to smoke inhalation.

Fig. 3. Effects of carbon monoxide toxicity.

operating room with a combination of respiratory and anatomic characteristics

Fig. 4. Recommended algorithm for airway management of burn patients.

Box 3: Indications for tracheostomy

end-expiratory pressure to maintain alveolar and airway patency [47]. At pre-

of transesophageal echocardiography (TEE) at a regional burn center over a 5-

Box 4: Pathophysiologic changes of burn injury that may alter drug

analgesics. Opioid tolerance may be apparent after as little as 2 weeks of unin-

Intraoperative fluid administration

studies are necessary to better define practices aimed at decreasing intraopera-

Local and regional anesthesia

throughout the remainder of the postoperative period, with care strategies

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