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454
J. L. Sparling and J. A. J. Martyn
thermal regulatory function of intact skin. Initial resuscitation is
a susceptible period, and consideration should be given to utilizing warmed fluids or an in-line fluid warmer. Subsequently,
dressing changes and dressing removal are an additional vulnerability. During the hypermetabolic phase, the inflammatory
response causes an increase in the hypothalamic temperature set
point, and hypermetabolism occurs to maintain this set point.
Shivering increases oxygen consumption, which exacerbates
catabolism in burn injury. Hypothermia below 35°C contributes
to coagulopathy through platelet inhibition [10], and hypothermia during surgery despite aggressive intraoperative warming is
correlated with the development of postoperative acute lung
injury (ALI). [11] Interventions to improve intraoperative body
temperature maintenance include increased ambient temperature (80–100 °F), use of underbody fluid warmers, forced air
warming blankets, radiant warmers, intravenous fluid warmers,
minimization of exposed skin, and wrapping exposed skin in
plastic insulation, especially the head. Patient temperature
should be communicated with the surgical and nursing teams
intraoperatively, so that, if necessary, surgery may be paused to
allow the patient to warm to acceptable levels.
Analgesia
Burns necessitate aggressive pain management, as many
aspects of burn treatment are inherently painful, including
dressing changes, excision and grafting procedures, and physical and occupational therapy. Pain severity depends not only
on the extent and depth of burns, but also on psychosocial
factors that influence a patient’s experience of pain. Inadequate
analgesia may provoke anxiety with subsequent procedures,
leading to a vicious cycle of pain and anxiety. Burn patients
may also develop hyperalgesia and allodynia in the affected
areas of burned skin and/or skin graft donor sites, in addition
to the tolerance and opioid-induced hyperalgesia that follows
from prolonged opioid therapy.
Opioids are the cornerstone of pain treatment in burn
patients. While long-term opioid dependence has been a con-
Chapter 22. Anesthesia forBurn Patients
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455
cern, addiction after therapeutic use of opioids for burn pain
is rare. Opioids may be delivered via continuous infusion in
ventilated patients, with intermittent IV boluses, enterally, or
via patient-controlled analgesia (PCA) pumps with or without a continuous background rate. Opioid requirements generally decrease significantly after successful wound closure,
which should be targeted as early as possible.
Myriad analgesic adjuncts have been reported in the
literature. Ketamine has been shown to counteract the
hyperalgesic effects of upregulated N-methyl-D-aspartate
(NMDA) receptors after burn, and it may also possess antiinflammatory effects [12]. Ketamine may be administered as
a continuous background infusion during anesthesia or in the
awake patient, or it may be administered via IV bolus for
painful bedside procedures. Ketamine has a superb margin of
safety in terms of dosing. Methadone offers the advantage of
concomitant opioid agonism and NMDA antagonism, limiting
opioid tolerance and opioid-induced hyperalgesia.
Methadone’s utility is limited, however, by its variable halflife due to cytochrome p450-dependent elimination and
potential for drug–drug interactions [13].
Dexmedetomidine is an intravenous α2-agonist with
sedative, anxiolytic, and analgesic properties; preoperative
administration reduced postoperative opioid requirements in
adults [14]. Dexmedetomidine use with ketamine can produce
adequate sedation and analgesia for pediatric patients
undergoing burn wound procedures, though its use is
consistently associated with hypotension and bradycardia [15,
16].
Perioperative use of gabapentinoids (i.e., gabapentin,
pregabalin) has an uncertain effect on pain and opioid
requirements, with a higher rate of dizziness and visual
disturbances [17]. Further, gabapentinoids have been associated
with potentiation of the respiratory depressant effects of
opioids [18, 19].
Acetaminophen has opioid-sparing effects demonstrated
for burn and other types of surgery, but generally must be
used in conjunction with other analgesics for all but the
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J. L. Sparling and J. A. J. Martyn
smallest burns. Nonsteroidal anti-inflammatory drugs
(NSAIDs) are generally avoided in the acute phase due to
the increased risk of peptic ulcers, gastrointestinal bleeds, and
renal impairment.
Regional anesthesia should be considered in all burn patients
to improve both intraoperative and postoperative analgesia and
facilitate early participation in physical and occupational therapy. Frequently, split-thickness skin graft donor sites are more
painful than the actual burn wound, which may be addressed
with either tumescent local anesthesia or regional nerve blocks.
The surface area covered by tumescent anesthesia is limited by
maximally allowable local anesthetic dose (e.g., lidocaine with
epinephrine 7mg/kg), but has been shown to be safe and effective with this constraint [20]. Regional nerve block may be
delivered as a single injection or via a continuous catheter.
Lateral femoral cutaneous block may be particularly useful as
the lateral thigh is a frequent donor site, and this block affects
only sensory innervation permitting early ambulation. This
block may be combined with a fascia iliaca block if coverage of
the anterior and medial thigh is also desired. Epidural analgesia
or truncal blocks—such as transversus abdominal plane (TAP),
rectus sheath, paravertebral, pectoralis I or II, or erector spinae
plane—may be utilized for wounds affecting the chest, abdomen, or back. Meticulous care must be taken during regional
anesthesia with respect to sterility and management of prophylactic and therapeutic anti-coagulation, according to nationally
recognized guidelines [21].
Echocardiography andPoint ofCare
Ultrasonography (POCUS)
Point of care ultrasonography (POCUS) and echocardiography
have many uses in the perioperative care of severely burned
patients. To date, small studies have examined the use of
transesophageal echocardiography (TEE) on burn patients.
These studies have reported reduced left ventricular (LV)
systolic function, impaired diastolic function, valvular
vegetation (i.e., with bacteremia), pulmonary hypertension,
pericardial effusion, fluid overload, and right heart failure
Chapter 22. Anesthesia forBurn Patients
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457
[22, 23]. TEE overcomes the challenges of access to the chest
in patients with anterior chest and abdominal burns, yet
placement of the TEE probe is invasive and may be difficult
in patients with acute facial burns. Transthoracic echocardiography (TTE) is more readily available at the bedside in
the Intensive Care Unit (ICU) and in many ORs.
Increasing attention has been given to perioperative use
of POCUS, with recent recommendations published by the
American Society of Regional Anesthesia and Pain Medicine
(ASRA) for use of POCUS by anesthesiologists [24]. The
ASRA recommendations include acquiring competency in
airway evaluation (for confirmation of endotracheal, orogastric, and nasogastric tube placement), lung evaluation (for
diagnosis of pneumothorax, complicated and uncomplicated
effusions, interstitial fluid, diaphragmatic paresis), cardiac
evaluation (as above), gastric ultrasound (for unknown
fasting status, characterization of stomach contents, and aspiration risk), and FAST examination (Focused Assessment
with Sonography for Trauma, for presence of abdominal
fluid). Gastric ultrasound, in particular, may be an important
tool to assess patients’ gastric volume and stratify risk of
aspiration. This evaluation may safely allow enteral nutrition
to be continued with shorter required fasting times preoperatively for nutritionally vulnerable burn patients.
Perioperative Communication andTeamwork
The critical nature of extensive burn injury makes
interprofessional communication and collaboration between
surgery, anesthesiology, and nursing clinicians essential.
Structured handoff procedures should be utilized for critically
ill patients preoperatively and postoperatively to ensure that
all essential information is conveyed and that the receiver is
adequately prepared to assume clinical responsibility for the
patient. During prolonged procedures, regular communication as to the progress of the surgical procedure, the patient’s
hemodynamic, fluid, and temperature status, and any recent
laboratory analysis should occur. This dialogue allows for
shared decision-making, for example—as to whether ongoing
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J. L. Sparling and J. A. J. Martyn
F . Intraoperative cognitive aid for burn anesthesia.
Cognitive aids standardize intraoperative approaches to management
of the critically ill burn patient and facilitate regular intraoperative
communications between surgical, anesthesia, and nursing teams to
align on patient status and inform shared clinical decision-making
debridement will be tolerated or should be terminated, or
whether a brief pause to allow for further fluid resuscitation
and active warming may occur. Cognitive aids posted in the
Chapter 22. Anesthesia forBurn Patients
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459
OR or embedded in the medical record may help facilitate
these communications. (See Fig.22.1.)
Anesthesia Implications, by System
Cardiovascular
Cardiac output is reduced immediately following a major
burn due to (1) a decline in effective blood volume secondary
to insensible and intravascular fluid loss from the burn in the
first 24–36h after major burn, (2) a decrease in venous return
due to circumferential burns of the chest and abdomen, (3)
impaired cardiac contractility, and (4) increased systemic
vascular resistance (SVR) [25, 26]. TEE may be a useful
adjunct to guide fluid resuscitation and administration of
vasopressors or inotropes in the acute setting [23]. In scenarios where adequate fluid resuscitation fails to normalize the
cardiac output, the impairment is likely due to a combination
of inflammation-mediated myocardial depression and elevated SVR due to release of endogenous vasopressin, painor anxiety-induced catecholamines, and elevated viscosity
due to hemoconcentration [25]. Early burn wound excision
may help to attenuate these inflammatory-mediated changes
and development of hypermetabolism [27].
Cardiac output in patients with substantial burns (e.g.,
involving more than 40% TBSA) evolves into a hypermetabolic phase within 3–5days following an acute burn [28]. A
deviance from these expected trends should prompt investigation into other causes of decreased cardiac output such as
persistent hypovolemia or a stress-induced cardiomyopathy.
Hypertension may occur during this phase due to increased
catecholamines (pain- or anxiety-induced), angiotensin II,
neuropeptide Y, vasopressin, and activation of the renin–
angiotensin–aldosterone system (RAAS) [25, 29, 30].
Adrenergic antagonists, such as propranolol, have been found
to modulate the hypermetabolic response in burn injury and
may be initiated early in the acute phase [31]. Elevated oxy-
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J. L. Sparling and J. A. J. Martyn
gen consumption associated with hypermetabolism is reduced
following complete excision and closure [32], but cardiac
output may continue to be elevated for up to 24months following injury [28].
Pulmonary
The American Burn Association’s National Burn
Repository reports a 10.3% incidence of inhalation injury
among burn patients, although this figure is likely higher
in those who present for anesthetic care in the acute phase
[33, 34]. Mortality increases more than ten-fold in those
patients with some degree of inhalation injury, and this
fact has not changed despite advances in diagnosis and
treatment [35]. Thermal damage is generally confined to
the upper (supraglottic) airways as heat is effectively dissipated in the oropharynx and nasopharynx, and the vocal
cords tend to close preventing heat from reaching the
lower airways [34, 36]. However, supraglottic edema
occurs within hours following injury, leading to airway
obstruction and difficult intubation. “Thermal epiglottitis”
may develop after intraoral scalds or ingestion of a toxic
agent [37, 38].
Conversely, subglottic inhalation injury typically arises
from the inhalation of noxious chemicals such as halogen
acids, unsaturated aldehydes, and formaldehydes, depending
on the type of product burnt. Inhaled nitrogen dioxide and
sulfur dioxide form nitric and sulfuric acid, respectively,
causing damage to the distal bronchi and alveoli. Hydrochloric
acid, sulfuric acid, and phosgene exist as aerosols and can
themselves reach the distal tracheobronchial tree and cause
disruption of surfactant and produce direct injury to the
alveolar membrane. These substances inflict direct irritation
and trigger inflammation via neuropeptide production leading to hyperemia, mucosal sloughing, loss of surfactant,
impaired mucociliary function, bronchospasm, and inducible
nitric oxide synthase (iNOS) activation impairing hypoxic
Chapter 22. Anesthesia forBurn Patients
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461
pulmonary vasoconstriction [39]. Cast formation can occur
due to the sloughing of damaged mucosal epithelium,
together with impaired mucociliary clearance; inhaled heparin and acetylcysteine have been studied to reduce airway
cast formation and mucous plugging, with mixed reports of
their efficacy [40].
Physical examination findings such as presence of facial
burns, singed nasal hairs, or carbonaceous sputum have traditionally been associated with inhalation injury, however,
these signs have poor discriminative value in predicting
patients with inhalation injury and poor agreement with
bronchoscopic diagnosis [41]. Clinical interventions for inhalation injury should rather be considered given a comprehensive assessment including estimated length of exposure,
degree of enclosure, type of material burned, and any
accompanying mental status changes. Flexible fiberoptic
bronchoscopy is a useful adjunct to evaluate for inhalation
injury, and more limited indirect (fiberoptic) laryngoscopy
may help to evaluate for laryngeal edema. Xenon-133 scan is
also a validated tool for diagnosis of inhalation injury, which
measures the delayed clearance of Xenon-133 via damaged
terminal airways, but its clinical utility is limited [42, 43].
Difficulty ventilating patients may arise due to reduced
chest wall compliance from circumferential chest or abdominal burns and rarely pleural effusion [26]. Optimization of the
functional residual capacity (FRC) through best positive endexpiratory pressure (PEEP) titration and recruitment maneuvers may improve ventilation-perfusion mismatching, but
escharotomy may ultimately be necessary to relieve elevated
thoracic or abdominal compartment pressures precluding
adequate ventilation. Hypoxemia may also develop in the
absence of direct inhalation injury, through the development
of cardiogenic or noncardiogenic pulmonary edema due to
fluid resuscitation or blood product transfusion (i.e.,
transfusion- associated circulatory overload (TACO)), or
transfusion-related acute lung injury (TRALI). Acute respiratory distress syndrome (ARDS) may also occur indepen-
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J. L. Sparling and J. A. J. Martyn
dent of inhalation injury. The PaO2/FiO2 ratio at presentation
predicts burn-related mortality [44].
Systemic poisoning from carbon monoxide (CO) or
cyanide may drive tissue hypoxia. Diagnosis may be
challenged by non-specific symptoms causing a delay in
diagnosis, and thus CO poisoning should be suspected in
enclosed (e.g., house) fires.
Renal
A variety of mechanisms may lead to acute kidney injury
(AKI) following substantial burns. Myoglobinuria is more
common following electrical burns and is associated with
high-voltage exposure, prehospital cardiac arrest, fullthickness burns, and compartment syndrome [45]. Patients
may present with some degree of prerenal AKI due to volume depletion and peripheral vasoconstriction caused by
catecholamine surge, activation of the RAAS, upregulation of
vasopressin receptors, and release of endothelin-1 and vasopressin [46]. Persistence of hypovolemia, hypotension, and
hypoxemia may lead to acute tubular necrosis (ATN) manifesting as intrinsic renal injury.
Initial fluid resuscitation and the release of these mediators
result in fluid retention commonly being seen in the first
2–5days following a burn, which is followed by diuresis and
an increase in glomerular filtration rate (GFR) concomitant
with the increase in cardiac output and basal metabolic rate.
However, this increase in GFR occurs even in the presence
of hypovolemia, as the tubular dysfunction may limit the
ability to concentrate urine. Thus, urine output may be a
poor indicator of intravascular volume status. This may be
reflected by a blood urea nitrogen (BUN) to creatinine ratio
greater than 20.
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463
Hepatic
Early liver injury may represent ischemic hepatopathy or
“shock liver” because of hypoperfusion, direct injury from
inhaled toxins, or reperfusion injury once intravascular volume has been adequately restored. Later liver injury may
occur as a sequelae of the proinflammatory cytokine cascade.
Functional assays such as the plasma disappearance rate of
indocyanine green (PDR
static laboratory tests in predicting mortality [47].
The hypermetabolic response to burns is characterized by
increased hepatic blood flow, hepatic oxygen uptake, synthesis of acute phase reactants, and gluconeogenesis [48, 49].
Other etiologies of later hepatic impairment include iatrogenic drug toxicity, blood transfusions, or sepsis. Fatty liver
may also develop due to peripheral lipolysis induced by the
hypermetabolic response, including in the absence of total
parental nutrition [50].
Alterations to the hepatic clearance of common anesthetic
medications are important to consider. Increased hepatic
blood flow and enzyme induction in the hypermetabolic
phase may decrease the half-life of perfusion-dependent (e.g.,
lidocaine, fentanyl) and enzyme-dependent (methadone,
diazepam) drugs [51]. Variation among many factors, including magnitude of burn, timeframe following burn injury, coadministration, degree of protein-binding, and volume of
distribution, make clinical studies of these drugs challenging
to interpret.
) may offer an advantage over
ICG
Central Nervous System
Central nervous system (CNS) injury may occur in burn
patients due to neurotoxin inhalation, hypoxic encephalopathy, sepsis, electrolyte abnormalities (particularly in the set-
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