1. Airway Management and
Respiratory Care of the
Burn Patient
Robert L. Sheridan, MD
The outcome, both for survival1 and for quality of life,2 has improved
dramatically for burn patients over the past 20 years. However, airway and
respiratory complications remain a common cause of morbidity and mor-
tality. Anticipation and skillful management of the airway in both the
acute and reconstructive burn patient is required if optimal outcomes are
to be regularly achieved.
Overall Management Strategy
Care of a large burn has four general phases (Table 1).3 The first
phase, the initial evaluation and resuscitation phase, occurs from day 1
through day 3 and requires an accurate fluid resuscitation and thorough
evaluation for other injuries and comorbid conditions. The second phase,
initial wound excision and biological closure, describes the maneuver that
attempts to change the natural history of the disease. This is typically
accomplished by a series of staged operations that are completed during
the first few days after injury. The third phase, definitive wound closure,
involves replacement of temporary wound covers with definitive covers
and closure and acute reconstruction of areas of small surface area but
high complexity, such as the face and hands. The final stage of care is
rehabilitation, reconstruction, and reintegration. Although this begins
during the resuscitation period, it becomes very time consuming and
involved toward the end of the acute hospital stay. There are unique
airway and respiratory issues relevant to all four phases of care.
Physiology of Burn Injury
Wound size and depth have a substantial influence on pulmonary
function. Wounds should be evaluated for extent, depth, and circumfer-
129

2. 130 Sheridan
Table 1. Phases of Burn Care
Phase Objectives
Initial Evaluation and Resuscitation Accurate fluid resuscitation
(0–72 hours) and thorough evaluation
Initial Wound Excision and Biological Accurately identify and excise
Closure (days 1–7) all full thickness wounds and
achieve biological closure
Definitive Wound Closure Replace temporary with definitive
(days 7–week 6) covers and close small complex
wounds
Rehabilitation, Reconstruction, and Initially to maintain range and reduce
Reintegration (entire edema, subsequently to strengthen
hospitalization) and prepare for return to
community
ential components (Table 2). As a general rule, burns are usually under-
estimated in depth on initial examination, even by experienced examin-
ers. There are predictable physiological changes that occur over the
course of a burn injury that also impact airway and respiratory manage-
Table 2. Evaluation of the Burn Wound
Extent
Lund-Browder Chart: Accounts for the changing body proportions with age and is the
preferred method of determining burn extent.
Rule of Nines: A rough estimate that assumes adult body proportions. The head and
neck are roughly 9%, the anterior and posterior chest are 9% each, the anterior
and posterior abdomen (including buttocks) are 9% each, each upper extremity is
9%, each thigh is 9%, each leg and foot is 9%, and the remaining 1% represents
the genitals.
Palmar Surface of the Hand: The palmar surface of the patient’s hand is
approximately 0.5% of the body surface over all age groups.
Depth
First Degree: Red, dry, and painful and are often deeper than they appear.
Second Degree: Red, wet, and very painful. There is a great variability in their depth,
ability to heal, and propensity to hypertrophic scar formation.
Third Degree: Leathery, dry, insensate, and waxy.
Fourth Degree: Involve underlying subcutaneous tissue, tendon, or bone.
Circumferential Components
Extremities: Progressive edema of tissue beneath nonelastic burns will threaten
extremity viability. Extremities at risk must be identified, closely monitored, and
promptly decompressed when distal circulation is compromised.
Neck: Although rare, deep circumferential neck burns can result in reduced venous
outflow from the head and should be decompressed when noted.
Torso: Chest compliance will be sharply reduced by near circumferential burns.
Prompt escharotomy in such patients will dramatically improve ventilation.

3. Airway Management of the Burn Patient 131
ment (Table 3). Those patients with burns over about 15% of the body
surface have a clinically important diffuse capillary leak that is felt to be
caused by wound-released mediators and is unique to burn-injured pa-
tients in its magnitude. This results in the extravasation of fluids, electro-
lytes, and moderate-sized colloid molecules into tissues adjacent to and
distant from the wound. A variety of formulas have been developed to
predict resuscitation volume requirements. However, there are multiple
variables that impact resuscitation requirements, including delay in ini-
tiation of resuscitation, inhalation injury, and the depth and vapor trans-
mission characteristics of the wound itself. No two injuries are exactly
alike, and no formula has yet been developed that can predict with ac-
ceptable accuracy the volume requirements necessary. Inaccurate volume
administration is associated with substantial airway, respiratory, and other
morbidity, and it is therefore essential that burn resuscitations be guided
by the hourly evaluation of resuscitation end-points, the formula serving
only to help determine initial volume infusion rate and to roughly predict
overall requirements.
Circumferential, or near circumferential, burn wounds of the torso
should be noted because they represent areas in which special monitor-
ing, and sometimes escharotomy, are essential. Constricting torso wounds
can reduce chest wall compliance as soft tissues swell beneath the inelastic
eschar. It is important that the need for escharotomy is recognized in a
timely way so effective intervention can follow. Dramatic improvement in
ventilation is common after needed escharotomy of the chest and abdo-
men (Fig. 1). In exceptional situations, bowel edema may result in ab-
dominal compartment syndrome in burn patients in the absence of ab-
dominal trauma. 4 This should be suspected based on physical
examination and clinical course and treated by abdominal decompres-
sion.5
After successful resuscitation, there is an abrupt decline in volume
requirements 18 to 24 hours after injury, as the diffuse capillary leak
Table 3. Predictable Physiologic Changes in Burn Patients
Time Predictable Changes Implications
Resuscitation Period Massive diffuse Fluid resuscitation is
(from day 0 to day 3) capillary leak required and airway
edema is pronounced
Post Resuscitation Hyperdynamic and Early wound closure
Period (from day 3 until hypercatabolic state with will reduce risk of
bulk of wound is relative sepsis; nutritional
definitively closed) immunosuppressed support is
status essential
Recovery Period Ongoing catabolic state Nutritional support
(from wound closure to remains essential;
about 1 year after anticipate and manage
injury) septic complications

4. 132 Sheridan
Figure 1. Improvement in chest wall compliance and ventilation can be dramatic after
escharotomy of the chest wall.
predictably abates. Subsequently, a systemic inflammatory state evolves,
characterized clinically by a hyperdynamic circulation, fever, and mas-
sively increased protein catabolism. These changes are thought to be
effected by a combination of wound colonization with release of bacteria
and their byproducts, translocation of similar substances through a com-
promised gastrointestinal barrier, foci of infection, and augmented re-
lease of the counter regulatory hormones cortisol, catecholamines, and
glucagon.
Serious burns are associated with severe and protracted metabolic
stress, and an important part of burn critical care involves support of this
physiology through accurate fluid and electrolyte repletion, nutritional
support, control of environmental temperature, prompt removal of non-
viable tissue with physiological wound closure, support of the gastrointes-
tinal barrier, and proper management of pain and anxiety. Techniques to
address all of these issues have evolved substantially. However, at present,
airway and respiratory complications associated with burn injury remain a
major source of morbidity and mortality.
Inhalation Injury
Inhalation injury is defined as the sequelae of aspiration of super-
heated gases, steam, or noxious products of incomplete combustion. Ap-

5. Airway Management of the Burn Patient 133
proximately 20% of patients admitted to regional burn centers have some
degree of inhalation injury. It has adverse effects on both gas exchange
and on hemodynamics, but the severity of individual injuries is only
roughly predictable based on history, examination, and currently avail-
able diagnostic tests. Inhalation injury has been demonstrated to have a
profound effect on mortality in multiple institutional reviews, with the
diagnosis as much as doubling mortality from that predicted based on age
and burn size alone.6 As there is no specific treatment for inhalation
injury, management involves providing the degree of support required to
compensate for decrements in gas exchange while the injured endobron-
chial and alveolar mucosa regenerate.
Physiology of Inhalation Injury
Inhalation injury involves the entire respiratory system, from the up-
per airway to the alveoli, to a variable and unpredictable degree. Super-
heated gas and liquid cause direct burning of the upper airway with re-
sultant mucosal edema and airway obstruction. This swelling is
exacerbated by the diffuse capillary leak associated with a cutaneous burn.
More distal injury is caused by chemicals adherent to fine particles
(smoke) that deposit in various parts of the respiratory system based on
the size of the particulate. Irritating gasses trigger bronchospasm. The
major airways are denuded of their normal mucosal layer and the ciliary
transport mechanism is therefore impaired. Small airways become ob-
structed with sloughed endobronchial debris and accumulated secretions
in the days after injury, as necrotic endobronchial mucosa sloughs. Pneu-
monia and tracheobronchitis frequently occur in partially obstructed lung
segments. The alveolar epithelium is disrupted by toxic products released
by burning synthetic products, resulting in alveolar flooding. The clini-
cally important problems that predictably occur include (1) loss of airway
patency secondary to mucosal edema, (2) bronchospasm, (3) intrapulmo-
nary shunting from small airway occlusion, (4) diminished compliance
secondary to alveolar flooding and collapse, (5) pneumonia secondary to
loss of ciliary clearance, (6) respiratory failure secondary to a combination
of the above factors, and (7) bronchiectasis and variable degrees of ob-
structive and restrictive defects in those who survive, particularly in serious
inhalation injuries.7
Diagnosis of Inhalation Injury
Most patients, even those with severe inhalation injuries, will have
little or no pulmonary dysfunction at initial presentation.8 The initial
chest radiograph is routinely normal. The noxious substances in structural
smokes are legion and generally unknown. Although there are a host of
diagnostic adjuncts reported for inhalation injury, none can reliably pre-

6. 134 Sheridan
dict injury severity or subsequent clinical course.9 Available diagnostics
include history, physical examination, chest radiograph, bronchoscopy,
admission arterial oxygen tension/inspired oxygen concentration ratio,
and radioisotope scanning. Inhalation injuries evolve over time and in-
volve the respiratory system from the upper airway to the alveoli to a
variable degree. Although nonspecific, most authors have based the diag-
nosis of inhalation injury on history and physical examination supple-
mented by bronchoscopy. The pertinent points of history include burns
sustained in a closed space or aspiration of hot steam or liquid. Physical
findings suggesting the diagnosis have included the presence of carbona-
ceous debris in the mouth or the sputum, singed nasal hairs, and facial
burns. Chest radiographs are generally normal initially, consistent with
the evolution of these injuries over time.
Invasive measures sometimes used to supplement history and physical
examination in the diagnosis of inhalation injury include bronchoscopy,
radioisotope scanning, and determination of serum carboxyhemoglobin
percentage. Despite its inability to determine parenchymal injury, most
clinicians use bronchoscopy as the gold standard for diagnosis of inhala-
tion injury. Bronchoscopic findings consistent with this diagnosis include
carbonaceous endobronchial debris, mucosal pallor, and mucosal ulcer-
ation (Fig. 2).10 Radioisotope imaging has been used to diagnose inhala-
tion injury in two forms: xenon-133 (administered intravenously) or tech-
Figure 2. Bronchoscopic findings consistent with inhalation injury include carbonaceous
endobronchial debris, mucosal pallor, and mucosal ulceration.

7. Airway Management of the Burn Patient 135
netium-99 (administered by inhalation). Both radioisotopes are rapidly
cleared by normal lungs,11 and asymmetric or delayed clearance is con-
sistent with the diagnosis of inhalation injury.12 Although physiologically
sound, xenon and technetium scanning have not been widely used be-
cause of logistic difficulty and expense. Tracheobronchial cytology and
biopsy have been reported to facilitate the diagnosis of inhalation injury
in small clinical series, but because of logistic difficulties and potential
complications, they have not been widely employed.13 In practical terms,
a clinical suspicion of inhalation injury, based on history and physical
examination and supplemented with bronchoscopy in selected patients, is
adequate information upon which to base transfer decisions and careful
monitoring for respiratory complications.
Management of the Airway in the Burn Patient
There are a few unique aspects of airway management in burn pa-
tients. These are detailed as they are typically encountered through the
course of the illness.
Initial Evaluation and Resuscitation Phase
The most important points of airway management in this phase are
assessment of current (and prediction of subsequent) airway patency and
documentation of the presence or absence of inhalation injury. Even
patients with incipient loss of airway patency from mucosal edema will
have open airways if they present to the hospital promptly after injury.
Loss of airway patency from mucosal edema usually only occurs after time
has passed and resuscitation fluid has been administered. The risk of
subsequent loss of airway patency is particularly acute in small children, in
whom moderate mucosal edema can lead to complete airway occlusion.
The use of heliox has been proposed as a way to avoid intubation in such
children.14 However, as subsequent intubation in those who fail on heliox
may be even more difficult, it seems wiser in most circumstances to pro-
ceed directly to careful intubation in burned small children with progres-
sive stridor.
Airway assessment is best done clinically, based on history and physical
examination and supplemented with laryngoscopy and bronchoscopy in
selected patients. Physical signs of particular importance are singed nasal
hairs, facial burns, and soot in the mouth and between the teeth (Fig. 3).
Stridor mandates intubation. In questionable cases, direct laryngoscopy
and fiberoptic bronchoscopy can be very useful; the bonchoscope can be
used as a stylet and intubation effected at the end of the diagnostic ex-
amination if indicated. Patients at risk for progressive edema should be

8. 136 Sheridan
Figure 3. Physical signs of particular importance in initial airway assessment are singed nasal
hairs, facial burns, and soot in the mouth and between the teeth.
admitted to the hospital and closely observed so that intubation can be
done in a timely fashion. If one waits until edema is advanced, intubation
can be very difficult. On occasion, hot liquids are aspirated by young
children and can lead to rapid and massive upper airway edema. If sus-
pected, immediate visualization of the airway and intubation is important
(Fig. 4). Such situations should be treated as thermal epiglottitis.15
Initial Wound Excision and Biological Closure Phase
During this phase of care, the principal burn-specific airway issue is
prevention of unplanned extubation. Unplanned extubation in the gen-
eral critical care setting is hazardous but not usually a cause of death or
permanent neurological injury. However, in the setting of massive face,
neck, and airway edema associated with burn resuscitation, reintubation
after unplanned extubation can be incredibly difficult, if not impossible.
The need for urgent reintubation is best avoided by compulsive attention
to adequate sedation and endotracheal tube security. Securing endotra-
cheal tubes in those with facial burns can be a challenge, but it can be
reliably done using umbilical tie harnesses (Fig. 5). Despite all proper
precautions, unplanned extubation will occur in some patients. Although
most can be reintubated using standard techniques, adjunctive techniques
may, on occasion, be lifesaving. These include laryngeal mask airway
(LMA) placement (with subsequent endotracheal intubation through the
LMA), fiberoptic intubation, needle cricothyroidotomy, and open crico-

9. Airway Management of the Burn Patient 137
Figure 4. On occasion, hot
liquids are aspirated by young
children and can lead to rapid and
massive upper airway edema. If
suspected, based on history or
examination of the burn pattern,
immediate visualization of the
airway and intubation is
important.
thyroidotomy. These techniques are detailed in other sections of this work.
Despite the most compulsive attention to this matter, deaths and adverse
events will occur because of the difficult nature of the clinical problem.
In selected patients, tracheostomy may be properly performed in this
phase of care, particularly if prolonged intubation is anticipated. It is ideal
if neck edema has subsided such that the procedure is not so technically
difficult and that there are no neck burns overlying the planned trache-
ostomy site.16,17 Tracheostomy in burned children is associated with a
high incidence of serious structural problems requiring airway reconstruc-
tion and is best avoided if possible.
Definitive Wound Closure Phase
In this phase of protracted intensive care, the issue of airway security
remains, although airway and facial edema are usually much reduced.
However, as facial edema subsides, pulmonary function often worsens in
those who have sustained significant parenchymal inhalation injury. A
unique problem that is seen in such patients is acute endotracheal tube

10. 138 Sheridan
Figure 5. In the setting of the
massive edema associated with
burn resuscitation, reintubation
after unplanned extubation can be
incredibly difficult and is best
prevented by compulsive attention
to endotracheal tube security.
obstruction from inspissated endobronchial debris (Fig. 6). Acute tube
occlusions or near occlusions are caused by wads of debris or even casts of
small airways lodging in the endotracheal tube. This problem is mini-
mized by the use of good humidification and frequent pulmonary toilet.
When it occurs, it is managed by prompt recognition and an initial at-
tempt to clear the tube with a relatively stiff suction catheter (especially if
facial edema predicts a difficult reintubation); extubation, mask ventila-
tion, and reintubation are used in those patients in whom the tube simply
cannot be cleared.
Reconstruction and Rehabilitation Phase
In this phase of care, there are two airway issues that occur with some
frequency: difficult elective intubations for reconstructive surgery and un-
suspected tracheal and subglottic stenosis.16,18 There are common con-
tractures that occur in burn patients that will predictably hinder safe
management of the airway on induction of anesthesia. Most notable are
flexion neck contractures and microstomia (Fig. 7). Adjuncts, such as

11. Airway Management of the Burn Patient 139
Figure 6. (A) A unique problem
that is seen in patients with severe
inhalation injury is acute
endotracheal tube obstruction from
inspissated endobronchial debris.
(B) Occasionally, total tube
obstruction is caused by the passage
of large endobronchial casts,
particularly in young children with
small tubes and severe inhalation
injury, as in this case in which
emergent extubation and
reintubation was required.
fiberoptic intubation or LMA can be useful in these patients. On occasion,
emergent sharp release is needed immediately after induction to allow for
mask ventilation and intubation. The surgeon should be in the operating
room prior to induction of anesthesia in patients with contractures of the
mouth or neck. Any contracture that precludes safe access to the airway
assumes a very high priority and should be addressed as soon as identified.
Patients are ideally not sent into rehabilitation settings until these are
addressed.
Patients who have required prolonged intubation or tracheostomy
have a low but important incidence of subglottic stenosis.19 This often
presents after discharge, either in the rehabilitation setting or at the time
of planned reconstructive operations. It should be suspected if slowly
progressive stridor develops or if a properly sized tube will not fit into the
trachea. Optimal diagnostic techniques are endoscopic, and management
is surgical.20

12. 140 Sheridan
Figure 7. There are common contractures that occur in burn patients that will predictably hinder
safe management of the airway on induction of anesthesia. Most notable are flexion neck
contractures and microstomia. On occasion, emergent sharp release is needed immediately after
induction to allow for mask ventilation and intubation. The surgeon should be in the operating
room prior to induction of anesthesia in patients with significant contractures of the mouth or neck.
Management of Inhalation Injury in the Burn Patient
Clinical management of inhalation injury is supportive only. Interest-
ingly, it is very typical that pulmonary function is relatively normal for the
first few days following the injury, with impaired gas exchange and com-
pliance occurring toward the end of the first week after injury. During this
interval, it is ideal to complete interfacility transfers and needed surgical
procedures. Prophylactic antibiotics and steroids are of no value.21,22 Af-
ter the airway has been secured (see above), there are five predictable
clinical problems that may need to be addressed in patients with inhala-
tion injury: bronchospasm, small airway obstruction, infection, respiratory
failure, and carbon monoxide (CO) poisoning.
Bronchospasm
In some patients, intense bronchospasm from aerosolized irritants
occurs during the first 24 to 48 hours, especially in young children. This
is well managed with in-line beta agonists in most patients, although some
will require intravenous bronchodilators such as terbutaline, low-dose

13. Airway Management of the Burn Patient 141
epinephrine infusions, or even parenteral steroids. Ventilatory strategies
should be designed to minimize intrinsic positive end-expiratory pressure
in this setting, much as one would do to ventilate a patient with status
asthmaticus.
Small Airway Obstruction
As necrotic endobronchial debris slough, increasing difficulty with
pulmonary toilet routinely occurs. An aggressive program of chest phys-
iotherapy and pulmonary toilet is an important component of care. Toilet
bronchoscopy can greatly facilitate clearance of the airways. Vigilant pul-
monary toilet is an essential component of the management of patients
with inhalation injury. Nebulized heparin and acetylcysteine has been
proposed as an adjunct to improve pulmonary toilet in patients with in-
halation injury,23 but available data do not seem adequate to recommend
the general use of this therapy as yet.
Pulmonary Infection
Approximately half of those with inhalation injury can be expected to
develop pulmonary infection, either pneumonia or purulent tracheobron-
chitis. Differentiating between these two entities can be difficult, but the
difference is of little practical importance. Infection typically occurs toward
the end of the first week following injury, and it is common to see patients
with serious inhalation injuries deteriorate at this time. A patient with a newly
purulent sputum, fever, and perhaps diminished gas exchange should be
treated with antibiotics based on sputum culture. The physiology of inha-
lation injury, involving injury to endobronchial mucosa with hampered
mucociliary clearance, makes good pulmonary toilet essential.
Respiratory Failure
Respiratory failure in burn patients is caused as often by sepsis as it is
by inhalation injury. Overly vigorous attempts to force high or even nor-
mal tidal volumes into such lungs will exacerbate the underlying injury.24
These patients do well with a pressure-limited ventilation strategy based
on permissive hypercapnia (Table 4).25 Burn patients who fail this ap-
proach are potential candidates for extracorporeal membrane oxygen-
ation26 or inhaled nitric oxide.27,28
Although weaning and extubation of burn patients follows the general
guidance presented elsewhere in this issue, there are some unique aspects
in this patient group that are important to know (Table 5). Of particular
importance is balancing the pain medication needs of those with large
wounds and donor sites with the need for an alert sensorium to protect
the airway and the frequent occurrence of severe upper airway edema in
those with inhalation injury.

14. 142 Sheridan
Table 4. Responses to Progressive Respiratory Failure in the Burn Patient
1. Address bronchospasm with nebulized beta-agonist agents.
2. Address poor chest wall compliance secondary to overlying eschar with
escharotomies.
3. Ensure ventilator synchrony with adequate opiate and benzodiazepine infusions.
Neuromuscular blockade may be required on occasion.
4. Reset end-point of ventilation to a physiological pH (7.2 or more). Allow gradual
onset hypercapnia as long as there is no head injury.
5. Reset end-point of oxygenation to an arterial saturation of at least 90%, typically
associated with an arterial oxygen partial pressure of 60 torr or greater.
6. Optimize inflating pressures.
A. Choose optimal positive end-expiratory pressure (PEEP). This is best done
by creating a pressure-volume curve with a graduated inflation and setting
PEEP just above the inflection point.
B. Choose optimal peak inflating pressure (PIP). This is best done by using
pressure controlled ventilation and targeting a tidal volume of 10–15
ml/kg, as long as total inflating pressures (PIP + PEEP) can be kept under
40 cm H2O. If this is inconsistent with meeting the reset end-points of
oxygenation and ventilation, then the pressure cap should be violated.
C. Choose optimal mean airway pressure (Pmaw). Lengthen expiratory time to
a target of 20 to 25 cm H2O, as long as intrinsic PEEP is not detectable.
7. In those few patients in whom these measures are not sufficient, consider the
use of innovative adjuncts, such as nitric oxide, partial liquid ventilation, or
extracorporeal support.
Carbon Monoxide Exposure
Carbon monoxide poisoning commonly occurs in conjunction with
inhalation injury. The obtunded state seen in many of these patients is
multifactorial, involving a combination of CO, anoxia, drugs, alcohol, and
Table 5. Important Considerations in Weaning and Extubation of Burn Patients
Sensorium: The patient must be awake and alert enough to guard their airway.
Airway patency: Upper airway edema must be resolved to the degree that there is
an audible airleak around the endotracheal tube (with cuff deflated if tube is
cuffed) at a moderate inflating pressure (20 to 30 cm H2O). A short course of
steroids (24 hours) may be useful in selected patients to reduce airway edema.
Muscle strength: Strength must be adequate for ventilation. An indirect measure of
this is a tidal volume (6 to 10 ml/kg) with continuous positive airway pressure of
5 cm H2O and a negative inspiratory force less than −20 cm H2O.
Compliance: Combined chest wall and lung compliance must be high enough that
the work of spontaneous breathing is not excessive. Indirect measures of this are a
measured static compliance of at least 50 ml/cm H2O and tidal volumes of at least
10 ml/kg with moderate inflating pressures (less than about 25 cm H2O).
Gas Exchange: An intrapulmonary shunt less than 20%, indicated by a PaO2/FIO2
ratio greater than 200, should be documented.
PaO2/FIO2 = arterial oxygen tension/inspired oxygen concentration.

15. Airway Management of the Burn Patient 143
hypotension. Hyperbaric oxygen has been proposed as a means of im-
proving the prognosis of those suffering serious CO exposures, but its use
remains controversial.29 To treat with 100% normobaric oxygen or with
hyperbaric oxygen is a decision that must be made if serious CO poisoning
is suspected or documented. Unfortunately, available data conflict, and
the efficacy of this therapy remains an open question.30–32
CO binds to iron-containing enzymes, particularly hemoglobin and
the cytochromes, which it thereby inactivates. The formation of carboxy-
hemoglobin results in an acute physiological anemia. The occurrence of
unconsciousness at a carboxyhemoglobin concentration of 50% implies
that other mechanisms are involved in the pathophysiology of CO injury.
It is likely that CO binding to the cytochrome system in the mitochondria,
interfering with oxygen utilization, is more toxic than CO binding to
hemoglobin. For unknown reasons, between 5% and 25% of patients with
serious CO exposures have been reported to develop delayed neurologi-
cal sequelae.32 These patients can be managed with 100% isobaric oxygen
or with hyperbaric oxygen. If serious exposure has occurred, manifested
by overt neurological impairment or a high carboxyhemoglobin level, then
hyperbaric oxygen treatment is probably warranted if it can be safely admin-
istered. Many patients with severe carbon monoxide exposure have also been
exposed to cyanide, which is released from burning synthetics. However, the
degree of exposure is rarely such that specific treatment is required.33
Most patients treated with hyperbaric oxygen receive their exposure
in a monoplace hyperbaric chamber. Treatment regimens vary, but the
typical regimens is 2 or 3 atmospheres for 90 minutes, with 3 10-minute
“air breaks” to decrease the incidence of oxygen toxicity seizures. Because
patient access is compromised in a monoplace chamber, unstable patients
are poor candidates. Other relative contraindications are wheezing or air
trapping, which increase the risk of pneumothorax, and high fever, which
increases the risk of seizures. Prior to placement in the chamber, endo-
tracheal tube balloons should be filled with saline to avoid balloon com-
pression–associated air leaks, and upper body central venous cannulation
should be avoided if possible to avoid sudden enlargement of an occult
pneumothorax during decompression. The decision whether to treat with
hyperbaric oxygen or 100% normobaric oxygen can be difficult to make
but is grounded in these considerations.
Conclusion
Airway and respiratory issues remain important sources of morbidity
and mortality in the burn unit. With fewer patients now succumbing to
wound sepsis, those with concomitant inhalation injury find airway and
respiratory issues the biggest threat to their life. Fortunately, the problems
associated with the injuries are predictable and can usually be successfully
managed by an informed burn care team.

16. 144 Sheridan
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