Pediatric Anesthesia 2009 19 (Suppl. 1): 147–154 doi:10.1111/j.1460-9592.2008.02884.

Review article
Inhalation burn injury in children
C H R I S T I N A W . FI D K O W S K I M D * , G E N N A D I Y F U Z A Y L O V
M D †, R O BE R T L. S H E R ID A N M D ‡ A N D C H A R L E S J .
C O T É M D †
*Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical
School, Boston, MA, USA, †Department of Anesthesia and Critical Care, Division of Pediatric
Anesthesia, The Mass General Hospital for Children, Massachusetts General Hospital, Harvard
Medical School, Boston, MA, USA and ‡Department of Surgery, Massachusetts General
Hospital, Harvard Medical School, Boston, MA, USA

Summary
With advances in burn care, many children are surviving severe burn
injuries. Inhalation injury remains a predictor of morbidity and
mortality in burn injury. Inhalation of smoke and toxic gases leads to
pulmonary complications, including airway obstruction from bron-
chial casts, pulmonary edema, decreased pulmonary compliance, and
ventilation–perfusion mismatch, as well as systemic toxicity from
carbon monoxide poisoning and cyanide toxicity. The diagnosis of
inhalation injury is suggested by the history and physical exam and
can be confirmed by bronchoscopy. Management consists of sup-
portive measures, pulmonary toilet, treatment of pulmonary infection
and ventilatory support as needed. This review details the patho-
physiology, diagnosis, and management options for inhalation injury.

Keywords: inhalation injury; burn injury; pediatric

from the impairment of mitochondrial metabolism

Introduction
Although children are less likely than adults to
experience significant smoke inhalation, it remains a
serious and life-threatening problem in the pediatric
population. Approximately 30% of patients with
burn injury have concomitant inhalation injury (1,2).
When victims are exposed to fires in an enclosed
space, they are at risk for inhalation injury. Inhala-
tion of flames, superheated air, smoke, and toxic
gases cause direct pulmonary damage as well as
systemic toxicities. Direct pulmonary damage results
from both heat injury and chemical irritation from
the products of combustion. Systemic toxicity results
Correspondence to: Dr G. Fuzaylov, Pediatric Anesthesia Service;
Massachusetts General Hospital, 55 Fruit Street, Clinics 309,
Boston MA 02155, USA (email: gfuzaylov@partners.org).
because of hydrogen cyanide and carbon monoxide
inhalation. It is important to recognize the presence
of inhalation injury as pulmonary complications
from inhalation injury markedly increase the mor-
bidity and mortality from burn injury from 3–10% to
20–30% (1,3). In the pediatric burn population in the
United States, the lethal burn area associated with
10% mortality is 73% total body surface area (TBSA)
without inhalation injury and 50% TBSA with
inhalation injury (2,4).
For isolated inhalation injury, the mortality rate is
about 3% (5). In this population, increased morbid-
ity from pulmonary complications is associated with
altered mental status from elevated carbon monox-
ide levels, rhonchi and dysphonia on initial exam-
ination, a positive bacteriologic sample, and a

 2008 The Authors

Journal compilation  2008 Blackwell Publishing Ltd 147
148 C.W. FIDKOWSKI ET AL.
requirement for bronchodilator agents for >24 h.
These risk factors are all suggestive that aspiration of
gastric contents at the time of burn injury may be an
inciting factor for increased morbidity and mortality
from pulmonary complications associated with
inhalation injury.
For combined inhalation and burn injury, predic-
tors of mortality include increasing age and increas-
ing TBSA burned (3,6). Increased fluid requirements
and the development of acute respiratory distress
syndrome are also shown to be associated with
increased mortality (6). While patients with com-
bined inhalation and burn injury have increased
fluid resuscitation requirements (7,8), there is no
clear correlation between the required amount of
fluid resuscitation for combined inhalation and burn
injury with disease severity or mortality (8). The
mortality rate also significantly increases if inhala-
tion injury is complicated by pneumonia (9,10).
Direct inhalation injury
Pathophysiology
The circumstances of the burn injury are quite
important in predicating inhalation injury. Burns
sustained in a closed space (house or automobile
fire) in particular are associated with inhalation
injuries as the heat in an enclosed space fire may
reach 538C (1000F) (11,12). As the respiratory
tract is an efficient heat exchanger, only the upper
airway is affected by thermal damage. The excep-
tion to this rule is if the victim is exposed to steam,
which has a much higher heat capacity than dry
air, particulate matter within smoke causes irrita-
tion and damage throughout the respiratory tract.
Particles >10 lm are deposited in the upper airway
(nasopharynx and larynx), particles 3–10 lm are
deposited in the conducting airways, particles 0.5–
3 lm are deposited in the distal airways and
alveoli, and particles <0.5 lm remain in the gas
and can be exhaled (13). Examples of products of
combustion, particularly from plastics and lami-
nated products that contribute to the chemical
airway injury from smoke inhalation include acet-
aldehyde, formaldehyde, acrolein, ammonia, hydro-
gen chloride, sulfur dioxide, nitrogen dioxide, and
hydrogen fluoride (13). The extent of the pulmo-
nary damage depends on the components of the
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
smoke, the length of the exposure, and the victim’s
minute ventilation (14).
The main pathophysiologic basis for the pulmo-
nary dysfunction from inhalation injury is because of
direct mucosal damage, increased bronchial blood
flow, decreased hypoxic pulmonary vasoconstric-
tion, activation of neutrophils, increased microvas-
cular permeability, destruction of goblet cells and
ciliated epithelium, and de-activation of surfactant
(15–18). These adverse effects on pulmonary func-
tion may last for many months after injury (19).
Localized injury caused by inhalation of super-
heated air is generally limited to the airway above the
carina. As a result of this airway burn, these children
should be considered to have airway obstruction
because of macroglossia, macro uvula, heat-induced
epiglottitis and croup all at one time because of the
marked burn induced edema (Figure 1). Any child
with a facial burn or one who is burned in a closed
space is likely to have an inhalation injury such that
the tongue, uvula, epiglottis and subglottic regions
will rapidly swell because of the heat injury. As a
high degree of airway support is likely, we recom-
mend the use of a cuffed endotracheal tube which
will allow better sealing of the airway should
positive end-expiratory pressure be required. Early
intubations is essential in such children as delayed
intubation will be more difficult and may not be
possible even several hours following injury as a
result of this massive swelling of the upper airway
structures. More distal mucosal damage from inha-
lation injury causes mucosal sloughing, impaired
mucociliary clearance, and development of a fibrin-
ous exudate, which lead to the formation of endo-
bronchial casts containing sloughed mucosal
endothelial cells and fibrin clots (Figure 2). This
injury is in part caused by the chemical reaction
combining NO2 and SO2 with exhaled H2O in the
airway that results in the formation of H2SO4 and
H2NO3, which then cause an acid burn of the distal
airway through the alveolar level. The cross-sectional
area of the bronchi, bronchioles, and respiratory
bronchioles is reduced by 29%, 11% and 1.2%,
respectively (20). Airway obstruction and broncho-
spasm result in higher ventilatory pressures that can
lead to barotrauma (15,16).
Both isolated burn injury and combined burn and
inhalation injury lead to increased production of
inflammatory mediators and cytokines such as
 2008 The Authors
 INHALATION BURN INJURY IN CHILDREN
(a)
(b)
Figure 1
(a and b). Early (a) and late (b) facial burn injury. Note the marked
edema of the face within hours of the burn injury.
tumor necrosis factor, interleukin (IL)-6, and IL-8.
These mediators are not further increased in com-
bined inhalation and burn injury compared with
isolated burn injury; therefore, an augmented anti-
inflammatory response alone may not explain the
pulmonary dysfunction from inhalation injury (21).
Immunosuppression and ⁄ or immunodysfunction
 2008 The Authors
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
149
Figure 2
Bronchus after inhalation injury. Note the carbonaceous material
at the level of the carina.
may explain the additional pulmonary dysfunction
as the levels of IL-7 and IL12p70, which regulate
T-cell function, are significantly different in com-
bined inhalation and burn injury (21). While the
exact pathophysiology of cytokine regulation in
inhalation injury remains unknown, evidence sug-
gests that alterations in IL-6, IL-10, and IL-7 are
potential markers for predicting mortality with
inhalation injury (22).
Bronchial blood flow is markedly increased after
smoke inhalation injury, combined smoke inhala-
tion, and cutaneous thermal injury (23,24). A postu-
lated mechanism for parenchymal damage is that
systemic mediators of inflammation from the dam-
aged bronchial mucosa are carried through the
bronchopulmonary circulation to directly injure the
pulmonary microvasculature and cause pulmonary
edema (15,23,24). In fact, ligation of the bronchial
artery in animal models decreases pulmonary
edema formation (23,24).
Inhalation injury also results in increased levels of
inducible nitric oxide synthase and nitric oxide (NO)
(15,16,25). With the increased NO levels, hypoxic
vasoconstriction is reduced (25), and patients sub-
sequently develop ventilation–perfusion mismatch
with an elevated alveolar-arterial oxygen gradient.
150 C.W. FIDKOWSKI ET AL.
Figure 3
Chest escharotomy. Note how the skin is separated, removing the
tourniquet effect around the chest. Multiple eschararotomys will
markedly improve chest wall compliance and reduce the work of
breathing.
The increased NO production caused by the inhala-
tion injury is also implicated in pulmonary micro-
vascular endothelial damage that leads to
pulmonary edema (26). Children with inhalation
injury may develop laryngospasm and broncho-
spasm from airway irritation. The loss of an intact
mucosal epithelium along with immunosuppression
leads to tracheobronchitis and pneumonia.
There is usually a 2–5 day initial period of near-
normal gas exchange prior to endobronchial slough,
shunting and compromised ventilation. Residual
reactive airway disease, bronchiectasis, bronchiolitis
obliterans, and interstitial fibrosis may occur. The
long-term consequences of prolonged tracheal
intubation (erosion of the ala nasae, granuloma
formation, subglottic stenosis, tracheomalacia,
tracheo-innominate artery fistula) are more likely
to occur in these children compared with children
without an inhalation injury (27,28).
Another consideration when evaluating the child
for an inhalation injury is a circumferential chest
burn. With this type of injury the skin shrinks,
causing a tourniquet-like effect and thereby reduc-
ing chest expansion; urgent multiple escharotomies
may be required to improve ventilation (Figure 3).
Diagnosis
The diagnosis of inhalation injury should be sus-
pected based on the history and physical examina-
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
tion. Singed nasal hairs, soot in the airway, stridor,
hoarseness, dyspnea, wheezing, and facial burns are
suggestive of inhalation injury (6,29). Chest radiog-
raphy is not useful in diagnosing inhalation injury as
it is often normal immediately following injury
(1,6,30). Xenon ventilation–perfusion scans were
previously used to diagnose inhalation injury; how-
ever, false positive results may occur in children
with underlying pulmonary disease (1,31). Bedside
fiberoptic bronchoscopy is often helpful in ascer-
taining the severity of inhalation injury (32,33).
Children with inhalation injury characteristically
have mucosal erythema, edema, ulcerations, partic-
ulate matter and soot in the airway, and areas of
necrotic mucosa (2,3,5,6). Methods for grading the
severity of inhalation injury based on bronchoscopy
findings have been developed (8,31) and may be
helpful in predicting the severity of disease, devel-
opment of acute lung injury, and mortality. Com-
puted Tomography (CT) scanning may also be
helpful in making the diagnosis (34,35) with findings
of ground glass opacities, atelectasis, and consolida-
tion adjacent to large airways, but this imaging is not
always practical in acutely burned children. CT
scanning is shown to predict severity of the inhala-
tion injury at 24 h postinjury in an ovine model (36).
Systemic toxicity
Carbon monoxide poisoning and cyanide toxicity
should be suspected in any child with inhalational
injury or with burns from open fires. Carbon
monoxide binds to heme-containing proteins, such
as hemoglobin, cytochromes, and myoglobin with
an affinity that is 200 times stronger than that of
oxygen (12,37,38). Carbon monoxide poisoning
decreases tissue oxygenation by displacing oxygen
from hemoglobin and cytochromes and by shifting
the oxygen dissociation curve to the left (37). Thus,
the available oxygen is more tightly bound and less
available for release to the tissues, and the total
amount of oxygen is reduced. For example, with a
40% level of carboxyhemoglobin, the amount of
available oxygen is reduced from 20 mlÆ100 g)1 of
hemoglobin to 12 mlÆ100 g)1 of hemoglobin. The
binding of carbon monoxide to myoglobin also
decreases oxygen tension in cardiac and skeletal
muscles, which may contribute to cardiac dysfunc-
tion and rhabdomyolysis.
 2008 The Authors
 INHALATION BURN INJURY IN CHILDREN
The diagnosis of carbon monoxide poisoning is
confirmed by elevated carboxy-hemoglobin levels
measured by cooximetry (38). Normal carboxy-
hemoglobin levels are in the range of 1–3%. Typi-
cally, children with a level <20% present with mild
symptoms such as lightheadedness, nausea and
headache (38). Children with 20–40% carboxyhemo-
globin may be confused and disoriented, whereas
those with higher levels (>60–70%) develop ataxia,
collapse, and coma with resultant seizures, cardio-
pulmonary arrest, and death (13,38). Treatment
should not be delayed. The half-life of carboxy-
hemoglobin is 40–80 min when breathing 100%
oxygen compared with 240–320 min when breathing
air (38). If there is any suspicion of carbon monoxide
poisoning, 100% oxygen should be administered
and supportive measures instituted (13). Treatment
for carbon monoxide poisoning with hyperbaric
oxygen is controversial but should be considered
for children who are hemodynamically stable and
whose airway is secured who also have a history of
loss of consciousness, neurologic sequela, or ongoing
metabolic acidosis. The half-life of carboxy-hemo-
globin decreases to 20 min when breathing 100%
oxygen at 2.5–3 atmospheres. It should be noted that
pulse oximetry will be inaccurate in children with
carbon monoxide poisoning with a resultant over
estimation of oxygen saturation as the standard
oximeter interprets carboxyhemoglobin as oxyhe-
moglobin (39,40). A new generation of pulse oxime-
ters (Rad-57 pulse Co-oximeter; Masimo, Inc., Irvine,
CA, USA) is able to quantitate carboxyhemoglobin
values and may be useful in assessing the efficacy of
treatment (41–44).
Cyanide toxicity results from inhalation of cya-
nide products of combustion, which are usually
contained, for example, in the glue that holds
laminates together (13,45,46). Cyanide poisoning is
suggested by an elevated venous oxygen level and a
lactic acidosis that does not improve with oxygen
administration. Cyanide binds to cytochrome oxi-
dase and impairs tissue oxygenation by converting
intracellular aerobic metabolism to anaerobic metab-
olism (47–51). Treatment consists of administration
of sodium thiosulfate, which serves as a sulfate
donor that increases the conversion of cyanide to the
nontoxic thiocyanate, and administration of nitrites,
such as amyl nitrite and sodium nitrite, that increase
the amount of methemoglobin, which then competes
 2008 The Authors
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
151
for cyanide binding from cytochrome oxidase
(47,51–53). The induction of methemoglobinemia
may be dangerous with inhalational injuries because
of co-existing carboxy-hemoglobin. Young children
are particularly sensitive to nitrite administration as
fetal hemoglobin more easily converts to methemo-
globin and as children have lower levels of methe-
moglobin reductase as compared with adults.
Hydroxocobalamin, which is a precursor to vitamin
B12, readily binds intracellular cyanide to form the
nontoxic cyanocobalamin (vitamin B12) (48,53,54).
Treatment with hydroxocobalamin may be more
advantageous in children with smoke inhalation as it
does not induce methemoglobinemia and has a
rapid onset of action. Empiric treatment for possible
cyanide exposure is not currently recommended.
Perioperative respiratory management
Although children may appear stable initially, air-
way edema can rapidly progress over the first 12–
24 h. As the typical physical examination findings of
inhalation injury, including stridor, hoarseness,
dyspnea, and dysphagia, are not predictive of the
need for intubation, it is imperative to err on the side
of intubation for some children who might not
require intubation rather than to delay intubation
only to encounter extreme difficulty when the
airway becomes distorted by edema (29). The pres-
ence of soot in the nares and oropharynx, facial
burns, and large body burns correlate with edema of
the true or the false vocal cords. Therefore, if a child
has facial burns, large body burns, or soot in the oral
cavity, the airway should be secured. If intubation is
required, it is safe to use the nondepolarizing muscle
relaxant, succinylcholine, within the first 24 h after
injury without the risk of developing lethal hyper-
kalemia (55). Our previous standard was to place
uncuffed endotracheal tubes in pediatric patients;
however, recent experience suggests that low pres-
sure high volume cuffed endotracheal tubes should
be used as the decreased pulmonary compliance and
increased ventilatory pressures may cause leaks
around the uncuffed tubes and result in an inability
to adequately ventilate and oxygenate the child (56).
In these circumstances, change to a cuffed tracheal
tube or a larger uncuffed tracheal tube would be
required, but places the child at risk for a disaster,
should reintubation prove difficult because of
152 C.W. FIDKOWSKI ET AL.
massive upper airway tissue edema. Unfortunately
we have been in such a position whereby even when
exchange of the tracheal tube took <30 s the child
was so compromised that cardiac arrest ensued. We
have also observed fatal loss of the airway in this
situation and it is for these reasons that we acknowl-
edge the greater potential for cuff induced airway
injury but balance this risk against a more serious
adverse outcome, should ventilation and oxygenation
prove inadequate with a small uncuffed tracheal tube.
A focus of care for children with inhalation injury
is aggressive pulmonary toilet, which includes chest
physiotherapy, therapeutic bronchoscopy in older
children, coughing, and, if possible, early ambula-
tion (57,58). If a child is mechanically ventilated,
attention should be paid to minimize barotrauma
and volutrauma by minimizing both peak airway
pressures and tidal volumes (57). Permissive hyper-
capnia may be indicated (59). High frequency
percussive ventilation is an alternative to conven-
tional mechanical ventilation and is shown to
decrease peak inspiratory pressures and work of
breathing in pediatric patients with inhalation injury
(60). This mode of ventilation does not, however,
improve shunt fraction, development of pneumonia,
or mortality (61).
Several pharmacologic treatments are also avail-
able for inhalation injury. As children with inhala-
tion injury develop bronchitis and reactive airways,
they benefit from inhaled bronchodilators. Nebu-
lized albuterol is effective in decreasing peak inspi-
ratory pressures, improving pulmonary compliance,
decreasing shunt fraction, and increasing the arterial
to alveolar oxygen gradient (62). These positive
effects of albuterol are attributed to its bronchodila-
tory effect as well as its anti-inflammatory effect.
Aerosolized epinephrine also has a bronchodilatory
effect along with a vasoconstrictive effect to reduce
mucosal edema (57).
As fibrin clots are one component of the debris
that creates airway obstruction, it is thought that
aerosolized anticoagulants will help attenuate the
respiratory, compromise that results from these
obstructions. Aerosolized antithrombin combined
with heparin is shown to decrease the degree of
airway obstruction in an ovine model of cutaneous
and inhalation burn (63). With the attenuated airway
obstruction, pulmonary mechanics also improve as
noted by decreased peak inspiratory pressures,
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
decreased shunt fraction, improved gas exchange,
and decreased lung water content. No systemic
anticoagulant effect is noted with the aerosolized
antithrombin and heparin. Aerosolized N-acetylcys-
teine combined with heparin is also shown to be
effective for treating inhalation injury in an animal
model as well as retrospectively in a pediatric
population (64,65). Prospective human data are
lacking.
Another potential mechanism for the management
of inhalation injury is aimed at reducing pulmonary
vascular permeability. In an ovine model, NO is
shown to decrease microvascular permeability by
decreasing pulmonary vascular pressures and by
decreasing the endovascular damage by reactive
oxygen species (66). NO also improves oxygenation
in children with severely impaired arterial oxygen-
ation and ventilation by decreasing ventilation–
perfusion mismatch (67).
A course of steroids is thought to reduce the
inflammatory response in inhalation injury. How-
ever, treatment with methylprednisolone in isolated
inhalation injury is shown not to improve long term
pulmonary function at 3 months postinjury (27).
Conclusion
Inhalation injury contributes to increased morbidity
and mortality from burn injuries. The diagnosis
should be suspected in individuals exposed to open
fires or those with characteristic physical examina-
tion findings. Those children with inhalation injury
should be treated aggressively with supportive
measures and pulmonary toilet. Further investiga-
tion is needed to fully elucidate the pathophysiology
of inhalation injury in order to provide targeted
treatment options.
References
1 Clark WR Jr. Smoke inhalation: diagnosis and treatment. World
J Surg 1992; 16: 24–29.
2 Barrow RE, Spies M, Barrow LN, et al. Influence of demo-
graphics and inhalation injury on burn mortality in children.
Burns 2004; 30: 72–77.
3 Edelman DA, White MT, Tyburski JG, et al. Factors affecting
prognosis of inhalation injury. J Burn Care Res 2006; 27: 848–
853.
4 Barrow RE, Przkora R, Hawkins HK, et al. Mortality related to
gender, age, sepsis, and ethnicity in severely burned children.
Shock 2005; 23: 485–487.
 2008 The Authors
 INHALATION BURN INJURY IN CHILDREN
5 Hantson P, Butera R, Clemessy JL, et al. Early complications
and value of initial clinical and paraclinical observations in
victims of smoke inhalation without burns. Chest 1997; 111:
671–675.
6 Darling GE, Keresteci MA, Ibanez D, et al. Pulmonary com-
plications in inhalation injuries with associated cutaneous
burn. J Trauma 1996; 40: 83–89.
7 Dai NT, Chen TM, Cheng TY, et al. The comparison of early
fluid therapy in extensive flame burns between inhalation and
noninhalation injuries. Burns 1998; 24: 671–675.
8 Endorf FW, Gamelli RL. Inhalation injury, pulmonary pertur-
bations, and fluid resuscitation. J Burn Care Res 2007; 28: 80–83.
9 Shirani KZ, Pruitt BA Jr, Mason AD Jr. The influence of
inhalation injury and pneumonia on burn mortality. Ann Surg
1987; 205: 82–87.
10 Edelman DA, Khan N, Kempf K, et al. Pneumonia after inha-
lation injury. J Burn Care Res 2007; 28: 241–246.
11 Trunkey DD. Inhalation injury. Surg Clin North Am 1978; 58:
1133–1140.
12 Fein A, Leff A, Hopewell PC. Pathophysiology and manage-
ment of the complications resulting from fire and the inhaled
products of combustion: review of the literature. Crit Care Med
1980; 8: 94–98.
13 Miller K, Chang A. Acute inhalation injury. Emerg Med Clin
North Am 2003; 21: 533–557.
14 Demling R, Lalonde C, Youn YK, et al. Effect of graded
increases in smoke inhalation injury on the early systemic
response to a body burn. Crit Care Med 1995; 23: 171–178.
15 Enkhbaatar P, Traber DL. Pathophysiology of acute lung
injury in combined burn and smoke inhalation injury. Clin Sci
(Lond) 2004; 107: 137–143.
16 Lentz CW, Peterson HD. Smoke inhalation is a multilevel
insult to the pulmonary system. Curr Opin Pulm Med 1997; 3:
221–226.
17 Murakami K, Traber DL. Pathophysiological basis of smoke
inhalation injury. News Physiol Sci 2003; 18: 125–129.
18 Nieman GF, Clark WR Jr, Wax SD, et al. The effect of smoke
inhalation on pulmonary surfactant. Ann Surg 1980; 191: 171–
181.
19 Park GY, Park JW, Jeong DH, et al. Prolonged airway and
systemic inflammatory reactions after smoke inhalation. Chest
2003; 123: 475–480.
20 Cox RA, Burke AS, Soejima K et al. Airway obstruction in
sheep with burn and smoke inhalation injuries. Am J Respir Cell
Mol Biol 2003; 29(3 Pt 1): 295–302.
21 Finnerty CC, Herndon DN, Jeschke MG. Inhalation injury in
severely burned children does not augment the systemic
inflammatory response. Crit Care 2007; 11: R22.
22 Gauglitz GG, Finnerty CC, Herndon DN, et al. Are serum
cytokines early predictors for the outcome of burn patients
with inhalation injuries who do not survive? Crit Care 2008; 12:
R81.
23 Soejima K, Schmalstieg FC, Sakurai H, et al. Pathophysiological
analysis of combined burn and smoke inhalation injuries in
sheep. Am J Physiol Lung Cell Mol Physiol 2001; 280: L1233–
L1241.
24 Abdi S, Herndon DN, Traber LD, et al. Lung edema formation
following inhalation injury: role of the bronchial blood flow.
J Appl Physiol 1991; 71: 727–734.
25 Westphal M, Cox RA, Traber LD, et al. Combined burn and
smoke inhalation injury impairs ovine hypoxic pulmonary
vasoconstriction. Crit Care Med 2006; 34: 1428–1436.
 2008 The Authors
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
153
26 Soejima K, Schmalstieg FC, Traber LD, et al. Role of nitric oxide
in myocardial dysfunction after combined burn and smoke
inhalation injury. Burns 2001; 27: 809–815.
27 Cha SI, Kim CH, Lee JH, et al. Isolated smoke inhalation
injuries: acute respiratory dysfunction, clinical outcomes, and
short-term evolution of pulmonary functions with the effects
of steroids. Burns 2007; 33: 200–208.
28 Cancio LC, Batchinsky AI, Dubick MA, et al. Inhalation injury:
pathophysiology and clinical care proceedings of a sympo-
sium conducted at the Trauma Institute of San Antonio, San
Antonio, TX, USA on 28 March 2006. Burns 2007; 33: 681–692.
29 Madnani DD, Steele NP, de VE. Factors that predict the need
for intubation in patients with smoke inhalation injury. Ear
Nose Throat J 2006; 85: 278–280.
30 Peitzman AB, Shires GT III, Teixidor HS, et al. Smoke inhala-
tion injury: evaluation of radiographic manifestations and
pulmonary dysfunction. J Trauma 1989; 29: 1232–1238.
31 Chou SH, Lin SD, Chuang HY, et al. Fiber-optic bronchoscopic
classification of inhalation injury: prediction of acute lung in-
jury. Surg Endosc 2004; 18: 1377–1379.
32 Irrazabal CL, Capdevila AA, Revich L, et al. Early and late
complications among 15 victims exposed to indoor fire and
smoke inhalation. Burns 2008; 34: 533–538.
33 Marek K, Piotr W, Stanislaw S, et al. Fibreoptic bronchoscopy
in routine clinical practice in confirming the diagnosis and
treatment of inhalation burns. Burns 2007; 33: 554–560.
34 Reske A, Bak Z, Samuelsson A, et al. Computed tomography –
a possible aid in the diagnosis of smoke inhalation injury? Acta
Anaesthesiol Scand 2005; 49: 257–260.
35 Koljonen V, Maisniemi K, Virtanen K, et al. Multi-detector
computed tomography demonstrates smoke inhalation injury
at early stage. Emerg Radiol 2007; 14: 113–116.
36 Park MS, Cancio LC, Batchinsky AI, et al. Assessment of
severity of ovine smoke inhalation injury by analysis of com-
puted tomographic scans. J Trauma 2003; 55: 417–427.
37 Douglas CG, Haldane JS, Haldane JBS. The laws of combina-
tion of hemoglobin with carbon monoxide and oxygen.
J Physiol 1912; 44: 275–304.
38 Kao LW, Nanagas KA. Carbon monoxide poisoning. Med Clin
North Am 2005; 89: 1161–1194.
39 Barker SJ, Tremper KK. The effect of carbon monoxide inha-
lation on pulse oximetry and transcutaneous PO2. Anesthesi-
ology 1987; 66: 677–679.
40 Tremper KK, Barker SJ. Pulse oximetry. Anesthesiology 1989; 70:
98–108.
41 Chee KJ, Nilson D, Partridge R, et al. Finding needles in a
haystack: a case series of carbon monoxide poisoning detected
using new technology in the emergency department. Clin
Toxicol (Phila) 2008; 46: 461–469.
42 Coulange M, Barthelemy A, Hug F, et al. Reliability of new
pulse CO-oximeter in victims of carbon monoxide poisoning.
Undersea Hyperb Med 2008; 35: 107–111.
43 Suner S, Partridge R, Sucov A, et al. Non-invasive pulse CO-
oximetry screening in the emergency department identifies
occult carbon monoxide toxicity. J Emerg Med 2008; 34: 441–
450.
44 Barker SJ, Curry J, Redford D, et al. Measurement of carbo-
xyhemoglobin and methemoglobin by pulse oximetry: a
human volunteer study. Anesthesiology 2006; 105: 892–897.
45 Barillo DJ, Goode R, Esch V. Cyanide poisoning in victims of
fire: analysis of 364 cases and review of the literature. J Burn
Care Rehabil 1994; 15: 46–57.
154 C.W. FIDKOWSKI ET AL.
46 Eckstein M, Maniscalco PM. Focus on smoke inhalation – the
most common cause of acute cyanide poisoning. Prehosp
Disaster Med 2006; 2(Suppl. 2): s49–s55.
47 Geller RJ, Barthold C, Saiers JA, et al. Pediatric cyanide poi-
soning: causes, manifestations, management, and unmet
needs. Pediatrics 2006; 118: 2146–2158.
48 Shepherd G, Velez LI. Role of hydroxocobalamin in acute
cyanide poisoning. Ann Pharmacother 2008; 42: 661–669.
49 Tinker JH, Michenfelder JD. Sodium nitroprusside: pharma-
cology, toxicology and therapeutics. Anesthesiology 1976; 45:
340–354.
50 Tinker JH, Michenfelder JD. Cardiac cyanide toxicity induced
by nitroprusside in the dog: potential for reversal. Anesthesi-
ology 1978; 49: 109–116.
51 Michenfelder JD, Tinker JH. Cyanide toxicity and thiosulfate
protection during chronic administration of sodium nitro-
prusside in the dog: correlation with a human case. Anesthe-
siology 1977; 47: 441–448.
52 Gracia R, Shepherd G. Cyanide poisoning and its treatment.
Pharmacotherapy 2004; 24: 1358–1365.
53 Borron SW, Baud FJ, Barriot P, et al. Prospective study of
hydroxocobalamin for acute cyanide poisoning in smoke
inhalation. Ann Emerg Med 2007; 49: 794–801.
54 Fortin JL, Giocanti JP, Ruttimann M, et al. Prehospital admin-
istration of hydroxocobalamin for smoke inhalation-associated
cyanide poisoning: 8 years of experience in the Paris Fire
Brigade. Clin Toxicol (Phila) 2006; 44(Suppl. 1): 37–44.
55 Martyn JA, Richtsfeld M. Succinylcholine-induced hyper-
kalemia in acquired pathologic states: etiologic factors
and molecular mechanisms. Anesthesiology 2006; 104: 158–
169.
56 Sheridan RL. Uncuffed endotracheal tubes should not be used
in seriously burned children. Pediatr Crit Care Med 2006; 7: 258–
259.
57 Mlcak RP, Suman OE, Herndon DN. Respiratory management
of inhalation injury. Burns 2007; 33: 2–13.
Corrigendum after online publication
The authors have declared no conflicts of interest.
Journal compilation  2008 Blackwell Publishing Ltd, Pediatric Anesthesia, 19 (Suppl. 1), 147–154
58 Arakawa A, Fukamizu H, Hashizume I, et al. Macroscopic and
histological findings in the healing process of inhalation injury.
Burns 2007; 33: 855–859.
59 Sheridan RL, Kacmarek RM, McEttrick MM, et al. Permissive
hypercapnia as a ventilatory strategy in burned children: effect
on barotrauma, pneumonia, and mortality. J Trauma 1995; 39:
854–859.
60 Mlcak R, Cortiella J, Desai M, et al. Lung compliance, airway
resistance, and work of breathing in children after inhalation
injury. J Burn Care Rehabil 1997; 18: 531–534.
61 Cortiella J, Mlcak R, Herndon D. High frequency percussive
ventilation in pediatric patients with inhalation injury. J Burn
Care Rehabil 1999; 20: 232–235.
62 Palmieri TL, Enkhbaatar P, Bayliss R, et al. Continuous nebu-
lized albuterol attenuates acute lung injury in an ovine model
of combined burn and smoke inhalation. Crit Care Med 2006;
34: 1719–1724.
63 Enkhbaatar P, Cox RA, Traber LD, et al. Aerosolized anticoag-
ulants ameliorate acute lung injury in sheep after exposure to
burn and smoke inhalation. Crit Care Med 2007; 35: 2805–2810.
64 Brown M, Desai M, Traber LD, et al. Dimethylsulfoxide with
heparin in the treatment of smoke inhalation injury. J Burn
Care Rehabil 1988; 9: 22–25.
65 Desai MH, Mlcak R, Richardson J, et al. Reduction in mortality
in pediatric patients with inhalation injury with aerosolized
heparin ⁄ N-acetylcystine [correction of acetylcystine] therapy.
J Burn Care Rehabil 1998; 19: 210–212.
66 Enkhbaatar P, Kikuchi Y, Traber LD, et al. Effect of inhaled
nitric oxide on pulmonary vascular hyperpermeability in
sheep following smoke inhalation. Burns 2005; 31: 1013–1019.
67 Sheridan RL, Zapol WM, Ritz RH, et al. Low-dose inhaled
nitric oxide in acutely burned children with profound respi-
ratory failure. Surgery 1999; 126: 856–862.
Accepted 4 November 2008
 2008 The Authors