Current Anaesthesia & Critical Care 19 (2008) 264–268

Contents lists available at ScienceDirect

Current Anaesthesia & Critical Care

journal homepage: www.elsevier.com/locate/cacc

FOCUS ON: BURNS CARE

The respiratory insult in burns injury

S. Singh, J. Handy*
Chelsea & Westminster Hospital, Imperial College London, 369 Fulham Road, London SW10 9NH, UK

s u m m a r y

Keywords: Inhalation injury may result from numerous noxious triggers and in association with other injuries, the
Inhalation most common being cutaneous burns. While patients with severe burns often require transfer to
Injury a regional unit for specialist management, this is not the case for those with inhalation injury associated
Burn
with minor burns or occurring in isolation. These latter patients may require management in a general
Management
intensive care unit and yet they present some unique challenges to the clinician that may otherwise go
Smoke
Toxins unnoticed. The aim of this review is to provide an overview of the pathophysiology, presentation and
management of patients with inhalation injury by way of a guide to those who manage such patients on
an infrequent basis.
Ó 2008 Elsevier Ltd. All rights reserved.

1. Introduction
Inhalation injury occurs in approximately 10–20% of patients
admitted to burn centres, with a report from north west England
highlighting an overall hospital admission rate to of 0.29/1000
population per year.1 Of the 5000 deaths from burns injuries in the
USA per annum, inhalation injury increases the odds ratio of
mortality independently by 2.6.2 Risk factors include delayed
extrication from enclosed or poorly ventilated spaces and the type
and dose of inhaled toxins.
Patients suffering burn injury may develop respiratory insults
from several causes: direct airway injury; hypoxic gas mixture
inhalation; inhalation of systemic toxins; inhalation of local (airway
and pulmonary) toxins; and injury resulting from the ensuing
Systemic Inflammatory Response Syndrome (SIRS). Despite esca-
lating interest and research into the pathophysiological processes
and treatments relevant to other forms of lung injury, there
remains a chasm of such knowledge and information when applied
to inhalation injury.3 There is, however, little reason to suppose that
the development of lung injury as a component of SIRS in these
patients is any different from that in other critically ill patient
groups.4 For this reason, this article will concentrate on the path-
ophysiology, recognition and management of airway and toxin-
related changes that occur in inhalation injury.
2. Pathophysiology of inhalation injury
The pathological processes initiated result from causes which
can be easily remembered using the mnemonic HOTT:
* Corresponding author.
E-mail address: j.m.handy@imperial.ac.uk (J. Handy).
 heat
 oxygen deficiency
 toxins – local
 toxins – systemic
2.1. Heat (thermal) injury
Thermal damage to the airway and subsequent airway
management are crucial, early considerations. The temperature
required to produce such injury will depend on the heat capacity
characteristics of the gas or vapour and the duration of exposure,
with dry gases having less injurious potential than a similar
exposure to saturated vapours. The heat-exchange capabilities of
the upper airway are so efficient that it is rare to suffer thermal
injury below the glottis unless super-heated particles have been
inhaled. This may occur when particulate matter from soot inha-
lation is transported beyond the protective upper airway.
The most significant effect of thermal injury to the upper
airways is the development of oedema with the potential for airway
obstruction. Oedema formation develops rapidly following burn
injury due to the generation of negative interstitial hydrostatic
pressures followed by increases in vascular permeability and
pressure.5–8 These changes develop as innate immune cellular
infiltration occurs, with release of oxygen free radicals, histamine,
bradykinin and prostaglandins.9–12 The process is less profound in
deep burns where the vascular supply is compromised due to the
thermal injury.13 In the absence of fluid resuscitation, the reduction
in intravascular volume and pressure will result in less oedema
formation than following fluid resuscitation. The use of base deficit
to guide resuscitation is associated with greater administered
volumes than when urine output alone is used and the risk of

0953-7112/$ – see front matter Ó 2008 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cacc.2008.09.008
 S. Singh, J. Handy / Current Anaesthesia & Critical Care 19 (2008) 264–268
worsened oedema and tissue oxygenation with over-hydration
highlights the need for more precise and considered end-points in
fluid resuscitation following burn injury.
2.2. Oxygen deficiency
Hypoxia is multi-factorial during inhalation injury and may be
immediate or delayed. During the burn incident:
 oxygen is consumed by combustion and thus ambient oxygen
concentrations can drop to potentially lethal levels
 airway obstruction due to oedema or loss of consciousness can
occur
 cytotoxic hypoxia may develop as a result of the inhalation of
carbon monoxide or hydrogen cyanide (discussed in Section
2.4)
Lung injury often takes between 24 and 48 h to develop and
thus results in delayed hypoxaemia. This is significant as it usually
coincides with the period of maximal tissue oedema. The combi-
nation of low capillary oxygen tension and reduced tissue oxygen
diffusion will compound tissue hypoxia and subsequent ‘reperfu-
sion’ may result in worsening of the injury.
2.3. Toxins – local (respiratory)
Smoke inhalation occurs through the inhalation of the products
of combustion of burning fuels. The two processes involved are
oxidation and pyrolysis (direct melting).
Many lower molecular weight constituents of smoke are toxic to
the lower airways and gas-exchange lung units as a result of their
pH or free radical potential. These include acrolein, formaldehyde,
chlorine, phosgene, perfluoroisobutylene, SO2, NO, and NO2. Soot
contains elemental carbon, and can adsorb toxins, thereby
increasing their distal delivery. Particles less than 4 mm in diameter
have greater propensity to reach the distal airways than the larger
smoke particles.14
2.4. Toxins – systemic
Smoke inhalation may lead to the absorption of carbon
monoxide and hydrogen cyanide. These molecules impair the
delivery and/or utilisation of oxygen and may result in systemic
tissue hypoxia and rapid death.
2.4.1. Carbon monoxide
Carbon monoxide is the leading cause of smoke-related fatali-
ties (up to 80% of deaths).14,15 The number of injuries directly
related to cyanide poisoning is less clearly defined, but its toxicity is
synergistic with that of carbon monoxide, and exposure may be
more common as parent compounds such as polyurethane, acry-
lonitrile, and nylon find increasingly numerous applications.
2.4.2. Cyanide
Hydrogen cyanide is a highly toxic compound that can be
formed in the high temperature combustion/pyrolysis of a number
of common materials such as polyurethane, acrylonitrile, nylon,
wool, and cotton. Cyanide binds to a variety of iron-containing
enzymes, the most important of which is the cytochrome a–a3
complex; this complex is critical for electron transport during
oxidative phosphorylation. By binding to this molecule, minute
amounts of cyanide can inhibit aerobic metabolism and rapidly
result in death.
265
3. Clinical presentation
Respiratory complications are more common following closed
space fires than after fires in the open. Risk factors for respiratory
complications include loss of consciousness and death of another
victim. Obvious signs on admission include facial burns or soot in
the nares or mouth, cutaneous burns on the neck, carbonaceous
sputum and wheezes or crackles on auscultation. Presence or
absence of these signs does not reliably predict the extent of
inhalation injury, nor the type of insult.16
The clinical effects of inhalation injury may be simplistically
divided into:
 effects above and below the glottis
 systemic effects
Particularly worrying signs are:
 any signs of upper airway compromise
 any neurological features that may indicate CO or cyanide
toxicity
The following features raise concern of thermal injury and its
attendant risk of asphyxiation:
 stridor
 use of accessory respiratory muscles
 respiratory distress
 hypoxia or hypercapnia
 deep burns to the face or neck
 blistering or oedema of the oropharynx
3.1. Carbon monoxide toxicity
Carbon monoxide (CO) is an odourless, tasteless, colourless,
non-irritating gas formed by the incomplete combustion of carbon-
containing compounds.14 The clinical findings of CO toxicity are
highly variable and largely non-specific. Symptoms and signs may
include headache, nausea, malaise, altered cognition, dyspnoea,
angina, seizures, cardiac dysrhythmias, congestive heart failure,
and/or coma.
Carboxyhaemoglobin levels correlate imprecisely with the
degree of poisoning and are not predictive of delayed neurologic
sequelae. Neurologic findings, particularly loss of consciousness,
impart a poorer prognosis.17
3.2. Cyanide toxicity
The typical clinical syndrome due to cyanide poisoning is one of
rapidly developing coma, apneoa, cardiac dysfunction, and severe
lactic acidosis in conjunction with a high mixed venous O2 and
a low arteriovenous O2 content difference.18
The toxicities of breathing hypoxic air (which decreases O2
supply), carbon monoxide (which primarily affects O2 delivery and
to a lesser extent O2 utilisation), and cyanide (which primarily
affects O2 utilisation) are synergistic. Some studies have docu-
mented levels of COHb and whole blood cyanide that are each
sublethal but appear fatal in combination.
4. Management
The ABCDE approach of a trauma primary survey is advisable for
assessment and management. Thus, immediate attention to the
adequacy of airway, breathing, and circulation is mandatory, whilst
specific causes of hypoxia should be sought and treated.
266 S. Singh, J. Handy / Current Anaesthesia & Critical Care 19 (2008) 264–268
4.1. Airway
The possibility of pending airway compromise must be consid-
ered continuously while administering high concentrations of
humidified oxygen. Airway oedema may not be maximal until up to
24 h after injury and is often precipitous following fluid
resuscitation.
If airway compromise develops or is anticipated, early endo-
tracheal intubation should be performed by experienced personnel
with prior preparation for the management of a difficult intubation
and surgical airway.
4.1.1. Airway obstruction is a clinical diagnosis
There is no place for pulse oximetry and blood gas analysis to
guide the need for intubation on the grounds of airway compromise
alone, as the latter will only show abnormalities at a pre-terminal
stage. Clinical signs that should alert the clinician to potential
airway obstruction include erythema and oedema of the mucosa in
the mouth; significant facial burns; carbonaceous sputum on deep
cough; singed nasal hair and hoarse voice.
Imminent signs of airway obstruction include:
 tracheal tug
 intercostal recession
 paradoxical (see-saw) breathing pattern
There is little substitute for repeated, meticulous assessments of
the airway, in particular with respect to voice quality as this not
only allows early recognition of airway inadequacy but can also
prevent unnecessary intubation and ventilation. Such clinical
monitoring should, however be performed in an environment
where the appropriate equipment, drugs and personnel are
immediately available should the need for definitive airway
management arise.
4.1.2. When to intubate?
If the findings of upper airway compromise are absent, the
oropharynx should be examined for erythema and laryngoscopy
performed. If oedema or blistering of the upper airway is appreci-
ated on laryngoscopic exam, intubation should be performed
without delay. In the absence of such findings, close observation is
warranted for 24 h with a low threshold to proceed to serial
laryngoscopies if there is a change in status.
If intubation is performed, a large lumen endotracheal tube
(ETT) should be placed to enable optimal management of secre-
tions, and oxygen should be humidified to avoid inspissation.
Changing the ETT in the presence of upper airway oedema is
dangerous, and the tube should be left in place until resolution of
upper airway oedema (generally 3–5 days). Repeated surgery or
persisting respiratory compromise may necessitate early
tracheostomy.
4.2. Breathing
Lung injury usually takes several hours or even days to progress
and the clinical course may reflect this. Radiographic changes often
do not appear until 24 h or more after the insult and thus a normal
chest radiograph at presentation does not exclude a significant
inhalation injury. Arterial blood gas analysis is invaluable for:
 assessing the state of respiratory adequacy
 excluding carbon monoxide toxicity
 raising suspicion of cyanide poisoning
Pulse oximetry should be performed continuously (this may
give an inappropriately high reading in the presence of
carboxyhaemoglobin.) The diagnosis of direct toxin damage is
based upon a compatible history, findings of bronchorrhea and
bronchospasm, and/or bronchoscopic visualisation of damaged
airway mucosa. Treatment involves aerosolised bronchodilators;
corticosteroids have no proven benefit in this setting.19
4.2.1. Carboxyhaemoglobin (COHb)
COHb levels greater than 10% should be treated with 100%
inspired oxygen therapy. The half life of COHb is reduced from
240 min at an inspired oxygen concentration (FiO2) of 21% to about
80 min at a FiO2 of 100%. Hyperbaric therapy should be considered
in patients with COHb greater than 40% or 20% if pregnant and in
patients who have had lowered conscious level from no other
cause. In practice though, due in part to logistic and technical
difficulties, hyperbaric therapy is rarely performed.
4.2.2. Ventilation
Supportive and ventilatory strategies associated with benefit in
non-burns acute lung injury (i.e. avoiding excessive volumes and
maintaining patency of recruited lung, once hypoxaemia has been
overcome) may be considered best clinical practice in the absence
of specific studies of ventilatory strategy in burns inhalational
injury.20 High-frequency percussive ventilation (HFPV) has been
reported to decrease both the incidence of pulmonary barotrauma
and pneumonia in inhalation injury. It has evolved into a ventila-
tory modality promoted to rapidly remove airway secretions and
improve survival of patients with smoke inhalation injury.21 Its
further evaluation is necessary before any specific recommenda-
tions can be made.
The use of vascularly inserted extracorporeal devices that assist
in the removal of carbon dioxide, whilst providing some additional
oxygenation are emerging. They are potentially useful in allowing
low tidal volume (LTV) ventilation, whilst maintaining the gas-
exchange functions of the lung, as a bridge to recovery. No robust
evidence to support their use yet exists, and they should be
considered only for named patients in a rescue setting. Interest-
ingly, a recent animal study of arteriovenous carbon dioxide
removal in conjunction with LTV ventilation showed improved
outcome over those supported by LTV or HFPV alone.22
Non-invasive positive pressure ventilation (NIV) is an important
technique which has been shown to prevent the need for intuba-
tion and improve respiratory weaning in a number of critical
pulmonary and cardiac conditions, such as chronic obstructive
pulmonary disease, respiratory failure due to pulmonary infection
in immunosuppressed patients and CPAP non-responsive cardio-
genic pulmonary oedema. While there is some evidence to support
its use in burned patients with respiratory failure,23 there is
a paucity of such evidence specifically aimed at the management of
those with inhalation injury.
4.2.3. Bronchoscopy
Some centres routinely perform bronchoscopy rather than
laryngoscopy. Although such an approach allows visualisation from
the mouth to the level of bronchopulmonary subsegments, the
appearance of the subglottic airways does not definitively affect
management and appears unreliable in predicting the need for
ventilator support.24,25 Lavage should be performed if pulmonary
contamination is present. Care should be maintained since exces-
sive saline lavage may induce lung injury. The safe volume is not
defined.
The use of local airway therapies such as nebulised unfractio-
nated heparin (300–1000 IU/kg per day for 3–5 days) or mucolytics
such as N-acetylcysteine to improve airway clearance of mucus
plugs or mucosal webs from sloughed airway lining (and as anti-
oxidants), whilst in use sporadically, have not been subjected to
rigorous trials.
 S. Singh, J. Handy / Current Anaesthesia & Critical Care 19 (2008) 264–268
4.3. Cardiovascular/disability/exposure
The assessment of these elements within the primary survey
will be greatly influenced by the presence or absence of other
injuries such as cutaneous burns or multiple trauma. Early clinical
signs of cardiovascular inadequacy include tachycardia, delayed
capillary return (greater than 2 s) and tachypnoea. Hypotension is
a late sign and will often occur with decreased skin perfusion (pale,
cold and clammy). Continuous electrocardiography (ECG) and
regular blood pressure monitoring should be instituted as a basic
standard of care, with continuous blood pressure monitoring
considered for the more severely ill. Decreased conscious level in
the absence of head injury should raise the possibility of critically
low oxygen delivery due to cardiovascular inadequacy or toxicity
through carbon monoxide or cyanide. In this context it is a pre-
terminal sign that warrants immediate action.
Both arterial and central venous blood gas analysis provide
useful information pertaining to oxygen delivery:
 increasing base deficit and blood lactate are suggestive of
inadequate tissue oxygenation which in the presence of
decreased central venous oxygen saturation (ScvO2) is likely
due to cardiovascular insufficiency
 if the ScvO2 is raised, cyanide toxicity should be considered and
treated empirically
 worsening acidosis; measurement of anion gap (corrected for
albumin and phosphate levels) and osmolar gap will aid in the
diagnosis of other acidifying toxins
Whole blood cyanide levels should be sent to confirm the
diagnosis, but the results of this test are generally not available in
a timely fashion and empiric treatment must be instituted if the
diagnosis is suspected.18
Sodium thiosulphate acts slowly by catalysing the metabolism
of cyanide. Sodium nitrite reduces cyanide binding by oxidation of
haemoglobin to methaemoglobin (MetHb). Methaemoglobin levels
of about 40% should be targeted. MetHb levels may require moni-
toring cyanide binding agents such as dicobalt edetate or hydrox-
ocobalamin may be used, though the former may induce cardiac
arrhythmias and instability if used in the absence of cyanide
poisoning. There are suggestions, albeit from one non-randomised
study, that early empirical treatment with hydroxycobalamin in
suspected cases of burns-related inhalational injury improves
survival rates.26
4.4. Other aspects of management
The overall management of such patients will largely be dictated
by the organ dysfunction that poses the greatest threat to life.
Standard established practices for the critically ill apply to burns
respiratory injury too. Thus, chest physiotherapy remains widely
accepted management despite a lack of evidence to support it.
Therapies employed in the management of long-term critically ill
and mechanically ventilated patients should be considered. Exam-
ples include the use of prophylaxis against venous thrombo-embo-
lism and gastrointestinal stress ulceration, and measures to reduce
ventilator associated pneumonia, (e.g. >30 head up). Patients who
have suffered inhalation injury are at risk of developing pulmonary
infections but there is no evidence to support the use of prophylactic
antibiotics. Meticulous surveillance, appropriate cultures and
conservative use of targeted antibiotic courses, with therapy guided
by close liaison with microbiology colleagues is encouraged.
Acute lung injury from any cause is associated with increased
energy expenditure requiring careful nutritional supplementation
in order to avoid protein-calorie malnutrition and its associated
increase in morbidity and mortality. This situation is significantly
267
exacerbated by the presence of other injuries; none more so than
cutaneous burns. These patients should have regular nutritional
assessment and the involvement of clinicians with appropriate
dietetic experience is advised.
4.4.1. Fluid management
There is little doubt that inhalation injury can result in large
fluid losses which require replacement and resuscitation. However
there is an increasing suggestion that patients with inhalation and
burn injury are experiencing over-resuscitation with detrimental
results. Over-hydration results in increased lung and tissue oedema
with decreased lung and chest wall compliance. These factors will
exacerbate existing impairment in gas exchange and ventilation
and can lead to worsened outcome. Currently there is interest in
utilising different end-points in fluid resuscitation in order to allow
a state of ‘permissive hypovolaemia’ for such patients27 though
there is an absence of large scale trials examining this strategy.
4.5. Future therapies
Exogenous surfactant, leukotriene inhibitors, and antioxidants
are a few compounds that have been investigated in animal models
of smoke inhalation. These, and experience extrapolated from
clinical trials (all of them negative) in acute lung injury raise the
possibility of these compounds having a future role in the treat-
ment of burns inhalation injury.
4.5.1. Exogenous surfactant
Exogenous administration of a surfactant preparation to dogs
immediately after wood smoke inhalation injury can improve gas
exchange and compliance in the first few hours.28
4.5.2. Antioxidants
The extent of oxidant stress (i.e. lipid peroxidation) in the lung
and systemically, correlates well with respiratory failure and
mortality in a rat model of burns inhalation injury.29 In a sheep
model, fluid resuscitation with a deferoxamine hetastarch complex
(a free iron and hydroxyl radical scavenger) attenuates both airway
and systemic inflammation.30
5. Conclusions
Inhalation injury is a disease process commonly associated with
burn injury that may require management in a general intensive
care unit setting. Despite a significant morbidity and mortality,
robust research data into the pathophysiology and optimum
management of this condition is limited. The mainstay of current
care involves aggressive attention to the trauma primary survey
and consideration and treatment of noxious gaseous toxins. This
should be followed by a multi-disciplinary approach with meticu-
lous attention to the ‘basics’ of critical care including prevention
and limitation of iatrogenic problems, nutritional and systemic
support and aggressive rehabilitation.
References
1. Rajpura A. Epidemiology of burns and smoke inhalation in secondary care:
a population-based study covering Lancashire and South Cumbria. Burns
2002;28(2):121–30 (abstract).
2. McGwin Jr G, George RL, Cross JM, Rue LW. Improving the ability to predict mortality
among burn patients. Burns; 2007 [Epub ahead of print; PMID: 17869427].
3. Palmieri T. Inhalation injury: research progress and needs. J Burn Care Res
2007;28(4):549–54.
4. Ware LB, Matthay MA. The Acute Respiratory Distress Syndrome. N Engl J Med
2000;342(18):1334–49.
5. Lund T, Wiig H, Reed RK. Acute postburn edema: role of strongly negative
interstitial fluid pressure. Am J Physiol 1988;255:H1069–74.
6. Arturson G. Microvascular permeability to macromolecules after thermal
injury. Acta Physiol Scand Suppl 1979;2:111–22.
268 S. Singh, J. Handy / Current Anaesthesia & Critical Care 19 (2008) 264–268
7. Lund T, Onarkeim H, Reed R. Pathogenesis of edema formation in burn injuries.
World J Surg 1992;16:2–9.
8. Lund T, Reed RK. Microvascular fluid exchange following thermal skin injury in
the rat: changes in extravascular colloid osmotic pressure, albumin mass water
content. Circ Shock 1986;20:91–104.
9. Matsuda T, Tanaka H, Reyes HM, Richter HM, Hanumadass MM, Shimazaki S,
et al. Antioxidant therapy using high dose vitamin C: reduction of post
resuscitation fluid volume requirements. World J Surg 1995;19:287–91.
10. Yoshioka T, Monafo W, Ayvazian VH, Deitz F, Flynn D. Cimetidine inhibits burn
edema formation. Am J Surg 1978;136:C81–5.
11. Nwariaku FE, Sikes PJ, Lightfoot E, Mileski WJ, Baxter C. Effect of a bradykinin
antagonist on the local inflammatory response following thermal injury. Burns
1996;22:324–7.
12. Barrow R, Ranwiez R, Zhang X. Ibuprofen modulates tissue perfusion in partial
thickness burns. Burns 2000;26:341–6.
13. Carvajal HF, Linares HA, Brouhard BH. Relationship of burn size to vascular
permeability changes in rats. Surg Gynecol Obstet 1979;149:193–202.
14. Ernst A, Zibrak JD. Carbon monoxide poisoning. N Engl J Med 1998;
339:1603–8.
15. Raub JA, Mathieu-Nolf M, Hampson NB, Thom SR. Carbon monoxide poisoning–
a public health perspective. Toxicology 2000;145(1):1–14.
16. Clark WR. Smoke inhalation: diagnosis and treatment. World J Surg
1992;16:24–9.
17. Seger D, Welch L. Carbon monoxide controversies: neuropsychologic testing,
mechanisms of toxicity, and hyperbaric oxygen. Ann Emerg Med
1994;24:242–8.
18. Klaassen CD, editor. Casarett and Doull’s toxicology: the basic science of poisons.
5th ed. New York: McGraw-Hill; 1996.
19. Robinson NB, Hudson LD, Riem M, Miller E, Willoughby J, Ravenholt O, et al.
Steroid therapy following isolated smoke inhalation injury. J Trauma
1982;22:876–9.
20. The Acute Respiratory Distress Syndrome Network. Ventilation with lower
tidal volumes as compared with traditional tidal volumes for acute lung
injury and the Acute Respiratory Distress Syndrome. N Engl J Med
2000;342:1301–8.
21. Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive
ventilation in inhalation injuries. J Burn Care Res 2007;28(3):396–400.
22. Schmalsteig FC, Keeney SE, Rudloff HE, Palkowetz KH, Cevallos M, Zhou X, et al.
Arteriovenous CO2 removal improves survival compared to high frequency
percussive and low tidal volume ventilation in a smoke/burn sheep acute
respiratory distress syndrome model. Ann Surg 2007;246(3):512–21.
23. Smailes S. Non-invasive positive pressure ventilation in burns. Burns
2002;28(8):795–801.
24. Bingham HG, Gallagher J, Powell MD. Early bronchoscopy as a predictor of
ventilatory support for burned patients. J Trauma 1987;27:1286–8.
25. American Burn Association. Inhalation injury: diagnosis. J Am Coll Surg
2003;196(2):307–12.
26. Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of
hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg
Med 2007;49:794–801.
27. Arlati S, Storti E, Pradella V, Bucci L, Vitolo A, Pulici M. Decreased fluid volume
to reduce organ damage: a new approach to burn shock resuscitation?
A preliminary study. Resuscitation 2007;72:371–8.
28. Nieman GF, Paskanik AM, Fluck RR, Clark WR. Comparison of exogenous
surfactant in the treatment of wood smoke inhalation. Am J Respir Crit Care Med
1995;152:597–602.
29. Demling R, Ikegami K, Lalonde C. Increased lipid peroxidation and decreased
antioxidant activity correspond with death after smoke exposure in the rat.
J Burn Care Rehabil 1995;16:104–10.
30. Demling R, Lalonde C, Ikegami K. Fluid resuscitation with deferoxamine
hetastarch complex attenuates the lung and systemic response to smoke
inhalation. Surgery 1996;119:340–8.