1. The respiratory insult in burns injury can result from inhalation of heat, oxygen deficiency, and toxins both locally in the airways and systemically. Thermal injury causes airway edema which can lead to obstruction, while toxins like carbon monoxide and cyanide impair oxygen delivery and utilization. 2. Clinical presentation may include signs of upper airway compromise, neurological features of toxin exposure, and respiratory distress. Management involves securing the airway, administering oxygen, treating specific toxins, and supporting ventilation while avoiding excessive lung volumes. 3. Intubation is indicated for impending airway obstruction from edema, while close monitoring is needed for delayed edema. High oxygen concentrations treat carbon monoxide toxicity

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

2. S. Singh, J. Handy / Current Anaesthesia Critical Care 19 (2008) 264–268 265
worsened oedema and tissue oxygenation with over-hydration 3. Clinical presentation
highlights the need for more precise and considered end-points in
fluid resuscitation following burn injury. 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
2.2. Oxygen deficiency victim. Obvious signs on admission include facial burns or soot in
the nares or mouth, cutaneous burns on the neck, carbonaceous
Hypoxia is multi-factorial during inhalation injury and may be sputum and wheezes or crackles on auscultation. Presence or
immediate or delayed. During the burn incident: absence of these signs does not reliably predict the extent of
inhalation injury, nor the type of insult.16
oxygen is consumed by combustion and thus ambient oxygen The clinical effects of inhalation injury may be simplistically
concentrations can drop to potentially lethal levels divided into:
airway obstruction due to oedema or loss of consciousness can
occur effects above and below the glottis
cytotoxic hypoxia may develop as a result of the inhalation of systemic effects
carbon monoxide or hydrogen cyanide (discussed in Section
2.4) Particularly worrying signs are:
Lung injury often takes between 24 and 48 h to develop and any signs of upper airway compromise
thus results in delayed hypoxaemia. This is significant as it usually any neurological features that may indicate CO or cyanide
coincides with the period of maximal tissue oedema. The combi- toxicity
nation of low capillary oxygen tension and reduced tissue oxygen
diffusion will compound tissue hypoxia and subsequent ‘reperfu- The following features raise concern of thermal injury and its
sion’ may result in worsening of the injury. attendant risk of asphyxiation:
stridor
2.3. Toxins – local (respiratory) use of accessory respiratory muscles
respiratory distress
Smoke inhalation occurs through the inhalation of the products hypoxia or hypercapnia
of combustion of burning fuels. The two processes involved are deep burns to the face or neck
oxidation and pyrolysis (direct melting). blistering or oedema of the oropharynx
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, 3.1. Carbon monoxide toxicity
chlorine, phosgene, perfluoroisobutylene, SO2, NO, and NO2. Soot
contains elemental carbon, and can adsorb toxins, thereby Carbon monoxide (CO) is an odourless, tasteless, colourless,
increasing their distal delivery. Particles less than 4 mm in diameter non-irritating gas formed by the incomplete combustion of carbon-
have greater propensity to reach the distal airways than the larger containing compounds.14 The clinical findings of CO toxicity are
smoke particles.14 highly variable and largely non-specific. Symptoms and signs may
include headache, nausea, malaise, altered cognition, dyspnoea,
angina, seizures, cardiac dysrhythmias, congestive heart failure,
2.4. Toxins – systemic and/or coma.
Carboxyhaemoglobin levels correlate imprecisely with the
Smoke inhalation may lead to the absorption of carbon degree of poisoning and are not predictive of delayed neurologic
monoxide and hydrogen cyanide. These molecules impair the sequelae. Neurologic findings, particularly loss of consciousness,
delivery and/or utilisation of oxygen and may result in systemic impart a poorer prognosis.17
tissue hypoxia and rapid death.
3.2. Cyanide toxicity
2.4.1. Carbon monoxide
Carbon monoxide is the leading cause of smoke-related fatali- The typical clinical syndrome due to cyanide poisoning is one of
ties (up to 80% of deaths).14,15 The number of injuries directly rapidly developing coma, apneoa, cardiac dysfunction, and severe
related to cyanide poisoning is less clearly defined, but its toxicity is lactic acidosis in conjunction with a high mixed venous O2 and
synergistic with that of carbon monoxide, and exposure may be a low arteriovenous O2 content difference.18
more common as parent compounds such as polyurethane, acry- The toxicities of breathing hypoxic air (which decreases O2
lonitrile, and nylon find increasingly numerous applications. supply), carbon monoxide (which primarily affects O2 delivery and
to a lesser extent O2 utilisation), and cyanide (which primarily
2.4.2. Cyanide affects O2 utilisation) are synergistic. Some studies have docu-
Hydrogen cyanide is a highly toxic compound that can be mented levels of COHb and whole blood cyanide that are each
formed in the high temperature combustion/pyrolysis of a number sublethal but appear fatal in combination.
of common materials such as polyurethane, acrylonitrile, nylon,
wool, and cotton. Cyanide binds to a variety of iron-containing 4. Management
enzymes, the most important of which is the cytochrome a–a3
complex; this complex is critical for electron transport during The ABCDE approach of a trauma primary survey is advisable for
oxidative phosphorylation. By binding to this molecule, minute assessment and management. Thus, immediate attention to the
amounts of cyanide can inhibit aerobic metabolism and rapidly adequacy of airway, breathing, and circulation is mandatory, whilst
result in death. specific causes of hypoxia should be sought and treated.

3. 266 S. Singh, J. Handy / Current Anaesthesia Critical Care 19 (2008) 264–268
4.1. Airway carboxyhaemoglobin.) The diagnosis of direct toxin damage is
based upon a compatible history, findings of bronchorrhea and
The possibility of pending airway compromise must be consid- bronchospasm, and/or bronchoscopic visualisation of damaged
ered continuously while administering high concentrations of airway mucosa. Treatment involves aerosolised bronchodilators;
humidified oxygen. Airway oedema may not be maximal until up to corticosteroids have no proven benefit in this setting.19
24 h after injury and is often precipitous following fluid
resuscitation. 4.2.1. Carboxyhaemoglobin (COHb)
If airway compromise develops or is anticipated, early endo- COHb levels greater than 10% should be treated with 100%
tracheal intubation should be performed by experienced personnel inspired oxygen therapy. The half life of COHb is reduced from
with prior preparation for the management of a difficult intubation 240 min at an inspired oxygen concentration (FiO2) of 21% to about
and surgical airway. 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
4.1.1. Airway obstruction is a clinical diagnosis patients who have had lowered conscious level from no other
There is no place for pulse oximetry and blood gas analysis to cause. In practice though, due in part to logistic and technical
guide the need for intubation on the grounds of airway compromise difficulties, hyperbaric therapy is rarely performed.
alone, as the latter will only show abnormalities at a pre-terminal
stage. Clinical signs that should alert the clinician to potential 4.2.2. Ventilation
airway obstruction include erythema and oedema of the mucosa in Supportive and ventilatory strategies associated with benefit in
the mouth; significant facial burns; carbonaceous sputum on deep non-burns acute lung injury (i.e. avoiding excessive volumes and
cough; singed nasal hair and hoarse voice. maintaining patency of recruited lung, once hypoxaemia has been
Imminent signs of airway obstruction include: overcome) may be considered best clinical practice in the absence
of specific studies of ventilatory strategy in burns inhalational
tracheal tug injury.20 High-frequency percussive ventilation (HFPV) has been
intercostal recession reported to decrease both the incidence of pulmonary barotrauma
paradoxical (see-saw) breathing pattern and pneumonia in inhalation injury. It has evolved into a ventila-
tory modality promoted to rapidly remove airway secretions and
There is little substitute for repeated, meticulous assessments of improve survival of patients with smoke inhalation injury.21 Its
the airway, in particular with respect to voice quality as this not further evaluation is necessary before any specific recommenda-
only allows early recognition of airway inadequacy but can also tions can be made.
prevent unnecessary intubation and ventilation. Such clinical The use of vascularly inserted extracorporeal devices that assist
monitoring should, however be performed in an environment in the removal of carbon dioxide, whilst providing some additional
where the appropriate equipment, drugs and personnel are oxygenation are emerging. They are potentially useful in allowing
immediately available should the need for definitive airway low tidal volume (LTV) ventilation, whilst maintaining the gas-
management arise. exchange functions of the lung, as a bridge to recovery. No robust
evidence to support their use yet exists, and they should be
4.1.2. When to intubate? considered only for named patients in a rescue setting. Interest-
If the findings of upper airway compromise are absent, the ingly, a recent animal study of arteriovenous carbon dioxide
oropharynx should be examined for erythema and laryngoscopy removal in conjunction with LTV ventilation showed improved
performed. If oedema or blistering of the upper airway is appreci- outcome over those supported by LTV or HFPV alone.22
ated on laryngoscopic exam, intubation should be performed Non-invasive positive pressure ventilation (NIV) is an important
without delay. In the absence of such findings, close observation is technique which has been shown to prevent the need for intuba-
warranted for 24 h with a low threshold to proceed to serial tion and improve respiratory weaning in a number of critical
laryngoscopies if there is a change in status. pulmonary and cardiac conditions, such as chronic obstructive
If intubation is performed, a large lumen endotracheal tube pulmonary disease, respiratory failure due to pulmonary infection
(ETT) should be placed to enable optimal management of secre- in immunosuppressed patients and CPAP non-responsive cardio-
tions, and oxygen should be humidified to avoid inspissation. genic pulmonary oedema. While there is some evidence to support
Changing the ETT in the presence of upper airway oedema is its use in burned patients with respiratory failure,23 there is
dangerous, and the tube should be left in place until resolution of a paucity of such evidence specifically aimed at the management of
upper airway oedema (generally 3–5 days). Repeated surgery or those with inhalation injury.
persisting respiratory compromise may necessitate early
tracheostomy. 4.2.3. Bronchoscopy
Some centres routinely perform bronchoscopy rather than
4.2. Breathing laryngoscopy. Although such an approach allows visualisation from
the mouth to the level of bronchopulmonary subsegments, the
Lung injury usually takes several hours or even days to progress appearance of the subglottic airways does not definitively affect
and the clinical course may reflect this. Radiographic changes often management and appears unreliable in predicting the need for
do not appear until 24 h or more after the insult and thus a normal ventilator support.24,25 Lavage should be performed if pulmonary
chest radiograph at presentation does not exclude a significant contamination is present. Care should be maintained since exces-
inhalation injury. Arterial blood gas analysis is invaluable for: sive saline lavage may induce lung injury. The safe volume is not
defined.
assessing the state of respiratory adequacy The use of local airway therapies such as nebulised unfractio-
excluding carbon monoxide toxicity nated heparin (300–1000 IU/kg per day for 3–5 days) or mucolytics
raising suspicion of cyanide poisoning such as N-acetylcysteine to improve airway clearance of mucus
plugs or mucosal webs from sloughed airway lining (and as anti-
Pulse oximetry should be performed continuously (this may oxidants), whilst in use sporadically, have not been subjected to
give an inappropriately high reading in the presence of rigorous trials.

4. S. Singh, J. Handy / Current Anaesthesia Critical Care 19 (2008) 264–268 267
4.3. Cardiovascular/disability/exposure exacerbated by the presence of other injuries; none more so than
cutaneous burns. These patients should have regular nutritional
The assessment of these elements within the primary survey assessment and the involvement of clinicians with appropriate
will be greatly influenced by the presence or absence of other dietetic experience is advised.
injuries such as cutaneous burns or multiple trauma. Early clinical
signs of cardiovascular inadequacy include tachycardia, delayed 4.4.1. Fluid management
capillary return (greater than 2 s) and tachypnoea. Hypotension is There is little doubt that inhalation injury can result in large
a late sign and will often occur with decreased skin perfusion (pale, fluid losses which require replacement and resuscitation. However
cold and clammy). Continuous electrocardiography (ECG) and there is an increasing suggestion that patients with inhalation and
regular blood pressure monitoring should be instituted as a basic burn injury are experiencing over-resuscitation with detrimental
standard of care, with continuous blood pressure monitoring results. Over-hydration results in increased lung and tissue oedema
considered for the more severely ill. Decreased conscious level in with decreased lung and chest wall compliance. These factors will
the absence of head injury should raise the possibility of critically exacerbate existing impairment in gas exchange and ventilation
low oxygen delivery due to cardiovascular inadequacy or toxicity and can lead to worsened outcome. Currently there is interest in
through carbon monoxide or cyanide. In this context it is a pre- utilising different end-points in fluid resuscitation in order to allow
terminal sign that warrants immediate action. a state of ‘permissive hypovolaemia’ for such patients27 though
Both arterial and central venous blood gas analysis provide there is an absence of large scale trials examining this strategy.
useful information pertaining to oxygen delivery:
4.5. Future therapies
increasing base deficit and blood lactate are suggestive of
inadequate tissue oxygenation which in the presence of Exogenous surfactant, leukotriene inhibitors, and antioxidants
decreased central venous oxygen saturation (ScvO2) is likely are a few compounds that have been investigated in animal models
due to cardiovascular insufficiency of smoke inhalation. These, and experience extrapolated from
if the ScvO2 is raised, cyanide toxicity should be considered and clinical trials (all of them negative) in acute lung injury raise the
treated empirically possibility of these compounds having a future role in the treat-
worsening acidosis; measurement of anion gap (corrected for ment of burns inhalation injury.
albumin and phosphate levels) and osmolar gap will aid in the
diagnosis of other acidifying toxins 4.5.1. Exogenous surfactant
Exogenous administration of a surfactant preparation to dogs
Whole blood cyanide levels should be sent to confirm the immediately after wood smoke inhalation injury can improve gas
diagnosis, but the results of this test are generally not available in exchange and compliance in the first few hours.28
a timely fashion and empiric treatment must be instituted if the
diagnosis is suspected.18 4.5.2. Antioxidants
Sodium thiosulphate acts slowly by catalysing the metabolism The extent of oxidant stress (i.e. lipid peroxidation) in the lung
of cyanide. Sodium nitrite reduces cyanide binding by oxidation of and systemically, correlates well with respiratory failure and
haemoglobin to methaemoglobin (MetHb). Methaemoglobin levels mortality in a rat model of burns inhalation injury.29 In a sheep
of about 40% should be targeted. MetHb levels may require moni- model, fluid resuscitation with a deferoxamine hetastarch complex
toring cyanide binding agents such as dicobalt edetate or hydrox- (a free iron and hydroxyl radical scavenger) attenuates both airway
ocobalamin may be used, though the former may induce cardiac and systemic inflammation.30
arrhythmias and instability if used in the absence of cyanide
poisoning. There are suggestions, albeit from one non-randomised 5. Conclusions
study, that early empirical treatment with hydroxycobalamin in
suspected cases of burns-related inhalational injury improves Inhalation injury is a disease process commonly associated with
survival rates.26 burn injury that may require management in a general intensive
care unit setting. Despite a significant morbidity and mortality,
4.4. Other aspects of management robust research data into the pathophysiology and optimum
management of this condition is limited. The mainstay of current
The overall management of such patients will largely be dictated care involves aggressive attention to the trauma primary survey
by the organ dysfunction that poses the greatest threat to life. and consideration and treatment of noxious gaseous toxins. This
Standard established practices for the critically ill apply to burns should be followed by a multi-disciplinary approach with meticu-
respiratory injury too. Thus, chest physiotherapy remains widely lous attention to the ‘basics’ of critical care including prevention
accepted management despite a lack of evidence to support it. and limitation of iatrogenic problems, nutritional and systemic
Therapies employed in the management of long-term critically ill support and aggressive rehabilitation.
and mechanically ventilated patients should be considered. Exam-
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