Current Anaesthesia & Critical Care 19 (2008) 264–268 Contents lists available at ScienceDirect Current Anaesthesia & Critical Care journal homepage: www.elsevier.com/locate/caccFOCUS ON: BURNS CAREThe respiratory insult in burns injuryS. Singh, J. Handy*Chelsea & Westminster Hospital, Imperial College London, 369 Fulham Road, London SW10 9NH, UK s u m m a r yKeywords: Inhalation injury may result from numerous noxious triggers and in association with other injuries, theInhalation most common being cutaneous burns. While patients with severe burns often require transfer toInjury a regional unit for specialist management, this is not the case for those with inhalation injury associatedBurn with minor burns or occurring in isolation. These latter patients may require management in a generalManagement intensive care unit and yet they present some unique challenges to the clinician that may otherwise goSmokeToxins 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 – localadmitted to burn centres, with a report from north west England toxins – systemichighlighting an overall hospital admission rate to of 0.29/1000population per year.1 Of the 5000 deaths from burns injuries in theUSA per annum, inhalation injury increases the odds ratio ofmortality independently by 2.6.2 Risk factors include delayed 2.1. Heat (thermal) injuryextrication from enclosed or poorly ventilated spaces and the typeand 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 temperaturefrom several causes: direct airway injury; hypoxic gas mixture required to produce such injury will depend on the heat capacityinhalation; 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 similarSystemic Inﬂammatory Response Syndrome (SIRS). Despite esca- exposure to saturated vapours. The heat-exchange capabilities oflating interest and research into the pathophysiological processes the upper airway are so efﬁcient that it is rare to suffer thermaland treatments relevant to other forms of lung injury, there injury below the glottis unless super-heated particles have beenremains 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 upperpatients is any different from that in other critically ill patient airways is the development of oedema with the potential for airwaygroups.4 For this reason, this article will concentrate on the path- obstruction. Oedema formation develops rapidly following burnophysiology, recognition and management of airway and toxin- injury due to the generation of negative interstitial hydrostaticrelated changes that occur in inhalation injury. pressures followed by increases in vascular permeability and pressure.5–8 These changes develop as innate immune cellular2. 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 thecan 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: firstname.lastname@example.org (J. Handy). volumes than when urine output alone is used and the risk of0953-7112/$ – 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 265worsened oedema and tissue oxygenation with over-hydration 3. Clinical presentationhighlights the need for more precise and considered end-points inﬂuid 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 another2.2. 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 orimmediate 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 compromisethus results in delayed hypoxaemia. This is signiﬁcant as it usually any neurological features that may indicate CO or cyanidecoincides with the period of maximal tissue oedema. The combi- toxicitynation of low capillary oxygen tension and reduced tissue oxygendiffusion will compound tissue hypoxia and subsequent ‘reperfu- The following features raise concern of thermal injury and itssion’ may result in worsening of the injury. attendant risk of asphyxiation: stridor2.3. Toxins – local (respiratory) use of accessory respiratory muscles respiratory distress Smoke inhalation occurs through the inhalation of the products hypoxia or hypercapniaof combustion of burning fuels. The two processes involved are deep burns to the face or neckoxidation and pyrolysis (direct melting). blistering or oedema of the oropharynx Many lower molecular weight constituents of smoke are toxic tothe lower airways and gas-exchange lung units as a result of theirpH or free radical potential. These include acrolein, formaldehyde, 3.1. Carbon monoxide toxicitychlorine, phosgene, perﬂuoroisobutylene, SO2, NO, and NO2. Sootcontains 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 aresmoke 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 neurologicmonoxide 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.17tissue hypoxia and rapid death. 3.2. Cyanide toxicity2.4.1. Carbon monoxide Carbon monoxide is the leading cause of smoke-related fatali- The typical clinical syndrome due to cyanide poisoning is one ofties (up to 80% of deaths).14,15 The number of injuries directly rapidly developing coma, apneoa, cardiac dysfunction, and severerelated to cyanide poisoning is less clearly deﬁned, but its toxicity is lactic acidosis in conjunction with a high mixed venous O2 andsynergistic with that of carbon monoxide, and exposure may be a low arteriovenous O2 content difference.18more common as parent compounds such as polyurethane, acry- The toxicities of breathing hypoxic air (which decreases O2lonitrile, and nylon ﬁnd increasingly numerous applications. supply), carbon monoxide (which primarily affects O2 delivery and to a lesser extent O2 utilisation), and cyanide (which primarily2.4.2. 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 eachformed 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. Managementenzymes, the most important of which is the cytochrome a–a3complex; this complex is critical for electron transport during The ABCDE approach of a trauma primary survey is advisable foroxidative phosphorylation. By binding to this molecule, minute assessment and management. Thus, immediate attention to theamounts of cyanide can inhibit aerobic metabolism and rapidly adequacy of airway, breathing, and circulation is mandatory, whilstresult in death. speciﬁc causes of hypoxia should be sought and treated.
266 S. Singh, J. Handy / Current Anaesthesia Critical Care 19 (2008) 264–2684.1. 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 damagedered 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.1924 h after injury and is often precipitous following ﬂuidresuscitation. 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 fromwith prior preparation for the management of a difﬁcult intubation 240 min at an inspired oxygen concentration (FiO2) of 21% to aboutand 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 in4.1.1. 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 technicalguide 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-terminalstage. Clinical signs that should alert the clinician to potential 4.2.2. Ventilationairway obstruction include erythema and oedema of the mucosa in Supportive and ventilatory strategies associated with beneﬁt inthe mouth; signiﬁcant facial burns; carbonaceous sputum on deep non-burns acute lung injury (i.e. avoiding excessive volumes andcough; 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 Itsthe 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 assistmonitoring should, however be performed in an environment in the removal of carbon dioxide, whilst providing some additionalwhere the appropriate equipment, drugs and personnel are oxygenation are emerging. They are potentially useful in allowingimmediately 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 be4.1.2. 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 dioxideoropharynx should be examined for erythema and laryngoscopy removal in conjunction with LTV ventilation showed improvedperformed. If oedema or blistering of the upper airway is appreci- outcome over those supported by LTV or HFPV alone.22ated on laryngoscopic exam, intubation should be performed Non-invasive positive pressure ventilation (NIV) is an importantwithout 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 criticallaryngoscopies 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 supportChanging the ETT in the presence of upper airway oedema is its use in burned patients with respiratory failure,23 there isdangerous, and the tube should be left in place until resolution of a paucity of such evidence speciﬁcally aimed at the management ofupper airway oedema (generally 3–5 days). Repeated surgery or those with inhalation injury.persisting respiratory compromise may necessitate earlytracheostomy. 4.2.3. Bronchoscopy Some centres routinely perform bronchoscopy rather than4.2. 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 affectand the clinical course may reﬂect this. Radiographic changes often management and appears unreliable in predicting the need fordo not appear until 24 h or more after the insult and thus a normal ventilator support.24,25 Lavage should be performed if pulmonarychest 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 togive an inappropriately high reading in the presence of rigorous trials.
S. Singh, J. Handy / Current Anaesthesia Critical Care 19 (2008) 264–268 2674.3. 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 appropriatewill be greatly inﬂuenced by the presence or absence of other dietetic experience is advised.injuries such as cutaneous burns or multiple trauma. Early clinicalsigns of cardiovascular inadequacy include tachycardia, delayed 4.4.1. Fluid managementcapillary return (greater than 2 s) and tachypnoea. Hypotension is There is little doubt that inhalation injury can result in largea late sign and will often occur with decreased skin perfusion (pale, ﬂuid losses which require replacement and resuscitation. Howevercold and clammy). Continuous electrocardiography (ECG) and there is an increasing suggestion that patients with inhalation andregular blood pressure monitoring should be instituted as a basic burn injury are experiencing over-resuscitation with detrimentalstandard of care, with continuous blood pressure monitoring results. Over-hydration results in increased lung and tissue oedemaconsidered for the more severely ill. Decreased conscious level in with decreased lung and chest wall compliance. These factors willthe absence of head injury should raise the possibility of critically exacerbate existing impairment in gas exchange and ventilationlow oxygen delivery due to cardiovascular inadequacy or toxicity and can lead to worsened outcome. Currently there is interest inthrough carbon monoxide or cyanide. In this context it is a pre- utilising different end-points in ﬂuid resuscitation in order to allowterminal 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 gasdiagnosis, but the results of this test are generally not available in exchange and compliance in the ﬁrst few hours.28a timely fashion and empiric treatment must be instituted if thediagnosis 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 lungof cyanide. Sodium nitrite reduces cyanide binding by oxidation of and systemically, correlates well with respiratory failure andhaemoglobin to methaemoglobin (MetHb). Methaemoglobin levels mortality in a rat model of burns inhalation injury.29 In a sheepof about 40% should be targeted. MetHb levels may require moni- model, ﬂuid resuscitation with a deferoxamine hetastarch complextoring cyanide binding agents such as dicobalt edetate or hydrox- (a free iron and hydroxyl radical scavenger) attenuates both airwayocobalamin may be used, though the former may induce cardiac and systemic inﬂammation.30arrhythmias and instability if used in the absence of cyanidepoisoning. There are suggestions, albeit from one non-randomised 5. Conclusionsstudy, that early empirical treatment with hydroxycobalamin insuspected cases of burns-related inhalational injury improves Inhalation injury is a disease process commonly associated withsurvival 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 surveyby 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 preventionaccepted 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-ples include the use of prophylaxis against venous thrombo-embo- Referenceslism and gastrointestinal stress ulceration, and measures to reduceventilator associated pneumonia, (e.g. 30 head up). Patients who 1. Rajpura A. Epidemiology of burns and smoke inhalation in secondary care: a population-based study covering Lancashire and South Cumbria. Burnshave suffered inhalation injury are at risk of developing pulmonary 2002;28(2):121–30 (abstract).infections but there is no evidence to support the use of prophylactic 2. McGwin Jr G, George RL, Cross JM, Rue LW. 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