Airway burns and smoke inhalation injuries

Out of all the possible complications of burns, the college examiners have been most interested in airway burns, and specifically in the various clinical features which alert you to the presence of such burns. Question 11 from the first paper of 2013, Question 13 from the second paper of 2006 and Question 11 from the second paper of 2000 are virtually identical: they all ask about airway burns, smoke inhalation injury and other forms of thermal damage to the upper respiratory tract. Question 23 from the second paper of 2017 is somewhat unique because it presented the candidates with a patient who has ARDS due to smoke inhalation, and who is ventilated with some profoundly stupid settings.

Features of history and examination associated with airway burns

Historical features associated with airway burns

• Explosions
• Fires in an enclosed space
• Exposure to heated steam
• Fires involving volatile solvents
• Corrosive ingestion
• Laryngeal surgery (using a laser)

Clinical features of airway burns

• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa
• Soot in sputum, nose, or mouth ("carbonaceous material"
• Singed vibrissae (the zoological term for innervated whisker hairs, misapplied to the coarse nasal hair which grows in human nostrils and has no role in tactile sensing)
• Bronchocopic findings of tracheal erythema, oedema or or ulceration.
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low pulse oximetry saturation or arterial oxygen tension) or increased carbon monoxide levels (>2%)

Pathophysiologic consequences of airway burns

Mechanisms organised by pathophysiological mechanism

Mechanism	Specific factors	Clinical features	Management
Thermal	Exposure to flames Splash with corrosives Inhalation of superheated smoke or steam	Facial burns Burns of the mucosa Soot on lips Carbonised material in the pharynx Carbonised material in sputum	Early assessment of airway patency Examination of the upper airway Serial assessments Upright positioning Suctioning of upper airway secretions Early elective intubation Referral to ENT for tracheostomy in case of severe burns, if strictures are anticipated
Inflammatory	Thermal damage to mucosa Effects of inhaled particles	Mucosal oedema Pharyngeal oedema Vocal cord oedema Tracheal oedema Difficulty swallowing Hoarse voice Cough Stridor Wheeze Increased work of breathing
Inhaled agents	Carbon monoxide Cyanide	"Cherry red" complexion Hypoxia despite normal SpO2 readings

Mechanisms organised by anatomical location

Mechanisms, Clinical Features and Management of Upper Airway Burns

Anatomical location	Mechanism	Clinical features	Management
Face	Exposure to flames Splash with corrosives	Facial burns	Early assessment of airway patency Examination of the upper airway Serial assessments Upright positioning Suctioning of upper airway secretions Early elective intubation Referral to ENT for tracheostomy in case of severe burns, if strictures are anticipated
Oral cavity	Exposure to flames Splash with corrosives	Soot on lips Burns of the mucosa Mucosal oedema
Pharynx	Inhalation of superheated smoke or steam	Carbonised material in the pharynx Pharyngeal oedema Difficulty swallowing
Larynx	Inhalation of superheated smoke or steam	Hoarse voice Cough Vocal cord oedema Stridor Increased work of breathing
Trachea	Inhalation of superheated smoke or steam	Stridor Wheeze Tracheal oedema Carbonised material in sputum
Lungs	Inhalation of superheated smoke or steam Exposure to toxic products of combustion	ARDS	Lung-protective ventilation Standard ARDS non-ventilatory management

ARDS due to inhaled products of combustion

 Question 23 from the second paper of 2017 offered the candidates a slightly singed miner, pulled out of some sort of underground conflagration. The question does not specifically ask about ARDS - rather, the candidates were asked as to why he might be so hypoxic. One of the main differentials would certainly be "inhalation injury resulting from exposure to pyrolysis and combustion atmospheres". The authors who have published the most helpful articles on this were Kimmel & Still (1999). They write mainly about the smoke inhalation experience of naval personnel, largely because military ships always seem to catch on fire and  "because of the extraordinary difficulties associated with escape and avoidance of ship-board fire atmosphere". In contrast, Akgun & Gorguner (2010) report that acute lung injury due to inhalation of flaming gas seems to be epidemiologically more common among miners, because of the combination of inescapable confinement and limited fresh gas supply.

In summary:

• The inhaled "fire atmosphere" can do damage by:
  • Heat damage
  • Chemical burn (eg. if it is corrosive)
  • Absorption of toxins, eg. asphyxiant agents such carbon monoxide
  • Blast damage, eg. in explosions
  • Asphyxiation, by absorbing all oxygen in an enclosed space
• The fire atmosphere can consist of:
  • Hot gases
  • Particles, which will cause injury at different points in the respiratory tract dependig on their size.
  • Aerosolised toxins (eg. by explosion)
  • Vacuum (eg. by process of combustion the partial pressure of gases can decrease in an enclosed space)
• The effect of this is:
  • Pulmonary oedema
  • Delayed pulmonary oedema, as in chlorine inhalation
  • Multiple pulmonary thromboses
  • Blast injury barotrauma
  • Mucus plugging due to sloughed epithelial lining

Question 23 from the second paper of 2017 asks for several differentials for hypoxia in a miner pulled from an underground fire. His ABG result demonstrates a severe metabolic and respiratory acidosis. Specific elements which arouse concern in that setting are:

• He's a miner, and therefore possibly exposed to exotic substances. Who knows what he was mining in there?
• He was underground, which as an enclosed space has two major consequences:
  • It amplifies blast waves
  • It concentrates heat
  • It limits the oxygen supply

The differentials therefore are:

• Inhalational burns injury
• Corrosive agent inhalation
• Asphyxiant agent exposure (eg. carbon monoxide or cyanide)
• "Blast lung" due to primary blast injury.
• Aspiration due to a decreased level of consciousness
• Pulmonary oedema due to primary myocardial damage