Inhalation Injury

OVERVIEW

• 20% in burn patients
• 60% in burns patients with central facial burns
• causes a massive increase in mortality

PATHOPHYSIOLOGY

Components of smoke that cause damage:

• heat
• particulates
• systemic toxins (CO and CN)
• respiratory irritants (ammonia, HCl, oxides of nitrogen, phosgene and aldehydes)

Thermal Injury

• oropharyngeal area
• lower airway affected if steam, volatile gases, explosive gasses or hot liquids are inhaled

Asphyxiation

• combustion utilises O2 -> low FiO2 -> hypoxaemia
• CO: tissue hypoxia, left shifted ODC, cytochrome oxidase binding, myocardial myoglobin binding with decreased contractility
• CN: poisoning of electron transport chain -> lactic acidosis
• MetHb: heat denaturation of Hb, oxides produced in fire, nitrites -> decreased O2 carrying capacity

Pulmonary Irritation

• direct tissue injury
• acute bronchospasm
• activation of inflammatory cascade
• oxygen radical and proteolytic enzymes
• mucosal damage
• bronchitis
• mucus plugging
• pulmonary oedema
• bronchospasm
• bronchorrhoea
• hypoxaemia/raised A-a gradient
• SIRS

CLINICAL FEATURES

• events: enclosed space, explosion, LOC, toxic gases, did you breathe fire, voice changes
• burns in face, especially around mouth/nose
• singed nasal hair
• carbonaceous sputum
• nasal deposits
• soot, charring, mucosal erythema/oedema/blistering/necrosis
• voice changes/hoarseness
• respiratory distress: hypoxaemia, raised A-a gradient, stridor, wheeze, tachypnoea, dyspnoea
• high CO levels – might look ‘cherry red’
• CN: bitter almond odour
• CO and CN toxicity: lactic acidosis, high SvO2, mental confusion, hypotension

INVESTIGATIONS

• CXR: diffuse atelectasis, pulmonary oedema, bronchopneumonia (not reliable investigation however)

MANAGEMENT

Prehospital

• minimise exposure time
• high flow O2

Inhospital

Airway

• proportional to severity
• acutely compromised airway: RSI, smaller ETT +/- surgical airway
• less severe: RSI or AFOI
• not compromised: nasal endoscopy, have low threshold for elective intubation
• leave tube uncut
• tie tube firmly (wire to teeth)
• elevate head (decreases oedema)
• adrenaline and steroids (controversial)

Breathing

• high flow O2 for 6 hours and until CO levels return to normal
• bronchospasm: B2 agonists (multiple benefits – bronchodilation, anti-inflammatory, improves airspace fluid clearance and stimulates mucosal repair)
• humidification
• NAC and heparin nebulisers (5000U heparin + 3mL of 20% NAC Q4 hrly for 7 days – reduced reintubation and mortality in children)
• aggressive toileting
• suction
• cultures
• protective lung ventilation strategy: low volume, high PEEP, permissive hypercapnia
• HFOV
• ECMO

Circulation

• no good data
• tendency to avoid increased fluids
• should be guided by urine output and haemodynamic parameters
• use dynamics parameters (pulse pressure variation, fluid responsiveness)
• early albumin after 24 hours

Carbon Monoxide Toxicity

• 100% oxygen
• rapid transport to a hyperbaric centre

Cyanide Toxicity

• sodium thiosulphate -> produces metHb which can bind CN and allows metabolism by liver enzymes
• hydroxocobalamin (vitamin B12) -> actively binds CN and allows renal elimination

Other Experimental Therapies

• nebulised heparin + antithrombin
• high dose IV heparin
• IV tPA
• anti-inflammatories
• NO inhibitors
• antioxidants (nebulized vitamin E)
• methylprednisolone
• phenytoin (for anti-inflammatory properties)
• endothelin-1 receptor antagonist (tezosentan)
• nebulized deferoxamine + pentastarch complex
• APC
• decontamination of lungs with amphorteric, hypertonic chelating agents

References and Links

• Toon, M. H. et al. Management of acute smoke inhalational injury Crit Care Resus, 2010;12: 53-61