Inhalational Injury
16/12/10
SP Notes
FANZCA Part II Notes
Toon, M. H. et al (2010) “Management of acute smoke inhalational injury” Crit Care Resus,
12:pages 53-61
- 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
Jeremy Fernando (2011)
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
Jeremy Fernando (2011)
- 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
Jeremy Fernando (2011)