Thermal Inhalation Injury
Most thermal energy is dissipated upon the high surface
area of the nasopharynx and oropharynx.
The least common but most deadly inhalation injury
Reflex closure of vocal cords to heat stimulus
Particle Inhalation Injury
Soot/dust/dirt is initially filtered by the nares.
Coughing up carbonaceous sputum & wheezing
The most common inhalation injury
Toxic Metabolic Byproducts from Combustion Inhalation
Carbon Monoxide and Cyanide Toxicity
Pulmonary Dysfuction Pathophysiology
Hypoxemia from V/Q Mismatch
Release of Pulmonary Smooth muscle Vascoconstrictors
Increased airway resistance
Increase in pulmonary neutrophilsàsuperoxide free radicals,
conjugated dienes
Pulmonary edema from increased alveolar capillary
permeability
Mucociliary elevator impaired and unable to clear
secretions, mucosal clumping.
Epithelial cells separated from basement membrane and
secrete protein exudateàfibrin
casts
Fibrin
casts can create “ball-valve” barotrauma.
Secondary bacterial pneumonia
Clinical Signs:
High index of suspiction (fire in an enclosed space)
Oropharygneal burn
Carbonaceous deposits in oropharynx or nares
Patient with impaired sensorium or agitation
Coughing up carbonaceous sputum, wheezing
Initial “honeymoon period” ranging from 24-72 hours prior
to respiratory difficulty.
Diagnosis:
Bronchoscopy:
Gold standard
Airway edema/erythema of
mid-bronchioles
Secondary secretions
Tissue loss/deposits
Carbonaceous sputum
1st degree: Erythema, Edema
2nd degree: Mucosal
disruption, Blistering, Exudates
3rd degree:
Hemorrhage, Ulceration
Treatment:
High-Flow Oxygen Therapy (100% NRB)
Humidified Air
Nebulized heparin and N-acetylcysteine alternating q4 for
5 days
- decreases formation of tracheobronchial casts
- decreases PIP
- decreased reintubation and mortality in children
Inhaled B-agonist to decrease bronchospasm
Pulmonary Toilet
Consider Daily Bronchoscopy
Mechanical Ventilation: limit PIP to <40cmH20, permissive hypercapnea,
pressure-limited modes
High frequency percussive ventilation (VDR) for severe
inhalation injury or as a rescue modality
Enables
recruitment of alveoli at lower airway pressures
Combines
standard tidal volume of conventional mode with smaller high-frequency
respirations
Loosens
inspissated secretions and improves pulmonary hygiene.
No role for steroids
No role for prophylactic antibiotics
Major References: Potenza, Guy, Cioffi
Carbon Monoxide Poisoning
Mortality as high as 31%
Leading cause of CO poisoning is automobile fumes
Smoke inhalation is 2nd leading cause
1.
Inhibits ability to oxygenate
2.
Deposits in CNS produce secondary potentially
life-long dysfunction
CO Hb%
|
Symptoms
|
10%
|
Asymptomatic, Headache
|
20%
|
Dizziness, nausea, dyspnea
|
30%
|
Visual disturbance
|
40%
|
Confusion, syncope
|
50%
|
Seizures and coma
|
>60%
|
Cardiopulmonary dysfunction and death
|
CO affinity to Hb is 200X that of O2 = Decreased PaO2
Hb-O2 dissociation curve is shifted to the left.
PulseOx (O2sat) does not differentiate between CO and O2
and may have inaccurate normal reading.
Cyanide Toxicity is a byproduct of CO.
Half-life of CO
|
|
Room Air
|
4-6 hrs
|
100% NRB
|
40-80 min
|
Hyperbaric O2 (3
ATM)
|
15-30 min
|
Delayed Sequelae (10% of patients with serious CO
exposure):
Headaches,
irritability, personality changes, confusion, memory loss, gross motor deficits
Will
need speech therapy consult for cognitive evaluation and possible therapy
