Inhalational injuries are a critical yet often overlooked aspect of trauma care, with far-reaching consequences in emergency medicine. These injuries can arise from various sources, including thermal injuries from fires, recreational activities such as smoke exposure during camping or outdoor events, and chemical inhalation in both industrial and household settings. Here, we present a unified approach with some special considerations to inhalational injuries in the acute care setting.

1. Thermal injuries
   • Airway burns
   • Intubation considerations
2. Recreational injuries
   • Vaping-Associated Lung Injury (VALI) 
   • Crack Lung
3. Chemical Injury
   • Chlorine gas
   • Hydrogen sulfide gas

1. Thermal Injury

Airway Burns

Pathophysiology

• In fires, it’s steam and smoke that cause airway injury, air does not hold heat as well
  1. Steam has 4,000X the relative heat capacity of air
  2. Smoke, which refers to heated soot suspended in air, is a pulmonary irritant and chemical asphyxiant via cyanide (CN) and carbon monoxide (CO)
• Greater heat capacity allows for injury deep within lower respiratory tract
• 3 components of airway injury:
  1. Thermal injury to supraglottic structures results in edema
     • Can rapidly lead to upper airway obstruction in initial hours post-exposure
  2. Chemical injury develops over the first 36 hrs
     • Small particles contained in smoke travel to the alveoli and trigger inflammatory reactions in the distal airways
       • Leads to bronchospasm, impaired gas exchange, pulmonary edema, ↓ lung compliance and ARDS 
  3. Systemic oxygenation impaired by toxic gases released (i.e. CN, CO)

On History: 

• Provide info about potential airway burn risk
  • Type & location of fire
  • Duration of smoke exposure
  • Any LOC
  • Condition of other victims

On Exam: 

• Face & neck burns
• Carbonaceous sputum
• Soot/edema in oropharynx
• Singed nasal hairs 
• Voice changes
• Wheezing

Management:

• Supplemental O2
• VBG (CO Hgb level & lactate)
• Consider intubation

Intubation Considerations:

• Systematic review and meta-analysis (Harshman et al, 2019) out of the Ross Tilley Burn Centre found that that up to 1/3 burn patients are unnecessarily intubated in the ED prior to arrival at a burn centre
  • Their definition of unnecessary intubation was when the patient was successfully extubated within 24 hrs of arrival
  • Others argue that perhaps unnecessary intubations are a necessary trade-off to avoid the devastating situation of losing the airway in a patient with a suspected airway burn
    • Initially well pts can rapidly deteriorate due to progressive and delayed edema and bronchoconstriction
    • As airway edema worsens, not only does the patient decompensate but intubation becomes more anatomically difficult
  • Experts caution that defining unnecessary intubation as a patient who is extubated within 24 hours of arrival to a burn centre is not completely appropriate
    • Perhaps a better definition for unnecessary intubations would have been patients extubated within 24 hours of arrival who had no concerning airway features prompting their intubation
• Harshman et al may have neglected to consider the realities of many of these patients’ analgesia requirements
  • Burn pts require high doses or infusions of Opioids and/or Ketamine to facilitate burn debridement and keep them comfortable during transfer
• We have new and advancing tools that can help guide us
  • In stable, cooperative pts, can use the B-flex scope to assess for oropharyngeal/glottic soot, erythema or edema

Intubation Recommendations

• No validated reference list for when airway burn patients should be intubated
• Through review of the literature and in consultation experts, below is a reasonable list of when intubation should be recommended or considered in potential airway burn patients

Recommended when:

• Signs of airway obstruction/respiratory distress: stridor, accessory muscle use, hoarseness, dysphagia
• Signs of respiratory compromise: inability to clear secretions, fatigue, poor oxygenation or ventilation
• Decreased LOC
• Soot, blisters/erythema or edema in oropharynx or glottis
• Deep burns to lower face or neck or oropharynx

Consider When:

• Extent of the burn (TBSA burn >40-50%)
• Requirement of large doses/infusions of Opioids/Ketamine
• Transfer of patient

Looking for Inspiration? Singed nasal hairs and/or facial burns ALONE are NOT indications for intubation

• My first key point of inspiration for you is that not all patients exposed to smoke or flames require intubation
  • Signs such as singed nasal hairs and facial burns ALONE are NOT indications for intubation in airway burns
  • Mild airway burn patients with normal SpO2, no signs of respiratory distress and no oropharyngeal/glottic soot, edema, erythema may be safely observed without fear of imminent decompensation

Transfer Considerations:

• The new Critical Care Services Ontario (CCSO) Guidelines (May 2024) highlight important updates in burn management
  • Recommendations surrounding inhalational injury have remained the same
    • Any inhalational injury should be discussed with a burn centre for potential transfer
  • Updates include that all full thickness burns (no longer dependent on size) should be considered for transfer
  • Similarly, partial thickness burns greater than or equal to 10% for any age (no longer just extremes of age)
  • New recommendations emphasize that only deep partial or full thickness burns to sensitive areas (i.e. face, hands, feet, joints, genitals) require consultation with a burn centre
  • Changes were made to better align with the American Guidelines for Burn Centre Transfer

Fluid Consideartions:

• Parkland/Modified Parkland Formulas for initial fluid resuscitation in burns are no longer recommended in ED setting per CCSO 2024 Guidelines
  • Burn experts consider this method to be too aggressive leading to over-resuscitation 
• Instead, for pts with significant burns ≥20% TBSA, CCSO recommends initial 500 cc/h of Ringer’s as maintenance
  • Avoid boluses unless pt is hypotensive
• Once patient stabilized, TBSA can be used to back-calculate amount of fluids pt requires
• Unfortunately, there are no guidelines/formulas specific to airway burns to prevent downstream complications of fluid overload   

Looking for Inspiration? Judicious fluid resuscitation is recommended with inhalational airway burns

• When your patient has significant non-inhalational burns ≥20% TBSA  proceed with 500 cc/h
  • However, if isolated or significant airway burn, start with a more judicious approach especially if patient not intubated
    • Reassess q1-2 using organ perfusion and urine output as guide

Post Intubation Considerations

• 100% FiO2 (given potential CO exposure)
• Inhaled beta agonists q4h (if bronchospasm)
• Bronchoscopy grading for severity of injury (used in discussion with burn centre for potential transfer)
• No evidence for prophylactic antibiotics or steroids
  • Linked to ↑ infection risk (especially fungal & resistant organisms)
• Evidence for Nebulized N-Acetylcysteine (NAC) & Nebulized Heparin in intubated pts
  • Interrupt the inflammatory and coagulation cascades in distal airways
  • ↓ mortality through improved lung compliance, ↓ pulmonary edema, ↓ duration of mechanical ventilation and ↓ re-intubation rates
    • Recommended by CCSO 2024 Guidelines
  • NAC breaks down mucous
    • Often used in combination with bronchodilators (as can cause bronchoconstriction, given airway irritant properties)
  • Heparin clears airways of fibrin casts and sloughed necrotic bronchial epithelium which cause airway obstruction/atelectasis leading to downstream infection
    • Limited systemic absorption, no increased bleeding risk
  • Not practical for us to be starting in ED, started by ICU 

2. Recreational Lung Injury

Vaping-Associated Lung Injury (VALI)

Background

• Although #s of VALI cases identified have ↓ dramatically since the epidemic of 2019-2020, cases are still occurring and the Covid pandemic has presented challenges in accounting for disease incidence
  • At least part of this decreased incidence secondary to increased regulations of vaping products
  • Canada has one of highest teen vaping rates in the world and vaping rates in Canada continue to increase 

Pathophysiology

• Vaping: inhaling an aerosol created by heating a liquid or wax containing various substances such as nicotine, cannabis, flavouring and additives
  • Various devices: e-cigarettes, vape pens, vape mods
• Toxicity is suspected to be related to Vitamin E acetate and specific heating mechanisms
• VALI is a form of acute lung injury that presents on spectrum of disease
• Should be suspected in vaping pts with progressive dyspnea and/or worsening hypoxemia
• Symptoms can initially mimic common pneumonia, but pts don’t respond to antibiotics
  • VALI ↑ risk of superimposed bacterial infection
    • Always ask about vaping hx/frequency in pt present sicker than expected with suspected viral/bacterial source

Clinical Features

• History:
  • Dyspnea
  • Cough
  • Chest pain (pleuritic)
  • Hemoptysis
  • Fevers, chills
  • N/V/D, abdo pain
• On Exam:
  • Tachycardia
  • Tachypnea
  • Hypoxia
  • Progression to respiratory failure

Imaging

• CXR: bilateral, diffuse, hazy consolidative opacities with basilar predominance
  • 85% pts will have CXR findings
  • All pts who’ve vaped in last 90 d should have CXR, even if resp symptoms are mild
• CT: most commonly diffuse bilateral ground glass opacities   
  • Wide variety of radiographic patterns
• Pneumothorax and pneumomediastinum well documented given high heat during inhalation

Diagnosis

• American Thoracic Society VALI diagnostic criteria:
  • Vaping in the past 90 days prior to symptom onset with
  • Infiltrates/opacities on CXR or CT and
  • Presentation is not better explained by infection/alternative dx

Management

• Supportive care 
  • ~25% of diagnosed VALI cases go on to require mechanical ventilation given risk of developing ARDS
• Empiric antibiotics
  • Infectious causes are often on the DDx
  • VALI ↑ risk of super-imposed bacterial infections
• Steroids (if severe)

Crack Lung

Background:

• Crack Lung: a syndrome of diffuse alveolar damage and hemorrhagic alveolitis 
• Crack Cocaine: cocaine powder boiled with baking soda and water into precipitate which is filtered and then can be smoked

Clinical Features:

• Occurs within 48 h of crack inhalation
• Acute onset of dyspnea, cough  can progress to respiratory failure
• Fever, chest/back pain (pleuritic), hemoptysis or melanoptysis (black sputum)
• Finger burns

Imaging:

• CXR: atelectasis, consolidation
• CT: ground-glass opacities, consolidation, emphysema
• Can again see pneumothorax or pneumomediastinum
  • Common practice among crack smokers to perform a Valsalva after inhalation

Looking for Inspiration? Vaping & Crack Cocaine increase risk for pneumothorax & pneumomediastinum

• Due to high heat exposures and Valsalva maneuvers performed at end of inhalation

Imaging Challenges in Recreational Lung Injury:

• Challenge with the diagnoses of VALI and crack lung is that imaging findings often show non-specific patterns of lung injury that can mimic a wide variety of infectious and inflammatory pathologies
  • Key to diagnosis is linking the imaging findings with a history of recreational use of vapes or crack cocaine
  • Limited information to guide us on when to seek further imaging
    • When should we not be satisfied with a simple viral/pneumonia picture on CXR as the sole presentation?
    • When should be not be satisfied with a normal CXR?
      • Experts recommend we rely on our core EM principles for choosing which pts require a dedicated CT chest
        

Looking for Inspiration? Maintain a low threshold to pursue CT chest with recreational exposure hx and abnormal: CXR, VBG, SpO2 or sicker than expected

Management:

• Supplemental O2  many pts go on to require ventilatory support
• Cessation of crack cocaine 
• Bronchodilators
• Empiric antibiotics
• Steroids not recommended

3. Chemical Injury

Chlorine Gas

Background:

• Cl reacts with water in resp tract to form toxic hydrochloric acid & hypochlorous acid 
• Common mechanisms of exposure include:
  • Pool chlorination/maintenance
  • Firefighters exposed during combustion of chlorinated hydrocarbons
  • Mixtures of household cleaning solutions:
    • Cl most commonly created through intentional or unintentional mixing of bleach (or other hypochlorites) with ammonia (found in cleaning solutions like Lysol).

Water Solubility

• High water solubility gases: cause more proximal airway damage
• Low water-solubility gases: cause more distal airway damage, lead to slower onset of injury
• Cl has intermediate water solubility, causing cause both upper & lower resp tract damage

Clinical Features:

• Mucosal irritation –> tearing, drooling, skin burning; which can progress to
• Alveolar injury –> cough, SOB, chest pain; can progress to
• Pulmonary toxicity more common at higher concentrations or enclosed space –> pulmonary edema, ARDS
  

Looking for Inspiration? Patients exposed to chlorine gas require 6h of monitoring from time of exposure

• Even in initially asymptomatic patients with normal vitals, resp exams and CXRs
• Due to slow-onset injury from production of hydrochloric and hypochlorous acid in the in lower respiratory tract, symptoms can be delayed up to 6 h after exposure

Management:

• Serial resp exams & SpO2
• Admission: abnormal CXR given risk of decompensation
• Discharge: asymptomatic with normal vitals at 6h 
• Supplemental O2, beta agonists for wheezing/cough
• Evidence for Nebulized Sodium Bicarbonate:
  • Experts recommend if ongoing symptoms despite 4-6 hrs supplemental O₂
• Steroids have poor evidence and are not routinely recommended   
  • Administer if respiratory failure/requiring intubation

Hydrogen Sulfide (H₂S) Gas

Background:

• Colourless, odour of rotten eggs
• Exposures: byproduct of microbial decomposition of organic matter (i.e. rotting fish guts, manure, sewage), pulp/paper mills, natural gas extraction/refining
• Also “Detergent Suicides”
  • Mixing of acidic cleaners such as Lysol as proton donor with insecticides/bath salts as sulfur source 
• Referred to as “Knock Down” Gas:
  • Knock Down Effect: person who discovers pt (i.e. friend, EMS) has sudden LOC

Clinical Manifestations Spectrum:

• If exposure in open, well-ventilated area (i.e. farmer shoveling manure outside)  H2S concentrations low, acts as a pulmonary irritant
  • Symptoms: dyspnea, cough, itchy eyes, sore throat, but can progress to cause hemorrhagic pulmonary edema & ARDS
• If exposure in confined, poorly ventilated area (i.e. shoveling manure inside barn, sewage exposure in manhole, detergent suicide)  H2S concentrations high, acts as a cellular toxin
  • Pts more likely to have fatal exposures
  • If survive to ED presentation, more likely to have systemic manifestations (i.e. cardiovascular collapse and AMS)

H₂S Mechanism of Action:

• Like CN, blocks complex IV of electron transport chain blocking oxidative phosphorylation
  • Forces body to relay on anerobic metabolism generating high lactate
• H2S binds reversibly, ox phos no longer blocked when pt removed from the exposure
  • May be improving upon hospital arrival
• CN continues to inhibit ox phos until antidote (Hydroxocobalamin) given

H₂S Triad:

1. Severe lactic acidosis (>8-10)
2. Altered mental status
3. Cardiovascular collapse

Management:

• Decontamination: remove clothing, skin irrigation
• High flow 100% O2 
• 4-6 h monitoring period
• Critically ill: often require intubation with circulatory support (fluids/pressors)
• Bicarbonate infusion (pH<7.1)
• If not improving, consider:
  • 1)  Na Nitrite 300 mg IV
    • Na nitrite facilitates binding of H2S to ferric acid in methemoglobin  generating sulfide methemoglobinemia
    • Worsens hypotension
  • 2) Hyperbaric O₂
    • Increases O₂ availability, interfering with H2S’s ability to block ox phos

Differentiating H₂S from CN Exposures:

• Really all comes down to history (i.e. what was patient doing during exposure)
• However, in an undifferentiated patient with unclear hx who’s altered with high lactate AGMA where you are questioning a potential Cyanide vs H2S exposure:
  • First draw your VBG up front so that administration of any antidotes does not interfere with your bloodwork analysis
  • Then proceed first with Hydroxocobalamin (cyanide antidote)
  • If no improvement, check CO level on VBG
    • If elevated CO: avoid Na Nitrite
      • As combination of high carboxyhemoglin and then generating sulfide-methemoglobinemia (from administering Na Nitrite) causes such severe left shift of O₂ dissociation curve
        • Essentially halts all O₂ delivery to tissues 
          • Causes severe chemical asphyxia  can precipitate death
    • If normal CO: proceed with a trial of Na Nitrite (if their BP can tolerate)
      • Na Nitrite has evidence in both CN and H2S exposures

Looking for Inspiration? Suspect H₂S with typical history OR severe lactic acidosis, AMS, cardiovascular collapse OR sudden LOC of bystander/first responder

Lung Story Short (Take Home Points)

1. Singed nasal hairs and/or facial burns ALONE are NOT indications for intubation
2. Judicious fluid resuscitation is recommended with inhalational airway burns
3. Vaping & Crack Cocaine increase risk for pneumothorax & pneumomediastinum
4. Low threshold to pursue CT chest with recreational exposure hx and abnormal: CXR, VBG, SpO2 or sicker than expected
5. Patients exposed to chlorine gas require 6h of monitoring from time of exposure
6. Suspect H₂S with typical history OR severe lactic acidosis, AMS, cardiovascular collapse OR sudden LOC of bystander/first responder