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Smoke Inhalation

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Overview

Smoke Inhalation

Quick Reference

Critical Alerts

  • Early intubation for airway compromise: Airway edema progresses rapidly
  • CO and cyanide toxicity often coexist: Treat empirically
  • 100% oxygen for all smoke inhalation: Displaces CO
  • Hydroxocobalamin for suspected cyanide: First-line antidote
  • Normal SpO2 does not exclude CO poisoning: Pulse ox unreliable
  • Burn + Smoke inhalation increases mortality significantly

Indicators for Intubation

FindingAction
StridorImmediate intubation
HoarsenessStrong consideration
Facial burns, singed nasal hairsAnticipate edema
Soot in oropharynxLower threshold
Upper airway edema on scopeImmediate
Deteriorating mental statusSecure airway

Emergency Treatments

ConditionTreatment
CO poisoning100% O2 via NRB or intubation; consider HBO
Cyanide poisoningHydroxocobalamin 5g IV
Airway edemaEarly intubation
BronchospasmNebulized albuterol

Definition

Overview

Smoke inhalation injury encompasses thermal injury to the upper airway, chemical injury to the tracheobronchial tree and alveoli, and systemic toxicity from carbon monoxide (CO) and hydrogen cyanide (HCN). It is a leading cause of death in fires. Management priorities include airway protection, high-flow oxygen, and treatment of CO and cyanide toxicity.

Types of Injury

TypeLocationMechanism
ThermalUpper airwayHeat; steam
ChemicalLower airway, alveoliCombustion products
SystemicCellularCO, Cyanide

Epidemiology

  • Leading cause of fire-related deaths
  • 50-80% of fire fatalities: Due to smoke inhalation (not burns)
  • Inhalation + Burns: Significantly increases mortality

Etiology

Toxic Products of Combustion:

ToxinSourceEffect
Carbon monoxideIncomplete combustionTissue hypoxia
Hydrogen cyanidePlastics, wool, silkCellular asphyxiation
AcroleinWood, paperMucosal irritation
AmmoniaNylon, silkMucosal injury
ChlorinePVCPulmonary edema
ParticulatesSootLower airway injury

Pathophysiology

Upper Airway (Thermal Injury)

  • Heat usually dissipates in upper airway
  • Exception: Steam (high heat capacity) → Reaches lower airway
  • Edema develops over hours → Airway obstruction

Lower Airway (Chemical Injury)

  • Combustion products cause mucosal injury
  • Bronchospasm, mucosal sloughing
  • ARDS may develop

Carbon Monoxide

  • Binds hemoglobin (COHb) with 200-250× affinity of O2
  • Left-shifts O2-dissociation curve
  • Tissue hypoxia despite normal PaO2

Cyanide

  • Inhibits cytochrome oxidase (mitochondria)
  • Blocks cellular respiration
  • Lactic acidosis

Clinical Presentation

Symptoms

FindingSignificance
DyspneaAirway or pulmonary injury
Hoarseness, stridorUpper airway edema
CoughMucosal irritation
WheezingBronchospasm
Confusion, HeadacheCO poisoning
Altered mental statusCO or cyanide

History

Key Questions:

Physical Examination

FindingSignificance
Facial burnsHigh risk for inhalation
Singed nasal hairsUpper airway exposure
Soot in nares, mouthBelow glottis exposure
Hoarseness, stridorUpper airway edema
Wheezes, rhonchiLower airway injury
Cherry-red skinCO (classic but rare)
Hypotension, acidosisCyanide

Enclosed space exposure
Common presentation.
Duration of exposure
Common presentation.
Loss of consciousness at scene
Common presentation.
Type of materials burning (plastics, synthetics)
Common presentation.
Associated burns
Common presentation.
Red Flags

Immediate Airway Management

FindingAction
StridorIntubate immediately
Progressive hoarsenessIntubate early
Facial/Neck burnsAnticipate edema
Upper airway edema on bronchoscopyIntubate
Mental status changeSecure airway

Cyanide Suspicion

FindingAction
Unexplained severe acidosis (lactate >0)Hydroxocobalamin
Hypotension + AcidosisHydroxocobalamin
Cardiac arrest after fireHydroxocobalamin

Diagnostic Approach

Laboratory

TestFinding
COHb levelElevated (co-oximetry required)
ABGMetabolic acidosis (cyanide), PaO2 may be normal
LactateElevated (>0 suggests cyanide)
Cyanide levelOften not available rapidly
CBCBaseline
BMPElectrolytes, renal function

Note: SpO2 unreliable (reads falsely normal with COHb)

Imaging

Chest X-ray:

FindingInterpretation
Often normal initiallyInjury may not be visible
Pulmonary edemaARDS developing
AtelectasisMucus plugging

Bronchoscopy

  • Direct visualization of airway
  • Edema, erythema, soot, mucosal sloughing
  • Helps predict severity

Treatment

Principles

  1. Secure airway early: Edema progresses
  2. 100% oxygen for all: Treats CO and maximizes O2 delivery
  3. Hydroxocobalamin for cyanide: Empiric if suspected
  4. Supportive care: Bronchodilators, fluids, monitoring

Airway Management

Indications for Intubation:

Finding
Stridor, hoarseness
Significant facial burns
Upper airway edema
Deteriorating mental status
Anticipated clinical course

Technique:

  • Use larger ETT if possible (can downsize later)
  • Video laryngoscopy may help visualization
  • Avoid succinylcholine if burn >24 hours (hyperkalemia)

Carbon Monoxide Treatment

InterventionDetails
100% O2Via NRB or ETT
Half-life of COHbRoom air: 4-5 hours; 100% O2: 60-90 min; HBO: 20-30 min
Hyperbaric oxygenConsider if COHb >5%, LOC, cardiac ischemia, pregnancy

Cyanide Treatment

Hydroxocobalamin (First-Line):

DoseNotes
5 g IV over 15 minMay repeat
Binds cyanide → Cyanocobalamin (excreted)
Safe; minimal side effectsSkin turns red

Cyanide Antidote Kit (Alternative):

ComponentsNotes
Amyl nitrite (inhaled)Induces methemoglobinemia
Sodium nitrite IVSame
Sodium thiosulfate IVEnhances cyanide excretion
CautionNitrites worsen CO toxicity

Bronchospasm

AgentDose
Albuterol nebulized2.5-5 mg q20min PRN
Ipratropium nebulized0.5 mg q4-6h

Supportive Care

InterventionDetails
IV fluidsBurns may need resuscitation
MonitorSerial exams, ABG, COHb
BronchoscopyConsider for soot clearance
Prophylactic intubationIf transfer needed and edema expected

Disposition

Admission Criteria

  • Significant smoke exposure
  • Elevated COHb
  • Respiratory symptoms
  • Suspected cyanide toxicity
  • Burns with inhalation injury

ICU Admission

  • Intubated
  • Hemodynamic instability
  • Severe acidosis
  • ARDS

Discharge Criteria

  • Brief exposure, minimal symptoms
  • Normal mental status
  • Normal COHb
  • Normal lactate
  • Observation × 4-6 hours without deterioration

Referral

IndicationReferral
BurnsBurn center
HBO considerationHyperbaric center
ARDSCritical care

Patient Education

Condition Explanation

  • "You inhaled smoke which can injure your lungs and cause poisoning from gases like carbon monoxide."
  • "We are giving you high-concentration oxygen to help clear the poison."

Prevention

  • Working smoke detectors
  • Fire escape plan
  • Avoid re-entering burning buildings
  • Crawl low in smoke (toxins rise)

Quality Metrics

Performance Indicators

MetricTargetRationale
100% O2 administered100%CO treatment
COHb level obtained100%Diagnosis
Early intubation for stridor100%Airway protection
Hydroxocobalamin for suspected cyanide>0%Empiric treatment

Documentation Requirements

  • Enclosed space exposure
  • Duration of exposure
  • Airway exam findings
  • COHb level
  • Treatment and response
  • Disposition rationale

Key Clinical Pearls

Diagnostic Pearls

  • SpO2 is unreliable in CO poisoning: Use co-oximetry
  • Lactate >10 suggests cyanide toxicity
  • Airway edema progresses over hours: Early intubation
  • Singed nasal hairs + Soot = High-risk airway
  • Normal CXR initially: Injury develops later
  • Cherry-red color is rare: Do not wait for it

Treatment Pearls

  • 100% O2 for all: Reduces COHb half-life
  • Early airway if any concern: Edema worsens rapidly
  • Hydroxocobalamin is safe: Give empirically if cyanide suspected
  • Avoid nitrite kit if CO poisoning also present: Worsens O2 delivery
  • HBO for severe CO: LOC, pregnancy, cardiac ischemia, COHb >25%

Disposition Pearls

  • Admit for significant exposure or symptoms
  • ICU for intubated or unstable
  • Burns + Inhalation = Burn center transfer
  • Observe asymptomatic × 4-6 hours before discharge

References
  1. Rehberg S, et al. Pathophysiology and treatment of inhalation injury. Burns. 2009;35(1):4-14.
  2. Weaver LK. Carbon monoxide poisoning. N Engl J Med. 2009;360(12):1217-1225.
  3. Baud FJ, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325(25):1761-1766.
  4. Borron SW, et al. Hydroxocobalamin for severe acute cyanide poisoning by ingestion or inhalation. Am J Emerg Med. 2007;25(5):551-558.
  5. Mlcak RP, et al. Respiratory management of inhalation injury. Burns. 2007;33(1):2-13.
  6. American Burn Association. Inhalation Injury Guidelines. 2018.
  7. Tintinalli JE, et al. Smoke Inhalation. Tintinalli's Emergency Medicine. 9th ed. 2020.
  8. UpToDate. Smoke inhalation injury. 2024.

At a Glance

EvidenceStandard
Last UpdatedRecently

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines