Inhalation Injury
1. Definition
Inhalation injury refers to damage to the respiratory tract and/or systemic toxicity resulting from inhalation of heat, smoke, toxic gases, or particulate matter, commonly associated with burns, especially closed-space fires.
It is a major determinant of mortality in burn patients and is an independent predictor of poor outcome, even after adjusting for TBSA burns.
2. Epidemiology & Clinical Importance
- Occurs in 10–30% of hospitalized burn patients
- Present in up to 60% of fire-related deaths
- Mortality increases 2–5 fold when inhalation injury coexists with burns
- Strongly associated with:
- ARDS
- Pneumonia
- Prolonged mechanical ventilation
- Multi-organ dysfunction
3. Pathophysiology
Inhalation injury is NOT a single entity. It consists of three distinct but overlapping components:
🔹 A. Thermal Injury (Upper Airway)
🔹 B. Chemical Injury (Lower Airway & Lung Parenchyma)
🔹 C. Systemic Toxicity (Carbon monoxide, Cyanide)
4. Types of Inhalation Injury
A. Thermal Injury (Supraglottic)
Mechanism
- Hot gases cause direct heat injury
- Heat is efficiently dissipated by:
- Nasopharynx
- Oropharynx
- Hence injury usually limited above vocal cords
Structures Involved
- Lips
- Tongue
- Oropharynx
- Epiglottis
- Vocal cords
Pathophysiology
- Mucosal edema
- Increased capillary permeability
- Progressive airway obstruction (worsens over 12–24 h)
B. Chemical Injury (Subglottic & Lung Parenchyma)
Mechanism
- Inhalation of:
- Smoke
- Toxic gases
- Combustion products
- Fine particulates (<5 μm)
Common Toxins
- Aldehydes
- Sulfur dioxide
- Nitrogen oxides
- Ammonia
- Phosgene
- Acrolein
Pathophysiology
- Ciliary dysfunction
- Mucosal inflammation
- Bronchorrhea
- Bronchospasm
- Fibrin casts formation
- Airway obstruction
- V/Q mismatch
- ARDS
C. Systemic Toxicity
1. Carbon Monoxide (CO)
Mechanism
- Binds Hb with 200–250× affinity of O₂
- Causes:
- Functional anemia
- Left shift of oxyhemoglobin dissociation curve
- Cellular hypoxia
Additional Effects
- Myocardial depression
- Arrhythmias
- Delayed neuropsychiatric syndrome
👉 Pulse oximetry is falsely normal
2. Cyanide (CN)
Sources
- Burning of:
- Plastics
- Polyurethane
- Synthetic materials
- Wool, silk
Mechanism
- Inhibits cytochrome oxidase (Complex IV)
- Blocks oxidative phosphorylation
- Causes histotoxic hypoxia
Hallmark
- Severe lactic acidosis
- High venous O₂ saturation
- Cardiovascular collapse
5. Risk Factors for Inhalation Injury
- Closed-space fire
- Prolonged smoke exposure
- Loss of consciousness at scene
- Facial burns
- Singed nasal hairs
- Soot in mouth/sputum
- Hoarseness
- TBSA >20–30%
6. Clinical Features (Systematic)
A. Upper Airway Signs
- Hoarseness
- Dysphonia
- Stridor
- Drooling
- Dysphagia
- Facial burns
- Edema of lips/tongue
B. Lower Airway Signs
- Cough
- Carbonaceous sputum
- Wheeze
- Tachypnea
- Hypoxemia
- Crackles
C. Systemic Features
- Headache
- Confusion
- Syncope
- Arrhythmias
- Metabolic acidosis
7. Diagnosis – Stepwise Approach
A. Clinical Suspicion (MOST IMPORTANT)
Diagnosis is clinical, supported by investigations.
B. Flexible Fiberoptic Bronchoscopy (GOLD STANDARD)
Findings
- Erythema
- Edema
- Ulceration
- Soot deposition
- Sloughing
- Fibrin casts
Severity Grading (Abbreviated Injury Score)
- Grade 0 – Normal
- Grade 1 – Mild erythema
- Grade 2 – Severe inflammation
- Grade 3 – Ulceration/necrosis
- Grade 4 – Massive necrosis
👉 Severity correlates with mortality & ventilator days.
C. Imaging
Chest X-ray
- Often normal initially
- Later:
- Atelectasis
- Infiltrates
- ARDS pattern
CT Chest
- Detects early airway wall thickening
- Not routine
D. Laboratory Evaluation
1. ABG
- Hypoxemia
- Metabolic acidosis
- Elevated lactate
2. Co-oximetry
- Carboxyhemoglobin level
- Essential in all suspected cases
3. Cyanide Levels
- Rarely available
- Diagnosis often clinical
8. Airway Management
Early Airway Protection is KEY
Indications for Early Intubation
- Hoarseness
- Stridor
- Progressive facial/neck edema
- Altered sensorium
- Extensive burns (>40% TBSA)
- Bronchoscopy-proven injury
- Anticipated transfer
👉 Do NOT wait for stridor
Preferred Tube
- Large bore ETT (≥8.0 mm)
- Facilitates bronchoscopy & suctioning
9. Mechanical Ventilation Strategy
Lung-Protective Ventilation
- Tidal volume: 6 ml/kg PBW
- Plateau pressure <30 cm H₂O
- Adequate PEEP
Adjuncts
- Frequent suctioning
- Bronchial toilet
- Bronchoscopy for cast removal
10. Pharmacologic Management
A. Oxygen Therapy
- 100% FiO₂ initially
- Reduces COHb half-life:
- Room air: ~4–5 h
- 100% O₂: ~60 min
- Hyperbaric O₂: ~20 min
B. Bronchodilators
- β₂-agonists (albuterol)
- Reduce bronchospasm
- Improve mucociliary clearance
C. Mucolytics
- N-acetylcysteine (NAC)
- Breaks disulfide bonds in mucus
- Used via nebulization
D. Anticoagulant Nebulization (Burn ICU Protocols)
Heparin Nebulization
- Prevents fibrin cast formation
- Often combined with NAC
👉 Evidence supports ↓ ventilator days (center-dependent)
E. Corticosteroids- NOT routinely recommended
- No mortality benefit
- ↑ infection risk
11. Management of Specific Toxicities
A. Carbon Monoxide Poisoning
Indications for Hyperbaric Oxygen
- COHb ≥25% (≥15–20% in pregnancy)
- Loss of consciousness
- Severe metabolic acidosis
- Ischemic ECG changes
- Neurological symptoms
B. Cyanide Poisoning
Antidotes
- Hydroxocobalamin (preferred)
- Forms cyanocobalamin (vit B12)
- Alternative:
- Sodium nitrite + sodium thiosulfate (less favored)
Clinical Clue
- Severe lactic acidosis (>8–10 mmol/L) with smoke inhalation
12. Complications
Pulmonary
- Pneumonia
- ARDS
- Atelectasis
- Bronchiolitis obliterans
- Tracheal stenosis
Systemic
- MODS
- Sepsis
- Delayed neurocognitive deficits (CO)
13. Prognostic Factors
- Severity of bronchoscopic injury
- COHb level
- Presence of cyanide toxicity
- TBSA burns
- Age
- Delay in airway management