13. Smoke / Inhalational Injury (incl. CO and Cyanide Toxicity)

Quick Recap

Nests under Acute Respiratory Failure. Final protocol in the Respiratory System (13/13). Covers thermal/chemical inhalation injury, carbon monoxide poisoning, and cyanide toxicity as a combined presentation typical of closed-space fire exposure.

1. Definition

Inhalation injury = airway and/or pulmonary parenchymal damage from inhaling heat, smoke particulates, and/or toxic combustion products (including CO and cyanide) in the setting of fire/smoke exposure, often complicating cutaneous burns. Three overlapping components to consider separately: (1) direct thermal/chemical injury to the upper airway and tracheobronchial tree, (2) systemic toxicity from inhaled gases (CO, cyanide), and (3) resulting ARDS/pulmonary parenchymal injury (may evolve over 24-72h).

2. Pathophysiology

Upper airway: direct thermal injury (mostly limited to above the vocal cords, as the upper airway efficiently dissipates heat) causes edema that can progressively obstruct over hours — injury may not be maximal at presentation, which is why early intubation is favored over a wait-and-see approach in high-risk patients.

Lower airway/parenchyma: chemical injury from soot/particulate-bound toxins (aldehydes, acrolein, and other combustion byproducts) causes mucosal inflammation, ciliary dysfunction, bronchorrhea, bronchospasm, and mucosal sloughing -> impaired secretion clearance, atelectasis, and risk of subsequent pneumonia/ARDS.

Carbon monoxide (CO): a byproduct of incomplete combustion; binds hemoglobin with ~200x the affinity of oxygen, forming carboxyhemoglobin (COHb), which both reduces oxygen-carrying capacity and shifts the oxyhemoglobin dissociation curve leftward (impairing peripheral O2 unloading) -> tissue hypoxia disproportionate to measured PaO2. COHb dissociates very slowly.

Cyanide: released from combustion of nitrogen-containing synthetic materials (common in modern furnishings/plastics); inhibits cytochrome c oxidase, blocking oxidative phosphorylation -> cellular/cytopathic hypoxia and a shift to anaerobic metabolism (lactic acidosis) despite adequate oxygen delivery. CO and cyanide toxicity frequently coexist in closed-space fire victims and their effects are additive/synergistic.

3. Immediate Stabilization (ABCDE)

Airway — the priority, and time-critical:

• Assess for hoarseness (signifies possible upper airway thermal injury), stridor, wheezing, carbonaceous sputum, singed nasal hairs/facial burns — hoarseness plus any of these should prompt strong consideration of early intubation, since airway edema is progressive and can become unmanageable within hours
• Risk factors for airway obstruction requiring especially low threshold for intubation: carbonaceous sputum, singed nasal hairs, deep burns >35-40% TBSA, burns involving face/neck/upper torso, need for prolonged transport
• If intubation needed: awake fiberoptic intubation in difficult cases; in-line cervical spine stabilization if trauma is a concern; call for experienced/difficult airway personnel early
• Do not wait for progressive obstruction to declare itself — intubate early and electively rather than emergently once edema is advanced

Breathing:

• 100% oxygen for ALL suspected inhalation injury/CO exposure patients immediately, regardless of measured SpO2
• Standard pulse oximetry is unreliable/falsely reassuring in CO poisoning — it cannot distinguish carboxyhemoglobin from oxyhemoglobin and will read falsely normal/high; confirm true oxygenation status with CO-oximetry on blood gas analysis, which directly measures COHb
• Oxygen saturation gap: if the SpO2 (pulse oximeter) and SaO2 (co-oximeter blood gas) differ by >5%, suspect an abnormal hemoglobin state — carboxyhemoglobin (CO), methemoglobinemia (cyanide/dapsone), or sulfhemoglobinemia (hydrogen sulfide)
• Wheeze/bronchospasm: treat with bronchodilators
• Ventilate per ARDSnet lung-protective strategy (Vt 6 mL/kg IBW, plateau pressure <30 cmH2O) once intubated; deep circumferential chest burns limiting chest wall mobility may require tolerating plateau pressures up to 40 cmH2O; frequent escharotomies can improve chest wall compliance and reduce airway pressures in circumferential torso burns

Circulation: IV access through unburned skin where possible; standard burn fluid resuscitation principles apply if cutaneous burns are present (beyond this protocol's scope — coordinate with burn unit).

Disability: depressed level of consciousness in a fire-exposure patient should immediately raise concern for CO and/or cyanide toxicity, in addition to trauma/head injury — keep a low threshold to treat empirically rather than waiting for confirmatory levels.

Checklist:

4. Focused History

Exposure circumstances (closed space vs open space — closed space fires carry much higher CO/cyanide risk), duration of exposure, loss of consciousness at scene, associated trauma, prior cardiopulmonary disease (worsens CO tolerance), pregnancy status (fetal hemoglobin has higher CO affinity — lower treatment threshold), materials burned if known (synthetic materials/plastics increase cyanide risk), time since exposure (affects COHb interpretation, as levels fall with any oxygen administered en route).

5. Examination + POCUS

Hoarseness, stridor, wheeze, carbonaceous sputum, singed nasal vibrissae, facial/perioral burns, soot in oropharynx, altered mental status, cherry-red skin discoloration (classic but insensitive/late CO sign — do not rely on it), signs of associated cutaneous burns/trauma.

POCUS: limited primary diagnostic role; useful to assess for concurrent cardiac ischemia (CO can precipitate myocardial ischemia/infarction even in patients without prior CAD) and to support general ICU assessment; bronchoscopy (not POCUS) is the definitive tool for grading inhalation injury severity (Section 9).

6. Syndrome Identification

Combined upper/lower airway thermal-chemical injury plus systemic toxic gas exposure (CO +/- cyanide) — treat as three simultaneous, interacting problems rather than a single diagnosis.

7. Differential Diagnosis

8. Severity Assessment

COHb level (does NOT reliably correlate with symptom severity — use clinically, not as a sole determinant):

• <10%: normal/baseline (higher in smokers)
• >40%: severe

Indications for hyperbaric oxygen (HBO2) therapy (thresholds not perfectly standardized, but most experts recommend for): loss of consciousness, neurologic abnormalities, cardiac ischemia, pregnancy (lower threshold given fetal Hb affinity for CO) — benefit is greatest when administered promptly, ideally within 6 hours of exposure, to reduce late neurologic sequelae.

Bronchoscopic grading of inhalation injury severity (erythema/edema/ulceration/sloughing/soot burden) is the most direct severity assessment tool for the airway component (Section 9).

9. Investigations

• Bedside: CO-oximetry ABG (COHb level, true SaO2), lactate (elevated out of proportion to shock severity suggests cyanide), EtCO2 (a compensatory drop can accompany cyanide-induced lactic acidosis)
• Bronchoscopy: establishes/grades inhalation injury — findings include erythema, edema, ulceration, mucosal sloughing, prominent vasculature, and infraglottic soot
• Imaging: CXR (often normal early despite significant inhalation injury — a normal initial CXR does NOT exclude significant injury; parenchymal changes/ARDS may evolve over 24-72h)
• ECG/troponin: screen for CO-induced myocardial ischemia, especially in patients with cardiac risk factors
• Do not delay empiric treatment (100% O2, antidotes) for confirmatory cyanide testing — cyanide levels are not rapidly available in most settings; treat on clinical suspicion

10. Evidence-Based Management

Carbon Monoxide Poisoning

• 100% oxygen (via NRB mask or ventilator if intubated) — mainstay; reduces COHb half-life substantially compared to room air
• Hyperbaric oxygen (HBO2): consider per indications in Section 8; most benefit when given within 6 hours of exposure; reduces late neurologic sequelae in appropriate candidates — requires transfer to a hyperbaric-capable center, so decision/logistics should be initiated early, not after prolonged stabilization attempts

Cyanide Toxicity

• Maintain a low threshold to treat empirically in any closed-space fire victim with altered consciousness, hemodynamic instability, or unexplained lactic acidosis — do not wait for confirmatory cyanide levels
• First-line antidotal combination: hydroxocobalamin + sodium thiosulfate — preferred in smoke-inhalation-associated cyanide toxicity (hydroxocobalamin does not induce methemoglobinemia, which is advantageous when CO co-poisoning may already be compromising oxygen-carrying capacity)
• Alternative (traditional cyanide antidote kit): amyl nitrite + sodium nitrite (induce methemoglobinemia, which binds cyanide) + sodium thiosulfate (sulfur donor for renal cyanide detoxification) — use nitrites cautiously/avoid in concurrent significant CO poisoning, since inducing methemoglobinemia further reduces functional oxygen-carrying capacity on top of COHb-related impairment; hydroxocobalamin is generally preferred when CO co-exposure is likely or unconfirmed

Airway/Pulmonary Injury Management

• Maintain open airway, maximize gas exchange, aggressive pulmonary toilet (suctioning, chest physiotherapy) in patients able to protect their airway and cough effectively — avoid unnecessary intubation in patients who can clear secretions well, but do not hesitate once respiratory failure appears imminent
• Frequent bronchoscopy may be needed to clear inspissated secretions/mucosal casts in more severe injury
• Bronchodilators for bronchospasm
• Adequate humidification of inspired gases
• Avoid corticosteroids for inhalation injury — associated with increased risk of bacterial infection without proven benefit, unlike some other inflammatory airway processes
• Ventilate per ARDSnet lung-protective principles once intubated (Section 3); consider escharotomy for circumferential chest burns limiting ventilation

11. Organ Support

100% oxygen/HBO2 for CO; hydroxocobalamin/thiosulfate for cyanide; lung-protective mechanical ventilation for evolving ARDS; standard burn/critical care supportive management (fluid resuscitation per burn protocols if cutaneous burns present, nutrition, infection surveillance) in coordination with a dedicated burn unit for major burns.

12. Consultation Matrix

13. Monitoring Framework

Serial COHb trend (should fall on 100% O2), serial lactate (cyanide toxicity resolution marker), continuous cardiac monitoring (arrhythmia/ischemia risk from CO), serial CXR/oxygenation trend over 24-72h (ARDS can evolve even with an initially normal CXR), airway exam trend if not yet intubated (progressive edema risk).

14. ICU Bundle Checklist (Daily)

15. Complications

Delayed airway obstruction (if intubation deferred inappropriately), ARDS evolving over 24-72h, ventilator-associated pneumonia (impaired mucociliary clearance predisposes), delayed neurologic sequelae from CO poisoning (impaired concentration, amnesia, depression — can manifest weeks to months later, more common without timely HBO2 in eligible patients), myocardial ischemia/infarction from CO, rhabdomyolysis/hepatic injury (less common CO complications), abdominal/intra-abdominal hypertension in extensively burned patients. Prevention: early proactive airway management, avoiding corticosteroids, prompt CO/cyanide antidotal therapy. Rescue: escharotomy for compliance-limiting chest burns, ECMO consideration for refractory ARDS per standard ARDS protocol criteria.

16. Escalation & De-escalation

Escalate: progressive airway edema/stridor -> intubate without further delay; worsening oxygenation/ARDS evolution -> lung-protective ventilation, consider ARDS rescue therapies per that protocol; persistent lactic acidosis despite adequate resuscitation -> continue/escalate cyanide antidotal therapy, reassess for other causes.

De-escalate: COHb normalized, lactate resolved, airway edema resolving (consider cuff leak test per Airway Emergencies protocol before extubation), oxygenation stable -> wean support, transition to burn unit/ward-level care per burn severity criteria.

17. ICU Discharge Criteria

Airway edema resolved and extubation criteria met (or definitively tracheostomy-dependent with a stable plan), COHb normalized, no ongoing cyanide toxicity evidence (lactate normalized), oxygenation stable, burn wound care plan established with burn unit if applicable, neurologic status assessed with a plan for delayed neurologic sequelae surveillance.

18. Documentation & Medicolegal Checklist

19. Key Guidelines / Reference Reviews

American Burn Association burn unit referral criteria; general inhalation injury/CO poisoning management as reflected in Washington Manual of Critical Care (Ch. 24, toxicology/environmental section) and ICU Protocols: A Step-wise Approach (Ch. 13, Burn Management).

20. Controversies

Optimal threshold and timing for HBO2 therapy remain incompletely standardized across guidelines/institutions, and access is often the practical limiting factor rather than a clear evidence-based cutoff. Choice between hydroxocobalamin and the traditional nitrite-based cyanide antidote kit in suspected combined CO-cyanide poisoning is influenced more by the theoretical concern about nitrite-induced methemoglobinemia compounding CO-related oxygen-carrying impairment than by direct comparative trial evidence in this specific combined-exposure population. Precise threshold for early elective intubation in less-severe inhalation injury (vs close observation) is judgment-based rather than protocolized, reflecting genuine practice variation.

21. References

1. Burn Management (inhalation injury, CO, cyanide sections). ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 13).
2. Toxicology/Environmental chapters (carbon monoxide poisoning). Washington Manual of Critical Care, 4th ed, 2025 (Ch. 24 region).
3. General Poisoning Management. ICU Protocols: A Step-wise Approach, 2nd ed. Springer; 2020 (Ch. 14) — antidote reference table including CO/cyanide.
4. American Burn Association. Burn unit referral criteria, current edition.