Episode 207: Smoke Inhalation Injury

Episode 207: Smoke Inhalation Injury

Author: Core EM April 2, 2025 Duration: 0:00

We discuss the injuries sustained from smoke inhalation.

Hosts:
Sarah Fetterolf, MD
Brian Gilberti, MD

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Show Notes

Table of Contents

00:37 – Overview of Smoke Inhalation Injury

00:55 – Three Key Pathophysiologic Processes

01:41 – Physical Exam Findings to Watch For

02:12 – Airway Management and Early Intervention

03:23 – Carbon Monoxide Toxicity

04:24 – Workup and Initial Treatment of CO Poisoning

06:14 – Cyanide Toxicity

07:19 – Treatment Options for Cyanide Poisoning

09:12 – Take-Home Points and Clinical Pearls


Physiological Effects of Smoke Inhalation:

  • Thermal Injury:
    • Direct upper airway damage from heated air or steam.
    • Leads to swelling, inflammation, and possible airway obstruction.
  • Chemical Irritation:
    • Causes bronchospasm, mucus plugging, and inflammation in the lower airways.
    • Increases capillary permeability, potentially causing pulmonary edema.
  • Systemic Toxicity:
    • Primarily involves carbon monoxide and cyanide poisoning.

Clinical Signs and Symptoms:

  • Physical Exam:
    • Facial burns, singed nasal hairs
    • Hoarseness, stridor (upper airway swelling)
    • Carbonaceous sputum (lower airway edema)
  • Systemic Symptoms:
    • Headache, dizziness, nausea
    • Syncope, seizures, altered mental status

Airway Management Considerations:

  • Not every patient requires immediate intubation.
  • Intubation should be performed early if airway compromise is suspected, as swelling can rapidly progress.
  • Close airway monitoring recommended for all patients.

Carbon Monoxide Poisoning:

  • Common cause of death post-smoke inhalation (50–75% of fire-related injuries).
  • Hemoglobin affinity 250 times greater for CO than oxygen, impairing tissue oxygenation.
  • Diagnosis:
    • Carboxyhemoglobin level via VBG (ensure proper lab ordering).
    • Pulse oximetry unreliable; falsely high readings.
  • Treatment:
    • Immediate high-flow oxygen administration.
    • Consider hyperbaric oxygen therapy for severe cases to reduce delayed neurocognitive sequelae.

Cyanide Poisoning:

  • Blocks cytochrome oxidase in electron transport chain, halting aerobic ATP production.
  • Patients present critically ill; notable features include:
    • Elevated lactate levels (>8–10 mmol/L)
    • Arterialization of venous blood
  • Treatment:
    • First-line therapy: hydroxocobalamin (Cyanokit) binds cyanide forming vitamin B12 for renal excretion.
    • Alternative: Cyanide antidote kit (amyl nitrite, sodium nitrite, sodium thiosulfate); induces methemoglobinemia and requires monitoring.
    • Important note: hydroxocobalamin turns blood and urine bright red; draw labs beforehand.

Key Takeaways:

  • Assess for airway compromise and signs of inhalation injury early.
  • Maintain a high index of suspicion for CO and cyanide poisoning in smoke inhalation victims.
  • Immediate, aggressive oxygen therapy and early antidote administration can significantly impact outcomes.

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