Episode 207: Smoke Inhalation Injury

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.