Episode 207: Smoke Inhalation Injury

We discuss the injuries sustained from smoke inhalation.

Hosts:

Sarah Fetterolf, MD

Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Smoke_Inhalation.mp3

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Tags: Environmental, Toxicology

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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