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
Download
Leave a Comment
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 excre...