Inhalation

A 4-year-old male is brought to the emergency department by EMS after being rescued from a house fire. He was found unconscious in a smoke-filled bedroom and is now minimally responsive with labored breathing. 

History
The child was trapped for several minutes in an enclosed room during a residential fire. The fire department reports heavy smoke inhalation, with no known burns. He was found obtunded, with shallow respirations and soot around his nose and mouth. His parents report he was healthy prior to this incident, with no history of seizures, asthma, or ingestions. No information is available about household chemicals present in the home. 

Physical Exam
Vitals: T 37.5°C, HR 130 bpm, RR 28/min, BP 92/55 mmHg, SpO₂ 99% on pulse oximetry. 
General: Minimally responsive, smells of smoke
HEENT: Soot in nares and oropharynx, singed nasal hairs
Lungs: Diffuse rhonchi, shallow breaths
Cardiovascular: Tachycardic, normal rhythm, cap refill 2–3 seconds
Abdomen: Soft, nontender
Neurologic: Unresponsive to voice, withdraws to pain, pupils sluggish
Skin: No external burns, skin pink with normal turgor

• Carbon Monoxide (CO) poisoning – Most common toxic exposure in enclosed fires; binds hemoglobin with high affinity, impairing oxygen delivery despite normal SaO₂ readings.
• Cyanide (CN) poisoning – Less common but highly lethal; results from combustion of synthetic materials (plastics, wool, foam). Cyanide inhibits mitochondrial respiration, causing lactic acidosis and rapid deterioration.
• Hypoxia from smoke inhalation and airway injury – Due to thermal and chemical irritation.
• Other toxic inhalants – May include oxides of nitrogen, sulfur dioxide, or household chemicals. 

In any pediatric fire victim with altered mental status, respiratory distress, or signs of shock, toxic inhalation must be assumed until proven otherwise. The two most concerning toxic exposures in enclosed-space fires are carbon monoxide (CO) and cyanide (CN). These can occur individually or together, often without external signs of injury. CO poisoning is common and interferes with oxygen delivery by binding hemoglobin, while cyanide disrupts cellular respiration, leading to rapid lactic acidosis and cardiovascular collapse. Because testing can be delayed or unavailable, especially for cyanide, clinicians must rely on clinical signs such as neurologic depression, high lactate, and fire exposure history to make early treatment decisions. Prompt administration of high-flow oxygen, empiric antidotes, and aggressive supportive care can be lifesaving. Time is critical — these patients can deteriorate rapidly without intervention. 

Initial Evaluation

• Point-of-care testing: 

• • Obtain point-of-care glucose to rule out hypoglycemia. 

• Laboratory evaluation: 

• • VBG or ABG with lactate level: elevated lactate (>8 mmol/L) suggests cyanide toxicity. 

• • Carboxyhemoglobin (COHb) level via co-oximetry to assess CO exposure. 

• • Basic labs such as CBC and CMP. 

• • Toxicology screen if ingestion or other exposures are suspected. 

• • ECG to assess for cardiac ischemia. 

• Imaging: 
• Chest X-ray to assess for smoke-related injury or aspiration. 

Management

• Rapid airway and breathing support: High-flow oxygen via non-rebreather mask or intubation if airway compromise is suspected (e.g., soot in airway, altered mental status, respiratory distress). 

• Treat carbon monoxide poisoning with 100% oxygen to reduce CO half-life. Hyperbaric oxygen therapy may be indicated for severe CO poisoning (e.g., neurologic symptoms, cardiac ischemia, COHb >25%). 

• Empirically treat cyanide poisoning in fire victims with significant lactic acidosis, coma, or cardiovascular collapse. Administer hydroxocobalamin (Cyanokit) IV — binds cyanide to form vitamin B12, which is excreted in urine. 

• Fluids and vasopressors as needed for hypotension. 

• Supportive care and monitor for respiratory decline or secondary complications. 

• Carbon monoxide poisoning is far more common than cyanide toxicity in fire victims, but both can coexist, especially in enclosed fires involving synthetic materials. 

• Pulse oximetry is unreliable in CO poisoning. Pulse oximetry reads normal because it cannot distinguish between oxyhemoglobin and carboxyhemoglobin. Co-oximetry is required for accurate measurement. 

• Empiric hydroxocobalamin is safe and effective in suspected cyanide poisoning. Administration should not be delayed for lab confirmation, especially in patients with coma, seizures, or high lactate. 

• An elevated lactate (>6-8) in a smoke inhalation victim is a red flag for cyanide toxicity. 

• Consider both CO and CN in any fire victim with neurologic depression, unexplained hypotension, or lactic acidosis. 

Answers

Q1. False. Pulse oximetry cannot detect COHb and will give falsely normal oxygen saturation readings.

Q2. False. In suspected cyanide poisoning, especially in fire victims, hydroxocobalamin should be given empirically.

Q3. B. This patient meets clinical criteria for empiric hydroxocobalamin due to exposure history, altered mental status, and high lactate level. 

• StatPearls – Inhalation Injury. 
• ACEP – Carbon Monoxide Poisoning
• Pediatric EM Morsels – Cyanide Poisoning