Smoke Inhalation and Carbon Monoxide Poisoning

Smoke Inhalation

Smoke inhalation produces injury through three mechanisms: heat (upper airway burn), toxic gases (CO, hydrogen cyanide, aldehydes), and particulates (lower airway irritation and inflammation).

Upper Airway Injury

Burns to the mouth, throat, and upper airway are surgical emergencies. Airway edema develops rapidly and can produce complete obstruction within hours of exposure.

Signs of upper airway involvement:

• Hoarseness or change in voice quality
• Stridor — a harsh, high-pitched sound on inhalation
• Drooling (too painful or too swollen to swallow)
• Burns to the face, lips, or inside the mouth
• Singeing of nasal hair

A patient with stridor or worsening hoarseness after smoke exposure is on a countdown to airway obstruction. This is a true emergency. Evacuation to surgical care is the only intervention — there is nothing field medicine can do once the airway closes.

While awaiting evacuation:

• Position upright or leaning slightly forward — this reduces edema pressure on the airway
• Supplemental oxygen at highest concentration available
• Keep the patient calm — crying, agitation, and exertion increase airway swelling
• Do not attempt anything in the mouth

Lower Airway Injury

Chemical and particulate injury to the bronchi and lungs causes bronchospasm, mucosal sloughing, and eventually pneumonia.

Signs: Productive cough with dark or sooty sputum, wheezing, and worsening respiratory function over 12-48 hours. Unlike upper airway injury, lower airway injury often has a delayed presentation — the patient may appear relatively well initially.

Field treatment:

• Remove from exposure
• 100% oxygen if available
• Albuterol inhaler for bronchospasm if available
• Evacuation for medical evaluation

Carbon Monoxide Poisoning

CO is produced by incomplete combustion — generators, charcoal grills, camp stoves, gas heaters, and running engines in enclosed or poorly ventilated spaces.

CO binds hemoglobin with 240 times the affinity of oxygen, blocking oxygen transport. It also binds mitochondria directly, impairing cellular oxygen use even where oxygen delivery is adequate. The result is cellular suffocation with apparently normal oxygen saturation.

Recognizing CO Poisoning

The dose-response pattern by carboxyhemoglobin level:

| COHb Level | Symptoms | |---|---| | 10-20% | Headache, mild exertional dyspnea | | 20-40% | Throbbing headache, nausea, weakness, confusion | | 40-60% | Severe confusion, syncope, seizures, chest pain | | Above 60% | Coma, cardiac arrest |

The practical presentation: Multiple people in the same enclosed space developing headache, nausea, and dizziness simultaneously. This pattern is characteristic. A single person with these symptoms in a space with a known combustion source should also raise immediate suspicion.

The pulse oximetry trap: A standard SpO2 reading is unreliable — it will read falsely normal. Do not use it to exclude CO poisoning. If the clinical picture suggests CO, treat as CO regardless of oximetry.

Treatment

Step 1: Remove from exposure. Move outside immediately. This is the first and most critical intervention.

Step 2: 100% oxygen by non-rebreather mask at 10-15 L/min. If no equipment, fresh air is still dramatically better than the CO environment. Continue oxygen for at least 4-6 hours.

Step 3: Assess severity.

• Mild (headache, nausea, no confusion, no syncope): 4-6 hours of 100% oxygen, observe for deterioration
• Moderate (confusion, syncope, chest pain): 100% oxygen, evacuate for medical evaluation and possible HBO
• Severe (loss of consciousness, seizures, cardiac symptoms): 100% oxygen, evacuate as emergency for hyperbaric oxygen therapy

Do not send the patient home to rest. CO poisoning causes ongoing neurological injury even after initial recovery. The "cognitive aftereffects" of significant CO exposure can persist for weeks. All patients with more than mild exposure require medical evaluation.

CO Poisoning Prevention in Preparedness Scenarios

The intersection of power outages and generators is where CO poisoning kills people in disasters.

Never run inside:

• Generators (even in a garage with the door open)
• Gas-powered tools (pressure washers, chainsaws)
• Charcoal grills, hibachi grills
• Camp stoves or lanterns (kerosene, propane, white gas)
• Vehicles warming up in attached garages

These are not hypothetical risks. CO poisoning is one of the leading causes of preventable death during and after natural disasters.

CO detectors are inexpensive and should be standard in any occupied shelter using combustion heating. Battery-powered models remain functional during grid-down scenarios.

Safe generator placement: Minimum 20 feet from any opening (window, door, vent). Exhaust pointed away from the structure. Outdoors only, regardless of weather.

Hydrogen Cyanide in Smoke

Modern building materials (foam insulation, synthetic carpets, plastics) release hydrogen cyanide when burned. Structural fires increasingly produce HCN in significant concentrations alongside CO.

HCN poisoning accelerates the cellular hypoxia of CO poisoning through a different mechanism (cytochrome oxidase inhibition).

Field treatment: Remove from exposure and administer oxygen. Hydroxocobalamin (Cyanokit) is the definitive antidote but is not available outside hospitals. For field purposes, high-concentration oxygen and removal from exposure are the interventions.

Suspect combined CO + HCN poisoning in any patient with severe metabolic acidosis, seizures, or cardiac arrest after structural fire exposure. These patients need immediate hospital-level care.