Assessing and treating smoke inhalation

It’s the winter season, and you know what that means: not only are we moving into our third year of the COVID-19 pandemic, it’s the cold and flu season as well. Whether we’ll be faced with a yet another variant or hybrid (flurona, anyone?) remains to be seen. Hand-in-hand with the cold and flu season and miserable weather comes a particularly nasty hazard we’ll also frequently encounter: structure fires.

A fire in a high-rise apartment building in the Bronx on January 9 killed 17 people, including eight children. Most of the victims died of smoke inhalation, which is the leading cause of death in structure fires. The suspected culprit in the Bronx fire was a malfunctioning electric space heater, but it could have just as easily been a dry Christmas tree, carbon monoxide poisoning from a faulty propane heater, running a gas range for heat, a curling iron left on in the bathroom, or someone forgetting to blow out a scented candle before they went to bed.

It doesn’t matter the source; all EMS providers, whether they are part of a fire department or not, need to be prepared to assess and treat patients poisoned with the byproducts of combustion. Care for electrical and thermal burns could spawn a series of articles in themselves, but in this article, we’ll confine ourselves to assessing and treating three types of toxic inhalations:

1. Cyanide poisoning
2. Carbon monoxide poisoning
3. Thermal inhalation injury

Cyanide Poisoning

Hydrogen cyanide and its analogues, such as cyanogen chloride, are colorless gases that result from the incomplete combustion of plastic-containing products – particularly polyvinyl chloride (PVC), vinyl or polyurethane – common in many households. When inhaled, cyanide binds to hemoglobin and circumvents the process of cellular respiration; it does not allow off-loading of oxygen at the cellular level.

Cyanide inhibits oxidative phosphorylation, the metabolic pathway essential for aerobic metabolism. The resultant histotoxic hypoxia causes lactic acidosis and greatly inhibits production of adenosine triphosphate (ATP), the fuel for our body’s metabolic processes.

Early signs and symptoms of cyanide poisoning include:

• Weakness and dizziness
• Headache
• Dyspnea
• Confusion
• Hypertension

Late signs of cyanide poisoning include:

• Hypotension
• Coma
• Seizures
• Metabolic acidosis
• Apnea
• Cardiac arrest

Traditionally, cyanide inhalation has been associated with the characteristic “bitter almond” smell, but keep in mind that a victim in a structure will likely be covered in multiple products of combustion, masking the smell of cyanide. Also, approximately 15% of the population cannot detect the smell of bitter almonds.

End-tidal CO2 may be low in cyanide poisoning due to the lack of cellular respiration, but there is little data on the subject [1,2]. In studies of sepsis patients, however, an EtCO2 of 25 mmHg or less was strongly associated with a lactate level of 4 mmol/L, and lactic acidosis is common in severe cyanide poisoning.

Treatment of cyanide poisoning includes high-flow oxygen, inhaled amyl nitrite and a combination of intravenous sodium nitrite and sodium thiosulfate. An antidote kit containing intravenous hydroxocobalamin (Cyanokit) is also available.

Carbon Monoxide Poisoning

Carbon monoxide (CO) is a byproduct of incomplete combustion that acts as an asphyxiant: it competitively binds with hemoglobin, eventually displacing all oxygen and causing systemic hypoxia. CO is lighter than air and rises from the point of origin.

One of the classic signs EMTs are taught to look for in carbon monoxide poisoning is cherry red skin, but be aware that this is an uncommon, and typically very late finding. Rather than have the pathologist note cherry red skin in an autopsy, here are more common signs and symptoms that will help you recognize CO poisoning while you can still do your patient some good:

• Headache
• Altered or decreased level of consciousness
• Fatigue and weakness
• Dizziness
• Nausea/vomiting
• Tachycardia
• Seizures

Traditional pulse oximetry is unreliable in carbon monoxide poisoning. The pulse oximeter only detects that hemoglobin is saturated; it is incapable of differentiating what the hemoglobin is saturated with. Some pulse oximeters have integrated carboxyhemoglobin sensors and may be useful in detecting elevated CO levels.

Here in hurricane country, we typically see several deaths each year from carbon monoxide poisoning unrelated to structure fires. Homeowners who are powering their homes with gasoline or diesel generators during power outages place the generators too close to their air conditioning intake, sucking up exhaust fumes rich in carbon monoxide and distributing it throughout the home. It is also a frequent occurrence in enclosed spaces where propane or kerosene space heaters are used without adequate ventilation. Whenever you see multiple victims with similar signs and symptoms, think carbon monoxide poisoning.

The first step in treating CO poisoning is to remove yourself and the patients from the source. Get the victims outside and into fresh air.

Once you have removed the patient from the potential source, administer high-flow oxygen. There is no specific antidote to carbon monoxide poisoning, but hyperbaric oxygen therapy has been demonstrated to limit oxidative stress better than normobaric oxygen, speeds the elimination of carboxyhemoglobin, and significantly diminishes the long-term neurological effects of carbon monoxide poisoning [3-5].

Thermal Inhalation Injury

Victims trapped in structure fires commonly inhale, along with the toxic gases previously mentioned, superheated air which induces inflammation and swelling of respiratory passages. Signs of thermal inhalation injury include:

• Stridor or hoarseness
• Coughing
• Burns to the face and throat
• Soot and particulate matter around the nose and mouth

Stridor is an ominous finding indicating significant upper airway edema. The swelling can continue, eventually necessitating a surgical airway. Sedation and prophylactic endotracheal intubation, even in conscious and spontaneously breathing patients, may be required before the airway is too swollen to accept an endotracheal tube. Administer high-flow oxygen and bronchodilators as necessary.

As much of the swelling in thermal inhalation injury occurs at or below the vocal cords, supraglottic airways will be of limited benefit; a subglottic airway – i.e., an endotracheal tube – is necessary. As many of these patients may also undergo hyperbaric oxygen therapy, consider filling the endotracheal tube cuff with sterile water or saline instead of air.

References

1. Hunter CL, Silvestri S, Dean M, Falk JL, Papa L. End-tidal carbon dioxide is associated with mortality and lactate in patients with suspected sepsis. American Journal of Emergency Medicine. 2013 Jan;31(1):64-71.
2. Hunter CL, Silvestri S, Ralls G, Stone A, Walker A, Papa L. A prehospital screening tool utilizing end-tidal carbon dioxide predicts sepsis and severe sepsis. American Journal of Emergency Medicine. 2016 May;34(5):813-9.
3. Ning K, Zhou YY, Zhang N, Sun XJ, Liu WW, Han CH. Neurocognitive sequelae after carbon monoxide poisoning and hyperbaric oxygen therapy. Med Gas Res. 2020 Jan-Mar;10(1):30-36. doi: 10.4103/2045-9912.279981. PMID: 32189667; PMCID: PMC7871936.
4. Liao SC, Shao SC, Yang KJ, Yang CC. Real-world effectiveness of hyperbaric oxygen therapy for delayed neuropsychiatric sequelae after carbon monoxide poisoning. Sci Rep. 2021 Sep 28;11(1):19212. doi: 10.1038/s41598-021-98539-y. PMID: 34584153; PMCID: PMC8479087.
5. Weaver LK. Hyperbaric oxygen therapy for carbon monoxide poisoning. Undersea Hyperb Med. 2014 Jul-Aug;41(4):339-54. PMID: 25109087.