by Justin Arnold, DO, MPH, FACEP, FACMT

Although us Floridian’s don’t have the freezing cold weather necessitating a nice fire in the fireplace or space heaters in every room, we still see victims of housefires presenting to our ED.  In fact, Florida has the third-highest number of properties at risk for fire due to natural disasters including hurricanes, flooding, and wildfires – only Texas and California pose more risk.

CYANIDE AND HOUSEFIRES

And though we certainly worry about thermal burns associated with a housefire, the culprit of those that succumb to a housefire is by and large smoke inhalation.  But when we talk about smoke inhalation – what exactly are we talking about?  Well, it depends really on what is burning!  In most house fires, patients are exposed to a variety of chemicals based on the combustion of the contents of the home.  These can include (but are not limited to):

• Carbon monoxide

• Cyanide

• Methane

• Volatile Organic Compounds (VOCs)

• Formaldehyde

• Benzene

• Acetic and Formic Acids

• Toluene

• Nitrogen Oxides

• Sulfur Dioxide

• Organic Carbon

• Trace Metals

Now that is quite a list, but what I want to focus on today is the real and immediate threat that we will see in the ED – and that is largely going to be Carbon Monoxide and Cyanide.  I think most people are fairly familiar with Carbon Monoxide toxicity and treatment but where we as toxicologists see things get interesting is in the assessment of Cyanide toxicity (most people are pretty good at treatment)!

So let’s review.

Recall that Cyanide (CN-) can exist as a gas, combined with hydrogen to produce hydrogen cyanide, as a salt, and as a solid as potassium cyanide.  In the United States, cyanide gas from housefires is the most common method of exposure.  Cyanide is considered a rapid knock-down agent, especially when inhaled.  Cyanide works by halting cellular respiration through inhibition of the electron transport chain by inhibition of cytochrome complex IV.  The result at a cellular level is ATP is not produced and cells cease to function without ATP present.

PRESENTATION

Clinically, this manifests with symptoms within 1-2 minutes if inhaled.   

Diagnostically, we would like to assess:

• CBC, CMP, lactate, and ABG with co-oximetry (to assess for CO exposure)

• CXR

• EKG

Also, symptoms of cyanide poisoning after smoke inhalation happen quickly!  You should see symptoms either before or shortly after arrival.  Decompensation hours after exposure is not likely due to cyanide poisoning.

MAKING THE DECISION TO TREAT (OR NOT)

So now that we know how cyanide is generated, mechanistically how it presents, and clinically what is seen, we arrive at the central question of this blog – how do we determine when to pull the trigger on Cyanokit (hydroxycobalamin) for a patient presenting from a housefire?

The answer is actually, quite simple!  The patient needs to :

• Present with symptoms of cyanide toxicity, which often include hemodynamic instability such as tachycardia, bradycardia or hypotension, seizures, or are unresponsive) after an exposure to smoke,

• Develop symptoms rapidly after exposure, AND

• Present with a lactate >8mmol/L

Now, if the patient present in extremis, clearly you’re not going to wait for a lactate to result – you will simply treat.  BUT – if you get a lactate back and it is LESS than 8 mmol/L, you really need to look for other causes of the patient’s symptoms – it’s unlikely to be cyanide.

Cyanokit (hydroxocobalamin) is the treatment available at most hospitals in the United States (Tampa General, included).  Hydroxocobalamin, when combined with cyanide, produces cyanocobalamin which is inert and renally eliminated.  It can cause an increase in blood pressure (which can be desirable in cyanide poisoning) and will result in red discoloration of the skin and bodily fluids.  Dosing is 70mg/kg (max 5 grams) IV infusion over 15 minutes.  The dose can be repeated once.

Additionally, hydroxocobalamin does not pose a risk for patients with concomitant carbon monoxide exposure the same way as the older cyanide antidote kit (amyl nitrite, sodium nitrite, and sodium thiosulfate) does.  The older cyanide antidote kit induces methemoglobinemia which when compounded with a significant carbon monoxide exposure, would pose a significant limitation of oxygenation of the patient.

SUMMARY

So, that’s it.  Surprisingly simple!  If a patient presents after a housefire, is clinically consistent with cyanide exposure and (if time permits) has a lactate > 8mmol/L, treat with hydroxocobalamin.  Rinse and repeat, if needed.  And don’t forget to assess and address CO. And, as always, please reach out to Poison Control at 800-222-1222 with all exposures!

REFERENCES

Cescon, D. W., & Juurlink, D. N. (2009). Discoloration of skin and urine after treatment with hydroxocobalamin for cyanide poisoning. CMAJ, 180(2), 251-251.

Graham, J., & Traylor, J. (2021). Cyanide Toxicity, Stat Pearls. Treasure Island (FL).

http://www.emdocs.net/em3am-cyanide-toxicity/

https://cyanokit.com/

ABOUT THE AUTHOR

Dr. Justin Arnold is the Medical Director of the Florida Poison Information Center in Tampa, Florida. He also leads the toxicology rotation at USF EM and is an Emergency Physician at Tampa General Hospital.