Carbon Monoxide, N.O.S.

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The Pre-brief

Most patients with carbon monoxide CO poisoning present to the emergency department with accidental exposures via indoor power tool use, faulty generators and heaters, house fires, or poorly ventilated garages with running vehicles.  Intentional poisonings are also common in the form of suicide via car exhaust in a closed garage.  Below, we will think outside the box though and discuss some atypical means to significant CO poisoning and unique oddities to keep in mind with CO cases.  Overall, CO poisoning is a common toxicologic problem leading to ~50,000 ED presentations and between 400 and 500 deaths in the U.S. annually.  Non-fatal CO poisonings lead to long-term morbidity in the form of delayed neurologic sequelae and in some cases cardiac dysfunction.  As a reminder, hyperbaric oxygen therapy (HBOT) is the primary therapy for CO poisoning and should be pursued when indicated (To dive or not to dive?) to reduce a patient’s risk of developing delayed neurologic sequelae.  

Suicide: acid cocktails and other methods 

A rare but frequently fatal suicidal method via CO is with an acid mixture with formic acid and sulfuric acid.  When formic acid is mixed with sulfuric acid (depicted below), CO is generated in a dangerously high concentration.   CO poisoning from this mixed acid cocktail is nearly universally fatal as caustic inhalation injury is combined with carboxyhemoglobin levels ranging from 64-93% in case reports.  Of important note, the acid mixture can also be harmful to first responders and ED providers, so decontamination of these patients and PPE for involved providers should be pursued as best as possible.  

Other suicide attempts via CO poisoning are unfortunately common.  Running a vehicle in a closed garage is a common method, though some patients go a step further and connect sealed tubing from the vehicle’s exhaust directly into the vehicle where they are sitting.  

Charcoal barbeque grills:

While charcoal grills are frequently involved in accidental CO poisonings when used in closed or poorly ventilated spaces, Bolechała and Strona recently reported an increasing frequency of mini barbeque grills being used indoors in suicide attempts in Europe and Asia.  


There is no denying that hookahs are becoming more popular.  A recent study on a college campus found that 48% of surveyed college freshmen had tried smoking hookah.  Hookah products are marketed as “tobacco-free” and therefore sold as having fewer harmful effects.  Some studies argue to the contrary though, suggesting CO levels and other toxic agents in hookah smoke to be similar or even worse relative to that of tobacco smoke.  In addition to burning the tobacco, hookah smoke is generated from burning charcoal (a lightweight carbon residue…).  Part of the very definition of CO is ‘a gas produced by incomplete combustion of carbon containing materials’!   In fact, the average CO exposure from hookah smoking is nearly 7 times that of a single cigarette.  This vast difference is chalked up to the typical time spent smoking hookah which can be hours at a time relative to the few minutes consumed by a single cigarette.  

Why then don’t college students drop and start seizing left and right at hookah bars?  The short answer is that we don’t know, but the problem is that some do.  An increasingly frequent presentation for CO poisoning is that of the syncopized or seizing patient who’s symptoms started while smoking hookah, and it is not uncommon to see carboxyhemoglobin (COHb)  levels in these cases in excess of 40%.  Patient education regarding the true risks of hookah smoke and prevention of these cases are therefore worthy efforts.          

Don’t forget the neuroimaging

Though quite rare, concurrent intracranial hemorrhage (ICH) is noted in several reported cases of CO poisoning.  Authors of prior case reports discuss the possibility of ICH being a downstream effect of the profound vasodilatory effects of CO leading to compromised integrity of cerebral endothelium.  Others argue that some cases of ICH with severe CO poisoning may be hemorrhagic conversion of stroke.  On a case by case basis, we must also ask the age old chicken or egg question; there are considerations in some cases that ICH (i.e. SAH with debilitating headache and/or mental status change) may precede and lead to accidental CO poisoning.  On the flip side, still other case reports also exist with CO suicide attempts with concurrent ICH.  These argue strongly, at least in some cases, that the CO likely preceded the ICH and that ICH is in fact a potential complication of severe CO poisoning.   

Both scenarios likely exist in which CO poisoning by some uncertain pathophysiologic mechanism leads to ICH and the inverse where ICH leads to accidental CO poisoning.  The overarching point here being to still pursue neuroimaging even if an altered or comatose patient has a COHb level of 40% to explain their depressed mental status as the finding of ICH obviously drastically alters management.  Typical management of ICH of any other cause should ensue.  Regarding HBOT which could be considered for the CO poisoning though, providers must take caution.  A patient with a new ICH is difficult but not impossible to dive and treat with HBOT.  In chamber risks such as seizure are elevated in this unique patient population, and a thorough risk vs. benefit conversation should be pursued with a hyperbaric team on a case by case basis.  

Treatment (briefly)

Again, see To dive or not to dive? for a more detailed discussion of when to pursue HBOT for CO poisoned patients.  In short, patients with syncope or seizure due to CO will almost always meet indications for HBOT regardless of CO level.  Patients with laboratory derangements suggestive of end organ damage (elevated lactate, CK, troponin, or acidosis) will also likely meet indications for HBOT.  Patients should be maintained on 100% via non-rebreather in interim to HBOT facility.  Treatment course typically will include three dives within a 24-hour period with the best outcomes coming when the first dive is started within 6 hours of exposure.  


  • Even when the typical history of CO exposure is not readily apparent, keep CO on the differential of the undifferentiated altered, syncope, seizure, or even comatose patients. 
  • Formic acid plus sulfuric acid is a rare but fatal suicide cocktail which produces highly concentrated CO and also causes caustic inhalational injury
  • Hookah pipes, though surging in popularity, are more dangerous than is typically appreciated and can cause significant CO poisonings
  • Very rare cases of CO poisoning can have concurrent intracranial hemorrhage.  Get neuroimaging even if labs are suggestive of a slam dunk CO poisoning
  • HBOT is the primary therapy for CO poisoning.  Call the poison control center or the nearest hyperbaric chamber for moderate to severe cases of CO poisoning.


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