Podcast 122 – Cardiac Arrest after the Toxicology of Smoke Inhalation with Lewis Nelson


We had a case a few months ago at Janus General–very sad and very scary. The patient came in after a house fire. He had some burns, but not enough to be the cause of his arrest. Instead, it had to be the asphyxia and possible toxicology of the smoke inhalation. I wanted to get a better idea of ideal care for these patients; for that I needed a toxicologist.

Lewis NelsonFew tox folks are smarter than Lewis Nelson, MD of the NYC Poison Center.

Note: In this episode we don’t deal with the thermal injury of smoke inhalation

Cyanide Toxicity

  • Empiric administration of  Hydroxocobalamin 5 g rapid IV drip x 1
  • Even better if this can be given at the scene as soon as the patient arrests or is profoundly hypotensive
  • Messes with labs that use colorimetric probes (cooximetry, lactate, LFTs, etc.) Get blood for cooximetry before giving the med if at all possible
  • Dr. Nelson doesn’t recommend giving sodium thiosulfate in addition to the Hydroxocobalamin
  • An IM version is in the pipeline–this will be easier for EMS/emergency use
You'll need 200 ml of Saline
You’ll need 200 ml of Saline

Carbon Monoxide

  • Put the patient on 100% fiO2
  • Not much to do beyond that until the patient stabilizes
  • See LITFL for more on CO


  • Caused by Hb oxidation from the heat of the fire
  • Administer Methylene Blue 2 mg/kg x 1 IVP
  • May be worthwhile to start a drip if patient has resistant hypotension, but this is an unproven therapy

Now on to the Podcast…

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  1. says

    Scott –

    Yes, you can give hydroxocobalamin (HCB), and it may save a life. Or may not – we just don’t know!

    The three clinical HCB studies out of France, as well as the abstract from Houston, were all case series, and so weren’t designed to prove any improvement in outcomes. None of them even had a historical control group, let alone randomization, so the best we can conclude from these studies is that giving HCB is feasible by EMS. (http://millhillavecommand.blogspot.com/2014/04/part-2-different-edit.html)

    Sure, there’s animal data suggesting that HCB can resuscitate cyanide-poisoned pigs. There is also evidence that epinephrine, along with ventilation and CPR, can achieve ROSC in a dog just as often as HCB. (http://millhillavecommand.blogspot.com/2014/04/cyanokit-whats-evidence-part-1.html)

    Lastly, although Dr Nelson simply states that HCB is “not particularly pricey”, at > $1200 a dose, this is a heavy hit for many EMS systems.

    Listen – we all use drugs and therapies that don’t have perfect evidence, or that have a significant pricetag. My concern about HCB, however, is that the rush to administer this expensive and (essentially) evidence-free drug will distract first-responders, and likely a few physicians, from interventions that actually HAVE been proven to save lives.

    So, before an EMS system or FD starts using this drug, they should make sure they know how to, say, immediately start compressions on a fully clad firefighter. I might wonder if they had already adopted all the principles of “pit-crew” CPR that has been shown to improve neuro-intact survival from arrest.

    Sorry for referencing my blog twice in one comment Scott. I hope the value of the references I provide outweighs my self-promotion!

    • says

      I think you hit the nail on the head as far as improving cardiac arrest care regardless of etiology: you have to start with high performance CPR and a system which demonstrates competence in the fundamentals. This will get you almost all of your survival gains.

      Because of this, once you’ve ensured the fundamentals are covered it will be rare to find another silver bullet, because statistically it probably won’t have nearly the same effect as CPR. I doubt we’d ever be able to generate the numbers necessary to answer the question, “does HCB improve survival to discharge neurologically intact in cardiac arrest due to cyanide toxicity?” Thus the NNT will be unknown, probably high, yet animal trials seem to hold that the NNH is at least as high or higher than the NNT.

      So if you’re a system with a proven track record of high survival to discharge, the addition of HCB in select patients is possibly helpful and may allow marginal gains. I use marginal in the economics sense rather than the patient-centric sense (any gain is significant in the patient-centric sense).

    • says

      Chris, You basically said exactly what I was going to, saving me having to type it.

      Brooks–Great Posts, here is Dr. Nelson’s response:

      Thanks for asking. We are all entitled to our opinion and there are no
      right answers for many of the issues raised. I agree that CPR (etc) is
      important, etc, but you can do all the CPR you want in a cyanide
      poisoned person and it wont help until the mitochondria can function
      again. That said, HCO is not going to save a dead person, so you still
      need all of the standard, high quality resusciation measures.

      Prices for HCO and for the Lilly/Taylor/CAK kits are all over the
      place and each pharmacy and system pays differently. Its a fairly
      small difference though. Hard to comment on cost when death is on the
      line. Regardless, its a lot less than new chemo that costs $100K and
      prolongs end of life by 12 weeks.

      Evidence will never be what people want esp for poisoning managment,
      and there will be the rarest of RCTs and almost never a high quality
      one (placebo controlled, blinded, etc). Not to mention that there are
      few enrollable patients. Thus so many decisions are based on other
      sources of merit and risk. Mechanistic understanding, animal models
      (animal rule via FDA), and summative clinical experience has been
      great. Added to this is the ease of use and reduced adverse effects
      which makes it a pretty clear choice over the prior kits. One of the
      great failures of EBM is that people’s expectation have become
      somewhat irrational and dogmatic. Anyway,I have no and never had any

      Thanks for asking,

  2. Dr James French says

    I had a case like this when I was a resident. I remember my boss, Dr Simon Mardel (one of the most interesting people in history; his life is like the film “Outbreak”, works for the WHO hunting Ebola and other nasties) walking into resus, looked at the burnt patient, ran out of resus and came back with HCB and poured it into her. She survived though it did turn her arm purple. True story…….

  3. Patrick Wanner says

    Thank you very much for the extremely interesting and informative interview! I recently had a case of smoke inhalation who ended up receiving HCB. Certain team members insisted on getting arterial and venous BGA to calculate the O2-gradient, a narrow one supposedly implicating CN-intoxication. Although an intuitive concept, does it have any diagnostic role, especially with concurrent CO-intoxication? Thanks!

  4. Patrick Wanner says

    Thank you very much for the extremely interesting and informative interview! I recently had a case of smoke inhalation who ended up receiving HCB. Certain team members insisted on getting arterial and venous BGA to calculate the O2-gradient, a narrow one supposedly implicating CN-intoxication. Although an intuitive concept, does it have any diagnostic role, especially with concurrent CO-intoxication? Thanks

  5. says

    There is a treatment;
    I’m not only a Paramedic for the past 15 years, but I used to work as a commercial Driver in the gulf of Mexico oilfield industry.
    I’ve had experience with treatment of CO poisoning. The CO binds with the hemoglobin and prevents gas exchange. If its available, a hyperbaric chamber that can deliver O2 during treatment can be used to send O2 directly into solution in the blood plasma, and allow oxygenation of the bodily tissues despite CO poisoning. this is done by compressing the patient to 60ft of depth seawater. and the patient breathing O2 via a mask similar to a C-PAP. care must be taken however as breathing o2 under high partial pressure in this way can cause O2 toxicity. there are two types that must be watched for, CNS O2 toxicity is characterized by altered mental status, slurred speech and seizures. Pulmonary O2 toxicity is slower onset ( can take 2-4 days) and is characterized by Pleurisy, chest pain, and flash Pulmonary Edema. In the case of the CNS type the patient should only be allowed to breathe the high partial pressure for 15-30 mins, with a 30-60 min air break between treatments, the air in the chamber must be cycled at the start of each air-break.

    It’s not a perfect solution but it is an alternative to doing nothing.

    Jeffrey Brown

  6. Bryan Swetel says

    I had two of these cases this week. The only difference was ROSC occurred within the first minute or two of chest compressions. What is your thought of administering HCB post cardiac arrest ? Now a days almost every structure fire victim is going to suffer from some level of cyanide poisoning. Scott, Thanks for all the excellent education opportunities !

  7. says

    Lewis –

    Great to have this dialogue. I suspect we’re not too far apart in either practice style, or dogma. After all, many of the tox attendings in my residency were trained through your fellowship, and I still have my textbook from my own NYCPC rotation years ago!

    Let me flip this discussion 180. Frankly, if I were arguing in favor of more routine HCB administration, I would describe the introduction of fomepizole, and of digoxin-specific Fab fragments. Neither one of those drugs had a supporting RCT, or even a strong case-control trial. Indeed, the important studies showing their benefit were open-label, and uncontrolled. (E.g. Brent 1999 “Fomepizole for the Treatment of Ethylene Glycol Poisoning,” and Antman 1990 “Treatment of 150 cases of life-threatening digitalis intoxication with digoxin-specific Fab antibody fragments.”). The low rate of adverse effects, and the strong mechanistic and animal data, however, along with the difficulty of conducting a true RCT, argued strongly in favor of using these drugs, despite active discussion regarding the costs. So it’s appealing to use a similar argument to support using HCB.

    These precedents, however, also suggest that recommendations for the routine administration of HCB are premature. The studies cited above were of far higher quality than the 3 French HCB studies. For example, both used prospective collection of data (rather than chart review), and both used clear criteria for the use of the antidotes. Given the high quality of the data, a valid comparison can then be made with historical cohorts.

    By contrast, the French studies are of very low-quality, based on chart reviews with unclear methods, and have plenty of missing data.

    This is especially true when it comes to the data regarding the use of HCB in cardiac arrest. As I highlighted in my review, study #1 had no data on the timing of HCB administration in patients found in cardiac arrest, so we have no idea if HCB “brought them back.” Study #3 is similar – 2 out of 13 cardiac arrests survived, but no other data is provided about the timing of HCB. Study #2 admitted that 4 out of the 5 survivors of cardiac arrest got HCB only *after* ROSC.

    With regard to cost, both fomepizole and Digibind were administered in the hospital, after careful evaluation bolstered a diagnosis of the specific toxidrome. By contrast, HCB has been delivered by EMS empirically, in the French and Houston experiences, to a broad swath of patients. The potential for far greater costs with this empiric approach should not be dismissed lightly. Perhaps FDNY can absorb these costs easily, but most small municipal, volunteer, and private EMS agencies will find the cost of stocking and replacing HCB to be a significant challenge.

    I think we both agree on a couple things, and one of those is that “HCO is not going to save a dead person.” There probably is a role for this relatively safe, specific, and (in pigs) effective drug. But just like no one is pushing fomepizole IV during a code on an undifferentiated OD patient, I’m not sure that empiric use of HCB can be justified just yet.

  8. Paul Barbara MD says

    This was a truly informative interview with one of the all-time greats. I have a background in EM and EMS, and actually helped craft the OOH protocol Dr. Nelson describes.

    I just want to remind the readers that we are forgetting one of HCB’s most important qualities — that it’s risks are greatly outweighed by its benefits. Yes it is pricey and can cause alteration in lab results, but we give medications and therapies routinely with a much worse risk/benefit profile.

    Another forgotten quality of HCB is the impact it may have on a first responder’s ability to survive an otherwise lethal inhalation. The comparisons to other EM and critical care modalities is important, but we should remember that deploying HCB in the prehospital arena will eventually save the life of a firefighter, EMT/medic, police officer, Good Samaritan, etc. Rarely do we as hospital providers and oversight physicians have the ability to impact our caregivers as well as the civilians they strive to save. We owe it to these brave men and women to be able to save their lives in the case of such an injury.

    $1200 is expensive per dose, as well as the underlying costs for supplies and training required to have it on scene for each fire job. However, in the current system, it is a small price when compared to the alternatives should that provider die in the line of duty.

    Concerning the route of administration concerns brought up by Dr. Nelson, has anyone heard or considered giving it through an intraosseus line? Given the recent move to proximal humeral IOs as the “go-to” line in situations with difficult access (including the new ability to use IOs on semi-conscious shock patients in NYC EMS), could the HCB be given through an IO? I don’t have the package insert to check but intuitively it should be ok.

    • says

      Disclaimer: this response only applies to the specific challenges when resuscitating a downed firefighter.

      My main concern in the resuscitation of a downed firefighter is that there are a few burdensome steps prior to even administering HCB.

      The turnout gear, bunker gear, PPE–whatever you want to call it–that a firefighter wears takes at least 2 minutes to doff in the best of conditions. In trials at my own department we’ve seen that it takes upwards of 5 minutes to remove the gear in folks who have not practiced.

      More typically firefighters collapse due to cardiovascular complications, but assuming it is a smoke inhalation exposure we’ve some timeline problems w.r.t. HCB administration:

      1. We’ve got to get them out. This takes time, quite a lot of time in fact, and if you read the NIOSH reports it is rarely under 10 minutes.

      2. Now that they’re out, we’ve got to get them out of their gear. This takes a lot of time.

      3. Now that they’re out of their gear, we need IV/IO access. This also takes time, but less with IO.

      My department (Leland Volunteer Fire/Rescue) has specifically looked at the challenge of step 2, which is the one we have the most control over in terms of removing variability. With a procedure in place to systematically doff the gear from an unresponsive firefighter, we can whittle the time down to about 2.5 minutes on average. I’ll ballpark a median of 10 minutes to remove the firefighter from the structure (in actuality it is much longer), so we’re looking at 12.5 minutes before chest compressions are initiated.

      With such a prolonged downtime in a primary respiratory etiology, it is unlikely that HCB will improve outcomes measurably. Spending money on HCB without spending money on the fundamentals is unlikely to save anybody. Therefore the application of HCB early in arrest should only be considered by departments who can demonstrate competence at removing the firefighter and initiating early CPR and advanced airway management (without interrupting CPR). Money spent on these endeavors is far more likely to measurably improve outcomes in the unlikely instance of a downed FF due to smoke inhalation.

      (I’m not against HCB and think it has a place, in fact another department in my area has been pursuing studying cyanide retention in bunker gear and have found elevated levels *inside* their coats during live burn evolutions. Hopefully they’ll get some funding and support to run trials with blood draws to see if that translates to actual exposure.)

  9. says

    Hey guys:

    Please for give me for interjecting a different topic than Hydroxocobalamin and smoke/heat inhalation injury. But I do have a burning question on a different important topic; SAH.
    In my ED shop, a small community hospital in rural Minnesota we do see a fair amounts of headaches like every body else. Last night I saw a middle-aged lady who woke up with a severe headache that reached a maximum intensity within minutes if not seconds of its onset. She denies any history of primary headaches or ever having a headache of this severity in her life. She tried to manage the headache with OTC’s such Advil to no avail. When she came our shop more than 10 hours from the onset of the headache she still had a severe headache(head pressure) with sharp neck pain. Her SBP was in the 200’s. She had no focal weakness or visual disturbances. She was not toxic, afebrile and with no AMS. My first impression was SAH. CT head was negative. Now I wanted to do LP but by then it was time to go home with change of shift and care was assumed by my colleague who thought LP was overkill given negative high resolution 64-slice CT. We discussed the possibility of this being due to so-called “sentinel bleed” from some sort of aneurysm and this being the opportunity to catch it now. The question my colleague asked which have also dogged me for a long time as well is the following: HOW LIKELY IS IT FOR INTRACRANIAL BLEED THAT CAUSES SO MUCH HEADACHE WITH SECONDS OF ITS ONSET TO BE SO SMALL THAT YOU CAN NOT SEE IT ON HIGH RESOLUTION CT?
    I understand as time goes the blood gets denatured and it is not as easily visible on CT but the question is even if she presented within minutes of the onset of her headache we would still go through the same protocol if we are concerned about SAH: CT head, if negative LP. MRA/CTA are less desirable because of the obvious possibility of findings an aneurysm that may not have been the cause of her headache with associated morbidity and mortality associated if corrective action taken by the specialist. Please educate me on this; I really would welcome your comments enthusiastically. Thank you very much indeed.

  10. Carlos Alfaro Iberico MD. GP working in ER on a tertiary hospital in Puerto Rico says

    uhmm. I listened the podcast yesterday. I am fan!. Do you think we could have make any difference if this patient was put into ECMO?. Maybe that could have give HCB a chance to work.


  1. […] inhalation and the potential for concomitant systemic toxicity, focussing on cyanide. Check out Podcast 122 – Cardiac Arrest after the Toxicology of Smoke Inhalation with Lewis Nelson. I also have a CCC entry on this topic here. […]

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