To Dive or Not to Dive?

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The Pre-brief

Outside of SCUBA diving injuries, carbon monoxide (CO) poisoning is the only other indication where hyperbaric oxygen therapy (HBOT) is considered primary therapy.  In addition to expediting CO elimination, HBOT can, more importantly, reduce a patient’s chances of developing delayed neurologic sequelae (DNS) following CO poisoning.  Even so, there are mixed recommendations as to whether HBOT should be recommended for CO poisoned patients based on conflicting results of trials.  In practice, many cases of CO poisoning are unclear whether HBOT is indicated, but there are certain features of cases, to be discussed herein, where a provider should strongly consider HBOT for the CO poisoned patient.   

Why we treat CO with HBOT: 

The two reasons we use HBOT to treat CO poisoning are expedited elimination of CO and reduction in risk for DNS.  While the half-life of carboxyhemoglobin (COHb) is markedly reduced with HBOT (23 min.) compared to a patient on room air (~5 hours) or non-rebreather (~75 min.), most patients will have cleared their COHb levels to normal or near-normal by the time they are treated in a hyperbaric chamber due to transfer time and other logistics.  This is not to say that immediate HBOT is not beneficial.  If a comatose patient is pulled from a garage full of car exhaust and a hyperbaric facility is a next door, by all means, dive them.  In most cases though, the markedly reduced half-life of COHb when treated with HBOT is not the primary reason why HBOT is recommended.  Instead, risk reduction for DNS is the primary goal.  

DNS occur 3-6 weeks following the poisoning in 25-50% of severely CO poisoned patients and can manifest as frequent headaches, neurocognitive deficits, or even personality changes.  The pathophysiology of DNS involves a complex cascade of inflammatory changes set in motion by the CO-induced leftward oxyhemoglobin shift and acute ischemic insult.  The details of this pathophysiology are beyond the scope of a single post but involve neuronal lipid peroxidation and alterations in myelin basic protein.  As implied by the name, the neurologic manifestations occur in a delayed fashion, and HBOT as acute therapy (within 24 hours of poisoning) can attenuate this inflammatory cascade.  

CO level, a binary approach?

While the correct answer to a CO-related board question is to treat with HBOT for COHb >25% or >15% in pregnant patients, actual hyperbaric practice is quite disparate from this approach.  Certainly, most cases with COHb >25% represent more severe exposures that would benefit from HBOT, but CO levels alone correlate poorly with morbidity and mortality.  For example, there are many patients with CO levels less than 25% who would still benefit from HBOT and there are some patients with levels >25% who don’t need HBOT.  In some ways, the COHb level can be considered a binary test that simply answers the question of whether there was a CO exposure or not.  Once there is a proven elevation in COHb (by blood only! Cutaneous co-oximeters are not reliable), it becomes a clinical question based on symptoms and laboratory data whether the patient would benefit from HBOT. 

End organ damage:

The ultimate question that needs to be answered is whether or not there is evidence of end-organ damage caused by acute CO toxicity.  When evidence of CO-associated end-organ damage is present, HBOT should be recommended.    

Workup should therefore include:

  • CBC, chemistry panel
  • Blood gas 
  • EKG and troponin
  • Lactate, CK, LFT’s
  • Pregnancy test in females (fetal Hb has even stronger affinity for CO than adult Hb)
  • Head CT in altered patients
    • First and foremost, to exclude alternative causes
    • Can demonstrate hypoattenuation in globus pallidus in severe CO toxicity

Slam dunk case features dive, dive, dive!

There are certainly case-by-case risk/benefit considerations and patient preferences to keep in mind, but CO cases with any of the following features should, in nearly all cases, receive HBOT given well-demonstrated increase in risk for DNS when these features are present.1  

  • Syncope
  • Mental status change or coma thought to be secondary to CO toxicity
  • Extremes of age 
  • Neurologic deficits on exam, particularly cerebellar findings
  • EKG changes, persistent tachycardia, or troponin elevation to suggest myocardial ischemia
  • Elevated lactate, CK, or LFT’s without other explanation
  • Severe acidosis 

Why the unclear recommendations?

ACEP recommendation:

“Emergency physicians should use HBO2 therapy or high-flow normobaric therapy for acute CO-poisoned patients. It remains unclear whether HBO2 therapy is superior to normobaric oxygen therapy for improving long-term neurocognitive outcomes.”


“Existing randomized trials do not establish whether the administration of HBO to patients with carbon monoxide poisoning reduces the incidence of adverse neurologic outcomes.”

There is certainly no claim to be made that randomized controlled trials (RCT’s) in support of HBOT for CO poisoning are abundant, but there are a few things to consider.  Performing a good, blinded RCT in hyperbaric medicine is nearly impossible given the difficulties in designing blinded and reliable controls, or “sham” hyperbaric treatments.  As such, double-blinded RCT’s are inherently few and far between in hyperbaric medicine.  While there are many retrospective and unblinded studies evaluating HBOT for CO poisoning, there are precisely two double-blinded RCT’s.  The discrepancy in recommendations stems, in part, from one of these arguing against a benefit from HBOT.

Scheinkestel et al. (1999)

This study argues that HBOT did not improve neurocognitive outcomes in CO poisoned patients, but also had the following features…

  • While cognitive outcomes at hospital discharge were reported (a few days after CO toxicity), no longer-term cognitive outcomes were reported.  DNS is expected to occur at 3-6 weeks post-CO poisoning!
  • The neurocognitive tool used in this study was unable to differentiate between depression and DNS, and over half of the patients in this study had CO toxicity as a result of a suicide attempt!
  • Poor follow-up: 46% at one month.  

Unfortunately, this study is often weighted similarly to the only other double-blinded RCT found here which employed more rigorous neuropsychological testing at legitimate follow-up timeframes and found a significant reduction in rates of DNS with HBOT.

The De-Brief:

  • Reduction in the incidence of DNS is the primary goal of using HBOT for CO poisoning.
  • Acute CO poisoning starts an inflammatory cascade, which ultimately causes the delayed neurologic injury.  This cascade can be attenuated with HBOT.
  • The decision to treat CO poisoned patients with HBOT can be a difficult one.  HBOT should be recommended if the history, exam, or workup reveals evidence of end-organ damage.  
  • While the evidence for HBOT in the reduction of DNS in CO poisoned patients is limited and mixed, it is important to consider that undue weight has historically been given to one of two existing double-blinded RCT’s which was riddled with major flaws.  


  1. Weaver LK. Clinical practice. Carbon monoxide poisoning. N Engl J Med. 2009 Mar 19;360(12):1217-25. doi: 10.1056/NEJMcp0808891. PMID: 19297574.
  2. Scheinkestel CD, Bailey M, Myles PS, Jones K, Cooper DJ, Millar IL, Tuxen DV. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomized controlled clinical trial. Med J Aust. 1999 Mar 1;170(5):203-10. doi: 10.5694/j.1326-5377.1999.tb140318.x. PMID: 10092916.
  3. Weaver LK, Hopkins RO, Chan KJ, et al.  Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J med.  2002 Oct 3;347(14):1057-1067.


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