burns xxx (xxxx) xxx–xxx

Available online at www.sciencedirect.com

journal homepage: www.elsevier.com/locate/burns

Hyperbaric oxygen treatment in carbon monoxide

poisoning – Does it really matter?

David Lysander Freytag a, Jennifer Lynn Schiefer b, Justus P. Beier c,

⁎
Gerrit Grieb a,c,
a
Department of Plastic Surgery and Hand Surgery, Gemeinschaftskrankenhaus Havelhoehe, Kladower Damm 221,
14089 Berlin, Germany
b
Department of Plastic, Reconstructive, Hand and Burn Surgery, Hospital Cologne Mehrheim, University of Witten,
Herdecke, Germany
c
Department of Plastic Surgery and Hand Surgery - Burn Center, University Hospital RWTH Aachen,
Pauwelsstrasse 30, 52074 Aachen, Germany

a rt i cl e in fo ab strac t

Article history: Carbon monoxide (CO) is an odorless and colorless gas that can lead to fulminant and life-
Accepted 12 June 2023 threatening intoxications. Besides an early diagnosis, an appropriate treatment of the in­
toxication is important. In this context the reduction of CO concentration in blood and
Keywords: tissues is crucial revealing hyperbaric oxygen treatment (HBO) as a highly promising tool.
Carbon monoxide However, the benefit of HBO in CO intoxications is still considered controversial. In this
Carbon monoxide intoxication review, we discuss the evidence of the role of HBO treatment in isolated CO intoxication.
Hyperbaric oxygen therapy © 2023 Elsevier Ltd and ISBI. All rights reserved.

Contents

1. Carbon monoxide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2
2. Hyperbaric oxygen therapy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2
3. HBO in CO intoxication treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .2
4. Conclusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .3
Declaration of Competing Interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .4

⁎
Corresponding author at: Department of Plastic Surgery and Hand Surgery, Gemeinschaftskrankenhaus Havelhoehe, Kladower
Damm 221, 14089 Berlin, Germany.
E-mail addresses: gerrit.grieb@havelhoehe.de, gerritgrieb@gmx.de (G. Grieb).

https://doi.org/10.1016/j.burns.2023.06.007
0305-4179/© 2023 Elsevier Ltd and ISBI. All rights reserved.
2 burns xxx (xxxx) xxx–xxx
1. Carbon monoxide
Carbon monoxide (CO) is an odorless, tasteless and colorless
gas, which is generated due to the incomplete combustion of
carbon-based compounds. It has an affinity to the he­
moglobin molecule that is approximately 240-fold higher
than that of oxygen forming carboxyhemoglobin (COHb) [1].
CO can lead to tissue hypoxia mostly affecting tissue areas of
high blood flow and oxygen need [2]. However, the reduction
of oxygen-carrying capacity is only one of the toxic effects of
CO, the main pathomechanism is the binding of CO to hem-
containing proteins, such as myoglobin or cytochrome oxi­
dase [3]. In addition, CO also inhibits the intercellular O2-
transfer, which results in O2 molecules remaining in the
blood stream not reaching the intracellular space for cellular
respiration [4]. Furthermore, CO inhibits the Krebs-Cycle
through inhibition of cytochrom-c-oxydases and thus re­
duces the intramitrochondrial metabolization of O2 [5].
On a cellular level, CO activates neutrophils and lympho­
cytes and can lead to peroxidation of lipids and mitochon­
drial dysfunction [6,7]. Furthermore, the formation of oxygen
radicals and oxidative stress is somehow comparable to an
ischemia/reperfusion injury [7,8]. Inflammatory mechnisms
can result in malfunction of granulocytes and intravascular
clotting [4].
Intoxication with CO can cause a broad spectrum of un­
specific symptoms, such as dyspnea, headache, and nausea
including vertigo and vomiting [9]. Specific symptoms can
affect the cardiovascular system (e.g., myocardial ischemia or
ventricular arrhythmia) [10,11] and the neurologic system
(e.g., status epilepticus, MS-like syndromes, and Parkinson´s
syndrome) [12]. Late and severe symptoms can include
chronic fatigue, emotional distress, memory deficits, sleep
disturbances, peripheral neuropathy, hearing loss, vestibular
abnormalities, dementia,and psychosis [4]. Since the variety
of symptoms can be so diverse and different in CO intoxica­
tion, a correct diagnosis is crucial.
The easiest and fastest way to detect CO intoxication is
the measurement of the percentage of COHb. This can be
performed through an invasive blood gas analysis or quickly
via non-invasive pulse CO-oximetry [13]. The level of COHb is
physiologically below 5% in non-smokers and up to 9% in
smokers [14]. Besides COHb measurement, laboratory mar­
kers, such as CRP serum concentration, liver enzymes, urea
and glucose levels, lactate blood level as well as leukocyte
count or pulmonary infiltrates on chest X-rays can give an
indication of the severity of an intoxication [9].
The treatment of CO intoxication includes inpatient
treatment in a specialized center as well as a detailed med­
ical history evaluation and physical examination [15]. Vital
parameters, such as blood pressure, heart rate, and electro­
cardiography should be monitored continuously. Cardiac is­
chemic parameters [16] and lactate level [17,18] of blood
should be checked. These ischemic parameters are not able
to detect a CO intoxication per se, but they allow an overview
about potential side effects and are able to rule out differ­
ential diagnoses [19]. Percutaneous oxygen saturation (with
CO-oximetry) and frequent blood gas analysis is re­
commended. Intubation and ventilation (100% O2) is required
if respiratory insufficiency occurs [9,20]. To determine neu­
rological status, the value of the Glasgow Coma Scale (GCS)
can be obtained easily [9]. Furthermore, cognitive function
should be checked regularly, especially after four to six
weeks, to evaluate the mid- and long-term effects of CO in­
toxication [21]. Due to its potential to quickly reduce the half-
life of COHb and other CO-hem-containing proteins, the use
of hyperbaric oxygen treatment (HBO) is a promising tool.
However, the use of HBO in treating CO intoxication is cur­
rently being debated and will be discussed further in the
following section.
2. Hyperbaric oxygen therapy
Hyperbaric oxygen therapy or hyperbaric oxygenation (HBO)
means breathing 100% oxygen under an elevated ambient
pressure of between 2 and 3 atm in a specific hyperbaric
oxygen chamber [22]. Arterial oxygen partial pressure in­
creases, in direct correlation with pressure elevation. At a
pressure of 2 atm absolute (ATA) oxygen dissolves in plasma,
increasing the arterial pO2 to 1400 mmHg, while at 3 ATA, it
increases arterial pO2 to approximately 2000 mmHg [23,24].
Increased arterial pO2 results in elevated tissue oxygenation
and may last for several hours [25]. However, the mechan­
isms of HBO activity at a molecular level are not yet fully
understood. HBO leads to vasodilation in hypoxic tissue and
to vasoconstriction in tissue with increased perfusion. How­
ever, HBO supports the preservation of ATP, the down­
regulation of pro-inflammatory cytokines and the
upregulation of anti-inflammatory cytokines. Furthermore,
HBO promotes an unspecific antibacterial effect since bac­
teria are not able to cope with high levels of oxygen [26,27].
While problems due to nasopharyngeal swelling in the
middle ear during HBO treatment may occur, side effects
such as paraesthesia or seizures are rare if an ATA of 3 atm is
not exceeded [22].
From a historical point of view, the first medical applica­
tion of HBO was done in 1622 and was used for the treatment
of anemia, tuberculosis and cholera [28]. Moreover, in 1895,
Haldaene et al. discovered the protective effect of highly
concentrated oxygen against CO [29]. Today HBO also is
commonly used in the surgical field including the treatment
of chronic wounds, diabetic ulcers and compromised flaps
and grafts [26]. Furthermore it is very promising in in vitro
and in vivo experimental settings [30].
However, the use of HBO treatment in CO intoxication is
still a controversial topic.
3. HBO in CO intoxication treatment
The higher the oxygen partial pressure in tissue, the shorter
the elimination time of CO. This leads to the hypothesis that
the use of HBO in CO intoxication treatment is extremely
promising [16,31]. However, pure elimination of CO from
hemoglobin is not the only therapeutic aspect of HBO. Dif­
ferent pathomechanisms of CO as the inhibition of the in­
tercellular O2-transfer, the cytochromec-coxidase, and the
intramitrochondrial metabolization of O2 are being reversed
[4]. Thus, intracellular hypoxia, oxidative stress, and tissue
 burns xxx (xxxx) xxx–xxx
Table 1 – Election of studies performed for Evidence of HBO in CO treatment.
Author Year Design
Raphael et al. [31] 1989 randomized
Scheinkestel et al. [33] 1999 double-blinded ranodmized controlled
Thom et al. [36] 1995 randomized
Weaver et al. [37] 2002 double-blinded randomized controlled
Huang et al. [39] 2017 retrospective multicenter
inflammation are reduced [32,33]. Furthermore, HBO induces
neuroprotective and neurogenetic effects [33]. This may ex­
plain the reduced occurrence of late neurologic sequelae
after HBO observed in clinical settings [34].
The most criticized aspects of HBO are its high costs,
complex logistics (a HBO center is not always near), and lack
of evidence. Indeed, studies are very heterogenous con­
cerning observation period, severity of intoxication, time
before starting treatment, and duration and intensity of HBO
treatment [35,36]. A selection of the studies is presented in
Table 1.
Some studies do not reveal any positive effect of HBO
treatment. An older study from 1989 could neither demon­
strate a positive nor a negative effect on neuropsychiatric
sequelae (asthenia, headaches, memory impairment, dis­
turbed sleep, visual disturbances) one month after intoxica­
tion with CO [37]. A randomized study evaluated the use of
HBO after domestic CO intoxication. No benefit from HBO
treatment could be shown compared to regular normobaric
applied oxygen. A second HBO session seemed to even
worsen the outcome (headaches, memory impairment, dis­
turbed sleep, visual disturbances) [38]. Scheinkestel et al.
performed a double-blinded randomized controlled trial and
could not prove any benefit of HBO one month after in­
toxication and showed instead that the outcome (headache,
fatigue, difficulty in thinking, dizziness, nausea) might even
be worse [39]. However, this study was conducted in Aus­
tralia and time from injury to treatment varied between pa­
tients because of long transportation times, which could
have affected the outcome and the conclusion of the study.
On the other hand, studies showing the positive effect of
HBO treatment in CO intoxication have been published
[31,40,41]. A prospective randomized trial demonstrated fa­
vorable neurological results and a delayed appearance of
neurological symptoms (headache and nausea/vomiting)
after HBO treatment [42]. One important trial supporting HBO
was published in the New England Journal of Medicine by
Weaver et al. [34]. In that study, normobaric (NBO) was
compared with HBO therapy with respect to cognitive se­
quelae after acute CO intoxication. The results revealed that
six weeks after CO poisoning, neurological pathologies (neu­
ropsychological tests, activities of daily living, geriatric de­
presseion scale) occurred at a significantly reduced frequency
in the HBO group compared to the NBO group (25 vs. 46.1%;
p = 0.007). A retrospective study by Rose et al. showed a re­
duced lethality after HBO treatment [43]. A retrospective
multicenter study including more than 20,000 patients with
CO intoxication demonstrated the benefit of HBO therapy on
long-term mortality [44].
Extremely few national and no international guidelines on
how to treat CO poisoning exist. According to the
3
No of subjects HBO beneficial in CO treatment (+/-)
629 no
191 no
60 yes
152 yes
25,737 yes
recommendations of the U. K. Department of Health and NHS
England, a COHb concentration of > 20% should be an in­
dication to consider HBO, and the decision should be taken
on the basis of specific indications namely neurological signs
or symptoms other than a headache, myocardial ischemia/
arrhythmia diagnosed using ECG, loss of consciousness at
any stage, or pregnancy [45,46]. The U.S. Centers for Disease
Control and Prevention has published the guideline “Clinical
Guidance for Carbon Monoxide (CO) Poisoning”, which states
that HBO therapy shall “be considered when the patient has a
COHb level of more than 25–30%, there is evidence of cardiac
involvement, severe acidosis, transient or prolonged un­
consciousness, neurological impairment, abnormal neu­
ropsychiatric testing, or the patient is ≥ 36 years of age. HBO
is also administered at lower COHb (< 25%) levels if suggested
by clinical condition and/history of exposure”. This points to
the high relevance of the clinical condition of a patient [47].
Moreover, in Germany, a national guideline under the
auspices of the DIVI (“German Interdisciplinary Association
for Intensive Care and Emergency Medicine, which re­
commends HBO in adults if signs of severe CO poisoning
occur (continued impaired consciousness, metabolic
acidosis, respiratory insufficiency, and/or cardiac ischemia)
and during pregnancy. HBO should be initiated within 6 h
after poisoning und should be performed three times within
the first 24 h [48].
However, the recommendations of the guidelines are
limited, since most of the published literature focus on iso­
lated CO intoxication. In a clinical setting most cases with CO
intoxication are combined with other inhalation injury
or burn.
Another limitation of the recommendation and the dis­
cussed studies might be the fact that only few clinical centers
have direct access to hyperbaric chambers and thus only few
clinicians are familiar with the potential, as well as the side
effects of HBO. This could explain the reason why few data
exist on this topic in general and many centers developed
own clinical approaches. However, international guidelines
based on further profound clinical trials will be necessary to
define the role of HBO in CO intoxication in the future.
4. Conclusion
Numerous hints concerning the benefit of HBO treatment in
CO intoxication exist. However, the definite benefit of HBO
has not been fully proven yet. National guidelines re­
commend HBO treatment in high COHb levels (> 20%) and
severe clinical cases, such as respiratory insufficiency, car­
diac ischemia, or particularly neurological deficits. CO in­
toxication is a diagnosis to always bear in mind and treat
4 burns xxx (xxxx) xxx–xxx
according to emergency standards. A long-term follow up
after discharge is recommended, since late sequelae might
occur.
Declaration of Competing Interest
All authors declare no conflict of interest.
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