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18 Hyperbaric Oxygenation Therapy KCE Reports 74
3.4.1.2 Summary of the evidence
This indication was accepted by the ECHM consensus conference as a type 1
recommendation supported by level B evidence (see Table 3 for definitions) in case of
CO intoxicated patients presenting with unconsciousness at or before admission or
with clinical neurological, cardiac, respiratory or psychological symptoms or signs, or in
case of pregnancy (level C evidence only). 9 The indication of CO intoxication is also
accepted by the UHMS, mainly based on in vitro studies, animal model studies and
occasional observational case series. 8 The UHMS recognises, however, that additionally
studies are required to clearly define benefits, optimal treatment indication, optimal
pressure, timing and number of sessions (one or more). 8
The condition of CO intoxication is sometimes mixed with cyanide poisoning in victims
of smoke inhalation, exhibiting a synergistic toxicity. However, it is thought that one
must be cautious with HBOT in this setting because the standard antidote for cyanide
poisoning involves the formation of met-haemoglobin through the infusion of sodium
nitrite. Those met-haemogolobin levels may be lowered by hyperoxia, possibly reducing
the efficacy of the antidotal therapy. 8 Pure cyanide poisoning is infrequent but a few
isolated reports suggested a potential benefit of HBOT in this condition. 8
The administration of oxygen, either normobaric or hyperbaric, is considered as the
corner stone of CO poisoning treatment, since it is assumed that oxygen will enhance
dissociation of CO from haemoglobin and induce enhanced tissue oxygenation. The
rationale for hyperbaric oxygenation therapy is that this rate of dissociation of CO from
haemoglobin could be expected to be greater that with normobaric oxygenation
therapy, and several historical and laboratory studies support this view. 8
Neither for hyperbaric nor for normobaric oxygen therapy, RCTs evaluating the shortterm
effects on CO poisoning have been carried out. A few RCTs evaluated the effect
of HBOT on long-term neurological sequels but presented conflicting results. A
Cochrane review from 2005 by Juurlink et al. 24 summarised the evidence from six RCTs
on the long-term neurological sequels of treatment of CO poisoning with HBOT. Four
of those studies found no benefit of HBOT on the reduction of neurological sequels
while two others did find a benefit (see Figure 2). All studies, however, had major flaws
in either design or analysis, and where very heterogeneous both in hyperbaric
treatment schemes and regarding comparative treatment. Some of the studies were
criticised because treatment pressures were considered too low and therefore it is felt
by some in the field that a meta-analysis combining those heterogeneous studies is
inappropriate.
The authors of the Cochrane review concluded that existing RCTs did not show that
HBOT in patients with carbon monoxide poisoning reduces the incidence of adverse
neurological outcomes, but that additional research is needed to better define the role,
if any, of HBOT in the treatment. A methodological problem is that there is never a
baseline assessment available prior to exposure to CO thus limiting the assessment of
symptoms after exposure and therapy. Ideally, randomisation should solve this problem
but cannot be relied upon completely in those small studies.