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