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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.
KCE Reports 74 Hyperbaric Oxygenation Therapy 19 Figure 2. Presence of symptoms or signs at 4-6 weeks, HBO vs. NBO Source: Juurlink et al. 24 Bennett’s thesis does not deal with this condition explicitly, 1 and neither the AHRQ horizon scan published in 2006 nor an overview of Silver et al. did identify further studies. 14, 43 The IECS study from December 2006 comes to similar conclusions and identifies no more additional studies on this indication. 38 The HAS report published in 2007, 37 repeats these same arguments and concludes that the different opinions are largely caused by the absence of clear evidence and that acceptance of this indication is mainly based on expert opinion and consensus, rather than on direct evidence. A recent RCT compared different HBOT schedules (different pressure and timing) but was too small (n=28) for definite conclusions and its main conclusion was that it is feasible to randomize CO-poisoned patients. 39 3.4.2 Decompression accidents 3.4.2.1 Short description of the condition Decompression sickness (DCS) was the very first indication for HBOT and arises from the generation of bubbles of gas in tissues or in blood during rapid decompression (either ascent from diving, flying or in a hyper- or hypobaric chamber). Those bubbles form when the speed of decompression is too fast for diffusion and perfusion to be able to reduce the partial pressure of the dissolved gas. Clinical manifestation includes pain in the joints, cutaneous eruptions or rashes, neurological dysfunction such as paralysis or loss of consciousness, cardiorespiratory symptoms and pulmonary oedema, shock and death. 8 These symptoms are thought to be caused by a combination of several pathophysiological mechanisms, such as mechanical disruption of the tissue, blood flow impairment, platelet disposition and coagulation activation, endothelial dysfunction etc. 1, 8 3.4.2.2 Summary of the evidence Recompression therapy (with air) has been used since 1896, and later on recompression with oxygen as an adjunct (HBOT) has become accepted standard practice although no formal RCTs has ever been conducted. Evidence of effectiveness for this indication is therefore mainly historical. Before it was used during the construction of the Hudson tunnel, the annual mortality from DCS among workers was 25%.
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KCE reports 33 Effects and costs of
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