Ketchum et al (1970) demonstrated rapid vascularization and increase in both
osteoclastic and osteoblastic activity in animals treated with hyperbaric oxygen in a controlled burn wound experiment. The daily elevation of oxygen tension in
hypoxic bone and soft tissues result in the ingrowth of capillaries (Hunt et al,
1969), fibroblastic proliferation, collagen synthesis (Hunt and Rai, 1972) and
capillary angiogenesis (Ketchum etal, 1970).
Mainous et al in 1973 were probably the first authors to suggest the use
of hyperbaric oxygen therapy for the treatment of osteoradionecrosis. Following its introduction and preliminary good results, it has been shown to promote
Chapter 2 - Literature Review - Section I - Osteoradionecrosis
healing in osteoradionecrosis, by promoting in theory neovascularity and neocellularity (Mainous and Boyne, 1974; Mainous and Hart, 1975; Hart and
Mainous, 1976; Davis et al, 1979; Tobey and Kelley, 1979; Mansfield at al,
1981; Marx and Ames, 1982; Epstein at al, 1987a; Farmer at al, 1987; Fattore
and Strauss, 1987; Daum and Negus, 1988; McKenzie atal, 1993).
Hart and Mainous (1976) used hyperbaric oxygen therapy at 2 to 2.5 atmospheres pressure for 1.5-2 hours per day for up to 84 sessions. They treated 46 patients, and their results showed that 80% were symptom-free after treatment, and 11% required further 20 sessions. However, 41% required some form of surgery for symptom control, and 9% required a mandibulectomy.
Mansfield at al (1981) treated twelve patients with HBO (2.4 Atm, 90 min.) for
an average of 75 sessions. Eight patients required sequestrectomy and one needed a bone graft.
Beehner and Marx (1983) showed that hyperbaric-oxygen induced angiogenesis becomes measurable by TcPOg after eight sessions, rapidly progresses to a plateau at 80% to 85% of nonirradiated tissue vascularity by 20 sessions, and remains at that level without further improvement with additional hyperbaric oxygen. However, it has to be remembered that TcPOg measurements are capable of measuring the oxygen levels only at the capifary loops of the skin, at a depth of less then 1 mm. These measurements can be used onlyîoverify the effects of hyperbaric oxygen on the skin, and not the underlying tissues. Therefore this method is unsuitable to investigate osteoradionecrosis, and these observations regarding the effects of HBO on osteoradionecrosis should be looked at very critically.
Marx (1983b) introduced a protocol for the treatment of
osteoradionecrosis that combines hyperbaric oxygen therapy (HBO) and surgery as its primary treatment modalities (Table 2.3). He concluded that hyperbaric oxygen alone cannot heal osteoradionecrosis wounds (only 15% responded to stage I), suggesting that hyperbaric oxygen without aggressive surgical management would not resolve the disease progress in most cases. Therefore, 8 patients (14%) needed sequestrectomies (Stage II), and 70%
required major reconstruction (Stage III). The reasons _ givgn for the low^ success rate were: (1) the degree of radiation tissue damage varies greatly between patients, even with identical doses and fractions, (2) hyperbaric oxygen cannot resurrect dead bone, and (3) hyperbaric oxygen cannot entirely reverse radiation injury. Therefore he recommends the combination of hyperbaric oxygen therapy and aggressive surgery. The high incidence of surgical treatment seemed to be unnecessary, since only conservative treatment can cure up to 60% of cases. Furthermore, if only 15% of his cases responded to HBO alone, and 70% required major surgery, there seems to be
no value in using hyperbaric oxygen therapy in osteoradionecrosis
management. Nevertheless, the use of HBO associated with surgery is
commonly described in the literature (Epstein et al, 1987a and b; McKenzie et
al, 1993; Mounsey etal, 1993; Merkensteyn et al, 1995).
McKenzie et al (1993) noted a 50% resolution of osteoradionecrosis with
HBO treatment, but over half of these patients had undergone a rwndfoulectomy in conjunction with HBO to achieve this resolution. In a retrospective study,
Mounsey et al (1993) analysed 41 patients with proven mandibular
osteoradionecrosis treated with HBO (Toronto Hospital). The results showed that 83% of the patients had a significant improvement, judged by at least 50% decrease in the size of the exposed bone, closing of the fistulous tract, or complete relief of symptoms. However 17% of the patients did not benefit. They conclude that only ‘mild’ cases of osteoradionecrosis can be cured with HBO, and the severe cases will need surgery to remove dead bone.
In 1995, Merkensteyn et al reported a series of 29 cases of
osteoradionecrosis treated with HBO. They found that HBO led to initial resolution of only 15 of 29 cases, and a second course of HBO improved the result to 20 of 29 cases (69%) Thirteen of these patients had mandibular discontinuities at the start of treatment, and two healed. The number of patients who lost continuity was 17 of 29, with 5 of 29 becoming discontinuous during HBO treatment. Undermining the supposed protective effects of HBO, was the fact that two patients had a second episode of osteoradionecrosis on the
Chapter 2 - Literature Review - Section I - Osteoradionecrosis
opposite side, which resulted in loss of mandibular continuity on the second site.
Contraindications and complications of hyperbaric oxygen therapy
An relevant contraindication of hyperbaric oxygen therapy in smokers is emphysema, and untreated pneumothorax. Side effects of HBO are uncommon but include transient myopia, seizures, and otic or pulmonary barotrauma, the latter potentially leading to air embolism. Concern has been expressed that
hyperbaric oxygen may exacerbate a variety of autoimmune and
immunosuppressive disorders, and viraemia (Giebfried etal, 1986), but there is
little supporting evidence.
Relative contraindications to hyperbaric oxygen therapy include upper respiratory tract infection, chronic sinusitis, epilepsy, chronic obstructive ainA/ays disease, high fevers, a history of spontaneous pneumothorax or thoracic or ear surgery, viral infections, congenital spherocytosis, a history of optic neuritis and claustrophobia (Scully and Epstein, 1996). The risk from hyperbaric oxygen therapy may be minimised by a careful pre-treatment assessment including
chest radiography and electrocardiography; some advise also an
otolaryngological and ophtalmological assessment (Giebfried etal, 1986).
The cost and lack of availability should also be mentioned as a potential problem related to HBO. Hyperbaric oxygen therapy is very time consuming,
and therefore expensive. Marx et al 1985 reported that the cost to treat one
patient with HBO is approximately 19,000 dollars per year, and combined with surgery, according to his protocol, 30,000 dollars per year (in 1985 values). In a more recent publication, daym an (1997) shows that the cost to treat one patient with HBO has reduced, but is still around 15,000 dollars (data courtesy
i ’ n’ 1
Hyperbaric Unit, Henry Ford Hospital, Detroit, Ml). There are only a few hospital or diving centres with the facilities of a hyperbaric camera in each country. Therefore it is not widely available, and can be even more expensive if the costs of travelling and accommodation are added.