HBOT AND DELAYED RADIATION INJURIES

Radiation can induce a non-healing, hypoxic wound which may occur in either soft
tissue or bone. The radiation damages the cellular and vascular components of
tissues resulting in a proliferative endarteritis. This results in a hypoxic, hypocellular
and hypovascular tissue.and a risk of non-healing following surgery. Successful
treatment with hyperbaric oxygen therapy is documented in post-radiation damage,
including chest wall necrosis, radiation-induced haemorrhagic cystitis, and central
nervous system radiation damage. A recent trial, however, found little evidence
for hyperbaric oxygen therapy in radiation-induced brachial plexopathy, though there
were some improvements in warm sensory threshold and long-standing arm
lymphoedema.
HBO2 increases vascular density and oxygenation in radiation-damaged tissue. It
also increases tissue angiogenesis which increases circulation to the injured area.
This increases oxygenation resulting in better wound repair by stimulating collagen
deposition. Marx has shown that tissue oxygen levels in irradiated areas approach
80% of normal tissue levels within about approximately 20 hyperbaric oxygen
therapy sessions. The benefits of HBOT are long lasting. In one study, three year
follow-up revealed pO2 levels that were still 80%-90% of those seen during the active
treatment cycles which improved tissue oxygen gradients and angiogenesis and
enhanced leukocyte bactericidal activity[78]. This facilitates healing and may enable
grafts to be placed. Mainous, reported a case of excellent improvement in
mandibular healing with HBO2 after radiotherapy[79]. Marx reported in 1985 that
prophylactic HBOT before tooth extractions in heavily irradiated mandibles prevented
mandibular osteoradionecrosis more effectively than penicillin. HBOT given
prophylactically prior to dental extraction is not 100% effective in preventing
osteoradionecrosis. If given before dental extractions in high risk patients, 5% still
develop osteoradionecrosis. However, where radionecrosis developed it was of a
minor nature and readily managed by simple surgery. Untreated radionecrosis
resulted in severe radionecrosis requiring sequestrectomies and resections of the
mandibula. For comparisons sake, when only penicillin is given, 30% of patients
develop osteoradionecrosis. Because it is much more economical to prevent
osteoradionecrosis than to treat it, prophylactic HBOT is still recommended. The
term “prophylactic” is misleading, however. Tissue for which HBO is provided in a
previously irradiated area prior to surgery contains late radiation tissue damage. The
HBO is applied to reverse the radiation tissue damage so that the tissue can
withstand the increased metabolic requirements of healing following surgery. It is
important to state that this is not prophylactic in the true sense of the word. It is
indeed therapeutic.
Neovius et al reported that patients with problem wounds following surgery and
radiotherapy had complete healing after treatment with hyperbaric oxygen therapy
and that hyperbaric oxygen therapy may reduce the incidence and progression of
soft tissue radionecrosis, such as laryngeal radionecrosis, although there is less
support for this in the literature than for osteoradionecrosis. Marx showed that, in
patients with previous radiation, “pre-operative hyperbaric oxygen therapy can
reduce wound dehiscence and infections, and improve healing in soft tissue flaps,
particularly in mandibular osteoradionecrosis, though randomized controlled trials
are lacking”.
Hyperbaric oxygen treatment for mandibular osteoradionecrosis is recommended by
the UHMS .