What Are Radiation-Induced Tissue Injuries?
Radiation-induced tissue injuries are the collective term for the pathological changes that develop in tissues exposed to radiation as part of cancer treatment.
Contrary to what patients often assume, tissue injury does not cease when radiotherapy ends. Chronic radiation injury may continue to progress for years, with new or worsening symptoms appearing long after the active treatment phase has been completed.
The condition may affect a wide range of tissues, depending on the irradiated area, including bones, soft tissues, mucous membranes, skin, nerves and blood vessels. The clinical presentation varies accordingly, ranging from chronic pain, stiffness and swelling to ulcers, tissue necrosis and severe functional impairment.
The common underlying feature of all forms of radiation-induced injury is the progressive depletion of the vascular supply and the resulting tissue hypoxia. This creates a biological environment that is unable to heal effectively or respond normally to everyday physical stress.
Pathophysiology and Characteristics of Radiation-Induced Tissue Injuries
The pathophysiology of radiation-induced tissue injury is commonly described through Marx’s model of “hypoxia, hypovascularity and hypocellularity”. Radiation damages the vascular endothelium, reduces the number of functioning blood vessels and depletes the tissue’s cellular population. The resulting tissue becomes biologically inactive in terms of its ability to respond, regenerate and heal.
A characteristic feature is its non-linear progression. Many patients remain clinically stable for months or years and then develop a serious complication, often following an apparently minor event.
This occurs because irradiated tissue has very limited biological reserve. It lacks the vascular infrastructure required to cope even with modest additional demands.
The severity of radiation-induced tissue injury is associated with the total radiation dose, the fractionation schedule, the radiosensitivity of the target tissue and the patient’s age at the time of treatment.
Clinical Studies
The use of hyperbaric oxygen therapy for radiation-induced tissue injuries is based on directly addressing the underlying pathology: the combined effects of hypoxia, hypovascularity and hypocellularity.
Clinical studies and systematic reviews have shown that hyperbaric oxygen therapy significantly improves oxygenation in irradiated tissues, stimulates VEGF-mediated neovascularisation and partially restores the tissue’s cellular population.
These findings have led the Undersea and Hyperbaric Medical Society (UHMS) and the European Committee for Hyperbaric Medicine (ECHM) to recognize several forms of radiation-induced tissue injury as approved indications, provided that treatment is delivered as part of comprehensive oncological care and under continuous medical supervision.
The Role of Hyperbaric Oxygen Therapy
In radiation-induced tissue injuries, hyperbaric oxygen therapy acts as a form of biological revitalization for irradiated tissue. It does not reverse the therapeutic effects of radiotherapy or adversely affect the patient’s oncological prognosis. Instead, it supports quality of life and functional capacity, both of which may have been significantly impaired.
By increasing tissue oxygen tension, hyperbaric oxygen therapy reactivates the mechanisms of neovascularisation, stimulates fibroblasts and progenitor cells, and creates a biological environment in which the tissue can once again respond and repair itself.
For patients who require surgery within previously irradiated areas, hyperbaric oxygen therapy may also provide important preoperative and postoperative support.
A typical treatment course consists of 30 to 40 sessions and is planned in collaboration with the oncologist and the relevant treating specialist.