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Delayed Radiation Injury
The cornerstone of therapy is to begin and complete (if possible) HBOT prior to any surgical intervention and then to resume HBOT as soon as possible after surgery. Only in this way is adequate time allowed for angiogenesis to support postoperative healing. For patients with a history of significant radiation exposure, but no exposed bone, who require oral surgery, many practitioners suggest 20 HBOT treatments prior to surgery and 10 treatments immediately following surgery. Feldmeier has published an excellent review of this literature. Soft tissue radionecrosis While soft tissue radionecrosis also is rare, it causes significant morbidity, depending on the site of injury. All of these injuries lead to significant local pain. Both radiation cystitis and radiation proctitis can result in severe blood loss with symptomatic anemia. Radiation cystitis may also cause obstructive uropathy secondary to fibrosis and blood clot formation. Radionecrosis of the neck and larynx can lead to dysphagia and respiratory obstruction. Irradiated skin develops painful, necrotic wounds that do not heal with standard wound healing care plans. For each of these subpopulations of soft tissue radionecrosis, published case series and prospective, nonrandomized clinical trials corroborate one another, providing a degree of external validity. Currently, the largest group of reported patients treated with HBOT for soft tissue radionecrosis are those with radiation cystitis. At least 15 publications, representing almost 200 patients, report a combined success rate in the 80% range. The two largest studies were published by Bevers and Chong. Radiation therapy causes acute, subacute, and delayed injuries. Acute and subacute injuries are generally self-limited. However, delayed injuries are often much more difficult to treat and may appear anywhere from 6 months to years after treatment. They generally are seen after a minimum dose of 6000 cGy. While uncommon, these injuries can cause devastating chronic debilitation to patients. Notably, they can be quiescent until an invasive procedure is performed in the radiation field. Injuries are generally divided into soft tissue versus hard tissue injury (osteoradionecrosis [ORN]). While the exact mechanism of delayed radiation injury is still being elucidated, the generally accepted explanation is that an obliterative endarteritis and tissue hypoxia lead to secondary fibrosis. Hyperbaric oxygen therapy (HBOT) was first used to treat ORN of the mandible. Based on the foundational clinical research of Marx, multiple subsequent studies supported its use. The success of HBOT in treating ORN then led to its use in soft tissue radionecrosis as well. |
Osteo-radionecrosis Marx demonstrated conclusively that ORN is primarily an avascular aseptic necrosis rather than the result of infection. He developed a staging system for classifying and planning treatment, which is largely accepted throughout the oromaxillofacial surgery community. See the following:
Treatment Protocol The cornerstone of therapy is to begin and complete (if possible) HBOT prior to any surgical intervention and then to resume HBOT as soon as possible after surgery. Only in this way is adequate time allowed for angiogenesis to support postoperative healing. For patients with a history of significant radiation exposure, but no exposed bone, who require oral surgery, many practitioners suggest 20 HBOT treatments prior to surgery and 10 treatments immediately following surgery. Feldmeier has published an excellent review of this literature. HBOT and carcinogenesis Practitioners and patients are often concerned that HBOT may foster recurrence of malignancy or promote the growth of an existing tumor. This is largely because of the known angiogenic effective of HBOT. Feldmeier has reviewed this subject extensively. Malignant angiogenesis appears to follow a different pathway than angiogenesis related to wound healing. His review of the literature suggests that the risk is low. |
