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Hyperbaric oxygen (HBO2) is used as an adjunct in the treatment of radiation injury at many sites, including the mandible, larynx, chest wall, bladder, and rectum. In these disorders, HBO2 is effective in stimulating neovascularization and reducing fibrosis. No previous publications report the application of HBO2 to radiation injuries of the extremities. From 1979 until 1997, 17 patients were treated at the Southwest Texas Methodist and Nix Hospitals for nonhealing necrotic wounds of the extremities within previously irradiated fields. All but one wound involved a lower extremity. Most of the patients had been irradiated for soft tissue sarcomas or skin cancers. The rest were irradiated for a variety of malignancies. HBO2 was delivered in a multiplace chamber at 2.4 atm abs daily for 90 min of 100% oxygen at pressure. This report is a retrospective, uncontrolled review of these patients. Eleven patients (65%) healed completely whereas five (29%) failed to heal and one (6%) was lost to follow-up. Three (60%) of those who failed were found to have local or distant recurrence of their tumor early in their course of hyperbaric treatment and were discontinued from therapy at that time. When last seen in the clinic, the wound of the patient who was lost to follow-up was improved but not completely healed. Four of those who failed (including the two with local tumor recurrence) required amputation. If we exclude those with active cancer and the patient lost to follow-up, the success rate was 11 of 13 or 85%. HBO2 was applied successfully with complete wound healing and the avoidance of amputation in a majority of these patients. The consequences of failure in patients suffering from radiation necrosis of the extremities (some complicated by the presence of tumor) are significant, with 80% of the five failures requiring amputation. In radiation injuries of the extremities as in delayed radiation injury at other sites, HBO2 is a useful adjunct and should be part of the overall management.

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Radiation therapy is often utilized as adjunctive or primary treatment for malignancies of the abdomen and pelvis. Radiation complications are infrequent, but can be life threatening or significantly diminish the quality of life. Radiation necrosis is an approved indication for hyperbaric oxygen (HBO2). Previous publications have reported results in treating delayed radiation injuries involving many sites. This paper reports the experience of a single physician group in treating delayed injuries of the abdomen and/or pelvis. Forty-four such patients have been treated since 1979. Of the 41 patients available for follow up, 26 have healed; 6 failed to heal; and 9 patients had an inadequate course of therapy (fewer than 20 treatments). Especially encouraging was the resolution of fistulae in six of eight patients with only three requiring surgery for closure. Overall, the success rate in patients receiving at least 20 HBO2 treatments was 81%. Hyperbaric oxygen is a useful adjunct in treatment of delayed radiation injuries of the pelvis and abdomen.

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Since 1979, 23 cases of radiation-induced chest wall necrosis have been treated in the Hyperbaric Medicine Departments of Southwest Texas Methodist Hospital and the Nix Hospital, San Antonio, Texas. Eight cases involved soft tissue only. Six of eight (75%) patients with soft tissue involvement healed without requiring surgical debridement, although four patients (50%) did have flaps or grafts. Fifteen patients had bony and soft tissue necrosis. Eight of these patients (53%) resolved with adjunctive hyperbaric oxygen (HBO), but all required aggressive surgical debridement including skeletal resection. Four (27%) had reconstructive flaps as well. Six patients (40%) with bony necrosis who had either no or incomplete debridement failed to heal. Three patients (13%)(two soft tissue and one bony) were found to have residual tumor during HBO and were discontinued from treatment. HBO is an effective adjunctive therapy for soft tissue chest-wall, radiation-induced necrosis, but must be coupled with appropriate debridement to include surgical removal of all necrotic bone to ensure a successful outcome of bony plus soft tissue necrosis.

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We reviewed all known published reports or studies related to a possible cancer-causing or growth-enhancing effect by hyperbaric oxygen. Published articles were retrieved using Medline searches for the period 1960-1993. Additional references were obtained from bibliographies included in those articles discovered in the computer search. Also, hyperbaric medicine text books and the published proceedings of international hyperbaric conferences were visually searched. Studies and reports discovered in this fashion and related to the topic were included in the review. Twenty-four references were found: 12 were clinical reports, 11 were animal studies, and 1 reported both an animal study and a clinical report. Three clinical reports suggested a positive cancer growth enhancement, whereas 10 clinical reports showed no cancer growth enhancement. Two animal studies suggested a positive cancer-enhancing effect, and 10 animal studies showed no such effect. (The report that included both animals and humans is counted in both groups). The vast majority of published reports show no cancer growth enhancement by HBO exposure. Those studies that do show growth enhancement are refuted by larger subsequent studies, are mixed studies, or are highly anecdotal. A review of published information fails to support a cancer-causing or growth-enhancing effect by HBO.

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Laryngeal necrosis is a rare complication of therapeutic radiation, but when it does occur there is no established, definitive treatment and laryngectomy is frequently required. This report is a retrospective review of all patients referred for hyperbaric oxygen (HBO) therapy to a single hyperbaric medicine unit for treatment of their laryngeal necrosis between 1980 and 1985. Nine patients were in this series. One patient had had a vertical hemilaryngectomy and another a supraglottic laryngectomy before referral. Eight of the nine patients had a Chandler grade IV necrosis and the ninth had a Chandler grade III necrosis. All nine patients were able to maintain their voice until death or last follow up. Seven of the nine patients maintained good voice quality while two exhibited some hoarseness. All patients with tracheostomies were able to be decannulated, and all patients with fistulae had these closed. No untoward reactions to HBO occurred. Based on this review, HBO is recommended as a therapeutic option whenever laryngeal necrosis occurs and there is a chance to save the larynx.

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A questionnaire was sent to 179 clinical hyperbaric medicine facilities to survey treatment policies and referral patterns for patients with a history of malignancy. Eighty-five surveys were returned. Most respondents indicated that they would accept patients with a history of malignancy for either adjuvant or emergent hyperbaric oxygen (HBO). Depending on specific circumstances, from about one third to one half of respondents believed that such patients should be informed of a theoretical potential for tumor acceleration or reactivation. An overwhelming majority had not personally attended nor had they been told by colleagues of cases of patients whose malignancy had been activated or accelerated by HBO. A large majority felt that referring physicians did not believe that HBO was carcinogenic, and that referrals were not prevented by such concerns. Seven percent believed that HBO is potentially carcinogenic. Forty-two percent of respondents felt that they might be at risk for malpractice litigation if a patient had reactivation or acceleration of a malignancy. Among respondents to the questionnaire, there is a consensus that HBO does not have cancer-promoting or accelerating properties.

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A single case of operatively proven spontaneous rupture of a normal stomach secondary to diving barotrauma is reported. The rupture was linear and located along the lesser curvature, as described most commonly in adults. Possible mechanisms to explain the closed loop obstruction required to produce this phenomenon are the swallowing of water and filling of the stomach with air, while trapped under water, at a depth of 27 meters. To the best of the authors' knowledge this case represents the first report of gastric rupture secondary to SCUBA (self-contained underwater breathing apparatus) diving. The presence of a normal abdominal examination by an experienced observed while compressed in the chamber does not preclude the diagnosis of a perforated viscus.

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Forty patients with chronic osteomyelitis were treated with hyperbaric oxygen as an adjunct to surgical therapy and antibiotics and followed for an average of 2 years with a recurrence rate of 15%. The mechanism of action of hyperbaric oxygen in osteomyelitis is probably an indirect one of improving local vascularity and potentiating phagocytosis. Many of these patients represent a refractory group with poor prognosis due to the etiology of the infection, site of involvement, and duration of infection prior to treatment. The recurrence rate following this mode of treatment seems to be primarily related to inadequate surgical management. There was no definite correlation between the site of the infection of pathologic organism and recurrence. Although this is a preliminary report, the results are encouraging. Hyperbaric oxygen may be indicated as an adjunct to good surgical and medical management, particularly in patients with refractory chronic osteomyelitis and in whom ablative surgery is under consideration as the only other means of controlling the infection.

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Radiation necrosis is a significant complication of surgery for previously irradiated head and neck malignant neoplasms. We used hyperbaric oxygen therapy (HBO) as adjunctive therapy in 52 cases of radiation necrosis. Thirty-nine cases involved the head and neck. Nineteen of 23 cases of osteoradionecrosis of the mandible remain arrested after as much as two years of follow-up. Fifteen of the 16 cases of soft-tissue radionecrosis of the head and neck were successfully managed with HBO therapy as an adjunct to surgery and antibiotics. Fibroblastic proliferation, collagen formation, and capillary budding require at least 20 to 30 mm Hg of wound Po2. This effect can be achieved in wounds that are rendered hypoxic by radiation endarteritis and ischemia with high-dose or hyperbaric oxygenation.

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Most cases of decompression sickness that occur at altitude resolve upon descent to lower altitudes. Before the use of hyperbaric therapy, cases that did not resolve accounted for some of the most difficult medical management problems in military aerospace medicine. On 27 March, 1941, the U.S. Navy Diving School successfully used hyperbaric therapy for a case of altitude-induced decompression sickness that did not resolve on return to ground level. Since then, over 145 such cases have been treated by hyperbaric therapy. At first, treatments involved using compressed air, with varying success. Current medical management of altitude-induced decompression sickness requires immediate compression to 2.8 ATA, equivalent to 60 ft of sea water (FSW) pressure, and a series of intermittent oxygen and air breathing periods during the subsequent slow decompression to surface. This report confirms the treatment recommendations set forth by Behnke and Downey, and crystallized by Goodman in 1964. Conclusions are based on treatment experience in the management of 120 cases in U.S. Air Force hyperbaric chambers, and a survey of hyperbaric facilities which have treated 25 other cases.

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Rat skin was irradiated with cyclotron-accelerated alpha particles with doses ranging from 210 rads to 6850 rads and monoenergetic electrons with doses ranging from 810 rads to 12,300 rads. The beams were modified so that the depth-dose curves were approximately identical with penetrations of about 1.0 mm. Tumors were counted every 4 weeks for 80 weeks, and at death or sacrifice the hair follicle damage was assessed by using "whole mounts" of separated epithelium. The RBE values determined from a comparison of the dose response curves were: acute skin injury, RBE = 3.0+/-1.0; hair follicle survival, RBE = 2.1 +/- 0.7; hair follicle damage, RBE = 2.6 = 0.4; tumor induction, RBE = 2.9+/- 0.5. Within the experimental error, these values were independent of the dose. For both types of radiation, the tumor incidence increased approximately as the square of time and at low doses approximately as the 4th power of dose. The histological characteristics of the tumors and the correlation between the incidence of tumors and damaged hair follicles were independent of the type of radiation. The results were consistent with the hypothesis that structural damage to the hair follicles is a factor in the tumor induction process.

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