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Radiation injury of the brain.

The clinical, radiologic, and pathologic findings in radiation injury of the brain are reviewed. Late radiation injury is the major, dose-limiting complication of brain irradiation and occurs in two forms, focal and diffuse, which differ significantly in clinical and radiologic features. Focal and diffuse injuries both include a wide spectrum of abnormalities, from subclinical changes detectable only by MR imaging to overt brain necrosis. Asymptomatic focal edema is commonly seen on CT and MR following focal or large-volume irradiation. Focal necrosis has the CT and MR characteristics of a mass lesion, with clinical evidence of focal neurologic abnormality and raised intracranial pressure. Microscopically, the lesion shows characteristic vascular changes and white matter pathology ranging from demyelination to coagulative necrosis. Diffuse radiation injury is characterized by periventricular decrease in attenuation of CT and increased signal on proton-density and T2-weighted MR images. Most patients are asymptomatic. When clinical manifestations occur, impairment of mental function is the most prominent feature. Pathologic findings in focal and diffuse radiation necrosis are similar. Necrotizing leukoencephalopathy is the form of diffuse white matter injury that follows chemotherapy, with or without irradiation. Vascular disease is less prominent and the latent period is shorter than in diffuse radiation injury; radiologic findings and clinical manifestations are similar. Late radiation injury of large arteries is an occasional cause of postradiation cerebral injury, and cerebral atrophy and mineralizing microangiopathy are common radiologic findings of uncertain clinical significance. Functional imaging by positron emission tomography can differentiate recurrent tumor from focal radiation necrosis with positive and negative predictive values for tumor of 80-90%. Positron emission tomography of the blood-brain barrier, glucose metabolism, and blood flow, together with MR imaging, have demonstrated some of the pathophsiology of late radiation necrosis. Focal glucose hypometabolism on positron emissin tomography in irradiated patients may have prognostic significance for subsequent development of clinically evident radiation necrosis.

Brain↗

[Radiation injuries of the bones during treatment of uterine cancer].

The data on 53 cases of bone injuries caused by radiation treatment for cancer of the uterus were analysed. The clinico-roentgenological signs of osteoradionecrosis (33), pathological fracture and dislocation (13), osteomyelitis (5) and radiation-induced sarcoma of bone (2) were considered. Lesions were found to occur most frequently in the upper flaring portion of the ilium and bones of the hip joints. Regular X-ray examinations of the pelvic bones are necessary for early detection of radiation injuries as well as conservative treatment to prevent such grave complications as pathologic fracture and osteomyelitis.

Adult↗

Radiation injury of the temporal bone.

Radiation injury of the temporal bone is a common occurrence following external beam treatments. Injuries can be mild, consisting of radiation otitis media, or more extensive, including bone and soft tissue necrosis with infection and intracranial complications. Pathogenesis of radiation-induced temporal bone injury along with treatment programs are discussed.

Humans↗

Role of mast cells in early and delayed radiation injury in rat intestine.

Mast cell hyperplasia is a characteristic feature of many inflammatory and fibrotic conditions, including intestinal radiation injury (radiation enteropathy). This study used mast cell-deficient rats to define the role of mast cells in the mechanisms underlying early radiation-induced mucosal injury and delayed intestinal wall fibrosis. Mast cell-deficient (Ws/Ws) mutant rats and mast cell-competent (+/+) littermates were used. A 4-cm loop of ileum was exposed to 21 Gy single-dose radiation. Irradiated and unirradiated intestine were examined at 2 or 26 weeks using quantitative histology and morphometry. Quantitative immunohistochemistry was used to assess transforming growth factor beta (Tgfb), myeloperoxidase, and epithelial and smooth muscle cell proliferation. Collagen content was measured colorimetrically, and steady-state Tgfb1 mRNA was determined with fluorogenic probe RT-PCR. Compared to +/+ rats, Ws/Ws animals exhibited strikingly exacerbated mucosal injury but minimal reactive intestinal wall fibrosis. Ws/Ws rats exhibited less radiation-induced intestinal smooth muscle cell proliferation and collagen accumulation than +/+ littermates. Tgfb expression increased to a similar extent in Ws/Ws and +/+ rats. Unirradiated intestine from Ws/Ws and +/+ rats did not differ significantly. Mast cells protected the intestinal mucosa during the early phase of radiation enteropathy and promoted intestinal fibrosis after the breakdown of the mucosal barrier. Mast cells may be required for Tgfb to exert its full fibrogenic effect in radiation enteropathy.

Animals↗

Radiation injury.

Despite advance radiotherapy techniques, long-term complications of radiation injury are still commonly seen. Acute effects are largely time dependent and can be controlled by alteration of therapy schedule. Chronic effects are dose dependent, and are associated with increased fibrosis and decreased vascularity which can lead to tissue necrosis, infection, and ulceration. The damaging effects of radiation therapy may not be clinically apparent for months or even years after treatment is given. The most commonly accepted theory explaining the effects of radiation injury on tissue healing has focused on decreased vascularity and hypoxia in affected tissues. More recently, impaired leukocyte function has been implicated as an additional factor in the pathophysiology of radiation injury. Reconstructive surgical plans may require alteration when operating in a radiated field, especially in the head and neck. Radiation wounds are best treated by standard, accepted techniques of thorough debridement and coverage with well-vascularized tissue. Hyperbaric oxygen may have a role in the management of early radiation injury or in prophylaxis against postoperative wound complications.

Chronic Disease↗

Hyperbaric oxygen an adjunctive treatment for delayed radiation injuries of the abdomen and pelvis.

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.

Abdominal Muscles↗

A semiquantitative histological method to estimate acute and chronic radiation injury in the small intestine of the cat.

To study the radiation injury in the small bowel of the cat after doses close to and above the threshold for chronic radiation injury (15 Gy), an attempt was made to quantify these changes. For this purpose a semiquantitative method was developed by using 13 different histological alterations that were considered to mirror the acute and chronic radiation changes in the mucosa. Fibrosis was difficult to quantify; micrometric measurements of the bowel wall and its different layers were therefore carried out. The histological alterations were tabulated in increasing degree of severity. The sum of points of registered alterations in the specimen yielded scores that together with the micrometric measurements made it possible to differentiate specimens irradiated with high doses from those irradiated with low doses. The method may be valuable in estimating radiation injury in surgical specimens and in experimental studies of radiation injury.

Animals↗

Hyperbaric oxygen therapy for delayed radiation injuries in gynecological cancers.

Delayed radiation-induced injuries are difficult to treat. The treatment of delayed radiation injuries with hyperbaric oxygen therapy (HBOT) is reported in small case series and case reports. This study reports the experience of a single institution with HBOT in delayed radiation injuries in patients with gynecological cancers. At least 20 sessions of 100% oxygen inhalation at 2.4 Atmospheric Absolutes (ATA) for 90 min in a hyperbaric chamber were carried out. Of the 14 patients included in the study, 10 patients have healed or showed improvement of more than 50%, resulting in a success rate of 71%. Mean follow-up was 31.6 months (range 6-70 months). The adverse events were acceptable. HBOT should be considered for patients with delayed radiation injuries, not responding to other treatments.

Adult↗

Surgical treatment of intestinal radiation injury.

A review of 43 consecutive patients requiring operation for serious intestinal radiation injury was undertaken to elucidate the efficacy of surgical treatment. The most common site of radiation injury was the rectum (19 cases), followed by the small bowel (13 cases), the colon (7 cases), and the combination of these (4 cases). The overall operative mortality was 14%; morbidity, 47%; and the postoperative symptom-free period, 18 +/- 30 months. Colostomy (N = 20) carried the lowest risk of mortality, 0%, as compared with resection (N = 17) and bypass procedure (N = 6), which were accompanied by the mortalities of 24% and 33%, respectively. During the follow-up (3-13 years) 12 patients (28%) died of recurrent cancer and 9 patients (21%) of persistent radiation injury, which yielded an overall mortality of 65% after resection and 50% and 65% after bypass and colostomy procedures, respectively. Continuing radiation damage led to 15 late reoperations. Ten of these were performed after colostomy, four after resection, and one after bypass. We conclude that colostomy cannot be regarded as a preferred operative method, because it does not prevent the progression of radiation injury and because it is, for this reason, associated with a higher late-complication rate. A more radical surgery is recommended but with the limitation that the operative method must be adapted to the operative finding.

Adult↗

Radiation injury of boron neutron capture therapy using mixed epithermal- and thermal neutron beams in patients with malignant glioma.

The purpose of this study was to clarify the radiation injury in acute or delayed stage after boron neutron capture therapy (BNCT) using mixed epithermal- and thermal neutron beams in patients with malignant glioma. Eighteen patients with malignant glioma underwent mixed epithermal- and thermal neutron beam and sodium borocaptate between 1998 and 2004. The radiation dose (i.e. physical dose of boron n-alpha reaction) in the protocol used between 1998 and 2000 (Protocol A, n = 8) prescribed a maximum tumor volume dose of 15 Gy. In 2001, a new dose-escalated protocol was introduced (Protocol B, n = 4); it prescribes a minimum tumor volume dose of 18 Gy or, alternatively, a minimum target volume dose of 15 Gy. Since 2002, the radiation dose was reduced to 80-90% dose of Protocol B because of acute radiation injury. A new Protocol was applied to 6 glioblastoma patients (Protocol C, n = 6). The average values of the maximum vascular dose of brain surface in Protocol A, B and C were 11.4+/-4.2 Gy, 15.7+/-1.2 and 13.9+/-3.6 Gy, respectively. Acute radiation injury such as a generalized convulsion within 1 week after BNCT was recognized in three patients of Protocol B. Delayed radiation injury such as a neurological deterioration appeared 3-6 months after BNCT, and it was recognized in 1 patient in Protocol A, 5 patients in Protocol B. According to acute radiation injury, the maximum vascular dose was 15.8+/-1.3 Gy in positive and was 12.6+/-4.3 Gy in negative. There was no significant difference between them. According to the delayed radiation injury, the maximum vascular dose was 13.8+/-3.8 Gy in positive and was 13.6+/-4.9 Gy in negative. There was no significant difference between them. The dose escalation is limited because most patients in Protocol B suffered from acute radiation injury. We conclude that the maximum vascular dose does not exceed over 12 Gy to avoid the delayed radiation injury, especially, it should be limited under 10 Gy in the case that tumor exists in speech center.

Adult↗

Assessment of gastrointestinal blood flow with laser Doppler flowmetry in patients with chronic radiation injury.

Laser Doppler flowmetry was used for pre- and intraoperative assessment of gastrointestinal blood flow and vascular damage in eight patients with late radiation injury of the gastrointestinal tract. The flowmeter recordings were compared with reference values previously obtained in unaffected tissue from corresponding gastrointestinal sites. Marked reduction of blood flow was demonstrated in macroscopic areas of radiation injury in all eight patients. Five also showed varying degrees of disturbed blood flow in adjacent macroscopically normal bowel segments with histologically varying severity of radiation injury. In a ninth patient radiation injury was clinically suspected but could not be demonstrated with laser Doppler flowmetry or histologically. The extent of radiation injury often is underestimated from clinical signs, and laser Doppler flowmetry during surgical treatment of late radiation injury to the gastrointestinal tract provides substantial information concerning the extent of vascular damage.

Adult↗