Radiation injury: imaging findings in the chest, abdomen and pelvis after therapeutic radiation
Radiation may be used as adjuvant or primary therapy in a variety of tumors in the chest, abdomen and pelvis.
Therapeutic radiation affects the malignant tumors but also surrounding normal tissues.
The risk of injury depends on the size, number and frequency of radiation fractions, volume of irradiated tissue, duration of treatment, and method of radiation delivery.
Concomitant chemotherapy can act synergistically to produce injury.
Other predisposing factors include infection, prior surgery and chronic illness like hypertension, diabetes mellitus and atherosclerosis.
Radiation changes vary with target organ and the time from completion of therapy.
Most serious complications related to radiotherapy are relatively uncommon.
There is a relatively long latency period for development of radiation changes.
Imaging studies frequently have findings that should be recognized as radiation related, permitting differentiation from other etiologies such as recurrent malignancy.
In the chest, the most common tumors that are treated with radiotherapy are cancers of the breast and lung.
In patients with breast cancer, the combination of lumpectomy and radiation therapy as primary treatment has become standard practice.
The standard portal used to treat the primary tumor and associated nodes include the breast, ipsilateral axilla and supraclavicular region.
For lung cancer, the primary tumor and associated areas of nodal drainage are irradiated.
Abdominal and pelvic tumors that are typically treated with radiation therapy include lymphoma, gastro-esophageal, and pancreatic carcinoma as well as tumors of the gastrointestinal tract, gynecologic tract and genitourinary tract.
Pelvic cancer treated with radiation alone at doses of 30–70 Gy or in conjunction with other therapies include colorectal, bladder, prostate and gynecologic malignancies.
Cervical cancer is generally treated with definitive radiation therapy in cases in which the primary lesion is large or has spread beyond the cervix.
Standard treatment usually includes external beam therapy as well as brachytherapy.
Cervical cancer patients are generally young and with higher long term survival rates allowing the manifestation of radiation change to be observed on serial follow-up studies.
Rectal cancers are often treated with radiation and chemotherapy, before or after surgery as neoadjuvant or adjuvant therapy respectively.
Doses of approximately 50 Gy are used to decrease the incidence of local recurrence after surgery.
Radiation is also used frequently in patients with bladder cancer and men with prostate cancer.
Radiation pneumonitis and fibrosis are expected changes in the lung.
Other more serious radiation complications in the chest such as myocardial infarction, pericardial effusion, brachial plexus neuropathy, bone and soft tissue necrosis, fractures and radiation-induced malignancy may also occur.
Radiation induced pneumonitis typically develops approximately 6–8 weeks after treatment with doses of 30–40 Gy.
Radiation pneumonitis is most extensive 3–4 months following the end of therapy and eventually becomes radiation fibrosis.
Fibrosis becomes a stable finding approximately 9–12 months after therapy.
Concomitant chemotherapy especially with drugs that have pulmonary toxicity such as bleomycin potentiates the effects of radiotherapy.
Other radiation enhancing drugs include actinomycin D, adriamycin, cyclophosphamide, mitomycin C and vincristine .
Radiation injury to the lungs does not follow anatomic boundaries.
It has sharp, well defined areas of air space consolidation with borders that conform to the radiation portals.
Less extensive radiation pneumonitis may appear as patchy consolidation in the irradiated field and manifest as indistinctness of the pulmonary vasculature.
Radiation fibrosis is generally seen in all patients who received therapeutic doses of radiation.
Radiation fibrosis may be associated with volume loss, bronchiectatic changes, pleural thickening, slight elevation of the hila or minor fissure, slight medial retraction of pulmonary vessels, minimal tenting of elevation of a hemidiaphragm and minor blunting of cardiophrenic angles.
Computed tomography (CT) demonstrates radiation injury changes earlier than conventional radiographs, due its greater sensitivity to minimal differences in radiographic density.
On CT, radiation change can appear as homogeneous consolidation, or patchy consolidation.
Homogeneous consolidation appears as ground glass opacity on CT.
Patchy consolidation is analogous to the findings on conventional radiographs.
Discrete consolidation is well demarcated but non-uniform with traction changes that likely represent fibrosis.
Solid consolidation is seen at doses higher than 50 Gy and is more uniform with volume loss and bronchiectatic change.
Conventional radiotherapy delivers higher doses to the
surrounding tissues because of radiation attenuation.
Three-dimensional conformal therapy is used to limit the amount of injury to the lung and surrounding tissues by using multiple smaller beams aimed at the tumor.
Three-dimensional conformal therapy results in injury that has different patterns: mass-like, modified conventional and scar-like
Recurrent disease is suspected in irradiated lung if there is alteration in the stable contours of radiation fibrosis, failure of contracture of an area of radiation pneumonitis or filling in of ectactic bronchi
Radiotherapy findings include hyperlucency of the irradiated lung, spontaneous pneumothorax, pleural effusions and calcification of lymph nodes.
Pleural effusions after radiation are frequently seen on CT within 6 months of therapy and are typically small, and resolve spontaneously.
Radiation injury to the heart can cause damage to the pericardium, myocardium and vasculature of the heart.
The incidence of pericardial disease is related to the dose, fraction size, volume irradiated:At doses below 40 Gy, the incidence is low ranging between 2 and 6%.
Moderate sized mediastinal fields have a 1% incidence of pericardial disease that rises to 17% when the fields are larger with treatment of extensive disease.
Radiation pericarditis generally presents 6–9 months after therapy, with both pericardial effusions and pericardial fibrosis occur.
The incidence of myocardial infarction is higher in patients treated for left breast carcinoma than in patients treated for right breast carcinoma as would be expected with radiation portals used.
Nerves are typically quite radio-resistant.
The incidence of neural damage after irradiation is directly related to the dose.
The concomitant use of chemotherapy increases the incidence of brachial plexus neuropathy.
Signs and symptoms of neural damage develops approximately 10 months after therapy and may range from mild to severe and debilitating.
The brachial plexus is best seen with magnetic resonance imaging, and the changes seen on MRI are decreased signal intensity of the fat in the axilla and supraclavicular regions.
This is most likely related to fibrosis which results in loss of clarity and distortion of the neurovascular bundle
Severe injury of the brachial plexus results in motor and sensory deficits in the upper extremity causing a flail arm or neuropathic changes in the shoulder.
Radiation injury to the lumbosacral plexus is not common and is only seen with doses higher than 70 Gy in the pelvis.
In children, the spine may be irradiated for Wilm’s tumor, neuroblastoma, Hodgkin lymphoma and acute lymphocytic leukemia with central nervous system relapse, often resulting in inhibition of vertebral growth and short stature, as well as kyphoscoliosis with asymmetric irradiation.
Osteitis and secondary fractures may also be observed.
Spine radiation for metastatic disease in adults may cause edema and necrosis of the marrow, with increased T2-signal intensity within days.
Conversion to fatty marrow results in T1-hyperintensity, occurring as early as 2 weeks post therapy and completed by 6–8 weeks in 90% of patients.
The brachial plexus changes seen on MRI are decreased signal intensity of the fat in the axilla and supraclavicular regions most likely related to fibrosis which results in loss of clarity and distortion of the neurovascular bundle after radiation.
Radiation injury to the lumbosacral plexus is not common and only seen with doses higher than 70 Gy are received in the pelvis.
The spine may be irradiated for Wilm’s tumor, neuroblastoma, Hodgkin lymphoma and acute lymphocytic leukemia with central nervous system relapse, and in children can result in inhibition of vertebral growth and short stature, as well as kyphoscoliosis with asymmetric irradiation.
In adults, the spine is usually irradiated for metastatic disease, and can result acutely in edema and necrosis of the marrow.
This results in increased T2-signal intensity on MRI within days.
Conversion to fatty marrow results in T1-hyperintensity change that occur as early as 2 weeks post therapy and completed by 6–8 weeks in 90% of patients.
Ionizing radiation is known to be carcinogenic: increased risk for the development of lung cancer in patients irradiated for breast carcinoma, particularly in smokers: Radiation-induced mesothelioma has also been described.
Skin changes such as atrophic ulceration and severe tissue necrosis requiring surgical resection is rare with a previously reported incidence of less than 0.5% with radiation.
The incidence of sarcomas after radiotherapy is reported to be about 0.1% and the sarcomas usually occur 10 or more years after therapy.
Radiation induced sarcomas usually occur around the shoulder and pelvis in women because of the more frequent use of radiotherapy for breast and gynecologic cancers and the better long term survival of these patients.
Radiation induced soft tissue sarcoma and sarcoma of bone may occur, with malignant fibrous histiocytoma is the most frequent histology of soft tissue sarcomas.
With bony sarcomas the most common imaging findings are a new soft tissue mass and bony destruction.
Liver, spleen and pancreas
The liver is usually included during radiation treatment to the stomach, pancreas or thoracolumbar spine.
The tolerance of the whole liver is 30–35 Gy in conventional fractionation, but parts of liver can be treated with doses in excess of 70 Gy with three-dimensional radiotherapy treatment planning.
Radiation-induced liver disease (RILD), or radiation hepatitis, is a clinical syndrome of anicteric ascites and hepatomegaly occurring 2 weeks to 4 months after hepatic irradiation, because of venoocclusive disease.
The irradiated liver appears hypodense with well-defined linear margins on non-contrast CT scans and can also be seen in patients who receive more than 45 Gy to a portion of the liver, regardless of whether they develop RILD.
Patients are usually asymptomatic if the non-irradiated liver is healthy.
In a fatty liver, the CT density pattern may be reversed.
The spleen may be irradiated to treat lymphoma, splenomegaly or hypersplenism.
The spleen is very radiosensitive and lymphoid tissues are destroyed within hours after a dose of 4–8 Gy.
At doses of 35–40 Gy, splenic fibrosis and atrophy may result.
The effects of splenic irradiation are usually not clinically significant,
But functional hyposplenism can occur.
Irradiation to the pancreas causes necrosis and fibrosis similar to chronic pancreatitis.
The pancreatic acinar epithelium is more sensitive than the islet cells and the imaging features are also similar to pancreatitis.
Pancreatic atrophy is eventually seen after radiotherapy.
The kidney is radiosensitive and 28 Gy to both kidneys in 5 weeks or less frequently leads to renal failure.
The risk of renal impairment increases with prior or concurrent chemotherapy.
Radiological changes to the kidney appear months to years after treatment, ultimately resulting in atrophic poorly functioning kidneys with smooth outlines.
Hypertrophy compensation of the non-irradiated contralateral kidney can develop. If only a portion of the kidney is irradiated, only that portion is affected.
Malignant hypertension may develop 1–10 years after renal irradiation due to renin overproduction, requiring nephrectomy relief.
The overall incidence of urologic complications after pelvic irradiation is reported to be approximately 21%, however, only 2.5% of such complications could be ascribed to the effects of radiation alone, since surgery and chemotherapy may have additive effects.
The incidence of radiation cystitis is reported to range from 3 to 12%.
The ureter is fairly radioresistant.
Ureteral injury, however, may not become apparent for many years after therapy.
The risk of ureteral stenosis in cervical cancer is 1% at 5 years, 1.2% at 10 years, 2.2% at 10 years, and 2.5% at 20 years .
The prostate and seminal vesicles typically become atrophic after radiation treatment.
Urethral strictures can occur in males in the prostatic and membranous portion of the urethra particularly after transurethral resection of the prostate.
In female patients, uterine atrophy can be seen in pre-menopausal women who receive therapeutic doses of radiation.
Cervical stenosis occurs rarely and can result in distension of the endometrial cavity with retained secretions.
The ovaries also become atrophic and fibrotic with loss of follicular cysts.
In the chest, the most common tumors that are treated with radiotherapy are cancers of the breast and lung.
Only the breast is treated when disease is limited.
For lung cancer, the primary tumor and associated areas of nodal drainage are irradiated.
Abdominal and pelvic tumors that are typically treated with radiation therapy include lymphoma, gastro-esophageal, and pancreatic carcinoma as well as tumors of the gastrointestinal tract, gynecologic tract and genitourinary tract.
Pelvic cancers treated with radiation alone at doses of 30–70 Gy or in conjunction with other therapies include colorectal, bladder, prostate and gynecologic malignancies.
Radiation pneumonitis and fibrosis are expected changes in the lung, but more serious complications such as myocardial infarction, pericardial effusion, brachial plexus neuropathy, bone and soft tissue necrosis, fractures and radiation-induced malignancy may also occur.
Radiation induced pneumonitis typically develops approximately 6–8 weeks after treatment, and is a well known early expected effect of therapy that is related to total dose and fractionation
Radiation pneumonitis is most extensive 3–4 months following the end of therapy.
Radiation pneumonitis eventually becomes radiation fibrosis.
Radiation fibrosis becomes a stable finding approximately 9–12 months after therapy
If changes occur after that time period, superimposed infection or recurrent tumor should be considered.
Concomitant chemotherapy especially with drugs that have known direct pulmonary toxicity such as bleomycin potentiates the effects of radiotherapy.
Radiation enhancing drugs include:actinomycin D, adriamycin, cyclophosphamide, mitomycin C and vincristine.
Radiation injury to the lungs does not follow anatomic boundaries, but has sharp, well defined areas of air space consolidation with borders that conform to the radiation portals.
Less extensive radiation pneumonitis may result in patchy consolidation in the irradiated field or manifest as indistinctness of the pulmonary vasculature.
Radiation fibrosis is generally seen after therapeutic doses of radiation, and volume loss is typical.
Bronchiectatic changes may also be seen after radiation.
Less obvious radiation changes include minimal pleural thickening, slight elevation of the hila or minor fissure, slight medial retraction of pulmonary vessels, minimal tenting of elevation of a hemidiaphragm and minor blunting of cardiophrenic angles.
Computed tomography (CT) demonstrates radiation injury earlier than conventional radiographs.
Computed tomography (CT) has greater sensitivity to minimal differences in radiographic density.
CT radiation change can appear as: homogeneous consolidation, patchy consolidation, discrete consolidation or solid consolidation.
Three-dimensional conformal therapy is used to limit the amount of injury to the lung and surrounding tissues by using multiple smaller beams aimed at the tumor.
Conformal therapy results in injury that has different patterns: mass-like, modified conventional and scar-like.
Other findings following radiotherapy include hyperlucency of the irradiated lung, spontaneous pneumothorax, pleural effusions and calcification of lymph nodes.
Therapeutic radiation can cause damage to the pericardium, myocardium and vasculature of the heart.
The incidence of pericardial disease is related to the dose, fraction size, volume irradiated and technique.
At doses below 40 Gy, the incidence is low ranging between 2 and 6%.
Moderate sized mediastinal fields have a 1% incidence of pericardial disease.
Increased radiation pericardia disease occurs rises when the fields are larger with treatment of extensive disease
Radiation pericarditis generally presents 6–9 months after therapy.
The majority of cases of radiation pericarditis occurs within 12–18 months of therapy.
Pericardial effusions and pericardial fibrosis can occur with radiation.
Fibrosis of the myocardium can also occur and is aggravated by the use of cardiotoxic chemotherapy with agents such as doxorubicin.
The incidence of myocardial infarction is higher in patients treated for left breast carcinoma than in patients treated for right breast carcinoma with radiation.
Nerves are typically quite radio-resistant.
The incidence of neural damage after irradiation is directly related to the dose.
The concomitant use of chemotherapy increases the incidence of neuropathy.
Signs and symptoms of brachial plexus neuropathy develop approximately 10 months after therapy and may range from mild and to severe and debilitating.
Severe injury of the brachial plexus results in motor and sensory deficits in the upper extremity causing a flail arm or neuropathic changes in the shoulder.
Radiation injury to the lumbosacral plexus is not common and is only seen with doses higher than 70 Gy in the pelvis
The spine may be irradiated in children for Wilm’s tumor, neuroblastoma, Hodgkin lymphoma and acute lymphocytic leukemia with central nervous system relapse.
Irradiation often results in inhibition of vertebral growth and short stature, as well as kyphoscoliosis with asymmetric irradiation, osteitis and secondary fractures.
In adults, the spine is irradiated for metastatic disease.
Spinal irradiation may result in edema and necrosis of the marrow resulting in increased T2-signal intensity within days
Conversion to fatty marrow results in MRI T1-hyperintensity, occurring as early as 2 weeks post therapy and completed by 6–8 weeks in 90% of patients.
Changes to bone after radiotherapy follow a characteristic pattern: first conventional radiographic sign of change is demineralization and osteopenia which develops approximately 12 months after therapy is completed and may be progressive.
Spontaneous fractures, aseptic necrosis and bony resorption may also occur within the radiation field.
In the chest, these changes typically involve the ribs, clavicle and shoulder.
The incidence of rib fracture after radiation therapy is approximately 1.8% and.
The rate of rib fractures is related to the radiation dose with doses greater than 50 Gy resulting in a higher incidence
The addition of chemotherapy to radiation may result in an increased rate of rib fractures.
In the pelvis, insufficiency fractures of the vertebral bodies, sacrum, and pubis can occur after radiotherapy.
In the past when ortho-voltage treatment was widely used, femoral neck fractures were more common, and avascular necrosis of the hips is also a known complication of radiotherapy.
Ionizing radiation is known to be carcinogenic:increased risk for the development of lung cancer in patients irradiated for breast carcinoma has been described, particularly in smokers; radiation-induced mesothelioma has also been described.
Skin changes such as atrophic ulceration and severe tissue necrosis requiring surgical resecti reported incidence of less than 0.5%.
The incidence of sarcomas after radiotherapy is reported to be about 0.1% and the sarcomas usually occur 10 or more years after therapy.
Radiation induced sarcomas usually occur around the shoulder and pelvis in women because of the more frequent use of radiotherapy for breast and gynecologic cancers.
Radiation induced soft tissue sarcoma and sarcoma of bone may occur.
Histologic proof of suspected malignant lesions should be obtained because the differential diagnosis would include metastases, infection and severe benign changes.
The liver is usually included during radiation treatment to the stomach, pancreas or thoracolumbar spine lesions.
The tolerance of the whole liver is 30–35 Gy in conventional fractionation.
Parts of liver can be treated with doses in excess of 70 Gy with three-dimensional radiotherapy treatment planning.
Radiation-induced liver disease is a clinical syndrome of anicteric ascites and hepatomegaly occurring 2 weeks to 4 months after hepatic irradiation, because of venoocclusive disease.
The irradiated liver appears hypodense on non-contrast CT scans.
Patients are usually remain asymptomatic if the non-irradiated liver is healthy.
The irradiated liver is hypodense with well-defined linear margins that conform to radiation portals.
The irradiated area can enhance more than adjacent liver, because of increased arterial flow or delayed clearance of contrast from radiation-induced venoocclusive disease.
Increased water within the irradiated liver causes T1-hypointensity and T2-hyperintensity.
The spleen may be irradiated to treat lymphoma, splenomegaly or hypersplenism, and is very radiosensitive as lymphoid tissues are destroyed within hours after a dose of 4–8 Gy.
At doses of 35–40 Gy, splenic fibrosis and atrophy may result.
Splenic irradiation is usually not clinically significant, although functional hyposplenism and fulminant pneumococcal sepsis can occur.
Irradiation to the pancreas causes necrosis and fibrosis.
The pancreatic acinar epithelium is more sensitive than the islet cells and the imaging features are also similar to pancreatitis.
Pancreatic atrophy is eventually seen.
The kidney is radiosensitive and 28 Gy frequently leads to renal failure
The risk of renal impairment increases with prior or concurrent chemotherapy.
Radiological changes appear months to years after radiation treatment: atrophic poorly functioning but non-obstructed kidneys with smooth outlines.
Malignant hypertension may develop 1–10 years after renal irradiation due to renin overproduction, requiring nephrectomy relief.
The overall incidence of urologic complications after pelvic irradiation is reported to be pproximately 2.5%.
The incidence of radiation cystitis is reported to range from 3 to 12%.
The ureter is fairly radioresistant.
Ureteral injury, however, may not become apparent for many years after therapy.
The risk of ureteral stenosis in cervical cancer is 1% at 5 years, 1.2% at 10 years, 2.2% at 10 years, and 2.5% at 20 years.
The prostate and seminal vesicles typically become atrophic after radiation treatment.
Urethral strictures can occur in males in the prostatic and membranous portion of the urethra, particularly after transurethral resection of the prostate.
Uterine atrophy can be seen in pre-menopausal women who receive therapeutic doses of radiation, and cervical stenosis occurs rarely and can result in distension of the endometrial cavity with retained secretions.
The ovaries also become atrophic and fibrotic with loss of follicular cysts after pelvic radiation.
Radiation fields used to treat malignancy in the chest, the esophagus may be injured and radiation-induced injury to the esophagus may be a limiting factor in therapy of thoracic neoplasms.
Esophageal injury typically occurs at doses higher than 45 Gy, with esophageal dysmotility the earliest and most common finding.
Mucosal changes edema, ulceration and fistula formation may also occur, and can be expected 4–12 weeks after completion of therapy.
Esophageal strictures typically occur 4–8 months after therapy.
Radiation induced esophageal carcinoma is rare.
The stomach and duodenum may be injured after radiation therapy to retroperitoneal structures such as the pancreas or lymph nodes.
The small intestine is quite radiosensitive and is potentially in the treatment field for all intra-abdominal, retroperitoneal and pelvic tumors.
The rapidly proliferating cells of the mucosa of the small intestine are most radiosensitive and therefore at highest risk for acute injury which occurs within weeks of radiation therapy and is rarely evaluated radiographically.
The terminal ileum is more commonly injured, as it is more fixed.
Acutely, small bowel dilation with edema and mucosal sloughing can occur and usually resolves.
Chronic bowel injury is caused by submucosal obliterative vasculitis that results in further ischemia and fibrosis.
Fibrotic strictures may cause small bowel obstruction.
Findings similarly occur in the colon:
CT bowel wall thickening related to submucosal edema, areas of stenosis and bowel obstruction.
Altered peristalsis may also be encountered, with mesenteric fibrosis that results in fixation of small bowel loops with tethering.
The overall incidence of chronic radiation injury to the bowel after radiotherapy to the pelvis is about 1%–5%.
The risk factor for injury to the gastrointestinal tract relates to the dose of radiation given.
Radiation damage to the colon can be shown radiographically as loss of distensibility with strictures of various lengths and degrees of narrowing.
Mucosucosal changes such as ulceration, polypoid protrusions or contour irregularities ranging from even circumferential lesions simulating malignancy are seen.
The endothelial lining of the microvasculature is the most radiosensitive portion of the vasculature.
Radiation damage results in intracellular edema with resultant vascular occlusion
Less severe radiation damage results in telangiectasia.
Arteriolar damage is frequent from radiation and consists of myointimal proliferation indistinguishable from atherosclerosis
Acute lymphocytic vasculitis affecting the media, intima and adventitia of medium sized vessels is also observed.
In medium and large arteries, atheromas and fibrosis are observed less often, resulting in stenosis.
Rupture of irradiated large vessels occurs mostly in the carotid arteries and less frequently in the aorta and femoral arteries.
Intensity modulated radiation therapy (IMRT) that may reduce the side effects of radiation on normal tissues: Compared to conventional radiation where multiple large beams pass through the body conforming to the target that needs to be treated, IMRT
This allows beams to be broken up into thousands of tiny pencil-thin radiation beams, each with a different intensity that enters the body from many more angles.
A complex irregular clinical target volumes can be irradiated while sparing adjacent normal tissues.
One of the major risks is that the high degree of conformation with IMRT may lead to misses of disease and recurrences especially for disease sites where positioning and motion play a large role.
Some studies have suggested that IMRT may almost double the incidence of second malignancies from about 1% after conventional radiation therapy to 1.75% after IMRT for patients surviving 10 years.
Proton therapy further improves in dose localization over photons (X-rays) and reduces the risk of second malignancies, while giving very low radiation dose to normal tissues while depositing high-energy radiation at carefully targeted tumors.
As protons edeposit a minimal amount of energy to the skin or tissues between the skin and the target volume.
Most of the energy is deposited in the target volume with only minimal dose passing beyond the target to normal tissues.
Proton beams have been shown to give less dose bladder, rectum and bone marrow in patients with prostrate cancer.
Radiation affects not only malignant tumors but also surrounding normal tissues with risks of injury depending on the size, number and frequency of radiation fractions, volume of irradiated tissue, duration of treatment, and method of radiation delivery.
Concomitant chemotherapy can act synergistically to produce injury.
Other predisposing factors include infection, prior surgery and chronic illness like hypertension, diabetes mellitus and atherosclerosis.
Radiation changes vary, based on the target organ and the time from completion of therapy.
Most serious complications related to radiotherapy are relatively uncommon, given the number of patients that are treated and the relatively long latency period for development of radiation changes, follow-up imaging studies frequently have findings that should be recognized as radiation related.
The spectrum of imaging findings after radiation injury permits differentiation from other etiologies such as recurrent malignancy.
In the chest, the most common tumors that are treated with radiotherapy are cancers of the breast and lung.
In patients with breast cancer, the combination of lumpectomy and radiation therapy as primary treatment has become more commonplace.
The standard portal used to treat the primary tumor and associated nodes include the breast, ipsilateral axilla and supraclavicular region.
Only the breast is treated when disease is limited.
For lung cancer, the primary tumor and associated areas of nodal drainage are irradiated.
Abdominal and pelvic tumors that are typically treated with radiation therapy include lymphoma, gastro-esophageal, and pancreatic carcinoma as well as tumors of the gastrointestinal tract, gynecologic tract and genitourinary tract.
Pelvic cancer treated with radiation alone at doses of 30–70 Gy or in conjunction with other therapies include colorectal, bladder, prostate and gynecologic malignancies.
Cervical cancer is generally treated with definitive radiation therapy in cases in which the primary lesion is large or has spread beyond the cervix.
Standard treatment usually includes external beam therapy as well as brachytherapy.
Colorectal cancers are often treated with radiation and chemotherapy, before or after surgery as neoadjuvant or adjuvant therapy respectively.
Doses of approximately 50 Gy are used to decrease the incidence of local recurrence after surgery.
Ionizing radiation is known to be carcinogenic.
An increased risk for the development of lung cancer in patients irradiated for breast carcinoma has been described, particularly in smokers.
Radiation-induced mesothelioma and sarcoma has occurred.
The incidence of sarcomas after radiotherapy is about 0.1%.
Such sarcomas usually occur 10 or more years after therapy.
Radiation induced soft tissue sarcoma and sarcoma of bone may also occur.
The liver is usually included during radiation treatment to the stomach, pancreas or thoracolumbar spine, with a tolerance of the whole liver at 30–35 Gy in conventional fractionation.
Parts of liver can be treated with doses in excess of 70 Gy with three-dimensional radiotherapy treatment planning.
Radiation-induced liver disease. or radiation hepatitis, is a clinical syndrome of anicteric ascites and hepatomegaly occurring 2 weeks to 4 months after hepatic irradiation, because of venoocclusive disease.
The irradiated liver appears hypodense on non-contrast CT scans.
The irradiated area can enhance more than adjacent liver,
from radiation-induced venoocclusive disease.
The spleen is very radiosensitive and lymphoid tissues are destroyed within hours after a dose of 4–8 Gy.
At doses of 35–40 Gy, splenic fibrosis and atrophy may result.
The effects of splenic irradiation are usually not clinically significant:
Functional hyposplenism and fulminant pneumococcal sepsis can occur.
Pancreas radiation causes necrosis and fibrosis similar to chronic pancreatitis, and imaging atrophy is eventually seen.
The kidney is radiosensitive and 28 Gy to both kidneys in 5 weeks or less frequently leads to renal failure.
In acute radiation nephritis, the kidney remains normal in size and shape, although glomerular damage is present histologically.
Radiological changes appear months to years after treatment, with atrophic poorly functioning but non-obstructed kidneys.
If only a portion of the kidney is irradiated, only that portion is affected.
Malignant hypertension may develop 1–10 years after renal irradiation due to renin overproduction, requiring nephrectomy relief.
The incidence of radiation cystitis is reported to range from 3 to 12% depending on the dose to the bladder.
The ureter is fairly radioresistant and radiation induced strictures are infrequent.
The risk of ureteral stenosis in cervical cancer is 1% at 5 years, 1.2% at 10 years, 2.2% at 10 years, and 2.5% at 20 years.
The prostate and seminal vesicles typically become atrophic after treatment.
The peripheral zone of the prostate loses its normal T2 hyperintensity and becomes uniformly low signal on T2 weighted images with radiation.
Urethral strictures can occur in males in the prostatic and membranous portion of the urethra particularly after transurethral resection of the prostate.
In female patients, uterine atrophy can be seen in pre-menopausal women who receive therapeutic doses of radiation.
Cervical stenosis can result in distension of the endometrial cavity with retained secretions.
The ovaries also become atrophic and fibrotic with loss of follicular cysts.
With radiation fields used to treat malignancy in the chest, the esophagus may be injured and radiation-induced injury to the esophagus..
Such injury may be a limiting factor in therapy of thoracic neoplasms.
Esophageal injury typically occurs at doses higher than 45 Gy.
Esophageal dysmotility is the earliest and most common finding of radiation injury, but mucosal changes such as edema, ulceration and fistula formation may also occur.
These esophageal findings can be expected 4–12 weeks after completion of therapy.
Esophageal strictures typically occur 4–8 months after therapy.
Radiation induced esophageal carcinoma is rare but has been described as occurring about 14 years after therapy is completed.
The stomach and duodenum may be injured after radiation therapy to retroperitoneal structures such as the pancreas or lymphnodes.
Radiographic findings include prepyloric and pyloric ulcers with deformity, fixed narrowing, deformity and an aperistaltic antropyloric region without ulceration can also
occur.
The small intestine is radiosensitive to treatment fields for all intra-abdominal, retroperitoneal and pelvic tumors.
The proliferating cells such as those in the mucosa of the small intestine are most radiosensitive and therefore at highest risk for acute injury which occurs within weeks of therapy.
The terminal ileum is more commonly injured with radiation exposure because it is more fixed.
Small bowel dilation, edema and mucosal sloughing can occur and changes in the vascular and interstitial connective tissues are more insidious and the initial injury leads to progressive ischemia of the intestinal wall.
Chronic bowel injury caused by submucosal obliterative vasculitis that results in further ischemia and fibrosis, and may cause small bowel obstruction, and fistulae.
The colon has similar findings after radiotherapy: Submucosal edema, fibrosis thickening and straightening of bowel folds and separation of adjacent loops.
Radiation changes may induce altered peristalsis by changes of mesenteric fibrosis resulting in fixation of small bowel loops with tethering.
The incidence of chronic radiation injury to the bowel after radiotherapy to the pelvis is about 1%–5%
The most important risk factor for injury to the gastrointestinal tract is the dose of radiation given.
Prostate cancer studies show that doses of more than 70 Gy raised the likelihood of rectal bleeding after therapy.
Radiation damage to the colon can be shown radiographically as loss of bowel distensibility with strictures and narrowing, with widening of the pre-sacral space.
Mucosal changes such as ulceration, pseudo-polypoid protrusions or contour irregularities ranging from tiny serrations to ragged margins and even circumferential lesions simulating malignancy occur after bowel radiation.
The possibility of radiation induced colon cancer is suggested.
The rectum is relatively radioresistant but is frequently injured because of its fixed location near organs in the pelvis that are frequently targeted for radiotherapy.
Radiation injury differs in small and large vessels.
The endothelial lining of the microvasculature is the most radiosensitive portion of the blood vessels and damage results in intracellular edema with resultant vascular occlusion.
Less severe damage results in telangiectasia.
Arteriolar damage consists of myointimal proliferation indistinguishable from atherosclerosis, and lymphocytic vasculitis affects the media, intima and adventitia of medium sized vessels is also observed.
In medium and large arteries, atheromas and fibrosis are observed less often, resulting in stenosis, and rupture of irradiated large vessels occurs mostly in the carotid arteries and less frequently in the aorta and femoral arteries.
Intensity modulated radiation therapy (IMRT) that may reduce the side effects of radiation on normal tissues.
IMRT allows beams to be broken up into thousands of tiny pencil-thin radiation beams, each with a different intensity that enters the body from many more angles.
The combined effect is to produce a high-dose volume with a sharp-dose gradient at its boundaries that can be designed into complex three-dimensional shapes.
Complex irregular clinical target volumes can be irradiated while sparing adjacent normal tissues.
IMRT decreases both acute and late bowel toxicity in patients treated to the pelvis.
In patients treated for prostrate cancers less rectal dose has been documented with IMRT.
The higher degree of conformation with IMRT may lead to geographic misses of disease and recurrences.
This is especially true for disease sites where positioning and motion changes in anatomy and biology take placeduring the course of radiation therapy.
The large volume of normal tissues receiving low dose radiation may increase the incidence of secondary malignancies outside the treatment fields.
Studies suggest that IMRT may almost double the incidence of second malignancies from about 1% after conventional radiation therapy to 1.75% after IMRT for patients surviving 10 years.
Proton beams offer further improvements in dose localization over photons (X-rays) and reduce the risk of second malignancies, as protons give very low radiation dose to normal tissues while depositing high-energy radiation at carefully targeted tumors.
As protons enter the body, there is a minimal amount of energy to the skin or tissues between the skin and the target volume, and only minimal dose passing beyond the target to normal tissues.
Proton beams have been shown to give less dose bladder, rectum and bone marrow in patients treated for prostrate cancer.