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DOI: 10.1055/s-0041-1735921
Imaging Features of Postradiotherapy Changes in Head and Neck Cancers
- Abstract
- Introduction
- Approach to Posttreatment Neck
- Routine Surveillance
- Expected Postradiation Changes: Early
- Expected Postradiation Changes: Late
- Unexpected Changes of Radiation Therapy
- Radiation-Induced Lung Changes
- Osteoradionecrosis
- Chondronecrosis
- Cerebral Radiation Necrosis
- Radiation-Induced Herpes Simplex Encephalitis
- Cranial and Brachial Neuropathy
- Radiation-Induced Vascular Changes
- New Primary Tumor and Radiation-Induced Neoplasms
- Recurrence after Radiation Therapy
- Conclusion
- References
Abstract
Radiation therapy is the mainstay in the treatment of head and neck cancers, in addition to surgery and chemotherapy. Expected radiotherapy changes evolving over time may be confused with recurrent tumor. Conversely, even residual or recurrent tumor in the setting of postradiotherapy changes may be difficult to identify clinically or even by radiological imaging. Therefore, it is important to be familiar with the temporal evolution of these changes. The purpose of this pictorial essay is thus to illustrate distinctly the expected radiotherapy changes and radiotherapy-related complications in the head and neck region and to differentiate them from tumor recurrence on routine cross-sectional imaging techniques (computed tomography and magnetic resonance imaging).
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Keywords
postradiotherapy changes - head and neck malignancy - head and neck squamous cell carcinoma - radiation complicationsIntroduction
With the diversity of tumors affecting the head and neck regions, radiotherapy (RT) protocols and their resultant changes are bound to vary. However, certain RT-related changes are inevitable. With the advent of newer RT techniques, such as three-dimensional conformal RT (3DCRT) and intensity-modulated RT (IMRT) replacing the conventional external beam RT (EBRT), the incidence of treatment-related complications have also reduced but it is still not negligible.[1] Tumor per se, as well as surrounding soft tissues, cartilages, and bones in the treatment field can undergo various changes over time. Early complications related to mucositis are usually detected clinically and are beyond the scope of imaging. Late-term effects of RT may be confused with recurrent disease or with treatment-related complications and usually warrant imaging diagnosis.
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Approach to Posttreatment Neck
The first step toward approaching a treated head and neck cancer scan is to review any previous imaging, including pretreatment scans. Adequate knowledge about type of surgery, including type of neck dissection and reconstructive flap used, is a must to be familiar with the expected changes. A knowledge of margins obtained at the time of surgery and primary histology of tumor by looking back at the surgical pathology report is just as important since some tumors have a high propensity for recurrence. Awareness of duration, dose, modality, location, and timing of RT is important. Finally, it is useful to know the reason for imaging, if there is any clinical suspicion of recurrence or only routine surveillance is required. Commonly used cross-sectional imaging modalities include computed tomography (CT), magnetic resonance imaging (MRI) and fluorodeoxyglucose positron emission tomography (FDG PET)–CT ([Table 1]). In most cases, CT is complementary to MRI to evaluate osseous involvement and laryngeal invasions.
Abbreviations: CT, computed tomography; FDG PET, fluorodeoxyglucose positron emission tomography; MRI, magnetic resonance imaging
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Routine Surveillance
Currently, no clear consensus exists among institutions regarding the optimum time of imaging or type of imaging modality to be routinely employed. The current National Comprehensive Cancer Network (NCCN) guidelines recommend baseline cross-sectional imaging at 8 to 10 weeks after treatment completion. But there are no recommendations for subsequent follow-up scan timings. If the specific clinical question is to look for residual or recurrent disease, following surgery or chemo-RT, the choice for baseline imaging is usually a contrast-enhanced CT scan of the neck and thorax or PET–CT study. Hence, in the surveillance setting too, there may be institutionalized protocols in place for time and type of imaging. In the author's institution, clinical examination and surveillance imaging are performed quarterly for the first 2 years, semiannually until 4 years and annually thereafter in the absence of a clinical suspicion.
This pictorial review aims to describe the early and late, expected, and unexpected changes of RT on standard CT and MRI examinations.
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Expected Postradiation Changes: Early
These changes are expected to be seen within 3 months of treatment, and sometimes as soon as 2 weeks of treatment initiation and are mostly attributed to interstitial edema of the soft tissues due to disruption of endothelial cell lining, affecting venous and lymphatic drainage.[2] These present as progressive thickening of skin and platysma ([Fig. 1]), subcutaneous reticulations ([Fig. 2]), and mucosal edema of pharyngeal and laryngeal walls. Sometimes, laryngeal edema can be very severe and life-threatening which should be alerted to the treating team ([Fig. 3]). There can also be fluid collections and edema of the retropharyngeal space which should not be mistaken for infectious processes ([Fig. 4]) as infective fluid collections are expected to have enhancing walls. Often, early radiation injury can involve the parotid and submandibular glands in a symmetric fashion which presents as diffuse enlargement and enhancement of the gland due to radiation-induced glandular hyperemia ([Fig. 5]). Sometimes, these changes manifest asymmetrically involving only one gland, depending on the radiation portal causing a painless enlargement of only one gland ([Fig. 6]). If superadded infection occurs due to poor oral hygiene, patients present with diffuse enlargement of the affected gland with pain and fever, termed as acute sialadenitis. Another expected change of RT includes fatty conversion of bone marrow and is one of the most common osseous alterations seen as a result of RT ([Fig. 7]).
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Expected Postradiation Changes: Late
These changes occur more than 3 months after RT completion and can persist for months to years and sometimes even resolve. Overtime, fibrosis and atrophy develop within the affected soft tissues lying in the radiation portal.[3] The salivary glands and thyroid undergo a similar process, eventually undergoing atrophy and being replaced by fat.
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Key point: expected tissue changes after RT appear symmetrical, unless the neck is irradiated using asymmetric radiation portals. Enhancement is homogenous without asymmetric expansion of affected soft tissues which helps differentiating from tumor recurrence.
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Unexpected Changes of Radiation Therapy
The risk factors for complications of RT can be multifactorial and may be related to radiation dose, duration and fractionation, radiation field size, local extent and histology of the neoplasm, concurrent use of chemotherapy, continued consumption of tobacco and alcohol, dental infections, and dental extractions.[1] These changes are seen for many months to years after therapy and generally follow a timeline ([Table 2]).
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Radiation-Induced Lung Changes
The lung apices are included in radiation treatment for head and neck malignancy to cover supraclavicular and level-IV cervical lymph nodes which result in bilateral apical radiation-induced changes.[4] These changes manifest as acute radiation pneumonitis (within 1–3 months of therapy) or late radiation lung fibrosis (within 6–12 months after therapy). Imaging findings of radiation pneumonitis are focal ground-glass attenuation or consolidations or both ([Fig. 8]). Radiation pneumonitis gradually resolves but it may progress to lung fibrosis if the damage is severe. Radiation lung fibrosis is seen on CT as a sharply delineated area of volume loss, linear scarring, and traction bronchiectasis.
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Osteoradionecrosis
It is the necrosis occurring in the bone within an irradiated field, with formation of fistula on the overlying skin and persistent nonhealing for more than 3 months when radiation doses exceed 60 Gy. At such high doses, osteoblastic function is impaired, resulting in decreased matrix production and increased bone resorption. Reparative processes ensue resulting in a mottled appearance with areas of patchy lucency, disorganized sclerosis, and coarsened trabeculae with or without bony expansion.[5] Over time, there can be progressive necrosis, secondary infection, and bony sequestration. The risk is highest in the first 6 to 12 months after therapy but may persist years after RT. Commonly affected bones include the mandible (due to its unique blood supply and superficial location), maxilla, hyoid, skull base, and temporal bone.[1] [6] Osteonecrosis of the skull base is a very serious complication of RT and is rather rare presently due to the optimized organ sparing radiation techniques. We have not seen any cases of radio necrosis of the skull base at the author's institution over the past years.
CT shows bizarre lysis, disorganized sclerosis, and cortical destruction with or without clear fistula onto the skin surface and with disorganized sclerosis being the most common finding. MRI shows the affected bone with mixed altered signal intensity and irregular patchy enhancement. Some reports in literature have described the use of FDG PET–CT in diagnosing and differentiating osteoradionecrosis from tumor recurrence, but significant overlap exists in the standardized uptake value (SUV) values and the two cannot be differentiated without the help of key CT features as described. Key differentiating points of osteoradionecrosis from tumor recurrence are the presence of associated measurable enhancing soft tissue mass corresponding to the site of new bone erosion or lysis in the latter ([Fig. 9]).
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Chondronecrosis
It is the collapse of cartilage within an irradiated field due to breach in the perichondrium by tumor and superadded infection resulting in necrosis. Late effects of radiation result in endothelial damage which impairs the vascular and lymphatic flow. Inflammatory changes ensue resulting in necrosis of the larynx and fistula formation with the overlying skin. Clinically, patients present with new onset odynophagia and hoarseness of voice. CT and MRI show fragmentation and collapse of affected cartilage ([Fig. 10]). Loss of high signal in the medullary space of ossified laryngeal cartilage on T1-weighted images, and enhancement of the affected cartilage after injection of gadolinium-contrast agents is observed.[7] Key differentiating features of chondronecrosis from tumor recurrence are presence of gas bubbles adjacent to the affected site of chondronecrosis, whereas presence of enhancing soft tissue clinches the diagnosis of tumor recurrence. Nevertheless, a coexistent tumor recurrence may be difficult to exclude depending on underlying tissue distortions.
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Cerebral Radiation Necrosis
Radiation-induced brain necrosis occurs with a latency period of at least 2 years. It was more commonly associated with older RT techniques such as EBRT and would affect the medial and inferior temporal lobes when RT was used for the treatment of skull base or nasopharyngeal cancers. Incidence has reduced significantly with newer techniques like IMRT as the brain is spared and contoured out of the radiation field.[8] It presents as a ring-enhancing lesion with perilesional edema involving the white matter on CT and MRI ([Fig. 11]). Oftentimes, there may only be white matter T2 hyperintensity due to myelin dysfunction and gliosis in the absence of any enhancement.[9] [10] Differentials, including high-grade glioma, metastases, and infections, can be differentiated on the basis of combination of diffusion, MR perfusion, and MR spectroscopy.
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Radiation-Induced Herpes Simplex Encephalitis
Although a rare phenomenon, herpes simplex encephalitis (HSE) in patients who have received RT for nasopharyngeal cancers has been reported in literature. It is postulated that cancer per se and related treatments, such as chemotherapy, RT, and corticosteroid, predispose to an immunosuppressive state resulting in an increased susceptibility to HSE due to disruption of blood brain barrier.[11] Early diagnosis of HSE is essential, as the prognosis is dependent on early treatment. MRI is more sensitive than CT, especially diffusion-weighted images or fluid-attenuated inversion recovery (FLAIR) images that can identify abnormal areas.[12] Unilateral temporal lobe and insular cortex involvement is the classic finding seen on imaging; however, bilateral involvement is also known to occur infrequently ([Fig. 12]). Cerebrospinal fluid (CSF) polymerase chain reaction (PCR) has a sensitivity of 98% and specificity of 94 to 100%, and is considered the gold standard for diagnosis.[12]. Early diagnosis and treatment remains the major prognostic indicator.
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Cranial and Brachial Neuropathy
These changes occur along the same timeline as radiation-induced brain changes. Radiation-induced lower cranial nerve palsy may occur rarely and is thought to be due to fibrosis around the carotid sheath carrying cranial nerves 9, 10, 11, and 12.[13] Radiation-induced brachial plexopathy is also uncommon and peaks 2 to 4 years after treatment and can present as thickening and enhancement of affected roots and trunks ([Fig. 13]).[14]
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Radiation-Induced Vascular Changes
Large vessel vasculopathy is far less common than small vessel disease. It is thought to be a combination of radiation-induced intimal hyperplasia and accelerated atherosclerosis. The changes are seen only after high-dose therapy and with a variable latency period. Accelerated atherosclerosis ([Fig. 14]), thrombosis of the internal jugular vein ([Fig. 15]), arterial stenoses, and occlusions of the intracranial or extracranial circulation are the most common findings.[15] [16] These are also now becoming rare due to newer carotid sparing intensity-modulated RT techniques (CSIMRT).[17] [18] Pseudoaneurysms and carotid arterial blowouts are known but are rare complications that can result in profound and lethal bleeding perorally[16] ([Fig. 16]).
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New Primary Tumor and Radiation-Induced Neoplasms
Positive association of head and neck squamous cell carcinomas with tobacco and alcohol consumption make these patients at an increased risk of a second primary neoplasm in the lungs or upper aerodigestive tract.
A radiation-induced secondary neoplasm is rare. It is imperative for the secondary tumor to be of a different histology than from the primary tumor and should occur at sites distant to the site of primary tumor and after a latency period of at least 5 years or more.[1] Some common tumor histology include meningiomas, sarcoma, squamous cell carcinoma of temporal bone, or external auditory canal and malignant peripheral nerve sheath tumors[19] ([Fig. 17]). Thyroid malignancies developing postradiation can pose a challenge in establishing a causal effect due to its inherently high prevalence. Some cases of thyroiditis, however, are reported in literature more commonly occurring than thyroid malignancies, whereby there is heterogeneous replacement of normal thyroid parenchyma, with the gland eventually undergoing atrophy and patients developing hypothyroidism ([Fig. 18]).
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Recurrence after Radiation Therapy
The development of a new expansile enhancing mass or new area of FDG avidity ([Fig. 19]) at the tumor bed or surgical flap margins, lymphadenopathy ([Fig. 20]), or evidence of new bone or cartilage destruction ([Fig. 21]) must be viewed with suspicion for recurrence. Recurrence can also occur uniquely in the head and neck region in the form of perineural spread ([Fig. 22]).
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Conclusion
RT continues to remain the workhorse in the treatment of head and neck carcinomas. Even with the newer RT techniques that are aimed at reducing therapy–related morbidities, some effects are inevitable. The most common and important findings encountered in the treated head and neck include changes in the mucosa, soft tissues, glands; changes in bony and cartilaginous structures; damage to nervous systems; and vascular systems and radiation-induced neoplasms. Many of these findings may be initially identified at imaging alone and therefore, familiarity with these spectrums of changes is important and so is differentiating them for tumor recurrence.
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Conflicting Interest
None declared.
Acknowledgments
The authors would like to thank Drs. Aditi Chandra and Dayananda Lingegowda for their contribution in design and conception. The authors would like to thank Drs. Priya Ghosh, Argha Chatterjee, and Bharat Gupta for reviewing the manuscript and for adding to the intellectual content.
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References
- 1 Saito N, Nadgir RN, Nakahira M. et al. Posttreatment CT and MR imaging in head and neck cancer: what the radiologist needs to know. Radiographics 2012; 32 (05) 1261-1282 , discussion 1282–1284
- 2 Peter M.Som, Eric M.Genden. The Posttreatment Neck: Clinical and Imaging Considerations. Peter M. Som and Hugh D. Curtin editors. Head and Neck Imaging. 2011. Mosby Elsevier. 5th edition. Volume 2; 2249-2250
- 3 Kim J, Shin ES, Kim JE, Yoon SP, Kim YS. Neck muscle atrophy and soft-tissue fibrosis after neck dissection and postoperative radiotherapy for oral cancer. Radiat Oncol J 2015; 33 (04) 344-349
- 4 Benveniste MF, Gomez D, Carter BW. et al. Recognizing radiation therapy-related complications in the chest. Radiographics 2019; 39 (02) 344-366
- 5 Alhilali L, Reynolds AR, Fakhran S. Osteoradionecrosis after radiation therapy for head and neck cancer: differentiation from recurrent disease with CT and PET/CT imaging. AJNR Am J Neuroradiol 2014; 35 (07) 1405-1411
- 6 Chrcanovic BR, Reher P, Sousa AA, Harris M. Osteoradionecrosis of the jaws–a current overview–part 1: physiopathology and risk and predisposing factors. Oral Maxillofac Surg 2010; 14 (01) 3-16
- 7 Glastonbury CM, Parker EE, Hoang JK. The postradiation neck: evaluating response to treatment and recognizing complications. AJR Am J Roentgenol 2010; 195 (02) W164-71
- 8 Dassarath M, Yin Z, Chen J, Liu H, Yang K, Wu G. Temporal lobe necrosis: a dwindling entity in a patient with nasopharyngeal cancer after radiation therapy. Head Neck Oncol 2011; 3: 8
- 9 Wang Y-XJ, King AD, Zhou H. et al. Evolution of radiation-induced brain injury: MR imaging-based study. Radiology 2010; 254 (01) 210-218
- 10 Shah R, Vattoth S, Jacob R. et al. Radiation necrosis in the brain: imaging features and differentiation from tumor recurrence. Radiographics 2012; 32 (05) 1343-1359
- 11 Zhao F, Bu L, Zhang W. et al. Herpes simplex encephalitis during radiation therapy in a patient with nasopharyngeal carcinoma. Transl Cancer Res 2017; 6 (06) 1149-1155
- 12 Sermer DJ, Woodley JL, Thomas CA, Hedlund JA. Herpes simplex encephalitis as a complication of whole-brain radiotherapy: a case report and review of the literature. Case Rep Oncol 2014; 7 (03) 774-779
- 13 Dropcho EJ. Neurotoxicity of radiation therapy. Neurol Clin 2010; 28 (01) 217-234
- 14 Warade AC, Jha AK, Pattankar S, Desai K. Radiation-induced brachial plexus neuropathy: A review. Neurol India 2019; 67 (suppl): S47-S52
- 15 Wilbers J, Kappelle AC, Kessels RP. et al. Long term cerebral and vascular complications after irradiation of the neck in head and neck cancer patients: a prospective cohort study: study rationale and protocol. BMC Neurol 2014; 14: 132
- 16 Suárez C, Fernández-Alvarez V, Hamoir M. et al. Carotid blowout syndrome: modern trends in management. Cancer Manag Res 2018; 10: 5617-5628
- 17 Choi HS, Jeong BK, Jeong H. et al. Carotid sparing intensity modulated radiotherapy on early glottic cancer: preliminary study. Radiat Oncol J 2016; 34 (01) 26-33
- 18 Gujral DM, Shah BN, Chahal NS, Senior R, Harrington KJ, Nutting CM. Clinical features of radiation-induced carotid atherosclerosis. Clin Oncol (R Coll Radiol) 2014; 26 (02) 94-102
- 19 Thiagarajan A, Iyer NG. Radiation-induced sarcomas of the head and neck. World J Clin Oncol 2014; 5 (05) 973-981
Address for correspondence
Publication History
Article published online:
06 October 2021
© 2021. Indian Radiological Association. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)
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References
- 1 Saito N, Nadgir RN, Nakahira M. et al. Posttreatment CT and MR imaging in head and neck cancer: what the radiologist needs to know. Radiographics 2012; 32 (05) 1261-1282 , discussion 1282–1284
- 2 Peter M.Som, Eric M.Genden. The Posttreatment Neck: Clinical and Imaging Considerations. Peter M. Som and Hugh D. Curtin editors. Head and Neck Imaging. 2011. Mosby Elsevier. 5th edition. Volume 2; 2249-2250
- 3 Kim J, Shin ES, Kim JE, Yoon SP, Kim YS. Neck muscle atrophy and soft-tissue fibrosis after neck dissection and postoperative radiotherapy for oral cancer. Radiat Oncol J 2015; 33 (04) 344-349
- 4 Benveniste MF, Gomez D, Carter BW. et al. Recognizing radiation therapy-related complications in the chest. Radiographics 2019; 39 (02) 344-366
- 5 Alhilali L, Reynolds AR, Fakhran S. Osteoradionecrosis after radiation therapy for head and neck cancer: differentiation from recurrent disease with CT and PET/CT imaging. AJNR Am J Neuroradiol 2014; 35 (07) 1405-1411
- 6 Chrcanovic BR, Reher P, Sousa AA, Harris M. Osteoradionecrosis of the jaws–a current overview–part 1: physiopathology and risk and predisposing factors. Oral Maxillofac Surg 2010; 14 (01) 3-16
- 7 Glastonbury CM, Parker EE, Hoang JK. The postradiation neck: evaluating response to treatment and recognizing complications. AJR Am J Roentgenol 2010; 195 (02) W164-71
- 8 Dassarath M, Yin Z, Chen J, Liu H, Yang K, Wu G. Temporal lobe necrosis: a dwindling entity in a patient with nasopharyngeal cancer after radiation therapy. Head Neck Oncol 2011; 3: 8
- 9 Wang Y-XJ, King AD, Zhou H. et al. Evolution of radiation-induced brain injury: MR imaging-based study. Radiology 2010; 254 (01) 210-218
- 10 Shah R, Vattoth S, Jacob R. et al. Radiation necrosis in the brain: imaging features and differentiation from tumor recurrence. Radiographics 2012; 32 (05) 1343-1359
- 11 Zhao F, Bu L, Zhang W. et al. Herpes simplex encephalitis during radiation therapy in a patient with nasopharyngeal carcinoma. Transl Cancer Res 2017; 6 (06) 1149-1155
- 12 Sermer DJ, Woodley JL, Thomas CA, Hedlund JA. Herpes simplex encephalitis as a complication of whole-brain radiotherapy: a case report and review of the literature. Case Rep Oncol 2014; 7 (03) 774-779
- 13 Dropcho EJ. Neurotoxicity of radiation therapy. Neurol Clin 2010; 28 (01) 217-234
- 14 Warade AC, Jha AK, Pattankar S, Desai K. Radiation-induced brachial plexus neuropathy: A review. Neurol India 2019; 67 (suppl): S47-S52
- 15 Wilbers J, Kappelle AC, Kessels RP. et al. Long term cerebral and vascular complications after irradiation of the neck in head and neck cancer patients: a prospective cohort study: study rationale and protocol. BMC Neurol 2014; 14: 132
- 16 Suárez C, Fernández-Alvarez V, Hamoir M. et al. Carotid blowout syndrome: modern trends in management. Cancer Manag Res 2018; 10: 5617-5628
- 17 Choi HS, Jeong BK, Jeong H. et al. Carotid sparing intensity modulated radiotherapy on early glottic cancer: preliminary study. Radiat Oncol J 2016; 34 (01) 26-33
- 18 Gujral DM, Shah BN, Chahal NS, Senior R, Harrington KJ, Nutting CM. Clinical features of radiation-induced carotid atherosclerosis. Clin Oncol (R Coll Radiol) 2014; 26 (02) 94-102
- 19 Thiagarajan A, Iyer NG. Radiation-induced sarcomas of the head and neck. World J Clin Oncol 2014; 5 (05) 973-981
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