The imaging presentation of head and neck oncologic emergencies

Special considerations in post-treatment patients

Post-treatment patients can have different etiologies of airway obstruction. Post-surgical airway compromise is not an uncommon phenomenon in the post-anesthesia care unit and relies heavily on clinical/endoscopic evaluation.^[7] On the other hand, radiation injury tends to arise more insidiously, requiring imaging to play a critical role in identification and subsequent management.

Radiation therapy, either alone or combined with chemotherapy or surgery, is utilized in the vast majority of squamous cell cancer (SCC) HNC patients. Radiation damages endothelial cells lining small blood vessels, leading to ischemia, edema, and ultimately fibrosis. In the early post-radiation period, this endothelial damage results in disruption of the venous and lymphatic drainage and results in significant interstitial edema, most commonly manifested on computed tomography (CT) as reticulations within the subcutaneous fat or thickening of the dermis along the port trajectory.^[8] Consequently, an emergent presentation can occur when there is an accumulation of laryngeal or retropharyngeal edema-resulting in acute airway compromise. Key clinical information that can help clarify the clinical scenario includes radiation timing and dosage. There is a significant increase in the risk of edema with increased radiation dose, leading some authors to recommend 43.5 Gy or below at 2 Gy/fraction to reduce this risk.^[9] Early edematous changes typically occur between 2 and 12 weeks of treatment [Figure 3] and chronic laryngeal edema has been found to have a median observation time of 36 weeks.^[10] Additional sequelae, such as osteoradionecrosis peak at 1 year after treatment, and are further discussed below.

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Figure 3:

A 62-year-old man with biopsy-proven squamous cell carcinoma status post high-dose radiation treatment. Computed tomography (CT) images demonstrate submucosal edema in the posterior pharyngeal wall causing supraglottic airway stenosis (b), which progressed from the prior CT soft tissues of the neck approximately 6 months prior (a). Imaging was obtained just over 2 weeks into the start of a 6-week radiation treatment course. (CT: computed tomography)

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Temporal variability in symptom onset

An important point must be considered when regarding the variability in the timing of the aforementioned post-radiation changes. For example, osteoradionecrosis has been reported in patients up to 50 years after treatment.^[11] While the typical onset of chronic laryngeal edema is less than a year as described above, [Figure 4] demonstrates an emergent presentation of a 63-year-old man who developed acute symptoms of increased dyspnea and inability to speak in full sentences which occurred 3.5 years after chemoradiation treatment.

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Figure 4:

A 63-year-old man with a history of p16 positive tonsillar squamous cell cancer s/p chemoradiation, completed 3.5 years prior. Serial outpatient cancer surveillance endoscopies showed stable curled epiglottis and arytenoid edema. Later, the patient presented acutely with several hours of increased dyspnea and inability to speak in full sentences. In (a and b) sagittal and axial contrast-enhanced computed tomography images demonstrate severe edema of the supraglottic airway (white arrow), bilateral aryepiglottic folds (white arrowhead), and vocal folds (white arrow). (c) Reformatted images of endoscopic view with left greater than right supraglottic obstruction (large white arrow). (d) Endoscopic images after emergent tracheostomy and 12 h of racemic epinephrine and Decadron still demonstrate significant edema through the supraglottic larynx and a curled “omega-shaped” epiglottis that collapses with inspiration (small white arrows).

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Venous occlusion/thrombus

As with most malignancies, HNC tumors exhibit a propensity for thrombogenicity. However, in contrast to most thrombogenic cancers that result in distant phlebitis or thromboembolism, HNC more commonly exerts local effects.^[12] While it is poorly understood why HNC is associated with local rather than distant thrombosis, this phenomenon is well demonstrated in clinical practice. For example, head and neck tumors more commonly result in venous obstruction secondary to external compression of the internal jugular vein (IJV) due to SCC metastatic lymph nodes [Figure 5]. Moreover, when venous thrombosis arises, particularly involving the lower IJV at the neck base, it becomes, especially important for the radiologist to follow the venous system down toward the superior vena cava (SVC) to look for evidence of SVC syndrome or mediastinal tumor involvement.

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Figure 5:

A 41-year-old woman with a history of metastatic melanoma status post-chemotherapy. (a) Sonography demonstrates a thrombus in the lower internal jugular vein (IJV), extending into the brachiocephalic vein. (b) Axial contrast-enhanced computed tomography image demonstrates a large necrotic lymph node (black arrow) compressing and nearly completely occluding the left IJV (black arrowhead).

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Extratumoral extension into vascular structures can also result in a tumor thrombus precipitating vascular compromise, and this has been described in both the carotid artery and IJV.^[13] Although infrequently seen with head and neck SCC, tumor thrombus has also been well described in the setting of differentiated thyroid cancer [Figure 6]. A key consideration in cases of suspected tumoral vascular invasion is utilizing the correct imaging modality. CT may provide high specificity, but there may be lower sensitivity when detecting vascular invasion, particularly when compared to other imaging modalities, such as ultrasound, which are readily available in the ED.^[14]

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Figure 6:

A 58-year-old man with a history of metastatic renal cell carcinoma presenting with palpable nodular enlargement of the thyroid gland as well as a left neck mass. (a) Axial computed tomography images demonstrate multinodular enlargement of the thyroid gland with extracapsular extension on the left into the adjacent visceral space, suspicious for tumor extension into the left internal jugular vein (IJV) (tumor thrombus, white and black arrows). (b and c) Ultrasound performed demonstrates contiguous extension of tumor from the thyroid into the left IJV with color Doppler showing increased vascularity throughout the tumor thrombus.

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Special considerations in post-treatment patients

Carotid blowout (CBO)

Common etiologies for CBO include radical resection, radiation necrosis, carotid exposure, wound infection, pharyngocutaneous fistula, and recurrent tumors. In addition, this can present after neck dissection (overall incidence of ~4.3%). While prior radiation has been shown to be an independent risk factor for CBO, overall risk has also been shown to increase substantially (7.6-fold) following neck dissection in patients with prior radiation.^[15] CBO is classically divided into three categories: Threatened, impending, and acute.^[16] Threatened CBO has imaging or clinical evidence of carotid at risk for rupture with the patient remaining asymptomatic. Common imaging findings include necrotic tissue/tumor adjacent to a vessel or the presence of a pharyngocutaneous fistula adjacent to a vessel. Impending CBO consists of transient bleeding that resolves spontaneously or with packing/pressure. Imaging may show a focal pseudoaneurysm without active bleeding or visible hematoma [Figure 7].^[17] Acute CBO is the presence of uncontrollable hemorrhage requiring surgical/endovascular intervention. Imaging often shows active contrast extravasation at the site of vessel injury. Although the radiologist has a key role in the workup of all three types, identifying a threatened CBO can be the most beneficial as this diagnosis may preclude clinical suspicion.

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Figure 7:

A 72-year-old man with a history of laryngeal squamous cell cancer after chemoradiation who subsequently developed laryngeal recurrence now status post salvage laryngectomy, pharyngectomy, and partial glossectomy is presenting with balance issues and ear pain. (a) Axial computed tomography angiogram of the neck demonstrates focal dissecting pseudoaneurysm of the right common carotid artery (CCA) (white arrow) with adjacent soft-tissue gas/necrosis (black arrowhead). Soft-tissue findings alone warrant prompt notification by the radiologist as this finding represents a threatened blowout. In this instance, a dissecting pseudoaneurysm elevates this to an impending blowout. (b) Digital subtraction angiography (DSA) demonstrates clear active extravasation from mid-CCA, representing an acute carotid blowout requiring intervention (black arrow). (c) DSA post-treatment shows covered stent graft placement.

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Carotid stenosis/occlusion

In the delayed phase, radiation increases the intima-media thickness and rapidly accelerates atherosclerosis,^[18] which can result in progressive stenosis or thrombotic occlusion. Occlusion has been reported up to 10 years after treatment,^[19] and can be seen in patients with no other concurrent risk factors.^[20] In addition, adjacent soft-tissue radiation changes such as perivascular circumferential soft-tissue formation may provide subtle clues of this particular etiology. Figure 8 demonstrates progressive carotid artery occlusion in a patient following chemoradiation. Fortunately, this patient demonstrated reconstitution of flow at the cavernous segment of the internal carotid artery due to the formation of collaterals.

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Figure 8:

A 77 year old male (a) Demonstrates atherosclerotic disease within the left internal carotid artery with a focal 60% stenosis of the proximal portion. (b) Demonstrates complete occlusion of the left internal carotid artery at this level approximately 1 year later. The images demonstrate the rapid rate of occlusive changes in patients with prior radiation. The patient received 60 Gy over 30 fractions to the right surgical bed and cervical lymph node levels I–V, as well as 52.5 Gy over 30 fractions to the left cervical lymph node levels II–IV.

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Special considerations in post-treatment patients

Osteoradionecrosis has been reported in the cervical spine following radiotherapy for HNC, of which nasopharyngeal carcinoma is most commonly described.^[23] Common presenting symptoms include neck pain, kyphosis, paresthesia, discitis/osteomyelitis, fracture, and cord compression. This often has a subacute or chronic course, occurring between 4 and 48 months after treatment. Key imaging findings are similar to discitis/osteomyelitis, with mixed sclerotic-lucent appearance and bone destruction. Often confounded by secondary discitis/osteomyelitis, a subtle differentiating imaging feature can be the absence of fluid in the disc spaces. However, tissue sampling is often needed to exclude the presence of infection as findings can be nearly identical. Figure 11 demonstrates progressive cervical destruction at the C5–6 level in subsequent outpatient images. This patient was noted to have negative blood cultures and even demonstrated no culture growth on biopsy. The patient was later taken for cervical decompression and fusion due to concern for spinal instability. This case emphasizes how unrecognized cervical spine osteoradionecrosis can result in instability necessitating surgical fixation. In addition, magnetic resonance imaging demonstrates no fluid in the intervertebral disc spaces, which is not a specific finding but can support the diagnosis of osteoradionecrosis over osteomyelitis.

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Figure 11:

A 56-year-old woman with a history of laryngeal cancer after total laryngectomy and adjuvant radiation completed 2 years prior presents with neck pain. (a-c) sagittal computed tomography neck in the bone window showing the progression of osteoradionecrosis 3, 7, and 10 months after radiation. (d and e) MRI images show heterogeneous short tau inversion recovery signal, a non-enhancing prevertebral collection spanning C4–C5, mixed sclerosis, and edema/enhancement with the C3–C5 vertebral body marrow. Notably, there is no fluid in the disc spaces, which would be more suggestive of infection.

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