Case Presentation:

A 63‐year‐old man with a history of locally advanced (T4 — deep muscle invasion, N2b — multiple ipsilateral neck lymph nodes, M0), left‐sided base‐of‐tongue squamous cell cancer presented to the emergency room with multiple episodes syncope over several weeks. He was treated with chemoradiation 6 months prior to current admission. Follow‐up imaging after chemoradiation showed progressive disease. He was then started on palliative cetuximab 1 month prior to current admission. During current admission, workup for syncope was commenced. EKG and cardiac enzymes were negative. There were no events on telemetry. Review of his last CT scan from 4 months prior to admission showed encasement of left carotid artery. A repeat CT scan of his neck was performed. It showed remarkable tumor progression with extensive lymphadenopathy and compression of both of his carotid arteries by a combination of tumor burden, lymph nodes, and postradiation edema. Surgical resection of the mass and local radiation therapy were both deemed inappropriate due to location of tumor and its relative radio‐resistance in the past. In addition, there was concern that radiation could cause worsening edema and precipitous worsening of patient's condition by causing complete occlusion of the carotid arteries. This information was discussed with patient and his wife and he is currently in home hospice. In the 2 weeks since discharge, he feels he has been able to minimize further episodes of syncope by limiting and modifying his activities.


Recurrent syncope due to malignancy is uncommon. Head and neck cancer can lead to recurrent syncope by 2 mechanisms. Neurally mediated syncope can occur due to carotid body invasion or involvement of the vagus nerve. Syncope due to reduced blood flow in carotid arteries is uncommon and requires involvement of both carotids. Although it is possible that our patient was passing out due to tumor pressure mediated firing of baroreceptors in his carotid bodies, we think reduced carotid blood flow was the more likely culprit. This is based on that he only started having syncopal events after involvement of his contralateral carotid artery. Finally, our case highlights the importance of imaging the carotid arteries in patients with history of head and neck cancer who present with syncope. Imaging of carotid arteries is not merited during routine diagnostic workup of syncope unless a neurological event is suggested by history or if focal signs and symptoms are present. However, such an evaluation should be considered in patients who have a history of head and neck cancer, especially if the cancer has been relatively resistant to treatment or locally advanced in the past.


Aggressive oropharyngeal cancer can lead to syncope. Our case illustrates a rare clinical scenario in which evaluation of carotid arteries is an appropriate part of syncope workup.