Deglutition Syncope: A Manifestation of Vagal Hyperactivity Following Carotid Enarterectomy

BACKGROUND: Transient hypotension and bradycardia following carotid endarterectomy (CEA) is related to increased barorecptor activity at the carotid bifurcation. These symptoms, mediated by afferent impulses through the nerve of Hering, result from increased vagal activity. We report a case of deglutition syncope following carotid endarterectomy.
CASE: A 61 year-old man presented with left amarousis fugax and bilateral >80% internal carotid artery stenoses. Past surgical history was significant for a right CEA 12 years previously. An uneventful left CEA was performed and upon completion of the procedure, he was hemodynamically stable and without neurologic deficits. On the first postoperative day, the patient experienced crushing chest pain, bradycardia, hypotension and bilateral vision loss as he began to eat breakfast. ECG, CT scan with PE protocol, cardiac isoenzymes, and echocardiogram were normal. His blood pressure, chest pain and vision loss responded initially to administration of pressors. Over the next day, he developed similar symptoms each time he attempted to eat. With initiation of anticholenergic medication, he was able to eat without symptoms. A barium swallow was obtained and was normal. The patient’s symptoms resolved and he was taken off the anticholenergic medication. Three months later, the patient underwent an uneventful right CEA. He was hemodynamically and neurologically stable during the procedure and postoperatively. The morning following his endarterectomy, he again developed diaphoresis, hypotension and tachycardia when eating breakfast. The patient was restarted on anticholenergic medications and all symptoms resolved within 48 hours.
RESULTS: The patient has been seen in follow up. He has had no further episodes of deglutition syncope or other neurologic symptoms. His endarterectomy sites are widely patent.
CONCLUSIONS: Increased vagal tone following CEA, mediated by hypersensitivity of the barroreceptors of the carotid sinus, is well described. The nerve of Hering, an afferent branch of the glossopharyngeal nerve, synapses with efferent fibers of the vagus nerve in the nucleus tractus solitanius within the medulla. The glossopharyngeal nerve also transmits afferent impulses from the esophagus. We hypothesize that following CEA, our patient had a transient increase in afferent activity to the nucleus tractus solitanius related to changes of the carotid barorecptor. With additional glossopharyngeal afferent activity associated with swallowing, he developed deglutition syncope. Deglutition syncope is felt to be an unusual manifestation of vasovagal episodes and usually has been reported in association with esophageal, cardiac, and thoracic aortic abnormalities. This patient is the first case of deglutition syncope reported following carotid endarterectomy. Because deglutition syndrome can be associated with esophageal abnormalities, a barium swallow should be obtained. Clinicians should be aware of and know how to address this rare complication of CEA.