Deglutition Syncope: A Manifestation of Vagal Hyperactivity Following Carotid Endarterectomy

Abstract

Background: Transient hypotension and bradycardia after carotid endarterectomy (CEA) is related to increased baroreceptor 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 after CEA. Case report: A 61-year-old man presented with left amaurosis fugax and bilateral >80% internal carotid artery stenoses. His surgical history was significant for a right CEA 12 years previously. After an uneventful left CEA, 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. Results of an electrocardiogram, computed tomography (CT) scan with pulmonary embolism protocol, cardiac isoenzyme analysis, and echocardiogram were normal. His blood pressure, chest pain, and vision loss responded initially to the administration of pressors. During the next day, similar symptoms developed each time he attempted to eat. With initiation of anticholinergic medication, he was able to eat without symptoms. Results of a barium swallow were normal. The patient's symptoms resolved, and the anticholinergic medication was discontinued. The patient underwent an uneventful right CEA 3 months later. He was hemodynamically and neurologically stable during the procedure and postoperatively. The morning after the CEA, diaphoresis, hypotension, and tachycardia again developed when he began eating breakfast. Anticholinergic medications were again initiated and all symptoms resolved ≤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 CEA are widely patent. Conclusions: Increased vagal tone after CEA, mediated by hypersensitivity of the baroreceptors 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 solitarius within the medulla. The glossopharyngeal nerve also transmits afferent impulses from the esophagus. We hypothesize that after CEA, our patient had a transient increase in afferent activity to the nucleus tractus solitarius related to changes of the carotid baroreceptor. With additional glossopharyngeal afferent activity associated with swallowing, deglutition syncope developed. Deglutition syncope is considered an unusual manifestation of vasovagal episodes and usually has been reported in association with esophageal, cardiac, and thoracic aortic abnormalities. To our knowledge, this patient is the first case of deglutition syncope reported after CEA. Because deglutition syndrome can be associated with esophageal abnormalities, a barium swallow should be evaluated. Clinicians should be aware of and know how to address this rare complication of CEA.