Dysphagia 20:238–240 (2005) DOI: 10.1007/s00455-005-0014-0
Case Report
Swallow-Induced Syncope in a Patient with Achalasia Ilker Turan, MD,1 Galip Ersoz, MD,2 and Serhat Bor, MD2 1
Department of Internal Medicine, and 2Division of Gastroenterology, Faculty of Medicine, Ege University, Bornova, Izmir, Turkey
Abstract. A 48-year-old man was referred for the evaluation of dysphagia and syncope. He suffered from both dysphagia and transient loss of consciousness when eating solid food, especially bread. An upper gastrointestinal barium examination and esophageal manometry suggested achalasia. Ambulatory ECG revealed marked sinus bradycardia when experiencing a syncopal episode following the ingestion of a solid meal. A permanent pacemaker was implanted and the patientÕs syncopal attacks were relieved following this procedure. However, the dysphagia and cardiac arrhythmia completely disappeared only following a successful pneumatic balloon dilatation for achalasia. This observation suggests that swallowing-induced sinus bradycardia and syncope might occur in the course of achalasia and these rhythm abnormalities could be relieved by successful treatment of the achalasia. Key words: Achalasia — Syncope — Arrhythmia — Esophagus — Deglutition — Deglutition disorders.
Swallow-induced syncope is a rare clinical condition. Deglutition or swallowing syncope is loss of consciousness on swallowing, which is thought to be associated with an abnormal vasovagal reflex that might be related to transient bradycardia [1–3]. An underlying abnormality of the esophageal or cardiac conduction system could be responsible in most cases [4,5]. We report an unusual achalasia patient in which syncope and dysphagia occurred soon after the ingestion of solid food.
Correspondence to: I. Turan, Department of Internal Medicine, Faculty of Medicine, Ege University, 35040, Bornova, Izmir, Turkey, E-mail:
[email protected]
Case Report A 48-year-old man had a two-year history of nonprogressive dysphagia, especially with solid foods, without odynophagia or weight loss. There was no history of medication. Upper gastrointestinal endoscopy revealed esophagitis (grade A). An upper gastrointestinal series showed tertiary contractions in the esophagus. Eighteen months later, transient loss of consciousness began to accompany the dysphagia when eating solid foods; this occurred once or twice a week. The patient sustained some episodes of minor head trauma during these syncope attacks. Cranial MRI showed an empty sella. The levels of cortisol, prolactin, FSH, LH, ACTH, and growth hormone were found to be within normal limits. The patient was referred to our hospital, at which time physical examination was unremarkable. The pulse rate was 72/ min. He was normotensive and had a normal cardiac examination. The body mass index was 27. Routine laboratory tests, including urinalysis and hematologic and biochemical tests, were within normal limits. Chest X-ray, upper abdominal ultrasonography, and upper gastrointestinal endoscopy yielded no abnormal findings. ECG (Fig. 1) and echocardiography were normal. The barium swallow study showed the esophageal body to be dilated: the barium column terminated in a tapered point, resembling a ‘‘birdÕs beak.’’ Fluoroscopy with a barium meal revealed no peristalsis in the esophageal body and complete clearing of the barium meal took 30 minutes. The lower esophageal sphincter (LES) pressure was 26 mmHg and relaxation was incomplete as assessed by esophageal manometry. There were no propagative waves and a complete low-amplitude simultaneous peristalsis sequence was observed (Fig. 2). Since the syncopal episodes were initiated by solid foods, the patient was asked to eat a slice of bread while he was being monitored by electrocardiograph. Five to ten seconds after the intake of bread, abrupt bradycardia and hypotension developed, and marked sinus bradycardia was detected on ECG (Fig. 3). Liquid foods (hot or cold) did not lead to bradycardia. Twentyfour-hour ambulatory ECG recordings revealed sinus bradycardia arrest only when he ate bread, with accompanying faintness on three occasions. His heart rate was 15 beats/min at these times (Fig. 4). A permanent pacemaker was implanted resulting in the resolution of syncopal attacks. However, dysphagia persisted. Pneumatic dilatation was performed and from two days thereafter the patient did not suffer from dysphagia with the intake of solid food. His heart rate did not change while being monitored by ECG and no triggering of the pacemaker was
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Fig. 1. ECG was normal at the time of admission.
Fig. 3. ECG monitoring during the meal. Marked sinus bradycardia was observed.
Fig. 2. Esophageal manometry showed simultaneous peristalsis without any propagative waves with swallows.
observed. The esophageal clearance was found to be within normal limits as assessed by barium swallow. The LES pressure dropped to 15 mmHg. The patient was discharged without symptoms and 24-hour Holter monitoring remained normal two months later. The patient remains asymptomatic after 18 months of followup.
Discussion A patient with achalasia who had serious syncopal attacks because of sinus bradycardia while eating solid foods has been presented. Initially, he suffered only from dysphagia. Syncopal attacks triggered by meals started 18 months after the start of dysphagia. Uncoordinated simultaneous contractions mimicking the configuration of ‘‘corkscrew esophagus’’ suggested diffuse esophageal spasm had been established in an upper gastrointestinal series at the beginning of the nonsyncopal period. At this time, both the radiologic appearance and the esophageal manometric study confirmed the presence of achalasia during the syncopal period. Pneumatic balloon dilatation was clearly successful in achieving the relief of dysphagia and possibly of the cardiac arrhythmias.
Fig. 4. Continuous recording of Holter monitoring while patient was swallowing revealed sinus bradycardia. The maximum pause detected in the tracing was 5s.
The latter claim is supported by two episodes of 24hour Holter monitoring over two months, both of which showed neither abnormalities of rhythm nor pacemaker beats. The most common cardiac pathologies associated with deglutitive syncope are ischemic heart disease, inferior myocardial infarction, and conduction disturbances producing heart block [6]. The arrhythmias provoked by swallowing which may lead to syncope include various degrees of A-V block, nodal or sinus bradycardia, ventricular asystole, and atrial fibrillation [7]. Our search of the literature revealed only one case in the English literature relating to syncope-associated dysphagia caused by achalasia [8]. The afferent pathway of the abnormal reflex is thought to involve the glossopharyngeal or vagus nerve in swallow-induced syncope [6,7,9]. The former may be associated with glossopharyngeal neuralgia [1], the latter may be a result of mechanical irritation caused by esophageal distension or spasm, thereby inducing intense vagal afferent activation [10–14]. Esophageal distension can be profound in achalasia; thus, esophageal compression can cause respiratory distress through the compression of the trachea and recurrent laryngeal nerve paralysis, especially in mega-esophagus
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caused by achalasia [15–18]. In our patient, syncope accompanied swallowing, suggesting that the afferent pathway is within the esophagus. The patient did not have glossopharyngeal neuralgia. Only solid meals, especially the eating of bread, induced the syncopal attack. The proposed mechanism responsible for reflex syncope might be activation of mechanoreceptors, which causes vagal afferent stimulation; it has been theorized that incoming sensory fibers along the vagus nerve may have artificially synapsed with efferent vagal fibers to the heart. This stimulation leads to sympathetic withdrawal and parasympathetic efferent activation resulting in peripheral vascular dilatation, hypotension, and sinus bradycardia or atrioventricular block [9,19,20]. References 1.
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