Swallow syncope after laparoscopic vertical sleeve gastrectomy

Rezvani, Masoud; Casillas, Sergio; Antanavicius, Gintaras

doi:10.1016/j.soard.2013.03.002

Cited by 3 publications

(4 citation statements)

References 9 publications

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“…The exact mechanism remains to be elucidated, however, excessive parasympathetic stimulation to the heart seems to be the central mechanism. The fact that atropine, a potent anticholinergic agent, prevents bradyarrhythmia effectively in cases of swallow syncope supports the theory of excessive vagal stimulations [5, 29, 66, 79].…”

Section: Discussionmentioning

confidence: 82%

Swallow syncope: a case report and review of literature

Siew

Tan

Hilmi

et al. 2019

BMC Cardiovasc Disord

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Background Swallow or deglutition syncope is an unusual type of neurally-mediated syncope associated with life-threatening bradyarrhythmia and hypotension. It is a difficult condition to diagnose with commonly delayed diagnosis and management. There is lack of review articles that elucidate the basic demographics, clinical characteristics and management of this rare condition. This publication systematically reviews the 101 case reports published since 1793 on swallow syncope. Case presentation A 59-year-old man presented with the complaint of recurrent dizziness associated with meals. A 24-h ambulatory ECG recording confirmed an episode of p-wave asystole at the time of food intake. Oesophagogastroduodenoscopy with balloon inflation in the mid to lower oesophagus resulted in a 5.6 s sinus pause. The patient’s symptoms resolved completely following insertion of a permanent dual chamber pacemaker. Conclusions Swallow syncope is extremely rare, but still needs to be considered during diagnostic workup. It is commonly associated with gastro-intestinal disease. Permanent pacemaker implantation is the first line treatment.

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Section: Discussionmentioning

confidence: 82%

Swallow syncope: a case report and review of literature

Siew

Tan

Hilmi

et al. 2019

BMC Cardiovasc Disord

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“…The studies evaluating the effects of bariatric surgery have consistently shown decreased orthostatic tolerance and increased propensity to NCS following both malabsorptive and restrictive surgical procedures (9)(10)(11)(12)(13)(14)(15)(16)(17). The impact of bariatric surgery on the predisposition to OI and NCS was indicated by the fact that the affected individuals had no relevant history prior to surgery, as well as by the reported resolution of postoperative symptoms of OI after removal or even simple adjustment of gastric band accompanied with weight regain (9,10,12).…”

Section: Bariatric Surgerymentioning

confidence: 99%

“…Onset of symptoms of OI has been reported to occur up to 3 years after bariatric surgery, although it appears to arise mostly within the first postoperative year . The main mechanism underlying OI after bariatric surgery is possibly inappropriate peripheral vasodilation, while excessive bradycardia or pauses have occasionally been reported as the cause of postoperative syncope .…”

Section: The Effects Of Body Weight Status On Orthostatic Intolerancementioning

confidence: 99%

“…Regarding the impact of body weight status on OI, crosssectional studies investigating the relationship between orthostatic responses and body mass index (BMI) found conflicting results (3)(4)(5)(6)(7)(8). Moreover, studies evaluating the effects of bariatric surgery have consistently reported increased OI and propensity to NCS after surgically induced weight loss, although these studies were only case reports or they had a small number of participants (9)(10)(11)(12)(13)(14)(15)(16)(17). No previous review article has investigated the issue of the effects of body weight status on OI and propensity to NCS.…”

Section: Introductionmentioning

confidence: 99%

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The effects of body weight status on orthostatic intolerance and predisposition to noncardiac syncope

Christou

Kiortsis

2017

Obesity Reviews

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Orthostatic intolerance (OI) is frequently the mechanism underlying the occurrence of noncardiac syncope (NCS) and is associated with substantial risk for injury. Body weight status appears to be a modifier of orthostatic responses and possibly influences the propensity to NCS. The majority of cross-sectional studies have found that the lower the body mass index (BMI) the greater the predisposition to OI is, accompanied with both down-regulation of sympathetic nervous system activity and up-regulation of parasympathetic nervous system activity. These changes appear to occur across the whole spectrum of BMI values from underweight to obesity, while they may be associated more strongly with central body fat than total body fat. Weight loss following bariatric surgery has been consistently found to increase OI, attributed first to the effects of weight loss per se, second to the specific type of surgical procedure and third to the potential postoperative autonomic neuropathy due to vitamin deficiency. The increased OI following bariatric surgery renders this intervention not easily tolerable for the affected individuals, mandating increased fluid and salt intake, pharmacological measures or surgical adjustments to attenuate OI. All future studies investigating orthostatic responses and NCS should implement a matching of the population arms for BMI and ideally for body fat.

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