AN INTERESTING CASE OF RECURRENT POSTPRANDIAL CARDIOGENIC SYNCOPE CAUSED BY TYPE III HIATAL HERNIA

Document Type

Conference Proceeding

Publication Date

6-23-2023

Publication Title

J Gen Intern Med

Abstract

CASE: 92 years-old female with past medical history of medium-size hiatal hernia (HH) presents with recurrent episodes of syncope, immediately after heavy meals, for 4 weeks. Patient denied any prodromal symptoms, bowel/bladder incontinence, tongue biting, or seizure-like activity. On presentation patient was hemodynamically stable, orthostatics negative, physical exam was unremarkable. EKG & cardiac telemetry were unremarkable. Lab work was remarkable for baseline anemia (Hb:8g/dl). CT brain did not show any acute changes. A CT scan chest, abdomen & pelvis showed a large HH with a largely intrathoracic stomach adjacent to left atria (LA) without gastric outlet obstruction.

IMPACT/DISCUSSION: Syncope is a sudden & brief loss of consciousness with spontaneous recovery. Detailed history & physical exam are pivotal in diagnosis. The differential diagnosis of syncope is broad. It includes neurologic & cardiovascular differentials. Precipitating factor aids in diagnosis. Deglutition syncope is either a neurally mediated syncope precipitated by vagal nerve stimulation during swallowing or caused by pressure on LA as a result of pressure from HH. HH is the protrusion of abdominal organs, mostly the stomach, into the mediastinum through diaphragmatic esophageal hiatus. It is usually asymptomatic & discovered incidentally. Type III HH is when both fundus & gastroesophageal junction herniate through the hiatus. In this case, the patient had no orthostatic hypotension, arrhythmias, or seizures, however, the history of HH & symptoms precipitated by large meals led to the hypothesis of deglutition syncope. In our patient, the size & location of HH led to postprandial cardiogenic syncope, by pressure on the LA compromising cardiac output. Symptomatic LA compression is a rare clinical condition causing left ventricular inflow obstruction resulting in low output, with symptoms such as syncope, and retrograde increase in pressure throughout the pulmonary vessels with subsequent dyspnea. Given poor surgical candidacy & patient preference, the patient was discharged on proton pump inhibitors along with the advice of eating small & frequent meals. The patient is compliant with recommendations with no recurrence of syncope.

CONCLUSION: Recurrent syncope in patients with a history of HH should prompt differential for HH leading to deglutition syncope. HH usually remains asymptomatic and sometimes is difficult to diagnose due to its various clinical presentations, the most common being gastroesophageal reflux, and less commonly chest pain, discomfort, or anemia. There are some unusual presentations that could be life-threatening. Management for HH is acid suppression & diet modifications. Surgical intervention is reserved for persistent symptoms/life-threatening emergencies.

Volume

38

First Page

S403

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