lower esophageal sphincter
Summary
The lower esophageal sphincter (LES) is a physiologic sphincter at the gastroesophageal junction that prevents reflux of gastric contents into the esophagus. It relaxes during swallowing to allow food passage into the stomach and remains contracted otherwise. Dysfunction leads to conditions like GERD (hypotensive LES) or achalasia (failure to relax).
Detail
The LES is not a true anatomic sphincter with distinct muscle bundles but rather a physiologic zone of increased tonic pressure (~10-30 mmHg) at the distal esophagus, maintained by the intrinsic smooth muscle of the esophagus, the sling fibers of the diaphragmatic crura (extrinsic component), and the angle of His. It is innervated by the vagus nerve, with relaxation mediated by nitric oxide and VIP released from inhibitory neurons of the myenteric plexus, while contraction is maintained by cholinergic input and intrinsic myogenic tone. During swallowing, receptive relaxation occurs via vagal reflex to allow bolus passage into the stomach, then tone returns to prevent reflux.
Clinical significance: LES hypotension or transient LES relaxations (TLESRs) are the primary mechanism behind GERD, contributing to symptoms like heartburn and regurgitation, and can lead to esophagitis, Barrett esophagus, and adenocarcinoma risk. Factors that decrease LES tone include fatty foods, caffeine, alcohol, chocolate, smoking, pregnancy (progesterone), anticholinergics, and calcium channel blockers. Factors that increase LES tone include gastrin and metoclopramide. Achalasia results from failure of LES relaxation due to loss of inhibitory neurons (nitric oxide/VIP) in the myenteric plexus, leading to functional obstruction, esophageal dilation, and symptoms of dysphagia to solids and liquids, regurgitation, and bird-beak sign on barium swallow. Diagnosis of both conditions involves esophageal manometry (measures LES pressure and relaxation) and pH monitoring for GERD. Treatment for GERD includes lifestyle modification, H2 blockers, PPIs, and fundoplication in refractory cases; achalasia is treated with pneumatic dilation, Heller myotomy, or botulinum toxin injection.
Sources
- First Aid for the USMLE Step 1
- Guyton and Hall Textbook of Medical Physiology
- Robbins and Cotran Pathologic Basis of Disease
- UpToDate: Pathophysiology of GERD and Achalasia
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