Overview

Length of high-pressure zone≈3–4 cm

Resting pressure≈10–30 mmHg above gastric

The LES has no discrete anatomical sphincter. Its tone comes from specialised circular "clasp" and oblique "sling" smooth-muscle fibres, held at a resting pressure about 10–30 mmHg above gastric pressure. Several other features add to the anti-reflux barrier. The right crus of the diaphragm wraps around the hiatus and pinches the oesophagus during inspiration (the extrinsic sphincter). The intra-abdominal segment is squeezed by positive abdominal pressure. The acute angle of His at the cardiac notch acts as a flap valve. A rosette of mucosal folds plugs the junction, and the phreno-oesophageal ligament anchors it below the diaphragm.

When a swallow begins, vagal inhibitory neurons in the myenteric plexus release nitric oxide and VIP. The LES relaxes ahead of the peristaltic wave (receptive relaxation), together with the proximal stomach.

Location: Gastro-oesophageal junction at about T11, just below the oesophageal hiatus, partly within the abdomen.

Anatomy

Innervation: Vagal preganglionic fibres act on myenteric neurons. Excitatory cholinergic neurons maintain tone; inhibitory nitrergic and VIP-ergic neurons produce relaxation. Sympathetic supply comes via the coeliac plexus.

Function

Prevents reflux of gastric acid and pepsin into the oesophagus.
Relaxes to let the bolus enter the stomach, and also to allow belching and vomiting.

Physiology: Transient LES relaxations are triggered by gastric distension through a vagovagal reflex, and they allow belching. They are the main mechanism of both physiological and pathological reflux. Tone is increased by ACh, gastrin, motilin, α-adrenergic agonists, protein meals and metoclopramide. Tone is decreased by fat, chocolate, peppermint, caffeine, alcohol, nicotine, progesterone (pregnancy), CCK, secretin, nitrates, calcium-channel blockers and anticholinergics.

Clinical significance

Achalasia

Inhibitory (NO/VIP) neurons of the myenteric plexus are lost, so the LES fails to relax and the oesophageal body loses peristalsis. Patients have dysphagia to both solids and liquids from the outset, regurgitation and weight loss. Barium swallow shows a "bird's beak" with a dilated oesophagus. Chagas disease (Trypanosoma cruzi) is a secondary cause. Treatment is pneumatic dilatation, Heller myotomy or POEM. There is a raised risk of squamous carcinoma.

Hiatus hernia

In a sliding hernia (about 95%) the gastro-oesophageal junction moves up into the thorax, disrupting the crural pinchcock and the angle of His and causing reflux. In a para-oesophageal (rolling) hernia the fundus herniates beside a junction that stays in place; these can strangulate.

GERD

An incompetent anti-reflux barrier lets acid reflux. See the system-level entry on GERD and Barrett oesophagus.

Test yourself

Approximately how far from the incisor teeth is the gastro-oesophageal junction (diaphragmatic constriction)?

15 cm
22.5 cm
27.5 cm
40 cm

Answer: 40 cm

The oesophageal constrictions lie about 15 cm (cricopharyngeus, C6), about 22.5 cm (aortic arch), about 27.5 cm (left main bronchus) and about 40 cm (oesophageal hiatus, T10) from the incisors. These distances guide endoscopy and explain where foreign bodies lodge.