Anatomy and Physiology of the Oesophagus

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🦴 Anatomy of the Oesophagus

The oesophagus is a muscular tube (~25 cm long) that transports swallowed material from the pharynx to the stomach. It begins at the pharyngoesophageal junction (lower border of the cricoid cartilage, C6) and ends at the gastro-oesophageal junction (GOJ) where squamous mucosa transitions to columnar gastric mucosa (the Z-line). Beyond being a “pipe”, it is a finely coordinated motor organ: it initiates peristalsis, generates a barrier against reflux, and coordinates sphincter relaxation to allow safe bolus transit. 🌊

📍 Position, Course, and Key Levels

• General course: Descends in the neck and posterior mediastinum, lying posterior to the trachea and anterior to the vertebral column, then passes through the diaphragm to join the stomach.
• Diaphragmatic passage: traverses the oesophageal hiatus at T10.
  Mnemonic: “I 8 10 Eggs At 12” → IVC T8, Oesophagus T10, Aorta T12
• Left atrial relation: In the thorax, the oesophagus lies close behind the left atrium (important for TOE/TEE and for symptoms from LA enlargement).
• Clinical landmarks for endoscopy: distances are often measured from the incisors to locate lesions/strictures.

🏷️ Anatomical Divisions

• Cervical oesophagus: Begins at C6 → thoracic inlet. Closely related to the trachea anteriorly and vertebral bodies posteriorly.
• Thoracic oesophagus: Thoracic inlet → diaphragm. Traverses the posterior mediastinum; intimately related to the aortic arch and left main bronchus (sites of narrowing).
• Abdominal oesophagus: Short (~1–2 cm) segment below the diaphragm → GOJ and gastric cardia.

🧭 Relations (High-yield Anatomy)

• Anterior: trachea (upper), then left main bronchus, then pericardium/left atrium (mid-lower thorax).
• Posterior: vertebral column; thoracic duct; azygos system (regional).
• Right side: azygos vein, mediastinal pleura (regional).
• Left side: aortic arch/descending thoracic aorta and mediastinal pleura (regional).
• At the hiatus: diaphragmatic crura form an external “pinch-cock” effect that contributes to the anti-reflux barrier.

🧩 Layers of the Oesophageal Wall (Structure ↔ Function)

• Mucosa: Non-keratinised stratified squamous epithelium — abrasion-resistant for bolus transit.
  Clinical: chronic reflux can drive metaplasia to columnar epithelium (Barrett’s).
• Submucosa: elastic tissue with mucous glands → lubrication and protection; contains the submucosal (Meissner) plexus.
• Muscularis externa: two coordinated layers generate peristalsis:
  • Inner circular layer: constricts behind the bolus.
  • Outer longitudinal layer: shortens the segment ahead of the bolus, reducing resistance.
  • Muscle type gradient: upper 1/3 skeletal, middle 1/3 mixed, lower 1/3 smooth — the anatomical basis for the transition from voluntary to involuntary propulsion.
• Adventitia: outer connective tissue anchoring the oesophagus to surrounding structures (note: unlike the stomach, much of the oesophagus is not fully peritonealised).

🚪 Sphincters & the Anti-reflux Barrier

The oesophagus has two functional sphincters: the upper oesophageal sphincter (UES) prevents air entry and aspiration, while the lower oesophageal sphincter (LES) and diaphragmatic hiatus create a high-pressure zone that prevents reflux. Importantly, the LES is not a discrete “ring” like a valve; it is a physiological high-pressure segment shaped by smooth muscle tone, the diaphragm, and the angle of the GOJ.

• UES: largely the cricopharyngeus muscle.
  • At rest: tonically contracted → prevents aerophagia and reflux into pharynx.
  • During swallow: relaxes and opens in synchrony with pharyngeal contraction.
• LES / GOJ complex:
  • Basal tone prevents gastric content reflux.
  • Relaxation is triggered by swallow-induced inhibitory neurons (NO/VIP mediated).
  • Additional components: diaphragmatic crura, the angle of His, and the intra-abdominal oesophageal segment (positive pressure zone).
  • Failure contributes to GORD/GERD, oesophagitis, stricture, and Barrett’s.

🩸 Blood Supply, Venous Drainage, Lymphatics & Innervation

• Arterial supply (segmental):
  • Cervical: inferior thyroid artery branches.
  • Thoracic: oesophageal branches from thoracic aorta ± bronchial arteries.
  • Abdominal: left gastric artery ± inferior phrenic branches.
• Venous drainage:
  • Cervical: inferior thyroid veins.
  • Thoracic: azygos/hemiazygos system.
  • Abdominal: left gastric vein → portal vein.
  • Key clinical concept: the distal oesophagus is a site of porto-systemic anastomosis → oesophageal varices in portal hypertension.
• Lymphatics: follow segmental pattern (cervical → deep cervical nodes; thoracic → posterior mediastinal; distal → left gastric/celiac).
  Clinical: this contributes to early lymphatic spread of oesophageal cancer and “skip” metastases.
• Innervation:
  • Vagus nerve: major parasympathetic control of peristalsis and sphincter function.
  • Enteric nervous system: myenteric (Auerbach) plexus coordinates smooth muscle contraction/relaxation.
  • Sympathetic: modulates blood flow and can influence motility (stress-related symptom exacerbation).
  • Pain referral: visceral afferents can refer discomfort retrosternally (reflux/oesophagitis can mimic cardiac pain).

⚙️ Physiology of Swallowing (Deglutition)

Swallowing is a coordinated sequence that protects the airway while propelling a bolus efficiently into the stomach. It has oral (voluntary), pharyngeal (reflex), and oesophageal (reflex) phases. The “swallowing centre” in the medulla coordinates cranial nerves and triggers a wave of peristalsis while transiently inhibiting respiration to prevent aspiration.

• Oral phase (voluntary): tongue propels bolus posteriorly → triggers swallow reflex.
• Pharyngeal phase (reflex):
  • Soft palate elevates to close nasopharynx.
  • Larynx elevates and vocal cords adduct; epiglottis helps protect the airway.
  • UES relaxes and opens; pharyngeal constrictors push bolus into oesophagus.
• Oesophageal phase (reflex): coordinated peristaltic wave + LES relaxation to allow entry into stomach.

🌊 Peristalsis & Motility (How the bolus moves)

• Primary peristalsis: initiated by swallowing; propagates from UES to LES.
• Secondary peristalsis: triggered by oesophageal distension/residual bolus; important for “clearing” refluxed acid.
• Mechanics: circular muscle contraction behind bolus + longitudinal shortening ahead reduces lumen resistance.
• Neurotransmitters:
  • Excitatory: acetylcholine/substance P → contraction.
  • Inhibitory: nitric oxide (NO) and VIP → relaxation (critical for LES relaxation).

🛡️ Mucosal Protection & Reflux Defence

The oesophagus is not built to tolerate acid long-term, so its defence relies on barrier mechanisms (LES + diaphragm + anatomy) and clearance mechanisms (peristalsis + saliva). When these fail or acid exposure is prolonged, inflammation and metaplastic change can occur.

• Barrier: LES tone, diaphragmatic crura, intra-abdominal oesophagus, angle of His.
• Clearance: secondary peristalsis + saliva (bicarbonate) neutralisation.
• Exposure factors: delayed gastric emptying, obesity, pregnancy, hiatus hernia, medications reducing LES tone.

📊 Physiological Narrowings (Constrictions) — High yield

These are common sites for food bolus impaction, pill injury, corrosive burns, and endoscopic “hold-ups”. They are also important radiological landmarks.

• 📌 Pharyngoesophageal junction (C6, cricoid/UES)
• 📌 Aortic arch impression (around T4)
• 📌 Left main bronchus impression (around T5/6)
• 📌 Diaphragmatic hiatus (T10)

🧪 Function at the Gastro-oesophageal Junction (Z-line & metaplasia)

• Z-line: transition from squamous oesophageal epithelium to columnar gastric epithelium.
• Barrett’s oesophagus: intestinal metaplasia from chronic reflux; increases oesophageal adenocarcinoma risk (clinical surveillance context).
• Strictures: chronic inflammation and scarring can narrow lumen → progressive dysphagia (solids then liquids).

🩺 Clinical Correlations (Anatomy + Physiology → Symptoms)

• Dysphagia:
  • Oropharyngeal (transfer problem) suggests neurological disease, structural pharyngeal pathology, aspiration risk.
  • Oesophageal (transport problem) suggests obstruction (stricture/cancer) or motility disorder (achalasia, spasm).
• Reflux (GORD/GERD): heartburn/regurgitation; complications include oesophagitis, strictures, Barrett’s.
• Achalasia physiology (core concept): failure of inhibitory neurons → impaired LES relaxation + absent peristalsis → dysphagia to solids and liquids, regurgitation (manometry diagnosis).
• Varices: portal hypertension → dilated submucosal veins in distal oesophagus → massive upper GI bleeding risk.
• TOE/TEE: oesophagus is a key “acoustic window” to the left atrium/mitral valve because of close posterior relation.
• Oesophageal cancer: often presents with progressive dysphagia and weight loss; common at physiological narrowings and at GOJ.

📝 Summary

The oesophagus is a 25 cm muscular conduit from C6 to the stomach that combines abrasion-resistant squamous mucosa with a sophisticated motility system. Swallowing triggers primary peristalsis and coordinated sphincter relaxation, while secondary peristalsis and saliva help clear refluxed acid. The anti-reflux barrier depends on LES tone plus diaphragmatic and anatomical supports at the GOJ; failure leads to GORD and complications such as strictures and Barrett’s. Clinically, dysphagia localises disease (transfer vs transport), and the distal oesophagus is a key porto-systemic site explaining variceal bleeding in portal hypertension.