Benign Esophageal Disease

A

General Description

• 1.

  The esophagus is an approximately 30-cm-long, muscular tube that begins 15 cm from the incisors at the cricopharyngeus muscle and ends at the gastroesophageal junction (GEJ) along the cardia of the stomach. There are three normal areas of anatomic narrowing: (1) the cricopharyngeal muscle (the narrowest point of the esophagus), (2) the aortic arch and left main stem bronchus, and (3) the diaphragmatic hiatus.

• 2.

  The cervical esophagus (5 cm) spans the C6 vertebra to T1–2. Recurrent laryngeal nerves lie in the tracheoesophageal groove on either side.

• 3.

  The thoracic esophagus (20 cm) begins at the thoracic inlet and lies between the trachea anteriorly and prevertebral fascia posteriorly. The azygous vein lies to the right and the thoracic aorta to the left of the esophagus.

• 4.

  The abdominal esophagus (2 cm) enters the abdomen at the esophageal hiatus at T11. Right and left vagal trunks also enter here.

B

Blood Supply and Nerves

• 1.

  Arterial supply is segmental from superior and inferior thyroid, aortic, bronchial, and esophageal branches, inferior phrenic, and left gastric arteries ( Fig. 27.1 ).

  

• 2.

  Venous drainage is to the submucosal venous plexus, with subsequent drainage to the inferior thyroid veins, azygos vein, hemiazygos vein, intercostal, gastric, and left and right phrenic veins. All are a potential source of varices if portal hypertension is present.

• 3.

  Innervation is from both parasympathetic and sympathetic systems. The cervical esophagus receives innervation from the recurrent laryngeal nerves. Damage to these nerves interferes with the function of the vocal cords, as well as the function of the cervical esophagus, predisposing to pulmonary aspiration with swallowing. The thoracic esophagus has both parasympathetic and sympathetic innervation via the vagus; these form the Auerbach plexus between muscle layers and the Meissner plexus within the submucosal layer. As the vagus nerve enters the abdomen, parasympathetic fibers form the left (anterior) and right (posterior) vagus nerves.

Pearl: LARP (l eft vagus lies a nteriorly and r ight vagus lies posteriorly) on the distal esophagus .

C

Histology

• 1.

  Mucosa is squamous epithelium, which becomes columnar epithelium of the stomach at the GEJ.

  Pearl: Squamous to columnar metaplasia is the hallmark of Barrett esophagus.

• 2.

  Submucosa contains glands, arteries, Meissner neural plexus, lymphatics, and veins.

• 3.

  Muscularis is composed of two layers, an outer longitudinal and an inner circular layer. Nerves and blood vessels run between the layers. The upper one-third is composed of striated muscle, and the lower two-thirds are smooth muscle.

• 4.

  No serosa. The lack of a serosal layer potentially contributes to an increase in anastomotic leaks and early mediastinal invasion by cancer.

A

Swallowing Mechanism

• 1.

  Oropharyngeal phase

  • a.

    Food is chewed and ready for swallowing.

  • b.

    Tongue pushes the food bolus into the hypopharynx.

  • c.

    Simultaneously, the soft palate elevates to prevent regurgitation of food into the nasopharynx and the hyoid bone moves anteriorly and superiorly to open the retrolaryngeal space.

  • d.

    Epiglottis moves over the larynx to prevent aspiration with the movement of the hyoid bone.

  • e.

    Rapid increase in the pressure of the hypopharynx and a subsequent relaxation of the upper esophageal sphincter (UES) (cricopharyngeus muscle) completes this phase.

• 2.

  Esophageal phase

  • a.

    Primary peristalsis is initiated by swallowing, relaxing the UES and simultaneous contraction of the posterior pharyngeal constrictors, which propels swallowed material from pharynx to stomach; food bolus is propelled by pressure differential between cervical esophagus and negative pressure of intrathoracic esophagus. Upper esophageal sphincter (UES) closes again to prevent reflux back into pharynx.

  • b.

    Secondary peristalsis is initiated by esophageal distention.

B

Sphincters

• 1.

  UES or cricopharyngeal muscle is approximately 3 cm long with resting pressure of 20–60 mm Hg.

• 2.

  Lower esophageal sphincter (LES)

  • a.

    The LES is not an anatomically defined sphincter in humans but a zone of high pressure that reduces gastric regurgitation and reflux. Located in the distal 3–5 cm of the esophagus, its normal resting pressure is 10–35 mm Hg.

  • b.

    LES pressure increases with inspiration and drug and/or hormone levels.

    • (1)

      Pressure is increased by gastrin, alpha-adrenergic drugs, bethanechol, and metoclopramide.

    • (2)

      Pressure is decreased by secretin, cholecystokinin, caffeine, glucagon, progesterone, alcohol, nitroglycerin, nicotine, anticholinergics, and beta-adrenergic drugs.

A

Achalasia

• 1.

  Aperistalsis and in complete relaxation of the LES.

• 2.

  Etiology can be idiopathic or infectious (i.e., Trypanosoma cruzi ) degeneration of Auerbach plexus; degeneration can lead to hypertension of LES, failure to relax, and progressive loss of peristalsis.

• 3.

  Symptoms include dysphagia, regurgitation, weight loss, retrosternal chest pain, nocturnal coughing, recurrent pulmonary infections. Progressing dysphagia beginning with liquids, then solids. Patient should eat carefully at meals and consume copious amounts of water.

• 4.

  Diagnosis: Barium swallow demonstrates “bird’s beak” narrowing of distal esophagus with proximal dilation; esophageal manometry is the gold standard for diagnosis—it will show aperistalsis and incomplete relaxation of the LES. LES resting pressure is often hypertensive, but it can be normotensive.

• 5.

  Treatment:

  • a.

    Medical management: nitroglycerin, calcium channel blockers, bougie dilation, Botox injection into the LES (symptoms frequently recur)

  • b.

    Surgical management:

    • (1)

      Heller myotomy with partial fundoplication

    • (2)

      Esophagectomy may be needed for sigmoid esophagus, failure after prior myotomy, or stricture refractory to dilation.

    • (3)

      POEM ( p er o ral e ndoscopic m yotomy) is a newer endoscopic treatment modality that creates an opening in the mucosa to access circular muscles, which are divided. No antireflux procedure is performed. Long-term outcomes are unknown at this time.

• 6.

  Approximately 1%–10% of patients experience development of squamous cell carcinoma after 15–25 years of disease.

B

Diffuse Esophageal Spasm

• 1.

  More common in women; repetitive, simultaneous contractions

• 2.

  Symptoms: chest pain, dysphagia; aggravated by reflux, cold liquids, and periods of emotional stress. Associated with other gastrointestinal (GI) complaints (e.g., irritable bowel syndrome [IBS], peptic ulcer disease [PUD])

• 3.

  Diagnosis: esophagram (“corkscrew esophagus”), manometry (simultaneous contractions with multiple peaks or long duration >2.5 seconds)

• 4.

  Treatment:

  • a.

    Medical (variable efficacy): elimination of trigger foods/drinks, acid suppression, nitrates, calcium channel blockers, anticholinergics, psychiatric evaluation

  • b.

    Surgical: for refractory dysphagia despite optimized medical therapy; long esophagomyotomy, including LES via left chest approach and partial fundoplication as LES is disrupted.

C

Nutcracker Esophagus

• 1.

  Hypermotility disorder: hypertensive peristalsis or high-amplitude peristaltic contractions; exact etiology unclear; commonly associated with gastroesophageal reflux disease (GERD) (>50%)

• 2.

  Symptoms: chest pain, dysphagia

• 3.

  Diagnosis: manometry—peristaltic esophageal contractions two standard deviations above normal amplitudes (i.e., >40 mm Hg); notably, LES pressure is normal and relaxes with each swallow

• 4.

  Treatment: medical management primarily. Treat GERD first. Calcium channel blockers, nitrates, antispasmodics can be used, but efficacy is low.

• 5.

  Surgical treatment can be performed in the setting of significant dysphagia. Outcomes poor for symptoms of pain alone

D

Hypertensive Les

• 1.

  Increased LES pressure greater than 35 mm Hg with normal LES relaxation; peristalsis typically normal

• 2.

  Symptoms: chest pain, dysphagia

• 3.

  Diagnosis: manometry, LES pressure greater than 35 cm with normal LES relaxation, normal peristalsis (50%)

• 4.

  Treatment:

  • a.

    Endoscopic management: Botox injection, balloon dilation

  • b.

    Surgical management: for those patients who fail endoscopic therapy and have severe symptoms; laparoscopic Heller myotomy with partial fundoplication

E