Chapter 10
Esophagus
William R. Alex
D. Bruce Panasuk
Richard N. Edie
I Introduction
A Anatomy
Location. The esophagus is approximately 24 cm in length. It extends from the C6 vertebral level to the T11 level.
It originates at the upper esophageal sphincter , which is essentially made up of the cricopharyngeal muscle, then courses behind the arch of the aorta, and descends into the thorax on the right.
It deviates anteriorly and enters the abdomen via the esophageal hiatus , which is formed by the right crus of the diaphragm.
The tubular esophagus meets the saccular stomach at the gastroesophageal junction, where the esophagus is anchored by the phrenoesophageal ligament. The gastroesophageal junction is approximately 40 cm from the incisors.
Histology
The esophageal mucosa consists of squamous cell epithelium except for the distal 1–2 cm, which is columnar epithelium.
There are two layers of muscle throughout the esophagus, an inner circular and outer longitudinal layer. The upper one third is striated muscle, whereas smooth muscle predominates in the lower two thirds.
The esophagus, unlike the rest of the gastrointestinal tract, lacks a serosal covering.
B Vasculature
Arterial supply to the esophagus is from branches of the inferior thyroid; the bronchial, intercostal, inferior phrenic, left gastric arteries; and direct esophageal branches from the aorta.
Venous return is more complicated.
An extensive subepithelial venous plexus empties superiorly into the hypopharyngeal veins and inferiorly into the gastric veins. The left gastric vein is also known as the coronary vein. Segmental drainage occurs also via the azygous and hemiazygous systems.
Lymphatic drainage is to the nearest lymph nodes. Lymphatics of the upper esophagus drain into the cervical or mediastinal nodes, whereas drainage of the distal lymphatics is more often to the celiac nodes.
C Innervation
The esophagus is supplied by the sympathetic and parasympathetic system via the pharyngeal plexus, the vagus, upper and lower cervical sympathetic, and splanchnic nerves. Meissner and Auerbach's plexuses are present in the normal esophagus.
D Physiology
The upper esophageal sphincter is a high-pressure zone at the upper border of the esophagus. It is 3–5 cm in length, and it relaxes during swallowing and contracts thereafter.
Peristalsis in the central portion of the esophagus consists of wavelike movements that pass down the body of the esophagus and become stronger toward the lower portion. Esophageal peristaltic pressures range from 25–80 mm Hg.
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The lower esophageal sphincter (LES) is a high-pressure zone at the lower portion of the esophagus. It is 3–5 cm in length and functions to prevent gastroesophageal reflux. LES pressure is influenced by several factors and substances.
LES pressure is increased by a protein meal, alkalinization of the stomach, gastrin, vasopressin, and cholinergic drugs.
LES pressure is decreased by secretin, nitroglycerine, glucagon, chocolate, fatty meals, and gastric acidification.
II Disorders of Esophageal Motility
A Cricopharyngeal dysfunction and Zenker's diverticulum
Pathophysiology
Cricopharyngeal dysfunction is caused by a failure of the upper esophageal sphincter to relax properly.
The problem may be an incoordination between relaxation in the upper esophageal sphincter and simultaneous contraction of the pharynx, which results in a pharyngoesophageal (Zenker's) diverticulum . This is a false diverticulum that consists only of mucosa that herniate posteriorly between the fibers of the cricopharyngeal muscle.
Cricopharyngeal dysfunction and Zenker's diverticulum is often associated with hiatal hernia and gastroesophageal reflux.
Symptoms of Zenker's diverticulum include dysphagia, halitosis, regurgitation of undigested food, nocturnal aspiration, and recurrent aspiration pneumonia.
Diagnosis
The history and physical examination are usually adequate to diagnose cricopharyngeal dysfunction.
Radiographs , which include a barium swallow, are helpful in delineating a diverticulum.
Endoscopy is contraindicated when Zenker's diverticulum has been documented by barium swallow because the risk of perforation is high. If a diverticulum is not seen on contrast studies, then endoscopy is indicated to rule out other esophageal disorders, including gastroesophageal reflux or neoplasm.
Treatment
Cricopharyngeal myotomy is the treatment of choice for cricopharyngeal dysfunction.
Resection or suspension of the diverticulum is combined with the myotomy.
B Achalasia
Pathophysiology
Achalasia is an esophageal disease of unknown etiology, although it may be secondary to ganglionic dysfunction, which causes:
High resting LES pressure
Failure of the LES to relax during swallowing
Absence of coordinated peristalsis in the body of the esophagus
The body of the esophagus becomes dilated, and the muscle hypertrophies in an attempt to force material through the dysfunctional LES. A similar symptom complex can be caused by Chagas disease , which is caused by the organism Trypanosoma cruzi.
Carcinoma of the esophagus is 10 times more common in patients with achalasia than in the general population.
Symptoms of achalasia include dysphagia, followed by regurgitation and weight loss. Frequently, respiratory symptoms caused by aspiration are present.
Diagnosis
Radiographic studies reveal a dilated esophagus with a bird's beaklike extension into the lower narrowed segment at the LES.
Esophageal manometry reveals the high resting LES pressure, failure of relaxation during swallowing, higher than normal resting pressure in the body of the esophagus, and absence of peristalsis.
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Esophagoscopy is required to rule out neoplasia and to document the extent of esophagitis.
Treatment for achalasia is palliative because LES function can never be restored to normal.
Nonsurgical treatment consists of forced pneumatic dilatation of the spastic lower esophageal sphincter, which is just above the gastroesophageal junction.
Surgical treatment is esophagomyotomy by the modified Heller procedure, via laparotomy/laparoscopy, or occasionally left thoracotomy. Care is taken not to disturb the vagus nerve attachments to the esophagus to prevent reflux. The myotomy is confined to the lower portion of the esophagus, usually 6–8 cm in length.
Surgical results with the Heller procedure are generally better than with pneumatic dilatation for relief of dysphagia.
Esophagomyotomy can be combined with an antireflux procedure if indicated.
C Diffuse esophageal spasm
Pathophysiology
Diffuse esophageal spasm is a disorder of esophageal motility that consists of strong nonperistaltic contractions.
Unlike achalasia, this condition has normal sphincteric relaxation and may be associated with gastroesophageal reflux.
Symptoms consist of chest pain, which can radiate to the back, neck, ears, jaw, or arms and may be confused with typical angina pectoris. The pain usually occurs spontaneously, and many patients are considered to have a psychoneurosis.
Diagnosis
Manometry reveals high-amplitude repetitive contractions with a normal sphincteric response to swallowing.
Radiographs are normal in one half of the cases but may reveal diverticula, segmental spasm, and a corkscrew appearance of the esophagus.
Treatment
Surgery is moderately effective with good results obtained in over two thirds of the patients. The best results are obtained in emotionally stable patients with severe disease and without associated lower gastrointestinal problems.
Surgery consists of a long esophagomyotomy that extends from the arch of the aorta to just above the LES.
Care is taken to preserve LES function, which is usually normal in these patients.
If significant gastroesophageal reflux is present, an antireflux procedure is performed.
Medical treatment. Calcium channel blockers and smooth muscle relaxants, such as nitrates, may ameliorate symptoms.
D Esophageal reflux
Etiology. Esophageal reflux is a common condition that may affect up to 80% of the population in varying degrees. Gastroesophageal reflux disease remains a multifactorial disease.
LES is a physiologic sphincter that is normally in an intra -abdominal position. Loss of LES pressure results in gastric reflux.
Esophageal motility, in the normal esophagus, causes refluxed secretions to be cleared by esophageal peristalsis.
Gastric secretions, gastric acid, pepsin, and bile reflux have been shown to produce severe esophagitis.
Symptoms of esophageal reflux are substernal pain, heartburn, and regurgitation, all of which may increase with bending and lying down.
Diagnosis is made by:
Manometry , which reveals decreased LES pressure
Esophagoscopy, which reveals varying degrees of esophagitis
Twenty -four hour pH measurements in the lower esophageal area, which demonstrate increased acidity
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Treatment
Medical treatment
Proton pump inhibitors and H2 -receptor antagonists to reduce acidity
Cisapride and metoclopramide, which increase both LES pressure and gastric motility, thus increasing the rate of gastric emptying
Antacids
Weight reduction
Abstinence from smoking and alcohol
Elevation of the head of the bed at night
Surgical treatment
Indications for surgery include:
Symptoms refractory to medical treatment
Additional problems, such as esophageal webs (see VII B ) or severe esophagitis, stricture formation, or Barrett's esophagus with severe dysplasia (i.e., replacement of the normal epithelial lining with columnar epithelium in the lower esophagus secondary to esophagitis)
Antireflux operations are designed to increase LES tone. All of the operations involve wrapping the lower esophagus with gastric fundus and restoring the distal esophagus to its original intra -abdominal position with the gastroesophageal junction below the diaphragm. The three most commonly used operations are:
The Nissen fundoplication, which is a 360 -degree wrap of the stomach around the esophagus performed through the abdomen. The procedure may now be successfully performed laparoscopically with minimal pain and a shorter recovery time.
Belsey Mark IV operation, which is a 270 -degree wrap performed through a left thoracotomy
The Hill repair , or posterior gastropexy, which uses the arcuate ligament to re-establish the intra -abdominal position of the distal esophagus.
III Esophageal Strictures
A Caustic stricture
Etiology. Caustic stricture is caused by the ingestion of caustic agents, such as lye, drain openers, and oven cleaners.
Diagnosis
The diagnosis may be made by the history of caustic ingestion and the presenting symptoms , which may be mild or very severe. Shock may ensue from severe burning or perforation of the esophagus. It is important to identify airway compromise early.
Endoscopy is indicated within 24 hours to determine the extent of damage.
Treatment
Broad -spectrum antibiotics are administered.
Corticosteroids are no longer indicated.
Radiographs of the esophagus are performed at 10–14 days to determine if strictures are developing.
Strictures occur in 5%–10% of patients who have ingested lye.
If strictures have formed, a program of dilatation, using esophageal dilators, is begun 3–4 weeks after ingestion.
Esophageal replacement with stomach or colon may be necessary.
B Strictures secondary to esophagitis and reflux
Pathophysiology. These strictures are caused by a recurrent alternating pattern of mucosal destruction secondary to gastric acid reflux and subsequent healing.
The strictures most often occur at the gastroesophageal junction.
In severe cases, a long stricture may result.
Diagnosis
A history of reflux symptoms and dysphagia is suggestive of strictures.
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Radiograph of the esophagus confirms the diagnosis.
Esophagoscopy is important to determine the extent of the disease and to rule out malignancy.
Treatment
Dilatation of the esophagus is attempted first, then an antireflux operation is performed.
If dilatation and an antireflux operation do not relieve the esophageal obstruction, a reconstructive procedure, using either the stomach or colon for esophageal replacement, may be necessary to restore adequate swallowing function.
IV Tumors of the Esophagus
A Benign tumors
Leiomyomas are intramural smooth muscle tumors that account for two thirds of all benign neoplasms of the esophagus.
Symptoms. Dysphagia occurs when leiomyomas exceed a diameter of 5 cm as they grow within the muscular wall, leaving the overlying mucosa intact.
Diagnosis
A history of dysphagia is typical.
A barium swallow reveals a localized smooth filling defect in the esophageal wall.
Esophagoscopy is performed to confirm the diagnosis.
Biopsy of the lesion is contraindicated because it violates the mucosa, making subsequent surgical therapy difficult.
Endoscopic ultrasound (EUS) is very helpful in confirming the intramural location of the lesion.
Surgical treatment
In symptomatic patients, the tumor is enucleated from the esophageal wall without violating the mucosa.
A limited esophageal resection is indicated if the tumor lies in the lower esophagus and cannot be enucleated.
Benign intraluminal tumors are usually mucosal polyps, lipomas, fibrolipomas , or myxofibromas.
Symptoms are dysphagia, occasional regurgitation, and weight loss.
Diagnosis
Radiographs of the esophagus suggest the diagnosis.
Esophagoscopy is performed to confirm the diagnosis and to rule out malignancy.
Surgical treatment
Esophagotomy, removal of the tumor, and repair of the esophagotomy comprise the surgical treatment.
Endoscopy should not be used to remove these tumors because of the possibility of esophageal perforation.
B Malignant tumors
Incidence. In the United States, the incidence of esophageal carcinoma ranges from 3.5 in 1 million for whites to 13.5 in 100,000 for blacks. The highest incidence of esophageal carcinoma is noted in the Hunan Chinese population, with as many as 130 in 100,000 individuals affected.
Etiology. The exact cause is unknown. Associated factors are tobacco use, excessive alcohol ingestion, nitrosamines, poor dental hygiene, and hot beverages. Certain pre -existing conditions also increase the likelihood of developing esophageal cancer, including achalasia and Barrett's esophagus.
Pathology
Type
Squamous cell carcinoma is the most common form.
Adenocarcinoma , the next commonest, is the type that occurs in patients with Barrett's esophagus.
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Rare tumors of the esophagus include mucoepidermoid carcinoma and adenoid cystic carcinoma.
Tumor spread. Esophageal malignancies metastasize through both the lymphatic system and the bloodstream, with metastases occurring in liver, bone, and brain.
Diagnosis
A history of dysphagia and weight loss is almost always present.
Contrast study of the esophagus demonstrates the location and extent of the tumor.
Computed tomography (CT) scan of the chest and abdomen is done to evaluate local lymphatic spread, and a thorough search is made for distant metastases.
Esophagoscopy is essential for tissue diagnosis and determination of the extent of the tumor.
EUS is done to assess the depth of the invasion and staging.
Bronchoscopy is performed in patients with proximal esophageal lesions to assess the possibility of invasion of the tracheobronchial tree.
Treatment
Overall, surgical therapy is associated with less than a 5% mortality rate. Several procedures are described for resection of the esophagus.
Transhiatal esophagectomy through a laparotomy and cervical incisions. A complete thoracic esophagectomy is performed bluntly with reconstruction of gastrointestinal continuity with the stomach or, rarely, the colon.
Ivor Lewis esophagectomy through a right thoracotomy and laparotomy. Reconstruction is
also accomplished with the stomach or, rarely, the colon.
Radiotherapy and chemotherapy are currently being investigated as adjuncts to surgery or as primary treatment modalities.
Neoadjuvant platinum-based chemotherapy in combination with X -Ray Therapy (XRT) given before surgical resection appears to shrink the tumor mass. Several studies have shown an impact on long-term survival. Clinical phase II and III studies are now under way.
Combination chemotherapy with cisplatin have shown up to a 50% response rate. However, a significant long-term survival has not been demonstrated.
Radiotherapy alone for carcinoma of the esophagus results in a 5-year survival of less than 10%.
In patients who have advanced disease with either invasion of the tracheobronchial tree or advanced metastases, palliative effects may be obtained by utilizing endoscopically placed metallic stents to allow swallowing of saliva and soft foods.
V Perforation of the Esophagus
A Etiology
Perforations of the esophagus have two basic causes:
Iatrogenic causes instrumentation (e.g., esophagoscopy or dilatation) account for 50% of all esophageal perforations.
Trauma , blunt or penetrating, 20%
Boerhaave's syndrome (postemetic rupture of the esophagus), 15%
Rupture of the esophagus results in acute mediastinitis, which if not corrected is almost always fatal.
B Diagnosis
History. Patients give a recent history of instrumentation of the esophagus or severe vomiting. All patients complain of severe chest pain, which is usually most prominent in the area of the rupture.
Physical examination
Crepitation in the neck results from mediastinal air.
Occasionally, a crunching sound can be heard over the heart (Hamman's sign), which is caused by air in the mediastinum behind the heart.
Septic shock can also occur.
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Chest radiograph reveals air in the mediastinum and, possibly, a widened mediastinum.
If the perforation is in the lower esophagus, air may be present under the diaphragm within the abdomen.
If the pleura has been violated, a hydropneumothorax may be present.
A barium swallow should be performed if perforation is suspected. This study is preferred over esophagoscopy for identifying a perforation.
CT scan is also a very useful diagnostic modality.
C
Treatment is to perform primary repair with tissue buttress reinforcement, combined with wide mediastinal and pleural drainage.
If mediastinal inflammation is severe and tissue integrity markedly is compromised, then esophageal resection with cervical esophagostomy and placement of a gastrostomy tube are performed. Esophageal reconstruction is performed at a later date when the patient has sufficiently recovered.
VI Mallory-Weiss Syndrome
A Pathophysiology
This condition presents as acute upper gastrointestinal hemorrhage. The bleeding occurs in the lower esophagus, usually near the gastroesophageal junction, and is secondary to a partial-thickness tear in the lower esophagus, which follows a prolonged period of severe vomiting and retching. The tear usually extends into the stomach and may involve the greater curvature of the cardia.
B
Diagnosis is made by endoscopy, which is performed to locate the tear and to rule out other causes of bleeding.
C
Treatment is by supportive measures, such as blood volume replacement, antacids, and gastric lavage.
In most cases, the bleeding subsides spontaneously.
Exploratory laparotomy is performed with gastrotomy and suture of the tear of the esophagus from within the stomach if the bleeding persists. The lacerations are closed using continuous nonabsorbable sutures. A recurrence is rare.
VII Esophageal Webs
A
Upper esophageal webs are part of the Plummer -Vinson syndrome women with atrophic oral mucosa, anemia, and dysphagia. The web Treatment is usually by esophageal dilatation.
, which presents in middle -age, edentulous occurs just below the esophageal introitus.
B
Lower esophageal webs, or Schatzki's rings , commonly occur in patients with reflux. Patients have dysphagia. Treatment consists of esophageal dilatation and an antireflux procedure.