Anatomy of Esophagus

• Muscular tube extends from the pharynx to the stomach – around 25 to 30cm long

• Divided in to four segments

  • • Pharyngoesophageal – Consists of superior, middle and inferior constrictors (Thyropharyngeus and cricopharyngeus), and stylopharyngeus muscles.

      • Killian’s triangle – Transition between oblique fibers of Thyropharyngeus and transverse fibers of Cricopharyngeus – Site of origin of Zenker diverticulum and also common site of perforation during esophagoscopy

    • Cervical – Posterior to the trachea, courses to left – Easily approachable via left sided neck incision

    • Thoracic – Up to diaphragmatic esophageal hiatus

    • Abdominal – Hiatus to cardia of stomach forming esophagogastric junction

• Has four constrictions

  • • At its beginning – caused by cricopharyngeus muscle (Upper esophageal sphincter) – Narrowest point of the gastrointestinal tract – around 15cm from the incisor teeth

    • Where it is crossed by the arch of the aorta – at 22.5 cm

    • Where it is crossed by the left main bronchus – at 27.5cm

    • Where it passes through the diaphragm – at 40cm

• Retroperitoneal but covered anteriorly and laterally by peritoneum

• Lacks serosa – surrounded by a layer of loose fibroalveolar adventitia

• Has internal circular and external longitudinal layers of muscle – superior third consists of skeletal muscle and inferior two-third composed of smooth muscle

• Auerbach plexus – connective tissue between two muscle layers containing blood vessels and ganglion cells

• Submucosa contains the mucous glands blood vessels, the meissner neural plexus and extensive lymphatic network

• Mucosa consists of squamous epithelium except for the distal 1 to 2cm

• Blood supply

  • • Cervical esophagus – Superior and inferior thyroid arteries

    • Thoracic – Esophageal arteries from aorta and collaterals from the inferior thyroid, intercostal, bronchial, inferior phrenic and left gastric arteries

• Venous drainage – Hypopharyngeal, azygous, hemiazygous, intercostals and gastric veins

• Nerve innervations – Left vagus – anterior and right vagus posterior at disphragmatic hiatus

Physiology of the Esophagus

• Air entry prevented by UES and gastric reflux by LES

• Upper esophageal sphincter – Tonically contracted at rest – Depressed during deep sleep or anesthesia and shows fluctuation with respiration. Relaxes by reflex mechanism coordinated through the swallowing center during swallowing

• Lower esophageal sphincter – Functional sphincter 3 to 5 cm in length in distal esophagus with elevated resting pressure ( Distal esophageal high pressure zone) – Relax by proximal esophageal distension. Normal resting pressure 10 to 20 mm Hg – No absolute value predicts competence or incompetence of the LES mechanism – varies with individual body habitus – Usually pressure less than 6 mm Hg and length less than 2 cm are likely to be associated with incompetence of the LES and Gastroesophageal refulx

• Contractions of Esophagus – Three types

  • Primary peristalsis – (2-6 cm/s) Progressive and triggered by voluntary swallowing

  • Secondary peristalsis – Progressive, generates with distension (Via Vagal reflexes mainly and also Myenteric nerve plexuses) and irritation – In smooth muscle only

  • Tertiary contractions – Non-progressive, may occur either after voluntary swallowing or spontaneously between swallows

• Sequence – Swallowed bolus – triggers primary peristaltic wave – propels food bolus to stomach – if the bolus not emptied to stomach – secondary peristaltic waves are initiated with local distension – continue until retained intra-esophageal contents are emptied in to stomach

• Tertiary contractions – non-progressive, nonperistaltic, monophasic or multiphasic, uncoordinated, responsible for “Corkscrew” appearance of esophageal spasm on barium swallow

• Table – Factors effecting distal esophageal sphincter pressure – Page 467 of Patric o’leary or page 1096 of Sabiston

Diseases

• Esophageal webs

  • Upper Esophageal webs (Plummer- Vinson Syndrome) – Associated with chronic iron-deficiency anemia. Premalignant condition – 10% develop carcinoma of the hypopharynx, oral cavity or esophagus. Treatment – esophageal dilatation and correction of the nutritional deficiency

  • Lower esophageal webs (Schatzki’s ring) – Annular stricture involving mucosa and submucosa at the squamocolumnar junction. May cause dysphagia if the ring dismeter leass than 20 mm ( Critical 13 mm) – Treatment – For only dysphagia – esophageal bougienage, for dysphagia and reflux – periodic dilatations and antireflux medical therapy. In refractory cases antireflux surgical procedure with intraoperative dilatation

  • Congenital – Rare

• Tracheo-esophageal fistula

• Disorders of Esophageal motility

  • Basic evaluation includes Barium swallow examination, esophagoscopy and other esophageal tests including manometry and intaesophageal pH reflux testing

    • Upper Esophageal Sphincter Dysfunction – Oropharyngeal dysphagia and Cricopharyngeal dysphagia

      • Have difficulty in swallowing liquids or solids – present as a lump in the throat. May be associated with expectoration of excessive saliva, Hoarseness, wt loss and symptoms of GERD (30 – 90%)

      • Causes –

        • General – Central and peripheral nerve system abnormalities, Metabolic and inflammatory myopathy, GERD and complications of neck or thoracic surgery

        • Anatomical – carcinoma, caustic stricture, cervical vertebral bone spurs, thyromegaly and trauma

        • Globus hystericus – Psychological – Diagnosis og exclusion

      • Diagnostic evaluation

        • Barium Swallow

        • Monometry

        • Acid reflux testing

        • Esophagoscopy

      • Treatment –

        • Cervical esophagomyotomy if documented abnormal UES

          • Operative technique – page 1098 Sabiston

        • Antireflux therapy for incompetent LES

        • Esophageal bougienage for neuromuscular conditions

    • Motor disorders of the body of the esophagus

      • Hypomotility – Achalasia

        • Most common functional disorder of the esophageal body and LES

        • Usual in middle age and equal in both sexes

        • Loss of ganglion cells in the intermyenteric (Auerbach’s) plexus of unknown etiology leading to dysfunctional or absent esophageal peristaltic waves, impaired relaxation and increased resting pressure of LES

        • May be associated with severe emotional stress, major physical trauma, drastic wt reduction and Chagas’ disease in south America

          • Chagas’ disease – page 1099 Sabiston

        • Premalignant – 2 to 8% Squamous cell carcinoma – secondary to long-standing mucosal irritation

        • Classic triad – Dysphagia, regurgitation and weight loss

        • Diagnostic tests

          • CXR – Air-Fluid level within a dilated esophagus

          • Barium swallow – Uniform esophageal dilatation with a distal tapering (Beak)

          • Manometric – Failure of the LES to relax reflexively

          • EGD – indicated to evaluate the severity of esophagus and to rule out secondary achalasia or pseudoachalasia due to a tumor or reflux stricture

        • Treatment – Purely palliative

          • Sublingual nitroglycerine

          • Dilatation

          • Esophagomyotomy

          • Botox injections

          • Page 1100 in Sabiston for discussion

      • Hypermotility – Diffuse esophageal spasm

        • Chest pain and/or dysphagia as a result of repetitive, simultaneous, high-amplitude esophageal contractions of unknown origin

        • Associated with emotional stress

        • 80% association of documented psychiatric disorders

        • Diagnostic evaluation

          • Intially as of chest pain

          • Barium swallow – classic curling or a corkscrew esophagus

          • EGD to rule out tumor, fibrosis and esophagitis

        • Treatment –

          • Reassurance – avoid stress and triggering food

          • Medical – Antispasmodics, calcium channel blockers and reflux treatment

          • Dilatation

          • Thoracic esophagomyotomy – only 50 to 60% success

      • Vigorous achalasia

      • Nutcracker or super squeeze Esophagus

        • Characterized by extremely high amplitude progressive peristaltic contractions, often of prolonged duration

        • Symptoms and management are same as of DES

      • Nonspecific neuromotor esophageal dysfunction – Seen in conditions associated with peripheral neuropathy (Diabetes, Alcoholism), Collagen vascular diseases ( Scleroderma, Dermatomyositis), myasthenia gravis, Multiple sclerosis and amyotropic lateral sclerosis

    • Tables from 1103 from Sabiston

• Esophageal diverticula

  • True vs False – True contains all layers of normal esophageal wall

  • Pulsion vs traction

    • Pulsion – false diverticula(Includes mucosa and submucosa) because of elevated intraluminal pressure

    • Traction – True diverticula because of traction of entire wall secondary to inflammation around the esophagus

  • Anatomical

    • Pharyngoesophageal (Zenker’s) – False pulsion diverticula

      • Most common esophageal diverticulum

      • Usually presents in older >60yrs

      • Arises from dorsal wall of the hypopharynxbetween oblique fibers of the posterior pharyngeal constrictor and the transverse fibers of the cricopharyngeus muscle of the UES, because of transient incomplete opening of UES

      • Refered to as cricopharyngeal achalasia

      • Symptoms – Usually asymptomatic and diagnosed in routine radiographic evaluation. Symtomatic patients complains of vague sensation or sticking in the throat, intermittent cough, excessive salivation, and intermittent dysphagia particularly with solid foods

      • Diagnostic evaluation

        • Plain X-ray shows air fluid levels

        • Barium swallow establishes the diagnosis

        • Manometric testing is usually normal and not indicated

      • Treatment –

        • Surgical or endoscopic esophagomyotomy with diverticulostomy or diverticulopexy – excellent results

        • Treat underlying motor abnormality

        • Discussion for methods – 1107 Sabiston

    • Parabronchial/ Midesophageal diverticula – True traction diverticula

      • Often wide mouthed and common on right side

      • Usually asymptomatic but can present with dysphagia, retrosternal pain, regurgitation, belching, epigastric pain, heartburn and wt loss

      • Barium swallow – diagnostic. May have manometric abnormalities

    • Epinephric – False pulsion diverticula

      • Within 10 cm of gastroesophageal junction and common on right side

      • Usually associated with a motility disorder

      • Rarely congenital (Ehlers-Danlos Syndrome) or may be from trauma

      • Ocassionally asymptomatic but most patients have a motility disorder and present with dysphagia, regurgitation , vomiting, chets and epigastric pain, anorexia, wt loss, cough, halitosis, and noisy swallowing

      • Diagnostic evaluation

        • Barium swallow

        • Motility studies necessary to rule out an underlying motor disorder

      • Treatment – Symptomatic patients with pouch greater than 3 cm – esophagomyotomy and resection of the diverticula

      • Discussion 1108 Sabiston

• Injury

  • Caustic

    • Alkali – Causes liquifactive necrosis resulting in deep burn

    • Acids – Coagulative necrosis forming an eschar that limits tissue penetration

    • Sites susceptibility to injury – Upper esophagus in the area of Cricopharyngeus, mid-esophagus where the aorta and left main stem bronchus impinge and the distal esophagus proximal to LES

    • Management

      • Verification of agent

      • Chest and abdominal radiographs to look for free air

      • EGD in 12 to 24 Hrs – to assess the severity of esophageal injury

        • First degree – Hyperemia and edema

        • Second degree – Ulceration

        • Third degree – Massive edema and eschar formation with or without full thickness necrosis

      • 48 hrs observation for first degree burns

      • For second and third degree burns without the evidence of perforation – ICU monitoring with NPO, I.V fluids, I.V antibiotics and anti reflux medication. Cortocosteroids may help in preventing strictures. Serial chest and abdominal x-rays required to look for perforation and barium swallow at 24 hrs. Consider stent placement or Gastrostomy

      • If perforated – Emergency ex-lap and Transhiatal esophagectomy with cervical esophagostomy and Jejunostomy

      • Complications – Stricture formation, tracheoesophageal fistula, hiatal hernia, reflux and esophageal carcinoma

      • Flow diagram in 1110 Sabiston

• • Perforation

    • Causes

      • Iatrogenic

        • Most common cause – endoscopic procedures

        • Most common site cricopharyngeal area

        • Also seen with biopsies, dilatation and rarely with endotraceal intubation, blind insertion of minitracheostomy, resection of lung cancer, blind dissextion of abdominal esophagus, operations on cervical spine, thyroidectomy and palliative intubation, stenting or laser treatment of esophageal tumors

      • Spontaneous

        • Most common – Boerhaave’s syndrome(Post emetic)

        • Most common site left posterior aspect

        • Also seen in Severe reflux, caustic ingestion, carcinoma and candidal, herpitic and immunodeficiency infections

      • Trauma – Penetrating or blunt trauma

      • Mallory-Weiss syndrome – mucosal laceration at the GE junction with hematemesis following retching or vomiting

    • Symptoms – Pain, Vomiting, Hematemesis and dysphagia

    • Signs – Tachypnea, tachycardia, fever, subcutaneous emphysema

    • Diagnostic evaluation

      • CXR – suggestive in 90%

      • Esophagogram – Use barium if the perforation is expected to communicate with abdominal cavity and use Gastrograffin if the perforation is expected to communicate with the abdomen

      • Chest CT

      • Esophagoscopy is not recommended

    • Treatment – Depends mainly on etiology, location and delay between rupture and treatment

      • Post-emetic perforation is the most morbid

      • Patients with perforation of the cervical esophagus have 94% survival, Thoracic have 66% and abdominal 71%

      • Needs fluid resuscitation and control of sepsis

        • Non-operative – for well contained leak in stable patient without evidence of sepsis or communication with pleural or peritoneal cavity

        • Operative –

          • Primary repair reinforced with vascularized tissue

          • Esophageal resection with cervical esophagostomy and enteral feeding tube

          • Adequate drainage of the mediastinum is important

• Tumors

  • Benign Tumors – Rare. 60% are leiomyomas, 20% are cysts and 5% are polyps

    • Leiomyomas

      • Typically occur between 20 and 50 years of age

      • More than 80% occur in the middle and lower thirds of the esophagus and rarely in cervical esophagus

      • Do not infiltrate the surrounding tissue- very rarely involve the mucosa

      • Usually symptomatic only with large tumors (Larger than 5 cm) – Present as dysphagia and vague retrosternal pressure or pain

      • Diagnostic evaluation

        • CXR may show posterior mediastenal mass

        • Barium swallow – well-localized mass with smooth surface and not circumferential

        • Endoscopy – Avoid biopsy

      • Treatment – Excise (enucleate) symptomatic or lager (>5 cm) leiomyomas by right thoracotomy for upper and middle third and left thoracotomy for lower third of the esophagus

  • Esophageal Cancer

    • Diagnosis

    • Staging

    • Treatment

  • Barrett’s esophagus

    • Columnar cell metaplasia of distal esophagus secondary to chronic gastroesophageal reflux.

    • Three types

      • Specialized intestinal metapalsia – Most common. Dysplasia and carcinoma are invariably associated with this type

      • Gastric fundic type epithelium

      • Junctional type epithelium

    • More common in males (3:1), blacks and elderly

    • Extent is related to status of the LES and degree of acid exposure

    • Can be found in 10 to 15% of patients who have endoscopic examinations for symptomatic GERD but most patients with Barrett’s esophagus may not have symptoms of GERD

    • Barrett’s esophagus is identified in 1 in 10 persons with erosive esophagitis and 1 in 3 persons with peptic esophageal stricture

    • Carcinogenesis in Barrett’s esophagus my involve activation of proto-oncogenes, dysfunction of tumor suppressor genes or both

    • True dysplastic change in Barrett’s esophagus is a neoplastic alteration and is a precursor of invasive malignancy – It is the best but not an ideal biomarker for malignancy because dysplasia is largely subjective and small foci can be missed

    • Prevalence of adenocarcinoma at the time of diagnosis of Barrett’s esophagus is approximately 8%

    • Management

      • Treat reflux esophagitis

      • Endoscopic surveillance – Flow chart in page 1143 Sabiston

      • Consider resection for high-grade dysplasia

Remember the best ABSITE review source for the 2009 and 2010 ABSITE is at http://www.clinicalreview.com/ABSITE.php.