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Benign Esophageal Disease

Benign Esophageal Disease

1. Anatomy of the esophagogastric junction

A. Phrenoesophageal membrane
1) Fascial attachments of the esophagus to the diaphragm
2) Attached to esophagus several centimeters above G-E jxn
3) Maintains intraabdominal esophagus

2. Hiatal herniae

A. Type I (sliding)
1) Phrenoesophageal ligament is stretched
2) G-E jxn can migrate to an intrathoracic position
3) G-E jxn remains cephalad to stomach
4) Reducible, unless esophagus is foreshortened from stricture
B. Type II (paraesophageal hiatal hernia)
1) Rare
2) Phrenoesophageal ligament remains firm, binding esophagus to preaortic fascia and median arcuate ligament
3) G-E jxn at or near normal location
4) Fundus and body of stomach roll into chest alongside esophagus
C. Type III (sliding and rolling hernia)
1)E-G jxn and most of greater curve and body of stomach herniate
D. Etiology
1) Most are acquired
2) Obesity and pregnancy increase intraabdominal pressure, stretching phrenoesophageal ligament

3. Pathophysiology of G-E reflux

A. LES - resting pressure, length, site
B. Esophageal clearance - gravity and esophageal peristalsis
C. Mucosal resistance
D. Salivary neutralization
E. Gastric secretion
1) Sensitivity to gastric acid, pepsin, alkaline bilious material
2) Additive effect
3) Gastric emptying (40% of pts w/reflux esophagitis
F. Complications
1) Anemia (chronic blood loss)
2) Stricture
3) Barrett’s esophagus
G. Pts w/G-E jxn incompetence should be treated the same as those w/ concomitant hiatal hernia

4. Symptoms

A. Most patients are free of symptoms
B. Very small risk of incarceration, strangulation, or obstruction of bowel (seldom involved)
C. Retrosternal pain, heartburn, postural regurgitation, gaseous eructation
D. Symptoms worse after a meal or when supine
E. Pain may radiate to jaw, neck, ears or arms
F. Respiratory involvement in 20%
1) Acid alone may exacerbate asthma
G. Shatzki ring
1) Membrane or diaphragm on swallow
2) Most are asymptomatic, but may produce intermittent or persistent dysphagia (solid > liquid)
3) Always associated with hiatal hernia
4) Squamous mucosa on top and gastric mucosa on bottom
5) Smooth muscle, fibrous tissue and scar between
6) Tx
a) Dilatation w/balloon or bougie
b) If symptomatic from hiatal hernia-repair hernia and dilate
H. Barrett’s esophagus
I. “Invariably” associated w/sliding hiatal hernia and severe GE reflux

5. Diagnosis

A. Radiographic - Ba swallow w/maneuvers to assess reflux
B. EGD for all respiratory or GER symptoms
C. Formal testing of esophageal function
1) Not necessary for typical symptoms of GER
2) 24hr pH monitoring and manometry prior to surgical intervention

6. Medical treatment

A. Lifestyle modification
1) Elevation of head of bed
a) Head 6-10 inches above the feet
b) Reduces number of reflux episodes and increases rate of clearance
2) Weight reduction - can improve symptoms
3) Smoking
a) Can decrease LES pressure and frequency of GER episodes
b) Cessation reduces frequency of episodes
4) EtOH - Lowers LES pressure and impairs peristalsis
5) Diet modification
a) Coffee, chocolate, peppermint and fatty foods - ¯ LES pressure
b) Citrus and tomato juice - direct mucosal irritation
c) Cola and milk products stimulate acid secretion
d) Timing of meals - avoid recumbency
6) Medications
a) Theophylline, dopamine, nitrates, opiates, diazepam, calcium channel blockers - all lower LES pressure
B. Pharmacologic therapy
1) Cytoprotective agents - sucralfate
a) Controversial data on efficacy
b) Primary use is adjunctive (add to acid suppression)
2) Antacids - increase LES pressure and alkalinize gastric acid
3) Acid suppression - H2 blockers
a) Decrease volume and concentration of gastric acid
b) Less effective for GER than for PUD
c) 50-60% healing in grade II-III esophagitis (cimetidine)
d) Healing is slow-treat for 3-6 months
4) Acid suppression - proton pump inhibitors - omeprazole
a) Suppresses basal and stimulated gastric acid secretion
b) Superior to placebo, ranitidine and cimetidine for GER
c) Recommendation is cessation after 2 months
5) Prokinetic agents
a) Metachlopramide-dopamine antagonist - disappointing
b) Cisapride- enhances acetylcholine release from myenteric plexus
(1) Better than placebo for GER symptoms
(2) w/ cimetidine is better than cimetidine alone
C. Strategy of medical therapy
1) First phase = lifestyle changes - behavior, food and drugs
2) Second phase = Pharmacologic management
a) H2-blocker, then add cisapride or sucralfate
b) Proton pump inhibitor for failure of combo tx
c) Continue tx for 3-6 months
d) Up to 90% will relapse by one year
3) Surgical treatment for failure of medical tx or complications (stricture, bleeding, severe ulceration)

7. Surgical therapy

A. Failure of medical tx or complications (stricture, bleeding, severe ulceration)
B. Significant symptoms and esophagitis in a young pt.
C. Operative approach
1) Restore 4-6cm of intraabdominal esophagus
2) Thoracic approach
a) Shortening of the esophagus - to immobilize esophagus
b) Prior esophageal procedure
c) Esophageal dysmotility requiring myotomy
d) Suggested mechanisms for improvements
1) LES manipulation
2) Accentuation of angle of His
3) Increased opening of the cardia
E. Procedures
1) Complete fundoplication - Nissen/Nissen-Rosetti
a) 87% free of symptoms long-term
b) 3cm loose Nissenà4% free from post-op symptoms
2) Partial fundoplication
a) Belsey Mark IV - 240° wrap
b) Lind - 300°
c) Toupet - 180°
3) Angelchick prosthesis
a) 20% persistent dysphagia
b) Migration

Barrett’s esophagus

1. Anatomy and physiology

A. Definition=esophagus is lined w/columnar mucosa more than 3cm proximal to the distal end of the muscular esophageal tube
B. 3 types of mucosa - gastric fundic, junctional, specialized columnar (80%)
C. Acid (and pepsin and gastrin) is produced, but amount is insufficient to explain peptic ulceration of Barrett’s

2. Pathogenesis

A. Nearly every patient has pathologic reflux
B. Metaplasia of pleuropotential cells in submucosa
C. Migration of gastric mucosa not felt to be mechanism

3. Epidemiology

A. 1% in pts w/o symptoms who undergo endoscopy
B. 10-20% in pts w/symptoms of reflux
C. 8-13% of children endoscoped for GER
D. Age 50-60
E. Men=3xwomen
F. Relative lack in African-Americans

4. Diagnosis

A. GER symptoms
B. Symptoms may improve with progression of Barrett’s
C. >80% - hiatal hernia
D. 75% - stricture
E. Nearly 50% - ulcer
F. Endoscopy
1) Irregular squamocolumnar junction
2) Strictures typically involve squamocolumnar junction
3) Biopsy at multiple levels
G. LES pressure is lower in pts w/Barrett’s than normal people and lower than pts w/reflux but w/o Barrett’s

5. Benign (non-neoplastic) complications

A. Stricture, bleeding, mucosal ulceration
B. Severe bleeding - 25% (rare in GER)
C. Penetrating ulcer in 10%
1) May be successfully treated w/acid suppression
2) Resection for mediastinal perforation

6. Dysplasia and adenocarcinoma

A. Persistent acid reflux responsible for Barrett’s is involved in dysplasia and malignant change
B. Other premalignant markers
1) Increased G2 tetraploidy
2) DNA aneuploidy
3) ras oncogenes (H- ras, K- ras, N- ras) - not a factor
C. Risk of malignant degeneration related to
1) Duration and severity of GER
2) Tobacco
3) Overall extent of columnar spread
D. Cancers
1) Arise almost exclusively in specialized columnar epithelium
2) Most have transmural extension with + nodes at time of dx
E. 1/140 pt years = 40x usual risk in this country = 10-20% of all esophageal ca

7. Medical management

A. Lifestyle changes - behavior, food and drugs
B. Medications
C. Resolution of symptoms does not correlate with regression of Barrett’s

8. Surveillance

A. Surveillance allows detection at an early stage and improves long-term survival
B. Endoscopy at least every year

9. Surgical treatment of benign disease

A. Indications = failure of medical tx or complications (same as for GERD)
B. Unknown whether regression of Barrett’s or reversion of dysplasia can be expected
C. Fundoplication and resection if necessary
1) Remove all Barrett’s mucosa
2) Cervical esophagogastrostomy (intrathoracic esophagogastrostomy carries a high
D. Surgical treatment of dysplasia and adenocarcinoma
1) High grade dysplasia (separate from carcinoma in situ)
2) Intensive med tx w/rebiopsy q 3months or resection
3) When resecting, remove all Barrett’s epithelium