PATHOLOGY OF THE ESOPHAGUS

Symptoms of the esophageal disorders Upper gastrointestinal bleeding (lacerations, varices) Odynophagia (painful swallowing)--infections, other inflammatory insults Dysphagia (difficulty swallowing)-disorders of motility (solids and liquids), obstructions such as tumors and benign strictures (solids first, progressing to liquids).

Disorders Hiatal hernia Achalasia Lacerations (Mallory-Weiss Syndrome) Varices Stenosis, webs and rings Esophagitis Esophageal carcinoma

ANATOMIC & MOTOR DISORDERS Hiatal hernia 1-20% of population; 9% symptomatic Characterized by separation of the diaphragmatic crura and widening of the space between the muscular crura and the esophageal wall. Complications: Ulceration, bleeding, perforation, reflux esophagitis.

Types of Hiatal hernia Type 1 (Sliding)--95%; protrusion of the stomach above the diaphragm creates a bell shaped dilation Type 2 (Paraesophageal)--stomach rolls along side of lower esophageal sphincter (LES), may strangulate or obstruct and thus is often managed surgically.

ACHALASIA Failure of relaxation with consequent dilatation of the esophagus Clinically progressive dysphagia and regurgitation Manifest in young adulthood but may appear in infancy or childhood Manometric studies show three major abnormalities of the achalasia: (1) aperistalsis, (2) partial or incomplete relaxation of the lower esophageal sphincter (LES) with swallowing, (3) increased resting tone of the LES.

Primary achalasia: primary degenerative changes in neural innervation Secondary achalasia: Chagas’ disease (Trypanosoma cruzi) causes destruction of the myenteric plexus of the esophagus, duodenum, colon, and ureter, with resultant dilatation of these structures Diseases of the vagal dorsal motor nuclei, particularly polio or surgical ablation, Diabetic autonomic neuropathy, Infiltrative disorders (malignancy, amyloidosis, sarcoidosis), Infectious diseases (pneumonia, candida albicans esophagitis).

Achalasia

Lacerations (Mallory-Weiss Syndrome) Longitudinal tears in the esophagus at the esophagogastric junction common in alcoholics 5 to 10% of upper gastrointestinal bleeding episodes.

Varices Portal hypertension  collateral bypass channels (wherever the portal and caval systems communicate) The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices. Two-thirds of all cirrhotic patients and are most often associated with alcoholic cirrhosis. No symptoms until they rupture. Massive hematemesis

Stenosis, Webs, and Rings Non-neoplastic constrictions (stenoses): Primary: developmental defects Secondary (severe esophageal injury): gastroesophageal reflux, radiation, scleroderma, caustic injury. Progressive dysphagia

Perforation of the esophagus Boerhaave syndrome Most commonly due to trauma (nasogastric tube) or excessive vomiting Gross: may be indistinct, or associated with a small amount of hemorrhage Complications: bacterial mediastinitis, which has a high mortality, even with the use of broad-spectrum antibiotics.

Plummer-Vinson syndrome (Paterson-Kelly syndrome): 1. microcytic hypochromic anemia, 2. esophageal webs (progressive dysphagia), 3. atrophic glossitis.

INFLAMMATORY DISORDERS ESOPHAGITIS Types Corrosive Infectious--CMV/Herpes/Candida Reflux. Injury to the esophageal mucosa with subsequent inflammation is common worldwide. In northern Iran, the prevalence of esophagitis is more than 80% (hot tea). It is also extremely high in regions of China.

Disease and Origin Reflux esophagitis, via reflux of gastric contents. Prolonged gastric intubation. Ingestion of irritants, such as alcohol, corrosive acids or alkalis (in suicide attempts), excessively hot fluids (i.e., hot tea in Iran), and heavy smoking. Cytotoxic anticancer therapy, with or without superimposed infection. Infection following bacteremia or viremia (herpes simplex viruses and cytomegalovirus are the more common offenders in the immunosuppressed).

Fungal infection in debilitated or immunosuppressed patients or during broad-spectrum antimicrobial therapy. Candidiasis is the most common; mucormycosis and aspergillosis may occur. Uremia. Radiation. Systemic conditions associated with decreased LES tone, including hypothyroidism, systemic sclerosis, and pregnancy. In association with systemic desquamative dermatologic conditions, such as pemphigoid and epidermolysis bullosa. Graft-versus-host disease.

In reflux esophagitis, three features are characteristic: Morphology The anatomic changes depend on the causative agent and on the duration and severity of the exposure: Simple hyperemia In reflux esophagitis, three features are characteristic: eosinophils, with or without neutrophils, in the epithelial layer basal zone hyperplasia elongation of lamina propria papillae .

The final common pathway for all is severe acute inflammation, superficial necrosis (erosion), ulceration with the formation of granulation tissue, accumulation of adherent purulent debris, and eventual fibrosis. In infectious dieseases: Candidiasis: gray-white pseudomembranes Herpes and cytomegalovirus: punched-out ulcers, inclusions Pathogenic bacteria: bacterial invasion with ulcerations.

Chemically induced injury ( acids, detergents): Irradiation: intimal proliferation with luminal narrowing in blood vessels, fibrosis and mucosal atrophy. Chemically induced injury ( acids, detergents): severe necrosis of the esophageal wall, hemorrhage severe inflammation. Graft-versus-host disease: karyorrhexis of basal epithelial cells, atrophy, fibrosis of the lamina propria with minimal inflammation.

Candida albicans Superficial, curdy, gray to white inflammatory membrane composed of matted organisms fibrinosuppurative exudate with an underlying erythematous inflammatory base Risk factors: Diabetes mellitus, neutropenia, immunoincompetent, AIDS, Xerostomia, antibiotic therapy.

Barrett’s Esophagus A premalignant condition in which the normal stratified squamous epithelium of the esophagus is replaced by a metaplastic columnar epithelium as a complication of chronic gastroesophageal reflux disease (GERD). The metaplastic epithelium of Barrett's esophagus is variously called Barrett's metaplasia, specialized columnar metaplasia intestinal metaplasia.

Red, velvety mucosa located between the smooth, pale pink esophageal squamous mucosa and the more lush, light brown gastric mucosa. Microscopically: the esophageal squamous epithelium is replaced by metaplastic columnar epithelium. dysplasia (the presumed precursor of malignancy)

Only about 5-10% of patients with Barrett's esophagus will progress to cancer. Endoscopy with biopsy is therefore recommended in patients who have long-standing or frequent gastroesophageal reflux disease (GERD) symptoms to determine whether or not Barrett's esophagus has developed.

Barret’s

Barrett's esophagus No malignancy Adenocarcinoma

TUMORS of the ESOPHAGUS Malignant tumors Squamous cell carcinoma (90%) Adenocarcinoma (associated with Barret’s esophagus) Benign tumors Rare

SQUAMOUS CELL CARCINOMA Risk factors Esophageal disorders Long standing esophagitis Achalasia Plummer-Vinson syndrome Life style Alcohol Tobacco Virus Human papillomavirus

Dietary Genetic disposition Hypovitaminosis (A,B,C) Deficiency of trace elements (zinc, molybdenum) Fungal contamination of foodstuff High contents of nitrits / nitrosamines Genetic disposition Tylosis (hyperkeratosis of palms and soles)

Squamous cell carcinoma Usually preceed by epithelial dysplasia and carcinoma in situ, Early lesions: small, gray-white mucosal thickenings, Three forms: 1. Polypoid exophytic 2. Necrotizing-ulcerative 3. Diffuse infiltrative Localization: Upper upper third (20%) Middle third (50%) Lower third (% 30).

Adenocarcinomas of the esophagus Barret’s esophagus Lower third Invasion of cardia Forms: Nodular Diffuse Infiltrative.

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