GI Case I - Diseases of the Esophagus

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Esophageal Webs --Define --Clinical Features --Demographic --Etiology?: ESOPHAGEAL WEBS
MECHANICAL OBSTRUCTION

--Rare, mucosal protrusions into esophageal lumen

--Episodic (intermittent) dysphagia, usually with solid food

--Pain Infrequent

--Women over 40

--Congenital OR

--Develops 2° to chronic reflux esophagitis, GVHD
Esophageal Webs --Location --Morphology: ESOPHAGEAL WEBS
MECHANICAL OBSTRUCTION

**Most often found in UE
-->Upper Esophagus called Webs
-->Lower Esophagus called Schatzi Rings

Morphology:
--> Upper Esophagus: Rare, ledge-like, eccentric, semicircumference protrusions of squamous mucosa with vascularized fibrous tissue core

--> Lower Esophagus: Concentric protrusion into lumen with undersurface of columnar gastric epithelium
Esophageal Webs --Complications: ESOPHAGEAL WEBS
MECHANICAL OBSTRUCTION

Complications:
Paterson-Brown Kelly or
Plummer Vinson syndrome:
when UE web accompanied by iron deficiency, anemia, glossitis, & cheilosis
Esophageal Stenosis --Define --Etiology --Demographic --Clinical Features --Morphology: ESOPHAGEAL STENOSIS
MECHANICAL OBSTRUCTION

Define: Fibrous thickening of esophageal wall, particularly the submucosa + atrophy of muscularis propria

Etiology: May be congenital, but most often 2° to severe injury w/inflammation scarring such as GERD, scleroderma, or caustic injury

Demographic: adults

Clinical Features: progressive dysplasia first with solids, then solids and liquids

Morphology: lining epithelium is thin, often ulcerated
ACHALASIA Characterized by... Pathogenesis Hallmark: MOTOR DYSFUNCTION
ACHALASIA

Characterized by:
a) aperistalsis- required for dx via manometry
b) incomplete relaxation of LES with swallowing
c) increased resting tone of LES

Pathogenesis:
1. Poorly understood
2. Thought to involve dysfunction of NO, VIP
3. South America, Chagas may cause 2Â° achalasia from destruction of myenteric plexus and resultant dilation
4. May also be caused by disorders of dorsal motor nuclei (polio) or diabetic autonomic neuropathy

Hallmark: â€œbird beakâ€ appearance on radiograph
ACHALASIA Morphology Clinical Presentation Complications: MOTOR DYSFUNCTION
ACHALASIA

Morphology: progressive dilation of the esophagus above LES
--esophageal wall thickness may be normal, thicker (hyperplasia) or thinner (from dilation)
--may exhibit loss of myenteric ganglia mucosal lining sometimes shows inflammation, ulceration or fibrotic thickening above LES

Clinical Presentation
--usually manifests in early adulthood with progressive dysphagia
--nocturnal regurg or aspiration of undigested food

Complications: esophageal squamous cell carcinoma, Candida esophagitis, lower esophageal diverticula, and aspiration w/pneumonia or obstruction
Hiatal Hernia Characterized by... Etiology Clinical Presentation Complications: MOTOR DYSFUNCTION
HIATAL HERNIA

Characterized by: separation of diaphragmatic crura, widened space between muscular crura and
esophageal wall

Sliding Hiatal Hernia (95%):
--dilated portion of gastric fundus slides through widened esophageal hiatus
--protruding stomach above DPH creates bell-shaped dilation

Paraesophageal hernia (5%): aka hiatal rolling hernia--> vascular supply to stomach comprimised when stomach herniates upwards through small opening--> leads to ischemia and infarction

Etiology: unknown, could be congenital or acquired

Clinical Presentation:
-<10% suffer from heartburn or regurg into mouth, although regurg esophagitis is very common

Complications: ulceration, bleeding, and perforation
Esophageal Diverticula Characterized by... Clinical Presentation: MOTOR DYSFUNCTION
ESOPHAGEAL DIVERTICULA

-diverticulum is an outpouching of the alimentary tract which contains all visceral layers

-Zenker: located immediately above UES Traction: near midpoint Epiphrenic: above LES

Clinical Presentation
Zenker: dysphagia, food regurg, mass in neck; at risk for aspiration pneumonia
Midesophageal: generally asymptomatic
Epiphrenic: massive amounts of nocturnal regurg
Mallory-Weiss Syndrome: MOTOR DYSFUNCTION
MALLORY-WEISS SYNDROME

-are Longitudinal lacerations at esophagogastric junction or gastric cardia
-thought to be a consequence of severe retching, particularly in EtOH abusers
-may be from failure of reflex esophageal relaxation immediately prior antiperistalsis, leading to massive dilation and tearing
-may only involve mucosa, or may perforate
-histology is non-distinctive, representing trauma with fresh hemorrhage, nonspecific infiltrate
-Complication Boerhaave syndrome = esophageal rupture, is a rare occurrence
Esophageal Varices: MOTOR DYSFUNCTION
ESOPHAGEAL VARICES

-prolonged or severe portal HTN induces collateral vessels traveling â†‘ esophagus
-produces dilated, tortuous submucosal veins in the lower esophagus
-dilated vessels cause protrusion of mucosa into lumen
-rupture produces massive hemorrhage; previous rupture is indicated by thrombosis and
superimposed inflammation

Clinical Presentation
-usually asymptomatic until rupture, then massive hematemesis treatment is usually required to stop bleeding (sclerotherapy or balloon tamponade)
Esophagitis - GERD: Esophagitis - GERD

Morphology
-may be hyperemia with no other findings
-may show inflammatory cells, including eosinophils,
neutrophils, lymphocytes
-shows basal zone hyperplasia
-elongated papillae of lamina propria

Clinical Presentation
-usually presents >40 y.o.
-dysphagia & heartburn, sometimes regurg of sour brash, hematemesis, melena
-anatomical damage correlates best with duration of exposure, not severity of symptoms
-complications include bleeding, ulceration, strictures, Barrett esophagusâ†’adenocarcinoma
Barrett's Esphagus: BARRETT'S ESOPHAGUS

Morphology
-red, velvety mucosa located between pale pink
esophageal and light brown gastric mucosae
-may display circumferential or patchy extension
-metaplastic mucosa may only contain gastric surface
and glandular cells, difficult to diff. from hiatal hernia;
definitive dx is made on presence of goblet cells
-search for dysplasia, recognized by enlarged, crowded,
or stratified hyperchromatic nuclei

Clinical Presentation
-usually 40-60 y.o. white males w/long hx of GERD
symptoms (heartburn), frequently more severe and
occurring more often
-may produce local ulceration and bleeding
INFECTIOUS & CHEMICAL ESOPHAGITIS: Infectious and Chemical Esophagitis

-causes include EtOH, suicidal acid/alkali, chemotherapy, infection, HSV, CMV, fungal, uremia

Morphology
-each cause develops uniquely, but all end with severe, acute inflammation, superficial necrosis, ulceration, granulation tissue, eventual fibrosis
candidiasis- patches of gray-white pseudomembranes w/matted fungal hyphae
HSV- punched- out ulcers CMV-linear ulcers
bacteria- invasion of lamina propria, necrosis of squamous epithelium
chemicals- erythema/edema, mucosal sloughing, or necrosis

Irradiation- submucosal and mural blood vessels show intimal proliferation, luminal narrowing; mucosal atrophy, flattened papillae

Clinical Presentation
-infections usually occur in immunocompromised pts.
Benign Neoplasms of the Esophagus: BENIGN NEOPLASMS of the esophagus

-usually mesenchymal, in esophageal wall
-Leiomyomas are most common
-mucosal polyps are composed of combo of fibrous, vascular and adipose tissue covered by mucosa
-squamous papillomas are sessile, have a central core of CT and papilliform squamous mucosa;
referred to as condyloma if 2° to HPV
Malignant Neoplasms of the Esophagus Squamous Cell Carcinoma: Squamous Cell Carcinomal of the Esophagus

Morphology
-begin as in situ lesions, much like SCC in other locations
-can appear anywhere along esophagus
-early lesions are small, plaque-like thickenings of mucosa; become masses which may encircle
lumen
-may adopt any of three morphologic patterns (protruded, polypoid, ulcerated)
-ulcerated type may excavate into respiratory tree (fistula) or aorta (exsanguinations)
-best if found when neoplasm is isolated to epithelium or lamina propria
-most are moderatelyâ†’well-differentiated, and are quite large at dx, invading wall and beyond
-rich lymphatic network promotes spread; local extension is common
-location along esophagus determines site of metastasis (cervical,
mediastinal/tracheobronchial/paratracheal, gastric/celiac)

Clinical Presentation
-insidious onset, producing dysphagia & obstruction
-pt. adaptation occurs by shifting solidâ†’liquid diet; weight loss from CA and malnutrition
-ulceration may produce hemorrhage & sepsis
-first indication may be aspiration via tracheoesophageal fistula
-resection is often successful, even if large when detected, although most will recur
Malignant Neoplasms of the Esophagus Adenocarcinoma: Clinical Presentation

-generally occur 40 y.o., usually in 60s
-more common in men
-present w/dysphagia, progressive weight loss, bleeding, chest pain, vomiting

-previous hx of long-standing heartburn, regurg, epigastric pain are present in about half of pts.

-pt. with low-grade dysplasia may not progress to full-blown adenoCA, and may actually regress
Malignant Neoplasms of the Esophagus Adenocarcinoma: Clinical Presentation
-generally occur 40 y.o., usually in 60s
-more common in men
-present w/dysphagia, progressive weight loss, bleeding, chest pain, vomiting

-previous hx of long-standing heartburn, regurg, epigastric pain are present in about half of pts.

-pt. with low-grade dysplasia may not progress to full-blown adenoCA, and may actually regress

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