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NORMAL ESOPHAGUS

NORMAL ENDOSCOPIC VIEW


OF ESOPHAGUS
NORMAL HISTOLOGY OF
ESOPHAGUS
ENDOSCOPIC VIEW OF
ESOPHAGEO GASTRIC
SYMPTOMATOLOGY OF
ESOPHAGEAL DISEASES
• Heart burn
• Dysphagia
• Pain
• Hematemesis
CONGENITAL ANOMALIES
• Ectopic tissue rests – stomach,
pancreas
• Congenital cysts – lower esophagus
usually
• Bronchogenic cyst
• Pulmonary sequestration
• Agenesis
• Atresias and fistulas
ATRESIAS AND FISTULAS
• ATRESIA – esophagus represented as
a thin non canalized cord
• Proximal blind pouch connected to
pharynx
• Distal lower pouch leading to
stomach
• Most commonly occurs at or near the
tracheal bifurcation
• Usually associated with a fistula –
ATRESIAS AND FISTULAS
• SINGLE UMBILICAL ARTERY
• Assoc with other diseases like CHD,
neurologic disease, genito urinary
diseases, GI malformations
• ASPIRATION PNEUMONIA
ATRESIAS AND FISTULAS
ESOPHAGEAL WEBS
• Ledge like mucosal protrusions into
esophageal lumen
• Semi circumferential
• Eccentric
• Upper esophagus common
• Can present as a cause of dysphagia
ESOPHAGEAL WEB
ESOPHAGEAL WEB
ESOPHAGEAL WEB
CAUSES
• Congenital
• Long standing reflux esophagitis
• Chronic GVHD
• Blistering skin diseases
• IRON DEFICIENCY ANEMIA
ESOPHAGEAL WEBS
• Iron deficiency anemia + glossitis +
cheilosis + post cricoid esophageal
webs = PLUMMER VINSON
SYNDROME / PATERSON BROWN
KELLY SYNDROME / SIDEROPENIC
DYSPHAGIA
• INCREASED RISK OF POST
CRICOID ESOPHAGEAL
CARCINOMA
ESOPHAGEAL RINGS
• Concentric plate of tissue
• Distal esophagus
• TYPE A RING : above the squamo
columnar junction
• TYPE B RING / SCHATZKI RING : at
the squamo columnar junction
ESOPHAGEAL STENOSIS
• Fibrous thickening of the esophageal wall
• Atrophy of muscularis propria
• Thin or ulcerated epithelium
• Causes :
5. Congenital
6. Inflammatory scarring
- gastro esophageal reflux
- radiation
- scleroderma
- caustic injury
. Progressive dysphagia – initially to solids
LESIONS ASSOCIATED WITH
MOTOR DYSFUNCTION
1. ACHALASIA
2. HIATAL HERNIA
3. MALLORY WEISS TEAR
ACHALASIA
• Failure to relax
• 3 major abnormalities
- Aperistalsis
- Partial / incomplete relaxation of LES
with swallowing
- Increased resting tone of LES
Two types : primary and secondary
Primary achalasia
• Dysfunction of inhibitory neurons
• Degenerative changes in neural
innervation – intrinsic / extrinsic
Secondary achalasia
• Chagas disease – trypanosoma cruzi
• Polio
• Surgical ablation of dorsal motor
nuclei
• Autonomic neuropathy
• Malignancy
• Amyloidosis
• Sarcoidosis
Morphology
• Progressive dilation of esophagus
above LES
• Wall – normal / thick / thin
• Absent myenteric ganglia in body
Clinical features
• Progressive dysphagia
• Nocturnal regurgitation
• Aspiration pneumonia
• Hazard of developing squamous cell
carcinoma
• Esophageal candidiasis
• Lower esophageal diverticulae
formation
HIATAL HERNIA
• Separation of the diaphragmatic
crura
• Widening of the space between the
muscular crura and esophageal wall
• Two anatomical types
4. Axial – sliding hernia
5. Non axial – paraesophageal hiatal
hernia
ESOPHAGEAL HERNIA
HIATUS HERNIA
HIATUS HERNIA -
ENDOSCOPY
Cause
• Congenital
• Acquired
Clinical features
• Heartburn
• Regurgitation of gastric juices in the
mouth when lying down or bending
forward
• Obesity
Complications
• Ulceration
• Bleeding
• Perforation
• Strangulation
• Obstruction
• Reflux esophagitis
DIVERTICULAE
• Outpouching of the alimentary tract
that contains ALL the visceral layers
• False diverticulum – only mucosa and
sub mucosa
• There are 3 types of esophageal
diverticulae
4. ZENKER DIVERTICULUM – PHARYNGO
ESOPHAGEAL DIVERTICULUM – UES
5. TRACTION DIVERTICULUM – MID
ESOPHAGUS
ZENKER DIVERTICULUM
• Disordered cricopharyngeal motor
dysfunction
• With or without GERD
• Diminished luminal size of UES
ESOPHAGEAL DIVERTICULAE
ESOPHAGEAL DIVERTICULAE
TRACTION DIVERTICULUM
• Scarring – post TB mediastinal
lymphadenitis
• Motor dysfunction
• Congenital lesion
ESOPHAGEAL DIVERTICULAE
ESOPHAGEAL DIVERTICULAE
ESOPHAGEAL DIVERTICULAE
Clinical features
• Accumulation of food in the
diverticulum
• Dysphagia
• Food regurgitation
• Neck mass
• Aspiration pneumonia
• Nocturnal regurgitation
MALLORY WEISS SYNDROME
• Longitudinal tear in the esophagus
• At the gastro esophageal junction
• Most common in alcoholics
• Due to severe retching / vomiting
• NO REFLEX RELAXATION OF THE LES
WITH THE ANTI PERISTALTIC WAVE OF
RETCHING / VOMITING
• Underlying hiatal hernia can be a
predisposing factor
MORPHOLOGY
• Linear irregular lacerations
• In the axis of the esophageal lumen
• Range in length from mm to cm
• Tear may involve partial thickness of
wall / full thickness - perforation
MALLORY WEISS SYNDROME
MALLORY WEISS TEAR -
ENDOSCOPY
CLINICAL FEATURES
• Sudden upper GI bleed
• Mild bleed / massive hemetemesis
• Heals with minimal or no residual
involvement
• Perforation = BOERHAAVE
SYNDROME
ESOPHAGEAL VARICES
• Dilated tortuous esophageal sub
epithelial and sub mucosal veins is
called as esophageal varices
• Causes : any cause of portal
hypertension
3. Alcoholic cirrhosis most common
cause.
4. Cirrhosis of other etiology also
manifest as varices
PORTAL
HYPERTENSION

DIVERSION OF PORTAL
BLOOD FLOW

CORONARY VEINS OF
STOMACH

ESOPHAGEAL SUB EPITHELIAL AND SUB


MUCOSAL VEINS

AZYGOS
VEINS

SYSTEMIC
CIRCULATION
MORPHOLOGY
• Dilated tortuous veins
• Distal esophagus and proximal stomach
• Sub mucosal and sub epithelial
channels massively dilated
• Mucosa irregularly protruding into the
lumen
• Mucosa normal / eroded and inflamed
• Rupture – massive hemorrhage into the
lumen and hemorrhage into the wall of
the esophagus
ESOPHAGEAL VARICES
ESOPHAGEAL VARICES
ESOPHAGEAL VARICES
ESOPHAGEAL VARICES
ESOPHAGEAL VARICES
ESOPHAGEAL VARICES
CLINICAL FEATURES
• Asymptomatic / massive
hemetemesis
• Death due to massive bleed / hepatic
coma triggered by hemorrhage
ESOPHAGITIS
• GERD / REFLUX
• MUCOSAL IRRITANTS – alcohol, corrosive acids, alkalis, excessive
hot fluids like tea, heavy smoking
• CYTOTOXIC ANTI CANCER THERAPY
• BACTERIA
• HSV VIRUS
• CMV VIRUS
• FUNGAL : immunosuppressed – candida, aspergillus, mucor
mycosis
• UREMIA
• RADIATION
• GVHD
• AUTO IMMUNE DISEASES
• PEMPHIGOID AND BULLOUS DISORDERS OF SKIN
• CROHN DISEASE
• DRUGS
GASTRO ESOPHAGEAL REFLUX
DISEASE (GERD) OR REFLUX
• Reflux of gastric contents into lower
esophagus most important cause
• Reduced LES tone / decreased
efficiency of anti reflux mechanisms
- CNS depressants
- Hypothyroidism
- Pregnancy
- Systemic sclerosing disorders
- Tobacco exposure
- Nasogastric tube
GERD
• Hiatal hernia – especially sliding
• Inadequate / slow clearance of refluxed
material
• Delayed gastric emptying
• Increased gastric volume
• Reduced reparative capacity of
esophageal mucosa by protracted
exposure to gastric juices
• Gastric juices +/- bile from duodenum
MORPHOLOGY
• Inflamed esophagus – “redness”
• Inflammatory cells in the epithelial
layer – eosinophils, neutrophils,
lymphocytes
• Basal zone hyperplasia
• Capillary congestion in lamina
propria with elongation of papillae
CLINICAL FEATURES
• Dysphagia
• Heartburn
• Regurgitation of sour material
• Hemetemesis
• Melena
• Chest pain
CONSEQUENCES
• Bleeding
• Ulceration
• Stricture formation
• Barrett esophagus formation
BARRETT ESOPHAGUS
• It is the metaplastic change
occurring in the distal esophageal
epithelium where in the squamous
epithelium is replaced by metaplastic
columnar epithelium.
• GERD IS THE SINGLE MOST
IMPORTANT CAUSE
• BARRETT ESOPHAGUS IS THE SINGLE
MOST IMPORTANT RISK FACTOR FOR
CRITERIA
1. Endoscopic evidence of columnar
epithelial lining above the gastro
esophageal junction
2. Histologic evidence of intestinal
metaplasia in the biopsy specimens
from the columnar epithelium
CLASSIFICATION
1. SHORT SEGMENT < 3cm cephalad
2. LONG SEGMENT > 3cm cephalad
from the manometric gastro
esophageal junction
ENDOSCOPIC VIEW OF
ESOPHAGEO GASTRIC
BARRETT ESOPHAGUS
BARRETT ESOPHAGUS
BARRETT ESOPHAGUS
BARRETT ESOPHAGUS
NORMAL GASTRO
ESOPHAGEAL JUNCTION
HISTOLOGY
• Definitive diagnosis is made when
the squamous epithelium is replaced
by columnar mucosa
• Also the columnar mucosa contains
intestinal goblet cells
• Low or high grade dysplasia can be
present
BARRETT ESOPHAGUS
BARRETT ESOPHAGUS-
DYSPLASIA
TUMORS OF ESOPHAGUS
• BENIGN:
2. EPITHELIAL
- Squamous cell papilloma
- Adenoma
2. MESENCHYMAL
- Leiomyoma
- lipoma
Tumors
• MALIGNANT
1. EPITHELIAL:
- Squamous cell carcinoma
- Adenocarcinoma
2. MESENCHYMAL
- leiomyosarcoma
CARCINOMA ESOPHAGUS
• Usually diagnosed late
• Aggressive spread
• Men > 50 years of age
• Varied incidence world wide
• Chinese and japanese common
• Bad prognosis
RISK FACTORS FOR CA
ESOPHAGUS
1. ESOPHAGEAL DISORDERS:
- Long standing eophagitis
- Barrett esophagus
- Achalasia
- Hiatus hernia
- Diverticula
- Plummer Vinson syndrome
2. DIET AND LIFE STYLE
- Smoking
- Alcoholism
- Deficiency of vitamins A,C, riboflavin,
thiamine, pyridoxine
- Trace element deficiency – zinc,
molybdenum
- Fungal contamination of food stuff
- High content of nitrites /
3. GENETIC FACTORS:
- Tylosis : hyperkeratosis of palms and
soles
- Inherited defects of cancer
MORPHOLOGY
• Squamous cell carcinoma and
adenocarcinoma are the 2 common
types
• SCC comprises almost 90% of cases
• Elderly men
• Most common in mid esophagus –
50%
lower esophagus – 30%
upper esophagus – 20%
PRECURSOR
• DYSPLASIA CARCINOMA IN SITU
INVASIVE CANCER
• BARRETT ESOPHAGUS LOW GRADE
DYSPLASIA HIGH GRADE DYSPLASIA
INVASIVE ADENOCARCINOMA
SCC
1. Polypoid fungating type
2. Ulcerating type
3. Diffuse infiltrative type
MICRO : well differentiated to poorly
differentiated squamous cell
carcinoma
ADENO CARCINOMA
• Usually arises in a setting of Barrett
esophagus
• Lower and mid esophagus common
sites
• Nodular, elevated masses in lower
esophagus
MICRO :
Most of them are well differentiated
mucin producing tumors
CLINICAL FEATURES
• Weight loss
• Anorexia
• Fatigue
• Weakness
• Pain during swallowing
• Dysphagia
• Spreads very soon because of the
extensive lymphatic network
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
CARCINOMA ESOPHAGUS
SQUAMOUS CELL CARCINOMA
ESOPHAGUS
CARCINOMA ESOPHAGUS -
STAGING