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 ESOPHAGUSDYSPLASIA
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