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Oesophagus
Epithelium lined muscular tube from 6th cervical 11th thoracic vertebra
Passes through 3 regions; neck, thorax and abdomen
Upper and lower sphincters
Three areas of narrowing; cricoid cartilage, left main bronchus and aortic arch,diaphragmatic hiatus
Orderly passage of food {solids & liquids} from mouth to stomach.
Diseases are subdivided into:
Congenital; oesophageal atresia, tracheoesophageal fistula, vascular ring,
webs, duplication Diverticuli; Zenkers, midoesophageal, epiphrenic
Inflammatory; acid & alkaline reflux, caustic ingestion, Barretts
oesophagus, candidiasis, Crohns disease
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Oesophagus
Benign tumours; Leiomyoma, fibrous polyp, lipoma, haemagioma, etc
Malignant tumours; Carcinoma, leiomyosarcoma, fibrosarcoma, melanoma
Motor abnormalities; Achalasia, primary spasm, scleroderma, etc.
Miscellaneous; Foreign bodies, cartilaginous spur, presbyesophagus, acquired
oesophageal web(Plummer-Vinson Syndrome)
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Oesophagus
Zenkers diverticulum.
Pulsion diverticulum
Compressible mass in the neck
Associated with gurgling sound, dysphagia, regurgitation and aspiration
Diverticulectomy
Upper oesophageal webs (Plummer-Vinson Syndrome)
Fissured lips(cheilosis), dry skin, smooth tongue, flat brittle nails(Koilonychia),
weight loss, dsyphagia, & Fe def. Anaemia.
Women
Diagnosis with Ba. Swallow & endoscopy Replace Fe
Bouginage
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Oesophagus
Midoesophageal Webs;
Congenital or acquired in origin ie., oesophagitis in association with Barretts
Long history of reflux(heartburn) & dysphagia
Ba. Swallow shows stricture in mid oesophagus often with Hiatus hernia
Lower oesophageal Webs (Schatzkis ring)
Common xray finding
Endoscopy reveals a white membrane with a concentric opening
Treated by dilatation, electrocautery through endoscope, or by balloon tamponade
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Oesophagus
Achalasia
Thomas Willis in 1674 first described it.
Other names ascribed simple ectasia, and Cardiospasm
Motility disorder characterised by absence of oesophageal peristalsis and failure of
lower oesophageal sphincter to relax on swallowing
Most common neuroanatomic change is a decrease or loss of myenteric ganglion
cells.
Incidence of 0.4 to 0.6 per 100,000 & prevalence 0f 8 per 100,000.
Described from infancy to 9th decade, but majority present between 20 to 40 years
Paediatric cases account for 2% - 5% of all cases Dyspahgia for solids mainly, with variable dysphagia for liquids
Regurgitation (60%-90%), chest pain (505-75%), weight loss, recurrent aspiration.
Distal oesophageal diverticulum may develop
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Oesophagus
Diagnosis
Endoscopic finding
Dilated, patulous esophageal body with extensive mucosal friability & ulcerations
LES appears puckered and fails to open with air insufflation, but is easily traversedwith minimal pressure
Presence of a hiatal hernia (4-14%) or epiphrenic diverticulum
Manometry
Gold standard
Absent peristaltis of distal smooth muscle
LES relaxation pressures are elevated >35 mm Hg
Radiographic findings
PFA; Mediatinal widening, air-fluid level (midesophagus), absence of gastric air
bubble, abnormal pulmonary marking due to repeated aspiration
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Oesophagus
Barium swallow; dilated esophageal body tapering to a Birds beak at the levelof LES
Esophageal emptying scans; impaired propulsion and emptying
Achalasia & carcinoma; squamous cell carcinoma in approx. 5% after 20
years of diagnosis. Present a decade earlier than general population ie 40 years.
Treatment
Drug therapy
Smooth muscle relaxants; nitrates, calcium channel blockers
Results inconsistent & disappointing overall
Oesophageal dilatation
Began 4 centuries ago, Fabricus ab Aquadendente (1537-1675) pushed a foreignobject into stomach
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Oesophagus
Dilatation with mercury filled dilators & polyethylene balloons(pneumatic)
Complications; GIT bleeding, intramural haemorrhage, perforation
Response to pneumatic dilatation 32%-98%, most studies 60%-80%
Remission is not durable; 60% are symptom free for 1 year, with recurrence in50% of these patients in 5 years
Surgery
Heller's Myotomy. Open or laparoscopic
Laparoscopic technique first described in 1991, little morbidity, shorter hospital
stay, and earlier return to daily activities Overall mortality rate
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Oesophagus
Botulinum toxin
Potent inhibitor of acetylcholine release from presynaptic nerve terminals
Short term efficacy
Advantages are noninvasive, ease of administration & minimal side effects
Disadvantages; need for repeated injections, lack of response in 1/3rd of patients,
diminution of response with repeat injections of BoTx
GORD & Hiatal Hernias
S&S; Typical, heartburn (pyrosis), regurgitation, dysphagia/odynophagia, waterbrash
Atypical; pulmonary aspiration, severe chest pain, pulmonary asthma(adult onset),chronic hoarseness, choking, difficulty initiating swallows, chronic cough
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Oesophagus
Types of Hiatus hernias;
Type 1 (Sliding)
Type 1p a postoperative hernia
Type II (paraoesophageal)
Type IIp a postoperative hernia
Type III ( combined sliding & paraoesophageal hernia)
Type IIIp a postoperative that has no sac
Patient evaluation
History
Upper GIT series
24 hour pH monitoring & manometry; Gold standard
OGD
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Oesophagus
Medical therapy
Main aims are eliminate symptoms, heal injured esophageal mucosa, and manageand/or prevent complications
Life style modifications eg, diet alterations, avoid eating 2-3 hours before bedtime,
elevation of head of the bed 6-10 inches during sleep, sleep in in left lateraldecubitus, wt. Loss, avoidance of drugs that inhibit LES pressure
PPIs eg, omeprazole & lansoprazole
H2 receptor antagonists eg, cimetidine, ranitidine, famotidine, nizatidine
Prokinetic agents Cisapride and Metoclopramide
Antacids
Sucralfate
Strictures Dilatation with bougies( mercury filled), wire guided dilators, hydrostaticballoons
Endoscopic procedures, endoscopic suturing device(EdnoCinch), submucosalinjection(polymethylmethacrylate, ethylene ethyl alcohol, radiofrequency energydelivery
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Oesophagus
Surgical therapy
Patient selection is crucial
Preoperative evaluation
Types of operations; Nissens fundoplication 1956 360-degree wrap
Toupets partial wrap 1963 Dors anterior fundoplication
Mark IV operation by Skinner and Belsey
Hills gastropexy
Principles of fundoplication Creation of fundoplication just proximal to gastroesophageal junction with fixation to
esophagus No tension and construction over a 60F bougie inside esophagus
A total fundoplication should measure about 2 cms anteriorly
The wrapped portion of esophagus must lie below the diaphragm
The diaphragmatic hiatus must be snugged around the esophagus above the fundoplication
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Oesophagus
Problems after surgery
Dysphagia
Misdiagnosed achalasia
Recurrent reflux Abdominal bloating
Chest pain
Diarrhoea
Reflux gastritis
Severe fibrosis or total failure of esophageal body function
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Barretts oesophagus
Macroscopically seen on endoscopy as pink epithelium extending well above
the squamocolumnar junction
Histologically goblet cells
22.6 per 100,000
S&S heartburn, regurgitation, dysphagia
Potential progression to carcinoma
Medical treatment; PPIs
Surgical; low grade dysplasia antireflux procedure, argon plasma coagulation
High grade dysplasia; thermal ablation, PDT, ultrasonic energy,oesophagectomy
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Carcinoma of oesophagus
Risk factors; alcohol, tobacco, vitamin and mineral deficiency, nitrosamines,
food and water contaminants, strong family history, multiple cancers, especially
head and neck cancers, corrosive esophagitis, Barretts esophagus, achalasia,
Plummer-Vinson syndrome
S&S; None, dysphagia, wt. Loss, chest pain, retrosternal pain, feeling of
obstruction, etc.
5 year survival rate is 6%-9%
Two histologic types; SCC & adenocarcinoma
Assessment; Radiologic: plain and Barium studies, CT scan, MRI
Endoscopy; rigid and flexible, endoscopic ultrasound
Treatment; Oesophagectomy, 2 or 3 stage, transhiatal.
Neoadjuvant chemotherapy/chemoradiation, downstage tumour, improved
survival, higher pathologic response with combined chemoradiation
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Carcinoma of oesophagus
Primary Tumour Regional LN Distant mets
Tx cannot be assessed NX cannot be assessed Mx cannot be assessed
TO No evidence of primarytumour
NO No regional nodes detected MO no mets
Tis Carcinoma in situ (highgrade dysplasia)
N1 regional nodes mets M1 distant mets
T1 invades lamina propria orsubmucosa
T2 invades muscularis propria
T3 invades adventitia
T4 invades adjacent structures
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Carcinoma of oesophagus
Endoscopic therapy;
Endoscopic mucosal resection
Laser & Photodynamic therapy
Endoscopic dilatation & Stenting
BICAP/Tumour probe
Local injections
Brachytherapy
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Stomach
Benign Diseases
Chronic Gastric ulcer
Chronic Duodenal ulcer
Gastrinoma (Zollinger Ellison syndrome)
Tumours
Malignant ie., Carcinoma of stomach
Miscellaneous gastric pathology
Gastric bezoar, Menetriers disease, Mallory-Weiss syndrome, gastric volvulus, etc
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Stomach
Chronic Gastric ulcers
Greater frequency in elderly
Four types
Type I; lesser curve ulcers, usually antral, near antral-fundic border, occur in Patientswith gastric stasis, poor emptying & low acid output
Type II; combination of type I & present or past DU. High prevalence of blood group
O, high acid output
Type III; prepyloric in location, 1-2 cms proximal to pylorus
Type IV; other areas of stomach, drug induced
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Stomach
S&S and Diagnosis
Epigastric pain, relieved by eating/antacids
Sometimes worsening of pain on eating, esp, pyloric ulcers.
Ba. Studies, OGD & biopsy
Treatment
Antacids
Surgical options
Type I ulcers; antrectomy and Billroth anastomosis, vagotomy & pyloroplasty
Type II & III; similar to DU
Type IV; stress ulceration, curlings & cushing ulcers, if bleeding point easilyidentified, truncal vagotomy, pyloroplasty & oversewing of bleeding ulcer. Otherwise
gastrectomy in seriously ill Patients. For less seriously ill patients, vagotomy & distal
gatrectomy
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Stomach
Chronic DU
Younger age group
Men more often than women
Epigastric or RUQ pain Ba. Series and endoscopy
Treatment
Antacids, H2 receptors blockers, PPIs, H pylori treatment
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Stomach
Operation Mortality Recurrence rate(%)
Advantages (%)Disadvantage(%)
2/3-3/4 distalgastrectomy
~1 elective 5-15% None Small gastricreservoir,dumping
Vagotomy &drainage
< 1 5 10% Gastric reservoir Dumping,diarrhoea
Vagotomy &
distalgastrectomy
~1 2 3% Lowest RR Dumping,
diarrhoea
Parietal cellvagotomy
0-
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Stomach
Complications of peptic ulcers
Perforation
Haemorrhage
Pyloric obstruction
Complication of gastric surgery
Mortality
Recurrent ulcers
Gastrojujenocolic fistula
Postgastrectomy syndromes
Dumping
Diarrhoea, afferent loop syndrome, efferent loop syndrome, alkaline gastritis,
weight loss, anaemia, bone disease, TB, gastric cancer
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Gastric carcinoma
Risk factors
Polycyclic hydrocarbons, dimethylnitrosamines
Miners, metal workers, rubber workers
Helicobacter pylori
Gastric polyps
Pernicious anaemia, atrophic gastritis, gastric ulcer,
Pathology
95% adenocarcinomas
Two types; intestinal & diffuse
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Stomach
S&S
Vague epigastric discomfort
Wt. Loss, anaemia, anorexia, vomiting
Virchows node
Sister Mary Joseph nodule, ascites, jaundice, liver or pelvic mass
Preoperative evaluation
Endoscopy
CT scanning
Endoscopic ultrasound
CEA levels
Laparoscopy
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Carcinoma of Stomach
Surgical treatment
Overall 5 year survival rate 10 21% in western series
Japanese series 50%
Adjuvant therapy
VASAG Thiotepa & fluxuridine no survival benefit
GITSG 5-FU and methyl CCNU
Neoadjuvant therapy Response rates vary from 21 31% clinical response rate to complete response
rate of 0-15%
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Carcinoma of Stomach
Tumour Node Metastasis
T1 invades laminapropria or submucosa
N0 no mets in LN M0 no distant mets
T2 invades muscularispropria or subserosa
N1 mets in perigastric LN within 3cms of tumour
M1 Distant mets
T3 penetrates serosa N2 mets in perigastric LN . 3cms fromtumour, or left gastric, common
hepatic, splenic, or coeliac arteries
T4 invades adjacentorgans
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Carcinoma of Stomach
Surgical options
Proximal tumours
Total or proximal subtotal gastrectomy with Roux N- reconstruction
Mid-body tumours
Total gastrectomy
Distal tumours
Distal subtotal gastrectomy with or without regional lymphadenectomy
Splenectomy
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