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HIATAL HERNIA

 Separation of the diaphragmatic crura and


widening of the space between the
muscular crura and the esophageal wall.
 This leads to portion of stomach entering
into thorax..
TYPES
 Sliding hernia :
Gastroesophageal junction and fundus of
stomach slide upward.

 Paraesophageal hernia :
Gastroesophgeal junction is fixed but part
of the stomach herniates into the chest.
Normal GE junction
Sliding hiatal hernia
Paraesophageal hernia
 Complications
- Gastric volvulus
- strangulation
- perforation
 Investigations
- Plain X – ray chest & abdomen
- Barium swallow study
- Endoscopy
 Treatment
- Medical
- Head end elevation
- Abstain from alcohol, smoking
- Antacids, PPI’s

- Surgery
- Reduction of hernial contents
- Nissen’s fundoplication
DIVERTICULA
 A diverticulum is an out pouching of the
alimentary canal that contains all the
layers.
 Types – true and pseudo
 Pseudo diverticulum only mucosa and
sub mucosa.
According to site
 Zenker diverticulum - pharyngoesophageal
 Traction diverticulum - midpoint of
esophagus because of inflammation
 Epiphrenic diverticulum – immediately
above LES.
symptoms
 Asymptomatic
 Dysphagia
 Food regurgitation
 Mass in the neck
 Halitosis
 Aspiration
Management
 Barium swallow study
 Endoscopy
 Diverticulectomy
Lacerations
 Mallory-weiss syndrome
 Boerhaave’s syndrome
BARRETT’s ESOPHAGUS
 The distal squamous mucosa is replaced
by metaplastic columnar epithelium as a
response to prolonged injury.
 Single most important risk factor for
esophageal adenocarcinoma.
 Occurs as a complication of long standing
GERD.
Types
 Long segment - involving > 3 cms
 Short segment – involving < 3 cms.
Criteria
 Endoscopic evidence – Indocarmine spray
 Histological evidence – multiple biopsies
Barrett’s esophagus
Pathogenesis
 Chronic irritation leads to change in the
differentiation program of stem cells of the
esophagus mucosa.
Clinical features
 Age – 40 to 60 yrs
 More common in white males.
 Symptoms of reflux esophagitis.
 Complications
Bleeding, Ulceration, Stricture and
development of Adenocarcinoma.
 Hence reflux esophagitis should be treated
aggressively with drugs and if needed
surgery to prevent Barretts’s esophagus
 Endoscopic surveillance should be done in
patients with Barrett’s esophagus
 Once high grade dysplasia is detected
treatment of choice is esophagectomy of
the segment
 Photodynamic laser, thermo-coagulative
mucosal ablation, and endoscopic
mucosal resection are being evaluated as
alternatives
TUMOURS
 Benign
Leiomyoma, fibroma, lipoma,
neurofibroma

 Maliganant
SCC, Adeno Ca, Carcinoid, Melanoma,
lymphoma.
Benign tumors
 The most common is leiomyoma
 Fibroma, neurofibroma, lipoma,
hemangioma may also arise.
 Polyps
 Inflammatory pseudotumor
Leiomyoma esophagus
Malignant
 Constitutes about 6% of GI malignancies.
 Majority are epithelial.
 Globally SCC is the commonest
esophageal carcinoma.
 In US the incidence is almost same for
SCC and Adenocarcinoma.
Squamous Cell Ca
 Most common type of carcinoma esophagus.
 Age – over 50 years.
 Incidence varies with country.
 Blacks are at more risk compared to whites.
 Seen in Upper & middle 1/3rd
 Constitutes about 40% of esophageal ca.
Adenocarcinoma
 The majority arises from barrett mucosa.
 Tobacco, obesity are the risk factor
 Usually located in lower end of esophagus
 In contrast to SCC whites are more
affected than blacks.
 5 year survival rate is under 20%.
 Incidence is about 45%
Staging - TNM classification
T – Tumour size
N - Nodal involvement
M - Metastasis

Grading – Histopathological
- Well differentiated
- Moderately differentiated
- Poorly differentiated
 Three morphological pattern
- Exophytic
- Flat
- Ulcerative.
 Most are moderate to well differentiated.
AETIOLOGICAL FACTORS for SCC
 Smoking
 Alcohol excess
 Chewing betel nuts or tobacco
 Coeliac disease
 Achalasia of the oesophagus
 Post-cricoid web
 Post-caustic stricture
 Tylosis (familial hyperkeratosis of palms and
soles)
 Aetiological factors
- Chronic GERD
- Barrett’s esophagus
- Tobacco & alcohol consumption
Clinical presentation

 Progressive dysphagia to first for solid


food then for liquids
 Weight loss
 Halitosis
 Regurgitation
 Hoarseness
 Hypercalcemia
Investigations

 Barium swallow
 Endoscopic biopsy
 Endo ultrasonography with tissue biopsy
 CT scan
 MRI
Ba swallow – Ca esophagus
Ca Esophagus
Ca Esophagus
Treatment
 Surgery remains the main stay with proper
clearance margin
 Local and distant recurrence is common.
 Five year survival rate is 75%.
 Surgery
- Esophagectomy with surrounding lymph
node excision

 Radiotherapy
- SCC more radiosensitive
- AdenoCa radioresistant
 Chemotherapy
- 5 FU
- Cisplatinum

 Palliative
- Metallic stenting
- Laser ablation