Hiatal Hernia

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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


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