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BIRG ANWAR UL HAQ
ENT SPECIALIST
CMH LAHORE
00923018513303
ACUTE OESOPHAGITIS
 It is acute inflammation of the oesophagus
 Causes
 Ingestion of
 Hot liquids
 Caustic corrosive agents
 Laceration due to swallowed foreign body
 Trauma of oesophagoscopy
 Monilial infection of oesophagus
 Systemic disorder
 Pemphigus.
ACUTE OESOPHAGITIS
Symptoms
 Dysphagia
 Retrosternal burning
 Haematemesis
Diagnosis
 History
 X-ray studies
 Oesophagoscopy.
PERFORATION OF OESOPHAGUS
 Aetiology
Instrumental trauma
 oesophagoscopy of dilatation of strictures
with bougies
Spontaneous rupture
 Follows vomiting
 involves mostly the lower third oesophagus.
Post-emetic rupture - Boerhaave's syndrome.
PERFORATION - DIAGNOSIS
Early diagnosis is imperative
Develops mediastinitis
Can rapidly prove fatal
PERFORATION - DIAGNOSIS
 Pain in the neck or interscapular region,
 Following oesophagoscopy
 The features of cervical oesophageal rupture
 Pain
 Fever
 Difficulty to swallow
 Local tenderness
 Surgical emphysema in the neck.
PERFORATION - DIAGNOSIS
 The features of thoracic oesophageal rupture
 Pain referred to the interscapular region
 fever 102-1 04°F(39-40°C)
 signs of shock
 surgical emphysema in the neck
 crunching sound over the heart (Hamman's sign,
 because of air in the mediastinum and pneumothorax).
 X-rays of the chest and neck are essen tial. They may
 reveal widening of the mediastinum and retrovisceral
 space, surgical emphysema, pneumothorax, pleural
effusion
 or gas under rhe diaphmgm.
PERFORATION - INVESTIGATIONS
 X-rays of the chest and neck are essential
 Widening of the
 Mediastinum
 Retrovisceral space
 Surgical emphysema
 Pneumothorax
 Pleural effusion
 Gas under the diaphram.
Treatment
 NPO
 Total parentral nutrition
 Massive doses of antibiotics
Cervical oesophagus –
 Conservative measures
 Drainage is required only if suppuration
develops
Treatment
Thoracic oesophagus
 Serious
 Conservative treatment rarely succeeds
Treatment
Within 6 hours
 Perforation is surgically closed
 Pleural cavity drained
If diagnosis is delayed
 Repair is not possible
 Drainage of the infected area.
CORROSIVE BURNS OF
OESOPHAGUS
Aetiology
 Acids
 Alkalies
 Other chemicals may be swallowed
accidentally by children
 Taken with the purpose of suicide in adults
CORROSIVE BURNS OF
OESOPHAGUS
Pathology
 Severity of oesophageal burns depends on the
 Nature of corrosive substance
 Quantity and concentration
 Duration of its contact with the oesophageal wall.
 Alkalies are more destructive and penetrate deep into
layers of the oesophagus
 Entire oesophagus and stomach may slough off
causing fatal mediastinitis and peritonitis.
CORROSIVE BURNS OF
OESOPHAGUS
 Oesophageal burns run through three stages:
 Stage of necrosis
 Stage of granulations
 Slough separates leaving granulating ulcer.
 Stage of stricture formation
 Stricture formation begins at 2 weeks
 continues for 2 months or longer.
CORROSIVE BURNS OF
OESOPHAGUS
 Evaluation of patient
 Determine the type of caustic ingested
 Signs and symptoms of shock
 Upper airway obstruction
 Mediastinitis
 Peritonitis
 Acid-base imbalance
 Associated burns of face, lips and oral cavity
 X-ray of the chest and soft tissue lateral view of
neck.
CORROSIVE BURNS OF
OESOPHAGUS
Management
 Hospitalize the patient.
 Treat shock
 Treat acid-base imbalance
 Monitor urine output for renal function
 Relieve pain
 Relieve airway obstruction
 Tracheostomy may be required.
CORROSIVE BURNS OF
OESOPHAGUS
 Neutralisation of the corrosive
 By appropriate weak acid or alkali
 Effective only if done within first 6 hours.
 Parenteral antibiotics
 Immediately
 Continued for 3- 6 weeks depending on the
degree of burns
CORROSIVE BURNS OF
OESOPHAGUS
 Pass a nasogastric tube
 Oesophagoscopy. - Contravertial
 with in 2 days to know
 Degree
 Extent
 Oesophagoscope is not passed beyond the first
severe circumferential burn.
 Steroids should be started
 within 48-96 hours for 4-6 weeks
CORROSIVE BURNS OF
OESOPHAGUS
 Oesophagogram and oesophagoscopy every
two weeks,
 If stricture develops it can be treated by
 Oesophagoscopy and prograde dilatations
 Gastrostomy and retrograde dilatation
 Oesophageal reconstruction or by-pass
 Life- long follow-up.
BENIGN STRICTURES OF
OESOPHAGUS
Aetiology
 Occur when muscular coat of the oesophagus
is damaged. The common causes are:
 Burns due to corrosive substances or hot
fluids.
 Trauma to oesophageal wall due to
 Impacted foreign bodies
 Instrumentation
 External injuries
BENIGN STRICTURES OF
OESOPHAGUS
Aetiology
Ulcerations due to reflux oesophagitis.
Ulcerations due to diphtheria, typhoid.
Sites of surgical anastomosis .
Congenital, usually in the lower third.
BENIGN STRICTURES OF
OESOPHAGUS
Clinical features and diagnosis
 Dysphagia
 First to solids and then to liquids
 Regurgitation
 When obstruction is complete
 Cough
 Malnourished.
BENIGN STRICTURES OF
OESOPHAGUS
Investigations
Barium swallow establishes the
diagnosis.
Oesophagoscopy to exclude
malignancy.
BENIGN STRICTURES OF
OESOPHAGUS
 Treatment
 Prograde dilatation with bougies.
 Gastrostomy
 Surgery.
 Excision of strictured segment
 Reconstruction of food passage using
 Stomach
 Colon
 Jejunum.
HIATUS HERNIA
 A hiatus hernia occurs when the
upper part of the stomach, which is
joined to the oesophagus moves up
into the chest through the hole
(called a hiatus) in the diaphragm.
 It is common and occurs in about 10
per cent of people.
HIATUS HERNIA
• Overweight
• Middle-aged
• Women and elderly people.
• It can occur during pregnancy.
• Diagnosis
• Barium meal x-rays
• Oesophgoscopy
HIATUS HERNIA
 Symptoms
Heartburn
Sudden regurgitation
Belching
Pain on swallowing hot fluids
Feeling of food sticking in the oesophagus
TREATMENT
Mainly it is surgical
Hernia is reduced
Diaphragmatic opening repaired
TREATMENT FOR HIATUS HERNIA
• Conservative treatment
• Early cases
• Unfit for surgery
• Sleeping with head and chest raised
• Use of drugs that reduce acidity (antacids and cimetidine)
• Losing weight
• Eating small but frequent meals
• Avoid actions which raise intra-abdominal pressure
• Avoidance of smoking
• Avoid spicy food
• Avoid hot drinks
• Avoid gassy drinks.
PLUMMER-VINSON SYNDROME
(PATTERSON BROWN-KELLY SYNDROME)
Classical features
 Dysphagia
 Iron-deficiency anaemia
 Glossitis
 Angular stomatitis
 Koilonychia (spooning of nails)
 Achlorhydria (atrophy of the mucous membrane)
Predominantly -females around 40
PLUMMER-VINSON SYNDROME
(PATTERSON BROWN-KELLY SYNDROME)
Investigations
 Barium swallow -
 Web in the post-cricoid region
 Subepithelial fibrosis
Oesophagoscopy
 Web in the post-cricoid region
 About 10% - develop post-cricoid carcinoma
 Predisposes to carcinoma
 Tongue, buccal mucosa, pharynx, oesophagus
and stomach.
Web
PLUMMER-VINSON SYNDROME
(PATTERSON BROWN-KELLY SYNDROME)
Treatment
 Correct anaemia
 Oral/parenteral iron
 Serum levels of iron are important than Hb%
 Dilatation of the web
 Oesophageal Bougies
 Oesophageal Baloons
GLOBUS HYSTERICUS
 Functional disorder
 Patient complains of "lump" in the throat
 No true dysphagia
 Feeling of lump is more marked between the
meals
 Rather than during a meal
 Fear of cancer in the throat.
 Clinical examination
 Pharynx, larynx and base of tongue is normal.
 Treatment is reassurance to the patient
when no cause has been found.
MOTILITY DISORDERS OF OESOPHAGUS
 Hypermotility disorder
 Cricopharyngeal spasm
 Diffuse oesophageal spasm
 Nut cracker oesophagus
 Hypomotility disorders
 Cardiac achalasia
 Gastro-oesophageal reflux
 May involve the
 Upper oesophageal sphincter
 Lower oesophageal sphincter
 Body of oesophagus.
CRICOPHARYNGEAL SPASM
 Failure of the upper oesophageal sphincter to relax properly
 Incoordination between
 Relaxation of the upper oesophageal sphincter
 Simultaneous contraction of the pharynx
 Common causes are
 Cerebrovascular accidents
 Parkinson's disease
 Bulbar polio
 Multiple sclerosis
 Muscular dystrophies.
DIFFUSE OESOPHAGEAL SPASM
 Strong non-peristaltic contractions of the body of
oesophagus while sphincteric relaxation is normal
 Symptoms
 Dysphagia
 Odynophagia
 Substernal chest pain - simulating angina pectoris.
 Barium swallow
 Segmented oesophageal spasms
 Rosary bead
 Cork-screw type of oesophagus,
DIFFUSE OESOPHAGEAL SPASM
 Manometry
 Normal relaxation of the sphincter on swallowing.
 Treatment
 Dilatation of lower oesophagus.
 Myotomy - severe cases
 From the arch of aorta to lower sphincter.
NUT-CRACKER OESOPHAGUS
 Strong, high amplitude oesophageal contractions
 Contractions remain peristaltic
 Spasm (contractions are non peristaltic)
Symptoms
 Dysphagia
 Substernal pain
CARDIAC ACHALASIA
 Absence of peristalsis in the body of oesophagus
 High resting pressure in lower oesophagal sphincter
 Lower oesophagal sphincterdoes not relax during
swallowing.
 Symptoms of cardiac achalasia
 Dysphagia,
 Which is more to liquids than solids
 Reverse of that seen in malignancy or strictures
 Regurgitation of swallowed food particularly at night.
CARDIAC ACHALASIA
 Diagnosis
 Barium swallow
 Dilated oesophagus with narrowed
 Rat tail lower end
 Bird-beak appearance
 Manometric studies
 Low pressure in the body of oesophagus
 High pressure at lower sphincter
 Failureof the sphincter to relax
 Endoscopy to exclude
 Benign stricture
 Development of carcinoma
CARDIAC ACHALASIA
 Treatment
 Modified heller's operation
 (Myotomy of the narrowed lower portion of the oesophagus).
 Forceful pneumatic dilatation of the loweroesophagus can be
done in those unfit for surgery.
Gastro-oesophageal Reflux
 Decreased function of lower oesophageal sphincter
 Permitting regurgitation of gastric contents into
oesophagus.
 Other causes
 Pregnancy
 Hiatus hernia
 Scleroderma
 Excessive use of tobacco
 Excessive use of alcohol
 Drugs that relax the smooth muscle
 Anticholinergic
 Beta-adrenergic drugs
 Calcium-channel blockers
Gastro-oesophageal Reflux
 symptoms
 Substernal Pain
 heartburn
 Regurgitation.
Gastro-oesophageal Reflux
Treatment
 Elevation of the head of bed at night.
 Avoiding food at least 3 hours before bed time.
 Antacids
 Drugs that increase tone of lower oesophageal
sphincter, e.g. Metoclopramide.
 H2 receptor antagonistse.g. Cimetidine and ranitidine.
 Avoiding smoking, alcohol, caffeine, chocolates, mints
and carbonated drinks.
 Antircflux surgery, e.g. Nissen's fundoplication.
COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX
Oesophageal
 Oesophagitis
 Oesophageal mucosal erosion and haemorrhage
 Benign oesophageal stricture
 Barrett's oesophagus (normal squamous epithelium of
oesophagus is replaced by columnar epithelium as a
result of continuous inflammation)
 Precancerous condition
COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX
Pulmonary
 Aspiration pneumonia
 Asthma
 Bronchiectasis
COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX
Laryngeal
 Posterior laryngitis - vague pain in throat
 Hoarseness and repeated throat clearing
 Pachydermia laryngitis
 Contact ulcers and granulomas
 Posterior glottic stenosis
 Paroxysmal laryngospasm
 Carcinoma larynx
COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX
Miscellenous
 • Globus hystencus
SCLERODERMA
 Systemic collagen disorder
 Primarily neural
 Secondarily weakening the smooth muscles of
 Lower two-thirds of oesophagus
 Lower oesophageal sphincter.
 Dysphagia may precede cutaneous lesions
 Barium swallow shows
 Absence of peristalsis in distal two third of oesophagus
 Many of these patients have hiatus hernia
 Reflux oesophagitis
 May develop stricture
 Distal part of the oesophagus
 Recurrent inflammatlon
SCHATZKI'S RING
 It occurs at the junction of
 Squamous epithelium
 Columnar epithelium
 At the lower end of oesophagus
 Called lower oesophageal ring
 Age - usually >50 years of age.
 Cause is unknown
SCHATZKI'S RING
Symptoms
 intermittent dysphagia
 bolus obstruction
 may be associated with hiatus hernia.
Treatment is oesophageal dilatation.
THANK
YOU

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DISEASES OF OESOPHAGUS

  • 1. BIRG ANWAR UL HAQ ENT SPECIALIST CMH LAHORE 00923018513303
  • 2.
  • 3. ACUTE OESOPHAGITIS  It is acute inflammation of the oesophagus  Causes  Ingestion of  Hot liquids  Caustic corrosive agents  Laceration due to swallowed foreign body  Trauma of oesophagoscopy  Monilial infection of oesophagus  Systemic disorder  Pemphigus.
  • 4. ACUTE OESOPHAGITIS Symptoms  Dysphagia  Retrosternal burning  Haematemesis Diagnosis  History  X-ray studies  Oesophagoscopy.
  • 5. PERFORATION OF OESOPHAGUS  Aetiology Instrumental trauma  oesophagoscopy of dilatation of strictures with bougies Spontaneous rupture  Follows vomiting  involves mostly the lower third oesophagus. Post-emetic rupture - Boerhaave's syndrome.
  • 6. PERFORATION - DIAGNOSIS Early diagnosis is imperative Develops mediastinitis Can rapidly prove fatal
  • 7. PERFORATION - DIAGNOSIS  Pain in the neck or interscapular region,  Following oesophagoscopy  The features of cervical oesophageal rupture  Pain  Fever  Difficulty to swallow  Local tenderness  Surgical emphysema in the neck.
  • 8. PERFORATION - DIAGNOSIS  The features of thoracic oesophageal rupture  Pain referred to the interscapular region  fever 102-1 04°F(39-40°C)  signs of shock  surgical emphysema in the neck  crunching sound over the heart (Hamman's sign,  because of air in the mediastinum and pneumothorax).  X-rays of the chest and neck are essen tial. They may  reveal widening of the mediastinum and retrovisceral  space, surgical emphysema, pneumothorax, pleural effusion  or gas under rhe diaphmgm.
  • 9. PERFORATION - INVESTIGATIONS  X-rays of the chest and neck are essential  Widening of the  Mediastinum  Retrovisceral space  Surgical emphysema  Pneumothorax  Pleural effusion  Gas under the diaphram.
  • 10. Treatment  NPO  Total parentral nutrition  Massive doses of antibiotics Cervical oesophagus –  Conservative measures  Drainage is required only if suppuration develops
  • 11. Treatment Thoracic oesophagus  Serious  Conservative treatment rarely succeeds
  • 12. Treatment Within 6 hours  Perforation is surgically closed  Pleural cavity drained If diagnosis is delayed  Repair is not possible  Drainage of the infected area.
  • 13. CORROSIVE BURNS OF OESOPHAGUS Aetiology  Acids  Alkalies  Other chemicals may be swallowed accidentally by children  Taken with the purpose of suicide in adults
  • 14. CORROSIVE BURNS OF OESOPHAGUS Pathology  Severity of oesophageal burns depends on the  Nature of corrosive substance  Quantity and concentration  Duration of its contact with the oesophageal wall.  Alkalies are more destructive and penetrate deep into layers of the oesophagus  Entire oesophagus and stomach may slough off causing fatal mediastinitis and peritonitis.
  • 15. CORROSIVE BURNS OF OESOPHAGUS  Oesophageal burns run through three stages:  Stage of necrosis  Stage of granulations  Slough separates leaving granulating ulcer.  Stage of stricture formation  Stricture formation begins at 2 weeks  continues for 2 months or longer.
  • 16. CORROSIVE BURNS OF OESOPHAGUS  Evaluation of patient  Determine the type of caustic ingested  Signs and symptoms of shock  Upper airway obstruction  Mediastinitis  Peritonitis  Acid-base imbalance  Associated burns of face, lips and oral cavity  X-ray of the chest and soft tissue lateral view of neck.
  • 17. CORROSIVE BURNS OF OESOPHAGUS Management  Hospitalize the patient.  Treat shock  Treat acid-base imbalance  Monitor urine output for renal function  Relieve pain  Relieve airway obstruction  Tracheostomy may be required.
  • 18.
  • 19. CORROSIVE BURNS OF OESOPHAGUS  Neutralisation of the corrosive  By appropriate weak acid or alkali  Effective only if done within first 6 hours.  Parenteral antibiotics  Immediately  Continued for 3- 6 weeks depending on the degree of burns
  • 20. CORROSIVE BURNS OF OESOPHAGUS  Pass a nasogastric tube  Oesophagoscopy. - Contravertial  with in 2 days to know  Degree  Extent  Oesophagoscope is not passed beyond the first severe circumferential burn.  Steroids should be started  within 48-96 hours for 4-6 weeks
  • 21. CORROSIVE BURNS OF OESOPHAGUS  Oesophagogram and oesophagoscopy every two weeks,  If stricture develops it can be treated by  Oesophagoscopy and prograde dilatations  Gastrostomy and retrograde dilatation  Oesophageal reconstruction or by-pass  Life- long follow-up.
  • 22. BENIGN STRICTURES OF OESOPHAGUS Aetiology  Occur when muscular coat of the oesophagus is damaged. The common causes are:  Burns due to corrosive substances or hot fluids.  Trauma to oesophageal wall due to  Impacted foreign bodies  Instrumentation  External injuries
  • 23. BENIGN STRICTURES OF OESOPHAGUS Aetiology Ulcerations due to reflux oesophagitis. Ulcerations due to diphtheria, typhoid. Sites of surgical anastomosis . Congenital, usually in the lower third.
  • 24. BENIGN STRICTURES OF OESOPHAGUS Clinical features and diagnosis  Dysphagia  First to solids and then to liquids  Regurgitation  When obstruction is complete  Cough  Malnourished.
  • 25. BENIGN STRICTURES OF OESOPHAGUS Investigations Barium swallow establishes the diagnosis. Oesophagoscopy to exclude malignancy.
  • 26. BENIGN STRICTURES OF OESOPHAGUS  Treatment  Prograde dilatation with bougies.  Gastrostomy  Surgery.  Excision of strictured segment  Reconstruction of food passage using  Stomach  Colon  Jejunum.
  • 27. HIATUS HERNIA  A hiatus hernia occurs when the upper part of the stomach, which is joined to the oesophagus moves up into the chest through the hole (called a hiatus) in the diaphragm.  It is common and occurs in about 10 per cent of people.
  • 28. HIATUS HERNIA • Overweight • Middle-aged • Women and elderly people. • It can occur during pregnancy. • Diagnosis • Barium meal x-rays • Oesophgoscopy
  • 29. HIATUS HERNIA  Symptoms Heartburn Sudden regurgitation Belching Pain on swallowing hot fluids Feeling of food sticking in the oesophagus
  • 30. TREATMENT Mainly it is surgical Hernia is reduced Diaphragmatic opening repaired
  • 31. TREATMENT FOR HIATUS HERNIA • Conservative treatment • Early cases • Unfit for surgery • Sleeping with head and chest raised • Use of drugs that reduce acidity (antacids and cimetidine) • Losing weight • Eating small but frequent meals • Avoid actions which raise intra-abdominal pressure • Avoidance of smoking • Avoid spicy food • Avoid hot drinks • Avoid gassy drinks.
  • 32. PLUMMER-VINSON SYNDROME (PATTERSON BROWN-KELLY SYNDROME) Classical features  Dysphagia  Iron-deficiency anaemia  Glossitis  Angular stomatitis  Koilonychia (spooning of nails)  Achlorhydria (atrophy of the mucous membrane) Predominantly -females around 40
  • 33. PLUMMER-VINSON SYNDROME (PATTERSON BROWN-KELLY SYNDROME) Investigations  Barium swallow -  Web in the post-cricoid region  Subepithelial fibrosis Oesophagoscopy  Web in the post-cricoid region  About 10% - develop post-cricoid carcinoma  Predisposes to carcinoma  Tongue, buccal mucosa, pharynx, oesophagus and stomach.
  • 34. Web
  • 35. PLUMMER-VINSON SYNDROME (PATTERSON BROWN-KELLY SYNDROME) Treatment  Correct anaemia  Oral/parenteral iron  Serum levels of iron are important than Hb%  Dilatation of the web  Oesophageal Bougies  Oesophageal Baloons
  • 36.
  • 37. GLOBUS HYSTERICUS  Functional disorder  Patient complains of "lump" in the throat  No true dysphagia  Feeling of lump is more marked between the meals  Rather than during a meal  Fear of cancer in the throat.  Clinical examination  Pharynx, larynx and base of tongue is normal.  Treatment is reassurance to the patient when no cause has been found.
  • 38. MOTILITY DISORDERS OF OESOPHAGUS  Hypermotility disorder  Cricopharyngeal spasm  Diffuse oesophageal spasm  Nut cracker oesophagus  Hypomotility disorders  Cardiac achalasia  Gastro-oesophageal reflux  May involve the  Upper oesophageal sphincter  Lower oesophageal sphincter  Body of oesophagus.
  • 39. CRICOPHARYNGEAL SPASM  Failure of the upper oesophageal sphincter to relax properly  Incoordination between  Relaxation of the upper oesophageal sphincter  Simultaneous contraction of the pharynx  Common causes are  Cerebrovascular accidents  Parkinson's disease  Bulbar polio  Multiple sclerosis  Muscular dystrophies.
  • 40. DIFFUSE OESOPHAGEAL SPASM  Strong non-peristaltic contractions of the body of oesophagus while sphincteric relaxation is normal  Symptoms  Dysphagia  Odynophagia  Substernal chest pain - simulating angina pectoris.  Barium swallow  Segmented oesophageal spasms  Rosary bead  Cork-screw type of oesophagus,
  • 41. DIFFUSE OESOPHAGEAL SPASM  Manometry  Normal relaxation of the sphincter on swallowing.  Treatment  Dilatation of lower oesophagus.  Myotomy - severe cases  From the arch of aorta to lower sphincter.
  • 42. NUT-CRACKER OESOPHAGUS  Strong, high amplitude oesophageal contractions  Contractions remain peristaltic  Spasm (contractions are non peristaltic) Symptoms  Dysphagia  Substernal pain
  • 43. CARDIAC ACHALASIA  Absence of peristalsis in the body of oesophagus  High resting pressure in lower oesophagal sphincter  Lower oesophagal sphincterdoes not relax during swallowing.  Symptoms of cardiac achalasia  Dysphagia,  Which is more to liquids than solids  Reverse of that seen in malignancy or strictures  Regurgitation of swallowed food particularly at night.
  • 44. CARDIAC ACHALASIA  Diagnosis  Barium swallow  Dilated oesophagus with narrowed  Rat tail lower end  Bird-beak appearance  Manometric studies  Low pressure in the body of oesophagus  High pressure at lower sphincter  Failureof the sphincter to relax  Endoscopy to exclude  Benign stricture  Development of carcinoma
  • 45. CARDIAC ACHALASIA  Treatment  Modified heller's operation  (Myotomy of the narrowed lower portion of the oesophagus).  Forceful pneumatic dilatation of the loweroesophagus can be done in those unfit for surgery.
  • 46. Gastro-oesophageal Reflux  Decreased function of lower oesophageal sphincter  Permitting regurgitation of gastric contents into oesophagus.  Other causes  Pregnancy  Hiatus hernia  Scleroderma  Excessive use of tobacco  Excessive use of alcohol  Drugs that relax the smooth muscle  Anticholinergic  Beta-adrenergic drugs  Calcium-channel blockers
  • 47. Gastro-oesophageal Reflux  symptoms  Substernal Pain  heartburn  Regurgitation.
  • 48. Gastro-oesophageal Reflux Treatment  Elevation of the head of bed at night.  Avoiding food at least 3 hours before bed time.  Antacids  Drugs that increase tone of lower oesophageal sphincter, e.g. Metoclopramide.  H2 receptor antagonistse.g. Cimetidine and ranitidine.  Avoiding smoking, alcohol, caffeine, chocolates, mints and carbonated drinks.  Antircflux surgery, e.g. Nissen's fundoplication.
  • 49. COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX Oesophageal  Oesophagitis  Oesophageal mucosal erosion and haemorrhage  Benign oesophageal stricture  Barrett's oesophagus (normal squamous epithelium of oesophagus is replaced by columnar epithelium as a result of continuous inflammation)  Precancerous condition
  • 50. COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX Pulmonary  Aspiration pneumonia  Asthma  Bronchiectasis
  • 51. COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX Laryngeal  Posterior laryngitis - vague pain in throat  Hoarseness and repeated throat clearing  Pachydermia laryngitis  Contact ulcers and granulomas  Posterior glottic stenosis  Paroxysmal laryngospasm  Carcinoma larynx
  • 52. COMPLICATIONS 0F GASTRO-OESOPHAGEAL REFLUX Miscellenous  • Globus hystencus
  • 53. SCLERODERMA  Systemic collagen disorder  Primarily neural  Secondarily weakening the smooth muscles of  Lower two-thirds of oesophagus  Lower oesophageal sphincter.  Dysphagia may precede cutaneous lesions  Barium swallow shows  Absence of peristalsis in distal two third of oesophagus  Many of these patients have hiatus hernia  Reflux oesophagitis  May develop stricture  Distal part of the oesophagus  Recurrent inflammatlon
  • 54. SCHATZKI'S RING  It occurs at the junction of  Squamous epithelium  Columnar epithelium  At the lower end of oesophagus  Called lower oesophageal ring  Age - usually >50 years of age.  Cause is unknown
  • 55. SCHATZKI'S RING Symptoms  intermittent dysphagia  bolus obstruction  may be associated with hiatus hernia. Treatment is oesophageal dilatation.