This presentation is made for undergraduate teaching purpose.

1. DYSPHAGIA
Dr. Juveria Majeed,
MS ENT

2. CLINICAL ANATOMY

3. Introduction
• Deglutition – is a process, whereby a bolus,
liquid or solid is transferred from the buccal cavity
to the stomach.
• 3 phases:
- Oral
- Pharyngeal
- Oesophageal

4. Stages of Swallowing
• Oral phase: voluntary
• Pharyngeal phase:
involuntary reflex
• Esophageal phase:
Peristalsis – Primary
wave- initiated by
impulses from
swallowing center.
Sec. waves are
initiated by a bolus in
the esophagus.
Tertiary contractions-
nonpropulsive,
irregular.

5. Dysphagia
• Defined as a sensation of sticking or obstruction of the
passage of the food in the mouth, pharynx or the
oesophagus.
• Dysphagia should be distinguished from:
Odynophagia- painful swallowing
Aphagia – Absolute dysphagia
Phagophagia – Fear or refusal to swallow
Globus Hystericus – Sensation of lump in the throat.

6. Aetiology of
Dysphagia
Pre-
oesophageal
Causes
Oral Phase
Pharyngeal
Phase
Oesophageal
Causes

7. Pre-oesophageal causes
• Oral Phase: Normally
food must be
masticated, lubricated
with saliva and
converted into a bolus.
Then its pushed by
tongue against hard
palate into pharynx.
Any disturbance in this
sequences will cause
dysphagia.

8. Oral causes
Disturbance in
mastication
Trismus, #mandible, Tumors of
upper or lower jaw, disorders of TM
joint.
Disturbance in
lubrication
Xerostomia foll. RT, Mickulicz
disease
Disturbance in
mobility of tongue
Paralysis of tongue, painful ulcers,
tumors of tongue,, lingual abscess
Defects of palate Cleft palate, oronasal fistula
Lesions of buccal
cavity and floor of
mouth
Stomatitis, ulcerative lesions,
ludwigs angina

9. Pharyngeal Phase
• For a normal swallow,
food should enter the
pharynx and then be
directed towards the
oesophageal opening.
All unwanted
connections into the
nasopharynx, larynx
and oral cavity should
be cut off.

10. Pharyngeal phase causes leading
to dysphagia
Obstructive
lesions of pharynx
Tumors of tonsil, soft palate, base of
tongue, supraglottic larynx, or even
obstructive hypertrophied tonsils
Inflammatory
Conditions
Ac.tonsillitis, peritonsillar abscess,
retro or parapharyngeal abscess,
ac.epiglottitis, edema larynx.
Spasmodic
conditions
Tetanus, rabies
Paralytic
conditions
Paralysis of soft palate due to
diphteria, bulbar palsy, CVA.They
cause regurgitation into nose.
Lesions of vagus and b/l SLN leading
to aspiration.

11. Oesophageal Causes
• Atresia, FB, Strictures,
Benign and Malignant
tumors
Lesions in the
lumen of
oesophagus
• Ac. Or Ch. oesophagitis
• Motility disorders- hypomotility
(achalasia,scleroderma)
• Hypermotility disorders-
cricopharyngeal spasm, diffuse
oesophageal spasm.
Lesions on the
wall of
oesophagus
• Hypopharyngeal diverticulum
• Hiatus Hernia
• Cervical osteophytes
• Thyroid lesions, eg enlargement, tumors,
hashimotos thyroiditis.
• Mediastinal lesions eg. Tumors, LN
enlargement, aortic aneurysm, cardiac
enlargement.
• Vascular rings- Dysphagia Lusoria.
Lesions
outside the wall
of oesophagus

12. HOW TO EVALUATE A CASE OF
DYSPHAGIA???

13. History
Clinical
Examination
Radiography Blood
Examination
Manometric
and pH
studies
Oesophagos
copy
Other
investigation
s

14. HISTORY
• Sudden or gradual onset?
• Progressive?
• Intermittent?
• More to liquids?
• More to solids, progressing to
liquids?
• Intolerance to acid foods?
• Associated symptoms- regurgitation
and heart burn, cough on lying
supine, aspiration into lungs.

15. Clinical Examination:
Examination of oral cavity
oropharynx,
hypopharynx
larynx to exclude pre
oesophageal causes of dysphagia.
Examination of neck, chest and nervous
system.

16. Radiography
• Xray chest
• Xray Neck lateral view
• Barium swallow

17. FB Oesophagus Oesophageal Stricture

18. BARIUM SWALLOW
Achalasia Cardia Ca. Oesophagus

19. Blood Investigations:
Hemogram – Plummer vinsons syndrome

20. Manometric and pH
studies:
These studies help in
motility disorders,
gastro-oesophageal
reflux and to find
whether oesophageal
spasms are
spontaneous or acid
induced.

21. Oesophagoscopy
It gives direct
examination of
oesophageal mucosa
and permits biopsy
specimens.
Flexible fibre optic or rigid
scopes.

22. Oesophageal webs and
rings

23. Other investigations
• Bronchoscopy (for bronchial carcinoma)
• Cardiac catheterisation (for vascular
anomalies
• Thyroid scan (for malignant thyroid)

24. NEOPLASMS OF OESOPHAGUS

25. Benign Neoplasms
• Rare compared to malignant ones.
• Leiomyomas – most common (2/3rds of all
benign neoplasms)
• Dysphagia
• Treatment is enucleation of the tumors by
thoracotomy.
• Other rare tumors- mucosal polyps,
lipomas, fibromas and hemangiomas.

26. Carcinoma Oesophagus
Incidence:
• High in China, Japan, USSR and south
Africa.
• In India, it constitutes 3.6% of all body
cancers

27. Aetiology:
Smoking and Alcohol
consumption
Dietary habits.
Pre-existing pathological
lesions such as strictures,
cardiac achlasia, diverticula
and hiatus hernia.
Barrets oesophagus

28. Barrett’s Oesophagus

29. Pathology
• SCC is the most
common (93%).
• Adenocarcinoma
(3%) is also seen,
but in the lower
esophagus, and
maybe an upward
extension of the
gastric ca.

30. Spread of Carcinoma
• Direct
• Lymphatic
• Blood borne

31. Clinical Features
• Substernal discomfort
• Progressive dysphagia and emaciation
• Vomitings
• Back Pain
• Aspiration problem

32. DIAGNOSIS
• Barium swallow
• Oesophagoscopy
• Bronchoscopy
• CT
• MRI
• PET- CT

33. Barium swallow

34. CT Scan

35. PET Scan

37. • Early stages- Endoscopic mucosal
resection(EMR) , Surgery.
• Surgery is the preferred method of
treatment for cancer of lower 2/3rd.
• Affected segment with wide margin along
with the fundus of the stomach can be
removed followed by primary
reconstruction.
• Surgery of upper 2/3rd is difficult due to
great vessels and involvement of
mediastinal nodes.
• Radiotherapy is the treatment of choice.

38. In advanced lesions, only palliation is possible. An
alternative food channel can be provided by:
• A by pass operation
• Oesophageal intubation with Celestin or
Mousseau Barbin or a similar tube.
• Permanent gastrostomy or a feeding jejunostomy
• Laser surgery: Oesophageal growth is burnt with
Nd:YAG lase to provide a food channel.

39. Surgery followed by
reconstruction

40. RADIOTHERAPY
• SCC of oesophagus are radiosensitive .
• Radiotherapy to a dose of 6000cGy is
employed for ca. esophagus.

41. CHEMOTHERAPY
• CT is used only as a palliative measure in
the locally advanced or disseminated
disease. Commonly in combination with
RT.
• Mtx, Bleomycin,5FU, Cisplatin have been
used in SCC.

42. COMBINED MODALITY TREATMENT
• Is the best modality for advanced
oesophageal ca.
• Improves five-year survival rate.
• Surgery + CT
• Surgery + RT
• CT+RT
• Radiochemotherapy+ Surgery
• Prognosis: Five-year survival rate not more
than 5-10%

43. THANK YOU