1. Esophageal Diseases By
Dr : RAMY A. SAMY

3. Anatomy of Esophagus
Hollow tube formed of striated muscle (upper part) and smooth muscle (lower part).
Length about cm in adults.
Fibers of the cricopharyngeus muscle represent the upper esophageal sphincter (UES).
In thoracic cavity it lies in posterior mediastinum, posterior to the trachea.
Leaves thorax through diaphragmatic hiatus
Lower esophageal sphincter (LES) about 3-5 cm long, ?physiological sphincter.

4. Esophageal Anatomy Upper Esophageal Sphincter (UES)
Esophageal Body (cervical & thoracic)
18 to 24 cm
Functionally the esophagus can be considered in three zones (UES, body, LES). The upper esophageal sphincter (UES) is tonically closed and contracts during inspiration, preventing air from entering into the gastrointestinal tract, and reflux. It relaxes during swallow, belching and vomiting. The lower esophageal sphincter (LES) maintains a steady baseline tone (~20 mm Hg) to prevent gastric contents from entering the esophagus. The LES also contracts during periods of increased intra-abdominal pressure, preventing reflux due to the pressure build up in the abdomen. The esophagus has 2 muscle layers: the inner circular layer and the outer longitudinal layer. The longitudinal muscle shortens the esophagus, while the circular muscle forms lumen-occluding ring contractions. The combination of these localized contractions is responsible for peristalsis. The proximal esophagus contains striated muscle and the distal esophagus smooth muscle, with a long transition zone between. Striated muscle is “faster”.
Lower Esophageal Sphincter (LES)

5. Microscopic Anatomy of esophagus
Mucosa:
Lined with stratified squamous epithelium, rich in glycogen.
Lamina propria
muscularis mucosa : thin layer of smooth muscle
Submucosa
The outer muscular layers: striated in the upper part and smooth in lower 2/3
No serosal covering.

6. Physiology UES: tonically closed, opens 0.2-0.3 sec after a swallow.
Peristaltic contractions,
duration less than 7 sec and
amplitude less than 150 mmHg,
velocity less than 8 cm/sec
LES: tonically closed at rest, pressure 20 mmHg, cholinergic mediated, relaxes with swallowing.
Transient LES relaxation, independent of swallowing is the major cause of reflux.

7. Normal Phases of Swallowing
Voluntary
oropharyngeal phase – bolus is voluntarily moved into the pharynx
Involuntary
UES relaxation
peristalsis (aboral movement)
LES relaxation
Between swallows
UES prevents air entering the esophagus during inspiration and prevents esophagopharyngeal reflux
LES prevents gastroesophageal reflux
peristaltic and non-peristaltic contractions in response to stimuli
capacity for retrograde movement (belch, vomiting) and decompression
Primary peristalsis is a wave that strips the esophagus proximal to distal, pushing the food bolus aborally toward the stomach. In the body, the wave travels at 3-4 cm/s. Secondary peristalsis is induced by esophageal distension from retained bolus, reflux, or swallowed air. It’s role is to clear the esophagus of retained food. Tertiary contractions are simultaneous (nonperistaltic), dysfunctional contractions and have no known physiologic role and are seen more often in the elderly and can be induced by stimuli (stress, reflux, etc.).

9. Esophageal Disorders Motility Anatomic & Structural Reflux Infectious
Neoplastic
Miscellaneous

10. Esophageal Motility Disorders

11. Motility Disorders upper esophageal esophageal body LES
UES disorders
neuromuscular disorders
esophageal body
achalasia
diffuse esophageal spasm
nutcracker esophagus
nonspecific esophageal dysmotility
LES
hypertensive LES
primary disorders
achalasia
diffuse esophageal spasm
nutcracker esophagus
nonspecific esophageal dysmotility
secondary disorders
severe esophagitis
scleroderma
diabetes
Parkinson’s
stroke
These can be further divided into hypomotlity and hypermotlity disorders.

12. Upper Esophageal Motility Disorders
cause oropharyngeal dysphagia (transfer dysphagia)
patients complain of difficulty swallowing
tracheal aspiration may cause symptoms
pharyngoesophageal neuromuscular disorders
stroke
Parkinson’s
Poliomyelitis
multiple sclerosis
diabetes
myasthenia gravis
dermatomyositis and polymyositis
upper esophageal sphincter (cricopharyngeal) dysfunction
These disorders tend to be considered separately from disorders of the body and LES because they are usually due to problems with striated muscle or its extrinsic innervation.

13. UES Disorders cricopharyngeal hypertension cricopharyngeal achalasia
elevated UES resting tone
poorly understood (reflex due to acid reflux or distension)
cricopharyngeal achalasia
incomplete UES relaxation during swallow
may be related to Zenker’s diverticula in some patients
clinical manifestations
localizes as upper (cervical) dysphagia
within seconds of swallowing
coughing, choking, immediate regurgitation, or nasal regurgitation
diagnosis: swallow evaluation & modified barium swallow

14. Motility Disorders of the Body & LES
symptoms: usually dysphagia (intermittent and occurring with liquids & solids)
diagnostic tests
barium esophagram
endoscopy
esophageal manometry
disorders
achalasia
diffuse esophageal spasm (DES)
nutcracker esophagus
hypertensive LES
nonspecific esophageal dysmotility
hypomotility
hypermotlity

15. Achalasia
Failure of relaxation of the LES with swallowing and aperistalsis in lower esophagus.
Due to decreased or absent intramural esophageal ganglion cells.

16. Symptoms of Achalasia
Dysphagia to fluids and solids, intermittent, long -standing.
Regurgitation of undigested food
Chest pain
Aspiration
Weight loss

17. Diagnosis of achalasia
Esophageal manometry:
Absent peristalsis
High LES pressure
Failure of relaxation of LES.
Radiographic studies
Endoscopy to exclude organic disease.

18. Normal Barium swallow

19. Radiology in Achalasia

21. Endoscopy in achalasia

22. TREATMENT OF ACHALASIA
Medical: Smooth muscle relaxants
Balloon Dilatation
Surgical myotomy

23. Diffuse Esophageal Spasm
frequent non-peristaltic contractions
simultaneous onset (or too rapid propagation) of contractions in two or more recording leads
occur with >30% of wet swallows (up to 10% may be seen in “normals”)
This condition is often split from the rest because the response to swallows is non-peristaltic.

24. Nutcracker Esophagus avg pressure in 10 wet swallows is >180 mm Hg
high pressure peristaltic contractions
avg pressure in 10 wet swallows is >180 mm Hg
33% have long duration contractions (>6 sec)
may inter-convert with DES

25. Nonspecific Esophageal Dysmotility
Hypertensive LES
Nonspecific Esophageal Dysmotility
high LES pressure
>45 mm Hg
normal peristalsis
often overlaps with other motility disorders
abnormal motility pattern
fits in no other category
non-peristalsis in 20-30% of wet swallows
low pressure waves (<30 mm Hg)
prolonged contractions
1/3 of pts with non-specific dysmotility will have LES hypertension.

26. Spastic Motility Disorders of the Esophagus
epidemiology
any age (mean age 40)
female > male
symptoms
dysphagia to solids and liquids
intermittent and non-progressive
present in 30-60%, more prevalent in DES (in most studies)
chest pain
constant % across the different disorders (80-90%)
swallowing is not necessarily impaired
can mimic cardiac chest pain
pyrosis (20%) and IBS symptoms (>50%)
symptoms and manometry correlate poorly
Pts often present with both sxs. Rare to see weight loss due to dysphagia here.

27. Spastic Motility Disorders of the Esophagus
diagnosis
manometry
barium esophagram
endoscopy
pH monitoring
treatment
reassurance
nitrates, anticholinergics, hydralazine - all unproven
calcium channel blockers - too few data with negative controlled studies in chest pain
psychotropic drugs – trazodone, imipramine and setraline effective in controlled studies
dilation - anecdotal reports, probable placebo effect
Some anecdotal evidence that the drugs can improve manometric findings, but clinical trials have been disappointing.
In the trazodone ( mg/d) study, a significant improvement was seen but it was not dependent on manometric improvement.
A JAMA trial of dilation found a positive effect equaled by a placebo dilator.

28. Hypomotilty Disorders
primary (idiopathic)
aging produces gradual decrease in contraction strength
reflux patients have varying degrees of hypomotility
more common in patients with atypical reflux symptoms
usually persists after reflux therapy
defined as
low contraction wave pressures (<30 mm Hg)
incomplete peristalsis in 30% or > of wet swallows

29. secondary scleroderma other “connective tissue diseases” diabetes
in >75% of patients
progressive, resulting in aperistalsis in smooth-muscle region
incompetent LES with reflux
other “connective tissue diseases”
CREST
polymyositis & dermatomyositis
diabetes
60% with neuropathy have abnormal motility on testing (most asx)
other
hypothyroidism, alcoholism, amyloidosis

30. Gastroesophageal Reflux

31. DEFINITIONS
Gasrtoesophageal reflux: Reflux of gastric contents to the esophagus
Gastroesophageal reflux disease (GERD): Any significant symptomatic clinical condition or histopathological changes resulting from reflux.
Reflux esophagitis: GERD patients with histopathologically demonstrable changes in the esophageal mucosa.

32. Epidemiology of GERD Heartburn is a very common condition:
3% of population experience heartburn daily
7% frequently
15% weekly
25% monthly
Most common in pregnant women: 80%
Common in obese and smokers

33. Mechanisms of GERD Transient LES relaxation Hypotensive LES
Decreased esophageal acid clearance
Hiatus hernia
Impaired salivation.

34. CLINICAL PICTURE OF GERD
ESOPHAGEAL SYMPTOMS
EXTRAESOPHAGEAL SYMPTOMS

35. ESOPHAGEAL SYMPTOMS OF GERD
HEARTBURN
REGURGITATION
Dysphagia
Chest pain
Water brash
Nausea and vomiting
Belching
Hicough

36. EXTRAESOPHAGEAL SYMPTOMS OF GERD
Chronic cough
Asthma
recurrent pneumonitis
nocturnal choking
hoarseness of voice
posterior laryngitis with ulceration and granuloma formation.
sore throat
dental disease
Earache
Globus sensation

38. Diagnosis of GERD Clinical picture. UGI endoscopy.
24 hour pH monitoring
Radioisotope scanning
Bernstein test : esophageal acid perfusion
Barium swallow.

39. Endoscopy: Normal Junction

40. Reflux esophagitis

41. Reflux esophagitis

42. Reflux esophagitis

43. Complications of GERD Stricture formation Chronic blood loss
Barrett’s epithelium
Adenocarcinoma

44. Esophageal stricture

45. Barrette’s epithelium

46. Natural history of GERD
May be acute condition in a small percentage
Mostly chronic condition with recurrent symptoms
Majority can be controlled on drugs
Majority may require a sort of acid suppressive therapy at 5 years
No clear relation exists between symptoms of reflux, amount of reflux or degree of esophagitis.

47. Management of GERD Life- style modification: avoid cigarette smoking
dietary manipulation: decrease fatty, spicy and acidic foods
decrease weight
elevation of the head of the bed
avoid tight abdominal binders
avoid constipation
avoid large meals
avoid drugs which decrease LES pressure
avoid sleeping after meals for at least 3 hours.

48. Pharmacologic therapy of GERD
Antacids:
Mg trisilicate
Aluminium hydroxide
Ca carbonate
sodium bicarbonate.
H2-blockers:
Cimetidine
ranitidine
famotidine
nizatidine

49. Pharmacologic therapy of GERD
Proton pump inhibitors:
Omeprazole
lansoprazole
pantoprazole
rabeprazole
Esomeprazole
Tenatoprazole
Prokinetic drugs:
metoclopramide
domperidone.

50. Endoscopic therapy for GERD
Sterrata procedure
Entyrex
Gate keeper anti-reflux repair
Gastric plication

51. Antireflux surgery
Indications:
complicated reflux
non compliance for medication
refractory GERD
patient’s preference
severe disease in young person
Most popular operation now is laparoscopic fundoplication

52. Treatment of Barrett’s epithelium
BE usually occurs in longstanding severe reflux disease
BE does not regress after fundoplication or PPI therapy
Screening for dysplasia?
If high grade dysplasia found: esophagectomy
Ablation of BE:
Photodynamic therapy
Argon plasma coagulation
Endoscopic mucosal resection

53. THANK YOU