ESOPHAGEAL DISORDERS

 GERD
 ESOPHAGITIS
 MOTILITY DISORDERS
Diseases of esophagus

 Functions of esophagus
 Transfer of food to stomach
 Prevention of reflux of stomach contents (LES)
Symptoms
 Dysphagia
 Sensation of sticking or obstruction of passage of food though mouth,
pharynx, or esophagus
 Heartburn
 Pyrosis
 Characteristic of reflux esophagitis
 Aggravated by bending straining or lying recumbent
 Worse after meals
 Bernstein test – 0.1 N HCL is infused to reproduce symptoms
 Odynophagia
 Painful swallowing
 Non-reflex esophgtitis
 Monilial, herpes, pill esophagitis, barrett’s ulcerr, carcinoma, caustic damage,
perforation.
 Esophagial pain
Esophagial pain

 Different from Heartburn, Odynophagia

 May occur with GERD or motility disorders like
Diffuse esophageal spasm (DES) called atypical
chest pain or non-cardiac chest pain.
 CAD must be ruled out
 A trial of PPI is given and motility study may be
done.
 Some respond to low dose antidepressants
Regurgitation

 Effortless appearance of gastric or

esophageal contents in mouth.
 Tasteless mucoid or undigested food
 Achalasia, diverticulum
 Sour or Bitter tasting material
 Severe GE reflux
 May result in chronic cough, laryngitis, laryngeal
aspiration, awaking pt. from sleep with choking
and coughing, aspiration pneumonia.
Diagnostic tests

 Barium swallow with fluoroscopy and

Esophagogram used for
 Structural disorders
 Motility disorders
 Videofluoroscopy sees
 Oral and pharyngeal phases of swallowing
 Esophageal peristalsis is best studied in lying down
position
 Double contrast esophagogram demonstrates
 Mucosal ulcers
 Early cancers
Video fluoroscopy
Double contrast esophagogram
Esophagoscopy

 Endoscopy is usually performed under

sedation
 Biopsy
 Carcinoma
 Esophagitis
 Eosinophilic esophagitis
Motility Studies

 Simultaneous recording of pressures from

different sites in lumen
 Pressure sensors 5 cm apart
 Diagnosis of achalasia, DES, scleroderma,
LES competence
Dysphagia

 Aphagia
 Bolus impaction, medical emergency
 Difficulty in initiating a swallow
 Voluntary phase disorder
 Odynophagia
 Globus Pharyngeus
 Sensation of lump in throat, but normal swallowing
 Misdirection of food
 Nasal, laryngeal, aspiration
 Phagophobia/Refusal to swallow
 Fear to swallow
 Rabies, tetanus, hysteria, pharyngeal paralysis
Physiology of swallowing
 Voluntary oral phase
 Preparatory phase
 Transfer phase
 Activation of oropharyngeal sensory receptors
 Initiation of deglutition reflex
 Propulsion of food into pharynx
 Prevention of entry into larynx
 Contraction of superior pharyngeal constrictor
against soft palate initiates peristalsis
 Primary peristalsis
 Peristalsis in response to swallow
 Secondary peristalsis
 In response to residual food
 Deglutitive inhibition
 Preceeds peristaltic contraction
Nerve supply

 Innervated by lower motor neurons of cranial

nerves V, VII, IX and XII
 UES
 Constrictor (cricopharyngeus) X th nv.
 Dilators (suprahyoid, geniohyoid) V th & VII th Nv
Dysphagia

 Mechanical
 Motor
 Oropharyngeal
 Esophageal
Approach to dysphagia
Difficulty in initiation, regurgitation through nose, coughing, choking

 Yes oropharyngeal type

 No Esophageal type
 Neromuscular findings
 Yes Motor oropharyngeal
 No Mechanical
 Mental status
 Normal VFSS
 Oral, Pharyngeal
 Dysphagia to solids, liquids
 Solids only
 Esophageal mechanical
 Both
 Esophageal motor
 Barium swallow,OGD,Motility study
 Episodic or progressive Rings/Carcinoma
 Prominent heartburn Scleroderma/Achalasia
GERD
 GERD
 15% have heartburn once a week, 7% have daily
 Due to back flow of acid into esophagus due to
incompetent barriers
 Normal antireflux mechanisms
 LES,
 Crural diaphragm,
 Anatomic location of LES below diaphragmatic hiatus
GERD

 Sustained hypotension of LES

 Primary
 Secondary
 Pregnancy, smoking, beta adrenergic agonists,
aminophylline, nitrates, CCB’s, phosphodiesterase
inhibitors
 Scleroderma
 Myopathy with chronic intestinal pseudoobstruction
 Surgical damage to LES
 Esophagitis
LES pressure

 Contraction
 Muscarinic M2, M3 receptor agonists
 Alpha adrenergic agonists
 Gastrin
 Substance P
 Prostaglandin F2a
LES relaxation
 Nicotine
 Beta adrenergic agonists
 Dopamine
 Cholecystokinin
Belching,
Gastric distention (vagovagal reflex)
 Secretin
Fatty meals
 VIP
Smoking
 Adenosine Beverages with high xanthine (tea,
 Prostaglandin E coffee, cola)
 Nitrates
 Phosphodiesterase
inhibitors (sildenafil)
 Reflux occurs when
 Gastric volume is increased
 After meals
 Pyloric obstruction
 Gastric stasis
 Acid hypersecretion states
 Gastric contents are near LES
 Recumbency
 Bending down
 Hiatal hernia
 Gastric pressure is increased
 Obesity
 Pregnancy
 Ascites
 Tight clothes
Esophageal exposure

 Amount of refluxed material per episode

 Frequency of reflux episodes
 Rate of clearing of esophagus by gravity and
peristalsis
 Impaired peristalsis
 Impaired salivary secretions
 Can enter pharynx, larynx, trachea
Reflux esophagitis

 Mucosal defenses are unable to counteract damage

 Mild esophagitis
 Microsopic changes
 Erosive esophagitis
 Clear mucosal damage
 Redness
 Friability
 Superficial linear ulcers and exudates
 Peptic strictures
 Short strictures 1-3 cm
 Long strictures
 Barrett’s esophagus may develop
 Clinical features
 Heartburn
 By contact of refluxed material with sensitized or
ulcerated esophageal mucosa
 Atypical chest pain
 Regurgitation of sour material into mouth
 In 1/3rd dysphagia is presenting symptom
 Bleeding due to mucosal erosions or barrett’s
ulcer.
 Many remain asymptomatic
 Many treat themselves without medical help
Extraesophageal
manifestations
 Chronic cough
 Laryngitis
 Pharyngitis
 Morning hoarsness
 Aggravation of chronic bronchitis, asthma,
pulmonary fibrosis, COPD, Pneumonia
 Chronic sinusitis and dental decay
Diagnosis
 History is most important
 Therapeutic trial with PPI for 1 week is
supportive
 Diagnostic studies indicated with persistent
symptoms on therapy or those with
complications
Diagnostic approach

 Documentation of mucosal injury

 Barium swallow, esophagoscopy, mucosal biopsy
 Biopsy should be performed at least 5 cm above LES
 Documentation and quantization of reflux
 Ambulatory pH testing 24-48 hr (pH sensitive
capsule {BRAVO})
 Endoscopic esophagitis does not correlate with
reflux
 Treatment
 Goals
 Symptom relief
 Heal erosive esophagitis
 Prevent complications
 Mild cases
 wt reduction, elevation of head end of bed 4-6 inches,
quit smoking, avoid fatty food, coffee, chocolate,
alcohol, mint, orange juice, anticholinergics, CCB’s,
Nitrates, avoid large quantities of fluids with meals
 Lifestyle changes with H2 blockers or PPI may be
sufficient
 PPI for 8 weeks heal erosive esophagitis in 90%
Treatment

 Refractory patients
 Double dose PPI
 Long term maintenance
 Acid suppression does not lead to resolution of
barrett’s metaplasia
 Anti reflux surgery
 Fundoplication (young patients are ideal
candidates)
Fundoplication
 Barrett’s esophagus
 Metaplasia of esophageal squamous to columnar
epithelium.
 Complication of severe reflux esophagitis
 Risk factor for esophageal adenocarcinoma
 Metaplasia occurs in continued acid reflux as
columnar epithelium is more resistant to acid-
pepsin damage than squamous.
 Long segment >2-3 cm 1-5% of GERD
 Short segment <2-3 cm10-15% of GERD
 Rate of cancer development 0.5% per year in long
segment
Barrett’s esophagus

 Progress occurs through low grade dysplasia(LGD),

high grade dysplasia(HGD).
 Optical methods of recognizing dysplasia being
developed.
 One time endoscopy in persistent GERD > 50 yrs is
recommended
 Dysplasia must be ruled out with multiple biopsies.
 HGD progresses to CA in 20%, so 3 monthly follow-
up
 In LGD 6 monthly for 1 yr, then every 3 years.
Inflammatory disorders
 Infectious esophagitis
 Viral
 Herpes simplex 1 & 2
 CMV
 VZV
 HIV
 Bacterial and fungal
 Lactobacillus
 Beta hemolytic streptococci
 Cryptosporidium
 Pneumocystic carinii
 Mycobacterium tubeculosis
 Candida esophagitis
 Other types of esophagitis
 Eosinophilic esophagitis
 Multiple concentric rings in esophagus
 Radiation esophagitis
 Doxorubicin
 Bleomycin
 Cyclophosphamide
 Cisplatin
 Corrosive esophagitis
 Pill induced esophagitis
 Doxycycline, tetracycline, oxytetracycline, minocycline
 Potassium chloride, ferrous sulphate, theophylline, ascorbic acid
 Bisphosphonates
Motor disorders of esophagus
 Achalasia cardia
 Loss of peristalsis and LES does not relax on
swallowing
 Loss of intramural neurons
 Primary
 Secondary
 Gastric CA, Lymphoma, Chaga’s disease, viral infections,
eosinophilic gastroenteritis, neurodegenerative disorders.
 Occurs at all ages in both sexes
 Chest pain and regurgitation
 Dysphagia Both to solids and liquids.
Achalasia

 Diagnosis
 Loss of gastric air bubble
 Tubular mass besides
aorta, air fluid level in
mediastinum
 Barium swallow
persistent beak like
narrowing
 CCK test – paradoxical contraction of LES
(loss of neurally trasmitted effect of CCK)
 Treatment
 Nitrates, CCB, Botulinum toxin injection, Balloon
dilatation,
 Heller’s extramural myotomy, Laparoscopic
myotomy with fundoplication
 Diffuse esophageal spasm (DES)
 DES shows non-peristaltic contractions
 Duration prolonged, repetitive, varying amplitude
 Non-peristaltic contractions
 Dysfunction of inhibitory nerves
 Patchy neural degenration
 Chest pain at rest, on swallowing, emotional stress
 Retrosternal, radiates to back, sides of chest, both
arms, sides of jaw, from seconds to minutes.
 Dysphagia may occur to solids and liquids
DES

 CAD must be ruled out

 Best diagnosed by manometry
 Barium
 Normal sequential peristalsis is
replaced by uncoordinated
simultaneous contractions
 Cork-screw esophagus
 Treatment
 Nitrates, CCB
Hypertensive motor
disorderas
 Nutcracker esophagus
 Normal peristalsis
 Hypertensive contractions
 Hypercontracting LES
 Normal relaxation followed by hypertensive
contraction
 Hypertensive LES
 Basal pressure is elevated
 Contraction and relaxation are normal
 Scleroderma esophagus
 CREST syndrome
 Atrophy of smooth muscle
 Weakness in lower 2/3rd of esophagus
 Incompetence of LES
 Wall is thin with patches of fibrosis
 Dysphagia to solids and liquids
 Heartburn, regurgitation
Scleroderma esophagus

 Barium
 Dilation, loss of peristalsis in the middle, patulous
LES
 Mucosal changes, ulceration, stricture
 Motility studies
 Reduced pressure of peristaltic contractions
 Decreased LES pressure
 Similar abnormalities found in other collagen
vascular disorders like Raynaud’s phenomenon
Boerhaave’s syndrome

 Spontaneous rupure of esophagus associated

with forceful vomiting or retching.
 Subcutaneous emphysema
 Retrosternal chest pain worsened by swallowing and
breathing
 Mediastinal crackling sounds on auscultation
 Pneumothorax
 Secondary infection
 Mediastinal abscess
 Pleural fluid has salivary amylase content