Diseases of the

Esophagus
R1 Sawanya/R3 Pisit/A.Rutti
Contents

▪ ANATOMY
▪ ESOPHAGEAL SYMPTOM ASSESSMENT
▪ ESOPHAGEAL TESTING
▪ ESOPHAGEAL DISEASE STATES THAT CAUSE DYSPHAGIA
▪ OTHER ESOPHAGEAL DISEASE STATE
▪ ESOPHAGEAL MANIFESTATIONS OF SYSTEMIC DISEASE
ANATOMY

▪ 25 CM
▪ Muscular tube
▪ Pharynx to the stomach
▪ Posterior to the Trachea
▪ Anterior to the thoracic aorta
▪ Pierces the diaphragm at T10 level
 ANATOMY

▪ Left-Right-Left pattern
▪ Bends to the left of the tracheal margin
▪ It crosses the midline behind the
aortic arch at T4
▪ Then turns to the right at T7
▪ Turns sharply to the left as it enters the
diaphragm  join the cardia of the
stomach at the gastroesophageal (GE)
junction
 HISTOLOGY

▪ Mucosa:
– Epithelium: nonkeratinized stratified squamous
epithelium g
– Lamina propria: fibrovascular connective tissue f
– Muscularis mucosae: smooth muscle bundles
oriented longitudinally
begins at cricoid cartilage and resemble
muscularis propria e
▪ Submucosa: loose connective tissue with vessels,
lymphatics, and white blood cells d
▪ Muscularis propria: inner circular c and
outer longitudinal layers b
▪ Adventitia: Loose connective tissue a
http://www.pathologyoutlines.com/topic/esophagusnormalhistology.html
ESOPHAGEAL SYMPTOM ASSESSMENT

▪ Primary symptoms
– Heartburn
▪ substernal burning sensation
▪ 30 minutes to 2 hours after meals
▪ worse by lying down or bending over
▪ Large meals
▪ strongly suggests the diagnosis of GERD
– Odynophagia
▪ pain caused by swallowing
▪ inflammatory condition
 ESOPHAGEAL SYMPTOM ASSESSMENT

 Primary symptoms
- Dysphagia
Oropharyngeal dysphagia Esophageal dysphagia

Difficulty in initiating a swallow Difficulty transporting food down

Disruptions of finely coordination secondary to Structural or neuromuscular defects

neuromuscular dysfunction

Upper esophagus, pharynx, UES, Body of the esophagus

Coughing, choking, gagging, or nasal regurgitation,

Neurodeficit

Liquids Solids and liquids

 ESOPHAGEAL SYMPTOM ASSESSMENT

▪ Primary symptoms
– Dysphagia
ESOPHAGEAL SYMPTOM ASSESSMENT

▪ Primary symptoms
– Regurgitation
– Acid or bitter taste in the mouth
– Severe at night , awakening with coughing and choking.
– Water brash : vagally mediated , Not regurgutation

▪ Other ancillary symptoms

▪ Noncardiac Chest pain
– longer duration, positional, related to meals, and associated with other GI symptoms

▪ Globus sensation
– feeling of a lump, fullness, or “tickle” in the throat

▪ Asthma, cough, hoarseness, sore throat, and repetitive throat clearing

 ENDOSCOPY

PROVOCATIVE ESOPHAGEAL
TESTING MANOMETRY

ESOPHAGEAL
TESTING
AMBULATORY
NEW 24-HOUR
TECHNOLOGIES ESOPHAGEAL
PH
AMBULATORY MONITORING
24-HOUR
BILE
MONITORING
ENDOSCOPY

▪ Evaluate the mucosa

▪ detect structural abnormalities
▪ Biopsy and treatment
▪ standard upper endoscope = 9 mm in diameter, smaller and larger
▪ local anesthetic sprayed and IV sedation
▪ swallow  relax the UES
 ENDOSCOPY

▪ Smooth and light pink mucosa

▪ Gastroesophageal junction (GEJ) :
proximal margin of the gastric folds
▪ Squamocolumnar junction :
irregular Z line
▪ Normally located at the same level
ENDOSCOPY
ENDOSCOPY : INDICATIONS

▪ Warning symptoms
– weight loss
– upper GI bleeding :
severe esophagitis , Mallory- Weiss tears , and esophageal varices
– dysphagia
– odynophagia
– chest pain
▪ Partial or no response to empiric therapy
▪ Evaluation for BE
 ESOPHAGEAL MANOMETRY

▪ Intraluminal pressures and coordination of the pressure activities of

▪ 1) LES : Resting LES pressure and relaxation
2) Esophageal body : Amplitude and duration of contractions and
peristalsis
3) UES : UES pressure and relaxation
– limited information : great variability
– barium radiography
▪ Standard for diagnosis of motor disorders of the esophageal body and LES
Normal Esophageal Manometry

▪ Progressive peristaltic contraction in the

body of esophagus
▪ Wave amplitude 30-180 mmHg
▪ LES relaxes completely to gastric baseline
at the end of peristalsis
ESOPHAGEAL MANOMETRY
AMBULATORY 24-HOUR ESOPHAGEAL PH MONITORING

▪ Diagnosis and management of GERD

▪ Detect and quantify gastroesophageal reflux and correlate
symptoms
▪ Primary indications
▪ 1) to document excessive acid reflux in patients with suspected
GERD but without endoscopic esophagitis
▪ 2) to evaluate the efficacy of medical or surgical therapy
 AMBULATORY 24-HOUR ESOPHAGEAL PH MONITORING

▪ Distal esophageal acid : probe 5 cm above the LES

alarm
C
– reflux episode : abrupt drop in pH below 4.0
– abnormal = total time that the pH is less than 4 exceeds 4.2% of the study period
– exclude artifact
▪ Record events on a diary card
– Normal diary activities
AMBULATORY 24-HOUR ESOPHAGEAL PH MONITORING

▪ Good correlation is considered to be 50%

▪ Confirmed only by the response to appropriate antireflux therapy
▪ Off therapy & On therapy
▪ Proximal esophageal pH probe
– 15 cm to 20 cm above the LES
– Abnormal = total time with pH below 4.0 is more than 1%
▪ Hypopharyngeal probe
– 2 cm above the UES
– more than 2 - 3 episodes
AMBULATORY 24-HOUR BILE MONITORING

▪ Bile and pancreatic enzymes  Duodenogastroesophageal reflux (DGER)

▪ Spectrophotometer : absorption band at 450 nm
▪ Bilirubin absorbance is greater than 0.14 %
▪ Clinical role is limited, and it is no longer available
NEW TECHNOLOGIES

▪ Wireless ambulatory pH monitoring

▪ Bravo
– Standard upper GI endoscopy with capsule probe placed 6 cm above the GEJ
– recording 48 hours of pH data.
– Passed in the stool after 4 to 10 days

1) prolonged monitoring (48 h vs. 24 h)

2) improved compliance
3) reduced impairment of daily activities
4) decreased catheter movement
during the study
NEW TECHNOLOGIES

▪ Restech
– minimally invasive device with colored light-emitting tip
– 1.5-mm oropharyngeal catheter
– assess patients with suspected extraesophageal reflux disease
NEW TECHNOLOGIES

▪ Multichannel intraluminal impedance (MII)

▪ Measures both acidic and nonacidic refluxate of liquid or gas consistency
▪ Evaluation of typical or atypical reflux symptoms refractory to acid
suppression
▪ Most accurate and detailed method
NEW TECHNOLOGIES

▪ clinical indications : still evolving

– Relevance of nonacid reflux in
specific clinical settings has to be
further discerned
– Paucity of quality blinded,
randomized, controlled studies are
available that have examined the
benefit of treating nonacid reflux
 PROVOCATIVE TESTING

▪ 0.1 N hydrochloric acid VS NSS in noncardiac chest pain Pt

▪ IV injection of edrophonium (80 ug/kg )
– esophageal manometric changes and chest pain in 20% - 30% of patients with
noncardiac chest pain

▪ Low sensitivity, wide variability and poor correlation between contractions

and chest pain
Esophageal disease that Other Esophageal Disease Esophageal Manifestations of
cause dysphagia States Systemic Disease

Esophageal Motility Gastroesophageal Reflux Disease

Abnormality Extraesophageal Systemic
Gastroesophageal Reflux Disease
• Achalasia
• Nonachalasia Motility Barrett Esophagus
Diseases
Disorders Neoplasia

Esophageal Diverticula
Stritures
Foreign Body Cutaneous
Rings and Webs Pill-Induced Infury Diseases and
Infectious Esophagitis The Esophagus
Eosinophilis Esophagitis Caustic INjury
Esophageal disease that
cause dysphagia

Esophageal Motility
Abnormality
• Achalasia
• Nonachalasia Motility
Disorders

Strictures

Rings and Webs

Eosinophilic Esophagitis
Esophageal Motility Abnormality

 4 Major patterns
1) Inadequate LES relaxation
2) Uncoordinated contraction
3) Hypercontraction
4) Hypocontraction
 Can overlap
Esophageal Motility Abnormality :
Achalasia

▪ Unknown etiology
▪ Insufficient LES relaxation and loss of esophageal peristalsis
▪ Hereditary, Degenerative, Autoimmune, and Infectious factors
Achalasia : Pathophysiology

Patchy inflammatory infiltrate of T lymphocytes, eosinophils, and

mast cells; loss of ganglion cells; and myenteric neural fibrosis

Selective loss of postganglionic inhibitory neurons

Sparing postganglionic cholinergic neurons of the

myenteric plexus

Unopposed cholinergic stimulation

High basal LES pressures

Insufficient LES relaxation

Achalasia : Symptoms

▪ Dysphagia :
– First solids  then progress to solids and liquids
– cervical or xiphoid areas
– Accommodations : lifting the neck or drinking carbonated beverages
▪ Regurgitation : 75 %
– Esophagus dilates with progression of the disease.
– Recumbent position
– Awakened by choking and coughing
▪ Chest pain : 40 %
 Achalasia : Investigation

▪ Barium esophagram with

fluoroscopy
– Best initial investigation
– Loss of primary peristalsis in the
distal 2/3 of the esophagus
– Heterogeneous air-fluid level at the
top of the barium column
– Closed LES : bird’s beak
– In late stage : massive dilation with
a sigmoid-like tortuosity
Achalasia : Investigation

▪ Esophageal manometry
– Establish the diagnosis
– In the body of the esophagus, aperistalsis is always present.
– Absence or incompleteness of LES relaxation with swallows
▪ 70% to 80%
▪ Complete relaxations but short duration
Normal Achalasia

▪ Elevated LES pressure

with minimal
relaxation

▪ Aperistalsis
– Isobaric contraction
without propagation
Achalasia : Investigation

▪ Upper endoscopy
– Findings
▪ Esophageal body appears dilated and tortuous
▪ Retained secretions and food debris may be encountered
▪ The LES appears puckered and remains closed with air insufflation
– Exclude pseudoachalasia
▪ Mimic both clinically and manometrically
▪ Tumor at the GEJ
– older age
– short duration
– significant weight loss
Achalasia : Treatments

▪ Surgery
– Pneumatic dilation
▪ endoscopically
▪ uses air pressure to dilate and disrupt the circular muscle fibers of the LES
▪ balloon dilators — 3, 3.5, and 4 cm
▪ followed by barium swallow to exclude esophageal perforation (2-5 %)
– Surgical myotomy
▪ Anterior myotomy across the LES (Heller myotomy)
– usually associated with an antireflux procedure
▪ Laparoscopy ; good to excellent response rate of 80% to 94%
▪ A potential complication is GERD (10% - 20% )
Achalasia : Treatments

▪ Medication
▪ High risk for pneumatic dilation or surgery
▪ Endoscopic injection of the LES with botulinum toxin
– inhibits the release of acetylcholine from nerve terminals
– effectiveness : 85% of patients
– Recurrence : more than 50% of patients at 6 months

▪ Pharmacologic treatment with nitrates or calcium channel blockers.

– reduce LES pressure and temporarily relieve dysphagia
– short acting, not provide complete symptom relief, efficacy decreases with time
– botulinum toxin injections fail
Esophageal Motility Abnormality :
Nonachalasia Motility Disorders

▪ Defined on the specific manometric criteria

▪ Clinical relevance is questionable
▪ Most : chest pain or dysphagia
Nonachalasia : Diffuse esophageal spasm

▪ Manometric changes
– simultaneous and repetitive contractions in the esophageal body
– some normal peristalsis is maintained.
– LES relaxation is also normal in diffuse esophageal spasm
Nonachalasia : Diffuse esophageal spasm
Nonachalasia : Diffuse esophageal spasm

▪ The classic finding on esophagram

– corkscrew esophagus
▪ chest pain, if the contraction amplitudes are high
▪ dysphagia, if the contraction amplitudes are low
▪ medications :
– nitrates and calcium channel blockers
– not completely effective

Corkscrew esophagus
Nonachalasia : Nutcracker esophagus

▪ Noncardiac chest pain

▪ It is defined by high-amplitude peristalsis
▪ This condition appears unlikely to be a true primary motility disorder
but is rather a marker for increased visceral pain perception
 Nonachalasia : Hypocontractile disorder

▪ Distal esophageal contraction amplitude of less than 30 mm Hg in 30% or more of wet swallows
▪ Higher incidence in patients with GERD, especially in those with respiratory symptoms
▪ Dysphagia : Food bolus may not be effectively transported
Esophageal disease that
cause dysphagia

Esophageal Motility
Abnormality
• Achalasia
• Nonachalasia Motility
Disorders

Strictures

Rings and Webs

Eosinophilic Esophagitis
 Esophageal Strictures

▪ Loss of lumen area within the esophagus

▪ The normal esophagus measures 20 mm in diameter
▪ Predominant symptom = dysphagia
– luminal diameter is less than 15 mm.
▪ Less severe strictures + large food pieces
– intermittent dysphagia
Esophageal Strictures : Etiology

Most common
▪ 60% to 70%
 Esophageal Strictures :
Esophagram

▪ Distal esophageal stricture

▪ The smooth taper of the distal esophagus
is consistent with a benign peptic
stricture
Esophageal Strictures : Treatments

▪ Main : Esophageal dilation

▪ Goal : diameter greater than 15 mm
– 1) mercury-filled rubber Maloney bougies Uncomplicated, short,
straight strictures

– 2) wire-guided rigid Savary-Gilliard dilators

– 3) balloon dilators

Long, tight,
or tortuous strictures
Esophageal Strictures : Treatments

▪ Complications :
– perforation (0.5%), bleeding (0.3%), and bacteremia (20% to 50%)
– higher risk with radiation-induced or malignant strictures
– To minimize risk : rule of threes
▪ 90% no recurrence at 24 months
– Diameter greater than 15 mm
Refractory Esophageal Strictures

▪ Lack of response to two or more dilations

▪ Causes
– ongoing insults from pills or NSAID drugs
– uncontrolled acid reflux
– inadequate lumen diameter achieved by dilations

▪ Treatment
– elimination of offending agents (pills and acid)
– gentle dilation to 15 mm
– Intralesional injection of steroids before dilation
– Surgery : fail to respond to aggressive medical therapy and dilation
▪ Preventing recurrence of acid-related strictures
– PPIs are superior to H2 blockers
Esophageal disease that
cause dysphagia

Esophageal Motility
Abnormality
• Achalasia
• Nonachalasia Motility
Disorders

Strictures

Rings and Webs

Eosinophilic Esophagitis
Esophageal Rings and Webs

▪ Common findings on upper endoscopy

▪ Symptoms
– asymptomatic
– intermittent solid food dysphagia
– aspiration
– regurgitation

Rings Webs
Circumferential Thin, eccentric lesion

Mucosa or muscle Always mucosal

Distal esophagus Proximal esophagus

Esophageal Webs

▪ Symptoms
– 5% of asymptomatic individuals
– When symptomatic : dysphagia

▪ Plummer-Vinson or Paterson-Kelly syndrome

– Triad that consists of proximal esophageal webs, iron deficiency anemia, and
dysphagia

▪ Investigation
– Barium radiography is the most sensitive
– Endoscopic visualization is also possible, and the web will appear as a thin, eccentric
lesion with normal-looking mucosa.

▪ Treatment : Symptomatic
– Mechanical disruption : Bougie or Balloon dilator
Esophageal Webs

The endoscopic view : Severe stenosis was

clearly visualized just beyond the esophageal
entrance
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6465006/
 Esophageal Rings

▪ The Schatzki ring or B-ring

– GEJ at the distal margin of the LES
– most common cause of intermittent solid food dysphagia
and food impaction
▪ Ring diameter less than 13 mm, the patient has symptoms
▪ Greater than 20 mm, the patient almost never has symptoms
▪ Between 13 and 20 mm, symptoms are variable : Most common
Esophageal Rings

▪ The pathogenesis : controversial

– congenital lesions
– GERD

▪ Investigation
– Barium swallow study :
The most sensitive test
– Endoscopy with air insufflation

▪ .
Esophageal Rings

▪ Treatment : symptomatic patients

– Mechanical bougienage is usually used
– Recurrent symptoms that require repeat dilation are not uncommon
▪ Some authorities recommend maintenance therapy with acid
suppression, given the possible association of a Schatzki ring with
GERD.
Esophageal Rings

▪ The second type of esophageal ring is the A-ring

– A muscular ring most commonly detected on barium swallow study
– Rarely symptomatic
– Proximal margin of the LES
2 cm proximal to the squamocolumnar junction
Esophageal disease that
cause dysphagia

Esophageal Motility
Abnormality
• Achalasia
• Nonachalasia Motility
Disorders

Strictures

Rings and Webs

Eosinophilic Esophagitis
 Eosinophilic Esophagitis

▪ Known as Ringed, feline, or corrugated esophagus

▪ Dysphagia and often food impaction, especially in young adults
▪ Endoscopic findings
– Multiple esophageal rings in patients with dysphagia

▪ Eosinophil density :
– More than 15 eosinophils per high-power field
on both proximal and distal esophageal biopsies

https://www.endoscopy-campus.com/en/classifications/eosinophilic-esophagitis/

▪ Associated with other atopic diseases and food allergies

Patients may also have a strong family history of atopy
Eosinophilic Esophagitis

▪ Given the limitations of the unknown natural history

▪ Lack of consensus on the therapeutic goal, a number of medical,
dietary, and endoscopic therapies are reported
▪ Treatment options
– acid suppression
– six-food elimination diet : milk, eggs, nuts, wheat, soy and seafood
– corticosteroid metered-dose inhaler
– esophageal dilation
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic INjury
Gastroesophageal Reflux Disease

▪ Chronic symptoms or mucosal damage secondary to the abnormal

reflux of gastric contents into the esophagus
▪ Spectrum
– Reflux esophagitis
▪ histopathologically demonstrated characteristic changes in the esophageal mucosa
30% to 40%
– Nonerosive reflux disease
▪ typical GERD symptoms
▪ without endoscopic findings of esophageal erosion
▪ 50% of cases
– BE
▪ 10% to 20%.
Gastroesophageal Reflux Disease

▪ Defects in the esophagogastric barrier transiently or

permanently
– Transient LES relaxation (TLESR)
▪ Primary mechanism in normal individuals and in patients with mild GERD
– LES incompetence
– Hiatal hernia
▪ severe GERD and complications
– Delayed gastric emptying
▪ gastroduodenal contents : acid, pepsin, bile acids, and trypsin
▪ esophageal defense break down  the severity of reflux increases
GERD : Symptoms

Heartburn • Retrosternal burning discomfort

• After meals
Acid regurgitation
• Recumbent

Dysphagia
Odynophagia
Belching
• Asthma
• Chest pain
Atypical GERD • Cough
• Laryngitis
• Dental erosions
GERD : Diagnosis

▪ No diagnostic gold standard

▪ Classic symptoms of acid regurgitation and heartburn are specific but
not sensitive for the diagnosis
▪ Initial empiric trial of antisecretory therapy in a patient with classic
GERD symptoms
▪ Further diagnostic testing should be considered
– does not respond to an empiric course of antisecretory therapy
– alarms signs : dysphagia, odynophagia, weight loss, chest pain, and choking
GERD : Diagnosis

▪ Endoscopy
– Evaluate the mucosa
– Reflux esophagitis : erosions or ulcerations at the squamocolumnar junction
▪ Los Angeles classification
GERD : Diagnosis

▪ Ambulatory 24-hour pH monitoring

– limitations
▪ Results are normal in 25% of patients with erosive esophagitis and in 33% of
patients with nonerosive reflux disease
– Useful to
▪ Quantitate esophageal acid exposure
▪ Allows for the correlation of symptoms to reflux events

▪ Clinical response to acid suppression is a good indication that a

patient’s symptoms may be due to GERD
GERD : Treatments

▪ Goals : relieve symptoms, heal the esophagitis, prevent

recurrence of symptoms, and prevent complications
▪ Lifestyle modifications
– Avoidance of precipitating foods (fatty foods, alcohol, caffeine)
– Avoidance of recumbency for 3 hours postprandially
– Elevation of the head of the bed
– Smoking cessation
– Weight loss
GERD : Treatments

▪ Medications
– PPIs
▪ Superior to H2 blockers
▪ Remission rate in 80% of patients
– H2 blockers : remission rate of 50%
▪ Step-down therapy
– Initially treated with PPIs
– Clinical improve  H2 blockers or PPIs on an as-needed basis
GERD : Treatments

▪ Medications
– Antacids and alginic
▪ Temporary relief of episodic heartburn
– Sucralfate
– Mild reflux esophagitis
– Few published data are available on the use of sucralfate in GERD
– Histamine receptor antagonists (H2 blockers)
▪ Standard divided : complete symptom relief in approximately 60% of patients
and heal esophagitis in about 50%
▪ Mild to moderate severity
▪ Poor in severe reflux esophagitis
GERD : Treatments

▪ Antireflux surgery
▪ Laparoscopic approach
▪ Candidate
– Patient with typical symptoms that respond completely to antisecretory therapy
▪ cost or potential adverse effects associated with long-term PPI therapy
– Patients with large hiatal hernias and predominant regurgitation symptoms
– GERD is refractory to acid suppression with high-dose PPI therapy
▪ Studies with impedance pH monitoring
▪ Possible benefit of surgery in those with continued nonacid reflux

▪ Not advised in patients with GERD unresponsive to PPIs who have no

evidence of esophageal acid exposure or nonacid regurgitation
GERD : Treatments

▪ Antireflux surgery
▪ Endoscopic suturing
▪ Injectable agents for bulking the GEJ
– Enteryx  Withdraw
– Gatekeeper Reflux Repair System from Medtronic (Minneapolis, MN)

▪ Radiofrequency energy delivery to the GEJ

▪ Role, Safety, Efficacy are not clear
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic Injury
 Extraesophageal Gastroesophageal Reflux
Disease

▪ GERD may manifest as symptoms other than heartburn and regurgitation

▪ Response to antireflux therapy : less predictable
▪ Empiric trial of twice-daily PPI therapy is indicated as initial treatment
▪ If treatment fails, full investigation with ambulatory pH testing is
recommended to ensure that medical therapy has been intensive enough
▪ The diagnosis of GERD can be confirmed only when the symptom is relieved
consistently with specific antireflux therapy
 Laryngitis

Dental Asthma
erosions
Extraesophageal
Gastroesophageal
Reflux Disease

Chronic
Chest pain
cough
 Laryngitis

▪ Laryngitis or laryngopharyngeal reflux : LPR

▪ Symptoms
– hoarseness, throat clearing, dysphagia, increased phlegm, and globus
sensation
▪ Laryngeal changes
– Erythema, edema, pharyngeal ulcerations,
vocal cord nodules and polyps, granulomas,
and even leukoplakia and cancer
– Exclude smoking, excessive alcohol use,
allergies, asthma, viral illnesses, or voice abuse
Laryngitis

▪ Three most common laryngeal findings

– Interarytenoid bar
– Arytenoid medial wall erythema
– Posterior pharyngeal wall cobblestoning

▪ Overdiagnosis of GERD because of the poor specificity

▪ 24-hour pH monitoring
– May not be the perfect test for diagnosing atypical GERD
– 50% of patients with abnormal laryngoscope
– Proximal and Distal probe  75% and 50% sensitive for classic GERD
– Conflict in predict clinical improvement
Laryngitis

▪ H2 blockers
– Mild to moderate improvements at best

▪ PPIs
– More effective
– First line of therapy in patients in suspected LPR
– Clinical response rates 60% to 98%

▪ Initial aggressive therapy with twice-daily PPI dosing followed by

tapering to once-daily PPI if response to therapy
Evaluation and Management of Laryngopharyngeal Reflux Disease: State of the Art Review
Otolaryngology–Head and Neck Surgery 2019, Vol. 160(5) 762–782
Asthma

▪ 70% to 80% of patients with asthma have GERD

▪ Pathophysiologic mechanisms
– Proximal esophageal reflux leads to microaspiration/bronchospasm
– Vagally mediated esophageal-bronchial reflex results in bronchospasm

▪ Patients with adult-onset asthma, no family history of asthma or atopy,

and heartburn, nocturnal wheezing and wheezing that is exacerbated by
meals, exercise, or the supine position
▪ Ambulatory pH monitoring for asthma : controversy
▪ Treatment of GERD in patients with asthma usually improves respiratory
symptoms in 69% of patients, and it reduces asthma medication use by 62%
Chest Pain

▪ Noncardiac chest pain angina-like substernal chest pain

▪ Cardiac workup results are negative
▪ Pulmonary, musculoskeletal, or esophageal cause
▪ GERD  40% to 60% of patients
▪ Initial therapy is a trial of PPIs for 3 months
▪ Endoscopy
– Dysphagia, odynophagia, and weight loss
Chronic Cough

▪ GERD is the third most common cause (after postnasal drip and asthma)
▪ Cough duration greater than 3 months
▪ Irritation of the upper respiratory tract or stimulation of an esophageal-
bronchial cough reflex
▪ normal CXR , Nonsmokers, No medications known to cause cough, such as
ACEI, : Diagnosis of Exclusion
▪ The best initial evaluation is a trial of PPI therapy 3 months
▪ Can take this long to resolve
▪ 24-hour pH monitoring may be helpful
– Correlation between reflux events and cough
Dental Erosion

▪ Dental erosion is a loss of tooth structure secondary to a chemical,

chronic exposure to acid
▪ Dental erosions in patients with GERD has varied from 17% to 68%
▪ Referral to a dentist can lead to prompt diagnosis and treatment of
dental lesions and institution of preventive dental therapy
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic Injury
 Barrette Esophagus
▪ Serious complication of long-
standing GERD.
▪ Normal stratified squamous
epithelium of the distal
esophagus has been replaced
by intestinal columnar
metaplasia
▪ Predisposes to the
development of esophageal
adenocarcinoma
▪ Endoscopic
– pale pink squamous mucosa of the
distal esophagus is replaced to
various length with salmon-pink
columnar mucosa
Barrette Esophagus

• Squamocolumnar junction is displaced proximal to the GEJ

• confirmed with a biopsy
• Intestinal metaplasia : mucin-containing goblet cells

Normal Barrett

Metaplasia
Barrette Esophagus

▪ Types
– Short segment : metaplasia is shorter than 3 cm
– Long segment : : metaplasia is longer than 3 cm
▪ 6% to 12% of patients who undergo endoscopy for GERD are found to have BE
▪ No specific symptoms
▪ Screening for BE : multiple risk for esophageal adenocarcinoma
– 50 years or older
– Male
– White race
– Chronic GERD
– Hiatal hernia
– Elevated body mass index (BMI)
– Intraabdominal distribution of body fat
Barrette Esophagus

▪ Endoscopic surveillance
– Detect the development of dysplasia and adenocarcinoma(0.12-0.5%)
– Early detection and Treatment in curable stage  Good prognosis
– Four-quadrant biopsies at 2-cm intervals along the entire length of the
affected area
– Biopsies at mucosal abnormalities
– Every 3 to 5 years
– Not perform : Uncontrolled active inflammation of GERD
Barrette Esophagus

▪ 1) Negative for dysplasia : every 3 to 5 years

▪ 2) Indefinite for dysplasia
▪ 3) Low-grade dysplasia every 6 to 12 months
– followed up for a mean of 26 months
– 28% progressed to high-grade dysplasia or adenocarcinoma
– 62% had regression of the dysplasia
– 12%continued to have low-grade dysplasia

▪ 4) High-grade dysplasia
– As high as 59% at 5 years and as low as 20% at 7 years
– 6% per patient per year
– Need Further investigations

▪ 5) Carcinoma
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic Injury
Neoplasia

Squamous cell carcinoma Adenocarcinoma

African-American men White men
Alcohol and tobacco abuse GERD and BE
Caustic injury
Achalasia, Plummer-Vinson syndrome, tylosis
History of head and neck SCC
HPV
Mid  distal  proximal Distal and GEJ
Locally invasive TE fistulas and RLN injury Less locally invasive
Distant metastases : lung, liver, bone, brain. More lymphatic and liver metastases
Neoplasia

▪ Symptoms
– Rapidly progressive solid food dysphagia (mechanical obstruction)
– Weight loss 75 %
– Less common : Odynophagia, iron deficiency, or hoarseness (RLN injury)
▪ CT : Accurately identify metastatic disease
▪ Endoscopic ultrasonography : Evaluation of the depth of invasion
Neoplasia

▪ T1 or T2 , N0 , M0 : Surgery alone
▪ T3 or N1 : Neoadjuvant chemotherapy and/or irradiation before surgery
▪ Late stage : Palliative treatment
– Repeated dilation
– Laser/photodynamic therapy ablation
– Esophageal stent placement
– Percutaneous endoscopy gastrostomy tube placement

▪ Increased screening and surveillance for BE in patients with GERD for

early detection of Adenocarcinoma
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic Injury
Esophageal Diverticula

▪ Sac that protrudes from the esophageal

wall.
▪ True diverticulum : all layers of the wall
▪ False diverticulum : mucosa and
submucosa
▪ Four categories :
– 1) Zenker diverticula
– 2) Midesophageal diverticula
– 3) Epiphrenic diverticula
– 4) Intramural pseudodiverticulosis
 Esophageal Diverticula
1 Zenker diverticulum

▪ Zenker diverticulum/esophageal diverticulum/ hypopharyngeal diverticulum

▪ Above the UES
▪ Killian triangle : Area of weakness
▪ Incomplete relaxation of the UES
▪ Oropharyngeal dysphagia, regurgitation of undigested food, halitosis, cough,
and aspiration pneumonia
▪ The barium swallow
▪ Treatment
– Open surgical resection of the diverticulum with division of the cricopharyngeus muscles
– Diverticulopexy
 Esophageal Diverticula
2 Midesophageal diverticula
▪ Midesophageal diverticula : most commonly asymptomatic
 Traction diverticula
 External pulling of the
esophageal wall
 The middle third of the
esophagus
 Only true diverticula in the
esophagus
 Pulsion diverticula
 Internal forces
 Relate to motility disorders
 Pathogenesis is similar to that
of Zenker and epiphrenic
diverticula
 Esophageal Diverticula
3 Epiphrenic diverticula

▪ Near the diaphragmatic hiatus, occur in the distal esophagus near the LES
▪ Result of a motility disorder ; achalasia or diffuse esophageal spasm
▪ Manometric studies : rule out an associated motility disorder
▪ Asymptomatic, chest pain or regurgitation
▪ Treatment
– Managing the underlying motility disorder
– Symptomatic diverticula ;
Diverticulotomy with or without myotomy
Esophageal Diverticula
4 Intramural pseudodiverticula

▪ Along Esophagus
▪ Multiple small outpouchings lesion
▪ Dilatated submucosal glands
▪ Associated with acid reflux, esophageal
strictures, and esophageal cancer
Zenker diverticulum Midesophageal Epiphrenic diverticula Intramural
diverticula pseudodiverticula
Above the UES Mid-esophagus Diaphragmatic hiatus, Along Esophagus
Killian triangle near the LES
Incomplete relaxation of External pulling Motility disorder Dilatated submucosal
the UES Traction diverticula glands
Internal forces
pulsion diverticula
Oropharyngeal Most commonly Asymptomatic, chest Associated with acid
dysphagia, regurgitation, asymptomatic pain or regurgitation reflux, esophageal
halitosis, cough, strictures, and
aspiration pneumonia esophageal cancer

Barium swallow Manometric studies

Open surgical resection, Underlying causes
diverticulopexy Diverticulotomy with or
without myotomy
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic Injury
Foreign Body

▪ Accidental or Intentional
▪ Pediatric patients, psychiatric patients, and prisoners
▪ Management : Nature of foreign body and its location
▪ Physiologic narrowing : the UES, Aortic arch, Diaphragmatic hiatus/LES
▪ True foreign body OR Food impaction
Foreign Body : Food impaction

▪ Benign structural abnormalities , history of intermittent solid food dysphagia

▪ Sudden onset of dysphagia after swallowing a large piece of food
▪ Chest pain and difficulty swallowing saliva
▪ CXR : PA ,Lateral
– Free air and look for bones

▪ Management
– Nonurgent endoscopy ( can swallow their own saliva ), preferably within 12 hours
– Gentle and safety push to the stomach
– Remove by piecemeal extraction : May use overtube
Foreign Body
Foreign Body food impaction

▪ Management
– Assessed for underlying pathology
– Inflammation : Dilation should be arranged at a later date
– No or only minimal inflammation : Dilation may be performed safely in the
same session
 Foreign Body : True foreign bodies

▪ Plain neck, chest, and abdominal radiographs

– Perforation and to attempt to localize a foreign body

▪ Sharp or long objects : should be removed regardless of location

– In the esophagus  emergency
– In the stomach  urgency
– Grasped from its blunt end, with its sharp end directed distally, to minimize the risk of perforation
– Not within reach of the endoscope : Close monitor and F/U Film
– Surgery : Perforation, Obstruction, or Non-progression

▪ Small blunt objects : can passed the esophagus  pass the GI tract
– Smaller than the usual esophageal diameter of 20 mm
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Injury

Infectious Esophagitis

Caustic INjury
Pill-Induced Injury

▪ Over 70 drugs
– Potassium chloride tablets, Doxycycline, Quinidine, NSAIDs, Iron, and
Alendronate

▪ Various mechanisms
Acidity, Size, and Contact time
▪ Acute self-limited esophagitis to refractory strictures
▪ The typical sites : The physiologic narrowings
▪ Symptoms
– Chest pain and odynophagia
– Dysphagia usually reflects a stricture within the inflammatory changes
Pill-Induced Injury

▪ Endoscopy : Ulcer formation, plaques (R/O Candida infection) and strictures.

▪ Management
– repeated dilations for strictures
– avoidance

▪ prevent further damage

– liquid form and with sufficient fluids
– upright for 15 - 30 minutes

▪ resolve within weeks after stops taking pill

Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Infury

Infectious Esophagitis

Caustic Injury
Infectious Esophagitis

▪ Immunosuppressed hosts
▪ Symptoms
– Odynophagia
– In immunodeficient : Heartburn, nausea, fever, and bleeding

1 Candida albicans
▪ Diabetes mellitus, alcoholism, and users of glucocorticoids, advanced
age, and motility disorders
▪ Oral thrush
 Infectious Esophagitis

▪ Endoscopy with biopsy and brushings

– White to pale yellow plaques ( not pathognomonic )
– Brushings of the plaques  Hyphae and budding yeast
▪ Treatment
– Antifungal therapy :
fluconazole : 100 - 200 mg per day for 10 to 14 days
– Mild immunologic deficiencies :
▪ Topical antifungals clotrimazole and nystatin (alternatives )
– Granulocytopenia and more severe
▪ Amphotericin B to prevent disseminated candida disease
 Infectious Esophagitis

2 CMV
▪ Infects the submucosal fibroblasts and endothelial cells
▪ Abdominal pain, nausea, vomiting, painful swallowing
▪ Endoscopic findings
– serpiginous erosions and ulcers, which may coalesce and form deep,
larger ulcers
▪ Tissue diagnosis : biopsy at bases of the ulcers
– Intranuclear and cytoplasmic inclusions and a halo surrounding the nucleus

▪ Viral culture : more sensitive

▪ Treatment
– Ganciclovir and Foscarnet
– Immunocompromised : Initial2-week full dose regimen then maintenance therapy for
several weeks
 Infectious Esophagitis

3 HSV
▪ Both immunocompetent and immunocompromised hosts.
▪ Endoscopy
– esophageal vesicles that rupture to create ulcers with raised edges

▪ Infects epithelial cells

▪ Tissue diagnosis : biopsy specimens must be taken from the ulcer margins
– Multinucleated giant cells and ground-glass intranuclear inclusion bodies

▪ Viral culture : more sensitive

▪ Treatment
– IV acyclovir : 5 to 10 mg/kg every 8 hours, until tolerate oral therapy
– 7 to 10 days
Other Esophageal Disease
States

Gastroesophageal Reflux Disease

Extraesophageal
Gastroesophageal Reflux Disease
Barrett Esophagus

Neoplasia

Esophageal Diverticula

Foreign Body

Pill-Induced Infury

Infectious Esophagitis

Caustic Injury
Caustic Injury

▪ Accidentally or attention
▪ Alkali or acids
▪ Early signs and symptoms often do not correlate with the severity and extent of
tissue injury
▪ Complication
– Upper airway obstruction
– Perforation and mediastinitis

▪ Management
– Intubation
– Upper endoscopy first 24 to 48 hours after ingestion
– Grading system
– Able to swallow without pain or vomiting  liquids can be started after 48 hours
Caustic Injury

Late complication
▪ Esophageal strictures
– Narrowed areas, More longer and tighter
– Dilation or surgery
▪ SCC
– More than 1,000 fold
– Mean time : 40 years
– Endoscopic surveillance for SCC
Esophageal Manifestations of
Systemic Disease

Systemic
Diseases

Cutaneous
Diseases and
The Esophagus
 Systemic Diseases : Scleroderma (PSS)

▪ Small-vessel vasculitis and proliferation of connective

tissue with fibrosis of multiple organs
▪ GI involvement occurs in 90%
▪ Heartburn, regurgitation, and dysphagia
▪ Affects smooth muscle in the GI tract  Motility
abnormalities and progressive loss of peristalsis
▪ Manometric findings : Aperistalsis in the distal 2/3 of
the esophagus and very low LES pressure
▪ Barium esophagrams : Dilated esophagus,
patulous GEJ, and free reflux into the proximal
esophagus
Systemic Diseases : Scleroderma (PSS)

▪ Severe, complicated GERD and sequelae : Barrett metaplasia esophagitis,

and strictures
▪ Treatment
– Aggressive acid suppression
– Dilations of strictures
– Surveillance of BE
– Control of the underlying disease
▪ Other connective tissue diseases
– Mixed connective tissue disease, inflammatory myopathies, SLE, RA,
and Sjögren syndrome

▪ The myopathies : Affect striated muscle

– Dysfunction in the oropharynx and proximal esophagus and oropharyngeal dysphagia
Systemic Diseases

Behçet disease Diabetes mellitus

▪ Idiopathic inflammatory disorder ▪ Predominantly decreased

peristalsis and esophageal
▪ Recurrent oral and genital emptying
aphthous ulceration
▪ Gastroparesis  in secondary
▪ Esophageal ulcerations, erosions, GERD symptoms
esophagitis, and perforation
▪ Treatment with
▪ Usually small bowel or colonic – Promotility agents : largely
ulceration : R/O Crohn disease ineffective for the esophageal
dysmotility
Systemic Diseases
Hypothyroidism
▪ Rare cause of dysphagia
▪ Manometry : decreased
amplitude and velocity of
peristalsis
▪ Thyroid replacement therapy
Amyloidosis
▪ Esophageal symptoms are rare
▪ Manometry : Aperistalsis,
hypomotility, an incompletely
relaxing LES, decreased LES
pressure
▪ Results from neurogenic
dysfunction
Esophageal Manifestations of
Systemic Disease

Systemic
Diseases

Cutaneous
Diseases and
The Esophagus
Dystrophic epidermolysis bullosa

▪ Autosomal dominant
▪ Blisters of the skin, mouth, and esophagus that develop during childhood
▪ Minor trauma from food  severe dysphagia and odynophagia.
▪ heal with fibrosis  esophageal strictures  malnutrition.
▪ Endoscopy : relatively contraindicated
– gentle dilation of strictures

▪ esophageal resection and replacement

▪ lifelong parenteral nutrition.
Bullous skin disease
Bullous pemphigoid
most common bullous skin
disease
subepidermal bullae
pruritic plaques that evolve
into bullae.
Rarely Esophageal
involvement
steroids
predispose to esophageal
carcinoma
Cicatricial pemphigoid Pemphigus vulgaris
autoimmune disease
mucosal surfaces Intraepidermal bullae
heal by fibrosis bullae and erosions along with
Bullae, webs and strictures the mouth
proximal esophagus
Esophageal involvement : < frequently involved
5%
steroids, steroids
stricture dilation
predispose to esophageal
carcinoma
Thank you