GERD and its

supraesophageal or
extraesophageal
manafestations

Dr. Varunsingh Saggu

 What is GERD

► A condition that occurs when

the lower esophageal
sphincter (LES) does not
close properly and stomach
contents leak back, or reflux,
into the esophagus.

► The LES is a ring of muscle

at the bottom of the
esophagus that acts like a
valve between the
esophagus and stomach.
 Prevalence of GERD

Approximately 20% of adults have frequent

"classic" symptoms of gastroesophageal reflux
(GER):

► Heartburn
► Regurgitation.
Clinical Presentations of GERD

►ClassicGERD
►Extraesophageal/Atypical GERD
►Complicated GERD
 What causes GERD?

► Noone knows why

people get GERD.

►A hiatal hernia may

contribute.
Other factors that may contribute to GERD

► Alcoholuse
► Overweight
► Pregnancy
► Smoking
Certain foods can be associated with reflux events

► Citrus fruits
► Chocolate
► Drinks with caffeine
► Fatty and fried foods
► Garlic and onions
► Mint flavorings
► Spicy foods
► Tomato-based foods, like spaghetti sauce, chili, and pizza
 What are the symptoms of GERD

► Persistent heartburn and acid

regurgitation.
► Belching
► Waterbrash (sudden excess of
saliva)
► Sour taste in the mouth
► Food stuck in throat
► Difficulty or pain when swallowing
► Chest pain
► Hoarseness
► Choking or throat tightness.
► Chronic sore throat
► Dry cough
► Bad breath
► Inflammation of the gums
► Erosion of tooth enamel (the
surface of the teeth)
 How is GERD diagnosed?

► Review of symptoms and a complete

physical examination, with Special
attention to alarming symptoms.

 Duration & severity of symptoms

 Anemia
 Dysphagia (Difficulty in swollowing)
 Weight loss
 When to Perform Diagnostic
Tests
► Uncertain diagnosis
► Atypical symptoms
► Symptoms associated with complications
► Inadequate response to therapy
► Recurrent symptoms
► Prior to anti-reflux surgery
 Diagnosis of supraesophageal Reflux

1. Heartburn and regurgitation

many of these patients fail to demonstrate the typical symptoms
of heartburn and regurgitation

2. The response of symptoms to an empirical trial of

antireflux therapy

3. Ambulatory, esophageal pH monitoring

4. Upper gastrointestinal endoscopy

Most do not have esophagitis when looked at endoscopically.
Clinical Presentations of GERD

►ClassicGERD
►Extraesophageal/Atypical GERD
►Complicated GERD
► pathophysilogy
 Food is passed from the
pharynx into the esophagus by a
mechanism called peristalsis. This
propelling motion is carried out
by the muscles and the central nervous
system. (Porth, 1998)
 Peristalsis continues in the
esophagus.

The food is carried

from the esophagus
to the stomach
where acid

production is formed.
(Porth,1998)

Image with permission from MDA

 “The esophagus is very
muscular and collapses
when empty.
It is 10 inches or 25cm in
length”
(Porth, 1998)
 The esophagus is sometimes
referred to as the “food tube”
or the gullet. It extends from the
pharynx, which is the back of the
throat and goes through the
diaphram to the stomach.
Clip Art derived from
Microsoft Office
The esophagus is posterior
to (behind) the trachea

Image with permission from Bristol-Meyers Squibb

 “The esophagus produces
bicarbonate and mucus”.(Kahrilas, 2003)

“The bicarbonate buffers the acid

and mucus forming a protective

barrier”.(Kahrilas, 2003)
Clip Art derived from
Microsoft Office
This creates an environment in the
esophagus of a higher pH than that
of the stomach. The pH in the
esophagus is normally about 7-8,
whereas the pH in the stomach is
generally 2-4. (Kahrilas, 2003)
 pH stands for potential of
hydrogen.
Hydrogen is what causes materials to
become acidic. 7 is considered
neutral; anything under 7 is
considered acidic. (Porth, 1998)
 There are specialized cells deep in the
stomach lining that affect the rate of
acid production. The primary cells
which contribute to acid production
are known as parietal cells. (Kahrilas, 2003)

Clip Art derived from

Microsoft Office
The binding of these 3 receptors in the
parietal cells initiates the process of
acid production. (Kahrilas, 2003)

PARIETAL
CELLS

Acetylcholine Gastrin Histamine

Each gastric parietal cell contains
about 1 million acid pumps.
“The primary function of the
activated pumps are to :
Exchange hydrogen ions from the
parietal cells to potassium using
energy derived from splitting ATP.”
(Kahrilas, 2003)

Clip Art derived from

Microsoft Office
Ions exchange at different rates based
on the permeability of the parietal
cells. The rate influences the
intracellular pH, resulting in
an environment of acidity or alkalinity
of the cells of the stomach. (Kahrilas,
2003)
 “The stomach produces an average of
2 liters of HCL a day, which in
combination with the protein-splitting
enzyme pepsin, breaks down
chemicals in food”. (Kahrilas 2003)

Clip Art derived from

Microsoft Office
There is a rare disorder, called
Zollinger-Ellison syndrome:
With this, the body produces an
excessive amount of acid, this
can increase the risk of
GERD. (CNN.com)
 The esophagus is divided into:

Upper Lower
It has a sphincter to It has a sphincter
prevent air from that opens while
entering the food is being
esophagus during passed into the
respirations. The stomach. It is
sphincter generally known as the LES,
only opens for food to lower esophageal
pass. sphincter.
( Porth, 1998)
 How is GERD treated?

► LifestyleChanges
► Medications
► Surgery
► Endoscopic options
Treatment Goals for GERD

► Eliminate symptoms
► Heal esophagitis
► Manage or prevent
complications
► Maintain remission
 Lifestyle Changes
► If you smoke, stop.
► Do not drink alcohol.
► Lose weight if needed.
► Eat small meals.
► Wear loose-fitting clothes.
► Avoid lying down for 3 hours after a meal.
► Raise the head of your bed 6 to 8 inches by
putting blocks of wood under the bedposts--
just using extra pillows will not help.
 Medications

► Proton pump inhibitors

 omeprazole (Prilosec)
 lansoprazole (Prevacid)
 pantoprazole (Protonix)
 rabeprazole (Aciphex)
 esomeprazole (Nexium)

► Prokinetics
 Bethanechol (Urecholine)
 Metoclopramide (Primpran)
 Domperidone (Motilium)
 Endoscopic GERD Therapy

► Endoscopic antireflux therapies

 Radiofrequency energy delivered to the LES
►Stretta procedure
 Suture ligation of the cardia
►Endoscopic plication
 Submucosal implantation of inert material in
the region of the lower esophageal sphincter
►Enteryx
 When to Discuss Anti-Reflux
Surgery with Patients

► Intractable GERD – rare

 Difficult to manage strictures
 Severe bleeding from esophagitis
 Non-healing ulcers
► GERD requiring long-term PPI-BID in a
healthy young patient
► Persistent regurgitation/aspiration symptoms
► Not Barrett’s esophagus alone
► Complications'
Long-term complications of GERD?

► Inflammation of the esophagus

► Bleeding or ulcers
► strictures
► Barrett's esophagus and adenoarcinoma
► Supraesphageal manafestations
 Asthma
 chronic cough
 pulmonary fibrosis
 ENT manafestations
 Symptoms of Complicated
GERD
► Dysphagia
 Difficulty swallowing: food sticks or hangs
up
► Odynophagia
 Retrosternal pain with swallowing
► Bleeding
 Extraesophageal disorders in GERD

Extraesophageal manifestations of gastroesophageal reflux disorder

(GERD) are frequent, and consist broadly of

► Noncardiac chest pain

► pulmonary diseases
 Asthma
 chronic cough
 recurrent bronchitis
 sleep apnea
 pulmonary fibrosis
► laryngeal diseases
 Laryngitis
 subglottic stenosis
 laryngeal cancer
► other ENT (ear, nose, throat) disorders
 Sinusitis
 Otitis media
 Pharyngitis
 dental erosion
 Noncardiac chest pain is associated with GERD

► Among patients with angina-like chest pain

 30% will have normal coronary arteries; of these, 40% to 50% have
objective evidence of GERD by endoscopy or ambulatory pH monitoring

► Prevalence of GERD symptoms is 23% to 100%

► Esophagitis is seen in 0% to 47%

► Abnormal ambulatory pH recordings noted in 20% to 63%

► Empiric trial of PPI

 78% sensitivity and 86% specificity , for diagnosing GERD association with
noncardiac chest pain.
 GERD and Chronic Cough

► Direct mucosal injury and/or

► Triggering vagally mediated mechanisms
 Increased airway secretions
 Bronchospasm
 Nonacid Gastroesophageal Reflux

► Reflux of gastric contents

 Food
 Nonacidic material.

► Symptoms that fail to respond to aggressive therapy with

proton-pump inhibitors may still improve after antireflux
surgery

► Traditional pH testing (which detects reductions in

intraesophageal pH from a baseline of pH 6-7) cannot
detect nonacidic reflux.
 Nonacid Gastroesophageal Reflux

► Nonacidic reflux was seen in both normal (healthy controls) subjects and GERD
patients

► Measured by multichannel intraluminal impedance (MII) monitoring

► Accounted for one third of all reflux events

► Occurred more commonly after meals and in recumbency

► Only 4% of nonacidic reflux events were due to bile reflux

► Three fourths of bile reflux episodes occurred in conjunction with acid reflux

► Compared with acid reflux events, nonacidic reflux typically did not extend as
far proximally and was cleared more quickly from the esophagus.
 importance of nonacidic reflux

► The true importance of nonacidic reflux in the

pathogenesis of both esophageal and extraesophageal
symptoms remains to be established.

► may be a factor in:

 Functional heartburn (ie, heartburn with normal esophageal pH
measurements)
 Nonerosive reflux disorders
 Extraesophageal disorders, whose symptoms persist despite
aggressive proton-pump inhibitor therapy.

► MII may be used to test for nonacidic reflux

 GERD and Chronic Cough

The mechanisms remain controversial.

 Microaspiration

 Stimulation of a vagally mediated esophageal-bronchial

reflex. That may also involve brainstem centers.
 GERD and Chronic Cough

► Establishing a definite cause-and-effect relationship between

GER and chronic cough is difficult.

► A normal esophageal pH study argues against acid GER as a

cause of chronic cough
► An abnormal pH study does not prove that acid reflux is the
cause of chronic cough.

► Only a minority of patients with proven GER have

improvement of cough after proton-pump inhibitor therapy.
 GERD and Chronic Cough

Empirical trial of high-dose therapy with PPI

 Uncontrolled trials
► 70% to 100% improvement

 The only published placebo-controlled trial reported

► 35% response rate.
 GERD and Chronic Cough

75 patients with chronic cough prospectively evaluated

 GER symptoms in 72%
 abnormal pH testing in 56% (42 of 75)
 20/42 had minimal or no reflux symptoms.

► Omeprazole was given to a subset of patients (n = 55)

with either GER symptoms and/or abnormal pH testing.

► After 3-6 months, significant improvement was noted 45%

► No symptom or pH parameter was predictive of

improvement.

Garrigues V, Bastida G, Bau I, et al. Gastroenterology. 2001;120:A-430. [Abstract #2195]

 GERD and Chronic Cough

Conclusions
► ambulatory esophageal pH testing still is of limited utility in the evaluation of patients
with chronic cough.

► A normal pH study with a low SI (symptom index) , probably excludes acid-related

cough, but a positive pH study does not prove a causal relationship.

► Many clinicians may choose to treat all patients with chronic cough with an empirical trial
of high-dose proton-pump inhibitors (eg, omeprazole 40 mg twice daily), even if
symptoms of reflux are absent.

► Cough usually responds within 2 weeks of therapy.

► An empirical trial is more cost-effective than formal evaluation with manometry and pH
testing.
 Laryngopharyngeal reflux

► 81% will have a normal-appearing esophagus

► 40% may have symptoms of heartburn

►
► Symptoms consistent with this diagnosis
 Dysphonia
 Globus sensation
 Throat clearing
 Halitosis
 Sore throat
 Cough.
 Hoarseness is a majer coplaint in 92% of patients with GERD-related
laryngitis
 > 50% of patients presenting to ENT specialists with hoarsness will
have a component of GERD contributing to their symptoms
 Reflux Laryngitis

► Posterior laryngitis at laryngoscopy is a typical finding of reflux

laryngitis

► Niether laryngoscopic findings nor positive pH studies have been found

to be of predictive value in identifying patients likely to respond to
proton-pump inhibitors.

► No agreement as to the optimal site of pharyngeal probe placement or

normal values of esophagopharyngeal reflux (EPR).

► EPR is also is detected in up to 20% of normal controls.

 Reflux Laryngitis

Study involved 62 cadidates

19 healthy controls
43 patients with suspected reflux laryngitis
 17 with symptoms but a normal ENT exam
 26 with posterior laryngitis.

► Videolaryngoscopy was performed in all subjects

► Dual-probe pH testing was performed, with the proximal probe located 1 cm above the
upper esophageal sphincter in the pharynx.

► Pharyngeal acid reflux occurred in

 26% of controls
 53% patients with ENT symptoms alone
 69% in patients with ENT symptoms and findings of posterior laryngitis

► However, there was no difference in symptoms between patients with abnormal and
normal pH values, or between patients with an abnormal or normal-appearing larynx.

Ylitalo R et al , Gastroenterology. 2001;120:A-426. [Abstract #2175]

 Reflux Laryngitis

► 49 patients with chronic ENT symptoms and abnormal laryngoscopic

examination underwent a questionnaire and dual-probe esophageal
(not pharyngeal) pH testing.

► After initial evaluation, patients were treated in an uncontrolled fashion

with either
 high-dose proton-pump inhibitors
 high-dose proton-pump-inhibitor therapy and bedtime ranitidine.

► At 4 months, improvement was noted in 32 of 49 (65%) of patients
treated with proton-pump inhibitors (with or without ranitidine).

► Symptoms, ENT findings, and pH parameters were not predictive of

response to proton-pump inhibitor therapy.

1. Vaezi M et al. Gastroenterology. 2001;120:A-118. [Abstract #636]