Almost everyone experiences a little acid reflux, particularly after
meals. Acid reflux irritates the walls of the esophagus, inducing a
secondary peristaltic contraction of the smooth muscle, and may produce
the discomfort or pain known as heartburn. Evidence indicates up to
36% of otherwise healthy Americans experience heartburn at least once
a month. Most episodes of acid reflux are asymptomatic.
After a meal, the lower esophageal sphincter (LES) usually remains
closed. When it relaxes at an inappropriate time, it allows acid and
food particles to reflux into the esophagus. Secondary peristalsis returns
approximately 90% of the acid and food to the stomach. Once peristalsis
ends, the LES closes again. The remaining acid in the esophagus is neutralized
by successive swallows of saliva, which is alkaline in nature, and then
cleared into the stomach.
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- What is GERD?
- I have never heard of GERD. Is it a new disease?
- What are some symptoms of GERD?
- How do people get GERD? What causes GERD?
- How many people are afflicted with GERD?
- Who is afflicted with GERD?
- Do children get GERD?
- What is the difference between GERD and GORD?
- What is the difference between heartburn and GERD?
- What is the difference between GERD and a hiatus hernia?
- What is endoscopy and when is it used in GERD patients?
- What are the complications of GERD?
- What makes GERD symptoms worse?
- Does eating spicy food cause GERD or make GERD worse?
- What about GERD and smoking?
- Do any medications make GERD worse?
- What should people with GERD avoid?
- Can GERD cause cancer?
- Are there long-term consequences of GERD?
- Is there a relationship between GERD and asthma?
- Can GERD cause inflammation of the throat?
- Can GERD be cured?
- I think I have GERD. What should I do?
- Where can I go for more information about GERD?
GERD stands for Gastroesophageal Reflux
Disease. Gastroesophageal reflux describes a backflow of acid from
the stomach into the swallowing tube or esophagus. This acid can irritate
and sometimes damage the delicate lining on the inside of the esophagus.
Almost everyone experiences gastroesophageal reflux at some time. The
usual symptom is heartburn, an uncomfortable burning sensation behind
the breastbone, most commonly occurring after a meal. In some individuals
this reflux is frequent or severe enough to cause more significant problems,
that is a disease. Thus, gastroesophageal reflux disease is a clinical
condition that occurs when reflux of stomach acid into the esophagus is
severe enough to impact the patientís life and/or damage the esophagus.
No. GERD has probably been around as long as heartburn. The
term is relatively new (about 20 years), however, and has really come
into common usage over the past few years. GERD is often called "reflux,"
"reflux esophagitis," or sometimes even "hiatus hernia" (although hiatus
hernia is a specific diagnosis that may or may not have anything to do
with GERD). GERD is the preferred term because it accurately describes
the problem - reflux of stomach acid up into the esophagus where it can
produce symptoms and sometimes damage. Many patients and health care professionals
are not familiar with GERD and its potential consequences, and thus may
not have heard the term previously.
The four major symptoms of GERD are:
Heartburn is the most common symptom of GERD. In some patients it may
be accompanied by other GERD symptoms, such as regurgitation of gastric
contents into the mouth, chest pain and difficulty swallowing. Pulmonary
manifestations, such as asthma, coughing, or intermittent wheezing and
vocal cord inflammation with hoarseness, occur in some GERD patients.
In addition, acid can be regurgitated into the lungs in some GERD patients,
causing wheezing or cough. Acid refluxed into the throat can cause sore
throat. If acid reaches the mouth, it can dissolve enamel of the teeth.
- Heartburn (uncomfortable, rising, burning sensation behind the breastbone).
- Regurgitation of gastric acid or sour contents into the mouth.
- Difficult and/or painful swallowing.
- Chest pain.
GERD is caused by reflux of stomach acid into the esophagus.
In most patients this is due to a transient relaxation of the gate
or sphincter that keeps the lower end of the esophagus closed when a person
is not swallowing food or liquids. This transient relaxation happens a
few times each day in people without GERD. Why it happens more frequently
in GERD patients isnít known. The esophagus is not able to cope with acid
as well as the stomach and is easily injured. It's the acid refluxing
into the esophagus that produces the symptoms and potentially damages
Recent statistics from the US Department of Health and Human
Services indicate that about seven (7) million people in the US alone
suffer from GERD.
(Source: Digestive Diseases in the United States: Epidemiology and
Impact, National Digestive Diseases Data Working Group, James E. Everhart,
MD, MPH, Editor, US Department of Health and Human Services, Public Health
Service, National Institutes of Health, NIH Publication No. 94-1447, May
GERD afflicts people of every socioeconomic class, ethnic group
and age. However, the incidence does seem to increase quite dramatically
above the age of 40. Greater than 50 percent of those afflicted with GERD
are between the ages of 45-64 (both male and female).
Yes. GERD is most common in adults over age 40 but virtually
anyone can get GERD, even infants.
The British spelling of esophagus is oesophagus. Hence, GERD
is GORD in many European countries.
GERD is a disease and heartburn is its most common symptom.
Heartburn is defined as a rising, burning sensation behind the breastbone
caused by reflux of stomach acid into the esophagus. Nearly everyone has
or will experience heartburn on occasion. Frequent heartburn that disrupts
one's lifestyle suggests the diagnosis of GERD.
Hiatus hernia refers to dislocation of the stomach through the
"hiatus" of the diaphragm and into the chest. This is a common condition
that increases in frequency with age. It may or may not be associated
with GERD. When GERD is severe enough to be complicated by erosive esophagitis,
seen as breaks in the lining of the esophagus, a hiatus hernia is usually
present. However, most patients with a hiatus hernia do not have GERD.
Basal LES pressure often is very low in patients who have large
hiatal hernias, and this LES hypotension predisposes to gastroesophageal
reflux. Also, the extrasphincteric anti-reflux mechanisms can be disrupted
when the stomach herniates into the chest through the diaphragmatic hiatus.
With a large hiatal hernia, the distal esophagus is no longer subject
to abdominal pressure. Furthermore, the diaphragmatic crurae no longer
pinch the distal esophagus during inspiration. Instead, approximation
of the crurae creates an intrathoracic pouch of stomach that may function
as a reservoir of material available for reflux. A recent study has shown
that the susceptibility to gastroesophageal reflux induced by abrupt elevations
of intra-abdominal pressure correlates significantly both with weak LES
pressure and with hiatal hernia size. Although it appears that hiatal
hernia often contributes importantly to GERD, hiatal hernia is neither
necessary nor sufficient for the development of reflux esophagitis. Patients
who have no hiatal hernia can have GERD, and hiatal hernia is not always
associated with reflux esophagitis.
Endoscopy is a diagnostic test wherein a thin, flexible tube
is swallowed by the patient to allow the physician to directly inspect
the lining of the upper gastrointestinal tract. This procedure can be
used to identify complications of GERD and to take small samples (biopsies)
for further analysis. GERD patients who have certain symptoms, such as
difficulty in swallowing or painful swallowing, should be considered for
endoscopy. Patients who fail to respond to therapy are also candidates
for endoscopy. Some physicians advocate endoscopy for all patients with
long-standing GERD in order to rule out Barrett's esophagus.
Only a minority of patients develop complications of GERD. These
complications include breaks in the lining of the esophagus (esophageal
erosions), esophageal ulcer, and narrowing of the esophagus (esophageal
stricture). In some patients, the normal esophageal lining or epithelium
may be replaced with abnormal (Barrett's) epithelium. This condition (Barrett's
esophagus) has been linked to cancer of the esophagus and must be carefully
watched. Lung (pulmonary) aspiration, asthma and inflammation of the vocal
cords or throat may also be caused by GERD.
The major factor is meals. Meals stimulate the stomach to produce
more acid that can reflux up into the esophagus. In some patients, lying
down or taking certain medications can worsen acid reflux.
Spicy foods do not cause GERD, although they do seem to worsen
GERD symptoms in some people. Food (in general) can make GERD worse. This
is because food fills the stomach and induces more transient relaxations
of the lower esophageal sphincter. In addition, all meals stimulate acid
production in the stomach to aid digestion and can increase reflux into
the esophagus in GERD sufferers. Any very large meal might be expected
to produce heartburn in some people. The spicy food story is so compelling,
however, that GERD sufferers often relate a spicy (or greasy) meal to
their symptoms. Often they are told to avoid certain foods whether or
not these foods have anything to do with their symptoms. In this way,
many GERD sufferers end up on a very restricted diet or end up blaming
their symptoms on dietary indiscretion. If avoiding spicy foods and/or
other dietary advice helps, that's great. If it doesn't, GERD sufferers
shouldn't feel that they are doing something wrong. They should seek medical
advice on managing their disease.
Smoking doesn't cause GERD and there is little evidence that
smoking significantly worsens GERD. Stopping smoking is a good idea anyway.
Yes. Medicines that delay emptying of acid from the stomach
or that increase acid backup into the esophagus can worsen GERD. If you
have, or suspect you have, GERD and you require medication for other conditions,
you should make sure you inform your doctor about all medications you
are taking including prescription and over-the-counter medications.
GERD is a disease that is caused by gastric acid. However, certain
foods can trigger symptoms in some patients. Lying down after a meal,
wearing tight-fitting clothing, and even performing certain activities,
such as bending over, can also trigger symptoms in patients. A good way
to identify these "triggers" is to keep a diary of GERD symptoms noting
when they occur. If symptoms follow a pattern and occur after certain
foods or activities, these foods or activities should be avoided. A diary
will also help patients continue to enjoy those foods or activities that
do not seem to provoke symptoms, so that their lifestyle is not restricted
unnecessarily. Patients should review their symptoms with their doctor,
who can evaluate their condition and advise an appropriate treatment plan.
Severe, long-standing GERD can damage the esophagus and cause
a condition known as Barrett's esophagus wherein the normal lining of
the esophagus is replaced by a lining more like that of the stomach or
intestine. It is thought that this replacement may be an attempt by the
body to protect itself from further injury by acid. The risk of esophageal
cancer appears to increase significantly in patients with Barrett's esophagus.
The only way to diagnose Barrett's esophagus is by endoscopy. Some studies
suggest that intensive treatment of Barrett's esophagus can reduce the
amount of abnormal lining in the esophagus. It is not yet clear whether
such treatment will prevent esophageal cancer in GERD patients, but this
is under active investigation.
Long-standing GERD can lead to damage of the esophagus. This
damage usually consists of breaks in the lining of the esophagus. In some
cases ulcers can develop. In some patients, such damage can result in
scarring and narrowing of the esophagus, making swallowing painful or
difficult. A condition called Barrett's esophagus is thought to result
from long-standing GERD in some patients. Barrett's esophagus is a risk
factor for the development of esophageal cancer. In some patients, acid
backup caused by GERD is thought to result in damage to the vocal cords
or teeth and may even cause asthma.
Many investigators believe that there is a link between asthma
and reflux of stomach acid up into the throat and then down into the lungs
in some patients. It appears that some patients who suffer from asthma
might benefit from treatment of GERD. This is a topic of active research
at the moment.
In some patients, acid can reflux into the throat causing inflammation
of the back of the throat which can lead to pharyngitis, or into the vocal
cords, which can lead to laryngitis and hoarseness. Although there are
many other causes for sore throat and laryngitis, GERD should be suspected
in a patient with chronic sore throat or other GERD symptoms or when no
other cause can be found.
Unfortunately, GERD, in general, cannot be cured at present.
In some cases, it may be a temporary condition associated with a specific
aggravating factor such as pregnancy. In such cases, GERD will go away
on its own when the pregnancy has ended. In most cases GERD is a chronic
condition. However, it can be effectively managed with medications and
lifestyle modifications in almost everybody. In severe cases, surgery
is an option. Surgery does not cure the underlying problem, but wraps
part of the stomach around the lower end of the esophagus to help keep
acid from getting back up into the esophagus. A doctor can evaluate the
condition and advise on an appropriate treatment plan.
See your doctor. Your doctor can establish the diagnosis and
work with you to get you symptom-free. Primary care and physicians of
many specialties are becoming increasingly familiar with GERD. Gastroenterologists
and some gastrointestinal surgeons are usually very familiar with GERD
and its treatment.
If you think you might have GERD - see your doctor who can determine
if you have GERD and, if so, can evaluate its severity. Additional information
is also available from the following organizations:
The American Gastroenterological Association (AGA)
7910 Woodmont Avenue, 7th Floor
Bethesda, MD 20814
E-mail the AGA at firstname.lastname@example.org
The American College of Gastroenterology (ACG)
P.O. Box 3099
Alexandria, VA 22302
Transient, inappropriate relaxation of the LES appears to be the most
important LES mechanism for gastroesophageal reflux. Unlike the brief
(3 to 10 seconds in duration), appropriate LES relaxations that accompany
primary peristalsis, so-called transient LES relaxations do not occur
during normal peristalsis and last for up to 30 seconds. In normal individuals,
brief episodes of gastroesophageal reflux (called physiologic reflux)
occur almost exclusively through the mechanism of transient LES relaxation.
In patients with GERD, transient LES relaxation is the most frequent,
but not necessarily the exclusive, cause of reflux. Transient LES relaxations
can occur spontaneously, after primary peristalsis, or with failed peristalsis.
In transient LES relaxation there is no swallow (absent pharyngeal
wave) and no activity in the body of the esophagus. For no apparent
reason, LES pressure collapses to O at which point the esophageal pH
records an episode of acid reflux.
Transient LES relaxation after primary peristalsis - there is a swallow
(evidenced by a pharyngeal wave) followed by peristalsis in the body
of the esophagus. The LES relaxes appropriately during the primary peristaltic
sequence and, when the peristaltic wave reaches the LES, the muscle
contracts appropriately. Rather than returning to baseline pressure
as is normal, however, the LES again relaxes completely after the primary
peristaltic sequence at which time acid reflux occurs (indicated by
the drop in esophageal pH).
Transient LES relaxation during failed peristalsis. There is a swallow
evidenced by the pharyngeal wave, and peristalsis proceeds to the proximal
esophagus. The peristaltic sequence fails, however, and does not advance
beyond the proximal esophagus. Nevertheless, the LES relaxes in anticipation
of a bolus that never arrives, and acid reflux follows.
In some patients with GERD, the resting pressure in the LES is so weak
that the sphincter does not pose an effective barrier to reflux. LES
pressure remains at or near 0, and the esophageal pH records multiple
episodes of acid reflux.
Acid reflux can be associated with a sudden increase in abdominal pressure
in a patient with a weak LES. Normally, increases in abdominal pressure
are attended by commensurate increases in LES pressure. This mechanism
ordinarily prevents gastroesophageal reflux during coughing, sneezing,
and straining. In patients whose LES is weak, however, sudden increases
in abdominal pressure may not be accompanied by similar elevations in
LES pressure. Note that the abrupt rise in abdominal pressure exceeds
the rise in LES pressure, and acid is propelled into the esophagus as
evidenced by the drop in esophageal pH.
Management of GERD begins with lifestyle modifications aimed at reducing
acid reflux and minimizing the duration of contact between refluxed
material and the esophageal mucosa.
The head of the bed is elevated on 4" to 6" blocks to exploit the effect
of gravity on esophageal clearance.
Obese patients are advised to lose weight with the rationale that obesity
may promote reflux by increasing abdominal pressure.
Tobacco and alcohol consumption should be avoided because these agents
may decrease LES pressure. Also, cigarette smoking decreases salivation
that is important for esophageal acid clearance.
Bedtime snacks can stimulate gastric acid production and trigger transient
LES relaxation, thereby promoting the nocturnal reflux of gastric acid.
Certain medications can decrease LES pressure and delay gastric emptying,
and these agents should be avoided if possible. These include drugs
that have anticholinergic effects (e.g. phenothiazines, tricyclic antidepressants),
theophylline preparations, and calcium channel blocking agents. NSAIDS
can be caustic to the esophageal mucosa, and these agents also should
be avoided if possible.
Fatty foods, chocolate, and peppermint contribute to GERD by decreasing
LES pressure, and fatty foods delay gastric emptying. Other restrictions
in diet and activities may be helpful in individual patients.
There are a number of different anti-reflux operations (e.g. Nissen
fundoplication, Belsey Mark IV repair, Hill posterior gastropexy), but
most share the common features. The hiatal hernia that usually accompanies
severe reflux esophagitis is reduced, a segment of intra-abdominal esophagus
is restored, and the diaphragmatic crurae are approximated. Also, a
portion of the gastric fundus is wrapped around the distal esophagus
(fundoplication). The operations differ primarily in the degree of fundoplication.
The mechanisms whereby these operations prevent reflux are disputed.
The surgery narrows the angle of His (the angle formed by the junction
of esophagus with stomach) which may create an anti-reflux flap-valve
effect, and restoration of the distal esophagus to the positive pressure
environment of the abdomen also may help to prevent reflux. With reduction
of the hiatal hernia and approximation of the diaphragmatic crurae,
the normal antireflux function of the crural diaphragm may be restored.
The fundoplication may act as a one-way valve and may prevent distention
of the gastric fundus that can trigger transient LES relaxations. Finally,
LES pressure increases after fundoplication for reasons that are not
clear. The importance of the latter mechanism also is disputed, however,
because the efficacy of antireflux surgery is not directly proportional
to the postoperative increase in LES pressure.
GERD - treatment guidelines
Current recommendations from the American College of Gastroenterology
regarding treatment guidelines for gastroesophageal reflux disease include
Patients who present with symptoms of gastroesophageal reflux disease
with mild symptoms should be treated with:
1. Lifestyle changes as previously described
2. Initial trial of patient-directed therapy with over-the-counter H2
antagonists or antacids
Lifestyle modifications include:
1. Accomplish weight loss if obese
2. Avoid lying down after meals
3. Avoid late night meals
4. Elevate the head of your bed by 6 inches. Preferably using wooden
blocks placed under the head of the bed.
5. Avoid wearing tight-fitting clothes
6. Avoidance of dietary irritants such as:
7. Avoid agents which lower the lower esophageal sphincter pressure:
A. Calcium channel blockers
C. Anticholinergic medications
8. Discontinuance of tobacco use
9. Stop or reduce alcohol use
10. Avoid non-steroidal antiinflammatory drugs
Should initial treatment with over-the-counter antagonists/antacids
and lifestyle modifications be effective, this treatment regimen is
recommended to be continued for an indefinite period.
If the patient develops more symptoms or has an inadequate response
then the following recommendations are made.
1. Continue lifestyle changes as previously noted
2. Initiation of prescription strength histamine 2 antagonist therapy,
proton pump inhibitor therapy or pro-motility agents
The medications used in this group are usually prescribed in the following
1. Histamine 2 receptor antagonist therapy:
A. Cimetidine 400 mg po bid
B. Ranitidine 150 mg po bid
C. Nizatidine 150 mg po bid
D. Famotidine 20 mg po bid
2. Proton pump inhibitors are usually prescribed in the following doses.
A. Omeprazole (Prilosec) 20 mg po qd
B. Lansoprazole (Prevacid) 30 mg po qd
C. Rabeprazole (Aciphex) 20 mg po qd
D. Pantoprazole (Protonix) 40 mg po qd
Pro-kinetic agents are of limited availability. The single agent in
this class that will be available during the rest of the year 2000 is
metoclopramide. Metoclopramide is prescribed as 10 mg ½ hour
before meals and at hours of bed.
Assessment of response is then reevaluated at 8-12 weeks worth of treatment.
If the patient does have an adequate response during this period of
time, patients may then be discontinued from this treatment regimen.
Should the patient relapse, reinstitution with this treatment regimen
for 8-12 weeks, endoscopic evaluation and consideration to maintenance
therapy with either histamine 2 receptor antagonists or proton pump
inhibitors is recommended. Titration of medication dose to the lowest
possible dose is recommended.
If patients do not have an adequate response to this, endoscopy should
be performed. Proton pump inhibitors should be prescribed if they have
not already been instituted. Consideration to increasing the dose of
proton pump inhibitors to a bid basis may be necessary. Some patients
respond to increasing the dose of histamine 2 receptor antagonists.
This may also be affective.
Jonathan E. Jensen, MD FACP
Colorado Center for Digestive Disorders
July 9, 2000