Guideline for

Management of Gastro-
oesophageal Diseases
(GERD)
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# Terminology and significance of reflux

(1) Normal reflux of gastric content into esophagus
(2) GERD: reflux exposes the patients to risk of physical
complications or symptoms that lead to a significant
impairment of well-being
(3) Impairment of well-being: 2 or more symptoms per week

# Epidemiology
(1) Reflux disease is the most common cause of heartburn and
indigestion in western society but heart-burn presentation
is not as usual in the Asian population
(2) Prevalence of GERD in Asia (reference 1)

Year Study group(Country) Prevalence

1979 Chen et al (Taiwan) 2% of 1000 pt (EGD)
1993 Kang et al (Singapore) 3% of 10000 pt (EGD)
1994 Lee et al (Korea) 3% (EGD)
1997 Hu et al (Hong Kong) 5% of 1558 pt
(questionnaire)
1997 Chang et al (Taiwan) 5% of 2044 pt (EGD)
17% > one symptom (+)
1997 Yeh et al (Taiwan) 14% of 464 pt (EGD)
1998 Yeom et al (Korea) 5% of 1010 pt (EGD)
2001 Cheng et al (Taiwan) 12% of 482 pt (EGD)
2003 Lien et al (Taiwan) 12% (EGD)
2004 Rosaida et al( Malaysia) 13.4% (EGD)
2005 Cho et al (Korea) 3.5% of 1417 pt (questionnaire)
2005 Huang et al (Taiwan) 16% (EGD) (reference 2)
** EGD(endoscope diagnosis)]

(3) Possible factors for lower prevalence of GERD in Asia

(reference 1)
a. Genetic factors
 1 Gastro-oesophageal Diseases (GERD)

b. Low maximal acid output/small parietal cell mass

c. High LES pressure
d. Low BMI (body mass index)
e. Lower consumption of alcohol, coffee, tea
f. Smoking
g. Fewer aggravated medicines used
h. Dietary factors: Lower dietary fat and chocolate
i. Lower consumption of carbonated soft drinks
j. Lower consumption of citric fruit drinks

# Classification for GERD

1. Erosive esophagitis
2. Non-erosive esophagitis (NERD)
3. Barrett’s esophagus
NERD: the presence of typical symptoms of GERD caused by
intra-esophageal acid, in the absence of visible
esophageal mucosa injury at endoscopes
Barrett’s esophagus: displacement of the squamocolumnar
junction proximal to the gastroesophageal junction with
the presence of intestinal metaplasia

# Defense mechanism against reflux

 Prevention of reflux:
tonic activity of the LES supported by curial diaphragm
 Esophageal mucosal defense

a) Prevention of reflux
Hill’s classification of Gatroesophageal flap valve(GEFV)
reference 3: (Hill LD. Gastrointest Endosc 1996)
(Grade I and II valves were classified as normal valves; grades III and
IV valves as considered abnormal valves)

Grade I: Prominent fold of tissue along the lesser curvature that

was closely apposed to the endoscope
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Grade II: Fold was present but there would be periods of opening
and rapid closing around the endoscope
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Grade III: Fold was not prominent and the endoscope was not
gripped tightly by the tissues

Grade IV: There was no fold and the lumen of the esophagus
gaped open, allowing the squamous epithelium to be
viewed from below
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b) Factors contributing to esophageal mucosal resistance against

injury by luminal acid

# Pathogenesis
1. Defective LES: transient LES relaxation (increase frequency of
reflux)
2. Impaired clearance function
3. Defective basal LES pressure (Lesser extent)
4. Acid-related symptoms appear to be a product of sensitivity
and susceptibility rather than any absolute baseline level of
acid.
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# Clinical features of GERD

Symptoms:
1. Directly related to reflux episodes
2. Caused by complications of reflux disease

Symptoms directly related to reflux episodes

1. Typical: Heartburn; Regurgitation
2. Atypical: Cardiac-type chest pain;Non-specific dyspepsia,
nausea, belching, bloating; hoarseness; sore throat, cough

Symptoms caused by complications of reflux disease

1. Respiratory symptoms
2. Dysphasia
3. Odynophagia
4. Hematemesis
5. Choking attack especially at night
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6. Weight loss

# Diagnosis
History taking is the most useful method for the diagnosis of
GERD
Heartburn: cardinal symptom
Symptoms overlapping: 2/3 with dyspepsia, 40% of IBS
Alarm symptoms: possible severe or complicated reflux
disease, another diagnosis?

(1) When to investigate?

Investigations are warranted if,
a) the diagnosis is unclear
b) symptoms persist or are refractory to treatment
c) complications suspected with presence of alarm symptoms
※Alarm symptoms: Melena, rectal bleeding
 BW loss > 10%
 Persistent vomiting
 Anemia, bleeding
 LN enlargement
 Abdominal mass
 Progressive dysphagia or odynophagia
 Family UGI cancer Hx

(2) Which investigation?

a) Barium swallow and meal: Inappropriate primary diagnostic
test may be useful in: persistent dysphasia caused by
suspected stricture or the assessment of large hiatus hernia
b) Endoscopes [high specific (90-95%)] (reference 4):
(i) Most sensitive test for reflux esophagitis, diagnosis of other
mucosal lesions
(ii) Only effective way to grade esophagitis
(iii) Only sensitive method for diagnosing Barrette’s esophagus
(iv) Recognition and management of peptic stricture

Endoscopic finding in Esophagitis:

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LA classification of esophagitis (reference 5)

Grade A: One or more mucosal break, each < 5 mm long confined

to he mucosal folds

Grade B: One or more mucosal break > 5 mm long, confined to

mucosal folds but not continuous the tops of two mucosal folds
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Grade C: One or more mucosal break continuous between the tops

of two or more mucosal folds but which involve < 75%
of the esophageal circumference

Grade D: Mucosal breaks which involve at least 75% of the

oesophageal circumference
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(3) 24-hour ambulatory pH monitoring: CLINICAL

APPLICATIONS
 Test whether symptoms are related to reflux (Heart-burn, acid
regurgitation, non-cardiac chest pain, respiratory symptoms and
ear, nose, and throat problems )
 Useful in whom the diagnosis is unclear after a therapeutic trail
(PPI) and negative for esophagitis by endoscopes
 The sensitivity (61%-85%) and specificity (71%- 100%),
(Especially if heartburn and acid regurgitation are dominant
complaints)
Interpretations for a diagnosis of GERD (especially NERD)
(1) Percentage time pH < 4.0 or esophageal acid exposure time
(2) Number of reflux episodes
(3) Mean duration of reflux episodes or acid clearance time
(4) Number of reflux episodes >=5 min
(5) Longest duration of reflux episode.
(These parameters are analyzed for upright, supine, and total periods)

# Current Management for GERD

 Life-style modification
 Medical therapy
 Endoscope therapy (reference 6)
• Endoscope suturing of ECJ (Endocinch)
• Radiofrequency thermal therapy (Stretta procedure)
• Injection therapy (Enterex procedure )
• Gatekeeper procedure
• Endoscopic Full-Thickness Plication (Plicator )
 Surgery
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(1) Lifestyle and Postural Measures

 Reducing body weight
 Cease smoking
 Avoid spicy or fatty food
 Avoid over food
 No snap
 Bed head elevation
 Avoid tight cloth

(2) Medical therapy for GERD

 Proton pump inhibitors (PPI) (reference 7)
 Irreversibly inhibit the H & K adenosine-triphosphate proton
pump of the parietal cells (Available in our hospital:
Esomeprazole, Panthoprazole,Lansoprazole)
 H2 receptor antagonists (H2RA): Blocks histamine stimulation
of the parietal cells (Available in our hospital:Famotidine,
Ranitidine, Cimetidine)
 Prokinetic agents: Less effective, side effects
 Antacids
 Combination therapy

* The frequency of acid-reflux symptoms is directly related to the time

that esophageal pH is below 4 (reference 8)
**The healing of reflux esophagitis is directly related to the proportion
of time during the 24-hour period for which the intra-gastric pH is
maintained above 4

Symptom Endpoint Definitions

1. Symptom resolution: No symptoms reported during a 24-hour
period
2. Sustained resolution: 7 consecutive days with no symptoms
3. Relief: Reduction in symptom severity or duration, while
“resolution” is the absence of symptoms
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Genval recommendations on first-line initial therapy for GERD:

1. Start with a proton pump inhibitor, with subsequent trial of step
down of the intensity of therapy.”
2. For endoscope-negative reflux disease there is an ascending level
of efficacy from either H2-receptor antagonist or prokinetics, to a
proton pump inhibitor.”
3. The most effective initial therapy for reflux disease is also the most
cost-effective.”

Medical cost-effectiveness for GERD Management

1. PPIs are more cost-effective than H2RA for in primary care setting
(references 9,10)
2. Initial treatment with a PPI, followed by step down to a low level
and less expensive therapy
3. On-demand PPI therapy is effective and can substantially reduce
cost (reference 11)
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Reasons for failed treatment in GERD

 Incorrect diagnosis
 Pill induced injury
 Inadequate compliance
 Zollinger-Ellison Syndrome
 Severe esophagitis (grade C & D) with nocturnal acid
breakthrough

Rescue therapy: Changing treatment protocol in nocturnal acid

breakthrough
 PPI once a day
 PPI plus H2RA at bedtime
 PPI BID
 PPI BID plus H2RA

# Endoscope treatment for GERD

 Endoscope suturing technique (gastroplication)
 Radiofrequency thermal therapy (Stretta procedure)
 Endoscope injection therapy (Enterex procedure )
 Gatekeeper procedure
 Endoscopic Full-Thickness Plication (Plicator )

# Anti-reflux Surgery
 Open anti-reflux surgery
 Laparoscopic anti-reflux surgery (reference 12)
(0.2-0.3% mortality rate, greater burdens of side effects (10%),
bloating, dysphasia and inability to vomit. Therefore, balance of
risks and benefits is necessary
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# GERD and Helicobacter Pylori Infection

H. Pylori infection and GERD (references 8, 13-15)
 Acid secretion and esophageal motility status are the cardinal
factors related to pathogenesis for GERD
 Compound mechanisms surrounding H. pylori and GERD exists
 Gastric acid hyper secretion may predispose to GERD in antral
predominant gastritis (DU)
 Decrease in gastric acid production helps to protect against
GERD in populations with atrophic corpus gastritis (GU,
pangastritis and gastric cancer)
 Eradication therapy in patients with H. pylori-positive dyspepsia
have no effect on QOL due to symptomatic GERD

Possible Roles of H. pylori Infection in GERD

 Potency of gastric refluxate by affecting patterns of gastritis and
gastric acid secretion
 Ammonia neutralizing the gastric acid
 Corpus gastritis and carditis associated with lower acid output
and increasing episodes of tLESR respectively
 Hypergastrinemia leading to increase esophageal sphincter
pressure and augmenting PPI effect
 Triggers esophageal dysmotility with complex mechanism and
variable results
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For the time being, datas support that:

 Substantial numbers of patients with H. pylori infection have
GERD
 Many patients whose H. pylori infection is treated do not
develop GERD
 Risk for GERD between who has had H. pylori eradicated and in
whom never had H. pylori infection is not ascertained
 Differing host, environmental, and dietary factors are not well
understood

Sophisticated relationship between Helicobacter pylori and GERD

 Development of GERD depends on interplay of multiple factors
(anti-reflux barrier, burden of acid reflux, acid clearance and
mucosal resistance)
 H. pylori infection reduces risk for GERD in trends
 Eradication of H. pylori infection is related to emergence of
GERD and its complications
 Eradication therapy is not recommended for most of GERD
patients with H. pylori infection

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