GERD - 2010 - Jacobi Medical Center

advertisement
Gastroesophageal
Reflux Disease
Arthur Harris, M.D.
GI Division, Jacobi Medical Center/NCBH
Assistant Professor of Medicine, AECOM
Objectives







Definition of GERD
Epidemiology of GERD
Pathophysiology of GERD
Clinical Manifestations
Diagnostic Evaluation
Treatment
Complications
Definition

American College of
Gastroenterology (ACG)
• Symptoms OR mucosal
damage produced by the
abnormal reflux of gastric
contents into the esophagus
• Often chronic and relapsing
• May see complications of
GERD in patients who lack
typical symptoms
Physiologic vs Pathologic

Physiologic GERD
•
•
•
•
•
Post-prandial
Short-lived
Often asymptomatic
TLSER’s
No nocturnal sx

Pathologic GERD
• Symptoms
• Mucosal injury
• Nocturnal sx
Epidemiology



About 44% of the US adult
population have heartburn at least
once a month
14% of Americans have symptoms
weekly
7% have symptoms daily
Pathophysiology



Primary barrier to
gastroesophageal
reflux is the lower
esophageal sphincter
LES normally works in
conjunction with the
diaphragm
If barrier disrupted,
acid goes from
stomach to esophagus
Clinical Manifestations

Most common symptoms
• Heartburn—retrosternal burning
discomfort
• Regurgitation—effortless return of
gastric contents into the pharynx
without nausea, retching, or
abdominal contractions
Clinical Manifestations
• Dysphagia—difficulty swallowing
• Other symptoms include:

Chest pain, water brash, globus sensation,
odynophagia, nausea
• Extraesophageal manifestations

Asthma, laryngitis, chronic cough
Diagnostic Evaluation
• If classic symptoms of heartburn and
regurgitation exist in the absence of
“alarm symptoms” the diagnosis of
GERD can be made clinically and
treatment can be initiated
Potential Oral and Laryngopharyngeal Signs
Associated with GERD

Edema and hyperemia
of larynx
• Vocal cord erythema,
polyps, granulomas,
ulcers





Hyperemia and
lymphoid hyperplasia
of posterior pharynx
Interarytenyoid
changes
Dental erosion
Subglottic stenosis
Laryngeal cancer
Alarms
• Alarm Signs/Symptoms







Dysphagia
Early satiety
GI bleeding
Odynophagia
Vomiting
Weight loss
Iron deficiency anemia
Trial of Medications

H2RA or PPI
• Expect response in 2-4 weeks
• If no response


Change from H2RA to PPI
Maximize dose of PPI
Trial of Medications

If PPI response inadequate despite
maximal dosage
• Confirm diagnosis


EGD
24 hour pH monitoring
Esophagogastrodudenoscopy

Endoscopy (with biopsy if
needed)
• In patients with alarm
signs/symptoms
• Those who fail medication trial
• Those who require long-term Rx



Lacks sensitivity for
identifying pathologic reflux
Absence of endoscopic
features does not exclude a
GERD diagnosis
Allows for detection,
stratification, and
management of esophageal
manifestations or
complications of GERD
Ambulatory pH Testing

24-hour pH monitoring
• Accepted standard for establishing or
excluding presence of GERD for those
patients who do not have mucosal
changes
• Trans-nasal catheter or a wireless,
capsule shaped device
Ambulatory 24 hour pH Monitoring -1


Physiologic study
Quantify reflux in
proximal/distal
esophagus
• % time pH < 4
• DeMeester score

Symptom
correlation
Ambulatory 24 hour pH Monitoring -2
Normal
GERD
Wireless, Catheter-Free Esophageal pH Monitoring
Potential Advantages
●Improved patient
comfort and acceptance
●Continued normal
work, activities and diet
during study
●Longer reporting
periods possible (up to
48 hours)
●Maintain constant
probe position relative to
SCJ
Esophageal Manometry
Limited role in GERD

Assess LES
pressure, location
and relaxation
• Assist placement of
24 hour pH catheter

Assess peristalsis
• Prior to anti-reflux
surgery
Patient with heartburn
Initiate Rx with H2RA or PPI
H2RA taken
BID
PPI taken QD
No
Good response
Good response
Yes
Yes
No
Yes
Frequent relapses
No
On demand Rx
Increase to
max dose QD
or BID
Maintenance therapy
with lowest effective dose
Yes
Symptoms persist
Good response
No
Consider EGD if
risk factors present
(> 45, white, male
and > 5 yrs of sx)
Confirm diagnosis
EGD, ph monitor
GERD vs Dyspepsia

Distinguish from Dyspepsia
• Ulcer-like symptoms-burning, epigastric
pain
• Dysmotility like symptoms-nausea,
bloating, early satiety, anorexia


Distinct clinical entity
In addition to anti-secretory meds
and an EGD, need to consider testing
for Helicobacter pylori
Treatment

Goals of therapy
• Symptomatic relief
• Heal esophagitis
• Avoid complications
Better Living

Lifestyle modifications
• Avoid large meals
• Avoid acidic foods (citrus/tomato), alcohol, caffeine,
chocolate, onions, garlic, peppermint
• Decrease fat intake
• Avoid lying down within 3-4 hours after a meal
• Elevate head of bed 4-8 inches
• Avoid meds that may potentiate GERD (CCB, alpha
agonists, theophylline, nitrates, sedatives, NSAID’s)
• Avoid clothing that is tight around the waist
• Lose weight
• Stop smoking
Treatment

Antacids
• O-T-C acid
suppressants and
antacids may be
appropriate initial
therapy
• Approx 1/3 of patients
with heartburn-related
symptoms use at least
twice weekly
• More effective than
placebo in relieving
GERD symptoms
Treatment

Histamine H2-Receptor Antagonists
• More effective than placebo and
antacids for relieving heartburn in
patients with GERD
• Faster healing of erosive esophagitis
when compared with placebo
• Can use regularly or on-demand
Treatment
AGENT
Cimetadine
Tagamet
EQUIVALENT
DOSAGES
400mg twice daily
DOSAGE
400-800mg twice daily
Famotidine
Pepcid
20mg twice daily
20-40mg twice daily
Nizatidine
Axid
150mg twice daily
150mg twice daily
Ranitidine
Zantac
150mg twice daily
150mg twice daily
Treatment

Proton Pump Inhibitors
• Better control of symptoms with PPI’s vs
H2RAs and better remission rates
• Faster healing of erosive esophagitis
with PPIs vs H2RAs
Treatment
AGENT
Esomeprazole
Nexium
EQUIVALENT
DOSAGES
40mg daily
DOSAGE
20-40mg daily
Omeprazole
Prilosec
20mg daily
20mg daily
Lansoprazole
Prevacid
30mg daily
15-30mg daily
Pantoprazole
Protonix
40mg daily
40mg daily
Rabeprazole
Aciphex
20mg daily
20mg daily
Treatment

H2RAs vs PPI’s
• 12 week freedom from symptoms

48% vs 77%
• 12 week esophagitis healing rate

52% vs 84%
• Speed of healing

6%/wk vs 12%/wk
Treatment Modifications for Persistent Symptoms

Improve compliance

Optimize pharmacokinetics
• Adjust timing of medication to 15 – 30 minutes
before meals (as opposed to bedtime)
• Allows for high blood level to interact with
parietal cell proton pump activated by the meal

Consider switching to a different PPI
Treatment

Anti-reflux surgery - Indications
• Failed medical management
• Patient preference
• GERD complications
• Medical complications attributable to a
large hiatal hernia
• Atypical symptoms with pathologic reflux
documented on 24-hour pH monitoring
Treatment

Anti-reflux surgery candidates
• EGD proven esophagitis
• ?Normal esophageal motility
• Incomplete response to acid suppression
Treatment

Anti-reflux surgery (laparoscopic)
• Tenets of surgery





Reduce hiatal hernia
Repair diaphragm
Strengthen GE junction
Strengthen anti-reflux barrier via gastric wrap
75-90% effective at alleviating symptoms of
heartburn and regurgitation
Treatment

Post-surgery
• 10% have solid food dysphagia
• 2-3% have permanent symptoms
• 7-10% have gas, bloating, diarrhea,
nausea, early satiety
• Within 3-5 years, up to 52% of patients
back on anti-reflux medications
Treatment

Endoscopic treatment
• Relatively new
• No clearly established indications
• Well-informed patients with well-documented
GERD responsive to PPI therapy may benefit

Three categories
• Radiofrequency application to increase LES
reflux barrier
• Endoscopic sewing devices
• Injection of a non-resorbable polymer into LES
region
Complications



Erosive esophagitis
Stricture
Barrett’s esophagus
Complications

Erosive esophagitis
• Responsible for 40-60% of GERD
symptoms
• Severity of symptoms often fail to
match severity of erosive esophagitis
Complications

Esophageal
stricture
• Occurs as a
result of healing
of erosive
esophagitis
• May need
dilation
Peptic Stricture
Barium swallow
Endoscopy
Complications

Barrett’s Esophagus
• Columnar metaplasia
of the esophagus
• Associated with the
development of
adenocarcinoma
Complications

Barrett’s Esophagus
• Acid damages lining of
esophagus and causes
chronic esophagitis
• Damaged area heals in
a metaplastic process
with abnormal columnar
cells replacing
squamous cells
• This specialized
intestinal metaplasia
can progress to
dysplasia and
adenocarcinoma
Complications
• Patient’s who need EGD



Alarm symptoms
Poor therapeutic response
Long symptom duration
• “Once in a lifetime” EGD for patient’s
with chronic GERD becoming accepted
practice
• Many patients with Barrett’s are
asymptomatic
Complications

Barrett’s Esophagus
• Manage in same manner as GERD
• EGD every 3 years in patient’s without
dysplasia
• In patients with dysplasia, annual to
even shorter interval surveillance is
recommended
Summary







Definition of GERD
Epidemiology of GERD
Pathophysiology of GERD
Clinical Manifestations
Diagnostic Evaluation
Treatment
Complications
?QUESTIONS?
Download