1

My Patient Isn’t Responding to

PPIs... Now What?

Crescent City GI, Endoscopy & Liver Disease Update

January 12, 2018

Michael S. Smith, MD, MBA

Chief of Gastroenterology and Hepatology

Mount Sinai West & St. Luke’s Hospitals

Associate Professor of Medicine

Icahn School of Medicine at Mount Sinai

Relevant Disclosures

• Endogastric Solutions—Consultant

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Gastroesophageal Reflux Disease(GERD)

Definition: Symptoms

and/or tissue damage

secondary to reflux of

normal gastric contents

Not all reflux is acid reflux!!!

GERD Pathogenesis• Esophageal causes

– Reduced saliva (e.g. anticholinergic medications)

– Reduced peristalsis (e.g. scleroderma)

– Lack of gravity (e.g. post-operative patient)

– Decreased mucosal resistance due to reduced secretion from

esophageal submucosal glands

• Lower esophageal sphincter dysfunction

– Inappropriate and prolonged LES relaxations

– Presence of a hiatal hernia

– Weak LES (e.g. old age, scleroderma, medications)

• Gastric Causes

– Slow gastric emptying

– Excess acid production

– Duodenogastric (bile) reflux

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What are the pathogenic factors

in reflux esophagitis?

• Volume of refluxed fluid

• Duration of reflux

• Type of refluxed fluid

• Clearing mechanisms

• Hiatal hernia

Normal Anatomy Prevents GERD

4

Effect of Hiatal Hernia

Acid Reservoir

LES and diaphragm

now separated

Seen by

Gastroenterologists

Seen by

Primary Care Physicians

Do Not Seek

Medical Attention

Chronic Symptoms

and Complications

Frequent

Symptoms

Mild Recurrent

Symptoms

Majority of Patients with GERD

Do Not Seek Medical AttentionGERD ICEBERG

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Heartburn is a ClassicSymptom of GERD

• Substernal burning and/or

regurgitation

• Postprandial

• Aggravated by change in

position

• Prompt relief by antacids

•ENThoarseness vocal cord granulomas/ulcers

cough laryngeal stenosisglobus laryngeal cancerhalitosis loss of dental enamel

•Pulmonaryasthma apnea

bronchitis atelectasisaspiration pulmonary fibrosis

pneumonia

•Non-Cardiac Chest Pain

Atypical GERD Symptoms

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Medical Options for GERD Treatment

• Dietary & Lifestyle Modification

• Antacids and Topicals

• Prokinetics

• Baclofen

• H2-receptor antagonists (H2RAs)

• Proton pump inhibitors (PPIs)

Dietary & Lifestyle ModificationsFrom the ACG Guidelines1:

• Weight loss is recommended for GERD patients who are overweight or

have had recent weight gain. (Conditional recommendation, moderate

level of evidence)

• Head of bed elevation and avoidance of meals 2–3 hours before bedtime

should be recommended for patients with nocturnal GERD. (Conditional

recommendation, low level of evidence)

• Routine global elimination of food that can trigger reflux (including

chocolate, caffeine, alcohol, acidic and/or spicy foods) is not

recommended in the treatment of GERD. (Conditional recommendation,

low level of evidence)

• Tobacco and alcohol cessation have not been shown to change either

GERD symptoms or esophageal pH 2-4

1 Katz PO, Gerson LB, Vela MF. Am J Gastroenterol 2013; 108:308 – 328.2 Schindlbeck NE , Heinrich C , Dendorfer A et al. Gastroenterology 1987 ; 92 : 1994 – 7.3 Waring JP , Eastwood TF , Austin JM et al. Am J Gastroenterol 1989 ; 84 : 1076 – 8.4 Kadakia SC , Kikendall JW , Maydonovitch C et al. Am J Gastroenterol 1995 ; 90 : 1785 – 90.

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Antacids & Topicals• Antacids:

– Examples: calcium carbonate, aluminum hydroxide, magnesium trisilicate

– Do not prevent GERD, only treat its symptoms by neutralizing gastric pH which

decreases the acidity of any refluxate

– Rapid onset of action (<5 minutes) but short duration of efficacy (<1 hour)

• Sucralfate:

– Available in both tablet and suspension form

– Adheres to esophageal wall and protects from peptic injury via unknown

mechanism

– Short duration of action, limited efficacy compared to PPIs

– ACG Guidelines: There is no role for sucralfate in the non-pregnant GERD

patient. (Conditional recommendation, moderate level of evidence)

• Sodium alginate:

– Derived from seaweed

– Forms a viscous gum which floats on the surface of gastric contents, reducing

the postprandial “acid pocket” in the proximal stomach 1

– Studies suggest it may be beneficial, especially with mild post-prandial

symptoms 1

1 Thomas E, Wade A, Crawford G et al. Aliment Pharmacol Ther 2014; 39: 595.

Prokinetics & Other Non-Acid Reducers• Prokinetics

– Examples include metoclopramide and domperidone

– Can increase lower esophageal sphincter pressures, improve peristalsis in

addition to promoting gastric emptying 1

– Metoclopramide CNS-based side effects include depression and tardive

dyskinesia (black box warning from FDA)

– Domperidone does not penetrate the blood-brain barrier but does carry a risk

of ventricular arrhythmia; also requires and IDA from the FDA

• Baclofen

– GABA(b) agonist shown to decrease TLESRs and reflux events 2-4

– Not currently approved by the FDA for treatment of GERD

– Lack of long-term data regarding efficacy in GERD

– Potential side effects of dizziness, somnolence, constipation

• ACG Guidelines:

– Therapy for GERD other than acid suppression, including prokinetic therapy

and/or baclofen, should not be used in GERD patients without diagnostic

evaluation. (Conditional recommendation, moderate level of evidence)

1 Champion MC. Can J Gastroenterol 1997; 11 (Suppl B): 55B – 65B.2 Grossi L , Spezzaferro M , Sacco LF et al. Neurogastroenterol Motil 2008 ; 20: 760 – 6.3 Koek GH , Sifrim D , Lerut T et al. Gut 2003 ; 52 : 1397 – 402.4 Vela MF , Tutuian R , Katz PO et al. Aliment Pharmacol Ther 2003 ; 17 : 243 – 51.

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H2Receptor Antagonists (H2RAs)• Act on type 2 histamine receptors on the basal side of the parietal

cell

• Faster onset of action than PPIs, but shorter half life

• Dosing for mild GERD generally is PRN or BID

• Studies have shown superiority of PPIs over H2RAs for relief of

heartburn in NERD patients (7 trials with RR of continued

heartburn 0.37 for PPIs, 0.77 for H2RAs, 95% CI 0.60-0.73) 1

• ACG Guidelines:

– H2RA therapy can be used as a maintenance option in patients without erosive

disease if patients experience heartburn relief. (Conditional recommendation,

moderate level of evidence).

– Bedtime H2RA therapy can be added to daytime PPI therapy in selected

patients with objective evidence of night-time reflux if needed, but may be

associated with the development of tachyphylaxis after several weeks of use.

(Conditional recommendation, low level of evidence)

1 van Pinxteren B , Sigterman KE , Bonis P et al. Cochrane Database Syst Rev : CD002095 .

Histamine

Acetylcholine

Gastrin

PGE2

ATPase

Antacids

Proton pump

inhibitors

H+

Therapeutic Modalities to Affect Gastric Acid Secretion

Histamine

Acetylcholine

Gastrin

Anticholinergic agents

H2-receptor antagonists

Gastric receptor antagonists

PGE2

ATPase

Antacids

Proton pump

inhibitors

H+

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Long-Term Esophagitis Remission100

90

80

70

60

50

40

30

20

10

00 2 4 6 8 10 12

Months

Pe

rce

nt

Pa

tie

nts

in

Re

mis

sio

n

Dent, J, et al. Gut 1994;35:593.

20 mg Omeprazole

every morning

20 mg Omeprazole

weekends

150 mg ranitidine

twice daily

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The Expanding Family of

Proton Pump Inhibitors

•Omeprazole (Prilosec) 1989

•Lansoprazole (Prevacid) 1995

•Rabeprazole (Aciphex) 1999

•Pantoprazole (Protonix) 2000

•Esomeprazole (Nexium) 2001

•Omeprazole/NaHCo3 (Zegerid) 2004

•Dexlansoprazole (Dexilant) 2009

• Response to PPI trial now has become an accepted

“first test” in suspected GERD

• “Red Flags” where empiric PPI should not be used:

– Age > 50

– Dysphagia

– Odynophagia

– Iron Deficiency Anemia

– Hematochezia

– Failure to respond to prior trial of acid reduction

Empiric PPI Therapy forSuspected GERD

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• Are they actually taking it?

• Are they taking it correctly? (30-60 min before meals)

• Are they taking the proper dose?

• Are they not responding to this particular PPI?

• Do they have refractory acid reflux?

• Do they have refractory GERD, but not excess acid?

• Are their symptoms not (just) due to GERD?

Why Hasn’t My Patient Improved on PPI?

• Do you have a compliant patient (diet, meds)?

• What exactly are the symptoms the patient has at this time, and have they improved or changed at all with PPI use?

– Typical (reflux, heartburn, regurgitation)

– Atypical

• How likely is it that the patient has GERD, and could there be another etiology for the symptoms (either primary cause or exacerbating factor for GERD)?

Step 1: Take a Great History

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• Trial the patient on BID PPI for at least 2-3 months before they are deemed a PPI failure, when GERD is suspected

• Atypical symptoms often take longer to resolve than typical symptoms, so make sure the patient knows to complete the whole trial rather than give up in 2 weeks if they don’t feel 100% better

Step 2: Complete a BID PPI Trial(if not already done)

• Make your best clinical guess—how likely is it that this patient really has reflux disease?

– At least partial response to PPI increases this

likelihood

– No change at all to a reasonably dosed BID PPI

decreases the likelihood

• This risk stratification affects the choice of subsequent quantitative reflux testing

Step 3: Risk Stratify the Patient for Having Refractory GERD

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• High resolution esophageal manometry with impedance

• Quantitative reflux testing

– 48 hour wireless pH-metry

– 24 hour pH-impedance

• Endoscopy

• Barium esophagram

• Gastric emptying scintigraphy

Step 4: Additional Testing to Quantify GERD and Assess for

Other Potential Etiologies

What is Esophageal Manometry?

• Mano = pressure, metry = measure

• Previous measurements taken with

water-perfused catheters

• Current high resolution models use

solid state transducers (36 at 1 cm

intervals)

• Catheters also include 18 impedance

transducers to evaluate for presence of

(conducting) liquids in the esophagus

• Catheter is placed transnasally and

patient is awake during the study

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What Does Manometry Evaluate?

• Upper esophageal sphincter (resting pressure and post-

deglutition/residual pressure)

• Esophageal contraction

– Presence or absence of contraction (skeletal and smooth muscle)

– Pattern of contraction

– Propagation velocity

– Amplitude of contraction

• Lower esophageal sphincter (resting pressure and post-

deglutition/residual pressure)

Normal Swallow on Manometry

Upper Esophageal

SphincterSkeletal Muscle

ContractionTransition Zone

Smooth Muscle

Contraction

Lower Esophageal

Sphincter

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Normal Manometry Line Tracing

Normal Manometry With Impedance

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The Chicago Classification

• Used to group motility disorders identified on manometry

• Provides a standardized nomenclature for describing

motility disorders of the esophagus

• Now on its third iteration

• Utilizes an algorithm to “read” studies and provide a

diagnosis:

1) Are there abnormalities of the lower esophageal sphincter/

esophago-gastric junction region?

2) Are there abnormalities of esophageal contractility?

3) Are there patterns of abnormal pressurization?

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Type I Achalasia

Type II Achalasia

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Type III Achalasia

EG Junction Outflow Obstruction

• Differential diagnosis:

– Mechanical obstruction

(subtle stricture or ring);

consider barium study

with a barium tablet or

barium-coated solid

object

– Incomplete achalasia

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Other Major Peristaltic Disorders

Diffuse Esophageal Spasm Jackhammer Esophagus

Absent Peristalsis/Contractility

• 100% failed swallows (DCI < 100 mmHg-cm-s)

• Normal IRP (< 15 mmHg)

• Includes scleroderma-like esophagus

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Treating Major Peristaltic Disorders

Overly Vigorous Peristalsis:

• Pharmacotherapy:

– PPI is preferred first option (is this effect of GERD?)

– Pain modulators (Tricyclics, SSRIs, SNRIs, Trazodone)

– Smooth muscle relaxants (CCBs, Nitrates, PDE-5 inhibitors)

• Botulinum toxin injection of distal esophagus

• Surgical (Heller) myotomy

• POEM (Per Oral Endoscopic Myotomy)

Absent Peristalsis:

• Management of GERD (PPI, Partial Fundoplication)

“Minor” Disorders of Peristalsis

• Ineffective Esophageal Motility: 50%+ ineffective swallows

(either failed or DCI < 450 mmHg-s-cm)

• Fragmented Peristalsis: 50%+ fragmented, DCI>450

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Treating Minor Peristaltic Disorders

• Mainstay of treatment is controlling GERD that is

exacerbated by these disorders

– Acid reduction therapy

– Partial fundoplication

• Could this be opioid-induced?

• Some believe in potential role for prokinetic therapy

– Tegaserod

– Bethanecol

– Pyridostigmine

– Buspirone

– Metoclopramide

– Erythromycin

Side effects and

potential for

tachyphylaxis

limit utility of

these agents

Transient

Lower

Esophageal

Sphincter

Relaxation

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• Low likelihood of GERD: 48 hour wireless pH-metry OFF

acid reducers

– Answer the key question: does this patient even have GERD in

the first place?

– Very unlikely patient has excess non-acid reflux if there is no

excess acid reflux

• Higher likelihood of GERD: 24 hour pH-impedance testing

ON BID PPI

– Quantifies reflux

Quantitative Reflux Testing Options

Wireless pH-Metry vs. pH-ImpedanceLikely GERD:

24 hourpH/impedance on BID PPI

Unlikely GERD:48 hour wirelesspH-Metry off PPI

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What Data Does pH Testing Provide?

48 hour wireless pH-Metry:

• # of acid reflux events

• % time pH < 4 (upright, supine, total)

• DeMeester score (predict response

to antireflux surgery)

• Correlation of symptoms with acid

reflux events

• Ability to expand to 96 hours of data

24 hour pH/impedance:

• # of acid reflux events

• # of weakly acidic/non-acidic events

• % time pH < 4 (upright, supine, total)

• Degree of esophageal stasis

• DeMeester score (predict response to

antireflux surgery)

• # of proximal reflux events

• Correlation of symptoms with acid

reflux events

• Correlation of symptoms with weakly

acidic and non-acidic reflux events

Evaluating GERD: Endoscopy

• Strengths- Esophagitis,

Barrett’s epithelium- Hiatal hernia,

strictures- Biopsy

• Limitations- Operator dependent- Cost

Endoscopy with biopsy is the best diagnostic

study for evaluating mucosal injury.

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Evaluating GERD: Radiology

BariumEsophagram

• 4 HOUR test to assess rate of gastric emptying

• Generally done with egg and toast meal (set portion), but

also can be done with a liquid version

• Key measurements: percent of meal retained at 2 hours

(normal <=60%) and at 4 hours (normal <=10%)

• Not an uncommon cause of (refractory) reflux, which

could be a primary symptom along with nausea, vomiting

and early satiety

Gastric Emptying Scintigraphy

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Relative Value of DiagnosticTests in GERD

Diagnostic tests should be performed in individualGERD patients to answer specific questions

Ambulatory

Barium pH

Swallow Endoscopy Monitoring Manometry

Dysphagia +++ ++ - +

Mucosal Injury + +++ - -

Quantitate reflux + - +++ -

Atypical symptoms + + +++ -

• Esophageal motility disorder

• Eosinophilic Esophagitis

• Peptic stricture

• Paraesophageal hernia causing outflow obstruction

• Gastroparesis

• Esophageal visceral hypersensitivity

• Functional dyspepsia

Step 5: Find your Diagnosis/es

TCAs, SSRIs, SNRIs,

Neuromodulators

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Tailor to the patient’s specific symptoms and their timing, if

testing confirms excess acid exposure despite BID PPI

• Double-dose H2-Receptor antagonist at bedtime

• Sodium alginate with meals

• Sucralfate to heal erosive esophagitis

Step 6: Augment Medical Management of Acid Reflux?

Surgical Alternatives

for Managing Refractory GERD

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Indications for Surgery in 2018

• Healthy GERD patient controlled on PPIs

– Cost of continuing lifelong PPI treatment

– Compliance with lifelong medication

– Ongoing side effects with current use

– Fear of side-effects of long term use

• Atypical GERD symptoms relieved on PPIs

• Esophagitis refractory to medical therapy

• Volume regurgitation and aspiration symptoms not

controlled on PPIs

– Large hiatal hernia

• Persistent symptoms documented to be caused by

refractory GERD (pH/impedance testing)

Nissen Fundoplication

• 360 degree wrap of fundus around the

esophago-gastric junction to bolster the

lower esophageal sphincter

• Mostly performed laparoscopically

• 10 year follow-up of VA study 1

– 62% of Nissens using medical therapy, vs. 92%

of non-surgical patients

• 12 year follow-up in separate study 2

– 53% of Nissens in remission, vs. 45% of PPIs

• Most common side effects:

– Gas-bloat (up to 15-20% of patients)

– Dysphagia (generally transient but not always)1 Spechler SJ , Lee E , Ahnen D et al. JAMA 2001 ; 285 : 2331 – 8 .2 Lundell L, Miettinen P, Myrvold HE et al. Clin Gastroenterol Hepatol 2009 ; 7: 1292 – 8 .

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Nissen Fundoplication versus PPI

Lundell et al. Am J Coll Surg 2001

Other Surgical Options

• Toupet Fundoplication:

– 270-300 degree wrap of fundus around the

esophago-gastric junction

– Thought to generate less dysphagia

– Preferred approach for refractory GERD in the

setting of known esophageal dysmotility

• Roux-en-Y Gastric Bypass:

– Creates physical separation between oxyntic

mucosa of the stomach and the esophagus

– Facilitates weight loss along with decreased

acid exposure to the distal esophagus

– May be the preferred option for long-term

GERD management in obese patients

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Magnetic Sphincter Augmentation

• Ring of titanium beads encasing magnetic cores

placed surgically at the level of the lower

esophageal sphincter

• Size of ring (number of beads) selected based on

esophageal measurement at time of placement

• Magnetic forces augment LES pressure to

approximately 15 mmHg

• Passage of a bolus through the esophago-gastric

junction allows for dynamic opening of the ring,

as pressure generated by the bolus overcomes that

of the beads

• Goal of this system is to allow for pressure-

induced opening of the LES, which is not possible

after suturing during a fundoplication (belching

and vomiting possible, less dysphagia, etc.)

• Data now available on 85 patients at 5 years

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Results at 5 Years

Ganz RA, Edmundowicz SA, Taiganides PA. Clin Gastroenterol Hepatol. 2016 ; 14(5) : 671 – 7.

ACG Guidelines• Surgical therapy is a treatment option for long-term

therapy in GERD patients. (Strong recommendation,

high level of evidence)

• Surgical therapy is as effective as medical therapy for

carefully selected patients with chronic GERD when

performed by an experienced surgeon. (Strong

recommendation, high level of evidence)

• Surgical therapy is generally not recommended in

patients who do not respond to PPI therapy. (Strong

recommendation, high level of evidence)

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ACG Guidelines II• Preoperative ambulatory pH monitoring is mandatory

in patients without evidence of erosive esophagitis. All

patients should undergo preoperative manometry to

rule out achalasia or scleroderma-like esophagus.

(Strong recommendation, moderate level of evidence)

• Obese patients contemplating surgical therapy for

GERD should be considered for bariatric surgery.

Gastric bypass would be the preferred operation in

these patients (Conditional recommendation, moderate

level of evidence)

Electrical Stimulation Therapy of LES

• Implantation performed with laparoscopy

• 2 small leads placed on LES

• Neurostimulator connected to leads sends mild

electrical signals throughout the day (not

generally sensed by patients) to improve LES

function

• 2 year data of multi-center trial1

– 21 patients with GERD partially responsive to GERD

and hiatal hernia 3 cm long or less made interim analysis

– Median GERD-HRQL scores dropped from 9 to 0

(comparing current to pre-EST scores on and off PPI)

– 16/21 patients totally off PPI

– 2/21 patients using PPI daily

– Median 24 hour distal acid exposure was 10% at baseline

and 4% (per protocol, p < 0.001)

– No serious adverse events reported

1Rodriguez et al. Surgery. 2015; 157(3): 566-7.

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Endosurgical Options

for Managing Refractory GERD

Radiofrequency Energy

• Ablation performed at 6 levels in the

region of the esophagogastric junction

• Outpatient endoscopic procedure

• Does not preclude use of other anti-

reflux measures in the future

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RF: Potential Mechanism of Action

• Increases gastric yield pressure in pig model vs. control 1

• Reduces transient LES relaxations (TLESRs) when applied

to the gastric cardia in dogs 2

• Randomized control study of 22 patients 3:

– RFA decreased GEJ compliance compared to sham patients

– Use of sildenafil (smooth muscle relaxant) 3 months after RFA

restored normal compliance, suggesting fibrosis is not the driving

force behind decreased compliance

1 Utley D et al. Gastrointest Endosc. 2000 ; 52 : 81 – 86. 2 Kim M et al. Gastrointest Endosc. 2003 ; 57 : 17 – 22.3 Arts J et al. Am J Gastroenterol. 2012 ; 107 : 222 – 230.

RF: Meta-analysis of 1,441 Patients

1 Perry K et al. Surg Laparosc Endosc Percutan Tech. 2012 ; 22(4) : 283 – 288.

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RF: Durability of Response

• 99 study patients with refractory GERD followed for 10

years

• PPI needs: 64% no longer required the same dose of PPI as pre-RF, and

41% remained off PPIs completely

• Normalization of GERD-HRQL scores (primary endpoint) in 70% of

patients

• Response rate in patients with variant anatomy and prior anti-reflux

surgery was the same as those with standard anatomy

1 Noar M, Squires P, Noar E et al. Surg Endosc. 2014. 28(8) : 2323 – 33.

RF: Endorsed by SAGES

http://www.sages.org/publications/guidelines/endoluminal-treatments-for-gastroesophageal-reflux-disease-gerd/

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Transoral Incisionless

Fundoplication (TIF)

• H-shaped fasteners applied for full-thickness plication to

recreate the gastroesophageal flap valve

• Final result is a 2-3 cm long valve of approximately 270

degrees

• Requires hiatal hernia of no more than 2 cm pre-TIF

Gastroenterology 2015

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TIF: Improvement Through 12 Months

Trad KS, Simoni G, Barnes WE et al. BMC Gastroenterol. 2014 ; 14: 174.

Trad KS, Barnes WE, Simoni G. et al. Surg Innov. 2015 ; 22(1) : 26 – 40.

52%

33%

54%

45%

5%

67%62%

77%

0%

71%

90%

82%

38%

85%90%

100%

0%

10%

20%

30%

40%

50%

60%

70%

80%

90%

100%

PPI Group (6mo) PPI Crossover (6mo after TIF) TIF Group (6mo) TIF Group (12mo)

Esophageal Acid Exposure (EAE) Complete Symptom Elimination Complete PPI Cessation Esophagitis Healed

• Randomized control trial of high-dose PPIs vs. TIF

• PPI patients crossed over to have TIF after 6 months

• 39 TIF and 21 crossover patients studied

• Significant improvement in symptom elimination (p < 0.001)

and healing of esophagitis (p < 0.018)

TIF: Durability Through 24 Months

Bell et al, Am Surg. 2014 ; 80(11) : 1093 - 1105.

• Prospective U.S. Registry to assess 2 year outcomes

• Primary endpoint: symtpom assessment

• 108 patients completed study

0

5

10

15

20

25

30

35

40

Screening 6-month 12-month 24-month

GERD - HRQL Regurgition RSI GERSS

To

tal S

co

res

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Ultrasonic Surgical Endostapler

• Disposable endoscopic system contains ultrasound sensor to

facilitate firing of 3 rounds of 4.8 mm titanium staples

• End result is a 150-180 degree anterior fundoplication

Pre-Procedure Post-Procedure

3rd Stapling

1

2

3

Still images from Dr. Ali Lankarani via https://youtu.be/fsuFKk5MlLc

Ultrasonic Endostapler: Key Data

1 Zacherl J et al Surg Endoscopy. 2015 ; 29(1) : 220 – 9.2 Kim HJ et al. Surg Endoscopy. 2016 ; 30(8) : 3402 – 8.

• 66 patients in multi-center trial (6 month data) 1

– 65% of patients off PPI

– 85% either off PPI or with 50%+ reduction in PPI use

• 34 patients in multi-center trial followed at least 4 years 2

– 69% remain off PPI at conclusion of study period

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Conclusions• PPIs remain the most potent acid-reducing agent in our

medical arsenal for treating GERD; switching to another

medication is unlikely to improve control of reflux (acid or non-

acid)

• If a patient continues to be symptomatic despite PPI therapy,

ensure they are taking their medication correctly and at the

proper dose, then confirm refractory GERD with 24 hour

pH/impedance testing on medication

• Prior to any mechanical intervention for reflux, check

esophageal function with manometry to exclude dysmotility

• Surgical intervention remains the best option for improving

the mechanical barrier to gastroesophageal reflux, as new

options show promise as alternatives to Nissen fundoplication

• Endoscopic techniques to bolster the anti-reflux barrier show

promise, with sample size and durability data forthcoming

Thank YouThank YouThank YouThank You!!!!

Michael.Smith1@mountsinai.orgMichael.Smith1@mountsinai.orgMichael.Smith1@mountsinai.orgMichael.Smith1@mountsinai.org