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36
Comments on Case 2: Dr. Sobin
This patient clearly does not have increased acid reux but appears to have reux
hypersensitivity. I give patients the “princess and the pea” analogy to explain their
heightened sensitivity. These patients are distinguished from those who have normal
24-h pH testing and no correlation between symptoms and pH reux episodes. This
is so-called functional heartburn. In both these instances, we think there is a func-
tional component to their symptoms.
In reux hypersensitivity, I would continue a PPI even though 24-h acid levels
are not increased, seeing how the patient’s symptoms are exacerbated when there
are episodes of reux. If the symptoms are severe, I might turn to a central neuro-
modulator. Trazodone and SSRIs have been used and found effective in treating
functional esophageal syndromes, although large population studies are lacking.
SSRIs have been found more helpful in treating functional esophageal disorders
than other functional disorders of gut-brain interaction. Tricyclics may also be tried,
as noted by Dr. Sanvanson.
P. Sanvanson
https://t.me/medicina_free
37© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_7
Chapter 7
Refractory GERD
W.HarleySobin
Case 1 A 41-year-old white man with a BMI of 26 presents with a history of chronic
acid reux symptoms for the past year. He has frequent heartburn and intermittent
regurgitation. He has taken occasional OTC Prilosec. You put him on esomeprazole,
40 mg a day, and see him back in 1 month. Despite therapy, he has ongoing
heartburn.
Is it surprising to you that the symptoms of heartburn aren’t gone after a
month of therapy?
Many people assume that PPIs universally clear up GERD symptoms, but only
60% of patients with GERD, at best, will become asymptomatic after a month of
PPI therapy.
When patients aren’t responding to PPIs what is the checklist you go
through?
I always review whether they are actually taking the medicine and timing it
appropriately. Many people take their PPIs with meals or HS which leads to poor
results. I consider alternative diagnoses: Could the patient have pill esophagitis—
are they taking minocycline, doxycycline, potassium pills, or alendronate? Might
there be an underlying motility disorder—either gastroparesis exacerbating GERD
or achalasia masquerading as GERD? Could it be eosinophilic esophagitis—is there
a history of food impactions or multiple allergies?
He had mistakenly been taking his PPI HS, so, instead, he starts to take his
esomeprazole 30min before breakfast and presents a month later with almost the
exact same complaints.
W. H. Sobin (*)
Division of Gastroenterology and Hepatology, Medical College of Wisconsin,
Milwaukee, WI, USA
e-mail: hsobin@mcw.edu
https://t.me/medicina_free
38
So now it has been 2 months since starting daily PPI and he is still symptom-
atic. How would you proceed?
At that time, I would investigate further with an EGD.However, I would want to
do the study off PPIs; if I do it on PPIs, I may get misleading information. Although
I will be looking for endoscopic evidence of reux esophagitis, I realize that the
majority of patients with true reux do not have erosive esophagitis on their index
endoscopy, only about 30% do. If I see erosive esophagitis, I have my diagnosis, but
since the majority of reux patients have NERD (non-erosive reux disease), I
would be prepared to do a pH study if the endoscopy is normal. I would have the
BRAVO probe ready to go. I would also do biopsies to rule out eosinophilic esopha-
gitis, etc.
You instruct him to taper his PPI off over a week to avoid acid rebound, and then,
he stays off it for a month. His symptoms go back to baseline. An EGD is performed,
and on EGD, the esophageal mucosa appears normal. Esophageal biopsies are
negative for EOE, Barrett’s esophagus, etc. The BRAVO probe is introduced and
shows time with pH<4 of 10%, a positive result.
How would you manage this?
At this time, I would go to bid PPI 30min before breakfast and before dinner. In
one study of pH results in patients with refractory heartburn, the pH results were
abnormal on one PPI daily in 31% of patients, but only 7% in patients on two PPI
daily [1].
If patients don’t respond sufciently to this, I will add an H2 blocker at bedtime.
This works well in many patients, but eventually a lot of them develop
tachyphylaxis.
The other thing I might do is switch PPIs. There is a gradation of potency of dif-
ferent products which goes-pantoprazole is weakest, omeprazole and esomeprazole,
somewhat stronger, rabeprazole and dexlansoprazole-the strongest.
In addition, there are patients who may have a genetic polymorphism in
CYP2C19. They may be hyper-metabolizers of PPIs who will do better on rabepra-
zole than most of the other PPIs. Esomeprazole should do better as well.
Another trick, in patients who suffer from nocturnal heartburn is giving Zegerid,
which is immediate release, not enteric coated, omeprazole-bicarbonate. This does
not have to be taken before meals; it may be taken at bedtime.
A common problem is that patients may have improvement in their heartburn but
still suffer from regurgitation. These patients generally have a signicant anatomic
defect, hiatal hernia, etc. I will reemphasize to these people the importance of ele-
vating the head of their beds and other anti-reux measures.
Are there other medical regimens that may improve regurgitation?
Taking baclofen before meals may be efcacious. Baclofen is a GABA-B ago-
nist, and GABA-B inhibits TLESRs. However, most patients don’t tolerate baclofen
well, certainly long term.
The patient does not respond to protonix 40mg bid and nighttime famotidine. He
is switched to rabeprazole and nds dramatic improvement. He is able to discon-
tinue his ranitidine and go to once daily rabeprazole before breakfast.
W. H. Sobin
https://t.me/medicina_free
39
Patient 2 A 38-year-old woman with chronic heartburn and regurgitation. Three
months earlier, she had an EGD because of melena at which time she was found to
have a hiatal hernia, reux esophagitis (LA grade A), and a small duodenal ulcer.
Biopsies were negative for Barrett’s esophagus and HP.She was started on PPIs.
After 2 months, the heartburn has improved, but she complains of severe regurgita-
tion. A repeat EGD is performed that demonstrates healing of the esophagitis and
duodenal ulcer. However, her LES appears quite lax, and she has a 3-cm sliding
hiatal hernia.
How would you approach this patient?
I think she is probably going to require anti-reux surgery to x the hernia and
correct the reux. Our surgeons do Nissen, Toupet, and LINX procedures to correct
these hernias. Their philosophy is outlined in the next chapter.
Reference
1. Charbel S, Khandwala F, Vaezi MF.The role of esophageal pH monitoring in symptomatic
patients on PPI therapy. Off J Am Coll Gastroenterol ACG. 2005;100(2):283–9.
7 Refractory GERD
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41© The Author(s), under exclusive license to Springer Nature
Switzerland AG 2023
W. H. Sobin et al. (eds.), Managing Complex Cases in Gastroenterology,
https://doi.org/10.1007/978-3-031-48949-5_8
Chapter 8
Surgery forGERD
JonGould
Case 1 A 40-year-old man, with 10 years of medically refractory reux, remains on
omeprazole. Despite omeprazole, he has severe regurgitation. When he stops
omeprazole, he has severe heartburn as well.
Workup reveals a 4-cm hiatal hernia, normal esophageal motility, and a positive
pH study with good symptom correlation. He has avoided having GERD surgery
because of horror stories on the Internet about difculties swallowing, not being
able to vomit after surgery, or having severe gas bloat.
Most patients with GERD are being treated medically. In a case like this, the
patient is really suffering despite medical therapy. Overall, is surgery
underused?
Tons of patients suffer from this condition; GERD is a really common disease.
Medical therapy with PPIs is frontline treatment, it’s used frequently. It’s accessible
to patients. They can prescribe it for themselves. Primary care doctors hand it out
frequently. We all prescribe it.
However, there are data that suggest that if you look at people who truly have a
well-established GERD diagnosis, who are on a PPI, as many as one-third of those
people are not completely satised with their treatment. We end up operating on a
very small subset of those patients, less than 1% of people who would meet surgical
criteria, which means symptoms of GERD refractory to medical therapy. We’ve got
a small subset of people getting surgical therapy, and we’ve got a lot of people that
are treading water, feeling like there’s got to be something better, but they’re not
ready to commit to surgery.
J. Gould (*)
Department of Surgery, Medical College of Wisconsin, Milwaukee, WI, USA
e-mail: jgould@mcw.edu
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Fundoplication outcomes can be excellent when done properly in the appropriate
patient. However, a lot of patients who have GERD interventions end up back on
PPIs. There are doctors who tell their patients to avoid fundoplication because they
only last a few years, and there are surgeons who have an opinion that these things
never fall apart. The truth is somewhere in the middle. These procedures are intended
to be lifelong interventions, but in the end, the bottom line is that you fail on
some people.
We can do an intervention, but the patient may be left with side effects. In the
end, are they better off? In some cases, no. There are some surgical failures. These
repairs can work for a while and then fall apart. There are some bad outcomes. The
wrong procedure might be done on the wrong patient.
The operations are not always as effective as we want them to be. So, we’ve got
this issue. We’ve got a prevalent disease with a lot of people who are suffering, who
aren’t completely happy with their current treatment. However, they’re not ready to
make the next leap because they don’t feel like there’s an ideal option for them.
The good news is that newer techniques and learning from past mistakes allow
us to have better surgical results.
You mention surgical repairs coming apart. Do the sutures loosen? Is that
what is happening here?
We used to think that the sutures that we placed in the hiatus were tearing and
the repair was disrupting. Now, we think that the repair doesn’t disrupt, and it
dilates over time. The hiatus stretches out, and then, the stomach herniates
through there.
So now, what people are trying to do is close it tight enough that when it stretches,
it doesn’t stretch too much. You make it tight enough to prevent recurrence but not
so tight that you get symptoms.
So, I tighten it to where I think it’s about right. My way of doing it is a little dif-
ferent from the next guy. It’s very much art, and it’s judgment. For what it's worth,
good judgment comes from having bad judgment a few times.
The 40-year-old patient described above seems to be a good candidate for
surgery. He has a 10-year history of symptoms, severe regurgitation in spite of
PPIs, and a disordered anatomy. I have always thought that the recommended
surgical therapy for these patients was a Nissen. If the patient had disordered
esophageal motility, you would do a Toupet instead. In this case the motility
looks normal so would you do a Nissen?
No, we had a multi-society GERD Consensus Conference [1] with GI and sur-
gery societies participating, and we reviewed a lot of data comparing Nissen with
Toupet. We looked at a lot of different outcomes that matter, including hiatal hernia
recurrence over time, dysphagia requiring an intervention, gas-bloat symptoms,
inability to vomit, and recurrence of reux symptoms at 1 year. What the data
showed is that patients did better with a partial wrap (Toupet) than a complete wrap
(Nissen). Our panel recommended that adult patients with GERD would benet
more from a partial wrap than a complete wrap. We shouldn’t be doing as many
Nissens as we do.
These studies also show that esophageal motility does not make much of a differ-
ence. If your motility is normal, a partial wrap has fewer side effects, with equal
J. Gould
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43
GERD outcomes to a full wrap. If your motility’s abnormal, same statement, it
probably doesn’t matter as much as we once thought. The only exception is those
cases with extreme dysmotility and real aperistalsis.
The bottom line is that the Toupet is better than the Nissen. The problem is that
surgeons in the USA haven’t been trained to do Toupets, and they only learn how to
do Nissens. We’re the only country in the world that does Nissens. Last month, I did
my rst Nissen in the last 5 years, and I’ve completely switched to partial wrap
fundoplication.
You mention esophageal manometry. Do you think everyone should get an
esophageal manometry prior to GERD surgery?
The guidelines say you should, and it’s nice to have a baseline, in case things
don’t go well. However, as I just pointed out, it doesn’t make as big a difference as
we once thought, unless there is severe aperistalsis. That being said, I do them in
about 75% of cases.
What do you think about the LINX anti-reux system, in comparison with
fundoplication?
I’m a fan. It’s an early technology, but so far, the data suggest that GERD may be
better treated with magnetic sphincter augmentation (MSA) than fundoplication.
So far, in terms of symptom recurrence, and perioperative complications, the
data suggest better outcomes with MSA.This includes dysphagia, which is counter-
intuitive, because the biggest problem with the LINX is concern about dysphagia.
When we look out over a longer time interval, at more than 2 years, quality of life
measures favor MSA.
The great thing about LINX is that it’s very easy to put in. The dissection is very
minimal compared to what you have to do for a wrap. You can put it in, and if there
are problems, you can take it out very easily. There are way fewer decision points,
and the technique is very standardized. There’s an established technique that’s
taught to every surgeon.
I think the physics at the diaphragm is different for a LINX than for a fundoplica-
tion. You don’t have this big bulky wrap pushing on the diaphragm. You’ve got a
magnet that’s sitting there without any tension. It’s not pushing as hard, and it even-
tually gets encapsulated in some scar tissue that helps hold it into place. So, you
don’t see the same rate of anatomic failures in hiatal hernias after a LINX that you
do after a fundoplication. What I say is “let’s do the least invasive option that leaves
us as many options as we can possibly still have on the table.”
What if you do a LINX and it’s not working well, is it permanently embed-
ded? And what about erosions with the LINX?
Most of the failures we see are people who develop dysphagia that doesn’t
improve. There is also a very small incidence of erosions about 0.2%. Most of the
erosions occurred on devices that were overly tight. The philosophy over time has
changed from making it tight to the point where you can see the things squeezing
the esophagus to actually having it loose enough that it doesn’t compress at all.
In terms of managing dysphagia, if you go in to remove the device a year later,
you nd that every bead has a perfectly formed scar on top of it. It’s like a little
capsule that you touch with a little cutter, and the magnet pops out and you grab the
magnet and you just ride around each side and you cut the wire.
8 Surgery forGERD
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However, what we’ve found is that even though you’ve removed the device,
there’s scar tissue remaining that changes the compliance there. When you take it
out and don’t do anything, the dysphagia is gone and about 75% of people don’t get
the reux back.
Do you take all patients with post-op dysphagia from the LINX back to
surgery?
No, there’s a reversal time frame, and at rst, you need to try and ride it out.
Some people will react to the implant with scarring, and you try to dilate it. You
might also prescribe a brief course of oral steroids to soften up the scar tissue.
You would try to manage it with dilation and steroids for a few months. If people
are struggling, asking to get them out, I would try to wait at least 2 or 3 months,
unless there’s a major issue. Most of these people will improve sufciently to avoid
surgery.
The patient under discussion has a 4-cm hiatal hernia. I thought that the
LINX was approved only for patients with a hiatal hernia under 3 cm. Does
that mean a LINX is contraindicated in this patient?
The original MSA studies only looked at patients with small hiatal hernias. Large
hernias were a relative contraindication because they were not studied in the pivotal
and premarket trials conducted to attain original FDA approval. Now, appropriate
studies have been done with larger hernias, and currently, the FDA indications for
LINX include larger hernias.
If that’s the case, would you prefer to do an MSA for most of your GERD
operations?
To be a candidate, the patient can't have any MSA contraindications, which
include a BMI>35, ineffective motility (IEM) on manometry, baseline dysphagia
that is moderate or worse, or an allergy to nickel. Insurance is a frequent obstacle,
Medicare and Medicaid don’t cover it; private insurance is about 50/50.
All else being equal, I would say that the MSA is simpler, more likely to be per-
formed without an overnight hospital stay, easily reversible, and may have a lower
failure rate. When MSA fails, Toupet is an option—not the other way around in my
opinion, so MSA saves options in the event of a failure. In the short term, however,
MSA is more likely than Toupet to cause dysphagia.
The advantages of the Toupet include that it is universally covered; it’s okay in
patients with IEM and dysphagia, and there’s no foreign body/implant, no worries
about MRI.
In my opinion, both are good options. All else being equal, I think a patient who
meets criteria and has access to either may be better off with the MSA due to the
long-term thoughts and preservation of options as described.
What are the concerns regarding MSA and MRIs?
The current generation of LINX is compatible with a 1.5 TESLA MRI.About
90% of the MRIs done in this country utilize an MRI 1.5T or weaker. Most of the
bone and joint and spine MRIs are all 1.5. However, some of the breast indications
use a 3 Tesla MRI, and those functional brain MRIs are 7.
If you use an MRI that’s stronger than the device is compatible with, it depolar-
izes the magnets. So instead of attracting each other, they repel, and people get their
reux back. That’s usually the worst thing that happens.
J. Gould
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45
Patients are educated and given a card. You would be amazed that someone could
have an operation and have a magnet implanted in their body, and then when they
go to get an MRI, they check the form saying “no implants.” I’ve had it happen to
two of my patients who didn’t follow our warnings.
Case 2 A 45-year-old man with a BMI of 22 has a long history of GERD well con-
trolled on PPI.His only symptom is heartburn, and it is totally relieved with PPI.He
had an EGD that showed a small hiatal hernia with a mildly lax lower esophageal
sphincter and Grade A esophagitis.
He is concerned about continuing PPIs long term because he read on the inter-
net that PPI use can cause cancer and dementia and wonders whether he should
just proceed with a hiatal hernia repair?
How do you feel about operating on patients whose symptoms are well con-
trolled on PPIs?
When I see people that are well controlled on PPIs but say that they want to get
off them, I’ll have a debate with them about whether that’s the right thing to do.
Because if their symptoms are completely under control, there’s a chance they’ll do
worse with surgery. I may give them a side effect from an operation that might ulti-
mately fail.
Of course, there’s potential downsides to PPIs, but things have been blown out of
proportion. For the patient who uses the C word (cancer), who doesn’t have Barrett’s
or dysplasia on endoscopy, I tell them that’s simply not a big concern. There’s
downsides to an invasive intervention. So, I’ll actually talk those people back.
I think that a patient who’s well managed medically on a PPI, who has symptoms
under control, whose quality of life as it relates to their GI symptoms is acceptable
to them is best left alone. Now, I might meet them in the future to discuss surgery if
things change, but for now I would counsel against surgery.
On the other hand, if I’m dealing with a patient whose main complaint is regur-
gitation, a PPI is not going to x that. Most people with bad regurgitation have a
signicant hiatal hernia. They have an anatomic issue.
Case 3 A 38-year-old woman has a long history of severe reux. She has a BMI of
40. On EGD, she has a 1-cm hiatal hernia. PPIs are not controlling her symptoms.
How do you manage GERD in the obese patient?
If a patient with a BMI of 40 has medically refractory reux, the best GERD
operation that I can do for them is a gastric bypass. We call it an esophageal discon-
nect instead, which is because many insurance companies will deny it if we call it a
bypass, claiming that they don’t cover cosmetic operations for obesity. So, I have to
get a medical doctor on the phone and tell him or her what I’m trying to accomplish.
We can usually get it covered if we call it a disconnect and have a peer-to-
peer review.
The reason it works so well is that we make a small pouch, about a 20-cc gastric
pouch, and there are very few parietal cells in there. Obviously, there’s no bilio-
pancreatic secretions that can get in there. There’s no pepsin that can get in there. So
that’s how it works to prevent reux. Of course, this patient is obese and will lose
weight, which is a factor for all these other things.
8 Surgery forGERD
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So, a gastric bypass or a disconnect is good in the high BMI patients. We know
that BMI is a risk factor for hiatal dilation leading to fundoplication failure. We also
prefer a gastric bypass for GERD in some patients with scleroderma and others with
profound motility problems. A bypass doesn’t rely on a valve that’s tight enough to
prevent reux, but not so tight that they’ll have a swallowing problem that gets
worse. It just diverts all that caustic stuff.
Case 4 A 63-year-old female, is 5 years status post an endoscopic TIF (transoral
incisionless fundoplication). Her symptoms prior to surgery were heartburn and
regurgitation refractory to medical therapy. She had a positive pH test, with no
hiatal hernia. Following the TIF, her symptoms resolved for 3 months, but after that
her symptoms came back, and they pretty quickly returned to baseline.
What is your impression of the new surgical-endoscopic hybrid procedure,
the transoral incisionless fundoplication (TIF)?
The word on the street is that because you’re doing it endoscopically, you don’t
burn any bridges whatsoever and that you leave everything on the table. You haven't
done anything to harm the patient, and you have every option that you would want
to have in your back pocket if that should fail.
However, the issue with TIF has always been that if a patient has a hiatal hernia,
it’s hard to do a wrap, have it in the chest, and have it work at all. So now people are
doing the cTIF, where they go in laparoscopically or robotically, x the hernia, and
then close all the incisions and step back and do a blind endoscopic TIF.
However, our Consensus Conference reviewed the data and found that as time
goes by the failure rate of a TIF is going to exceed the failure rate of a fundoplica-
tion. Therefore, we recommended that adult patients with GERD would get greater
benet from fundoplication than TIF.
We need to come up with an endoscopic treatment for medically refractory
reux; we have to do it. Of all the things that are out there, TIF is really the closest
thing I think, to what we do in surgery. We’re not there yet.
In terms of the ease of a redo, if the TIF fails, I nd that these are really hard
things to undo. The people that claim that it’s easy are cutting corners and putting
wraps on top of TIFs. However, this stuff is bound to fail. The only technique that
works is to do a minimally invasive hernia repair with takedown of the TIF and
conversion to a Toupet. It’s really hard to remove all those TIF anchors. I would
rather redo a fundoplication any day of the week than someone who had a TIF.
Reference
1. Slater BJ, Collings A, Dirks R, Gould JC, Qureshi AP, Juza R, Rodríguez-Luna MR, Wunker
C, Kohn GP, Kothari S, Carslon E.Multi-society consensus conference and guideline on the
treatment of gastroesophageal reux disease (GERD). Surg Endosc. 2023;37(2):781–806.
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