Gastroparesis Patient Seminar – Parham Doctors’ Hospital

Gastroparesis Patient Seminar – Parham Doctors’ Hospital


– Hi, I’m Dr. Matt Brengman
and I’m gonna talk to you a little bit about gastroparesis today. I do gastroparesis
therapies in my practice, about 50% of my practice is gastroparesis and it’s an unusual therapy, I think. I do some talks nationally for this and I did one in the summer of 2015, which we broadcast on Periscope, which some followers on Twitter saw, and there were some people
who missed it and, you know, if you know Periscope, it kind
of goes away after 72 hours. So I thought we’d put something together, put it on the website, and hopefully this is informative to you. First thing we probably should do is just define what gastroparesis is. Gastroparesis is a slowing of
the emptying of the stomach that’s not related to a blockage. Clearly, if there’s a mechanical blockage of the first part of the intestine or the end of the stomach
by a tumor or scarring, that’s gonna lead to gastric slowing, but that’s not what we’re talking about. What we’re talking about is somebody who appears to have a normal stomach, but it’s not emptying properly
for a functional reason. So delayed gastric emptying can lead to all kinds of symptoms,
and generally speaking, people experience bloating and fullness, nausea with or without vomiting, acid reflux, and abdominal pain. Now, you think about those
symptoms, they’re pretty generic. There’s lots of different things that can give you those symptoms. You can get those symptoms
from gallbladder disease, gastritis, hiatal hernia, H. Pylori, gastric ulcers, duodenal ulcers, so the problem with the upper abdomen is almost everything gives
you those types of symptoms, and so generally speaking,
people are gonna go through a long process of self-treatment and then some diagnostic
workup by their doctors before they get diagnosed
with gastroparesis. The underlying cause of the slowing is what we’re a little more interested in. Slowing is basically a symptom
of other disease processes. We think of gastroparesis as being diabetic and non-diabetic. Non-diabetic has another
term called idiopathic, which means we don’t know what causes it. When we look at diabetics, about 5% of the type one diabetics will develop gastroparesis that’s symptomatic over their lifetime. About 1% of type two
diabetics will get it. Now, diabetic gastroparesis
is a type of neuropathy, and so for the diabetics out there, you know neuropathy can mean painful feet, tingling in the feet or in the hands, and other types of like retinopathy. So it takes awhile to get it, so most people are gonna have
diabetes for about 10 years or more before they develop
significant gastroparesis. We don’t think of it commonly in people who are just diagnosed with diabetes, unless they’ve been untreated
for a long period of time and they’ve just come to therapy, so that’s how most people in this country. For the idiopathic gastroparesis, it’s a much smaller number, it’s about 0.2% of the total population, but there’s just way more people that are non-diabetic in
this country, so in all, there’s actually more people
with idiopathic gastroparesis out there than there are diabetics. Unfortunately, most
physicians don’t think of it as being a very common disease and they’ll think of
diabetic gastroparesis when a diabetic comes in
with nausea or vomiting, but because of all the other crossover with other diseases that
are much more common, again, gallbladder diseases,
ulcers, gastritis, et cetera, they won’t think of gastroparesis as the first item of interest when a patient presents
with those symptoms. Diabetics and non-diabetic
or idiopathic gastroparesis, they present differently. They’re kind of different
disease processes. And so the diabetics tend to
have more nausea and vomiting, bloating symptoms, but less pain. The idiopathics tend to have
nausea with less vomiting, but a much higher incidence
of epigastric abdominal pain as a component, and so
that’s pretty clearly seen when we look at these populations and so that can help direct somebody when they see a patient
with these symptoms. A common statement I hear
from the patients I see is I’ve had pain for so long,
my doctors aren’t trusting me in my symptoms, and
they say that, you know, pain doesn’t come with gastroparesis and that’s clearly not the case if we look at the literature
around gastroparesis, especially idiopathic gastroparesis. 80% to 90% of patients
who come to medical care for gastroparesis will complain of abdominal pain as
one of their symptoms. Now, a much smaller
percentage, only about 20% are gonna have that as
their primary complaint, but if you do a good history, they’ll describe nausea,
vomiting, bloating, oh, yeah, I also get pain after I eat. It’s just not the primary
presenting symptom. So the purposes of this
conversation we’re having, we’re gonna divide gastroparesis up into kind of three big buckets, the diabetic gastroparetics, and then the idiopathic gastroparetics we’re gonna put into two subgroups. There is post-viral and
then the post-surgical. They’re treated slightly differently and so it’s important to try
to figure out who has what. As I mentioned when we were
talking about incidence, the biggest number of patients is gonna be the idiopathic gastroparetics. These are typically middle-aged
women or younger women, 35 to 45 at presentation. Many of them are gonna have an antecedent or preceding viral illness, whether it’s respiratory
or gastrointestinal, and the flu, for lack of a better term, and then after that, develop
significant nausea, vomiting that sometimes leads to hospitalization and it just persists, it keeps on going on and then the physicians are
sort of at their wit’s end to try to figure out what’s going on. That’s the most common presentation. When we look at post-viral gastroparesis, there’s been lots of studies. The one thing we know is it
can get better over a year and some people are gonna
experience spontaneous remissions. And so typically, as somebody
who does gastroparesis therapy as part of my work, you know,
I’ll wait on those people until they’ve had to just make sure it’s not gonna get better on its own. Now, most people who come to me have had symptoms for multiple years and so we know that they’re not
gonna resolve spontaneously, but some don’t, and for those, we wait, and we do other therapies
that you’ll hear about a little bit later in this talk. There’s been some studies on looking at the viruses that can cause this. Cytomegalovirus, or
CMV, Epstein-Barr virus, herpes or herpes zoster,
those can all be associated with the development of gastroparesis, and so if you have had those diagnoses and now you’re having
significant abdominal pain or nausea or vomiting,
there’s a possible link there. Less common in numbers but
dramatic in presentation are the folks who have
post-surgical gastroparesis, and that’s a physical
disruption of the nerves that go to the stomach at surgery. And this used to be really
common with ulcer surgery, you know, back 25 years ago, we did a lot of surgery for ulcers and one of the major
procedures that was done involved dividing the nerves
that go to the stomach. Now, we don’t do ulcer surgery
that frequently any longer ’cause we have great
medications that allow us to not have to do it,
but we do other surgeries where we work around the
food tube or the esophagus and we’re working around these nerves, and those are mostly done for gastroesophageal reflux
disease or heartburn and then hiatal hernias. And, you know, if you just
look at the surgical series, there is at least a 1% incidence of damage to these nerves
during these procedures. They can be hard to identify. Sometimes the anatomy is very abnormal when these procedures are being done. And if they’re damaged, they can lead to significant gastroparesis symptoms. A final cause of gastric slowing that’s not really gastroparesis is drug-induced gastric slowing. This is clearly most common
with the narcotic pain medicines like Percocet and Dilaudid
and morphine and the others. You know, narcotics have a
direct effect on the bowel and have direct slowing of the bowel, so somebody who’s on
chronic narcotic therapy, most commonly for back pain, those people can often
see chronic constipation and chronic gastric slowing,
and the mainstay therapy there is to see if there’s another medication that could work versus the narcotic, ’cause if you can get
them off the narcotic, many times, it’ll just get totally better. There are other medicines
that can do it, too, anticholinergic medicines,
those are mostly antiemetics like Phenergan and
Compazine, scopolamine patch, Cyclosporine and anti-transient medicine will do this the same, and interestingly, a medicine called Byetta, or
in the other GLP-1 analogs, these medicines are used for diabetes, they are a synthetic form of
a naturally-occurring hormone that the intestine makes
that helps your body digest and absorb glucose and
sugars from your body, and we know that through some studies that were done a long time ago that direct infusions of that
hormone cause gastric slowing and so the main side effect of Byetta is gastric slowing and nausea. And so we use it in diabetics and so some diabetics have gastroparesis, now we can exacerbate it by
using one of the medicines. So somebody who’s a
diabetic gets put on Byetta and they start vomiting like crazy or they have a lot of food
intolerance, you know, they’re gonna need to
come off that medicine and maybe try a different medicine and the symptoms will resolve with cessation of the medication. So how do we make the
diagnosis of gastroparesis? Well, the gold standard really is called a gastric emptying study, which, in this day and age,
is a pretty vague test. It’s a nuclear medicine
test, so the patient eats, either like an egg salad
sandwich or some oatmeal, it’s been labeled with
a radioactive protein, and they sit or lay down in
front of a big Geiger counter, for lack of a better
term, just a big disc, and it measures the
radioactivity in the stomach. And over time, we see that
radioactivity decrease and we know that the food is
moving through, and typically, we want to see about 50%
of the radioactive material move out of the stomach
in a four-hour period. Ideally, the test is done over four hours. Lots of time, it’s done over two hours with extrapolation after four hours. That’s fine if it’s really abnormal, but if it’s close and
there’s some concerns, then probably a four-hour
study is the best thing. There are some other
tests that have been done. They’re really not the gold standard. There’s breath testing,
there is wireless capsules, where you eat a capsule and you see how long it stays in the
stomach and the change in the pH that’s sensed by a remote sensor tells us. Endoscopy can be quite helpful, though, so if you have to have an
endoscopy for any reason, and nausea’s a good reason
to have an endoscopy, and your endoscopist goes
down into your stomach and they’ve made sure that you
didn’t eat anything overnight so it’s been at least
12 or maybe 18 hours, and they see that your
stomach’s full of food, almost by definition,
unless there’s a medication causing some sort of a side effect, that would be diagnostic
of poor gastric emptying. There’s some pictures you’ll
see on these next slides of images of what gastric
emptying tests look like. You can see it’s not super scientific, but it’s what we have and it seems to work to get people in the
door for the diagnosis. Then, it’s really up to
the clinician to say, okay, what kind of gastroparesis is this and how are we best gonna treat it? Treatment of gastroparesis
is multi-factorial, and honestly, the majority of patients are gonna improve with
just dietary therapy. So avoiding the foods
that slow the stomach and then not eating large meals so the food has time to
empty, although slowly, before it causes any side effects. And so typically we’ll tell patients to avoid raw fruits and vegetables, that tends to slow stomach emptying, caffeine, high-fat foods,
that can also mean spicy foods because most spicy foods, even if they’re not perceived as high-fat, they have a lot of oil in
them to carry that spice and then things like smoking that also decrease gastric emptying. So you want to take all the
confounding variables out, small meals, maybe five
or six meals per day, liquid to softer-based,
majority of patients are gonna do fine with that. You know, does that mean that patients are gonna eat that all the time? No, that’s totally unrealistic, right? So people go on holiday and whatever, but then they can manage it, right? So if they say, like, I’m gonna have pizza ’cause I want pizza, I know
I might feel bad afterwards, you know, they make that choice, but they have the tool
to manage their symptoms, and so dietary therapy is a mainstay and basically every
patient with gastroparesis should see a dietitian with
some expertise in the disease, just to go through their
diet and see if there’s a way to manage the disease without
even using medications. One of the reasons that gastroparesis is really, I guess, relatively shunned by many physicians is we
don’t have great drug therapy. So if you’re in your office and
you’re a primary care doctor and you are seeing lots
of different diseases, you want to be able to treat them, and when you can’t, it’s hard. It’s hard for the patient,
it’s hard for the physician. Right now we only have one FDA medication that’s approved for gastroparesis and that’s a medicine
called metoclopramide, or the trade name is Reglan. Unfortunately, it has a
black box warning around it, so any time there’s a black box warning, you know, physicians don’t really want to prescribe it too much
’cause there’s some liability, and there’s a lot of side effects. So Reglan can be very effective, it’s usually very effective
when people initiate therapy, but there tends to be some
accommodation to the therapy where the effect wears off over time, leading to increasing doses, and there’s a dose dependence
side effect profile that involves involuntary movements, involuntary movement facial
motions, jitteriness, and if those things occur,
the medicine has to be stopped because if it goes on prolonged, those side effects can become permanent and so very important to
recognize those limitations, and when they are recognized, get the patient off the
medication as quickly as possible. Unfortunately, then, what
are you gonna do for them? ‘Cause they were sick
enough to need medications, what are our other choices? There’s a medicine that’s available outside the United States
called Domperidone, was kind of available in
the United States for awhile through overseas pharmacies in Canada and India and Australia. The FDA has really come down on people that were importing this drug, even though it works pretty well and it’s generally pretty safe. It’s not FDA-approved
and the FDA finally did kind of come down on several
pharmacies and practitioners, and so much more difficult
to get than it used to be. And so while we still see people use it, not quite as much as we used to. There’s a side effect profile, too. Probably the most important one is it elevates the prolactin level. There’s a rare incidence of
pituitary tumor formation, and for women, that can mean
that they start lactating and if that happens, clearly, the medicine needs to be
stopped, even if it’s beneficial. Some medicines that are
used in the hospital more are a medicine, Erythromycin,
which is an antibiotic. It is structurally similar
to a molecule in the body called modalin, so it has a direct effect on the stomach to increase emptying. It’s why the major side effect
of Erythromycin is nausea, is because people get this sort of hyperactive stomach nausea and they can’t tolerate the medicine. Well, for some of you whose
stomach doesn’t empty very well, Erythromycin can be beneficial. It works pretty well IV
in the acute setting. There’s very rapid
accommodation to the effects, so it typically won’t work
longer than about four weeks and so prescribing it as an outpatient is not gonna work for most people, although it generally is tried, but it can be helpful in the hospital, so if somebody comes in with an acute gastroparesis exacerbation, IV infusions of Erythromycin are indicated and can be helpful and
have been shown to be so in some of the medical literature. That’s it for the medications, and I didn’t say anything
that sounded super good, so that’s why we are here, I guess, to talk about other therapies. The next step in a lot
of people’s algorithms is to place an enteral tube, so that’s a tube that goes
in the body somewhere, into the stomach or intestines so that nutrition can be delivered by liquid directly to the intestine. It’s about as good as it sounds. It can be really helpful
in the acute management of people who have had
gastroparesis for a long time who present very ill
and very malnourished, not ready to have any type
of surgical intervention or just need to have their
nutrition balanced out to see what happens, and I’ve
seen patients in the past who’ve had acute gastroparesis just have come in very malnourished, immune system depressed
from their malnourishment, just sick as a dog, for
lack of a better term, brought them into the hospital, got them on enteral nutrition, usually through a jejunostomy tube, got their nutrition back, and
had them completely recover because the malnutrition was just exacerbating the problem so much that you have to sort
those two things out. So the person who shows
up very malnourished, enteral therapy is really indicated, and probably six weeks, you know, a good trial, checking the laboratories, making sure the vitamin levels are normal, making sure the protein levels are normal, getting their immune system
back to where it needs to be, and that person can sometimes
not need any therapy and that does happen on occasion. So enteral therapy can be very helpful. Enteral therapy, however,
is not what we call a destination therapy. What we mean by destination therapy is a long-term solution to the problem. First of all, enteral
therapy requires a way to get the food to the intestine. So if it’s not going to be surgically, that means a tube through the
nose that goes all the way through the stomach into the intestine. The date on that is just terrible. Those are okay things
to do in the hospital, where the patient is not going anywhere, but outside the hospital,
those tubes are really tiny, they tend to get clogged,
they tend to migrate back into the stomach, worsening the problem, you can imagine delivering
a bunch of liquid nutrition into somebody whose stomach
is not working great, that’s not gonna be too good, or they get pulled out on accident. People are asleep, they grab at things, and then, you know, it just
doesn’t work out very good. So a temporary therapy with
a tube in the nose is okay. Longer than six weeks, there’s
almost nobody who makes it longer than six weeks
with this kind of therapy. So if we’re gonna consider
doing enteral therapy as an outpatient, like
do it, get them home, let them recover, we’re almost always talking about a jejunostomy tube, and so as you’re gonna
see in these slides, there’s several pictures
of jejunostomy tubes. A jejunostomy tube is
a surgical procedure, typically speaking. Some people will do them in endoscopy, but that’s not as frequent,
usually with surgery. It’s a tube that goes through the skin, and there’s a picture you’ll
see, into the intestine. This disease affects a lot of young women. There’s a lot of body image issues with having a tube hanging
out of your stomach. It’s not a good thing and they hurt. They always leak a little bit. There’s always a little
bit of seepage around it. It kind of smells bad and it’s gross. And so as a destination
therapy, it’s not what we want. I mean, sometimes we
end up in that corner, but we should have exhausted
many other therapies that you’ll hear about in a
minute before we end up there. So it’s good for the short-term, not great for the long-term. Another short-term therapy if the patient can’t get enteral therapy is IV nutrition, total parenteral nutrition,
or TPN is what it’s called. That requires an implantable IV catheter. That has its own problems
with infections and implants. And then the nutrition just cannot be as balanced as enteral therapy. Enteral therapy is sort of
naturally-occurring compounds and there’s lots of little micronutrients that we can’t create in a
bag solution that to help. And then the IV nutrition,
the infections are a problem. So long-term IV therapy
should really be a rarity. It’s very expensive,
lots of complications, the catheters usually
have to be changed out due to infection over time,
and for somebody who’s young, 30s or 40s, we should be
looking for another answer for that person than long-term IV therapy, if we can find it, if we can find it. The next therapy which is not surgical is injection of the pylorus, or the muscle at the end of the stomach, with Botox. Botox is a naturally-occurring
compound that, when injected into muscle,
essentially paralyzes the muscle. And so Botox makes that muscle
at the end of the stomach open all the time, and so if your stomach is not emptying properly,
we don’t want a valve at the end of the stomach
that’s closed, right? We want it to be open all the time so at least gravity will
help the food go out. And so Botox injection’s
been around for a long time. It’s been studied on many occasions. There’s a lot of controversy
about whether it works or not. In my experience, I don’t
do Botox injections, but I see lots of patients
who’ve had Botox injected. It works about 20% of the time and based on what we know about
pyloroplasty as a therapy, Botox injections should
work more frequently. And so I think the problem
with Botox injection is not so much that it’s
theoretically a bad thing, I think theoretically, it should work, I think it’s very hard to deliver from the end of an endoscope
directly into the muscle at the right location to get it to relax. I think it’s a little bit of a crap shoot, for lack of a better term,
to get it in the right spot. And so when it works
for people, it’s great. When it doesn’t work, it doesn’t. Typically, what I see is for
when it does work with people, they get one, two, or three
injections, and by the third, they’re starting to get this accommodation to the effect and it’s not
working like it used to, and so then we’ll pursue
a surgical therapy. But it can be, and it usually
works for about six months and so I think it’s
worth doing for people, but I also don’t think it’s a permanent solution for most people. So now we’re gonna talk
about surgical therapies. Full disclosure, I’m a surgeon, so I know probably more about
this than anything else, although I do plenty of other therapies. I treat lots of people, though. I don’t think just because
you have gastroparesis, you need surgery, and most people don’t. We’ve already talked about
diets and medications and lots of people are gonna be better or even waiting and doing nothing. Some people will come to surgery. It’s a smaller percentage,
and we’re gonna go in the order of history
rather than frequency, just to give you a better sense of how things have evolved over time. The first surgical therapy
we’re gonna talk about is gastric electrical stimulation. This is probably better known
as the gastric pacemaker. The trade name is Enterra, E-N-T-E-R-R-A. It’s a device. It was introduced and approved
in this country around 2001. I was in one of the initial
training classes from Medtronic, the company that makes it, and it’s a modified pacemaker
and initially what was thought was we were gonna take
a modified pacemaker and take some wires,
just like we take wires from a pacemaker, put them in the heart, put them on the stomach,
turn this thing on, and then the stomach is gonna
start pumping the food out. And what we know for sure is
it doesn’t work like that, that this is truly neural stimulation. It comes back to sort of what’s
the problem in gastroparesis or in some forms of gastroparesis? And the problem is is
the nerves are damaged. And so what do the
nerves do in the stomach? Well, autonomic nerves or
nerves that go to the intestine are not like are skeletal muscle nerves. Our skeletal muscle nerves,
the ones that move our arms and our hands, when the nerve fires, the electrical impulse causes
the muscle to contract, and it’s the exact
opposite in the intestine. When the nerves fire, it
causes the muscle to relax. And so you can imagine
that in the stomach, if the nerves are injured, then the muscle is not relaxing at the right time and maybe it even spasms
when the patient eats. And that’s why sometimes we see patients who smell food and all of a
sudden become very nauseated and have retching, or
they eat like one bite and all of a sudden they’re
vomiting like crazy. It’s not like they had a giant
meal and they’re vomiting. It can be really only one bite. And so this denervation
effect can be very prominent and the stimulator renervates. It gives electrical
stimulation to the stomach. And there’s certainly a subgroup of people who think that it increases
a combination, that is, it helps the stomach relax
when the food comes down. This is born out by some of the evidence in which the majority of
patients who have a stimulator, their stomach doesn’t empty better. If we measure gastric emptying before and we measure gastric emptying after, it’s actually the same. There’s a minority that
will have improved emptying, but the majority do not, and yet, the vast majority of people
who get a stimulator, 75%, will experience significant
improvement in their symptoms. And so we think about the
problem as denervation, then gastric stimulation seems
to make a lot more sense. Like I said, about 75% of
people are gonna improve. This therapy is much more
effective in diabetics than it is in idiopathic patients. My experience is about 80% of diabetics are gonna have improvement
and about 50% of folks who are idiopathic gastroparetics are gonna have an improvement, not that it can’t work,
but it’s not as effective. And so for gastric stimulation, that’s my first line
therapy for the patient who has a diabetic gastroparesis, especially the ones that
sort of have symptoms that sound like denervation gastric spasm, and so those people would
generally do pretty well with a gastric stimulator. And so we’ll often add
as first line therapy and then we’ll progress with therapy if they need something else. Now, the gastric stimulator
is a device, right? So it’s a battery pack and it’s wires that go through the abdominal
wall into the stomach. The battery has a lifetime,
just like any battery, a battery in your car or your cell phone. That battery has to be replaced,
depending on the settings, between five and eight
years after it’s placed. And so, you know, you talk about putting a gastric stimulator in a patient who’s 40 years old, they’re
potentially looking at multiple replacements of the device. It’s one of the reasons
now we will commonly use adjunctive therapy or adjunctive
surgery with the stimulator and we’ll talk about
pyloroplasty in a minute, so most people will now do a pyloroplasty at the same time as a stimulator, trying to get as much effect as possible and maybe decreasing the frequency with which the stimulator
needs to be changed. There are very few complications
with the stimulator. Your provider can give you
a lot more detail on this, but it’s generally a safe operation, done with a video laparoscope. I keep people overnight, but some people will send home the same
day, and that’s fine. The next therapy we’re gonna talk about is laparoscopic pyloroplasty, and this is a relatively new procedure. If you go to our site, there’s
another little slideshow you can read through that
has a lot more information on pyloroplasty with some references, and I encourage that if
you want to know more. This is a procedure that’s been around for about three years now commonly, maybe a little bit longer,
and based on some information out of the University of Oregon, who was really the first
group to publish on this, where they just took a bunch of people who had gastroparesis,
and laparoscopically, they cut the muscle at
the end of the stomach. Now, if you think about the
Botox data a little bit, you would think it probably
wouldn’t work that frequently. If Botox is working great,
20% of people respond, then we should expect 20% of people who have the muscle
physically cut with surgery should also respond, and I think everybody in the group of people I
know are really impressed that it works much more
frequently than that. The published data is 75% to
80% improvement in symptoms and improvement in gastric emptying. So remember, with the stimulator, there was no improvement
in gastric emptying. With pyloroplasty, improvement
in gastric emptying as well. And so for those folks
that have bad reflux from retained gastric secretions, this is a better procedure for them. And so I started doing this
procedure several years ago. I use it routinely on the idiopathics ’cause those people seem to do better. There’s been additional information over the last couple years
on looking at pylorus and pyloric function in patients with idiopathic
gastroparesis, and turns out, not surprisingly, that the
muscles in the patients who have idiopathic gastroparesis tend to be higher pressure,
they’re squeezing harder, and they’re hypertrophic, they’re thicker than
they’re supposed to be, and this may be part of the ideology or the cause of idiopathic gastroparesis. So when you eliminate
that, you cut that muscle, that spasm or that high
pressure, that is eliminated and patients feel much better. And so my experience has been similar to that of the medical literature. Many, many people improved
quite dramatically. It’s a laparoscopic operation. It’s an overnight
hospital stay in my hands. It’s cutting the intestine, so there’s a little bit of risk, bleeding, infections,
rare incidents of leakage, but it’s no implant, so there’s
no adjustments afterwards, there’s no batteries to be changed, and so it has that benefit. So it’s a nice little procedure, it works really well for people,
there’s few side effects, and so we like doing this, and again, I think the consensus opinion now is that even for diabetics, who
are gonna have a stimulator, we add pyloroplasty to that
to get the added benefit of increased emptying and see that result. Those two therapies work great together. You can do them sequenced,
you can do them together, and they seem to really
improve people’s life and get them back onto
eating normal foods. Again, the destination
for all these therapies is eating normal foods. Now, does that mean
chicken wings every night? It doesn’t mean chicken
wings every night, right? It means maybe chicken wings. What it does mean is that
you can eat solid food with your family and not be ostracized to some sort of minuscule
diets or boring liquid diets or things that really take away from the quality of life, right? I mean, we live so much of
our life around the table. So many of our meaningful events
in life are around eating. It’s our obligation to try to help people get to a point where they can eat normally and so these procedures
really provide that, and so really, these are good therapies. Now, not every single
person is gonna get better with those two therapies,
and in my experience, it’s really the very severe diabetics who don’t have a hypertensive
stomach any longer, they have a completely flaccid stomach, there’s no emptying at
all, we’ll sometimes see on the gastric emptying setting what’s called an ascending curve. They don’t see it empty at all over the course of four hours. Sometimes even cutting the muscle or putting a stimulator is
not gonna help those people and they can benefit from
having their stomach removed and the stomach is removed in an operation that looks similar to a gastric bypass, where we create a very small pouch at the top of the stomach,
bring intestine up, so if you look at the diagrams that you’ll see on your screen, the food is coming down the food tube, into the small pouch and
directly into the intestine. It never enters the stomach, and that stomach is then removed so that it can’t cause any of
the symptoms the patient has. This has also been studied,
more aggressively now that we’re seeing more patients
for gastroparesis therapy, and it can work very well. Is this a first line
therapy for most people? I don’t think so. I think most people are
gonna get better without it. This is really a therapy as an
end stage, highly effective, but there’s some management involved. Those patients who require this therapy will behave very similar to
weight-loss surgery patients, and generally speaking,
somebody who gets this therapy, they don’t need to lose weight, right? That is not the problem. The problem is that they
can’t keep their weight on. And so we have to work pretty
intensely with those folks and they’re diabetic, so they’re gonna see a dramatic alteration in
their insulin metabolism. They’re not gonna be hungry,
so we really gotta help them. If a patient has a jejunostomy
tube already, we’ll keep it to help them through
the adjustment period, but people are getting
admitted every month to the hospital for severe symptoms. We can make that better
and this is a good therapy for that in the right patient. It’s a big therapy,
though, and I don’t think the patient comes to the office the first time and we sit down and say, hey, you need to have
your stomach out, right? It’s a process. It’s getting to know one another, understanding what the disease
is, trying some therapies. If somebody gets to that
screen and it works, it works well, but in my opinion,
not a first line therapy. So a final therapy that’s surgical that we offer for gastroparesis is actually gastric bypass,
which you are probably more familiar with in
terms of weight-loss. Paradoxically, we will see some patients with very severe gastroparesis, lots of nausea and vomiting, who are significantly overweight. And while sometimes
people can’t understand how that can happen, remember, gastroparetics, when
they’re able to eat food, it’s typically high-calorie
liquids and low-fiber foods. Those tend to have a lot of added sugar, lots of carbohydrates, and
for some people’s metabolism, that will lead to obesity
very, very quickly. And we’ll see a
subpopulation who are obese or morbidly obese, with a
body mass index over 35, who need therapy for gastroparesis, and in that group, we’ll
offer them gastric bypass. And you can see on your
screen the picture of that. It looks very similar to
the subtotal gastrectomy, except that we leave the stomach part in. This is well-studied. It works very well. It leads to weight loss,
which is much healthier for the patient, for the diabetics. It frequently leads to
remission of their diabetes, their high blood pressure,
their sleep apnea, and a resolution to the
nausea, so that again, they’re able to eat more normal foods, healthier, high-quality
foods, higher in protein, some raw vegetables, and
so we use that therapy in this group and it seems to work well. It’s a minority population,
but still important to mention. And that leads us to
our treatment algorithm, kind of how do we do it? So typically, when we see a new patient, we’re gonna go through the
dietary recommendations, refer them to a dietitian,
take a good history. For the diabetics, once
they’ve been through that, if they’re not improved,
we’re gonna offer them pyloroplasty and stimulator together. For the idiopathic patients, we’re gonna do pyloroplasty alone. Most people, 75%, 80%, are
gonna be good at that stage. For the folks that are
still very symptomatic, still getting admitted to the hospital, having involuntary weight-loss,
we’ll either progress to the addition of a
stimulator for the idiopathics or to subtotal gastrectomy
or gastric bypass. And that algorithm seems to work well. One, it gives people hope. You know, we have a therapy
at the end of the day that’s gonna get people to
where they can eat again, they can enjoy their quality of life, and we’re gonna take it
in a risk-averse approach, doing the least risk items up front, medium risk in the middle, and saving the highest risk items for those people who
absolutely must have it. Okay, well, that wraps it up. I hope you’ve enjoyed the content today and it’s been informative. If you have questions or comments, you can get me at my contact information, which will be on the screen, and we hope to hear from you another day.

12 Replies to “Gastroparesis Patient Seminar – Parham Doctors’ Hospital”

  1. If you suspect you have this, ask for a gastric emptying test and stomach ultrasound ASAP. My doctor made me go through (and pay for) SO MANY other tests looking for an obstruction that wasn't there.
    (The ultrasound will show them if there are gallstones, etc, the gastric emptying will prove your stomach is digesting way too slowly.) You may also need an upper endoscopy. If you have Diabetes you'll have a much easier time getting your correct diagnosis of GP!

    Lastly: When you are symptomatic GO TO THE ER. The doctors at the ER are top notch and they can give you strong medications that other doctors shy away from. Tell the doctor straight up that you suspect GP.
    If I hadn't gone to the ER (twice) and met a doctor with the balls to give me Reglan and Bentyl, I'd still be in the hospital right now puking my guts up.

    PS. Never be afraid to fire your doctor. Keep moving to a new doctor until you find the one who will listen to you.

  2. is it possible that a BEZOAR is mistaken for food in the stomach after a 12 – 16 hour fast and that most MD's are just ignorant about BEZOARS ?

  3. Metoclopramide is an awful drug. Tardive dyskinesia and mental and sexual side effects should not be taken lightly.

    Also, they suspect Domperidone might lead to heart complications.

  4. im not diabetic i got severe pain cant eat cant drink nausea all the time..took my gallbladder out 5 weeks ago even sicker now anyway over it,,

  5. I find your video well presented especially to the nub patient/and support system, so thank you for that! I have had GP for about 9ish years which started after a chronic pancreatitis dx 13years ago. It’s been hell!! I underwent major surgery for CP in 2011 to remove my total pancreas/spleen/gallbladder/duodenum and had an islet cell transplantation into my liver in hopes to lessen my post op diabetes. Did suffer many complications and my severity of GP is one of them!! I am insulin dependent and just recently have been placed on an insulin pump and CGM which have been game changers for me!! Anyway…the reason I wanted to post is to say that in some cases no feeding tubes are sometimes a long term option!!! I’ve had one for 3 years(switched sides with new tube every 8 weeks) due to fighting a abscess/mesh infection in my abdomen for over 18 months from attempting to place a surgical J tube thru my mesh. I went septic a few times, ugh!! So now I have a solid piece of mesh and tummy tubes are a NONO!!! I wish not but that’s my reality. Thanks again for the video!!

  6. My daughter has this and when it acts up left side under her breast swells up real big. They did a test and they said its her intestines swollen. Dont know how to stop this

  7. The moment you said Epstein Barr…. I have had Epstein barr since age 16 and now possibly have Gastroparesis with procedures scheduled next month!! Cannot keep food down and I've lost 75 pounds in the last 6 months.😢

  8. What happens when you end up gastroparesis but you are Type 1 diabetic with brittle diabetes . I have been diagnosed with gastroparesis and in the last month I have been in ICU 4 times this month .

  9. Does he see patients from other states? I am in North Alabama and no gastrologist will see me around here. I have a gj tube. I have pots, SMAS, GERD, MALS, Gastroparesis , and Nutcracker phenomenon. As soon as I tell them my problems. They say no I cant see you. You are to complicated and I have no idea how to take care of a gj tube.

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