Dr GI Joe

Welcome to the Deep Dive.

Today we're tackling, well, a really tough area in gastroenterology.

Those upper GI conditions with that miserable mix of symptoms, nausea, feeling full all the time, Vomiting.

It's confusing.

Yeah, so our goal here is to try and map this out.

We want a clear symptom-based way to tell apart five tricky disorders , gastropsis, gastric outlet.letstruction, GOO, Rination Syndrome, cyc Vomiting syndrome, CV and cannabinoid hyis syndrome, CH.

If you've ever felt these just blur together, hopefully this will help pinpoint the key differences.

Exactly.

And getting that difference right is crucial because, you know, the treatments are worlds apart.

You can't fix a blockage with motility drugs.

So maybe think about it this way, mechanistically..

We've got mechanical problems.

That's your GOO, maybe a bazor, then motility, that's gastropsis.

And there's a behavioral one rumination syndrome.

And finally, the episodic conditions, CV and CHS.

The key really is pattern recognition.

It's all about the timing and the specific clues in the patient's story.

Right, the history.

Yeah.

Okay, let's start unpacking the workup then.

Patient comes in, chronic vomiting, constant fullness.

The source mate material seems pretty clear.

We have to rule out structure first before even thinking motility.

So where do we begin?

The absolute first step, pretty much non-negotiable here, is an EGD .

An esophago gastrodude denoscopy.

You have to look inside.

Why the EGD specifically?

Because you need to visually confirm there's no mechanical blockage.

Are we dealing with a subtle stcture, a bazaar, you know, that clump of stuff?

Or the really critical one?

Malignancy.

Those all potentially fall under gastric outlet obstruction.

But sometimes you see people jumping to imaging first, right?

Like a CT scan or maybe a broad upper GI series.

Is that missing the point?

Oh, absolutely.

That's a big track.

The EGD is better because you get direct visualization.

And importantly, you can do things right, then take biopsies, maybe even dilate a benign structure.

If you skip that EGD, assume it's gastroposis, put them on a prochonetic , what if it's actually a slow growing tumor blocking the exit?

You've lost critical time and missed the real diagnosis.

So, EGD first, structure function.

Always.

Perfect.

So, EGD is done, it's clean.

Anatomy looks totally normal.

Now we're at that fork in the road.

How do you do decide, is this an esophagus problem, like food getting stuck going down?

Yeah.

Or is it a stomach problem, food not leaving the stomach properly?

Barium swallower, gastric emptying study next?

It really comes down to the main symptom.

What's bothering the patient most?

If they're saying dysphagia, that feeling of fooding, catching in the throat or chest , that points straight to the esophagus.

Your next test, then is the barium swallow, the esophogram.

You're looking for things like acylia, maybe a spasm, a structural issue there.

But if the story is more about nausea, getting full, really fast, bloating and vomiting, especially, you know, hours after they've eaten, that pattern screams, delayed gastric emptying.

Right.

In that case, you skip the esoph tests and go right for the gastric emptyingography, the GES.

This is where I think it gets muddy for a lot of us.

We have these three contrast tests that sound kind of similar, Bum Swallow, Gastric emptying Study, and the UGI series.

Can you just really break down what each one tells us?

Why aren't they entertainchangeable?

Yeah, good question.

Let's sort out that trio.

First, bum swallow.

Think esophagus specialist.

It's dynamic, real time .

You watch the swallow, how the barier moves down, perfect for subtle structural things like functional issues, like esophm.

It gives you a really detailed look at the path from mouth to stomach.

Okay, esophagus focusocus.

Second, gastric emptying synigographyhy, the GES.

This is all about function , Physiology.

It's the gold standard for diagnosing gastroparesis.

The radioactive egg sandwich test.

That's the one, usually.

A standardized meal tag with a tracer.

We track how much is left in the stomach over four hours, the key number.

More than 10% retention at four hours means delayed emptying.

It's quantit.

It gives you an objective measure.

Got it. 10% at four hours.

And third , the upper GI series, or UGI.

This is more of a broad anatomical map desophagus, stomach, duodenum.

It's okay for a quick look, maybe if you suspect a really typel itage like in the Pylus or Duadino.

But, and this is crucial, it's not sensitive enough to catch the subtle motility problems you'd see on a barium swallow, and it's definitely not quantitative like the GES.

It won't tell you how fast the stomach's emptying.

If you need that rate, you need the GES, period.

That's super helpful.

Okay, so EGD clear.

We've picked the right motility study based on symptoms.

Now, it really sounds like the diagnosis comes down to the patient's story.

Let's shift to the clinical picture, the timing, the nature of the symptoms, how that splits these gastric disorders apart.

Exactly.

Now we play detective with the history.

We need to separate that chronicility issue of gastropis from a structural block, GOO, so gastropis.

It's chronic, it's persistent.

You get that classic triad, naea, early fullness, and vomiting, typically out, often digest, like, empty , butatomy on.

And it causes?

Well, classically, diabetic autonomic neuropathy is a big one.

Postal cases seem to be increasing, too.

And medications are a huge factor now, especially chronic opioid use and definitely the GLP one agonists, the weight loss drugs, which are designed to slow emptying.

Right the GLP ones.

So how do we reliably tell that apart from gastric out obstruction ?

Both cause vomiting hours after eating, both chronic?

The key differences are the mechanism and often the progression.

GOO is usually progressive because there's a physical blockage scar tissue from an ulcer, a bizarre growing, or maybe a tumor. Doesn't usually get better on its own.

And along in itself. To be food, often undigest because it just sat there blocked .

But the real clinical, the bedside finding that can clinch GO versus gastis.

It's the succussion splash.

Ah, the c secccussion splash.

Tell us about that sloshing sound.

Right.

If you place your stethoscope over the patient's abdomen and gently rock their hips side to side, you might hear this splashing or sloshing sound .

It's large amount ofained flu and food just sitting in the stomach, unable to drain because of a physical.

And you wouldn't hear that in gastropis.

Generally, no, gastrsis is a functional problem, a motility failure, not a physical dam.

So finding that splash strongly points towards structural GO, it's a really valuable sign.

That's a great clinical distinction.

Okay, we've got the two chronic delayed conditions sorted .

What about the real outlier here?

Rumination Syndrome?

It seems totally different in timing.

Completely different.

Rumination is behavioral.

It's defined by this effortless regurgitation, not vomiting of undigested food, happening super quickly after eating, usually within 10 to 15 minutes.

Effortless.

So no nausea beforehand.

Exactly.

No nausea, no retching, none of that awful prelude to vomiting.

What happens is the person , often without realizing it, contracts their abdominal wall muscles, squeezing the stomach, increasing the pressure dramatically, and the food just coming back up.

It's a learned, though often subconscious physical manuver.

The timing minutes, nots, is the dead giveaway.

Okay, minutes, effortless, undigested food.

Got it.

Now for the episodic pair.

Cyclic Vomiting Syndrome, CVS, and canabinoid Hyperis Syndrome, CH.

The defining feature has to be the well interval, right?

They're not sick all the time.

Precisely.

That's the absolute hallmark of both CV and CHS, the cyclical pattern.

They have these intense, stereotyped episodes of severe vomiting lasting hours or days .

But crucially, these episodes are separated by well intervals, periods where they feel completely completely normal, 100% symptom free.

That immediately rules out the constant symptoms of gastroperesis or ga.

Right.

So if you have well intervals, you're thinking CVS or CHS.

Differentiating between those two then comes down purely to the history .

CBS is often considered idiopathic, maybe linked to migraines, often has triggers like stress or illness.

But CHS, the cannabis one, the history is usually pretty striking if you ask the right questions.

What's that classic triad again?

Oh, yeah.

The CHS Triad is hard to miss once you know it.

One , chronic, heavy cannabis use.

We're talking dam daily, near daily, usually for years, two, the selic vomiting pattern we just discussed, and three, the really specific clue.

Finding relief from the nausea and vomiting with compulsive hot bathing.

The hot showers.

Why does that help?

Patients describe spending hours in hot water, sometimes until the hot water runs out, sometimes even getting skin burns.

The intense heat seems to provide temporary relief.

Theory involvesritation and possibly affects onPV receptors in the skin and g.

So, young, chronic cannab user, in the shower during episodes.

That's CH until proven.

Okay, we've m mapped the diagnoses really well.

Let's switch to treatment.

Since these conditions are so different, mechanical, behavioral, motility, episodic, accep, I assume the treatments don'tap much.

Yeah.

What are the core strategies, especially if inial therapies don't work?

You're right.

The treatments are very distinct, targeting the specific underlying problem, very little overlap.

Let's start with rumination.

Since it's learned behavior, first line is not meds, it's diaphratic breathing training, maybe biofeedback.

Teaching the patient to relax their abdominal muscles during and after eating , to consciously prevent that pressure surge.

Any role for meds or procedures?

Medications like blofin are sometimes tried in refractory cases, maybe helps relax the lower esophagus, but it's not primary.

And critically, absolutely no role for surgery and rumination.

It's not a structural fix.

Okay.

What about CHS ?

Patients in the middle of a terrible episode?

What helps acutely and what's the actual cure?

The only definitive cure is stopping cannis completely.

Easier said than done, that's the c.

Ac, during an attack, anti-as like on Datron often don't work very well.

So what does?

Surprisingly, low dose halo paradol, like 0.5 to 2 milligrams IV or IM , can be quite effective.

Also, topical capsus and cream applied to the abdomen, it sort of mimics the hot shower effect, that counter iritation.

Interesting.

Okay, moving to gastrois.

What's the approach there?

It starts with diet.

Small, frequent meals, low and fat, low in fiber.

Medically, the maineneticic is, maybe milligrams three times a day .

But this is a big, the risk of tive dysia is serious, so we try to limit use ideally less than 12 weeks.

And if that doesn't cut it, refractory gastropis.

Then we escalate.

A really effective option now is GPM gastric paral endoscopic myodomy.

It's an endoscopic procedure where we cut the pyoric muscle, the the valve at the stomach outlet to help it relax and improve empty .

For severe cases with malnutrition, sometimes a ju feeding tube, a tube is needed topass the stomach entirely for nutrition.

GPOM seems counterintuitive, almost fixing the exit for a stomach muscle problem.

It does, but often in gastropricis, even though the main stomach muscle, the funus is weak, the pyorus can be tight or spasming, contributing significantly to the blockage , so relaxing that outlet can make a huge difference.

It's often very effective for a refractory symptoms.

Then for CVS, the cyclic vomiting, the key is prophyllaxis preventing the ep..

First line is often a tricyclic antidepressant, usually apt line aiming for 51 milligrams.

It seems to work well, possibly due to the link with migr pathways.

And during an acute CV attack.

Aggressive supportive care .

4V fluids are crucial.

Antics often need in.

Sometimes benziazepines like lepam or even if theres migraine components to try and break the cycle.

And finally, GOO gastric outlet obstruction.

Purely mechanical, so the fix must be mechanical too.

Exactly.

Acute management is often an NG tube for decomression, letting the stomach rest the underlying .

If it's a benignure endoscopic balloon dilation usually works.

If it's malign, maybe endoscopicenting for pallation,y of the patient's a candidate, you have to physically open the passage.

This has been incredibly clear.

I think the main takeaway for everyone listening is that nailing the history is paramount .

The timing of symptoms, the presence or absence of, well, intervals, those specific triggers like cannabis or behaviors like abdominal straining, that's how you navigate this complex map.

Absolutely.

But before we finish, there's one more crucial differential we have to mention.

It lives right next gastis and causes a lot of confusion, functional dyssia, or FD.

FD, right.

Patients with FD almost identical symptoms gastis, that, discomfort eating,ating.

They sound the same.

But the key difference, the thing that separates them entirely is the diagnostic test .

Which is?

Patients with functional dyss have a completely normal gastric emptying.

Their stomach empties normally.

The problem isn't motility.

It's thought to be more about hypersivity of the stomach or maybe impaired accommodation how the stomach stretches with food.

So same symptoms, normal emptying study.

Exactly.

That makes empty a diagnosis of exclusion .

And importantly, because the emptying is normal, you don't treat it with procetics like metoppide.

Treatment is symptomatic, often using neuromodulators likece or busone.

Getting that GE result is critical to distinguish from gastaresis.

That distinction is vital.

Normal emptying, but same symptoms a major potential pitfall.

Okay, let's wrap up with the final thought for our listeners, something quite relevant right now.

We touched on medication-induced gastaresis, particularly with GPists.

Given how incredibly common drugs like seoglutide and tappetite are becoming for weight loss, and we knowificant delay gastric emptying.

How are clinicians going to handle this increasing overlap?

How do you sort out drug symptoms versus underlying idiopathic gastr?

That's a huge question.

Yeah, and how do do you advise a patient to potentially stop a drug that's helping them lose weight and improve metabolic health if it's also causing debilitating nausea and viting?

That is the clinical tightrope we're walking right now.

It's blurring the lines significantly .

Is this now the most common cause of gastropsis symptoms we're seeing?

Probably.

Managing that is going to be a major challenge in the coming years.

Definitely something to watch.

We really hope this deep dive helps bring some clarity to these often overlapping and frustrating upper GI conditions.

Remember the timing, look for well intervals, ask about cannabis and hot showers , and maybe keep your stuff as scope bandy for that succocian splash.

Until next time.