Diagnostic and Management Pathways for Gastric Motility and Vomiting Disorders
1.0 Initial Patient Assessment: Symptom-Based Triage
1.1. Introduction to Symptom-Directed Diagnosis
A meticulous clinical history is the cornerstone of an accurate diagnosis for upper gastrointestinal disorders. While imaging and physiological tests are essential, the patient's own description of their symptoms provides the critical initial roadmap. After a structural evaluation has ruled out obvious anatomical issues, the specific cluster of symptoms—what the patient feels, when they feel it, and what makes it better or worse—becomes the primary guide for selecting the most appropriate and high-yield diagnostic tests. This symptom-directed approach prevents unnecessary procedures and efficiently navigates the complex landscape of motility and functional GI disorders.
1.2. Symptom Cluster Triage Framework
The following framework provides initial clinical triage based on the dominant symptoms reported by the patient:
Primary Symptom: Dysphagia (Difficulty Swallowing)
- Most likely origin: Esophageal disorder
- Initial diagnostic direction: Barium swallow to evaluate structure and motility
- Key considerations: Progressive vs. intermittent, solids vs. liquids
Primary Symptom: Nausea with Early Satiety
- Most likely origin: Gastric motility disorder
- Initial diagnostic direction: Gastric emptying study after excluding obstruction
- Key considerations: Timing relative to meals, medication history
Primary Symptom: Effortless Regurgitation
- Most likely origin: Rumination syndrome
- Initial diagnostic direction: Clinical diagnosis, manometry if confirmation needed
- Key considerations: Timing (within 10-15 minutes), absence of nausea
Primary Symptom: Episodic, Stereotyped Vomiting
- Most likely origin: Cyclic vomiting syndrome vs. cannabinoid hyperemesis
- Initial diagnostic direction: Detailed social history, rule out red flags
- Key considerations: Cannabis use, hot bathing behavior, episode patterns
Primary Symptom: Progressive Vomiting with Weight Loss
- Most likely origin: Mechanical obstruction
- Initial diagnostic direction: Urgent EGD and/or imaging
- Key considerations: Succussion splash, bilious vs. non-bilious vomit
1.3. Concluding Transition
This initial symptom-based triage points toward a likely origin, but before proceeding with specialized motility testing, it is imperative to conduct a foundational evaluation to rule out any physical blockage, which is the universal first step in every diagnostic pathway.
2.0 Core Diagnostic Pathway: From Presentation to Diagnosis
2.1. The Foundational Role of Initial Evaluation
Ruling out a mechanical obstruction is the non-negotiable first step in the diagnostic workup. Symptoms of delayed gastric emptying can be caused by a functional motility issue or a physical blockage, such as a stricture or tumor. Labeling a patient with a motility disorder like gastroparesis before definitively excluding a mechanical cause is a critical diagnostic error. Therefore, the central pillar of the algorithm is to ensure the "pipes" are open before investigating the "pump."
Clinical Pearl: Gastroparesis is a diagnosis of normal anatomy plus delayed emptying. Gastric Outlet Obstruction is a diagnosis of abnormal anatomy plus impaired passage.
2.2. Step-by-Step Diagnostic Algorithm
Step 1: Exclude Mechanical Obstruction
The initial evaluation requires an Esophagogastroduodenoscopy (EGD) to exclude mechanical causes. The EGD allows for direct visualization to rule out intrinsic blockages like strictures, malignancy, peptic ulcer scarring, or bezoars.
If there is suspicion of extrinsic compression (e.g., from a pancreatic mass), a CT scan of the abdomen serves as a crucial adjunct to assess the anatomy surrounding the stomach and duodenum.
Step 2: Proceed Based on Normal EGD and Dominant Symptoms
After ruling out mechanical obstruction with a normal EGD, the clinician must select the next diagnostic test based on the dominant symptom profile.
A. If Dysphagia Dominates:
- The next step is a Barium Swallow (Esophagram) to evaluate esophageal structure and motor function in real-time. This can reveal subtle rings, webs, or motility patterns like achalasia.
- If the esophagram is non-diagnostic but suspicion for a motility disorder remains high, Esophageal Manometry is performed to directly measure muscle contractions.
B. If Nausea, Early Satiety, and Postprandial Fullness Dominate:
- The next step is a Gastric Emptying Scintigraphy (GES). This nuclear medicine test is the gold standard for quantifying the rate at which the stomach empties solid food.
- The diagnostic criterion for gastroparesis is >10% retention of a radiolabeled solid meal at 4 hours.
C. If Effortless Regurgitation is the Key Feature:
- The diagnosis of Rumination Syndrome is often made clinically based on a classic history.
- If physiological confirmation is required, the definitive test is High-Resolution Manometry with Impedance. This test can identify the characteristic, subconscious rise in intra-abdominal pressure that precedes the regurgitation event.
D. If Episodic, Stereotyped Vomiting is the Pattern:
- Cyclic Vomiting Syndrome (CVS) and Cannabinoid Hyperemesis Syndrome (CHS) are diagnoses of exclusion, requiring a workup to rule out dangerous mimics.
- Essential "red flag" investigations include:
- Labs: Complete Blood Count (CBC), Comprehensive Metabolic Panel (CMP), lipase, urinalysis (UA), and a pregnancy test.
-
- Imaging: CT or MRI of the brain to rule out a mass or increased intracranial pressure.
-
- Metabolic Screens: A serum cortisol to rule out adrenal insufficiency and a urine porphobilinogen to screen for acute intermittent porphyria.
-
2.3. Concluding Transition
Following this structured diagnostic algorithm allows for the precise identification of the underlying disorder, which is the necessary prerequisite for creating a targeted and effective management plan.
3.0 Disorder-Specific Diagnostic Profiles
3.1. Introduction to Differentiating Key Syndromes
Understanding the distinct clinical signatures and underlying pathophysiology of each disorder is essential for accurate diagnosis. While symptoms can overlap, key features in the history, physical exam, and diagnostic testing allow for clear differentiation, which in turn guides targeted and effective therapy.
3.2. Profile: Gastroparesis vs. Functional Dyspepsia
These two conditions can present with nearly identical symptoms, but they are physiologically distinct.
Gastroparesis:
- Pathophysiology: Impaired gastric motility leading to delayed stomach emptying
- Key Symptoms: Nausea, early satiety, postprandial fullness, delayed vomiting (often hours after eating)
- Diagnostic Test: Abnormal gastric emptying scintigraphy (>10% retention at 4 hours)
- Common Causes: Diabetes, post-surgical (especially after vagotomy), medications (opioids, GLP-1 agonists)
- Management Focus: Prokinetic agents, dietary modification, symptom control
Functional Dyspepsia:
- Pathophysiology: Normal EGD and gastric emptying but altered gastric accommodation or hypersensitivity
- Key Symptoms: Identical to gastroparesis (nausea, early satiety, postprandial fullness)
- Diagnostic Test: Normal gastric emptying scintigraphy
- Common Triggers: Stress, certain foods, unclear etiology in many cases
- Management Focus: Acid suppression, tricyclic antidepressants, lifestyle modification
3.3. Profile: Gastric Outlet Obstruction (GOO)
GOO is not a primary motility disorder but a true mechanical blockage. It is the most critical mimic of gastroparesis to exclude, as their symptoms can be nearly identical but their management is radically different.
Clinical Clues: The classic physical exam finding is a succussion splash—a sloshing sound heard when shaking the abdomen, caused by retained fluid and gas. Patients often report progressive, large-volume, non-bilious vomiting and associated weight loss.
Etiologies: Causes can be intrinsic (e.g., scarring from chronic peptic ulcer disease, bezoars—a mass of trapped indigestible material like plant fiber or hair) or extrinsic (e.g., compression from a pancreatic head cancer or an intrinsic gastric tumor).
Diagnostic Modalities: The diagnosis is confirmed with EGD, CT scan, or a Barium Upper GI Series showing a physical blockage.
3.4. Profile: Rumination Syndrome
This is a behavioral disorder, not a primary digestive disease.
Pathophysiology: Rumination is a learned, subconscious behavior involving contraction of the abdominal wall muscles. This action raises intra-abdominal pressure and forces recently ingested food back up into the mouth.
Clinical Hallmark: The key feature is the effortless, non-nauseated regurgitation of undigested or partially digested food, typically occurring within 10-15 minutes of finishing a meal.
Common Misdiagnosis: It is frequently misdiagnosed as refractory gastroesophageal reflux disease (GERD) or a primary vomiting disorder.
3.5. Profile: Cyclic Vomiting Syndrome (CVS) vs. Cannabinoid Hyperemesis Syndrome (CHS)
These syndromes are characterized by severe, episodic vomiting with periods of complete wellness in between.
Cyclic Vomiting Syndrome (CVS):
- Characterized by stereotyped episodes of intense nausea and vomiting that are similar in timing and duration each time they occur.
- Patients experience complete wellness between episodes.
- There is a strong association with a personal or family history of migraines.
Cannabinoid Hyperemesis Syndrome (CHS):
- Diagnosed based on a clinical triad:
- A history of chronic, heavy cannabis use.
-
- A pattern of cyclic nausea and emesis.
-
- A learned, compulsive behavior of taking hot showers or baths for symptom relief.
-
- Complete resolution of symptoms upon cessation of cannabis use is confirmatory.
3.6. Concluding Transition
A precise diagnosis is the foundation of targeted therapy. We now transition from the 'what' to the 'how,' detailing the tiered management protocols for each established syndrome.
4.0 Tiered Management Protocols
4.1. Introduction to a Structured Therapeutic Approach
Effective management of these complex disorders requires a step-wise, "laddered" approach. Therapy should begin with conservative lifestyle and dietary measures, escalating to pharmacotherapy and, in refractory cases, more advanced endoscopic or surgical interventions. This structured escalation is based on patient response, disease severity, and the specific underlying pathophysiology of the disorder.
4.2. Management: Gastroparesis
Lifestyle & Diet: The foundation of treatment is dietary modification, including small, frequent meals that are low in fat and fiber. It is also critical to review and discontinue, if possible, medications that delay gastric emptying, such as opioids, anticholinergics, and GLP-1 receptor agonists.
Pharmacotherapy:
- Prokinetics: Metoclopramide (5–10 mg three times daily before meals), with use preferably limited to less than 12 weeks due to the risk of tardive dyskinesia. Erythromycin (50–250 mg three times daily) can also be used, though its effectiveness may wane over weeks.
- Antiemetics: Ondansetron (4–8 mg every 8 hours as needed) is used for symptomatic control of nausea.
Refractory Disease: For patients who do not respond to conservative measures, options include G-POEM (gastric peroral endoscopic myotomy) to open the pylorus, Gastric Electrical Stimulation for severe nausea and vomiting, or Jejunostomy tube feeding to ensure adequate nutrition.
4.3. Management: Gastric Outlet Obstruction (GOO)
Acute Management: Initial stabilization requires making the patient NPO (nothing by mouth), placing a nasogastric (NG) tube for stomach decompression, and administering intravenous (IV) fluids to correct dehydration and electrolyte imbalances.
Definitive Treatment (by cause):
- Benign Strictures: Endoscopic balloon dilation is the primary treatment.
- Malignant Obstruction: Palliative treatment with an endoscopic stent or surgical bypass (gastrojejunostomy) may be performed to restore oral intake.
4.4. Management: Rumination Syndrome
First-Line: The cornerstone of therapy is behavioral modification, specifically diaphragmatic breathing training. This technique teaches patients to relax their abdominal muscles after meals, breaking the subconscious cycle of pressurization and regurgitation.
Second-Line: Biofeedback and cognitive-behavioral therapy can be used to reinforce proper breathing techniques and address any associated anxiety or stress triggers.
Refractory Pharmacotherapy: For refractory cases, Baclofen (5–10 mg three times daily) may be trialed. There is no surgical role in the management of rumination syndrome.
4.5. Management: Cyclic Vomiting Syndrome (CVS)
Acute Episode Abortive Therapy: During an attack, treatment focuses on supportive care and symptom control with IV fluids, antiemetics such as Ondansetron (4-8 mg IV), and benzodiazepines like Lorazepam (0.5–2 mg IV), which can help abort an episode. Triptans may be effective in patients with a strong migraine phenotype.
Prophylactic Therapy: To prevent future episodes, daily medication is often required. First-line therapy is Amitriptyline, started at a low dose (10–25 mg at bedtime) and titrated up. Other options include Propranolol, Topiramate, and Cyproheptadine.
4.6. Management: Cannabinoid Hyperemesis Syndrome (CHS)
Acute Symptomatic Relief: During an episode, supportive care includes IV fluids. Unlike in other vomiting disorders, standard antiemetics like ondansetron are often ineffective. Haloperidol (0.5-2 mg IV/IM) and topical capsaicin cream applied to the abdomen may provide relief. Compulsive hot showers provide temporary relief; this unusual behavior is thought to be mediated by the activation of TRPV1 receptors in the skin, which may modulate central nausea pathways in the hypothalamus.
Definitive Treatment: The only definitive and curative treatment for CHS is the complete and permanent cessation of cannabis use.
4.7. Concluding Transition
Mastering these specific treatment protocols is essential, but equally important is the ability to recognize high-yield clinical clues and avoid common diagnostic traps that can lead to misdiagnosis and ineffective therapy.
5.0 High-Yield Clinical Pearls and Pitfall Avoidance
5.1. Introduction to Recognizing Clinical Traps
In clinical practice, especially with complex cases where symptoms overlap, the ability to recognize classic "buzzwords" and common diagnostic pitfalls is a hallmark of an expert clinician. This awareness allows for more efficient and accurate decision-making, preventing unnecessary tests and ensuring patients are placed on the correct diagnostic and therapeutic pathway from the outset.
5.2. Diagnostic Traps and Buzzword Associations
High-Yield Clinical Buzzwords:
"Succussion Splash"
- Clinical Association: Gastric outlet obstruction
- Key Point: Pathognomonic for mechanical blockage; absent in functional gastroparesis
- Action: Urgent EGD or imaging to identify obstruction
"Hot Shower Relief"
- Clinical Association: Cannabinoid hyperemesis syndrome
- Key Point: Compulsive bathing behavior is virtually diagnostic
- Action: Detailed cannabis use history, counseling for cessation
"Effortless Regurgitation Within 10-15 Minutes"
- Clinical Association: Rumination syndrome
- Key Point: No nausea or retching; behavioral, not organic
- Action: Behavioral therapy, not medications or surgery
"Stereotyped Episodes with Well Intervals"
- Clinical Association: Cyclic vomiting syndrome
- Key Point: Complete wellness between episodes; often migraine-associated
- Action: Migraine prophylaxis, trigger identification
Common Diagnostic Traps to Avoid:
Trap #1: Diagnosing Gastroparesis Without Excluding GOO
- Problem: Symptoms are nearly identical
- Solution: Always perform EGD first to rule out mechanical causes
- Pearl: "Check the pipes before blaming the pump"
Trap #2: Missing CHS in Cyclic Vomiting
- Problem: Patients may not volunteer cannabis use history
- Solution: Direct, non-judgmental questioning about all substance use
- Pearl: Hot bathing behavior is the key diagnostic clue
Trap #3: Over-medicalizing Rumination Syndrome
- Problem: Treating as GERD or motility disorder with medications
- Solution: Recognize the behavioral pattern; focus on breathing techniques
- Pearl: No nausea = think rumination, not gastroparesis
Trap #4: Using Gastric Emptying Study Too Early
- Problem: Ordering GES before ruling out mechanical obstruction
- Solution: EGD must come first in the algorithm
- Pearl: GES is only valid with normal anatomy
Trap #5: Missing Red Flag Causes of Vomiting
- Problem: Assuming functional cause without proper workup
- Solution: Rule out intracranial, metabolic, and endocrine causes first
- Pearl: CVS and CHS are diagnoses of exclusion
5.3. Concluding Summary
The diagnostic and management pathways for these complex disorders are built upon a simple but rigid foundation: a symptom-first approach must always be followed by the meticulous exclusion of mechanical obstruction. Adherence to this core principle prevents the misattribution of structural problems to functional disorders and is the bedrock of accurate diagnosis. By carefully differentiating between mechanical, motility, episodic, and behavioral syndromes, clinicians can move beyond symptom management to provide precise, effective, and targeted therapies.
What is Dr GI Joe?
I'm Dr. Joseph Kumka, Gastroenterology Fellow, educator, and creator of this podcasts. Whether you're a resident gearing up for the boards, a fellow diving deep into subspecialty topics, or a practicing clinician hungry for high-yield updates—you’re in the right place.
Subscribe, engage, and let's raise the bar together.
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.