Diarrhea

Diarrhea

Podcast Episode Introduction

Welcome back to GI Insights, the podcast dedicated to bringing clarity to complex clinical topics in gastroenterology. Today, we're tackling one of the most universal challenges in all of medicine: the patient with diarrhea. It’s a chief complaint that can signify anything from a benign, self-limited illness to a life-threatening condition. The differential is vast, and it’s easy to get lost in a sea of unnecessary tests or, worse, miss a critical diagnosis.

The goal of this episode is to move beyond rote memorization and equip you with a clear, systematic, and actionable mental framework for triaging, diagnosing, and managing these patients. We'll build a clinical reasoning model that you can apply at the bedside, whether you're in the emergency department, a primary care clinic, or on the GI consult service. Over the next few minutes, we’ll cover the core frameworks for initial triage, the five pathophysiologic buckets that organize your differential, a step-by-step diagnostic pathway, a special deep dive into malabsorption, and finally, a pragmatic treatment ladder for when the initial workup is unrevealing. Let’s get started.

1. The First Sort: Triage, Time, and Temperature

The initial moments of a patient encounter are critical for triage. Before diving into complex pathophysiology, the clinician's first job is to determine acuity and chronicity. These two factors—how sick is the patient right now, and for how long has this been going on?—dictate the entire pace and direction of the workup, telling you whether to admit, scope urgently, or proceed with a measured outpatient evaluation.

Critical Red Flags

The first and most important question is "sick or not sick?" The presence of any of the following alarm features should trigger a more urgent evaluation, and often, admission.

• Hemodynamic Instability: Hypotension, tachycardia, or marked volume depletion.
• Systemic Toxicity: High fever or severe abdominal pain, especially with peritoneal signs.
• Significant Bleeding: Grossly bloody stool.
• Host Factors: Immunocompromised status (e.g., transplant recipients, patients on chemotherapy) or extremes of age.
• Key Historical Clues: Unintentional weight loss or nocturnal diarrhea that awakens the patient from sleep.

Define the Clinical Time Course

The next crucial sort is based on duration. This simple classification helps narrow the differential diagnosis significantly.

• Acute Diarrhea: Symptoms lasting less than 14 days. This is most often infectious, toxin-mediated, or drug-induced.
• Persistent Diarrhea: Symptoms lasting between 14 and 30 days. This category often includes unresolved infections, post-infectious syndromes, or the initial presentation of inflammatory bowel disease (IBD).
• Chronic Diarrhea: Symptoms lasting more than 4 weeks. For these patients, thinking in pathophysiologic categories becomes essential.

Once you’ve established that the patient is stable and their condition is chronic, the next step is to classify the type of diarrhea to systematically narrow the differential.

2. The Core Mental Model: The Five Pathophysiologic Buckets

The "five buckets" framework is the central organizing principle for any chronic diarrhea workup. Rather than chasing down dozens of individual diagnoses, the goal is to first identify the primary pathophysiologic category the patient falls into. This is the single most important step, as it directly informs the subsequent diagnostic strategy, from which stool tests to order to whether an endoscopy is required.

2.1. Osmotic Diarrhea

This type of diarrhea occurs when non-absorbed, osmotically active solutes remain in the intestinal lumen, pulling water in with them. The classic analogy is a sponge in the gut. Because it is driven by ingested substances, it characteristically improves or resolves completely with fasting.

• Hallmarks and Examples
  • Clinical Clues: Smaller stool volume, symptoms cease with fasting, high stool osmotic gap (>100 mOsm/kg).
  • Representative Examples: Lactose intolerance, magnesium-containing antacids or supplements, poorly absorbed sugar alcohols (sorbitol, mannitol, xylitol), and SIBO with carb malabsorption.

2.2. Secretory Diarrhea

Secretory diarrhea is caused by a net increase in intestinal secretion of electrolytes and water, or an inhibition of normal absorption. Unlike osmotic diarrhea, it is driven by internal processes and is not dependent on what the patient eats. This results in a high-volume, watery diarrhea that persists even when the patient is fasting.

• Hallmarks and Examples
  • Clinical Clues: Large stool volume, persists with fasting, often occurs at night, low stool osmotic gap (<50 mOsm/kg).
  • Representative Examples: Bile acid malabsorption (e.g., post-cholecystectomy), microscopic colitis, hormone-secreting tumors (e.g., VIPoma), stimulant laxative abuse, and post-surgical short bowel or high output ileostomy.

2.3. Inflammatory / Exudative Diarrhea

This category results from disruption of the mucosal lining of the intestine, leading to an exudation of mucus, protein, and blood into the lumen. These patients are often systemically unwell and present with symptoms beyond just loose stool, such as fever and abdominal pain.

• Hallmarks and Examples
  • Clinical Clues: Blood and/or mucus in the stool, fever, abdominal pain, elevated fecal calprotectin or lactoferrin.
  • Representative Examples: Inflammatory bowel disease (Crohn's disease, ulcerative colitis), invasive infections (e.g., Shigella, Campylobacter, C. difficile), ischemic colitis, and radiation colitis.

2.4. Fatty Diarrhea (Malabsorption / Maldigestion)

Also known as steatorrhea, this type of diarrhea is caused by the failure of normal fat digestion (maldigestion) or absorption (malabsorption). Because fat is a major source of calories, patients with significant steatorrhea almost always present with weight loss and deficiencies of fat-soluble vitamins.

• Hallmarks and Examples
  • Clinical Clues: Bulky, pale, greasy, foul-smelling stools that are difficult to flush; associated with weight loss and nutritional deficiencies.
  • Representative Examples: Pancreatic exocrine insufficiency (maldigestion), celiac disease (malabsorption), extensive small bowel Crohn's disease, and lymphatic obstruction.

2.5. Disordered Motility / Functional Diarrhea

In this category, the primary problem is altered intestinal transit time, often without any identifiable mucosal inflammation or structural abnormality. This is frequently a diagnosis of exclusion after ruling out the other four buckets, and there is significant overlap with Irritable Bowel Syndrome with Diarrhea (IBS-D).

• Hallmarks and Examples
  • Clinical Clues: Normal labs, imaging, and endoscopy; symptoms often overlap with classic IBS criteria.
  • Representative Examples: IBS-D, hyperthyroidism, diabetic autonomic neuropathy, and post-vagotomy states.

Understanding these five fundamental mechanisms is key. Now, let's turn to the practical steps of how to determine which bucket a patient belongs in, starting with the clinical evaluation.

3. The Diagnostic Pathway: From History to Histology

A systematic diagnostic process prevents missed diagnoses and avoids a costly, inefficient battery of unnecessary tests. This pathway is a journey, moving logically from the patient's story to targeted lab work and, only when necessary, to endoscopic evaluation for a definitive tissue diagnosis.

3.1. Phenotyping the Diarrhea Through History

The patient’s history is the most powerful tool for phenotyping their diarrhea and placing them into one of the five buckets. The right questions can differentiate watery, inflammatory, and fatty diarrhea before you order a single test.

Key Historical Inquiries

• Stool Characteristics: "Can you describe the stool? Is it purely watery, greasy and floating, or does it contain blood or mucus?"
• Timing and Triggers: "Does it happen at night, waking you from sleep? Does it go away if you don't eat for a day? Is it worse with certain foods, like dairy or coffee?"
• Associated Symptoms: "Have you had any fevers, severe abdominal pain, unintentional weight loss, or joint pains?"
• Contextual Clues: "Has anyone else you know been sick? Have you traveled recently? Did this start after a new medication, supplement, or surgery like a gallbladder removal?"
• Dietary Habits: "Do you regularly consume sugar-free gum, mints, or 'keto' products? What about magnesium supplements or 'calm' drinks?"

3.2. Decoding the Initial Lab Panel

Before you order a single fancy test, a basic screening lab panel can tell you an enormous amount about where to look next. After the history, this panel serves to identify alarm features, reveal nutritional consequences, and screen for common etiologies. Let's break down what we're hunting for with each one.

• Complete Blood Count (CBC) A CBC helps assess for inflammation, bleeding, and malabsorption. Microcytic anemia (low iron) points toward chronic blood loss (IBD, neoplasia) or malabsorption in the proximal small bowel (celiac disease). Macrocytic anemia suggests B12 or folate malabsorption from ileal or pancreatic disease. An elevated white blood cell count can signal infection or severe inflammation, while eosinophilia may suggest a parasitic infection or eosinophilic gastroenteritis. This finding is a direct trigger for proceeding to endoscopy, even in the absence of other alarm features.
• Comprehensive Metabolic Panel (CMP) The CMP reveals the metabolic severity of the diarrhea and provides clues to its origin. Electrolyte abnormalities and elevated creatinine indicate significant dehydration. Low albumin is a major red flag, suggesting malnutrition or a protein-losing enteropathy (as seen in IBD or lymphatic disease). This critical finding shifts the differential away from functional disorders and necessitates a search for organic diseases like IBD, lymphatic obstruction, or celiac disease. A cholestatic pattern of liver function tests is also a key clue, as severe cholestasis leads to poor bile acid delivery and therefore fat malabsorption.
• Thyroid-Stimulating Hormone (TSH) This is a simple but crucial test to rule out a non-GI cause. Hyperthyroidism can cause chronic diarrhea and weight loss by increasing gut motility. A normal TSH allows you to confidently set aside this diagnosis and continue focusing on a primary gastrointestinal pathology.
• Celiac Serologies Given that celiac disease is common, treatable, and can present with a wide variety of symptoms mimicking IBS, celiac serologies (such as anti-tissue transglutaminase IgA) are a critical part of the initial screening for nearly any patient with chronic diarrhea or suspected malabsorption.

3.3. The Role of Endoscopy: When and How to Scope

Endoscopy is not required for every patient with diarrhea. It is generally not needed in cases of acute, self-limited diarrhea in a stable patient without alarm features, or when an obvious reversible trigger (like a new medication) is identified. The decision to scope is reserved for specific clinical scenarios.

Indications for Colonoscopy

A colonoscopy is warranted in patients with chronic diarrhea that remains unexplained after initial testing, or in the presence of alarm features, including:

• Blood in the stool
• Unintentional weight loss
• Nocturnal symptoms
• Iron deficiency anemia
• Elevated fecal calprotectin
• Suspicion for IBD or malignancy

Indications for Upper Endoscopy (EGD)

An upper endoscopy is the procedure of choice when the clinical picture points toward a proximal small bowel cause. Key indications include:

• Suspected malabsorption (steatorrhea, weight loss, nutritional deficiencies)
• Positive celiac serologies
• Unexplained iron deficiency anemia

The Biopsy Strategy

Obtaining the right biopsies is non-negotiable. Rule #1: For chronic watery diarrhea, even with a normal-appearing colon, random biopsies from both the right and left side are mandatory to rule out microscopic colitis. Rule #2: For suspected malabsorption, systematic duodenal biopsies are mandatory to rule out celiac disease, as the mucosa can appear deceptively normal.

With our general diagnostic pathway established, let's take a deeper look into one of the most complex buckets: malabsorption.

4. Deep Dive: Understanding Malabsorption

Malabsorption is more than just diarrhea; it's a clinical syndrome characterized by fatty diarrhea (steatorrhea) plus the systemic nutritional consequences of failing to absorb nutrients. This distinguishes it from purely watery diarrheas, as the presence of weight loss, anemia, and specific vitamin deficiencies points directly to a failure of the small intestine's primary function.

The "Three-Level" Framework for Malabsorption

To diagnose the cause of malabsorption, it's helpful to think about the three critical phases where nutrient handling can fail.

1. Luminal Phase Problems (Maldigestion) This is a failure to properly break down nutrients within the intestinal lumen, most often due to a lack of enzymes or bile. Examples include pancreatic exocrine insufficiency (from chronic pancreatitis or cystic fibrosis) and advanced cholestatic liver disease where bile delivery is inadequate.
2. Mucosal Phase Problems (True Malabsorption) Here, nutrients are properly digested, but the small bowel lining is damaged and cannot absorb them. This is a problem at the level of the enterocyte. Examples include celiac disease, extensive Crohn's disease of the small bowel, and infiltrative diseases like Whipple disease or amyloidosis.
3. Postmucosal / Lymphatic Problems In this rarer category, nutrients (especially fats) are successfully absorbed by the intestinal cells but cannot be transported away due to a blockage in the lymphatic drainage system. This is a problem after the enterocyte.

A Closer Look at Postmucosal Malabsorption

The concept of postmucosal or lymphatic malabsorption is key for understanding cases with profound protein loss and edema. The mechanism is essentially a plumbing problem: absorbed fats are packaged into chylomicrons, which are supposed to exit via intestinal lymphatic channels called lacteals. When lymphatic outflow is blocked, pressure builds, the lacteals dilate and leak, and patients develop both fat malabsorption and a severe protein-losing enteropathy. This can be caused by primary (congenital) intestinal lymphangiectasia or by secondary obstruction from conditions like lymphoma, constrictive pericarditis, or extensive retroperitoneal disease.

Having explored the complexities of diagnosis, let's now pivot to the practical realities of management, especially for the common scenario where a clear diagnosis remains elusive.

5. The Empiric Treatment Ladder for Chronic Watery Diarrhea

This pragmatic ladder is designed for the common clinical scenario of a stable outpatient with chronic, non-inflammatory, watery diarrhea whose initial workup—including labs, celiac serologies, and often a colonoscopy with biopsies for microscopic colitis—has returned negative. It is a pragmatic, step-wise escalation of therapy that is both diagnostic and therapeutic.

The 4-Rung Ladder

1. Rung 1: Remove Triggers & Provide Symptomatic Control The first step is to eliminate obvious offenders. This involves a thorough review and removal of potentially causative medications and dietary triggers (e.g., magnesium, sugar alcohols, high caffeine intake). Concurrently, provide baseline symptomatic control with an anti-diarrheal agent like loperamide, often taken on a scheduled basis before meals rather than reactively.
2. Rung 2: The Bile Acid Sequestrant Trial If symptoms persist, the next step is an empiric trial of a bile acid sequestrant like cholestyramine or colestipol. This intervention targets suspected bile acid diarrhea, a common cause of chronic watery diarrhea, especially in patients who have had their gallbladder removed or who have limited disease of the terminal ileum. A dramatic positive response within a few days is highly suggestive of the diagnosis and serves as effective therapy.
3. Rung 3: Address IBS-D / SIBO Overlap For patients whose symptoms have features of IBS-D (bloating, gas, crampy pain) or SIBO, the next rung involves therapies targeting these conditions. This may include a course of a non-absorbable antibiotic like rifaximin or the implementation of a structured low-FODMAP diet to reduce the intake of highly fermentable carbohydrates.
4. Rung 4: Re-evaluate the Diagnosis If a patient fails to respond to the first three rungs of the ladder, the next step is not more empiric therapy. It is time to pause, step back, and fundamentally reconsider the diagnosis. Ask the critical question: "What did I miss?" This may prompt a search for rarer etiologies like endocrine tumors, a repeat endoscopy if biopsies were suboptimal, or further evaluation for pancreatic insufficiency.

Before even needing this ladder, however, many cases can be solved by identifying common but often overlooked dietary triggers.

6. Practical Pearls: Unmasking "Stealth" Dietary Culprits

Often, chronic diarrhea is caused or significantly exacerbated by common consumer products that both patients and clinicians overlook. Before launching a complex workup, a careful dietary history focused on these "stealth" culprits can be incredibly high-yield.

Categorizing Common Offenders

• Sugar-Free Products: Sugar-free gum, mints, cough drops, and "keto" or diabetic sweets are often loaded with sugar alcohols like sorbitol, mannitol, xylitol, maltitol, and erythritol, which are potent osmotic agents.
• Vitamins & Supplements: Many patients don't consider supplements to be "medication." Key offenders include magnesium citrate or oxide (often found in "calm" powders) and high-dose Vitamin C.
• Beverages: The daily liquid intake can be a major driver. Culprits include high volumes of coffee, energy drinks, large fruit smoothies, and alcohol.
• "Gut Health" Items: Ironically, products marketed for gut health can cause diarrhea in sensitive individuals. Examples include apple cider vinegar, aloe vera juice, MCT oil, large volumes of kombucha, and fiber bars with added inulin or chicory root.
• Over-the-Counter Products: Patients often forget to mention products they don't consider "medicine," such as magnesium-containing antacids (e.g., Maalox, Mylanta) or herbal laxative teas containing senna.

An Actionable Patient Approach to a Low-FODMAP Trial

For patients with a suspected functional component, a full, strict low-FODMAP diet can be overwhelming. A simplified approach is often more practical and sustainable:

1. First, "Dial way down on the 5 big groups for 2-4 weeks." Advise the patient to significantly reduce their intake of: lactose-heavy dairy; wheat, onion, and garlic; beans and lentils; certain high-fructose fruits (apples, pears); and sugar alcohols. The goal isn't perfection, but a substantial reduction to see if the gut "quiets down."
2. Second, "Reintroduce one group at a time to identify personal triggers." Once symptoms have improved, the patient can add back one food group per week to see which specific categories provoke symptoms. This transforms the diet from a restrictive one to a personalized tool for long-term management.

Identifying these culprits often solves the case by unmasking a classic Osmotic Diarrhea that was hiding in plain sight in the patient's daily habits.

7. Episode Summary & Key Takeaways

We’ve covered a lot of ground today, moving from initial triage to the nuances of malabsorption and empiric therapy. The central message is that a chaotic and broad differential can be tamed by applying a consistent, systematic framework. By layering these mental models—triage, pathophysiology, and a structured diagnostic pathway—you can approach any patient with diarrhea with confidence and clarity.

To summarize, here are the key takeaways from today’s episode:

1. Triage First: Sick vs. Not Sick, Acute vs. Chronic. Before all else, determine the patient's stability and the duration of their symptoms. This initial sort dictates the urgency and setting of the entire workup.
2. Find the Bucket: Classify the Pathophysiology. For any chronic diarrhea, classify it as Osmotic, Secretory, Inflammatory, Fatty, or Functional. This step is the most powerful tool for narrowing the differential and guiding your diagnostic choices.
3. Follow the Pathway: History, Labs, then Scope. A targeted history and a simple screening lab panel (CBC, CMP, TSH, Celiac Serologies) can often solve the case or point you directly to the next best step. Reserve endoscopy for patients with alarm features or when the diagnosis remains unclear.
4. Trust the Ladder for Unexplained Watery Diarrhea. When the workup is negative, use a pragmatic, step-wise empiric treatment ladder: start by removing triggers and using loperamide, then trial a bile acid sequestrant, address IBS/SIBO overlap, and finally, re-evaluate the diagnosis if all else fails.

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.

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Please not that that these are AI generated podcasts curated from most up to date resources.

Welcome back to The Deep Dive.

Today we're taking on a topic that is, well, it's universally common, incredibly disruptive, and as it turns out, surprisingly complex for clinicians.

It really is.

We're talking about chronic diarrhea, and our mission today is to peel back the layers on the diagnostic framework.

Exactly.

The goal is to turn what feels like this endless list of causes into a really structured systematic map.

For the patient, it's just a symptom, right?

It's urgency, it's misery.

Right.

But for us, the clinician, it's a diagnostic puzzle.

So we're going to give you the exact framework, the clinical buckets that we use to narrow things down fast.

Okay, so to start, let's establish the playing field.

When does loose stool actually become, you know, clinical diarrhea?

Yeah, we need a solid definition.

It's technically increased stool water plus increased frequency or volume.

Okay.

Operationally, what that really means is more than three loose or watery stools a day, or, and this is key, a stool weight over by 200 to 250 grams per day.

That volume piece matters a lot.

And the first most important fork in the row, the first move you make is all about time.

Why is that 30-day mark so critical?

Because time just completely changes the probabilities.

It dictates the likely pathology.

So we sorted immediately into three buckets.

Right.

Acute, which is under 14 days that's usually infectious, then persistent from 14 to 30 days, and then chronic.

Anything over a month.

Anything over four weeks.

And once you cross that line , the chance of it being a simple bug just plummets.

You have to pivot immediately and start hunting for an underlying organic cause.

And those are the five big frameworks we're building today.

Osmotic, secretary, inflammatory, fatty., and then mertility or functional.

So we have the time buckets.

Let's talk about bedside triage.

A new patient comes in with chronic symptoms.

What are the two or three questions just running through your head before you even think about order?

Dering a test?

First, I'm confirming time.

Is this truly chronic?

Second, and this is the critical safety question .

Are they sick or not sick?

Are there any red flags?

And third, just based on the story, which of those path of physiologic buckets does this kind of smell like?

Let's zoom in on those red flags.

The signals that just scream, stop, this is urgent.

We need to work this up now.

These are the things that mean you have to be aggressive.

We're looking for signs of a systemic illness.

So significant volume depletion, dehydration, a high fever, really severe abdominal pain, or obviously, if there's blood in the stool.

Right.

Beyond the acute stuff, we look for chronic alarms .

So unintentional weight loss, anemia, high inflammatory markers on their labs, and one really profound sign nocturnal stools.

Nocturnal stools.

Why is that such a clear sign that this is an organic problem and not, say, just functional?

Because functional issues like IBS, they typically turn off when the patient's asleep but get settles down.

It sounds.

If the diarrhea is bad enough to wake you up at 2 in the morning , that implies there's an active process, a secret pump that doesn't care if you're resting.

It's always on.

And also, you can never ignore age.

If someone over 50 develops new chronic symptoms, you have to move fast to rule out things like like malignancy or a scheicitis.

That distinction is just so key.

Okay, so let's shift to chronic watery diarrhea.

For a clinician, the biggest split here is telling osmotic from secretary .

How do you do that at the bedside?

This is all about the history and sometimes some simple chemistry.

So osmodic diarrhea is caused by non absorbed salutes, things that are physically pulling water into the gut and keeping it there.

Like lactose intolerance.

Perfect example.

Lactose or too much magnesium from supplements, or sugar alcohols like sorbbitol.

So the telltale sign is, if they stop eating and the diar,rhea stops, you're thinking osmotic, you took away the thing that was pulling in the water.

Exactly.

The hallmark is that stool volume falls dramatically with fasting.

And if you do the chemistry, you calculate what's called the stool osmotic gap .

A high gap, over 100, basically confirms there's some unsorbed agent driving the whole thing.

Okay, hold on.

For those of us who don't have that formula memorized, what does a hyosmotic gap actually tell you clinically?

It's pretty straightforward.

It just means there's a big chunk of stuff in the stool that's not supposed to be there.

It's that unabsorbed salute.

The cult..

The culp.

It immediately points you toward laxative abuse, a specific food intolerance, or maybe a supplement they forgot to mention.

It's often the easiest one to fix.

Okay, so contrast that with secretary diary.

The Secretary is completely different.

It's a net increase in active intestinal secretion.

The pump is stuck in the on position.

I see.

Think of rare hormal tumors., mor,rosc hall that, which is really large volume, iting because thechanism doesn't care what you.

And the chemistry would be the opposite then.

Exactly.

The osmic gap is low, usually less than 50.

This tells you the stool volume is all just electrolytes and water that the body is actively kicking out.

And this is the type that is almost always nocturnal.

Got it.

Okay.

What about the other two core types, inflammatory and fatty?

So inflammatory or exitiv means the mucosal lining is disrupted.

It's damaged.

So the clinical picture is blood , pus, pain, fever, and you get a really strong lab signal, a high fecal cowprotein.

The protein from neutrophils.

Exactly.

So if you see that, you're hunting for IBD, a nasty infection like C diff or maybe a schemicitis.

And then fatty diarrhea or strhea, that signals a huge failure in how we handle nutrients.

Correct.

A total failure to digest or absorborb fat, and the stools are classic .

Bulky, pale, really foul smelling, greasy, they're hard to flush.

And this almost always comes with significant, unintentional weight loss.

Let's zoom in on that fatty diarrhea bucket for a minute, because localizing the problem here gets pretty sophisticated.

You use a three-le frame, right?

Luminal nucosal, and postnucosal.

That's the one.

And most of us get the first two.

Migestion is a problem.

The isn't broken down, right?

Usually a pancreatic enzymes .sor isucosing is damaged celi disease.

But what's really fascinating, and I think less discussed, is that third category, postmucosal, or lymphatic malabsorption.

Okay.

Here, the gut cell, the interterocy, it absorbs the fat just fine.

The problem is, the plumbing is backed up .

The fat gets packaged into calomicrons, but it can't leave the gut to get into the circulation because the lymphatic drainage is blocked.

So the vessels that are supposed to carry the fat fat away are obstructed, what would cause that?

Well, the classic cause is congenital thing, primary intestinal lymphagantasia , but it can be secondary to something else, putting on pressure.

Like a tumor.

Like a lymphoma or extensive retro peritonal disease.

Or, and this is the really wild connection, from high systemic venus pressure, like in severe right heart failure or constrictive pericarditis.

Wait, wait.

Constrictive caracarditis , a heart problem is causing GI symptoms.

That sounds like a systemic catastrophe.

It is.

It connects cardiology, right to gastenterology.

High pressure in the ve veins backs up into the lymphhatics, and they start to leak.

Into the gut.

Right into the gut lemon.

Yeah.

And because they're leaking, you don't just get starerhea.

You get what's called a protein losingathy.

Meaning the body is just dumping crucial proteins through the gut wall.

Precisely.

And this shows up as a classic diagnostic triad.

You get disproportionate hypoalbumemia, very low protein in the blood.

Which leads to swelling.

Profound peripheral edema. Swollen legs otes.

And often you see lymphopia, a lack of circulating lymphocites, because those are being lost, too..

That unique combo is a massive alarm bell for lymphatic costs.

Wow.

Okay, let's connect this back to Secretary diarrhea.

We have to talk about how the location of the damage, specificallyally in the ileium, completely changes the pathology, the Ial split.

This is a beautiful concept.

The length of the distal ileium that's damaged have been recsected changes everything.

So let's say you have limited damage less than centimeters.

Okay.

The liver's still making plenty of bile acids, but the remaining i can't reorb all of it.

So the excess bile spills into the colon, which is super irritating and causes a bacid induced secretary diarrhea.

And that causes that terrible urgency in spasticity, right?

The treatment is just a binder.

Simple as that?

You use colus gamine to mop up the extra bile.

But if the rection is extensive, say 100 centimeters or more , the body can't recycle its biosalt pool anymore.

The liver can't keep up.

So you run out of bile.

You become bile acid deficient.

And then you jump buckets completely..

The patient shifts from a simple secretary diarrhea to true fat malabsorption starrhea because they don't have enough bile to break down fat in the first place.

Yeah.

It's a total flip in strategy.

So we've mapped the categories.

Now we have to turn this into action.

Before we even think about scoping, what about the initial blood work?

We're not just ordering a panel, we're hunting for specific clues.

Absolutely.

Targeted hunts.

Yeah.

You start with this CBCBC, the complete blood count.

You're looking for anemia.

Okay.

Is it microcidic?

That suggests iron deficiency from blood loss, maybe IBD or cancer ?

Or is it macroic that suggests B12 or fate malaborption, which points you to theium or maybe CO?

And the CMP, the metabolic panel.

That gives us two things.

First, severity.

How dehydrated are they?

But second, and more importantly, nutrition, that albumen level screens for that critical protein losing ineropathy we talked about.

Pushing you towards lymphangjectasia.

Right, or severe IBD.

And we also check LFTs, looking for liver disease that might be impairing bileflow.

And TSH , it's so simple, but we just can't miss hyperthyroidism.

We have to screen for it.

Hyperthyroidism is this great mimic it causes incre gut motility, loose stools, weight loss.

It looks just like a primary GI disease.

A TH check is an easy way to close that door.

And, of course, celierogies.

Essential.

It's a common, treatable cause of all absorption that so often gets mislabeled as IBS .

A positive test there sends you right to an upper endoscopy instead of wasting months on diet changes.

Speaking of scoping, when do you actually pull that trigger?

I mean, not every person with chronic diarrhea needs a scope, right?

Not at all.

If you have a young patient, no red flags, and the story really fits a functional disease , you manage that conservatively first.

You scope when the diary is unexplained or when those alarm features are there.

Blood, weight loss, nocturnal stool.

Anemia, or if they're over 50 with new symptoms, that's when you have to look.

And if we do scope, the biopsy protocol is everything, isn't it?

Especially when the gut looks totally normal, we're looking for invisible disease.

This is a high stakes moment, for a colonoscopy, if you're looking for microscopic colitis, a super common cause of secret diarrhea, you must take random biopsies from the right and the left colon.

Even if it looks perfectly healthy..

Especially if it looks perfectly healthy, if you don't take those biopsies, you will miss the diagnosis 100% of the time.

And what about for an upper endoscopy, say, for a suspected celiac?

Same principle.

Even if the duadenome looks completely normal, the protocol is at least four biopsies from the second part of the duodunum and two from the duad in the bulb.

Why the bulb specifically?

Because celiac disease could be patchy , and sometimes the only changes are way up there in the bull..

If you skip that spot, you might undample and get a false negative.

It's a common diagnostic trap.

Let's pivot to the everyday causes people miss, the stealth culprits.

Before we're writing prescricriptions, what are the common things people are eating or drinking that are causing all this?

Oh, this is huge.

We're looking at things people think are harmless or even healthy.

The first big one is sugar-free products.

The sugar alcohol.

Sorbol, manit, xylotol,th.

They're in gum, mints, cough drops, protein bars, keto snacks .

They are powerfully osmic.

They pull in water.

And the patient never thinks to the 10 cough drops they have every day.

That is such a critical teaching point.

What about supplements?

Hidos magnesium is the number one offender.

People take magnesium citrate or oxide for sleep or muscle cramps or stress , and they are potentsmotic laxatives.

Also, huge doses of powdered vitamin C or some of those physilectrolyte mixes can do it too.

Okay, so we've ruuled out the big organic causes.

We've eliminated the sneaky culprits.

What's the simple step-by-step empiric treatment ladder for that chronic, watery, and non-bloody diarrhea?

We move systematically, assuming the basic labs and red flag screen are negative.

Wrong one. Is just that .

Remove the offending meds and supplements and try a simple diet change.

We'll often do a two to four week trial of reducing FODMIM, lactose, wheat, onion, garlic, and of course, those sugar alcohol.

Wung, too.

Symptomatic control.

This would be scheduled, low dose l , and stress scheduled.

If you take it as needed, you'reasing the syptom.

Scheduleses give the gut a predictable pattern and improve quality of life so much more.

Okay, Rung three, the trial of Bile acid binders.

This is a crucial diagnostic and therapeutic step. Trial cholesteroles tabl secret syms are still there if they' their gallbladder out oralisease.

And this is where the patient's response is actually diagnostic, right?

It confirms the problem.

Absolutely.

Excess bile acids cause this profound urgency, spasticity, and that awful feeling of incomplete evacuation called tenesus.

If the binder takes that away, if the patient says, the urgency and spasticity just melted, you've confirmed a bilacid component.

It's an incredibly powerful clue.

So RU 4, if all that has failed.

If the workup is still normal, now we're really in the land of IBSD or maybe CO.

So here you might try a Courser for Faximen, the non-absorbed antobiotic, or a more structured, long-term low FODM map diet.

And the final and maybe most important step, rung 5..

Run 5 is reassessment.

If the patient is still miserable after all that, you've removed offenders , tried lopperide, tried a binder, tried refaxmen, you have to stop escalating.

That persistent failure is a huge diagnostic signal.

It means you missed something.

It means you almost certainly missed an organic disease.

You have to stop managinging symptoms and go back to the drawing board.

Reassess the need for those critical biopsies for microscopic colitis or celiac disease.

So, to wrap this all up, our systematic approaches , triage by time and severity, then phenotype the diarrhea into watery, fatty, or inflammatory.

Then you run target of testing based on that phenotype.

And finally, you use a treatment knowing when to stop.

And I think if we connect this to the bigger picture for you, the learner, the real clinical art here, beyond the empiric treatment, is in that initial meticulous venotyping and just keeping a really high index of suspicion for those hidden organic diseases, the invisible ones, like celiac and microscopic colitis.

That's the key takeaway.

And the most provocative thought to leave you with is this .

The failure of that carefully planned empiric ladder is not a therapeutic failure.

It is, in fact, a powerful diagnostic signal.

It's demanding that you go back and look harder.

If the ladder fails, you are no longer dealing with the functional problem, you are dealing with a missed organic disease.