By: A Person Who Has Seen Some Things

Let’s be adults for a second. We’ve all been there.

You just completed the morning ritual. You feel lighter. You feel accomplished. You reach for the handle to banish the evidence, but then… you pause. You look back. It’s still there.

It’s bobbing. It’s weaving. It’s treading water like a tiny, brown Olympic swimmer refusing to touch the bottom of the pool.

You stare at it, and it stares back (metaphorically). Why? you wonder. Is this a sign of my superior health? Have I evolved into a being of pure light and air? Or is my body slowly dissolving from the inside out?

Well, put down the WebMD search, because we are about to dive deep (too deep?) into the hydrodynamics of doo-doo. It turns out, the reason your poop floats isn’t magic. It’s math. And sometimes, it’s a cry for help from your pancreas.

Part 1: It’s Not Magic, It’s Just Marshmallows

First, let’s get the science out of the way so we can get back to the jokes.

You remember Archimedes? The Greek guy who shouted “Eureka!” in the bathtub? Legend says he was figuring out displacement, but let’s be honest: he probably just noticed something floating and went, “Whoa, physics.”

Here is the equation: Water has a density of 1.0.

A “normal,” healthy poop is dense. It’s compact. It’s got business to do. It sinks like a stone because it’s heavier than water.

A floating poop, however, has been corrupted. It has been infiltrated by forces that lower its density. To understand this, imagine a marshmallow. A marshmallow is mostly air and sugar, so it floats. Your floater? It’s basically a biological marshmallow.

But what inflated the marshmallow? There are two suspects, and one of them is significantly grosser than the other.

Part 2: The “Happy Floater” (Your Gut Bacteria Are Throwing a Rave)

The most common reason your poop is floating is that you have essentially become a blimp.

Somewhere in your recent history, you ate a bean burrito. Or a bowl of broccoli. Or maybe you just drank a liter of Mountain Dew.

Here is what happens inside you: Your body is lazy. It can’t digest complex fibers or certain sugars (like the ones in beans or milk) on its own. So, it pushes them down to the colon, where your microbiome—the trillions of bacteria living in your gut—waits like a pack of starving hyenas.

The bacteria eat the fiber. They love it. It’s a party. And like any good party, this produces gas. We’re talking methane, hydrogen, carbon dioxide—the whole greenhouse gang.

This gas gets trapped inside the stool. It turns your waste into a foam dart.

In the 1970s, a group of scientists at the University of Minnesota actually proved this. (Yes, someone got a grant for this). They took floating poop samples and squeezed the gas out of them. Once the air was gone, the poop sank immediately.

So, if your poop floats, congrats! It just means you ate a vegetable and your bacteria are working overtime. You are a gas-filled, buoyant miracle of nature. Go you.

Part 3: The “Sad Floater” (The Exxon Valdez Scenario)

Okay, put the party hat down. We need to talk about the other reason poop floats.

If your poop floats because of gas, it’s fluffy. It looks like a cloud.

But if your poop floats because of fat, it is not a cloud. It is an oil slick.

This is called Steatorrhea. Say it with me: Stee-uh-toe-ree-uh. It sounds like a spell Harry Potter would cast, but it’s actually a nightmare.

Normally, your body digests fat with the help of your pancreas (which makes enzymes) and your liver (which makes bile). Bile is like dish soap; it breaks up the grease so you can absorb it.

If your pancreas goes on strike, or your liver decides to stop making soap, the fat doesn’t get absorbed. It goes right through you. It comes out oily, pale, yellowish, and shiny.

This poop floats because fat is lighter than water. But the real tell is the aftermath. If you flush and the bowl is coated in a grease that requires a Brillo pad and a prayer to remove? That’s not gas. That’s malabsorption.

Red Flags Your Floater is “Sad”:

1. It smells like a rotting corpse wrapped in burning tires. (Normal poop smells bad; this smells like evil).
2. It’s sticky. It clings to the bowl like it’s holding on for dear life.
3. It’s pale or clay-colored. (Brown is good; grey is bad).
4. You’re losing weight without trying. (This is the “Oh crap” moment).

If you have the “Sad Floater,” stop reading this blog and go see a doctor. Your pancreas needs a pep talk.

Part 4: How to Tell the Difference (Without Poking It)

You don’t need a lab kit to diagnose your buoyant bowel movement. You just need to look at your life choices.

Scenario A:

• Yesterday’s dinner: Large salad, two bean burritos, a broccoli cheddar soup, and a soda.
• Poop status: Floating.
• Verdict: You are fine. You are just a human fermentation tank. Drink some water and maybe lay off the beans for a day.

Scenario B:

• Yesterday’s dinner: Normal toast.
• Poop status: Floating, oily, smells like a chemical war, and you had to flush three times.
• Verdict: Go to the doctor. This is not a diet issue; this is a mechanical failure.

Part 5: Conclusion – Just Flush It

At the end of the day, a floating poop is usually a sign of a healthy, fiber-fueled gut. It’s your bacteria saying, “Thank you for the brunch!”

But if your poop looks like it should be in the Smithsonian Museum of Natural History as a sample of “Industrial Grease,” get that checked out.

So, the next time you stand up and see the Brown Dolphin bobbing in the waves, don’t panic. Check the texture. Check the color. Check your memory of the burrito.

And then, for the love of all that is holy, wash your hands.

Flushing emoji. Toilet emoji. Face with medical mask emoji.

But wait—you didn’t think we were just making this stuff up, did you? While the blog post was the “digestible” version (pun absolutely intended), the actual rabbit hole of research went significantly deeper. We spelunked into the dark corners of medical history, revisited the terrifying University of Minnesota degassing studies of the 1970s, and analyzed the fluid dynamics of the lower intestine with the scrutiny of a NASA engineer.

Below, we present the source material for your viewing pleasure (or horror). It is the full, unadulterated Ph.D. dissertation that serves as the scientific backbone for everything you just read. It is rigorous, heavily cited, and terrifyingly accurate. If you have ever wanted to read a 2,000-word treatise on specific gravity, methane-producing archaea, and the tragic heroism of the Bristol Stool Scale, today is your lucky day. Behold: The Hydrostatic Anomalies of Fecal Matter.

THE HYDROSTATIC ANOMALIES OF FECAL MATTER:

A Multidisciplinary Inquiry into the Phenomenon of Buoyant Defecation, the Scourge of Malabsorption, and the Gut Microbiome’s Unrelenting Production of Methane

A DISSERTATION
SUBMITTED TO THE FACULTY OF THE GRADUATE SCHOOL
IN PARTIAL FULFILLMENT OF THE REQUIREMENTS
FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY IN SCATOLOGICAL PHYSICS

BY
A. N. ONYMOUS, B.S., M.S.

ADVISOR:
PROFESSOR I. P. FREELY, Ph.D.

THE UNIVERSITY OF THE LOWER BOWEL
DEPARTMENT OF GASTROINTESTINAL HYDRODYNAMICS
MAY 2025

ABSTRACT

The phenomenon of stool buoyancy—colloquially termed “The Floater”—represents a significant intersection of fluid dynamics, organic chemistry, and existential dread. While the lay observer often interprets a floating bowel movement as a benign curiosity or a victory over gravity, a rigorous scientific analysis suggests a more complex etiology involving trapped methane, undigested lipids, and the occasional systemic failure of the exocrine pancreas.

This dissertation employs a multidisciplinary approach to interrogate the mechanisms governing fecal density. Through a critical review of the literature, specifically the degassing studies of the 1970s which proved that squeezing the gas out of a turd causes it to sink, we establish that gas, rather than fat, is the primary agent of buoyancy in the vast majority of cases. However, we also explore the pathological nuances of steatorrhea, a condition in which the stool floats not because it is airy, but because it is a greasy, lipid-laden insult to plumbing.

We examine the impact of high-fiber diets, the methanogenic tendencies of Brassica oleracea (broccoli), and the specific gravity of various foodstuffs. Furthermore, we investigate the diagnostic criteria for malabsorption syndromes, including the utility of fecal elastase testing and the sheer, unadulterated misery of the 72-hour fecal fat collection protocol. Finally, we offer a heuristic framework for the terrified layperson: if it floats and smells like a vegetable, eat a banana; if it floats and smells like a chemical spill, call a gastroenterologist immediately.

DEDICATION

To the toilet. The unsung hero of modern sanitation. The porcelain confidant. The silent witness to our darkest, most gaseous moments. May your water pressure never falter and your trap never clog.

ACKNOWLEDGMENTS

I would like to thank my thesis advisor, Dr. Freely, for not resigning when I explained my research topic. I thank the subjects of the Minnesota Degassing Study for their, uh, contributions. I thank my cats, for ignoring me completely, which provided the solitude necessary to write 200 pages about poop. And finally, I thank the human microbiome, without whose relentless production of hydrogen sulfide this research would have been significantly less pungent.

TABLE OF CONTENTS

Chapter 1: Introduction – The Porcelain Problem
    1.1 The Vexation of the Bobbing Stool
    1.2 The “Floater” vs. The “Sinker”: A Binary World
    1.3 Research Question: Is It Gas, Grease, or Magic?

Chapter 2: Literature Review – A History of Squeezing Poop
    2.1 Archimedes and the Urge to Submerge
    2.2 The University of Minnesota Degassing Experiments (1972)
    2.3 The Bristol Stool Scale: From Type 1 to Type 7 (The Type 4 Utopia)

Chapter 3: Theoretical Framework – The Physics of Flotation
    3.1 Specific Gravity and the Density of Water (1.0 g/mL)
    3.2 The Role of Trapped Gas: Methanogenesis as a Lift Force
    3.3 Lipids and Hydrophobicity: Why Oil Doesn’t Mix with Toilet Water

Chapter 4: The “Happy Floater” – Dietary Indiscretions
    4.1 The Fiber Fiasco: Beans, Lentils, and the Bacterial Rave
    4.2 Lactose Intolerance: The Milk Betrayal
    4.3 Aerophagia: Swallowing Air and Why Chewing Gum is for Fools

Chapter 5: The “Sad Floater” – Pathophysiology of Malabsorption
    5.1 Steatorrhea: When Your Stool Becomes an Oil Slick
    5.2 Exocrine Pancreatic Insufficiency (EPI): The Pancreas on Strike
    5.3 Bile Acid Deficiency: The Liver’s Forgotten Detergent
    5.4 Celiac Disease and Crohn’s: When the Intestine Attacks Itself

Chapter 6: Diagnostic Methodologies – Probing the Abyss
    6.1 Fecal Elastase: Searching for Enzymes in a Haystack
    6.2 The 72-Hour Stool Collection: The Psychological Toll
    6.3 Imaging: CT Scans of the Guts (and Why We Prefer Not To)

Chapter 7: Special Populations – Kids, Old People, and Spinal Cords
    7.1 Pediatric Malabsorption: Why Kids Can’t Describe Their Poop
    7.2 Neurogenic Bowel Dysfunction: When the Wires are Crossed
    7.3 Geriatric Considerations: The Metabolic Slowdown

Chapter 8: Discussion – So, What Do We Do With This Information?
    8.1 The Symptom Clusters of Doom
    8.2 To Flush or Not to Flush?
    8.3 Clinical Recommendations for the Hypochondriac

Chapter 9: Conclusion – Gravity Always Wins

References

CHAPTER 1: INTRODUCTION – THE PORCELAIN PROBLEM

1.1 The Vexation of the Bobbing Stool

The act of defecation is, ostensibly, a straightforward biological transaction. The body processes fuel, extracts nutrients, and expels the waste. Ideally, this waste—hereafter referred to as “stool,” “feces,” “scat,” or “the morning deposit”—should obey the fundamental laws of physics. Specifically, it should sink.

Water has a density of approximately 1.0 gram per milliliter. A healthy, well-formed stool, composed of ~75% water and ~25% solid matter (bacteria, fiber, and sloughed intestinal cells), typically possesses a density greater than water. Therefore, according to the hydrostatic principles established by the ancient Greeks, the stool should descend to the bottom of the toilet bowl, resting peacefully upon the porcelain until the handle is depressed.

However, for a disturbingly large segment of the population, this law is violated. The stool floats. It bobs. It navigates the surface tension like a stubborn cork. It refuses to sink, creating a moment of post-defecatory anxiety that reverberates throughout the day. The subject stares into the bowl, brow furrowed, asking the silent question that has plagued humanity since the invention of indoor plumbing: Why?

1.2 The “Floater” vs. The “Sinker”: A Binary World

In the realm of scatological observation, the world is divided into two camps. The “Sinkers”—individuals who produce dense, compact, well-behaved stools—and the “Floaters”—those whose fecal matter possesses a stubborn buoyancy.

While Sinkers walk with the quiet confidence of those whose bowels are in mechanical harmony, Floaters live in a state of perpetual doubt. Is their buoyancy a sign of a healthy, high-fiber diet? Is it a sign of a super-charged microbiome producing abundant gas? Or, terrifyingly, is it the first symptom of pancreatic cancer, cystic fibrosis, or celiac disease?

This dissertation seeks to bridge the gap between anxiety and empiricism. By dissecting the biochemical composition of the stool and the mechanics of the gastrointestinal tract, we aim to provide a definitive taxonomy of the floating stool.

1.3 Research Question: Is It Gas, Grease, or Magic?

The central hypothesis of this work is that floating stool is not magic. It is physics. Specifically, it is the result of density reduction caused by either:

1. Gas Entrapment: The incorporation of gases (methane, hydrogen, carbon dioxide) produced by bacterial fermentation.
2. Lipid Excretion: The presence of excess, undigested dietary fat (steatorrhea), which is less dense than water and hydrophobic.

We shall explore these two divergent paths to buoyancy, examining the “Happy Floater” (the gas-filled result of a bean burrito) and the “Sad Floater” (the grease-filled result of a dying pancreas).

CHAPTER 2: LITERATURE REVIEW – A HISTORY OF SQUEEZING POOP

2.1 Archimedes and the Urge to Submerge

One cannot discuss floating poop without acknowledging the father of hydrostatics, Archimedes. While his famous “Eureka” moment in the bathtub concerned a gold crown and the concept of displacement, the principle applies equally well to a bowel movement. An object will float if the weight of the fluid it displaces is greater than its own weight.

For centuries, this principle was largely applied to naval engineering rather than gastroenterology. It was not until the mid-20th century that the scientific community turned its collective eye toward the buoyancy of human waste.

2.2 The University of Minnesota Degassing Experiments (1972)

The watershed moment in scatological physics occurred in the early 1970s at the University of Minnesota. A team of intrepid gastroenterologists, driven by a curiosity that borders on the sociopathic, conducted a series of experiments on stool samples from 39 volunteers (and, presumably, themselves).

These researchers collected fecal samples and subjected them to a process of degassing. They essentially squeezed the poop until the gas came out. The results were definitive and, in a way, beautiful. When the gas was removed, the samples that previously floated sank with a satisfying thud.

This study proved, once and for all, that gas is the primary driver of stool buoyancy. The fat content of the stool was found to be insufficient to cause floating on its own in the absence of gas. This discovery shifted the diagnostic focus from lipids to aerophagia and fermentation.

2.3 The Bristol Stool Scale: From Type 1 to Type 7 (The Type 4 Utopia)

No discussion of stool mechanics is complete without referencing the Bristol Stool Scale (BSFS). Developed in 1997 at the University of Bristol, this chart classifies human feces into seven categories based on shape and consistency.

• Type 1: Separate hard lumps (The “Rabbit Droppings”).
• Type 2: Lumpy sausage (The “Backlog”).
• Type 3: Sausage with cracks (The “Almost There”).
• Type 4: Smooth, soft sausage (The “Holy Grail”).
• Type 5: Soft blobs with edges (The “Warning Shot”).
• Type 6: Mushy pieces (The “Emergency”).
• Type 7: Liquid (The “Disaster”).

Buoyancy can occur across types, but it is most commonly associated with Type 5 and Type 6, where the high water content and high bacterial activity create a frothy, gas-filled matrix. However, the oily “Type Slick” associated with steatorrhea defies standard classification and represents a pathological outlier.

CHAPTER 3: THEORETICAL FRAMEWORK – THE PHYSICS OF FLOTATION

3.1 Specific Gravity and the Density of Water (1.0 g/mL)

To understand why poop floats, one must understand density.

• Water Density: ~1.00 g/mL.
• Healthy Stool Density: ~1.06 g/mL (It sinks).
• Floating Stool Density: <1.00 g/mL.

When stool sinks, it is doing its job. It is compact, relatively dehydrated, and dense. When it floats, its specific gravity has been compromised. Something has infiltrated the stool matrix to lower its overall density.

3.2 The Role of Trapped Gas: Methanogenesis as a Lift Force

The human colon is a fermentation vat. It is inhabited by trillions of bacteria—the microbiome—that act as a biological recycling plant. When dietary fiber reaches the colon (having survived the enzymatic assault of the small intestine), these bacteria feast.

Through the process of bacterial fermentation, fiber is broken down into Short-Chain Fatty Acids (SCFAs) and gas. The specific gases produced include hydrogen, carbon dioxide, and, in some lucky individuals, methane.

Methane producers possess a specific gut composition dominated by Methanobrevibacter smithii. These archaea are highly efficient at scavenging hydrogen and converting it into methane. While this is energetically efficient for the host, it produces a gas that is easily trapped within the viscous matrix of the stool.

Think of the stool as a biological Styrofoam cup. The “foam” is the bacterial gas. The “cup” is the fiber. If enough gas is produced, the density drops below that of water, and the stool achieves lift-off.

3.3 Lipids and Hydrophobicity: Why Oil Doesn’t Mix with Toilet Water

If gas is the primary cause of floating, fat is the secondary, more nefarious cause.

In a healthy digestive system, dietary fats (triglycerides) are emulsified by bile and broken down by pancreatic lipase into free fatty acids and monoglycerides. These are absorbed in the small intestine.

If this system fails—due to a lack of enzymes or bile—fat passes through the intestine undigested. Fat has a density lower than water, but more importantly, it is hydrophobic. It repels water.

Steatorrheic stool (fatty stool) is not just floating; it is often difficult to flush. It adheres to the porcelain like a greasy mechanic to a wrench. It may appear pale or clay-colored (due to the lack of stercobilin, the pigment that makes poop brown) and emits an odor that can only be described as “unforgiving.”

CHAPTER 4: THE “HAPPY FLOATER” – DIETARY INDISCRETIONS

4.1 The Fiber Fiasco: Beans, Lentils, and the Bacterial Rave

The most common cause of floating stool is a diet rich in fermentable fiber. The offender is often the legume family. Beans, peas, and lentils contain oligosaccharides (specifically raffinose and stachyose) that the human enzyme repertoire cannot digest.

When these arrive in the colon, the bacteria go wild. It is a feeding frenzy. The result is a prodigious production of gas.

• Beans: 10/10 buoyancy potential.
• Broccoli/Cauliflower/Brussels Sprouts: While healthy, these cruciferous vegetables are also gas factories. They are the “silent but deadly” contributors to floating stools.
• Carbonated Beverages: Drinking a liter of soda introduces massive amounts of carbon dioxide directly into the gastrointestinal tract. While much is belched out, the residual gas contributes to the buoyancy of the stool.

This type of floating stool is the “Happy Floater.” It is the result of a functional, albeit gassy, digestive system. It is a sign that you are eating your vegetables (even if the social consequences are severe).

4.2 Lactose Intolerance: The Milk Betrayal

Lactose intolerance is a global phenomenon. A significant portion of the adult human population lacks the enzyme lactase, required to break down the sugar in milk.

When lactose-intolerant individuals consume dairy, the undigested sugar draws water into the colon (osmosis) and serves as a feast for bacteria. The dual result is diarrhea (high water content) and gas. A loose, gas-filled stool is the ultimate recipe for buoyancy. It floats not because it is light, but because it is essentially a frothy bubble bath.

4.3 Aerophagia: Swallowing Air and Why Chewing Gum is for Fools

Aerophagia is the medical term for swallowing air. It happens when you eat too fast, talk while eating, or chew gum constantly.

While much of the swallowed air is eructated (burped), some persists into the intestines. This air, comprised mostly of nitrogen and oxygen, mixes with the stool. While nitrogen is less soluble than carbon dioxide, it still contributes to the overall volume of the gas within the bolus. Chewing gum is a double whammy: you swallow air, and the artificial sweeteners (sorbitol, xylitol) are poorly absorbed, acting as osmotic laxatives and feeding the gas-producing bacteria.

CHAPTER 5: THE “SAD FLOATER” – PATHOPHYSIOLOGY OF MALABSORPTION

5.1 Steatorrhea: When Your Stool Becomes an Oil Slick

We move now from the benign to the pathological. Steatorrhea is the medical term for excess fat in the stool. It is the “Sad Floater.”

The hallmark of steatorrhea is not just floating; it is grease. The stool is often described as “oily,” “shiny,” or “foul-smelling.” It may leave a residue on the toilet bowl that is difficult to clean. It floats because fat is lighter than water, but it is also voluminous, loose, and pale.

Steatorrhea indicates a failure of digestion (maldigestion) or absorption (malabsorption). It is a red flag. It is your body screaming, “I am broken.”

5.2 Exocrine Pancreatic Insufficiency (EPI): The Pancreas on Strike

The pancreas is the workhorse of digestion. It secretes a cocktail of enzymes—amylase for carbs, protease for proteins, and lipase for fats.

Exocrine Pancreatic Insufficiency (EPI) occurs when the pancreas fails to produce enough lipase. Without sufficient lipase, fats remain as large triglycerides, too big to be absorbed.

• Causes: Chronic pancreatitis, cystic fibrosis, pancreatic cancer, or simply the ravages of time and alcohol.
• Mechanism: The fat stays in the gut. It passes through to the stool. The stool becomes fatty.
• Consequence: Nutrient deficiencies, weight loss, and floating stool.

Diagnosis is typically confirmed via the Fecal Elastase Test. Elastase is another pancreatic enzyme. If its levels in the stool are low (<200 µg/g), the pancreas is slacking off.

5.3 Bile Acid Deficiency: The Liver’s Forgotten Detergent

Bile is the dish soap of the gut. Produced by the liver and stored in the gallbladder, bile salts emulsify fats, breaking large globules into smaller droplets that lipase can attack.

If bile production is compromised (liver cirrhosis) or delivery is blocked (gallstones, bile duct obstruction), fats cannot be digested.

• Primary Biliary Cholangitis (PBC): An autoimmune disease that destroys the bile ducts.
• The Result: The toilet bowl becomes a crime scene of undigested fat.

5.4 Celiac Disease and Crohn’s: When the Intestine Attacks Itself

Malabsorption can also stem from damage to the absorptive surface of the intestine.

• Celiac Disease: An autoimmune reaction to gluten destroys the villi (finger-like projections) in the small intestine. This reduces the surface area for absorption. Fat, along with other nutrients, passes through unabsorbed.
• Crohn’s Disease: Inflammation can affect any part of the GI tract. If it hits the small intestine or the area where the bile ducts empty, fat absorption suffers.

In both cases, floating stool is often accompanied by other symptoms: abdominal pain, bloating, and fatigue.

CHAPTER 6: DIAGNOSTIC METHODOLOGIES – PROBING THE ABYSS

6.1 Fecal Elastase: Searching for Enzymes in a Haystack

The Fecal Elastase-1 (FE-1) Test is the gold standard for diagnosing EPI. It is relatively simple: the patient provides a stool sample (in a jar, thankfully, not by hand), and the lab measures the concentration of elastase.

• >200 µg/g: Normal. Your pancreas is working.
• 100–200 µg/g: Indeterminate. Your pancreas is maybe thinking about retiring.
• <100 µg/g: Severe EPI. Your pancreas has left the building.

This test is superior to the 72-hour fecal fat collection because it is not dependent on the patient accurately collecting every single poop for three days, a feat that 90% of the population finds abhorrent.

6.2 The 72-Hour Stool Collection: The Psychological Toll

Historically, to measure fat malabsorption, doctors required the patient to collect every bowel movement for 72 hours while adhering to a high-fat diet (100g of fat per day).

The samples would then be analyzed for fat content. If more than 7g of fat was excreted per day, steatorrhea was confirmed.

This test is the “Dark Souls” of gastroenterology. It is arduous, embarrassing, and requires a dedication to one’s own fecal matter that borders on the psychotic. It is rarely performed today, relegated to the archives of medical torture, replaced by the sensible fecal elastase test.

6.3 Imaging: CT Scans of the Guts (and Why We Prefer Not To)

When malabsorption is suspected, imaging may be employed to look for structural causes.

• CT Enterography: A CT scan of the small intestine, often performed after the patient drinks a large volume of contrast material (a “shake” that tastes like radioactive chalk). It can visualize inflammation, strictures, or masses in Crohn’s disease.
• MRI: Useful for visualizing the pancreas and biliary tree without radiation.

While high-tech, these methods cannot “see” the fat in the stool directly. They only look for the cause of the fat. The diagnosis of the floating stool itself remains a clinical observation, or as we prefer to call it, “The Porcelain Assessment.”

CHAPTER 7: SPECIAL POPULATIONS – KIDS, OLD PEOPLE, AND SPINAL CORDS

7.1 Pediatric Malabsorption: Why Kids Can’t Describe Their Poop

Diagnosing malabsorption in children is a nightmare, partly because children are terrible historians.

• “Does your poop float?” is a question met with blank stares or a detailed story about a dinosaur.
• The 3-D Stool Model Study: Research has shown that children have significant difficulty classifying stool consistency. They often mistake loose stools for normal ones because they lack the tactile experience of the “Type 4 Utopia.”

In pediatrics, “failure to thrive” (poor weight gain) is the red flag that prompts a workup for Celiac disease or Cystic Fibrosis. The floating stool is often a symptom that the parents notice (if they are brave enough to look) or report based on the child’s complaints of “potty bubbles.”

7.2 Neurogenic Bowel Dysfunction: When the Wires are Crossed

Patients with spinal cord injuries (SCI) or neurological disorders (Multiple Sclerosis, Parkinson’s) suffer from Neurogenic Bowel Dysfunction (NBD).

In these individuals, the nerves controlling the colon are damaged. This leads to dysmotility—stool moves too slowly (constipation) or too quickly (incontinence). In the context of floating stool, the dysmotility can lead to bacterial overgrowth (SIBO) and fermentation, causing gas and buoyancy.

Furthermore, managing NBD often involves laxatives, fiber, and stool softeners, all of which contribute to a looser, gassier, potentially floating stool.

7.3 Geriatric Considerations: The Metabolic Slowdown

As the human body ages, the digestive system slows down. Peristalsis weakens. The production of digestive enzymes declines.

Elderly patients are prone to “SIBO” (Small Intestinal Bacterial Overgrowth), where bacteria migrate up from the colon into the small intestine. These bacteria ferment food before it is fully digested, leading to gas and bloating. This fermentation can cause floating stool, which is often misdiagnosed as “just getting old” rather than a treatable bacterial imbalance.

CHAPTER 8: DISCUSSION – SO, WHAT DO WE DO WITH THIS INFORMATION?

8.1 The Symptom Clusters of Doom

Differentiating the “Happy Floater” from the “Sad Floater” relies on symptom clustering.

• Happy Floater Profile:
  • Floating is intermittent.
  • Associated with a recent change in diet (e.g., “I ate a burrito the size of a baby”).
  • No weight loss.
  • Abdominal pain is mild/bloating/gas-related.
  • Stool looks normal (brown, formed).
• Sad Floater Profile:
  • Floating is persistent.
  • Stool is greasy, oily, or shiny.
  • Stool is pale or clay-colored.
  • Stool is foul-smelling (beyond normal).
  • Patient has weight loss, diarrhea, or abdominal pain.
  • Patient experiences foul-smelling gas.

If you check any box in the “Sad Floater” profile, do not consult a dissertation. Consult a physician.

8.2 To Flush or Not to Flush?

The psychological impact of floating stool is not to be underestimated. It induces shame. It induces uncertainty.

However, the act of flushing is the final acceptance of the outcome. A “Happy Floater” flushes with a satisfying whirlpool. A “Sad Floater” may require a secondary flush, or even the use of a toilet brush, adding insult to injury.

We must normalize the inspection of one’s stool. It is a biological dashboard. A “Check Engine” light shaped like a floating turd is not something to be ignored, but neither is it something to be panicked over in isolation.

8.3 Clinical Recommendations for the Hypochondriac

For the reader who is currently convinced they have pancreatic cancer because their poop floated after a salad:

1. Relax. Gas is good. It means you have bacteria.
2. Evaluate your diet. Have you increased fiber? Are you chewing gum? Drinking soda?
3. Wait. If it persists for weeks, then worry.
4. Stop Googling. Dr. Google will convince you that floating stool is caused by alien parasites. It is usually just beans.

CHAPTER 9: CONCLUSION – GRAVITY ALWAYS WINS

In this dissertation, we have explored the buoyancy of fecal matter with the rigor it deserves. We have established that the primary determinant of floatation is gas volume, a result of bacterial fermentation of indigestible carbohydrates. We have acknowledged the secondary, pathological role of fat, specifically in the context of steatorrhea and pancreatic insufficiency.

We have reviewed the literature of poop-squeezing (Minnesota) and the classification of turds (Bristol). We have investigated the diagnostics of enzyme deficiency (Fecal Elastase) and the horror of the 72-hour collection.

The phenomenon of the “Floater” is a testament to the complexity of the human gut. It is a reminder that we are hosts to a universe of microscopic organisms, fermenting our lunch and inflating our waste. It is a reminder that the pancreas and liver are essential organs, and when they fail, the consequences are visible in the toilet bowl.

Ultimately, whether the stool sinks or floats, the digestive system has performed its duty: it has moved the waste from the inside to the outside. The physics of the flush are a problem for the plumber. The physics of the buoyancy are a problem for the gastroenterologist.

Gravity usually wins. But occasionally, with the help of a hearty bean chili, the poop wins.

REFERENCES

1. The Levitating Defecation: A Comparative Analysis of Gas vs. Fat. J. Scatol. Phys. (1972). University of Minnesota Press.
2. Archimedes’ Principle Applied to Organic Solids in Aqueous Solutions. Greek Journal of Hydrostatics, 250 BC.
3. The Bristol Stool Form Scale: A Guide for the Perplexed. Heaton, K. W., et al. (1997). Scand J Gastroenterol.
4. Exocrine Pancreatic Insufficiency: Why Your Enzymes Are on Vacation. Domínguez-Muñoz, J. E. (2019). United European Gastroenterol J.
5. Steatorrhea: The Greasy Truth. Azer, S. A., & Sankararaman, S. (2023). StatPearls Publishing.
6. Fecal Elastase: A Non-Invasive Look Into Your Pancreas. Löser, C., et al. (1996). Pancreas.
7. The 72-Hour Stool Collection: A Form of Torture or Just Really Gross Medicine? Van de Kamer, J. H., et al. (1949). J Clin Invest.
8. Beans, Beans, The Musical Fruit: An Analysis of Raffinose Oligosaccharides. Suarez, F. L., et al. (1999). Am J Gastroenterol.
9. Why Kids Can’t Describe Poop: The 3-D Model Study. Saps, M., et al. (2013). Rev Gastroenterol Mex.
10. Neurogenic Bowel: When Your Spine Stops Your Colon. Emmanuel, A. (2019). F1000Res.

VITA

A. N. Onymous was born in a small town in the Midwest. He received his B.S. in Biology from the University of Why Did I Pick This Major, and his M.S. in Gastrointestinal Physiology from the Institute of What Goes In Must Come Out.

He currently resides in a house with a very good toilet and a dog who occasionally eats poop, reminding him daily that nature is weird and nothing is sacred. His research interests include the specific gravity of different types of chili and the aerodynamics of the flush.

This dissertation is his magnum opus. He hopes you enjoyed it. He hopes you flushed.

THE END.
(Please flush the document when finished.)

Real Actual Research Processed

Keeping 35 items:
✓ Physical principles of stool buoyancy
✓ Density comparison between stool and water
✓ Gas content as primary factor in buoyancy (degassed stool weight studies)
✓ Fat content contribution to buoyancy in steatorrhea cases
✓ Relationship between stool composition and water displacement
✓ Dietary factors influencing stool buoyancy
✓ High-fiber diet effects on bacterial fermentation and gas production
✓ Specific gas-producing foods (beans, broccoli, cauliflower, cabbage, onions, bran)
✓ Carbonated beverages and air swallowing mechanisms
✓ Lactose-containing dairy products and carbohydrate malabsorption
✓ Pathophysiological mechanisms of malabsorption
✓ Fat malabsorption (steatorrhea) and undigested fat accumulation
✓ Carbohydrate malabsorption processes (lactose, fructose, starch)
✓ Bile production and delivery system for fat digestion
✓ Pancreatic enzyme secretion and function in nutrient breakdown
✓ Organ system disorders associated with floating stool
✓ Pancreatic disorders (pancreatitis, pancreatic cancer, exocrine pancreatic insufficiency)
✓ Liver and biliary system diseases (bile duct blockage, cirrhosis, primary biliary cholangitis)
✓ Small intestine disorders (celiac disease, Crohn’s disease, tropical sprue)
✓ Gastrointestinal infections (giardiasis, bacterial infections)
✓ Clinical characteristics of pathologic floating stool
✓ Greasy/oily appearance and adherence to toilet bowl
✓ Foul odor and pale or clay-colored stool presentation
✓ Stool consistency patterns (bulky, loose, difficult to flush)
✓ Symptom clusters requiring medical evaluation
✓ Diagnostic evaluation methods for floating stool
✓ Fecal fat analysis and 72-hour stool collection protocols
✓ D-xylose test for intestinal absorption assessment
✓ Blood tests for nutrient deficiencies and organ function markers
✓ Imaging studies for gastrointestinal structure evaluation
✓ Differentiation between normal and concerning floating stool
✓ Frequency and duration thresholds for clinical concern
✓ Dietary correlation assessment techniques
✓ Accompanying symptoms indicating pathology (weight loss, dark urine, chronic diarrhea)
✓ Population-specific considerations in symptom interpretation
Generating replacement items for removed topics…

No changes made to research outline. Continuing with original outline.

Deep Research Mode: Activated

I’ll search for comprehensive information about your query. This might take a moment…

Research Cycle 2: Search Queries

Query 1: Gas content primary factor stool buoyancy degassed weight studies
Topic: Gas content as primary factor in buoyancy

Query 2: Steatorrhea undigested fat malabsorption stool buoyancy mechanism
Topic: Fat malabsorption (steatorrhea) and undigested fat accumulation

Query 3: High-fiber diet bacterial fermentation gas production stool buoyancy
Topic: High-fiber diet effects on bacterial fermentation and gas production

Query 4: Pathological floating stool diagnostic criteria symptom clusters medical evaluation
Topic: Differentiation between normal and concerning floating stool

Site: https://www.bbc.com/future/article/20231221-why-does-your-poop-float-it-might-be-down-to-your-gut-health

Tokens: 2267

Search query: Gas content primary factor stool buoyancy degassed weight studies

Skip to content Home News Israel-Gaza War War in Ukraine US & Canada UK UK Politics England N. Ireland N. Ireland Politics Scotland Scotland Politics Wales Wales Politics Africa Asia China India Australia Europe Latin America Middle East In Pictures BBC InDepth BBC Verify Sport Business Executive Lounge Technology of Business Future of Business Innovation Watch Documentaries Technology Science & Health Artificial Intelligence AI v the Mind Culture Watch Documentaries Film & TV Music Art & Design Style Books Entertainment News Arts Watch Documentaries Arts in Motion Travel Watch Documentaries Destinations Africa Antarctica Asia Australia and Pacific Caribbean & Bermuda Central America Europe Middle East North America South America World’s Table Culture & Experiences Adventures The SpeciaList Earth Watch Documentaries Natural Wonders Weather & Science Climate Solutions Sustainable Business Green Living Audio Podcast Categories Radio Audio FAQs Video Watch Documentaries BBC Maestro Live Live News Live Sport Documentaries Home News Sport Business Innovation Culture Arts Travel Earth Audio Video Live Documentaries Weather Newsletters Watch Live Why does your poo sometimes float? It might be down to your gut health 26 December 2023 Share Save Richard Gray Share Save Getty Images The reason your poo sometimes floats is down to the make-up of bacteria inside your guts (Credit: Getty Images) The mystery of why our number twos sometimes bob to the surface of the toilet water while others sink without trace has been solved – and it could be a window into the health of the bacteria living in our guts. Before we dive in, Nagarajan Kannan has a question: “Are you a floater or a sinker?” It’s a surprisingly intimate thing to ask someone you’ve only exchanged emails with, but it is exactly this line of thinking that has led to something of a passion project for the director of the Mayo Clinic’s stem cell and cancer biology laboratory in Rochester, Minnesota. Most of his day job is spent studying the cellular and molecular mechanisms that lead to breast cancer. But during rare idle moments, Kannan has found himself wrestling with another puzzle – why do faeces sometimes float. Most of us have probably experienced it at some point: the poo that simply refuses to flush, bobbing around on the surface of the water like an incriminating brown buoyancy aid. At other times, however, our number twos simply sink without trace. A mystery indeed. The answer to this scatological conundrum, however, offers some surprising insights about what is going on inside our bodies and the health of the microbes that live there, Kannan believes. It had initially been thought that the reason for the occasional floating unmentionable was something to do with the levels of fat that made their way into it . But in the early 1970s a couple of gastroenterologists at the University of Minnesota with time on their hands decided to put it to the test with a series of experiments. After subjecting the excrement from 39 volunteers – and some of their own solid waste for good measure – to a barrage of tests, the answer they came up with was that it was not fat, but gas . More precisely the amount of gas found within a stool can vary to such degrees that they can either float to the surface or sink like a brick (along with a fair bit of mid-bowl drifting in-between). If the gas in a floater was compressed out, the researchers discovered, they would sink. Could our ‘number twos’ be the answer to some of the world’s biggest problems? The reason for the difference, they concluded, was too much methane production. In other words, excessive flatulence. And this is where Kannan enters the increasingly whiffy arena. In the intervening years, medical science has revealed the enormous role that our microbiota play in many aspects of our health – from obesity to heart disease . Kannan suspected that changes in the make up of the 100 trillion bacteria, fungi and other microorganisms that ca…

Site: https://www.ncbi.nlm.nih.gov/books/NBK541055/

Tokens: 2863

Search query: Steatorrhea undigested fat malabsorption stool buoyancy mechanism

Warning: The NCBI web site requires JavaScript to function. more… The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Bookshelf Search database Books All Databases Assembly Biocollections BioProject BioSample Books ClinVar Conserved Domains dbGaP dbVar Gene Genome GEO DataSets GEO Profiles GTR Identical Protein Groups MedGen MeSH NLM Catalog Nucleotide OMIM PMC Protein Protein Clusters Protein Family Models PubChem BioAssay PubChem Compound PubChem Substance PubMed SNP SRA Structure Taxonomy ToolKit ToolKitAll ToolKitBookgh Search term Search Browse Titles Advanced Help Disclaimer –> NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. StatPearls [Internet]. Show details Treasure Island (FL): StatPearls Publishing ; 2025 Jan-. Search term Steatorrhea Samy A. Azer ; Senthilkumar Sankararaman . Author Information and Affiliations Authors Samy A. Azer 1 ; Senthilkumar Sankararaman 2 . Affiliations 1 King Saud University, King Khalid UH 2 University Hospitals Rainbow Babies & Children’s Hospital, Cleveland Last Update: May 16, 2023 . Continuing Education Activity The management of steatorrhea is complex and new approaches have been introduced. To achieve satisfactory outcomes, the basic and clinical aspects of steatorrhea must be clearly defined. This activity reviews the evaluation and management of steatorrhea and highlights the role of the interprofessional team in evaluating and improving care for patients suffering from steatorrhea. Objectives: Identify the etiology of steatorrhea. Describe the clinical features of steatorrhea. Review the management of steatorrhea. Identify interprofessional team strategies for improving care coordination and outcomes in patients suffering from steatorrhea. Access free multiple choice questions on this topic. Introduction The definition of steatorrhea is an increase in fat excretion in the stools. Steatorrhea is one of the clinical features of fat malabsorption and noted in many conditions such as exocrine pancreatic insufficiency (EPI), celiac disease, and tropical sprue. An increase in the fat content of stools results in the production of pale, large volume, malodorous, loose stools. Screening for steatorrhea may be carried out by examining stool samples for the presence of fat by Sudan III staining. However, quantitative fecal fat estimation is required to confirm the diagnosis. Among the macronutrients, digestion and absorption of fat involve a complex mechanism. Fat absorption requires bile acids, digestive enzymes, and a normally functioning small intestinal mucosa. Dietary lipids, mostly as triacylglycerols, are initially emulsified by bile acids and then hydrolyzed by the pancreatic lipases and colipases into free fatty acids and monoglycerides. In the proximal small bowel, these hydrolyzed lipids form micelles by the action of bile acids. The micelles are then absorbed across the intestinal villi and transported as chylomicrons via the intestinal lymphatics. Therefore, any defects in the availability or function of bile acids, pancreatic digestive enzymes, or absorptive villi will lead to steatorrhea. [1] Etiology The causes of steatorrhea are numerous and subclassified under three broad categories: Conditions leading to exocrine pancreatic insufficiency (EPI) Bile acid deficiency states Diseases affecting the small intestine. Most notable disorders in each category are given below [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] : EPI due to chronic pancreatitis, cystic fibrosis (CF), and conditions resulting in pancreat…

Site: https://seed.com/cultured/what-does-your-poop-say-about-you/

Tokens: 2982

Search query: High-fiber diet bacterial fermentation gas production stool buoyancy

Share How To Read Your Poop (And Why You Should) The ultimate defecation decoder: Learn how to read the information hidden in plain sight in your poop to gauge the state of your diet, stress levels, digestive functioning, and more. 11 minutes 39 Citations Share By the time poop makes a touchdown in your toilet, it’s had to maneuver 20-30 feet of the intestinal tract, face liters of highly acidic juice in the stomach, and traverse up to 100 trillion bacterial cells in the gut. 1 , 2 , 3 Its shape, color, size, consistency, and odor can tell you a lot about the status of all these biological touchpoints and then some. Stool is a vital diagnostic tool that gets delivered right to us multiple times a week. But it’s up to us to interpret it before we flush. Ready to decode your defecation? Here’s how to scan your poop’s shape, color, size, and more for clues about your digestive health. Consistency and Shape Your stool is around 75% water and 25% solid waste (primarily undigested plant fibers but also fats, proteins, mucus, bile, and microbial matter). 4 So, its appearance on any given day can tell you quite a bit about whether you’re drinking enough water or consuming enough nutrient-dense foods. Consulting the Bristol Stool chart can give you a quick read on the composition and consistency of your stool. 5 Developed in 1997 and now used in clinical and research settings around the world, the chart classifies human poop into seven categories: TYPE 1: Separate hard lumps TYPE 2: Lumpy and sausage-like TYPE 3: Sausage shape with cracks TYPE 4: Smooth, soft sausage shape TYPE 5: Soft blobs with clear edges TYPE 6: Mushy consistency TYPE 7: Liquid consistency Your stool type can change by the week and in some cases, by the day. Here’s how to interpret all seven: Types 1 and 2: Lacking in liquid If your stools appear lumpy, dry, and sausage-like, or small and hard like pebbles, it could be a sign that your GI system is clogged. During digestion, the intestines remove excess water and nutrients from your stool before it makes its way out. If your stool is sitting in the colon for a long time , it may lose too much water and become dry and difficult to pass. Here are a few ways you can loosen up those harder BMs: Drink more water Up your fiber intake Exercise and walk after meals Types 3, 4, and 5: The superstars of stool Sausage or snake-like in shape, stool types 3, 4, and 5 are not watery or dry, and they’re expelled easily without strain. If you spot one of these in the bowl, keep doing what you’re doing! Types 6 and 7: Need time to tighten up If your stools have a mushy or liquid texture, it’s a sign that your colon is not extracting enough water from your food. (This likely means you’re not absorbing proper nutrients from your food, either). 4 , 6 Loose stools can happen when digested food material doesn’t spend enough time in the GI tract. They can also occur if something you eat draws water into the colon. Gluten and lactose are common culprits, particularly in people with food intolerances. 4 Here are a few ways to slow things down and bulk things up if you’ve just passed a 6 or 7: Drink more water Up your fiber intake If loose stools are recurring, get tested for food intolerances Probiotics for all Research suggests that if you tend to fall on either end of the Bristol Stool chart, taking a probiotic may help you return to middle ground. Having a diverse, microbe-rich gut environment has been strongly associated with firmer stools. Translation: Those with types 6 or 7 may benefit from a daily probiotic. 7 Conversely, if your stools are firm and difficult to pass (types 1 or 2), taking a probiotic can deliver the specific types of bacteria you need to get things moving. Certain probiotic strains produce short-chain fatty acids (SCFAs) that support mucus production and strengthen the gut lining, and other responses that help stool move through the body more quickly and efficiently. 8 Case in point: In a double-blind, randomized,…

Site: https://www.ncbi.nlm.nih.gov/books/NBK553106/

Tokens: 2789

Search query: Pathological floating stool diagnostic criteria symptom clusters medical evaluation

Warning: The NCBI web site requires JavaScript to function. more… The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Bookshelf Search database Books All Databases Assembly Biocollections BioProject BioSample Books ClinVar Conserved Domains dbGaP dbVar Gene Genome GEO DataSets GEO Profiles GTR Identical Protein Groups MedGen MeSH NLM Catalog Nucleotide OMIM PMC Protein Protein Clusters Protein Family Models PubChem BioAssay PubChem Compound PubChem Substance PubMed SNP SRA Structure Taxonomy ToolKit ToolKitAll ToolKitBookgh Search term Search Browse Titles Advanced Help Disclaimer –> NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. StatPearls [Internet]. Show details Treasure Island (FL): StatPearls Publishing ; 2025 Jan-. Search term Malabsorption Syndromes Tyesha Zuvarox ; Eric Goosenberg ; Chris Belletieri . Author Information and Affiliations Authors Tyesha Zuvarox 1 ; Eric Goosenberg 2 ; Chris Belletieri . Affiliations 1 Lower Bucks Hospital 2 Temple University School of Medicine Last Update: July 7, 2025 . Continuing Education Activity Malabsorption syndromes encompass a wide spectrum of conditions resulting from impaired digestion or absorption of essential nutrients. Dysfunction in any of the key phases of absorption—luminal, mucosal, and postabsorptive—results in common malabsorption disorders such as fat malabsorption, exocrine pancreatic insufficiency, bile acid malabsorption, celiac disease, and conditions affecting intestinal lymphatic flow. This activity provides clinicians with a in-depth review of the gastrointestinal mechanisms involved in nutrient assimilation, highlighting the interdependent processes of digestion and absorption. The course outlines pediatric-specific conditions, congenital malabsorption disorders, and the systemic implications of vitamin and mineral deficiencies, as well as, differentiating malabsorption from maldigestion and selecting appropriate diagnostic studies based on clinical presentation. By examining diverse causes—from enzymatic defects to mucosal injury and anatomical disruptions—clinicians will be better equipped to diagnose, manage, and coordinate care for patients with nutrient absorption disorders. This activity for healthcare professionals is designed to enhance the learner’s competence in identifying malabsorption syndromes, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing these conditions to improve patient outcomes and quality of life. Objectives: Identify the clinical features of malabsorption syndromes. Determine the appropriate evaluation to diagnose malabsorption syndromes accurately. Assess the management approaches available for malabsorption syndromes. Apply interprofessional team strategies to improve care coordination and outcomes for patients with malabsorption syndrome. Access free multiple choice questions on this topic. Introduction The gastrointestinal tract plays a crucial role in absorbing essential nutrients, including fats, carbohydrates, proteins, vitamins, minerals, and trace elements. Malabsorption refers to impaired nutrient absorption at any point where nutrients are absorbed, and maldigestion refers to impaired nutrient digestion within the intestinal lumen or at the intestinal brush border. Although malabsorption and maldigestion differ, digestion and absorption are interdependent, and the term “malabsorption” often refers to either process of this interdependence. Malabsorption can arise from any defect in the d…

Research Analysis (Cycle 2)

This cycle confirmed that gas content from bacterial fermentation is the primary factor in stool buoyancy, as explicitly stated in Result 1. The results validated that high-fiber diets and gut bacteria directly impact gas production affecting buoyancy. Steatorrhea’s role in buoyancy was supported by Result 2. Result 3 provided detailed stool composition data (75% water, 25% solid) and introduced the Bristol Stool Chart as a classification system. However, the results lack specific diagnostic criteria for pathological floating stool and detailed physical principles explaining buoyancy. New topics about gut bacteria composition and stool composition percentages emerged as critical factors in understanding why poop floats.

Topics Completed:
✓ Stool consistency patterns (bulky, loose, difficult to flush)
✓ Gas content as primary factor in buoyancy (degassed stool weight studies)
✓ High-fiber diet effects on bacterial fermentation and gas production
✓ Fat content contribution to buoyancy in steatorrhea cases

Topics Partially Addressed:
⚪ Density comparison between stool and water
⚪ Physical principles of stool buoyancy
⚪ Diagnostic evaluation methods for floating stool
⚪ Pathophysiological mechanisms of malabsorption
⚪ Differentiation between normal and concerning floating stool
…and 4 more

New Topics Discovered:

• Gut bacteria composition as primary factor in stool buoyancy
• Bristol Stool Chart classification system for stool consistency
• Stool composition (75% water, 25% solid waste) and its implications

Remaining Topics:
□ Pancreatic enzyme secretion and function in nutrient breakdown
□ Carbonated beverages and air swallowing mechanisms
□ Density comparison between stool and water
□ Dietary factors influencing stool buoyancy
□ Physical principles of stool buoyancy
…and 29 more

Research Cycle 3: Search Queries

Query 1: Stool specific gravity measurement water displacement buoyancy principles
Topic: Density comparison between stool and water

Query 2: Exocrine pancreatic insufficiency enzyme secretion stool density correlation
Topic: Pancreatic enzyme secretion and function in nutrient breakdown

Query 3: Fecal fat analysis 72-hour collection buoyancy clinical correlation
Topic: Fecal fat analysis and 72-hour stool collection protocols

Query 4: Pancreatic liver disorders floating stool pathological differentiation criteria
Topic: Differentiation between normal and concerning floating stool

Site: https://courses.lumenlearning.com/suny-physics/chapter/11-7-archimedes-principle/

Tokens: 2697

Search query: Stool specific gravity measurement water displacement buoyancy principles

Archimedes’ Principle Learning Objectives By the end of this section, you will be able to: Define buoyant force. State Archimedes’ principle. Understand why objects float or sink. Understand the relationship between density and Archimedes’ principle. When you rise from lounging in a warm bath, your arms feel strangely heavy. This is because you no longer have the buoyant support of the water. Where does this buoyant force come from? Why is it that some things float and others do not? Do objects that sink get any support at all from the fluid? Is your body buoyed by the atmosphere, or are only helium balloons affected? (See Figure 1.) Figure 1. (a) Even objects that sink, like this anchor, are partly supported by water when submerged. (b) Submarines have adjustable density (ballast tanks) so that they may float or sink as desired. (credit: Allied Navy) (c) Helium-filled balloons tug upward on their strings, demonstrating air’s buoyant effect. (credit: Crystl) Answers to all these questions, and many others, are based on the fact that pressure increases with depth in a fluid. This means that the upward force on the bottom of an object in a fluid is greater than the downward force on the top of the object. There is a net upward, or buoyant force on any object in any fluid. (See Figure 2.) If the buoyant force is greater than the object’s weight, the object will rise to the surface and float. If the buoyant force is less than the object’s weight, the object will sink. If the buoyant force equals the object’s weight, the object will remain suspended at that depth. The buoyant force is always present whether the object floats, sinks, or is suspended in a fluid. Buoyant Force The buoyant force is the net upward force on any object in any fluid. Figure 2. Pressure due to the weight of a fluid increases with depth since P = hρg . This pressure and associated upward force on the bottom of the cylinder are greater than the downward force on the top of the cylinder. Their difference is the buoyant force F B . (Horizontal forces cancel.) Just how great is this buoyant force? To answer this question, think about what happens when a submerged object is removed from a fluid, as in Figure 3. Figure 3. (a) An object submerged in a fluid experiences a buoyant force F B . If F B is greater than the weight of the object, the object will rise. If F B is less than the weight of the object, the object will sink. (b) If the object is removed, it is replaced by fluid having weight w fl . Since this weight is supported by surrounding fluid, the buoyant force must equal the weight of the fluid displaced. That is, F B = w fl ,a statement of Archimedes’ principle. The space it occupied is filled by fluid having a weight w fl . This weight is supported by the surrounding fluid, and so the buoyant force must equal w fl , the weight of the fluid displaced by the object. It is a tribute to the genius of the Greek mathematician and inventor Archimedes (ca. 287–212 B. C.) that he stated this principle long before concepts of force were well established. Stated in words, Archimedes’ principle is as follows: The buoyant force on an object equals the weight of the fluid it displaces. In equation form, Archimedes’ principle is F B = w fl , where F B is the buoyant force and w fl is the weight of the fluid displaced by the object. Archimedes’ principle is valid in general, for any object in any fluid, whether partially or totally submerged. Archimedes’ Principle According to this principle the buoyant force on an object equals the weight of the fluid it displaces. In equation form, Archimedes’ principle is F B = w fl , where F B is the buoyant force and w fl is the weight of the fluid displaced by the object. Humm … High-tech body swimsuits were introduced in 2008 in preparation for the Beijing Olympics. One concern (and international rule) was that these suits should not provide any buoyancy advantage. How do you think that this rule could be verified? Making Connec…

Site: https://pmc.ncbi.nlm.nih.gov/articles/PMC6432881/

Tokens: 2792

Search query: Exocrine pancreatic insufficiency enzyme secretion stool density correlation

Note: This result was initially filtered but is used as a fallback.

Skip to main content Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( Lock Locked padlock icon ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites. Search PMC Full-Text Archive Search in PMC Journal List User Guide New Try this search in PMC Beta Search PERMALINK Copy As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice Clin Exp Gastroenterol . 2019 Mar 21;12:129–139. doi: 10.2147/CEG. S168266 Exocrine pancreatic insufficiency: prevalence, diagnosis, and management Gabriele Capurso Gabriele Capurso 1 Pancreato-Biliary Endoscopy and Endosonography Division, Pancreas Translational and Clinical Research Centre, San Raffaele Scientific Institute, Vita Salute San Raffaele University, Milan, Italy, capurso.gabriele@hsr.it Find articles by Gabriele Capurso 1, ✉ , Mariaemilia Traini Mariaemilia Traini 1 Pancreato-Biliary Endoscopy and Endosonography Division, Pancreas Translational and Clinical Research Centre, San Raffaele Scientific Institute, Vita Salute San Raffaele University, Milan, Italy, capurso.gabriele@hsr.it Find articles by Mariaemilia Traini 1 , Matteo Piciucchi Matteo Piciucchi 2 Digestive and Liver Disease Unit, Sant’Andrea Hospital, Sapienza University, Rome, Italy Find articles by Matteo Piciucchi 2 , Marianna Signoretti Marianna Signoretti 2 Digestive and Liver Disease Unit, Sant’Andrea Hospital, Sapienza University, Rome, Italy Find articles by Marianna Signoretti 2 , Paolo Giorgio Arcidiacono Paolo Giorgio Arcidiacono 1 Pancreato-Biliary Endoscopy and Endosonography Division, Pancreas Translational and Clinical Research Centre, San Raffaele Scientific Institute, Vita Salute San Raffaele University, Milan, Italy, capurso.gabriele@hsr.it Find articles by Paolo Giorgio Arcidiacono 1 Author information Article notes Copyright and License information 1 Pancreato-Biliary Endoscopy and Endosonography Division, Pancreas Translational and Clinical Research Centre, San Raffaele Scientific Institute, Vita Salute San Raffaele University, Milan, Italy, capurso.gabriele@hsr.it 2 Digestive and Liver Disease Unit, Sant’Andrea Hospital, Sapienza University, Rome, Italy ✉ Correspondence: Gabriele Capurso, Pancreato-Biliary Endoscopy and Endosonography Division, Pancreas Translational and Clinical Research Centre, San Raffaele Scientific Institute, Vita Salute San Raffaele University, IRCCS, Via Olgettina 60, 20132 Milan, Italy, Tel +39 02 2643 6548, E-mail capurso.gabriele@hsr.it Collection date 2019. © 2019 Capurso et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/ ). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. PMC Copyright notice PMCID: PMC6432881 PMID: 30962702 Abstract Exocrine pancreatic insufficiency (EPI) is a condition caused by reduced or inappropriate secretion or activity of pancreatic juice and its digestive enzymes, pancreatic lipase in particular. EPI can result in clinical manifestation and biochemical alterations causing reduced quality of life and life-threating complications. EPI is common in pancreatic disorders, where it should be suspected and actively investigated, and in many extrapancreatic conditions. There are various tests available to diagnose EPI, with indirect, noninvasive ones, such as concentration of fecal elastase being more commonly emp…

Site: https://ltd.aruplab.com/Tests/Pub/2002356

Tokens: 2631

Search query: Fecal fat analysis 72-hour collection buoyancy clinical correlation

Skip to main content News Careers Contact Us | Connect Sign In News Careers Contact Us Testing Test Directory Test Updates Clinical Decision Support | ARUP Consult ® Resources Featured Test Categories Search Our Test Directory Search Search our extensive Laboratory Test Directory to find test codes, ordering recommendations, specimen stability information, Test Fact Sheets, and more. Changes and New Tests Explore the most recent updates to our Laboratory Test Directory in one convenient location. Review important information about upcoming or current Hotlines, CPT code changes, new tests, and immediate activations. Test Resources Find general guidance on ARUP specimen preparation and handling, specimen transportation, test turnaround times, critical alerts, billing practices, patient forms, and more. Changes and New Tests Explore the most recent updates to our Laboratory Test Directory in one convenient location. Review important information about upcoming or current Hotlines, CPT code changes, new tests, and immediate activations. CPT Code Updates Find information about our annual and biweekly updates to CPT codes. Test Resources Find general guidance on ARUP specimen preparation and handling, specimen transportation, test turnaround times, critical alerts, billing practices, patient forms, and more. Performed/Reported Find information about updates to the Performed schedule and the Reported turnaround time. ARUP Consult ® Our clinical decision support resource, ARUP Consult, empowers clinicians with robust information, algorithms, and tools for informed patient care decisions. Choose the Right Test Testing Algorithms Test Fact Sheets Test Resources Find specimen instructions, test turnaround times, patient forms, test codes, and more. Specimen Handling CPT Codes Z-Codes LOINC Codes Test Turnaround Time and Contingency Plan Critical Values and Urgent Notifications View All Test Resources Comprehensive Diagnostic Solutions Discover the benefits of our testing for each featured test category. Explore highlighted updates, articles, video spotlights, and more. This section highlights our specialized offerings and is separate from our Laboratory Test Directory. Autoimmune Neurologic Disease Genetics Hematopathology Infectious Disease View All Search the Laboratory Test Directory Clinical Decision Support | ARUP Consult ® Services Healthcare Advisory Services Drug and Clinical Research Services Research and Innovation Tailored Solutions and Advisory Services Optimize your laboratory by partnering with ARUP Healthcare Advisory Services. Discover our solutions, including process streamlining, outreach business planning, laboratory stewardship, and more. Laboratory Outreach Solutions and Business Planning Workflow Solutions and Space Planning Laboratory and Pharmacy Stewardship Solutions Laboratory Analytics and Reporting Tools | ARUP AnalyticsDx TM View All Advisory Services For Researchers: Clinical Research Services Our team of experienced project managers is available to assist you in companion diagnostic development, clinical trial studies, academic research, and expert pathology review. Clinical and Academic Research Our Clinical Trials group supports a variety of research efforts, including academic research initiatives, and serves clients from central laboratories, clinical research organizations (CROs), in vitro device (IVD) manufacturers, and more. Discover all of our services. Pharmaceutical Services ARUP offers companion diagnostics and central pathology review services as part of our comprehensive pharmaceutical services. Explore our capabilities and more. View All Clinical Research Services ARUP Institute for Research and Innovation in Diagnostic and Precision Medicine™ We accelerate the development and adoption of cutting-edge diagnostic and prognostic technologies advancing patient care through groundbreaking science and engineering. The Sherrie Perkins Research and Innovation Collaboration Grant The Sherrie Perkins Re…

Site: https://www.ncbi.nlm.nih.gov/sites/books/NBK553106/

Tokens: 2789

Search query: Pancreatic liver disorders floating stool pathological differentiation criteria

Warning: The NCBI web site requires JavaScript to function. more… The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Bookshelf Search database Books All Databases Assembly Biocollections BioProject BioSample Books ClinVar Conserved Domains dbGaP dbVar Gene Genome GEO DataSets GEO Profiles GTR Identical Protein Groups MedGen MeSH NLM Catalog Nucleotide OMIM PMC Protein Protein Clusters Protein Family Models PubChem BioAssay PubChem Compound PubChem Substance PubMed SNP SRA Structure Taxonomy ToolKit ToolKitAll ToolKitBookgh Search term Search Browse Titles Advanced Help Disclaimer –> NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. StatPearls [Internet]. Show details Treasure Island (FL): StatPearls Publishing ; 2025 Jan-. Search term Malabsorption Syndromes Tyesha Zuvarox ; Eric Goosenberg ; Chris Belletieri . Author Information and Affiliations Authors Tyesha Zuvarox 1 ; Eric Goosenberg 2 ; Chris Belletieri . Affiliations 1 Lower Bucks Hospital 2 Temple University School of Medicine Last Update: July 7, 2025 . Continuing Education Activity Malabsorption syndromes encompass a wide spectrum of conditions resulting from impaired digestion or absorption of essential nutrients. Dysfunction in any of the key phases of absorption—luminal, mucosal, and postabsorptive—results in common malabsorption disorders such as fat malabsorption, exocrine pancreatic insufficiency, bile acid malabsorption, celiac disease, and conditions affecting intestinal lymphatic flow. This activity provides clinicians with a in-depth review of the gastrointestinal mechanisms involved in nutrient assimilation, highlighting the interdependent processes of digestion and absorption. The course outlines pediatric-specific conditions, congenital malabsorption disorders, and the systemic implications of vitamin and mineral deficiencies, as well as, differentiating malabsorption from maldigestion and selecting appropriate diagnostic studies based on clinical presentation. By examining diverse causes—from enzymatic defects to mucosal injury and anatomical disruptions—clinicians will be better equipped to diagnose, manage, and coordinate care for patients with nutrient absorption disorders. This activity for healthcare professionals is designed to enhance the learner’s competence in identifying malabsorption syndromes, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing these conditions to improve patient outcomes and quality of life. Objectives: Identify the clinical features of malabsorption syndromes. Determine the appropriate evaluation to diagnose malabsorption syndromes accurately. Assess the management approaches available for malabsorption syndromes. Apply interprofessional team strategies to improve care coordination and outcomes for patients with malabsorption syndrome. Access free multiple choice questions on this topic. Introduction The gastrointestinal tract plays a crucial role in absorbing essential nutrients, including fats, carbohydrates, proteins, vitamins, minerals, and trace elements. Malabsorption refers to impaired nutrient absorption at any point where nutrients are absorbed, and maldigestion refers to impaired nutrient digestion within the intestinal lumen or at the intestinal brush border. Although malabsorption and maldigestion differ, digestion and absorption are interdependent, and the term “malabsorption” often refers to either process of this interdependence. Malabsorption can arise from any defect in the d…

Research Analysis (Cycle 3)

This cycle confirmed the physical basis of stool buoyancy through Archimedes’ principle (Result 1), establishing that stool floats when its density is less than water’s density (1 g/mL). Result 3 provided detailed clinical protocols for fecal fat analysis, while Result 4 offered context on malabsorption syndromes affecting stool density. Result 2 was minimally informative. We determined carbonated beverages and air swallowing are irrelevant as swallowed air rarely reaches the colon in significant amounts, and the D-xylose test is too specific to directly relate to buoyancy mechanisms. The physical principles are now well-understood, shifting focus toward clinical differentiation of pathological causes.

Topics Completed:
✓ Density comparison between stool and water
✓ Physical principles of stool buoyancy
✓ Gut bacteria composition as primary factor in stool buoyancy
✓ Relationship between stool composition and water displacement
✓ Stool composition (75% water, 25% solid waste) and its implications
✓ Fecal fat analysis and 72-hour stool collection protocols
✓ Fat content contribution to buoyancy in steatorrhea cases
✓ Stool consistency patterns (bulky, loose, difficult to flush)
✓ Gas content as primary factor in buoyancy (degassed stool weight studies)
✓ High-fiber diet effects on bacterial fermentation and gas production
✓ Bristol Stool Chart classification system for stool consistency

Topics Partially Addressed:
⚪ Pancreatic enzyme secretion and function in nutrient breakdown
⚪ Dietary factors influencing stool buoyancy
⚪ Carbohydrate malabsorption processes (lactose, fructose, starch)
⚪ Specific gas-producing foods (beans, broccoli, cauliflower, cabbage, onions, bran)
⚪ Diagnostic evaluation methods for floating stool
…and 20 more

Irrelevant/Distraction Topics:
✗ Carbonated beverages and air swallowing mechanisms
✗ D-xylose test for intestinal absorption assessment

Remaining Topics:
□ Pancreatic enzyme secretion and function in nutrient breakdown
□ Dietary factors influencing stool buoyancy
□ Carbohydrate malabsorption processes (lactose, fructose, starch)
□ Specific gas-producing foods (beans, broccoli, cauliflower, cabbage, onions, bran)
□ Diagnostic evaluation methods for floating stool
…and 20 more

Research Cycle 4: Search Queries

Query 1: Lactose fructose malabsorption gas production stool buoyancy specific foods
Topic: Carbohydrate malabsorption processes and gas-producing foods

Query 2: Primary care floating stool evaluation algorithm pathological symptom clusters
Topic: Diagnostic evaluation methods for floating stool

Query 3: Bile acid malabsorption steatorrhea stool buoyancy pathophysiology presentation
Topic: Liver and biliary system diseases related to floating stool

Query 4: Celiac Crohn’s disease floating stool malabsorption differentiation approach
Topic: Small intestine disorders and pathological floating stool differentiation

Site: https://www.health.com/condition/digestive-health/what-does-it-mean-when-your-poop-floats

Tokens: 2206

Search query: Lactose fructose malabsorption gas production stool buoyancy specific foods

–> ​ Ad Why Does Poop Float? What It Could Say About Your Health By Maxine Lipner Maxine Lipner Maxine Lipner is a veteran health and medical journalist with more than 30 years of experience contributing to magazines and medical trade journals. As a health writer, Maxine strives to provide the latest information on medical breakthroughs and health trends in a reader-friendly way. health’s editorial guidelines Updated on June 13, 2025 Medically reviewed by Qin Rao, MD Medically reviewed by Qin Rao, MD Qin Rao, MD, is a board-certified physician based in New York City. He currently works as a gastroenterologist and hepatologist at Manhattan Gastroenterology. learn more Follow Us On In This Article View All In This Article Floating vs. Sinking Common Causes Conditions Treatment Prevention When To Seek Care FAQs Jonathan Kirn / Getty Images Poop can float due to eating foods that produce a lot of gas or a condition that causes malabsorption. Your stool absorbs gas or fats, which causes it to float. Floating poop is generally not cause for concern. A healthcare provider can diagnose any underlying causes. Should My Poop Float or Sink? You will usually see poop sink to the bottom of the toilet, but it is normal for poop to float every now and then. Floating poop is often a sign of excess gas or dietary changes. Stools that float are sometimes a sign of an infection or a condition. Common Causes of Floating Poop Poop may float for a few reasons. Some of these causes may work together or separately to cause floating poop. Excess Gas Extra gas can end up in the digestive tract if you swallow too much air, known as aerophagia. The swallowed air may come from consuming drinks with fizz or chewing gum. Fiber Fiber will pass through the small intestine undigested and into the large intestine (colon), where bacteria break it down. Gasses are released into the colon and can get trapped inside stools, which makes them buoyant. High-fiber foods include: Beans, peas, and lentils Cruciferous vegetables, like broccoli and collard greens Fruits, such as apples and pears Whole grains High Fat Content Floating poop may indicate steatorrhea (oily stool). Your stool may also be large, pale, and have an unpleasant odor. Eating fatty foods or conditions that affect fat digestion cause steatorrhea. Even a tiny amount of fat you eat could end up in your poop due to malabsorption. Sugar Intolerances People with certain intolerances cannot digest sugars, which may cause extra gas in the colon. Common sugar intolerances include: Fructose: Found in fruits and juices Lactose: Found in milk, ice cream, yogurt, and cheese Sorbitol: Found in “sugar-free” items, such as chewing gum Conditions That Affect Digestion and Absorption Some conditions may cause your poop to float, such as bile duct blockages, celiac disease, or those that affect the pancreas. Bile Acid-Related Conditions Without enough bile to break down food, extra fat ends up in your stools and causes them to float. Conditions that may reduce the amount of bile include: Gallbladder removal: Changes in bile production and fat absorption may lead to diarrhea and floating poop Gallstones: Hardened deposits of bile that build up in the gallbladder Liver failure: May cause decreased bile production Primary sclerosing cholangitis: Can cause scarring and block the liver, which produces bile Bile Duct Blockages Conditions that block the bile duct may allow fat to build up and cause your poop to float. Bile duct blockages may cause a build-up of bilirubin, or dark yellow-brown substance in bile. High bilirubin levels may cause jaundice , or yellowing of the skin and eyes. Celiac Disease Celiac disease damages the small intestine in response to gluten . This condition can lower the small intestine’s ability to absorb fats and other nutrients. Crohn’s Disease Crohn’s disease is a type of inflammatory bowel disease (IBD) that causes inflammation of the digestive tract. It may cause malabsorption, which can lead t…

Site: https://pubmed.ncbi.nlm.nih.gov/22356614/

Tokens: 1989

Search query: Primary care floating stool evaluation algorithm pathological symptom clusters

Note: This result was initially filtered but is used as a fallback.

This site needs JavaScript to work properly. Please enable it to take advantage of the complete set of features! Clipboard, Search History, and several other advanced features are temporarily unavailable. Skip to main page content The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Search: Search Advanced Clipboard User Guide Save Email Send to Clipboard My Bibliography Collections Citation manager Display options Display options Format Abstract PubMed PMID Save citation to file Format: Summary (text) PubMed PMID Abstract (text) CSV Create file Cancel Email citation Subject: 1 selected item: 22356614 – PubMed To: From: Format: Summary Summary (text) Abstract Abstract (text) MeSH and other data Send email Cancel Add to Collections Create a new collection Add to an existing collection Name your collection: \/]” title=”The following characters are not allowed in the Name field: “&= /” maxlength=”100″ data-ga-category=”save_share” data-ga-action=”create_collection” data-ga-label=”non_favorties_collection”> Name must be less than 100 characters Choose a collection: Unable to load your collection due to an error Please try again Add Cancel Add to My Bibliography My Bibliography Unable to load your delegates due to an error Please try again Add Cancel Your saved search Name of saved search: \/]” title=”The following characters are not allowed in the Name field: “&= /”> Search terms: Test search terms Would you like email updates of new search results? Saved Search Alert Radio Buttons Yes No Email: ( change ) Frequency: Monthly Weekly Daily Which day? The first Sunday The first Monday The first Tuesday The first Wednesday The first Thursday The first Friday The first Saturday The first day The first weekday Which day? Sunday Monday Tuesday Wednesday Thursday Friday Saturday Report format: Summary Summary (text) Abstract Abstract (text) PubMed Send at most: 1 item 5 items 10 items 20 items 50 items 100 items 200 items Send even when there aren’t any new results Optional text in email: Save Cancel Create a file for external citation management software Create file Cancel Your RSS Feed Name of RSS Feed: \/]” title=”The following characters are not allowed in the Name field: “&= /”> Number of items displayed: 5 10 15 20 50 100 Create RSS Cancel RSS Link Copy Full text links Wiley Full text links Actions Cite Collections Add to Collections Create a new collection Add to an existing collection Name your collection: \/]” title=”The following characters are not allowed in the Name field: “&= /” maxlength=”100″ data-ga-category=”collections_button” data-ga-action=”create_collection” data-ga-label=”non_favorties_collection”> Name must be less than 100 characters Choose a collection: Unable to load your collection due to an error Please try again Add Cancel Display options Display options Format Abstract PubMed PMID Share Permalink Copy Full text links Cite Display options Display options Format Abstract PubMed PMID Abstract Background: Current diagnostic criteria for functional gut disorder are based on symptom clusters observed after sporadic onset. It remains unclear whether symptoms group similarly in functional disorders of postinfectious etiology. We utilized observational data from the Walkerton Health Study (WHS) to: (i) determine groupings of functional gastrointestinal symptoms among patients exposed to acute gastroenteritis (GE), and (ii) assess the stability of these symptoms grouping over time. Methods: WHS participants 16 years of age and older at the time of the outbreak were included, if they had completed a modified Talley’s Bowel Disease Questionnaire (BDQ) and responded ‘yes’…

Site: https://www.ncbi.nlm.nih.gov/books/NBK541055/

Tokens: 2295

Search query: Bile acid malabsorption steatorrhea stool buoyancy pathophysiology presentation

Note: This result was initially filtered but is used as a fallback.

Dietary counseling should be done by nutritionist regarding intake of fat and fat-soluble vitamins. It was advised earlier to decrease fat intake in patients with exocrine pancreatic insufficiency that helps in decreasing stool volume but it has been found that it causes malnutrition. So normal to high-fat diet with pancreatic enzyme replacement is advised in such patients. Similarly, dietary counseling in patients with celiac disease is essential. Pearls and Other Issues Untreated steatorrhea leads to malnutrition and other complications such as fat-soluble vitamin deficiencies (A, D, E, and K). Identifying the cause of steatorrhea is vital for proper management and prevention of these complications. [31] Enhancing Healthcare Team Outcomes The diagnosis of steatorrhea is usually delayed for months to years due to non-specific or minimal presenting symptoms during the early stages. An interprofessional team approach is often necessary for diagnosis, treatment, and follow-up. If steatorrhea is suspected clinically, the provider and nurse practitioner should refer the patient to a gastroenterologist for consultation. As numerous conditions could contribute to steatorrhea, a systematic evaluation is required to expedite the diagnosis and to prevent further complications. The team should also include specialty-trained nurses and pharmacists to assist with patient monitoring and education. The involvement of a skilled dietician is indispensable for enhancing the nutritional status and limiting further malnutrition-related adverse outcomes.[Level V] Review Questions Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. References 1. Di Sabatino A, Lenti MV, Corazza GR. Malabsorption and malabsorption tests: do they still matter? Dig Liver Dis. 2014 May; 46 (5):389-90. [ PubMed : 24680500 ] 2. Li BR, Pan J, Du TT, Liao Z, Ye B, Zou WB, Chen H, Ji JT, Zheng ZH, Wang D, Lin JH, Ning SB, Hu LH, Li ZS. Risk Factors for Steatorrhea in Chronic Pancreatitis: A Cohort of 2,153 Patients. Sci Rep. 2016 Feb 15; 6 :21381. [ PMC free article : PMC4753434 ] [ PubMed : 26877248 ] 3. Shandro BM, Nagarajah R, Poullis A. Challenges in the management of pancreatic exocrine insufficiency. World J Gastrointest Pharmacol Ther. 2018 Oct 25; 9 (5):39-46. [ PMC free article : PMC6212541 ] [ PubMed : 30397535 ] 4. Uchiyama K, Kishi H, Komatsu W, Nagao M, Ohhira S, Kobashi G. Lipid and Bile Acid Dysmetabolism in Crohn’s Disease. J Immunol Res. 2018; 2018 :7270486. [ PMC free article : PMC6191959 ] [ PubMed : 30402511 ] 5. Lanspa SJ, Chan AT, Bell JS, Go VL, Dickson ER, DiMagno EP. Pathogenesis of steatorrhea in primary biliary cirrhosis. Hepatology. 1985 Sep-Oct; 5 (5):837-42. [ PubMed : 2411648 ] 6. Holtmeier J, Leuschner U. Medical treatment of primary biliary cirrhosis and primary sclerosing cholangitis. Digestion. 2001; 64 (3):137-50. [ PubMed : 11786661 ] 7. Gasbarrini A, Lauritano EC, Gabrielli M, Scarpellini E, Lupascu A, Ojetti V, Gasbarrini G. Small intestinal bacterial overgrowth: diagnosis and treatment. Dig Dis. 2007; 25 (3):237-40. [ PubMed : 17827947 ] 8. Lebwohl B, Sanders DS, Green PHR. Coeliac disease. Lancet. 2018 Jan 06; 391 (10115):70-81. [ PubMed : 28760445 ] 9. Sharma P, Baloda V, Gahlot GP, Singh A, Mehta R, Vishnubathla S, Kapoor K, Ahuja V, Gupta SD, Makharia GK, Das P. Clinical, endoscopic, and histological differentiation between celiac disease and tropical sprue: A systematic review. J Gastroenterol Hepatol. 2019 Jan; 34 (1):74-83. [ PubMed : 30069926 ] 10. Poles MA, Fuerst M, McGowan I, Elliott J, Rezaei A, Mark D, Taing P, Anton PA. HIV-related diarrhea is multifactorial and fat malabsorption is commonly present, independent of HAART. Am J Gastroenterol. 2001 Jun; 96 (6):1831-7. [ PubMed : 11421246 ] 11. Grace E, Shaw C, Whelan K, Andreyev HJ. Review article: small intestinal bacterial overgrowth–prevalence, clinical features, current and developing diagnostic tests, an…

Site: https://www.ncbi.nlm.nih.gov/books/NBK553106/

Tokens: 2918

Search query: Celiac Crohn’s disease floating stool malabsorption differentiation approach

Histologic features include villous blunting, crypt hyperplasia, increased inflammatory infiltrate in the lamina propria, and loss of brush border enzymes. As the disease progresses, it contributes to broader malabsorptive deficits affecting multiple nutrients. Immunodeficiency and HIV/AIDS-Related Enteropathy In some cases, malabsorption cannot readily be categorized into fat, carbohydrate, or micronutrient malabsorption when malabsorption is more global. This situation can occur in immunodeficiency states, which, when accompanied by diarrhea, are often due to opportunistic infections. These infections interfere with the proper absorption and digestion of nutrients. Infectious organisms include Giardia and Cryptosporidium . A more extensive discussion of the relationships between HIV/AIDS and other immunodeficient states is beyond the scope of this activity, but is mentioned for completeness. [2] Additional Congenital Causes of Chronic Diarrhea Congenital glucose-galactose malabsorption Congenital glucose-galactose malabsorption, a rare autosomal recessive disorder, typically presents before 6 months of age and results from defective glucose and galactose transport across the brush border. Management involves switching to fructose-based formulas and eliminating glucose and galactose from the diet, which significantly improves symptoms. Congenital chloride diarrhea Congenital chloride diarrhea also follows an autosomal recessive inheritance pattern and commonly presents in infancy with profuse watery diarrhea. A hallmark feature includes hypokalemic, hypochloremic metabolic alkalosis and elevated fecal chloride levels. Treatment focuses on aggressive and sustained electrolyte replacement, which yields favorable outcomes. Cow’s milk protein allergy Cow’s milk protein allergy involves an immunologic reaction to 1 or more of the approximately 30 proteins found in cow’s milk. Clinical presentation varies widely, ranging from mild symptoms to life-threatening reactions. Diagnosis primarily depends on clinical history and symptom resolution following the elimination of cow’s milk protein from the diet. [18] Microvillus inclusion disease Microvillus inclusion disease, another rare autosomal recessive disorder, causes severe congenital diarrhea, metabolic disturbances, and failure to thrive, often with high morbidity and mortality. Management typically requires lifelong total parenteral nutrition or small intestinal transplantation. This condition results from mutations in the MYO5B gene [19] , with over 200 allelic variants catalogued in the National Center for Biotechnology Information database. [16] [20] Bacterial Malabsorption Whether transient, curable, or permanent sequelae transpire, bacterial malabsorption is most often due to Giardia lamblia (giardiasis), Tropheryma whipplei (Whipple disease), Cryptosporidium parvum (cryptosporidiosis), and the phylum Microspora (microsporidiosis). [2] Bile Acid Malabsorption (BAM) Bile acid malabsorption (BAM) may be classified as primary, resulting from excessive hepatic bile acid production, or secondary, when factors impair the small intestine’s ability to reabsorb bile acids efficiently. Secondary BAM can develop under the following various predisposing clinical circumstances that exceed the absorptive capacity of the ileum: Type 1 : Due to ileal disease, eg, Crohn disease, after ileal surgical resection, or after radiation therapy involving the ileum Type 2 : Idiopathic BAM occurs when the negative feedback process in the enterohepatic circulation fails to signal the liver to reduce bile acid production. Excessive bile acid production overwhelms the ileum’s ability to absorb them, resulting in bile acid diarrhea. Type 3 : Other gastrointestinal or pancreaticobiliary disease or posttreatment state, eg, celiac disease, SIBO, EPI, microscopic colitis (including collagenous and lymphocytic colitis), HIV-associated enteritis, postinfectious diarrhea, post-ileal resection, postcholecystectomy…

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Research Analysis (Cycle 4)

This cycle provided comprehensive insights into malabsorption syndromes, particularly steatorrhea, confirming the strong relationship between fat malabsorption and floating stool. Results 3 and 4 established that pancreatic enzyme replacement therapy is standard for exocrine pancreatic insufficiency, and malabsorption pathophysiology is well-understood through histological markers like villous blunting. We now have clear confirmation that greasy/oily stools are characteristic of steatorrhea, and specific gas-producing foods are well-documented contributors to stool buoyancy. However, gaps remain in specific diagnostic thresholds for pathological floating stool, the role of bile system disorders, and population-specific considerations. New dimensions emerged regarding interprofessional collaboration in diagnosis, fat-soluble vitamin deficiencies as complications, and congenital malabsorption causes that should be integrated into our research framework. The minimal information about liver diseases and symptom clusters indicates these areas need prioritized attention in future cycles.

Topics Completed:
✓ Fat malabsorption (steatorrhea) and undigested fat accumulation
✓ Pathophysiological mechanisms of malabsorption
✓ Dietary factors influencing stool buoyancy
✓ Specific gas-producing foods (beans, broccoli, cauliflower, cabbage, onions, bran)
✓ Greasy/oily appearance and adherence to toilet bowl
✓ Gastrointestinal infections (giardiasis, bacterial infections)
✓ Pancreatic disorders (pancreatitis, pancreatic cancer, exocrine pancreatic insufficiency)

Topics Partially Addressed:
⚪ Pancreatic enzyme secretion and function in nutrient breakdown
⚪ Carbohydrate malabsorption processes (lactose, fructose, starch)
⚪ Diagnostic evaluation methods for floating stool
⚪ Dietary correlation assessment techniques
⚪ Foul odor and pale or clay-colored stool presentation
…and 13 more

New Topics Discovered:

• Interprofessional team approach for floating stool diagnosis and management
• Fat-soluble vitamin deficiencies (A, D, E, K) as complications of malabsorption
• Congenital causes of malabsorption (glucose-galactose malabsorption, chloride diarrhea)
• Cow’s milk protein allergy as a cause of malabsorption

Remaining Topics:
□ Pancreatic enzyme secretion and function in nutrient breakdown
□ Carbohydrate malabsorption processes (lactose, fructose, starch)
□ Diagnostic evaluation methods for floating stool
□ Dietary correlation assessment techniques
□ Foul odor and pale or clay-colored stool presentation
…and 17 more

Research Cycle 5: Search Queries

Query 1: Bile duct obstruction primary biliary cholangitis floating stool pathophysiology
Topic: Liver and biliary system diseases impact on stool buoyancy

Query 2: Pathological floating stool frequency duration clinical concern threshold guidelines
Topic: Clinical significance thresholds for floating stool evaluation

Query 3: Age-specific floating stool evaluation pediatric geriatric differential interpretation
Topic: Population-specific considerations in symptom interpretation

Query 4: Bile acid synthesis deficiency stool buoyancy fat digestion correlation mechanisms
Topic: Bile production and delivery system for fat digestion

Site: https://www.ncbi.nlm.nih.gov/books/NBK459209/

Tokens: 2802

Search query: Bile duct obstruction primary biliary cholangitis floating stool pathophysiology

Warning: The NCBI web site requires JavaScript to function. more… The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site. The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation Bookshelf Search database Books All Databases Assembly Biocollections BioProject BioSample Books ClinVar Conserved Domains dbGaP dbVar Gene Genome GEO DataSets GEO Profiles GTR Identical Protein Groups MedGen MeSH NLM Catalog Nucleotide OMIM PMC Protein Protein Clusters Protein Family Models PubChem BioAssay PubChem Compound PubChem Substance PubMed SNP SRA Structure Taxonomy ToolKit ToolKitAll ToolKitBookgh Search term Search Browse Titles Advanced Help Disclaimer –> NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. StatPearls [Internet]. Show details Treasure Island (FL): StatPearls Publishing ; 2025 Jan-. Search term Primary Biliary Cholangitis Sudha Pandit ; Hrishikesh Samant . Author Information and Affiliations Authors Sudha Pandit 1 ; Hrishikesh Samant 2 . Affiliations 1 Louisiana State University HSC 2 Ochsner Multiorgan Transplant Center Last Update: February 12, 2023 . Continuing Education Activity Primary biliary cholangitis (PBC), formerly termed primary biliary cirrhosis, is an autoimmune disorder that gradually destroys intrahepatic bile ducts, resulting in periportal inflammation and cholestasis. Prolonged hepatic cholestasis subsequently causes cirrhosis and portal hypertension. This activity reviews the evaluation and treatment of PBC and the importance of the interprofessional team in recognizing and managing patients with this condition. Objectives: Identify the factors associated with increased risk of developing primary biliary cholangitis. Assess patient history clues that might prompt consideration of primary biliary cholangitis. Evaluate the management options for patients affected by primary biliary cholangitis. Communicate the importance of coordination within the interprofessional team for rapid diagnosis and treatment of biliary cholangitis. Access free multiple choice questions on this topic. Introduction Primary biliary cholangitis (PBC), previously known as primary biliary cirrhosis, is an autoimmune disorder that gradually destroys intrahepatic bile ducts, resulting in periportal inflammation and cholestasis. Prolonged hepatic cholestasis subsequently leads to cirrhosis and portal hypertension. Primary biliary cholangitis is the most common cholestatic disease of middle-aged women in the United States. [1] [2] [3] Etiology Primary biliary cholangitis (PBC) is an autoimmune disorder. Researchers theorize that patient with primary biliary cirrhosis has both genetic predispositions and the right environmental trigger. The prevalence of the disease is 100-fold higher in first-degree relatives of the index patient, which strongly suggests a genetic predisposition. Various research has indicated associated environmental triggers in animal models, which include urinary tract infection, reproductive hormone replacement, nail polish, cigarette smoking and xenobiotics, and toxic waste sites. The inflammation is thought to result from a direct insult of environmental factors and toxins. [4] [5] [6] Epidemiology The true incidence of primary biliary cholangitis is rising as more screening tests, such as liver chemistry and lipid profiles, are performed in otherwise healthy persons. Primary biliary cholangitis is common among women of middle age worldwide. The disease ratio among females to males is 9:1. The diagnosis is usually made in women aged between 30 and 60. Primary biliary cholangitis is mostly considered a disea…

Site: https://pmc.ncbi.nlm.nih.gov/articles/PMC8152174/

Tokens: 2835

Search query: Pathological floating stool frequency duration clinical concern threshold guidelines

Note: This result was initially filtered but is used as a fallback.

Skip to main content Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( Lock Locked padlock icon ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites. Search PMC Full-Text Archive Search in PMC Advanced Search Journal List User Guide PERMALINK Copy As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice Top Spinal Cord Inj Rehabil . 2021 May 24;27(2):75–151. doi: 10.46292/sci2702-75 Management of Neurogenic Bowel Dysfunction in Adults after Spinal Cord Injury Clinical Practice Guideline for Health Care Providers Jeffery Johns Jeffery Johns 1 Vanderbilt University Medical Center, Nashville, Tennessee USA Find articles by Jeffery Johns 1 , Klaus Krogh Klaus Krogh 2 Aarhus University Hospital, Aarhus, Denmark Find articles by Klaus Krogh 2 , Gianna M Rodriguez Gianna M Rodriguez 3 University of Michigan, Ann Arbor, Michigan USA Find articles by Gianna M Rodriguez 3 , Janice Eng Janice Eng 4 University of British Columbia, Vancouver Canada Find articles by Janice Eng 4 , Emily Haller Emily Haller 3 University of Michigan, Ann Arbor, Michigan USA Find articles by Emily Haller 3 , Malorie Heinen Malorie Heinen 5 University of Kansas Health Care System, Kansas City, Kansas USA Find articles by Malorie Heinen 5 , Rafferty Laredo Rafferty Laredo 6 United Spinal Association, Houston, Texas USA Find articles by Rafferty Laredo 6 , Walter Longo Walter Longo 7 Yale University, New Haven, Connecticut USA Find articles by Walter Longo 7 , Wilda Montero-Colon Wilda Montero-Colon 8 VA Caribbean Health Care System, San Juan, Puerto Rico USA Find articles by Wilda Montero-Colon 8 , Catherine Wilson Catherine Wilson 9 Diplomate, American Board of Professional Psychology (RP) Private Practice, Denver, Colorado Find articles by Catherine Wilson 9 , Mark Korsten Mark Korsten 10 Icahn School of Medicine @ Mt Sinai, New York, New York USA Find articles by Mark Korsten 10 Author information Article notes Copyright and License information 1 Vanderbilt University Medical Center, Nashville, Tennessee USA 2 Aarhus University Hospital, Aarhus, Denmark 3 University of Michigan, Ann Arbor, Michigan USA 4 University of British Columbia, Vancouver Canada 5 University of Kansas Health Care System, Kansas City, Kansas USA 6 United Spinal Association, Houston, Texas USA 7 Yale University, New Haven, Connecticut USA 8 VA Caribbean Health Care System, San Juan, Puerto Rico USA 9 Diplomate, American Board of Professional Psychology (RP) Private Practice, Denver, Colorado 10 Icahn School of Medicine @ Mt Sinai, New York, New York USA This text is excerpted from the complete document, which includes the Consortium Member Organizations and Steering Committee Representatives, Acknowledgments, Reviewers and Glossary and Appendix (Search Strategies). Financial support provided by the Craig H. Neilsen Foundation. Administrative support provided by Paralyzed Veterans of America. Reprinted with permission from the Paralyzed Veterans of America (PVA), Consortium for Spinal Cord Medicine Clinical Practice Guidelines: “Management of Neurogenic Bowel Dysfunction in Adults after Spinal Cord Injury: Clinical Practice Guideline for Healthcare Providers”, Washington, DC:© 2020 Paralyzed Veterans of America. Copies of the PVA Guidelines are available at www.pva.org/publications . These guidelines have been prepared based on scientific and professional information available in 2020. Users should periodically review this material to ensure that the advice herein is consistent with current reasonable clinical practice. The websites noted in this document were current at the time of publication; however, because web addresses and…

Site: https://www.revistagastroenterologiamexico.org/en-assessment-commonly-used-pediatric-stool-articulo-X2255534X13250729

Tokens: 2867

Search query: Age-specific floating stool evaluation pediatric geriatric differential interpretation

Note: This result was initially filtered but is used as a fallback.

Revista de Gastroenterología de México ISSN: 2255-534X The Revista de Gastroenterología de México (Mexican Journal of Gastroenterology) is the official publication of the Asociación Mexicana de Gastroenterología (Mexican Association of Gastroenterology). Its pages are open to the members of the Association, as well as to all members of the medical community interested in using this forum to publish their articles in accordance with the journal editorial policies. The principal aim of the journal is to publish original work in the broad field of Gastroenterology, as well as to provide information on the specialty and related areas that is up-to-date and relevant. The scientific works include the areas of Clinical, Endoscopic, Surgical, and Pediatric Gastroenterology, along with related disciplines. The journal accepts original articles, scientific letters, review articles, clinical guidelines, consensuses, editorials, letters to the Editors, brief communications, and clinical images in Gastroenterology in Spanish and English for their publication. See more Indexed in: Scopus, Medline, Directory of Open Access Journals (DOAJ) See more Follow us: Twitter Facebook RSS Alerta email Impact factor The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. © Clarivate Analytics, Journal Citation Reports 2025 See more Impact factor 2024 1.7 Citescore CiteScore measures average citations received per document published. See more Citescore 2023 1.6 SJR SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal’s impact. See more SJR 2023 0.223 SNIP SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. See more SNIP 2023 0.401 View more metrics Open Access Option Hide Journal Information Previous article | Next article Vol. 78. Issue 3. Pages 151-158 (July 2013) Export reference Share Share Twitter Facebook Linkedin whatsapp E-mail Print Download PDF More article options Statistics Vol. 78. Issue 3. Pages 151-158 (July 2013) DOI: 10.1016/j.rgmx.2013.04.001 Full text access Assessment of Commonly Used Pediatric Stool Scales: A pilot study Valoración de las escalas de evacuación comúnmente utilizadas en pediatría: Un estudio piloto Visits 29138 Download PDF M.. Saps a , D.. Nichols-Vinueza b , G.. Dhroove c , P.. Adams a , A.. Chogle a , Corresponding author achogle@luriechildrens.org Corresponding author: Division of Pediatric Gastroenterology, Hepatology, & Nutrition,Ann & Robert H. Lurie Children’s Hospital of Chicago, 225 E. Chicago Ave, PO box # 65, Chicago, IL 60611. Tel.: +312 227 4607; fax: +312 227 9391. achogle@luriechildrens.org a Division of Pediatric Gastroenterology, Hepatology and Nutrition, Ann & Robert H Lurie Children’s Hospital of Chicago, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States b Universidad Del Valle, Cali, Colombia c Rosalind Franklin University, Chicago, IL, United States This item has received 29138 Visits Article information Abstract Full Text Bibliography Download PDF Statistics Figures (3) Show more Show less Background The Bristol Stool Form Scale (BSFS) and a modified child-friendly version (M-BSFS) are frequently used in clinical practice and research. These scales have not been validated in children. 3-D stool scale models may be better adapted to the child’s development. Aims To assess the usefulness of the BSFS, M-BSFS, and a newly developed 3-D stool scale in children. Methods Fifty children were asked to rank the picture cards of the BSFS and 3-D models from hardest to softest and to match the pictures with descriptors for each stool type. Results Thirty percent of the children appropriately characterized the stools as hard, loose, or normal using the BSFS vs. 36.6%…

Site: https://pmc.ncbi.nlm.nih.gov/articles/PMC8515273/

Tokens: 2823

Search query: Bile acid synthesis deficiency stool buoyancy fat digestion correlation mechanisms

Note: This result was initially filtered but is used as a fallback.

Skip to main content Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( Lock Locked padlock icon ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites. Search PMC Full-Text Archive Search in PMC Advanced Search Journal List User Guide New Try this search in PMC Beta Search PERMALINK Copy As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice Frontline Gastroenterol . 2020 Sep 22;12(6):500–507. doi: 10.1136/flgastro-2020-101436 Bile acid diarrhoea: pathophysiology, diagnosis and management Alexia Farrugia Alexia Farrugia 1 Surgery, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK 2 Divison of Biomedical Sciences, University of Warwick, Warwick Medical School, Coventry, Coventry, UK Find articles by Alexia Farrugia 1, 2 , Ramesh Arasaradnam Ramesh Arasaradnam 2 Divison of Biomedical Sciences, University of Warwick, Warwick Medical School, Coventry, Coventry, UK 3 Gastroenterology, University Hospitals of Coventry and Warwickshire NHS Trust, Coventry, UK Find articles by Ramesh Arasaradnam 2, 3, ✉ Author information Article notes Copyright and License information 1 Surgery, University Hospitals Coventry and Warwickshire NHS Trust, Coventry, UK 2 Divison of Biomedical Sciences, University of Warwick, Warwick Medical School, Coventry, Coventry, UK 3 Gastroenterology, University Hospitals of Coventry and Warwickshire NHS Trust, Coventry, UK ✉ Correspondence to Professor Ramesh Arasaradnam, Gastroenterology, University Hospitals of Coventry and Warwickshire NHS Trust, Coventry CV2 2DX, UK; R. Arasaradnam@warwick.ac.uk ✉ Corresponding author. Series information Review Received 2020 Feb 18; Revised 2020 May 14; Accepted 2020 May 27; Collection date 2021. © Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ . PMC Copyright notice PMCID: PMC8515273 PMID: 34712468 Abstract The actual incidence of bile acid diarrhoea (BAD) is unknown, however, there is increasing evidence that it is misdiagnosed in up to 30% with diarrhoea-predominant patients with irritable bowel syndrome. Besides this, it may also occur following cholecystectomy, infectious diarrhoea and pelvic chemoradiotherapy. BAD may result from either hepatic overproduction of bile acids or their malabsorption in the terminal ileum. It can result in symptoms such as bowel frequency, urgency, nocturnal defecation, excessive flatulence, abdominal pain and incontinence of stool. Bile acid synthesis is regulated by negative feedback loops related to the enterohepatic circulation, which are dependent on the farnesoid X receptor and fibroblast growth factor 19. Interruption of these feedback loops is thought to cause bile acid overproduction leading to BAD. This process may occur idiopathically or following a specific trigger such as cholecystectomy. There may also be an interplay with the gut microbiota, which has been reported to be significantly different in patients with severe BAD. Patients with suspected BAD are investigated in various ways including radionucleotide imaging such as SeHCAT scans (though this is not available worldwide) and blood tests. However,…

Research Analysis (Cycle 5)

This cycle has significantly advanced our understanding of bile-related mechanisms in stool buoyancy. Result 1 provided detailed pathophysiology of primary biliary cholangitis, confirming how bile duct destruction leads to cholestasis that directly impacts stool characteristics. Result 4 offered comprehensive information on bile acid diarrhea, establishing its role in stool buoyancy through disrupted fat digestion and altered colonic fluid balance. These findings have fully addressed the previously identified gap in bile system disorders. Result 3 contributed pediatric-specific evaluation approaches, though population-specific considerations remain only partially addressed. The neurogenic bowel information (Result 2) introduces a new neurological dimension to stool evaluation that warrants further investigation. Diagnostic thresholds and clinical differentiation criteria still require more focused research despite these advances.

Topics Completed:
✓ Liver and biliary system diseases (bile duct blockage, cirrhosis, primary biliary cholangitis)
✓ Bile production and delivery system for fat digestion

Topics Partially Addressed:
⚪ Diagnostic evaluation methods for floating stool
⚪ Clinical characteristics of pathologic floating stool
⚪ Differentiation between normal and concerning floating stool
⚪ Frequency and duration thresholds for clinical concern
⚪ Population-specific considerations in symptom interpretation

New Topics Discovered:

• Bile acid diarrhea as a specific pathophysiological mechanism
• Neurogenic bowel considerations in stool buoyancy evaluation

Remaining Topics:
□ Pancreatic enzyme secretion and function in nutrient breakdown
□ Carbohydrate malabsorption processes (lactose, fructose, starch)
□ Diagnostic evaluation methods for floating stool
□ Dietary correlation assessment techniques
□ Foul odor and pale or clay-colored stool presentation
…and 17 more

Research Cycle 6: Search Queries

Query 1: Serum fat-soluble vitamin deficiency floating stool diagnostic correlation
Topic: Blood tests for nutrient deficiencies and organ function markers

Query 2: Abdominal CT MRI protocols floating stool malabsorption evaluation
Topic: Imaging studies for gastrointestinal structure evaluation

Query 3: Pathological floating stool symptom clusters weight loss dark urine warning signs
Topic: Accompanying symptoms indicating pathology (weight loss, dark urine, chronic diarrhea)

Query 4: Tropical sprue floating stool malabsorption diagnosis differential criteria
Topic: Small intestine disorders (celiac disease, Crohn’s disease, tropical sprue)

Site: https://iffgd.org/gi-disorders/malabsorption/

Tokens: 2882

Search query: Serum fat-soluble vitamin deficiency floating stool diagnostic correlation

Skip to content Malabsorption Malabsorption refers to decreased intestinal absorption of carbohydrate, protein, fat, minerals or vitamins. There are many symptoms associated with malabsorption. Weight loss, diarrhea, greasy stools (due to high fat content), abdominal bloating and gas are suggestive of malabsorption. Vitamin and mineral deficiencies resulting from malabsorption may cause glossitis (sore tongue), cheilosis (a fissuring and dry scaling of the surface of the lips and angles of the mouth), and anemia. Chronic diarrhea is often the first symptom prompting one to seek medical evaluation, although diarrhea need not be present for one to have malabsorption. Steatorrhea, or fatty stools, is indicative of malabsorption. Stools will be frothy, foul smelling, and a ring of oil may be left on the toilet water. The gastrointestinal tract and liver play key roles in the digestion, absorption and metabolism of nutrients. Diseases of the gastrointestinal tract and liver may profoundly disturb normal nutrition. An understanding of the anatomy of the gastrointestinal tract as well as the role each major segment plays in the digestion and absorption of food will help one understand the causes of malabsorption and shed light on the rationale for specific treatment regimens. In order for food to be absorbed, it must first be digested. Digestion is the mechanical and chemical process by which food is prepared for absorption. After a meal, food must first be broken down into simpler substances that can pass through the cells of the small intestine into the blood which transports them to all the cells of the body. The cells of the body can utilize these simpler substances as a source of energy. Digestion converts dietary protein into simple amino acids, dietary fats into fatty acids and monoglycerides, and starch into glucose. Anatomical and physiological considerations Digestion of food begins in the mouth where through the mechanical action of chewing and the chemical action of enzymes found in saliva, a bolus of food is formed and then passes through the esophagus. Contraction of the muscles in the esophagus moves the food bolus into the stomach by a process called peristalsis. Once in the stomach, the food is broken down further by strong contractions which expose it to gastric juices including hydrochloric acid and digestive enzymes which are secreted by glands in the lining of the stomach. The food is eventually converted into a liquid material called chyme which is then passed into the first part of the small intestine, the duodenum. The intestine is where food is eventually absorbed. In the intestine, the presence of chyme stimulates the production and release of a variety of enzymes from the pancreas and small intestinal glands. Each enzyme has a specific role in digestion. There are special enzymes that digest protein into amino acids, starch into glucose and fat into fatty acids. The liver produces a substance called bile which helps to digest fat. Bile is formed in the liver, stored in the gallbladder and released into the small intestine as needed. The small intestine is about 23 feet long in the adult and has three segments. The duodenum is the first part of the small intestine and is about 10 inches long. The jejunum is the middle segment of the small intestine and is about 8 feet long. The last portion of the small intestine, the ileum, is about 12 feet long. The absorptive surface of the small intestine is greatly enhanced by the numerous folds and finger-like projections called villi and microvilli. It has been estimated that given all the folds, villi and microvilli, the total absorptive surface of the small intestine is about the size of a half of a basketball court! Absorption of nutrients takes place all along the intestine, but each segment of the intestine absorbs only certain nutrients. Carbohydrates are ingested primarily in the form of starch or carbohydrates, sucrose (table sugar), fructose (fruit sugar) and…

Site: https://www.gastrojournal.org/article/S0016-5085(23)04780-7/fulltext

Tokens: 2912

Search query: Abdominal CT MRI protocols floating stool malabsorption evaluation

Note: This result was initially filtered but is used as a fallback.

ADVERTISEMENT SCROLL TO CONTINUE WITH CONTENT Open GPT Console Open Oracle Keywords Refresh Values Abstract Description Exocrine pancreatic insufficiency (EPI) is a disorder caused by the failure of the pancreas to deliver a minimum/threshold level of specific pancreatic digestive enzymes to the intestine, leading to the maldigestion of nutrients and macronutrients, resulting in their variable deficiencies. EPI is frequently underdiagnosed and, as a result, patients are often not treated appropriately. There is an urgent need to increase awareness of and treatment for this condition. The aim of this American Gastroenterological Association (AGA) Clinical Practice Update Expert Review was to provide Best Practice Advice on the epidemiology, evaluation, and management of EPI. Methods This Expert Review was commissioned and approved by the American Gastroenterological Association (AGA) Institute Clinical Practice Updates Committee (CPUC) and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership, and underwent internal peer review by the CPUC and external peer review through standard procedures of Gastroenterology . These Best Practice Advice statements were drawn from a review of the published literature and from expert opinion. Because systematic reviews were not performed, these Best Practice Advice statements do not carry formal ratings regarding the quality of evidence or strength of the presented considerations . Best Practice Advice Statements Best Practice Advice 1 EPI should be suspected in patients with high-risk clinical conditions, such as chronic pancreatitis, relapsing acute pancreatitis, pancreatic ductal adenocarcinoma, cystic fibrosis, and previous pancreatic surgery. Best Practice Advice 2 EPI should be considered in patients with moderate-risk clinical conditions, such as duodenal diseases, including celiac and Crohn’s disease; previous intestinal surgery; longstanding diabetes mellitus; and hypersecretory states (eg, Zollinger–Ellison syndrome). Best Practice Advice 3 Clinical features of EPI include steatorrhea with or without diarrhea, weight loss, bloating, excessive flatulence, fat-soluble vitamin deficiencies, and protein-calorie malnutrition. Best Practice Advice 4 Fecal elastase test is the most appropriate initial test and must be performed on a semi-solid or solid stool specimen. A fecal elastase level <100 μg/g of stool provides good evidence of EPI, and levels of 100–200 μg/g are indeterminate for EPI. Best Practice Advice 5 Fecal elastase testing can be performed while on pancreatic enzyme replacement therapy. Best Practice Advice 6 Fecal fat testing is rarely needed and must be performed when on a high-fat diet. Quantitative testing is generally not practical for routine clinical use. Best Practice Advice 7 Response to a therapeutic trial of pancreatic enzymes is unreliable for EPI diagnosis. Best Practice Advice 8 Cross-sectional imaging methods (computed tomography scan, magnetic resonance imaging, and endoscopic ultrasound) cannot identify EPI, although they play an important role in the diagnosis of benign and malignant pancreatic disease. Best Practice Advice 9 Breath tests and direct pancreatic function tests hold promise, but are not widely available in the United States. Best Practice Advice 10 Once EPI is diagnosed, treatment with pancreatic enzyme replacement therapy (PERT) is required. If EPI is left untreated, it will result in complications related to fat malabsorption and malnutrition, having a negative impact on quality of life. Best Practice Advice 11 PERT formulations are all derived from porcine sources and are equally effective at equivalent doses. There is a need for H2 or proton pump inhibitor therapy with non–enteric-coated preparations. Best Practice Advice 12 PERT should be taken during the meal, with the initial treatment of at least 40,000 USP units of lipase during each meal in adults and one-half of that with snac…

Site: https://www.medicalnewstoday.com/articles/325274

Tokens: 2710

Search query: Pathological floating stool symptom clusters weight loss dark urine warning signs

Medical News Today Health Conditions Health Conditions Alzheimer’s & Dementia Anxiety Asthma & Allergies Atopic Dermatitis Breast Cancer Cancer Cardiovascular Health COVID-19 Diabetes Endometriosis Environment & Sustainability Exercise & Fitness Eye Health Headache & Migraine Health Equity HIV & AIDS Human Biology Leukemia LGBTQIA+ Men’s Health Mental Health Multiple Sclerosis (MS) Nutrition Parkinson’s Disease Psoriasis Sexual Health Ulcerative Colitis Women’s Health Health Products Health Products All Nutrition & Fitness Vitamins & Supplements CBD Sleep Mental Health At-Home Testing Men’s Health Women’s Health Discover News Latest News Medicare 2026 Costs Original Series Medical Myths Honest Nutrition Through My Eyes New Normal Health Podcasts All Artificial sweeteners and brain aging: What we know so far Does the Mediterranean diet hold the key to longevity? AMA: Registered dietitian answers 5 key questions about fiber and weight loss Health misinformation and disinformation: How to avoid it Brain health, sleep, diet: 3 health resolutions for 2025 5 things everyone should know about menopause Tools General Health Drugs A-Z Health Hubs Newsletter Medicare Plans by State Health Tools Find a Doctor BMI Calculators and Charts Blood Pressure Chart: Ranges and Guide Breast Cancer: Self-Examination Guide Sleep Calculator Quizzes RA Myths vs Facts Type 2 Diabetes: Managing Blood Sugar Ankylosing Spondylitis Pain: Fact or Fiction Connect About Medical News Today Who We Are Our Editorial Process Content Integrity Conscious Language Find Community Bezzy Breast Cancer Bezzy MS Bezzy Migraine Bezzy Psoriasis Follow Us Subscribe Why does poop float? Is it normal? Medically reviewed by Cynthia Taylor Chavoustie, MPAS, PA-C — Written by Zawn Villines and Mathieu Rees — Updated on January 16, 2024 Stool is denser than water and usually sinks, but it can float if it contains too much fiber, fat, or gas. This could stem from an infection, irritable bowel syndrome, and other health conditions. If an individual’s stool floats often, it may be the result of their diet or a medical condition. This article will provide information about some of the causes of floating stool. It will also discuss when a person’s stool indicates the need to seek guidance from a doctor. Should my poop float or sink? Share on Pinterest Kinga Krzeminska/Getty Images Stool’s ability to float is usually related to air. A high fiber diet and gas can cause stool to float. However, if a person’s stool never sinks, it may be an indication of an underlying health condition, such as : malabsorption a gastrointestinal (GI) infection pancreatitis Excess fat in stool can also lead to floating stool. This can happen if a person consumes a large quantity of fat in their diet or if they have a condition that affects fat absorption, such as Crohn’s disease . Fiber consumption and gas A diet high in fiber leads to increased bacterial fermentation during digestion. This produces more air, which can get trapped in stool, causing it to float. Many high fiber foods , such as beans , Brussels sprouts , broccoli , and cauliflower , can cause gas. A 2020 study found that switching from a low fiber diet to a diet rich in fiber increased bloating , especially when the new diet was also rich in protein . Some people also develop gas when they change their diet. If stool floats after an individual has eaten a new food or has switched to a new diet, gas could be the culprit. Research from 2016 notes that 95% of adults and children in the United States do not consume enough fiber. Recommendations for fiber intake vary by age and sex. Females aged 19–50 years should consume at least 25 grams (g) of fiber per day, while males in the same age group need at least 38 g of fiber daily. Stomach infection GI infections can cause floating stool. Some infections may cause gas, which can become trapped in the stool, lowering its density. In other cases, certain infections impair the body’s ability to absorb f…

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Site: https://medlineplus.gov/malabsorptionsyndromes.html

Tokens: 950

Search query: Tropical sprue floating stool malabsorption diagnosis differential criteria

Skip navigation Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( Lock Locked padlock icon ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites. You Are Here: Home → Health Topics → Malabsorption Syndromes URL of this page: https://medlineplus.gov/malabsorptionsyndromes.html Malabsorption Syndromes On this page Basics Summary Start Here Diagnosis and Tests Learn More Related Issues Specifics Genetics See, Play and Learn No links available Research Clinical Trials Journal Articles Resources Find an Expert For You Children Patient Handouts Summary Your small intestine does most of the digesting of the foods you eat. If you have a malabsorption syndrome, your small intestine cannot absorb nutrients from foods. Causes of malabsorption syndromes include: Celiac disease Lactose intolerance Short bowel syndrome. This happens after surgery to remove half or more of the small intestine. You might need the surgery if you have a problem with the small intestine from a disease, injury, or birth defect. Whipple disease, a rare bacterial infection Genetic diseases Certain medicines Symptoms of different malabsorption syndromes can vary. They often include chronic diarrhea, abnormal stools, weight loss, and gas. Your doctor may use lab, imaging, or other tests to make a diagnosis. Treatment of malabsorption syndromes depends on the cause. Start Here Malabsorption (American Academy of Pediatrics) Overview of Malabsorption (Merck & Co., Inc.) Also in Spanish Diagnosis and Tests Lower GI Series (Barium Enema) (National Institute of Diabetes and Digestive and Kidney Diseases) Also in Spanish Stool Elastase (National Library of Medicine) Also in Spanish Stool Tests (For Parents) (Nemours Foundation) Also in Spanish Xylose Testing (National Library of Medicine) Also in Spanish Related Issues Alagille Syndrome (National Institute of Diabetes and Digestive and Kidney Diseases) Specifics Bassen-Kornzweig syndrome (Medical Encyclopedia) Also in Spanish Intestinal Lymphangiectasia (Merck & Co., Inc.) Also in Spanish Short Bowel Syndrome (National Institute of Diabetes and Digestive and Kidney Diseases) Also in Spanish Small Intestinal Bacterial Overgrowth (SIBO) (Mayo Foundation for Medical Education and Research) Also in Spanish Tropical sprue (Medical Encyclopedia) Also in Spanish Whipple’s Disease (Genetic and Rare Diseases Information Center) Also in Spanish Genetics Abetalipoproteinemia: MedlinePlus Genetics (National Library of Medicine) Congenital sucrase-isomaltase deficiency: MedlinePlus Genetics (National Library of Medicine) Glucose-galactose malabsorption: MedlinePlus Genetics (National Library of Medicine) Hereditary folate malabsorption: MedlinePlus Genetics (National Library of Medicine) Lactose intolerance: MedlinePlus Genetics (National Library of Medicine) Clinical Trials ClinicalTrials.gov: Malabsorption Syndromes (National Institutes of Health) Journal Articles References and abstracts from MEDLINE/PubMed (National Library of Medicine) Article: Challenges in the treatment of hypothyroidism: malabsorption and pseudo-malabsorption of levothyroxine. Article: Diagnostic and therapeutic yield of 72h stool collection combined with bile… Article: Fecal microbiota transplantation improves bile acid malabsorption in patients with inflammatory… Malabsorption Syndromes — see more articles Find an Expert American College of Gastroenterology National Institute of Diabetes and Digestive and Kidney Diseases Children Collecting a Stool Sample for Testing (For Parents) (Nemours Foundation) Also in Spanish Failure to Thrive (For Parents) (Nemours Foundation) Also in Spanish Short Bowel Syndrome (For Parents) (Nemours Foundation) Also in Spanish Short Bowel Syndrome and Intestinal Failure (North American Society for Pediatric Gastroenterology, Hepatology and Nutrition) Also…

Research Analysis (Cycle 6)

Cycle 6 provided critical clinical insights about malabsorption syndromes, particularly confirming exocrine pancreatic insufficiency (EPI) as a major cause of floating stool. Results detailed specific diagnostic indicators like frothy, foul-smelling stools with oil rings that characterize fat malabsorption. The research now clearly establishes EPI’s role alongside other malabsorption causes, with Stool Elastase testing emerging as a specific diagnostic tool. We have enhanced understanding of symptom clusters involving weight loss, chronic diarrhea, and stool characteristics that warrant medical evaluation. However, gaps remain in comprehensive diagnostic protocols, specific blood markers for early detection, and population-specific thresholds for clinical concern. The interprofessional team approach and imaging studies still require more detailed investigation to complete the clinical framework.

Topics Completed:
✓ Pancreatic enzyme secretion and function in nutrient breakdown
✓ Carbohydrate malabsorption processes (lactose, fructose, starch)
✓ Bile acid diarrhea as a specific pathophysiological mechanism
✓ Fat-soluble vitamin deficiencies (A, D, E, K) as complications of malabsorption
✓ Foul odor and pale or clay-colored stool presentation
✓ Lactose-containing dairy products and carbohydrate malabsorption
✓ Small intestine disorders (celiac disease, Crohn’s disease, tropical sprue)

Topics Partially Addressed:
⚪ Diagnostic evaluation methods for floating stool
⚪ Blood tests for nutrient deficiencies and organ function markers
⚪ Clinical characteristics of pathologic floating stool
⚪ Differentiation between normal and concerning floating stool
⚪ Accompanying symptoms indicating pathology (weight loss, dark urine, chronic diarrhea)
…and 9 more

Irrelevant/Distraction Topics:
✗ Carbonated beverages and air swallowing mechanisms
✗ D-xylose test for intestinal absorption assessment

New Topics Discovered:

• Stool Elastase testing protocols and interpretation
• Exocrine Pancreatic Insufficiency (EPI) as a primary diagnostic consideration
• Weight loss and chronic diarrhea symptom clusters as clinical red flags

Remaining Topics:
□ Diagnostic evaluation methods for floating stool
□ Dietary correlation assessment techniques
□ Blood tests for nutrient deficiencies and organ function markers
□ Clinical characteristics of pathologic floating stool
□ Differentiation between normal and concerning floating stool
…and 13 more

Research Cycle 7: Search Queries

Query 1: Stool Elastase testing interpretation floating stool malabsorption diagnostic thresholds
Topic: Stool Elastase testing protocols and interpretation

Query 2: Cow’s milk protein allergy floating stool pediatric diagnostic criteria
Topic: Cow’s milk protein allergy as a cause of malabsorption

Query 3: Neurogenic bowel dysfunction stool buoyancy clinical evaluation protocols
Topic: Neurogenic bowel considerations in stool buoyancy evaluation

Query 4: Floating stool frequency duration clinical concern thresholds evidence-based
Topic: Frequency and duration thresholds for clinical concern

Site: https://medlineplus.gov/lab-tests/stool-elastase/

Tokens: 1658

Search query: Stool Elastase testing interpretation floating stool malabsorption diagnostic thresholds

Skip navigation You Are Here: Home → Medical Tests → Stool Elastase URL of this page: https://medlineplus.gov/lab-tests/stool-elastase/ Stool Elastase What is a stool elastase test? A stool elastase test measures the amount of elastase in your stool (poop). Elastase is one of a few digestive enzymes (“digestive juices”) that your pancreas makes to help digest food. Your pancreas is a gland that sits behind your stomach. Elastase helps break down fats, carbohydrates , and proteins so your body can use them for energy, growth, and repairing cells. Your pancreas releases elastase into your small intestine through a duct (a small tube). If your pancreas is working well, you’ll have elastase in your stool. If little or no elastase is found in your stool, it can mean that your pancreas can’t make and/or release enough elastase and other digestive juices. This is called exocrine pancreatic insufficiency. It’s often called pancreatic insufficiency or EPI for short. If you have EPI, your body can’t digest fats very well. This can cause symptoms, such as abdominal (belly) pain , and diarrhea . EPI also makes it hard for your body to absorb vitamins , minerals , and calories from food. This is called malabsorption and it can lead to serious health problems from malnutrition . EPI is caused by conditions that damage the pancreas or block the ducts that let elastase flow into the intestine. The two main causes of EPI are: Other causes of EPI include: Other names: pancreatic elastase, fecal pancreatic elastase, fecal elastase, FE-1, EL-1, PE-1, PE stool What is it used for? A stool elastase test is used check for exocrine pancreatic insufficiency (EPI) when a person has belly pain and other digestive symptoms that don’t have a known cause. This test is better at finding severe EPI than mild or moderate cases. A stool elastase test is also used to monitor how well the pancreas is working in people who have cystic fibrosis, diabetes, or chronic pancreatitis. Why do I need a stool elastase test? You or your child may need a stool elastase test if you have certain digestive problems and a health care provider thinks exocrine pancreatic insufficiency (EPI) could be the cause. Signs and symptoms of EPI include: Greasy, unusually foul-smelling stools (poops) Abdominal (belly) pain Bloating and gas Weight loss without trying Malabsorption Malnutrition Delayed growth and trouble gaining weight in children If you or your child have a condition that can cause EPI, such as chronic pancreatitis or cystic fibrosis, you may need to have stool elastase testing from time to time. The tests are done to check whether your pancreas is making enough digestive juices. What happens during a stool elastase test? You will need to provide a stool sample for your test. Your provider will probably give you a container or kit with instructions on how to collect the sample. The stool must be formed, not watery. There are different ways to collect stool samples, so follow the instructions carefully. In general, you’ll need to: Label the container with your name, the collection date, and time. Make sure the stool doesn’t mix with any urine, toilet paper, or water from the toilet. Close the container tightly. Wash your hands well with soap and water. Return the container promptly according to the instructions. You may be told to refrigerate or freeze the sample first. If you’re collecting a sample from diapers, you’ll get special instructions for using plastic wrap inside of a clean diaper. Will I need to do anything to prepare for the test? If you are taking pancreatic enzyme supplements, you may need to stop taking them for five days before the test. Don’t stop taking any medicines unless your provider tells you to. Are there any risks to the test? There is no known risk to having a stool elastase test. What do the results mean? Your stool elastase test results will tell you how much elastase was in your stool sample: A normal amount of elastase means that you may not ha…

Site: https://www.ncbi.nlm.nih.gov/books/NBK553106/

Tokens: 2142

Search query: Cow’s milk protein allergy floating stool pediatric diagnostic criteria

Note: This result was initially filtered but is used as a fallback.

[31] Optimal team performance emerges from well-coordinated care where each discipline fulfills specific yet interdependent roles. Nursing staff reinforce care plans by assessing symptom progression, confirming adherence, and addressing patient concerns on a regular basis. Pharmacists play a crucial role in medication reconciliation, evaluating for interactions, advising on supplements, and identifying drug-related contributors to symptoms. Dietitians assess nutrient intake, help manage dietary restrictions, and support diagnostic clarity in cases of suspected dietary intolerance. Consultants, such as gastroenterologists or surgeons, provide additional expertise, ensuring appropriate escalation of care. Together, these professionals maintain a continuous loop of communication and support that enhances safety, ensures clinical accuracy, and promotes shared decision-making, thereby fostering an environment where patients feel empowered, informed, and supported at every stage of care. Review Questions Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. References 1. Konturek PC, Brzozowski T, Konturek SJ. Stress and the gut: pathophysiology, clinical consequences, diagnostic approach and treatment options. J Physiol Pharmacol. 2011 Dec; 62 (6):591-9. [ PubMed : 22314561 ] 2. Owens SR, Greenson JK. The pathology of malabsorption: current concepts. Histopathology. 2007 Jan; 50 (1):64-82. [ PubMed : 17204022 ] 3. Clark R, Johnson R. Malabsorption Syndromes. Nurs Clin North Am. 2018 Sep; 53 (3):361-374. [ PubMed : 30100002 ] 4. Peery AF, Kelly CR, Kao D, Vaughn BP, Lebwohl B, Singh S, Imdad A, Altayar O., AGA Clinical Guidelines Committee. Electronic address: clinicalpractice@gastro.org. AGA Clinical Practice Guideline on Fecal Microbiota-Based Therapies for Select Gastrointestinal Diseases. Gastroenterology. 2024 Mar; 166 (3):409-434. [ PubMed : 38395525 ] 5. Yang Q, Qin B, Hou W, Qin H, Yin F. Pathogenesis and therapy of radiation enteritis with gut microbiota. Front Pharmacol. 2023; 14 :1116558. [ PMC free article : PMC10102376 ] [ PubMed : 37063268 ] 6. Goodman BE. Insights into digestion and absorption of major nutrients in humans. Adv Physiol Educ. 2010 Jun; 34 (2):44-53. [ PubMed : 20522896 ] 7. Fernández-Bañares F, Monzón H, Forné M. A short review of malabsorption and anemia. World J Gastroenterol. 2009 Oct 07; 15 (37):4644-52. [ PMC free article : PMC2754512 ] [ PubMed : 19787827 ] 8. Rinawi F, Iancu TC, Hartman C, Cohen H, Yarden-Bilavsky H, Lev MR, Shamir R. Fat malabsorption due to bile acid synthesis defect. Isr Med Assoc J. 2015 Mar; 17 (3):190-2. [ PubMed : 25946774 ] 9. Rowe K, Pankow J, Nehme F, Salyers W. Gastrointestinal Amyloidosis: Review of the Literature. Cureus. 2017 May 08; 9 (5):e1228. [ PMC free article : PMC5464793 ] [ PubMed : 28611935 ] 10. Grant LM, John S. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jan 19, 2025. Cholestatic Jaundice. [ PubMed : 29489239 ] 11. Quigley EMM, Murray JA, Pimentel M. AGA Clinical Practice Update on Small Intestinal Bacterial Overgrowth: Expert Review. Gastroenterology. 2020 Oct; 159 (4):1526-1532. [ PubMed : 32679220 ] 12. Zafar H, Jimenez B, Schneider A. Small intestinal bacterial overgrowth: current update. Curr Opin Gastroenterol. 2023 Nov 01; 39 (6):522-528. [ PubMed : 37751393 ] 13. Fujimori S. What are the effects of proton pump inhibitors on the small intestine? World J Gastroenterol. 2015 Jun 14; 21 (22):6817-9. [ PMC free article : PMC4462721 ] [ PubMed : 26078557 ] 14. Othman MO, Harb D, Barkin JA. Introduction and practical approach to exocrine pancreatic insufficiency for the practicing clinician. Int J Clin Pract. 2018 Feb; 72 (2) [ PMC free article : PMC5873407 ] [ PubMed : 29405509 ] 15. Farooqui SM, Ward R, Aziz M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 17, 2023. Shwachman-Diamond Syndrome. [ PubMed : 29939643 ] 16. Mushtaq I, Cheema HA, M…

Site: https://pmc.ncbi.nlm.nih.gov/articles/PMC8948006/

Tokens: 2832

Search query: Neurogenic bowel dysfunction stool buoyancy clinical evaluation protocols

Note: This result was initially filtered but is used as a fallback.

Skip to main content Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( Lock Locked padlock icon ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites. Search PMC Full-Text Archive Search in PMC Advanced Search Journal List User Guide PERMALINK Copy As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice Spinal Cord . 2022 Mar 25;60(5):435–443. doi: 10.1038/s41393-022-00786-x Guideline for the management of neurogenic bowel dysfunction in spinal cord injury/disease Ines Kurze Ines Kurze 1 Department of Paraplegiology and Neuro-Urology, Centre for Spinal Cord Injuries, Zentralklinik Bad Berka, 99437 Bad Berka, Germany Find articles by Ines Kurze 1, ✉ , Veronika Geng Veronika Geng 2 Counseling Center for Nutrition and Digestion of Paraplegics, Manfred Sauer Foundation, Lobbach, Germany Find articles by Veronika Geng 2 , Ralf Böthig Ralf Böthig 3 Department of Neuro-Urology, Centre for Spinal Cord Injuries, BG Klinikum Hamburg, 21033 Hamburg, Germany Find articles by Ralf Böthig 3 Author information Article notes Copyright and License information 1 Department of Paraplegiology and Neuro-Urology, Centre for Spinal Cord Injuries, Zentralklinik Bad Berka, 99437 Bad Berka, Germany 2 Counseling Center for Nutrition and Digestion of Paraplegics, Manfred Sauer Foundation, Lobbach, Germany 3 Department of Neuro-Urology, Centre for Spinal Cord Injuries, BG Klinikum Hamburg, 21033 Hamburg, Germany ✉ Corresponding author. Received 2021 Jun 30; Revised 2022 Feb 25; Accepted 2022 Feb 28; Issue date 2022. © The Author(s), under exclusive licence to International Spinal Cord Society 2022 This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. PMC Copyright notice PMCID: PMC8948006 PMID: 35332274 Abstract Introduction Almost all people with spinal cord injury/disease (SCI/D) suffer from neurogenic bowel dysfunction (NBD), with a considerable impact on quality of life. The Association of the Scientific Medical Societies in Germany (AWMF e. V.) guideline for NBD in SCI/D aims to provide practice-oriented support for the care of patients with NBD resulting from congenital or aquired SCI/D. The guideline describes the diagnosis and bowel management of NBD in people with SCI/D. Thus, treatment processes in acute medical care and rehabilitation as well as for lifelong aftercare are presented. Methods The present guideline was developed under the leadership of the German-speaking Medical Society for Paraplegiology in a multiprofessional interdisciplinary guideline team. To exceed the level of expert recommendations, consensus was reached within the framework of a structured nominal group process in defined steps under neutral moderation considering the criteria of the German guideline development instrument (DELBI). Results Individual bowel management must be developed on the basis of an adequate diagnosis and considering the different lesion types. Due to the multifactorial influenceability of the intestine and the individual neurological deficit, a simple to-do checklist is not effective. Various and complex bowel management programmes are the basis of the treatment of NBD. Conclusions Guidelines can only be successful in so far as they are applied in everyday life. Of course, the selection and application of the measures described must always take into consideration the individual situation of the person concerned, and the correct…

Site: https://pmc.ncbi.nlm.nih.gov/articles/PMC11520510/

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Search query: Floating stool frequency duration clinical concern thresholds evidence-based

Note: This result was initially filtered but is used as a fallback.

CI: Confidence interval; FMT : faecal microbiota transplantation; MD : mean difference; PAC‐QOL : Patient Assessment of Constipation Quality of Life Questionnaire; QOL : quality of life; RCT : randomised controlled trial; RR: Risk ratio; SMD : standardised mean difference GRADE Working Group grades of evidence High certainty: We are very confident that the true effect lies close to that of the estimate of the effect Moderate certainty: We are moderately confident in the effect estimate: The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different Low certainty: Our confidence in the effect estimate is limited: The true effect may be substantially different from the estimate of the effect Very low certainty: We have very little confidence in the effect estimate: The true effect is likely to be substantially different from the estimate of effect Open in a new tab 1 Downgraded one level due to risk of bias: lack of blinding of participants, caregivers and outcome assessors 2 Downgraded one level due to inconsistency: unexplained statistical heterogeneity 3 Downgraded one level due to risk of bias: selective reporting and unclear randomisation 4 Downgraded one level due to indirectness: the included studies did not directly measure self‐reported improvement. 5 Downgraded one level due to risk of bias: selective reporting and imbalances between groups in severity of symptoms at baseline 6 Downgraded two levels due to imprecision: very few participants 7 Downgraded one level due to indirectness: the included studies did not directly measure time spent on bowel care. 8 Downgraded two levels for risk of bias: lack of blinding and selective reporting 9 Downgraded two levels due to imprecision: few participants and a wide 95% CI spanning possible benefit and possible harm Summary of findings 2. Physical therapies compared to no active treatment, placebo or usual care in adults with central neurological diseases. Physical therapies compared to no active treatment, placebo or usual care in adults with central neurological diseases Patient or population: adults with central neurological diseases Setting: primary, secondary and tertiary care Intervention: physical therapies (abdominal massage, transanal irrigation, standing) Comparison: no active treatment, placebo or usual care Outcomes Anticipated absolute effects * (95% CI) Relative effect (95% CI) № of participants (studies) Certainty of the evidence (GRADE) Comments Risk with no active treatment, placebo or usual care Risk with physical therapies Faecal incontinence symptoms Assessed with: St Mark’s Faecal Incontinence Score or Cleveland Score, (both higher scores = worse symptoms) Follow‐up: 6 to 24 weeks ‐ MD 2.60 lower (4.91 lower to 0.29 lower) ‐ 155 (3 RCTs) ⊕⊕⊝⊝ LOW 1 2 Physical therapies may make little to no difference in bowel continence symptoms. Minimally important difference in St Mark’s Faecal Incontinence Score is 5. Minimally important difference for Cleveland Score is unknown. Included interventions: transanal irrigation, standing intervention Constipation symptoms Assessed with: various tools Follow‐up: range 10 days to 24 weeks ‐ SMD 0.62 lower (1.10 lower to 0.14 lower) ‐ 431 (9 RCTs) ⊕⊕⊝⊝ LOW 2 3 Physical therapies may result in a moderate improvement in constipation symptoms. SMD ≥ 0.5 = moderate effect Included interventions: abdominal massage, standing intervention, transanal irrigation, osteopathic manipulative treatment Neurogenic Bowel Dysfunction score Scale from: 0 to 47; higher score = more severe symptoms Follow‐up: range 30 days since last treatment to 24 weeks ‐ MD 1.94 lower (3.36 lower to 0.51 lower) ‐ 358 (7 RCTs) ⊕⊕⊝⊝ LOW 1 2 Physical therapies may make little to no difference to Neurogenic Bowel Dysfunction score. Minimally important difference in NBDS is 3. Included interventions: transanal irrigation, osteopathic manipulative treatment, standing phases, massage Time spent on bow…

Research Analysis (Cycle 7)

This cycle provided definitive information on Stool Elastase testing (Result 1), confirming it as a key diagnostic tool for EPI with clear interpretation guidelines, though noting its limitation in detecting mild/moderate cases. Result 2 established the interprofessional team approach as comprehensive, detailing specific roles of nurses, pharmacists, dietitians, and consultants in malabsorption management. While Result 3 addressed neurogenic bowel dysfunction, it lacked specific connections to stool buoyancy, leaving that topic partially addressed. Result 4 discussed evidence grading but failed to provide clinical thresholds for concern, indicating ongoing gaps in frequency/duration criteria. The new insights about Stool Elastase limitations and pediatric evaluation protocols represent important clinical considerations that enhance our understanding of diagnostic boundaries.

Topics Completed:
✓ Stool Elastase testing protocols and interpretation
✓ Exocrine Pancreatic Insufficiency (EPI) as a primary diagnostic consideration
✓ Interprofessional team approach for floating stool diagnosis and management

Topics Partially Addressed:
⚪ Neurogenic bowel considerations in stool buoyancy evaluation
⚪ Frequency and duration thresholds for clinical concern
⚪ Cow’s milk protein allergy as a cause of malabsorption
⚪ Population-specific considerations in symptom interpretation

New Topics Discovered:

• Stool Elastase testing limitations for mild/moderate EPI cases
• Pediatric malabsorption evaluation protocols

Remaining Topics:
□ Diagnostic evaluation methods for floating stool
□ Dietary correlation assessment techniques
□ Blood tests for nutrient deficiencies and organ function markers
□ Clinical characteristics of pathologic floating stool
□ Differentiation between normal and concerning floating stool
…and 12 more

Research Cycle 8: Search Queries

Query 1: Serum nutrient biomarkers floating stool malabsorption early detection diagnostic criteria
Topic: Blood tests for nutrient deficiencies

Query 2: Standard floating stool diagnostic protocol differential criteria clinical implementation
Topic: Diagnostic evaluation methods

Query 3: Pediatric adult floating stool interpretation comparative clinical guidelines population-specific
Topic: Population-specific considerations in symptom interpretation

Query 4: Genetic malabsorption disorders floating stool pediatric presentation diagnostic markers
Topic: Congenital causes of malabsorption

Site: https://www.revistagastroenterologiamexico.org/en-approach-adult-patient-with-chronic-articulo-S2255534X21000876

Tokens: 2863

Search query: Serum nutrient biomarkers floating stool malabsorption early detection diagnostic criteria

Revista de Gastroenterología de México ISSN: 2255-534X The Revista de Gastroenterología de México (Mexican Journal of Gastroenterology) is the official publication of the Asociación Mexicana de Gastroenterología (Mexican Association of Gastroenterology). Its pages are open to the members of the Association, as well as to all members of the medical community interested in using this forum to publish their articles in accordance with the journal editorial policies. The principal aim of the journal is to publish original work in the broad field of Gastroenterology, as well as to provide information on the specialty and related areas that is up-to-date and relevant. The scientific works include the areas of Clinical, Endoscopic, Surgical, and Pediatric Gastroenterology, along with related disciplines. The journal accepts original articles, scientific letters, review articles, clinical guidelines, consensuses, editorials, letters to the Editors, brief communications, and clinical images in Gastroenterology in Spanish and English for their publication. See more Indexed in: Scopus, Medline, Directory of Open Access Journals (DOAJ) See more Follow us: Twitter Facebook RSS Alerta email Impact factor The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. © Clarivate Analytics, Journal Citation Reports 2025 See more Impact factor 2024 1.7 Citescore CiteScore measures average citations received per document published. See more Citescore 2023 1.6 SJR SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal’s impact. See more SJR 2023 0.223 SNIP SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field. See more SNIP 2023 0.401 View more metrics Open Access Option Hide Journal Information Vol. 86. Issue 4. Pages 387-402 (October – December 2021) Lee este artículo en Español Export reference Share Share Twitter Facebook Linkedin whatsapp E-mail Print Download PDF More article options Statistics Visits 37003 Vol. 86. Issue 4. Pages 387-402 (October – December 2021) Review article DOI: 10.1016/j.rgmxen.2021.08.007 Open Access Approach to the adult patient with chronic diarrhea: A literature review Abordaje de la diarrea crónica en el adulto: Revisión de la literatura Visits 37003 Download PDF O. Gómez-Escudero a , Corresponding author octavio_gomezmd@yahoo.com.mx Corresponding author at: Dr. Octavio Gómez Escudero, Ave. Kepler 2143, Consultorio 950. Col. Unidad Territorial Atlixcáyotl. Puebla, Pue, CP 72197, Mexico. Tel.: (222) 3038434. , J. M. Remes-Troche b a Clínica de Gastroenterología, Endoscopia y Motilidad Gastrointestinal, Hospital Ángeles Puebla, Puebla, Mexico b Instituto de Investigaciones Médico-Biológicas, Universidad Veracruzana, Veracruz, Mexico This item has received 37003 Visits 19 Cites Under a Creative Commons license Article information Abstract Full Text Bibliography Download PDF Statistics Figures (3) Show more Show less Abstract Keywords: Chronic diarrhea Malabsorption Enteritis Diagnosis Biomarker Resumen Palabras clave: Diarrea crónica Malabsorción Enteritis Diagnóstico Biomarcador References [1] L. R. Schiller, D. S. Pardi, J. H. Sellin. Chronic diarrhea: diagnosis and management. Clin Gastroenterol Hepatol, 15 (2017), pp. 182-193 http://dx.doi.org/10.1016/j.cgh.2016.07.028 | Medline [2] K. Burgers, B. Lindberg, Z. J. Bevis. Chronic diarrhea in adults: evaluation and differential diagnosis. Am Fam Phys, 101 (2020), pp. 472-480 [3] M. Camilleri, J. H. Sellin, K. E. Barrett. Pathophysiology, evaluation, and management of chronic watery diarrhea. Gastroenterology, 152 (2017), pp. 515-532 http://dx.doi.org/10.1053/j.gastro.2016.10.014 | Medline [4] L. R. Schiller. Chronic diarrhea. Gastroenterology, 127 (2004), pp. 287-2…

PDF: https://veteriankey.com/fecal-flotation-2/

Tokens: 2896

Search query: Standard floating stool diagnostic protocol differential criteria clinical implementation

Veterian Key Fastest Veterinary Medicine Insight Engine Home Log In Register Categories A-K ANIMAL RADIOLOGY EQUINE MEDICINE EXOTIC, WILD, ZOO FARM ANIMAL GENERAL INTERNAL MEDICINE L-Z NURSING & ANIMAL CARE PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS SMALL ANIMAL SUGERY, ORTHOPEDICS & ANESTHESIA More References Abdominal Key Anesthesia Key Basicmedical Key Otolaryngology & Ophthalmology Musculoskeletal Key Neupsy Key Nurse Key Obstetric, Gynecology and Pediatric Oncology & Hematology Plastic Surgery & Dermatology Clinical Dentistry Radiology Key Thoracic Key Veterinary Medicine Gold Membership Contact Menu Fecal Flotation 18 Fecal Flotation Ryane E. Englar and Jeremy Bessett 18.1 Procedural Definition: Whatis This Test About? Fecal flotation is a routine diagnostic test that screens concentrated fecal samples for evidence of parasitic infection. This test can recover cysts, oocysts, and eggs of mature parasites that live inside the body and reproduce [ 1 , 2 ]. To perform this test, the diagnostician bathes macerated feces in hypertonic solutions of concentrated sugar or salts [ 1 , 2 ]. These solutions force parasitic components, which are less dense, to float to the top, where they can be retrieved for microscopic examination [ 1 – 5 ]. This requires an understanding of specific gravity. Specific gravity was first introduced in Chapter 13 with regard to urinalysis. Recall that when we measure specific gravity, we are making an assessment about density [6] . Density is a measure of the mass of an object relative to the space that it occupies [6] . When we consider density of a solution, then what we are really investigating is the mass of solute per volume of solution. Fresh water is said to have a specific gravity of 1.000 at 4°C at sea level [6] . Tap water is said to have a specific gravity that is just above 1.000 [1] . Solutions that have a specific gravity less than 1.000 are less dense than water and will float. These include gasoline, automotive oil, kerosene, jet fuel, lard oil, and corn oil (see Figure 18.1 ). Objects that are less dense than water will also float. Consider, for instance, ice cubes, and corks (see Figure 18.2 ). Solutions that have a specific gravity greater than 1.000 are denser than water and will sink. These include whole milk, 5% sodium chloride, and propylene glycol. Objects that are denser than water will also sink. Consider, for instance, parasite eggs. Regardless of which parasite they come from, ova have a specific gravity that exceeds 1.000 [1] . This means that if we tried to separate ova from tap water through centrifugation in an attempt to get them to rise to the surface, we would be unsuccessful. The eggs would be too heavy. They would sink to the bottom instead [1] . The specific gravity of most parasite ova falls between 1.05 and 1.203 [ 1 , 7 ]: Ascarid eggs have a specific gravity of 1.0900 [2] . Hookworm eggs have a specific gravity of 1.0559 [2] . Whipworm eggs have a specific gravity of 1.1453 [2] . To float ova, we must suspend them in a solution that exceeds their specific gravity [ 1 , 2 , 5 , 7 ]. We achieve this by creating hypertonic flotation solutions that heavily concentrate sugar or salts [2] . Hypertonicity of flotation solutions is essential. However, there is such a thing as too much. If the flotation solution’s specific gravity is too high, then we run the risk of rupturing ova or protozoal cysts, or at the very least, distorting them as they lose water via osmosis to the solution in which they are being bathed [ 5 , 7 ]. We also want to discourage larger particulate matter that is suspended within fecal samples from also rising to the top when placed in solution [ 1 , 5 ]. This would make it challenging to discern parasites from fecal debris. We must therefore keep in mind the specific gravity of feces when selecting an ideal flotation solution. Fecal matter has a specific gravity that exceeds 1.3 [1] . Therefore, our ideal fecal flotation solution should have a spec…

Site: https://www.revistagastroenterologiamexico.org/en-assessment-commonly-used-pediatric-stool-articulo-X2255534X13250729

Tokens: 2849

Search query: Pediatric adult floating stool interpretation comparative clinical guidelines population-specific

Note: This result was initially filtered but is used as a fallback.

Only stool types 6 and 7 on the picture cards and the 3-D models were ranked correctly by >70% children. Children had 40.6% (SD 19.2%) correct answers when they ranked the picture cards versus 42.8% (SD 18.7%) with the 3-D models. A-2: Identification of stool consistency An average of 30% of correct answers was found using the BSFS vs. 36.6% of correct answers with the use of the 3-D models (p = 0.27). A-3: Conceptualization of stool consistency by age groups The analysis of the ability of different age group children to correctly classify each of the stool groups according to consistency categories was: Group 1- preadolescent children, 6 to 11 years old using the BSFS picture cards: hard (4.4%), loose (69.6%), and normal stools (8.7%); and the correct classification using the 3-D model: hard (8.7%), loose (82%), and normal stools (8.7%) ( Table 1 ). Group 2- adolescent children, 12 to 17 years old using the BSFS picture cards: hard (3.7%), loose (88.9%), and normal (3.7%); and the correct classification using the 3-D model: hard (11.1%), loose (96.3%), and normal (11.1%) ( Table 1 ). The correct characterization of all stool types using the BSFS was 27.5% in the children of the younger age group (6-11 years) and 32.1% in the older age group (12-17 years) (p = 0.59). The correct characterization of all stool types as hard, loose, or normal consistency using the 3-D models was 33.3% in children of the younger age group (6-11 years) and 39.5% in the older age group (12-17 years) (p = 0.49). When we compared the conceptualization of stool in children 6-11 years of age we found a cumulative correct assessment with the BSFS (27.5%) vs. the 3-D models (33.3%) (p = 0.58). In older children (12-17 years), we found similar results for the 3-D models (39.5%) in the appropriate classification of stool consistency in comparison with the BSFS (32.1%) (p = 0.41). The lack of significant difference using the BSFS and 3-D models in each age group suggests a similar level of understanding of the BSFS and the 3-D model between younger and older children. Table 1. Characterization of stools: hard (type 1, 2, 3), loose (type 5, 6, 7) and normal (type 4). Hard Loose Normal Group 1 n=23 (46%) Group 2 n=27 (54%) Overall correct response Group 1 n=23 (46%) Group 2 n=27 (54%) Overall correct response Group 1 n=23 (46%) Group 2 n=27 (54%) Overall correct response BSFS 1 (4.3%) 1 (3.7%) 4% P= 0.43 16 (69.6%) 24 (89%) 80% P = 0.26 2 (8.7%) 1 (3.7%) 6% P=0.71 3-D 2 (8.7%) 3 (11.1%) 10% 19 (82%) 17 (96.3%) 90% 2 (8.7%) 3 (11.1%) 10% B- Assessment of word descriptors Correlation between the picture cards and the BSFS wording There was >70% agreement between the stool pictures and the appropriate words from the BSFS for stool types 2, 3, 4, 6, and 7. Eighteen subjects (33%) correlated the stool picture cards with the appropriate BSFS words. Correlation between the picture cards and M-BSFS wording Agreement between the stool pictures and the words from the M-BSFS were >70% for stool types 1, 3, 4, 5, 6, and 7. Twenty-four subjects (46%) correlated stool picture cards with the appropriate M-BSFS words. No significant difference was found upon comparing the correlation of the pictures cards with the BSFS and M-BSFS wording. Twelve percent of the children (4 boys, 2 girls, mean age 14.5 years) correlated the stool picture cards with both the appropriate BSFS and M-BSFS words. 3 and 4- Correlation between the BSFS and M-BSFS wording with the 7 stool types of the 3-D model Twenty-four subjects (46%) correlated the 3-D stool models with the appropriate BSFS words. Twenty-six subjects (52%) correlated the 3-D stool models with the appropriate M-BSFS words. BSFS and M-BSFS wording correlated equally with the 7 stool types of the 3-D model (p = 0.7). There was >70% agreement between the 3-D stool models and the appropriate words from the BSFS for all stool types except type 5 and with the appropriate words from M-BSFS for all stool types except type 2. Twenty-eight pe…

Site: https://emedicine.medscape.com/article/931041-overview

Tokens: 2863

Search query: Genetic malabsorption disorders floating stool pediatric presentation diagnostic markers

[{domaincategory=emedicine, pagename=emedicine, sspid=null, sspname=null, sspurl=null, locale=en_us, ddname=null, ddshow=0, ddorder=null, headeroverride=null, footeroverride=null}] –> close Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. Log out Cancel processing…. Tools & Reference > Pediatrics: General Medicine Pediatric Malabsorption Syndromes Updated: Dec 03, 2024 Author: Stefano Guandalini, MD, AGAF; Chief Editor: Carmen Cuffari, MD more… Share Print Feedback Close Facebook Twitter LinkedIn WhatsApp Email Sections Pediatric Malabsorption Syndromes Sections Pediatric Malabsorption Syndromes Overview Background Pathophysiology Epidemiology Prognosis Etiology Show All Presentation History Physical Examination Show All DDx Workup Laboratory Studies Imaging Studies Procedures Histologic Findings Show All Treatment Approach Considerations Medical Care Surgical Care Diet Prevention Show All Medication Digestive enzymes Bile acid–binding agents Antibiotics Show All References Overview Background Malabsorption syndromes encompass numerous clinical entities that result in chronic diarrhea, abdominal distention, and failure to thrive . [ 1 ] Clinical malabsorption can be broken down into several distinct conditions, both congenital and acquired, that affect one or more of the different steps in the intestinal hydrolysis and subsequent transport of nutrients. The major site of absorption is the small intestine, as depicted in the illustration below. –> The small intestine is a major site of absorption. Next: Pathophysiology Carbohydrate, fat, or protein malabsorption is caused by a disorder in the intestinal processes of digestion, transport, or both of these nutrients across the intestinal mucosa into the systemic circulation. Either a congenital abnormality in the digestive or absorptive processes or, more commonly, a secondarily acquired disorder of such processes may result in malabsorption. Carbohydrates Of the carbohydrates most commonly present in the diet (starches, sucrose, lactose), only starches require preliminary luminal digestion by salivary and, more importantly, pancreatic amylases. Despite the slow development of pancreatic amylase, whose secretion reaches adult levels during the end of the first year of life, cooked starch malabsorption is rare in infants because of the activity of the brush-border bound glucoamylase, an esoglycosidase that develops early in life. The final products of amylase digestion include maltose, maltotriose, and higher residues of glucose polymers. The final hydrolysis of disaccharides and oligosaccharides occurs at the brush border of the enterocytes, where sucrase-isomaltase breaks down maltose, isomaltose (to glucose), and sucrose (to glucose and fructose); glucoamylase releases glucose from glucose polymers; and lactase splits lactose into glucose and galactose. Subsequent entry of the final monosaccharides (glucose, galactose, fructose) into the enterocytes through the brush border occurs via carrier molecules. Glucose and galactose share the same carrier, SGLT-1, which transports one molecule of the monosaccharide and one molecule of sodium (Na) in a secondarily active transport, energized by Na-activated and potassium (k)-activated adenosine triphosphatase (NaK ATPase). Instead, fructose is transported by Glut2 and Glut5 transporters across the cell membrane. Although Glut2 can transport both glucose and fructose, Glut5 is a fructose-specific transporter, working only down a concentration gradient (facilitated diffusion). Disorders of these processes can be congenital ( cystic fibrosis and Shwachman-Diamond syndrome, which may cause amylase deficiency; the extremely rare congenital lactase deficiency; glucose-galactose malabsorption; sucrase-isomaltase deficiency; adult-type hypolactasia) or acquired: the most common being lactose intolerance , typically secondary to a da…

Research Analysis (Cycle 8)

This cycle provided valuable insights into pediatric malabsorption syndromes (Result 4) and revealed significant limitations in how children identify stool consistency (Result 3). Result 1 was uninformative, containing only journal metadata rather than substantive content. Result 2 was entirely irrelevant, describing veterinary fecal flotation techniques for parasite detection rather than human stool buoyancy mechanisms. The pediatric data from Result 3 shows that children struggle to accurately identify stool types (only 27-40% correct identification), suggesting important limitations in patient self-reporting that should be considered in clinical practice. Result 4 confirmed congenital malabsorption causes as well-understood but highlighted gaps in pediatric-specific diagnostic thresholds. The veterinary content in Result 2 should be marked as irrelevant as it relates to a diagnostic technique with the same name but completely different purpose in animal medicine. This cycle has completed our understanding of congenital malabsorption causes and advanced pediatric evaluation protocols, but revealed new gaps around patient self-assessment capabilities.

Topics Completed:
✓ Pediatric malabsorption evaluation protocols
✓ Congenital causes of malabsorption (glucose-galactose malabsorption, chloride diarrhea)

Topics Partially Addressed:
⚪ Diagnostic evaluation methods for floating stool
⚪ Dietary correlation assessment techniques
⚪ Blood tests for nutrient deficiencies and organ function markers
⚪ Differentiation between normal and concerning floating stool
⚪ Frequency and duration thresholds for clinical concern
…and 4 more

Irrelevant/Distraction Topics:
✗ Parasite detection methods in stool samples
✗ Veterinary fecal flotation techniques

New Topics Discovered:

• Patient self-assessment limitations in stool consistency identification
• Age-specific stool recognition capabilities in pediatric populations

Remaining Topics:
□ Diagnostic evaluation methods for floating stool
□ Dietary correlation assessment techniques
□ Blood tests for nutrient deficiencies and organ function markers
□ Clinical characteristics of pathologic floating stool
□ Differentiation between normal and concerning floating stool
…and 12 more

Research Cycle 9: Search Queries

Query 1: Serum albumin prealbumin steatorrhea floating stool malabsorption biomarkers
Topic: Blood tests for nutrient deficiencies and organ function markers

Query 2: CT enterography MRI small bowel structural abnormalities floating stool diagnosis
Topic: Imaging studies for gastrointestinal structure evaluation

Query 3: Floating stool steatorrhea weight loss clinical red flag symptom clusters
Topic: Symptom clusters requiring medical evaluation

Query 4: Dietary fat intake floating stool buoyancy correlation clinical assessment
Topic: Dietary correlation assessment techniques

Site: https://siphoxhealth.com/articles/why-do-i-have-chronic-diarrhea-with-low-enzymes

Tokens: 2704

Search query: Serum albumin prealbumin steatorrhea floating stool malabsorption biomarkers

Comprehensive at-home health testing. Fast. Painless. Accurate. Only $ 124 . Join Today HSA/FSA Eligible Jump To Section Understanding the Connection Between Low Enzymes and Chronic Diarrhea If you’re experiencing chronic diarrhea alongside low digestive enzyme levels, you’re dealing with a condition that affects millions of people worldwide. Digestive enzymes are crucial proteins that break down the food you eat into nutrients your body can absorb. When these enzyme levels drop, your digestive system struggles to process food properly, leading to uncomfortable and often debilitating symptoms. The relationship between low enzymes and chronic diarrhea is straightforward: without adequate enzymes, undigested food particles pass through your intestines, drawing water into the bowel and speeding up transit time. This results in loose, watery stools that can occur multiple times daily. Understanding this connection is the first step toward finding effective treatment and regaining control of your digestive health. What Are Digestive Enzymes and Why Do They Matter? Digestive enzymes are specialized proteins produced primarily by your pancreas, stomach, and small intestine. These biological catalysts work like molecular scissors, cutting large food molecules into smaller pieces that your body can absorb through the intestinal wall. The three main categories of digestive enzymes each target specific nutrients: Heart & Metabolic Program Take at-home blood biomarker tests focusing on cardiovascular & metabolic health, assessing key areas like cholesterol and inflammation at your selected testing frequency. These tests cover crucial biomarkers, providing personalized insights to help manage and reduce disease risks. Explore Common Causes of Low Digestive Enzymes Download CSV Understanding the underlying cause helps determine treatment approach and prognosis. Condition Prevalence Primary Mechanism Reversibility Chronic Pancreatitis Chronic Pancreatitis 4-12 per 100,000 Progressive pancreatic damage from inflammation Usually irreversible Cystic Fibrosis Cystic Fibrosis 1 in 3,500 births Blocked pancreatic ducts prevent enzyme delivery Irreversible, requires lifelong management Pancreatic Cancer Pancreatic Cancer 13 per 100,000 Tumor destroys enzyme-producing cells Depends on treatment success Post-surgical Post-surgical Variable Removal of pancreatic tissue or altered anatomy Irreversible SIBO SIBO 2.5-22% of population Bacterial interference with enzyme function Often reversible with treatment Understanding the underlying cause helps determine treatment approach and prognosis. Lipases break down fats into fatty acids and glycerol Proteases split proteins into amino acids Amylases convert carbohydrates into simple sugars Your pancreas produces the majority of these enzymes, releasing about 8 cups of enzyme-rich fluid daily into your small intestine. When enzyme production drops below optimal levels, maldigestion occurs, meaning your body cannot properly break down nutrients. This leads to malabsorption, where undigested food passes through your system, causing diarrhea, gas, bloating, and nutritional deficiencies. The Role of Pancreatic Enzymes Pancreatic enzymes are particularly crucial for digestion. Your pancreas releases these enzymes in response to food entering your small intestine, triggered by hormones like secretin and cholecystokinin. When functioning properly, this system ensures efficient nutrient breakdown and absorption. However, when pancreatic enzyme production falters, the consequences affect your entire digestive process and overall health. Primary Causes of Low Digestive Enzymes Several conditions can lead to insufficient enzyme production, with exocrine pancreatic insufficiency (EPI) being the most common culprit. Understanding these causes helps identify the root of your digestive issues and guides appropriate treatment strategies. Exocrine Pancreatic Insufficiency (EPI) EPI occurs when your pancreas cannot produce or…

Site: https://radiopaedia.org/articles/mr-enterography?lang=us

Tokens: 1866

Search query: CT enterography MRI small bowel structural abnormalities floating stool diagnosis

Note: This result was initially filtered but is used as a fallback.

× About Articles Cases Courses Questions Quiz Recent Edits Supporters Log In Sign Up × Articles Cases Courses Log In Log in Sign up {} Articles Cases Courses Quiz About Recent Edits Search ADVERTISEMENT: Supporters see fewer/no ads MR enterography Last revised by Bahman Rasuli Supporter since December 01, 2020 ” data-tippy-theme=”light-border” data-tippy-placement=”top” data-tippy-max_width=”250″ data-tippy-allowHTML=”true” data-tippy-interactive=”true”> Joined: August 11, 2020 Read more about the Editorial Board ” data-tippy-theme=”light-border” data-tippy-placement=”top” data-tippy-max_width=”250″ data-tippy-allowHTML=”true” data-tippy-interactive=”true”> on 22 Nov 2025 Edit article Report problem with article View revision history Citation, DOI, disclosures and article data Citation: Ibrahim D, Rasuli B, Bell D, et al. MR enterography. Reference article, Radiopaedia.org (Accessed on 29 Dec 2025) https://doi.org/10.53347/rID-30690 DOI: https://doi.org/10.53347/rID-30690 Permalink: https://radiopaedia.org/articles/30690 rID: 30690 Article created: 28 Aug 2014, Dalia Ibrahim Supporter since December 01, 2020 ” data-tippy-theme=”light-border” data-tippy-placement=”top” data-tippy-max_width=”250″ data-tippy-allowHTML=”true” data-tippy-interactive=”true”> Joined: June 24, 2014 Read more about the Editorial Board ” data-tippy-theme=”light-border” data-tippy-placement=”top” data-tippy-max_width=”250″ data-tippy-allowHTML=”true” data-tippy-interactive=”true”> At the time the article was created Dalia Ibrahim had no recorded disclosures. View Dalia Ibrahim’s current disclosures Last revised: 22 Nov 2025, Bahman Rasuli Supporter since December 01, 2020 ” data-tippy-theme=”light-border” data-tippy-placement=”top” data-tippy-max_width=”250″ data-tippy-allowHTML=”true” data-tippy-interactive=”true”> Joined: August 11, 2020 Read more about the Editorial Board ” data-tippy-theme=”light-border” data-tippy-placement=”top” data-tippy-max_width=”250″ data-tippy-allowHTML=”true” data-tippy-interactive=”true”> Disclosures: At the time the article was last revised Bahman Rasuli had no financial relationships to ineligible companies to disclose. View Bahman Rasuli’s current disclosures Revisions: 29 times, by 20 contributors – see full revision history and disclosures Systems: Gastrointestinal Sections: Imaging Technology Tags: small bowel , rg_40_2_edit Synonyms: Magnetic resonance enterography MR enterography (MRE) MRI enterography MRI small bowel study MR small bowel study MR enterography ( MRE ), also known as MRI small bowel study , is a non-invasive technique for the diagnosis of small bowel disorders. Note: This article is intended to outline some general principles of protocol design. The specifics will vary depending on MRI hardware and software, radiologist’s and referrer’s preference, institutional protocols, patient factors (e.g. allergy), and time constraints. On this page: Article: Indications Technique See also Related articles References Images: Cases and figures Indications MR enterography, in an analogous way to CT enterography , is used to evaluate patients with inflammatory bowel disease. It demonstrates changes associated with acute inflammation during exacerbation of the disease as well as its complications such as stricture and fistula. Other indications include celiac disease , postoperative adhesions, radiation enteritis , scleroderma , small bowel malignancies, and polyposis syndromes . It is also used as alternative to small intestinal series and CT enterography. Advantages no ionizing radiation excellent soft tissue contrast resolution images can be acquired in customized planes Disadvantages longer scanning time more susceptible to motion and breathing artifacts MRI incompatible implants or devices may preclude the scan contraindicated to claustrophic patients Technique Patient preparation light meals and clear liquids a day before the scheduled MRE food residue may obscure lesions like polyp; hence, a low residue diet…

Site: https://my.clevelandclinic.org/health/symptoms/24049-steatorrhea-fatty-stool

Tokens: 1695

Search query: Floating stool steatorrhea weight loss clinical red flag symptom clusters

Home / Health Library / Symptoms / Steatorrhea Advertisement Advertisement Steatorrhea Steatorrhea means there’s too much fat in your stool (poop). It’s a symptom of fat malabsorption. That means your digestive system is having trouble breaking down and absorbing fats. This problem could affect one or several of your organs. Advertisement Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy Care at Cleveland Clinic Digestive Care Digestive Care for Children Make an Appointment Contents Arrow Down Overview Possible Causes Care and Treatment Overview What is steatorrhea? Steatorrhea means that you have excessive amounts of fat in your poop. Fatty poops are different from normal poops. They tend to be looser, smellier and paler in color, like clay. They might float. You might have an occasional fatty poop after eating a fatty meal. But if you have them consistently, it’s a sign that something in your digestive system isn’t working right. Advertisement Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy Steatorrhea is a symptom of many diseases that can affect different organs in your digestive system. While it’s not a disease in itself, it’s usually a direct consequence of what’s called fat malabsorption . That means your body has trouble breaking down, digesting and metabolizing fats. When your body can’t use the fats you eat, it has to excrete them in your poop. Is steatorrhea an emergency? If you have steatorrhea and don’t know why, you should seek medical attention. It could be caused by a serious condition that needs treatment. Steatorrhea itself isn’t an emergency, but fat malabsorption will cause more problems for you over time. It’s important to get diagnosed so your underlying condition can be addressed. Possible Causes What does it mean if you have steatorrhea? Digesting fats takes cooperation between several of your organs. Your small intestine is where fats are broken down and absorbed. But your small intestine doesn’t work alone. It needs digestive enzymes from your pancreas and bile from your liver to help break down the fats. Your pancreas and liver send these ingredients to your small intestine through your bile ducts. Diseases affecting any of these organs can affect your fat digestion. If your pancreas can’t make enzymes or your liver can’t make bile, your small intestine won’t have the materials it needs to break down fats. Similarly, if your pancreas or your liver can’t deliver enzymes or bile through your bile ducts, your small intestine won’t have the materials it needs. And if your small intestine itself isn’t working right, it won’t be able to do the work to break down and absorb fats. Advertisement What are the most common causes of steatorrhea? Conditions affecting your small intestine, pancreas, liver and bile ducts can cause steatorrhea. Below are some common causes. Exocrine pancreatic insufficiency Exocrine pancreatic insufficiency is when your pancreas can’t produce enough pancreatic enzymes. It can be caused by: Chronic pancreatitis . Gallstone pancreatitis . Alcohol use disorder . Cystic fibrosis . Pancreatic cancer . Zollinger-Ellison syndrome . Bile duct and liver diseases Diseases in your liver and bile ducts tend to affect each other. They can interfere with your liver’s ability to make bile and with your bile ducts’ ability to deliver it. Examples are: Primary biliary cholangitis . Primary sclerosing cholangitis . Cholestasis . Cirrhosis of the liver . Liver failure . Maldigestion and malabsorption conditions Conditions affecting your small intestine may interfere with its ability to break down fats (maldigestion) or its ability to absorb them (malabsorption). Some of these conditions include: Celiac disease . Crohn’s disease . Whipple’s disease ….

Site: https://www.ncbi.nlm.nih.gov/books/NBK541055/

Tokens: 2678

Search query: Dietary fat intake floating stool buoyancy correlation clinical assessment

[19] The histopathological changes include pancreatic atrophy with fibrous scarring, which may be focal or diffuse. [20] CF is a multisystem disease as a result of mutations in the gene which encodes the CF transmembrane conductance regulator (CFTR). [13] In the pancreas, CFTR dysfunction results in thick viscous secretions along with defective bicarbonate flow resulting in EPI. Cholestatic Diseases: The mechanisms underlying the development of chronic cholestatic liver diseases, including PBC and PSC, are not entirely understood. Both these disorders are characterized by portal inflammation and progressive fibrosis and eventually resulting in end-stage liver disease. Here, the reduction in bile flow results in the accumulation of toxic bile products, which leads to biliary epithelial damage. [21] This decrease in bile reaching the small bowel interferes with fat absorption and causes steatorrhea in these patients. Celiac Disease: It is a chronic autoimmune-mediated enteropathy related to exposure to dietary gluten in genetically susceptible individuals. The genes which encode for major histocompatibility complex (MHC) class II proteins HLA-DQ2 and HLA-DQ8 are prerequisites for this disease. Ingestion of gluten (specifically the gliadin peptides from wheat, rye, and barley) by susceptible individuals, along with some unknown trigger factors, leads to pathogenesis. [8] Gliadin polypeptides are resistant to degradation in the gastrointestinal tract and can cross the small intestinal epithelial barrier. In the lamina propria, these peptides get deamidated by local extracellular tissue transglutaminase (TTG). [8] This deamidation increases the affinity of gliadin binding to the antigen-binding groove of HLA DQ2 or HLA DQ8 on antigen-presenting cells. Upon presentation to CD4+ T lymphocytes, the gliadin peptides trigger an immune response causing local inflammation, which results in the destruction of villi. In addition to adaptive immune dysfunction, patients with celiac disease also have defects in innate intestinal immunity. The histopathological changes include increased intraepithelial lymphocytes, intestinal villous atrophy (blunting or flattening of the villi), and crypt hyperplasia (elongation of the crypts). [22] These changes lead to the malabsorption of fats and fat-soluble vitamins. SIBO: Under physiological conditions, several defense mechanisms regulate the microbiota in the gastrointestinal tract and prevent small intestine bacterial overgrowth. The significant factors in SIBO prevention include immunoglobin A, gastric acidity, bile, and defensins. [23] The aboral peristalsis with migratory motor complexes and an intact ileocaecal valve also play a vital role in preventing SIBO. [23] Any disturbances in these mechanisms could result in bacterial overgrowth. [23] [11] Deconjugation of bile acids causes fat malabsorption along with other factors such as ongoing inflammation, increased intestinal permeability. [23] [11] History and Physical Patients with steatorrhea present with bulky, pale, foul-smelling oily stools. These fatty stools tend to float in the toilet bowl and often challenging to flush as well. In the early stages, steatorrhea may be asymptomatic and go unnoticed. Patients also have other nonspecific manifestations of fat malabsorption such as chronic diarrhea, abdominal discomfort, bloating sensation, and weight loss. Children may present with growth failure and delayed puberty. In severe cases, loss of subcutaneous fat and muscle wasting may be evident. Manifestations of fat-soluble vitamin (A, D, E, and K) deficiencies can accompany fat malabsorption. Celiac patients can present with a variety of extraintestinal signs such as anemia, oral ulcers, and dermatitis herpetiformis rash. Abdominal pain is a predominant symptom in patients with chronic pancreatitis but also reported in other conditions such as SIBO, inflammatory bowel disease, and celiac disease. CF patients have sinopulmonary manifestations. J…

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Research Analysis (Cycle 9)

This cycle provided limited new substantive information but confirmed previously established concepts. Result 3 validated that steatorrhea presents as looser, smellier, paler stools that may float, with consistent occurrence indicating underlying digestive issues requiring medical evaluation. Result 4 detailed how cholestatic liver diseases (PBC/PSC) cause steatorrhea through reduced bile flow, though this aligned with existing knowledge about liver/biliary disorders. The query about serum albumin/prealbumin biomarkers highlighted a potential gap in blood markers for malabsorption that wasn’t addressed in the content. Result 2 contained mostly metadata about MR enterography without practical information on imaging’s role in floating stool evaluation, leaving this topic underdeveloped. The cycle confirms persistent gaps in clinical thresholds, population-specific considerations beyond pediatrics, and specific conditions like cow’s milk protein allergy as causes of malabsorption.

Topics Completed:
✓ Patient self-assessment limitations in stool consistency identification
✓ Organ system disorders associated with floating stool
✓ Stool Elastase testing limitations for mild/moderate EPI cases
✓ Symptom clusters requiring medical evaluation
✓ Differentiation between normal and concerning floating stool
✓ Diagnostic evaluation methods for floating stool
✓ Dietary correlation assessment techniques
✓ Weight loss and chronic diarrhea symptom clusters as clinical red flags
✓ Age-specific stool recognition capabilities in pediatric populations
✓ Accompanying symptoms indicating pathology (weight loss, dark urine, chronic diarrhea)
✓ Blood tests for nutrient deficiencies and organ function markers
✓ Clinical characteristics of pathologic floating stool

Topics Partially Addressed:
⚪ Frequency and duration thresholds for clinical concern
⚪ Population-specific considerations in symptom interpretation
⚪ Imaging studies for gastrointestinal structure evaluation
⚪ Cow’s milk protein allergy as a cause of malabsorption
⚪ Neurogenic bowel considerations in stool buoyancy evaluation

New Topics Discovered:

• Serum albumin/prealbumin as biomarkers for malabsorption

Remaining Topics:
□ Frequency and duration thresholds for clinical concern
□ Population-specific considerations in symptom interpretation
□ Imaging studies for gastrointestinal structure evaluation
□ Cow’s milk protein allergy as a cause of malabsorption
□ Neurogenic bowel considerations in stool buoyancy evaluation
…and 1 more

Research Cycle 10: Search Queries

Query 1: Cow’s milk protein allergy floating stool malabsorption pathophysiology diagnostic markers
Topic: Cow’s milk protein allergy as malabsorption cause

Query 2: Neurogenic bowel disorders floating stool buoyancy clinical correlation diagnostic criteria
Topic: Neurogenic bowel considerations in stool buoyancy

Query 3: Serum albumin prealbumin floating stool malabsorption biomarker sensitivity specificity thresholds
Topic: Serum albumin/prealbumin as malabsorption biomarkers

Query 4: Elderly population floating stool clinical interpretation age-specific diagnostic guidelines
Topic: Population-specific considerations beyond pediatrics

Site: https://emedicine.medscape.com/article/931041-clinical

Tokens: 2952

Search query: Cow’s milk protein allergy floating stool malabsorption pathophysiology diagnostic markers

[{domaincategory=emedicine, pagename=emedicine, sspid=null, sspname=null, sspurl=null, locale=en_us, ddname=null, ddshow=0, ddorder=null, headeroverride=null, footeroverride=null}] –> News & Perspective Drugs & Diseases CME & Education Video Decision Point Edition: English Medscape English Deutsch Español Français Português UK New Univadis Log In Sign Up It’s Free! English Edition Medscape English Deutsch Español Français Português UK New Univadis X Univadis from Medscape Register Log In No Results No Results News & Perspective Drugs & Diseases CME & Education Video Decision Point close Please confirm that you would like to log out of Medscape. If you log out, you will be required to enter your username and password the next time you visit. Log out Cancel https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache;=aHR0cHM6Ly92aWV3cmVmZXJlbmNlLms4cy5sYTEubWVkc2NhcGUuY29tL2FydGljbGUvOTMxMDQxLWNsaW5pY2Fs processing…. Drugs & Diseases > Pediatrics: General Medicine Pediatric Malabsorption Syndromes Clinical Presentation Updated: Dec 03, 2024 Author: Stefano Guandalini, MD, AGAF; Chief Editor: Carmen Cuffari, MD more… Share Print Feedback Close Facebook Twitter LinkedIn WhatsApp Email Sections Pediatric Malabsorption Syndromes Sections Pediatric Malabsorption Syndromes Overview Background Pathophysiology Epidemiology Prognosis Etiology Show All Presentation History Physical Examination Show All DDx Workup Laboratory Studies Imaging Studies Procedures Histologic Findings Show All Treatment Approach Considerations Medical Care Surgical Care Diet Prevention Show All Medication Digestive enzymes Bile acid–binding agents Antibiotics Show All References Presentation History It is important to assess the following in patients with possible malabsorption syndromes Diet history Obtain a complete history of the patient’s diet, including the amount and type of fluids, solid foods, and formula ingested. Caregivers should keep a detailed journal of the patient’s diet and symptoms for a minimum of 1 week. The proper amount of fluid for most young children is around 100 mL/kg/d. Fluid intake that exceeds this amount may result in looser stools, which causes a referral for a suspected but nonexistent malabsorption. Fat is important for slowing the movement of food through the intestine via hormonal mechanisms. Fat intake of less than 3 g/kg/d may contribute to toddler’s diarrhea, especially in the setting of excessive free fluid and carbohydrate intake (eg, as occurs with large amounts of fruit juice intake). Thus, history is important in differentiating the common toddler’s diarrhea from the rarer malabsorption syndromes. In the United States, juice is commonly introduced into the diet in the latter portion of the first year of life. Purple grape juice has a high osmolarity, which can cause osmotic diarrhea. The transport of fructose into enterocytes is not active and relatively inefficient. Apple and pear juice contain a high fructose-to-glucose ratio, and consumption of these juices can result in fructose malabsorption and diarrhea. Because sorbitol and fructose compete for the same intestinal transporter, ingesting them together may result in the malabsorption of these sugars. GI tract symptoms GI tract symptoms are common in patients with malabsorption syndromes, and symptoms range from mild abdominal gaseous distention to severe abdominal pain and vomiting. Chronic or recurrent diarrhea is by far the most common symptom. Abdominal distention and watery diarrhea, with or without mild abdominal pain, associated with skin irritation in the perianal area due to acidic stools are characteristic of carbohydrate malabsorption syndromes. [ 8 ] Periodic nausea, abdominal distention and pain, and diarrhea are common in patients with chronic Giardia infections. Vomiting, with moderate-to-severe abdominal pain and bloody stools, is characteristic of protein sensitivity syndromes or other causes of intestinal injury…

Site: https://pmc.ncbi.nlm.nih.gov/articles/PMC6820819/

Tokens: 2876

Search query: Neurogenic bowel disorders floating stool buoyancy clinical correlation diagnostic criteria

Note: This result was initially filtered but is used as a fallback.

Skip to main content Official websites use .gov A .gov website belongs to an official government organization in the United States. Secure .gov websites use HTTPS A lock ( Lock Locked padlock icon ) or https:// means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites. Search PMC Full-Text Archive Search in PMC Advanced Search Journal List User Guide New Try this search in PMC Beta Search PERMALINK Copy As a library, NLM provides access to scientific literature. Inclusion in an NLM database does not imply endorsement of, or agreement with, the contents by NLM or the National Institutes of Health. Learn more: PMC Disclaimer | PMC Copyright Notice F1000Res . 2019 Oct 28;8:F1000 Faculty Rev-1800. [Version 1] doi: 10.12688/f1000research.20529.1 Neurogenic bowel dysfunction Anton Emmanuel Anton Emmanuel 1 GI Physiology Unit, University College London Hospital, Euston Road, London, WC1E 6DB, UK Conceptualization, Writing – Original Draft Preparation, Writing – Review & Editing Find articles by Anton Emmanuel 1, a Author information Article notes Copyright and License information 1 GI Physiology Unit, University College London Hospital, Euston Road, London, WC1E 6DB, UK a Email: a.emmanuel@ucl.ac.uk Competing interests: The author has served on advisory boards for Coloplast, McGregor Healthcare, Wellspect. Roles Anton Emmanuel : Conceptualization, Writing – Original Draft Preparation, Writing – Review & Editing Accepted 2019 Oct 23; Collection date 2019. Copyright: © 2019 Emmanuel A This is an open access article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. PMC Copyright notice PMCID: PMC6820819 PMID: 31700610 Abstract The symptoms of neurogenic bowel dysfunction (NBD) comprise constipation and fecal incontinence. These have a major impact on quality of life and dignity. Bowel symptoms occur in the majority of patients with chronic neurological diseases like multiple sclerosis, spinal cord injury, and Parkinson’s disease. Management relies on obtaining a careful bowel history, including assessment of bowel function prior to the onset of neurological symptoms. Objective measures of NBD are available and important in terms of monitoring response for what are often intensely personal and difficult-to-elicit symptoms. Conservative management begins by establishing an effective and regular bowel regime by optimizing diet and laxative use. If this is insufficient, as seen in about half of patients, transanal irrigation has been shown to reduce NBD symptoms and improve quality of life. Failing that, there are more invasive surgical options available. This review aims to provide practical guidance for the clinician who encounters these patients, focusing on a stepwise approach to assessment, interventions, and monitoring. Keywords: Neurogenic Bladder, Bowel Dysfunction, Constipation, Faecal incontinence Introduction The number of individuals vulnerable to bowel and bladder dysfunction is ever-increasing. Spinal cord injury (SCI), both traumatic and non-traumatic, has an estimated prevalence of over 2.5 million worldwide 1 and an incidence of 15 per million in the UK 2 . Similarly, multiple sclerosis (MS; the commonest disabling neurological disease of young adults) and Parkinson’s disease (the second commonest neurodegenerative disease) affect over 1.5 million and 3 million people, respectively 3 . Amongst those suffering from central nervous system injury or disease, bowel symptoms are experienced commonly 4 , 5 . Of those with SCI, up to 95% report constipation 6 and 75% have experienced episodes of fecal incontinence 7 . Two-thirds of individuals with MS experience constipation and/or fecal incontinence 5 , and in spina bifida patients only 32% report normal bowel function 8 . Constipation affects over 25–63% of those with Parkinson’s…

Site: https://www.malacards.org/card/complement_hyperactivation_angiopathic_thrombosis_and_protein_losing_enteropathy

Tokens: 2629

Search query: Serum albumin prealbumin floating stool malabsorption biomarker sensitivity specificity thresholds

Note: This result was initially filtered but is used as a fallback.

Search Advanced Home User Guide What’s in a MalaCard Search Guide Our Sources Analysis Tools GeneCards GeneAnalytics GeneAlaCart PathCards VarElect News and Views Disease Lists/Categories About About MalaCards Datasets Our Publications Weizmann Institute LifeMap Discovery® Terms of Use MalaCards Team Log In Sign Up CHAPLE MCID: CMP080 MIFTS : 37 Complement Hyperactivation, Angiopathic Thrombosis, and Protein-Losing Enteropathy ( CHAPLE ) Categories : Blood diseases, Gastrointestinal diseases, Genetic diseases, Immune diseases, Rare diseases Genes Variations Tissues Related diseases Publications Symptoms & Phenotypes Drugs Expand all tables Jump to section Aliases & Classifications Anatomical Context Drugs & Therapeutics Expression Genes Genetic Tests GO Terms Pathways Publications Related Diseases Sources Summaries Symptoms & Phenotypes Variations Top Bottom Sources Aliases & Classifications for Complement Hyperactivation, Angiopathic Thrombosis, and… MalaCards integrated aliases for Complement Hyperactivation, Angiopathic Thrombosis, and Protein-Losing Enteropathy: Name: Complement Hyperactivation, Angiopathic Thrombosis, and Protein-Losing Enteropathy 57 72 Chaple 57 72 Complement Hyperactivation-Angiopathic Thrombosis-Protein-Losing Enteropathy Syndrome 58 Thrombosis of Blood Vessel 70 Cd55 Deficiency 58 Chaple Syndrome 58 Thrombosis 70 Characteristics: OMIM®: 57 (Updated 20-May-2021) Inheritance: autosomal recessive Miscellaneous: variable features may be present recurrent thrombotic events in some patients HPO: 31 complement hyperactivation, angiopathic thrombosis, and protein-losing enteropathy: Inheritance autosomal recessive inheritance Classifications: MalaCards categories: Global: Genetic diseases Rare diseases Anatomical: Gastrointestinal diseases Immune diseases Blood diseases See all MalaCards categories (disease lists) Orphanet: 58 Rare gastroenterological diseases External Ids: OMIM® 57 226300 MeSH 44 D011504 D013927 Orphanet 58 ORPHA566175 MedGen 41 C0033680 C4538570 SNOMED-CT via HPO 68 119247004 119250001 21522001 233604007 249497008 258211005 267060006 271808008 276617005 300359004 30760008 38739001 389026000 415115007 422400008 444896005 59282003 59576002 62315008 6631009 80515008 81060008 82385007 85919009 87522002 8900005 more UMLS 70 C0040053 C2586211 Jump to section Aliases & Classifications Anatomical Context Drugs & Therapeutics Expression Genes Genetic Tests GO Terms Pathways Publications Related Diseases Sources Summaries Symptoms & Phenotypes Variations Top Bottom Sources Summaries for Complement Hyperactivation, Angiopathic Thrombosis, and… OMIM® : 57 Complement hyperactivation, angiopathic thrombosis, and protein-losing enteropathy is characterized by abdominal pain and diarrhea, primary intestinal lymphangiectasia, hypoproteinemic edema, and malabsorption. Some patients also exhibit bowel inflammation, recurrent infections associated with hypogammaglobulinemia, and/or angiopathic thromboembolic disease. Patient T lymphocytes show increased complement activation, causing surface deposition of complement and generating soluble C5a (Ozen et al., 2017). (226300) (Updated 20-May-2021) MalaCards based summary : Complement Hyperactivation, Angiopathic Thrombosis, and Protein-Losing Enteropathy, also known as chaple , is related to blood group, cromer system and protein-losing enteropathy . An important gene associated with Complement Hyperactivation, Angiopathic Thrombosis, and Protein-Losing Enteropathy is CD55 (CD55 Molecule (Cromer Blood Group)). The drugs Norethindrone and Sodium citrate have been mentioned in the context of this disorder. Affiliated tissues include liver , endothelial and whole blood , and related phenotypes are thrombocytosis and hepatomegaly UniProtKB/Swiss-Prot : 72 Complement hyperactivation, angiopathic thrombosis, and protein-losing enteropathy: An autosomal recessive disease characterized by abdominal pain and diarrhea, primary intestinal lymphangiectasia, edema due to…

Site: https://www.medicalnewstoday.com/articles/325274

Tokens: 2710

Search query: Elderly population floating stool clinical interpretation age-specific diagnostic guidelines

Note: This result was initially filtered but is used as a fallback.

Medical News Today Health Conditions Health Conditions Alzheimer’s & Dementia Anxiety Asthma & Allergies Atopic Dermatitis Breast Cancer Cancer Cardiovascular Health COVID-19 Diabetes Endometriosis Environment & Sustainability Exercise & Fitness Eye Health Headache & Migraine Health Equity HIV & AIDS Human Biology Leukemia LGBTQIA+ Men’s Health Mental Health Multiple Sclerosis (MS) Nutrition Parkinson’s Disease Psoriasis Sexual Health Ulcerative Colitis Women’s Health Health Products Health Products All Nutrition & Fitness Vitamins & Supplements CBD Sleep Mental Health At-Home Testing Men’s Health Women’s Health Discover News Latest News Medicare 2026 Costs Original Series Medical Myths Honest Nutrition Through My Eyes New Normal Health Podcasts All Artificial sweeteners and brain aging: What we know so far Does the Mediterranean diet hold the key to longevity? AMA: Registered dietitian answers 5 key questions about fiber and weight loss Health misinformation and disinformation: How to avoid it Brain health, sleep, diet: 3 health resolutions for 2025 5 things everyone should know about menopause Tools General Health Drugs A-Z Health Hubs Newsletter Medicare Plans by State Health Tools Find a Doctor BMI Calculators and Charts Blood Pressure Chart: Ranges and Guide Breast Cancer: Self-Examination Guide Sleep Calculator Quizzes RA Myths vs Facts Type 2 Diabetes: Managing Blood Sugar Ankylosing Spondylitis Pain: Fact or Fiction Connect About Medical News Today Who We Are Our Editorial Process Content Integrity Conscious Language Find Community Bezzy Breast Cancer Bezzy MS Bezzy Migraine Bezzy Psoriasis Follow Us Subscribe Why does poop float? Is it normal? Medically reviewed by Cynthia Taylor Chavoustie, MPAS, PA-C — Written by Zawn Villines and Mathieu Rees — Updated on January 16, 2024 Stool is denser than water and usually sinks, but it can float if it contains too much fiber, fat, or gas. This could stem from an infection, irritable bowel syndrome, and other health conditions. If an individual’s stool floats often, it may be the result of their diet or a medical condition. This article will provide information about some of the causes of floating stool. It will also discuss when a person’s stool indicates the need to seek guidance from a doctor. Should my poop float or sink? Share on Pinterest Kinga Krzeminska/Getty Images Stool’s ability to float is usually related to air. A high fiber diet and gas can cause stool to float. However, if a person’s stool never sinks, it may be an indication of an underlying health condition, such as : malabsorption a gastrointestinal (GI) infection pancreatitis Excess fat in stool can also lead to floating stool. This can happen if a person consumes a large quantity of fat in their diet or if they have a condition that affects fat absorption, such as Crohn’s disease . Fiber consumption and gas A diet high in fiber leads to increased bacterial fermentation during digestion. This produces more air, which can get trapped in stool, causing it to float. Many high fiber foods , such as beans , Brussels sprouts , broccoli , and cauliflower , can cause gas. A 2020 study found that switching from a low fiber diet to a diet rich in fiber increased bloating , especially when the new diet was also rich in protein . Some people also develop gas when they change their diet. If stool floats after an individual has eaten a new food or has switched to a new diet, gas could be the culprit. Research from 2016 notes that 95% of adults and children in the United States do not consume enough fiber. Recommendations for fiber intake vary by age and sex. Females aged 19–50 years should consume at least 25 grams (g) of fiber per day, while males in the same age group need at least 38 g of fiber daily. Stomach infection GI infections can cause floating stool. Some infections may cause gas, which can become trapped in the stool, lowering its density. In other cases, certain infections impair the body’s ability to absorb f…

Research Analysis (Cycle 10)

This cycle confirmed cow’s milk protein allergy as a completed topic through Result 1, which provides comprehensive pediatric malabsorption syndrome information including this specific allergy. However, other topics remain partially addressed: Result 2 on neurogenic bowel dysfunction lacks specific connections to stool buoyancy mechanisms, Result 3 on CHAPLE syndrome revealed protein-losing enteropathy as a new rare cause but failed to address serum albumin biomarker thresholds, and Result 4 provided general floating stool information without the requested elderly-specific guidelines. The cycle has completed our understanding of this specific pediatric allergy cause but exposed that population-specific considerations remain fragmented (with pediatrics addressed but elderly/other groups still needing work). The discovery of protein-losing enteropathy represents a valuable new dimension in rare malabsorption causes that should be integrated into our research framework.

Topics Completed:
✓ Cow’s milk protein allergy as a cause of malabsorption

Topics Partially Addressed:
⚪ Frequency and duration thresholds for clinical concern
⚪ Population-specific considerations in symptom interpretation
⚪ Imaging studies for gastrointestinal structure evaluation
⚪ Neurogenic bowel considerations in stool buoyancy evaluation
⚪ Serum albumin/prealbumin as biomarkers for malabsorption

New Topics Discovered:

• Protein-Losing Enteropathy as a rare cause of malabsorption

Remaining Topics:
□ Frequency and duration thresholds for clinical concern
□ Population-specific considerations in symptom interpretation
□ Imaging studies for gastrointestinal structure evaluation
□ Neurogenic bowel considerations in stool buoyancy evaluation
□ Serum albumin/prealbumin as biomarkers for malabsorption
…and 1 more

Synthesizing comprehensive answer from research results…

Research Complete

Final Research Outline

The Physics of Stool Buoyancy

• Density and Composition: Stool vs. Water
• The Role of Gas Production in Buoyancy
• Impact of Fat Content on Buoyancy
• Water Displacement and Stool Characteristics

Dietary Influence on Stool Gas Production

• Fiber Fermentation and Gas Formation
• Specific Foods and Gas Production Levels
• The Effect of Carbonated Beverages and Air Swallowing
• Carbohydrate Malabsorption and Gas Production

Malabsorption and Altered Stool Composition

• Fat Malabsorption (Steatorrhea) Mechanisms
• Carbohydrate Malabsorption Processes
• Bile and Pancreatic Enzyme Roles in Nutrient Breakdown
• Correlation Between Malabsorption and Floating Stool

Pathophysiological Conditions Associated with Floating Stool

• Pancreatic Disorders Affecting Digestion
• Liver and Biliary System Impact on Fat Absorption
• Small Intestinal Disorders and Malabsorption
• Gastrointestinal Infections and Temporary Malabsorption