Chapter 43: The Child With a Gastrointestinal Alteration

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Welcome back to the Deep Dive.

We are pulling a heavy one off the shelf today.

We're looking at Chapter 43 from Maternal Child Nursing, and the title is The Child with a Gastrointestinal Alteration.

It sounds a little dry on the surface, doesn't it?

It sounds incredibly dry.

Yeah.

It sounds like a lot of diaper changes and tummy aches, but when you actually get into the source material, the articles, the clinical alerts, the diagrams, this is probably one of the highest stakes chapters we've covered.

It really is.

I think people underestimate GI because, well, everyone vomits eventually.

Everyone gets a stomach bug.

It feels familiar.

Right.

But in pediatrics, the margin for error is razor thin.

We aren't just talking about messy cleanups or a kid who ate too much candy.

We're talking about congenital defects where the plumbing literally isn't connected, right?

We're talking about metabolic crises that can stop a heart.

And that's our mission today.

We're going to map out the entire pediatric GI landscape as it's presented in Chapter 43.

We're starting with the anatomy,

specifically why a kid isn't just a mini -adult.

Then we'll move into the structural defects, the things that happen before birth.

We've got issues,

infections, obstructions, the really scary mechanical blockages, and we'll finish with the liver.

It's a full roadmap.

And if there's one theme I want you, the listener, to hold onto, it's the detective work.

GI symptoms in children are often so vague.

My tummy hurts.

He's throwing up.

Yeah.

That tells you nothing.

Nothing.

The nurse's job is to take those vague signals and figure out if this is a laundry problem or a surgical emergency.

Safe practice means knowing the difference.

So let's start right at the foundation.

Section one, the pediatric difference.

The text emphasizes this idea that children are physiologically distinct from adults.

It's not just size.

Right.

It's function.

And the clinical reference section in the text throws some numbers at us that are honestly startling.

Look at stomach capacity.

This one blew my mind.

A newborn day one.

What are we working with?

10 to 20 milliliters.

10 to 20.

That is what, a tablespoon?

Roughly.

It's the size of a large marble or a walnut.

I mean, it's tiny.

Now compare that to an adult stomach, which can hold 2 ,000 to 3 ,000 milliliters.

So two to three liters.

Yeah.

That is a massive, massive discrepancy.

It changes everything about how you feed a baby.

So when we talk about small, frequent feedings for a newborn, that's not a lifestyle choice.

Right.

It's physics.

It's a volumetric requirement.

If you try to feed a newborn four ounces, which is about 120 millimiles, you are literally overfilling the tank by 600%.

It has nowhere to go but back up.

Which makes perfect sense.

And that leads us to the next point, which is peristalsis.

The movement of the gut.

The text mentions that in infants, this is faster.

Much faster.

Food moves through the stomach really quickly, which, you know, contributes to that need for frequent feeding.

But here's the fact that the valves can easily reverse an infant.

Reverse, you mean?

Yeah.

Coming back up.

Vomiting.

Regurgitation and vomiting.

Exactly.

The valve systems aren't fully mature yet.

In adults, it's a one -way street usually.

But in infants, that lower esophageal sphincter is loose.

It's a bit more of a two -way street.

So all that spitting up we see, it's not always a sign of illness.

Not at all.

Sometimes it's just a sign of a full tank and a loose lid.

That explains a lot of laundry.

Okay.

What about the liver?

We usually think of the liver as this like powerhouse detoxifier.

In adults, yes.

But the neonatal liver is immature.

It's really inefficient at detoxifying things.

This has huge implications for medication administration.

Right.

You can't dose a baby like an adult because their liver just can't break down the drugs as fast.

It also affects their vitamin storage.

They just don't have the reserves we do.

And one thing that really stood out to me in that clinical reference section was fluid balance.

We all know dehydration is a big risk for kids, but the text explains specifically why.

And it comes down to the large intestine.

In an infant, it's relatively short and it has less epithelial lining to absorb water.

So less surface area for absorption.

Exactly.

So stools are naturally softer and they move faster.

They lose water much more easily than we do.

And kids have a higher metabolic rate too, don't they?

That's the other piece of the puzzle.

They burn through fluid faster.

So if you combine a short bowel that doesn't absorb water well with a high metabolic rate, and then you add a stomach virus on top of that.

That sounds like a perfect storm for dehydration.

It's a cascading failure.

An infant can slide into dangerous dehydration much, much faster than an adult would.

So given this really fragile anatomy, the text highlights a nursing quality alert about assessment.

It basically says don't just write vomiting in the chart.

Vomiting tells me nothing.

If you call a physician and say the kid is vomiting, the first thing they're going to do is grill you.

You need the characteristics.

Is it bilious?

That means green, right?

From bile.

Bright green.

That tells us the blockage is likely below the bile duct.

And that is a surgical emergency.

Or is it bloody?

Is it just dribbling out or is it projectile?

And the volume.

I love the tip in the book about estimating volume on a bed sheet.

Right.

If you can't measure it in a basin, you ask how big was the circle on the sheet?

Was it the size of a saucer?

A dinner plate?

That gives you a tangible metric to estimate fluid loss.

It turns a vague complaint into actual clinical data.

Okay, let's move to section two.

Disorders of prenatal development.

So these are things that happen, you know, before the baby's even born.

And the first one is cleft lip and palate.

This is the most common congenital craniofacial deformity.

It's a failure of the KIPP or the palate to fuse during those really early weeks of pregnancy.

It's actually pretty prevalent, especially in Asian and Native American populations.

And visually, it's very obvious, especially the cleft lip.

But the text really emphasizes that the primary nursing priority isn't cosmetic at all.

It's nutritional.

Absolutely.

Think about how a baby eats.

They need to create suction, a vacuum, to pull milk from a nipple.

Right.

If you have a cleft, a hole in the lip, or especially in the palate, you cannot create that seal.

You just can't generate suction.

So they can literally starve even if they're trying to eat.

Exactly.

They are working hard, burning calories, but getting nothing.

Or worse, the milk that does get in goes up into the nasal cavity, which leads to aspiration.

So the nurse's role is educating parents on special feeding techniques.

The text mentions specialized bottles.

Yes, like the Haberman feeder.

These bottles utilize compression rather than suction.

You gently squeeze the milk into the baby's mouth so they don't have to generate that vacuum.

You're essentially doing the work for them while they learn to swallow safely.

And then comes the surgery.

The post -op care seems incredibly strict here.

It has to be.

You have a very delicate suture line on the lip or inside the mouth.

The rule is, protect the site.

No straws, no spoons, no hard pacifiers, and definitely no fingers in the mouth.

I can imagine that's so tough with a toddler or an infant who just wants to self -soothe.

It's incredible.

Now, moving to another structural defect that just sounds like a true emergency.

Esophageal atresia, or EA,

and tracheosophageal fistula, PEF.

Can you kind of explain the mechanics here?

Yeah, so this is a failure of the plumbing to separate during development.

Normally, the trachea, your wind pipe, and the esophagus, your food pipe, are two completely separate tubes.

Right.

In esophageal atresia, the esophagus is a blind pouch.

It just ends.

It doesn't connect to the stomach.

So food has nowhere to go.

Nowhere.

And in TEF, which often happens with it, there's a fistula and abnormal connection between the trachea and the esophagus.

The most common type, which is shown in figure 43 .2, involves that blind esophageal pouch and then a fistula connecting the stomach directly to the trachea.

That sounds incredibly dangerous.

The source material has a very specific safety alert for this, the three Cs.

Yes.

Every nursing student needs to memorize these.

Coughing, choking, and cyanosis.

So if a newborn is feeding for the first time and they start coughing, choking, and turning blue.

You stop immediately.

That is a massive red flag for TEF.

The fluid is either overflowing from that blind pouch and spilling into the lungs or it's passing through the fistula from the stomach into the lungs.

It is an aspiration nightmare.

What's the immediate action?

What do you do?

First, stop the feed.

The baby needs to be NPO nothing by mouth.

You elevate the head of the bed to 30 or 40 degrees.

That helps keep any gastric juices down in the stomach and not refluxing up through the fistula into the lungs.

And then you prepare for surgery.

This is a surgical fix.

And post -op, these kids often end up with a G -tube, right?

A gastrostomy tube.

Often, yes.

A G -tube goes directly into the stomach to bypass the healing esophagus.

The patient -centered teaching section in the text talks about teaching parents how to clean the site.

And interestingly, the importance of using pacifier during G -tube feeds.

Why a pacifier if they aren't eating by mouth?

That seems counterintuitive.

This is so crucial for development.

We call it sham feeding or non -nutritive sucking.

We want the infant to associate the feeling of a full stomach with the act of sucking.

It preserves that developmental reflex.

Oh, I see.

So that when they can eat orally, they still know how.

It connects the brain to the belly.

It's not just about calories.

It's about wiring the nervous system correctly.

That's fascinating.

Okay, let's slide into section three.

Motility disorders.

This is where things aren't necessarily blocked, but they just aren't moving right.

And first up is reflux.

G -E -R versus G -E -R.

Right.

I feel like every parent says their baby has reflux.

But there's a really important distinction in the text between physiologic G -E -R and pathologic G -E -R.

It's a huge difference.

G -E -R is what we call the happy spitter.

The baby eats, they spit up some formula, but they're gaining weight.

They aren't crying in pain and they're hitting all their milestones.

That's a laundry problem, not a medical one.

And G -E -R.

G -E -R is when it becomes a disease.

The D stands for disease.

This child is failing to thrive.

They aren't gaining weight.

They are irritable, arching their back in pain during fees because of the acid burn from the reflux.

They might even have respiratory issues like apnea or asthma because that acid is constantly irritating the airway.

And the cause is that lower esophageal sphincter, the LES.

Right.

In infants, it's short and immature.

I like to describe it as a loose drawstring on a bag.

It just doesn't stay cinched tight.

So how do we manage it?

The text mentions diet and positioning first.

Right.

You always start with the most conservative measures.

Small frequent feedings, again.

Thickening the formula with a little bit of rice cereal.

It just makes it heavier, so it's more likely to stay down.

And then positioning, keeping the baby upright after feeds for at least 30 minutes.

What about sleeping?

I've heard different things about that.

This is a tricky one.

Prone positioning, so on the tummy, actually decreases reflux events,

but we never ever recommend it for sleep due to the risk of esides.

Okay, that's critical.

The risk of sudden infant death syndrome far outweighs the benefit for reflux.

So prone position is only for when the baby is awake and you are directly supervising them.

And if all of that doesn't work.

Then we move to medications like proton pump inhibitors, PPIs like omeprazole, and in the most severe cases, surgery.

A Nissen fund application.

What is that exactly?

They essentially take the top part of the stomach, the fundus, and wrap it around the lower esophagus to create a new, tighter valve.

Wow.

Okay, let's talk about the other end of the motility spectrum.

Constipation.

A very, very common problem in pediatrics.

The text describes this cycle of pain.

I think this is so important for parents and nurses to understand.

It's not just the child being stubborn.

No, it's physiological.

It starts with one painful stool.

Maybe they were a little dehydrated or their diet changed.

It hurt to poop.

So the next time the urge comes, the child voluntarily holds it in to avoid that pain.

Which just makes the stool sit in the rectum longer.

Exactly.

And the colon's job is to absorb water.

So that retained stool gets harder, drier, and bigger.

The rectum stretches out to accommodate it.

Over time, the sensation to go, that urge, it fades.

So when they finally do have to go, it hurts even more.

And the cycle just reinforces itself.

And this leads to something called encaprisis.

Can you define that?

Encaprisis is so often misunderstood.

It's the leakage of loose, liquid stool around a hard, impacted mass of stool in the rectum.

Parents often think the child has diarrhea, or they think the child is soiling themselves on purpose out of it.

They can't.

The liquid stool is just seeping past the blockage.

And they can't control it because the rectum is so distended, they've lost that normal sensation.

That's just heartbreaking.

So the success in management, the tech says, can take months.

Oh yes.

It's bowel retraining.

It's a long process.

You have to clear the impaction first, often with enemas or high -dose laxatives.

Then you start daily stool softeners like polyethylene glycol to keep things moving, plus plenty of fluids and fiber.

But you have to give that distended rectum time to shrink back down and for the child to relearn the sensation.

It's a marathon, not a sprint.

Moving on to section four, inflammatory and infectious conditions.

Let's talk about the classic stomach bug,

infectious gastroenteritis.

Rotavirus, norovirus, bacteria, parasites.

It's extremely common.

But in kids, as we discussed in the anatomy section, the real enemy is dehydration.

What are the key signs you're looking for?

The classic signs are sunken fontanels.

That soft spot on a crying.

Poor skin turgor.

If you gently pinch the skin on the abdomen, it stays tinted up.

And dry mucus membranes like a tacky or dry mouth.

The text suggests a really useful assessment method called ACCT.

Right.

Amount, color, consistency, and time.

Nurses need to track every single stool and vomit episode using ACCT to accurately gauge fluid loss.

A lot of poop isn't measured.

Three large watery green stools in the last hour is clinical data.

And the treatment of choice is ORT, oral rehydration therapy.

This is the gold standard.

Small amounts frequently.

We're talking five millimiles in a syringe or on a spoon every five to 10 minutes.

If you give a dehydrated, nauseous kid a full bottle, they will almost certainly vomit it right back up.

You have to go slow.

And what about giving them juice or soda?

I remember getting ginger ale as a kid when I was sick.

Yeah, that's a common misconception.

The text actually advises strongly against that.

High sugar drinks like colas or apple flus have a very high osmolarity.

They can actually pull more water into the gut via osmosis and make the diarrhea worse.

Oh, wow.

You want to stick to an oral rehydration solution like Pedialyte, which has the right balance of electrolytes and a small amount of sugar to help with absorption.

That's really good to know.

Now let's talk about appendicitis.

This is a classic surgical emergency.

It is inflammation of the appendix.

It typically starts with this vague, dull pain around the belly button.

And then over several hours, it migrates and localizes to the right lower quadrant.

To McBurney's point.

Exactly.

McBurney's point.

That's about midway between the right anterior superior iliac crust, the front of the hip bone and the umbilicus.

You often get rebound tenderness there.

It hurts more when you let go of the pressure than when you press down.

There is a very specific and frankly scary danger sign in the text.

The false hope.

This is so critical for nurses to know.

A child comes into the ER, they're screaming in pain, writhing, inconsolable.

And then suddenly they stop crying and say, I feel better.

The pain is all gone.

Well, the parents think, oh, thank goodness it was just gas after all.

But the nurse should be thinking, the appendix just ruptured.

When it perforates, the intense pressure is released and the pain stops for a moment.

But now all that infectious bowel content is spilling into the peritoneum.

Peritonitis and sepsis are coming next.

That moment of relief is actually the calm before the storm.

That is terrifying.

So if that happens, it's an immediate trip to the OR.

Absolutely.

And IV antibiotics and a much longer, more complicated hospital stay.

And another key point, we never apply heat to the abdomen if we suspect appendicitis.

Heat increases blood flow and inflammation and can actually cause a non -ruptured appendix to rupture.

Okay, let's touch on chronic inflammation, inflammatory bowel disease, or IBD.

The text breaks it down into Crohn's and ulcerative colitis.

What's the quick distinction for our listeners?

The easiest way to remember is location, location, location.

Ulcerative colitis, or UC, is limited to the colon and rectum.

It's continuous inflammation starting at the rectum and moving up.

Crohn's disease can affect any part of the GI tract from the mouth to the anus.

And it has what we call skip lesions.

So you'll see a patch of healthy bowel, then a diseased patch, then another healthy patch.

It's patchy.

And for kids, the text says growth failure is a major sign.

It's a huge sign.

If you have chronic inflammation and malabsorption in your gut, you aren't getting the nutrients you need to grow.

Sometimes short stature or delayed puberty is the very first sign, even before the major GI symptoms get really bad.

And what about the psychosocial impact?

That has to be immense.

It's profound.

Imagine being a teenager who needs to use the bathroom 20 times a day, sometimes with urgency, or having a temporary ostomy bag, or taking high dose steroids that give you a puffy moon face.

The body image issues, the social isolation.

It's a huge part of the disease.

Nursing care has to include that mental and emotional health support.

Absolutely.

Okay, let's get into the mechanics of section five, obstructive disorders.

So now something is physically blocking the way.

First up, hypertrophic pyloric stenosis.

This usually hits infants around three to five weeks of age.

The pylorus, which is the muscle at the bottom of the stomach that lets food into the small intestine, it thickens.

It becomes huge, hypertrophied.

The text calls it the olive.

Yes, because a skilled examiner can sometimes palpate a hard, mobile, olive -shaped mass in the right upper quadrant.

That's the thickened muscle.

It clamps shut.

So the stomach tries to push food through, but it can't.

And the result is vomiting.

But not just any vomiting.

Projectile.

We are talking three to four feet across the room.

It's impressive and scary.

And it's non -dilious because the blockage is before the bile decks.

And the key thing is the baby is hungry, even ravenous, immediately after vomiting because they didn't digest a thing.

And there's a key metabolic consequence here too, isn't there?

Yes, metabolic alkalosis.

They are vomiting up pure stomach acid, so they're losing a ton of acid, and their body's pH rises, becoming alkalotic.

You have to correct those electrolytes with IV fluids before they can safely go to surgery for the fix, which is a pyloromyotomy.

Okay, next obstruction.

Intussusception.

I always struggle to say that word.

It's a mouthful.

Intussusception.

The glove analogy in the text really helped me visualize it.

It's the perfect analogy.

Imagine taking a rubber glove and pushing one of the fingers inside out back into the hand of the glove.

That's what the bowel does.

One portion telescopes into another.

Usually it's the ileum into the cecum.

And this cuts off the blood supply to that part of the bowel.

Right.

It causes edema, inflammation, and eventually necrosis.

The classic triad of symptoms here is, first, sudden paroxysmal pain.

The child is playing happily, then suddenly screams and pulls their legs up to their chest, and then a few minutes later they're fine again.

Okay.

Second, you can feel a sausage -shaped mass in the abdomen.

And third, the hallmark sign.

Current jelly stools.

Current jelly.

What does that mean?

It's a mix of blood and mucus from the ischemic bowel.

It looks exactly like dark red jelly.

If you see that in a diaper, you should immediately think intussusception.

And the treatment is actually really cool.

It's not always surgical.

That's right.

Often they can fix it with a hydrostatic reduction.

They do an air enema or a barium enema.

The pressure of the air or the fluid literally pushes the telescoped bowel back out.

It unfolds it.

So it's diagnostic and therapeutic at the same time.

Exactly.

If it works, the child often passes a normal brown stool and you know the reduction was successful and surgery has been avoided.

That is amazing.

Okay.

The last obstruction in this section, Hirschsprung disease,

also known as congenital aganglionic megacolon.

This is a nerve problem.

During fetal development, the nerve cells, the ganglion cells that are supposed to tell the bowel to squeeze and relax, they don't migrate all the way to the end of the colon.

So you have a segment of colon, usually near the rectum, that has no nerves.

So it just sits there.

It can't move.

It stays clamped shut.

There's no peristalsis in that segment.

So it acts like a functional blockage.

Stool backs up behind it, causing the healthy part of the colon above the blockage to stretch out and become huge, which is where the megacolon part of the name comes from.

And a tailtail newborn sign.

Failure to pass meconium in the first 24 to 48 hours of life.

Every newborn should poop within two days.

If they don't, you have to have a high index of suspicion for Hirschsprung.

And later on, if it's not caught, the schools are described as ribbon -like.

Yes, because they're being squeezed through that tiny narrow clamped down aganglionic segment.

They come out flat and are often very foul smelling.

The treatment is surgery to remove that bad section of bowel.

A temporary colostomy may be needed while everything heals.

Okay, section six, malabsorption disorders.

We touched on this with IBD, but let's talk specifically about celiac disease.

This is so often misunderstood as just an allergy or a diet fad.

It is a serious autoimmune response to gluten, the protein found in wheat, barley, and rye.

And what actually happens inside the gut when someone with celiac eats gluten?

The gluten triggers an immune attack on the villi, the tiny finger -like projections in the small intestine that absorb all our nutrients.

They get flattened and destroyed,

atrophied.

So you lose all that crucial surface area you need to absorb food.

So you could be eating a healthy diet, but you're essentially starving because you can't absorb it.

Exactly.

The classic symptoms include statorrhea, which are fatty, foul smelling, floating stools because you aren't absorbing fat.

You see muscle wasting, a distended abdomen, and anemia.

And there is something mentioned called a celiac crisis.

That sounds serious.

It is.

If a child with undiagnosed celiac gets a GI infection or even just eats a large amount of gluten, they can have profuse watery diarrhea and vomiting that leads to severe dehydration and metabolic acidosis.

It's a medical emergency that requires IV fluids.

And the education here is lifelong, right?

There's no cure.

Lifelong, stripped, 100 % gluten -free diet.

And it's the nurse's job to really explain to the won't hurt situation.

Every exposure to gluten causes damage to the gut.

Another malabsorption issue is short bowel syndrome or SBS.

This is usually a result of surgery.

Maybe an infant had NC necrotizing enterocolitis or a volvulus, a twisting of the bowel, and surgeons had to remove a large portion of the small intestine.

The bowel is now physically too short to absorb enough nutrients to sustain life.

So how do these children survive?

Total parenteral nutrition or TPN, which is given through a central line.

All their nutrition goes directly into the bloodstream, bypassing the gut entirely.

But TPN has major risks associated with it.

It does.

The risk of a central line infection is constant and can be life -threatening.

But also long -term TPN is incredibly hard on the liver.

It can cause TPN -associated cholestasis and eventually liver failure.

So what's the goal?

The goal is always to transition to enteral feeds, even tiny amounts, as soon as possible.

Giving food to the gut, even a trickle, stimulates it to grow and adapt.

The hope is that the remaining bowel will eventually lengthen and become more efficient at absorption.

Which brings us perfectly to our final section, hepatic disorders.

Let's talk about the liver, starting with biliary atresia.

This is a blockage or even a complete absence of the extra hepatic bile ducts.

So bile is made in the liver, but it can't get out to the intestine to help digest fat.

It just backs up in the liver.

Causing damage.

Yes, it causes inflammation and cirrhosis, which is scarring very, very quickly.

The classic signs are jaundice that persists past two weeks of life, and the stools, they are acolic.

Acolic.

What does that mean?

It means pale, clay -colored, or even white.

Bile is what gives poop its normal brown color.

If bile is blocked from reaching the gut, the poop has no color.

At the same time, the urine gets very dark, almost like tea, because the body is trying to excrete all that excess bilirubin through the kidneys.

And the treatment is the COSI procedure.

Yes, it's a hepatoportoenterostomy.

Surgeons connect a loop of the child's own intestine directly to the liver to try and create a new drainage path for the bile.

But, frankly, it's often a bridge.

It buys time for the child to grow big enough and strong enough for a liver transplant, which is the ultimate cure.

And finally, cirrhosis.

We usually associate this with alcohol use in adults, but kids get it too, often as a result of something like biliary atresia.

It's the end stage of liver damage.

The liver tissue is replaced by scar tissue, and it becomes hard and lumpy.

Blood can't flow through it easily anymore.

Which leads to a condition called portal hypertension.

Right.

High pressure in the portal veins system.

This causes three big complications that nurses need to be watching for constantly.

One is a sites a massive fluid buildup in the abdomen.

Two is esophageal varices.

And these are swollen veins in the throat?

Yes, in the esophagus.

And because of high pressure, they can burst.

If they burst, it is a catastrophic, life -threatening bleed.

You'll see bloody emesis.

It's a true emergency.

And what's the third complication?

Hepatic encephalopathy.

A healthy liver clears toxins like ammonia from the blood.

When the liver is failing, ammonia builds up and goes to the brain.

The child becomes confused, lethargic, irritable, and can progress to a coma.

We treat it with a medication called lactulose, which helps them poop out the excess ammonia.

Also, a really important safety alert.

No Tylenol.

Absolutely no acetaminophen.

It's hepatotoxic.

It's metabolized by the liver.

If your liver is already failing, even a normal dose of Tylenol can be dangerous.

Wow.

We have covered an immense amount of ground.

For the mouth, with cleft lip, all the way down to the rectum with Hirschbrunn, and then the accessory organs.

It's a full journey through the system.

To wrap this all up, let's go back to that outro thought.

The nursing process.

How does it all tie together?

It always comes back to this.

Recognize cues.

Your assessment.

Analyze cues.

Your nursing diagnosis.

Take action.

Your interventions.

You have to see the sunken fontanel to know it's dehydration.

You have to recognize that the current jelly stool is a sign of in exception.

You have to hear that a child's sudden relief from pain might mean a ruptured appendix.

The assessment is everything.

And the final takeaway from the chapter regarding family education.

The nurse is the bridge from the hospital to home.

Whether it's teaching a parent how to manage a new G -tube, or how to read labels for a gluten -free diet, or just how to spot the early signs of dehydration, the nurse is the one who determines if that family feels safe and competent going home.

You empower them to care for their child.

And that's one of the most important things we do.

That's a powerful note to end on.

Thank you for walking us through this really complex, but super important deep dive.

My pleasure.

It was great.

And to our listener, take this knowledge, digest it, and use it to keep your patients safe.

From the Last Minute Lecture Team, thank you and good luck.