Chapter 42: Alterations of Musculoskeletal Function in Children

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Hello deep divers.

Have you ever really stopped to think about how a child's body, especially their bones and joints, handles,

problems, it's such a dynamic system?

It really is.

And any issue, injury or disease, can genuinely reshape their future in ways you just don't see in adults.

Exactly.

So today, we're taking a deep dive into alterations of musculoskeletal function in children.

We're pulling insights straight from Understanding Pathophysiology, the seventh edition.

Right.

You there, McCants, Brashers and Rote.

Good stuff.

Our goal here is pretty simple.

Give you a clear, structured handle on some key pediatric musculoskeletal conditions.

What they are, why they're different in growing bodies, you know, what the impact is.

Yeah, without needing the textbook right in front of you, we'll cover things kids are born with, infections, even tumors,

and non -accidental trauma.

And really focus on how these conditions develop differently in kids.

That immature skeleton is key.

It reacts completely differently to injury and treatment than an adult one.

Absolutely.

The growth plates, the cartilage, the way bone remodels, it all plays a massive role and can lead to, well, unique long -term issues that need specific understanding.

OK, let's unpack this.

Starting with conditions present at birth.

First up, club foot.

Or talipesiquinovirus, technically speaking.

Right.

And this isn't just one thing.

It's a range of deformities where the foot points inward and downward.

Yeah, imagine the heel turned in, that's the varus part, and the whole foot pointing down like they're on tiptoes, the plantar flexion.

And treatment has changed dramatically, hasn't it?

Oh, completely.

The Punzetti method.

It's truly revolutionized outcomes.

Instead of big surgeries.

Exactly.

Before you had these extensive surgeries that could leave a lot of scarring, stiffness.

Now it's a series of gentle casts.

How does that work?

Like, how many?

Usually about six to eight casts applied one after the other.

Each one stays on for maybe five to seven days.

So over weeks, it gradually corrects the position.

Precisely.

It harnesses the growth potential.

Sometimes the Achilles tendon needs a little lengthening procedure, but often it's just the casting and then bracing afterwards.

Amazing.

A real testament to early non -invasive methods.

Definitely.

Okay, moving up the leg a bit to the hip.

Developmental dysplasia of the hip or DDH.

Right.

Imperfect development of that hip joint.

It could be the femur, the socket, the acetabulum, or both.

And it's a spectrum, right?

From just a bit loose to fully dislocated.

Exactly.

And this brings up a really key point.

Why early diagnosis is so crucial here.

Because the hip is still developing?

Yes.

It has incredible potential to remodel itself, but only if that ball, the femoral head, is sitting correctly in the socket early on.

So how do doctors check for that?

In a relaxed baby, they'll do specific gentle maneuvers.

Looking for the Barlow sign, meaning the hip is in, but can be topped out, or the Ortolani sign, meaning it's out, but could be popped back in with a little plunk.

Okay.

And if they find it early?

If it's caught in the first, say, four months, a simple pablic harness often works wonders.

That's the soft brace.

Yeah.

Holds the baby's hips and knees, bend and angled outwards, keeping the hip joint in the right spot.

Highly successful, like 90 % of the time.

But if you miss that window...

The prognosis really declines.

Delaying treatment can lead to permanent changes, maybe needing casting or even surgery later, and a much higher risk of lifelong problems like arthritis.

That window really is critical.

Okay, now let's talk about bones that are just too fragile.

Osteogenesis imperfecta, OI.

Brittle bone disease.

It's a genetic condition affecting collagen.

The main protein in bone.

And blood vessels, actually, which is why you see issues beyond just fractures.

Right.

So the classic signs are low bone mass, lots of fractures, bones might be bowed or deformed.

But the spectrum is huge.

Type 2 can be fatal very early on.

Type 3 is severe, often with short stature, maybe blue sclerae.

The whites of the eyes look blue, poor teeth.

And milder types.

Type I and IV are milder.

But even type IV, with its frequent fractures, can sometimes be tragically mistaken for child abuse.

That's horrifying.

What about treatment?

It's supportive.

Managing the fractures, often with intramedullary rotting, putting rods inside the long bones for support.

Do those grow with the child?

Some newer ones are telescoping, which helps.

But kids often need multiple surgeries.

And then there are medications, like bisphosphonates, that can help increase bone density by slowing down bone breakdown.

But they don't fix the underlying collagen issue.

No, not yet.

Genetic counseling is really important for families.

Okay, let's shift gears now.

From congenital conditions to infections.

First up, osteomyelitis.

Infection in the bone.

Usually bacterial.

Yes, Staphylococcus aureus is a common culprit.

Birth regular staph and MRSA, the resistant kind.

And MRSA makes it worse.

Definitely.

Since the 80s, MRSA has really increased the severity, the morbidity, even mortality from osteomyelitis.

It's a bigger challenge now.

And how does it happen in kids?

Does it start differently?

Often it starts in the metaphysis.

That's the wider part of a long bone, near the growth plate, where blood flow is a bit sluggish and abscess forms there.

And then it spreads.

It can rupture out and spread along the shaft.

But in infants, under one year old, it has this unique ability to actually cross the growth plate and get into the end of the bone, the epithesis.

Which could damage growth.

Potentially, yes.

And the infection can cut off blood supply, causing bone death.

You might see this walled off dead bone called an involucrum on x -rays after a few weeks.

So diagnosis needs more than just an x -ray early on.

Right.

MRI is crucial early on to see the extent of it.

Clinically, kids might have pain, swelling,

warmth, maybe fever, poor appetite.

Labs show inflammation markers like CRP and ESR is usually high.

And treatment.

Antibiotics are key.

Usually a long course, like six weeks.

And if it's MRSA or if there are bone changes on MRI suggesting dead bone, surgery to clean it out is often necessary.

Okay.

Now, a related infection, but maybe even more urgent, septic arthritis.

Yes.

Infection inside the joint space itself.

And this is always, always a surgical emergency.

That's so urgent.

Because the bacteria in the body's inflammatory response to them can just destroy the joint cartilage incredibly quickly.

The smooth lining of the joint.

Exactly.

Gone.

And in kids, remember how we said some growth areas are inside the joint capsule?

Like in the hip.

Yes.

Hip, shoulder, places like that.

So the infection could damage the growth plate too.

It can lead to lifelong disability very fast.

I don't think I present.

Usually the child looks quite sick.

Severe joint pain.

They refuse to move the limb.

This is called pseudo paralysis.

Very guarded.

Can't bear weight.

Malaise.

Diagnosis must be tricky sometimes.

Differentiating it from other things.

It can be.

The COTRA criteria help things like high white count, fever, can't bear weight, high inflammation markers like ESR and CRP.

But the gold standard is aspirating fluid from the joint.

Sticking a needle in.

Carefully.

Yes.

If the white cell count in that fluid is high, it's likely septic arthritis.

Culture tells you the bug often staph or is again, maybe MRSA or increasingly congellic congay in toddlers.

And treatment is immediate surgery.

Immediate surgical washout, cleaning out the joint, followed by antibiotics, maybe for two, three weeks.

Long -term follow -up is essential.

Okay.

Moving from infections to inflammation.

Juvenile idiopathic arthritis, JIA.

Right.

Sometimes thought of as the childhood version of rheumatoid arthritis, but it's distinct.

How so?

Well, JIA typically affects large joints more often.

Knees, ankles, wrists.

And a big difference is the risk of chronic uveitis.

Inflammation in the eye.

Yes.

In the front part of the eye.

It can be silent, no symptoms, but lead to vision loss if it's not caught.

Kids with JIA, especially if they have a positive ANA blood test, need regular eye exams.

That's crucial.

Any other differences?

Rheumatoid factor can be negative, unlike in many adults.

But if it is positive, the prognosis tends to be worse.

JIA can also affect growth and sometimes cause fusion in the neck vertebrae later on.

So treatment isn't curative?

No, it's supportive.

Aiming to control the inflammation, prevent joint damage and deformity.

Usually starts with NSAIDs, maybe methotrexate or newer biologic drugs if needed.

Got it.

Now let's talk about a group called osteochondroses.

What's the common thread here?

Blood supply.

These are basically avascular diseases affecting growing bones, often areas under repetitive stress.

Avascular meaning not enough blood.

Exactly.

For some reason, maybe trauma, maybe genetics, maybe clotting issues, the blood supply gets interrupted, part of the bone might die, gets weak, can develop tiny frashers.

And the body tries to fix it.

It does.

Over months or even years.

It tries to resorb the dead bone and lay down new bone.

But sometimes the shape doesn't recover fully, leaving deformity.

Okay.

And the most well -known example is?

Leg Calvipirthes disease, LCP, affecting the hip.

Right.

The top of the femur, the femoral head, usually in kids aged, what, three to ten?

Yeah.

Peak age around six.

More common in boys.

What happens is that blood supply to the femoral head gets cut off, maybe repeatedly.

So the bone starts to die.

The top part, yes.

It becomes necrotic.

Then the body starts a long process, two to five years sometimes, of removing the dead bone and replacing it with new bone.

You can see this on x -rays.

Oh, yes.

You see the femoral head kind of flatten, fragment, and then slowly, hopefully regain a rounder shape as it heals and remodels.

How does it present?

A limp.

Often a limp, yeah.

And pain, which is tricky because it can be felt in the hip, groin, inner thigh, or even referred down to the knee.

Usually worse with activity, better with rest.

And the treatment goal is?

Preserve the shape of that femoral head as much as possible and keep it well -seated in socket.

Maintain that joint congruity.

How do you do that?

Anti -inflammatories for pain,

activity modification,

serial x -rays to monitor.

If the head starts to deform badly or slip out of the socket, surgery might be needed to reposition things.

Does age matter for prognosis?

Big time.

Kids older than six when it starts tend to have worse outcomes, less potential for the bone to reshape itself well.

They're more likely to need surgery to prevent early severe osteoarthritis down the road.

Hip replacement by 40?

Wow.

It's a serious long -term consequence if not managed well.

Maintaining that joint shape during healing is paramount.

Okay.

Similar concept, but in the knee.

Ah, it was good shlatter.

Right.

Osteochondrosis of the tibial tubercle that bump just below the kneecap where the patellar tendon attaches.

Plus tendonitis.

Common in sporty kids.

Very common, especially pre -teens and teens, more often boys doing lots of running and jumping.

The tendon pulls repeatedly on that growing area.

Causing pain and swelling there.

Yeah, the tubercle can become quite prominent and tender.

In severe cases, there can actually be some separation of that growth area, the apophysis, due to the stress and maybe compromised blood flow.

Treatment is mainly rest.

Rest from aggravating activities, yeah.

NSAIDs, stretching, maybe a strap below the knee, sometimes immobilization if it's bad.

Return to sport has to be gradual, usually after skeletal maturity.

And there's one for the heel,

too.

Severed disease.

Same idea, but it's the Achilles tendon pulling on the growth plate of the calcaneus, the heel bone.

Common in, say, young soccer players.

Exactly.

Especially those aged 8, 12, maybe with tight Achilles tendons.

Usually gets better with rest, stretching, heel lifts in the shoes.

Okay, let's shift to the spine now.

Scoliosis.

A rotational curvature.

It's not just sideways bending.

The vertebrae actually twist along the curve.

And there are different types.

Broadly, non -structural caused by something else, like posture or leg length difference, which goes away if you fix the cause, and structural with a curve is fixed in the bone.

And structural is the main concern.

Usually, yes.

Within structural, you have congenital cause by malformed vertebrae from birth or teratologic link to other syndromes, but the vast majority, 80%, is idiopathic.

Meaning we don't know the cause.

Right.

Tends to show up in adolescents.

Much more common for girls to develop significant curves over 10 degrees.

And these curves tend to get worse during growth spurts.

So treatment depends on the curve size and how much growing the child has left.

Exactly.

For idiopathic curves over, say, 25 degrees in a kid who's still growing,

bracing is the main non -operative treatment.

To stop it getting worse.

To try and slow or stop progression, yes.

And compliance is key.

Studies show the more hours a day the brace is worn, the better the chance of avoiding surgery.

What about other things, like physical therapy or chiropractic?

The evidence just isn't there to show they changed the natural history of idiopathic scoliosis.

Bracing is the only proven non -operative method.

And if the curve gets too big?

Curves over 50 degrees, especially after skeletal maturity, usually need surgery, spinal fusion, to prevent further progression, which can eventually impact lung function.

Congenital or teratologic curves often need surgery earlier, as they don't respond well to That bracing compliance sounds like a huge challenge.

Okay, moving on to neuromuscular disorders.

Inherited conditions affecting muscle.

Right.

Progressive muscle fiber loss, weakness, leads to significant disability, lifelong issues.

Genetic testing is now crucial for diagnosis.

And the most common is Duchenne muscular dystrophy, DMD.

Yes, X -links, so mainly boys.

About 1 in 3 ,500 male births, caused by mutations in the gene for dystrophin.

What does dystrophin do?

It's like a shock absorber or anchor for muscle fibers.

Without it, the fibers get damaged and tear just during normal contraction.

They die off, get replaced by fat and scar tissue.

When does it usually show up?

Often noticed around age 3 or 4.

Parents see gait problems, maybe a waddling gait, difficulty getting up from the floor.

They might use the gaur sign.

Or they kind of walk their hands up their legs.

Exactly.

Calf muscles might look big, but it's false hypertrophy, pseudo hypertrophy.

Weakness starts in the hips and legs, then moves to the shoulders.

And the progression is relentless.

Historically, yes.

Loss of walking usually between 12 and 15.

Then progressive respiratory problems, heart muscle problems,

cardiomyopathy.

Scoliosis is common.

Cognitive issues can occur too.

What's the lifespan typically?

Used to be early 20s, often due to respiratory failure.

But things are changing.

How so?

Corticosteroids are standard now.

They can prolong walking by 2T5 years, improve strength and increase life expectancy.

Plus, multidisciplinary care, managing, breathing, heart, nutrition, rehab is crucial.

And gene therapies are developing rapidly.

Offering real hope.

Yes.

Real hope to slow progression and improve quality of life.

It's a much more optimistic outlook than even a decade ago, though still a huge challenge.

Are there other muscular dystrophies we should mention?

Briefly, yes.

Spinal muscular atrophy, SMA, it's degeneration of motor neurons in the spinal cord.

Also seeing huge advances with gene therapies.

Facioscapular humeral, FSH, dystrophy.

Slower progression, often starts later, affects face and shoulders first.

Lifespan usually near normal.

Myotonic muscular dystrophy, MMD, multi -system.

The key feature is myotonia difficulty relaxing muscles.

Can affect heart, brain, endocrine system too.

Severity varies a lot.

All right.

Let's turn now to musculoskeletal tumors in children.

Benign first.

Benign bone tumors are much more common than malignant ones.

The most common is osteochondroma or exostosis.

That's like an extra bony bump.

Yeah.

Usually near a growth plate, like at the end of the femur or top of the humerus, grows as the child grows and stops.

Usually harmless unless it causes pain or pressure.

Any others?

Nossifying fibroma is also very common.

Maybe 50 % of benign tumors.

It's a fibrous lesion inside the bone cortex.

Most are found, incidentally, and don't need treatment unless they get very large and weaken the bone.

Okay.

Now for the malignant ones.

Less common, but serious.

Yes.

Typically appear in adolescents.

The top two are osteosarcoma and Ewing sarcoma.

Osteosarcoma is the most common malignant one.

Correct.

Originates from bone -forming cells, usually in the metaphysis of long bones during rapid growth, spurts distal femur.

Proximal tibia are common spots.

Do they make bone?

Yes.

That's a key feature.

It produces oscuroid abnormal bone tissue.

You can often see this on x -ray.

It's bulky, can break out into soft tissues, and sadly often spreads to the lungs early via the bloodstream.

Presentation is usually pain.

Pain, especially night pain that wakes the child, is very common.

Swelling, warmth maybe.

Diagnosis needs a biopsy.

And Ewing sarcoma, second most common.

Yes,

and considered the most lethal.

Also often diagnosed in teens, maybe a bit younger sometimes, it's a malignant round cell tumor.

Different origin.

Yes.

Arises from bone marrow, often found in the mid -shaft of long bones, or in flat bones like the pelvis.

And unlike osteosarcoma, it doesn't make bone.

On x -ray, it looks more destructive, moth -eaten.

Does it also spread early?

Very much so.

It metastasizes early and widely lungs, other bones, lymph nodes, almost anywhere.

Often metastases are present at diagnosis or appear soon after.

So treatment for both needs to be aggressive.

Absolutely.

Combination therapy,

surgery, often limb sparing now, avoiding amputation when possible, plus chemotherapy.

For Ewing, radiation is often added too.

Has survival improved?

Grammatically, with combined therapy.

Five -year survival is now over 60 -75 % for localized disease, depending on the type.

But metastasis still worsens the prognosis significantly.

Okay.

Our final topic,

a difficult one, non -accidental trauma, NAT.

Child abuse and its skeletal signs.

It's a grim reality over 1 .5 million kids abused annually in the US.

Health care providers are mandated reporters.

And failure to report can be fatal.

Tragically, yes.

An abused child returned to that environment without intervention has a roughly 10 -15 % chance of dying from subsequent abuse.

So recognizing the signs is critical.

What are the skeletal red flags?

A key one.

Any long bone fracture in an infant who isn't walking yet?

That has a greater than 75 % chance of being NAT.

That high.

That high.

Also, certain fracture types are highly specific, though less common.

Corn or metaphysiol fractures.

Tiny fractures.

Right at the end of the bone near the growth plate.

Posterior rib fractures are also very suspicious.

What about multiple fractures?

Fractures at different stages of healing, some new, some old, are also a huge red flag.

Of course, you have to rule out things like osteogenesis imperfecta.

So evaluation needs to be thorough.

Absolutely.

Full skeletal survey.

Especially in kids under two.

Careful physical exam for bruises, burns,

detailed history, bone scan can pick up subtle fractures, brain imaging for subdural hematomas, eye exam for retinal hemorrhages, and involving child protective services early.

It's not just treating the fracture.

Not at all.

The fracture often heals well in kids.

It's the potential neurologic injury and the underlying social situation that are much harder to fix and have devastating long -term consequences.

Maintaining a non -judgmental approach is vital, providing support for both child and family.

Wow.

Okay, that brings us to the end of our deep dive today.

What a journey through these pediatric musculoskeletal conditions.

It really covers a huge range.

From those congenital issues like clubfoot and DDH, where early intervention is everything.

Through the urgency of infections like osteomyelitis and septic arthritis, where rapid diagnosis and treatment are key.

To inflammatory conditions like JIA, the blood supply issues and osteochondrosis like perthase.

The complexities of scoliosis, the challenges of neuromuscular disorders like Duchenne.

And finally, that critical need to recognize non -accidental trauma.

And the consistent theme is how different these all are in a growing, changing body compared to an adult.

Exactly.

Children are not just small adults.

They're bones, joints, muscles.

They're dynamic.

Understanding these differences is fundamental to providing good care.

It highlights both the incredible resilience and the unique vulnerability of a child's body.

So for you, our listener, we hope this deep dive gives you a clear picture of these intricate pediatric conditions.

It really underscores the importance of early diagnosis, specialized treatment, and just understanding the unique nature of growth.

Yeah, how pathology interacts with that growth process.

So maybe something to think about as you go about your day.

How could we better harness that developmental plasticity, that inherent ability to grow and remodel in treating these conditions?

Instead of just reacting to symptoms, could we be more proactive in guiding growth?

Interesting thought.

What new approaches might that open up?

Food for thought.

Thank you so much for joining us on this deep dive into alterations of musculoskeletal function in children.

We really appreciate you spending your time with us.

We hope you feel a bit more informed and maybe even more curious about the incredible complexities of the growing human body.