Chapter 46: Concepts of Care for Patients With Arthritis and Total Joint Arthroplasty

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Welcome back to The Deep Dive.

We're here to break down those really dense chapters into the key info you actually need to remember.

Yep, making it stick.

Today we're tackling a big

arthritis and total joint arthroplasty or TJA.

It's pretty central to musculoskeletal nursing.

Absolutely.

And the best way to get a handle on this chapter, I think, is to understand the framework it uses.

Okay.

So arthritis just means joint inflammation,

but the chapter really splits it into two main types, using them as exemplars for core nursing concepts.

You've got osteoarthritis or OA, which is the model for mobility.

Right, the wear and tear one.

Exactly.

And then there's immunity, a completely different beast.

Okay.

Mobility versus immunity.

That's a helpful starting point.

So our mission today is to walk through the core details, path, risks, how they look clinically, and crucially, the nursing management for both OA and RA, and then wrap up with TJA care.

That's the plan.

And honestly, if you can nail the core difference, OA being localized, mechanical wear versus RA being systemic,

autoimmune destruction, you're already halfway there.

Got it.

Let's start with OA then, the mobility exemplar.

It's the most common, right?

Degenerative joint disease, DJD.

What's actually happening inside that joint?

Well, it's really about the mechanics failing over time.

It's a progressive breakdown, a loss of that smooth, articular cartilage, and even the bone underneath.

Okay.

What happens is the cartilage starts to lose water, and these key molecules, proteoglycans that keep it spongy,

then enzymes get released that actually chew up the cartilage matrix.

So the cushion just kind of deflates and wears away.

Yeah.

And that narrows the joint space, right?

That's where those bones spurs, the osteophytes.

Precisely.

Osteophytes form as the bone tries to sort of stabilize itself.

And here's something really important for when you're assessing patients.

The cartilage itself.

No nerve endings.

Okay.

So the pain isn't from the disappearing cartilage.

Right.

The pain comes from other things.

Stress on the joint capsule, the soft tissues getting irritated, muscle spasms trying to protect the joint.

Sometimes you get secondary inflammation of the joint lining, senobitis.

Oh, and those little bits of bone and cartilage floating around.

That's what causes crepitus.

That grating sound or feeling.

Okay.

That distinction about the pain source is really useful.

What about risk factors?

There's primary and secondary OA.

Yeah.

Primary OA is mostly just getting older and genetics playing a role.

It tends to hit weight -bearing joints, hips, knees, spine, also hands.

And secondary.

Secondary OA is where lifestyle and history matter more.

It's often from a specific joint injury maybe years ago or trauma.

Also, jobs with heavy, repetitive stress.

And obesity is a huge factor, especially for knees and hips.

It just puts so much extra load on them.

Makes sense.

Any difference between men and women?

There is.

Yeah.

Men under 55 often get it from sports injuries.

But women over 55, much higher rates.

It might be linked to hormones post -menopause, maybe obesity rates, or even just anatomical differences like wider hips affecting joint alignment.

So when a patient comes in, what are the classic signs you look for?

What screams OA?

The absolute classic is chronic joint pain and stiffness.

And here's a key differentiator.

Early on, the pain gets better with rest and worse with activity.

And the stiffness usually lasts less than 30 minutes after they wake up or after sitting for a while.

Okay.

Less than 30 minutes stiffness.

What about physically seeing it?

You'll often see the joint looks bigger, enlarged.

That's the bony hypertrophy.

And specifically in the hands, especially in women, look for Heberden nodes out near the fingertips, the DIP joints, and Bouchard nodes closer to the knuckles, the PIP joints.

Got it.

Heberden's distal, Bouchard's proximal.

So history and physical point towards OA.

X -rays confirm the structural changes.

Labs are usually normal.

Generally, yes.

Your ESR and C -reactive protein might be slightly up if there's some secondary inflammation synovitis, but OA itself isn't primarily inflammatory, which leads us straight into pain management.

Right.

Since it's not mainly inflammatory, what's the go -to drug?

This is a huge safety point.

The primary drug of choice is acetaminophen, regular Tylenol, because we're not fighting massive inflammation systemically.

Okay.

Start simple.

Exactly.

And this is critical.

You have to counsel on the dose.

The standard max is 4 ,000 milligrams a day.

But the sources really emphasize caution, especially in older adults or anyone with liver issues.

Often, keeping it under 3 ,000 milligrams a day is safer to prevent liver damage.

Okay.

Acetaminophen first.

Watch the dose.

What if that doesn't cut it?

Then you might move to topical things like lidocaine patches or salicylate creams or oral NSAIDs like silicoxib, a KOX2 inhibitor.

But you have to weigh the risks.

NSAIDs carry cardiovascular and GI side effect warnings.

And non -drug approaches are just as important.

Absolutely vital.

Simple things like positioning.

Use small pillows.

Critically, don't put big pillows under the knees.

That encourages flexion contractures.

Good tip.

Heat or cold?

Heat is generally better for OA stiffness and muscle tension, like a warm shower or heating pad.

Cold is used less, maybe to numb acute pain or decrease some secondary inflammation.

And of course, weight loss for those weight -bearing joints.

Even modest weight loss makes a difference.

Any newer therapies?

Yeah.

Things like stem cell injections or platelet -rich plasma, PRP, are being explored.

Trying to actually repair the cartilage, maybe delay needing surgery.

Still evolving though.

Which brings us nicely to surgery.

When all that conservative stuff isn't enough and pain and mobility are really bad,

total joint arthroplasty, TJA.

TJA, yeah.

Total hip replacement, THA.

Or total knee replacement, TKA.

It's the last resort when quality of life is suffering.

Any major reasons someone couldn't have it?

The big contraindications are pretty straightforward.

Any active infection anywhere in the body can't risk seeding the new joint.

And also, really unstable or uncontrolled medical problems, like severe heart failure or diabetes.

Okay.

Before the surgery, what are the priorities?

Seems like infection and clots are big concerns.

Huge.

There's a big push for the joint coach idea, having a designated family member or friend involved from the start to help with everything, especially after discharge.

Makes sense.

And infection prevention is protocol driven.

An IV antibiotic, usually a cephalosporin, within one hour before the first cut.

Plus, things like using nasal muperosin whitement beforehand and washing with chlorhexidine CHG.

And planning for VTE prevention too.

Definitely.

Figuring out how to manage their usable anticoagulants, if they're on any.

Teaching them about early movement post -op, getting them ready for compression devices.

Okay, let's jump to post -op care.

Starting with the hip, THA.

What's the absolute number one risk we need to prevent?

Dislocation.

The artificial ball coming out of the socket.

The risk level depends a bit on how the surgeon went in the perforolateral approach has the highest risk.

So how do we stop that?

Positioning.

Positioning is key.

The action alert is keep them mostly supine, head slightly up,

use an abduction pillow or regular pillows between the legs to prevent the leg crossing the midline, that abduction movement.

And if it does dislocate, what are the immediate warning signs?

It's usually sudden and pretty obvious.

Intense pain, maybe sudden agitation.

You might see the leg is rotated funny, either inward or outward, or it looks shorter than the other leg.

Needs immediate attention.

Okay, besides dislocation, what's the next major post -op priority for THA?

Preventing VTE blood clots, WT or PE.

It's a major risk after orthopedic surgery.

And the strategy for that is the PAC -C approach.

Right, PAC -C helps you remember.

Pharmacology, ambulation, compression.

Pharmacology is anticoagulants, low molecular weight heparin, maybe newer factor Zod inhibitors.

Ambulation means getting them moving early and often, at least three times a day.

And compression means using those sequential devices or stockings.

Are there specific exercises too?

Yes, simple but effective ones.

Heel pumps just pointing and flexing the feet.

And quad sets tightening of the thigh muscles.

Both help blood flow and muscle tone.

And we can't forget neurovascular checks.

Absolutely critical.

The neurovascular monitoring action alert reminds us.

Check color, temperature, capillary refill, pulses, movement and sensation in that surgical leg frequently.

Catching problems early prevents permanent damage.

So for discharge after THA, what are those key hip precautions they absolutely must follow?

It depends slightly on the approach, but the common ones, especially for postural lateral, are don't cross your legs past the middle of your body.

Don't bend your hip more than 90 degrees means using raised toilet seats, careful sitting.

Don't twist your body when your foot is planted.

And use your walker or crutches as instructed.

Got it.

Now, shifting to the knee, TKA.

Is dislocation a big worry there?

Much, much rarer in knees.

So the positioning focus changes.

Keep the leg neutral, maybe slightly elevated on pillows, but, and this is a key difference, avoid putting a pillow directly under the replace knee.

Why not under the knee?

Big risk of causing a flexion contracture.

You want that knee to be able to get fully straight.

Swelling and pain are usually more intense immediately after TKA.

So how do we manage that?

Cryotherapy is huge right away.

Ice packs are often those special cold therapy units that circulate cold water, helps reduce swelling and hematoma.

And what about that CPM machine, the continuous passive motion device?

Ah, yes, the CPM.

Its use is a bit debated now, but if it is prescribed, the goal is to prevent arthrofibrosis.

Which is?

Excessive scar tissue building up inside the knee, making it stiff and limiting motion.

It's a major reason for poor outcomes and readmission.

If using a CPM, nurses need to check the padding, make sure the settings, range of motion, speed are correct, check it every eight hours or so, and importantly, turn it off during meals.

Okay, and the big readmission risks for TKA are infection, DVT, and that arthrofibrosis.

Those are the main culprits, yes.

Pain control is also managed multimodally opioids, NSAIDs, maybe nerve blocks, plus non -drug things like guided imagery or music.

All right, that gives us a solid picture of OA and TJA.

Now let's pivot completely.

If OA is different, it's the immunity exemplar.

How?

Fundamentally different.

RA is a chronic, progressive, systemic, autoimmune inflammatory disease.

Systemic is the key word.

Meaning the body's attacking itself.

Exactly.

The immune system mistakenly creates antibodies, called rheumatoid factors, or RFs, that target the synovium, the lining of the joints.

This triggers massive inflammation.

And that inflammation does the damage.

It creates this abnormal tissue called panus.

Panus is aggressive stuff.

It grows over the cartilage and actually erodes right into the cartilage and bone, destroying the joint.

Wow.

And because it's systemic,

it's not just joints.

Not at all.

It affects connective tissue everywhere.

Patients have periods of remission where things calm down and exacerbations or flare -ups.

But over time, that systemic inflammation can hit blood vessels, vasculitis, skin, eyes, lungs, heart, pretty much anywhere.

So how does RA look different from OA when it first shows up?

Early signs.

Big differences.

Unlike OA's often one -sided pain, early RA typically presents as bilateral and symmetric joint inflammation.

Often starts in the small joints of the hands of our SPIPs, MCPs, and crucially, it comes with systemic symptoms.

Feeling weak, tired all the time, loss of appetite, maybe a persistent low -grade fever.

That systemic feeling is key.

What about later signs as it progresses?

Then you see more severe joint inflammation and pain.

The morning stiffness is profound, can last for hours, not just under 30 minutes like OA.

You get the characteristic deformities,

swan neck and boutonnier fingers,

and subcutaneous nodules, little bumps under the skin, often along the forearm.

And more systemic stuff too.

Yeah, like Sjogren's syndrome, the classic dry eyes, dry mouth, dry vagina.

Vasculitis can cause skin ulcers or even organ damage.

Respiratory and cardiac issues can pop up too.

There was a critical rescue alert mentioned about the neck and RA.

That sounds serious.

It is potentially life -threatening.

RA can affect the cervical spine, causing instability, particularly between C1 and C2.

If that subluxation happens, it can press on the spinal cord or critically compromise the phrenic nerve, which controls the diaphragm.

So breathing problems.

Exactly.

If a patient with RA reports new neck pain, stiffness, or neurological changes, the immediate nursing action is, keep their neck straight, in a neutral position, don't let them move it around, and notify the provider immediately.

It's an emergency.

Wow, okay.

Good to know.

How do we diagnose RA definitively?

It's often a combination of clinical picture and labs.

Blood tests will likely show a positive rheumatoid factor, RF, although not always.

Elevated ESR and CRP show inflammation and are used to track disease activity.

A more specific marker, especially for early or aggressive disease, is anti -CCP.

Any other tests?

Sometimes arthrocytesis drawing fluid from the joint.

In RA, the fluid is typically cloudy and has a high white blood cell count, indicating inflammation.

Given how destructive RA is, management must be pretty aggressive, right?

Focusing on controlling that inflammation.

Absolutely.

The goal is to slow the disease progression and prevent joint destruction.

This relies heavily on drug therapy.

What's the cornerstone drug class?

DRMARD's disease -modifying anti -hermetic drugs.

The main player here is methotrexate, MTX.

It's usually given once a week, low dose.

But it comes with serious warning.

Oh yes.

Three huge safety alerts you absolutely must know for methotrexate.

One,

increased risk of infection because it suppresses the immune system.

Two, liver toxicity risk is significant, so patients must avoid alcohol completely.

Three,

it's highly teratogenic causes birth defects, so strict birth control is mandatory for women of childbearing potential.

Infection liver teratogenicity.

Got it.

What if MTX isn't enough?

Then we often move to the newer class, the BRM's biological response modifiers or biologics.

Drugs like intanarcept or infliximab.

They're more targeted, neutralizing specific inflammatory chemicals like TNF -alpha.

Sounds effective, but more risks.

Definitely more potent immunosuppression.

The big safety alert with BRM's is an even higher risk for serious infections.

Crucially, because of this, every patient must be screened for latent tuberculosis TB with a PPD skin test before starting a biologic.

You don't want to reactivate TB.

Okay, TB screening is mandatory pre -BRM.

What about steroids?

Glucocorticoids like prednisone are used for quick anti -inflammatory effects during flares.

They work fast, but chronic use is bad news, risk of diabetes, osteoporosis, cataracts, thin skin, impaired immunity.

So usually use short -term or as a bridge.

Makes sense.

Beyond drugs, what about self -management?

Hugely important for quality of life.

Adequate rest is crucial.

Using heat, especially for that severe morning stiffness.

Proper positioning to protect joints.

And teaching energy conservation techniques is key.

Energy conservation.

Yeah, helping patients pace activities, set priorities, maybe schedule short naps.

The fatigue with RA can be overwhelming.

And also psychosocial support, listening, validating their experience, and pushing back against outdated negative stereotypes about an arthritis personality.

That's really important.

Okay, we've covered a lot of ground.

Bringing it all together, what's the absolute core takeaway contrasting OA and RA?

It boils down to that conceptual framework.

OA is localized joint wear and tear, a mobility issue.

Management focuses on pain relief, function, and eventually maybe joint replacement like TJA.

RA is a systemic autoimmune attack on the Johnson body, an immunity issue.

Management requires aggressive immunosuppressive drugs like DRRs and biologics to prevent irreversible damage system -wide.

And clinically, the absolute must -knows for nursing students.

For TJA.

Preventing hip dislocation post -THA with proper positioning.

Preventing VTE using that PAC approach.

And never skipping those neurovascular checks.

For RA, knowing the methotrexate safety alerts, infection liver birth defects, and the mandatory TB screening before starting biologics.

Huge infection risks with both.

Perfect.

And the final thought.

Just that both are chronic conditions.

So patient education is everything.

Teaching them how to manage their meds safely, how to protect their joints, like using larger joints instead of smaller ones.

For tasks, that self -management piece is what truly helps maintain function and quality of life long -term.

That really clarifies the key differences and priorities.

Understanding that core distinction between OA and RA really sets you up for success with this material.

Thanks so much for joining us on this Deep Dive.

My pleasure.

And a warm thank you from the Last Minute Lecture team to you, our listeners, for tuning in.