Chapter 14: Antiepileptic Drugs

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Welcome to the Deep Dive.

Today we're jumping right into a really complex but vital area, anti -epileptic drugs or AEDs.

Yep, we're digging into seizure management using pharmacology and nursing process as our guide.

We'll be looking at how seizures happen, how these drugs work, the key players like Fanny Toyne, and the critical nursing points you absolutely need to know.

Exactly.

The goal is to cut through the complexity.

We want to give you the core pathophysiology, the drug mechanisms, the main classes, side effects, and what you as the caregiver need to do.

Think of it as a clinical shortcut.

Okay, first things first, language.

People mix these terms up all the time, right?

Epilepsy, seizure, convulsion.

Let's clarify for the listener.

Good place to start.

So epilepsy is the big picture, the chronic disorder, the pattern of recurrent seizures.

And a seizure.

That's the specific event,

a brief episode where there's abnormal electrical firing in the brain's nerve cells.

Which sometimes leads to a convulsion.

Right.

A convulsion is the physical part.

We often picture that severe seizure with the involuntary spasms and contractions.

But we use AED, anti -epileptic drug, because they treat more than just convulsions.

Precisely.

AED covers meds for all types of seizure activity, not just the ones that involve shaking.

It's a much better term.

So let's talk causes.

Why do these electrical storms happen in the brain?

Well, fundamentally, it's dysfunction in the central nervous system.

You get this excessive electrical discharge, mainly in the cerebral cortex.

Neurons just get hyperactive.

And where does that come from?

Is it always something identifiable?

Not always.

About half the cases are what we call primary or idiopathic.

Meaning, we can't pinpoint a specific cause.

Might be genetic.

And the other 50%.

That's secondary or symptomatic epilepsy.

There, you can point to a cause.

Maybe a head injury, a stroke, an infection, a tumor.

Something acquired.

Does knowing the cause change the drug treatment much?

It definitely guides the overall strategy.

But AEDs are usually needed for both types.

Now, how we classify the seizures themselves has changed.

And that does impact drug choice significantly.

Right.

We've moved on from terms like grand mal and petty mal.

We have.

The newer ILA classification from 2017 is much more descriptive.

It focuses on where the seizure starts in the brain.

So what are the main categories now?

We talk about generalized onset, focal onset, which used to be called partial and unknown onset.

And knowing if it's focal matters,

because?

Because if you know it starts in one specific area, you can often use more targeted drugs, maybe with fewer side effects.

It really refines the treatment approach.

Okay.

Within generalized, there's the tonic -clonic type, the stiffening, then jerking phase.

Everyone kind of knows that one.

Yes.

That's the classic presentation.

Tonic phase is the contraction.

Clonic is that alternating contraction and relaxation.

But there's a major complication we need to highlight.

The really dangerous one.

Absolutely.

Status epilepticus.

This is a critical medical emergency.

What exactly happens in status?

It's basically multiple seizures happening one after another with no recovery time in between.

The brain just keeps firing abnormally.

And the consequences.

Severe.

It can lead to hypoxia, lack of oxygen to the brain, permanent brain damage, and even death if it's not stopped quickly.

Time is absolutely critical.

So what do you use to break that cycle right away?

The go -to drugs are diazepam and lorazepam, usually IFE.

Why those two specifically?

Because they work fast, they enhance GABA, the brain's main inhibitory neurotransmitter.

Essentially hitting the brakes on that excessive electrical activity immediately.

You need to stop the seizure now.

Okay.

So that covers the why and the immediate emergency.

Let's talk about the long -term goals and how these AEDs actually work day to day.

Right.

The main goal isn't always zero seizures, though we achieve that for about 70 % of patients on just one drug, which is pretty good.

So what is the main goal then?

It's really about quality of life.

Trying to reduce seizure frequency as much as possible while, and this is key, minimizing the side effects and toxicity from the drugs.

These are often lifelong meds, remember?

Makes sense.

Let's get into the mechanism of action, the MOA.

How do they actually quiet down those overactive nerves?

It mostly comes down to controlling the movement of ions across the nerve cell membranes, things like sodium, potassium, magnesium.

So manipulating the electrical signal.

Exactly.

The idea is to stabilize those membranes, make them less excitable.

This leads to three main effects.

Okay.

What are they?

One, they raise the threshold for activity in the motor cortex.

So it takes more stimulation to make a nerve fire.

Two, they limit the spread of a seizure if one does start.

And three, they slow down the speed of nerve impulse conduction.

And you mentioned GABA earlier, the brain's brake pedal.

That's important too.

Hugely important.

Many AEDs work by boosting GABA levels or making GABA receptors work better.

It enhances the brain's natural inhibitory system to counteract the hyper excitability.

This delicate balance, the way these drugs work, it seems like getting the dose just right would be critical.

Absolutely.

Which brings us straight to therapeutic drug monitoring, or TDM.

It's essential for several key AEDs.

Why is TDM so vital here?

Because many of these drugs have a really narrow therapeutic index.

That means the difference between a dose that works and a dose that's toxic or doesn't work at all is tiny.

So you need to check blood levels regularly.

Yes.

For certain ones, we have established ranges we aim for.

Like phenytoin, it's usually 10 to 20 micrograms per ml.

Phenobarbital is 10 to 40.

Carbamazepine, 4 to 12.

Valproic acid, 50 to 125.

What do those levels tell you?

Well, if the level is too low, it might mean the patient isn't taking the medication correctly or the dose isn't high enough.

If it's too high, there's a serious risk of toxicity, and you need to let the prescriber know immediately.

You mentioned the narrow window.

Does that cause issues with generic versions of these drugs?

That's actually a really significant concern flagged in our sources.

Professional groups have raised questions about whether generic AEDs are always truly bioequivalent to the brand name ones.

Meaning they might not be absorbed or work exactly the same?

Potentially yes.

So the practical takeaway for you, the caregiver, is if a patient switches from a brand name to a generic, or even between generics, you need to be extra vigilant.

Increased monitoring, watching for any change in seizure control or new side effects is definitely warranted.

Okay, that's a crucial point.

Let's dive into the specific drug classes now, starting with the older, traditional ones.

The hydantines, particularly phenytoin or dilantin.

Ah, phenytoin, a classic first -line drug, but notoriously tricky to manage.

What makes it so tricky?

Well, first the side effects.

You can get lethargy, confusion, cognitive slowing.

Long -term, the really specific ones are gingival hyperplasia, that overgrowth of the gum.

Requires really good dental hygiene.

Absolutely meticulous.

And then things like acne, hirsutism, excess hair growth, and something called dilantin facies, a sort of coarsening of facial features.

And what happens if the levels go above that 20 -milti -GML target?

Toxicity signs appear pretty quickly.

Nostagmus, those jerky eye movements, ataxia, which is poor coordination.

And in severe cases, encephalopathy, which is brain dysfunction.

You mentioned it's tricky kinetically too.

What does that mean?

Two big things.

One, it's highly protein -bound.

So if a patient has low albumin levels in their blood, maybe they're malnourished or have liver disease,

more of the drug is free and active, increasing the risk of toxicity, even if the total level seems okay.

And the second thing?

It's a major hepatic enzyme inducer.

It revs up the liver enzymes that break down other drugs.

Like?

The big one is oral contraceptives.

Phenytoin can make them less effective.

That's a critical piece of patient teaching, especially for women of childbearing age.

And giving phenytoin intravenously.

That has some serious warnings attached.

Oh, absolutely.

Critical nursing knowledge here.

RD -phenytoin must be given slowly, no faster than 50 milligrams per minute in adults.

Why so slow?

And it must be diluted only in normal saline, no dextrose.

And use a filter.

Okay, saline only, filter, slow push.

What happens if it's given wrong, like into the tissue?

It's incredibly caustic.

If it infiltrates or is given subcutaneously, it can cause severe tissue damage, necrosis, slapping, even leading to amputation in the worst cases.

It's a high alert medication for IV use.

Which is why phosphenytoin was developed, I assume, to avoid that IV risk.

Exactly.

Phenytoin, brand name Cerebix, is a pro drug.

It gets converted to phenytoin in the body, but it's water soluble and much less irritating to veins.

So it's safer to give IV.

Much safer.

You can give it faster to up to 150 milligrams of phenytoin equivalents, or PE, per minute.

And it can be given intramuscularly if needed.

But still needs caution.

Oh yes.

It has its own black box warning regarding cardiac monitoring during infusion and limiting that rate.

Still needs careful handling.

Okay, moving on.

What about the barbiture?

It's like phenobarbital.

Phenobarbital and its cousin primidone, which gets metabolized to phenobarbital.

These are older, very low cost, so you still see them used a lot globally.

Advantages.

Disadvantages.

Big advantage.

Very long half -life.

Often allows for just one sedate dosing, which is great for adherence.

Main downside is sedation, although people often develop tolerance to that.

Any specific populations to watch out for?

Yes, children.

They can sometimes have a paradoxical reaction.

Instead of getting sleepy, they might become restless, agitated, or excited.

And like phenytoin.

It's also a potent hepatic enzyme inducer.

Same issue speeds up the metabolism of other drugs, so you always have to check for interactions.

Got it.

Now, the aminostobines.

Carbamazepine or tagretol.

Another first -liner.

Yes, for focal and generalized seizures.

But important caveat, it can actually make certain types, like myoclonic or absent seizures, worse.

So diagnosis is key.

And carbamazepine has that unique kinetic property.

Autoinduction.

Right.

Autoinduction.

This is really important.

For the first couple of months of therapy, the drug actually stimulates the liver enzymes that break itself down.

So the drug levels can drop over time, even if the patient takes it correctly.

Exactly.

You might see effectiveness decrease after the first month or two.

It means you need to anticipate this, monitor levels, and potentially increase the dose proactively.

Any food interactions to warn patients about?

Yes.

A big one.

Avoid grapefruit and grapefruit juice completely.

It inhibits carbamazepine metabolism and can sharply increase levels, leading to toxicity.

No grapefruit.

Is oxcarbazepine similar?

It's a chemical cousin, yes.

But a key difference is that oxcarbazepine is not a significant hepatic enzyme inducer like carbamazepine.

So fewer drug interactions.

Generally, yes.

That often makes it a preferred choice if the patient is on multiple other medications.

Okay, let's shift gears to some other key AEDs.

Maybe one's known for specific risks.

Valproic acid.

Valproic acid, depakine.

Very useful for generalized seizures.

Also used a lot in bipolar disorder.

But it comes with serious warning.

It does.

The two major ones are hepatotoxicity, liver damage, and pancreatitis.

Both can be life -threatening.

Requires careful monitoring of liver function and watching for abdominal pain.

Any specific administration tips for valproic acid?

Yes.

The oral forms, tablets, or capsules should not be taken with milk or carbonated drinks, as it can affect absorption or cause irritation.

Usually take with food or water.

All right.

What about Lamontregeny?

Lamontregeny is used for various seizure types, including Lennox -Gastaut syndrome.

But the absolute critical thing here is the rash risk.

Not just any rash, right?

No, this is the potential for Stevens -Johnson syndrome, or SJS.

It's a severe, potentially fatal skin reaction.

Looks almost like a burn.

How do you minimize that risk?

Slow, slow titration.

The dose has to be increased very gradually over roots.

Starting too high or increasing the dose too quickly is what dramatically increases the risk of SJS.

Patience is key.

Let's touch on lymiteracetam, or Kepra.

Seems very popular, often well tolerated.

It is popular.

Its exact mechanism isn't fully unemployed, which is interesting.

And a convenience is that routine blood level monitoring usually isn't needed.

But there's a catch.

Yes.

The main thing to watch for is behavioral or psychiatric changes.

Things like increased anxiety, agitation, hostility, irritability,

and sometimes even suicidal thoughts or actions.

That's serious.

Is that risk unique to Kepra?

Well, all AEDs carry a black box warning about increased risk of suicidal thoughts and behavior, but it seems particularly noted as something to monitor closely with lymiteracetam.

Okay.

And quickly, gabapentin and pregabalin.

Neurontin and Lyrica.

Right.

While they can be used as add -on therapy for seizures, you probably know them better for treating other things.

Neuropathic pain.

Exactly.

Gabapentin is chemically related to GABA, used a lot for nerve pain.

Pregabalin, which is a Schedule V controlled substance, is used for nerve pain, posterpac neuralgia, and fibromyalgia.

Side effects, mostly CNS.

Yeah.

Primarily dizziness, drowsiness, fatigue.

Generally considered to have a better side effect profile than many of the older AEDs, but still need monitoring.

This is a lot to keep track of.

Which brings us squarely to the nursing process.

Before giving any AED what's essential in the assessment.

Okay.

Baseline is key.

Get a full health history allergies, other meds, any contraindications like liver or kidney disease,

then a thorough neuroassessment.

What does that involve?

Checking reflexes, vision, their gait, how they speak, and really listen if they describe an aura.

The warning sign before a seizure.

Yes.

That specific feeling or sensation.

Documenting that is really important.

And baseline labs are crucial too.

CBC, liver function, kidney function, clotting studies, especially for drugs like carbamazepine and valproic acid with known organ toxicity risks.

Okay.

Assessment done.

Now implementation actually giving the meds.

What's the absolute number one rule?

Never ever stop AEDs abruptly.

Can't emphasize that enough.

Suddenly stopping them is a major trigger for withdrawal seizures, potentially even status epilepticus.

So tapering off is essential if they need to be stopped or changed.

Always under medical supervision.

And for ongoing therapy, consistency is vital.

Dosing needs to be around the clock to maintain stable blood levels.

Not just, you know, three times a day whenever specific timing matter.

Administration tips for early doses.

Generally take them with food and about six to eight ounces of fluid to minimize stomach upset, unless there's a specific reason not to.

If it's a suspension, shake it really well before measuring.

And no crushing long acting pills.

Definitely not.

Extended release or long acting tablets or capsules should never be crushed, broken or chewed.

There are some exceptions like Depakote sprinkles, which can be put on soft food, but generally altering the formulation messes up the release mechanism.

Let's talk about managing an active seizure.

What are the immediate priorities?

Seizure precautions.

Priority one is always airway.

Maintain an open airway chin lift, jaw thrust if needed.

Get the person onto their side immediately the recovery position.

This helps prevent aspiration if they vomit.

And the thing not to do.

The myth we need to bust.

Do not try to force anything into their mouth.

No tongue blades, no fingers, no wallets.

You can't swallow your tongue.

That's a myth.

Trying to pry open a clenched jaw is likely to cause injury, broken teeth, bitten fingers to both the patient and you.

Just protect their head and let the seizure run its course while ensuring the airway is clear.

Okay.

Crucial safety point.

Moving to patient teaching for long -term management and safety at home.

What do female patients need to know?

This is high stakes counseling.

First, because many AEDs can potentially cause birth defects,

any woman of childbearing potential needs to talk to her provider before planning a pregnancy.

It's crucial.

And the birth control issue.

Yes.

Because those enzyme -inducing AEDs like phenytoin, phenobarbital, carbamazepine can make hormonal contraceptives less effective, you absolutely must counsel them on using reliable alternative or barrier methods of birth control.

An unintended pregnancy while on these meds carries significant risk.

What about general safety advice for anyone on AEDs?

First, that black box warning again.

Report any suicidal thoughts, deepening depression, or unusual mood changes immediately.

Avoid things that can lower the seizure threshold, mainly alcohol, but also excessive caffeine and smoking are generally discouraged.

And practical tips for around the house.

Think about reducing risks.

Maybe using an electric stove instead of gas.

Putting heat control devices on faucets to prevent burns if they have a seizure while washing, not locking the bathroom door.

Ensuring supervision during activities like swimming or bathing.

Little things that improve safety.

And wearing medical ID.

Absolutely.

A medical alert bracelet or necklace stating they have epilepsy and are on AEDs is really important in an emergency.

Finally, evaluation.

How do we know the therapy is working?

Success isn't necessarily a complete cure, remember, it's control.

Therapeutic response means seizure activity is decreased or hopefully absent, but you're constantly monitoring any changes in mental status, mood, effect, coordination, vision.

Those need follow -up.

So we've covered a huge amount of the basics of seizures, the mechanisms of AEDs, the major drug classes like hideantines, barbiturates, immunostal bins, valproic acid, and the newer agents.

Plus that vital nursing process piece.

Yeah, from the acute treatment of status epilepticus with diazepam or lorazepam to the long -term management challenges like phenytoin's kinetics or the metrogenase rash risk and those critical IV safety protocols.

It really underscores the need for vigilance.

It does.

So here's something for you, the listener, to think about.

We talked about the narrow therapeutic window for many AEDs and the concerns about generic bioequivalence.

Given all that, what practical steps should you take?

What increased vigilance is needed when one of your patients is switched from a brand name AED to a generic?

How do you best ensure their continued safety and seizure control during that transition?

Something definitely worth considering.

We hope this deep dive provided you with the clarity you needed.

A warm thank you from the Last Minute Lecture team.