Vous êtes sur la page 1sur 31

Chapter 21

Drugs Treating Seizure Disorders

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Seizures
What are they ?

How are they caused?

Which patients can have a seizure?

How are they treated ?

What are the side effects or precautions for


the patient ?

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Epilepsy
• Epilepsy is a group of neurologic disorders in which CNS
neurons display hyperexcitability
• Seizures are a result of excessive neurologic activity.
Manifestations are displayed as either:
loss of consciousness with generalized muscle
twitching
mild alterations in consciousness with repetitive
blinking.
• Patients with patterns of seizures who are diagnosed
with epilepsy are treated with antiepileptic drugs.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Pharmacodynamics of Antiepileptic Drugs
• The 3 main ways that antiepileptic drugs work:
– Decreasing the rate at which sodium flows into the cell
Prototype : Phenytoin
– Inhibiting calcium flow rate into the cell through specific
channels
Prototype: Ethosuximide
– Increasing the effect of the neuroinhibitor gamma-
aminobutyric acid (GABA)
Prototype: Benzodiazepines

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Physiology

• Action potentials within neurons are initiated by an influx


of sodium into the cell.
• Influx of calcium through specialized voltage-dependent
channels also plays a role in creating an action potential.
• When the cell fires, there is a release of
neurotransmitters into the synaptic cleft.
• The neurotransmitter glutamate produces excitation.
• GABA normally acts as a counterbalance to glutamate,
preventing hyperexcitation ( Inhibitory neurotransmitter)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Physiology of Neurotransmitters

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Pathophysiology
• When a group of neurons exhibits coordinated, high-frequency
discharge, it is termed a focus.
• The causes of a focus include:
head trauma tumor growth
hypoxia inherited birth defects

• Seizures result from :


a focus which spreads to other areas of the brain
additional neurons join in the hyperactivity

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Pathophysiology

• Seizures may result from either:


high levels of glutamate
low levels of GABA
Classification of seizures depends on how widespread is the
neural hyperactivity
• Partial seizures occur when focus activity is limited to a
specific area of the brain

• Generalized seizure occurs when focus activity spreads within


both hemispheres of the brain

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Classifications of Seizures
• Partial - involves only one hemisphere of brain
Simple ( consciousness not impaired)
Complex ( consciousness impaired)
• Generalized - involves both hemispheres
loss of consciousness
tonic-clonic phase ( grand mal)
 initially stiffness & rigidity
 LOC, massive muscle spasms
 urinary / bowel incontinence
 post ictal state follows convulsion
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Emergency : Status Epilepticus

• One seizure follows another


• No recovery of consciousness in between seizures
• Any grand mal seizure that lasts longer than 5 minutes
Any grand mal seizure has the potential to become status
epilepticus

Most common reasons for status epilepticus:


alcohol withdrawal
stopping antiepileptic drug therapy
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Febrile Seizures in Children

• Febrile Seizures occur in children with high fevers


• Generalized seizure activity occurs
• These are common and do not increase the risk of
developing epilepsy

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Other causes of generalized seizure
activity
• Seizures may also occur from known and reversible causes:
( any patient has the potential to develop a seizure)
Metabolic abnormalities:
hypoglycemia
electrolyte imbalance
brain infection ( meningitis)
uremia
pre-eclampsia or toxemia of pregnancy
drug and alcohol abuse

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Antiepileptic Drugs That Decrease Sodium
Influx

• Control seizures by  sodium influx into the cells.


Remember :
• Sodium influx into the cells produces an action potential
• Action potential causes neurons to fire

• Prototype drug: phenytoin (Dilantin)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin: Core Drug Knowledge

• Pharmacotherapeutics
– Control partial and generalized seizures
– Prevent and treat seizures post neurosurgery
– Treat status epilepticus after administering a benzodiazepine
– Normal blood level : 10-20 mcg/ ml
– Small changes in the dose may produce larger than expected
changes in the serum concentration of the drug
 Great variability exists among how individuals metabolize this
 Slight deviations from the therapeutic range may produce: non-
therapeutic effects or adverse effects

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin (Dilantin)
• Pharmacokinetics
 Absorbed slowly orally ( but common route )
 IM absorption very erratic … precipitates at the
injection site
IV administration effective : can’t be mixed with
Dextrose
Highly protein bound (90%)
Half life at therapeutic levels is 20 – 60 hours
• Metabolized in the liver ( to an inactive metabolite)
• How quickly this biotransformation occurs has a limit 

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin ( Dilantin)
• Pharmacodynamics
primary site of action : motor cortex
binds to Na channels (while in the inactive state)
delays the return of the channel to an active state
(remember Na can only enter the channel and initiate an
action potential when the channels are in an active state)
time between action potentials is lengthened
neurons cannot fire now at an excessive rate
excessive muscle contractions (as in grand mal seizures
are prevented)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin: Core Drug Knowledge (cont.)
• Contraindications and precautions
– Bradycardia and heart block ( because it can also affect
the Na channels in the cardiac cells as well)
– Do not stop the drug abruptly
• Adverse effects ( most frequent occur in CNS)
– Nystagmus, ataxia, dysarthria, slurred speech, mental
confusion, tremor
– gingival hyperplasia-
– Blood dyscrasias
– Rare but fatal : Stevens Johnson syndrome, lupus
• Drug interactions: induces P 450 enzyme system
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins
Phenytoin: Core Patient Variables
• Health status
– Assess allergies and any cardiac conditions
• Life span and gender
– Pregnancy category D ( controversial topic )
– Antiepileptic drugs increase the metabolism of hormonal
contraceptives,  effectiveness, risk for unplanned pregnancy
• Lifestyle, diet, and habits
– Alcohol intake and nutritional status ( assess protein intake)
– Absorption  if administered with continuous tube feedings
– May increase blood glucose levels.
– Be careful driving until effects of drug are known

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin: Nursing Diagnoses and
Outcomes
• Disturbed Sensory Perception related to adverse effects of
drowsiness and sedation
– Desired outcome: the patient will not experience adverse
effects to the degree that sensory perception is altered
enough to impair quality of life.
• Altered Oral Mucous Membrane related to the adverse effect of
gingival hyperplasia
– Desired outcome: the patient will demonstrate knowledge
of optimal oral hygiene and experience no deterioration in
dental health.
• Risk for Injury related to adverse effects of blood dyscrasias
– Desired outcome: the patient will return for follow-up blood
work while taking phenytoin and will have no life-threatening
blood disorders.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin: Planning & Interventions
• Maximizing therapeutic effects
– Monitor blood levels of the drug.
– Titrate the dose upward gradually.
• Minimizing adverse effects
– Monitor blood levels—narrow therapeutic range.
– Administer IV push phenytoin( during an active seizure)
no faster than 50 mg/minute in adults or 1 to 3
mg/kg/minute in neonates
– Too rapid administration may cause:
hypotension and arrhythmias

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Phenytoin: Teaching, Assessment &
Evaluations
• Patient and family education ( p. 339 Box 21-4)
– Ensure proper administration of medication.
– Take medication with food to decrease GI upset.
– Monitor for & notify physician of any adverse effects.
– Do not abruptly stop taking this medication
• Ongoing assessment and evaluation
– Ongoing assessments include:
– monitoring patients closely for:
therapeutic responses, seizure control, adverse effects

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Ethosuximide: Core Drug Knowledge
• Pharmacotherapeutics
– Used to treat absence type seizures ( petit mal)
– Hypothalmic neurons are responsible for these
– Brief LOC ( < 1 minute) : eye blinking, staring
– Occur commonly in children ( 100 /day)
• Pharmacokinetics
– Administered: oral. Metabolism: liver. Excreted:
kidneys.
– Peak: 3-7 hours. T½: 30-60 hours.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Ethosuximide: Core Drug Knowledge
(cont.)
• Pharmacodynamics – inhibits the influx of Ca ions
• Contraindications and precautions
– Hypersensitivity to succinimides
• Adverse effects
– Drowsiness, dizziness, lethargy, nausea,
– blood dyscrasias
• Drug interactions
– Known to interact with some of the other antiepileptic drugs

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Ethosuximide: Core Patient Variables
• Health status
– Assess allergies, history of renal or hepatic dysfunction
• Life span and gender
– Pregnancy category C ( but used only for absence
seizures)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Ethosuximide: Nursing Diagnoses and
Outcomes
• Imbalanced Nutrition: Less than Body Requirements related to
adverse GI drug effects of anorexia, abdominal complaints, nausea,
and vomiting
– Desired outcome: the patient will not experience major
nutritional imbalances while receiving ethosuximide.
• Risk for Injury from falls related to CNS adverse effects of
ethosuximide
– Desired outcome: the patient will not sustain an injury while
receiving ethosuximide.
• Risk for Injury from blood dyscrasias related to adverse effects of
ethosuximide
– Desired outcome: the patient will not experience major
changes in his or her complete blood cell counts.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Ethosuximide: Planning & Interventions

• Maximizing therapeutic effects


– Monitor drug levels at the start of therapy and when
changing dosage.
• Minimizing adverse effects
– Assess CBC, UA, and LFT.
– Taper dose gradually if needed to discontinue drug.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Ethosuximide: Teaching, Assessment &
Evaluations

• Patient and family education


– Teach patients to take the drug with milk or food if
GI upset occurs.
– Notify provider of adverse effects.
• Ongoing assessment and evaluation
– Ongoing assessments include monitoring patients
closely for therapeutic responses, seizure control,
and adverse effects of drug therapy.

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Antiepileptic Drugs that Increase Effects
of GABA
• Benzodiazepines ( first line drugs for status epilepticus)
• Diazepam – Valium ( given PO or IV )
highly lipid soluble ( crosses BBB)
highly protein bound ( 98%)
Diazepam onset IV 10- 20 seconds
Duration of action is short
Used as an “adjunct therapy”
IV injection is slow ( not > 5 mg /minute)

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Drugs Different Than the Benzodiazepines
• Phenobarbital ( Luminal Sodium)
CNS depressant –suppresses sensory cortex
decreases motor activity
alters cerebellar function
produces drowsiness, sedation and hypnosis
• Stimulates GABA receptors : affecting CNS transmitters
• Tolerance does not occur to the seizure effects : only the
sedative effects

Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins


Drugs Different from the Benzodiazepines
Phenobarbital ( Luminal)
• Absorbed GI tract
• Moderately protein bound (40%)
• Long half life
• Pregnancy Category D
• Induces the P 450 enzyme system
• Adverse effects are related to: ( dose dependent)
CNS depression and respiratory depression
 Can also produce “paradoxical effect” in children and
older adults
Copyright © 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins

Vous aimerez peut-être aussi