Approach to epilepsy POWER POINT---EDITED.ppt

7/27/2019 Approach to epilepsy POWER POINT---EDITED.ppt

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Approach to epilepsy

evaluation and treatment of seizuresin ER

history of epilepsy or first seizure e.g.

poorly controlled epilepsy comesafter a seizure and has recovered to

normal interictal stateAggressive lumbar punture repeatscans may not be necessary
http://professionals.epilepsy.com/page/emergency_approach.htmlhttp://professionals.epilepsy.com/page/emergency_approach.html


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.

You cant attribute fever, focal

weakness, or altered awareness to

the post-ictal state

may signal new or deteriorating

disorders

Individuals with epilepsy are still

human and can any other disease


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.emergency EEG is useful in:-

to distinguish successful resolution of

convulsive status epilepticus from a

conversion to subtle status epilepticus

to rule out seizures as a cause of unusualbehavior or movements

If muscle and movement artifacts present

difficulty in interpreting these events, video-

EEG can be extremely useful


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Emergency neuroemaging CT or

MRI

Any change in the patients seizure

pattern or type

prolonged postictal confusion or

worsening mental status. patients

who have epilepsy with recurrent

seizures whenever the physician

suspects a serious structural lesion.


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e.g

new focal deficits

persistent altered mental status (with or withoutintoxication with alcohol other substance)

fever

recent trauma

persistent headache

vomiting

history of cancer

history of anticoagulation

suspicion of acquired immunodeficiency syndrome(AIDS)
http://professionals.epilepsy.com/page/emergency_approach.htmlhttp://professionals.epilepsy.com/page/emergency_approach.htmlhttp://professionals.epilepsy.com/page/emergency_approach.htmlhttp://professionals.epilepsy.com/page/emergency_approach.html


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.

If an MRI scan --seizure protocol

thin coronal cuts through the

amygdala,

hippocampus,

mesial temporal regions,

T1, T2, and FLAIR pulse sequences


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Neck immobilization

Spinal immobilization in individuals

after seizures is rarely necessary. In

one retrospective study, 1,656 cases

over a 10-year period were reviewed,and no spinal injuries were found.[25]
http://professionals.epilepsy.com/page/emergency_ref.htmlhttp://professionals.epilepsy.com/page/emergency_ref.html


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Communication

Contacting the patients treating

physician is vital to good quality and

continuity of care.

In one study, AED therapy was

altered by the ED in nearly 20% of

epilepsy patients who were evaluated

and discharged from an ED,


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Driving, swimming, cooking

alone, working in risky areas

e.g.moving machines, scaffoldReview issues of compliance with the

patient, and inform him or her about

the state laws that pertain to driving.

Some countries by law you have to

inform Department of Motor Vehicles


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, Figure: EEG demonstrating a single generalized

polyspike-and-wave in second 2 and brief burst of

generalized spike-and-waves in second 7


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What is strong of evindence of drug

resistant epilepsy


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Status epilepticus is a neuologic

.

Status epilepticus is a neurologicemergency associated

with high mortality and long-termdisability. Recent advances

in our understanding of thepathophysiological

mechanisms involved in the initiationand perpetuation of

seizure activity have revealed thatstatus epilepticus is a

dynamic and evolving process.


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,

PATHOPHYSIOLOGY

Status epilepticus represents a failure ofinherent cellular

mechanisms to prevent sustained seizureactivity.22 These

mechanisms are believed to fail secondaryto either persistent

excitation of a cellular focus or ineffectiveinhibition of

sustained seizure activity.


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,

Results of experiments on brain slice

preparations suggest that sustained seizureactivity

requires the development of a reverberating circuit

betweenentorhinal and hippocampal structures. #Thisappears

to occur as an all-or-none phenomenon,# with

seizuresbecoming self-sustaining after 15 to 30 minutes of

stimulation.


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,

These findings suggest that SE involves both anactivation

and a maintenance phase.24 Activation may beinitiated

by the presence of excessive excitatorystimulation. This

concept was supported by the clinical observationof the

development of SE in individuals after they

inadvertentlyingested domoic acid, an analogue of anexcitatory amino

acid.


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,

Induced seizures may be sustained byfailure of -

aminobutyric acid (GABA)-mediated

suppression of anactivated focus. This resistance maydevelop through seizure-

induced formation of varying isoforms of

the GABAtype A (GABAA) receptor in thehippocampus.


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,

Alternatively, SE may be perpetuatedby sustained Nmethyl-

D-aspartate (NMDA)-mediated

neuronal stimulation.27 In animal models, SE developed asensitivity toNMDA

simultaneously with the developmentof progressive GABAAresistance.28,29


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,

It is believed that earlypharmacological administration

of medication leads to termination of

seizures withmuch smaller doses and withsubsequent less risk to the

patient than would be required ifseizures were allowed to

progress.


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.

important consideration in thetreatment of SE

is the immediate need for EEG

monitoring. Electrographicseizure activity has been reported tocontinue in up to 15%

of patients whose overt clinicalseizures are pharmacologically

controlled.


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.

out-of-hospital administration ofbenzodiazepines, a

randomized double-blind trial comparingintravenous (IV)

diazepam (5-10 mg) or lorazepam (2-4 mg)In many circumstances, IV access

may be unavailable during emergencytransport; in

these settings, rectal or intramuscularadministration of

benzodiazepines may be effective.


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,

Initial management of SE follows the principles of basic

life support.2,8 The first priority is ensuring an adequate

airway. Most patients with SE maintain adequate ventilation

as long as an adequate airway is present.# Oral or

nasopharyngeal devices supplemented with oxygen

deliveredvia a nasal cannula or bag mask ventilation are usually

adequate to maintain oxygenation and avoid hypoxemia;

prolonged seizures, however, lead to loss of pharyngeal

tone and increase the risk of aspiration. The timing of oral

or nasal tracheal intubation is a clinical decision, but mostpatients who receive large doses of benzodiazepines or

other sedative medications will require mechanicalventilatory support.


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.

Intubation can be problematic for patients with GCSE

who may require neuromuscular blockade. If neuromuscular

blockade is required, a short-acting nondepolarizing

agent such as rocuronium bromide is preferred. If there is a

possibility of rhabdomyolysis, succinylcholine chloride

should be avoided because of potentialhyperkalemicinduced

cardiac arrhythmias. Adequate peripheral IV access

is needed to provide drugs and fluid resuscitation.

Central access may be required if inotropes are needed for

blood pressure support.


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,

All patients should have continuous

pulse oximetry and

electrocardiographic monitoring. Of

Cardiac arrhythmias


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.

sudden death can occur in SE, presumably secondary to

sympathetically mediated cardiac damage Hypoxemia is

common and has many etiologies including apnea, airway

obstruction, aspiration, and neurogenic pulmonary

edema. Frequent monitoring of blood pressure and urinary

output is crucial because hypotension is a commonadverse effect of several of the medications used to control

seizures. More invasive monitoring may be required if the

patient becomes hemodynamically unstable. Continuous

EEG monitoring is required in all patients who receive

long-term neuromuscular paralytic agents, have a prolongedpostictal period, are being treated for refractory SE

(RSE), or have atypical features to their seizures suggestive

of pseudoseizures.


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,

Routine laboratory evaluation includes serum electrolytes,glucose, magnesium, calcium, liver function tests,

complete blood cell count, creatine kinase, toxicology

screen, and antiepileptic medication levels. Treatment

should be based on the findings of this evaluation. A bedside

glucose level should be attained as soon as possibleand 100 mg of thiamine and 50 mL of 50% glucoseadministered

if hypoglycemia is present.


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,

In GCSE, a metabolicacidosis inevitably is found and reflects sustained muscular

activity. This acidosis is self-correcting once seizures are

controlled and rarely requires treatment. Arterial blood gas

testing may reveal hypoxia or a respiratory acidosis that

requires ventilatory support.Hyperthermia augments

neuronal damage due to sustained seizure activity and

should be treated aggressively with active cooling


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.

A full diagnostic evaluation should be initiated on thepatients arrival at the emergency department. Pertinent

historical features include any recent change in medication,

alcohol or drug use, previous epilepsy, or neurologic insult.

If witnessed, a description of the onset and initial features

of the seizure may be helpful. In the absence of a knownseizure disorder, computed tomography of the head should

be performed once the patient is stabilized and seizures are

controlled. The threshold for obtaining cerebrospinal fluid

should be low.

MPsUrine toxic screen


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,

Benzodiazepines.

Benzodiazepines are an antiepilepticmedication used for the initial treatment of SE. They

are a class of drugs that act at the GABAA receptor.Stimulation

of this subunit leads to inhibition of neural transmission

through hyperpolarization of the resting cell membrane.This is accomplished through the GABA-induced

opening of chloride channels, which allows for intracellular

chloride influx.


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.

At higher concentrations, benzodiazepines reduce repetitiveneuronal firing by a mechanism

similar to that of phenytoin and carbamazepine.

Diazepam achieves higher brain concentrations and has a

slightly faster onset of action,

although , Because of high lipidsolubility, diazepam is redistributed rapidly to peripheral

fat stores. This property limits its clinical effectiveness to

only 20 to 30 minutes and accounts for its large relapse

rate


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.

Phenytoin and Fosphenytoin.

Phenytoin (5,5-diphenyl-2,4-imidazolidinedione) is a barbiturate-like drug that

is effective in controlling seizure activity. It limits the

repetitive firing of action potentials through the slowing of

the rate of recovery of voltage-activated sodium channels.

Phenytoin is formulated with propylene glycol and ethanoland is adjusted to pH 12 with sodium hydroxide. It is highly

protein-bound with only the free portion being metabolically

active. Maintaining appropriate drug levels can be

problematic because of multiple drug interactions and the

saturable pharmacokinetics of hepatic metabolism andprotein binding.


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.

The loading dose of phenytoin for SE is 20 mg/kg innonglucose-containing solutions administered at a maximal

rate of 50 mg/min

A gram of phenytoin is commonly

given, but this is an insufficient loading dose for

most adult patients.In the absence of clinical effect, an

additional 10 mg/kg is given because many patients may

require serum levels of approximately 25 to 30 gm/mL to

achieve seizure control.


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. phenytoin

adverse effects SE are cardiovascular, includinghypotension, QT prolongation,

cardiac dysrhythmias. Most can be attenuated

by reducing the infusion rate. The effects are attributable to

a direct effect of both the medication and the propylene

glycol used as a diluent.14The most problematic adverse effect is severe tissue

reaction that can occur with extravasation of phenytoin into

adjacent tissue. The purple glove syndrome, a variant of

this reaction, occurred in up to 5.9% of patients in one

Mayo series.57


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.

Despite this rapid administration, it is

unclear whether

fosphenytoin controls seizures faster

than phenytoin.


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.

Phenobarbital.

Phenobarbital is a barbiturate thatprevents seizure activity by increasing GABAA-mediated

cellular inhibition

third-line drug in algorithms designed to

treat SE because of its serious adverse effect profile.14

Phenobarbital profoundly depresses respiration andconsciousness

level with a half-life of more than 48 hours. In

addition, it causes severe hypotension secondary toperipheral

vasodilation and decreased cardiac contractility.


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RECENT ADDITION

IV Valproic Acid and Other Medications.

Valproicacid is a short-chain fatty acid with anticonvulsant properties.

similar to phenytoin in that

prolonged recovery of

activated voltage-gated sodium channels. Other

mechanismson

neuronal calcium channels or through its effects on GABA

metabolism.55 Valproate has been used previously

Rectal form


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NO LONGER USED

Lidocaine hydrochloride and

paraldehyde have been


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nonpharmacological

Including

vagal nerve stimulation,

plasmapheresis,

electroconvulsive therapy,

and surgical resection of cortical

tissue,


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. refractory status epilepticus

require treatment with anesthetic

doses of benzodiazepines,

short-acting barbiturates, or propofol.


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.

, isoflurane, a volatile

Ketamine hydrochloride in controlling

recalcitrant seizures

neuroprotective because it

simultaneously controls seizures

and blocks glycine-activated NMDA

receptors.


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,AIM

20 minutes of treatment and did not

return for at least 40

minutes.


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THE FUTURE

We need :-

may involve both a GABA agonist to

prevent seizures and an

NMDA antagonist to prevent neuronal

damage

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