Transcript Approach to fits and faints

CLINICAL APPROACH TO FITS
AND FAINTS
HSAJB
OBJECTIVES
• Know how to approach a patient with seizure/fits
• Know how to approach a patient with syncope
• Differentiate between fits and faints, and make a
provisional diagnosis
• Recognize the different type of seizure
• Initiate the correct therapy for fits or faints
• Know when and how to stop the anti-epileptic
drugs
APPROACH TO FITS AND FAINTS
• Ask the witness
• Before the attack
HISTORY
– General sense of the patient's state of health and
hydration on the day of the event
– Patient's appearance before the event (whether eyes
were open or shut)
– Posture immediately before loss of consciousness
– Any warning?
• Epileptic aura or cardiac pre-syncope
• Prodromal symptoms (eg, seeing sparks, tunnel vision,
nausea, sweating or feeling warm/hot, muffled hearing, or
a feeling of lightheadedness) in the moments just before
the attack-syncope
• Before the attack
HISTORY
– What sort of circumstances it occur?
– While watching TV, sleep deprivation, alcohol withdrawal,
drug misuse - epilepsy
– Change in position, loud noises, jumping into water,
phlebotomy, "emotional” stress, prolonged standing or
dehydration, low salt intake, raised intrathoracic pressure
(e.g., during coughing), and carotid sinus stimulationsyncope
– Can the patient prevent the attacks?
– Any family history of similar attacks? (Cardiac
disease/epilepsy)
– Current medication that may have contributed to TLoC (for
example, diuretics, antihistamines-causes prolonged QT
interval)
HISTORY
• During the attack
• Any loss of awareness? Is it a loss of consciousness (LOC)
or fall to the ground without LOC? how the patient fell
• Any injury? Loses of postural tone with LOC and little or no
wounding-syncope. Head injury, shoulder dislocation, and
severe lateral tongue biting-epilepsy.
• Does the patient move? Stiff or floppy? Exact details of
movements(e.g. (strange behavior, focal rhythmic
movement-twitching, jerking, thrashing, automatisms of
the face & extremities, expiratory groan or cry)
HISTORY
• During the attack
• Any incontinence?(epilepsy, but can occur also in syncope)
• Any change of complexion? Cyanosis-epilepsy? Pale-syncope?
Red-arrhythmia / temporal lobe seizure?
• Did he bite side of his tongue? (epilepsy)
• Associated symptoms- palpitations, sweats, pallor, chest pain,
dyspnoea
• How long does the attack last?(onset to regaining
consciousness)
• Details of any previous TLoC, including number and frequency
• If a drop attack, is the patient always sleepy?(Narcolepsy)
HISTORY
• After the attack
– Were they sleepy, confused, or alert?
– How long did they take to recover completely
• Rapid recovery(eye-contact re-established in few
seconds) without neurological deficits, with fatigue,
nausea, pallor, and persisting diaphoresis-epilepsy
– Weakness down one side during the recovery
period
HISTORY
• Past medical history
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IHD
Arrhythmia
History of implanted defibrillator (ICD) or pacemaker
Epilepsy
Drug compliance
PHYSICAL EXAMINATION
• Vital signs
• Lying and standing blood pressure
• Cardiovascular examination
• Pulse-rate & rhythm
• Palpate for ICD or pacemaker
• Neurological examination
• GCS, neurocutaneous stigmata, meningism, focal neurological
deficit, raised ICP, UMNL
• Venepuncture track marks, tatoo
• Suggestive of IVDU with drug intoxication
INVESTIGATIONS
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GM stat-hypoglycaemia
Haemoglobin levels -anaemia or bleeding
Buse/Creat-Sodium level(hyponatremia)
Calcium level-hypocalcemia
LFT
TFT-hyperthyroidism
Urine and blood toxicology
Trop-T, Cardiac enzyme
INVESTIGATIONS
• Repeat 12-lead ECG and obtain and examine previous
ECG recordings
• Cardiac arrhythmias may present as syncope or
seizures and may be life threatening, so correct
diagnosis is important, particularly since a number of
AEDs can affect cardiac conduction.
• Red flag
– conduction abnormality (for example, complete right or
left bundle branch block or any degree of heart block)
– evidence of a long or short QT interval
– any ST segment or T wave abnormalities
INVESTIGATIONS
• Echocardiography is useful only at the
presence of a positive cardiac history or an
abnormal ECG
INVESTIGATIONS
• EEG
– Helpful to support a diagnosis of epilepsy in
people in whom seizures are considered likely
– Help in classification of seizures by demonstrating
focal or generalized epileptic abnormalities
– Because of its low sensitivity, EEG should not be
used to exclude the diagnosis of epilepsy
• possibility of a false-positive result
INVESTIGATIONS
• Neuroimaging
– used to identify structural abnormalities that cause certain epilepsies
• MRI
– Imaging modality of choice
– It identifies abnormalities capable of causing epilepsy that are not
apparent on CT scanning (such as focal cortical dysplasia, cavernoma,
mesial temporal sclerosis)
– Scanning may not be necessary in people in whom a clear diagnosis of
genetic generalized epilepsy has been made
– Important in those :
» Who develop epilepsy before the age of 2 years or in adulthood
» Who have any suggestion of a focal onset on history, examination
or EEG (unless clear evidence of benign focal epilepsy)
» In whom seizures continue in spite of first-line medication
• CT SCAN
INVESTIGATIONS
– Where MRI scanning is contraindicated (e.g. in people with cardiac
pacemakers), it may be necessary to rely on a CT scan.
– Appropriate for initial imaging to aid management in the situation
where the patient presents acutely with seizures.
– Urgent imaging is indicated in those in whom a focal intracranial lesion
is suspected, for example
» Those in whom recovery is delayed,
» People with a recent history of head trauma,
» Those with new or progressive focal neurological signs
» Those with new focal onset seizures
» In people with persistent altered mental state
» Malignancy
» Immunocompromised
» HIV infection
» Fever
» Alcoholism
» Bleeding diathesis.
HOW TO DIFFERENTIATE BETWEEN
FITS AND FAINTS
CLINICIANS “ART OF LISTENING”
IS VITAL
-time-consuming
-a challenge during a time limited consultation
FEATURES NOT SUGGESTIVE OF
EPILEPSY
• Prodromal symptoms that on other occasions
have been abolished by sitting or lying down
• Sweating before the episode
• Prolonged standing that appeared to
precipitate TLoC
• Pallor during the episode
SYNCOPE
DEFINITION
• A sudden loss of consciousness resulting from
decreased cerebral blood flow, usually with
prompt recovery during a period of seconds to
minutes.
• The underlying mechanism is transient global
cerebral hypoperfusion
• Syncope is almost ten times commoner than
epilepsy in particular when considering the
elderly population.
CAUSES OF SYNCOPE
CARDIAC vs NON CARDIAC SYNCOPE
• A screening rule suggestive of a cardiac
etiology based on
– History of exertional syncope
– TLOC has occurred after exercise, it could suggest a reflex
syncope, and if during exercise, a cardiomyopathy or an
intracardiac conduction defect.
– Family history of cardiac disease
– Abnormal physical examinations findings
– Abnormal ECG findings
WHEN TO REFER FOR URGENT CVS
ASSESSMENT
• Red flags
– TLoC who also has any of the following:
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ECG abnormality
Heart failure (history or physical signs)
TLoC during exertion
Family history of sudden cardiac death in people aged younger
than 40 years
• Inherited cardiac condition
• New or unexplained breathlessness
• Heart murmur
• Consider referring within 24 hours
• Anyone aged older than 65 years who has experienced TLoC
without prodromal symptoms
SPECIALIST CARDIOVASCULAR
ASSESSMENT AND DIAGNOSIS
SPECIALIST CARDIOVASCULAR
ASSESSMENT AND DIAGNOSIS
SPECIALIST CARDIOVASCULAR
ASSESSMENT AND DIAGNOSIS
Criteria to determine type of ambulatory ECG
• For people who have:
– TLoC at least several times a week, offer Holter
monitoring (up to 48 hours if necessary).
– TLoC every 1–2 weeks, offer an external event
recorder.
– TLoC infrequently (less than once every 2 weeks),
offer an implantable event recorder.
– A Holter monitor should not usually be offered unless
there is evidence of a conduction abnormality on the
12-lead ECG
SPECIALIST CARDIOVASCULAR
ASSESSMENT AND DIAGNOSIS
• SUSPECTED NEURALLY MEDIATED
(VASOVAGAL SYNCOPE)
SPECIALIST CARDIOVASCULAR
ASSESSMENT AND DIAGNOSIS
• SUSPECTED NEURALLY MEDIATED (CAROTID
SINUS SYNCOPE)
DIAGNOSE UNCOMPLICATED FAINT
(UNCOMPLICATED VASOVAGAL
SYNCOPE)
• The 3 'P's
• No features that suggest an alternative diagnosis
– (note that brief seizure activity can occur during
uncomplicated faints and is not necessarily diagnostic of
epilepsy)
• Posture – prolonged standing, or similar episodes that
have been prevented by lying down
• Provoking factors (such as pain or a medical procedure)
• Prodromal symptoms (such as sweating or feeling
warm/hot before TLoC).
DIAGNOSE SITUATIONAL SYNCOPE
• No features from the initial assessment that
suggest an alternative diagnosis
• Syncope is clearly and consistently provoked
by straining during micturition (usually while
standing) or by coughing or swallowing
MANAGEMENT OF UNCOMPLICATED
FAINT OR SITUATIONAL SYNCOPE
• If there is nothing in the initial assessment to raise
clinical or social concern, no further immediate
management required
• Advice
– Reassure the person that their prognosis is good
– Explain the mechanisms causing their syncope
– Advise people on possible trigger events and strategies to
avoid them
– To keep a record of their symptoms, when they occur and
what they were doing at the time to help understand
trigger events
– To consult their GP if they experience further TLoC,
particularly if this differs from their recent episode
DIAGNOSE ORTHOSTATIC
HYPOTENSION
• To measure lying and standing blood pressure – repeat
measurements while standing for 3 minutes
• When to suspect orthostatic hypotension
– There are no features from the initial assessment that suggest
an alternative diagnosis and the history is typical
• Consider likely causes, including drug therapy
• Advice
– Explain the mechanisms causing their syncope
– Discuss and review possible causes, especially drug therapy
– Discuss the prognostic implications and treatment options
available
– Advise people what to do if they experience another TLoC
UNEPLAINED CAUSE OF SYNCOPE
If the cause of TLoC remains uncertain
• If a person has persistent TLoC, consider psychogenic non-epileptic
seizures (PNES) or psychogenic pseudosyncope if, for example:
• the nature of the events changes over time
• there are multiple unexplained physical symptoms
• there are unusually prolonged events
• The distinction between epilepsy and non-epileptic seizures is
complex; therefore, refer for neurological assessment if either PNES
or psychogenic pseudosyncope is suspected
• Advise people to try to record any future TLoC events
– (for example, a video recording or a detailed witness account of the
event), particularly if diagnosis is unclear or taking a history is difficult
• If after further assessment the cause of TLoC remains uncertain or
the person has not responded to treatment, consider other causes,
including the possibility that more than one mechanism may co-exist
(for example, ictal arrhythmias)
EPILEPSY
DEFINITIONS
• Epileptic seizure is a transient occurrence of signs
and/or symptoms due to abnormal excessive or
enhanced synchronous neuronal activity in the
brain.
DIAGNOSIS
• Diagnosis of epilepsy depends on the
occurrence of two nonprovoked seizures
RED FLAGS
• Should be seen by the specialist within 2 weeks
– Bitten tongue.
– Head-turning to one side during TLoC.
– No memory of abnormal behaviour that was witnessed before, during
or after TLoC by someone else.
– Unusual posturing.
– Prolonged limb-jerking (note that brief seizure-like activity can often
occur during uncomplicated faints).
– Confusion following the event.
– Prodromal déjà vu, or jamais vu
– Consider that the episode may not be related to epilepsy if any of the
following features are present.
– Prodromal symptoms that on other occasions have been abolished by
sitting or lying down.
– Sweating before the episode.
– Prolonged standing that appeared to precipitate the TLoC.
– Pallor during the episode.
TO TREAT OR NOT TO TREAT AS
EPILEPSY
• Patients should not be treated if there is
uncertainty about the diagnosis
• The wisdom would be to “wait and see" for the next event
• If further events are frequent and the diagnosis is still
doubtful, video-EEG monitoring is helpful when trying to
reproduce a T-LOC
• When there is high risk of further seizures,
medication may be started after a single seizure.
• Development of epilepsy secondary to a cerebral tumour
• Presence of active epileptic changes on EEG in people with
genetic generalized epilepsy.
• Seizures associated with cavernous haemangiomata -high
risk of recurrence
TO TREAT OR NOT TO TREAT AS
EPILEPSY
• Trials of treatment should not normally be
undertaken.
• Rare exceptions occur in which the diagnosis is difficult
to confirm
– For example in elderly people living alone (provided there is a
compatible history and cardiac causes have been ruled out)
– In the case of focal seizures without loss of awareness, in
which even ictal epileptic activity may not be apparent on
scalp electrode EEG recordings.
TO TREAT OR NOT TO TREAT AS
EPILEPSY
• Nature of the seizures
• The need to start treatment for seizures not causing loss of
awareness may be less pressing than for other seizures,
unless driving is an issue)
• Timing of seizure
• Tonic clonic seizures in sleep are associated with an
increased risk of sudden unexpected death in epilepsy
(SUDEP)
• Other co-morbidities
• The likelihood of pregnancy
• The wishes of the patient
FACTORS THAT MAY LOWER SEIZURE
THRESHOLD
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Alcohol excess
Sleep deprivation
Fever/acute systemic illness
Hyponatremia/other metabolic disturbance
Abrupt withdrawal of antiepileptic drugs
Proconvulsant medication (includes much
psychotropic medication as well as some
recreational drugs)
COUNSELLING PEOPLE WITH EPILEPSY
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Nature of epilepsy
Precipitating factors for seizures
Driving laws
Need to avoid potentially dangerous situations
Sudden unexpected death in epilepsy (SUDEP)
Need (or not) for medication
Adverse effects of medication
Interactions of medication with other drugs including
oral contraceptive
• Pregnancy and teratogenicity
• Employment/leisure
SAFETY PRECAUTIONS IN EPILEPSY
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Avoid unguarded heights
Avoid unguarded fires, radiators etc
Shower rather than bath where possible
Avoid swimming alone: an observer should
always be alerted to the possibility of a seizure
before swimming
• When waiting for a train, wait at the back of the
platform till the train pulls in
• Avoid working with unguarded machinery
GENERAL PRINCIPLES OF
PHARMACOLOGICAL TREATMENT OF
EPILEPSY
• Initial treatment should be a first-line drug appropriate for
their epilepsy syndrome and seizure type(s).
• Started at a low dosage and gradually increased until either
the patient becomes seizure-free, or they develop adverse
effects.
• If the patient has ongoing seizures despite adequate doses
of an appropriate AED for their seizure type or syndrome,
the diagnosis should be reconsidered.
• Is the diagnosis correct? Correct seizure type?
– If yes, a second first-line drug appropriate for the epilepsy should be added
– The dosage being gradually increased as before.
– Once an appropriate dosage has been reached, the dosage of the AED used
initially should be gradually tapered.
• Only if at least two appropriate first-line drugs have failed
independently to control the seizures should two or more drugs be
prescribed concurrently.
: PHARMACOLOGICAL TREATMENT
BY SEIZURE TYPE
Other AEDs that may
be considered on
referral to tertiary care
Seizure type
First-line AEDs
Adjunctive AEDs
Generalised tonic–clonic
Carbamazepine
Lamotrigine
Oxcarbazepinea
Sodium valproate
Clobazama
Lamotrigine
Levetiracetam
Sodium valproate
Topiramate
Tonic or atonic
Sodium valproate
Lamotriginea
Rufinamidea
Topiramatea
Absence
Ethosuximide
Lamotriginea
Sodium valproate
Ethosuximide
Lamotriginea
Sodium valproate
Clobazama
Clonazepam
Levetiracetama
Topiramatea
Zonisamidea
Do not offer AEDs
(may worsen seizures)
(If there are absence or
myoclonic seizures, or if
juvenile myoclonic
epilepsy suspected)
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
Carbamazepine
Gabapentin
Oxcarbazepine
Pregabalin
Tiagabine
Vigabatrin
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
Myoclonic
Levetiracetama
Sodium valproate
Topiramatea
Levetiracetam
Sodium valproate
Topiramatea
Clobazama
Clonazepam
Piracetam
Zonisamidea
Focal
Carbamazepine
Lamotrigine
Levetiracetam
Oxcarbazepine
Sodium valproate
Carbamazepine
Clobazama
Gabapentina
Lamotrigine
Levetiracetam
Oxcarbazepine
Sodium valproate
Topiramate
Eslicarbazepine acetatea
Lacosamide
Phenobarbital
Phenytoin
Pregabalina
Tiagabine
Vigabatrin
Zonisamidea
Prolonged or repeated
seizures and convulsive
status epilepticus in the
community
Buccal midazolam
Rectal diazepamb
Intravenous lorazepam
Convulsive status
epilepticus in hospital
Intravenous lorazepam
Intravenous diazepam
Buccal midazolam
Intravenous midazolamb
Propofolb (not in children)
Thiopental sodiumb
Refractory convulsive
status epilepticus
Intravenous phenobarbital
Phenytoin
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
PHARMACOLOGICAL TREATMENT
BY EPILEPSY SYNDROME
Epilepsy syndrome
First-line AEDs
Adjunctive AEDs
Other AEDs that
may be considered
on referral to tertiary Do not offer AEDs
care
(may worsen seizures)
Childhood absence epilepsy or Ethosuximide
other absence syndromes
Lamotriginea
Sodium valproate
Ethosuximide
Lamotriginea
Sodium valproate
Clobazama
Clonazepam
Levetiracetama
Topiramatea
Zonisamidea
Juvenile absence epilepsy or
other absence syndromes
Ethosuximide
Lamotriginea
Sodium valproate
Ethosuximide
Lamotriginea
Sodium valproate
Clobazama
Clonazepam
Levetiracetama
Topiramatea
Zonisamidea
Juvenile myoclonic epilepsy
Lamotriginea
Levetiracetama
Sodium valproate
Topiramatea
Lamotriginea
Levetiracetam
Sodium valproate
Topiramatea
Clobazama
Clonazepam
Zonisamidea
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
Epilepsy with generalised
tonic–clonic seizures only
Carbamazepine
Lamotrigine
Oxcarbazepinea
Sodium valproate
Idiopathic generalised epilepsy
Lamotriginea
Sodium valproate
Topiramatea
Infantile spasms not due to
tuberous sclerosis
Discuss with, or refer to, a
tertiary paediatric epilepsy
specialist
Steroid (prednisolone or
tetracosactidea) or vigabatrin
Discuss with, or refer to, a
tertiary paediatric epilepsy
specialist
Vigabatrin or steroid
(prednisolone or
tetracosactidea)
Carbamazepinea
Lamotriginea
Levetiracetama
Oxcarbazepinea
Sodium valproate
Infantile spasms due to
tuberous sclerosis
Benign epilepsy with
centrotemporal spikes
Clobazama
Lamotrigine
Levetiracetam
Sodium valproate
Topiramate
Lamotriginea
Levetiracetama
Sodium valproate
Topiramatea
Carbamazepinea
Clobazama
Gabapentina
Lamotriginea
Levetiracetama
Oxcarbazepinea
Sodium valproate
Topiramatea
Clobazama
Clonazepam
Zonisamidea
Eslicarbazepine
acetatea
Lacosamidea
Phenobarbital
Phenytoin
Pregabalina
Tiagabinea
Vigabatrina
Zonisamidea
Carbamazepine
Gabapentin
Oxcarbazepine
Phenytoin
Pregabalin
Tiagabine
Vigabatrin
Panayiotopoulos syndrome
Carbamazepinea
Lamotriginea
Levetiracetama
Oxcarbazepinea
Sodium valproate
Carbamazepinea
Clobazama
Gabapentina
Lamotriginea
Levetiracetama
Oxcarbazepinea
Sodium valproate
Topiramatea
Late-onset childhood occipital
epilepsy (Gastaut type)
Carbamazepinea
Lamotriginea
Levetiracetama
Oxcarbazepinea
Sodium valproate
Carbamazepinea
Clobazama
Gabapentina
Lamotriginea
Levetiracetama
Oxcarbazepinea
Sodium valproate
Topiramatea
Eslicarbazepine
acetatea
Lacosamidea
Phenobarbital
Phenytoin
Pregabalina
Tiagabinea
Vigabatrina
Zonisamidea
Eslicarbazepine
acetatea
Lacosamidea
Phenobarbital
Phenytoin
Pregabalina
Tiagabinea
Vigabatrina
Zonisamidea
PHARMACOKINETICS OF ANTI EPILEPTIC DRUGS
ADVERSE EFFECTS OF AEDs
AED
SIDE EFFECTS
POSSIBLE DRUG INTERACTIONS
Carbamazepine
Drowsiness, agitation, diplopia, benign
leukopenia, hepatic failure
↓level= phenytoin, phenobarbital,
valproic acid.
↑ level= erythromycin, diltiazem,
Isoniazid, cimetidine.
Phenytoin
Dose related= nausea, vomiting,
sedation, nystagmus, ataxia. Non –
dose related=gingival hyperplasia,
acne, hirsutism, hepatic failure,
osteomalacia
↑level =cimetidine,
chloramphenicol, isoniazid,
trimethoprim, sulfonamides.
↓ level effectiveness of= OCP,
theophylline, valproic acid
Valproic acid
Weight gain, hepatotoxicity,
thrombocytopenia, alopecia, tremor,
pancreatitis, rash
↓ level=phenytoin, phenobarbital,
meropenem, carbamazepine
↑level= amitriptyline
Lamotrigine
Insomnia, rash that could progress to
SJS
↓level= acetaminophen, OCP,
carbamazepine, phenobarbital,
phenytoin, rifampicin
↑level= valproic acid
ADVERSE EFFECTS OF AEDs
AED
SIDE EFFECTS
POSSIBLE DRUG INTERACTIONS
Ethosuximide
GI upset, sedation, headaches
↓ level= carbamazepine, phenytoin,
phenobarbital, valproic acid,
nevirapine
Levetiracetam
Somnolence, tiredness, dizziness, URTI
None
Phenobarbital
Lethargy, sedation, ↓ cognition, ↓
attention, hyperactivity, depression
Valproic acid
Gabapentin
Drowsiness, ataxia, weight gain,
behavioural changes
None
Oxycarbazepine Hyponatremia, nausea, rash
↓ level= carbamazepine, phenytoin,
phenobarbital, valproic acid
↓ efficacy of= OCP, felodipine,
lamotrigine
WITHDRAWAL OF PHARMACOLOGICAL
TREATMENT OF EPILEPSY
• After a full discussion of the risks and benefits of
withdrawal, risk of seizure recurrence on and off
treatment in relation with the epilepsy syndrome,
prognosis and lifestyle.
• Seizure free for at least 2 years.
• Should be carried out slowly (at least 2–3
months) and one drug should be withdrawn at a
time.
• If seizures recur, the last dose reduction is
reversed and medical advice is sought.
REFERRAL FOR COMPLEX OR
REFRACTORY EPILEPSY
• Epilepsy is not controlled with medication within
2 years
• Management is unsuccessful after two drugs
• Child is aged under 2 years
• Experiences, or is at risk of, unacceptable side
effects from medication
• Unilateral structural lesion
• Psychological and/or psychiatric co-morbidity
• Diagnostic doubt as to the nature of the seizures
and/or seizure syndrome.
TREATING CONVULSIVE STATUS
EPILEPTICUS-ADULT
• Investigations
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ABG
GM stat & RBS
LFT
Renal function test
Coagulation profile
TDM of antiepileptic drugs
Toxicology-blood & urine
CXR- Possible aspiration
Others-brain imaging/Lumbar puncture
Emergency AED therapy for convulsive
status epilepticus
Premonitory stage
(pre-hospital)
Diazepam 10−20 mg given rectally, repeated once 15 minutes later if
status continues to threaten, or midazolam 10 mg given buccally.
If seizures continue, treat as below.
Early status
Lorazepam (intravenous) 0.1 mg/kg (usually a 4 mg bolus, repeated
once after 10−20 minutes; rate not critical).
Give usual AED medication if already on treatment.
For sustained control or if seizures continue, treat as below.
Established status
Phenytoin infusion at a dose of 15–18 mg/kg at a rate of 50
mg/minute or fosphenytoin infusion at a dose of 15−20 mg phenytoin
equivalents (PE)/kg at a rate of 50–100 mg PE/minute and/or
phenobarbital bolus of 10–15 mg/kg at a rate of 100 mg/minute.
Emergency AED therapy for convulsive
status epilepticus
Refractory status
(60/90 minutes after the initial therapy)
General anaesthesia, with one of:
- propofol
(1–2 mg/kg bolus, then 2–10
mg/kg/hour) titrated to effect
-midazolam
(0.1–0.2 mg/kg bolus, then 0.05–0.5
mg/kg/hour) titrated to effect
- thiopental sodium
(3–5 mg/kg bolus, then 3–5 mg/kg/hour)
titrated to effect; after 2–3 days infusion
rate needs reduction as fat stores are
saturated
-anaesthetic continued for 12−24 hours
after the last clinical or electrographic
seizure, then dose tapered.
Emergency AED therapy for convulsive
status epilepticus
• AED therapy must be given in parallel with emergency treatment.
• The choice of drug depends on previous therapy, the type of
epilepsy, and the clinical setting.
• Any pre-existing AED therapy should be continued at full dose, and
any recent reductions reversed.
• If phenytoin or phenobarbital has been used in emergency
treatment, maintenance doses can be continued orally or
intravenously guided by serum level monitoring.
• Other maintenance AEDs can be started also, with oral loading
doses.
• Once the patient has been free of seizures for 12−24 hours and
provided that there are adequate plasma levels of concomitant
AEDs, then the anaesthetic should be slowly tapered
• Monitoring
– Regular neurological observations
– Vital signs measurements
– ECG, biochemistry, blood gases, clotting, blood
count, drug levels.
– EEG monitoring is necessary for refractory status.
• The primary end-point is suppression of epileptic
activity on the EEG, with a secondary end-point of
burst-suppression pattern
Treating convulsive status epilepticus
in children
• The approach to the child who presents with a
tonic–clonic convulsion lasting more than 5
minutes should be the same as the child who
is in "established" status – to stop the seizure
and to prevent the development of status
epilepticus
Time
0 mins
(1st step)
Seizure starts
Check ABC, high flow O2 if available
Check blood glucose
Confirm clinically that it is an
epileptic seizure
5 mins
(2nd step)
Midazolam 0.5 mg/kg buccally
or
Lorazepam 0.1 mg/kg if intravenous access
established
Midazolam may be given by
parents, carers or ambulance
crew in non-hospital setting
15 mins
(3rd step)
Lorazepam 0.1 mg/kg intravenously
This step should be in hospital
Call for senior help
Start to prepare phenytoin for
4th step
Re-confirm it is an epileptic
seizure
25 mins
(4th step)
Phenytoin 20 mg/kg by intravenous
infusion over 20 mins
or (if on regular phenytoin)
Phenobarbital 20 mg/kg intravenously over
5 mins
Paraldehyde 0.8 ml/kg of mixture
may be given after start of
phenytoin infusion as directed by
senior staff
Inform intensive care unit and/or
senior anaesthetist
45 mins
(5th step)
Rapid sequence induction of anaesthesia
using thiopental sodium 4 mg/kg
intravenously
Transfer to paediatric intensive
care unit
• Contraception
WOMEN & EPILEPSY
• In women of childbearing potential
• Hepatic enzyme-inducing antiepileptic drugs-(carbamazepine, phenytoin,
phenobarbital, topiramate)
• affect the efficacy of the OCP through their enzyme-inducing effect
• increasing the hepatic synthesis of sex hormone binding globulin decreasing the
unbound, active progestagen.
• Other methods of contraception, such as barrier methods, depot injection
of medroxyprogesterone or hormone releasing intrauterine contraceptive
devices, may be suitable alternatives
• The copper-bearing intrauterine device is the only method of emergency
contraception not affected by liver enzyme-inducing drugs.
• Lamotrigine
– not thought to induce liver enzymes.
– COCP increases the clearance of lamotrigine and may reduce its plasma
concentration by 50%, such that increased dosage of lamotrigine may be
necessary.
– women taking the COCP in addition to lamotrigine may develop symptoms of
lamotrigine toxicity when they discontinue the COCP
WOMEN & EPILEPSY
• Pregnancy & teratogenicity
– Pre-conceptual counselling is essential for women with epilepsy
• most if not all antiepileptic drugs carry a risk of teratogenicity
– treated with a single AED if possible
– take folic acid 5 mg daily before pregnancy and for the first
trimester, to reduce the risk of teratogenicity
– ideally be treated with AEDs carrying a low rate of major
congenital malformations (MCMs)
• Carbamazepine, lamotrigine, levetiracetam
• Sleep deprivation in the post-partum period may increase the
risk of seizures
– Advice about childcare
•
•
•
•
feed the infant while sitting on a floor cushion,
change the infant on a changing mat on the floor,
avoid bathing the infant when alone in the house
use a carrycot if it is necessary to carry the infant upstairs.
PSYCHOGENIC SEIZURE
(DISSOCIATIVE CONVULSION).
DEFINITION
• Transient behavioral disturbance without any organic
basis.
• Constitute by far the most common (>90%) condition
misdiagnosed as epilepsy, at least at referral epilepsy
centers
• In the DSM-IV (American Psychiatric Association,
1994),classified as a somatoform disorder
• The ICD-10 classification (World Health Organisation,1992)
it is classified as dissociative convulsion in the group of
conversion disorders
– “the common theme shared by dissociation disorders is a
partial or complete loss of the normal integration between
memories of the past, awareness of identity and immediate
sensations and control of bodily movements”
• The behaviour during the convulsion is important
since a recent study showed that having the eyes
closed during the tonic clonic phase predicted a
dissociative seizure with a sensitivity of 96% and a
specificity of 98%
• Enquire about dissociative symptoms such as
depersonalization and derealization
• If a dissociative convulsion is suspected,48-h
video-EEG monitoring may be sufficient to
document an episode
FEATURES SUGGESTIVE OF
PSYCHOGENIC SEIZURE
• Resistance to AEDs
– Have received AEDs for some time before the correct diagnosis is made
• A very high frequency of seizures (multiple daily episodes) that is
completely unaffected by AEDs.
• Specific triggers that are unusual for epilepsy (e.g., stress, getting upset,
pain, certain movements, sounds), especially if they are alleged to
consistently trigger a seizure
• The circumstances in which attacks occur
– tend to occur in the presence of an audience, and occurrence in the
physician’s office or waiting room
– tend not to occur in sleep, although they may seem to and be reported as
doing so
• Presence of ‘‘fashionable” diagnoses, such as fibromyalgia or diagnoses
suggesting somatization
• The psychosocial history, including associated psychiatric diagnoses
FEATURES SUGGESTIVE OF
PSYCHOGENIC SEIZURE
• Witnesses’ accounts are rarely detailed
enough to describe these accurately, and in
fact, even seizures witnessed by physicians are
often wrongly diagnosed.
• Assess the mental status, general demeanour,
affect, level of concern, over dramatization,
and histrionic features
• an attack more likely to occur during the history taking
or examination
SLEEP-WAKE TRANSITION
DISORDERS
• If a sleep disorder is suspected, videopolysomnography should be organized
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