CLINICAL 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

HISTORY• Ask the witness• Before the attack

– 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

HISTORY• Before the attack

– 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 stimulation-syncope

– 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• 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

• 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

INVESTIGATIONS• CT SCAN

– 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:

• 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



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


• SUSPECTED NEURALLY MEDIATED (VASOVAGAL SYNCOPE)


• 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 SYNCOPEIf 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


• 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.


• 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

• 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

• 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

• 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

Seizure type First-line AEDs Adjunctive AEDs

Other AEDs that may be considered on referral to tertiary care

Do not offer AEDs (may worsen seizures)

Generalised tonic–clonic Carbamazepine Lamotrigine Oxcarbazepinea Sodium valproate

Clobazama Lamotrigine Levetiracetam Sodium valproate Topiramate

(If there are absence or myoclonic seizures, or if juvenile myoclonic epilepsy suspected) Carbamazepine Gabapentin Oxcarbazepine Phenytoin Pregabalin Tiagabine Vigabatrin

Tonic or atonic Sodium valproate Lamotriginea Rufinamidea Topiramatea

Carbamazepine Gabapentin Oxcarbazepine Pregabalin Tiagabine Vigabatrin

Absence Ethosuximide Lamotriginea Sodium valproate

Ethosuximide Lamotriginea Sodium valproate

Clobazama Clonazepam Levetiracetama Topiramatea Zonisamidea

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 phenobarbital Phenytoin

Refractory convulsive status epilepticus

Intravenous midazolamb Propofolb (not in children) Thiopental sodiumb

PHARMACOLOGICAL TREATMENT BY EPILEPSY SYNDROME

Epilepsy syndrome First-line AEDs Adjunctive AEDs

Other AEDs that may be considered on referral to tertiary care

Do not offer AEDs (may worsen seizures)

Childhood absence epilepsy or other absence syndromes





Juvenile absence epilepsy or other absence syndromes





Juvenile myoclonic epilepsy Lamotriginea Levetiracetama Sodium valproate Topiramatea

Lamotriginea Levetiracetam Sodium valproate Topiramatea

Clobazama Clonazepam Zonisamidea


Epilepsy with generalised tonic–clonic seizures only

Carbamazepine Lamotrigine Oxcarbazepinea Sodium valproate

Clobazama Lamotrigine Levetiracetam Sodium valproate Topiramate

Idiopathic generalised epilepsy Lamotriginea Sodium valproate Topiramatea

Lamotriginea Levetiracetama Sodium valproate Topiramatea

Clobazama Clonazepam Zonisamidea


Infantile spasms not due to tuberous sclerosis

Discuss with, or refer to, a tertiary paediatric epilepsy specialist Steroid (prednisolone or tetracosactidea) or vigabatrin

Infantile spasms due to tuberous sclerosis

Discuss with, or refer to, a tertiary paediatric epilepsy specialist Vigabatrin or steroid (prednisolone or tetracosactidea)

Benign epilepsy with centrotemporal spikes

Carbamazepinea Lamotriginea Levetiracetama Oxcarbazepinea Sodium valproate

Carbamazepinea

Clobazama

Gabapentina

Lamotriginea

Levetiracetama

Oxcarbazepinea

Sodium valproate Topiramatea

Eslicarbazepine acetatea Lacosamidea

Phenobarbital Phenytoin Pregabalina Tiagabinea

Vigabatrina

Zonisamidea

Panayiotopoulos syndrome Carbamazepinea Lamotriginea Levetiracetama Oxcarbazepinea Sodium valproate

Carbamazepinea

Clobazama

Gabapentina

Lamotriginea

Levetiracetama

Oxcarbazepinea




Vigabatrina

Zonisamidea

Late-onset childhood occipital epilepsy (Gastaut type)

Carbamazepinea Lamotriginea Levetiracetama Oxcarbazepinea Sodium valproate

Carbamazepinea

Clobazama

Gabapentina

Lamotriginea

Levetiracetama

Oxcarbazepinea




Vigabatrina

Zonisamidea

PHARMACOKINETICS OF ANTI EPILEPTIC DRUGS

ADVERSE EFFECTS OF AEDsAED 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 AEDsAED 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• 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.


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.


• 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

Time0 mins (1st step)

Seizure startsCheck ABC, high flow O2 if availableCheck blood glucose

Confirm clinically that it is an epileptic seizure

5 mins (2nd step)

Midazolam 0.5 mg/kg buccallyorLorazepam 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 hospitalCall for senior helpStart to prepare phenytoin for 4th stepRe-confirm it is an epileptic seizure

25 mins (4th step)

Phenytoin 20 mg/kg by intravenous infusion over 20 minsor (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 staffInform 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

WOMEN & EPILEPSY• Contraception

• 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, video-polysomnography should be organized

THANK YOU

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CLINICAL APPROACH TO FITS AND FAINTS