SEIZURES AND EPILEPSIES

•	Seizures in infants and childhood.
•	Neonatal seizures.
•	Febrile fits.
•	Epilepsies in school age child.
•	Non-epileptic disorders of childhood.
•	Management of convulsions.
•	Status epilepticus.

Seizures in infants and childhood

1.	Seizure is an episodic involuntary alteration in:

a.	Consciousness.

b.	Motor activity.

c.	Sensory perception.

d.	Autonomic function.

e.	Behavior.

2.	Biochemical changes during seizures

a.	Cerebral metabolism:

i.	increase need for oxygen and substrate.

ii.	compromised cerebral blood flow leading to hypoxia.

b.	Loss of intracellular K and migration of Na into cells, precipitating SIADH.

c.	Derangement of neurotransmitter function:

i.	excess of excitatory neurotransmitters.

ii.	lack of inhibitory neurotransmitters. 

3.	Factors determining Seizure threshold

a.	Genetic: determine the tendency to convulse.

b.	Physiological:

i.	REM sleep.

ii.	illness.

iii.	fatigue.

iv.	premenstrual period.

c.	Time: 

i.	certain periods of life are move vulnerable to seizures.

ii.	usually between 6 months and 3 years of life and puberty.

d.	Pathological:

i.	any prior brain damage, esp. to the cortex.

ii.	cerebral malformation.

4.	Incidence in childhood

a.	Overall 6.7% of all children before 5 years of age.

b.	Usually 1.2% of newborn have poor prognosis.

c.	Cerebral palsy:

i.	hemiplegia: 35%.

ii.	quadriparesis: 50%/

d.	Mentally retarded children: 20%.

5.	Types of Fits by age group

Age	Fits	
Birth – 1 week	Neonatal seizure.	
1 week - 6 months	Infantile seizures.	
6 months - 5 years 	Febrile fits	
5 years – adolescence	Epilepsy	

6.	Common seizure types

Seizure type	Features	
Generalized:
Tonic – clonic	
•	May follow a partial seizure, idiopathic or induced by infections, stress or drugs.
•	Tonic phase:
       - Sudden loss consciousness.
       - Tonic contraction.
       - Apnoea.
       - Cyanosis.
       - Eyes roll backwards.
       - Clonic phase:
•	Clonic phase:
       - rhythmic contractions of all muscle groups.
       - tongue biting.
       - sphincter control loss.
•	Post-ictal: semi-conscious for 30 minutes to 2 hours.	
Absence	•	Sudden loss of awareness.
•	No motor activity.
•	Eyelid fluttering.
•	No postical phase.
•	Last < 30 seconds.
•	Complex: myotonic movements and loss of mody tone. 
•	EEG: 3/sec generalized spike and wave. 	
Myoclonic	•		
Clonic	•		
Tonic	•		
Ataxic	•		
Partial
Simple	
•	Consciousness preserved.
•	Usually focal motor or sensory disturbance.	
Complex	•	Altered consciousness.
•	Automatism: lip smacking, chewing, drooling.	
Secondarily generated	•		

7.	History

a.	Detailed description of the fit by eye-witness:

i.	pre-ictal.

ii.	ictal.

iii.	post-ictal.

b.	Any associated illness:

i.	fever.

ii.	vomiting / diarrhoea.

iii.	starvation.

iv.	behavioral changes.

v.	headaches: meningitis, brain tumor, trauma.

vi.	ear discharge.

c.	Drug history: phenothiazines.

d.	Abnormal birth and developmental history.

e.	Head trauma.

f.	Past history of fits.

g.	Medical illness:

i.	bleeding disorders: hemophilia may bleed into brain causing sudden focal fit.

ii.	CHD: SBE predisposes to brain abscess.

iii.	diabetes mellitus: hypoglycaemia.

h.	Family history of fits and mental retardation.

8.	Clinical examination

a.	Neurological signs: generalized or localized.

b.	Signs of cerebral palsy.

c.	Signs of mental retardation.

d.	Dysmorphism.

e.	Neurocutaneous stigmata. 

9.	Causes of seizures in children

Perinatal conditions	•	Birth trauma.
•	Asphyxia.
•	Hemorrhage.	
Congenital malformations	•	AVM.
•	Cerebral malformation.	
Degenerative disease	•	Decreased mental capacity and milestones.	
Genetic grand-mal	•	Tuberous sclerosis.
•	Other neurocutaneous syndrome.	
Infection	•	Meningitis.
•	Encephalitis.
•	Brain abscess.	
Metabolic	•	Aminoaciduria.
•	Hypoglycaemia.
•	Hypocalcaemia.	
Systemic disorders	•	SLE.
•	Vasculitis.
•	Hypertension.
•	Renal failure.
•	Hepatic encephalopathy.	
Others	•	Toxins: heavy metals & drugs.
•	Trauma.
•	Tumor.
•	Fever.	

Neonatal seizures

1.	Clinical features

a.	Tonic spasm: stiffening, apnoea, cyanosis.

b.	Clonic: focal, multifocal, generalized.

c.	Tonic – clonic: rare.

d.	Myoclonic.

e.	Subtle manifestations:

i.	facial grimacing.

ii.	pallor. 

iii.	apnoea.

iv.	eye deviation.

v.	sucking movements.

vi.	cycling of lower limbs.

2.	Causes of fits in 1st 3 days of life

a.	Hypoxic-ischaemic insult.

b.	Birth trauma.

c.	Intracranial haemorrhage.

d.	Hypoglycaemia.

e.	Normophosphataemic hypocalcaemia.

f.	Pyridoxine deficiency. 

g.	Cortical dysplasia.

3.	Causes of fits at the end of first week

a.	Hyperphosphataemic hypocalcaemia.

b.	Hypomagnesaemia.

c.	Infections:

i.	meningitis.

ii.	encephalitis.

iii.	septicaemia.

iv.	intrauterine infections: TORCH.

d.	Genetic causes:

i.	neurocutaneous syndromes.

ii.	benign familial neonatal fits: dominantly inherited disorder with good prognosis.

e.	Metabolic disorders:

i.	galactosaemia.

ii.	aminoaciduria.

4.	Prognosis

a.	Earlier presentation (Day 1 – 3): 1/3 die.

b.	Later presentation (Day 4 – 7): 10% die.

c.	Sequelae in survivors: 

i.	mental retardation.

ii.	cerebral palsy.

iii.	epilepsy.

5.	Investigations

a.	Infection screen:

i.	lumbar puncture.

ii.	blood culture.

iii.	urine culture.

iv.	eye, nasal, umbilical, skin and anal swabs for culture.

b.	Intrauterine infection screen:

i.	TORCH.

ii.	hepatitis B.

iii.	coxsackie serology.

c.	Metabolic screen:

i.	blood sugar.

ii.	urea and electrolytes.

iii.	acid-base.

iv.	blood gases.

v.	lactate / pyruvate.

vi.	urine and blood aminograms.

vii.	urine reducing sugars.

d.	Cerebral imaging:

i.	skull x-rays: intracranial calcifications.

ii.	CT scan: calcifications, malformations and bleeding.

e.	EEG.

6.	There are two categories of patients:

a.	Those in which the cause is irreversible and treatment is ineffective.

b.	Those in which treatment is effective:

i.	hypoglycaemia.

ii.	hypocalcaemia / hypomagnesaemia.

iii.	pyridoxine dependency.

iv.	acquired infections.

7.	Management

a.	Stop seizures with high dose phenobarbitone.

b.	Reduce cerebral edema secondary to trauma, bleeding, infection and hypoxia:

i.	intravenous mannitol.

ii.	hyperventilation: keep pCO2 at 25 – 28 mmHg.

c.	Treat primary treatable cause.

d.	Nutritional and cardiorespiratory support.

Infantile spasms

1.	Epidemiology

a.	Incidence: 1:3000.

b.	Peak incidence: 3 – 6 months.

c.	The earlier the onset, the worse the prognosis.

d.	More common in boys than girls.

e.	Associated with arrested development.

2.	Clinical features

a.	Sudden onset.

b.	Characteristically occur in clusters of several within a minute or two, and episodes may be repeated many times a day.

c.	May be preceded or accompanied by a cry.

d.	Sudden bilateral myoclonic jerks:

i.	sudden drawing of the legs on the abdomen.

ii.	hunching forward of the neck and shoulders.

iii.	arms are often flung out in extension.

e.	Opisthotonic or extensor spasms are less common.

f.	Occurs in the twilight period of sleep or upon wakening. 

3.	Causes

a.	Idiopathic (1/3):

i.	milestones delayed before onset of fits: bad prognosis.

ii.	milestones delayed after onset of fits: intermittent.

b.	Secondary (2/3):

Prenatal	•	Intrauterine infections.
•	Cerebral malformation.
•	Tuberous sclerosis.
•	Sturge Weber’s.
•	Phenylketouria.
•	Tay-Sach’s disease.
•	Pyridoxine deficiency.	
Perinatal	•	Birth trauma.
•	Hypoxia.
•	Asphyxia.
•	Intracranial hemorrhage.	
Postnatal	•	Kernicterus.
•	Trauma.
•	Infection. 	

4.	Complications

a.	Gross motor delay.

b.	Mental retardation.

c.	Antisocial / autistic behavior.

5.	Investigations

a.	Metabolic screen.

b.	CT scan: tuberous sclerosis and cerebral malformation.

c.	EEG

i.	hypsarrhythmia

ii.	disorganized pattern of generalized high voltage slow wave, sharp wave and spike activity.

6.	Treatment

a.	Treatment doesn’t affect outcome or prognosis.

b.	Spasms can be controlled by administration of oral prednisolone 2 mg/kg/day or ACTH 40 units/day IM for 1 – 2 months with slow withdrawal.

c.	Nitrazepine / Clonazepam / Vigabatrin have been used with varying degree of success.

d.	Fits usually stop by itself by 2 – 4 years of age and replaced by grand mal epilepsy.

7.	Prognosis

a.	Rests heavily on underlying brain pathology; most have poor prognosis: severe mental retardation.

b.	A normal child has better prognosis than one with brain damage; 10 – 15% will succumb.

c.	Even without treatment, the fits get less severe and ceases after months or years, some giving way to focal seizures, grand mal seizures or minor motor seizures.

d.	Motor function usually is delayed but eventually most patients learn to sit and walk.

e.	Intellectual disability is present in 70 – 80% even with early and adequate therapy.

8.	West syndrome is characterized by a triad of:

a.	Infantile spasms.

b.	Hypsarrhythmias.

c.	Mental retardation.

Febrile Fits

1.	Definition

a.	An event in infancy or childhood, usually occurring between 3 months and 5 years of age, associated with fever but without evidence of intracranial infection or defined cause.

b.	Seizures with fever in children who have suffered a previous nonfebrile seizure are excluded.

c.	A benign condition including:

i.	complex febrile seizures.

ii.	metabolic or toxic encephalopathy.

iii.	early epilepsy which requires precipitation by fever.

2.	Characteristics of simple febrile fits

a.	Age of presentation:

i.	6 months to 6 years.

ii.	peak incidence: 2nd year of life.

iii.	1st seizure most commonly occurs in infancy to 3 years of life.

iv.	60% under 2 years of age.

v.	20% between 2 – 3 years of age.

vi.	20% after 3 years of age. 

b.	Temperature:

i.	threshold is > 38.5C.

ii.	rapidly rising.

c.	Seizure:

i.	within 12 hours of onset of fever.

ii.	one generalized seizure.

iii.	last less than 15 minutes.

d.	No history of afebrile seizures.

e.	Postictally, no neurological or sensorial deficits.

f.	No evidence of CNS infection.

g.	EEG normal in between fits. 

h.	Family history:

i.	in 15 – 20% of patients.

ii.	polygenic inheritance.

iii.	inheritance of a low seizure threshold.

3.	Complex febrile fits

a.	Focal seizures and / or Todd’s paralysis.

b.	Seizures longer than 15 minutes.

c.	More than one seizure within 24 hours.

4.	Causative infections

a.	Viral URTI.

b.	Urinary tract infection.

c.	Viral exanthem.

d.	Gastroenteritis.

5.	Exclusion of other diagnoses

a.	Meningitis must be excluded: 

i.	it presents as febrile fits in 15% of cases, esp. in child < 2 years.

ii.	no signs are present in 35%.

b.	Lumbar puncture in:

i.	suspicious meningitis.

ii.	< 2 years.

iii.	1st febrile fit.

iv.	if recovery is slow. 

c.	Acute encephalopathy.

d.	Inborn errors of metabolism.

e.	Epileptic seizures precipitated by fever.

f.	Pseudoseizures: rigors.

6.	Management

a.	Supportive:

i.	isolate child; remove sharp objects from vicinity.

ii.	place in left lateral position.

iii.	do not put anything into mouth. 

b.	Control fever:

i.	use of antipyretic agents.

ii.	sponging head, axilla and groin.

c.	Stop seizure:

i.	rectal or IV diazepam 0.25 mg/kg/BW.

ii.	IV valium or phenobarbitone.

d.	Frequent recurrences > 3 episodes:

i.	prophylaxis with diazepam suppositories.

ii.	effective in reducing recurrence rate by 50% and number of prolonged fits. 

e.	Family education and counseling:

i.	seizure first aid.

ii.	management of fever.

iii.	long-term outlook.

7.	Prognosis

a.	Good mental development.

b.	Few have neurological deficits.

c.	Recurrence risk:

i.	30 – 40%: second attack.

ii.	5 – 10%: multiple attacks.

iii.	2 – 5%: frequent epilepsy.

iv.	most recurrences occur within 3 years of onset.

d.	Risk factors associated with increased risk of afebrile fits:

i.	prior neurodevelopmental disorder.

ii.	age of onset < 15 months.

iii.	epilepsy in parents / sibling.

iv.	complex first seizure.

e.	Implications of complex febrile fit:

i.	association with pre- or perinatal problems.

ii.	association with abnormal neurological examination.

iii.	3 x higher incidence of subsequent epilepsy.

f.	Implications of previous neurodevelopmental delay:

i.	associated with earlier age of onset.

ii.	increased risk of complex seizures.

iii.	increased risk of later epilepsy.

iv.	increased risk of intellectual deficits.

v.	increased incidence of EEG abnormalities. 

8.	Indications for anticonvulsant therapy

a.	Atypical, complex fit.

b.	Presence of structural brain damage: CP & MR.

c.	Previous afebrile seizures.

d.	Abnormal development antedating the first fit.

e.	Family history of afebrile fit or epilepsy. 

Lennox-Gastaut syndrome

1.	These comprise a heterogeneous group of seizure disorders with a mixed seizure pattern dominated by ‘small attacks’: myoclonic, tonic and atypical absence seizures.

2.	Etiology

a.	Idiopathic.

b.	Hypoxic-ischaemic brain injury.

c.	Metabolic disturbances.

d.	Brain malformations and degenerative diseases.

e.	Often evolves from infantile spasms.

3.	Clinical features

a.	Head nods and drop attacks, with sudden loss of postural control.

b.	Momentary loss of consciousness.

c.	Myoclonic jerks of the arms and shoulders.

d.	Intellectual disability.

4.	Management and prognosis

a.	Drugs of choice:

i.	sodium valproate.

ii.	lamotrigine.

iii.	benzodiazepines.

b.	Ketogenic diet, corticosteroids and corpus callosotomy may be used in resistant cases.

c.	Prognosis is usually poor because of difficulty in controlling seizures, and the frequent association of retarded intellectual development.

Grand Mal Epilepsy

1.	Clinical features

a.	Abrupt onset of muscular spasms with loss of consciousness.

b.	Tonic phase:

i.	apnoea and bradycardia.

ii.	up-rolled eyes.

iii.	clenched teeth.

iv.	loss of posture: patient will fall if standing or sitting.

c.	Clonic phase:

i.	generalized coarse rhythmic jerking.

ii.	bowel and bladder contraction.

iii.	lasts a few minutes. 

c.	Post-ictal:

i.	sleep.

ii.	headache.

iii.	confusion.

d.	Aura do not occur; if present, the seizure is of partial origin, with secondary generalization.

e.	Often occur during sleep, following sleep deprivation or during periods of stress or illness. 

2.	Treatment

a.	Sodium valproate or carbamazepine are used.

b.	If not successful, phenytoin or a benzodiazepine may be tried.

3.	Prognosis: seizure control is usually possible, but several years of being seizure free should elapse before medication is withdrawn.

Petit Mal Epilepsy

1.	Incidence

a.	Commence between 5 and 10 years of age.

b.	Rare before age of 3.

c.	Females are affected more commonly than males.

2.	Clinical features

a.	Sudden cessation of activity with staring, usually lasting only 5 – 10 seconds.

b.	Blinking, upward deviation of the eyes, slight mouthing movements and some fidgeting hand movements may occur.

c.	The child does not fall and is rarely incontinent.

d.	Many attacks usually occur in a day and rarely they may be almost continuous.

e.	Attacks usually can be precipitated by hyperventilation.

3.	EEG: 3 per second generalized spike and wave activity.

4.	Treatment

a.	Sodium valproate.

b.	Ethosuximide.

c.	Lamotrigine.

5.	Prognosis

a.	More than 50% of children outgrow their seizures.

b.	Some continue to have absence and other generalized seizure types in adolescence and adult life.

c.	Intellectual development is usually normal.

Benign partial epilepsy of childhood

1.	Incidence

a.	Most common form of epilepsy in childhood.

b.	Onset: 5 – 10 years of age.

2.	Clinical features

a.	Focal disturbance: paraesthesiae of the side of the face, mouth and tongue.

b.	Motor: 

i.	twitching of one side of the face.

ii.	jerking movements of the jaw.

iii.	mouthing movements, gurgling and choking noises.

c.	Consciousness is unimpaired, but there is often inability to speak during attacks.

d.	Attacks may progress to involve the arm and leg and may secondarily generalized.

e.	Most commonly nocturnal.

3.	Treatment

a.	Because some children have only 1 or 2 attacks, anticonvulsant medication is often recommended only if they are continuing to occur.

b.	They usually respond well to carbamazepine.

c.	Treatment can often be successfully discontinued after 1 year.

4.	Prognosis

a.	Excellent due to good response to anticonvulsants.

b.	Seizures usually cease by age of 12 – 15 years.

Temporal lobe Epilepsy

1.	Etiology

a.	Due most commonly to scarring of the medial temporal lobe – hippocampal sclerosis.

b.	In some children, it is associated with prolonged febrile convulsions or meningitis in early childhood.

c.	Developmental malformations of the temporal lobe and tumors are found in one third of children.

2.	Clinical features

a.	Preictal:

i.	aura: irritability, butterfly stomach, fear and hallucination.

ii.	consciousness often impaired, but rarely completely lost.

iii.	cannot control.

iv.	know of forthcoming episodes.

v.	often sits down to prepare. 

b.	Ictal:

i.	lasts 2 – 10 minutes.

ii.	stares in a searching manner > 1 minute.

iii.	unilateral motor: repeated rubbing or fidgeting hand movements; dystonic posture of the upper extremity.

iv.	autonomic: facial flushing or pallor, lip smacking, salivation, chewing and vomiting, abdominal discomfort, belching or vomiting.

v.	psychic: unreal dream states, feeling of familiarity, fear, distortion of visual images. 

c.	Postictal:

i.	amnesia.

ii.	know what’s happening but unable to respond.

d.	Seizures commonly occur in clusters over several days, alternating with seizure free periods of days or weeks.

e.	Cognitive and behavioral problems are very common.

3.	Treatment

a.	Carbamazepine is the drug of first choice.

b.	Second line drugs:

i.	lamotrigine.

ii.	vigabatrin.

iii.	sodium valproate.

iv.	phenytoin.

c.	Temporal lobectomy.

4.	Prognosis

a.	Difficult in obtaining complete seizure control.

b.	Associated behavioral and learning difficulties are common.

c.	Complex partial seizures can arise in other lobes of the brain and have a similar course.

Non-epileptic episodic disorders of childhood

1.	Breath holding attacks

a.	Usually commences in the first or second year of life.

b.	Attacks are precipitated by either:

i.	physical trauma: fall or knock.

ii.	emotional distress: fright, anger, frustration.

c.	Clinical features:

i.	attacks usually commence with crying.

ii.	apnoea then occurs, with either cyanosis or pallor.

iii.	the attack may terminate without apparent loss of consciousness.

iv.	incontinence may occur.

v.	recovery is usually rapid. 

d.	Attacks usually cease by the third or fourth year of life but occasionally not so until 6 or 7 years.

e.	They are not a cause of death, epilepsy, intellectual disability or cerebral damage in later life. 

2.	Syncope

a.	Associated with syncope in children:

i.	vomiting illnesses.

ii.	prolonged standing.

iii.	venepuncture.

iv.	injury.

b.	Clinical features:

i.	brief tonic stiffening, clonic jerking and incontinence can follow loss of consciousness.

ii.	preceding light headness or visual loss, subsequent sweating and tachycardia.

c.	Syncope without an obvious precipitant or syncope during exercise should prompt concern about a cardiac cause such as prolonged QT syndrome or aortic stenosis. 

Management of Seizures

1.	Principles

a.	Distinguish epileptic seizures from non-epileptic attacks.

b.	Determine the type(s) of epileptic seizures the child is having.

c.	Try to make an epilepsy syndrome diagnosis when the child is having recurrent seizures.

2.	EEG is used in distinguishing:

a.	Partial from generalized seizures.

b.	Various epilepsy syndromes.

3.	Indications of MRI

a.	Partial seizures.

b.	Focal EEG abnormalities.

c.	Evidence of neurological impairment.

d.	Uncontrolled seizures.

e.	Clinical evidence of a specific brain lesion, e.g. tuberous sclerosis.

4.	Use of anticonvulsants

a.	If epilepsy is difficult to control it is often necessary to change drugs and to adjust dosage before control is obtained.

b.	Seizures can usually be controlled with one medication at an optimal dose.

c.	Children vary greatly in their dosage requirements and tolerance of anticonvulsants.

d.	Appropriate drugs are commenced singly and in low dosage and then increase gradually to a level where control is obtained. 

e.	Use of serum levels for monitoring anticonvulsant medications is useful if seizure control is inadequate: barbiturate and phenytoin.

f.	Duration of therapy depends on the epilepsy syndrome diagnosis, degree of seizure control and patient’s lifestyle.

5.	Medications and seizure types

Seizure type	Anticonvulsant	
Partial	•	Carbamazepine.
•	Lamotrigine.
•	Vigabatrin.
•	Sodium valproate.	
Generalized tonic-clonic	•	Sodium valproate.
•	Ethosuximide.
•	Lamotrigine.	
Absence	•	Sodium valproate.
•	Ethosuximide.
•	Lamotrigine.	
Myoclonic, atonic, tonic	•	Sodium valproate.
•	Lamotrigine.
•	Benzodiazepine.	
Infantile spasms	•	Predisolone.
•	ACTH.
•	Vigabatrin.
•	Benzodiazepine.	
Neonatal seizures	•	Phenobarbitone.
•	Phenytoin.
•	Clonazepam.	

6.	Side effects of anticonvulsants

Anticonvulsant	Side effects	
Most	•	Drowsiness.
•	Confusion.
•	Nausea and vomiting.
•	Ataxia, tremor, nystagmus, dysarthria.	
Carbamazepine	•	Rash.
•	Leukopenia.
•	Hyponatraemia.
•	Irritability.
•	Depression.	
Valproate	•	Weight gain.
•	Alopecia.
•	Acute hepatic failure.
•	Pancreatitis.	
Lamotrigine	•	Rash.
•	Severe hypersensitivity syndrome.	
Vagabatrin	•	Psychosis.
•	Behavior disturbance.
•	Weight gain.	
Clonazepam	•	Severe behavioral changes.
•	Increased bronchial and salivary secretions.	
Phenytoin	•	Rash.
•	Gum hypertrophy.	
Phenobarbitone	•	Behavioral disturbances.	

7.	Surgery

a.	Useful in children with intractable epilepsy.

b.	Best results have been with anterior temporal lobectomy for temporal lobe epilepsy.

c.	Corpus callostomy, hemispherectomy and extratemporal resections have a role in certain other epilepsy syndromes. 

8.	Social 

a.	Education and vocation.

b.	Emotional disorders associated with epilepsy.

c.	Safety issues.

d.	First aid treatment of seizures.

Status Epilepticus

1.	Definition

a.	More than 30 minutes of continuous seizure or two or more seizures without full recovery of consciousness in between.

b.	Generalized convulsive status epilepticus is the most common and dangerous type of status epilepticus.

2.	Precipitating factors

a.	Sudden withdrawal of anticonvulsants in a known epileptic.

b.	Acute infection: CNS / systemic.

c.	Acute insult to the brain.

d.	Brain tumor.

3.	Generalized convulsive status epilepticus may produce brain damage by:

a.	Hypoxic-ischaemic brain injury.

b.	Excessive metabolic requirements of cerebral neurons.

c.	Excess of excitatory amino acids.

d.	The underlying cause of the status epilepticus.

4.	The longer the status epilepticus is allowed to continue, the less likely the patient is to respond to further anticonvulsant therapy and the greater the likelihood of an adverse outcome.

5.	Complications

a.	Mortality (8 – 33%):

i.	aspiration asphyxia.

ii.	cerebral edema.

iii.	tissue anoxia.

iv.	electrolyte disturbances and metabolic acidosis.

b.	Morbidity:

i.	mental deficits: 30 – 50%.

ii.	neurological sequelae: 20 – 35%.

iii.	normal: 20 – 25%.

6.	First aid advice

a.	Keep airways open by posture: either side or prone so tongue does not fall back.

b.	Protect from physical harm:

i.	put on level surface.

ii.	do not restrain.

iii.	do not force anything into mouht.

7.	Protocol for Treatment

Time	Procedure	
0 – 5 mins	•	ABCs of life support.
•	Quick history and examination.	
6 – 9 mins	•	Draw blood for laboratory investigations.
•	Set up IV with normal saline.	
10 – 30 mins	•	IV glucose & IV thiamine if hypoglycaemic.
•	IV benzodiazepine (diazepam or lorazepam).
•	IV phenytoin 20/mg/kg at 1 mg/kg/min.	
30 – 40 mins	•	Can repeat IV diazepam.
•	IV phenytoin up to 30 mg/kg.
•	IV phenobarbitone 20 mg/kg.	
1 hour	•	If seizures persist, use high doses of barbiturates, abolish all seizure activity with EEG monitoring. 	

8.	Use of Anticonvulsants

a.	Phenytoin:

i.	should be injected slowly and directly into a large vein through a large-gauge needle or IV catheter.

ii.	each injection should be followed by a ‘flushing’ injection of sterile saline through the same needle.

iii.	avoid continuous infusion. 

iv.	loading dose of 20 mg/kg in children over 20 minutes.

b.	Phosphenytoin:

i.	a water-soluble prodrug for phenytoin.

ii.	it is rapidly converted to phenytoin in the body.

iii.	can be absorbed rapidly after IM injection without causing tissue necrosis and pain.

iv.	can be given by rapid IV injection.

c.	Other drugs:

i.	midazolam.

ii.	rectal diazepam: 0.5mg/kg.

iii.	IV valproic acid.