ARTICLE IN PRESS

Current Paediatrics (2005) 15, 324–332

www.elsevier.com/locate/cupe

Status epilepticus: Beyond guidelines

Helen Basu, Finbar O’Callaghan

Department of Paediatric Neurology, Bristol Royal Hospital for Children, Upper Maudlin Street,
Bristol BS2 8BJ, UK

KEYWORDS Summary Status epilepticus is the most common neurological emergency in

Convulsive status paediatric practice. If convulsive status epilepticus is prolonged (i.e. greater than
epilepticus; 30 min) then there is a loss of cerebral autoregulation that results in cerebral
Refractory status oedema and ischaemic injury to the brain. There may be permanent neurological
epilepticus; sequelae. The aims of treatment are to terminate the seizure as rapidly as possible
Non-convulsive and to identify and treat any underlying causes. Treatment guidelines for established
status epilepticus convulsive status epilepticus have recently been developed by the Status Epilepticus
Working Party, have been endorsed by the National Institute of Clinical Excellence
(NICE) and are recommended here. The treatment of refractory convulsive status
epilepticus and the less well recognised non-convulsive status epilepticus is
problematic but management options are discussed in this article.
& 2005 Elsevier Ltd. All rights reserved.

Introduction status epilepticus can reduce mortality and

Status epilepticus encompasses a range of epileptic
seizure types with different aetiologies, clinical
presentations and outcomes. Convulsive status
epilepticus is the most common neurological
emergency in paediatric practice and carries a risk
of permanent neurological sequelae. Data have
suggested that between 4 and 8 children per 1000
may experience an episode of convulsive status
epilepticus before the age of 15 years.1 The
outcome may be dependent on aetiology but
prompt and appropriate treatment of convulsive
Corresponding author. Tel.: +44 117 342 0187.
E-mail address: finbar.ocallaghan@bristol.ac.uk
(F. O’Callaghan).
morbidity.
Types of status epilepticus
Status epilepticus can be considered in two broad
groups: convulsive and non-convulsive. Convulsive
status epilepticus can be physiologically or electro-
graphically generalised (affecting the whole brain)
or focal (partial—affecting part of the brain).
Generalised status epilepticus includes tonic, to-
nic–clonic, clonic and myoclonic seizure types.
Generalised convulsive (tonic–clonic) status epi-
lepticus has been defined as a generalised convul-
sion lasting 30 min or longer, or repeated
tonic–clonic convulsions occurring over a 30 min
period without recovery of consciousness between

0957-5839/$ - see front matter & 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.cupe.2005.04.003
 ARTICLE IN PRESS
Status epilepticus: Beyond guidelines
each convulsion.2 As status epilepticus continues
the tonic phase may become less obvious and the
seizure evolves into continuous clonic status epi-
lepticus. Consciousness is impaired. Afterwards the
child is usually drowsy but gradually regains full
consciousness. If this does not occur after a
reasonable time the possibility of continuing brain
epileptic activity without ongoing motor signs must
be considered. This electroclinical dissociation may
constitute ‘subtle’ convulsive or non-convulsive
status epilepticus manifested by just twitching,
blinking or no movement at all. An electroence-
phalogram (EEG) may be needed to help with
diagnosis.
In tonic status epilepticus there is continuous
contraction usually of the extensor muscles and
it may be associated with hypoventilation and
cyanosis. This rare type of status epilepticus
may be seen in children with Lennox–Gastaut
syndrome.
Myoclonic status epilepticus is characterised
by persistent myoclonic jerks. It may occur in
children with a previous history of myoclonic
epilepsy or it may be associated with acute brain
injury and anoxia in which case the prognosis is
much worse.
In focal convulsive status epilepticus there is
usually rhythmic jerking of one part of the body,
often the upper limb. The convulsive activity does
not spread to the whole of the affected side. There
may be more subtle movements such as eye
blinking or trunk rotation. Secondary generalisation
may occur.
Epilepsia partialis continua is a type of focal
motor status, notably seen in Rasmussen’s ence-
phalitis. There is regular or irregular jerking of a
body part, most commonly the face or hand. It may
continue for hours, days or weeks.
Non-convulsive status epilepticus will be consid-
ered later.
Aetiology
Four aetiological groups can be identified: febrile,
idiopathic, remote symptomatic and acute sympto-
matic.
Febrile status epilepticus occurs in children aged
6 months to 5 years. It is precipitated by fever in
children with no history of previous afebrile
seizures and no evidence of central nervous system
(CNS) infection or other cause. There is a genetic
predisposition.
Idiopathic status epilepticus occurs without a
CNS or systemic insult in otherwise neurologically
325
normal children. It may present as a first seizure or
as part of an established seizure disorder.
Remote symptomatic status epilepticus occurs in
children with a known neurological insult such as
cerebral palsy, previous stroke or previous head
trauma. They may or may not have had previous
seizures.
There are many causes of acute symptomatic
epilepsy including CNS infection, head trauma,
cerebrovascular disturbance, e.g. arterial ischae-
mic stroke and intracranial haemorrhage. Other
causes include hypoxia, metabolic and electrolyte
disturbances (hypoglycaemia and hyperglycaemia)
and drug intoxication, e.g. cocaine, theophylline,
tricyclic antidpressants, amphetamines and insulin.
Acute withdrawal of antiepileptic drugs may pre-
cipitate seizures. Status epilepticus also occurs in
some progressive neurological disorders, e.g. brain
tumours and neurodegenerative diseases.
Pathophysiology
In generalised convulsive status epilepticus there
are widespread systemic and metabolic changes.3
Tachycardia, hypertension and increased cardiac
output are the results of increased sympathetic
outflow. Hyperthermia and hyperglycaemia also
occur. Initially the increased metabolic demands
of the brain are met by increased cerebral blood
flow. As the lactic acid level rises a metabolic
acidosis develops. After about 30–60 min decom-
pensation occurs and cerebral autoregulation is
impaired. Cerebral perfusion falls as hypotension
develops. Serum glucose and bicarbonate decrease
and serum potassium rises. Antiepileptic drugs may
become less effective and cardiac arrhythmias may
ensue. Hypoventilation and respiratory failure may
result from the status epilepticus and from the
medications given to treat it. Pulmonary oedema
and aspiration may contribute to hypoxaemia and
hypercarbia. Venous stasis and cerebral vein
thrombosis can result from hypotension and volume
depletion. In prolonged status epilepticus, rhabdo-
myolysis and myoglobinuria with renal failure may
occur.
Loss of cerebral autoregulation may result in
ischaemic injury and cerebral oedema.
In addition to the loss of autoregulation neuronal
hyperexcitability probably also contributes to
neuronal damage, which tends to occur in selec-
tively vulnerable areas such as the hippocampus.
The neuronal hyperexcitability may be mediated by
failure of the inhibitory neurotransmitter gamma-
aminobutyric acid (GABA). The failure of the
 ARTICLE IN PRESS
326
inhibitory effects of the GABA system is partly
responsible for the initiation and continuation of
status epilepticus. Excitatory amino acids such as
glutamate probably also contribute to the increase
in excitation and prolongation of status epilepticus
in addition to contributing to neuronal injury.
Activation of the N-methyl-D aspartate (NMDA)
receptor by glutamate results in calcium influx
and intracellular calcium increases. Destructive
calcium-dependent enzymes are activated result-
ing in neuronal damage.4
Since the loss of cerebral autoregulation and the
shift towards brain hyperexcitability seems to
occur approximately 30 min after seizure onset,
treatment protocols are directed towards termi-
nating the seizure before this time in an attempt to
prevent irreversible neurological damage.
Differential diagnosis of convulsive
status epilepticus
Before any treatment is instituted for status
epilepticus it is important to be certain of the
diagnosis. Several conditions can mimic convulsive
status epilepticus. A brief history and clinical
examination should help to differentiate these.
1. Decerebrate or decorticate posturing in a child
with increased intracranial pressure and im-
pending herniation may be mistaken for status
epilepticus as may an acute dystonic reaction in
response to drugs such as phenothiazines and
butyrophenones. Consciousness is usually pre-
served in acute dystonic reactions.
2. Movement disorders including chorea, hemibal-
lismus or a paroxysmal dyskinesia may be
difficult to distinguish from status epilepticus
especially if they develop in the context of an
acute encephalopathic illness or following head
trauma.
3. Benign neonatal sleep myoclonus may also
mimic status epilepticus.5 This is a self-limiting
movement disorder characterised by neonatal-
onset myoclonic jerks only during sleep with an
absence of concomitant electrographic changes
suggestive of seizures.
4. Non-epileptic seizures or psychogenic seizures
may take the form of prolonged pseudo-status
epilepticus.
In cases where there is doubt about the diagnosis
of status epilepticus an EEG is necessary for
confirmation.
H. Basu, F. O’Callaghan
Management of convulsive status
epilepticus
Aims
The aim of treatment is to terminate the seizure as
rapidly as possible and to identify and treat any
underlying cause. A child who presents with a
tonic–clonic convulsion lasting more than 5 min
should be treated in the same way as a child who is
in established status epilepticus. A treatment
guideline for an acute tonic–clonic convulsion
including established convulsive status epilepticus
was developed by the Status Epilepticus Working
Party and has recently been endorsed by NICE.2,6
The guideline is shown in Fig. 1.
During the initial evaluation of a child with
potential or suspected status epilepticus a history,
brief clinical examination and some basic investi-
gations should be performed in order to confirm the
diagnosis and if possible identify any underlying
cause. However, any necessary support for the
airway, breathing and circulation should not be
delayed.
History
The history should include enquiry about recent
trauma, infection, ingestion, previous seizures and
medication.
Examination
The examination should include assessment of
airway, breathing, circulation, temperature, ex-
ternal signs of trauma, skin rashes, neurocutaneous
stigmata and neurological status. Close monitoring
of oxygen saturation, pulse, blood pressure, re-
spiratory rate and depth and electrocardiogram
(ECG) should be established. The type of ictal
behaviour and its duration should be observed and
documented.
Investigations
The probable aetiology of the status epilepticus
may determine the investigations but all children
should have blood tests for glucose, urea, electro-
lytes, calcium, magnesium and blood gas analysis.
Blood tests for antiepileptic drug levels may be
appropriate. If infection is suspected a full blood
count and blood culture should be performed.
Further tests such as plasma amino acids, urine
organic acids, blood lactate and ammonia may be
considered if a metabolic disorder is suspected.
 ARTICLE IN PRESS
Status epilepticus: Beyond guidelines 327

Airway Breathing Circulation

Give high flow oxygen

Measure blood glucose

Confirm epileptic seizure

IMMEDIATE IV ACCESS NO IV ACCESS

1. LORAZEPAM 0.1 mg/kg IV 1. DIAZEPAM 0.5 mg/kg PR

(Give over 30–60 seconds)

Seizure continuing at 10 min IV ACCESS Seizure continuing at 10 min

2. LORAZEPAM 0.1 mg/kg IV 2. PARALDEHYDE 0.4 ml/kg PR

(Give over 30–60 seconds) (Give with same volume of olive oil)

Seizure continuing at 10 min Seizure continuing at 10 min

after commencing Step 2 after commencing Step 2

CALL FOR SENIOR HELP

3. PHENYTOIN 18 mg/kg IV over 20 min

OR

If already on PHENYTOIN give PHENOBARBITONE 20 mg/kg IV over 10 min

(use intraosseous route if still no IV access)

AND

PARALDEHYDE 0.4 ml/kg PR + same volume of olive oil if not already given

AND

CALL ON-CALL ANAESTHETIST OR INTENSIVE CARE PHYSICIAN

Seizure continues 20 min after commencing Step 3

4. RAPID SEQUENCE INDUCTION OF ANAESTHESIA USING THIOPENTAL 4 mg/kg IV

TRANSFER TO INTENSIVE CARE UNIT

Figure 1 Treatment guideline for an acute tonic–clonic convulsion including established convulsive status epilepticus.
IV, intravenous (modified from Appleton et al.2).

Blood and urine for toxicological screening may be the status epilepticus has been effectively treated
necessary if the cause of the status epilepticus is and the level of consciousness improved or until
unclear. Lumbar puncture should be deferred until cerebral oedema and a mass lesion have been
 ARTICLE IN PRESS
328
excluded. Indications for urgent brain imaging with
CT scan include status epilepticus associated with
head trauma, focal seizures, focal neurological
signs or focal EEG abnormalities. Children with a
previous history of epilepsy who have been thor-
oughly investigated do not need repeat brain
imaging with every episode of status epilepticus.
However each child should be carefully evaluated
as new pathology may occur. EEG may be necessary
if the diagnosis of status epilepticus is uncertain.
General management
Initially 100% oxygen should be administered and
the airway should be supported as necessary.
Breathing should be assessed and supported with
ventilation via a face mask or endotracheal tube as
appropriate. A nasogastric or orogastric tube may
aid stomach decompression and reduce the risk of
aspiration. Circulation may need support with
intravenous fluids but overhydration should be
avoided. If infection is suspected antibiotics and
acyclovir should be commenced and antipyretics
given.
Drug treatment in status epilepticus
The drug treatment of convulsive status epilepticus
in children is outlined in Fig. 1.
Benzodiazepines are potent and effective for the
initial management of status epilepticus and have a
rapid onset of action. They bind to the benzodia-
zepine binding site on the GABA receptor complex
increasing GABAergic transmission. This results in
inhibition of sustained and repetitive neuronal
discharges.
Step 1
If rapid intravenous access is not achieved, rectal
diazepam should be administered in a dose of
0.5 mg/kg. This has a rapid onset of action but as it
is highly lipid-soluble it quickly redistributes to
other fatty tissues causing brain and blood con-
centrations to fall rapidly. If intravenous access can
be achieved rapidly, the first line agent to be
administered is lorazepam (0.1 mg/kg). Lorazepam
has a rapid onset of action and a longer duration of
action than diazepam as it is less lipophilic. Both
diazepam and lorazepam can cause respiratory
depression and hypotension.
Step 2
After 10 minutes if the seizure has not stopped a
second dose of intravenous lorazepam 0.1 mg/kg
should be given. If diazepam was given initially, a
H. Basu, F. O’Callaghan
first dose of lorazepam can be given. If intravenous
access still has not been achieved and the child is
still convulsing at 10 minutes after an initial dose of
rectal diazepam a dose of rectal paraldehyde
0.4 ml/kg mixed with an equal volume of olive oil
can be given.
Step 3
If the seizure is continuing 10 minutes later, a
longer-acting anti-epileptic drug such as phenytoin
or phenobarbital is used. Phenytoin is preferred as
it causes less respiratory depression and CNS
depression.2 Side effects include cardiac arrhyth-
mias and hypotension. A dose of 18 mg/kg should be
administered intravenously over 20 min. The infu-
sion rate should not exceed 1 mg/kg/min and ECG
monitoring should be performed.
If a child is on oral maintenance therapy with
phenytoin there may be a risk of phenytoin toxicity
if intravenous phenytoin is used. Therefore, in this
situation, intravenous phenobarbitone 20 mg/kg
infused over 10 min is recommended. Barbiturates
potentiate the inhibitory action of GABA. Respira-
tory and CNS depression are common and may be
severe enough to warrant mechanical ventilation.
If intravenous access has not been achieved the
intraosseous route can be used.
Step 4
If convulsive status epilepticus is continuing 20 min-
utes after commencement of Step 3 then rapid
sequence induction of anaesthesia should be
performed using intravenous thiopentone (the
dosage will depend on the cardiovascular status of
the child). If neuromuscular blockade is necessary,
a short-acting agent should be used in order not to
mask ongoing convulsive activity. The child should
be transferred to a paediatric intensive care unit
(PICU) for further management.
Refractory status epilepticus
If convulsive status epilepticus is continuing despite
the measures outlined in Steps 1–4 above it is
considered to be refractory. There are no clear
guidelines for further drug treatment since rando-
mised clinical trials have not been done in
refractory status epilepticus, but a number of
different agents have been used. These include
midazolam, propofol, phenobarbitone, pentobarbi-
tal, lidocaine, ketamine, intravenous chlormethia-
zole, inhalational agents such as isoflurane and
desflurane, high-dose intravenous lorazepam, in-
travenous valproate and topiramate. At this stage
 ARTICLE IN PRESS
Status epilepticus: Beyond guidelines
care should be ongoing on a PICU under the joint
supervision of a paediatric neurologist. Supportive
therapy should be continued in order to maintain
and support the airway, breathing and circulation
and further diagnostic tests may need to be
considered if not already completed. Serum crea-
tinine kinase and urine myoglobin levels should be
monitored due to the risk of rhabdomyolosis in
refractory convulsive status epilepticus.
Thiopentone
Thiopentone is a barbiturate anaesthetic agent
traditionally used in the treatment of status
epilepticus. It has antiepileptic effects but has a
tendency to accumulate and cause hypotension,
which may require vasopressor therapy.
Midazolam
Midazolam has been reported to be an effective
and safe agent for the treatment of refractory
status epilepticus.7–9 It is a potent fast-acting
benzodiazepine with a short elimination half-life.
Its action is short-lived and therefore a loading dose
is usually administered followed by a continuous
infusion, the rate titrated to achieve seizure
suppression. Tachyphylaxis may occur necessitating
large dose increases after 24–48 h in order to
maintain seizure control. Midazolam accumulates
with prolonged infusion and this may result in a
long time to awakening. Side effects include
hypotension and respiratory suppression.
Propofol
Propofol is an intravenous anaesthetic agent with
antiepileptic properties. It is highly lipophilic and
has a rapid onset of action. Recovery is rapid when
it is discontinued. It has been found to be effective
in the treatment of refractory status epilepti-
cus.10,11 However, propofol has been associated
with a higher mortality rate than treatment with
midazolam.12 Long-term propofol infusion may
cause lipaemia, acidosis and rhabdomyolosis and
the risks may be higher in children than in adults.13
It is currently not routinely used in paediatric
practice.
Phenobarbitone
Phenobarbital may be effective in refractory status
epilepticus. It has a rapid onset of action but is
eliminated slowly and there is a risk of accumula-
tion necessitating blood level monitoring if therapy
329
is prolonged. Side-effects include sedation, re-
spiratory depression and hypotension. Since seda-
tion can be prolonged clinical assessment may be
difficult.
Pentobarbital
Pentobarbital is a barbiturate with a shorter half-
life than phenobarbital and, therefore, it may be
more suitable than phenobarbitone in refractory
status epilepticus as it allows more rapid clinical
assessment. Pentobarbital may be an effective
treatment in some cases14,15 but may be associated
with significant hypotension requiring vasopressor
therapy.16 It is not licensed in the UK.
Sodium Valproate
Intravenous loading with sodium valproate has been
found to be safe and effective in refractory status
epilepticus.17 It has fewer cardiovascular side
effects than some other agents18 and is relatively
non-sedating.
Lignocaine
Intravenous lignocaine has been used in refractory
status epilepticus.19 Sodium channel blockade and
decreased membrane excitability are thought to be
responsible for its antepileptic properties. At high
levels, lignocaine may cause CNS toxicity including
confusion, drowsiness, tremulousness, tinnitus and
psychosis.
Inhalational agents
Isoflurane and desflurane, inhalational anaesthetic
agents, have been reported to be effective in
stopping epileptic discharges in adult patients with
refractory status epilepticus and prolonged treat-
ment was well tolerated.20
High dose intravenous lorazepam
High dose intravenous lorazepam given as either a
continuous infusion or frequent intermittent bo-
luses has been reported to be effective in stopping
clinical or electrographic seizures in patients with
refractory status epilepticus.21
Topiramate
Topiramate administered via a nasogastric tube
was reported to be effective in terminating
refractory status epilepticus within 24 h of
 ARTICLE IN PRESS
330
initiating maintenance therapy in three children.22
These children had failed to respond to treatment
with benzodiazepines, phenytoin, phenobarbitone,
midazolam or pentobarbital.
Pyridoxine
A trial of intravenous pyridoxine in a dose of 100 mg
should be given to all children presenting up to the
age of 2 years with refractory status epilepticus
that has not responded to other antiepileptic drugs.
Vitamin B6-dependent seizures are due to an
autosomal recessive disorder and typically present
in the neonatal period. However they may begin as
late as 2 years of age and usually respond quickly to
intravenous pyridoxine.
EEG monitoring
The goal of treatment of refractory status epilepti-
cus is the termination of seizures, but by this stage
convulsive activity may be very subtle. Ideally all
children with refractory status epilepticus should
have continuous EEG monitoring in a PICU setting.
Continuous EEG monitoring has several advantages
including reasonable spatial resolution (i.e. activity
in different brain regions can be assessed simulta-
neously) and good temporal resolution (2–4 ms).23
At the very least, daily intermittent EEG recordings
should be performed but there is a danger of over-
or under-treatment.
There is no general consensus on the goal
regarding EEG activity. The traditional aim has
been the attainment of a burst-suppression pattern
but seizure control is achieved in some patients
with a background of continuous slow wave
activity.24
Long-term antiepileptic drug therapy
The need for long-term antiepileptic drug therapy
after convulsive status epilepticus has been con-
trolled depends on the underlying aetiology and an
assessment of the risk of recurrence. For example,
patients with known idiopathic generalised epi-
lepsy or a structural brain lesion are likely to need
long-term therapy unlike those in whom status
epilepticus occurred in the context of a transient
metabolic disturbance.
Non-convulsive status epilepticus
Types of non-convulsive status epilepticus include
typical absence, atypical absence, focal status
H. Basu, F. O’Callaghan
epilepticus with sensory symptomatology, focal
status epilepticus with affective symptomatology,
complex partial status epilepticus, continuous
spike and wave during slow-wave sleep and status
epilepticus in coma.
Typical absence status epilepticus is rare in
children. It is characterised by a prolonged period
of diminished responsiveness or confusion asso-
ciated with generalised spike and slow wave
discharges on the EEG.25 There may be associated
movements including eyelid flutter and rhythmical
facial or upper extremity movements.
Atypical absence epilepsy occurs more fre-
quently in childhood and is associated with Len-
nox–Gastaut syndrome, myoclonic astatic epilepsy
and severe myoclonic epilepsy of infancy. Children
may present with a change in personality, apparent
loss of contact with their environment, decreased
cognition, drooling, feeding difficulties, impaired
speech and unsteady gait.
Simple focal non-convulsive status epilepticus
may present with sensory or affective symptoms
including auditory sensations and fear.
Complex partial status epilepticus has been
defined as a ‘prolonged epileptic episode in which
focal fluctuating or frequently recurring electro-
graphic epileptic discharges, arising in temporal or
extratemporal regions, result in a confusional state
with variable clinical symptoms.’26 These include
fluctuating level of consciousness, impaired inter-
action with familiar people, staring, automatisms
and speech arrest.
Electrical status epilepticus in slow-wave sleep is
characterised by spike and wave discharges in at
least 85% of non-rapid eye movement (REM) sleep.
It is associated with Landau–Kleffner syndrome and
Lennox–Gastaut syndrome. The child may present
with language regression, behavioural changes and
neuropsychological problems.
Non-convulsive status epilepticus can occur in
coma either following convulsive status epilepticus
or associated with other pathologies in which the
significance of the EEG abnormalities may be
difficult to interpret as they may represent wide-
spread cortical damage rather than true epileptic
activity.27
The diagnosis of non-convulsive status epilepti-
cus is based on the clinical presentation together
with a supportive EEG. The clinical features may be
subtle and difficult to interpret especially in
children with existing learning disability.
The differential diagnosis of non-convulsive
status epilepticus includes a postictal state,
metabolic encephalopathy, psychogenic or conver-
sion disorder, alcohol or drug intoxication, psycho-
sis, hyperglycaemia and diabetic ketoacidosis,
 ARTICLE IN PRESS
Status epilepticus: Beyond guidelines
psychogenic mutism, depression, stroke, emotional
lability and psychosis.
Management of non-convulsive status
epilepticus
Typical absence status epilepticus usually responds
to benzodiazepines, which may be given orally or
intravenously, e.g. lorazepam, clonazepam, diaze-
pam. Intravenous valproate has also been used
successfully.28
Atypical absence status epilepticus may be more
difficult to treat and intravenous benzodiazepines
may not only be less effective but may precipitate
tonic status epilepticus. Oral treatment may be
preferred initially and valproate, lamotrigine,
topiramate, clonazepam and clobazam have all
been used effectively. Oral ketamine has also been
used successfully.29
Complex partial status epilepticus may be effec-
tively treated with oral benzodiazepines. More
resistant cases may require intravenous benzodia-
zepines or intravenous phenytoin. If more aggres-
sive therapy is needed such as intravenous infusions
of clonazepam or midazolam the child should be
closely monitored in a high dependency unit or
PICU. This allows the early recognition of severe
side effects including cardiorespiratory suppres-
sion. Continuous EEG monitoring would ideally be
used to assess treatment efficacy.
Electrical status epilepticus during slow-wave
sleep may respond to oral benzodiazepines. If these
are ineffective steroids may be tried. In some
resistant cases surgical options such as multiple
subpial transaction may be helpful.
Outcomes
A mortality rate of 30% has been described in
children with severe refractory convulsive status
epilepticus30 although other estimates have been
lower. Mortality is related to the aetiology, with the
highest rates occurring in the acute symptomatic
and progressive encephalopathy groups. Morbidity
is low following febrile, idiopathic and remote
symptomatic status epilepticus.
The long-term effects of non-convulsive status
epilepticus are not well understood. Typical ab-
sence status epilepticus may have a good prognosis
but there may be long-term memory deficits
following complex partial status epilepticus.31
Non-convulsive status epilepticus in coma asso-
331
ciated with acute medical illness has a poor
prognosis with a high mortality rate.32
Conclusions
Status epilepticus is a common paediatric neurolo-
gical emergency. There is an established protocol
for the treatment of convulsive status epilepticus in
the UK but the management of refractory status
epilepticus and non-convulsive status epilepticus is
more difficult. The outcome of status epilepticus
depends to a large extent on the aetiology, but
early and aggressive treatment of convulsive status
epilepticus reduces morbidity and mortality.
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