Management of Convulsive Status Epilepticus in Children - UpToDate

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Manejo del estado epiléptico convulsivo

en niños
Autor: Dr. Angus Wilfong
Editores de sección: Douglas R. Nordli, Jr., MD, Dra. Susan B. Torrey
Editores adjuntos: John F. Dashe, MD, PhD, James F. Wiley, II, MD, MPH
Todos los temas se actualizan a medida que se dispone de nueva evidencia y se

completa nuestro proceso de revisión por pares .
Revisión de la literatura actual hasta: octubre de 2022. | Última

actualización de este tema: 23 de noviembre de 2021.
INTRODUCCIÓN
El estado epiléptico convulsivo generalizado (SE) es una

emergencia médica grave y potencialmente mortal que requiere
una intervención inmediata.
El manejo de SE en niños se revisa aquí. La definición, la

fisiopatología, los factores de riesgo y el resultado de este
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trastorno se analizan por separado. (Consulte "Características

clínicas y complicaciones del estado epiléptico en niños" .)
DEFINICIÓN Y DIAGNÓSTICO DIFERENCIAL
● Estado epiléptico : una definición aceptada para los fines de

la práctica clínica define el EE como una convulsión única que
no remite que dura más de cinco minutos o como
convulsiones clínicas frecuentes sin un retorno interictal al
estado clínico inicial. La ventana de cinco minutos se
corresponde con el momento en que debe comenzar el
tratamiento urgente. Si SE continúa más allá de los 30
minutos, pueden ocurrir consecuencias a largo plazo que
incluyen lesión neuronal, alteración de las redes neuronales
y muerte neuronal. (Ver "Características clínicas y
complicaciones del estado epiléptico en niños", sección sobre
'Definición' ).
El SE se clasifica según si la actividad convulsiva es focal o

generalizada. En muchos casos, sin embargo, el SE
convulsivo generalizado no se puede separar fácilmente en
casos con un inicio principalmente generalizado frente a
aquellos con inicio focal y generalización secundaria. Tanto el
SE generalizado como el focal se pueden clasificar según si la
actividad convulsiva clínica es convulsiva o no convulsiva (
tabla 1 ).
● Estado epiléptico convulsivo: el SE convulsivo es el foco de

este tema y es un diagnóstico clínico, confirmado en la
mayoría de los casos por la presencia de actividad motora
tónica y clónica generalizada sostenida y rítmica que dura
más de cinco minutos o ataques convulsivos repetitivos sin
retorno a la línea de base. conciencia entre convulsiones.
Aunque el diagnóstico de SE convulsivo suele ser obvio, un
examen neurológico detallado es importante para hacer el
diagnóstico de formas más sutiles o focales de SE.
● Estado epiléptico no convulsivo: el SE no convulsivo se

define como un estado epiléptico sin síntomas motores
prominentes. (Consulte "Estado epiléptico no convulsivo:
clasificación, características clínicas y diagnóstico" .)
● Convulsiones generalizadas breves: no se considera que

los niños con convulsiones motoras generalizadas breves y
una conciencia interictal relativamente conservada tengan
SE; la mayoría de estos pacientes no tendrán convulsiones al
llegar al departamento de emergencias y no requieren
medicación intravenosa de emergencia [ 1 ]. Los escenarios
comunes incluyen:
• Convulsiones febriles: las convulsiones febriles son el

tipo más común de convulsiones breves y generalizadas
en los niños y, en ausencia de signos de meningitis o
encefalitis, no requieren una evaluación de laboratorio

extensa ni terapia anticonvulsiva. (Consulte

"Características clínicas y evaluación de las convulsiones
febriles" y "Tratamiento y pronóstico de las convulsiones
febriles" .)
• Convulsión afebril por primera vez : una primera

convulsión afebril requiere una historia cuidadosa, un
examen físico y una evaluación enfocada para excluir
afecciones médicas no epilépticas que pueden haber
provocado la convulsión, como fiebre, infección grave,
traumatismo craneoencefálico, hipoglucemia, alteración
de electrolitos, arritmia cardíaca , o una lesión
intracraneal ocupante de espacio.
Si no se puede encontrar una causa médica aguda

durante la visita al departamento de emergencias,
entonces el niño puede estar experimentando la
convulsión inicial de un trastorno epiléptico. Estos
pacientes justifican la derivación a un neurólogo
pediátrico. La mayoría de los niños diagnosticados con
convulsiones no provocadas o epilepsia de etiología
desconocida necesitarán un electroencefalograma (EEG)
programado y neuroimagen, preferiblemente con
resonancia magnética. (Consulte "Convulsiones y
epilepsia en niños: clasificación, etiología y características
clínicas" y "Convulsiones y epilepsia en niños: tratamiento
inicial y seguimiento" .)
Los niños con una primera convulsión no provocada, en

particular los pacientes con EEG y neuroimagen normales,
no suelen recibir medicamentos anticonvulsivos.
(Consulte "Convulsiones y epilepsia en niños: tratamiento
inicial y seguimiento", sección sobre 'Primera convulsión
no provocada' ).
• Convulsiones intercurrentes en niños con epilepsia

conocida : los niños con un trastorno convulsivo conocido
pueden tener convulsiones convulsivas intercurrentes
breves que comúnmente son causadas por una
enfermedad intercurrente o niveles anticonvulsivos
subterapéuticos. Muchos de estos pacientes pueden
manejarse mediante el ajuste de la terapia anticonvulsiva
oral después de consultar con el neurólogo pediátrico
que los recetó.
● Convulsiones focales : las convulsiones que no son

convulsivas generalizadas (tónicas, clónicas, tónico-clónicas)
requieren un enfoque diferente para la evaluación y el
tratamiento, como se analiza por separado. (Consulte
"Epilepsia focal: causas y características clínicas" y
"Convulsiones y epilepsia en niños: tratamiento inicial y
seguimiento" .)
● Convulsiones no epilépticas psicógenas: las convulsiones

no epilépticas psicógenas (PNES, por sus siglas en inglés)

suelen ser eventos de comportamiento dramáticos en un

individuo consciente que a menudo se diagnostican
erróneamente como ataques epilépticos y, a veces, se tratan
con grandes dosis de medicamentos anticonvulsivos. La
historia y la presentación pueden proporcionar pistas para el
diagnóstico. Las CPNE ocurren típicamente en pacientes
adolescentes, predominantemente en mujeres, con
trastornos afectivos o de ansiedad, y puede haber
antecedentes familiares de convulsiones. Muchos pacientes
que tienen CPNE también tienen o han tenido ataques
epilépticos, por lo que no se debe usar un historial médico
previo de CPNE para descartar la posibilidad de un estado
epiléptico. Las CPNE incluyen una variedad de
manifestaciones clínicas, algunas de las cuales son
indicativas, aunque no diagnósticas independientes, para
distinguir las CPNE de otros diagnósticos
diferenciales. tabla 2 ); estos se discuten en detalle en otra
parte. (Consulte "Convulsiones psicógenas no epilépticas:
etiología, características clínicas y diagnóstico", sección
"Manifestaciones clínicas" ).
En muchos pacientes, PNES se puede distinguir de SE en

función de las características clínicas o la respuesta a
estímulos dolorosos breves (p. ej., presión en el lecho
ungueal). Cuando existe incertidumbre clínica, PNES se
puede distinguir definitivamente de SE por un EEG urgente

(ver 'Electroencefalografía' a continuación). Es posible que

sea necesario iniciar la terapia antes de que se pueda
obtener un EEG, especialmente en pacientes con ataques
epilépticos previos. En este caso, se debe evitar la
medicación sedante, si es posible. La fosfenitoína o el
valproato son alternativas razonables a las benzodiazepinas
en este contexto.
El PNES y otros trastornos paroxísticos no epilépticos se

analizan en detalle por separado. (Consulte "Trastornos
paroxísticos no epilépticos en niños" y "Convulsiones
psicógenas no epilépticas: etiología, características clínicas y
diagnóstico" .)
RECONOCIMIENTO RÁPIDO DEL ESTADO EPILÉPTICO
El diagnóstico de SE convulsivo es clínico y se confirma verificando

la presencia de una crisis generalizada incesante que dura más de
cinco minutos o crisis frecuentes sin retorno interictal al nivel de
conciencia inicial. (Consulte 'Definición y diagnóstico diferencial'
más arriba).
Los pacientes con convulsiones motoras generalizadas que son

frecuentes o están separados por un período de alteración
significativa de la conciencia o que son médicamente inestables
requieren evaluación y tratamiento inmediatos en un entorno de

cuidados intensivos (servicio de urgencias o unidad de cuidados

intensivos).
EVALUACIÓN ENFOCADA URGENTE
Durante el curso de la reanimación, el médico o la persona

designada debe obtener un historial específico de un padre o
cuidador para determinar:
● Administración prehospitalaria de benzodiazepinas y

cualquier otro medicamento anticonvulsivo
● Historial de epilepsia del paciente
● Factores precipitantes previos a la convulsión (p. ej.,
enfermedad febril, posible exposición tóxica, traumatismo,
cambio de medicamentos anticonvulsivos) (ver
"Características clínicas y complicaciones del estado
epiléptico en niños", sección sobre 'Causas' )
● Medicamentos actuales, incluido el uso anterior o actual de
medicamentos anticonvulsivos
● Para pacientes con SE previo, historial de respuesta al
tratamiento (ver 'Factores que influyen en la elección del
agente' a continuación)
● Otros diagnósticos médicos activos, especialmente aquellos
asociados con hipoglucemia ( tabla 3 ), hiponatremia o
hipocalcemia ( tabla 4 )
● Alergias a cualquier medicamento.
En pacientes con SE, la exploración física inicial es limitada.

Además de evaluar los signos vitales, las vías respiratorias, la
respiración y la circulación, el médico debe identificar:
● Signos de traumatismo craneoencefálico (p. ej., hinchazón,

equimosis o laceraciones)
● Signos de sepsis o meningitis (p. ej., fiebre, mala perfusión o
erupción cutánea [p. ej., petequias, eritrodermia o celulitis])
● Seizure characteristics (eg, focal or generalized) (see "Clinical
features and complications of status epilepticus in children",
section on 'Classification')
IMMEDIATE SUPPORTIVE CARE
Approach — In children with convulsive SE, rapid supportive care

must occur simultaneously with prompt administration of
antiseizure medications ( algorithm 1).
The main goals of treatment are [2]:
● Establish and maintain adequate airway, breathing, and

circulation (see 'Airway and breathing' below)
● Identify and treat hypoglycemia ( table 5)
● Stop the seizure and thereby prevent brain injury (see
'Emergency antiseizure treatment' below)
● Identify and treat life-threatening causes of SE such as
trauma, sepsis, meningitis, encephalitis, or structural brain
lesion
Monitoring — All patients with generalized convulsions should

have continuous monitoring of heart rate and rhythm, breathing,
and pulse oximetry along with periodic measurement of blood
pressure and temperature. However, myoclonic jerks may
interfere with the ability of electronic monitors to detect
abnormalities. Thus, frequent clinical assessment of breathing,
pulse, and color must supplement monitor readings to ensure
rapid detection of apnea, cyanosis, or shock.
Airway and breathing — Important airway interventions in

children with SE include:
● Open the airway and maintain it through positioning

( picture 1), jaw thrust ( picture 2), and/or airway
adjuncts (eg, nasopharyngeal ( picture 3) or oropharyngeal
( picture 4) airways) as needed.
● Suction secretions using a Yankauer (tonsil tip) suction

catheter; have an additional large-bore suction device
available in case the patient vomits.
● Administer 100 percent oxygen; use pulse oximetry and

visual appearance to assess for cyanosis. When feasible,
quantitative, sidestream end-tidal CO2 (EtCO2) monitoring
can help supplement the visual assessment of respiratory
rate and ventilation when the wave form is used to interpret
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the EtCO2 reading. Myoclonus may interfere with the

accuracy of monitor readings.
For children with transient apnea or hypoxemia, the clinician

may use bag-mask ventilation as long as the airway can be
maintained and spontaneous breathing with adequate
oxygenation resumes within a short period of time. Two
rescuers are typically necessary to maintain the airway
during bag-mask ventilation in children with SE ( picture 5).
The patients with any one of the following should undergo

rapid sequence endotracheal intubation (RSI) and mechanical
ventilation:
● Unprotected or unmaintainable airway

● Apnea or inadequate ventilation
● Hypoxemia
● SE lasting 30 minutes
The tables provide a rapid overview of RSI in children ( table 6)

and initial settings for volume-controlled ( table 7) and pressure-
controlled ( table 8) mechanical ventilation. Emergency
endotracheal intubation in children and pediatric RSI are
discussed in detail separately. (See "Emergency endotracheal
intubation in children" and "Rapid sequence intubation (RSI)
outside the operating room in children: Approach".)

Special considerations for children with SE undergoing RSI

include:
● Propofol and midazolam have antiepileptic properties, and

either agent may be used for induction in hemodynamically
stable patients. Propofol has a shorter onset of clinical effect.
● Short-acting muscle relaxants, either rocuronium or, in

patients without contraindications, succinylcholine should be
given so that visual confirmation of continued seizures is
preserved once the brief paralysis resolves. However, an
urgent EEG should be obtained to look for electrographic
seizures if prolonged paralysis is indicated, as may be the
case for patients with hyperthermia or rhabdomyolysis.
Circulation and vascular access
● Establish venous access – Patients with SE require timely

vascular access for sampling of blood and administration of
medications and fluids. Peripheral intravenous (IV) access
should be established as soon as possible. Alternative routes
of antiseizure medication administration (eg, rectal,
intramuscular, buccal, or intranasal) should be used if IV
administration is not possible within the first five minutes; an
intraosseous (IO) line should be placed if IV access is further
delayed.

For patients whose seizures do not resolve with

benzodiazepine therapy, a second IV access should be
obtained to facilitate the administration of two separate
antiseizure medications and/or continuous anesthetic
infusions.
● Hemodynamic support – Most children with SE initially have

elevated blood pressure and do not require circulatory
support. Heart rate and blood pressure may be elevated in
patients with SE but typically normalize once seizures resolve
[2].
In general, SE does not independently cause systemic

hypotension. The presence of low blood pressure in children
presenting with SE should prompt consideration of an
underlying systemic illness, traumatic hemorrhage, or
infection. These patients warrant rapid infusion of isotonic
crystalloid (eg, normal saline or Ringer lactate) and further
treatment based upon the type of shock that is present
( algorithm 2). (See "Initial management of shock in
children".)
In addition, the presence of bradycardia, hypotension, and

poor perfusion are warning signs that point to hypoxia.
Children with these signs require immediate attention to
improve oxygenation and ventilation and, if not already
done, RSI with mechanical ventilation [2].

Clinicians should anticipate hypotension for children who

require continuous infusions of medications for refractory SE.
Rapid infusion of isotonic crystalloid (eg, 20 mL/kg of normal
saline or Ringer lactate) followed by a continuous infusion of
a vasopressor such as epinephrine or norepinephrine are
frequently necessary to maintain adequate tissue perfusion
and blood pressure.
Initial studies — Initial blood and urine studies should be

obtained for rapid determination of:
● Plasma glucose and a rapid "finger-stick" or point-of-care

glucose
● Serum electrolytes and calcium
● Serum antiseizure medication levels, if applicable
● If substance use or poisoning is suspected, urine and blood
toxicology
● In postmenarchal females, qualitative pregnancy test (urine
or blood)
Other studies may also be indicated based upon the most likely
underlying cause. (See 'Additional studies' below.)
Plasma glucose, serum electrolytes, and antiseizure medication

serum levels (for children receiving them) are the most helpful in
guiding initial care for children with SE. In a systematic review of
20 observational studies (almost 2100 children with SE), the yield
of preliminary testing was as follows [3]:
● 6 percent had abnormal electrolyte or glucose levels

● 3.6 percent had evidence of toxin ingestion
● Of children receiving antiseizure medications, almost 33
percent had subtherapeutic levels
While the yield of routine measurement of electrolytes, glucose,

and qualitative toxin screens was relatively low in this study,
abnormal findings affect management strategies and outcomes.
The utility and interpretation of testing for drugs of abuse screen
is discussed in detail separately. (See "Testing for drugs of abuse
(DOAs)".)
● Electroencephalogram (EEG) – When there is uncertainty

regarding the presence of SE, an urgent portable EEG should
be obtained. In the emergency department, this can be a
limited study, with application of only a few electrodes to
determine if the background is consistent with a normal
awake individual (ie, psychogenic nonepileptic seizure) or the
diffusely slow and depressed background of SE. (See
"Psychogenic nonepileptic seizures: Etiology, clinical features,
and diagnosis".)
If an urgent EEG cannot be obtained, or is not considered

necessary in the case of an obvious clinical diagnosis of
convulsive SE, an EEG should still be done to evaluate
background activity as soon as possible after the seizure
stops for patients with first-ever seizures or convulsive SE.

Patients with known epilepsy who return to baseline may not

require an EEG. (See 'Electroencephalography' below.)
● Neuroimaging – Neuroimaging is generally deferred until

the patient is stabilized. (See 'Neuroimaging' below.)
Correct hypoglycemia and metabolic

abnormalities — Hypoglycemia may provoke seizures and
convulsive SE. Although uncommon, either severe hyponatremia
or hypocalcemia may cause SE that is refractory to antiseizure
medication and requires timely correction. Metabolic acidosis is
often present in patients with SE and can be severe, but it usually
resolves without treatment once seizures are controlled.
● Hypoglycemia – All children with SE should have

measurement of a fingerstick or rapid point-of-care
measurement of plasma glucose as soon as possible. In
children with SE, including those who are just initiating the
ketogenic diet for seizure control, hypoglycemia should be
treated as outlined in the rapid overview table ( table 5).
For patients who are stable on the ketogenic diet for seizure
control and present in SE, a plasma glucose ≤40 mg/dL (2.2
mmol/L) warrants treatment for hypoglycemia. Continued
seizures, especially in the setting of hypoxemia, may lower
brain glucose levels as the metabolic demands outstrip the
supply, worsening brain lactic acidosis and leading to further
neuronal damage if prolonged; this emphasizes the

importance of ensuring adequate plasma glucose levels [4].

(See "Approach to hypoglycemia in infants and children" and
"Ketogenic dietary therapies for the treatment of epilepsy".)
Children with diabetes and hypoglycemia may present in the

emergency department with generalized or focal seizures, or
focal syndromes such as hemitonic posturing and
hemiparesis, which may mimic seizures or a postictal state,
respectively. These children should be treated with glucose,
not anticonvulsants. This situation emphasizes the
importance of obtaining a rapid assessment of blood glucose
in a child with seizures in order to provide appropriate
therapy.
Most children with acute seizures have elevated blood

glucose levels that do not require treatment. However,
nonketotic or ketotic hyperglycemia can occasionally
precipitate SE and may be an early manifestation of diabetes
[5,6].
● Hyponatremia – Severe symptoms, including seizures, are

most commonly seen in children with severe hyponatremia
(serum sodium <120 mEq/L) that develops acutely (over less
than 48 hours). Initial therapy consists of 3 to 5 mL/kg of 3
percent saline administered over 15 minutes. After the initial
hypertonic saline infusion, point-of-care serum sodium
should be remeasured and, if seizures are ongoing, the

infusion should be repeated. (See "Hyponatremia in children:

Evaluation and management", section on 'Acute symptomatic
hyponatremia'.)
● Hypocalcemia – Seizures in the setting of hypocalcemia

require therapy with IV calcium. The recommended dose of
elemental calcium is 5 to 7 mg/kg. Dosing in this range can
be achieved by giving 0.6 mL/kg of calcium gluconate 10
percent, which provides 5.6 mg/kg of elemental calcium or
0.2 mL/kg of calcium chloride 10 percent (must be given
through a central venous line), which provides 5.4 mg/kg of
elemental calcium. The maximum single dose is 540 mg of
elemental calcium. The calcium should be administered over
5 to 10 minutes in patients with spontaneous circulation.
(See "Primary drugs in pediatric resuscitation", section on
'Calcium'.)
The causes of hyponatremia or hypocalcemia in children are

discussed separately. (See "Hyponatremia in children: Evaluation
and management" and "Etiology of hypocalcemia in infants and
children".)
Temperature control — Fever at presentation lowers the seizure

threshold and requires treatment with acetaminophen in children
with SE.
Ongoing monitoring of temperature is essential to detect

hyperthermia associated with excess muscle activity during SE. If
present, then the resuscitation team should rapidly stabilize

airway, breathing, and circulation, and initiate cooling measures
(eg, evaporative cooling supplemented by a cooling blanket) and
assess for rhabdomyolysis and end-organ damage. Antipyretics
are ineffective. Hyperthermia and rhabdomyolysis caused by
persistent SE may require rapid sequence intubation and ongoing
paralysis and necessitate continuous portable EEG monitoring to
guide seizure management. (See "Heat stroke in children", section
on 'Hospital management' and "Heat stroke in children", section
on 'Diagnostic evaluation'.)
Suspicion for isoniazid poisoning — In addition to

benzodiazepine administration, children with SE possibly due to
isoniazid poisoning should receive pyridoxine 70 mg/kg IV, up to 5
g at a rate of 0.5 per minute, which should be repeated if seizures
continue. A dose of 1 gram pyridoxine per gram of isoniazid
ingested can be used (and may be necessary) after ingestion of a
known quantity of isoniazid. (See "Isoniazid (INH) poisoning".)
EMERGENCY ANTISEIZURE TREATMENT
Approach — Although many protocols are available for treatment

of pediatric SE, comparative data are limited, and these
approaches have not been validated by clinical trials [7-9]. The
approach presented below applies to children older than four
weeks of age (ie, not newborns) with generalized convulsive SE
(tonic-clonic, clonic, or tonic) is generally consistent with

guidelines published by the Neurocritical Care Society [8]. The
overall treatment approach is summarized in the algorithm
( algorithm 1). The treatment of neonatal seizures is discussed
separately. (See "Treatment of neonatal seizures".)
Clinically obvious convulsive SE should be treated immediately

with a benzodiazepine, without waiting for an EEG or other
studies. Treatment delay is associated with increased morbidity
and mortality [10-12]. (See 'First therapy: Benzodiazepines' below.)
If seizures continue for 10 minutes after at least two injections of a

benzodiazepine, a second therapy with a long-acting antiseizure
medication should be given ( table 9). (See 'Second therapy:
Antiseizure medications' below.)
In patients with ongoing convulsive SE lasting longer than 30

minutes despite two initial doses of benzodiazepine and a second
therapy antiseizure medication, preparation for a continuous
infusion of midazolam or pentobarbital should occur
simultaneously with administration of a different antiseizure
medication. At this stage, the patient will require endotracheal
intubation and mechanical ventilation (if not already performed),
neurologic consultation, and transfer to a pediatric intensive care
unit with continuous EEG monitoring capability, as described
below. (See 'Refractory status epilepticus' below.)

There is controversy about whether to treat nonconvulsive SE

(NCSE) as aggressively as convulsive SE. In all patients with NCSE, a
concerted effort should be made to diagnose and treat seizures as
quickly as possible but with minimal sedation to avoid inducing or
prolonging coma and respiratory depression that requires
endotracheal intubation and mechanical ventilation. In general,
any fluctuating or unexplained alteration in behavior or mental
status warrants consideration of NCSE and evaluation with EEG.
The evaluation and treatment of NCSE is discussed in detail
separately. (See "Nonconvulsive status epilepticus: Classification,
clinical features, and diagnosis", section on 'Evaluation' and
"Nonconvulsive status epilepticus: Treatment and prognosis".)
First therapy: Benzodiazepines — For children presenting with

convulsive SE, we recommend immediate treatment with a
benzodiazepine ( algorithm 1). Benzodiazepines are the first-line
treatment for SE because they can rapidly control seizures (see
'Benzodiazepine efficacy and pharmacokinetics' below). The three
most commonly used benzodiazepines to treat SE are lorazepam,
diazepam, and midazolam.
Prior to hospital arrival, benzodiazepine treatment may occur in

the home or be performed by emergency medical services
according to prehospital, pediatric seizure protocols. In these
patients, the first dose of benzodiazepines given in the hospital
counts as the second dose of benzodiazepines as long as
prehospital dosing was appropriate and, in children who continue
with SE, a second antiseizure medication should be given

( table 9).
Prehospital treatment — Treatment of SE out-of-hospital by

prehospital emergency responders appears to be safe and
effective in children. Intramuscular (IM) midazolam (5 mg for
children whose weight is 13 to 40 kg and 10 mg for those over 40
kg) or intravenous (IV) lorazepam (0.1 mg/kg) can be safely and
effectively used in this setting. Additional options include
intranasal midazolam, 0.2 mg/kg of parenteral solution per dose,
or buccal midazolam, 0.3 to 0.5 mg/kg. (See 'Benzodiazepine
efficacy and pharmacokinetics' below.)
In-hospital treatment — Benzodiazepines can be administered

by a variety of routes. However, if IV access is available, drugs
administered by this route are more effective [13]. (See "Seizures
and epilepsy in children: Refractory seizures", section on 'Home
rescue therapy (transmucosal antiseizure medications)'.)
● When IV or IO access is available – Lorazepam 0.1 mg/kg

intravenously (IV/intraosseous [IO]) up to a maximum of 4
mg should be administered by slow IV push over one minute
and its effect assessed over the next five to ten minutes [14].
An equally effective alternative is diazepam, although it has a
shorter duration of action (<20 minutes) [14,15]. The
recommended dose of diazepam is 0.2 mg/kg IV or IO
(maximum dose 10 mg). Treatment with benzodiazepine

doses that are lower than recommended has been

associated with a decreased likelihood of seizure cessation
[16]. Some UpToDate experts use a higher dose of diazepam
(0.3 mg/kg) based upon clinical experience, recognizing that
higher doses increase the risk of respiratory depression.
If seizures continue after five minutes, additional doses of

lorazepam or diazepam can be given ( table 9). The risk of
respiratory depression increases after administration of
more than two doses of benzodiazepines [13,17]. (See
'Benzodiazepine efficacy and pharmacokinetics' below.)
If IV access is not rapidly obtained, then IO placement should

be performed. (See "Intraosseous infusion".)
● When IV and IO access are unavailable – Placement of an

intravenous catheter may be difficult in some patients. When
IV and IO access cannot be achieved within the first three
minutes, alternative first-line agents include [14,18]:
• Intranasal midazolam – Intranasal midazolam 0.2 mg/kg

of parenteral solution per dose, divide dose between
nares, maximum single dose 10 mg (mucosal atomizer
device recommended), may repeat once in 10 minutes;
for children ≥12 years, midazolam nasal spray 5 mg (one
spray) into one nostril, may repeat in 10 minutes.

• Intranasal diazepam – Intranasal diazepam dosing is

fixed and varies by age and weight; for children age 6 to
11 years, the dose is 0.3 mg/kg ( table 10); for children
age 12 or older, the dose is 0.2 mg/kg ( table 11).
• Rectal diazepam – Rectal diazepam 0.5 mg/kg, maximum

20 mg.
• Intramuscular midazolam – IM midazolam 0.2 mg/kg

once, maximum 10 mg; alternative fixed dosing is 5 mg
for patients 13 to 40 kg, or 10 mg for patients >40 kg.
• Buccal midazolam – Buccal midazolam 0.3 to 0.5 mg/kg

once, maximum 10 mg.
Among these alternatives, IM midazolam is rapidly effective.

Buccal or intranasal midazolam may be more effective than
rectal diazepam but may raise the risk of aspiration [14]. (See
"Seizures and epilepsy in children: Refractory seizures",
section on 'Home rescue therapy (transmucosal antiseizure
medications)'.)
Benzodiazepine efficacy and

pharmacokinetics — Benzodiazepines are the first-line treatment
for SE because they can rapidly control seizures [4,8]. The three
most commonly used benzodiazepines to treat SE are lorazepam,
diazepam, and midazolam; for first-line IV therapy, lorazepam or
diazepam are the preferred agents. Lorazepam has a longer
duration of action, which may provide continued seizure control

until a loading dose of a second agent can be completed. For that
reason, lorazepam is preferred by most pediatric experts for in-
hospital treatment of SE.
The efficacy of lorazepam and diazepam was demonstrated in a

multicenter trial in which 273 children (aged 3 months to 18 years)
with convulsive SE were randomly assigned to receive lorazepam
(0.1 mg/kg IV) or diazepam (0.2 mg/kg IV) upon presentation to
the emergency department [15]. Half of the initial dose was
repeated at 5 minutes if necessary, and fosphenytoin was
administered if seizures continued at 12 minutes. The primary
outcome measure was cessation of SE by 10 minutes without
recurrence in 30 minutes. SE was successfully terminated in 73
percent of those treated with lorazepam and 72 percent of those
treated with diazepam (95% CI -11.4 to 9.8 percent). There was no
difference in the rate of assisted ventilation for patients treated
with lorazepam versus diazepam (17.6 versus 16 percent; 95% CI
-9.9 to 6.8 percent). Patients treated with lorazepam were more
likely to be sedated (67 versus 50 percent) and had a longer time
to return of baseline mental status.
These results contrast with prior observational studies and one

small randomized trial in children, which suggested that
lorazepam was more effective than diazepam in the treatment of
SE and caused less respiratory depression [19-21]. Randomized
trials in adults with convulsive SE have found a trend toward
improved efficacy of lorazepam over diazepam and similar safety

profiles [22-24].
Additional pharmacokinetic and dosing considerations

include the following:
● Lorazepam – The time from injection to lorazepam's

maximum effect can be as long as two minutes. The effective
duration of action, as long as four to six hours, is longer than
diazepam because of its less pronounced redistribution into
adipose tissue. The half-life of lorazepam (which is much
longer than the period of seizure suppression) is significantly
prolonged in newborns (approximately 40 hours) compared
with older children or adults (10 and 13 hours, respectively)
[25-27].
As with diazepam, rectal administration of lorazepam can be

effective when IV access cannot be achieved. An intranasal
formulation of lorazepam is another probably effective
treatment option [28].
● Diazepam – Diazepam has high lipid solubility, rapidly

crosses the blood-brain barrier, and is highly effective in
terminating seizures. An effect upon seizure activity can be
seen as early as 10 to 20 seconds after administration;
cerebrospinal fluid (CSF) concentrations reach one-half of
their maximum value in three minutes. However, because of
subsequent redistribution of the drug into adipose tissue,
the duration of diazepam's acute anticonvulsant effect is

typically <20 minutes.
Diazepam has been the drug of first choice in many settings,

especially outside the emergency department, because it is
stable in liquid form for long periods at room temperature.
Therefore, diazepam is available in resuscitation kits in
premixed form, whereas lorazepam, midazolam, and
phenytoin are not.
A rectal gel formulation of diazepam (Diastat) provides rapid

delivery when IV access is problematic. Some families and
caregivers will have this at home and may have already
administered to the child prior to evaluation in the
emergency department. A nasal spray formulation of
diazepam is also available; it is approved by the US Food and
Drug Administration (FDA) for the acute treatment of
intermittent, stereotypic episodes of frequent seizure activity
(ie, seizure clusters, acute repetitive seizures) in patients age
six years and older [29].
● Midazolam – Midazolam is also very effective in acutely

terminating seizures, frequently in less than one minute, but
it has a short half-life in the central nervous system. In
addition to IV administration, it can be given by the IM,
intranasal, oral, buccal, or rectal routes [4,30,31]. Thus, it is a
useful agent when intravenous access cannot be established

[18]. (See "Seizures and epilepsy in children: Refractory

seizures", section on 'Buccal therapy'.)
In a clinical trial of 893 patients (including 120 children

younger than 18 years) treated in the prehospital setting, IM
midazolam was shown to be at least as effective as IV
lorazepam in terminating SE [32,33]. Overall, seizure
remission upon arrival to the emergency department was
more likely in patients treated with IM midazolam compared
with IV lorazepam (73 versus 63 percent) [32]. In a secondary
analysis limited to patients <18 years of age, seizure
remission rates were similar for midazolam versus
lorazepam (68 versus 72 percent) [33]. The dose of
midazolam was 5 mg for children whose weight was 13 to 40
kg and 10 mg in those over 40 kg. While lorazepam
treatment was associated with a shorter median time from
active treatment to cessation of convulsions (1.6 versus 3.3
minutes) among responders, this was offset in the
prehospital setting by a longer median time to active
treatment administration in the lorazepam group (4.8 versus
1.2 minutes) because of the need to place an IV catheter. The
need for endotracheal intubation, recurrence of seizures, and
other adverse event rates were similar in the two treatment
groups. (See 'Prehospital treatment' above.)
Buccal administration of midazolam was found in one study

of 177 children to be more effective than rectal diazepam in
terminating seizures [30]. Fewer children required further

antiseizure medication treatment in the midazolam
compared with the diazepam-treated group. (See "Seizures
and epilepsy in children: Refractory seizures", section on
'Home rescue therapy (transmucosal antiseizure
medications)'.)
Nasal midazolam is approved by the FDA for the acute

treatment of intermittent, stereotypic episodes of frequent
seizure activity (ie, seizure clusters, acute repetitive seizures)
in patients age 12 years and older [34].
Midazolam can be given as a continuous infusion for

refractory SE, but this mode of administration is not
recommended as a first-line treatment for SE. (See
'Midazolam' below.)
● Clonazepam – Clonazepam has been used to treat SE

outside the United States in settings where intravenous
formulations are available. It has effects similar to those of
other benzodiazepines, with a rapidity of onset that is
intermediate between that of lorazepam and diazepam and a
more prolonged duration of action than diazepam.
Second therapy: Antiseizure medications — If seizures continue

for 10 minutes after at least two injections of lorazepam or
diazepam, a second therapy with a long-acting antiseizure
medication is indicated. Levetiracetam, phenytoin/fosphenytoin,
and valproate are reasonable choices in this setting [9]. The onset
of action is delayed with these drugs. Therefore, it may be helpful
to give an additional dose of a benzodiazepine as the antiseizure
medication is being administered. (See 'In-hospital treatment'
above.)
In patients with ongoing SE lasting longer than 30 minutes despite

two initial doses of benzodiazepine and a second therapy
antiseizure medication, preparation for a continuous infusion of
midazolam, propofol, or pentobarbital should occur
simultaneously with administration of a different second therapy
antiseizure medication. At this stage, the patient will require
endotracheal intubation, mechanical ventilation, transfer to a
pediatric intensive care unit, and, if not already obtained,
emergency neurologic consultation. (See 'Refractory status
epilepticus' below.)
Choosing an agent — For children with SE that continues for 10

minutes after at least two doses of a benzodiazepine, we suggest
treatment with levetiracetam rather than another antiseizure
medication.
● When IV or IO access is available – We begin treatment

with levetiracetam 60 mg/kg IV/IO (maximum single dose
4500 mg), which we prefer over phenytoin because of ease of
use, more rapid administration, and equivalent efficacy. (See
'Antiseizure medication efficacy' below.)

Alternatively, fosphenytoin can be given at a dose of 20 mg

phenytoin equivalents (PE)/kg IV or IO and a rate of 2 mg
PE/kg per minute (maximum rate 150 mg PE/min)
( table 9). Although high-quality evidence is lacking, some
UpToDate experts give fosphenytoin at a higher initial dose
of 30 mg PE/kg IV, which in their experience is associated
with excellent seizure control and tolerability. If seizures
persist, an additional 5 to 10 mg PE/kg IV of fosphenytoin
can be given 10 minutes after the loading dose. The
maximum suggested single dose in children is 1500 mg.
Phenytoin and fosphenytoin may be less effective for the

treatment of seizures due to toxins or drugs (eg, children
with seizures caused by lidocaine, cocaine, amphetamines,
lindane, or theophylline); in such cases, an alternative such
as levetiracetam, phenobarbital, or valproate should be used.
Valproate or phenobarbital IV/IO may also be used as initial

therapy in children who did not respond to levetiracetam or
fosphenytoin in previous episodes of SE or in children with a
hypersensitivity to phenytoin. The clinician should anticipate
respiratory depression and apnea when phenobarbital is
given with benzodiazepines.
In addition, valproate may also be used as the initial

treatment in children on chronic valproate therapy who are

known to have had recent nonadherence and in whom

valproate levels are suspected to be low.
● When IV and IO access are not available – When either IV

or IO access is delayed or unavailable, fosphenytoin can be
given by intramuscular injection.
Factors influencing choice of agent — Knowledge of the

patient's previous response to antiseizure medications and current
medication use may guide the approach to management. In
deciding initial antiseizure therapy for SE, the following issues
should be considered:
● Previous response – If the child has a history of previous SE,

knowing which antiseizure medication was effective in
arresting the seizures is helpful. If the child did not respond
to phenytoin or fosphenytoin, for example, another drug,
such as phenobarbital or valproate, would be preferable.
● Trauma – In the setting of trauma, levetiracetam is generally

the preferred antiseizure medication for treating SE, and
fosphenytoin is also a reasonable choice. Concerns about
adverse effects of phenobarbital (sedation) and valproate
(thrombocytopenia and other coagulation disturbances)
make them less useful in for patients with trauma.
● Antiseizure medication adherence – If the child is on long-

term antiseizure medication therapy, it should be
determined whether the medication has been recently

missed or if prescriptions have not been refilled. Serum
antiseizure medication levels obtained upon admission may
not be available for many hours, and initial treatment
decisions may be made without them. If, for example,
valproate has provided good seizure control and the child is
known to have missed one or more doses, intravenous
valproate, rather than phenytoin, should be considered as
initial treatment.
Low antiseizure medication levels may contribute to SE in up

to one-third of patients [3]. In one series of 51 children with
SE, at least one or all antiseizure medication levels were
therapeutic in 82 and 66 percent, respectively [35]. In
addition to nonadherence, there are a number of other
clinical scenarios that may lead to an unexpectedly low
serum level of an antiseizure medication. These include
medical conditions such as vomiting or malabsorption and
administration of concomitant medications that may
increase clearance of a particular antiseizure medication.
● Paradoxical effects of antiseizure medications – Elevated

levels of certain antiseizure medications, including
phenytoin, carbamazepine, gabapentin, tiagabine, and
vigabatrin, can paradoxically trigger generalized convulsive
SE, particularly the myoclonic type, as well as nonconvulsive
(absence) SE. The underlying mechanisms are poorly
understood [36]. When suspected, paradoxical seizures

caused by phenytoin or carbamazepine should be managed
with benzodiazepines and phenobarbital. (See
"Carbamazepine poisoning" and "Phenytoin poisoning".)
Even benzodiazepines can rarely worsen seizures and

precipitate tonic SE, particularly in children with Lennox-
Gastaut syndrome [37], although this should not alter the
standard initial approach to therapy.
Some antiseizure medications commonly used to treat SE

may worsen seizures caused by illicit drugs. As an example,
phenytoin could worsen the toxicity of lidocaine or cocaine,
because both block sodium channels [38].
Selected antiseizure medications may also precipitate or

worsen other types of seizures [36]:
• Carbamazepine, phenytoin, and lamotrigine may worsen

myoclonic seizures.
• At high serum levels, carbamazepine and phenytoin may

worsen focal seizures with impairment of consciousness
(previously called complex partial seizures) and increase
generalized tonic-clonic seizures.
• Carbamazepine is known to precipitate drop attacks,

often with atypical absence seizures.

• Carbamazepine and lamotrigine may worsen seizures in

patients with Dravet syndrome. (See "Dravet syndrome:
Management and prognosis".)
● Change in antiseizure medications – Seizures may be

worsened or precipitated even when antiseizure medication
blood levels are in the therapeutic range [39]. If a new
antiseizure medication has been added or the dose has been
increased in the previous months, the drug may be causing
seizures and should not be used in an attempt to control SE.
● Nonprescription and illicit drugs – Nonprescription

medications, including over-the-counter drugs such as
antihistamines or other agents with anticholinergic effects,
illicit substances, and, rarely, herbal preparations, can
precipitate seizures. Specific questioning may uncover the
use of these substances, especially illicit drug use. Since this
information is typically unavailable early in the course of
managing SE, we obtain a urine drug screen as part of the
initial evaluation in at-risk patients (eg, adolescents and older
school children, and younger children if there is suspicion for
illicit drug exposure). (See 'Initial studies' above.)
Antiseizure medication efficacy — Mounting evidence from

randomized controlled trials and observational studies suggests
that levetiracetam, fosphenytoin/phenytoin, and valproate have
similar efficacy for convulsive SE in children [40,41]. Phenytoin and

fosphenytoin may be less effective for the treatment of seizures

due to toxins or drugs and may intensify seizures caused by
cocaine, other local anesthetics, theophylline, or lindane [42-44].
In such cases, levetiracetam, valproate, or phenobarbital should
be used.
● Comparative efficacy – Among the antiseizure medications

that can be loaded intravenously, the Established Status
Epilepticus Treatment Trial (ESETT) found that fosphenytoin,
valproate, and levetiracetam are equally effective and have
similar rates of adverse effects [45]. The trial enrolled 384
children (aged 2 to 17 years) and adults with convulsive SE
refractory to benzodiazepines. The patients were randomly
assigned to receive levetiracetam (n = 145), fosphenytoin (n =
118), or valproate (n = 121). The trial was stopped early when
an interim analysis met criteria for futility. The composite
outcome (cessation of SE and improvement in the level of
consciousness at 60 minutes) was achieved in 47 percent
(95% CI 39-55) of the levetiracetam group, 45 percent (95% CI
36-54) of the fosphenytoin group, and 46 percent of patients
(95% CI 38-55) in the valproate group. Although not
statistically significant, there were more episodes of
hypotension and intubation in the fosphenytoin group and
more deaths in the levetiracetam group compared with the
other groups. Limitations to the ESETT include a substantial
rate (approximately 50 percent) of unblinding of

investigators and clinicians to permit choosing a second

antiseizure medication for ongoing seizures, inadvertent
enrollment of patients without SE, including patients with
psychogenic nonepileptic seizures (approximately 10 percent
of the study population), and absence of confirmatory
electroencephalography.
In an extension of ESETT, which enrolled an additional 78

children with SE, there was no difference in the efficacy of
levetiracetam, fosphenytoin, or valproate by age group
comparing children, younger adults (ages 18 to 65 years),
and older adults (age >65 years) [40].
Data from two open-label trials suggest that levetiracetam is

equivalent but not superior to phenytoin for the treatment of
convulsive SE. The ConSEPT trial randomly assigned 233
children (aged 3 months to 16 years) presenting to
emergency departments with convulsive SE who failed initial
benzodiazepine treatment to phenytoin 20 mg/kg infusion
(IV or IO) over 20 minutes or levetiracetam 40 mg/kg infusion
(IV or IO) over 5 minutes [46]. At five minutes after the end of
infusion, the proportion of patients with clinical cessation of
seizure activity in the phenytoin and levetiracetam groups
was similar (60 versus 50 percent, respectively; risk
difference -9.2 percent, 95% CI -21.9 to 3.5), and there was no
difference between groups in any of the other primary or
secondary outcomes. Similarly, the EcLiPSE trial evaluated
286 children (aged 6 months to 18 years) with convulsive SE

requiring second-therapy treatment who were randomly
assigned to levetiracetam 40 mg/kg IV over 5 minutes or
phenytoin 20 mg/kg IV over at least 20 minutes [47]. There
was no significant difference between groups in any of the
prespecified outcomes. The proportion of patients with
cessation of convulsive SE was similar for the levetiracetam
and phenytoin groups (70 and 64 percent), as was the
primary outcome of median time to cessation of SE with
levetiracetam and phenytoin (35 and 45 minutes, hazard
ratio 1.20, 95% CI 0.91-1.60). In both trials, levetiracetam and
phenytoin had similar safety profiles [46,47].
In one of the larger retrospective series, 78 children (median

age 31 months) with SE refractory to initial benzodiazepines
and two second-therapy antiseizure medications (phenytoin
and phenobarbital) were treated with either levetiracetam
(20 mg/kg IV at 5 mg/kg per minute, maximum 3 grams) or
valproate (20 mg/kg IV), prior to continuous infusional
therapy [48]. The rate of seizure control was similar for
levetiracetam and valproate (78 versus 63 percent, p = 0.12).
An adjusted analysis was not presented. No specific adverse
effects were ascribed to levetiracetam; valproate caused
reversible liver enzyme elevation in four patients (13
percent).

● Levetiracetam – The ConSEPT and EcLiPSE trials both used

levetiracetam 40 mg/kg dosing for convulsive SE [46,47],
while most earlier and smaller reports used a dose of 20 to
30 mg/kg [48-52]; single doses of up to 60 mg/kg had been
endorsed by at least two guideline panels [8,9].
Levetiracetam is available in intravenous as well as oral
formulations.
● Fosphenytoin and phenytoin – Phenytoin is a long-acting

drug that has been widely used to treat acute and chronic
seizures in children [4]. Its principal advantage is in
preventing recurrence of SE for extended periods of time.
• Fosphenytoin – Fosphenytoin is a pro-drug of phenytoin

that is preferred over phenytoin in the treatment of SE
because it has a better safety profile and can be infused
more rapidly than phenytoin. Fosphenytoin is highly
water soluble at neutral pH and therefore unlikely to
precipitate during intravenous administration. Compared
with phenytoin, the drug has fewer side effects, including
a reduced risk of local irritation at the site of infusion;
therefore, fosphenytoin can be infused much more
rapidly. Hypotension and cardiac arrhythmias remain a
risk, so cardiac monitoring is still required.
Little information is available on the pharmacokinetics of

fosphenytoin in infants and children. Subtherapeutic free

phenytoin levels may occur rarely in children after

fosphenytoin infusion [53].
Since fosphenytoin is converted on a 1:1 molar basis to

phenytoin, the dosing of fosphenytoin in terms of moles
is identical. However, the molecular weight of
fosphenytoin is greater than that of phenytoin; hence, a
greater weight of fosphenytoin must be given in order to
yield the same concentration of phenytoin. To eliminate
potential confusion, fosphenytoin is prescribed as
milligrams of phenytoin equivalent (PE); as an example,
20 mg PE/kg load, at a rate of 2 mg PE/kg per minute.
• Phenytoin – If fosphenytoin is unavailable, phenytoin can

be given in an initial dose of 20 mg/kg IV at a rate of 1
mg/kg per minute (maximum rate 50 mg/min). Phenytoin
is not water soluble; in order to have a liquid preparation,
it is dissolved in propylene glycol at a very high pH. This
contributes in large part to the phenytoin's side effects of
hypotension and cardiac arrhythmias. Thus, heart rate
and blood pressure should be monitored during the initial
infusion. However, these complications are less common
in children than adults and can be minimized by an
infusion rate that does not exceed 1 mg/kg per minute
(maximum 50 mg per minute) [4]. Phenytoin must not be
infused along with a dextrose containing IV fluid, as it
may form a precipitate.
The risks of local pain and injury, including venous

thrombosis and the purple glove syndrome, also increase
with more rapid rates of infusion. The purple glove
syndrome is characterized by edema, discoloration, and
pain in the extremity distal to the site of phenytoin
infusion. Severe cases can lead to skin necrosis and limb
ischemia, sometimes requiring amputation. More
common in older adults, a few cases have been reported
in children, usually late in the first decade, and
adolescents. Venous extravasation must be avoided
because the high pH and osmolality of this drug cause
tissue inflammation and necrosis.
● Valproate – Valproate can be used if seizures continue for 10

minutes after at least two doses of a benzodiazepine.
Valproate is given in a loading dose of 20 to 40 mg/kg IV
(diluted 1:1 with normal saline or 5 percent dextrose in
water) over 5 to 10 minutes (maximum 3000 mg per dose)
and may be repeated after 10 to 15 minutes [54].
Valproate usually is well tolerated, even in clinically unstable

patients, and is less sedating than barbiturates [4,55]. Severe
hypotension was reported in an 11-year-old girl following
intravenous administration [56].
● Phenobarbital – Phenobarbital slowly infused IV (maximum

infusion rate 2 mg/kg per minute with a ceiling of 50

mg/min) in an initial dose of 20 mg/kg, and followed by

repeated increments of approximately 8 to 10 mg/kg every
30 minutes, can achieve high levels and seizure control,
usually without significant hypotension or respiratory
depression.
Phenobarbital is a long-acting antiseizure medication that

has been used for many years to treat seizures. Side effects
of IV administration include sedation and respiratory
depression, especially when it is preceded by a
benzodiazepine. As a result, phenobarbital is considered a
second-line long-acting agent after levetiracetam,
fosphenytoin or phenytoin, and valproate, and usually is
used only when these agents are not effective. Respiratory
and cardiac monitoring should be performed because
endotracheal intubation and mechanical ventilation may be
needed. The risk of prolonged sedation with phenobarbital is
greater than with the other anticonvulsants because its half-
life is 87 to 100 hours, and often longer in newborns [57].
REFRACTORY STATUS EPILEPTICUS
Medications for refractory status epilepticus — If convulsive SE

persists for 30 minutes after initial measures are instituted
(immediate benzodiazepine treatment followed by second therapy
with an antiseizure medication), further pharmacologic therapy
(third therapy) is required ( algorithm 1), usually with continuous

infusion of midazolam (preferred) or pentobarbital [58].
Among these, midazolam is the most frequent first-choice

sedative-anesthetic agent, followed by pentobarbital. Although
propofol has been used to treat SE, data are limited, and
significant associated complications have been reported. Propofol
should not be used in children on the ketogenic diet; a report of a
fatality in a 10-year-old boy illustrates the incompatibility of these
treatments, which both involve fatty acid metabolism [59].
The patient's hemodynamic status will bear on the choice, because

pentobarbital and propofol may exacerbate cardiovascular
complications including hypotension. Dosing of these agents and
important contraindications are discussed below. (See 'Specific
agents' below.)
At this stage, the patient will require endotracheal intubation,

mechanical ventilation, emergency neurologic consultation if not
already obtained, and transfer to a pediatric intensive care unit
with continuous EEG capability. The clinician should also anticipate
the need to treat iatrogenic hypotension. Rapid infusion of
isotonic crystalloid (eg, 20 mL/kg of normal saline or Ringer
lactate) followed by a continuous infusion of a vasopressor such as
epinephrine or norepinephrine are frequently necessary to
maintain adequate tissue perfusion and blood pressure.

Continuous EEG monitoring — Continuous EEG (cEEG)

monitoring is critical during the treatment of refractory SE. The
longer convulsive SE continues, the less convulsive it appears
clinically, and continuous electroencephalogram (cEEG)
monitoring should be instituted. Once infusion of midazolam or
pentobarbital has begun, cEEG monitoring is necessary to confirm
that seizures have been treated adequately; to guide use of
antiseizure medications and assess the level of suppression
achieved; and to monitor for relapse of seizures and SE, especially
when infusions are tapered.
Goals of therapy — The primary goal of therapy is to stop both

clinical and electrographic seizures. There is no conclusive
evidence that a burst-suppression EEG pattern is necessary, and
more suppression equates to more sedation and a longer
intensive care unit course of treatment. The cEEG must be
followed closely, as recurrent seizures often appear on the EEG
before they are evident clinically. However, the optimal
electroclinical endpoint of treatment has not been studied
rigorously.
Specific agents
Midazolam — Midazolam can be given as a continuous

intravenous (IV) infusion for refractory SE and is usually associated
with minimal cardiovascular side effects [60-64]. Midazolam is
given as an initial bolus infusion of 0.2 mg/kg IV followed by a

continuous infusion of 0.05 to 2 mg/kg per hour; for breakthrough

seizures, additional 0.1 to 0.2 mg/kg boluses can be given and the
continuous infusion rate increased by 0.05 to 0.1 mg/kg per hour
every three to four hours [8].
Hypotension may be less common than with pentobarbital but

commonly occurs at higher doses of midazolam. The short half-life
of midazolam (one to four hours) can increase markedly after days
of use. Tachyphylaxis is common, and the anticonvulsant effects of
midazolam can cease rapidly when it is stopped. Withdrawal
seizures and recurrent SE are therefore an important concern.
In a prospective multicenter study of 54 children with refractory SE

who underwent continuous infusion of an anesthetic drug, 78
percent received midazolam as the first-choice agent [58].
Pentobarbital was the most commonly used therapy after
midazolam failure (82 percent). Seizure termination was achieved
in 30 out of 42 patients (71 percent) who received first-line
midazolam, and an additional eight patients achieved seizure
termination with one more drug (mostly pentobarbital). The
median length of intensive care unit stay was 10 days in the entire
cohort, and 28 percent of patients required vasopressor support.
Pentobarbital — Pentobarbital is given as an initial bolus

infusion of 5 to 15 mg/kg IV followed by a continuous infusion of
0.5 to 5 mg/kg per hour [4].

Significant side effects include respiratory depression,

hypotension, myocardial depression, and reduced cardiac output.
Thus, intubation and mechanical ventilation with intravascular
pressure monitoring are required prior to treatment, and inotropic
agents frequently are needed. Other important potential
complications include pulmonary edema, ileus, and prolonged
sedation.
Propofol — Propofol is rarely used for the treatment of SE in

children because doses and duration of therapy necessary to
control refractory seizures are associated with life-threatening
propofol infusion syndrome characterized by one or more of
severe metabolic acidosis, rhabdomyolysis, and ECG changes, with
or without cardiovascular collapse, hyperlipidemia, renal failure,
elevated liver enzymes, or elevated lactate [65-67]. Risk factors for
the propofol infusion syndrome include high infusion doses (>67
mcg/kg per minute or >4 mg/kg per hour), prolonged
administration (>48 hours), and administration to children on the
ketogenic diet [59]. Others have found that propofol may be used
without severe adverse effects if the dose is not titrated above 5
mg/kg per hour and with continuous monitoring and stopping the
infusion if side effects appear [68]. However, these doses may be
insufficient to control refractory SE.
Other therapies — In addition to levetiracetam, observational

data suggest that other antiseizure medications, including
lacosamide, and topiramate, may play a role in the management
of SE, particularly in the refractory setting. Other emerging

therapies include ketamine [69] and the ketogenic diet [70-72].
(See "Ketogenic dietary therapies for the treatment of epilepsy",
section on 'Super-refractory status epilepticus'.)
● Lacosamide – Lacosamide is also available in both oral and

intravenous formulations, and there are an increasing
number of case reports and case series describing its utility
in adults with refractory SE [73-75]. The bolus dose most
often used in adults is 200 to 400 mg IV infused over three to
five minutes [73]. Published data in children are limited [76-
79]. One small, retrospective case series suggests that
infusions of 50 mg or 100 mg in children and young adults
can be effective in cases of refractory tonic SE [77]. Another
cases series of nine patients treated with a mean initial
loading dose of 8.7 mg/kg reported no serious adverse
effects and one episode of bradycardia [78].
● Topiramate – Topiramate has a broad spectrum of efficacy

against many seizure types. Case reports and small case
series report that it may be efficacious in refractory SE [80-
82]. Some have used low initial doses [80,81], others a higher
loading dose [82]. There is no formulation for parenteral
administration. Further prospective study is needed to define
the role of topiramate in SE.

Duration of continuous infusions — Continuous infusions of

sedative-anesthetic agents for refractory SE require management
by pediatric neurology and critical care specialists in a pediatric
intensive care unit.
Therapy with midazolam (preferred) or pentobarbital is titrated to

induce cessation of clinical and electrographic seizures, as
confirmed by cEEG monitoring. The dose is then slowly reduced
while monitoring to ensure that seizures do not reappear. If
seizures recur, the dose is increased to achieve seizure
suppression again for a period of time, followed by attempts to
reduce the infusion while maintaining control of seizures.
POSTICTAL RECOVERY AND FURTHER EVALUATION
Pace of recovery — Most children begin to recover

responsiveness within 20 to 30 minutes after generalized
convulsions, although there is a broad range of duration. Close
monitoring during the immediate postictal phase is critical,
particularly for respiratory status. This is a vulnerable time, as
some patients may not be able to maintain their airway without
basic airway maneuvers such as a jaw thrust or chin lift or
insertion of airway adjuncts such as a nasopharyngeal or oral
airway; monitoring the end-tidal CO2 can help assess adequacy of
ventilation. (See "Basic airway management in children".)

The two most common reasons for delayed postictal recovery are
sedation from medications and ongoing nonconvulsive seizures
[83], and these two causes can be impossible to distinguish
clinically. Note that benzodiazepine reversal with flumazenil is
contraindicated in this setting, as reversal can precipitate seizures.
All children who do not return to a normal level of consciousness

within a few hours after initial treatment of SE should therefore
undergo an emergency EEG; continuous EEG monitoring and
escalation of treatment is indicated if the routine EEG shows
nonconvulsive SE. (See 'Electroencephalography' below and
"Nonconvulsive status epilepticus: Classification, clinical features,
and diagnosis" and "Nonconvulsive status epilepticus: Treatment
and prognosis".)
History and physical examination — During the postictal

recovery period. it is important to perform a detailed history,
physical examination, and a full neurologic examination that looks
for asymmetric or focal findings or signs of increased intracranial
pressure that may suggest clues to the underlying etiology.
The causes of SE and the evaluation and diagnosis of seizures in

children are discussed in detail separately. (See "Clinical features
and complications of status epilepticus in children", section on
'Causes' and "Seizures and epilepsy in children: Clinical and
laboratory diagnosis".)

Electroencephalography — For patients with SE as the first

presentation of seizures or epilepsy, an EEG should be done to
evaluate background activity as soon as possible after the seizure
stops, ideally within one to two hours. An EEG may not be
necessary for patients with known epilepsy who are recovering
normally from SE if the clinicians are confident the clinical seizures
have stopped and there is no other independent reason that the
child would benefit from ongoing EEG monitoring. Useful clues to
the cessation of a clinical seizure are eye closure and resumption
of a normal breathing pattern. An EEG may be useful if the eyes
remain open or there is any lingering doubt as to the continuation
of subclinical seizures.
EEG monitoring may be useful if the patient does not return to

normal mentation in an appropriate time after cessation of SE. The
clinician may also elect to perform cEEG in patients with acute
symptomatic causes where the etiology could potentially cause
further neurologic injury (eg, meningitis, trauma, etc.).
The EEG background usually remains abnormally slow for hours or

even days after generalized convulsive or prolonged partial SE, but
it is normal in psychogenic nonepileptic seizures unless large
doses of sedating antiseizure medications have been given. If the
patient has not regained a relatively normal mental state within a
few hours after SE has stopped, an EEG should be performed to
evaluate the possibility of subclinical electrographic seizures [84].

Studies of critically ill children who undergo continuous EEG

monitoring indicate that electrographic seizures are present in
approximately 30 to 40 percent of recordings, often without
clinical accompaniment [85-87]. Similar findings have been
reported in critically ill adults. The benefit of continuous EEG
monitoring in unselected patients is unclear. However, the
possibility of nonconvulsive seizures should be considered in such
patients when the degree of coma is not adequately explained by
their underlying condition.
Neuroimaging — A neuroimaging study is essential when SE is

the first presentation of epilepsy as well as in children whose
recovery from SE does not follow the expected course [88,89].
Computed tomography may be performed in the emergency
department setting, but magnetic resonance imaging has superior
yield for determining the underlying etiology. (See "Clinical
features and complications of status epilepticus in children",
section on 'Causes'.)
Additional studies — Additional laboratory studies may be

warranted for selected patients with SE based upon the most likely
etiology as discussed separately:
● Septic shock. (See "Systemic inflammatory response

syndrome (SIRS) and sepsis in children: Definitions,
epidemiology, clinical manifestations, and diagnosis", section
on 'Laboratory studies'.)

● Meningitis or encephalitis. (See "Bacterial meningitis in

children older than one month: Clinical features and
diagnosis", section on 'Evaluation' and "Viral meningitis in
children: Clinical features and diagnosis", section on
'Evaluation'.)
● Metabolic studies for inborn errors of metabolism in infants

younger than six months of age or children with other
suggestive indicators. (See "Seizures and epilepsy in children:
Clinical and laboratory diagnosis", section on 'Laboratory and
genetic testing in undiagnosed epilepsy'.)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from

selected countries and regions around the world are provided
separately. (See "Society guideline links: Seizures and epilepsy in
children".)
SUMMARY AND RECOMMENDATIONS
● Clinical presentation – Convulsive status epilepticus (SE) is a

clinical diagnosis, confirmed in most cases by the presence of
sustained and rhythmic generalized tonic and clonic motor
activity lasting for longer than five minutes or repetitive
convulsive seizures without a return to baseline
consciousness between seizures. Although the diagnosis of

convulsive SE is usually obvious, a detailed neurologic
examination is important in making the diagnosis of more
subtle or focal forms of SE. (See 'Definition and differential
diagnosis' above and 'Urgent focused evaluation' above.)
● Supportive care – The initial assessment, stabilization, and

treatment of a child presenting with SE should proceed in
quick succession and include the following ( algorithm 1):
• A brief physical examination to assess respiratory and

circulatory status, with immediate interventions as
necessary, and a rapid neurologic examination to confirm
the presence of SE. (See 'Rapid recognition of status
epilepticus' above and 'Immediate supportive care'
above.)
• Maintenance of an adequate airway, breathing, and

circulation, along with continuous pulse oximetry and
cardiac monitoring performed simultaneously with
initiation of emergency antiseizure treatment. (See
'Immediate supportive care' above.)
• Laboratory studies ( table 12) including (see 'Initial

studies' above):
- Plasma glucose and a rapid "finger-stick" or point-of-

care glucose
- Serum electrolytes and calcium

- Serum antiseizure medication levels, if applicable
- If substance use or poisoning is suspected, urine and
blood toxicology
- In postmenarchal females, qualitative pregnancy test
(urine or blood)
• Clinically obvious SE should be treated immediately,

without waiting for an EEG. When there is uncertainty
regarding the presence of SE, an urgent EEG should be
obtained. In the emergency department, this can be a
limited study. (See 'Approach' above and
'Electroencephalography' above.)
● Management – The management of convulsive SE in

children is summarized in the algorithm ( algorithm 1).
• First therapy – For children presenting with convulsive

SE, we recommend immediate treatment with a
benzodiazepine (Grade 1B). For children with intravenous
(IV) access, the preferred benzodiazepines are either
lorazepam 0.1 mg/kg IV (maximum 4 mg per dose) or
diazepam 0.2 mg/kg IV (maximum 10 mg per dose),
administered by slow IV push over one minute. The dose
can be repeated in 5 to 10 minutes if seizures persist. (See
'First therapy: Benzodiazepines' above and
'Benzodiazepine efficacy and pharmacokinetics' above.)

In the prehospital setting, or if IV access is delayed or

impossible, an alternative to IV lorazepam or IV diazepam
for initial therapy is intramuscular (IM) midazolam at a
dose of 0.1 to 0.2 mg/kg up to a maximum of 10 mg.
Other options if IV access cannot be established are
intranasal midazolam, intranasal diazepam, rectal
diazepam (0.5 mg/kg, maximum 20 mg), and buccal
midazolam (0.2 mg/kg, maximum 10 mg). (See
'Prehospital treatment' above and 'In-hospital treatment'
above.)
• Second therapy – For children with SE that continues for

10 minutes after at least two doses of a benzodiazepine,
additional antiseizure medication is required; for such
patients, we suggest treatment with levetiracetam rather
than another antiseizure medication (Grade 2C).
Levetiracetam is given at a dose of 60 mg/kg IV.
Fosphenytoin is our preferred alternative to levetiracetam
except for toxin-induced seizures. Phenobarbital and
valproate are additional antiseizure medications for
second therapy in this setting. (See 'Second therapy:
Antiseizure medications' above and 'Choosing an agent'
above and 'Antiseizure medication efficacy' above.)
• Refractory status epilepticus – If SE persists for 30

minutes after initial measures are instituted, further
pharmacologic therapy usually consists of continuous
infusion of midazolam (preferred) or, if hemodynamic

status permits, pentobarbital. At this stage, the patient
will require intubation, mechanical ventilation, neurologic
consultation if not already obtained, and transfer to a
pediatric intensive care unit with continuous EEG
capability. (See 'Refractory status epilepticus' above.)
● Postictal recovery – Most children begin to recover

responsiveness within 20 to 30 minutes after generalized
convulsions, although there is a broad range of duration.
Close monitoring during this period is critical. An emergency
EEG should be obtained in all children who do not return to a
relatively normal mental state within a few hours after SE has
stopped to evaluate for the possibility of subclinical seizures.
(See 'Postictal recovery and further evaluation' above.)
During the postictal recovery period, it is important to

perform a detailed history, physical examination, and a full
neurologic examination that looks for asymmetric or focal
findings or signs of increased intracranial pressure that may
suggest clues to the underlying etiology. The causes of SE
and the evaluation and diagnosis of seizures in children are
discussed in detail separately. (See "Clinical features and
complications of status epilepticus in children", section on
'Causes' and "Seizures and epilepsy in children: Clinical and
laboratory diagnosis".)

Use of UpToDate is subject to the Terms of Use.
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events. Epilepsia 2019; 60:2095.
88. Singh RK, Stephens S, Berl MM, et al. Prospective study of

new-onset seizures presenting as status epilepticus in
childhood. Neurology 2010; 74:636.
89. Yoong M, Madari R, Martinos M, et al. The role of magnetic

resonance imaging in the follow-up of children with
convulsive status epilepticus. Dev Med Child Neurol 2012;
54:328.
Topic 6192 Version 59.0

GRAPHICS
Formas de estado epiléptico
Convulsivo
generalizado Focal
Estado epiléptico convulsivo Focal motor SE (incluye epilepsia

generalizado parcial continua)
SE convulsivo
generalizado primario
SE convulsivo
generalizado secundario
(inicio focal)
mioclónico
Tónico (también puede tener un

inicio focal)
Clónico (también puede tener

inicio focal)
Atónico (muy raro para SE en

adultos; también puede tener
un inicio focal)
no convulsivo
Ausencia típica ("clásica") NCSE NCSE de inicio focal con

alteración de la conciencia
Otro NCSE primario
generalizado NCSE de inicio focal con
Ausencia atípica NCSE características no motoras (p. ej.,
Otro NCSE generalizado, con un cognitivas o sensoriales)

inicio focal
SE: estado epiléptico; NCSE: estado epiléptico no convulsivo.
Gráfico 97140 Versión 5.0

Principales características clínicas de las crisis

tónico-clónicas en comparación con el tipo
convulsivo de crisis psicógenas no epilépticas
(CPNE)
Crisis epilépticas
tónico-clónicas SNP convulsivo
generalizadas
Frecuencia Variable PNES poco frecuentes

son inusuales
Duración Usualmente <2 min Breve PNES son

excluyendo la fase inusuales
postictal
Ojos Abierto/medio abierto Normalmente

cerrado
Actividad del Tono generalizado Movimiento

motor seguido de actividad alternante o temblor,
clónica generalizada ocasionalmente
paliza, arqueamiento
de la espalda,
movimiento de la
cabeza de lado a lado;
características tónicas
poco comunes
Vocalización Inicial, inarticulado, Durante y después de

sin rasgos la convulsión,
emocionales transmite angustia
Signos Signos de excitación e Cianosis

autonómicos hiperventilación,
enrojecido, pálido
Fase postictal Somnolencia, A menudo vuelve al

confusión, sueño, estado de alerta
dolor de cabeza rápidamente;
severo angustia
incontinencia de Reportado y Comúnmente

orina observado reportado
Eventos de sueño Comúnmente Comúnmente

informado/observado, reportado/observado,
los eventos pueden pero no verificado
ocurrir solo durante el por EEG; eventos
sueño informados que
ocurren durante el
sueño solo muy
inusuales
Lesión Comúnmente Reportado/observado

reportado/observado con menos frecuencia
quemaduras Térmico Fricción
Lesión en la Mordedura en la Mordedura reportada

lengua/boca lengua lateral o en el en la punta de la
interior de la mejilla, lengua
lesión observada
estereotipia Habitual Común

No todas las características distinguen entre convulsiones tónico-

clónicas y el tipo convulsivo de PNES; ninguna característica
individual es lo suficientemente sensible o específica para usarse
sola.
EEG: electroencefalograma.
Cortesía de Roderick Duncan, MD, PhD, FRCP.

Causas de la hipoglucemia en bebés y niños
MIM Grupo de edad

Trastorno
# típico
mediado por insulina
hiperinsulinismo
Congénito Neonatal, infancia
KATP hyperinsulinism 256450,

601820
GLUD1 hyperinsulinism 606762
GCK hyperinsulinism 602485
Perinatal stress-induced Neonatal

hyperinsulinism
Syndromic
hyperinsulinism
Beckwith-Wiedemann 130650 Neonatal, infancy

syndrome
Kabuki syndrome 147920 Neonatal, infancy
Insulinoma
Associated with MEN1 131100 Adolescence
Factitious hypoglycemia Any age
Congenital disorders of glycosylation
Phosphomannomutase 212065 Infancy, childhood

2 deficiency
Phosphoglucomutase 614921 Any age

1 deficiency
Mannosephosphate 602579 Infancy

isomerase deficiency
Fatty acid oxidation disorders
Medium-chain acyl-CoA 201450 Infancy

dehydrogenase
20+ other disorders All ages
Ketotic hypoglycemia
Disorders of glycogen metabolism
Glycogen storage disease 240600 Early childhood

type 0
Glycogen storage disease 232400 Infancy

type III

type VI

type IX
Hormone deficiencies
Growth hormone Infancy, early

deficiency childhood
Cortisol deficiency Childhood
Ketone utilization defects 245050,

Early childhood
203750,
616095

Idiopathic ketotic Early childhood

hypoglycemia
Disorders of gluconeogenesis
Glycogen storage type I* 232200 Infancy
Fructose-1,6-bisphosphatase 229700 Infancy, early

deficiency childhood
Pyruvate carboxylase 266150 Infancy

deficiency
PEPCK deficiency 261650 Infancy
Galactosemia 230400;
Infancy
others
Hereditary fructose 229600 Infancy, childhood

intolerance
Other causes
Ingestions Early childhood, all

ages
Oral hypoglycemic
Ethanol Adolescence
Salicylates
Beta blockers
Pentamidine
6-mercaptopurine
Ackee/lychee fruit
Liver failure All ages

Sepsis Infancy, childhood
MIM: Mendelian Inheritance in Man database; KATP: ATP-sensitive

potassium channel; GLUD1: glutamate dehydrogenase 1 gene; GCK:
glucokinase gene; MEN1: multiple endocrine neoplasia type 1;
PEPCK: phosphoenolpyruvate carboxykinase.
* Also, disorders of glycogen metabolism.
Graphic 103015 Version 7.0

Causes of hypocalcemia in children
Low PTH (hypoparathyroidism)
Impaired synthesis or secretion of PTH
Genetic
DiGeorge syndrome
Genetic mutations interfering with the production of

PTH (autosomal dominant, autosomal recessive)
HDR syndrome (hypoparathyroidism, deafness, renal

anomaly)
Sanjad-Sakati or Kenny-Caffey syndromes
Mutations of the CaSR and related proteins (autosomal

dominant hypocalcemia)
Mutations interfering with parathyroid gland

development (X-linked)
Mitochondrial disorders (eg, MELAS syndrome, Kearns-

Sayre syndrome, mitochondrial trifunctional protein
deficiency)
Autoimmune
APS1
Other
Parathyroid or thyroid gland surgery

Infiltration of parathyroid gland (eg, iron overload)
High PTH
Deficient calcium intake or intestinal absorption
Deficient vitamin D intake, intestinal absorption and/or dermal

synthesis
Defects in vitamin D metabolism
Hepatic dysfunction
Severe liver disease
Drugs that increase cytochrome P450 activity, which

accelerate catabolism of vitamin D to inactive
metabolites (eg, antiseizure medications, isoniazid, and
rifampin)
Renal dysfunction
Genetic disorders
25-hydroxylase deficiency
1-alpha-hydroxylase deficiency (previously known as

vitamin D-dependent rickets type 1 or pseudovitamin
D-deficient rickets)
Increased catabolism of vitamin D (gain-of-function

variants in the CYP3A4 gene)
Defects in vitamin D action
Hereditary resistance to vitamin D (previously known as

vitamin D-dependent rickets type 2)
End-organ resistance to PTH (pseudohypoparathyroidism)

Type 1 (1a, 1b, and 1c)
Type 2
Miscellaneous
Hungry bone syndrome
Osteopetrosis
Sepsis or acute severe illness
Hyperphosphatemia
Alkalosis
Intravenous products with citrate or lactate
Pancreatitis
Fluoride poisoning
Drugs – Bisphosphonates, denosumab, calcimimetics (cinacalcet),

foscarnet, and some chemotherapeutic drugs
Hypomagnesemia
PTH: parathyroid hormone; HDR: hypoparathyroidism, deafness,

renal anomaly; CaSR: calcium-sensing receptor; MELAS:
mitochondrial encephalomyopathy with lactic acidosis and stroke-
like episodes; APS1: autoimmune polyglandular syndrome type 1.

Approach to treatment of convulsive status epilepticu


This algorithm summarizes our suggested approach to antiseizure treatm

unremitting seizure lasting >5 minutes or frequent clinical seizures withou
with CSE require simultaneous, rapid initiation of monitoring, including fre
recognition and treatment of hypoglycemia and other potential underlying
infection, sepsis, and traumatic brain injury. Refer to UpToDate topics on p
EMS: emergency medical services; IV: intravenous; IO: intraosseous; ICP: in

intensive care unit; RSI: rapid sequence endotracheal intubation; NCSE: no
* Rapid sequence intubation should be performed if airway, ventilation, or
¶ For ancillary studies to obtain in children with status epilepticus, refer to
Δ Common causes of pediatric CSE are listed here. If isoniazid poisoning is

discussion of causes of CSE in children, refer to UpToDate's topic on pediat
◊ Additional evaluation may include neuroimaging if CSE is the first presen

increased ICP, or prolonged duration of depressed consciousness (ie, for >
with CSE, refer to UpToDate topics on pediatric CSE.
§ Refer to text for dosing intranasal midazolam.

¥ Phenytoin and fosphenytoin may be less effective for the treatment of se

theophylline, or lindane. In such cases, levetiracetam, valproate, or pheno
‡ With fosphenytoin administration, the rate of infusion should not exceed

phenytoin may be used (20 mg/kg IV; do not exceed 1 mg/kg per minute; m
† When administering phenobarbital, the maximum infusion rate is 2 mg/k

Rapid overview for diagnosis and treatment of

hypoglycemia in adolescents and children (other
than neonates) in the Emergency Department
Clinical features
Any patient with acute lethargy or coma should have an immediate
measurement of blood glucose to determine if hypoglycemia is a
possible cause
Other findings of hypoglycemia are nonspecific* and vary by age:
Infants Older children and adolescents
Irritability Neurogenic Neuroglycopenic

Lethargy (autonomic) response
Jitteriness response Irritability
Feeding Sweating Confusion
problems Tachycardia Uncharacteristic
Hypothermia Palpitations behavior
Hypotonia Tremor Weakness
Tachypnea Nervousness Lethargy
Cyanosis Hunger Loss of
Apnea Paresthesias consciousness
Seizures Pallor Seizures

Coma
Occasionally,
transient focal
neurologic
deficits
Diagnosis
Obtain rapid bedside point-of-care glucose concentration (and

beta-hydroxybutyrate, if available as a point-of-care
measurement)
Confirm the presence of hypoglycemia with a plasma glucose
measurement (drawn close in time to the point-of-care
sample)
Treat, as outlined below, if the bedside value is low (<70
mg/dL [3.89 mmol/L]) in symptomatic patients
For all infants and young children who are not being treated
for diabetes mellitus or do not have a known cause for
hypoglycemia, obtain a blood sample for additional diagnostic
studies prior to glucose administration, if possible, and collect
the first voided urine after the hypoglycemic event.¶
Treatment
Do not delay treatment if symptomatic hypoglycemia is

suspected. However, every reasonable effort should be made
to obtain a rapid plasma glucose measurement (fingerstick or
point-of-care device) prior to administering glucose.
Give glucose based upon the patient's level of
consciousness and ability to swallow safely (ie, alert
enough to do so and with intact gag reflex) as follows:
Conscious and able to drink and swallow safely:
Administer 0.3 g/kg (10 to 20 g) of a rapidly-

absorbed carbohydrate. May repeat in 10 to 15
minutes.
Options include any one of the following:
Glucose tablets (5 g per tablet)

Glucose gel (15 g per tube)

Sweetened fruit juice: 12 g carbohydrate per 4 oz

(120 mL)
Regular soda (not diet): 18 g carbohydrate per 6
oz (180 mL)
Honey: 17 g carbohydrate per 1 tablespoon (15
mL)
Table sugar (granulated sugar): 12.5 g sugar per 1
tablespoon
Altered mental status, unable to swallow, or does
not respond to oral glucose administration within 15
minutes:
Give an initial IV bolus of glucose of 0.25 to 0.5 g/kg

of dextrose (maximum single dose 25 g).Δ The
volume and concentration of glucose bolus is
infused slowly at 2 to 3 mL per minute and based
upon age:
Infants and children up to 12 years: 2.5 to 5 mL/kg

of 10% dextrose solution (D10W), or 1 to 2 mL/kg
of 25% dextrose (D25W). D10W is typically used in
infants and children <5 years of age. (10%
dextrose is 100 mg/mL; 25% dextrose is 250
mg/mL.)
Adolescents ≥12 years: 1 to 2 mL/kg of D25W
Unable to receive oral glucose and unable to obtain
IV access:
Give glucagon 0.5 mg (for <25 kg body weight) or 1

mg (for ≥25 kg body weight) IM or SQ (maximum
dose 1 mg):◊
Perform blood glucose monitoring every 10 to 15

minutes as the effects of glucagon may be
transient
Establish vascular access as soon as possible; if
unable to achieve access and hypoglycemia
persists or is recurrent, ensure the airway is
protected and, if not, secure it with rapid
sequence intubation. Then place a nasogastric
tube and administer 0.2 to 0.25 g/kg dextrose
using volume and concentration guidance for IV
administration above.
After initial hypoglycemia is reversed, provide additional
glucose and treatment based upon suspected etiology:
For patients with type 1 diabetes mellitus: Give a normal
diet; initiate IV dextrose-containing fluids if intake is
inadequate.
For patients with an underlying hypoglycemic disorder or
with an unknown cause of hypoglycemia: Administer an
intravenous infusion of dextrose 10%:
For infants, start with initial glucose infusion rate (GIR)
of 5 to 6 mg/kg/minute
For older children, start with GIR of 2 to 3
mg/kg/minute
Calculation to convert target GIR to infusion rate:
Rate of dextrose infusion (mL/hr) = GIR
(mg/kg/minute) × 6 × weight (kg) ÷ dextrose
percentage of fluid (eg, 5 for 5% dextrose [D5W] or
10 for D10W)
Titrate infusion to maintain plasma glucose in a safe
and appropriate range (70 to 120 mg/dL [3.89 to 8.33
mmol/L]).
Patients who have ingested a long-acting hypoglycemia
agent such as a sulfonylurea may require prolonged
treatment until the effect wears off. Selected patients may

also warrant treatment with octreotide. (Refer to
UpToDate topic on sulfonylurea poisoning.)
Measure a rapid plasma glucose 15 to 30 minutes after the
initial IV glucose bolus and then monitor every 30 to 60
minutes until stable (minimum of four hours) to ensure that
plasma glucose concentration is maintained in the normal
range (>70 to 100 mg/dL [>3.89 to 5.55 mmol/L])
Obtain pediatric endocrinology consultation for patients with
persistent hypoglycemia and for hypoglycemia of unknown
cause
Obtain medical toxicology consultation for patients with
ingestion of oral hypoglycemic agents by calling a regional
poison control center.§
Admit the following patients:
Cannot maintain normoglycemia with oral intake
Hypoglycemia of unknown cause
Ingestion of long-acting hypoglycemic agents
Recurrent hypoglycemia during the period of observation
IV: intravenous; IM: intramuscular; SQ: subcutaneous; D10W: 10%

dextrose in water; D25W: 25% dextrose in water; D50W: 50%
dextrose in water; GIR: glucose infusion rate.
* These findings may also occur in infants with sepsis, congenital

heart disease, respiratory distress syndrome, intraventricular
hemorrhage, other metabolic disorders, and in children and
adolescents with a variety of underlying conditions.
¶ Specific laboratory studies to obtain in children include blood

samples for glucose, insulin, C-peptide, beta-hydroxybutyrate,
lactate (free flowing blood must be obtained without a tourniquet),

plasma acylcarnitines, free fatty acids, growth hormone, and

cortisol.
Δ Higher doses of glucose (eg, 0.5 to 1 g/kg [5 to 10 mL/kg of 10%

dextrose in water or 2 to 4 mL/kg of 25% dextrose in water]) is
recommended by the Pediatric Advanced Life Support course and
may be needed to correct hypoglycemia caused by excess insulin
administration or sulfonylurea ingestion. (For more detail, refer to
UpToDate topic on sulfonylurea agent poisoning.)
◊ Glucagon will reverse hypoglycemia caused by excess

endogenous or exogenous insulin and will not be effective in
patients with inadequate glycogen stores (prolonged fasting),
ketotic hypoglycemia, or are unable to mobilize glycogen (glycogen
storage diseases). Of note, children may exhaust their glycogen
stores in as little as 12 hours. Other conditions in which glycogen
cannot be effectively mobilized include ethanol intoxication in
children, adrenal insufficiency, and certain inborn errors of
metabolism (eg, a disorder of glycogen synthesis and glycogen
storage diseases).
§ To access a regional poison control center in the United States, call

1-800-222-1222. Contact information for poison centers around the
world is available at the following website:
https://www.liquidglassnanotech.com/poison-emergency-center-
contact-numbers/.

Head-tilt/chin-lift maneuver
To relieve upper airway obstruction, the clinician uses two hands to extend
patient's neck. While one hand applies downward pressure to the patient's
forehead, the tips of the index and middle fingers of the second hand lift t
mandible at the chin, which lifts the tongue from the posterior pharynx. Th
head-tilt/chin-lift maneuver may be used in any patient in whom cervical s
injury is NOT a concern.

Jaw-thrust maneuver
The jaw-thrust maneuver is used to relieve upper airway obstruction

by moving the tongue anteriorly with the mandible, minimizing the
tongue's ability to obstruct the airway. With the patient supine and
the clinician standing at the head of the bed, the technique is
performed by placing the heels of both hands on the parieto-
occipital areas on each side of the patient's head, then grasping the
angles of the mandible with the index and long fingers, and
displacing the jaw anteriorly. The jaw-thrust maneuver may be used
in the patient in whom cervical spine injury is a concern.

Nasopharyngeal airway insertion
The nasopharyngeal airway (NPA) should be coated with water-soluble lub

anesthetic jelly. The device is then inserted along the floor of the naris into
posterior pharynx behind the tongue. Clinicians should note that the floor
naris inclines in a caudad orientation approximately 15 degrees. The tube
rotated slightly if resistance is encountered.

Oropharyngeal airway sizing
A rough method for choosing the correct oropharyngeal airway (OPA)

size is to hold the airway beside the patient's mandible, orienting it with
the flange at the patient's mouth and the tip directed toward the angle
of the mandible. The tip of an appropriately sized OPA should just reach
the angle of the patient's mandible.

Two rescuer bag-mask ventilation
Two rescuers may be necessary to provide ventilation. One rescuer

may need both hands to open the airway and make the seal
between the child's face and the mask. The second rescuer is then
needed to provide positive pressure ventilation.

Rapid sequence intubation in children: Rapid

overview of emergency management
Preparation – Utilize an active checklist to:
Begin preoxygenation as described below.
Identify conditions that will affect choice of medications (eg,

increased intracranial pressure, septic shock, bronchospasm,
status epilepticus, or, if succinylcholine use is planned, absolute
contraindications for its use as listed below).
Identify conditions that will predict difficult intubation or bag-

mask ventilation (eg, small chin, inability to fully open the mouth,
upper airway trauma, or infection).
Assemble equipment and check for function.
Develop contingency plan for failed intubation (refer to UpToDate

topics on devices for difficult endotracheal intubation).
Preoxygenation
Begin preoxygenation as soon as rapid sequence intubation is

potentially needed:
Spontaneously breathing: 100% FiO2 (>7 L/min oxygen
flow) by nonrebreather mask for 3 minutes
Apneic or inadequate breathing: Bag-mask ventilation with
small tidal breaths using 100% FiO2
During induction and paralysis, provide apneic
oxygenation via nasal cannula at flow rate of 1 L/kg/min
(maximum flow 15 L/min)
Administer oxygen at the highest concentration available.

Pretreatment (optional)
Atropine: Although not routinely recommended, many experts

suggest atropine as pretreatment for:
Children ≤1 year
Children in shock
Children <5 years receiving succinylcholine
Older children receiving a second dose of succinylcholine
Dose: 0.02 mg/kg IV without a minimum dose (maximum single

dose 1 mg; if no IV access, can be given IM).
Induction (sedation)
Etomidate:
Safe with hemodynamic instability, neuroprotective,
transient adrenal cortico-suppression. Do not use routinely
in patients with septic shock.
Dose: 0.3 mg/kg IV.
Ketamine:
Safe with hemodynamic instability if patient is not
catecholamine depleted. Use in patients with
bronchospasm and septic shock. Use with caution in
hypertensive patients with increased intracranial pressure.
Dose: 1 to 2 mg/kg IV (if no IV access, can be given IM
dose: 3 to 7 mg/kg).
Propofol:
Causes hypotension. May use in hemodynamically stable
patients with status epilepticus.
Dose 1 to 1.5 mg/kg IV.
Midazolam:

May use in hemodynamically stable patients with status

epilepticus. Time to clinical effect is longer; inconsistently
induces unconsciousness. May cause hemodynamic
instability at doses required for sedation.
Dose: 0.2 to 0.3 mg/kg IV (maximum dose 10 mg; onset of
effect requires 2 to 3 minutes).
Fentanyl:
Optional for cardiogenic shock or catecholamine-depleted
shock (eg, persistent hypotension despite vasopressor
therapy). Limited evidence in children.
Dose 1 to 5 mcg/kg titrated to effect. Start at lower end of
range in hypotensive patients. Give over 30 to 60 seconds
to avoid respiratory depression or chest wall rigidity.
Paralytic
Rocuronium:
Use for children with contraindication for succinylcholine
or as primary paralytic if sugammadex is immediately
available.
Dose: 1 mg/kg IV.*
Succinylcholine:
Do not use with extensive crush injury with
rhabdomyolysis, chronic skeletal muscle disease (eg,
Becker muscular dystrophy) or denervating neuromuscular
disease (eg, cerebral palsy with paralysis); 48 to 72 hours
after burn, multiple trauma, or denervating injury; patients
with history or malignant hyperthermia; or pre-existing
hyperkalemia.
Dose: Infants and children ≤2 years: 2 mg/kg IV, older
children and adolescents: 1 to 1.5 mg/kg IV (if IV access

unobtainable, can be given IM, dose: 4 mg/kg)¶ .
Protection and positioning
Maintain manual cervical spine immobilization during intubation

in the trauma patient.
If cervical spine injury is not potentially present, put the patient

in the "sniffing position" (ie, head forward so that the external
auditory canal is anterior to the shoulder and the nose and
mouth point to the ceiling).
Utilize external laryngeal manipulation or, in infants, gentle

cricoid pressure to optimize the view of the glottis during direct
laryngoscopy if the initial view is suboptimal or inadequate
despite correct laryngoscope blade positioning.Δ
Positioning, with placement
Confirm tracheal tube placement with end-tidal CO2 detection

and auscultation.
Postintubation management
Obtain a chest radiograph to confirm the depth of tracheal tube

insertion.
Provide ongoing sedation (eg, midazolam), analgesia (eg,

fentanyl 1 mcg/kg), and, if indicated, paralysis.◊
If IV access is not rapidly obtained, intraosseous administration of

drugs is an acceptable alternative.
IM: intramuscularly; IV: intravenously; CO2: carbon dioxide; FiO2:

fraction of inspired oxygen.
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* Sugammadex in a dose of 16 mg/kg can provide immediate

reversal of paralysis when given approximately 3 minutes after a
single dose of rocuronium or vecuronium. Vecuronium may be used
in children with contraindications to succinylcholine and when
rocuronium is not available. Suggested dose for rapid sequence
intubation: vecuronium 0.15 to 0.2 mg/kg. Patients may experience
prolonged and unpredictable duration of paralysis at this dose.
¶ Defasciculating agents (eg, rocuronium or vecuronium at one-

tenth of the paralyzing dose) are not routinely recommended for
children receiving succinylcholine. Onset of paralysis is slower by the
IM route; the clinician must ensure full pre-oxygenation prior to
administration, whenever possible, and be prepared to perform
bag-mask ventilation if desaturation occurs before the patient is
fully paralyzed for endotracheal intubation.
Δ Bimanual laryngoscopy, also called external laryngeal

manipulation (ELM), entails manipulating the thyroid cartilage or
hyoid bone with the right hand during laryngoscopy in order to
improve the view of the glottis. For a description of how to perform
ELM, refer to UpToDate topics on emergency endotracheal
intubation in children and rapid sequence intubation in children.
◊ If decompensation occurs after successful intubation, use the

DOPE mnemonic to find the cause:
D: Dislodgement of the tube (right mainstem or esophageal)
O: Obstruction of tube
P: Pneumothorax
E: Equipment failure (ventilator malfunction, oxygen
disconnected or not on)

Initial settings for volume-controlled mechanical

ventilation in children*
Infant
Toddler/child
Adolescent
(<1 year (1 to 12
(>12 years)
of age) years)
Tidal volume 5 to 8 5 to 8 mL/kg 5 to 8 mL/kg

(mL) mL/kg (healthy lungs) (healthy
(healthy lungs)
lungs)
3 to 6 3 to 6 mL/kg 3 to 6 mL/kg
mL/kg (lung protective (lung
(lung strategy) protective
protective strategy)
strategy)
Rate 20 to 30 15 to 25 12 to 20
(breaths/minute)
PEEP (cm H2O) 3 to 8 3 to 8 3 to 8
Pressure support Minimum 6 Minimum 6 to Minimum 6 to

(cm H2O)¶ to 10 10 10
Peak inspiratory Adjusted to Adjusted to fit Adjusted to fit

flow (L/minute) fit desired desired desired
inspiratory inspiratory time inspiratory
time time
Inspiratory time 0.4 to 0.6 0.7 to 0.9 0.9 to 1.2

(seconds)
Targeted, based

upon changes to
inspiratory flow
FiO2 (%)Δ Start with Start with 1.0, Start with 1.0,
1.0, rapidly rapidly wean to rapidly wean
wean to ≤0.6 to ≤0.6
≤0.6
Flow trigger 0.25 to 0.5 0.8 to 2 0.8 to 2

(L/minute)
Pressure support 10 to 25% 10 to 25% of 10 to 25% of

cycle of peak peak flow rate peak flow rate
flow rate
PEEP: positive end-expiratory pressure; FiO2: fraction of inspired

oxygen.
* Consultation with an expert in the mechanical ventilation of

children (eg, pediatric intensivist or pediatric anesthesiologist) is
strongly encouraged. Regardless of ventilator settings employed,
the physician must assess ventilator settings shortly after initiation
and frequently thereafter and adjust them as needed to meet
oxygenation and ventilation goals as the natural course of the
underlying pathophysiology evolves.
¶ Adjust according to endotracheal tube size: 3 to 3.5 mm: 10 cm

H2O; 4 to 4.5 mm: 8 cm H2O; ≥5 mm: 6 cm H2O.
Δ Wean to 0.6 or below to maintain arterial oxygen tension (PaO2)

60 to 80, oxygen saturation (SpO2) 92 to 97% when required PEEP is
<10 cm H2O; if required PEEP is ≥10 cm H2O, then targeted oxygen
saturation may be reduced to 88 to 92% for those patients with
pediatric acute respiratory distress syndrome (PARDS).


Initial settings for pressure-controlled mechanical

ventilation in children*
Infant
Toddler/child
Adolescent
(<1 year (1 to 12
(>12 years)
of age) years)
PIP (cm H2O)¶ 16 to 25 16 to 25 16 to 25
PEEP (cm H2O)¶ 3 to 7 3 to 7 3 to 7
Rate 20 to 30 15 to 25 12 to 20
(breaths/minute)
Inspiratory time 0.4 to 0.6 0.7 to 0.9 0.9 to 1.2

(seconds)
Pressure support Minimum Minimum 6 to Minimum 6 to

(cm H2O)Δ 6 to 10 10 10
FiO2 (%)◊ Start with Start with 1.0, Start with 1.0,
1.0, rapidly rapidly wean to rapidly wean
wean to ≤0.6 to ≤0.6
≤0.6
Flow trigger 0.25 to 0.5 0.8 to 2 0.8 to 2

(L/minute)
Pressure support 10 to 25% 10 to 25% of 10 to 25% of

cycle of peak peak flow rate peak flow rate
flow rate
PIP: peak inspiratory pressure; PEEP: positive end-expiratory

pressure; FiO2: fraction of inspired oxygen.

* Consultation with an expert in the mechanical ventilation of

children (eg, pediatric intensivist or pediatric anesthesiologist) is
strongly encouraged. Regardless of ventilator settings employed,
the physician must assess ventilator settings shortly after initiation
and frequently thereafter and adjust them as needed to meet
oxygenation and ventilation goals as the natural course of the
underlying pathophysiology evolves.
¶ Initial pressure settings can be established based upon pressures

identified during manual ventilation with a bag and a
manometer/standalone respiratory mechanics monitor prior to
switching to the ventilator.
Δ Adjust according to endotracheal tube size: 3 to 3.5 mm: 10 cm

H2O; 4 to 4.5 mm: 8 cm H2O; ≥5 mm: 6 cm H2O.
◊ Wean to 0.60 or below to maintain arterial oxygen tension (PaO2)

60 to 80, oxygen saturation (SpO2) 92 to 97% when required PEEP is
<10 cm H2O; if required PEEP is ≥10 cm H2O then targeted oxygen
saturation may be reduced to 88 to 92% for those patients with
pediatric acute respiratory distress syndrome (PARDS).

Initial shock management in children in settings with


ICU: intensive care unit; HR: heart rate; BP: blood pressure; HFNC: high-flow
intravenous; IO: intraosseous; US: ultrasound; ECHO: echocardiography; PT
thromboplastin time; ECG: electrocardiography; e-FAST: extended focused
* A trial of HFNC or NIV, such as continuous positive airway pressure venti

need for endotracheal intubation in selected patients. Patients with hemod
shock prior to or during intubation. Refer to UpToDate content on HFNC, N
¶ Ancillary studies are determined by patient presentation and suspected

may also be indicated based upon the suspected underlying condition tha
Δ Fluid volume should be calculated based upon ideal body weight (eg, 50t
◊ When performed by trained and experienced physicians, bedside ECHO

dysfunction due to obstructive shock.

§ Patients with signs of fluid overload who continue to receive fluid boluse
clinician should have a low threshold for endotracheal intubation and mec
¥ Suggested vasoactive therapy depends upon type of shock and clinical fi

shock in children.

Initial management of status epilepticus in

children
Supportive Seizure
Timeline* Assessment
care therapy
0 to 5 Obtain initial vital Open airway Benzodiazepine:

minutes signs, including
Suction Lorazepam 0.1
temperature
secretions mg/kg IV or IO,
maximum 4 mg
Administer 100%
O2 OR
Identify airway Place continuous Diazepam 0.2

obstruction and cardiorespiratory mg/kg IV or IO,
hypoxemia monitors and maximum 10 mg
pulse oximetry
IV or IO access
Identify impaired Perform bag- not achieved
oxygenation or valve-mask within 3
ventilation ventilation, as minutes:
needed Buccal
Prepare for RSI* midazolam 0.3
to 0.5 mg/kg,
Obtain rapid Establish IV or IO
maximum 10 mg
bedside blood access
glucose and OR
other studies, as IM midazolam
indicated¶ 0.1 to 0.2 mg/kg,
Evaluate for Treat maximum 10 mg
signs of hypoglycemia (IV OR
sepsis/meningitis

dextrose 0.25 to Rectal

0.5 g/kg) diazepam
(Diastat gel or
Evaluate for Treat fever
injection solution
signs of head (acetaminophen
given rectally)
trauma 15 mg/kg
0.5 mg/kg,
rectally)
maximum 20 mg
5 to 10 Reevaluate vital Maintain Benzodiazepine:

minutes signs, airway, monitoring, second dose
breathing, and ventilatory
circulation support, and
vascular access
Evaluate for Give antibiotics if

signs of trauma, signs of sepsis or
sepsis, meningitisΔ
meningitis, or
encephalitis
10 to 15 Reevaluate vital Maintain Levetiracetam

minutes signs, airway, monitoring, 60 mg/kg IV or
breathing, and ventilatory IO, maximum
circulation support, and single dose 4500
vascular access mg
Place second IV OR
RSI potentially Fosphenytoin

indicated* 20 mg PE per kg
IV or IO,
maximum single
dose 1500 mg◊
OR

Valproate 20 to
40 mg/kg IV or
IO
OR
Phenobarbital
20 mg/kg IV or
IO, maximum 1 g
(expect a
respiratory
depression with
apnea)¥
15 to 30 Reevaluate vital Maintain Fosphenytoin (if

minutes signs, airway, monitoring, not already
breathing, and ventilatory given) 20 mg PE
circulation support, and per kg IV or IO◊
vascular access
Obtain OR
continuous EEG
Valproate (if not
monitoring, if
already given) 20
available to 40 mg/kg IV
or IO
OR
Phenobarbital
(if not already
given) 20 mg/kg
IV or IO,
maximum 1 g
(10 mg/kg if
phenobarbital
already given)¥

OR
Levetiracetam
(if not already
given) 60 mg/kg
IV or IO
AND
Pyridoxine 100
mg IV or IO in
infants <1 year of
age
Pyridoxine 70
mg/kg IV or IO,
maximum 5 g, if
INH poisoning
suspected
Obtain
pediatric
neurology
consultation‡
RSI: rapid sequence endotracheal intubation; IV: intravenous; IO:

intraosseous; IM: intramuscular; O2: oxygen; PE: phenytoin
equivalents; EEG: electroencephalogram; INH: isoniazid.
* Rapid sequence intubation should be performed if airway,

ventilation, or oxygenation cannot be maintained and if the seizure
becomes prolonged.
¶ For ancillary studies to obtain in children with status epilepticus,

refer to UpToDate topics on status epilepticus in children.

Δ Empiric antibiotic regimens vary depending on patient

susceptibility and likely pathogen.
◊ Do not exceed 2 mg PE/kg per minute (maximum rate: 150 mg

per minute). If fosphenytoin not available, may use phenytoin 20
mg/kg IV, do not exceed 1 mg/kg per minute (maximum rate: 50 mg
per minute). Both fosphenytoin and phenytoin infusion require
cardiac monitoring. Phenytoin and fosphenytoin may be less
effective for the treatment of seizures due to toxins or drugs and
may intensify seizures caused by cocaine, other local anesthetics,
theophylline, or lindane. In such cases, levetiracetam, valproate, or
phenobarbital should be used.
¥ When administering phenobarbital, the maximum infusion rate is

2 mg/kg per minute with a ceiling of 50 mg/min. Anticipate
respiratory depression.
‡ In patients with ongoing seizure activity despite two initial doses

of benzodiazepine and a second-therapy antiseizure medication,
preparation for a continuous infusion of midazolam, propofol, or
pentobarbital should occur simultaneously with administration of a
third-therapy antiseizure medication.

Intranasal diazepam dosing for children 6 to 11

years of age
Quantity
and type of Number of
Weight Dose (mg)
nasal sprays
device
10 to <19 kg 5 mg One 5 mg 1 spray in 1

device nostril

device nostril
38 to <56 kg 15 mg Two 7.5 mg 2 sprays

devices delivered as 1
spray in each
nostril
56 to 74 kg 20 mg Two 10 mg 2 sprays
spray in each
nostril
Intranasal diazepam dosing varies with age and weight.
Reproduced with permission from: Lexicomp online. Copyright © 1978-2022

Lexicomp, Inc. All Rights Reserved.

Intranasal diazepam dosing for children ≥12 years

and adolescents
Quantity
and type of Number of
Weight Dose (mg)
nasal sprays
device

device nostril

device nostril
51 to <76 kg 15 mg Two 7.5 mg 2 sprays

spray in each
nostril
≥76 kg 20 mg Two 10 mg 2 sprays

spray in each
nostril
Intranasal diazepam dosing varies with age and weight.
Reproduced with permission from: Lexicomp online. Copyright © 1978-2022

Lexicomp, Inc. All Rights Reserved.

Laboratory studies in child with status epilepticus
Patient
Studies
population
All patients Serum electrolytes
Serum calcium, phosphate, and magnesium
Serum glucose and a rapid point-of-care glucose
Brain imaging (CT or MRI)*
EEG
Postmenarchal Qualitative pregnancy test (urine or blood)

females
Epilepsy Antiseizure medication level

patients
maintained on
antiseizure
medications
Febrile CBC with differential

patients
Blood culture
Urinalysis, urine culture
CSF culture (once seizures stopped and if brain

imaging excludes increased intracranial pressure)
Substance use Serum and urine toxicology screen for drugs of

or poisoning abuse and prescription drugs (eg, tricyclics,
suspected antipsychotics)¶
Aspirin level

Venous or arterial pH and pCO2
EKG once seizures stop
Infants <6 Blood gas

months of
Plasma ammonia
ageΔ
Plasma amino acids
PT, PTT
Serum AST, ALT, LDH, alkaline phosphatase
Blood lactate and pyruvate
Urinalysis
Urine for reducing substances
Check newborn urine screening results if infant

from country where instituted
CT: computed tomography; MRI: magnetic resonance imaging; EEG:

electroencephalogram; CBC: complete blood count; CSF:
cerebrospinal fluid; PCP: phencyclidine; pCO2: partial pressure of
carbon dioxide; EKG: electrocardiogram; PT: prothrombin time; PTT:
partial thromboplastin time; AST: aspartate aminotransferase; ALT:
alanine aminotransferase; LDH: lactate dehydrogenase.
* Neuroimaging is essential when status is the first presentation of

epilepsy as well as in children whose recovery does not follow the
expected course.
¶ Los niños con sospecha de envenenamiento y estado epiléptico

pueden requerir pruebas toxicológicas más completas de sangre y
orina con fines diagnósticos o forenses, aunque estas pruebas no
están disponibles de manera oportuna y, a menudo, no cambian el
manejo. Se recomienda consultar con un toxicólogo médico o un

centro regional de control de envenenamiento para ayudar con la

selección de pruebas específicas basadas en características clínicas
e identificar laboratorios capaces de realizar estas pruebas.
Δ Se recomienda enfáticamente la consulta con un neurólogo

pediátrico y/o un especialista metabólico. Los ensayos de detección
en recién nacidos son muy completos y deberían detectar la gran
mayoría de los errores metabólicos congénitos potencialmente
tratables; la mayoría de los trastornos metabólicos se diagnostican
genéticamente.

Contributor Disclosures
Angus Wilfong, MD Grant/Research/Clinical Trial Support: Data Safety
Monitoring Board [Epilepsy]; Marinus [Epilepsy]; Zogenix [Epilepsy].
Consultant/Advisory Boards: LivaNova [Epilepsy].
Speaker's Bureau:
LivaNova [Epilepsy].
All of the relevant financial relationships listed have
been mitigated. Douglas R Nordli, Jr, MD Grant/Research/Clinical Trial
Support: Shire[ADHD].
Consultant/Advisory Boards:
AstraZeneca[Dyslipidaemia].
All of the relevant financial relationships
listed have been mitigated. Susan B Torrey, MD No relevant financial
relationship(s) with ineligible companies to disclose. John F Dashe, MD,
PhD No relevant financial relationship(s) with ineligible companies to
disclose. James F Wiley, II, MD, MPH No hay relación(es) financiera(s)
relevante(s) con compañías no elegibles para revelar.
El grupo editorial revisa las divulgaciones de los contribuyentes en busca

de conflictos de intereses. Cuando se encuentran, estos se abordan
mediante la investigación a través de un proceso de revisión de múltiples
niveles y mediante los requisitos para que se proporcionen referencias
para respaldar el contenido. Se requiere que todos los autores tengan
contenido referenciado de manera adecuada y debe cumplir con los
estándares de evidencia de UpToDate.
Política de conflicto de intereses

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8/11/22, 10:45 Management of convulsive status epilepticus in children - UpToDate

Reimpresión oficial de UpToDate ®

Manejo del estado epiléptico convulsivo

Todos los temas se actualizan a medida que se dispone de nueva evidencia y se

Revisión de la literatura actual hasta: octubre de 2022. | Última

El estado epiléptico convulsivo generalizado (SE) es una

El manejo de SE en niños se revisa aquí. La definición, la

trastorno se analizan por separado. (Consulte "Características

DEFINICIÓN Y DIAGNÓSTICO DIFERENCIAL

● Estado epiléptico : una definición aceptada para los fines de

El SE se clasifica según si la actividad convulsiva es focal o

● Estado epiléptico convulsivo: el SE convulsivo es el foco de

● Estado epiléptico no convulsivo: el SE no convulsivo se

● Convulsiones generalizadas breves: no se considera que

• Convulsiones febriles: las convulsiones febriles son el

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extensa ni terapia anticonvulsiva. (Consulte

• Convulsión afebril por primera vez : una primera

Si no se puede encontrar una causa médica aguda

Los niños con una primera convulsión no provocada, en

• Convulsiones intercurrentes en niños con epilepsia

● Convulsiones focales : las convulsiones que no son

● Convulsiones no epilépticas psicógenas: las convulsiones

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suelen ser eventos de comportamiento dramáticos en un

En muchos pacientes, PNES se puede distinguir de SE en

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(ver 'Electroencefalografía' a continuación). Es posible que

El PNES y otros trastornos paroxísticos no epilépticos se

RECONOCIMIENTO RÁPIDO DEL ESTADO EPILÉPTICO

El diagnóstico de SE convulsivo es clínico y se confirma verificando

Los pacientes con convulsiones motoras generalizadas que son

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cuidados intensivos (servicio de urgencias o unidad de cuidados

EVALUACIÓN ENFOCADA URGENTE

Durante el curso de la reanimación, el médico o la persona

● Administración prehospitalaria de benzodiazepinas y

En pacientes con SE, la exploración física inicial es limitada.

● Signos de traumatismo craneoencefálico (p. ej., hinchazón,

IMMEDIATE SUPPORTIVE CARE

Approach — In children with convulsive SE, rapid supportive care

The main goals of treatment are [2]:

● Establish and maintain adequate airway, breathing, and

Monitoring — All patients with generalized convulsions should

Airway and breathing — Important airway interventions in

● Open the airway and maintain it through positioning

● Suction secretions using a Yankauer (tonsil tip) suction

● Administer 100 percent oxygen; use pulse oximetry and

the EtCO2 reading. Myoclonus may interfere with the

For children with transient apnea or hypoxemia, the clinician

The patients with any one of the following should undergo

● Unprotected or unmaintainable airway

The tables provide a rapid overview of RSI in children ( table 6)

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Special considerations for children with SE undergoing RSI

● Propofol and midazolam have antiepileptic properties, and

● Short-acting muscle relaxants, either rocuronium or, in

Circulation and vascular access

● Establish venous access – Patients with SE require timely

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For patients whose seizures do not resolve with

● Hemodynamic support – Most children with SE initially have

In general, SE does not independently cause systemic