Medscape Status Epilepticus

7/31/2019 Medscape Status Epilepticus

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MEDSCAPEPediatric Status Epilepticus Follow-up

Author: Grace M Young, MD; Chief Editor: Richard G Bachur, MD

Background

Status epilepticus is defined as recurrent or continuous seizure activity lasting longer

than 30 minutes in which the patient does not regain baseline mental status.[1]

Pathophysiology

Seizures result from rapid abnormal electrical discharges from cerebral neurons. This

presents clinically as involuntary alterations of consciousness or motor activity. Consumption

of oxygen, glucose, and energy substrates (eg, ATP, phosphocreatine) is significantly

increased in cerebral tissue during seizures. Optimal delivery of these metabolic substrates to

cerebral tissue requires adequate cardiac output and intravascular fluid volume.

Prolonged seizures are associated with cerebral hypoxia, hypoglycemia, and

hypercarbia and with concurrent and progressive lactic and respiratory acidosis. When

cerebral metabolic needs exceed available oxygen, glucose, and metabolic substrates

(especially during status epilepticus), neuronal destruction can occur and may be irreversible.

Hypoxia, hypercarbia, hyperthermia, tachycardia, hypertension, hyperglycemia,

hyperkalemia, andlactic acidosisresult from massive sympathetic discharge.

Epidemiology

Frequency

United States

Seventy percent of children younger than 1 year who are subsequently diagnosed with

epilepsy present with status epilepticus as the initial symptom of their illness. In children with

epilepsy, 20% have status epilepticus within 5 years of diagnosis. Five percent of children

with febrile seizures present with status epilepticus.International

Rates are similar to those in the United States.Mortality/Morbidity

In the United States, the overall mortality is 10-15%.Sex

No sexual predilection is recognized.Age

Status epilepticus is common at any age. Certain etiologies are more prevalent in selected age

groups (see Causes).

History

In the initial presentation of status epilepticus, a directed history suffices. Obtain a more

detailed history after stabilization, including the following details:

The course of current seizure activity - Time and nature of onset of seizure activity;involvement of extremities or other body parts; nature of movements (eg, eye

movements, flexion, extension, stiffening of extremities), including any focal

movements and details of postictal neurologic deficit; incontinence; cyanosis (perioral

or facial); duration of seizure activity prior to medical attention; mental status after

cessation of seizure activity

Fever or intercurrent illnesses
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Prior history of seizures - If present, specify medications, anticonvulsant use, andcompliance.

Head injury (recent and remote) Central nervous system (CNS) infection or disease (eg, meningitis, neurocutaneous

syndrome)

Intoxication or toxic exposure (see Causes for examples) Other CNS abnormality (eg, ventricular-peritoneal shunt, prior CNS trauma) Birth history and developmental delay (eg, anoxic encephalopathy, cerebral palsy) Other medical history (eg, acquired immunodeficiency syndrome, systemic lupus

erythematosus, type 1 diabetes mellitus)

Physical

Perform a rapid, directed physical and neurologic examination during status

epilepticus, followed by a detailed examination when the child is stabilized.

Signs of sepsis or meningitis include the following:

Temperature more than 38.5C; in patients younger than 2-3 months, more than38.0C

Respiratory distress Cyanosis Poor peripheral perfusion Bulging fontanelles in infant Meningismus (in children >12-18 mo) Presence of petechiae or purpura, herpetic vesicles

Evidence of head or other CNS injury includes the following:

Bradycardia, tachypnea, and hypertension (Cushing triad for signs of increasedintracranial pressure)

Poor pupillary response Asymmetry on neurologic examination Abnormal posturing Gross deformity or soft tissue injury to head

Hallmarks of neurocutaneous syndromes (eg, port wine stain) may be noted.

Causes

Neonates (first month of life) Birth injury (eg, anoxia, hemorrhage) and congenital abnormalities Metabolic disorders (eg, hypoglycemia, hypocalcemia, hyponatremia) and inborn errors of

metabolism (eg, lipidoses, amino acidurias)

Infection (eg, meningitis)Early childhood (< 6 y)

Birth injury Febrile convulsions (3 mo to 6 y) Infection Metabolic disorders Trauma Neurocutaneous syndromes Cerebral degenerative diseases Tumors Idiopathic

Children and adolescents (>6 y) Birth injury


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Trauma Infection Epilepsy with inadequate drug levels Cerebral degenerative disease Tumor Toxins Idiopathic

Toxins and medications

Topical anesthetics (eg, lidocaine) Anticonvulsant overdose Camphor Hypoglycemic agents (eg, insulin, ethanol) Carbon monoxide Cyanide Heavy metals (eg, lead) Pesticides (eg, organophosphate)

Cocaine Phencyclidine Belladonna alkaloids Nicotine Sympathomimetics (eg, amphetamines, phenylpropanolamine [recalled from US market]) Tricyclic antidepressants

Differential Diagnoses

Herpes Simplex Herpes Simplex Encephalitis

Neoplasms, Brain Pediatrics, Bacteremia and Sepsis Pediatrics, Febrile Seizures Pediatrics, Meningitis and Encephalitis Toxicity, Amphetamine Toxicity, Anticholinergic Toxicity, Antidepressant Toxicity, Carbon Monoxide Toxicity, Cocaine Toxicity, Cyanide Toxicity, Cyclic Antidepressants Toxicity, Heavy Metals Toxicity, Lead Toxicity, Local Anesthetics Toxicity, Medication-Induced Dystonic Reactions

Toxicity, Methamphetamine Toxicity, Organophosphate and Carbamate
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Toxicity, Phencyclidine Toxicity, Sympathomimetic

Laboratory Studies

Obtain laboratory studies based on age and likely etiologies.

Blood glucose level using immediate bedside testing (eg, Dextrostix), particularly ifthe child or other household members are dependent on insulin or other hypoglycemic

agents

Electrolyte levels Calcium and magnesium levels, particularly in neonates ABG levels Toxicology screen Anticonvulsant levels (if indicated by history of ingestion or existent therapy) WBC count: An elevated WBC count may be due to demargination, returning to

reference ranges over 12-24 hours.

Carboxyhemoglobin levels

Imaging Studies

Stabilize all children before CT scanning or other imaging studies are performed.

Obtain imaging studies based on likely etiologies.

Cervical spine radiographs, if potential trauma is suspected.

A head CT scan is the best diagnostic imaging study, particularly if the following are

suspected:

Hemorrhage

Midline shift Mass lesionMRI is not a diagnostic tool, unless it is immediately available and the child's

cardiorespiratory status is stable.

Other Tests

Electroencephalography

For unremitting status epilepticus Usually performed in a critical care setting

ProceduresLumbar puncture with opening pressure

For prolonged status epilepticus of unknown etiology For immunocompromised patients

Prehospital Care

Secure the airway. Administer supplemental 100% oxygen. Infuse isotonic intravenous fluids and glucose. Immobilize the cervical spine in patients with possible trauma.
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Consider rectally administered diazepam (0.5 mg/kg/dose) or intramuscularlyadministered midazolam (0.1-0.2 mg/kg/dose; not to exceed a cumulative dose of 10

mg).[2]

Emergency Department Care

The principles of treatment are to terminate the seizure while resuscitating the patient,treating complications, and preventing recurrence.

Assessment and stabilization of ABCs concurrent with management of the seizure is

imperative. Administer 100% oxygen by facemask, assist ventilation, and use artificial

airways (eg, endotracheal intubation) as needed. Suction secretions and decompress the

stomach with a nasogastric tube. Immobilize the cervical spine if trauma is suspected.

Closely monitor vital signs, cardiorespiratory function, and oxygen saturation. Perform rapid

blood glucose assay (eg, Dextrostix) at bedside.

Establish intravenous access. Use intraosseous (IO) infusion if intravenous access is not

immediately available in the child younger than 6 years. Most available anticonvulsants may

be administered intravenously or intraosseously.

Infuse isotonic intravenous fluids 20 mL/kg with glucose (eg, 200 mL dextrose 5% in normal

saline [D5NS] intravenously over 1 h for a 10-kg child).

Consider treatment with the following agents: Dextrose - 0.25-0.5 g/kg/dose (1-2 mL of 25% dextrose) intravenously for hypoglycemia; not

to exceed 25 g/dose

Naloxone - 0.1 mg/kg/dose intravenously preferably (if needed may administerintramuscularly/subcutaneously) for narcotic overdose

Thiamine - 100 mg intramuscularly for possible deficiency Pyridoxine - 50-100 mg intravenously/intramuscularly for possible deficiency Antibiotics - If meningitis is strongly suspected, initiate treatment with antibiotics prior to

cerebrospinal fluid (CSF) analysis or CNS imaging.

Administer anticonvulsant medication. The optimal protocol for management of status

epilepticus begins with a benzodiazepine. In the United States, lorazepam is the first drug of

choice in patients with intravenous or intraosseous access. For patients without parenteral

access, intramuscular midazolam is best. If the seizures cease, no further drugs are

immediately necessary, and the etiology of status epilepticus should be investigated. If

seizures continue, administer intravenous phenytoin or parenteral fosphenytoin. If these are

not effective, administer intravenous phenobarbital titrated to induce barbiturate coma.

Finally, consider general anesthesia with pentobarbital or midazolam.

The goal is prompt cessation of seizure activity. Patiently allow infused anticonvulsants to actbefore using additional anticonvulsants. Proceed to the next drug if seizure activity continues.

Lorazepam (0.05-0.1 mg/kg intravenously/IO slowly infused over 2-5 min) has rapid onset

and long duration of anticonvulsant action. It is preferred over diazepam.

Phenytoin (18-20 mg/kg intravenously/IO) or fosphenytoin (15-20 mg/kg intravenously/IO)

loading doses: These long-acting anticonvulsants usually are infused if benzodiazepines do

not stop the seizures. Phenytoin and fosphenytoin are effective for most idiopathic

generalized seizures and for posttraumatic, focal, or psychomotor status epilepticus. Use a

slow rate of infusion (< 1 mg/kg/min or < 50 mg/min) to avoid hypotension or cardiac

arrhythmias. A full loading dose should be delivered unless the patient is known to have a

current therapeutic level.


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Midazolam (0.1-0.2 mg/kg intramuscularly) is most effective when intravenous or

intraosseous access is not immediately available.[3]

Midazolam is the only benzodiazepine

that can be administered safely intramuscularly with equivalent rapid onset and moderate

duration of action.

Phenobarbital (20-25 mg/kg intravenously/IO) is effective for febrile and neonatal status

epilepticus and may be infused after lorazepam or other benzodiazepines if the child is likely

to have these types of seizures. Phenobarbital's major disadvantages are that it significantly

depresses mental status and causes respiratory difficulty. Obtain serum anticonvulsant levels

prior to administering additional long-acting anticonvulsants such as phenytoin or

fosphenytoin.

General anesthesia

Pentobarbital (5-10 mg/kg intravenously/IO loading dose followed by 0.5-3 mg/kg/h)

or midazolam (0.2 mg/kg intravenously/IO loading dose followed by 0.75-10 mcg/kg/min)

All children must be intubated and paralyzed, have continuous cardiorespiratory and EEG

monitoring, and be in a pediatric critical care setting.

Consultations

After initial emergency stabilization, consider consultation with the following specialists:

Pediatric emergency or critical care specialist or general pediatrician Pediatric neurologist Pediatric neurosurgeon if needed

Medication Summary

Benzodiazepines, hydantoins, and barbiturates have anticonvulsant properties. Choose

a parenteral preparation with rapid onset and long duration of action with the least amount of

sedation and respiratory depression. Titrate for clinical response by waiting an adequate

length of time for attainment of therapeutic levels in the brain.

Benzodiazepines

Class Summary

By increasing the action of GABA, which is a major inhibitory neurotransmitter in the

brain, may depress all levels of CNS, including limbic and reticular formation.

In one study, no difference in efficacy was observed between caregiver-administered

intranasal midazolam and rectal diazepam for terminating sustained seizures (ie, >5 minutes)

in children at home. Caregiver's satisfaction was higher with the inhaled midazolam (easier to

administer) and the median time from medication administration to seizure cessation was 1.3

minutes less for inhaled midazolam compared with rectal diazepam.[4]

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life.

Preferred over diazepam because of significantly longer duration of action and equivalent

rapid onset of action.

Important to monitor patient's blood pressure after administering dose. Adjust prn.
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Diazepam (Valium)

For treatment of seizures. Depresses all levels of CNS (eg, limbic and reticular formation),

possibly by increasing GABA activity. Effective for prehospital use as PR administration. Has a long

half-life but rapidly redistributes from the CNS. Requires administration of the longer-acting

phenytoin or phenobarbital because of very short duration of seizure control.

Do not administer >1-2 mg/min IVP in children or > 5 mg/min in adults.

Midazolam (Versed)

Used as alternative in termination of refractory status epilepticus. Because midazolam is

water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician

must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose.

DOC for child without immediate IV or IO access (available IM).

Barbiturates

Class Summary

These agents suppress CNS from reticular activating system (presynaptic and postsynaptic).

Phenobarbital (Barbita, Luminal)

Effective for febrile and neonatal status epilepticus. Can be administered PO. In status

epilepticus, it is important to achieve therapeutic levels as quickly as possible. IV dose may require

approximately 15 min to attain peak levels in the brain. If injected continuously until convulsions

stop, brain concentrations may continue to rise and can exceed that required to control seizures

resulting in subsequent toxicity. Important to use minimal amount required and wait for

anticonvulsant effect to develop before administering a second dose.

If IM route chosen, administer into areas with little risk of encountering a nerve trunk

or major artery such as one of the large muscles (eg, gluteus maximus, vastus lateralis). A

permanent neurologic deficit may result from injecting into or near peripheral nerves.

Restrict IV use to conditions in which other routes are not possible, either because patient is

unconscious or because prompt action is required.

IV administration should be < 50 mg/min. Parental product contains 68% propylene glycol.

Ensure monitoring for hypotension, bradycardia, and arrhythmias upon administration.

Hydantoins

Class Summary

These agents stabilize neuronal membranes and decrease seizure activity.

Fosphenytoin (Cerebyx)

Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin.

Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde, and

phenytoin.

To avoid need to perform molecular weight-based adjustments when converting between

fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents

(PE). Although can be administered IV and IM; IV route is route of choice and should be

used in emergency situations.
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Concomitant administration of an IV benzodiazepine usually is necessary to control status

epilepticus. Full antiepileptic effect, whether administered as fosphenytoin or parenteral

phenytoin, is not immediate. Not currently recommended for acute control of status

epilepticus because of its slow onset of action. Prepare drug in 100 mL of NS or D5W.

Phenytoin (Dilantin)

May act in motor cortex where may inhibit spread of seizure activity. Activity of brain stem

centers responsible for tonic phase of grand mal seizures also may be inhibited. Effective for

idiopathic, posttraumatic, focal, and psychomotor status epilepticus. Individualize doses. Administer

larger dose before retiring if dose cannot be divided equally.

Administer only in saline solutions (incompatible when mixed with dextrose-containing

solutions).

General anesthetics

Class SummaryAll children must be intubated and paralyzed and must have continuous cardiorespiratory and

EEG monitoring in a pediatric critical care unit. Pentobarbital may be required when seizures

persist despite appropriate administration of other antiseizure agents.

Pentobarbital (Nembutal)

Short-acting barbiturate with sedative, hypnotic, and anticonvulsant properties. Can

produce all levels of CNS mood alteration. Acts primarily on cerebral cortex and reticular formation

through decreased neuronal synaptic activity.

Further Inpatient CareMost children with an episode of status epilepticus should be admitted for inpatient

observation, evaluation, and treatment.

Any child with persistent altered mental status (despite cessation of seizure activity) or with

prolonged status epilepticus should be admitted to a pediatric critical care unit.

Inpatient & Outpatient Medications

A child who has a single generalized tonic-clonic seizure for the first time often does not

receive long-term anticonvulsant therapy. Consult a pediatric neurologist.

Transfer

Transfer is prudent unless the hospital facility has a pediatric critical care unit and staff

familiar with the risks and complications of status epilepticus in children.

Deterrence/Prevention

Patients should avoid exposure to specific causes.

Complications

Complications of status epilepticus may include the following:
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Anoxic brain damage Aspiration Head trauma Minor soft tissue trauma Joint dislocation: Posterior shoulder dislocation is a classic complication and is

difficult to diagnose in the unconscious patient. Complications as a result of the underlying cause

Prognosis

Outcome depends on the underlying cause.

Patient Education

Patients should follow instructions from the pediatric neurologist.

Patients should maintain compliance with anticonvulsant therapy.

For excellent patient education resources, visit eMedicine's Brain and Nervous System

Center. Also, see eMedicine's patient education articleEpilepsy.

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