Status Epilepticus

Victoria Goretty405080197

PROBLEM 3EMERGENCY MEDICINE BLOCK

GROUP 15FACULTY OF MEDICINE

TARUMANAGARA UNIVERSITY JAKARTA

TUESDAY, OCTOBER 16TH 2012

GROUP 15• Tutor : dr. Intan, Sp.Kk• Leader : Angela Putri 405090139• Secretary : Hsu Chong Jen 405090054• Writer : Vinnie Juliana 405090058• Members : Riana Chandra 405080073

Donny Firdaus 405080086 Lili Juniarti 405080120 Victoria Goretty 405080197 Kevin Keenan 405090118 Ivan Michael 405090161 Agnes 405090173 Vivian Otha 405090216

A 21 y.o. male patient had recurrent transient attack of loss of consciousness with general seizures for less than 5 minutes since 6 months ago. Before the attack, no changes such as headache, dizziness/ vertigo, or other certain things felt by the patient. After the attacks, he doesn’t feel either strange or confused. However, he doesn’t remember ehat happened to him. There is no history of febrile seizure, head injury, CNS infection or brain tumor. He didn’t receive any specific medical treatment. He had about 4 attacks during 30 minutes before he was brought to Emergency Departement.

Physical examination: Unconscious (GCS E2M5V2), BP 130/90 mmHg, HR 92 beats per minute, RR 22 breaths per minute, temperature 36.6C, heart/ lung normal, liver/ spleen unpalpatable, pupils isocoric 3/3 mm eith light reflex (+)/(+), meningeal signs (-), signs of increased of intracranial pressure (-), cranial nerves are normal, sensoric/ motoric normal, physiological reflex normal, pathological reflex (-)/(-).

Please discuss this problem!

Mind Mapping

Learning Objective

Definition of Status Epilepticus

• more than 30 minutes of continuous seizure activity or 2 or more seizures in this period without full recovery of consciousness

EtiologyPrimary neurologic lesion Non-primary neurologic lesion

Neurovascular (stroke, artery – venous malformation, hemorrhage)

Hypoxia / ischemia

Tumor (primary, metastatic) Drugs/ chemical toxicity (antibiotic, antidepressant, antipsychotic, bronchodilator, local anesthesia, immunosuppressant drugs, cocaine, amphetamine)

CNS Infection (Abscess, Meningitis, Encephalitis)

Drug withdrawal (barbiturate, benzodiazepine, opioid, alcohol)

Inflammation disease (vasculitis, acute disseminated encephalomyelitis)

Febrile seizures

Capitis trauma (contusion, hemorrhage) Metabolic disturbances

Primary epilepsy

RISK FACTOR

• Anticonvulsant withdrawal or noncompliance• Previous incident of status epilepticus (SE)• Refractory epilepsy• Head trauma• Metabolic disturbances• Drug toxicity• CNS infection; tumors

• Cerebrovascular disease• Fever (especially in children)• Medications that lower the seizure threshold

ANTIBIOTICS LITHIUM

ANTIHISTAMINES MEPERIDINE

ANTIDEPRESSANTS PROPOXYPHENE

BACLOFEN THEOPHYLLINE

FENTANYL

FLUMAZENIL

KETAMINE

LIDOCAINE

Sign and symptoms• Generalized SE

– Overt convulsions– After 30–45 minutes of uninterrupted seizures,

signs may become increasingly subtle.• Mild clonic movements of only the fingers• Fine, rapid movements of the eyes• Paroxysmal episodes of tachycardia,

hypertension, and pupillary dilation– Patients who remain unresponsive following

termination of overt convulsions may remain in nonconvulsive SE, a condition often detectable only by electroencephalogram (EEG).

Cause of Seizure

Major Cause

Common Cause

Less Common

• Low Levels of AED• Cerebrovascular

Disease : Acute or Remote Stroke and Hemorrhage

• alcohol withdrawal• Metabolic abnormalities• anoxia• Hypoxia• Tumors• CNS infections

• Drug overdose• Traumatic Brain

Injuriesa

Cause & Epidemiology of Seizure

Mechanism & Pathology of SE

• The central pathophysiology of SE is failure of the normal mechanisms that terminate an isolated seizure.

• Excessive excitation, ineffective inhibition, or a combination of the two may play a role in the origin of prolonged seizures (most cases), but the exact mechanisms are poorly understood.

Mechanism & Pathology of SE

• Excessive excitation can be modeled by domoic acid, a glutamate analogue. Patients who accidentally ingest mussels (remis, kepah) contaminated with domoic acid develop prolonged SE.

• Several inhibitory mechanisms may play a role in SE, including :– calcium-dependent potassium currents

Mechanism & Pathology of SE

– magnesium blockade of NMDA channels– inhibitory neurotransmitters such as adenosine and

GABA.• As SE becomes prolonged, functional changes in the

GABA receptor lead to failure of GABA mediated inhibition.

Mechanism & Pathology of SE• SE-induced neuronal damage is mediated by

excitotoxicity or excessive release of excitatory amino acids such as glutamate

• Glutamate release causes an influx of sodium, depolarization of the cell membrane, and cell swelling.

• Excessive calcium enters neurons via glutamate activated NMDA, kainate, and a -amino-3-hydroxy-5-methylisoxazole-4-proprionic acid AMPA receptors. Intracellular calcium induces a cascade of events cell damage/neuronal death.

Mechanism & Pathology of SE

• Excessive calcium enters neurons via glutamate activated NMDA, kainate, and a -amino-3-hydroxy-5-methylisoxazole-4-proprionic acid AMPA receptors. Intracellular calcium induces a cascade of events cell damage/neuronal death.

Classification

Convulsive (GCSE) convulsions that are associated with rhythmic jerking of the extremities

Non-convulsive (NCSE) seizure activity seen on electroencephalogram(EEG) without clinical findings associatedwith GCSE.

Refractory SE (RSE) Patients who do not respond to standard treatmentregimens for status epilepticus

Convulsive Non-convulsiveGeneralized Tonic-clonic

TonicMyoclonic

LenaAtypical lenaAtonic

Partial Partial motoric (epilepsy partialis continua)

AphasiaNonmotoric simple partialComplex partial

Secondary generalized Partial seizures with secondary generalization

Subtle / coma

Generalized Convulsive SE• GCSE is the most common form of SE.• GCSE is characterized by paroxysmal or continuous

tonic and/or clonic movements with coma or profound impairment of consciousness.

• Typically, the seizures begin as individual discrete seizures, which gradually merge to produce a continuous ictal state.

GCSE

• Most GCSE is secondarily generalized, with seizures beginning in one part of the brain and spreading to generalized convulsions.

• As SE progresses, motor manifestations become more subtle or may disappear entirely. EEG is usually necessary to make the diagnosis of subtle GCSE.

GCSE

• GCSE has high morbidity and mortality. Mortality ranges between 10% and 30% with higher rates in:– the elderly,– acute symptomatic SE– SE lasting more than 2 hours.

GCSE

• Morbidity includes:– cognitive impairment– focal neurological deficits– epilepsy.

Nonconvulsive SE

• NCSE can be divided into two subcategories:– absence (generalized) NCSE and– Partial NCSE

• Absence SE, sometimes called an epileptic ‘‘twilight state’’, is characterized by mild impairment of consciousness and a characteristic EEG pattern of generalized spikes at 3 Hz.

NCSE

• Most absence SE occurs in patients with a history of absence seizures or primary generalized epilepsy. Atypical absence SE, characterized by more variable impairment of consciousness and spikes at repetition ratesless than 3 Hz on EEG, occurs in patients with the Lennox-Gastaut syndrome.

NCSE

• Partial NCSE is divided into :– Simple partial SE– complex partial SE– Electrographic partial SE

• Simple partial SE is characterized by continuous or repetitive focal motor, sensory, special sensory, autonomic, or psychic symptoms without impairment of consciousness.

• Complex partial SE is characterized by alteration of consciousness, often with oral or limb automatisms or focal motor movements. Impairment of consciousness ranges from mild confusion to coma.

• Electrographic partial SE occurs in comatose patients without overt clinical seizure activity in reveals focal ictal discharges lasting 30 minutes or more.

NCSE

• Outcomes of patients with NCSE are highly variable. Patients with absence SE tend to have good prognoses regardless of the duration of seizure activity, whereas those with partial NCSE have widelyvarying outcomes.

• A retrospective review of 100 patients with NCSE showed a mortality of 18% in the groupwith acute medical problems but only 3% in those with NCSE secondary to epilepsy.

NCSE

• The level of consciousness during NCSE may also predict outcome.

• Severe mental status impairment is associatedwith higher morbidity (39%) than milder cognitive impairment (7%).

Refractory SE

• RSE is defined as SE that fails to respond to treatment.

• SE becomes more difficult to treat as its duration increases.

• Outcome of RSE is extremely poor, with mortality at almost 50% and only a small fraction of patients returning to their premorbid functional baseline.

RSE

• RSE is associated with:– increased mortality– increased functional deterioration– increased hospital length of stay.

Management