meidy case 3
TRANSCRIPT
• Convulsion– Intense paroxysm of involuntary repetitive muscular contractions
• Seizure– Paroxysmal excessive electrical nervous discharges affects
consciousness, alteration of perception, impairment of psychic function, convulsive movements, disturbance of sensation, combination of thereof
• Epilepsy– Condition of recurrent unprovoked seizures
• Status epylepticus – Prolonged or repeated convulsive seizures for ≥30 minutes
Pathophysiology• Hyper-activity from neuron as pace-makers• Repetitive hyper-excitation of neurotransmitter (glutamic
acid & aspartic)• Reduced inhibition activity of GABAHyper-excitation of neurons stimulates surrounding
neurons seizureDistribution area of hyper-excitated neurons determines the type of the seizure
– Epileptic focus partial seizure– Spreading to both hemisphere generalized seizure– Continuous hyperexcitation status epylepticus
Pre-ictal Phenomenon
• Apathetic• Depressed• Irritable• Ecstatic• Myoclonic jerks of trunk or limbs
• Usually strikes “out of the blue” without warning
Post-ictal Phenomenon
• Movements have ended• Patiet lies still and limp, in deep coma• Pupils : equal/unequal contract to light• Breathing : quiet/stertorous• Open eyes bewildered / confused / agitated• Drowsy, falls asleep (several hours), wake with
pulsatile headache• Anatomical abnormalities (burns, fractures,
haemorrhages, etc)
EtiologyPrimary neurologic disorders Systemic disorders
Benign febrile convulsions of childhood Hypoglycemia
Idiopathic/cryptogenic seizures Hyponatremia
Cerebral dysgenesis Hyperosmolar states
Symptomatic epilepsy Hypocalcemia
Head trauma Uremia
Stroke or vascular malformations Hepatic encephalopathy
Mass lesions Porphyria
CNS infections Drug toxicity
Encephalitis Drug withdrawal
Meningitis Global cerebral ischemia
Cysticercosis Hypertensive encephalopathy
HIV encephalopathy Eclampsia
Hyperthermia
Major categories of drugs reported to cause seizures.
Antibiotics (quinolones, penicillins, isoniazid)
Anticholinesterases (organophosphates, physostigmine)Antidepressants (tricyclic,monocyclic, heterocyclic; selective serotonin reuptake inhibitors)
Antihistamines
Antipsychotics (phenothiazines, butyrophenones, clozapine)
Chemotherapeutics (etoposide, ifosfamide, cisplatinum)
Cyclosporine, FK 506
Hypoglycemic agents (including insulin)
Hypoosmolar parenteral solutions
Lithium
Local anesthetics (bupivacaine, lidocaine, procaine, etidocaine)
Methylxanthines (theophylline, aminophylline)
Narcotic analgesics (fentanyl, meperidine, pentazocine, propoxyphene)
PhencyclidineSympathomimetics (amphetamines, cocaine, ephedrine, MDMA1 “ecstasy,” phenylpropanolamine, terbutaline)
Epidemiology
• Approximately 100,000 new cases in the United States each year. – 6 - 10 % individuals experience at least one seizure
during their lives.• 1 - 2 % are subject to recurrent seizures.
– Incidence rates highest < 20 years old. second peak > 60 years
old.– There is a slightly higher male predominance.
Classification
Generalized seizures:–Classically tonic-clonic (grand
mal)–Begins as myoclonic jerks
followed by loss of consciousness–Sustained generalized skeletal
muscle contractions–Nonconvulsive generalized
seizures:– Absence seizures (petit mal); brief
episodes of sudden immobility and blank stare
Partial seizures• Simple:
• Brief sensory or motor symptoms without loss of consciousness (i.e., jacksonian)
• Complex :• Mental and psychological symptoms• Affect changes• Confusion• Automatisms• Hallucinations• Associated with impaired consciousness
• Secunder Generilized
http://www.easyhealth.org.uk/cmsimages/Seizure-types-1_1255.gif
Seizure EEG• A. Onset of a tonic seizure showing
generalized repetitive sharp activity with synchronous onset over both hemispheres.
• B. Burst of repetitive spikes occurring with sudden onset in the right temporal region during a clinical spell characterized by transient impairment of external awareness.
• C. Generalized 3-Hz spike-wave activity occurring synchronously over both hemispheres during an absence (petit mal) attack
Test
STATUS EPILEPTICUS
• Prolonged seizure activity lasting greater than 30 minutes
• Or, recurrent seizures without the interval of recovery (consciousness) lasting greater than 30 minutes
• Aktivitas kejang berkepanjangan yang berlangsung lebih dari 30 menit
• Atau, kejang berulang tanpa interval pemulihan (kesadaran) yang berlangsung lebih dari 30 menit
DEFINITION
Etiology
• 3 groups of etiology:– an exacerbation of a pre-existing seizure disorder– the initial manifestation of a seizure disorder– insult other than a seizure disorder
• Primary neurological lesion– Neurovascular– Tumor– Infection of the CNS– Inflammation– Trauma capitis– Primary epilepsy
• Non-neurological lesion– Hypoxia/ischemia– Chemical toxicity– Seizure of medications– Infections (Febrile seizures)– Metabolic disorders
Etiology (Pediatric)The etiology of SE tends to vary by the age of the child (ie,
younger than versus older than 6 years). Causes of SE in early childhood (< 6 y) may include the following:
• Birth injury• Febrile convulsions (3 mo to 6 y)• Infection• Metabolic disorders• Trauma• Neurocutaneous syndromes• Cerebral degenerative diseases• Tumors• Idiopathic
Causes in children and adolescents (>6 y) may include the following:
• Birth injury• Trauma• Infection• Epilepsy with inadequate drug levels• Cerebral degenerative disease• Tumor• Toxins• Idiopathic
Etiology
The main causes of status epilepticus arelow blood concentrations of antiepileptic
drugs in patients with chronic epilepsy (34%)remote symptomatic causes (24%)cerebrovascular accidents (22%)anoxia or hypoxia (~10%)metabolic causes (~10%), andAlcohol and drug withdrawal (~10%)
Acut repetitive seizure
Seizure mechanisms
• Excessive excitation
• Deficient inhibition
PathophysiologyGlutamate• Neurotransmitter rangsang yang paling umum• Eksitasi Kelebihan dimediasi melalui• N-methyl-D-aspartate (NMDA) Reseptor• faktor-faktor yang meningkatkan aktivitas glutamat
dapat menyebabkan kejang
Huff JS, Fountain NB. Emerg Med Clin N Am. 29 (2011) 1-13.
PathophysiologyGamma-aminobutyric acid (GABA)• Neurotransmitter inhibisi paling umum• GABAA reseptor mencegah kelebihan eksitasi• Obat-obatan yang mengikat reseptor GABAA
menjadi kurang efektif sebagai SE terus• Antagonis GABA dapat menyebabkan SE - misalnya
Penisilin, antibiotik lain
Huff JS, Fountain NB. Emerg Med Clin N Am. 29 (2011) 1-13.
Pathophysiology - SE continued
• SSP kerusakan dapat terjadi - mekanisme:• penembakan neuron yang tidak terkontrol ->
kelebihan glutamat -> ini masuknya tinggi yang berkelanjutan ion kalsium ke dalam neuron menyebabkan kematian sel ("excitotoxicity")
• GABA dirilis untuk melawan ini, tetapi reseptor GABA akhirnya rasa mudah terpengaruh
• efek ini memburuk jika hipertermia, hipoksia, atau hipotensi
Status Epilepticus
Pathophysiology • Seizures are sustained by excess excitation and reduced
inhibition– Glutamate : excitatory neurotrasmitter– NMDA (N-methyl-D-aspartate) receptor subtype– GABA : inhibitory neurotrasmitter
Status Epilepticus : Pathophysiology
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
SE phases
• Phase 1– Increased metabolic demand :
• Increased BP and blood glucose level, sweating, salivation, hyperpyrexia
• 2nd phase– 30 minutes after the 1st phase
• Failure of cerebral auto-regulation, cerebral hypoperfusion, increased ICP, systemic hypotnesion
Temporal changes which occur as tonic-clonic status epilepticus progresses.
Status Epilepticus
Physical Examination• body temperature (reach 42oC)• Prominent systemic arterial pressure BP • Papilledema : sign of intracranial pressure : mass
lesion/brain infection• Patient who doesn’t have improving level of consciousness
within 20-30 minutes consider as subtle SE
Status Epilepticus
Laboratory Studies• Electrolytes• Calcium• Magnesium• Glucose• Complete blood count
• Renal function tests• Toxicologic screening• Anticonvulsant levels• Liver function tests
Status Epilepticus
Arterial Blood Gas• To monitor oxygenation & ventilation efficacy and to
discover any acid-base abnormalities
EEG• complex partial status
epilepticus originating in the right temporal lobe,
• a patient with history of intractable partial epilepsy.
• On clinical observation, the patient was lethargic, sluggish, and vague, with variable responsivity to examiners
CT-scan
• Membantu dalam mengevaluasi untuk lesi struktural (misalnya, tumor otak, infark, abses, perdarahan) yang mungkin mendasari SE.
• Noncontrast CT adalah prosedur pencitraan pilihan untuk pasien gawat darurat dengan SE.
• Pencitraan sering ditangguhkan jika pasien diketahui memiliki epilepsi
Lumbar Puncture
• Jika infeksi SSP adalah dalam diagnosis diferensial, pertimbangkan pungsi lumbal (setelah pencitraan kepala yang tepat untuk memastikan keselamatan).
• Memulai terapi antibiotik jika SSP atau infeksi sistemik diduga kuat.
Algoritma tatalaksana pada status epileptikus
PRINCIPLES OF MANAGEMENT STATUS EPILEPTICUS
1. Stabilization of the patient with the principles of ABC's
a) Airway --> intubation after a seizure lasting 15 minutes or unstable or if the obstruction occurs before
b) Breathing : disturbed --> need help breathingc) Circulation : secure the venous line to anticipate
hypotension, take blood (check glucose, electrolytes)d) Drugs --> adjust the patient's treatment is undertaken when
possible
2. Stop seizures and look for the cause simultaneously
3. Prevent recurrent seizures, overcome complications
4. Overcome trigger 5. > 60 minute --> refractory --> ICU
STATUS EPILEPTICUS
Airway
Breathing
Circulation
Drugs & Differential Dx/
3) Rule out hypoglicemia
1) Protect the airway
2) Insert an IV catheter
4) Pharmacological Protocol Therapy
5) Measure Arterial Blood Gases and pH
6) Maintain Ventilation
7) Rule Out Meningitis
8) Search for the underlying cause
Secondary survey
After acute seizures stopped• ABC• CT scan see blood disorders, tumors, or other
structure• lumbar puncture if suspected meningitis / not
recover to the initial neurological function• Unstable patients treated in hospital again• Stable patients can be discharged but given a
maintenance phenytoin 300 mg / day and prohibited driving
Refractory status epilepticus• Secara umum, 80% dari pasien dengan status epileptikus
kejang dapat dikontrol dengan pemberian benzodiazepin / fenitoin.
• Jika kejang masih berlangsung Status epileptikus refrakter perawatan di ICU untuk anestesi
When to Refer
• episode perilaku adalah alam pasti.• Kejang sulit untuk mengontrol atau memiliki
fitur fokus.• Ada menyertai tanda-tanda neurologis.• Ada gangguan neurologis progresif.
SE Complication
• CNS– Cerebral hypoxia, edema, hemorrhage
• CVS– MI, arrhythmia, cardiac arrest
• Respiratory system– Aspiratory pneumonia, Pulmonary hypertension,
pulmonary emboli• Metabolic changes
– Dehydration, electrolyte changes, acute tubular necrosis
Prognosis• Prognosis tergantung pada:?-Yang mendasari etiologi
kejang kejang dapat secara efektif dihentikan sebelum kerusakan neurologis ireversibel telah terjadi-apakah?.
• Angka kematian keseluruhan adalah sekitar 20% bagi mereka yang mencapai status epilepticus (SE) .
• Bahwa angka kematian tertinggi untuk mereka yang berusia lebih 75 tahun, neoplastik, dan patologi vaskular.
• Sebanyak 50% dari pasien dengan epilepsi akan mengalami kejang berulang meskipun terapi medis. Sebanyak 25% pasien dengan kejang umum pertama kali akan memiliki kekambuhan dalam waktu 2 tahun.