Status Epilepticus

67,108 views 24 slides Feb 23, 2017
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About This Presentation

Useful explanation regarding SE


Slide Content

Dr. Kamran Khan PG Medicine Year 1 STATUS EPILEPTICUS

DEFINITIONS A condition characterized by epileptic seizures that are sufficiently prolonged or repeated at sufficiently brief intervals so as to produce and unvarying and enduring epileptic condition. (WHO 1973) A seizure that persists for a sufficient length of time or is repeated frequently enough that recovery between attack doesn’t occur. (ILAE Commission 2001)

Status epilepticus is a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms, which lead to abnormally, prolonged seizures (after time point t 1 ). It is a condition, which can have long-term consequences (after time point t 2 ), including neuronal death, neuronal injury, and alteration of neuronal networks, depending on the type and duration of seizures . (ILAE 2015)

CLASSIFICATION OF STATUS EPILEPTICUS Generalized convulsive status epilepticus Tonic Clonic Status epilepticus Clonic Status epilepticus Tonic Status epilepticus Myoclonic Status epilepticus Generalized non convulsive Status epilepticus Absence Status epilepticus

CLASSIFICATION OF STATUS EPILEPTICUS Simple partial (focal) Status epilepticus Complex partial Status epilepticus

PATHOPHYSIOLOGY On a neurochemical level, seizures are sustained by excess excitation and reduced inhibition. Glutamate is the most common excitatory neurotransmitter and the NMDA (N-methyl-D-aspartate) receptor subtype is involved.

Gamma- aminobutyric acid (GABA) is the most common inhibitory neurotransmitter. Failure of inhibitory processes is increasingly thought to be the major mechanism leading to status epilepticus . However, changes in gene expression that are induced by SE result in alterations in the number or subunit composition of ion channels, receptors, cell metabolism, and neuronal connectivity.

Neuronal death probably results from the inability to handle large increases in intracellular calcium brought about by prolonged exposure to excitatory neurotransmitters. More prolong the status, the poorer the prognosis

Neuronal Death occurs after 30 mins of continuous seizures. High mortality related to Rhabdomyolysis Aspiration Metabolic/lactic acidosis Respiratory failure Neurogenic pulmonary edema Myocardial injury

ETIOLOGY In adults, the most common precipitant was cerebrovascular disease (25%), whereas this factor caused only 3% of pediatric cases . SE vary significantly with age. DeLorenzo et al reported that in patients younger than 16 years, the most common cause was fever and/or infection (36%); in contrast, this accounted for only 5% of SE in adults.    Only 25% of people who experience seizures or status epilepticus have  epilepsy .

Stroke (remote or acute) Hypoxic injury Tumor Subarachnoid hemorrhage Head trauma Drugs eg , cocaine,  theophylline , isoniazid (INH) may cause seizures and is unique in having a specific antidote, pyridoxine (vitamin B-6 ), Flouroquinolones , Flumazenil

Alcohol withdrawal Electrolyte abnormalities ( eg ,  hyponatremia ,  hypernatremia,hypoglycemia , hyperglycemia, hypocalcemia,hepatic encephalopathy, Uremia) Neoplasms CNS infections ( eg , meningitis, brain abscess, encephalitis) Toxins, notably sympathomimetics

PRESENTATION The event usually begins with a series of generalized tonic, clonic , or tonic- clonic seizures that often are dramatic . If the condition is not treated or is treated inadequately, SE persists, and the motor manifestations become less dramatic than before. Eventually, only subtle movements ( eg , nystagmoid jerks of the eyes or twitching of the shoulder) may be seen—that is, subtle SE. If SE continues, all motor activity may stop, though EEG seizures persist ( ie , electrical generalized convulsive SE).

 Among patients with established epilepsy, noncompliance with medications is the rule rather than the exception. In roughly one third of cases, status epilepticus is the initial presentation of a seizure disorder.

simple partial status epilepticus By clinical history, nonmotor simple partial SE involves subjective sensory disturbances, including the following: Focal or unilateral paresthesias or numbness Focal visual changes, usually characterized by flashing lights Focal visual obscuration or focal colorful hallucinations Olfactory or gustatory hallucinations Atypical rising abdominal sensations

Complex partial status epilepticus Complex partial SE often begins with a history of recurrent or prolonged simple partial seizures, or it may follow or precede a generalized convulsive seizure. Patients are often confused and have variable responsiveness. Memory of the event is usually impaired. Behavior may fluctuate or be bizarre. Many patients have clinical automatisms, as with typical complex partial seizures, including repetitive lip-smacking, fumbling, or swallowing movements. Subtle nystagmus may be observed.

EXAMINATION FINDINGS Needle track marks might suggest SE secondary to the use of illicit, or street, drugs Papilledema , a sign of increased intracranial pressure, suggests a possible mass lesion or brain infection Associated injuries that may be present in patients with seizures include tongue lacerations (typically lateral), shoulder dislocations, head trauma, and facial trauma.

DIFFERENTIAL DIAGNOSES Encephalitis Heatstroke Hypernatremia in Emergency Medicine Hyperosmolar Hyperglycemic Nonketotic Coma Hypocalcemia in Emergency Medicine Hypoglycemia Hyponatremia Medication-Induced Dystonic Reactions Neuroleptic Malignant Syndrome Neurological Manifestations of Uremic Encephalopathy Withdrawal Syndromes

Laboratory Studies Laboratory studies that should be obtained on an emergency basis include the following: Electrolytes Calcium Magnesium Glucose Complete blood count Renal function tests Toxicologic screening Anticonvulsant levels Liver function tests

EEG ABGs CT Scan MRI Chest Radiography Lumbar Puncture

MANAGEMENT In 2016, the American Epilepsy Society (AES) issued new guidelines for the treatment of SE . In the stabilization phase, standard first-aid for seizures should be initiated. In the initial therapy phase, a benzodiazepine (specifically IM midazolam, IV lorazepam , or IV diazepam) is recommended as initial therapy. In the second phase, options include IV fosphenytoin , valproic acid, or levetiracetam . If none of these is available, IV phenobarbital is a reasonable alternative. In the third phase, if a patient experiences 40+ minutes of seizure activity, treatment considerations should include repeating second-line therapy or anesthetic doses of thiopental, midazolam, pentobarbital, or propofol .