I. Definition.
Multiple consecutive seizures with 2 seizures during which the patient does not regain consciousness; epileptic seizures lasting more than 30 minutes.
II. Clinical manifestations and classification.
1, generalized convulsive status epilepticus: including generalized tonic-clonic status epilepticus, tonic status epilepticus, clonic status epilepticus and myoclonic status epilepticus. The most important and common one is generalized tonic-clonic status epilepticus. The clinical manifestations are recurrent generalized tonic-clonic seizures, unconsciousness during two seizures, or one seizure lasting for more than 30 minutes. The seizures are characterized by generalized convulsions and respiratory arrest, which can cause cerebral hypoxia, congestion, edema, and in severe cases, brain herniation or even death. The death rate and disability rate are high.
2, generalized non-convulsive epilepsy persistent status: there are mainly petit mal seizures persistent status. It is a persistent disorder of consciousness of different degrees for more than 30 minutes, mostly seen in children. The milder ones may appear to be “normal”, or just “lack of efficiency” in work or study, mostly showing drowsiness, unresponsiveness, reduced spontaneous movements and speech, and the more severe ones are in a comatose state. It may be accompanied by myoclonus or automatism. The EEG shows a wide range of 3Hz spike and slow wave integrated sustained issuance.
3, simple partial seizure persistence: mainly simple partial motor seizure status, manifested as a part of the body continued non-stop convulsions for hours, days or even months, but no impairment of consciousness, can develop into secondary generalized epilepsy, the seizure termination may leave the seizure site of paralysis.
4, complex partial seizure persistence: manifested as a prolonged state of confusion or only vague memory, may be accompanied by automaticity, lasting for days or months. Sometimes it can appear immediately after a generalized tonic-clonic seizure and can be easily misdiagnosed as generalized tonic-clonic epilepsy persistence. The EEG shows limited epileptiform discharges in the temporal lobe or temporal frontal lobe.
5, myoclonic epilepsy persistent status epilepticus: manifested as continuous myoclonic seizures for several hours or days, often without impaired consciousness, sometimes with impaired consciousness.
6, hemiplegic status epilepticus: mostly seen in infants and young children, manifested as hemiplegic clonic convulsions, often accompanied by ipsilateral hemiplegia, known as hemiplegic-hemiplegic syndrome.
7. Neonatal persistent status epilepticus: its seizure form is often different from that of adults. The clinical manifestations are extremely atypical, mostly with mild twitching and strange tonic movements of the limbs. The seizure form is not fixed, often shifting from one limb or one muscle group to another limb or another muscle group, or presenting hemiplegic convulsive seizures. The seizures are characterized by pauses in breathing and unconsciousness. EEG changes also have specificity, showing 1~4Hz slow waves, interspersed spike waves, or 2~6Hz rhythmic spike and slow wave synthesis, δ waves in tonic seizures, and spike and sharp waves issued in clonic seizures.
III. Etiology.
The etiology of persistent status epilepticus is often closely related to or identical to the etiology of epilepsy itself, and therefore both are described simultaneously.
1. Etiology of epilepsy.
(1) Primary (idiopathic): may be closely related to genetic factors (about 50% of the etiology is unknown)
(2) Secondary (symptomatic): mainly includes congenital malformations, prenatal and perinatal diseases, sequelae of febrile convulsions, craniocerebral injury, infection, poisoning, intracranial tumors, cerebrovascular disease, nutrition, metabolic diseases and degenerative diseases.
2. Etiology of persistent status epilepticus.
(1) Patients who have been diagnosed with epilepsy, discontinued or reduced medication, metabolic disorders, and aggravation of underlying diseases. (1) Patients with diagnosed epilepsy, discontinuation or reduction of medication, metabolic disorders, and aggravation of underlying diseases.
(2) Those without previous epilepsy are often caused by acute encephalopathy, most commonly traumatic brain injury, cerebrovascular disease, brain tumors, acute poisoning and metabolic diseases, hypoxia, and fever.
IV. Pathophysiological changes.
Significant pathophysiological changes can occur during SE, and these changes may cause damage to peripheral organs or multiple systems, increasing the disability rate of SE and even mortality.
1. Blood pressure and heart rate.
A full-blown attack causes changes in systemic arterial blood pressure in both animals and humans, with blood pressure and heart rate reaching their peak within 1 minute. Blood pressure gradually returns to baseline levels after 1 hour, while heart rate is only rarely reduced. As SE progresses, blood pressure drops below baseline levels, at which point there may be a risk of cerebral hypoperfusion.
2. Acidosis.
Acidosis is an obvious concomitant symptom of SE. This convulsion-induced acidosis is significantly reduced with the use of inotropic agents, suggesting that anaerobic metabolism of muscles producing large amounts of lactic acid is its main cause.
3. Hypoxemia.
The arterial partial pressure of oxygen is significantly reduced in SE. There is actually evidence that the hypoxia present in convulsions may have a neuroprotective effect. It is thought that the protective effect of hypoxia is due to a reduction in the intensity of the convulsive episode.
4. Effects on respiratory function.
SE affects not only the flow of gas in and out of the lungs, but also the flow of fluid through the capillary bed. The main clinical abnormality that appears at this time is postictal pulmonary edema.
5. Effects on body temperature.
Hyperthermia is a major component of convulsive SE. There are two components of elevated body temperature during seizures: extreme muscle contraction until depletion results and driven by central sympathetic.
6. Leukocytosis.
It is common to see elevated peripheral leukocyte counts in SE, often reaching 12,700 to 28,800/mm3.
7, Acute disability rate and mortality.
SE has a fairly high rate of disability and mortality. Recent studies have confirmed a mortality rate of 8% to 32%. Some common sequelae of SE include: mental retardation, persistent neurological deficits, and recurrent convulsive episodes. Neuropathological studies have shown that the prolonged electrical activity of CNS (more than 60 minutes) causes irreversible neuronal damage.
V. Treatment principles.
1, accurate diagnosis and typing: select the appropriate antiepileptic drugs to rapidly terminate the seizures, and it is advisable to use drugs with rapid effect, strong action and low adverse effects for intravenous administration.
2. Perform cardiac monitoring, maintain stable vital signs, and prevent and treat complications.
3. Etiological treatment: actively search for the cause, treat the primary disease and avoid triggering factors.
4. Prevention of recurrence: After seizure control, appropriate antiepileptic drugs should be given for maintenance and systematic antiepileptic drug therapy to prevent recurrence.
6. chronological development of treatment procedures.
1. 0 minutes: Observe the seizure and ask for medical history to make a diagnosis. Do EEG as soon as possible, but should not wait for EEG delay.
2. 5 minutes: Establish intravenous access, use saline (glucose can precipitate phenytoin sodium) to do routine blood and biochemical tests. Measure drug blood concentration. Do rapid blood glucose, if there is hypoglycemia. Give vitamin B1 100mg by static push, followed by 50% glucose intravenous injection.
3. 10 minutes: Adults give Valium 10mg intravenously (push rate <2mg/min), not intramuscularly. If ineffective, repeat once in 10-20 minutes until the seizure is terminated or the total dose reaches 20mg.
4. 25 minutes: If the seizure does not stop, start phenytoin sodium (20mg/kg) intravenously (rate <50mg/min). Monitor blood pressure and electrocardiogram. If the seizure still does not stop, add 5mg/kg, and if necessary, add another 5mg/kg until the maximum dose is 30mg/kg.
5.60 minutes: If the seizure still does not stop, after tracheal intubation, administer sodium phenobarbital intravenously (20mg/kg, <100mg/min).
6.90 minutes: If the seizure is still not terminated, use barbiturate coma (anesthesia), give more sodium phenobarbital or pentobarbital (5~15mg/kg) slowly intravenously, maintenance amount 0.5~5mg/kg/h), and monitor blood pressure, ECG and respiratory function at the same time.
Seven, commonly used drug therapy methods.
1, Valium plus Valium therapy: Valium is preferred for adult patients, 10~20mg intravenous injection, not inotropic injection, injection rate <2mg/min, if the effect is not obvious, 10~20min later can be repeated once. If effective, Valium 80~100mg will be added to 500ml of saline and maintained by slow intravenous infusion for 12 hours. If it is ineffective, it is necessary to switch to other drugs.
2, phenytoin sodium therapy: phenytoin sodium 14-18mg/(kg.times) into saline 500ml intravenous drip, the speed does not exceed 50mg/min, the elderly and cardiopulmonary disease do not exceed 5-10mg/min, because of its 70-95% and plasma protein binding, only about 10% has antiepileptic effect, high dose can lead to arrhythmia, blood pressure High dose can lead to arrhythmia, blood pressure reduction and heart block, so heart rate and blood pressure should be monitored. After the seizure has stopped, it should be given orally or intranasally. The advantage is that it does not affect consciousness.
3, Valium plus phenytoin sodium therapy: as phenytoin sodium brain to reach the peak of 15-30min, so you can first use Valium sedation, after the effective sedation of Valium, followed by phenytoin sodium intravenous drip, the specific method as before.
4, Depakene therapy: for patients who have not been treated with sodium valproate, 5-10mg/(kg.times) in 3-5min by sedation, followed by 1-1.5mg (kg.h) for maintenance, not more than 3 d, and later changed to oral. For patients who have used sodium valproate, 7mg/(kg.times) in 3-5min by sedation, and later maintained with 0.5-1mg (kg.h). Active liver disease, familial liver disease, and sodium valproate allergy are prohibited.
5, chloral hydrate therapy: 10% chloral hydrate 20-30ml nasal feeding or add equal amount of saline retention enema, this drug is safer.