Treatment of status epilepticus in St. Petersburg: help and relief of symptoms

Status epilepticus is a condition in which epileptic seizures are repeated or continuous over a fairly long period of time (about 30 minutes). The patient does not have time to recover from the previous seizure before the next one overtakes him. The patient's consciousness is unclear, breathing is difficult, and signs of a coma are observed.

Causes of status epilepticus

The action of medications taken by a patient with epilepsy is aimed at inhibiting seizures. If the patient independently refuses medications prescribed for treatment, then this action can trigger the occurrence of ES.

Epistatus can also occur, for example, with brain pathologies:

Malignant neoplasms;
Withdrawal syndrome;
Infections, intoxications, hematomas and encephalopathy;
Peripheral circulation disorders.

Status epilepticus can also occur in patients with diabetes. Diabetes is scary because of its complications, including ES.

Types and stages of status epilepticus

The variability and diversity of types of epileptic seizures is the main basis for the formation and identification of forms of epileptic seizures, characterized by general signs of the clinical picture of the disease. They are divided into two groups: non-convulsive and convulsive. Classifying the types of ES, we can distinguish:

Generalized non-convulsive seizure. In this case, a short-term loss of consciousness is observed. The patient seems to freeze with interrupted activities (eating, talking, writing...), or thinking about something. In this case, the eyes are focused on one point, the face becomes pale, and the connection with the outside world is interrupted. The absence seizure stops as suddenly as it started.
Incompletely generalized status epilepticus is characterized by muscle cramps, the patient completely loses consciousness, cardiovascular activity is disrupted, and breathing becomes unstable.
Tonic SE is typical for children of different ages with rare and severe forms of epilepsy.
Clonic ES, accompanied by high fever and convulsions in children and infants.
Myoclonic ES is expressed in episodic twitching of muscle tissue.

Epileptic seizures are characterized by short duration. Usually a seizure lasts several seconds, or several tens of seconds, less often - a minute. After status epilepticus, relief occurs spontaneously, without outside intervention. Therefore, they are called self-limited epileptic seizures. Serial attacks following one after another are often encountered.

In medicine, each stage of epistatus, which is a complication of epileptic syndrome, has its own name:

The duration of the pre-status stage can last from 1 to 10 minutes;
The initial stage is characterized by the duration of the attack from 10 to 30 minutes;
Expanded - from 30 to 60 minutes;
The stage, which lasts more than an hour, is called refractory.

Epistatus is a state of a person when he does not regain consciousness during alternating epileptic seizures. Before one attack has finished, the next one begins. The second variant of epistatus is no less dangerous, and is a seizure lasting more than 30 minutes.

Features of the condition in children

Very often, epistatus that occurs in children is a sign of the onset of epilepsy, but it happens that convulsive attacks appear already in the later stages of the course of this disease.

In newborns, a seizure occurs with partial loss of consciousness, while the reaction to external stimuli remains intact.

Generalized SE can manifest itself as tonic-clonic, clonic, myoclonic convulsions.

In nonconvulsive SE, electroencephalography is used to detect peak-wave stupor and slow waves, which reflect a state of epileptic stupefaction. Partial ES can be simple, somatomotor, or dysphasic.

In complex partial epistatus, stable preservation of epileptic twilight of consciousness is observed.

With generalized SE, the main property of an epileptic seizure is disrupted - it does not go away on its own.

The number of attacks can reach several tens or even hundreds per day. In this case, respiratory function and hemodynamics are disrupted, metabolic processes in the brain are disrupted, and the coma state can deepen until death occurs.

Symptoms of status epilepticus

Symptoms of epistatus are expressed in circulatory disorders, disturbances of consciousness (the person “switches off”), and disruption of the respiratory system. Symptoms of status epilepticus are a consequence of previous seizures from which the patient does not recover.

Epistatus can be characterized by a frequency of attacks up to 20 per hour. The patient does not regain consciousness at the onset of the subsequent seizure; his condition can be described as numbness bordering on coma.

The comatose state worsens in direct proportion to the duration. Tonic spasms affect the muscles of the back, arms and legs. High blood pressure suddenly drops. Increased reflexivity is also unexpectedly replaced by a complete lack of reaction.

Respiratory and circulatory disorders become obvious. When the seizures disappear, epileptic prostration occurs.

The duration of the epistatus is at least 30 minutes. Usually, as expected, we draw a line between this condition and episodic seizures with partial restoration of physiology and consciousness (full or partial).

There are two phases that characterize epileptic convulsive status with the following features:

Compensatory changes in the circulatory and metabolic system, expressed in high blood pressure, vomiting and nausea, uncontrolled urination and defecation.
Coming in about half an hour/hour, it is a maladaptation of compensatory changes, which is expressed in acute renal failure (and liver failure), a sharp decrease in pressure, disruption of the respiratory system, and arrhythmia.

Epistatus, the course of which is not accompanied by convulsions, is characterized by complete immobility of the patient and a feeling of detachment. Usually the patient lies with his mouth open, his blank gaze does not express anything.

Introduction

Doctors of various specialties deal with status epilepticus: neurologists, epileptologists, neurosurgeons, psychiatrists, general anesthesiologists and resuscitators, neuroreanimatologists, psychoreanimatologists, sometimes even obstetricians and infectious disease specialists.
There is no clear attribution of this condition to any medical discipline. Most often, the question of who will treat such a patient is determined by random reasons (for example, distance to the nearest medical facility). In this brief guide, attention is focused on the treatment of those patients who come to the attention of psychoreanimatology. The material is based on twenty years of experience in the intensive care unit (Moscow Regional Center for Psychoreanimatology) at the Moscow Regional Psychiatric Hospital No. 23. According to this unit, patients with status epilepticus make up no more than 3% of the total flow of emergency patients admitted there, but the severity of their condition, requiring intense and dramatic work of staff, are in one of the first places. These recommendations do not constitute exhaustive rules to which there is nothing to add. Each patient can, with his or her individuality, force us to make adjustments to treatment. Each unit of psychoreanimatology has its own differences in traditions, approaches and equipment. Therefore, the material presented here is best used as a story from experienced people about what and in what sequence they usually do when treating epistatus - a story that should in no way hinder the creativity of a practicing doctor.

Emergency care for status epilepticus

First aid for status epilepticus, before the arrival of doctors, is the need to protect the patient from receiving mechanical injuries. There is no need to crowd around the patient, blocking free access to clean air.

Our recommendations:

Place the patient on a non-traumatic surface with something soft (jacket, sweater) under his head;
To avoid choking on saliva, carefully turn your head to the side;
Remove the tie, belt, unbutton the collar so that nothing interferes with the patient’s ability to breathe freely;
Remove all sharp and traumatic objects located nearby;
If your teeth are clenched, there is no need to unclench them;
If your mouth is open, place any soft cloth between your teeth.

You should not place sharp, metal or other objects between your teeth that could cause injury to an unconscious person.

Emergency care for status epilepticus should be provided very carefully. You should not hold the patient too tightly so as not to damage his bones (in this condition the likelihood of fractures is very high).

Complications of status epilepticus

Epistatus is characterized by irreparable consequences. Statistics. With symptomatic ES, mortality is 30–50%. With ES in patients with epilepsy - 5%.

If ES lasts more than an hour, then patients will face serious consequences:

Diffuse saturation of brain tissue with fluid, called cerebral edema and accompanied by oxygen starvation;
Critically low blood pressure;
Excessive levels of lactic acid, called lactic acidosis;
Violation of water-salt balance;
For children, characteristic signs are delays in the development and formation of the psyche, which can lead to mental retardation.

Non-convulsive epistatus is considered less dangerous compared to generalized epistatus. Nevertheless, complications of status epilepticus often find expression in disturbances of perception, attitude, thinking, memory, and understanding.

NSICU.RU neurosurgical intensive care unit website of the intensive care unit of the N.N. Research Institute Burdenko

Introduction

Status epilepticus is a serious complication of the postoperative period in patients with neurosurgical pathology, significantly worsening the prognosis of the underlying disease and increasing the risk of an unfavorable outcome. Brain tissue damaged during neurosurgical intervention or severe traumatic brain injury can cause the formation of a focus of pathological electrical activity of brain cells, such as usually manifested by various types of convulsive seizures. The frequency of this complication during neurosurgical interventions reaches 5% - 20%, depending on the location of the tumor (7,15,16). The leading ones in this regard are cortical or meningeal lesions, and the main manifestation of this condition is partial or generalized epileptic seizures. However, in a certain situation, pathological electrical activity of brain cells can occur without characteristic clinical manifestations, but is realized by a non-convulsive attack or even non-convulsive status epilepticus (45,50,53,71). An asymptomatic (non-convulsive) epileptic attack, and in particular status epilepticus, can cause an increase in general cerebral and focal neurological symptoms, up to the development of a coma. In such a clinical situation, identifying the cause of the coma is difficult. Delayed administration of anticonvulsants is also likely, which can lead to the formation of a persistent epileptogenic focus and severe secondary brain damage as a result of neuronal death. The concept of nonconvulsive status epilepticus (NSE) was first introduced by Celesia in 1976 (17). The purpose of this work is to summarize the main clinical characteristics of BES and attract the attention of clinicians to the serious problem of diagnosis and treatment of BES.

Definition

The most accurate definition of BES, proposed by the Epilepsy Reseach Foundation Workshop, includes the following provisions: Clinically detectable changes in the level of consciousness or other equivalents: changes in the position of the eyeballs, nystagmus, autonomic manifestations (hyperhidrosis, tachycardia, changes in skin color). The presence of characteristic spike manifestations detected during EEG monitoring. The positive effect of anticonvulsant therapy in the form of normalization of the EEG and the disappearance of clinical symptoms. BES has attracted increasing attention in recent years, since some of its aspects have been poorly developed, in particular in various acute cerebral lesions, when BES significantly worsens forecast. In such a situation, based on the clinical picture of the disease, it is usually difficult to suspect BES: EEG data are crucial for diagnosis. Frequency of occurrence. The frequency of occurrence of BES varies according to various authors and ranges from 7.5 to 65 and even 89% in the studied series of patients (7,25,38,44,45,59,61,67,70). This depends to a large extent on the diagnostic methods used and on the patient population. Among patients with acute cerebral injuries, the incidence of BES is much higher compared to patients with other pathologies. In patients with brain tumors, after neurosurgical interventions, BES occurs in 20% of cases of all status epilepticus (7). In patients in a septic state who are in coma, non-convulsive seizures were detected in 10% of cases (6). In victims with severe TBI, BES was detected in 3% of patients (8). With subarachnoid hemorrhage, BES was diagnosed in 8% of cases (9,20). The development of BES after subarachnoid hemorrhage in most cases led to an unfavorable outcome (7,20). With parenchymal hemorrhage, the development of BES was combined with an increase in displacement of the midline structures and clinical deterioration (70). The main reason for unfavorable patient outcomes is late diagnosis and initiation of therapy for BES caused by acute cerebral damage. The pattern of prognosis and outcomes for BES is the same as for convulsive ES: the longer the status, the worse the prognosis. J. Yong et al. (71) based on multivariate regression analysis, they found that the development of BES in acute brain injury increases the risk of death by 46%. ###Etiology The cause of BES is a number of very different clinical conditions, manipulations and the use of pharmacological drugs: surgery of skull base tumors, pneumaticcephaly (7), the use of third generation cephalosporins (1,28,48), theophylline (55), lithium salts ( 41), phosphamide (42), tiagabine (33,36,43), carbamazepine (50), traumatic brain injury (8), chronic hemo- (32) and peritoneal dialysis (18), Creutzfeldt-Jakob disease (19 ), spontaneous subarachnoid and intraventricular hemorrhages [25,45], sclerosing encephalitis [10], abnormalities of brain development [1], herpetic encephalitis [29], necrotizing leukoencephalitis [26], consequences of electroconvulsive therapy [57] and temporal lobectomy [16, 22], and finally, withdrawal of benzodiazepines [56]. Perhaps the list of these reasons for the development of NES is not even complete, but even in its current form it is impressive and suggests the nonspecificity of NES.

Pathogenesis

Epileptiform activity leads to an unconscious state as a result of excessive excitation of cerebral activity, corresponding to an increased concentration of excitatory neurotransmitters (glutamate, aspartate) and a decrease in the content of inhibitory neurotransmitters (GABA) in the brain. Local cortical hyperperfusion was detected in 78% of patients in BES according to perfusion CT ( PCT) (30) and this was consistent with transient clinical symptoms and EEG changes, but was most likely a consequence of BES rather than its underlying cause.

Clinic

Clinical manifestations of BES include depression of consciousness, the degree of which may vary, agitation, abnormal movements of the eyeballs (including eyeball deviations and nystagmus), aphasia, and pretentious posturing of the limbs. Transient severe anterograde amnesia has been described in patients with BES after temporal lobectomy (22). In a patient with frontal BES, clinical symptoms began with somatic hallucinations (66). Patients with BES demonstrated a wide variety of clinical symptoms, ranging from subtle memory loss and unusual behavior to acute psychosis and coma (40,62). This diversity has determined the lack of a generally accepted classification of clinical manifestations of nonconvulsive epilepsy at present (37).

Classification of BES

BES is divided (52-58,64,81) into: Generalized status:

A). Typical absence seizure;
B). Atypical absence syndrome;
IN). Late absence status

Partial status:

A). Simple partial;
B). Complex partial;
IN). Silent (hidden) non-convulsive status.

Below we provide a more detailed clinical description of the various variants of BES.

Typical absence status is characterized by varying degrees of impairment of consciousness, decreased spontaneous activity, slowed speech, hallucinations, and rhythmic twitching of the eyelids. It usually occurs suddenly and lasts from several minutes to weeks. Typical absence status can be started or completed with the help of generalized convulsive status, provoked by tachypnea, hyperventilation, and fever. A non-seizure EEG appears to be normal baseline activity. An EEG study during BES reveals a 3 Hz spike - wave activity, which begins to gradually slow down over time. Atypical absence status. Additional clinical manifestations of this variant of BES are primarily eyelid fluttering and grimacing. Patients often feel their thoughts slow down. A risk factor for the development of this variant of BES is Lennox-Gastaut syndrome (pharmaco-resistant symptomatic generalized epilepsy) (51). The provoking factor is the prescription of carbamazepine, phenytoin, vigabatrin for idiopathic generalized epilepsy. Sudden EEG is characterized by continued generalized slowing. An EEG study during BES reveals a 3 Hz spike-wave activity. Late absence status. This variant of generalized BES is characterized by prolonged episodes of confusion in elderly patients, ranging from mild amnesia to stupor. The typical age of manifestation of this variant of BES is 6-7 decades of life. In this case, mental illnesses are often misdiagnosed. Interestingly, 50% of patients with this variant of BES had idiopathic generalized epilepsy in adolescence. The provoking factor may be intoxication with psychotropic drugs. An EEG study during BES reveals frequent, irregularly shaped 0.5 – 4 Hz spike wave activity (51). Simple partial status. This variant of BES proceeds without motor manifestations in only 5–10% of cases. At the same time, consciousness is preserved; sometimes patients’ complaints are difficult to confirm with an objective examination. There may be auditory, aphasic, sensory, gustatory, olfactory, mental, autonomic, visual symptoms and altered behavior. This variant of BES can develop against the background of long-standing focal epilepsy. An EEG study during BES reveals regional spikes and spike-wave complexes, with a mesiotemporal focus, often negative (51). Complex partial status. This variant of BES is characterized by depression of consciousness, oral and/or manual automatisms. A common clinical manifestation is a frozen gaze with an aura. Clinical symptoms fluctuate with a gradual increase in focal symptoms. Temporal and frontal attacks often occur. An EEG study during BES reveals regional spikes, spike-waves, rhythmic delta activity, often bilateral patterns (40,51). A silent (hidden) non-convulsive status develops in patients in a coma. This variant is characterized by “hidden” motor manifestations (twitching of the eyelids, deviation of the eyeballs). The EEG shows continued electrographic seizure activity. It is characteristic that pathological patterns in this form of BES are not sensitive to photostimulation.

Diagnosis of BES

The main diagnostic criteria for BES are various options for decreased levels of wakefulness and disturbances of consciousness, accompanied by epileptiform changes on the EEG. According to a study by Al-Mefty et al., (7) which included 7 patients operated on for tumors of the base of the skull and in the postoperative period in a non-convulsive state, the main clinical manifestation of this condition was coma. Upon examination, there were no focal neurological symptoms and data from additional methods (CT, MRI, MR angiography, TCD, laboratory diagnostic methods) did not explain the causes of the coma. And only video-EEG monitoring carried out within 24 hours revealed pathological seizure activity in the form of 1-3 Hz slow wave activity. The EEG picture in BES against the background of acute cerebral lesions looks like this: epileptiform discharges are superimposed on a deformed and normal slow-motion background. As for the EEG epileptiform pattern, it is represented by virtually unilateral hemispheric discharges, which can be accentuated according to the lesion and have the character of acute-slow wave complexes, with a frequency of approximately 1-1.5 Hz. (11,40,44). Previously, a similar EEG pattern was described as hemispheric lateralized epileptiform disorders (PLEDS), but was regarded as a phenomenon and not a manifestation of BES. However, in 12-24% of patients, generalized discharges may also occur, which is prognostically unfavorable. Therefore, the diagnosis of BES requires a high degree of clinical alertness, especially in patients with a decreased level of wakefulness in the neurointensive care unit and can only be confirmed using EEG monitoring.

Differential diagnosis

Differential diagnosis includes encephalitis, migraine with aura, post-traumatic amnesia, post-attack confusion, mental illness, intoxication with various substances, and global transient amnesia (40,44).

Therapy

Therapy for BES is not fundamentally different from the treatment of convulsive status epilepticus (48,51). Initial therapy for BES is preferable with intravenous lorazepam at a dose of 0.1 mg/kg. You can start with low doses of lorazepam - 4 mg and repeat this dose if the status continues according to EEG monitoring. A single 4 mg dose of lorazepam was effective in 80% of patients with status epilepticus. If IV lorazepam is not available, IV diazepam 10 mg should be given instead, followed immediately by phenytoin 18 mg/kg or an equivalent dose of fosphenytoin. Phenytoin should be administered as a continuous infusion at a rate of 50 mg/min. Treatment of resistant generalized convulsive and non-convulsive status epilepticus is recommended to begin immediately with an infusion of midazolam (0.2 mg/kg IV bolus, followed by 0.1-0.4 mg /kg/hour IV) or propofol (2 - 3 mg/kg IV bolus, followed by 1 - 2 mg/kg, and then 5 - 10 mg/kg/hour IV) or thiopental (3 - 5 mg/kg bolus, then further bolus of 1 - 2 mg/kg every 2 - 3 minutes until attacks stop, then continued infusion at a rate of 3 - 7 mg/kg/hour).

The effectiveness of therapy is confirmed by EEG monitoring; burst suppression is required to be achieved, which must be maintained for 24 hours. Therapy for refractory complex partial status epilepticus includes: Pentobarbital: at the beginning, an IV bolus of 20 mg/kg or 50 mg /min; Valproic acid: IV bolus of 25 – 45 mg/kg IV or at a rate of 6 mg/kg/min; Levetiracetam: IV bolus 1000 – 3000 mg over 15 minutes. Currently, due to the lack of comparative studies, it is not entirely clear which of these drugs is more effective.

Conclusion

Thus, BES is a serious, life-threatening condition that can lead to coma and death. In acute brain lesions, BES complicates the underlying disease quite often on average in 20% of patients, which significantly worsens the prognosis of the disease. Due to diagnostic difficulties - the lack of specific clinical manifestations - BES often remains unrecognized and, accordingly, its therapy is ineffective. The only reliable method for diagnosing latent epileptiform activity is continuous EEG monitoring.

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Relief of status epilepticus. Drugs

We usually relieve status epilepticus using a number of measures. At the very first stage, we provide the patient with the opportunity to breathe freely. This is followed by oxygen treatment - oxygen therapy.

We administer Diazepam intravenously, not exceeding the daily dose, which is 40 mg. A serious side effect of this medication is insufficient pulmonary ventilation.

Our doctors carry out further treatment of status epilepticus using Depakine, Diazepam, Feniton and other drugs, the choice of which depends on the stage of SE. Like all medications, medications administered to a patient for ES have side effects.

The most common of which are:

A sharp decrease in potassium in the body;
Sclerosis of veins;
Acute toxic hepatitis;
A sharp decrease in blood pressure, accompanied by dizziness, drowsiness, and often visual disturbances.

If the stage is advanced, then we treat ES using the drugs Phenobarbital, Lorazepam and others.

The measures carried out by our doctors during the refractory stage of epistatus boil down to intubation, artificial ventilation of the lungs, and correction of the water-salt balance of the body.

In case of critical condition of the patient, we provide barbiturate anesthesia. Over 20 seconds, the doctor administers 100 to 250 mg of sodium thiopental as an intravenous injection. The duration of anesthesia can range from 12 hours to a whole day.

We administer Dexamethasone and Mannitol by injection to prevent brain swelling. Our doctors use drugs such as Magnesia and others with similar effects to restore metabolism and proper circulation of cerebrospinal fluid.

Worth a try

There is evidence that lorazepam is more effective than diazepam in epistatus. A parenteral dosage form of valproic acid (Depakine) has appeared, specifically intended for the treatment of epistatus.

Work has been carried out indicating the prospects of using hemosorption in the treatment of severe forms of epistatus.

There are observations that intravenous laser irradiation of blood increases the effectiveness of other measures for epistatus.

There is evidence of the effectiveness of electroconvulsive therapy for intractable forms of epistatus.