Treatment of mixed crisis in myasthenia gravis. Treatment of acute conditions in myasthenia gravis

Myasthenic crisis is characterized by life-threatening weakness of the respiratory and bulbar muscles, leading to respiratory arrest.

Treatment. During a crisis, the first step is to ensure patency respiratory tract, remove mucus from the throat using an electric suction or using a body position with the head down. Then it is necessary to carry out mechanical ventilation by everyone accessible ways. The use of masks during mechanical ventilation in patients is not recommended due to existing dysphagia. To quickly stop the crisis, proserin is administered - 0.5-1.5 mg (1-3 ml of 0.05% solution) intravenously with preliminary administration of 0.6 mg of atropine (proserin administered intravenously can cause cardiac arrest), after 15 minutes 0.5 mg of proserine is administered subcutaneously. It is possible to administer 60 mg of neostigmine (proserine) into the endotracheal tube or 2.5 mg intramuscularly. Throughout critical period Airway drainage is mandatory. As additional help, prednisolone 90-120 mg per day, immunoglobulin 0.4 mg per day, cardiotonic and symptomatic drugs are used.

To remove autoantibodies to acetylcholine receptors from the body, plasmapheresis and hemosorption are used.

Cholinergic crisis, resulting from an overdose of anticholinesterase drugs (proserin, neostigmine, kalimin, mestinon), is manifested by miosis, excessive salivation, bronchospasm, sweating, agitation, muscle weakness, abdominal pain, diarrhea, fibrillations and fasciculations.

When this condition is diagnosed, all anticholinesterase drugs are immediately discontinued, 1-2 mg (1-2 ml of 0.1% solution) of atropine is administered subcutaneously or intravenously every hour, monitoring the diameter of the pupils. Mechanical ventilation is performed with intermittent positive pressure through an endotracheal tube, the airways are sanitized.

According to the severity of the injury, traumatic brain injury is divided into concussion, contusion and contusion with compression, which determines the tactics and scope of emergency care.

Treatment. All patients with traumatic brain injury are subject to inpatient treatment and observation. If vital functions are preserved, the patient needs to be provided with rest, cold on the head, symptomatic therapy (painkillers, sedatives, hypnotics) and correction of microcirculatory disorders (venotonics, vasoactive drugs, antiplatelet agents). It is advisable early appointment antibacterial therapy.

The use of antipsychotics and narcotic analgesics for prehospital stage and until exclusion intracranial hematoma Not recommended.

Gradual depression of consciousness is usually a sign of intracranial hematoma, compression, edema or herniation of the brain, which require surgical intervention, hemostatic therapy (intravenous 1 ml of 12.5% ​​dicinone or etamsylate solution with an interval of 6 hours) and dehydration therapy. Development psychomotor agitation, hyperthermia, comatose state requires nonspecific emergency treatment.

Under the editorship prof. A. Skoromets

"Myasthenic crisis" and other articles from the section

Some nervous diseases When doctors first visit patients, it is quite difficult to diagnose them. These diseases include myasthenia gravis. The initial complaints voiced by the patient are rapid fatigue. But after rest, muscle fatigue decreases short time recedes, and the patient feels quite normal again.

Meanwhile, myasthenia gravis is a violation of neuromuscular signal transmission from the central nervous system into the striated muscles, causing abnormal cyclic fatigue after minor exercise.

Information about the disease

There are immune-dependent myasthenia gravis and myasthenic syndromes.

The cause of the first is autoimmune diseases; the development of syndromes is caused by a combination of developmental defects: postsynaptic and presynaptic.

These defects are nothing more than disruptions in the synthesis necessary for normal life body substances and defects in the sensory organs. Due to pathologies of organic processes, the function of the thymus gland is disrupted.

Push to launch autoimmune diseases or violations biochemical processes there may be all factors in the body that weaken immune status, namely infectious diseases, stress or injury.

You can select following forms myasthenia gravis:

• ophthalmic;
• bulbar;
• generalized.

Some doctors believe that bulbar myasthenia is combined with ocular myasthenia, and how separate state it is not classified.

The first symptoms of myasthenia gravis eye-shaped- damage to the muscles of the eyelids. Patients complain of drooping eyelids, rapid eye fatigue, and image doubling.

Then signs of bulbar myasthenia appear - the pharyngeal muscles, also innervated by the cranial nerves, atrophy.

Chewing and swallowing functions are impaired, the timbre of the voice will subsequently change, and the ability to articulate speech will disappear.

With generalized myasthenia, all muscles are gradually blocked - from top to bottom - from the cervical and scapular to the dorsal, then the muscles of the extremities are affected. Drooling appears, the patient finds it difficult to care for himself or perform the simplest actions, and a feeling of weakness occurs in the limbs.

The progression of symptoms can stop at any stage.

In children, the disease does not appear before six months of age; in most cases, it is diagnosed in boys over 10 years of age. For them, it takes up to 2 years from the first symptoms – weakness of the eyelid muscles – to the next ones

In adulthood, between 20 and 40 years of age, women are more likely to get sick, and at the age of over 65, the manifestation of the disease no longer depends on gender.

Types of myasthenic syndrome

There are several myasthenic syndromes caused by genetic defects.

All of them are inherited autosomal recessively, except for the autosomal dominant syndrome, which is caused by the slow closure of immune channels:

1. Lambert-Eaton syndrome is more often diagnosed in men over 40 years of age. Its main symptoms are weakness of the proximal muscles of the extremities while sparing the bulbar and extraocular muscles. Symptoms may precede clinical manifestations, at physical activity– playing sports, muscle weakness can be stopped;
2. Congenital myasthenic syndrome. Signs – violation of symmetrical movement eyeballs and ptosis of the eyelids;
3. Symptoms: weakness of facial and skeletal muscles, sucking function is impaired;
4. Muscle hypotonia and underdevelopment of the synaptic apparatus causes a rare myasthenic syndrome, in which tendon reflexes are reduced. Typical signs conditions – asymmetry of the face, mammary glands and torso;
5. Myasthenic syndromes can be caused by taking certain drugs: D-penicillamine and antibiotics: aminoglycosides and polypeptides. Improvement occurs 6-8 months after discontinuation of the drug.

The syndrome caused by slow closure of ion channels has the following symptoms:

• weakness of the extraocular muscles;
• muscle atrophy;
• weakness in the limbs.

Treatment of each case of myasthenia gravis is carried out according to a specific algorithm.

Can be used:

• corticosteroids;
• antibiotics;
• anticholinesterol drugs;
• plasmapheresis and other types of specific therapy.

Drugs used for one form of the disease are ineffective for other forms.

Myasthenic crisis

Main symptoms myasthenic crisis– extensive dysfunction of the bulbar muscles, which includes the respiratory muscles, up to the onset of apnea.

The intensity of symptoms increases at a critical rate - brain hypoxia can occur within half an hour.

If emergency treatment is not provided for sudden myasthenic crisis, the patient will suffocate.

The reasons for the development of a crisis may be the following factors:

• stressful conditions;
• increased physical activity;
• flu;
• acute respiratory diseases;
• metabolic disorders;
• intoxication of various etiologies.

These factors provoke blocking neuromuscular conduction, cause loss of excitability in muscles and tendons.

Patients with myasthenia gravis always have a note with them on which it is written that they suffer from such and such a form of the disease and what medications are needed to provide first aid. In most cases, patients carry medications with them - these are proserin and canevin.

If among those around you who have seen a myasthenic crisis develop, there is at least 1 person who knows how to give injections, the person’s life will be saved. But you still need to call an ambulance.

Crisis treatment

The method of treating myasthenic crisis is completely determined by the patient’s condition and how quickly emergency assistance was provided by the specialist who arrived at the scene. brigade.

As quickly as possible, the victim must be placed in intensive care and connected to a ventilator - artificial respiration. Artificial ventilation should be performed for at least 24 hours.

Plasmapheresis effectively restores the condition, but may require intravenous administration immunoglobulin. Together with immunoglobulin, methylprednisolone and potassium chloride are used.

Joint treatment with immunoglobulin, potassium chloride and methylprednisolone is used if there is a history of inflammatory processes.

Antioxidants are used - lipoic acid in particular. They reduce the amount free radicals, accumulated in the blood, reduce the severity of oxidative stress in the body of patients.

Myasthenic crisis is a sudden onset critical condition, the cause of which is a violation of neuromuscular conduction like a competitive block. MK occurs in 13-27% of cases, during the first 3 years of the disease, regardless of the patient’s age, form and course of the disease. Most formidable complications- breathing difficulties in the bulbar form, risk of aspiration of food or “valvular asphyxia” due to retraction of the tongue and weakness of the epiglottis, and with spinal form- due to shutdown of the diaphragm and weakness of the intercostal muscles. In cardiac forms of crisis, acute cardiovascular failure. A cholinergic crisis is caused by an overdose of ACEP and superficially resembles a myasthenic crisis.

A reliable diagnostic test is repeated intravenous administration of 1 ml of 0.05% proserine solution: in myasthenic crisis there is a regression of symptoms, in cholinergic crisis there is an increase in symptoms.

Treatment. In case of myasthenic crisis, treatment begins with subcutaneous or intravenous administration of 2 ml of 0.05% proserin solution 3 times every 30 minutes (or 2 times every 45 minutes 3 ml). Lack of effect is an indication for mechanical ventilation. Mechanical ventilation is also indicated for tachypnea - more than 35 breaths per minute, a decrease in vital capacity by 25%, an increase in physiological dead space and with hypoxemia combined with hypercapnia. If the need for mechanical ventilation persists for more than a week, a tracheostomy is performed. To reduce salivation and bronchial secretion, 1 ml of 0.1% atropine sulfate solution is administered. If swallowing is impaired, nutrition is provided through a nasoesophageal tube.

At severe forms myasthenic crisis, pulse therapy is carried out: 1000-2000 mg of prednisolone hemisuccinate is administered intravenously, for less severe ones - the drug is administered at the rate of 1.5-2 mg/kg (on average 100-200 mg) per day. At the same time, potassium preparations are prescribed (intravenous drip of 30 ml of 10% potassium chloride solution per 500 ml of isotonic sodium chloride solution at a rate of 20 drops per minute). Plasmapheresis or hemosorption is effective.

Timoptin (a drug from thymus peptide fractions) is administered subcutaneously in a dose of 100 units of dry matter, diluted in 1 ml of isotonic sodium chloride solution per injection. The course includes 5 injections with an interval of 3 days. In 1/3 of cases, improvement is noted after the first injection, in the rest - after the 2-3rd injection. Improvements in neuromuscular transmission and the action potential state of skeletal muscle motor units have been repeatedly confirmed by EMG data. This made it possible to reduce the dose of ACEP.

There are no side effects observed with the administration of thyoptin. For partial cardiac or generalized myasthenic crises with severe cardiovascular disorders, 6 ml (50-100 mg) of cocarboxylase, 10 ml of a 10% panangin solution, 1 ml of a 0.06% solution of corglycon, diluted by 10-20 ml of 20% or 40% glucose solution, subcutaneously - 1 ml of 10% sodium caffeine benzoate solution or 1 ml of cordiamine. If ineffective the listed activities plasmapheresis (3-5 sessions) and hemosorption (1 session) are used.

When treating patients with cholinergic crisis, ACEP should be discontinued. 0.5-1 ml of a 0.1% solution of atropine sulfate is injected intravenously, then again (after 1-1.5 hours) 1 ml subcutaneously (until mydriasis and dry mouth appear).

Introducing the cholinesterase reactivator dipyroxime—1 ml of a 15% solution under the skin or into the muscle—is effective. After 1 hour, the injection at the same dose is repeated. If signs of respiratory failure increase, the patient is transferred to mechanical ventilation. Sometimes it is enough to stop taking ACEP for 16-24 hours and perform mechanical ventilation during this time. If these measures are ineffective, plasmapheresis is indicated.

Target adjuvant therapy at long-term treatment– improve the synthesis and release of acetylcholine, muscle function and reduce side effect corticosteroids. The first task is accomplished by adrenomimetics, calcium preparations, methionine, ATP, glutamic acid, vitamins B, D and E, riboxin, phosphoden, adaptogens (schizandra tincture and eleutherococcus).

To prevent osteoporosis during long-term corticosteroid therapy, a 5% solution of retabolil is prescribed 1 ml intramuscularly 6 times with a break of 3 days between injections. Then the intervals between injections are increased to 5, 7, 10, 15, 20 and 30 days and then switched to a maintenance dose (1 ml of 5% solution once every 2 months) for several years. Side effect long-term use retabolil is virilization. The drug is not recommended for young women and men with adenoma prostate gland. To prevent osteoporosis, a fluorine-containing drug corebiron (ossin) is also used, 0.5-1 g 3 times a day.

Myasthenic syndromes

Clinical manifestations of myasthenic syndrome are similar to those of myasthenia gravis. Disruption of neuromuscular transmission in this disease occurs at the presynaptic level. Myasthenic syndromes occur with carcinomatous neuromyopathies (Lambert-Eaton syndrome), with systemic diseases connective tissue, botulism. The main differential diagnostic feature of these syndromes is the “training symptom” - an increase in the amplitude of subsequent evoked action potentials when stimulated with medium (10-20 pulses/s) and especially high (40-50 pulses/s) frequencies when recording EMG. For myasthenic syndrome, along with therapy for the underlying disease, calcium supplements, ACEP, and guanidine are prescribed.

Myasthenic syndrome as a complication drug treatment occurs as a result of blockade of neuromuscular transmission at the presynaptic level when prescribing aminoglycoside antibiotics (gentamicin, kanamycin, lincomycin, neomycin, etc.), streptomycin, tetracyclines, curare-like drugs(ditylin, tubocurarine, diplacin, melliktin), D-penicillamine, some anticonvulsants(trimethine, clonazepam, barbiturates), lithium and quinine preparations.

Treatment begins with the abolition of the medications that caused the development of the syndrome; detoxification therapy, vitamins, ACEP, and potassium-containing drugs are prescribed.

In addition to those listed medicines, in patients with myasthenia gravis and myasthenic syndromes, muscle relaxants, tranquilizers, antipsychotics, antidepressants, morphine and barbiturates are contraindicated long acting, magnesium-containing laxatives, sulfonamides.

The cause of a myasthenic crisis is usually a sudden worsening of a pre-existing myasthenia gravis due to a medication error or an intercurrent illness, most often an infection. Only in in rare cases Myasthenic crisis is the debut manifestation of myasthenia gravis. There are acute crises with respiratory failure And sudden stop breathing, heart failure due to severe violations heart rate caused by myocarditis, and subacute crisis with decompensation functionality acetylcholine receptors and weakness of the respiratory and/or bulbar muscles.

Symptoms and signs of myasthenic crisis

Ptosis and diplopia may be observed. Reflexes and sensitivity are not impaired.

Dyspnea. At first glance, there is no impression that the patient's condition is serious. The combination of facial expression and weakness of the respiratory muscles creates a false impression of the patient’s satisfactory condition.

Tabloid violations carry potential danger violations protective function upper respiratory tract and the development of aspiration pneumonia.

Fatigue and respiratory failure lead to the development of coma.

Taking penicillamine (can cause the development of a syndrome identical to idiopathic myasthenia gravis).

Common predisposing factors for myasthenic crisis

Infection, surgical interventions, reception medicines. Note! Glucocorticoids used to treat myasthenia gravis may initially lead to exacerbation.

Severity rating

The most important indicator of the severity of the crisis is the vital capacity of the lungs. Gases arterial blood- an insufficiently sensitive criterion; their determination makes it possible to detect hypercapnia at a late stage.

Tabloid violations. Cholinergic crisis.

Sometimes it is not possible to differentiate between myasthenia gravis and the excessive effect of anticholinesterase therapy (which leads to muscle weakness as a result of depolarization blockade) on the basis of clinical data alone. The issue of discontinuing anticholinesterase drugs is decided only after consultation with a neurologist. It should be remembered that cholinergic crisis is much less common than myasthenic crisis.

Treatment of myasthenic crisis

Stabilize the patient's condition. You should make sure that there are no electrolyte disturbances (decreased potassium and calcium concentrations, increased magnesium concentrations), and that the patient is not taking medications that aggravate muscle weakness.

Treatment is aimed at maintaining vital important functions, which includes intubation and connection to a ventilator. Towards measures symptomatic therapy, and differential diagnosis with cholinergic crisis, includes the administration of an anticholinesterase agent short acting- edrophonium chloride. If the condition improves, treatment is continued with longer-acting anticholinesterase agents administered parenterally or orally (for example, pyridostigmine (kalimine)).

When switching from oral to intravenous administration, it is necessary to remember that the ratio of equivalent doses administered intravenously and orally is 1:30!

At the same time, additional measures are carried out: the prescription of anticholinergic drugs (atropine) if available large quantity mucus, adequate replenishment of potassium deficiency (plasma concentration should be at upper limit norms), treatment concomitant diseases. After recovery from the acute condition, immunomodulatory therapy is prescribed.

The issue of conducting a test with edrophonium (tensilone test) is decided. Anticholinesterase therapy is effective provided that a cholinesterase crisis is excluded. If there is no effect after administration of edrophonium, the correctness of the diagnosis is assessed. All anticholinesterase drugs are discontinued for 72 hours. The edrophonium test can be repeated after some time.

Immunosuppressive therapy should be carried out under the supervision of a neurologist: prescribing prednisolone according to an alternating regimen leads to improvement. However, such treatment must be carried out with caution, since at the beginning of treatment with glucocorticoids there may be muscle weakness. High doses glucocorticoids are prescribed until remission is achieved. Azathioprine is also used for maintenance therapy, but the effect is achieved only after several months of taking it.

Plasmapheresis removes circulating antibodies from the bloodstream. Usually a replacement of 50 ml/(kg/day) is carried out over several days.

Long-term therapy with cholinesterase inhibitors is prescribed by a neurologist. The choice of drug determines the patient's response to therapy, but treatment should always begin with pyridostigmine at a dose of 60 mg every 4 hours. The drug can be administered through a tube or, if intramuscular administration is necessary, replace it with neostigmine (at the rate of 1 mg neostigmine per 60 mg pyridostigmine).

Relative contraindication - bronchial asthma and arrhythmias. Atropine should be administered before the test, since the administration of edrophonium (belongs to the group of cholinesterase inhibitors) may be accompanied by a severe cholinergic reaction, such as symptomatic bradycardia.

Prepare and label two 1 ml syringes: one with saline solution, and the other with 10 mg edrophonium.

Select a muscle to be monitored and ask colleagues to evaluate the strength of the muscle being tested before testing.

The contents of both syringes are injected, and neither the patient nor the doctor should know in what sequence they were injected. Ask the observer to reassess muscle strength after injecting the contents of each syringe.

Initially, edrophonium 2 mg (0.2 ml) is administered as a bolus and the patient is assessed for adverse cholinergic effects. If the patient has tolerated this dose, the remaining 0.8 mg (0.8 ml) of the drug is administered after 1 minute.

An increase in muscle strength after administration of edrophonium-3 indicates the presence of a myasthenic rather than a cholinergic crisis in the patient.

Myasthenic crisis is a suddenly developed critical condition in patients with myasthenia, which indicates not only a quantitative, but also a qualitative change in the nature of the process. The pathogenesis of the crisis is associated not only with a decrease in the density of cholinergic receptors of the postsynaptic membrane due to their complement-mediated destruction, but also with a change functional state remaining receptors and ion channels.

Heavy generalized myasthenic crises appear varying degrees depression of consciousness, pronounced bulbar disorders, increasing respiratory failure, severe weakness of skeletal muscles. Breathing disorders progress steadily over hours, sometimes minutes. At first, breathing becomes frequent, shallow, with the inclusion of auxiliary muscles, then - rare, intermittent. Subsequently, the phenomenon of hypoxia develops with facial hyperemia, followed by cyanosis. Anxiety and excitement appear. Developing motor restlessness, then complete cessation of breathing, confusion and loss of consciousness. Impaired cardiovascular activity at the time of crisis is expressed by an increase in heart rate to 150-180 per minute and an increase in blood pressure to 200 mm. rt. Art. Subsequently, the pressure decreases, the pulse becomes tense at first, then arrhythmic, rare, thread-like. Intensifying autonomic symptoms– salivation, sweating. At extreme severity loss of consciousness is accompanied involuntary urination and defecation. In severe generalized myasthenic crises, hypoxic encephalopathy develops with the appearance of unstable pyramidal symptoms (symmetrical increase in tendon reflexes, the appearance of pathological foot signs). According to our observations, pyramidal symptoms persist long time after the crisis has subsided.

Cholinergic crisis - this is a condition that has a special development mechanism, caused by excessive activation of nicotinic and muscarinic cholinergic receptors due to an overdose of anticholinesterase drugs. With this type of crisis, along with the development of generalized muscle weakness, a whole complex of side cholinergic effects is formed. At the basis of motor and autonomic disorders During a cholinergic crisis, there is hyperpolarization of the postsynaptic membrane and desensitization of cholinergic receptors, which is associated with a pronounced blockade of acetylcholinesterase and the resulting excess supply of acetylcholine to the cholinergic receptors of the postsynaptic membrane. Cholinergic crises are quite rare (in 3% of patients) and develop more slowly than myasthenic crises. In all cases, their occurrence is associated with an overdose of anticholinesterase drugs. Over the course of a day or several days, the patient’s condition worsens, weakness and fatigue increase, the patient cannot maintain the previous interval between doses of anticholinesterase drugs, individual signs cholinergic intoxication, then, after the next injection or enteral administration of anticholinesterase drugs (at the height of their action - usually after 30-40 minutes), a picture of a crisis develops, simulating myasthenic disorders. The difficulty of differential diagnosis of cholinergic crisis is that in all cases there is generalized muscle weakness with bulbar and respiratory disorders, observed in myasthenic crisis. Diagnosis is aided by the presence of various cholinergic manifestations and signs of chronic cholinergic intoxication according to medical history. The diagnosis of cholinergic crisis is based on a paradoxical decrease in muscle strength (without previous provocation by physical effort) in response to the usual or increased dose of anticholinesterase drugs.

Differentiation of crises in myasthenia gravis is based on assessing the effectiveness of the test with the introduction of an adequate dose proserina. In myasthenic crisis, the test is positive, and according to our data, complete compensation of the motor defect is observed in 12%, and incomplete compensation in 88% of patients. In case of cholinergic crisis, the test is negative, however, in 13% of patients, partial compensation. Most often (in 80% of cases) partial compensation is observed with a mixed nature of the crisis, and in 20% of cases incomplete compensation is observed.

Treatment: Artificial pulmonary ventilation (ALV). Plasmapheresis Immunoglobulins G (HUMAGLOBIN, OCTAGAM, BIAVEN, VIGAM, INTRAGLOBIN, Antioxidants (thioctaacid)

3 . Secondary purulent meningitis- a disease of the meninges, which is based on various etiological factors(pneumococci, staphylococci, etc.). Occurs more often when there is another infectious focus. The process spreads hematogenously, as well as per continuitatem (for example, otogenic process), with cracks and fractures of the skull bones.

Clinically, it is often difficult to distinguish from epidemic meningitis; clarifies the diagnosis bacteriological examination. Develops quite early meningeal syndrome, in children - convulsions, photophobia.

In the cerebrospinal fluid there is pleocytosis, numbering in tens of thousands of polynuclear cells, protein up to 10%, sugar content is reduced.

In the blood there is leukocytosis with a shift of the formula to the left.

From separate forms secondary purulent meningitis In first place in frequency are otogenic and pneumococcal.

Otogenic secondary meningitis is a consequence of chronic purulent otitis. The process penetrates the cranial cavity usually through the cells temporal bone. The clinical picture is practically no different from other types of purulent meningitis. Research is important cerebrospinal fluid, in particular regarding the presence of meningococcus.

Treatment. First of all, it is necessary to eliminate the primary focus operationally; at purulent process in the ear produce an emergency radical surgery with wide exposure of hard tissue meninges middle and back cranial fossae. Early surgery promotes favorable current diseases and prevents new complications, in particular such dangerous ones as sinus thrombosis. Massive doses of antibiotics are indicated (see Meningococcal meningitis, treatment).

Penicillin at the rate of 200,000-300,000 units per 1 kg of patient weight per day (i.e. 18,000,000-24,000,000 units per day, in equal doses every 3-4 hours), and for children under 3 months - 300,000- 400,000 units per 1 kg of body weight per day. The patient's condition improves after 10-12 hours; consciousness clears up, disappears headache. The temperature drops on the 1st-3rd day. Meningeal signs usually disappear by 4-10 days of treatment. The cerebrospinal fluid is sanitized by the 4th-8th day, less often - by the 10th-12th day. The average duration of penicillin therapy is 5-8 days in adults and 4 days in children. The criterion for sanitation of the cerebrospinal fluid and the indication for the abolition of penicillin is a decrease in the cytosis of the cerebrospinal fluid below 100 cells with a lymphocyte count of at least 75%. In some cases, they resort to the use of chloramphenicol (chloramphenicol succinate, chloracid) or tetracyclines (tetracycline, morphocycline) alone or combined with penicillin. However, tetracycline drugs are sharply painful when intramuscular injection, and their infusion into a vein is often complicated by phlebitis.

Antibiotics - macrolides (erythromycin, etc.) poorly penetrate the blood-brain barrier and are not used to treat purulent meningitis.

In addition to penicillin, sulfamonomethoxine, a long-acting sulfonamide administered orally (after clearing consciousness), can be used. As a rule, along with antibiotics for patients with meningococcal meningitis it is necessary to introduce fluids, electrolytes, vitamins, and dehydrating agents.

To reduce body temperature, antipyretics (pyrabutol, or reopirin intramuscularly) and ice packs on the head are used. Common with meningitis convulsive syndrome treated with injections of seduxen or transfusion of gamma-hydroxybutyric acid (GHB).