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

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

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

Plasmapheresis and hemosorption are used to remove autoantibodies to acetylcholine receptors from the body.

The cholinergic crisis, as a result of an overdose of anticholinesterase drugs (prozerin, neostigmine, kalimin, mestinon), is manifested by miosis, excessive salivation, bronchospasm, sweating, agitation, muscle weakness, abdominal pain, diarrhea, fibrillations and fasciculations.

When diagnosing this condition, all anticholinesterase drugs are immediately canceled, 1-2 mg (1-2 ml of a 0.1% solution) of atropine is administered subcutaneously or intravenously every hour, controlling the diameter of the pupils. IVL is carried out with intermittent positive pressure through the endotracheal tube, sanitize the airways.

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

Treatment. All patients with traumatic brain injury inpatient treatment and observation. With the preservation of vital functions, the patient must be provided with rest, cold on the head, symptomatic therapy (painkillers, sedatives, hypnotics) and correction of microcirculatory disorders (venotonics, vasoactive drugs, antiplatelet agents). expedient early appointment antibiotic therapy.

The use of neuroleptics and narcotic analgesics for prehospital stage and before 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 (intravenously, 1 ml of 12.5% ​​solution of dicynone or etamsylate with an interval of 6 hours) and dehydration therapy. Development psychomotor agitation, hyperthermia, coma requires non-specific emergency treatment.

Ed. prof. A. Skoromets

"Myasthenic crisis" and other articles from the section

Some nervous diseases at the initial treatment of patients by doctors, it is quite difficult to diagnose. These diseases include myasthenia gravis. Initial complaints, voiced by the patient, of rapid fatigue. But after rest, muscle fatigue on short time recedes, and the patient again feels quite normal.

Meanwhile, myasthenia gravis is a violation of the neuromuscular transmission of signals from the central nervous system into striated muscles, resulting in abnormal cyclic fatigue after minor exertion.

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 due to a combination of developmental defects: postsynaptic and presynaptic.

These defects are nothing more than violations of the synthesis necessary for normal life organism of substances and defect of organs of perception. Due to pathologies of organic processes, the function of the thymus gland is disrupted.

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

Can be distinguished the following forms myasthenia:

• eye;
• bulbar;
• generalized.

Some physicians believe that myasthenia gravis is combined with the eye, and how separate state it is not classified.

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

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

Chewing and swallowing functions are violated, in the future the timbre of the voice will change, the ability to articulate speech will disappear.

With generalized myasthenia gravis, all muscles are gradually blocked - from top to bottom - from the cervical and scapular to dorsal, then the muscles of the limbs are affected. Salivation appears, it becomes difficult for the patient to serve himself, perform the simplest actions, there is a feeling of weakness in the limbs.

The increase in symptoms can stop at any stage.

In children, the disease does not manifest itself before the age of six months, in most cases it is diagnosed in boys older than 10 years. They have up to 2 years from the first symptoms - weakness of the muscles of the eyelids - to the next ones.

In adulthood, in the period from 20 to 40 years, 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 in an autosomal recessive manner, except for the autosomal dominant syndrome, which is caused by the slow closing of immune channels:

1. Lambert-Eaton syndrome is more often diagnosed in men over 40 years of age. Its main features are weakness of the proximal limb muscles while maintaining 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 the facial and skeletal muscle, the sucking function is impaired;
4. Muscle hypotension 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.

Syndrome due to slow closure of ionic channels has the following symptoms:

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

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

Can be applied:

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

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

myasthenic crisis

Main symptoms myasthenic crisis- extensive violations of the functions of the bulbar muscles, which include the respiratory, 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 care is not provided for a sudden myasthenic crisis, the patient will suffocate.

The reasons for the development of the crisis can be the following factors:

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

These factors lead to blockage neuromuscular conduction cause loss of excitability in muscles and tendons.

Patients with myasthenia always have a note with them, which says that they suffer from such and such a form of the disease and what drugs are needed for first aid. In most cases, patients carry drugs with them - these are prozerin and canevin.

If among those around, in whose eyes a myasthenic crisis developed, there is at least 1 person who knows how to inject, a person's life will be saved. But you still need to call an ambulance.

Crisis treatment

The method of treatment of a myasthenic crisis is completely determined by the patient's condition and how quickly emergency care was provided to the specialist who arrived at the place of the call. brigade.

As soon as possible, the victim must be placed in intensive care and connected to a ventilator - artificial respiration. Artificial ventilation of the lungs should be carried out within 24 hours, no less.

Effectively restores the state of plasmapheresis, but may be required intravenous administration immunoglobulin. Together with immunoglobulin, methylprednisolone and potassium chloride are used.

Joint treatment with immunoglobulin, potassium chloride and methylprednisolone is used in the presence of 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 situation, the cause of which is a violation of neuromuscular conduction by the type of competitive block. MK occurs in 13-27% of cases, during the first 3 years of the disease, regardless of the age of the patient, the form and course of the disease. Most formidable complications- respiratory failure with bulbar form, the 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 the switching off of the diaphragm and weakness of the intercostal muscles. In cardiac forms of a crisis, acute cardiovascular failure. The cholinergic crisis is caused by an overdose of AHEP and outwardly resembles a myasthenic crisis.

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

Treatment. In myasthenic crisis, treatment begins with subcutaneous or intravenous administration sequentially 3 times every 30 minutes with 2 ml of a 0.05% solution of proserin (or 2 times every 45 minutes with 3 ml). Lack of effect serves as an indication for IVL. IVL is also indicated for tachypnea - more than 35 breaths per 1 min, a decrease in VC 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 a 0.1% solution of atropine sulfate is administered. If swallowing is disturbed, nutrition is provided through the nasoesophageal tube.

At severe forms myasthenic crisis, pulse therapy is carried out: 1000-2000 mg of prednisolone hemisuccinate is administered intravenously, in less severe cases, the drug is administered at the rate of 1.5-2 mg / kg (average 100-200 mg) per day. At the same time, potassium preparations are prescribed (intravenously drip 30 ml of a 10% solution of potassium chloride per 500 ml of isotonic sodium chloride solution at a rate of 20 drops per 1 minute). Plasmapheresis or hemosorption is effective.

Timoptin (preparation from thymus peptide fractions) is administered subcutaneously at a dose of 100 IU of dry matter diluted in 1 ml of isotonic sodium chloride solution per injection. The course is prescribed 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 2nd-3rd injection. Improvement in neuromuscular transmission and action potential status of skeletal muscle motor units has been repeatedly confirmed by EMG data. This made it possible to reduce the dose of AHEP.

Side effects with the introduction of thymoptin are not observed. In case of partial cardiac or generalized myasthenic crises with severe cardiovascular disorders, 6 ml (50-100 mg) of cocarboxylase, 10 ml of a 10% solution of panangin, 1 ml of a 0.06% solution of corglicon diluted by 10-20 ml of 20% or 40% glucose solution, subcutaneously - 1 ml of 10% caffeine-sodium benzoate solution or 1 ml of cordiamine. With inefficiency listed activities apply plasmapheresis (3-5 sessions), hemosorption (1 session).

When treating patients with a cholinergic crisis, AHEP 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) subcutaneously 1 ml (until mydriasis and dry mouth appear).

It is effective to introduce the cholinesterase reactivator dipiroxime - 1 ml of a 15% solution under the skin or into the muscle. After 1 hour, the injection at the same dose is repeated. With an increase in signs of respiratory failure, the patient is transferred to mechanical ventilation. Sometimes it is enough to stop taking AHEP for 16-24 hours and to carry out mechanical ventilation at this time. With the ineffectiveness of these measures, 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 served by adrenomimetics, calcium preparations, methionine, ATP, glutamic acid, vitamins of groups B, D and E, riboxin, phosphoden, adaptogens (schisandra tincture and eleutherococcus).

In order to prevent osteoporosis during long-term corticosteroid therapy, a 5% solution of retabolil, 1 ml intramuscularly, is prescribed 6 times with a break between injections of 3 days. 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 a 5% solution once every 2 months) for several years. side effect long-term use retabolil is virilizing. The drug is not recommended for young women and men with adenoma prostate. For the prevention of 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. Violation 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 sign of these syndromes is the "workability symptom" - an increase in the amplitude of subsequent evoked action potentials during stimulation with medium (10-20 pulses/s) and especially high (40-50 pulses/s) frequencies during EMG recording. In myasthenic syndrome, along with the therapy of the underlying disease, calcium preparations, AHEP, 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(dithylin, tubocurarine, diplacin, mellictin), D-penicillamine, some anticonvulsants(trimetin, clonazepam, barbiturates), lithium preparations and quinine.

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

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

The cause of a myasthenic crisis is usually a sudden worsening of a pre-existing myasthenia due to an error in treatment or an intercurrent disease, most often an infection. Only in rare cases myasthenic crisis is the debut manifestation of myasthenia gravis. There is an acute crisis with respiratory failure and sudden stop respiration, 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 seen. Reflexes and sensitivity are not disturbed.

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.

The tabloid violations bear potential danger violations protective function upper respiratory tract and the development of aspiration pneumonia.

Fatigue and respiratory failure lead to the development of coma.

Reception of penicillamine (may 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 exacerbate.

Severity score

The most important indicator of crisis severity is lung capacity. gases arterial blood- insufficiently sensitive criterion, their determination allows to detect hypercapnia already at a late stage.

Boulevard violations. cholinergic crisis.

Sometimes it is impossible to differentiate between progressive myasthenia gravis and an excess effect of anticholinesterase therapy (which leads to muscle weakness as a result of depolarization blockade) on the basis of clinical data alone. They decide on the abolition of anticholinesterase drugs only after consultation with a neurologist. It should be remembered that a cholinergic crisis is much less common than a myasthenic one.

Treatment of myasthenic crisis

Stabilize the patient's condition. It should be ensured that there are no electrolyte disturbances (decrease in the concentration of potassium, calcium, increase in the concentration of magnesium), and also that the patient is not taking drugs that aggravate muscle weakness.

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

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

At the same time, additional measures are taken: the appointment of anticholinergics (atropine) in the presence of a large number mucus, adequate replenishment of potassium deficiency (plasma concentration should be at upper bound norms), treatment concomitant diseases. After removal from the acute state, immunomodulatory therapy is prescribed.

Decide whether to conduct a test with edrophonium (tensilon test). Anticholinesterase therapy is effective if a cholinesterase crisis is excluded. If there is no effect after the introduction of edrophonium, the correctness of the diagnosis is assessed. Cancel all anticholinesterase drugs for 72 hours. The test with the introduction of edrophonium can be repeated after a while.

Immunosuppressive therapy should be carried out under the supervision of a neurologist: the appointment of prednisone according to an alternating regimen leads to improvement. However, such treatment should 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 a few months of its use.

Plasmapheresis removes circulating antibodies from the bloodstream. Usually, a replacement of 50 ml / (kgxday) is carried out for 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 be started with pyridostigmine at a dose of 60 mg every 4 hours. The drug can be administered through a tube or, if necessary, replace it with intramuscular injection with neostigmine (at the rate of 1 mg of neostigmine per 60 mg of pyridostigmine).

Relative contraindication - bronchial asthma and arrhythmias. Before the test, atropine should be administered, due to the fact that 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 and the other with 10 mg of edrophonium.

The muscle to be observed is selected and colleagues are asked to evaluate the strength of the muscle being tested before the test.

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

First, 2 mg (0.2 ml) of edrophonium is injected in a stream and assessed for adverse cholinergic effects. If the patient tolerated this dose, the remaining 0.8 mg (0.8 ml) of the drug is administered after 1 min.

An increase in muscle strength after the appointment 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 gravis, 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 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, severe bulbar disorders, increasing respiratory failure, severe weakness of skeletal muscles. Respiratory disorders progress steadily over hours, sometimes minutes. At first, breathing becomes frequent, shallow, with the inclusion of auxiliary muscles, then rare, intermittent. In the future, the phenomenon of hypoxia develops with flushing of the face, followed by cyanosis. There is anxiety, excitement. Developing restlessness, then complete cessation of breathing, confusion and loss of consciousness. Violation of cardiovascular activity at the time of the crisis is expressed by an increase in heart rate up to 150-180 per minute and an increase in blood pressure up to 200 mm. rt. Art. In the future, the pressure decreases, the pulse becomes tense at first, then arrhythmic, rare, thready. Are getting stronger autonomic symptoms- salivation, sweating. At extreme severity loss of consciousness is accompanied involuntary urination and defecation. In severe generalized myasthenic crises, the phenomena of hypoxic encephalopathy develop with the appearance of intermittent 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 mechanism of development, due to excessive activation of nicotinic and muscarinic cholinergic receptors due to an overdose of anticholinesterase drugs. In this type of crisis, along with the development of generalized muscle weakness, the whole complex of side cholinergic effects is formed. At the heart of motor and autonomic disorders in 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. Within a day or several days, the condition of patients worsens, weakness and fatigue increase, the patient cannot withstand the previous interval between taking anticholinesterase drugs, appear individual features cholinergic intoxication, then, after another 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 complexity of the differential diagnosis of a cholinergic crisis is that in all its cases there is a generalized muscle weakness with bulbar and respiratory disorders observed in myasthenic crisis. Assistance in the diagnosis is provided by the presence of various cholinergic manifestations, signs of chronic cholinergic intoxication according to the anamnesis. The diagnosis of a cholinergic crisis is based on a paradoxical decrease in muscle strength (without prior exercise provocation) in response to a normal or increased dose of anticholinesterase drugs.

Differentiation of crises in myasthenia gravis is based on the evaluation of the effectiveness of the test with the introduction of an adequate dose prozerina. 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 a cholinergic crisis, the test is negative, however, 13% of patients may experience 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 noted.

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

3 . Meningitis secondary purulent- a disease of the meninges, which is based on various etiological factors(pneumococci, staphylococci, etc.). It often occurs 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 bones of the skull.

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

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

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

From individual forms secondary purulent meningitis Otogenic and pneumococcal are in the first place in frequency.

Otogenic secondary meningitis is a consequence of chronic purulent otitis media. The process enters the cranial cavity, usually through cells temporal bone. The clinic practically does not differ from other types of purulent meningitis. important research cerebrospinal fluid in particular with respect to the presence of meningococcus.

Treatment. First of all, it is necessary to eliminate the primary focus operational way; at purulent process in the ear produce an emergency radical operation with a wide outcrop of hard meninges middle and back cranial pits. Early surgical intervention promotes favorable course diseases and prevents new complications, in particular such a dangerous one as sinus thrombosis. Massive doses of antibiotics are shown (see Meningitis meningococcal, treatment).

Penicillin at the rate of 200,000-300,000 IU per 1 kg of the patient's weight per day (i.e., 18,000,000-24,000,000 IU per day, in equal doses after 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, disappears headache. The temperature drops on the 1-3rd day. meningeal signs usually disappear by the 4-10th day of treatment. The liquor is sanitized by the 4th or 8th less often - by the 10th-12th day. The duration of penicillin therapy averages 5-8 days in adults and 4 days in children. The criterion for the rehabilitation of CSF and the indication for the abolition of penicillin is a decrease in CSF cytosis below 100 cells with a number of lymphocytes of at least 75%. In some cases, they resort to isolated or combined with penicillin administration of levomycetin (levomycetin succinate, chloracid) or tetracyclines (tetracycline, morphocycline). 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, sulfamonometoxin, a long-acting sulfanilamide administered orally (after consciousness has cleared), can be used. As a rule, along with antibiotics, patients with meningococcal meningitis it is necessary to introduce fluids, electrolytes, vitamins, dehydrating agents.

To reduce body temperature, antipyretics are used (pirabutol, or reopirin intramuscularly), ice packs on the head. Uncommon in meningitis convulsive syndrome they are stopped by injections of seduxen or transfusion of gamma-hydroxybutyric acid (GHB).