G40-G47 Episodic and paroxysmal disorders. Paroxysmal tachycardia Paroxysmal state according to ICD

Lymph nodes are organs of the lymphatic system that perform a protective function. Thanks to the lymph nodes, the infection from the bloodstream is not able to spread throughout the body. With inflammation of the lymph nodes, lymphadenitis develops. Treatment of lymphadenitis depends on the cause of the disease. Pathology can be primary or secondary.

In the case when the symptoms of the disease occur against the background of other infections, they speak of secondary lymphadenitis. In some cases, the disease occurs as a complication of tuberculosis, actinomycosis. In medicine, such inflammation of the nodes is called specific lymphadenitis. Most often, the nodes become inflamed in the inguinal and axillary region, under the jaw and on the neck.

ICD code

According to the international classification of ICD 10, lymphadenitis, depending on the localization, is divided into:

Face, neck, head - code L04.0.
Torso - ICD code 10 L04.1.
Shoulders, armpit - ICD code 10 L04.2.
Lower limbs, pelvic area - ICD code 10 L04.3.
Other areas - L04.8.
Unspecified type - L04.9.

Nonspecific forms of lymphadenitis according to ICD 10 are divided into:

Mesenteric (acute and chronic) - I88.0 according to ICD 10.
Chronic course (except for mesenteric lymphadenitis) - I88.1 according to ICD 10.
Another non-specific inflammation - I88.8 according to ICD 10.
The unspecified nature of nonspecific inflammation is I88.9 according to ICD 10.

Classification and origin

Based on the severity and duration of the course, several forms of pathology are distinguished:

spicy;
chronic;
specific;
non-specific;
serous.

By the number of inflammatory foci are distinguished:

unit;
multiple.

Nonspecific lymphadenitis causes a pathogenic pyogenic infection. Most often, infectious agents enter the lymph nodes with blood flow from abscesses (furuncle, carbuncle, abscess), purulent foci located in the respiratory tract (tonsillitis, bronchitis, laryngitis, etc.). Pathology can occur against the background of erysipelas or trophic disorders and the formation of trophic ulcers. A purulent infection causes acute lymphadenitis.

Specific inflammation occurs in diseases such as:

Tuberculosis.
Mycoses.
Syphilis.
Viral infections.

Lymph nodes can become inflamed at the first stage of the underlying disease, thereby signaling hidden pathological processes in the body. Vaccinal inflammation is also distinguished. Most often, against the background of the underlying disease, chronic lymphadenitis develops with periods of exacerbations and remissions.

Development of the disease

Symptoms of the disease begin to appear after the infection from the primary focus enters the lymph node with blood or lymph flow. When the level of infectious elements exceeds the norm, the barrier function of the node is impaired. Toxins of microorganisms in the lymph nodes begin to affect the surrounding tissues, causing an inflammatory reaction. In the future, purulent fusion of the affected node occurs.

Nonspecific lymphadenitis can also be caused by other causes - trauma and injury to the lymph node. This route of infection is called contact. Favorable conditions for the occurrence of inflammation are: hypothermia, deficient states of immunity, stress.

In some cases, the lymph nodes increase without inflammation. The reasons for the increase are associated with an excess number of lymphocytes that are produced to fight infection when foreign agents enter the body. This condition does not apply to pathological processes and indicates the implementation of the barrier function of the lymphatic system.

Symptoms

Symptoms in the serous nature of inflammation are manifested by a violation of general well-being. The patient may complain of nagging pain in the affected area. Lymph nodes may be slightly enlarged and firm. The skin over the affected node is not changed. If the disease is not treated at this stage, the inflammation begins to progress. Lymphatic tissue is destroyed during this process.

As a result of suppuration, purulent acute lymphadenitis develops. Patients complain of sharp pain, sometimes pulsating. The skin in the area of inflammation is reddened. When feeling the lymph node, pain appears. With a purulent process, the lymph nodes can merge with each other and become immobile.

Purulent diffuse inflammation is called adenophlegmon. The patient has symptoms:

pronounced redness;
edema;
fever with chills;
signs of intoxication (headache, lethargy);
tachycardia.

Chronic lymphadenitis develops as a result of improper treatment of acute inflammation. Usually the disease proceeds without severe symptoms. Characteristic symptoms may appear during exacerbation. The patient's temperature rises and there is a slight swelling at the site of the affected node. In some cases, a fistula is formed through which purulent contents flow during an exacerbation.

Chronic lymphadenitis often accompanies other specific infectious processes or oncological diseases. Therefore, if symptoms of inflammation appear, a doctor's consultation and examination is necessary.

Manifestations of the disease depending on the localization

The causes of inflammation of the lymph nodes in the neck are associated with diseases of the upper respiratory tract. Most often, such a pathology occurs in childhood with acute respiratory infections, influenza. In adults, inflammation of the lymph nodes in the neck may indicate tuberculosis or syphilis.

Symptoms of inflammation of the submandibular nodes indicate tonsillitis or dental diseases. A brighter clinical picture develops with axillary lymphadenitis. Enlargement and inflammation of the lymph nodes behind the ears can develop against the background of ENT diseases, eye pathology, mycoses, lymphoma and oncological processes in the brain. With pediculosis, the occipital lymph nodes can become inflamed.

Inguinal lymphadenitis develops as a result of infectious processes of the reproductive system, the lower part of the peritoneum and the perineum. The causes of the disease may be associated with cystic formations. Symptoms appear:

dull pain in the groin;
intense pain after exercise or while walking.

With tuberculosis, tumors, autoimmune diseases, a generalized lesion of the lymph nodes is often found. The disease is accompanied by an increase in lymph nodes of all groups. In the case of increased capillary permeability, the lymph node is saturated with blood. Hemorrhagic inflammation occurs in anthrax.

Reactive inflammation of the lymph nodes occurs against the background of local disorders in the body. The reactive form accompanies any acute inflammation against the background of a weakened immune system. Manifestations of this form can be observed in children after the Mantoux test. A characteristic feature of reactive lymphadenitis is the rapid development of the process, which is suppressed with normal immunity.

There are cases of damage to the nodes of the mesentery of the intestine. Pathology occurs with pain in the abdomen in the navel. The patient's condition worsens as the disease progresses. There is vomiting, fever, diarrhea. If you do not seek help in time and do not treat the disease, complications may occur (abscess, sepsis, intestinal obstruction). The causes of inflammation are associated with intestinal infections, viruses, tuberculosis.

Treatment

Treatment of lymphadenitis depends on the nature and location of inflammation. At the initial stage of inflammation, rest conditions are created for the affected area, treated with antibiotics, anti-inflammatory drugs. Treatment with antibiotics begins after the cause of the disease is established. In therapy, antibacterial agents of the penicillin series (Cefuroxime, Rovamycin), as well as antibiotics are used:

Sumamed.
Amoxiclav.
Amoxicomb.
Augmentin.
Amoxicillin.
Clamox.
Flemoklav.

For children under 10 years old, the dosage is calculated taking into account the weight and state of immunity. Antibiotics are prescribed only by a doctor after establishing the cause of inflammation and analyzing the sensitivity of microbes to the action of the drug. With specific inflammation, the treatment of lymphadenitis is to eliminate the cause of the pathology. Patients are prescribed drugs that stop the symptoms of the underlying disease (syphilis, HIV, mycoses, tuberculosis, etc.). If the symptoms of the disease are caused by oncological processes, chemotherapy, radiation and other methods are prescribed as indicated.

In the case when nonspecific lymphadenitis is complicated by purulent fusion, an operation is indicated. The affected node is opened, conditions are created for the outflow of pus (drained). Subsequent treatment consists in treating the wound and prescribing anti-inflammatory therapy.

The complex therapy includes local remedies and physiotherapeutic procedures. Patients are prescribed compresses with Dimexide, anti-inflammatory ointments (Ichthyol). In order to improve regenerative processes in the subacute period, electrophoresis, UHF are shown. Patients are prescribed general strengthening drugs (vitamins and drugs that increase immunity).

It is forbidden to treat inflammation of the lymph nodes on their own. Uncontrolled use of drugs can lead to the spread of infection and complications such as phlegmon, sepsis, inflammation of the meninges (especially with posterior cervical localization), osteomyelitis, and elephantiasis.

Features of the action of non-selective B-blockers
Indications for use
Contraindications for treatment
Methods of treatment
Side effect
What to know
Conclusion

Propranolol was one of the first B-blockers that began to be used for the treatment of cardiovascular pathology. This drug is better known as anaprilin. Since the drug is a non-selective blocker of B-adrenergic receptors, its use is currently limited. But there are situations when this medicine has advantages.

Features of the action of non-selective B-blockers

Like any drug in this group, anaprilin blocks B1-adrenergic receptors located in the heart and kidneys. Due to this, the formation of renin decreases and the activity of the RAAS is suppressed. Propranolol reduces the frequency of heart contractions, their intensity, which is accompanied by a decrease in cardiac output. Through these mechanisms, the drug helps lower blood pressure.

Anaprilin reduces the activity of the sinoatrial node, as well as foci of pathological activity located in the atria, AV junction, and ventricles. The drug has a membrane-stabilizing effect. That is why the drug can be used for rhythm disturbances.

Since the strength of heart contractions and their frequency decreases, the need for oxygen in the heart muscle decreases, due to which angina attacks occur less often.

Unlike selective B-blockers, anaprilin additionally acts on B2-adrenergic receptors, which are located in the wall of the bronchi, uterus, intestines, in the smooth muscles of arteries, in skeletal muscles, salivary glands, eyes and other organs. That is why blocking the stimulating effect of catecholamines leads to the corresponding effects. Propranolol increases the tone of the uterus, lowers intraocular pressure, due to which the indications for the use of the drug are expanding compared to selective B-blockers. But the number of adverse reactions also increases significantly.

After oral administration, propranolol is absorbed fairly quickly. Already after 1-1.5 hours, the concentration of the active substance in the blood reaches a maximum. The hypotensive effect lasts up to a day. Bioavailability is about 30%, but after a meal it increases. The half-life is two to three hours. It binds to plasma proteins by 90-95%. The drug is excreted mainly by the kidneys. Penetrates into breast milk and through the placental barrier.

Indications for use

You can take anaprilin in tablets for many diseases:

Elevated blood pressure in essential and symptomatic hypertension.
IHD: stable and unstable angina, myocardial infarction (from the fifth day).
Tachyarrhythmias, including against the background of various diseases. Propranolol helps to effectively deal with sinus tachycardia. Treatable: supraventricular tachycardia, extrasystole, atrial fibrillation.
Heart disease: subaortic stenosis, mitral valve prolapse, hypertrophic cardiomyopathy.
Autonomic disorders: sympathetic-adrenal crises in patients with diencephalic syndrome, neurocirculatory dystonia, panic attacks, autonomic disorders during menopause.
Portal hypertension syndrome in liver cirrhosis.
Thyrotoxicosis - to eliminate tachycardia, relieve thyrotoxic crisis, in preparation for surgical treatment.
Essential tremor.
Complex treatment of pheochromocytoma (mandatory with alpha-blockers).
withdrawal syndrome.
Prevention of migraine attacks.
Primary weakness of labor activity and prevention of postpartum complications.
Hemangiomas in newborns.

Contraindications for treatment

Anaprilin can be used only in the absence of contraindications:

low pressure;
sinoatrial and AV blockade of 2-3 degrees;
Heart rate less than 55 per minute;
SSS (sick sinus syndrome);
severe heart failure (acute and chronic);
variant angina (Prinzmetal);
bronchial asthma and a tendency to bronchospasm;
cardiogenic shock;
the first days after acute myocardial infarction;
circulatory disorders in the peripheral arteries (Raynaud's disease, etc.);
hypersensitivity.

Take pills with caution in the following conditions:

diabetes mellitus and a tendency to hypoglycemia;
chronic diseases of the bronchopulmonary system, emphysema;
disruption of the liver and kidneys;
psoriasis;
spastic colitis;
muscle weakness;
advanced age;
pregnancy;
lactation period.

Methods of treatment

In the presence of high pressure, tablets begin to take 40 mg in the morning and evening. Gradually increase the dosage to the required. The daily dose can be divided into 2 or 3 doses. Such treatment is most effective at the initial stage of hypertension or an episodic increase in blood pressure, accompanied by a rapid heartbeat. Preferably used in young people.

If you have to treat angina pectoris, then start with 20 mg 3 times a day. The dosage can be increased over time to a maximum, but not more than 240 mg.

You can take anaprilin and with essential tremor, and for the prevention of migraine attacks. Small doses are used: 40 mg 2-3 times a day, maximum 160 mg. Do not forget that propranolol lowers blood pressure, as a result of which the use of large doses can cause hypotension.

The drug is sometimes used to stimulate labor, as well as to prevent postpartum complications, as it stimulates uterine contractions. Doses are small: 20 mg three to six times a day.

There is an injectable form of the drug. It is used to stop arrhythmias and angina attacks. The medicine is administered intravenously. There are also eye drops that help with glaucoma.

Side effect

The negative consequences after taking anaprilin are much greater than those of selective B-blockers.

First of all, the drug acts on the cardiovascular system, often causing a pronounced decrease in the frequency of heart contractions, intracardiac blockade, hypotension, heart failure. Violated peripheral circulation due to spasm of the arteries.
The reaction of the nervous system is manifested in the form of dizziness, headaches, sleep disturbances. There are nightmares. Emotional lability is often observed, the speed of mental and motor reactions decreases. Hallucinations, depression, disorientation in space and time, short-term amnesia, sensory disturbances and paresthesias are possible.
The gastrointestinal tract reacts to the medication with dyspeptic disorders, which is manifested by nausea, vomiting, and stool disorders. Since the drug increases the tone of the smooth muscles of the intestines, as well as the arteries, abdominal pains appear. Mesenteric artery thrombosis and ischemic colitis may develop.
The respiratory organs also respond with a characteristic reaction to the drug. Increased muscle tone of the bronchi manifests itself in the form of bronchospasm and laryngospasm, shortness of breath, cough, chest pain.
Eye changes: keratoconjunctivitis, visual disturbances and dry eyes.
Disturbances in the blood system: a decrease in the content of leukocytes, agranulocytosis, thrombocytopenic purpura, an increase in liver parameters, cholesterol and its atherogenic fractions.
Other reactions: skin manifestations in the form of rashes, alopecia, itching, exacerbation of psoriasis; sexual dysfunction up to impotence; Peyronie's disease; pain in the joints; hypoglycemia and fever.

What to know

If propranolol has to be used for a long time and it becomes necessary to cancel it, then this should be done very carefully. The dosage is reduced gradually. If you stop taking the pills immediately, then a withdrawal syndrome occurs. This is manifested in an increase in the symptoms of the underlying disease.

It is necessary to constantly monitor blood glucose in patients with diabetes mellitus, so as not to miss hypoglycemia. This condition is much more dangerous than high sugar, because the brain suffers from a lack of energy.

Given that propranolol lowers the reactivity of the body (motor and mental), people who drive a vehicle or work in hazardous conditions should be especially careful.

You can not use the drug simultaneously with certain drugs:

antipsychotic and anxiolytics;
calcium channel blockers (diltiazem and verapamil);
alcoholic products.

Various antihypertensive drugs, sympatholytics, MAO inhibitors, anesthetics enhance the ability to lower blood pressure. Reduce the effectiveness of treatment with NSAIDs, glucocorticoids and estrogens.

Propranolol itself increases the activity of thyreostatic drugs and drugs that tone the uterus. But reduces the effectiveness of allergy medications. Slows down the excretion of lidocaine and aminophylline, prolongs the action of coumarins and non-depolarizing muscle relaxants.

If surgical treatment is planned using anesthesia (chloroform, ether), treatment should be discontinued.

If the treatment of coronary heart disease with the help of this B-blocker is planned to be carried out for a long time, then it is advisable to take cardiac glycosides at the same time.

Tablets may contain 10 and 40 mg of the active substance. One package contains 30 or 50 pieces. The shelf life is 4 years.

Conclusion

Anaprilin has its own niche for use. But if its additional effects are not needed, then the drug should be replaced with a selective B-blocker. How long the treatment will last, what dose to take, only a doctor can determine. He is able to take into account all the risks from such therapy, which the patient himself cannot do. Self-medication is dangerous and often leads to a deterioration in the course of the underlying disease, as well as the general condition.

The question of the tactics of treating patients with paroxysmal tachycardia is decided taking into account the form of arrhythmia (atrial, atrioventricular, ventricular), its etiology, the frequency and duration of attacks, the presence or absence of complications during paroxysms (cardiac or cardiovascular failure).
Most cases of ventricular paroxysmal tachycardia require emergency hospitalization. The exception is idiopathic variants with a benign course and the possibility of rapid relief by administering a specific antiarrhythmic drug. With a paroxysm of supraventricular tachycardia, patients are hospitalized in the cardiology department in case of acute cardiac or cardiovascular failure.
Planned hospitalization of patients with paroxysmal tachycardia is carried out with frequent, 2 times a month, attacks of tachycardia for an in-depth examination, determination of therapeutic tactics and indications for surgical treatment.
The occurrence of an attack of paroxysmal tachycardia requires the provision of urgent measures on the spot, and in case of primary paroxysm or concomitant cardiac pathology, a simultaneous call to an ambulance cardiological service is necessary.
To stop the paroxysm of tachycardia, they resort to vagal maneuvers - techniques that have a mechanical effect on the vagus nerve. Vagal maneuvers include straining; Valsalva test (an attempt to exhale vigorously with the nasal fissure and oral cavity closed); Ashner's test (uniform and moderate pressure on the upper inner corner of the eyeball); Cermak-Goering test (pressure on the area of one or both carotid sinuses in the area of the carotid artery); an attempt to induce a gag reflex by irritating the root of the tongue; wiping with cold water, etc. With the help of vagal maneuvers, it is possible to stop only attacks of supraventricular paroxysms of tachycardia, but not in all cases. Therefore, the main type of assistance with developed paroxysmal tachycardia is the introduction of antiarrhythmic drugs.
As an emergency, intravenous administration of universal antiarrhythmics is indicated, effective for any form of paroxysm: novocainamide, propranolola (obzidan), aimalin (giluritmal), quinidine, rhythmodan (disopyramide, rhythmilek), ethmozine, isoptin, cordarone. With prolonged paroxysms of tachycardia that are not stopped by drugs, they resort to electrical impulse therapy.
In the future, patients with paroxysmal tachycardia are subject to outpatient monitoring by a cardiologist, who determines the amount and schedule of antiarrhythmic therapy. The appointment of anti-relapse antiarrhythmic treatment of tachycardia is determined by the frequency and tolerance of attacks. Carrying out continuous anti-relapse therapy is indicated for patients with paroxysms of tachycardia that occur 2 or more times a month and require medical assistance for their relief; with more rare, but prolonged paroxysms, complicated by the development of acute left ventricular or cardiovascular failure. In patients with frequent, short episodes of supraventricular tachycardia that resolve spontaneously or with vagal maneuvers, indications for anti-relapse therapy are questionable.
Long-term anti-relapse therapy of paroxysmal tachycardia is carried out with antiarrhythmic drugs (quinidine bisulfate, disopyramide, moracizin, etacizin, amiodarone, verapamil, etc.), as well as cardiac glycosides (digoxin, lanatoside). The selection of the drug and dosage is carried out under electrocardiographic control and control of the patient's well-being.
The use of β-blockers for the treatment of paroxysmal tachycardia can reduce the likelihood of the transition of the ventricular form to ventricular fibrillation. The most effective use of β-blockers in conjunction with antiarrhythmic drugs, which allows you to reduce the dose of each of the drugs without compromising the effectiveness of the therapy. Prevention of recurrence of supraventricular paroxysms of tachycardia, reduction in the frequency, duration and severity of their course is achieved by continuous oral administration of cardiac glycosides.
Surgical treatment is resorted to with a particularly severe course of paroxysmal tachycardia and the ineffectiveness of anti-relapse therapy. As a surgical aid for paroxysms of tachycardia, destruction (mechanical, electrical, laser, chemical, cryogenic) of additional pathways for impulse conduction or ectopic foci of automatism, radiofrequency ablation (RFA of the heart), implantation of pacemakers with programmed modes of paired and “exciting” stimulation, or implantation of electrical defibrillators.

Questions from users

How is Propanorm combined with β-blockers and calcium antagonists?

Propanorm is well combined with beta-blockers and calcium antagonists, especially in patients with coronary artery disease (without cicatricial changes) and arterial hypertension, but we must not forget that Propanorm is also effective in patients with vagotonic arrhythmias (when atrial fibrillation occurs at night or early morning against the background of relative bradycardia) and in this case, drugs that can slow down heart rate (which include beta-blockers and calcium antagonists) will reduce the antiarrhythmic effect of Propanorm, so it is better not to combine them in such patients.

If, when taking a loading dose of Propanorm, the relief of AF paroxysm is ineffective, what are our further actions? Can other antiarrhythmics, etc., be administered intravenously?

Zakharov Alexander Yurievich, Novorossiysk

If Propanorm did not stop the arrhythmia, it is necessary to wait 7-8 hours (since the antiarrhythmic effect of the drug is up to 8 hours and the rhythm can be restored before this time), the patient can take a beta-blocker for normosystole rhythm and reduce the symptoms of arrhythmia. After 8 hours, you can repeat the loading dose of Propanorm (450-600 mg at a time) or administer another antiarrhythmic drug.

Until this time, it is advisable not to use other antiarrhythmic drugs to exclude a proarrhythmic effect.

If hemodynamically unstable, electrical cardioversion should be used and not wait 8 hours.

The patient takes Propanorm 450 mg/day for prophylactic purposes. At the same time, his rhythm periodically breaks down. Is it possible to stop the paroxysm of atrial fibrillation with the same Propanorm ("pill in your pocket")? What dose of Propanorm to use?

Emergency cardiologist from Ryazan

First of all, it is necessary to evaluate the dynamics of the recurrence of paroxysms. If they have become more frequent only recently, look for the cause in the progression of the underlying disease (perhaps arterial hypertension is out of control or CHF is progressing).

If there is no deterioration from the side of the underlying disease, and the rhythm still breaks down at a constant dose of 450 mg / day, most likely this amount of propafenone is not enough to maintain sinus rhythm. In this case, for full prevention, the daily dose of the antiarrhythmic may be increased.

The resulting paroxysm can be stopped with the same Propanorm at a dose of 450 to 600 mg once, but it is necessary to take into account what dose of Propanorm the patient has already taken from the beginning of the day. The highest daily dose of propafenone is 900 mg.

Specify, what is the tactics of using Propanorm in AV blockade of I-II degree?

Anna Alekseevna from Sergiev Posad

The initial AV blockade of the I degree is not a contraindication for the appointment of Propanorm (AV blockade of the II-III degree is a common contraindication for all antiarrhythmics). If the drug is prescribed to a patient with 1st degree AV block, then after 3-5 days it is necessary to conduct a HM ECG to exclude its progression to the 2nd degree. If AV blockade of the 1st degree has passed into the 2nd degree, then according to the XM ECG it is necessary to assess when it appears and what are the pauses:

If the blockade appears only at night, then the drug can be continued, because. a tendency to blockade may be due to increased vagal influence on the sinus node and AV node at night.
If the pauses are more than 2500-3000 seconds, then it is better to cancel the drug. In this case, the tactics of managing the patient is as follows: if the drug prevents AF episodes well, it is necessary to implant the pacemaker and continue treatment with Propanorm. You can also try to continue treatment with the drug, but transfer the evening dose approximately to the early evening time - 18 hours (not at night), and take 2 tablets directly at night. bellataminal or Zelenin drops, after which, against this background, it is imperative to conduct an HM ECG again to control the effect.
If, against the background of stopping AF with the help of Propanorm, a pause of 2500 or more occurred (1500 ms is not scary), then a TPES test should be performed to exclude SSSU.

If AV blockade of the 1st degree appeared during treatment with Propanorm, it should be regarded as a side effect of the drug. In this case, it is better to cancel Propanorm.

What is the efficacy and safety of propafenone compared to sotalol?

Foreign (Reimold, 1993) and Russian (Almazov Research Institute of Cardiology, Tatarsky B.A.) comparative studies have shown that sotalol is somewhat inferior to propafenone in terms of antiarrhythmic efficacy, while against the background of its use, side effects are recorded 3 times more often (in including proarrhythmic effects - 1.5 times more often). It was also noted that due to side effects, sotalol has to be canceled 1.5 times more often.

More significant regarding the dangers of the use of sotalol is evidence of reports of cases of cardiac arrest and deaths obtained in a number of comparative studies of sotalol with propafenone.

How does propafenone differ from other widely used class 1C drugs (etacizin, allapinin)?

O.E. Dudin from Moscow

The range of properties of propafenone is much wider than that of allapinin and ethacizin, since it has not only class IC properties, but also has the characteristics of class II, III and IV antiarrhythmics. In addition to the main electrophysiological effect associated with the blockade of transmembrane sodium channels, propafenone is also characterized by β-blocking properties, explained by the structural similarity of the molecule with β-blockers. In addition, the main metabolites of propafenone (5-hydroxypropafenone and N-dipropylpropafenone) have a moderate calcium channel blocking effect. Thus, the antiarrhythmic effect of Propanorm is associated not only with the blockade of sodium channels, but also with the blockade of slow calcium channels and β-adrenergic blocking properties, which allows the drug to be widely used to treat various cardiac arrhythmias.

For a practicing physician, the most important factor remains that, unlike allapinin and etacizine, propafenone remains the only class 1C antiarrhythmic available in Russia, which for many years has been included in both international and Russian guidelines for the management of patients with arrhythmias. When prescribing allapinin and etatsizin, the doctor acts on the basis of his own empirical experience and small local studies, which does not allow him to be protected by international experience and recommendations of professional associations, which is unsafe in such a complex area as arrhythmology.

In addition, the cost of therapy with allapinin and etacizin is higher than treatment with Propanorm.

Recently I was on an improvement cycle with an emphasis on arrhythmology, I learned about Propanorm. So far, she has not prescribed “pure” antiarrhythmics - she was afraid of a proarrhythmic effect.

Ovchinnikova O.P. from Moscow

Unfortunately, when taking any antiarrhythmic drug, a proarrhythmic effect can occur. But against the background of taking propafenone, this side effect develops less frequently. Due to the fact that the efficacy and safety of propafenone has been proven in numerous studies, it is included as a priority drug in the official international and Russian recommendations for AF and PNT.

When prescribing Propanorm, it must be remembered that it is not prescribed for myocardial infarction, unstable coronary artery disease and severe CHF with reduced left ventricular EF (less than 50%).

Is there a proven way to transfer from Allapinin to Propanorm? What difficulties may arise in this case?

Terenina E.M. from Moscow

In the cardiological aspect, the transfer of a patient from Allapinin to Propanorm does not require special preparation: after Allapinin is canceled, Propanorm is immediately prescribed.

If the patient, while taking Allapinin, has managed to form an alkaloid dependence, manifested by such autonomic symptoms as tachycardia, a feeling of lack of air, it will be useful to prescribe small doses of anaprilin (10-20 mg).

In cases of more serious addiction (dependence) of the patient on Allapinin, a psychiatrist's consultation is necessary.

Recently, quite a lot of patients have contacted me, who, while taking Amiodarone, developed thyroid dysfunction in various manifestations (often hypothyroidism). Is it possible to transfer from Amiodarone to Propanorm? If this is possible, how can it be done in practice?

Kuzmin M.S. from Moscow

Indeed, taking amiodarone quite often causes extracardiac side effects. If you decide to transfer the patient from amiodarone to Propanorm, then this is possible.
It must be remembered that an important condition for the appointment of Propanorm is the preservation of the contractile function of the myocardium - EF> 40%.
Most likely, rhythm disturbance (more often extrasystole or AF) is the result of the course of diseases such as hypertension, coronary artery disease, CHF, or cardiomyopathy. We know that in all of the above diseases complicated by arrhythmia, along with antiarrhythmics, ?-blockers are prescribed as the main drugs that reduce the risk of sudden death.
When Amiodarone is canceled, it is necessary to increase the dose of?-blocker!
Since amiodarone is excreted from the body slowly (from 10 to 15 days), the moment at which Propanorm can be added to?-blockers is decided individually and depends on the heart rate.
If a patient has a tendency to tachycardia (heart rate more than 75-80 beats / min) after amiodarone withdrawal, one can think that amiodarone has already been metabolized and “does not work”. This moment serves as a signal for the appointment of Propanorm.
Ideally, of course, it is necessary to control the concentration of amiodarone in the blood and prescribe Propanorm at the moment when there is no more amiodarone left in the body, but, unfortunately, such a study is practically not done in Russia.

Is it advisable to use Propafenone as a second-line drug after an unsuccessful attempt at medical cardioversion with Amiodarone? The rhythm disruption occurred more than 48 hours ago, but the patient has been under medical supervision all this time and is receiving antiplatelet therapy. Is there a need for transesophageal echocardiography and subsequent 3-week preparation of the patient with indirect anticoagulants?

If an attack of atrial fibrillation lasts more than 48 hours, it is imperative to prescribe Warfarin and conduct an emergency EchoCG to make sure there are no blood clots. If, for example, an emergency EchoCG was done on the 4th day and it was made sure that there were no blood clots, then electrical cardioversion (with current) can be performed, but then continue taking warfarin for 3-4 weeks. If there are blood clots, then Warfarin should be continued for 4 weeks, then the state of emergency should be repeated again

EchoCG and decide on cardioversion.

If intravenous Kordaron fails to restore sinus rhythm, then after 4-6 hours, when Kordaron no longer works, you can use the Propanorm 450-600 mg regimen once.

If the patient took Kordaron in tablets to restore the rhythm and has already received a saturating dose, then Propanorm should not be used against this background, since Kordaron is excreted from 28 to 150 days. You can get proarrhythmic or other side effects with an unfavorable outcome.

How long can Propanorm be taken as a preventive measure?

Low organotoxicity combined with high efficiency are undeniable arguments in favor of prescribing propafenone for the maximum duration required.

Paroxysm of atrial fibrillation mkb 10

Nosological form Atrial fibrillation Atrial fibrillation ICD-10 diagnosis code I48 Phase primary diagnosis. Stage everything. In ICD-10, ARF and CRHD are classified as diseases of the circulatory system, class IX and. With paroxysms of atrial fibrillation, accompanied by. However, in modern classifications of mental illness ICD-10. functional class; rare paroxysms of atrial fibrillation with.

At the moment of paroxysm, relatively normal state of health in interictal. Patients meeting criteria I48 according to ICD-10 were included. Gordeev S. A. New relationship in the pathogenesis of atrial fibrillation.

Wed, 10/31/2012 - - admin. Paroxysm of atrial fibrillation less than a day old, age up to 60 years, including individual. Paroxysms in atrial fibrillation and atrial flutter after restoration of sinus rhythm; With creatinine clearance in the range of 10-30 ml / min dose. Nosological classification ICD-10. Vuchetich, 10-A. postoperative complications such as hypertensive crisis, paroxysmal atrial fibrillation and pneumonia, as well as pulmonary embolism and. In the international classification of sleep diseases, there are about 80. Less frequent 10-60% nocturnal asthma attacks, decreased libido and potency. and paroxysms of atrial fibrillation from regular became single.

Atrial fibrillation emergency care in the dentist's chair

Bibliography: Golikov A.P. and Zakin A.M. emergency care, p. 95, M. 1986; Mazur N.A. Fundamentals of clinical pharmacology and pharmacotherapy in cardiology, p. 238, M. 1988; Guide to cardiology, ed. R.I. Chazova, vol. 3, p. 587, M. 1982; Smetnev D.S. and Petrova L.I. Emergency conditions in the clinic of internal diseases, p. 72, M. 1977.

1. Small medical encyclopedia. - M. Medical Encyclopedia. 1991-96 2. First aid. - M. Great Russian Encyclopedia. 1994 3. Encyclopedic dictionary of medical terms. - M. Soviet encyclopedia. - 1982-1984

Servella syndrome
Heart race

INFLAMMATORY DISEASES OF THE CENTRAL NERVOUS SYSTEM (G00-G09)

G00 Bacterial meningitis, not elsewhere classified

Includes: arachnoiditis)
leptomeningitis)
meningitis) bacterial
pachymeningitis)
Excludes: bacterial:
meningoencephalitis ( G04.2)
meningomyelitis ( G04.2)

G00.0 Influenza meningitis. Meningitis due to Haemophilus influenzae
G00.1 Pneumococcal meningitis
G00.2 Streptococcal meningitis
G00.3 Staphylococcal meningitis
G00.8 Meningitis caused by other bacteria
Meningitis caused by:
Friedlander's wand
Escherichia coli
Klebsiella
G00.9 Bacterial meningitis, unspecified
Meningitis:
purulent NOS
pyogenic NOS
pyogenic NOS

G01* Meningitis in bacterial diseases classified elsewhere

Meningitis (for):
anthrax ( A22.8+)
gonococcal ( A54.8+)
leptospirosis ( A27. -+)
listeriosis ( A32.1+)
Lyme disease ( A69.2+)
meningococcal ( A39.0+)
neurosyphilis ( A52.1+)
salmonellosis ( A02.2+)
syphilis:
congenital ( A50.4+)
secondary ( A51.4+)
tuberculosis ( A17.0+)
typhoid fever ( A01.0+)
Excludes: meningoencephalitis and meningomyelitis due to bacterial
diseases classified elsewhere ( G05.0*)

G02.0* Meningitis in viral diseases classified elsewhere
Meningitis (caused by a virus):
adenovirus ( A87.1+)
enteroviral ( A87.0+)
herpes simplex ( B00.3+)
infectious mononucleosis ( B27. -+)
measles ( B05.1+)
mumps (mumps) B26.1+)
rubella ( B06.0+)
chicken pox ( B01.0+)
shingles ( Q02.1+)
G02.1* Meningitis with mycoses
Meningitis (for):
candidiasis ( Q37.5+)
coccidioidomycosis ( B38.4+)
cryptococcal ( B45.1+)
G02.8* Meningitis in other specified infectious and parasitic diseases classified elsewhere
Meningitis due to:
African trypanosomiasis ( B56. -+)
Chagas disease ( B57.4+)

G03 Meningitis due to other and unspecified causes

Includes: arachnoiditis)
leptomeningitis) due to other and unspecified
meningitis) causes
pachymeningitis)
Excludes: meningoencephalitis ( G04. -)
meningomyelitis ( G04. -)

G03.0 Non-pyogenic meningitis. Non-bacterial meningitis
G03.1 chronic meningitis
G03.2 Benign recurrent meningitis [Mollare]
G03.8 Meningitis due to other specified pathogens
G03.9 Meningitis, unspecified. Arachnoiditis (spinal) NOS

G04 Encephalitis, myelitis and encephalomyelitis

Includes: acute ascending myelitis
meningoencephalitis
meningomyelitis
Excludes: benign myalgic encephalitis ( G93.3)
encephalopathy:
NOS ( G93.4)
alcoholic genesis ( G31.2)
toxic ( G92)
multiple sclerosis ( G35)
myelitis:
acute transverse ( G37.3)
subacute necrotizing ( G37.4)

G04.0 Acute disseminated encephalitis
encephalitis)
Encephalomyelitis) post-immunization
If necessary, identify the vaccine
G04.1 Tropical spastic paraplegia
G04.2 Bacterial meningoencephalitis and meningomyelitis, not elsewhere classified
G04.8 Other encephalitis, myelitis and encephalomyelitis. Postinfectious encephalitis and encephalomyelitis NOS
G04.9 Encephalitis, myelitis or encephalomyelitis, unspecified. Ventriculitis (cerebral) NOS

G05* Encephalitis, myelitis and encephalomyelitis in diseases classified elsewhere

Includes: meningoencephalitis and meningomyelitis in diseases
classified elsewhere

If it is necessary to identify the infectious agent, use an additional code ( B95-B97).

G06.0 Intracranial abscess and granuloma
Abscess (embolic):
brain [any part]
cerebellar
cerebral
otogenic
Intracranial abscess or granuloma:
epidural
extradural
subdural
G06.1 Intravertebral abscess and granuloma. Abscess (embolic) of the spinal cord [any part]
Intravertebral abscess or granuloma:
epidural
extradural
subdural
G06.2 Extradural and subdural abscess, unspecified

G07* Intracranial and intravertebral abscess and granuloma in diseases classified elsewhere

brain abscess:
amoebic ( A06.6+)
gonococcal ( A54.8+)
tuberculosis ( A17.8+)
Cerebral granuloma in schistosomiasis B65. -+)
Tuberculoma:
brain ( A17.8+)
meninges ( A17.1+)

G08 Intracranial and intravertebral phlebitis and thrombophlebitis

Septic(s):
embolism)
endophlibitis)
phlebitis) intracranial or intravertebral
thrombophlebitis) venous sinuses and veins
thrombosis)
Excludes: intracranial phlebitis and thrombophlebitis:
complicating:
abortion, ectopic or molar pregnancy ( O00 -O07 , O08.7 )
pregnancy, childbirth or the postpartum period ( O22.5, O87.3)
non-purulent origin ( I67.6); non-purulent intravertebral phlebitis and thrombophlebitis ( G95.1)

G09 Sequelae of inflammatory diseases of the central nervous system

Note This rubric should be used to refer to
conditions primarily classified under headings

G00-G08(excluding those marked with *) as the cause of consequences that are themselves attributed to
Other headings The term “sequelae” includes conditions specified as such or as late manifestations or effects existing for a year or more after the onset of the causing condition. When using this rubric, one should be guided by the relevant recommendations and rules for coding morbidity and mortality given in v.2.

SYSTEMIC ATROPHY AFFECTING PREFERENTIALLY THE CENTRAL NERVOUS SYSTEM (G10-G13)

G10 Huntington's disease

Huntington's chorea

G11 Hereditary ataxia

Excludes: hereditary and idiopathic neuropathy ( G60. -)
cerebral palsy ( G80. -)
metabolic disorders ( E70-E90)

G11.0 Congenital non-progressive ataxia
G11.1 Early cerebellar ataxia
Note Usually starts in people under 20 years of age
Early cerebellar ataxia with:
essential tremor
myoclonus [Hunt's ataxia]
with preserved tendon reflexes
Friedreich's ataxia (autosomal recessive)
X-linked recessive spinocerebellar ataxia
G11.2 Late cerebellar ataxia
Note Usually starts in people over 20 years of age
G11.3 Cerebellar ataxia with impaired DNA repair. Teleangiectatic ataxia [Louis-Bar syndrome]
Excludes: Cockayne syndrome ( Q87.1)
pigment xeroderma ( Q82.1)
G11.4 Hereditary spastic paraplegia
G11.8 Other hereditary ataxia
G11.9 Hereditary ataxia, unspecified
Hereditary (th) cerebellar (th):
ataxia NOS
degeneration
disease
syndrome

G12 Spinal muscular atrophy and related syndromes

G12.0 Infantile spinal muscular atrophy, type I [Werdnig-Hoffmann]
G12.1 Other hereditary spinal muscular atrophies. Progressive bulbar palsy in children [Fazio-Londe]
Spinal muscular atrophy:
adult form
child form, type II
distal
juvenile form, type III [Kugelberg-Welander]
scapular-peroneal form
G12.2 Motor neuron disease. Familial motor neuron disease
Lateral sclerosis:
amyotrophic
primary
Progressive(s):
bulbar paralysis
spinal muscular atrophy
G12.8 Other spinal muscular atrophies and related syndromes
G12.9 Spinal muscular atrophy, unspecified

G13* Systemic atrophies affecting predominantly the central nervous system in diseases classified elsewhere

G13.0* Paraneoplastic neuromyopathy and neuropathy
Carcinomatous neuromyopathy ( C00-C97+)
Neuropathy of the sense organs in the tumor process [Denia-Brown] ( C00-D48+)
G13.1* Other systemic atrophies affecting predominantly the central nervous system in neoplastic diseases. Paraneoplastic limbic encephalopathy ( C00-D48+)
G13.2* Systemic atrophy in myxedema, affecting predominantly the central nervous system ( E00.1+, E03. -+)
G13.8* Systemic atrophy affecting predominantly the central nervous system in other disorders classified elsewhere

EXTRAPYRAMID AND OTHER MOTOR DISORDERS (G20-G26)

G20 Parkinson's disease

Hemiparkinsonism
shaking paralysis
Parkinsonism or Parkinson's disease:
NOS
idiopathic
primary

G21 Secondary parkinsonism

G21.0 Malignant neuroleptic syndrome. If necessary, identify the drug
use an additional external cause code (class XX).
G21.1 Other forms of secondary drug-induced parkinsonism.
G21.2 Secondary parkinsonism caused by other external factors
If necessary, to identify an external factor, use an additional code of external causes (class XX).
G21.3 Postencephalitic parkinsonism
G21.8 Other forms of secondary parkinsonism
G21.9 Secondary parkinsonism, unspecified

G22* Parkinsonism in diseases classified elsewhere

syphilitic parkinsonism ( A52.1+)

G23 Other degenerative diseases of the basal ganglia

Excludes: polysystemic degeneration ( G90.3)

G23.0 Hallervorden-Spatz disease. Pigmentary pallidar degeneration
G23.1 Progressive supranuclear ophthalmoplegia [Steele-Richardson-Olshevsky]
G23.2 Striatonigral degeneration
G23.8 Other specified degenerative diseases of the basal ganglia. Calcification of the basal ganglia
G23.9 Degenerative disease of basal ganglia, unspecified

G24 Dystonia

Includes: dyskinesia
Excludes: athetoid cerebral palsy ( G80.3)

G24.0 Drug induced dystonia. If necessary, identify the drug
use an additional external cause code (class XX).
G24.1 Idiopathic familial dystonia. Idiopathic dystonia NOS
G24.2 Idiopathic non-familial dystonia
G24.3 Spasmodic torticollis
Excludes: torticollis NOS ( M43.6)
G24.4 Idiopathic oro-facial dystonia. Oro-facial dyskinesia
G24.5 Blepharospasm
G24.8 Other dystonias
G24.9 Dystonia, unspecified. Dyskinesia NOS

G25 Other extrapyramidal and movement disorders

G25.0 Essential tremor. familial tremor
Excludes: tremor NOS ( R25.1)
G25.1 Drug induced tremor
If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.
G25.2 Other specified forms of tremor. Intention tremor
G25.3 Myoclonus. Drug-induced myoclonus. If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.
Excludes: facial myokymia ( G51.4)
myoclonic epilepsy ( G40. -)
G25.4 drug-induced chorea
If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.
G25.5 Other types of chorea. Chorea NOS
Excludes: chorea NOS with cardiac involvement ( I02.0)
chorea of Huntington ( G10)
rheumatic chorea ( I02. -)
chorea of Sidenhen ( I02. -)
G25.6 Drug-induced tics and other organic tics
If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.
Excludes: de la Tourette syndrome ( F95.2)
tick NOS ( F95.9)
G25.8 Other specified extrapyramidal and movement disorders
Restless legs syndrome. Chained Man Syndrome
G25.9 Extrapyramidal and movement disorder, unspecified

G26* Extrapyramidal and movement disorders in diseases classified elsewhere

OTHER DEGENERATIVE DISEASES OF THE NERVOUS SYSTEM (G30-G32)

G30 Alzheimer's disease

Includes: senile and presenile forms
Excludes: senile:
brain degeneration NEC ( G31.1)
dementia NOS ( F03)
senility NOS ( R54)

G30.0 Early Alzheimer's
Note The onset of the disease is usually in people under the age of 65 years.
G30.1 Late Alzheimer's disease
Note The onset of the disease is usually in people over the age of 65 years.
G30.8 Other forms of Alzheimer's disease
G30.9 Alzheimer's disease, unspecified

G31 Other degenerative diseases of the nervous system, not elsewhere classified

Excludes: Reye's syndrome ( G93.7)

G31.0 Limited atrophy of the brain. Pick's disease. Progressive isolated aphasia
G31.1 Senile degeneration of the brain, not elsewhere classified
Excludes: Alzheimer's disease ( G30. -)
senility NOS ( R54)
G31.2 Degeneration of the nervous system caused by alcohol
Alcoholic:
cerebellar:
ataxia
degeneration
cerebral degeneration
encephalopathy
Alcohol-induced autonomic nervous system disorder
G31.8 Other specified degenerative diseases of the nervous system. Gray matter degeneration [Alpers disease]
Subacute necrotizing encephalopathy [Leig's disease]
G31.9 Degenerative disease of nervous system, unspecified

G32* Other degenerative disorders of the nervous system in diseases classified elsewhere

G32.0* Subacute combined degeneration of the spinal cord in diseases classified elsewhere
Subacute combined degeneration of the spinal cord with vitamin deficiency AT 12 (E53.8+)
G32.8* Other specified degenerative disorders of the nervous system in diseases classified elsewhere

DEMIELINIZING DISEASES OF THE CENTRAL NERVOUS SYSTEM (G35-G37)

G35 Multiple sclerosis

Multiple sclerosis:
NOS
brain stem
spinal cord
disseminated
generalized

G36 Other form of acute disseminated demyelination

Excludes: postinfectious encephalitis and encephalomyelitis NOS ( G04.8)

G36.0 Neuromyelitis optica [Devic's disease]. Demyelination in optic neuritis
Excludes: optic neuritis NOS ( H46)
G36.1 Acute and subacute hemorrhagic leukoencephalitis [Hurst's disease]
G36.8 Another specified form of acute disseminated demyelination
G36.9 Acute disseminated demyelination, unspecified

G37 Other demyelinating diseases of the central nervous system

G37.0 diffuse sclerosis. Periaxial encephalitis, Schilder's disease
Excludes: adrenoleukodystrophy [Addison-Schilder] ( E71.3)
G37.1 Central demyelination of the corpus callosum
G37.2 Central pontine myelinolysis
G37.3 Acute transverse myelitis in demyelinating disease of the central nervous system
Acute transverse myelitis NOS
Excludes: multiple sclerosis ( G35)
neuromyelitis optica [Devic's disease] ( G36.0)
G37.4 Subacute necrotizing myelitis
G37.5 Concentric sclerosis [Balo]
G37.8 Other specified demyelinating diseases of the central nervous system
G37.9 Demyelinating disease of the central nervous system, unspecified

episodic and paroxysmal disorders (G40-G47)

G40 Epilepsy

Excludes: Landau-Kleffner syndrome ( F80.3)
convulsive seizure NOS ( R56.8)
epileptic status ( G41. -)
paralysis todd ( G83.8)

G40.0 Localized (focal) (partial) idiopathic epilepsy and epileptic syndromes with seizures with focal onset. Benign childhood epilepsy with EEG peaks in the central temporal region
Pediatric epilepsy with paroxysmal activity, no EEG in the occipital region
G40.1 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with simple partial seizures. Seizures without change of consciousness. Simple partial seizures turning into secondarily
generalized seizures
G40.2 Localized (focal) (partial) symptomatic epilepsy and epileptic syndromes with complex partial seizures. Seizures with altered consciousness, often with epileptic automatism
Complex partial seizures progressing to secondary generalized seizures
G40.3 Generalized idiopathic epilepsy and epileptic syndromes
Benign(s):
myoclonic epilepsy in early childhood
neonatal seizures (familial)
Childhood epileptic absences [pycnolepsy]. Epilepsy with grand mal seizures on awakening
Juvenile:
absence epilepsy
myoclonic epilepsy [impulsive petit mal]
Nonspecific epileptic seizures:
atonic
clonic
myoclonic
tonic
tonic-clonic
G40.4 Other types of generalized epilepsy and epileptic syndromes
epilepsy with:
myoclonic absences
myoclonic-astatic seizures

Baby spasms. Lennox-Gastaut syndrome. Salaam teak. Symptomatic early myoclonic encephalopathy
West syndrome
G40.5 Special epileptic syndromes. Epilepsy partial continuous [Kozhevnikova]
Epileptic seizures associated with:
drinking alcohol
use of medicines
hormonal changes
sleep deprivation
stress factors
If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.
G40.6 Seizures grand mal, unspecified (with or without minor seizures)
G40.7 Minor seizures, unspecified without grand mal seizures
G40.8 Other specified forms of epilepsy. Epilepsy and epileptic syndromes not defined as focal or generalized
G40.9 Epilepsy, unspecified
Epileptic:
convulsions NOS
seizures NOS
seizures NOS

G41 Status epilepticus

G41.0 Epileptic status grand mal (convulsive seizures). Tonic-clonic status epilepticus
Excludes: continuous partial epilepsy [Kozhevnikova] ( G40.5)
G41.1 Zpileptic status of petit mal (small seizures). Epileptic status of absences
G41.2 Complex partial status epilepticus
G41.8 Other specified status epilepticus
G41.9 Epileptic status, unspecified

G43 Migraine

Excludes: headache NOS ( R51)

G43.0 Migraine without aura [simple migraine]
G43.1 Migraine with aura [classic migraine]
Migraine:
aura without headache
basilar
equivalents
familial hemiplegic
hemiplegic
With:
aura with acute onset
long aura
typical aura
G43.2 migraine status
G43.3 Complicated migraine
G43.8 Another migraine. Ophthalmoplegic migraine. retinal migraine
G43.9 Migraine, unspecified

G44 Other headache syndromes

Excludes: atypical facial pain ( G50.1)
headache NOS ( R51)
trigeminal neuralgia ( G50.0)

G44.0 Histamine headache syndrome. Chronic paroxysmal hemicrania.

"Histamine" headache:
chronic
episodic
G44.1 Vascular headache, not elsewhere classified. Vascular headache NOS
G44.2 Tension headache. Chronic tension headache
Episodic tension headache. Tension headache NOS
G44.3 Chronic post-traumatic headache
G44.4 Headache due to medication, not elsewhere classified
If it is necessary to identify the medicinal product, an additional code of external causes (class XX) is used.
G44.8 Other specified headache syndrome

G45 Transient transient cerebral ischemic attacks [attacks] and related syndromes

Excludes: neonatal cerebral ischemia ( P91.0)

G45.0 Syndrome of the vertebrobasilar arterial system
G45.1 Carotid Syndrome (hemispheric)
G45.2 Multiple and bilateral cerebral artery syndromes
G45.3 transient blindness
G45.4 Transient global amnesia
Excludes: amnesia NOS ( R41.3)
G45.8 Other transient cerebral ischemic attacks and related syndromes
G45.9 Transient cerebral ischemic attack, unspecified. Spasm of the cerebral artery
Transient cerebral ischemia NOS

G46* Cerebral vascular syndromes in cerebrovascular diseases ( I60-I67+)

G46.0* Syndrome of the middle cerebral artery ( I66.0+)
G46.1* Syndrome of the anterior cerebral artery ( I66.1+)
G46.2* Posterior cerebral artery syndrome ( I66.2+)
G46.3* Stroke syndrome in the brain stem ( I60-I67+)
Syndrome:
Benedict
Claude
Fauville
Miyart-Jublé
Wallenberg
Weber
G46.4* Cerebellar stroke syndrome ( I60-I67+)
G46.5* Pure motor lacunar syndrome ( I60-I67+)
G46.6* Purely sensitive lacunar syndrome ( I60-I67+)
G46.7* Other lacunar syndromes ( I60-I67+)
G46.8* Other cerebrovascular syndromes in cerebrovascular diseases ( I60-I67+)

G47 Sleep disorders

Excluded: nightmares ( F51.5)
sleep disorders of non-organic etiology ( F51. -)
night terrors F51.4)
sleepwalking ( F51.3)

G47.0 Sleep disturbances and sleep maintenance [insomnia]
G47.1 Sleepiness disorders [hypersomnia]
G47.2 Sleep and wake cycle disorders. Delayed sleep phase syndrome. Sleep-wake cycle disorder
G47.3 sleep apnea
Sleep Apnea:
central
obstructive
Excludes: Pickwickian syndrome ( E66.2)
sleep apnea in newborns P28.3)
G47.4 Narcolepsy and cataplexy
G47.8 Other sleep disorders. Kleine-Levin syndrome
G47.9 Sleep disorder, unspecified