Hospital therapy. Rheumatism (rheumatic fever) Rheumatism etiology pathogenesis clinic diagnostics treatment

Hypothermia, genetic predisposition, malnutrition, physical and mental overwork play a certain role in the development of rheumatic processes. The infectious-allergic origin of rheumatism has been scientifically proven.

The primary causative agent of the disease is streptococcus. The root cause of rheumatism can be angina (1-3% chance of risk) or scarlet fever (very rare). The protein shell of group A beta-hemolytic streptococcus provokes the formation of M-antibodies and lysis (destruction) of leukocytes. At the same time, streptococcus secretes toxic substances, including streptolysin, which has a cardiotoxic effect. In 2/3 cases, streptococcus is detected by sowing from the pharynx.

In addition to hemolytic streptococcus, a certain reaction of the body is necessary for the development of inflammation (allergic theory). Rheumatic inflammation develops only after angina, scarlet fever in 2-3 weeks. Therefore, the pathogenesis of rheumatism is divided into 3 stages:

1. Lasts about 2 weeks from acute sore throat to symptom onset.
2. Acute rheumatism is manifested by severe hyperergic reactions, severe symptoms.
3. Autosensitization - the formation of secondary antibodies that support recurrent inflammation in connection with non-specific infections or with repeated entry into the body of streptococcus.

Rheumatism can be secretive for a long time. Symptoms are determined by localization inflammatory process and very varied.

The pathogenesis of the rheumatic process is very complex, and many of its aspects have not yet been elucidated. However, the main links in the pathogenesis of the disease have been clarified. The leading role is assigned to the direct damaging effect of streptococcal toxins on the tissue structures of the heart and other organs, as well as the violation of immunogenesis and the mechanisms of neuroendocrine regulation, etc.

Currently great importance in the development of rheumatism, a perversion of the reactions of immunological reactivity as a result of hereditary or acquired characteristics of the organism is assigned. Exposure to streptococcal toxins results in the production of anti-streptococcal antibodies. Under the influence of streptococcal toxins (first of all, antistreptolysin), their decay products are released on the heart tissues, which, together with toxins, form autoantigens.

The main significance in the defeat of the heart in rheumatism is given to the influence of streptococcal toxins on the tissues of the heart and impaired immunogenesis with the development of allergic and autoimmune reactions against the background of genetic predisposition in conditions of impaired neuroendocrine regulation.

Intracellular soluble streptococcal antigens have a tropism for the connective tissue of the heart and blood vessels, due to their antigenic relationship. This contributes to the permanent and predominant damage to the heart, as well as the long-term persistence of streptococcus in the body and tissues of the patient. Streptococcal toxins damage the membranes of lysosomes of cells in the focus of inflammation, which leads to the release of enzymes (proteases, nucleases, phosphatases) from them, causing depolymerization of connective tissue elements with the destruction of its protein-polysaccharide complexes (glucosaminoglycans with proteins).

Morphofunctional changes in the cellular elements of the connective tissue develop, in particular mast cells- their number changes, degranulation intensifies, the severity of which reflects the activity of the rheumatic process. As a result, biological substances enter the tissue and microvasculature. active substances inflammatory mediators (histamine, serotonin, bradykinin, etc.)

Genetically determined (hereditary) features of tissues, organs, as well as protective mechanisms for fighting streptococcal infection play a role (increased tendency to sensitization, increased response to irritant antigens, unusual rapid proliferation of lymphoid and plasma cells, a tendency to hyperproduction of antibodies and perversion of immunological reactions ).

Various elements of the connective tissue of the vascular wall and myocardium are affected (myocyte-sarcolemma, sarcoplasm, discs and intercalary plates, valve glycoprotein, etc.). There is a splitting of myofibrils, smoothness of their transverse structure, rupture and fusion of cells, which is clearly expressed in the acute phase of the disease.

Arising under the influence of prolonged intoxication and other adverse factors, disorders of the central and vegetative nervous system, as well as the functions of the endocrine glands (pituitary gland, adrenal glands) lead to a change in the neuroendocrine regulation of immunological reactivity and other processes in the body and, as a result, to a violation of adaptation mechanisms.

In the complex mechanism of the development of the rheumatic process, a significant role is given to immunological reactions, which in this disease often proceed as immediate in acute and delayed - with a protracted, sluggish course. Immunological reaction on immediate type it is caused by humoral factors — antibodies and intracellular soluble antigens of a streptococcus.

It leads to the development of the exudative component of the rheumatic process, which determines the severity of clinical manifestations, the severity of the course and the activity of the disease. The immunological reaction of the delayed type is due to cellular factors and antibodies to intracellular soluble streptococcal antigens. At the same time, a specific component of the rheumatic process develops - a granuloma, on which the outcome of the disease depends.

Etiology: microflora of the gastrointestinal tract.

Pathogenesis: meat food - meat chyme
activates MF, making it pathogenic.

Modern neurovascular theory
(angioneurotic, Ricker's theory):
the process of vascular spasms begins
with muscle spasms, disturbed
blood circulation, hypoxia, stole.
vascular permeability, mo intrude
in the wall, inflammation.

1. Acute simple - the initial form (anemia,
edema, hemosiderin deposition - result
circulatory disorders, pain
syndrome).

2. superficial appendicitis - in depth
crypt, a small focus of inflammation occurs
(primary effect).

3. phlegmonous appendicitis - inflammatory
process from the primary affect on the environment
tissue, pus affects most
process walls.

4. apostematous (abscess) - in the wall
the process forms an abscess;
accumulates a large amount
leukocytes, focus of necrosis, leukocyte
enzymes liquefy necrosis, cavity pus,
aposteme (abscess).

5. primary gangrenous - as a result
prolonged vasospasm, embolism.

6.secondary gangrenous - inflammation
captures the wall of blood vessels to the intima,
the vessel is thrombosed, necrosis.

More severe changes occur in
distal part of the process.

1. sclerosis (with uneven sclerosis in the wall
process m. diverticula - protrusions).

2. obliteration (overgrowth) - distal
part is almost completely separated from
proximal, bag of pus.

3. empyema of the process

4. dropsy process - filling with liquid.

5.preserving mucosal areas
membranes - mucus fills the distal
part, sac of mucus, mucocelium.

6.pyliflebitis, typhlitis.

Hypertension is a chronic
disease, the main clinical
a symptom of which is prolonged
and a persistent increase in blood pressure (hypertension).

It is also called essential hypertension.

Rarely, hypertension is
a symptom of some other disease
it is called secondary (symptomatic)
hypertension.

1. Renal hypertension - kidney damage
- chr.pyelonephritis, o. and hr. glomerulonephritis,
diabetic nephropathy, tumors
kidneys, renal artery stenosis.

2. Endocrine - disease or symptom
Itsenko-Cushing, pheochromocytoma (tumor
adrenal gland - excess catecholamines)

3. Neurogenic - increased intracranial
pressure (trauma, tumor, abscess,
hemorrhage), damage to the hypothalamus.

4. Others - coarctation of the aorta and other vessels.

Etiology of GB. Risk factors -

Multifactorial disease - combination
genetic predisposition and
factors environment. Greatest
the value of psycho-emotional overstrain
(stress, conflicts), excessive
NaCl intake, smoking, sedentary
Lifestyle.

Affects gender, age, cholesterol level
blood, smoking, hypercholesterolemia,
diabetes, obesity increases the development
GB.

Pathogenesis

1. t. Myasnikova - reducing the brake
influence of the cerebral cortex on the subcortical
vegetative centers, especially
pressor - overexcitation of these
centers vascular
spasmincrease
ADswitch on
renal endogenous mechanism
regulation of blood pressure. Reduced brake
the influence of the cortex is due to long-term
stressful situations.

2. Membrane t. Postnova - initial
factor in the development of HD - generalized
consequential defect in membrane ionic
cell pumps. Decreased activity
Sa pump. Excess Ca 2 and Na in the cytoplasm of smooth muscle cells
causes them to spasm, and increase
sensitivity to pressor factors.

The point of application for GB is the arteries and
arterioles.

Stress  violation of the central regulation of blood pressure  increased activity of the sympathetic-adrenal
systemshypersecretion
catecholamines - due to persistent
vascular spasm is activated
renin-angiotensin c-a (ischemia) increased cardiac output - increased
systolic pressure - benign
courserelease of reninangiotensin II, stimulation of production
aldosteroneretention of Na and H2Opersistent vasoconstriction and increased
HELL.

Etiology and pathogenesis of rheumatism

The role of B-hemolytic streptococcus group A in the development of rheumatism is generally recognized. Rheumatism has long been associated with acute and chronic streptococcal diseases (tonsillitis, pharyngitis, tonsillitis, scarlet fever, etc.), which are detected in approximately 80% of patients with rheumatism. Re-exacerbation of chronic focal infections or layering of acute streptococcal diseases is the decisive moment, leading after 2 to 3 weeks directly to the development of the rheumatic process.

The streptococcal ethnology of rheumatism is evidenced by the frequent sowing of streptococcus from the contents of the crypts of the tonsils and blood, the detection of streptococcal antigens in the blood and urine of patients with rheumatism and the increase in the titer of antistreptococcal antibodies (antistreptolysin O, antihyaluronidase, antifibrinolysin-antistreptokinase), positive skin tests with streptococcal toxin, as well as a significant reduction in the frequency of primary incidence of rheumatism, its exacerbations and relapses in children who received rational antistreptococcal therapy for the purpose of prevention.

A certain importance in the development of rheumatism, especially in protracted and sluggish forms of the disease, is currently assigned to L-forms of streptococcus, filtered through bacterial filters and formed under the influence of damaging factors (V. D. Timakov and G. Ya. Kagan, 1962). The etiological role of viruses, including Coxsackie Ai3, both as an independent factor and in combination with streptococcus (G.D. Zalessky) has not yet received convincing confirmation and requires further study.

3. empyema of the process

The course of the disease may be benign
(benign hypertension) and
malignant (malignant)
hypertension).

malignant hypertension. More often
occurs after a period of benign
flow, which continues on average
10 years. Rarely malignant course
observed from the very beginning.

Initial clinical manifestations
visual disturbances, severe headaches
pain, hematuria. diastolic pressure
above 130 mm Hg diagnostic criterion,
allowing differentiation of malignancy.

from benign - disc edema
optic nerve, with albuminous effusion,
retinal hemorrhage.

Dominant in malignant form
symptoms characteristic of hypertension
crisis, i.e. a sharp increase in blood pressure.

Morphological changes - corrugation
and destruction of endothelial basement membranes,
arrangement of endothelial cells
palisades, plasma impregnation
arteriole walls, fibrinoid necrosis
walls, joining thrombosis. Per
due to this, heart attacks develop,
hemorrhages.

1. preclinical - transient hypertension
- period 1 BP, well amenable to correction.
Moderate compensatory hypertrophy
left ventricle of the heart.

2. stage of widespread changes
arteries. Characterized by persistent
an increase in blood pressure. Changes in arterioles
the most typical symptom is hyalinosis
(arteriosclerosis). The most common are the kidneys
brain, pancreas,
intestines, adrenal glands.

Changes in the arteries of the muscular,
musculo-elastic and muscular types
– elastofibrosis and atherosclerosis, elastofibrosis
- splitting of the internal elastic
membranes and its sclerosis. atherosclerosis on
background GB has features - more
widespread, involved
arteries of the muscular type (which is not typical
for atherosclerosis in its pure form),
fibrous plaques are circular, and
non-segmental character, which leads to
development of stenosing atherosclerosis.
Most often in the arteries of the heart, brain,
kidneys, vertebral arteries.

Myocardial hypertrophy increases, thickness
left ventricle - 2-3 cm. Occurs
relative insufficiency
myocardial blood supply, which
the occurrence of diffuse small focal
cardiosclerosis

and signs of heart failure
insufficiency.

3. Stage of change in internal organs.
Secondary organ changes can
develop slowly, leading to
development of parenchymal atrophy and sclerosis
stroma.

There may be acute or complicated
changes due to the addition of thrombosis,
prolonged persistent spasm, fibrinoid
necrosis (during a crisis) - heart attacks,
hemorrhages. in vessels, especially
microaneurysms develop in the brain
which leads to intracerebral
hemorrhages.

O
effusion pericarditis say then,
when accumulates in the heart sac
exudate. The nature of the exudate
effusion pericarditis
distinguish: serous-fibrinous; serous; purulent; hemorrhagic.

Cluster
fluid in the pericardial cavity creates
pressure on the outer surface of the heart
and that part of the vessels that lies in
cavity of the pericardial sac. it
the pressure gets stronger the more
amount of fluid in the pericardium
it builds up faster. Usually
intrathoracic pressure
negative and consistent
approximately 80-100 mm of water column.

in the superior and inferior vena cava, and
in the right atrium during diastole
pressure is also negative - 30-40
mm water column. Thereby
lumen of the vena cava and right atrium
keeps open. Comparatively enough
small and rapid increase in pressure
in the pericardial sac to make it difficult
blood flow to the right heart.

AT
result of exudative pericarditis
failure develops
blood circulation, the basis of pathogenesis
which lies the compression of the mouths of the hollow
and hepatic veins, right atrium
and difficulty in ventricular diastole.

Complaints
sick. Heat(more
38°-40°), sweating, weakness, headache
pain - symptoms of intoxication; dyspnea,
difficulty swallowing (squeezing
esophagus), nausea, vomiting (irritation
diaphragm), pressing pain in the area
hearts, palpitations (stagnation in the veins -
Bayi-Bridge sign).

At
examination reveals pallor of the skin
integument, cyanosis of the lips, puffiness
face, swelling of the jugular veins. Shortness of breath in
rest. Breitman's position
(kneeling position
patient).

AT
areas of the heart - protrusion of the intercostal
gaps, or heart hump.
The apex beat is weak and is
in the middle of cardiac dullness (because
pushed up by exudate
vertical position of the patient). AT
severe conditions may increase
abdomen due to ascites.

Palpation.
Pulse weak tension, frequent, soft.
Blood pressure is reduced -
less than 100/60 mm Hg Art. Venous pressure
increased to 300-400 mm of water column.
The apex beat is weak, determined
in the center of cardiac dullness.

Percussion.
The boundaries of the heart expand into everything
sides take the form of a triangle
or a trapezoid. Relative disappears
dullness of the heart, smoothed out
cardio-hepatic angle. Revealed
absolute sign of the presence of fluid
in the pericardial cavity, when the left border
cardiac dullness does not coincide with
heart impulse.

Auscultation.
Heart sounds are weakened due to
the presence of fluid in the pericardial
bag; pericardial friction rub with slight
the amount of exudate is heard more often
in zone III-IV
intercostal space on the left.

ECG
- low voltage curve (occurs
short circuit of potentials due to liquid).
ST shift is noted upward
from the isoelectric line in many
leads (concordant type of displacement).

At
X-ray examination shadow
the heart is evenly dilated
across and takes the form
equilateral trapezoid.

3. Vascular
failure. Classification,
etiology, clinic.

Mismatch
between the capacity of the vascular bed
and circulating blood volume due to
lack of vascular tone
and/or volume of circulating blood
(hypovolemia). Venous return deficit
(blood filling of the heart) can disrupt
pumping function of the heart. In such cases
changes are predominantly
according to the type of left ventricular failure
ejection with symptoms of cerebral ischemia,
heart, kidneys and other organs
hypovolemia - with centralization
circulation. Possible development
disseminated syndrome
intravascular coagulation.

Vascular
deficiency is a condition
arising from a decrease in tone, i.e.
e. constant tension of smooth muscles
vascular walls. Decreased tone
vessels leads to the fact that the extensibility
their walls increases: respectively
increases the capacity of the vascular bed,
that you lead the first place to the fall
blood pressure (hypotension).

Distinguish
acute and chronic vascular
failure.

Acute
vascular insufficiency appears
in the form of fainting and collapse.

Fainting occurs
due to acute short-term
disorders of the blood supply to the brain
brain. Fainting is observed in some
violations heart rate, in patients
with lesions of the vessels of the neck, feeding
brain (so-called
vertebrobasilar insufficiency)
at certain head turns,
in some cases (in debilitated patients
in some diseases of the nervous system,
in patients taking certain
medicines) with a sharp transition from
horizontal position to vertical.

Collapse -
it is usually more severe than
syncope, a form of acute vascular
insufficiency. Causes of the collapse
may be sharp infectious diseases,
in which the "center" is affected,
regulating vascular tone and located
in one part of the brain
(medulla), as well as walls
vessels; very severe pain (traumatic
shock);

extensive burns (while developing
collapse is involved not only
pain as such, but also some
toxic substances produced in
dead tissues): massive blood loss
(vascular tone during blood loss reflexively
rises to prevent falling
blood pressure, then
falls catastrophically). acute
allergic reaction to ingestion
blood of a foreign protein substance
(anaphylactic shock); acute cardiac
insufficiency in myocardial infarction
(cardiogenic shock) and extremely severe
arrhythmias (arrhythmogenic shock); overheating
(sun and heat stroke).

Causes of rheumatism and the mechanism of its development

CLASSIFICATION

Rheumatism is characterized by a variety of clinical manifestations, as well as alternating periods of exacerbation and attenuation of the process. Almost all organs can be affected, however, the cardiovascular system, joints, serous membranes, and the central nervous system are most often involved in the process.

In 1964, it was proposed working classification rheumatism (A.I. Nesterov), which was based on determining the phase of the rheumatic process and the degree of its activity, the features of changes in the heart and other organs, the nature of the course of the disease and the functional characteristics of blood circulation.

1 If possible, you should clarify the main localization of the heart lesion (myocarditis, endocarditis, pericarditis, pancarditis, coronarig), indicate the number of attacks, and also note whether there is a valvular defect (which one).

3. empyema of the process

The Russian rheumatological school strictly distinguishes true R. from the group of rheumatic diseases (Sokolsky-Buyo disease), investing in this concept not only acute episodes (“acute rheumatic fever”), but also all stages of the development of the disease with its tendency to relapse and the formation of valvular defects hearts. The latest version of the classification and nomenclature of R.

adopted at the symposium of the All-Union Scientific Society of Rheumatologists in December 1964. There are active and inactive phases of the disease. At the same time, the possibility of the transition of an active rheumatic process to the inactive phase of the disease and the division of the active phase into three degrees of activity are recognized. As the main component of the concept of "activity" is meant, first of all, the inflammatory rheumatic process in organs and tissues in its clinical and laboratory display.

At the same time, it is taken into account that the concept of "activity", like the concept of "disease", is not limited to inflammation, but certainly includes elements of damage, dystrophy, and a multifaceted protective and adaptive, including immune, response of the body. According to the nature of the course, acute, subacute, protracted, continuously recurrent and latent course of the rheumatic process are distinguished.

It should be noted that in the modern course of rheumatism, recurrent myocarditis sometimes, especially in childhood, can be without heart disease, as well as the inactive phase is characterized by the absence of changes in the heart (myocardiosclerosis or heart disease). In the active phase of the disease, among the lesions of other organs and systems, polyarthritis, serositis (pleurisy, peritonitis, abdominal syndrome), chorea, encephalitis, meningoencephalitis, neuropsychiatric disorders, nephritis, hepatitis, skin lesions, etc.

To characterize the features of the course of R., the clinical-temporal principle was used, in accordance with the Crimea, the active phase of the disease (rheumatic attack) can have an acute, subacute, and three variants of a chronic course: protracted, continuously recurrent, and latent (Table 2).

Thus, the working classification allows us to evaluate R. as a pathogenetically multifaceted disease in a particular patient with differentiation according to the degree of activity, the nature of the course, indicating the primary or recurrent nature of the rheumatic process, which greatly helps the doctor in determining the tactics of managing the patient and organizing an individualized dispensary observations.

Symptoms and Causes

After streptococcal angina, the disease may appear only after a few weeks. Main symptoms:

• increase in body temperature;
• the appearance of small nodules under the skin;
• chest pain;
• voluntary muscle twitches;
• skin rash;
• cardiopalmus.

In arthritis, rheumatism affects the joints. They swell, hurt, their redness, a local increase in temperature, and the formation of a liquid inside are observed. The course of treatment can last from 2 weeks.

Carditis - rheumatism of the heart, initially manifested by the symptoms described above. Then there is a rapid heartbeat, pain in chest. Perhaps the development of heart failure, characterized by shortness of breath, barking cough, abdominal pain, nausea and vomiting. The course of treatment is up to 5 months.

Abdominal syndrome has the following symptoms: nausea, vomiting, sharp migrating pains in the abdomen, stool disorders. More common in children.

The defeat of the lungs is accompanied by the development of rheumatic pneumonia or pulmonary vasculitis. In the second case, in addition to coughing and shortness of breath, hemoptysis can be observed.

Kidney damage is manifested by the development of glomerulonephritis, postinfectious nephritis, congestive kidney (in rare cases).

Rheumatic chorea - meningoencephalitis. Inflammatory changes in brain segments are more likely to develop in pregnant women and girls. The main symptom is muscle hypotension. Difficulty swallowing, patient cannot sit or walk. Rheumatism in this case is also manifested by aggressiveness, fatigue and absent-mindedness, emotional instability.

At the same time, drugs are prescribed to relieve inflammation, reduce destructive processes. The treatment regimen is selected only by a doctor based on the results of a diagnostic examination.

Pathogenesis

DIAGNOSIS CRITERIA FOR RHEUMATISM

Ticket
№ 29.

1. Inspection,
percussion and auscultation of the abdomen.
carried out in a standing and lying position.
Standing examination gives an idea of
able abdominal wall. Wherein
may show shape changes.
abdomen, retractions, bloating and asymmetric
plots. When examining lying in asthenics
in the region stomach are sometimes detected
normal peristaltic movements
stomach.

Pathological is gross
peristaltic movements in the form
shafts (deep waves coming from the left
hypochondrium to the right) periodically
lifting regions of the stomach and observed
in cases where there is difficulty
to promote gastric contents
due to narrowing of the exit from the stomach (
spasi, tumor, scar). Great importance
have visible peristaltic
bowel movements that cause
bizarre changes in the relief of the abdomen.

Always associated with the feeling of pain
stop with the passage of gases,
rumbling. Palpation Palpation
the most important diagnostic sign.
First, a superficial
palpation, i.e. indicative, for
this soft in a circular motion
consistently palpate the abdominal
wall of the right and left iliac
paraumbilical, subcostal areas,
then epigastrium, oculo-umbilical,
suprapubic areas.

At the same time, it is possible
identify local pain and
muscle tension in the abdominal wall, hernia
and tumors.
deep methodically sliding
palpation according to the model of the hand
lay flat and slightly bent
fingers during inhalation tend to
penetrate to the posterior abdominal wall.
Reaching it or the organ under study
slide the tops of the fingers in the direction
transverse to the axis of the organ under study
or to its edge.

Starting with the sigmoid
intestines. Blind, iliac. transverse colon
intestine. The sigmoid is palpable in the left
iliac region, mobile, painless,
thickness c thumb hands, smooth.
Blind in the form of a smooth, two fingers
thick rumbling, painless,
moderately movable cylinder.
deep palpation in people with stomach ulcers
and 12 intestines pain points are revealed:

dot
Boas in the region of the body of the 10th and 12th thoracic vertebrae.
At the same time, pain to the left of the vertebrae
indicates the localization of the ulcer
on the lesser curvature, to the right of the vertebrae
ulcer of the pylorus or 12 intestines.

dot
herbst - in the region of the transverse processes
3 lumbar vertebrae.

points
Openhovsky in the region of the spinous processes
7 and 10 vertebrae.

Percussion. By
Mendel definition of sensitivity
abdominal wall. Pain on impact
on the rectus abdominis muscles speaks of an ulcer
12 guts.

Auscultation.

listening
peristaltic bowel sounds.

Despite the polymorphism of R.'s clinical manifestations, clear patterns are noted in its development, which make it possible to single out the disease as a strictly defined nosological form. These, in particular, include R.'s connection with streptococcal infection (the presence of a latent period between the end of the infection and the initial symptoms of the disease). R. is also characterized by a tendency to polysyndromic clinical manifestations, the existence of typical variants of the onset and course of the disease, the presence in the clinical picture of the first identified A.A.

Kisel "absolute signs of rheumatism" and, finally, R.'s tendency to exacerbations and relapses. In a significant part of cases, the classic acute forms of R. end in complete recovery. At the same time, mainly with a protracted course and relapses of R., conditions may arise that contribute to the subsequent transition of the disease into a chronic, torpid, often aggravated process.

AI Nesterov (1973) identifies three periods in the development of the rheumatic process. The first (hidden) period usually lasts 2-4 weeks after the end of the streptococcal infection until the initial manifestations of a rheumatic attack. It is characterized by processes of toxic-infectious damage to connective tissue structures and immunological restructuring of the body in response to streptococcal antigenic effects.

Clinically, this period proceeds either asymptomatically or with manifestations characteristic of a period of prolonged convalescence. The second period is the period of hyperergic tissue reactions with distinct and characteristic clinical manifestations of the disease (rheumatic attack). It is important to note that even against the background of adequate anti-rheumatic therapy, the regression of the clinical symptoms of an attack does not occur simultaneously.

After the disappearance of the bright inflammatory manifestations of the disease, its transition to a latent phase with a gradual normalization of immunological and biochemical parameters is natural. The third period is manifested by various forms of recurrent R. It is characterized by a certain tendency to further disruption and qualitative changes in protective and compensatory reactions with an increase in immunological disorders, progression of dystrophic processes.

There are also primary and recurrent R. Primary R., as a rule, occurs in childhood and adolescence, is characterized mainly by acute and subacute variants of the course of the disease (in 88% of patients, according to 3. P. Annenkova, 1981). There is a clear age pattern in the development of primary R.: infants, as a rule, do not get sick, two-, three-year-olds get sick extremely rarely, and in subsequent years the incidence increases, reaching a maximum in children 7-14 years old and adolescents. In childhood, there are usually no gender differences in the incidence of primary R.; among adolescents, females are more likely to fall ill with R..

The initial clinical manifestations of acute primary R. include fever, migratory polyarthritis (in 50-60% of patients, according to the materials of the Institute of Rheumatology of the USSR Academy of Medical Sciences) or pronounced arthralgia, relatively rarely - serositis and signs of damage to other organs and systems. There is an association between high fever, polyarthritis and serositis. Carditis, even severe, can occur only with a moderate increase in temperature or at normal body temperature.

Primary chronic variants of R.'s course are relatively rare. The question of the specific gravity of the primary latent course in the structure of the incidence of R.

Primary R. is characterized by generalized exudative inflammatory reactions, however, over the past 20-25 years (since the end of the 50s), primary R.'s evolution has been noted towards mitigation of bright exudative-hyperergic forms of the disease. Comparatively rare now are acute inflammatory lesions of all membranes of the heart (pancarditis), primary exudative pleurisy, pericarditis, acute meningoencephalitis. Primary rheumatic pneumonia, annular erythema, rheumatic nodules are much less common, and rheumatic chorea is milder.

There are age-related features of the course of primary R. So, in preschoolers, a protracted course prevails, and in primary school age - subacute. The greatest danger is represented by 12-14-year-old age, at Krom more often than in other age groups, the acute and subacute, and sometimes and continuously and relapsing course is found. At the same time, in this, as well as at an older age (15-18 years), a primary latent course is often observed with involvement of the heart valves in the process.

Recurrent R. as a manifestation of the third period of the development of the disease is characterized by a particular tendency to exacerbations and relapses, progressive disorders of trophism and regulatory processes with a predominance of protracted, continuously recurrent variants of the course. Based on the materials of the Institute of Rheumatology of the USSR Academy of Medical Sciences (V. A. Nasonova, I. A. Bronzov, 1978), among 200 patients with primary R.

Like primary, recurrent R. can be manifested by polyarthritis, involvement in the inflammatory process of the serous membranes, lungs, nervous system, and other organs. However, the most persistent is carditis, clinical course to-rogo most often determines the nature of the flow of recurrent R. as a whole. At the same time, as new exacerbations occur, along with a decrease in the frequency and weakening of the severity of joint damage, there is a progressive worsening of cardiac pathology due to an increase in damage to the valves and myocardium of the heart. A continuously relapsing course is much more common.

Rheumatic carditis (rheumatic carditis)

Rheumatic carditis is the leading manifestation of active R., which determines the severity of the course and the prognosis of the disease. The features of rheumatic carditis include a tendency to sequential or simultaneous inflammatory damage to the myocardium, endocardium and pericardium (see Pancarditis). Due to the difficulty of distinguishing lesions of individual membranes of the heart in clinical practice the generalized term "rheumatic heart disease" has become widespread.

Primary rheumatic heart disease, according to various researchers, is recognized in 80-90% of children and in 95-100% of adults with R. Despite the existence of certain age-related features, there are no fundamental differences in the clinical manifestations of primary rheumatic heart disease in children, adolescents and adults . The symptomatology of rheumatic heart disease is largely determined by the predominant lesion of one or another shell of the heart - the myocardium, endocardium and pericardium.

Despite advances in the development of modern diagnostic methods, often establishing a reliable diagnosis of R., especially its initial manifestations, is far from an easy task for the doctor. The absence of specific clinical and laboratory diagnostic tests determines the need for a syndromic approach to establishing the diagnosis of R. The essence of the latter lies in the reasonable idea that the nosological specificity of the disease can be established when a characteristic combination of nonspecific syndromes is detected.

It was this principle that formed the basis of the proposed by A. A. Kisel diagnostic criteria acute R. Pointing out the diagnostic significance of the syndromes of carditis, polyarthritis, chorea, rheumatic nodules, annular erythema characteristic of this disease, he drew attention to the importance of their combinations for reliable recognition of R. Later, the same five syndromes were attributed by the American cardiologist Jones (T. D.

TREATMENT

Treatment for rheumatism depends on the phase and degree of activity of the process, the depth of organ damage, the nature of the course of the disease, as well as the degree of circulatory disorders. Treatment should be aimed at actively fighting streptococcal infection, suppressing the inflammatory process, and reducing sensitization (autosensitization).

In our country, a method of staged treatment of patients with rheumatism has been developed and widely implemented in practice: in a hospital (first stage), in a sanatorium (second stage) and in a cardio-rheumatology room of a polyclinic (third stage).

Patients in the active phase of rheumatism are subject to hospitalization. Bed rest is prescribed, combined with individualized complexes of physiotherapy exercises, a rational diet.

In the acute course of rheumatism with a pronounced activity of the process, the patient should be on bed rest for 3-6 weeks. With a rapid improvement in the general condition, normalization of laboratory tests and a significant improvement in the patient's heart, it is possible to transfer to a semi-bed rest earlier than the specified period. And, conversely, in protracted cases or with the development of circulatory failure II-III degree, this period should be extended.

Caring for a sick child is of great importance, especially with prolonged bed rest. It is necessary to ventilate the room well. With excessive sweating, you should often change clothes and wipe the skin with a solution of vinegar or cologne. Mandatory daily morning toilet, oral care. It is necessary to monitor the stool (if the stool is delayed every other day, put a cleansing enema or prescribe a laxative).

With severe symptoms of circulatory failure, an elevated position in bed is necessary. To prevent prolonged bed rest from being a burden to the child, you should think about board games, books, drawing pencils, embroidery threads, etc. Exercise therapy is shown to children even with bed rest in the supine position, later exercises are performed while sitting, and then standing.

The nutrition of patients should be complete, but not too plentiful, since energy consumption is minimal during bed rest. Preferably four meals a day. The food must be rich in vitamins. With hormone therapy, you should increase the intake of potassium from food. Potassium-rich foods include baked potatoes, cabbage, raisins, apricots, prunes, oatmeal, and buckwheat, cottage cheese, milk.

Of the antibacterial agents aimed at combating streptococcal infection, penicillin preparations are successfully used. In the acute period of rheumatism, potassium or sodium salt benzylpenicillin intramuscularly in the usual age doses for 10 days, then they switch to injections of bicillin-1 once every 10 days.

Anti-inflammatory therapy of patients with rheumatism is currently carried out with non-hormonal and hormonal drugs. Among the first, the most widely used drugs salicylic acid, first of all - acetylsalicylic acid at a dose of 0.2 - 0.3 g per year of life (no more than 2 g per day); pyrazolone derivatives - amidopyrine, analgin at a dose of 0.15 - 0.2 g per year of life (no more than 2 g per day).

For the treatment of patients with rheumatism, the anti-inflammatory drug indomethacin (methindol) is also used at a dose of 10-20 mg 2-3 times a day, followed by an increase in dose to 50-150 mg / day. It is justified to use Brufen for rheumatism - 20 mg 4 times a day for 1.5 - 2 months. Unfortunately, these drugs are side effect. With prolonged use of acetylsalicylic acid, intestinal bleeding may occur as a result of tissue necrosis (ulcers).

Long-term use of amidopyrine can lead to the development of agranulocytosis; butadione and its derivatives - to the defeat of the urinary tract (hematuria). Therefore, in the course of treatment, careful monitoring of the condition of patients and repeated laboratory research blood and urine. Glycocorticosteroids - prednisolone, dexamethasone, triamcinolone - have good efficiency, especially in severe cases and high activity of the rheumatic process.

Prednisolone is prescribed at the rate of 0.5 - 1 (less often 2) mg / day, dexamethasone and triamcinolone - at a lower dose, according to their comparative effectiveness (dexamethasone - 7 times, triamcinolone - 2 times more active than prednisolone). After 10 days of treatment, the daily dose of prednisolone is gradually reduced (every 5-7 days - 5 mg).

When determining the dose and duration of the use of hormonal drugs, one should focus on the degree of activity of the process and the nature of the course. In an acute course with a pronounced activity, the dose of drugs is the highest, the duration of treatment should be an average of 6 weeks, with a protracted course - longer. On the contrary, with a subacute or sluggish course, a short (2-3-week) course of hormone therapy can be prescribed. In such patients, ef. the effectiveness of steroid therapy is low.

In patients with symptoms of circulatory insufficiency PB - III degree, hormone therapy should be carried out with caution. It is advisable to start treatment with low doses of steroid drugs (for example, prednisone 5-10 mg / day), and then within 7-10 days to increase to age doses, followed by a gradual decrease.

In acute course and high activity of the rheumatic process, the administration of steroid hormones in combination with nonsteroidal drugs, most often - prednisolone and acetylsalicylic acid. With a small activity of the process, treatment is carried out only with nonsteroidal drugs in maximum doses. With continuously recurrent and protracted course of rheumatism, quinoline preparations (delagil, rezochin, plaquenil) are used at a dose of 5–10 mg/kg/day for 3–6 months. The treatment is carried out for a long time, it can be combined with the intake of salicylates or steroid hormones.

Steroid drugs reduce the immunological reactivity of the body, so when they are taken, exacerbations of chronic foci of infection can be observed. To prevent this, hormonal preparations under the guise of antibiotics: first, penicillin is used, and then bicillin.

In patients with rheumatism, especially during hormonal therapy, the content of ascorbic acid and B vitamins in the body decreases, so it is necessary to prescribe them additionally. Cardiac agents are used only for symptoms of circulatory failure.

Treatment in a hospital is carried out for 40 - 60 days with a gradual change of bed rest to half-bed.

After the rheumatic process subsides and discharge from the hospital, the patient continues to be treated in a rheumatic cardiology sanatorium or at home. If the disease was acute, the child needs a sanatorium regimen for a month. With a sluggish course, this period can be somewhat reduced, and with a protracted course, it can be extended to 8-12 weeks.

The daily routine of the patient after a rheumatic attack should be strictly individualized depending on the nature of the course of the process, the time elapsed after discharge from the hospital, the functional state of the cardiovascular system.

The question of school attendance should be decided taking into account the distance from home to school. If the school is close, visiting it can be allowed within a month after the end of the acute period, but if it is far away, you can organize a school at home. In some cases, the child is given an additional day off. Patients in the active phase of rheumatism are exempted from exams.

In the absence of signs of rheumatism activity and a satisfactory response to physical activity, after 4-6 months, exercises can be allowed according to the complex of the preparatory group. A year later, the child can be admitted to physical education in the volume of the main group, excluding various competitions and distance running. If for three years there have been no exacerbations of rheumatism or circulatory failure, you can be allowed to play some sports.

When deciding on the acceptable physical activity It is necessary to take into account the presence and nature of heart disease.

A child who has had rheumatism should be registered in the dispensary in the rheumatic cardiological room of the children's clinic, and in rural areas - in the district hospital or first-aid post. During the year after the attack, he is examined monthly, and then once every 3 months. The examination should include studies of the functional state of the cardiovascular system and laboratory indicators of the activity of the rheumatic process.

With persistent arthralgia, treatment with mud and hydrogen sulfide baths is indicated in the resorts of Odessa, Evpatoria, Matsesta and others 10-12 months after the attack. In other cases, patients should be healthier in a planned manner in local sanatoriums and pioneer camps of a sanatorium type.

The idea of ​​R. as a systemic disease with a predominant lesion of the cardiovascular system, clinical and morphological data on the staging of its development, taking into account the etiological role of group A p-hemolytic streptococcus, substantiated the creation of a domestic system of three-stage treatment of R. Put forward in the 60-70s A. I. Nesterov clinical and immunological direction in the study of R.

made a significant contribution to its further development. AT modern form this system includes: treatment of the active phase of the disease in the hospital, continuation of treatment after discharge from the hospital in the rheumatology room of the polyclinic for adults, or the cardio-rheumatology room of the children's polyclinic, or in a suburban sanatorium with the connection of rehabilitation measures, subsequent long-term dispensary observation and preventive outpatient care.

More than twenty years of experience in the fight against rheumatism in the USSR has confirmed the high efficiency of three-stage treatment and systematic long-term follow-up of patients in a polyclinic. The success of treatment depends on how individualized its program is, depending on the degree of activity, the course of the rheumatic process, the severity of carditis, the severity of valvular and muscular damage to the heart, and the presence of streptococcal infection.

4B. Atherosclerosis of the vessels of the brain, kidneys, intestines, lower extremities: pathology, complications.

3. empyema of the process

Atherosclerosis of the arteries of the brain
also manifests itself slowly progressive
course with the development of atrophy of the cortex
brain, manifested by a decrease
memory, intelligence up to development
senile insanity.

Complicated manifestations - ischemic
cerebral infarction develops
relevant neurological
symptomatology.

4. Atherosclerosis of the renal arteries -
formation of wedge-shaped ischemic
heart attacks, followed by scarring
- large-tuberous atherosclerotic
primary shriveled kidney.

in stenosing atherosclerosis
due to ischemia of the renal tissue occurs
symptomatic hypertension.

5. Atherosclerosis of the arteries of the intestine -
complicated manifestations of gangrene
intestines due to thromboembolism or
thrombosis of the mesenteric arteries.

6. Atherosclerosis of the arteries of the extremities -
more often affected femoral arteries —
stenosing atherosclerosis in
insufficient collateral blood flow
leads to the development of the syndrome of intermittent
lameness (pain in the muscles when walking, atrophy
limb muscles). With thrombosis -
gangrene develops lower extremities.

Prevention of rheumatism

Prevention of rheumatism is carried out in the direction of preventing the disease (primary prevention) and preventing relapses in those who have been ill (secondary, anti-relapse prevention).

Primary prevention includes general health measures: hardening of the body, physical education, sports. Importance is attached to the active fight against streptococcal infection, i.e., the sanitation of foci of a chronic inflammatory process (tonsillitis, otitis media, dental caries, sinusitis, cholecystocholangitis). It is necessary to eliminate the effect of sensitizing factors (irrational nutrition, improper vaccination).

With angina and exacerbation of chronic tonsillitis, pharyngitis, bed rest and a course of treatment with antibacterial and anti-inflammatory drugs (penicillin for seven days, followed by the introduction of bicillin-1) are prescribed with the simultaneous administration of acetylsalicylic acid, multivitamins, desensitizing drugs. A blood test is repeated. Discharge to a children's institution is allowed only if normal blood and a healthy state of the cardiovascular system.

In chronic tonsillitis, it is necessary to carry out conservative treatment, and if it is ineffective, especially in children with a toxic-allergic background, resort to tonsillectomy. In case of tonsillogenic intoxication, it is recommended to prescribe acetylsalicylic acid or amidopyrine for the prevention of rheumatism in spring and autumn for three weeks.

Secondary prevention is based on increasing the body's reactivity by prescribing hardening procedures, a sparing training regimen, and physiotherapy exercises. Active detection and systematic planned remediation of outbreaks should be carried out widely. chronic infection, including the use of antibiotics and, if indicated, tonsillectomy.

Patients with signs of heart damage and the consequences of primary rheumatic heart disease, who have had chorea with a protracted course, recurrent rheumatic heart disease, are prescribed monthly continuous administration of bicillin-1 for five years. For children who have had primary rheumatic heart disease without the formation of a defect or chorea without obvious changes in the heart, the period of monthly year-round administration of bicillin-1 is limited to three years, and seasonal prophylaxis is carried out in the next two years.

In children with frequent respiratory infections it is justified from the onset of the disease to use repeated 2–3-week courses of mefenamic acid (0.2–0.3 g 3–4 times a day), which has anti-inflammatory, desensitizing and interferonogenic effects. As a result of anti-relapse treatment, the number of repeated exacerbations has now decreased by 3-4 times, the number of patients with the formation of heart defects has sharply decreased.

Identification of the role of streptococcal infection in the occurrence of R. and its relapses allows for the primary prevention of the disease. It consists of measures aimed at the systematic and reasonable hardening of the body, the development of physical culture and sports, the implementation of extensive sanitary and hygienic measures that reduce the possibility of streptococcal infection of the population, primarily children's groups.

Secondary prevention is aimed at preventing relapse and progression of the disease in people who have already undergone R. In addition to activities related to primary prevention, it includes methods of year-round and seasonal bicillin-drug prevention of relapses, carried out by rheumatologists of outpatient facilities or district doctors.

In the spring and autumn periods for 4 weeks. acetylsalicylic acid is additionally prescribed for adults at a dose of 2.0 g, for children 1.0-1.5 g per day or another non-steroidal anti-inflammatory drug. After 3 years of year-round bicillin prophylaxis, in the absence of relapses, seasonal prophylaxis is prescribed for the next 2 years. It is carried out in spring and autumn for 6-8 weeks with bicillin-5 at a dose of 1,500,000 IU administered monthly in combination with acetylsalicylic acid at a dose of 2.0 g per day.

Among rehabilitation actions the important place belongs to operational treatment of heart diseases, results to-rogo largely depend on the preoperative preparation carried out by rheumatologists and postoperative observation of patients.

See also Collagen diseases.

Rheumatism prognosis

Currently, there are almost no cases of the disease with a catastrophic course and death. The outcome of the disease is affected by the age of the patient, the nature of the course of the first attack of rheumatism and the quality of dispensary care.

Severe cases of the disease are more common among young children. The severity of the first attack usually determines the further course of the disease. Timely rational treatment in the active phase and regular anti-relapse therapy in the inactive phase of the disease are of great importance for the prognosis. As a rule, the prognosis is aggravated by repeated relapses of the disease.

Early diagnosis, timely prescribed adequate therapy, the correct use of all stages of staged treatment contribute to the suppression of the activity of the rheumatic process, the prevention of the formation of heart disease, and a significant reduction in the recurrence of the disease. R.'s forecast is defined by hl. arr. the outcome of heart damage, most often valvular endocarditis (valvulitis).

Therefore, predicting the outcome of primary rheumatic valvulitis is of paramount importance for R.'s prognosis as a whole. H. N. Kuzmina, A. V. Trufanova, T. G. Glazkova (1978) developed with the help of a computer prognostic tables for the children's contingent of patients with R., which make it possible to predict the outcome of the disease based on the results of clinical and instrumental examination;

The etiological relationship of group A streptococci with rheumatism can be briefly confirmed by the following facts. First, numerous clinical and epidemiological studies have demonstrated a close relationship between group A streptococcal infection and rheumatism. Firstly, in the acute phase of rheumatism, immunological signs of a previous streptococcal infection are almost always found (increased titers of antibodies to streptococcal antibodies). Moreover, prospective long-term studies have shown that rheumatism worsens only after intercurrent streptococcal infection. Third, both primary and recurrent attacks of rheumatic fever can be prevented by adequate treatment or prophylaxis of streptococcal infection with antibiotic therapy. The gate of infection at the beginning of the rheumatic process is the pharynx. Streptococcal lesions of the skin or throat caused by some group A strains seem to almost never cause rheumatism.

The mechanism by which group A streptococci trigger the pathological process remains unknown. Rheumatism develops in a relatively small percentage of people who have had strep throat. After a few days or weeks after an acute streptococcal infection, rheumatism develops, microorganisms are no longer found in the affected organs. No causal relationship has been established between any of the components of streptococcus and the subsequent development of the disease. None of them act as a direct tissue toxin or antigen that causes a hypersensitivity reaction. Cross-reactivity of several streptococcal antigens with tissues of the heart and other organs has been identified. However, their direct relationship to the pathogenesis of rheumatism has not been proven, and the autoimmune response caused by streptococcus remains the only popular but unproven pathogenetic concept that explains the mechanism of the rheumatic process.

Rheumatism: pathological changes.

Morphological changes in rheumatism affect the entire body. At the same time, selective tropism for connective tissue is noted. Local inflammatory foci occur mainly around small blood vessels.

Rheumatism: changes in the cardiovascular system.

Rheumatism: non-cardiac lesions.

RHEUMATISM- systemic inflammatory disease connective tissue with predominant localization in the heart. It affects mainly children and young people. Women get sick about 3 times more often than men.

Etiology, pathogenesis of rheumatic fever. The main etiological factor is group A beta-hemolytic streptococcus. In patients with prolonged and continuously recurrent forms of rheumatic heart disease, the association of the disease with streptococcus often cannot be established. In such cases, heart damage, which fully meets all the main criteria for rheumatism, apparently has a different nature - allergic (out of touch with streptococcus or infectious antigens in general), infectious-toxic, viral.

Allergy is of great importance in the development of rheumatism, although the specific stages of pathogenesis have not been elucidated. It is assumed that sensitizing agents (streptococcus, virus, nonspecific allergens, etc.) can lead in the first stages to allergic inflammation in the heart, and then to a change in the antigenic properties of its components with their transformation into autoantigens and the development of an autoimmune process. An important role in the development of rheumatism plays a genetic predisposition. The systemic inflammatory process in rheumatism is morphologically manifested in characteristic phase changes in the connective tissue (mucoid swelling - fibrinoid change - fibrinoid necrosis) and cellular reactions (infiltration by lymphocytes and plasma cells, formation of Ashofftalalaev granulomas). These cellular reactions are considered as a histological reflection of allergy in this disease. Starting from the stage of fibrinoid changes, complete tissue repair is impossible, and the process ends with sclerosis.

Symptoms, course of rheumatism. In typical cases, the disease develops 1-2 weeks after a sore throat or other infection. With repeated attacks, this period may be shorter. In some patients, even primary rheumatism occurs 1 to 2 days after cooling without any connection with infection. Relapses of the disease often develop after any intercurrent diseases, surgical interventions, physical exertion. As a rule, the patient can relatively accurately indicate the day of onset of the disease.

In the first period of the disease, there is often fever(usually subfebrile); the general condition suffers relatively little. Severe condition and high relapsing fever up to 38 - 40 ° C with daily fluctuations of 1-2 ° C and strong sweats (but, as a rule, without chills) have been observed very rarely in recent years - in individual patients with polyarthritis or serositis.

The most common manifestation of rheumatism is an inflammatory lesion of the heart. Any membranes of the heart can be involved in the process, but primarily the myocardium. At the same time, rheumatism not so rarely proceeds without any obvious cardiac changes. The older the patient who initially fell ill with rheumatism, the less serious the rheumatic heart disease.

In some patients in childhood, the so-called diffuse rheumatic myocarditis. It is manifested by violent allergic inflammation of the myocardium with its pronounced edema and dysfunction. From the very beginning of the disease, patients complain of severe shortness of breath, forcing them to take the orthopnea position, constant pain in the heart area, and palpitations. Characterized by "pale cyanosis", swelling of the jugular veins. The heart is significantly and diffusely dilated, the apex beat is weak. Tones are sharply muffled, a clear III tone (protodiastolic gallop rhythm) and a distinct but soft systolic murmur are often heard. The pulse is frequent, weak filling. Blood pressure is significantly lowered, a collaptoid state may develop. Venous pressure rises rapidly, but with the onset of collapse it also falls. The ECG shows a decrease in the voltage of all teeth, an increase in the systolic index, a decrease in the T wave and ST interval, and atrioventricular block. Very characteristic of diffuse myocarditis is the development of circulatory failure both in the left ventricular and right ventricular types. This variant of rheumatic myocarditis in adults is currently practically not found.

rheumatic endocarditis, flowing in isolation, very poor in symptoms (especially general ones). An essential sign of endocarditis is a clear and even more coarse systolic murmur with sufficient sonority of tones and the absence of signs of pronounced damage to the myocardium. Even more important is the variability of already existing noises and especially the emergence of new ones with unchanged heart boundaries. This symptom is most indicative in patients with primary rheumatic heart disease with normal heart size. Light and rather quickly disappearing diastolic murmurs, sometimes heard at the beginning of a rheumatic attack on the projection of the mitral valve or vessels, can also be partly associated with endocarditis. The appearance of a soft proto-diastolic murmur on the aorta is particularly suggestive of endocarditis (aortic semilunar valves). These noises appear, apparently, in connection with thrombotic overlays on inflammatory valves. These overlays occasionally serve as a source of embolism in the vessels of the small or large circulation with the development of infarctions of the lungs, kidneys, spleen, gangrene of the extremities, central paralysis, etc. Patients in whom endocarditis is the only or at least the main localization of rheumatism, for a long time maintain good general health and ability to work, constituting a group of patients with the so-called outpatient course of rheumatism. Only hemodynamic disorders due to an imperceptibly formed heart disease make such patients see a doctor for the first time.

Pericarditis in the clinic of modern rheumatism very rare. Dry pericarditis is manifested by constant pain in the region of the heart and a pericardial friction rub, heard more often along the left edge of the sternum (usually in both phases of the cardiac cycle). The ECG is characterized by an upward shift in the ST interval in all leads at the onset of the disease. In the future, these intervals gradually return to the isoline, at the same time biphasic or negative T waves are formed. Sometimes ECG data are not indicative.

Exudative pericarditis characterized by the accumulation of serofibrinous exudate in the heart sac and is essentially a further stage in the development of dry pericarditis. Characterized by shortness of breath, aggravated in the supine position. The region of the heart in large numbers the exudate swells somewhat, the intercostal spaces are smoothed, the apex beat is not palpable. The heart is greatly enlarged and takes characteristic shape trapezoid or round decanter. The pulsation of the contours during fluoroscopy and especially X-ray kymography is small. Tones and noises give the impression of being very deaf (due to the presence of effusion). The pulse is frequent, small filling. BP is reduced. Venous pressure is almost always increased, there is swelling of the cervical and even peripheral veins. The ECG is basically the same as in dry pericarditis; an additional symptom is only a marked decrease in the voltage of the QRS complex. Since the presence of fluid in the pericardial cavity limits the diastolic expansion of the heart, there is insufficient blood flow to the heart, which leads to stagnation in the small and especially in the systemic circulation.

The outcome of rheumatic pericarditis is often small adhesions between both sheets or the outer sheet with surrounding tissues. Much less often, there is a complete fusion of the sheets of the heart bag (adhesive, obliterating pericarditis, "armored heart").

Rheumatic vascular lesions. Arteritis of the internal organs is the basis of the clinical manifestations of rare rheumatic visceritis: these are nephritis, meningitis, encephalitis, etc. Symptoms of peripheral arteritis (mainly of the limbs), which are extremely rare, are pain and weakening of the pulse on the corresponding artery. The existence of rheumatic phlebitis itself has not been proven.

Rheumatic affections of the joints. Relatively rare in recent years, acute rheumatic arthritis is characterized by increasing acute pain in the joints, aggravated by movement and palpation. Within a few hours, the pain becomes very sharp and, in especially severe cases, causes a forced position on the back with maximum sparing of the affected joints. Very quickly, objective symptoms of inflammation of the joints join arthralgia - swelling, rarely hyperemia. Symmetrical lesions of large joints and volatility of arthritis are considered characteristic. Rheumatoid arthritis is completely reversible: all articular manifestations (regardless of their severity at the onset of the disease) pass without a trace.

In recent years, the picture of articular lesions in many patients differs from that described above. Often there are only severe arthralgia without further addition of swelling of the joints. The peculiarity of the course of rheumatic polyarthritis can also be manifested in the slow increase or reverse development of its symptoms (even despite antirheumatic treatment), in mild or no volatility, in the predominant inflammation of small joints. Often there is no symmetry of the lesion. Occasionally, during the entire disease, only one joint is affected, that is, we are talking about rheumatic monoarthritis. As an exception, there is mild muscle atrophy around long-term inflamed joints.

Rheumatic myositis itself is very rare, manifested by severe pain in the corresponding muscle groups.

Skin lesions in patients with rheumatism occur in the form of rheumatic nodules, annular or nodular erythema, urticaria, etc., but their diagnostic value and pathogenetic relationship with the underlying disease are completely different. Rheumatic nodules are usually located in the affected joints, over bony prominences, in the occipital region, on the forearms and legs. These are small (about the size of a pea) dense, painless formations, localized shallowly under the skin in groups of 2-4 each. Under the influence of treatment, and sometimes spontaneously, they disappear within a few days. Almost never seen in recent years.

Annular erythema is a pink ring-shaped elements, never itchy, located mainly on the skin of the inner surface of the arms and legs, abdomen, neck and trunk. Like rheumatic nodules, this is a sign that is almost pathognomonic for rheumatism, but is found only in 1-2% of patients. Erythema nodosum is very rare in rheumatism, is not typical for it, and is much more common in other allergic diseases. Other skin changes in rheumatism are even more nonspecific and rare: urticaria, unstable spots and papules, hemorrhages.

Rheumatic lesions of the lungs. Rheumatic pneumonia is extremely rare and usually occurs already against the background of the developed disease. the only hallmark rheumatic pneumonia is their resistance to antibiotics and good effect from the use of antirheumatic drugs (without antibacterial). Only under this condition can the diagnosis be considered justified.

Rheumatic pleurisy its manifestations are also non-specific. Its diagnosis is possible only when combined with other signs of rheumatism. It is often bilateral and is characterized by good reversibility. Exudate in rheumatic pleurisy is serofibrinous and always sterile. Rivalta's test is positive. At the beginning of the disease, neutrophils predominate in the exudate, later - lymphocytes; admixture of erythrocytes, endothelial cells and eosinophils is also possible. The first, and even more so the only sign of rheumatism, pleurisy usually does not happen. In some patients, pleurisy is one of the components of the defeat of several or all serous membranes - rheumatic polyserositis, which is an indicator of particularly active rheumatism.
Rheumatic nephritis is rare, they are characterized by persistent and pronounced changes in urinary sediment and proteinuria; hypertension and edema are not common. Antirheumatic treatment gives a distinct effect, although it is sometimes possible for acute rheumatic nephritis to become chronic. Very rarely, patients with rheumatism have developed nephrotic syndrome.

Rheumatic lesions of the digestive system have no significant clinical significance. Gastritis and especially ulceration of the stomach and intestines are usually the result of long-term use of drugs, especially steroid hormones. Children with rheumatism sometimes experience severe abdominal pain associated with rapidly reversible allergic peritonitis. Pain can be very sharp and, combined with positive symptom Blumberg, make you think about acute surgical disease abdominal cavity. Distinctive features of rheumatic peritonitis are the diffuse nature of pain, their combination with other signs of rheumatism (or indications of this disease in history), a very rapid effect of antirheumatic therapy; often the pain disappears on its own in a short time. In some patients with rheumatism with a high activity of the process, an increase in the liver occurs in combination with its mild soreness (without circulatory failure). This is due to interstitial hepatitis. Elements of parenchymal hepatitis with more or less pronounced direct bilirubinemia are even less common.

Rheumatic changes in the nervous system. Chorea minor (pathognomonic "nervous form" of rheumatism) occurs predominantly in children, especially girls. It is manifested by a combination of emotional lability with muscular hypotension and violent fanciful movements of the torso, limbs and mimic muscles. These movements increase with excitement and disappear during sleep. Chorea minor can occur with relapses; however, by the age of 17-18, it almost always ends. The features of this form are relatively small damage to the heart and slightly pronounced laboratory indicators of rheumatism activity (including often normal ESR).
Actually, rheumatic lesions of the central nervous system are very rare and usually proceed as a combination of signs of encephalitis and meningitis. They are almost always combined with other signs of rheumatism and respond well to antirheumatic therapy. Residual effects of rheumatic meningoencephalitis are clinically manifested by headaches, in exceptional cases - epileptiform seizures. "Rheumatic psychoses" do not seem to exist. At the onset of the disease, vegetative symptoms such as sweating, pulse lability, rapid red dermographism, and asymmetry in blood pressure indicators are not uncommon.

Laboratory data. Neutrophilic leukocytosis, reaching 12 - 15 103 in 1 µl, occurs only in patients with maximum activity process. In this case, there is usually a shift of the leukogram to the left due to an increase in stab leukocytes, much less often due to the appearance of metamyelocytes and myelocytes. In most patients, the number of leukocytes and the leukogram are not significant. The number of platelets in the acute period of the disease is increased, but subsequently decreases, and in some patients with a chronic course of the disease, it is kept at subnormal numbers. In most patients with rheumatism, an increase in ESR is noted, reaching maximum numbers (40-60 mm / h) with polyarthritis and polyserositis.

Shifts in immunological indicators deserve attention. These include a frequent increase in titers of antistreptococcal antibodies: antistreptohyaluronidase and antistreptokinase more than 1: 300, antistreptolysin-O more than 1: 250. An increase in the level of these antibodies reflects the body's response to exposure to streptococci and therefore often occurs after any streptococcal infections (as well as detection in the blood or urine streptococcal antigens). The height of titers of antistreptococcal antibodies and their dynamics do not reflect the degree of activity of rheumatism. In addition, in many patients with chronic forms of rheumatism, signs of streptococcal infection are not observed at all.

All known biochemical parameters activities of the rheumatic process are nonspecific and occur during various types inflammation and tissue decay, so they are unsuitable for nosological diagnosis. Only in cases where the diagnosis of rheumatism is justified by clinical and instrumental data, the complex of these indicators is very useful for judging the presence or absence of disease activity (but not the disease itself). These include an increase in the level of plasma fibrinogen above 4000 mg/l, an increase in alpha-2 globulins above 10%, gamma globulins above 20%, hexose above 1250 mg/l, ceruloplasmin above 0.26 optical. units, seromucoid and indicators of diphenylamine reaction - above 0.21 optical. units, plasma hydroxyproline - above 9.5 mg / l, the appearance in the blood C-reactive protein etc. In most cases, biochemical indicators of activity are parallel to the values ​​of ESR, which remains the best laboratory sign of the activity of rheumatism, including its dynamics.

Handbook of a practitioner / Ed. A. I. Vorobiev. - M.: Medicine, 1982

1. Rheumatism. Etiology and pathogenesis

Rheumatism (Sokolsky-Buyo disease) is a systemic inflammatory disease of the connective tissue with a predominant localization of the process in cardiovascular system, which develops in individuals predisposed to it (as a rule, these are young people) due to acute infection with group A b-hemolytic streptococcus.

This definition of the disease was given in 1989 by V. A. Nasonov.

The defeat of other organs and systems in rheumatism is of secondary importance and does not determine its severity and subsequent prognosis.

Etiology. Group A beta-hemolytic streptococci cause damage to the upper respiratory tract. That is why the onset of rheumatism is usually preceded by angina, exacerbation of chronic tonsillitis, and in the blood of patients with an increased amount of streptococcal antigen and anti-streptococcal antibodies (ASL-O, ASG, ASA, antideoxyribonuclease B (anti-DNase B)).

Age and social factors play a role in the development of rheumatism (unfavorable living conditions, malnutrition), genetic predisposition also matters (rheumatism is a polygenically inherited disease, the existence of "rheumatic" families is well known), which consists in a hyperimmune response to streptococcus antigens, the propensity of patients to autoimmune and immunocomplex processes.

Pathogenesis. In rheumatism, a complex and diverse immune response (hypersensitivity reactions of immediate and delayed types) to numerous streptococcal antigens occurs. When an infection enters the body, antistreptococcal antibodies are produced and immune complexes are formed (streptococcus antigens + antibodies to them + complement), which circulate in the blood and settle in the microcirculatory bed. Streptococcus toxins and enzymes also have a damaging effect on the myocardium and connective tissue.

Due to a genetic defect immune system streptococcal antigens and immune complexes are not completely and quickly eliminated from the body of patients. As a result, autoimmune processes develop according to the type of delayed-type hypersensitivity, and lymphocytes reacting with cardiac tissue are found in the blood of patients. These cells are of great importance in the origin of organ lesions (mainly the heart).

In the connective tissue with rheumatism, phase changes occur: mucoid swelling - fibrinoid changes - fibrinoid necrosis. The morphological expression of immune disorders are cellular reactions - infiltration by lymphocytes and plasmocytes, the formation of rheumatic, or Ashofftalalaevskaya, granuloma. The pathological process ends with sclerosis.

When the heart is affected, the inflammatory process can spread to all the membranes of the heart (pancarditis) or in isolation to each of the membranes.

2. Clinical picture of rheumatism

All manifestations of the disease can be divided into cardiac and extracardiac. It is possible to describe the clinical picture of the disease from these positions.

Stage I: the connection of the disease with the transferred infection is revealed. In typical cases, 1-2 weeks after a sore throat or acute respiratory disease body temperature rises, sometimes up to 38-4 ° C, with fluctuations during the day within 1-2 C and strong sweat (usually without chills).

The most common manifestation of rheumatism is heart damage - rheumatic heart disease: simultaneous damage to the myocardium and endocardium. Patients complain of mild pain or discomfort in the region of the heart, slight shortness of breath during exercise, interruptions or palpitations are much less common.

Rheumatic heart disease in young patients, as a rule, is severe: from the very beginning of the disease, severe shortness of breath during exercise and at rest, constant pain in the heart, and palpitations are noted.

Pericarditis, as well as extracardiac manifestations of rheumatism, is rare. With the development of dry pericarditis, patients note only constant pain in the region of the heart. With exudative pericarditis, characterized by the accumulation of serous-fibrinous exudate in the heart sac, the pain disappears, as the inflamed pericardial layers are separated by the accumulating exudate.

The most characteristic of rheumatism is the defeat of the musculoskeletal system in the form of rheumatic polyarthritis.

Rheumatic lesions of the kidneys are also extremely rare, detected only in the study of urine.

Abdominal syndrome (peritonitis) occurs almost exclusively in children and adolescents with acute primary rheumatism.

At stage II of the diagnostic search, the detection of signs of heart damage is of little importance.

In primary rheumatic heart disease, the heart is usually not enlarged. Auscultation reveals a muffled I tone, sometimes the appearance of a III tone, a soft systolic murmur at the apex. This symptomatology is due to changes in the myocardium.

In case of damage to the aortic valve, a proto-diastolic murmur at the Botkin point may be heard, and the sonority of the II tone may be preserved.

In patients with polyarthritis, joint deformity is noted due to inflammation of the synovial membrane and periarticular tissues, pain on palpation of the joint.

Annular erythema (a sign that is almost pathognomonic for rheumatism) is extremely rare (in 1-2% of patients).

At the III stage of the diagnostic search, the data of laboratory and instrumental studies allow us to establish the activity of the pathological process and clarify the damage to the heart and other organs.

Acute phase indicators: neutrophilia with a shift leukocyte formula blood to the left; an increase in the content of 2-globulins, followed by an increase in the level of globulins; increase in fibrinogen content; the appearance of C-reactive protein; ESR increases. Immunological indicators, increased titers of anti-streptococcal antibodies (anti-hyaluronidase and antistreptokinase more than 1: 300, anti-O-streptolysin more than 1: 250).

3. Diagnosis of rheumatism

With the gradual onset of rheumatism, the syndromic diagnosis proposed by AI Nesterov in 1973 (see Table 1) matters: clinical and epidemiological syndrome; cardiovascular syndrome (see Table 2).

Table 1

table 2

4. Differential diagnosis of rheumatism

Rheumatic polyarthritis must be differentiated from non-rheumatic ones (see table).

5. Treatment of rheumatism

The whole complex of treatment of rheumatism consists of antimicrobial and anti-inflammatory therapy, measures that are aimed at restoring immunological homeostasis. It is recommended to use a rational balanced diet, focus on adaptation to physical activity, preparation for labor activity, timely surgical treatment patients with complex heart disease. All patients during the active phase of rheumatism are shown penicillin (1,200,000-1,500,000 IU for 6 doses per day, every 4 hours), which has a bactericidal effect on all types of A-streptococcus. The course of treatment is 2 weeks during the active phase of rheumatism, in the future, a transfer to the prolonged drug bicillin-5 (1,500,000 units) is required. With intolerance to penicillin, erythromycin 250 mg 4 times a day can be prescribed.

Drugs with anti-inflammatory effect, which are used in the modern treatment of the active phase of rheumatism, are glucocorticosteroids, salicylic, indole derivatives, derivatives of phenylacetic acid, etc.

Prednisolone is used at 20-30 mg per day (for 2 weeks, then the dose is reduced by 2.5-5 mg every 5-7 days, in total for a course of 1.5-2 months) for primary and recurrent with III and II degree activity of the process of rheumatic heart disease, with polyserositis and chorea, with the development of heart failure due to active carditis.

Corticoid agents affect water-salt metabolism, therefore, potassium chloride 3-4 g / day, panangin and others should be used in the treatment, with fluid retention - aldosterone antagonists (veroshpiron up to 6-8 tablets per day), diuretics (la-zix 40-80 mg / day, furosemide 40-80 mg / day, etc.), with euphoria - tranquilizers, etc.

Non-steroidal anti-inflammatory drugs are also widely used for rheumatism: the average doses of acetylsalicylic acid are 3–4 g per day, less often 5 g per day or more.

Acetylsalicylic acid is used 1 g 3-4 times a day after meals for 1-3 months or more with normal tolerance and with control over side effects.

The successful use of an indolacetic acid derivative - indomethacin in rheumatism for more than 20 years. It has a pronounced healing effect: subjective symptoms of carditis (cardialgia, palpitations, shortness of breath) disappear by the 8-10th day of therapy, and objective signs - by the 14-16th day. The disappearance of polyarthritis and polyserositis occurs even faster.

In the treatment of rheumatism, a combination of three main stages is important: hospital - clinic - resort.

At stage I, treatment is carried out with the drugs listed above. After reducing the activity of rheumatism and normalizing the patient's condition, they are transferred to stage II - treatment in a rheumatological sanatorium.

The main goal of this stage is to continue treatment with non-steroidal anti-inflammatory drugs.

Stage III includes dispensary observation and preventive treatment.

6. Classification of cardiomyopathies. Etiology of Dilated Cardiomyopathy (DCM)

Cardiomyopathies are primary isolated non-inflammatory myocardial lesions of unknown etiology (idiopathic), they are not associated with valvular defects or intracardiac shunts, arterial or pulmonary hypertension, ischemic disease heart or systemic diseases (such as: collagenoses, amyloidosis, hemochromatosis, etc.), and in the final stage of the disease, severe congestive heart failure and complex cardiac arrhythmias and patency develop.

The classification of cardiomyopathies is as follows:

1) dilated cardiomyopathy:

a) idiopathic;

b) toxic;

c) infectious;

d) with collagenoses;

2) hypertrophic;

3) restrictive;

4) arrhythmic dysplasia of the right ventricle;

5) a combination of one of the 4 types of cardiomyopathies with arterial hypertension.

Dilated cardiomyopathy (DCM) is a disease of the heart muscle characterized by a diffuse expansion of all chambers of the heart (mainly the left ventricle), in which the pathology of the pumping function of the heart is in the foreground and, as a result, chronic heart failure (hence the second name is congestive, when the heart is not able to fully pump blood and it "stagnates" in the tissues and organs of the body). The muscular wall of the heart remains either unchanged or hypertrophied to varying degrees.

Diseases and factors that preceded the development of DCMP are described in the table below (see table).

Diseases and factors that preceded the development of DCMP

This is the most common form of damage to the heart muscle. The incidence is 5-8 cases per 100,000 people per year. There is no clear family history for these patients. Men get sick 2-3 times more often than women.

7. Pathogenesis of dilated cardiomyopathy (DCM)

Pathogenesis. As a result of the inflammatory process in the heart muscle (myocarditis), individual cells die in its various parts. Inflammation in this case is viral in nature, and the cells affected by the virus become foreign agents for the body. Accordingly, when antigens appear in the body, a complex of immune response reactions develops, aimed at their destruction. Gradually, the dead muscle cells are replaced by connective tissue, which does not have the ability to extensibility and contractility inherent in the myocardium. As a result of the loss of the main functions of the myocardium, the heart loses its ability to function as a pump. In response to this (as a compensatory reaction), the chambers of the heart expand (i.e., they dilate), and thickening and thickening occurs in the remaining part of the myocardium (i.e., its hypertrophy develops). To increase the delivery of oxygen to the organs and tissues of the body, a persistent increase in heart rate (sinus tachycardia) occurs.

This compensatory response only temporarily improves the pumping function of the heart. However, the possibilities of myocardial dilatation and hypertrophy are limited by the amount of viable myocardium and are individual for each specific case of the disease. With the transition of the process to the stage of decompensation, chronic heart failure develops. However, at this stage, another compensatory mechanism comes into play: the tissues of the body increase the extraction of oxygen from the blood compared to a healthy body. But this mechanism is insufficient, since a decrease in the pumping function of the heart leads to a decrease in the supply of oxygen to organs and tissues, which is necessary for their normal functioning, while the amount of carbon dioxide in them increases.

In 2/3 of patients in the cavities of the ventricles in the late stages of the disease, parietal thrombi form (due to a decrease in the pumping function of the heart, as well as uneven contraction of the myocardium in the chambers of the heart), followed by the development of embolism in the pulmonary or systemic circulation.

Pathohistological and pathomorphological changes in the heart. The shape of the heart becomes spherical, its mass increases from 500 to 1000 g, mainly due to the left ventricle. The myocardium becomes flabby, dull, with noticeable whitish layers of connective tissue, there is a characteristic alternation of hypertrophied and atrophic cardiomyocytes.

Microscopically, diffuse fibrosis is detected, it can be combined with both atrophy and hypertrophy of cardiomyocytes, in which there is a significant increase in the volume of nuclei, the number of mitochondria, hyperplasia of the Golgi apparatus, an increase in the number of myofibrils, free and associated with the endoplasmic reticulum ribosomes, an abundance of glycogen granules.

8. Clinical picture and diagnosis of dilated cardiomyopathy (DCM)

There are no specific signs of the disease. Clinical picture polymorphic and defined:

1) symptoms of heart failure;

2) rhythm and conduction disturbances;

3) thromboembolic syndrome.

In most cases, the prognosis of the disease is determined by the defeat of the left ventricle of the heart. Before the onset of heart failure, DCM is latent. The most frequent complaints of already onset heart failure are complaints of decreased performance, increased fatigue, shortness of breath during exertion, and then at rest. At night, he has a dry cough (the equivalent of cardiac asthma), later - typical asthma attacks. Patients present with characteristic anginal pain. With the development of congestion in the systemic circulation, heaviness appears in the right hypochondrium (due to an enlarged liver), swelling of the legs.

Diagnostics. When diagnosing a disease important sign is a significant increase in the heart (signs of valvular heart disease or hypertension are absent). Cardiomegaly is manifested by the expansion of the heart in both directions, determined by percussion, as well as the displacement of the apex beat to the left and down. In severe cases, a gallop rhythm, tachycardia, murmurs of relative insufficiency of the mitral or tricuspid valves are heard. In 20% of cases, atrial fibrillation develops. Arterial pressure usually normal or slightly elevated (due to heart failure).

Biochemical studies of blood and urine can detect various toxic substances, as well as vitamin deficiencies. Instrumental research methods make it possible to detect:

1) signs of cardiomegaly;

2) changes in indicators of central hemodynamics;

3) rhythm and conduction disturbances. Phonocardiogram confirms auscultatory data in the form of a gallop rhythm, a fairly common detection of systolic murmur.

X-ray reveals a significant increase in the ventricles and stagnation of blood in the pulmonary (small) circulation.

Echocardiography helps to detect dilatation of both ventricles, hypokinesia of the posterior wall of the left ventricle, paradoxical movement of the interventricular septum during systole.

A radioisotope study of the heart (myocardial scintigraphy) is performed to clarify the state of the pumping function of the heart, as well as to determine the zones of the dead myocardium.

Angiocardiographically, the same changes are detected as on the echocardiogram. Live myocardial biopsy is not informative for determining the etiology of cardiomyopathy. In some cases, a viral antigen or an increase in the content of LDH, as well as a decrease in energy production by mitochondria, can be detected in the biopsy.

9. Differential / diagnosis of dilated cardiomyopathy (DCM)

It is produced primarily with myocarditis and myocardial dystrophies, i.e. with those conditions that are sometimes unreasonably called secondary cardiomyopathies.

Myocardial biopsy provides significant assistance in the differential diagnosis of dilated cardiomyopathy and heart disease, occurring with a pronounced increase in it:

1) with severe diffuse myocarditis, cellular infiltration of the stroma is found in combination with dystrophic and necrotic changes in cardiomyocytes;

2) with primary amyloidosis occurring with heart damage (the so-called cardiopathic variant of primary amyloidosis), there is a significant deposition of amyloid in the interstitial tissue of the myocardium, combined with atrophy of muscle fibers;

3) with hemochromatosis (a disease caused by a violation of iron metabolism), deposits of iron-containing pigment are found in the myocardium, various degrees of dystrophy and atrophy of muscle fibers, and proliferation of connective tissue are observed.

As a variant of DCM, drug-induced and toxic cardiomyopathies can be considered.

Numerous agents can cause toxic damage to the myocardium: ethanol, emetine, lithium, cadmium, cobalt, arsenic, isoproterenol and other poisons. Histopathological changes in the tissues of the heart muscle appear as focal dystrophies. The most striking example of toxic cardiomyopathy is cardiomyopathy, which occurs in people who consume excessive beer. In the acute stage of the course of cobalt cardiomyopathy, the presence of hydropic and fatty degeneration, destruction of intracellular organelles, and focal necrosis of cardiomyocytes are noted.

Alcoholic cardiomyopathy. Ethanol has a direct toxic effect on cardiomyocytes.

Macroscopically, the myocardium is flabby, clay-like, sometimes small scars are observed. coronary arteries intact. Microscopic examination shows a combination of dystrophy (hydropic and fatty), atrophy and hypertrophy of cardiomyocytes, possibly the presence of foci of cardiomyocyte lysis and sclerosis. The affected areas of the myocardium contrast with unchanged ones. Electron microscopic examination of heart biopsy specimens shows cystic expansion of the sarcoplasmic reticulum and the T-system of cardiomyocytes, which is characteristic of alcoholic cardiomyopathy. Complications of alcoholic cardiomyopathy - sudden death as a result of ventricular fibrillation or chronic heart failure, thromboembolic syndrome.

10. Treatment and prevention of dilated cardiomyopathy (DCM)

The general principles for the treatment of DCM do not differ significantly from the treatment of chronic heart failure. In cases of secondary DCM, the treatment of the previous disease (valvular heart disease, etc.) is additionally carried out, and all measures are taken to eliminate the causes of DCM.

Peripheral vasodilators are quite effective, especially with concomitant anginal syndrome (nitrong, sustak, nitrosorbide). With anginal syndrome, it becomes necessary to use antianginal drugs, preferably prolonged nitrates (sustak, nitrong, nitrosorbide). Adrenoblockers are effective (they are prescribed in the absence of signs of heart failure).

From modern methods surgical treatment DKMP is the most effective heart transplantation (transplantation). However, the possibilities of carrying out this operation are significantly limited. For this reason, as an alternative to heart transplantation in modern treatment, to increase the life expectancy of patients with DCM, there have been developed and are being produced reconstructive operations which are aimed at eliminating insufficiency of the mitral and tricuspid valves of the heart. An alternative to heart transplantation in patients with DCM is partial removal left ventricle to reduce its size (Baptiste operation).

Not so long ago, for the treatment of patients with DCMP, special models of pacemakers were developed, they allow you to make the work of the ventricles of the heart synchronous. This leads to an improvement in the filling of the ventricles of the heart with blood and an increase in the pumping function of the heart.

DCM in children is 5-10 cases per 100,000 children per year. The greatest effect of the treatment of dilated cardiomyopathy in children early age achieved with a combination of corticosteroids and glycosides (prednisolone and digoxin). Against the background of monotherapy with prednisolone, a decrease in heart rate occurs. Monotherapy with digoxin leads to a decrease in tachycardia and dyspnea. Given the inadvisability of prescribing cytostatic drugs in young children, since a significant number of treatment complications were observed, it is more optimal in pediatrics to use long-acting cardiac glycosides in combination with corticosteroid hormones in dilated cardiomyopathy.

Prevention. Prevention of DCMP consists in the exclusion of alcohol, cocaine, as well as careful monitoring of cardiac performance during tumor chemotherapy.

It is useful to harden the body from an early age. Complete abstinence from alcohol in alcoholic DCM improves heart contractility and may eliminate the need for a heart transplant.

42. Rheumatism. Classification. Clinic of rheumatic polyarthritis

Rheumatism is a systemic inflammatory disease of the connective tissue with a characteristic lesion of the heart.

Etiology, pathogenesis. The main etiological factor in acute forms diseases - β-hemolytic streptococcus group A. In patients with prolonged and continuously recurrent forms of rheumatic heart disease, it is often not possible to establish a connection between the disease and streptococcus. In the development of rheumatism, immune disorders are of particular importance.

It is assumed that sensitizing agents in the body (streptococcus, viruses, nonspecific antigens, etc.) can lead at the first stages to the development of immune inflammation in the heart, and then to a violation of the antigenic properties of its components with their transformation into autoantigens and the development of an autoimmune process. A special role in the development of rheumatism plays a genetic predisposition.

Classification. It is necessary to identify a previously inactive or active phase of the disease.

Activity can be minimal (I degree), medium (II degree) and maximum (III degree).

To determine the degree of activity, the severity of clinical manifestations, as well as changes in laboratory parameters, are used.

Classification according to the localization of the activity of the rheumatic process (carditis, arthritis, chorea, etc.), the state of the blood circulation and the course of the disease.

Allocate an acute course of rheumatism, a subacute course, a protracted course, a continuously relapsing course and a latent course of the disease. The allocation of a latent course is justified only for the retrospective characteristics of rheumatism: the latent formation of heart disease, etc.

Clinic. Most often, the disease develops 1-3 weeks after suffering a sore throat, sometimes another infection.

With relapses, this period may be shorter. Relapses of the disease often develop after any intercurrent diseases, surgical interventions, physical overload. A manifestation of rheumatism is a combination of acute migratory and completely reversible polyarthritis of large joints with moderately severe carditis. The onset of the disease is acute, stormy, rarely subacute. Polyarthritis develops rapidly, accompanied by remitting fever up to 38–40 ° C with daily fluctuations of 1–2 ° C, severe sweating, but more often without chills.

The first symptom of rheumatic polyarthritis is acute pain in the joints, increasing and intensifying with the slightest passive and active movements. The pain is accompanied by swelling of the soft tissues in the area of ​​​​the joints and at the same time an effusion appears in the joint cavity. Skin over the affected joint are hot, on palpation of the joint there is a sharp pain, the range of motion is limited due to pain.

A characteristic feature is a symmetrical lesion of large joints - more often knee, wrist, ankle, elbow. The "volatility" of inflammatory changes is typical, manifested in the rapid and reverse development of arthritic manifestations in some joints and the same rapid increase in other joints. All articular changes disappear without a trace even without treatment, they last no more than 2-4 weeks.