Rheumatic Fever Heart Cardiology Adrenal corticosteroid

Section 4. Rheumatic Fever

Rheumatic fever is a late onset of immune after infection with group A hemolytic streptococcus. There are non-bacterial inflammations in various organs, and clinical manifestations are multiple migratory arthritis, carditis, circular erythema on the skin and subcutaneous nodules. It is characterized by repeated episodes of rheumatic activity. If it affects the heart, it causes permanent damage to the heart valve, leading to rheumatic heart disease.

 

The disease mostly occurs in the winter and spring seasons with changing climates. It occurs more frequently in humid and crowded environments. The age of onset is 5-15 years, and the recurrence is mostly within 3-5 years after the initial onset. Recurrence can lead to increased heart damage. In recent years due to the application and residence of antibiotics. With the improvement of nutritional conditions, the incidence has decreased significantly.

 

Pathogenesis of Rheumatic Fever

I. Research on Streptococcus

Observing the structure of streptococcal cells through an electron microscope can be divided into the following:

 

(A) Capsule is the outermost layer of hyaluronidase of streptococcus. Its structure is similar to human hyaluronidase. The complete and sticky capsule can resist cell phagocytosis and is not antigenic.

 

Streptococcal antigen structure map

(B) The cell wall: from the outside to the inside can be divided into three layers:

1. Protein antigen is a specific antigen containing M, T, R, S, and antigenic components. Among them, M antigen is related to pathogenicity, and it has cross-antigenicity with human heart muscle and tropomyosin.

 

2. The polysaccharide component contains M-acetylglucosamine, which has cross-antigenicity with human heart valve glycoproteins.

 

3. Mucopolypeptide is composed of alanine, etc., has antigenicity and is related to nodular damage to connective tissue.

 

(C) Cell membranes are formed by lipoproteins and have cross-antigenicity with human myocardium.

 

The pathogenesis of rheumatic fever

The pathogenesis of rheumatic fever is currently proposed by the theory of toxic immunity and viral infection, which are described below:

(1) Poisoning and Immunology: Rheumatic fever is caused by streptococcal infection 2 to 3 weeks, which is exactly the reaction process of body fluids after the body is infected. The body’s heart muscle and connective tissue have similar immune structures to streptococcus. After infection, the body’s heart muscle and connective tissue components change, and also have antigenicity. They also produce autoantibodies.

In the presence of streptococcal antigen and its own tissue antigen, antibodies bind to it to produce a cross immune response. The antigen-antibody immune complex activates complement, attracts white blood cells to aggregate, granulocytes decompose, isolates hydrolase, and produces tissue damage and inflammation.

(2) Viral infection theory: Some people have found that Coxsackie B4 can cause pancarditis and rheumatoid disease in Java monkeys through animal experiments and viral antibody tests, and similar Aschoff’s granulomas can occur in the myocardium. In young patients with mitral stenosis before surgery, coxsackie B3 and B4 antibody titers increased significantly.

 

Pathology of Rheumatic Fever

The pathological changes of rheumatism can involve collagen fibers in connective tissues throughout the body. Joints, heart, blood vessels, and serosa are the most common, but heart disease is the most important. It can affect the endocardium, myocardium, and pericardium. The development process of inner collagen fibers and blood vessels can be divided into three stages.

   1.   Degeneration and exudation

The colloidal fibers were swollen and degenerate, with lymphocytes and garden cells infiltration and serous exudation. This issue can last from January to February.

 

    2.   The proliferation period

The main lesion is the Aschoff body (Aschoff body), which is a characteristic lesion of rheumatic fever. The center of the body has colloidal fibrous degeneration and necrosis, surrounded by oval polymorphic cells, large in volume, and cytoplasmic. There was infiltration of lymphocytes and plasma cells. This period lasted from March to April.

 

   3.   The hardening period

The degeneration and necrotic substance absorption in the central body of A Shaofu body, the surrounding inflammatory cells are reduced, the lesion is fibrotic, and scar tissue is formed.

Due to the recurrence of the disease and the chronic delay process, the above three phases often cross.

Rheumatic lesions can affect all parts of the heart, and myocarditis and endocarditis are the most common and important. Typical Aschaff bodies can be seen in the myocardium, mainly in the connective tissue around the myocardial interstitial blood vessels.

Endocarditis mainly affects the valve, causing the valve to swell and thicken, small vegetations appear on the surface, and the valve leaflets are closed. There is fibrin deposition, forming inter-leaflet adhesions.

Repeated episodes of rheumatism can aggravate valve lesions, cause inter-leaflet adhesions, shorten deformation, and increase tendon and papillary muscle adhesions to increase deformation and form valve stenosis. After the pericardial serous exudates and absorbs, the light cases can fully recover. In most cases repeatedly delay the onset of the heart valve deformation and myocardial scar formation. Arthritis is mainly exudative, and it does not remain after the inflammation subsides.

 

Clinical Manifestations of Rheumatic Fever

Rheumatic fever is mainly manifested as multiple arthritis, carditis, circular erythema of the skin, subcutaneous nodules and chorea, etc., which occur individually or in different combinations after streptococcal infection. With the progress of society and the improvement of nutritional conditions in medical and health living, the clinical manifestations of rheumatic fever have been significantly different from before.

In addition to the decrease in incidence, atypical and mild cases increase. The number and severity of heart invasions are significantly reduced.

 

The onset period is 1-4 weeks, and about 1/2 of the patients have acute pharyngitis, tonsillitis, fever, fatigue, sweating, anemia, weight loss, etc., and some people do not have any discomfort.

 

I.                  Carditis

As the most serious disease, it is more common in adolescents with rheumatic fever. The incidence and severity of cardiac inflammation gradually decreases with the onset of age. Mild cases are asymptomatic, pericardium, myocardium and endocardium can be individually affected. Or three levels of involvement at the same time are called pancarditis.

 

(1) The symptoms of myocardial inflammation depend on the extent and extent of myocardial invasion, and may have palpitation and discomfort in the precardiac area. Severe cases are complicated by heart failure, cough, dyspnea, sweating, etc., and are often the main cause of death in children with acute stage.

Examination: There may be tachycardia that is not proportional to body temperature, the heart generally increases, the first heart sound of the apex decreases, diastolic gallops, heart murmurs, and other signs of heart failure can appear. Electrocardiograms include atrioventricular block, premature beats, atrial fibrillation, flat or inverted T waves, downshift of the ST segment and prolonged Q-T, suggesting myocardial damage.

 

(2) There are no obvious signs in the acute phase of endocarditis. The initial rheumatic fever may be caused by accelerated blood flow, enlarged heart, or valvular edema, and inflammatory response. The heart murmur mostly originates from the mitral valve, and a small part originates from the aortic valve. Mid-diastolic murmur due to cardiomyopathy and mitral valve inflammation, also known as Carey-Coombs murmur.

Acute murmurs often need to be tracking and observation, and mild cases can disappear with rheumatic heat control. If repeated rheumatic activities can cause permanent valve damage, murmurs can persist. It usually takes more than two years to produce permanent damage. About half of the patients with cardiac inflammation are initially asymptomatic and eventually develop chronic heart valve disease.

 

(3) Pericarditis is part of rheumatic pancarditis or serositis. Fibrin exudation often occurs first, the patient has chest pain, pericardial friction sounds can be heard, followed by serous exudation to form pericardial effusion. But the amount of fluid is often small. It may be accompanied by pleurisy or pneumonia. The ECG can have ST segment up and T wave inversion.

According to statistics, about one third of patients with carditis have no obvious symptoms and eventually develop chronic heart valve disease. This is more common in adults.

 

II.               Arthritis

It is the most common main manifestation of rheumatic fever. As the patient gets older, arthritis is more common, asymmetry, migratory, major arthritis. The severity varies widely, with mild joint pain and no inflammation. Typical patients may have redness, swelling and heat pain, and limited mobility. No joint dysfunction remains after the inflammation subsides. Arthritis is not related to the severity of heart inflammation. Adult rheumatic fever patients are mostly characterized by arthritis, while adolescents and young children are mainly affected by heart disease.

 

III.            Skin Performance

Circular erythema and subcutaneous nodules are characteristic. Ring-shaped erythema mostly occurs on the inner side of the trunk or limbs. It is a pale red ring-shaped erythema with a clear and easy to fade outline. It may have erythematous rash on the periphery and pale central, often transient. Subcutaneous nodules are 2-5 mm indurated nodules, round or oval, do not stick to the skin, no tenderness, and can be moved. It often appears on the extensor side of large joints, especially the elbow, knee, and wrist joints, the occipital region, or the spinous process of the thoracolumbar spine. Subcutaneous nodules often coexist with carditis. Subcutaneous nodules have been relatively rare in recent years.

 

IV.            Chorea

It is rare in adults and the incidence is very low in children. It is more common in girls. Appears months after streptococcal infection. Caused by rheumatic cerebrovascular disease, unconscious and uncoordinated hand and foot movements. Sometimes facial twitches often coexist with carditis.

 

V.              Other Performance

Other extracardiac rheumatism activities such as:

  1.       Rheumatic pneumonia or pleurisy
  2.       Peritonitis mainly with abdominal pain
  3.       Rheumatic nephritis, whose renal function is normal, may have proteinuria and hematuria
  4.       Rheumatic vasculitis, which can occur in large and small arteries, such as lung and cerebral arterioles can cause pulmonary and cerebral infarction Angina can occur in the coronary arteries.

 

Laboratory and other inspections

I. Indicators reflecting streptococcal infection

(1) Fresh specimens of pharyngeal swabs should be taken and cultured immediately after collection. Positive cases only indicate infection with the bacteria, negative cases cannot rule out rheumatic fever.

 

(2) Determination of streptococcal antibodies commonly used are anti-streptolysin O or ALSO (Anti-Streptolysin O). It started to increase at 2 weeks after infection, reached its peak at 5 and 6 weeks, and declined slowly, and the anti-O titer ≥500u was meaningful. The level of titer and the rate of decline have nothing to do with the severity and prognosis of the disease. The increase only indicates a recent hemolytic streptococcal infection and is not a specific diagnosis of the disease.

 

Others include anti-hyaluronidase (AH), anti-streptococcal kinase (ASK), and anti-DNA (anti-DNase). The latter remain positive for longer.

If> 200,000 u / L (> 200 u / ml), strep infection is indicated.

 

II. Reflect non-specific inflammation indicators

1. The white blood cell count and neutrophil ratio increased, and there was anemia.

2. Increased erythrocyte sedimentation may be related to elevated globulin and fibrinogen. The former is related to immune response, and the latter is related to inflammatory response. ESR can be normal during heart failure.

3. Mucin is elevated, the normal is 30-70g / L (30-70mg / ml).

4. C-reactive protein is positive. C-reactive protein is a protein that appears in blood during inflammation. Erythrocytes increased rapidly during anemia, C-reactive protein was negative, and patients with heart failure had normal erythrocyte sedimentation, and C-reactive protein was positive.

 

The above laboratory inspection indicators should be jointly conducted and comprehensively analyzed.

 

Diagnosis of Rheumatic Fever

Rheumatic fever lacks a specific diagnostic method, mainly referring to the revised Jones standard.

There are two major manifestations or one major plus two minor manifestations of streptococcal infection, then rheumatic fever is very likely.

Additional recommendations for rheumatic fever diagnosis at the Northeast Northeast Cardiovascular Collaborative Conference of 1981: ECG except for prolonged P-R, may have ST-T changes, Q-T prolonged or arrhythmia, rheumatic pneumonia, pleurisy, peritonitis, vasculitis , Rheumatic encephalopathy, rheumatic nephritis, etc., as diagnostic reference conditions.

 

In recent years, due to the relatively mild and atypical rheumatic fever, the revised Jones standard is insufficient in sensitivity and specificity. The following aspects should be noted when diagnosing rheumatism:       Major manifestations Minor manifestations Support for streptococcal infection

  1.         Cardiitis Clinical anti-streptococcal antibodies, anti-streptolysin O and other titers increased
  2.           Polyarthritis have had rheumatic fever or rheumatic heart disease
  3.          Chorea disease Arthralgia Streptococcus aureus pharyngeal culture positive
  4.           Marginal erythema fever with recent scarlet fever
  5.           Subcutaneous nodule experiment
  6.           Acute phase reaction
  7.           ESR
  8.          C-reactive protein
  9.           Leukocytosis
  10.          P-R interval extended

* If there are two primary criteria, or one primary criterion plus two secondary criteria, based on a group A streptococcal infection, this indicates a high probability of acute rheumatic fever.

 

1. When cardiac inflammation is the main clinical manifestation, if there is no obvious murmur, attention should be paid to distinguish it from viral myocarditis.

 

2. The main clinical manifestations of arthritis, fever, and rapid erythrocyte sedimentation should be distinguished from rheumatoid arthritis, tuberculosis allergic arthritis (Poncet’s syndrome), and connective tissue disease.

 

3. The condition is mild after streptococcal infection, the heart is not invaded, only joint pain, often the state after streptococcal infection.

 

4. There are chronic rheumatic valvular diseases, the diagnostic reference conditions for judging the presence or absence of rheumatism:

 

(i) The nature of the original organic murmur changes or there is a new pathological murmur.

 

(ii) Recently, there is no obvious cause of enlarged heart or heart failure.

 

(iii) Heart failure is difficult to control, digitalis tolerance is reduced, and poisoning manifests.

 

(iv) Sinus tachycardia> 100 beats / min in the case of recent arrhythmia, or in the quiet condition without using digitalis.

 

(v) ESR is normal during heart failure, and the rate of erythrocyte sedimentation caused by other causes can be excluded after the heart failure is controlled or after cardiac surgery.

 

(vi) Recently, fever, sweating, fatigue, joint pain, and heart failure symptoms appear or worsen.

 

(vii) Extracardiac manifestations of rheumatic fever.

 

(viii) The condition improved significantly after anti-rheumatic test treatment.

 

Treatment of Rheumatic Fever

Control inflammation, prevent recurrence and protect the heart.

I. General Treatment

In the acute phase, bed rest should be performed. Those with carditis should stay in bed strictly to reduce the burden on the heart until the symptoms of rheumatic activity disappear and the indicators return to normal. The diet should be easy to digest and nutritious.

 

II. Antibiotics

Apply penicillin daily for two weeks. Erythromycin can be used if you are allergic to penicillin.

 

III. Salicylic acid preparations

This medicine can inhibit the synthesis of prostaglandins. Thereby reducing the inflammatory response. Adults 4-6g daily, pediatric 100-150mg / kg body weight, orally divided into 3-4 times. After the symptoms are controlled, the dosage can be reduced as appropriate, and the drug can be discontinued 2 to 4 weeks after the rheumatism is stopped. Its side effects are bleeding or / and gastrointestinal reactions.

 

IV. Adrenal corticosteroids

Can reduce tissue response, suitable for high fever, carditis, heart failure, or complete atrioventricular block asthma syndrome. In emergencies, dexamethasone may be administered intravenously 5-10 mg each time or hydrocortisone 50-100 mg each time, 2-4 times daily. Generally, 30-60 mg of prednisone can be taken orally daily, and the dosage should be reduced after 2 weeks.

The total course of treatment is 6-8 weeks. When hormone therapy is reduced or discontinued, there may be a “bounce” phenomenon. The milder disappears in 2-3 days and sometimes lasts for 1-2 weeks. At this time, it should still be treated as rheumatic activities.

 

Prevention and control of streptococcal infection

Mainly for the prevention and control of streptococcal infections:

  •       Pay attention to cold protection and warmth, and strengthen resistance.
  •       For those who have suffered from rheumatic fever, intramuscular injection of long-acting penicillin should be applied once a day. In the season of onset, and followed up regularly.
  •      After rheumatism is stopped, chronic lesions can be removed.

  

Section 5. Chronic Rheumatic Valvular Disease

Rheumatic heart valve disease is due to repeated episodes of rheumatic carditis, and the heart valve and its ancillary structures (tendon cords, papillary muscles) have become damaged, resulting in valve stenosis and insufficiency of the valve function abnormality, resulting in hemodynamic disorders, that is, chronic Rheumatic valvular disease, patients with heart valve damage often have a history of repeated rheumatic activities, but nearly one-half of the patients have no clear history of rheumatic fever and develop heart valve disease. This disease is one of the common heart diseases in the world and is more common in adults aged 20-40.

 Rheumatic heart valve disease is the second most common type of valve, followed by aortic valve, the latter often coexisting with mitral valve disease is called combined valve disease. The susceptibility to invasion of the mitral and aortic valves may be related to the large pressure load on the two. The main cause of valve dysfunction is rheumatic fever, but it can also be caused by non-rheumatic, which needs identification.

 

Section VI. Infective Endocarditis

Endocarditis is mainly inflammation of heart valves. There are two types of infectious and non-infectious (such as rheumatic, lupus and rheumatoid).

Clinically, it is mainly infectious, most of which are caused by bacterial infections, so it is also called bacterial endocarditis.

 

Infective endocarditis is divided into acute and subacute according to its pathogenesis and different bacterial virulence. However, due to the individual differences between bacterial virulence and human resistance, the same bacteria can have different clinical differences in different patients.

In addition, in recent years, the widespread use of antibiotics, the clinical manifestations of the two have no clear boundaries. It is difficult to distinguish strictly.

 

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