rheumatic fever
Introduction
Introduction to rheumatic fever Rheumatic fever is a common recurrent episode of acute or chronic connective tissue inflammation, mainly involving the heart, joints, central nervous system, skin and subcutaneous tissue. The clinical manifestations are mainly carditis and arthritis, which may be accompanied by fever, toxemia, rash, subcutaneous nodules, and chorea. It usually occurs 2 to 4 weeks after streptococcal infection. It is an allergic disease of pharyngeal group A hemolytic streptococcus infection. It is usually obvious when arthritis is acute, but rheumatoid carditis at this stage. Can cause death of the patient. Cardiac damage of varying severity often remains after an acute attack. basic knowledge Sickness ratio: 0.05% Susceptible people: no special people Mode of infection: non-infectious Complications: heart failure, rheumatic disease
Cause
Rheumatic fever cause
Streptococcal infection and immunoreactivity (20%):
Although the etiology and pathogenesis of rheumatic fever have not yet been fully elucidated, it is currently recognized that rheumatic fever is an autoimmune disease caused by pharyngeal infection of Streptococcus A, and it has been confirmed that certain structures of human tissue and streptococcus have Cross-antigenicity, so the body can mistakenly think that streptococci are "autologous", and do not produce a normal immune response to remove it; once the body's immune function changes, streptococcus enters the human body as an antigen to produce corresponding antibodies, which can be detected at present. A variety of autoantibodies, such as anti-myocardial antibodies, anti-M protein antibodies, anti-cardiac valve polysaccharide antibodies, anti-neuronal antibodies, etc., such antibodies not only react with streptococcal-associated antigens, but also act on their own myocardium, heart valves The related antigens of nerve tissue and connective tissue cause autoimmune reaction, leading to corresponding tissue damage and causing rheumatic fever. In the process of rheumatic fever, cellular immune mechanism also plays an important role, confirmed by immunohistochemical techniques. Rheumatic fever lesions are mainly infiltrated by T lymphocytes, and patients with rheumatic fever have lymphatic circulation Increased cellular response and activation of a series of cellular immune response markers, such as interleukin (IL-1, IL-2), increased tumor necrosis factor-gamma (TNF-), enhanced inhibition of leukocyte migration, natural killer cells (NK) and Increased monocyte toxicity, enhanced T cell response to streptococcal antigens, free radicals by phagocytic cells, and increased procoagulant activity in peripheral blood and cardiac tissue cells indicate that cellular immunity plays an important role in the pathogenesis of rheumatic fever.
Virus infection theory (20%):
In recent years, scholars have paid more attention to the theory of viral infection, and believe that rheumatic fever may be related to Coxsackie B3, B4 virus infection. In recent years, relevant scholars have paid more attention to the theory of viral infection, and believe that rheumatic fever may be related to Coxsackie B3, B4 virus infection, based on:
1. The titer of Coxsackie B3 and B4 antibodies was significantly increased in the serum of some patients with rheumatic heart disease.
2. Rheumatoid virus was found in the left atrium and heart valve of patients with rheumatic heart disease.
3, when the Javanese monkey infected with Coxsackie B4 virus, it can produce pathological changes similar to rheumatic heart disease, but this theory has not been generally accepted, and it is difficult to explain that penicillin does have a significant effect on preventing recurrence of rheumatic fever. Many scholars believe that the virus Infection may create conditions for streptococcal infection and act as an inducer in the development of rheumatic fever.
Genetic factors (20%):
Recently, genetic markers have been found in patients with rheumatic fever. A serum containing 883 B cell alloantigen (allogeneicantigen) was used, and approximately 72% of patients with rheumatic fever were positive. Recently, it has been found that there are genetic markers in patients with rheumatic fever. A serum containing 883 B cell alloantigen (allogeneicantigen) is used. About 72% of patients with rheumatic fever are positive, and the same antigen for B cells has also been produced. Clone antibody D8/17, 80%100% of patients with acute rheumatic fever were positive, while only 15% of the control group was positive. Therefore, it is possible to use monoclonal antibodies to screen vulnerable people with acute rheumatic fever. In patients with rheumatic fever and their relatives, there are special antigen expressions on the cells of the immune system. Most of the reports are accompanied by an increase in the frequency of HLA-DR4. In addition, the frequency of HLA-DQAl and DQB1 is increased. The progress of this study may be In the general population, rheumatic fever and easy patients are found for targeted prevention. Most scholars believe that genetic factors can be used as one of the risk factors, but the most likely causes of multiple members in the same family are the same as the living environment. Easy to get involved in each other.
Immune function (20%):
Changes in immune function status may also be involved in the occurrence of rheumatic fever. Changes in immune function may also be involved in the occurrence of rheumatic fever. Immunoglobulin IgG, IgA and IgM are often elevated during rheumatic fever and rheumatism; although leukocytosis is elevated in blood, phagocytosis is reduced, and lymphocyte transformation test results It shows that the conversion rate of lymphocytes to the original lymphocytes is decreased, indicating that there is a defect in cellular immune function, and in addition, the cell-mediated immune response is also important in the course of the disease.
As for the theory of malnutrition, the relationship between trace elements and rheumatic fever (currently found to be closely related to the immunopathological mechanism of zinc deficiency and rheumatic fever and rheumatic heart disease), endocrine disorders, etc., continue to explore, in short, the pathogenesis of rheumatic fever Intricate, it is the result of a combination of factors such as streptococcal pharyngeal infection and immune status.
Pathology: Rheumatic fever is systemic connective tissue inflammation, which can be divided into three phases according to the process of pathogenesis.
1. Denatured exudation period: Collagen fibers in connective tissue divide, swell, form glassy and cellulose-like degeneration, and there are cell infiltration of lymphocytes, plasma cells, eosinophils, neutrophils and other inflammatory reactions around degenerative lesions. This period can last for 1 to 2 months, and resume or enter the second and third phases.
2, proliferative period: on the basis of the above-mentioned lesions, rheumatoid granuloma or rheumatoid body (Aschoff body), which is a characteristic lesion of rheumatic fever, is the basis for pathological diagnosis of rheumatic fever and indicators of rheumatic activity, small body There is cellulose-like necrosis in the center, lymphocytes and plasma cells infiltrated at the edges, and rheumatoid cells. The rheumatoid cells are round, elliptical or polygonal, and the cytoplasm is rich in basophilic, nucleus empty, with obvious nucleus. Ren, sometimes occurs in the formation of giant cells in the form of binuclear or multinuclear, and enters the hardening phase, which lasts for 3 to 4 months.
3. Hardening period: The degeneration and necrotic substances in the center of the rheumatoid body are gradually absorbed, the inflammatory cells exuded are reduced, the fibrous tissue is proliferated, and scar tissue is formed in the granuloma.
Because the disease often recurs, the development of the above three phases can be staggered, it takes 4 to 6 months, the first phase and the second phase are often accompanied by serous exudation and inflammatory cell infiltration, this exudative lesion is To a large extent, it determines the occurrence of various clinical symptoms. The pathological changes in joints and pericardium are mainly exudative, while the formation of scars is mainly limited to the endocardium and myocardium, especially the valve.
The inflammatory lesions of rheumatic fever involve collagen fibers in the connective tissue of the whole body. In the early stage, the joints and the heart are involved, and then the heart damage is dominant. The lesions in each stage are concentrated in the affected organs, such as exudation in the joints and pericardium. , the formation of arthritis and pericarditis, after the exudate can be completely absorbed, a few pericardial exudate absorption is incomplete, polarization forms part of the adhesion, in the myocardium and endocardium is mainly proliferative lesions, after the formation of scar proliferation, heart valve Proliferative lesions and adhesions often lead to chronic rheumatic valvular disease.
Prevention
Rheumatic fever prevention
Rheumatic fever is a preventable disease, and its relationship with streptococcus is very close, so preventing the epidemic of streptococcal infection is one of the most important steps to prevent rheumatic fever.
First, prevention of primary rheumatic fever
1, to prevent upper respiratory tract infections, injection health, often participate in physical exercise, improve health.
2, for scarlet fever, acute tonsillitis, pharyngitis, otitis media and lymphadenitis and other acute streptococcal infections, should be actively and thoroughly antibiotic treatment in the early stage, with penicillin as the first choice, those who are allergic to penicillin can choose erythromycin.
3, chronic tonsillitis repeated acute authors (onset 2 times a year), surgery should remove the tonsils, 1 day before surgery to 3 days after surgery to prevent infection with penicillin, after tonsil removal, hemolytic streptococcal pharyngitis can still occur, It should be treated promptly.
4. Prevention and early detection in closed collective groups (military camps, schools, kindergartens, etc.), early diagnosis of streptococcal infection, establishment of necessary health care system, may completely eliminate the prevalence of streptococcal infection, and greatly reduce the incidence of rheumatic fever.
Second, prevent recurrence of rheumatic fever
Patients who have suffered from rheumatic fever should actively prevent streptococcal infection. It is generally recommended to use 1.2 million units of benzylpenicillin (long-acting Xilin), once a month for intramuscular injection. For those who are allergic to penicillin, sulfadiazine or sulfisoxazole can be used. Children 0.25 ~ 0.5g per day, adults 0.5 ~ 1.0g per day, oral orally, it is generally believed that the duration of prophylaxis, patients under the age of 18 with rheumatic fever must continue to prevent medication, patients over the age of 18 without heart involvement in rheumatic fever, from At least 5 years after the last episode of rheumatic fever, patients with rheumatic fever who have suffered from heart disease can easily cause rheumatism after re-infection with streptococcus, and are prone to onset of carditis. Therefore, strict preventive treatment is required. Studies have shown that the level of preventive medication is high. In contrast to the proportion of patients with streptococcal infection, the proportion of streptococcal infections in the no-prevention or irregular-prevention group was three times higher than that in the complete prophylaxis group, and it is particularly noteworthy that patients with rheumatic activity without the preventive or irregular prophylaxis group The proportion is 10 times higher than that of the complete preventive medication group, and even if the irregular preventive medication has a certain effect.
Complication
Rheumatic fever complications Complications, heart failure, rheumatic diseases
In the rheumatic heat treatment process or rheumatic heart disease repeated rheumatic fever activities, patients are prone to lung infections, severe heart failure, sometimes complicated by endocarditis, hyperlipidemia, hyperglycemia, hyperuricemia, Elderly patients with rheumatic heart disease will also have coronary heart disease and acute myocardial infarction. Rheumatic heart disease is the most common complication of this disease.
Symptom
Rheumatic fever symptoms common symptoms unexplained fever
[clinical manifestations]
1, prodrosis: 2 to 5 weeks before the typical clinical symptoms of rheumatic fever, often have clinical manifestations of upper respiratory tract infection such as pharyngitis or tonsillitis, such as fever, sore throat, submandibular lymph nodes, cough, etc. Symptoms, after treatment symptoms disappear, there is no discomfort, the infection can be light without obvious clinical symptoms, sometimes mild patients will completely forget the history, only 1/3 ~ 1/2 patients with rheumatic fever can complain about the recent A history of upper respiratory tract infections.
2, typical clinical manifestations: the most common fever, arthritis and carditis, ring erythema, subcutaneous nodules and chorea are also occasionally seen.
(1) Fever: 50% to 70% of patients have fever, irregular heat type, high fever is more common in children and adolescents, adults have moderate fever, mild cases often only have low fever, or even no fever, low fever sometimes only in regular regular test Wen was only discovered.
(2) Arthritis: Typical arthritis is migratory and multiple, and several large joints are invaded at the same time. Knee, ankle, elbow, wrist and shoulder joints are more common. The affected joints are red, swollen and hot during an acute attack. , pain and tenderness, limited activity, no joint deformation after the acute phase, typical rheumatic migratory arthritis refers to arthritis (pain) can be transferred from one site to a short period of time, such as 24-48 hours In another position, joint symptoms are greatly affected by the climate and are very sensitive to weather changes. Often, there is obvious joint pain before the weather changes (especially cold and rainy days), the symptoms are relieved after the climate is stable, and the salicylic acid preparations are applied to the wind joints. Inflammation has excellent curative effect, and the condition is relieved in more than 48 hours after administration. For patients with mild arthritis, it is often necessary to check carefully. The palpation of joints one by one can reveal the existence of arthritis. The mild patients can only have joints. Pain, occasionally manifested as hip, phalangeal joint, cervical vertebrae, mandibular joint or sterno-articular pain, chest rib joint pain is often misdiagnosed as myocarditis, cardiac neurosis, intercostal neuralgia, recent cases, joints About 57%, about 70% of joint pain.
(3) Carditis: typical patients with carditis often complain of heart palpitations, shortness of breath, discomfort in the anterior region, pain, etc. When valvitis is present, there may be a new high-pitched apex area, and a squeaky murmur during the systolic period. Vulnerability, but does not change with body position and breathing; there may also be short-term low-grade diastolic middle murmur in the apical region. This diastolic murmur is called Carey Coombs's murmur. The difference between this murmur and mitral stenosis is that the former does not have left atrium and left. Significant pressure gradient between the ventricles, such as the ablation of the aortic valve area at the bottom of the heart (left sternal border), a soft, squeaky murmur in the middle of the diastolic phase, especially in the case of acute rheumatic carditis without mitral murmur. Caused by inflammation, myocarditis often accompanied by apical systolic and diastolic murmurs, tachycardia (still more than 100 beats / min after falling asleep) is an early manifestation of myocarditis, progressive palpitations after upper respiratory tract infection, gas Promote cardiac dysfunction, should be closely followed to rule out early myocarditis, severe symptoms can have symptoms and signs of congestive heart failure such as tachycardia, difficulty breathing, cough, Sitting breathing, and even pulmonary edema, which is caused by left ventricular volume overload, X-ray or echocardiography can show heart enlargement, pericarditis can be expressed as distant heart sounds, pericardial friction or chest pain, mitral regurgitation The murmur can sometimes be covered by the pericardial friction sound, until the pericarditis subsides, the echocardiogram can detect the pericardial effusion, the electrocardiogram can have a low voltage, the ST segment elevation of the chest lead, the X-ray can have a heart shadow increase Large, when sitting in the standing position, the lower part of the heart shadow is enlarged as a flask; when lying down, the bottom of the heart is obviously widened, and the heart is gone. In recent years, the incidence of carditis is about 45%.
(4) ring erythema: rare in clinical, its incidence in rheumatic fever varies from 6% to 25%, with a reddish red blush, central pale, mostly distributed in the proximal end of the trunk or limb When the time is hidden, sometimes a few erythema merge into an irregular ring, the size of which varies, the itch is not obvious, and the pressure fades.
(5) Subcutaneous nodules: It is also rare. According to statistics, the incidence rate ranges from 2% to 16%. It is a slightly hard, painless small nodule. It is found in the subcutaneous tissue on the extension side of the joint, especially in the elbow. Knee, wrist, occipital or thoracic and lumbar spinous processes, no adhesion to the skin, no redness and inflammation, often appear in carditis.
(6) chorea: occurs in children, 4 to 7 years old children are more common, adults rarely occur, generally occur 2 months or more after the first streptococci infection, caused by rheumatic fever inflammation invading the basal ganglia, A purposeless, involuntary torso or limb movement, such as facial expressions such as squeezing the eyebrows, blinking, shaking the head and turning the neck, licking the tongue, the limbs appearing straight and flexing, adduction and abduction, pronation and supination, etc. Irregular alternating movements, exacerbated when excited, disappeared during sleep, and often unstable mood is one of its characteristics. It must be differentiated from other neurological choreas. Because it appears in the later stage of rheumatic fever, it is often accompanied by other obvious The clinical manifestations of rheumatic fever, domestic reports have a incidence of about 3%, foreign reports can be as high as 30%.
(7) Other manifestations: progressive fatigue, fatigue, anemia, myalgia, sweating, nosebleeds, ecchymoses, etc. are also quite common. The atypical manifestations of the skin may be nodular erythema and polymorphous erythema, sometimes severe Abdominal pain, similar to acute appendicitis and acute abdomen, this may be due to rheumatic vasculitis, if rheumatoid nephritis, there may be urinary red blood cells and protein, as for rheumatic pneumonia, pleurisy and encephalitis, has been relatively rare in recent years.
3. Clinical classification of rheumatic fever: According to the disease process of rheumatic fever, it can be divided into the following four types:
(1) fulminant: This type is more common in children, acute onset, dangerous condition, often due to severe carditis, congestive heart failure, rheumatic pneumonia is equal to death in the short term, this type is rare in the country, but in Western countries, Due to the absence of new cases for a long time in the past, the population's immunity has declined. In recent years, this type of case has been reported.
(2) recurrent type: this type is the most common, with repeated clinical manifestations in recurrence, recurrence is often the most likely within 5 years after initial onset of rheumatic fever, the following cases have higher recurrence rate: 1 previous rheumatoid Sexual heart disease; 2 patients with a history of recurrent rheumatic fever; 3 symptoms of pharyngeal streptococcal infection, strong immune response (such as ASO and other antibody titers); 4 this streptococci infection from the previous rheumatism The onset time of fever is less than 2 years; 5 is younger; 6 can not adhere to secondary prevention, and the recurrence rate is 18% to 58% in one or more of the above cases. The prognosis of patients with simple arthritis is good. There is no joint malformation, the prognosis of patients with carditis and the number of recurrent episodes, the severity of each episode, whether it can adhere to secondary prevention and early anti-rheumatic treatment.
(3) Chronic type (or prolonged type): The course of disease lasts for more than half a year, often with carditis as the main manifestation. During the course of the disease, the symptoms are relieved and aggravated repeatedly, and there is a heart involvement, especially a heart enlargement or The incidence of valvular disease is higher, but there are also those with initial rheumatic fever. Those who can adhere to secondary prevention and adequate treatment for anti-rheumatic treatment have a better prognosis. Those who give up prevention and treatment have a poor prognosis. Chronic patients with valve involvement die within 6 years of giving up prevention or treatment.
(4) subclinical type (recessive rheumatic fever): This type generally has no characteristic clinical manifestations, sometimes only fatigue and fatigue, pale, low fever, limb pain, may have a history of sore throat or pharyngeal discomfort, only found in the examination There is submandibular lymph node tenderness (prompt to have tonsillitis in the near future), laboratory tests often have ESR acceleration, -glycoprotein increased, ASO titer increased, serum circulating immune complex (CIC) continued to increase, anti-myocardial antibody positive, ECG Normal or mild PR interval prolongation, after a period of time, typical clinical manifestations may occur due to increased rheumatic activity, or the condition may be concealed, and chronic rheumatic heart disease may occur several years later.
Rheumatic carditis is the most important clinical manifestation of rheumatic fever. It usually occurs within 2 weeks after arthritis. The pericardium is often exudative inflammation, which may have symptoms such as friction and chest pain. Constrictive pericarditis is rare, and myocardium often has lymph. Infiltration of cells and focal necrosis. The Aschoff body of the myocardium is a pathological feature of rheumatic heart disease. It is a fibrin-like swelling and degeneration of collagen fibers in connective tissue, followed by inflammatory cell infiltration. Granuloma, a new gentle reflux heart murmur suggesting valvular inflammation, a verrucous lesion formed by cell infiltration and fibrosis at the edge of the leaflet is characteristic of valvitis, a scorpion on the mitral valve leaflet Lesions can cause mild diastolic murmurs (Carey Coombs murmurs), valvitis most often involves the mitral valve, followed by the aortic valve, rarely involving the tricuspid and pulmonary valves, and electrocardiographic changes in carditis include ST or T waves. Change; sometimes there is abnormal heart conduction and may cause syncope.
Examine
Rheumatic heat check
[Laboratory Inspection]
1. Tests that reflect recent streptococcal infection and related immunity
(1) Determination of anti-streptolysin O (ASO): It is generally considered that ASO titer >500U is valuable, but some people think that adult >250U, children over 5 years old >333U, should consider its titer Increased, it is currently considered that the results of a trial are of little significance for diagnosis. If multiple trials (preferably once every 2 weeks) gradually increase the results, the diagnosis of rheumatic fever and rheumatism is of great value, such as long-term constant antibody in high units. Mostly inactive, if the high unit gradually declines, it is the disease remission period, the antibiotics or hormones used in the early stage of the disease, ASO may not increase, in addition, suffering from certain hepatitis, nephritis, nephrotic syndrome and multiple osteomyelitis ASO can also be non-specifically increased.
(2) Determination of anti-streptococcal cell wall polysaccharide antibody (ASP): According to the common antigenic property of streptococcal cell wall polysaccharide and human heart valve glycoprotein, ELISA method for determination of ASt-IgM, IgG, rheumatic valvular heart disease The rate is as high as 80% or more. On the contrary, the positive rate of non-rheumatic valvular heart disease, streptococcal infection, acute nephritis and viral myocarditis is only about 10% to 13%. This test is superior to blood sedimentation in reflecting rheumatic fever activity. The immune response after reflecting streptococcal infection is better than ASO, and has higher sensitivity and specificity.
(3) Determination of anti-streptokinase (ASK): ASK titer increased during rheumatic fever, often >800U.
(4) Determination of antihyaluronidase (AHT): When the rheumatic fever is hot, it is often >128U.
(5) Determination of anti-Streptococcus deoxyribonuclease B (ADNase B): When rheumatic fever, children often >250U, adults >160U.
(6) Anti-Streptococcus diphosphate pyridine nucleotidase (ASDA) assay: more than 1:275 U indicates rheumatic fever or rheumatic activity.
It is generally considered that two items in the above Streptococcal antibody test can be simultaneously examined, once every two weeks. If one of the two dilution tubes or two or more dilution tubes of the test has an increased antibody titer, it is rheumatic fever or rheumatism. Strong evidence.
2, reflect the blood white, globulin changes test
(1) ESR: increased, associated with decreased albumin in blood, elevated - and 2-globulin, when rheumatic fever combined with heart failure or application of salicylic acid, hormones may not increase.
(2) C-reactive protein (CRP): positive, indicating that there is a globulin in the serum that can precipitate the C polysaccharide on the S. pneumoniae membrane. Although this test has no specificity, its level is directly proportional to the degree of rheumatic activity.
3. Experiments reflecting the destruction of connective tissue collagen fibers
(1) Serum mucin test: serum mucin > 40 mg / L (4 mg / dl) is positive.
(2) Serum diphenylamine reaction > 0.25 optical density unit.
(3) Increase in serum glycoprotein: a1>20%, a2>38%, in addition, serum protein hexose increased (normal value l210 21mg/L); aminoglycose increased (normal value was 830 41mg/L).
4, serum circulating immune complex test
(1) Complement test: serum complement C3 is increased, immunoglobulin IgA, IgG can also be increased.
(2) Peripheral blood lymphocyte procoagulant activity test: based on rheumatic fever with cellular immunity, using streptococcal cell membrane or cell wall polysaccharide antigen as specific antigen, stimulating peripheral blood lymphocytes of patients, found that its blood coagulation activity increased, positive rate More than 80% (normal people, simple streptococcal infection, viral myocarditis, coronary heart disease, positive rate is only 4% to 14%), can be used as evidence of rheumatic fever or rheumatism.
(3) Anti-myocardial antibody assay: The principle is that the streptococcal membrane has common antigenicity with mammalian myocardium, and can adsorb specific anti-myocardial antibodies in the serum of patients with rheumatic fever, and the positive rate can be as high as 70%, especially for judging whether there is any Cardiac involvement is of great significance.
5, other
In serum rheumatoid myocarditis, serum phosphocreatine kinase (CPK) and its isoenzyme (CPK-MB) and aspartate aminotransferase (GOT) can be increased, and the degree of increase is parallel with the severity of myocarditis.
Film degree exam
1, ECG examination
Patients with rheumatic carditis typically change to atrioventricular block (prolonged PR interval), atrial and ventricular premature contractions, and ST-T changes, atrial fibrillation and pericarditis may occur. In the past, it was considered that the PR interval was prolonged, even as high as 70% to 80%. In recent years, only about 1/3 of cases have been seen.
2, echocardiography
Since the 1990s, the application of two-dimensional echocardiography and Doppler echocardiography for rheumatic fever and rheumatic carditis has made great progress, not only for carditis with obvious clinical symptoms, but also for heart valve ultrasound changes. High positive rate, Vasan RS also found 2 cases of acute rheumatic fever, although there is no clinical symptoms of carditis (polyarthritis and chorea), there are changes in mitral ultrasound, small nodules in the anterior mitral valve, After follow-up after treatment, this nodular change disappeared, so the author believes that these changes should be an acute cardiomyelitis manifestation of acute rheumatic fever. The most diagnostic ultrasound changes are currently considered to be:
(1) valve thickening: can be diffuse valve leaf thickening or focal nodular thickening, the former can be as high as 40%, the latter can be as high as 22% to 27%, both with mitral valve more common, followed by The aortic valve, focal nodule size is about 3 ~ 5mm, located in the body and / or tip of the valve leaflet, these nodular thickening is the most characteristic morphological changes, more considered rheumatic It is related to the formation of neoplasms, and its morphology and activity are different from those of infective endocarditis.
(2) mitral valve prolapse: the incidence of each report varies widely, can be as high as 51% to 100%, as low as 5% to 16%, this difference is considered to be related to the examiner's technical proficiency and vigilance Valve prolapse is more common in the anterior mitral regurgitation (51% to 82%), and the posterior mitral valve (7%) and the aortic valve (15%) prolapse are less common.
(3) valvular regurgitation: is the most common valve change, mitral regurgitation is much more common than aortic valve and tricuspid regurgitation, for the skilled practitioner can accurately distinguish the physiological and pathological range of reflux, such as Combined with color Doppler ultrasound, the accuracy is higher. According to statistics, the incidence of mitral regurgitation is as high as 84% to 94%, and severe reflux can reach 25% in recurrent rheumatic fever.
(4) Pericardial effusion: mostly a small amount of effusion, which occurs in 7% of initial rheumatic fever and 29% of recurrent rheumatic fever. It is worth noting that although there are rheumatic fever, there may be multiple echocardiograms mentioned above. Performance, but in the absence of clinical evidence of carditis, it is not easy to make a diagnosis of rheumatic fever or rheumatic carditis by some positive changes in echocardiography, so as to avoid other causes such as primary mitral valve prolapse, Various non-rheumatic valvular heart disease, cardiomyopathy, and ultrasound changes caused by pericarditis are confused.
3, X-ray chest examination
Clinically, only severe carditis can be detected at the time of physical examination when the heart is significantly enlarged. The heart enlargement of most rheumatic carditis is mild. It is difficult to find without X-ray examination. Sometimes it must be passed. The reduction of heart shadow after treatment confirmed that the heart enlargement of the original carditis had existed.
It can show prolongation of PR interval or sinus tachycardia. ST-T changes indicate that there may be myocarditis. Conventional lead (except AVR) is elevated in horseshoe down ST suggesting that there may be pericarditis.
Diagnosis
Rheumatic fever diagnosis
Diagnostic performance
So far, there is no specific diagnostic method for rheumatic fever, and the revised Jones diagnostic criteria are clinically used.
1, mainly for carditis, polyarthritis, chorea, marginal erythema, subcutaneous nodules.
2, secondary manifestations of fever, joint pain, past history of rheumatic fever or rheumatic heart disease.
3, streptococcal infection according to: ASO or other anti-streptococcus antibodies increased, pharyngeal group A streptococcus culture positive, recent occurrence of scarlet fever.
4, with 2 main performances, or 1 major performance and 2 secondary performance, such as the support of previous streptococcal infection, suggesting the possibility of rheumatic fever.
Differential diagnosis
First, other causes of arthritis
1, rheumatoid arthritis: for multiple symmetry refers to small arthritis and spondylitis, characterized by "morning stiffness" and finger spindle swelling, late joint deformity, clinically less heart damage, but ultrasound Cardiac examination can detect pericardial lesions and valvular lesions early, X-ray shows joint surface destruction, joint space narrowing, osteoporosis adjacent to bone tissue, serum rheumatoid factor positive, immunoglobulin IgG, IgM and IgA increased.
2, exoccal arthritis caused by sepsis: often have signs of primary sensation, blood and bone marrow culture is positive, and intra-articular exudate has a tendency to purulent, and pathogens can be found.
3, tuberculous arthritis: mostly involved in a single joint, occurs in the regular activities of friction or weight-bearing joints, such as the hip, thoracic vertebrae, lumbar or knee joints, joint pain but no redness, heart without lesions, often other parts Tuberculosis, X-ray shows bone destruction, nodular erythema can occur, anti-rheumatic treatment is ineffective.
4, tuberculosis infection allergic arthritis (Poncet disease): the body has a specific tuberculosis infection in the non-articular area, often repeated arthritis, but generally good, X-ray shows no bone destruction, salicylate drugs The symptoms can be alleviated but recurrent, and the symptoms subsided after anti-tuberculosis treatment.
5, lymphoma and granuloma: leukemia can be reported in 10% of cases of fever and acute polyarthritis symptoms, and arthritis can be preceded by changes in the surrounding blood, resulting in misdiagnosis, other lymphoma and benign granulomatosis are similar Report.
6, Lyme disease (Lyme disease): This disease is an epidemic caused by sputum, usually 3 to 21 days after the bite occurs symptoms, clinical manifestations of fever, chronic migratory skin erythema, recurrent Asymmetric arthritis, which occurs in large joints, can have heart damage, affecting the conduction system, ECG shows different degrees of atrioventricular block, and can also have neurological symptoms such as chorea, meningoencephalitis, myelitis, facial nerve spasm Etc., laboratory tests for circulating immune complexes positive, ESR increased, serum specific antibody determination can be identified.
Second, subacute infective endocarditis
More common in the original heart valve disease, there are progressive anemia, splenomegaly, sputum, ecchymosis, clubbing, can be found in different valves such as brain, kidney or lung.
Third, viral myocarditis
There are often respiratory or enterovirus infections before or during the onset of the disease. The main affected parts are in the myocardium. Occasionally, the pericardium may be involved. The endocardium is rarely invaded. The fever time is short. There may be joint pain but no arthritis. The first heart of the apical area Low sound and secondary systolic murmur, arrhythmia is common; no ring erythema, subcutaneous nodules, etc., laboratory tests show that leukopenia or normal, erythrocyte sedimentation rate, ASO, C-reactive protein are normal, complement binding test and neutralizing antibody positive Myocardial biopsy can isolate the virus.
Fourth, the status of streptococcal infection (streptococcal infection syndrome)
At the same time of acute streptococcal infection or 2 to 3 weeks after infection, low fever, fatigue, joint pain, increased erythrocyte sedimentation rate, ASO-positive, electrocardiogram may have a premature beat or mild ST-T change, but no heart enlargement or Obvious murmur, after antibiotic treatment of infection control, the symptoms quickly disappeared, no longer relapse.
Five, systemic red spotted wolf
The disease has joint pain, fever, carditis, kidney disease, etc., similar to rheumatic fever; but symmetrical facial butterfly erythema, decreased white blood cell count, ASO negative, blood or bone marrow smear can be found to help diagnose the lupus cells.
