subacute infective endocarditis
Introduction
Introduction to subacute infective endocarditis Subacute infective endocarditis often occurs in rheumatic valvular heart disease, ventricular septal defect, patent ductus arteriosus and other heart diseases. It can also occur in patients without heart disease. The pathogens are mainly bacteria, followed by fungi and Gram, chlamydia and virus. Mainly manifested as low-to-moderate fever, progressive anemia, fatigue, night sweats, hepatosplenomegaly, clubbing (toe), vascular embolism, young and middle-aged patients, in recent years, the disease was found in the mitral valve On the basis of sag, cardiac catheterization and cardiac surgery, as well as senile valvular degeneration, there is an increasing trend, and the age of onset has gradually increased. Streptococcus viridans is the most important pathogen of the disease, but it has been significantly reduced in recent years. Various staphylococci, hemolytic streptococcus, enterococci and Gram-negative bacteria have become the main pathogens. basic knowledge The proportion of illness: 0.013% Susceptible people: young adults Mode of infection: non-infectious Complications: arrhythmia
Cause
The cause of subacute infective endocarditis
(1) Causes of the disease
Almost all pathogenic microorganisms can cause infective endocarditis, such as mitral and aortic regurgitation, and certain congenital heart diseases such as ventricular septal defect, patent ductus arteriosus and bicuspid aortic valve In recent years, the pathogenic aspect of infective endocarditis has undergone major changes. For a long time, it has been recognized that Streptococcus viridans is an infective endocarditis, especially a subacute infective endocardium. The most important pathogens of inflammation accounted for 90% to 95% before the advent of antibiotics. In recent years, it has dropped to 20% to 40%. Some scholars have counted 81 cases of infection diagnosed from the First Affiliated Hospital of Zhongshan Medical University from 1975 to 1985. In endocarditis (the same below), there was no case of blood culture, and there was no case of Streptococcus viridans. Many scholars at home and abroad believed that the proportion of Streptococcus viridans as a pathogen of endocarditis has gradually decreased. In 1958, In 1964, in 1982, domestic scholars reported 69%, 49%, and 53% respectively. Japans Sheng Zhengxiao reported that in 323 to 1970, 323 cases of subacute infective endocarditis in the country accounted for 71.8% of the bacteria, from 1971 to 1978. 679 patients with subacute infective endocarditis The bacteria decreased to 56.7%. During this period, 836 cases of IE were collected from foreign countries, accounting for 25.8%. Among the 54 cases of SIE diagnosed by the First Affiliated Hospital of Sun Yat-sen University of Medical Sciences from 1990 to 1995, 22 cases were positive for blood culture. In 3 cases (13.6%), it is generally believed that the proportion of Streptococcus viridans as a pathogen of IE has decreased to 25% to 40% since the 1990s.
Staphylococcus including Staphylococcus aureus, Staphylococcus aureus, Staphylococcus aureus and Staphylococcus epidermidis can cause acute, subacute infective endocarditis. The incidence of endocarditis in the past 30 years has been Elevation, related to cardiac surgery at home and abroad, extensive use of artificial heart valves, interventional cardiac diagnosis and treatment technology, drug users increased by intravenous drug addicts (IVDA) and other factors, domestic scholars reported in 1964 10%, increased to 35.7% in the early 1980s, 55.8% of 81 cases of infective endocarditis reported in 1985, and 31.8% of 54 cases of infective endocarditis reported in 1996. Cocci can invade normal and damaged heart valves, and the valve is quickly damaged, and the effect on drug treatment is poor. In recent years, the proportion of endocarditis caused by it has been rising, accounting for 5% to 7.6% in China. The 51 cases of infective endocarditis accounted for 9.1%, and the proportion is higher in foreign countries. This strain is one of the three major pathogens of infective endocarditis in the United States, especially in older males and young women.
(two) pathogenesis
Subacute bacterial endocarditis is predisposed to organic heart disease and may be related to the following factors:
1. There are valves or endocardium that may adhere to pathogens. It is well known that normal human blood flow often has transient bacteremia. The bacteria mainly come from the mouth, respiratory tract, urinary tract, gastrointestinal tract, or other ways to invade the bloodstream. Under normal circumstances, bacteria or other pathogens that invade the bloodstream are eliminated at any time due to the action of the body's defense mechanism. It is not easy to cause subacute infective endocarditis. When the endocardium, especially the heart valve endothelium, is damaged, the collagen fibers under the endothelium are exposed. Promotes platelet aggregation and fibrin deposition, forming a sterile platelet protein plug, which is a necessary condition for the development of infective endocarditis. In addition, the surface is rough and the bacteria or other pathogenic microorganisms are easily retained. Breeding and breeding provide a foothold and are therefore prone to subacute bacterial endocarditis.
2. The effects of temperature and blood flow in bacteria and pathogens that adhere to the valve confirm that a bacterial aerosol can be formed into a gas stream through a Venturi agar tube to form a characteristic colony distribution. The largest sediment ring appears in front of the exit orifice, the so-called Winter force effect, according to which the part of the invasion of bacteria or pathogenic microorganisms can often be explained in front of the narrow channel of blood flow, such as mitral regurgitation and subacute infection. Endocarditis often invades the left atrial surface, ventricular septal defect and subacute infective endocarditis often in the right ventricular surface, aortic stenosis in the aortic intima, aortic regurgitation Left ventricular surface, patent ductus arteriosus in the intima of the pulmonary artery, etc., in addition, any pathogen or pathogenic microorganism that can cause infective endocarditis must have the characteristics of colonization on the valve surface and must be tolerated The bactericidal power of serum complement is not affected by platelets, only such pathogens can cause IE, clinically common such as Streptococcus viridans, Staphylococcus, Enterococcus and certain leather Lan-negative bacilli have strong adhesion to the valve or endocardium, so it is easy to cause IE. On the contrary, such as diphtheria-like bacilli, acne short-stick bacterin, etc. lack the ability to adhere to the valve, so it rarely causes IE.
3. Whether the blood flow pressure step effect is susceptible to SIE is related to the strength of the Winter force effect, and also has a significant relationship with the blood flow pressure step. When the blood flow, this can explain why heart disease complicated with atrial fibrillation, congestive In patients with heart failure or severe mitral stenosis, SIE is not easy to occur, because atrial fibrillation, heart failure or severely narrow, the blood flow velocity is slowed down and/or the pressure gradient is small, and turbulence and jet flow are not easy to occur. Therefore, the jet effect and the Winter force effect are weak, which is not conducive to the formation of neoplasms, so SIE is less likely to occur. For this reason, the risk of common IE can be easily classified.
4. The role of immune mechanism The immunopathological mechanism of infective endocarditis has attracted attention. Repeated temporary bacteremia causes the body to produce specific agglutinating antibodies, which promote the accumulation of pathogenic microorganisms such as bacteria and adhere to the endocardium. Or the role of valve damage, enhance the ability of pathogen invasion, serum antigen stimulates the immune system to cause non-specific hypergammaglobulinemia, antigen-antibody immune complexes to produce rheumatoid factor, anti-nuclear factor, anti-myocardial antibody, etc. 72% of IE patients over 6 weeks have rheumatoid factor. In some cases, bacteremia such as Streptococcus viridans, Streptococcus mutans and Candida can produce specific antibodies, and non-specific antibodies in serum can cause immunoglobulin. Increased concentrations of IgG, IgM, cryoglobulin and macroglobulin, renal complications of infective endocarditis, in addition to renal embolism, immunoglobulin has a special affinity for the glomerular basement membrane, blood vessel wall, etc., so it can be concurrent Focal, diffuse proliferative and membranous proliferative type 3 nephritis, in addition, serum complement C3, C9, C4 and CH50 are often decreased in patients with longer disease duration, The development of the Ming infectious endocarditis, the immune mechanisms involved in the pathological role.
(three) pathology
The pathological changes in the heart valve or endocardium are caused by the formation of neoplasms. The neoplasms are composed of fibrin, platelets and white blood cells. The bacteria are hidden in them, where there are no capillaries and less phagocytic infiltration. Drugs are difficult to reach deep, and bacteria are difficult to be swallowed, which is why bacteria are long-lived.
Prevention
Subacute infective endocarditis prevention
1. Health education insists on prevention, and publicizes the basic heart disease, predisposing factors, pathogenesis, clinical manifestations and harmfulness of the disease, and advises people to stay away from drugs. For those who have intravenous drug addicts, they are advised to actively detoxify. An important way to reduce infective endocarditis in the heart, prevention and education of the disease should be carried out in susceptible people. For patients with congenital heart disease who have undergone surgery, if hemodynamic changes remain, care must be taken to prevent it. For patients with persistent congenital heart disease and acquired valvular heart disease, patients should be informed about the prevention of the disease and the specific use of antibiotics. At the same time, all medical personnel should be familiar with the necessity and specificity of prevention of high-risk patients. method.
2. Preventive medication due to the disability rate of this disease, the mortality rate is high, therefore, effective preventive measures should be taken actively, and primary prevention is the most important, rheumatic valvular disease or congenital heart disease, need to pay attention to oral hygiene, Timely treatment of various infectious lesions, antibiotics should be given before surgery or device examination. Endocarditis often occurs about two weeks after surgery. Because of the bacteremia in the early stage of the disease, the first step is to prevent bacteremia. At the beginning, many scholars have found that temporary bacteremia often occurs after tooth extraction, especially in the case of periodontal disease or simultaneous removal of many teeth. Many oral bacteria can enter the blood through the wound, but in the grass green Streptococcus is the most common, digestive tract and genitourinary system trauma and infection often cause enterococci and Gram-negative bacilli, staphylococcal bacteremia is seen in the skin and infections away from the heart, bacteria do not necessarily disease after entering the blood circulation , but it may pose a serious threat to patients with underlying heart disease. Because this disease can occur on the basis of organic heart disease, it can also be Invasive surgical procedures, but whether the incidence and invasion of pathogenic microorganisms, heart valve disease and hemodynamic changes, the body's immunity and other factors are related, so the use of antibiotics to prevent this disease should be active, but also to avoid abuse.
Complication
Subacute infective endocarditis complications Complications arrhythmia
Complications of infective endocarditis can be broadly classified into two categories: cardiovascular itself and other organ involvement, the former including heart failure, arrhythmia, myocardial and/or pericardial abscesses and infectious aneurysms; Organ embolism and neuropsychiatric complications are described as follows:
1. Heart failure (referred to as heart failure)
Heart failure is the most common complication of infective endocarditis and the leading cause of death. Early infective endocarditis is still light due to valve involvement, and cardiac function can be compensated. As the disease progresses, once the valve is perforated Or under-valve devices such as papillary muscles, chordae rupture, can cause acute valvular insufficiency, or increase the original valvular lesions, leading to severe hemodynamic disorders and increased cardiac load (especially preload), often can produce Progressive heart failure, if not treated in time, due to refractory heart failure, especially the prognosis of severe aortic regurgitation is the worst, once the diagnosis of severe valve damage is established, the author believes that active anti-infection, anti-heart failure (such as On the basis of limiting water, sodium and cardiotonic, diuretic, vasodilators, etc.), early surgery should be pursued. On the contrary, one-sided emphasis on medical antibacterial therapy, anticipation of improvement in internal medicine or stable surgery, often loses the opportunity for surgery because Severe valve damage medication can only temporarily improve heart function, it can not ~ 6 months, depending on the condition to continue medical follow-up treatment or elective surgery is better, Infected endocarditis complicated with heart failure In addition to the above reasons, infection with toxins, myocarditis, myocardial abscess, arrhythmia, and even myocardial infarction caused by coronary embolism, etc., can cause and / or aggravate heart failure, in the treatment of heart failure It should also be considered and treated accordingly. It must be pointed out that sometimes infective endocarditis can also produce progressive heart failure, which may be related to the following factors: 1 Infective endocarditis is invaded by heart valve Scar contracture or valve distorted deformity, resulting in valve dysfunction; 2 infective endocarditis invaded valve is more fragile, can be perforated or ruptured at any time; 3 aortic valve swelling tumor formation, especially combined with aorta When the valve is incomplete, it can affect the valve opening and closing function. Once this happens, surgery is often needed.
2. Arrhythmia
According to statistics, there are 1/3 to 1/2 patients with infective endocarditis who have various arrhythmias. Of course, some arrhythmias may be related to the original basic heart disease, and arrhythmia caused by infective endocarditis. Pre-sexual contraction is the most common, followed by atrial fibrillation, and atrioventricular block and bundle branch block are rare, and most occur in infective endocarditis involving the aortic valve, when infective endocarditis Concurrent heart failure, especially in refractory heart failure, the incidence of arrhythmia also increases, especially ventricular arrhythmia is the most common, both can cause aggravation of the disease, many infective endocarditis The patient is killed by severe ventricular arrhythmia, so it must be actively treated. The treatment principle is similar to that of other heart disease. Frequent ventricular premature contraction can be achieved with amiodarone 0.2g or mexiletine 0.15~0.2. g, 3 times / d, until the ventricular premature contraction control reduction, ventricular tachycardia preferred lidocaine 50 ~ 100mg intravenous injection, can also be used amiodarone 150 ~ 250mg plus 50% glucose 20ml intravenous injection If necessary, electric shock cardioversion, the first electric energy is 100 ~ 150J (focal ), ventricular fibrillation according to cardiac arrest, infective endocarditis with third degree or high atrioventricular block, causing a significant reduction in cardiac output, temporary pacemaker should be placed, can also be used in the base layer 0.5 ~ 1mg isoproterenol is added to the 500ml infusion intravenously. In addition, atropine, anisodamine, etc. may also be used as appropriate.
3. Myocardium and (or) pericardial abscess
Mostly caused by Staphylococcus aureus or other virulence of pyogenic bacteria, myocardial abscess can be multiple or single, clinically more common in acute infective endocarditis, with the progress of the disease can also be combined into a single abscess Large abscesses, even leading to perforation of the heart, pericardial abscesses are mostly caused by myocardial abscesses, spread or ulceration into the pericardial cavity, multiple small focal myocardial abscess mainly for the cause, using large doses of sensitive antibiotics, for individual A huge myocardial abscess, based on active internal medicine anti-infection, some people advocate puncture drainage, pericardial abscess can be treated according to suppurative pericarditis, if necessary, pericardial puncture or incision drainage, often can achieve better results.
4. Infectious aneurysms
Fungal infective endocarditis is most likely to be complicated by infectious aneurysms, so it is more common in elderly and frail patients after surgery. Occasionally, infective endocarditis can also cause aneurysms. Aneurysms can occur in the body. Arteries in the site, but especially in the aorta and middle arteries, especially the arteries that supply the vital organs such as the heart, brain, kidney, etc., can produce corresponding local compression symptoms. The aneurysm can also be asymptomatic before it breaks. Hemorrhagic shock or the symptoms of insufficient or even necrosis of the corresponding organs. Diagnosis of infectious aneurysms depends on improving the understanding of the complications of the disease and raising vigilance. If necessary, echocardiography, CT or angiography should be performed. Before the aneurysm is not broken, it will not affect the human body too much. It is mainly for the treatment of infective endocarditis. After the control of infective endocarditis, regular follow-up or elective aneurysm removal or blood vessel is performed as appropriate. Transplantation, for large thin-walled aneurysms, especially those with a tendency to rupture at any time, should be combined with vascular surgeons to develop treatment plans, if necessary, as soon as possible, surgery Once ruptured aneurysm, the prognosis is more serious and more, conditional units can be emergency surgical repair.
5. Organ embolism
Mostly, subacute infective endocarditis is caused by embolization of the arteries with blood flow. Clinically, embolism of the brain, kidney, and spleen is the most common and most important. It is caused by subacute infective endocarditis. Important reasons for disability, in recent years, right heart infective endocarditis has an increasing trend, so pulmonary embolism has caused increasing clinical concern, once embolization occurs, it can produce the corresponding clinical manifestations of blood supply and infarction of organs, it must be pointed out that Small embolization can be asymptomatic, clinically difficult to diagnose, and sometimes only found in autopsy. In addition, organ embolism does not necessarily occur in the subacute infective endocarditis active period, but also in the stationary phase, Zhongshan The First Hospital of the University had encountered a subacute infective endocarditis that had been cured for 3 years. Patients with cerebral embolism caused by sudden shedding of neoplasms left on the aortic valve, therefore, subacute infective endocarditis Even if it is cured, as long as there is a neoplasm in the endocardium, it may cause embolism of the organs. The vast majority of the endocardial neoplasms are poorly treated with antibiotics. In order to kill, some people tried to reduce the volume of neoplasms by applying anticoagulants to improve the efficacy of antibiotics and reduce the embolism of organs. Although new anticoagulants have been introduced in recent years, the value of anticoagulant therapy needs further study. Whether anticoagulant is applied to patients who have undergone embolization is inconclusive. There are indications that anticoagulants may have a certain effect on pulmonary embolism caused by RHIE, but in the application process, the condition should be closely observed, pay attention to bleeding tendency. Some patients with splenic embolism advocate splenectomy, and embolization of the extremities has been able to remove emboli by surgery.
6. Neuropsychiatric complications
For general neuropsychiatric symptoms, such as headache, irritability, dizziness and other symptoms of poisoning, symptomatic treatment, neuropsychiatric symptoms caused by cerebral embolism, the treatment method is basically the same as other causes of cerebral embolism.
Symptom
Subacute infective endocarditis symptoms Common symptoms Finger or toe nails flaky hemorrhage Relaxation heat night sweats Muscle sore high fever low heat intermittent heat bacteremia chills fatigue
symptom
Most cases have slow onset, low fever, fatigue, fatigue, a few onset, chills, high fever or embolism. Some patients have oral surgery, respiratory infection, abortion or childbirth history before onset. The clinical manifestations of SIE include The following three aspects:
First, systemic infection fever is the most common, often unexplained persistent fever for more than a week, irregular low fever, can also be intermittent heat or relaxation heat, accompanied by fatigue, night sweats, progressive anemia splenomegaly, late can have sputum Finger.
(1) fever: 80% to 88% of cases have fever, heat type is variable, irregular fever is more common, mostly between 37.5 °C-39 °C, can be intermittent heat or relaxation heat, many cases It is characterized by low fever, which may be accompanied by chills or sweating. In recent years, many patients have no fever, which may be related to early use of antibiotics. Older patients may be associated with poor reactivity.
(2) Other symptoms associated with infection: such as fatigue, loss of appetite, weight loss, progressive anemia, excessive sweating and muscle soreness.
(3) clubbing (toe): more than 1 to 2 months after the onset of the disease, and no cyanosis, in the past about 1/3 of cases, and as one of the important signs of IE, but in recent years has been greatly reduced, liver, Splenomegaly is generally mild to moderately enlarged. In the past, at least half of the patients had splenomegaly, and 1/4 of the patients had hepatomegaly. However, in recent years, liver and splenomegaly were also significantly reduced.
Second, the performance of the heart depends on the type of heart disease, the type of pathogen and the degree of damage to the valve or endometrium. Due to the growth or shedding of the neoplasm, the destruction of the valve, the chordae, the murmur, or the appearance of new murmurs. In the case of murmur, endocarditis cannot be excluded. Heart failure can occur in the late stage. When the infection affects the atrioventricular bundle or interventricular septum, it can cause atrioventricular block and bundle branch block. It can have premature beat or atrial fibrillation. Abnormalities are not common in subacute infective endocarditis, most of which are ventricular premature contractions, followed by atrial fibrillation and prolonged PR interval, 4% of cases can have high atrioventricular block, severe arrhythmia has become this An important cause of death.
Third, embolism and vascular lesions
(1) Skin and mucous membrane lesions are caused by infectious toxins acting on capillaries to increase fragility and rupture and hemorrhage, or microembolism. In the limbs, the skin and eyelids may be combined with the membrane, and the oral mucosa may appear in batches. The purple or red Osler nodules slightly above the surface may appear on the palm of the toe, and there may be nodular nodules (Janewey nodules) in the palm or foot, without tenderness.
(B) cerebrovascular lesions can have the following performance:
1 meningoencephalitis similar to tuberculous meningitis, increased cerebrospinal fluid pressure, increased protein and white blood cell count, normal chloride or sugar quantification, 2 cerebral hemorrhage with persistent headache or meningeal irritation, caused by bacterial aneurysm rupture, 3 brain Embolism in patients with fever, sudden paralysis or blindness, 4 central retinal embolism can cause sudden blindness.
(3) renal embolism is the most common, accounting for 1/2 cases, with gross or microscopic hematuria, severe renal insufficiency often due to bacterial infection, antigen-antibody complex deposition in the renal glomus, causing renal glomerulonephritis the result of.
(4) Pulmonary embolism is common in congenital heart disease and infective endocarditis. The neoplasm is mostly located in the right ventricle or pulmonary intima, with acute onset, chest pain, difficulty breathing, hemoptysis, cyanosis or shock, if infarction The area is small and there are no obvious symptoms.
In addition, there may be coronary embolism, which is characterized by acute infarction, spleen embolism with left upper abdominal pain or left rib pain, fever and local friction, mesenteric artery embolism, acute abdomen, bloody stool, etc. The embolization limb is pale and chilly, the arterial pulse is weakened or disappeared, and the limb ischemic pain.
Examine
Subacute infective endocarditis
There are several methods for examining this disease:
1. Blood culture positive blood culture has decisive diagnostic value and provides a basis for treatment. Foreign countries report that the positive rate of subacute infective endocarditis blood culture is as high as 85%, while the domestic is far below this number, the first hospital of Sun Yat-sen University The positive rate of 81 cases of subacute infective endocarditis reported was 53%. In recent years, the positive rate of blood culture has a downward trend. The reason may be related to the following factors:
(1) Most antibiotics have been used before blood culture.
(2) The increase in the number of pathogens and the variation of the bacteria itself, but most hospitals still routinely culture and lack a variety of training methods.
(3) Specimen collection techniques are defective, such as insufficient blood draw, lack of continuous blood draw or insufficient blood draw.
(4) Subacute infective endocarditis can be intermittently sterilized, and there is a sterilized period. If the blood is taken out during the above period, it can be cultured negative. Some people think that the fever is prone to be positive during the prodromal period, while fever Most of the bacteria or pathogenic microorganisms in the blood have been phagocytosed by phagocytic cells, and it is difficult to obtain positive results. At present, many units of blood cultures are often carried out during fever. In order to improve the positive rate of blood culture, the following measures can be taken: 1 Try to fight for antibiotics For pre-blood culture, blood is usually taken 3 to 5 times within 24 to 48 hours, but the amount of blood should be 10 ml or more per time; 2 if antibiotics have been used, if the condition permits, blood culture should be done 1 week after stopping the drug. However, many patients can not wait because of the condition, the blood sample of antibiotics should be diluted 20 times with the medium to dilute the concentration of antibiotics and reduce the effect of antibodies against specific pathogenic microorganisms; 3 conditional units carry out various cultures Means, including aerobic and anaerobic cultures and special cultures and fungal cultures; 4 appropriate extension of culture time.
2. routine and serological examination
(1) blood routine: often with progressive anemia, leukocytosis, nuclear left shift, occasionally normal or low, sometimes visible poisoning particles.
(2) ESR: About 90% of cases are elevated. If it is normal, it does not support infective endocarditis.
(3) urinary routine: half of the patients have microscopic hematuria and proteinuria, gross hematuria suggests renal infarction, sometimes visible tubular and a large number of proteinuria, suggesting renal damage or combined immune complex glomerulonephritis.
(4) Looking for phagocytic monocytes in blood samples: The diameter of the cells is 20-30 m. The cytoplasm may contain bacteria or red blood cells degenerated at various stages, and sometimes tissue cells or reticuloendothelial cells may be seen. The increase of the above cells indicates The reticular endothelial system is over-stimulated.
(5) Rheumatoid factor-positive: Infective endocarditis with a course of more than 6 weeks, about half of the cases are positive for rheumatoid factor, and related to the degree of the disease. In addition, the syphilis serum reaction can also be positive.
(6) Positive blood circulation immune complex: more than 90% of patients are positive, often more than 100mg / L (100m / ml), can be used as one of the identification points of sepsis patients with non-infective endocarditis, in addition, still Specific pathogens can be directly assayed, including direct assays such as immunoprecipitation assays and complement binding assays.
1. The electrocardiogram lacks specificity. When the ventricular septal abscess is present, different degrees of atrioventricular block may occur. In addition, various arrhythmias and atrioventricular hypertrophy may be found, and the electrocardiogram changes of the strain may be found.
2. X-ray examination, in addition to the corresponding characteristic changes of the original basic heart disease, is also non-specific, only indirect signs can be found, such as pulmonary congestion, aortic dilatation caused by bacterial aneurysm, right heart infective endocarditis Can have the performance of pulmonary embolism.
3. Cardiac catheterization and cardiovascular angiography are rarely used for the diagnosis of infective endocarditis, and may lead to the risk of spastic detachment, only used to understand the severity of valvular damage and hemodynamic changes.
4. Echocardiography (UCG) examination of UCG can detect the neoplasms on the valve, which is of great help in the diagnosis of infective endocarditis. The detection rate of sputum is 70%-80%, sensitivity is 90. %, specificity 89%; on the other hand, UCG did not find neoplasms can not rule out infective endocarditis, which may be due to the small size of the neoplasm (diameter <2mm), or the location of the neoplasm is not easy to be ultrasonically probed Caused by the difference in the resolution of the instrument, the intensity of the echo density and the skill level of the operator, on the contrary, a variety of conditions such as valve calcification, sputum, fibrosis, tumor, thrombosis, etc. can also produce similar infections. Endocarditis echoes of neoplasms. Therefore, UCG diagnosis of infective endocarditis must be combined with clinical comprehensive analysis. In addition, UCG is also difficult to judge whether pathogens in surviving organisms survive and whether the lesions are active, and should be combined with clinical comprehensive judgment. In UCG, the mites are fluffy, fluted or smoked, dense, clump-like echoes that are tightly attached to the leaflets. The mites can move with the heart's contraction, and large sputum can sometimes lead to stenosis or Valve incarceration, special The latter can cause one of the causes of shock or sudden death of the patient. The activity of the valve itself is not limited. The two-dimensional UCG can see the whole process of the activity of the mass of the mites in the cardiac cycle, and estimate the size and position of the scorpion. Shape, activity, and number of neoplasms, thereby increasing the sensitivity of detection. Indirect signs of infective endocarditis in UCG include destructive changes in the valve and its subvalvular devices, such as chordae rupture, perforation of the leaflets Destruction and changes in the valvular leaflets, as well as abnormal hemodynamic changes due to valve damage, occasionally visible signs of peri-infection, such as mitral annulus abscess, ventricular septal abscess, aortic root abscess, etc., must be noted, Early infective endocarditis (within 2 weeks of disease) is often difficult to detect neoplasms, so patients with suspected infective endocarditis should be followed up for observation to improve the detection rate.
5. Radionuclide examination, such as 67 gallium (67Ga) heart scan, because 67Ga can be concentrated in heart inflammation and neoplasms, has a reference value for the diagnosis of infective endocarditis.
Diagnosis
Diagnosis and identification of subacute infective endocarditis
diagnosis
The symptoms and signs of infective endocarditis are often systemic. Combined with laboratory tests, typical cases are not difficult to diagnose. Due to the use of antibiotics and pathogens, epidemiological and clinical manifestations, atypical cases increase. The following conditions should be suspected of the occurrence of infective endocarditis: 1 valvular heart disease patients with unexplained fever for more than 1 week; 2 new occurrence of reflux murmur or original heart murmur properties significantly changed; 3 unknown Causes of arterial embolism; 4 unexplained heart failure; 5 sustained fever after cardiac surgery for more than 1 week; 6 prosthetic patients at any time with fever or valvular insufficiency; 7 intravenous drug addicts with fever especially with cough and chest pain, where In case of the above conditions, blood culture and echocardiography should be performed in time to confirm the diagnosis. In addition to the typical manifestations, the clinical diagnosis of this disease is difficult. In 1981, the diagnostic criteria of Beth Israel proposed by Von Reyn et al. were widely used, but On the one hand, the standard does not classify intravenous drug addicts (IVDA) as a risk factor for infective endocarditis, and on the other hand ignores echocardiography. Diagnostic role; at the same time, less than one-third of patients need to undergo surgery in the acute phase of infection. Therefore, only a very small number of patients can be truly diagnosed with this standard, especially those with negative blood culture. Sex.
In 1994, Durack et al. proposed the Duke diagnostic criteria, which are described below:
1. Determined infective endocarditis
(1) Pathological diagnosis criteria: histological changes in acute endocarditis are accompanied by neoplasms, myocardial abscesses or neoplasms, pathological examination of peripheral emboli or culture of pathogenic microorganisms.
(2) Clinically confirmed criteria: meet the following two main criteria; or one primary criterion and three secondary criteria; or five secondary criteria.
2. Possible infective endocarditis between the determination and exclusion.
3. Invasive endocarditis that can be ruled out has a positive other diagnosis; short-term antibiotics ( 4 days) symptom relief or no evidence of infective endocarditis in surgery and autopsy.
4. In addition, the primary and secondary criteria in the Duke diagnostic criteria are as follows.
(1) Main criteria:
1 Positive blood culture with diagnostic significance for infective endocarditis (any of the following conditions):
A. Two independent blood cultures were found: a. Streptococcus viridans, Streptococcus bovis or HAECK, b. Community-free Staphylococcus aureus or Enterococcus.
B. persistent bacteremia: a. no more than two times of blood culture positive for more than 12h interval, b. 3 times blood culture all positive, 4 or more blood cultures are mostly positive, of which 1 The second and last interval is 1h.
2 endocardial involvement (one of the following conditions):
A. Signs of echocardiography: a. movable neoplasms attached to the valve, subvalvular structures or implant surfaces, b. abscesses, c. newly emerging lobes.
B. New valvular regurgitation.
(2) Secondary criteria:
1 heart susceptibility factors or intravenous drug addicts.
2 fever, > 38 ° C.
3 vascular signs: arterial embolism, septic lung infarction, bacterial aneurysm, intracranial hemorrhage, conjunctival hemorrhage, Janeway damage.
4 immune damage: glomerulonephritis, Osler nodules, Roth plaque rheumatoid factor positive.
5 Evidence of microbial infection: serological evidence of intermittent bacteremia or acute infection.
6 Atypical echocardiographic signs associated with infective endocarditis.
Differential diagnosis
1. Rheumatic fever can have fever, heart valve damage and other symptoms, sometimes difficult to identify with this disease, patients with organic heart disease have unexplained fever for more than a week, need to consider the possibility of this disease, anemia of rheumatic fever Light, prolonged PR interval is more common, anti-rheumatic treatment is effective; and skin blemishes, clubbing, splenomegaly, hematuria, embolism, progressive anemia, blood culture positive and echocardiographic valves have neoplasms, etc. Found in endocarditis, sometimes infective endocarditis can coexist with rheumatic fever, such as adequate treatment of sensitive antibiotics and still not fever, suspected and combined rheumatism activities, if necessary, try anti-rheumatic treatment.
2. Left atrial myxoma may have fever, embolism and heart murmur; but blood culture is negative, no splenomegaly, echocardiography can show tumor and its moving images.
3. Cerebrovascular accidents such as infective endocarditis with cerebral embolism as the main performance, often easy to deny the diagnosis of lupus erythematosus, typhoid fever, tuberculosis, brucellosis and malignant tumors.
4. In addition, infective endocarditis should also pay attention to the identification of the following conditions;
(1) Febrile diseases such as rheumatic fever, systemic lupus erythematosus identification.
(2) Identification of other infections associated with heart disease, such as rheumatic heart disease, congenital heart disease patients with lungs, gastrointestinal or genitourinary tract infections with fever.
(3) Patients with fever with the main manifestations and mild cardiac signs need to be identified with typhoid, malaria and tuberculosis.
(4) Identification of embolism caused by other causes: such as cerebral embolism, need to be associated with cerebral thrombosis, stroke identification; renal embolism, need to be differentiated from kidney stones, acute glomerulonephritis; limb arterial embolism, need to Identification of vasculitis; mesenteric artery embolization, need to be differentiated from acute abdomen; coronary embolism, need to be associated with coronary atherosclerosis or coronary arteritis caused by angina pectoris, myocardial infarction.
