Infective endocarditis refers to inflammation of the endocardium of the heart valves or ventricular wall due to direct infection by bacteria, fungi and other microorganisms such as viruses, rickettsia, chlamydia, spirochetes, etc. It is distinct from non-infective endocarditis due to rheumatic fever, rheumatoid fever, systemic lupus erythematosus, etc. In the past, the disease was referred to as bacterialendocarditis, which is no longer used because it is not comprehensive enough. The typical clinical manifestations of infective endocarditis include fever, murmurs, anemia, embolism, skin lesions, splenomegaly, and positive blood cultures.
[Etiology
Infective endocarditis often occurs in hearts with pre-existing disease, but in recent years it is increasingly occurring in patients without pre-existing cardiac disease, especially in patients receiving prolonged intravenous therapy, addiction to intravenous narcotics, and immune suppression caused by drugs or disease. There has also been an increase in infective endocarditis after prosthetic valve replacement.
Endocarditis of the left heart mainly involves the aortic and mitral valves, especially in those with mild to moderate insufficiency of closure. Endocarditis in the right side of the heart is less common and mainly involves the tricuspid valve. Among the various congenital heart diseases, arteriovenous ductus arteriosus, ventricular septal defect, and tetralogy of Fallot occur most frequently. Among the individual valve lesions, bilobed aortic stenosis is most likely to occur, and valve prolapse (aortic and mitral valves) is also prone to infective endocarditis. Pathological examination of specimens removed by prosthetic valve replacement in 82 cases of infective endocarditis between 1980 and 1995 at Zhongshan Hospital in Shanghai showed that congenital bilobed aortic valve malformation accounted for 20 cases (36%) and aortic valve prolapse for 10 cases (18%) of the 55 cases with pre-existing organic cardiac pathology. Hypertrophic obstructive cardiomyopathy, degenerative valve lesions, and coronary artery disease have also been reported.
Acute infective endocarditis is often caused by the invasion of septic bacteria into the endocardium, mostly due to infection by more virulent pathogens. Staphylococcus aureus accounts for more than 50% of cases. Subacute infective endocarditis is caused by 80% of non-hemolytic streptococci, mainly Streptococcus griseus, before antibiotics are used in clinical practice. In recent years, due to the widespread use of broad-spectrum antibiotics, the pathogenic species have changed significantly, and almost all known pathogenic microorganisms can cause the disease, and the same pathogen can produce an acute course as well as a subacute course. And there has been an increase in cases of drug-resistant microorganisms that were rare in the past. The incidence of Streptococcus oxalis is decreasing, but still predominates. The proportion of Staphylococcus aureus, Enterococcus, Staphylococcus epidermidis, gram-negative bacteria or fungi is significantly higher. Anaerobes, actinomycetes, and listeria are occasionally seen. Mixed infections of both bacteria are sometimes found. Fungi are especially seen in patients addicted to cardiac surgery and intravenous anesthetic drugs. Long-term application of antibiotics or hormones, immunosuppressants, and intravenous catheter infusion of highly nutritious fluids can increase the chance of fungal infections. Among them, Candida spp., Aspergillus spp. and Histoplasma spp. are more common.
In heart valve lesions, congenital cardiovascular malformations or acquired arteriovenous fistulas, there is an abnormal blood pressure step difference, causing strong blood jets and eddies. The jet impact of blood flow causes endothelial damage and collagen exposure in the endocardium, resulting in platelet-fibrin thrombosis. Vortex flow can cause bacteria to settle on the damaged endocardium proximal to the low pressure chambers and at the abnormal blood outflow. Although a few bacteria in normal human blood flow from time to time invade from wounds such as the oral cavity, nasopharynx, gums, examination operations or surgery causing bacteraemia, most of them are temporary and are quickly eliminated by the body and are of little clinical significance. However, repeated temporary bacteremia causes the body to produce circulating antibodies, especially lectins, which can prompt a small number of pathogens to aggregate into clusters that can easily adhere to platelet-fibrin thrombi and cause infection.
The common sites of infection in aortic valve insufficiency are the left ventricular surface of the aortic valve and the mitral tendon; in mitral valve insufficiency, the foci of infection are on the atrial surface of the mitral valve and the endocardium of the left atrium; and in ventricular septal defect, on the endocardial surface of the right ventricular septal defect and the ventricular surface of the pulmonary valve. However, the disease is less likely to occur when the defect is large enough that there is no pressure step difference between the left and right ventricles or when there is a combination of pulmonary hypertension that reduces fractional flow. It is also less likely to occur in congestive heart failure and atrial fibrillation because of reduced blood ejection and eddy currents.
It has also been suggested that receptor attachment is responsible for the inflammation of the endocardium because certain gram-positive pathogenic bacteria, such as Enterococcus, Staphylococcus aureus, and Staphylococcus epidermidis, have a surface component that reacts with receptors on the endocardial cell surface.
Contaminated prosthetic valves, suture materials, instruments, and hands are important causes of prosthetic valve endocarditis. Pathogens enter the body from infected chest wounds, urinary tract and various arteriovenous cannulae, tracheotomy, and postoperative pneumonia to form bacteremia, while phagocytosis is disrupted after blood is diverted through extracorporeal circulation, weakening the body’s ability to clear pathogens is also a cause.
[Symptoms
The incidence of infective endocarditis accounts for about 2.1%, which is 2 to 3 times higher than that of those undergoing other types of cardiac surgery. The incidence of PVE after double valve replacement is higher than that after single valve replacement, with PVE in the aortic valve being higher than that in the mitral valve, which may be due to the longer duration of aortic valve replacement surgery, the large pressure step difference across the aortic aneurysm, and the formation of local turbulence. In those with preoperative pre-existing natural valve endocarditis, the chance of postoperative PVE is increased 5-fold. The incidence of PVE is the same for mechanical and prosthetic bioprosthetic valves at approximately 2.4%. The incidence of early PVE is higher in mechanical valves than in prosthetic valves, and the morbidity and mortality rate of PVE is higher, around 50%. Early PVE (within 2 months after surgery) has a higher morbidity and mortality rate than late PVE (after 2 months after surgery). The former pathogens are mainly staphylococci, accounting for 40% to 50%, including Staphylococcus epidermidis, Staphylococcus aureus. Diphtheria-like bacilli, other gram-negative bacilli, and mycobacteria are also more common. The incidence has decreased since preoperative prophylactic antibiotic therapy was given. Late stage PVE is similar to natural valve endocarditis and is mainly caused by various streptococci (predominantly Streptococcus straw green), enterococci, and Staphylococcus aureus, with Staphylococcus epidermidis being more sensitive to antibiotics than Staphylococcus epidermidis in early stage PVE. Fungi (most commonly Candida albicans, followed by Aspergillus), gram-negative bacilli, and diphtheria-like bacilli are also nonuncommon.
The clinical presentation of prosthetic valve endocarditis is similar to that of natural valve endocarditis, but is less sensitive and specific as a basis for diagnosis. Because postoperative bacteremia, indwelling various intubations, thoracic surgical wounds, pericardiotomy syndrome, postperfusion syndrome, and anticoagulation therapy can cause fever, bleeding spots, and hematuria. more than 95% of patients have fever, elevated white blood cell counts of about 50%, and anemia are common, but skin lesions rarely occur in early PVE. Splenomegaly is mostly seen in late stage PVE. Sometimes serum immune complex titers may be increased and rheumatoid factor may be positive, but the presence of PVE cannot be excluded in those with negative serology.
Regurgitant murmurs are present in approximately 50% of patients with infective endocarditis. Prosthetic bioprosthetic valve endocarditis primarily causes disruption of the valve leaflets, producing a murmur of incomplete closure, and rarely an annular abscess. Infection of mechanical valves is mainly at the annulus attachment site, causing the sutures at the annulus and valve suture to fall off and split, resulting in a perivalvular leak and a new murmur of incomplete closure and hemolysis, worsening anemia, and diffuse infection of the annulus or even complete tearing of the prosthetic valve. When an annular abscess is formed, it can easily extend to adjacent cardiac tissue and develop complications similar to natural valve endocarditis. In the early stages of PVE, when the valve is not yet significantly damaged, there may be no murmur, and thus the diagnosis should not be delayed because no new murmur is heard. The murmur of valve stenosis can be caused when the valve orifice is occluded by a superfluous organism. Embolization of the body circulation can occur at any site, and in fungal PVE (especially in Aspergillus), embolization may be the only clinical finding. Other complications of PVE, like natural valve endocarditis, can include cardiac insufficiency, embolism, myocardial abscesses, and fungal aneurysms. The prosthetic valve has a weakened closing tone, abnormal oscillations and displacements of the prosthetic valve with angles greater than 7° to 10°, and double shadowing (stinson “s sign) due to annular dehiscence are seen on x-ray. The presence of a redundant organism on 2-dimensional echocardiography is diagnostic. Blood cultures are often positive. The causative agent of PVE is often hospital-derived and therefore easily resistant to drugs.
(b) Staphylococcal endocarditis is mostly acute and sinister, so it is mostly acute, and only a few are subacute. It is usually caused by penicillin G-resistant Staphylococcus aureus. It is more likely to attack the normal heart and often causes severe and rapid valve damage, resulting in aortic and mitral regurgitation. The presence of metastatic infections and abscesses in multiple organs and tissues is important in the diagnosis.
(iii) Enterococcal endocarditis is most often seen in patients with prostate and genitourinary tract infections. It is devastating to the heart valves, and most often has a significant murmur, but often appears in a subacute form.
(D) fungal endocarditis due to the increased application of broad-spectrum antibiotics, hormones and immunosuppressive agents, long-term use of intravenous fluids, indwelling of vascular and intracardiac catheters, the widespread development of direct cardiac surgery and the increase in addiction to intravenous anesthetic drugs in some countries, the incidence of fungal endocarditis is gradually increasing, with about 50% occurring after cardiac surgery. The causative organisms are mostly Candida, Histoplasma, Aspergillus spp. or Aspergillus. The onset of fungal endocarditis is acute, a few are more insidious, and the incidence of embolism is high. The redundant organisms are large and brittle and can easily dislodge, causing embolization of larger arteries such as the femoral and iliac arteries. Occurring in right-sided endocarditis can cause fungal pulmonary embolism. Huge bulky organisms that obstruct the valve orifice and form a stenosis of the valve orifice can cause severe hemodynamic disturbances. Fungal endocarditis may present with skin lesions, such as subcutaneous ulcers in histoplasma infections, and lesions of the oral and nasal mucosa, which are often diagnostically important when examined histologically. Infection with Aspergillus spp. can also cause diffuse intravascular coagulation.
(v) Endocarditis involving the right side of the heart is seen in congenital heart disease with left-to-right shunts and after prosthetic tricuspid valve replacement, urinary tract infections, and infected abortions. It can also be caused by cardiac pacing, right heart catheterization, and normal delivery. The incidence of right-sided heart endocarditis has increased significantly in some countries in recent years, about 5% to 10%, due to an increase in addiction to intravenous narcotics. Most of the drug addicts originally did not have heart disease and may be related to contaminated drugs, non-observance of aseptic practice and damage to the tricuspid valve by special substances in the intravenous material. Bacteria are mostly Staphylococcus aureus, followed by fungi, yeast, Pseudomonas aeruginosa, Pneumococcus, etc. Gram-negative bacilli can also be caused. Infective endocarditis of the right side of the heart mostly involves the tricuspid valve and, rarely, the pulmonary valve. Most of the superfluous organisms are located in the tricuspid valve, the right ventricular wall, or the pulmonary valve. Fragmentation of the superfluous organisms causes pulmonary inflammation, septic arteritis of the pulmonary artery branches, and bacterial pulmonary infarction. If caused by Staphylococcus aureus, the site of infarction may be transformed into a pulmonary abscess. Splenomegaly, hematuria and skin lesions are rare because the clinical manifestations are mainly in the lungs. Patients may have cough, sputum, hemoptysis, pleuritic chest pain, and shortness of breath.
Due to the small pressure step difference between the right atrium and the right ventricle (except in cases of organic heart disease with pulmonary hypertension), the tricuspid systolic murmur is short and very soft, easily mixed with respiratory noise or mistaken for a hemodynamic murmur, but an increase in murmur intensity during deep inspiration is highly suggestive of the presence of tricuspid regurgitation. A mid-diastolic murmur due to pulmonary regurgitation can be heard if the pulmonary valve is involved. Heart enlargement or right heart failure is uncommon. Chest X-rays show nodular or segmental inflammatory infiltrates in both lungs, which may cause pleural effusion. Lung abscesses or necrotizing pneumonia may also lead to pneumothorax. The most common causes of death in right-sided cardiac endocarditis are pulmonary valve closure insufficiency and respiratory distress syndrome caused by recurrent septic pulmonary embolism. Uncontrolled sepsis, severe right heart failure and simultaneous left-sided valve involvement are rare causes of death. With early diagnosis, early application of antibiotics or surgical treatment, and timely management of complications, the prognosis for infective endocarditis of the right side of the heart alone is good.
(vi) Recurrence and relapse of infective endocarditis Recurrence refers to the reproduction of signs of infection or positive blood cultures within 6 months after the end of antibiotic therapy or during the treatment period, with a relapse rate of about 5% to 8%. Early relapse is mostly within 3 months. It may be due to the fact that the bacteria deep inside the superfluous organisms are not easily killed or that there is a long course of disease before treatment or the previous antibiotic treatment is not sufficient, thus increasing bacterial resistance and having serious complications, such as embolism of the brain and lungs. Dual infections may also occur due to broad-spectrum antibiotic application.
Six months after the initial episode is cured, all cardiac manifestations of infective endocarditis and the reproduction of positive blood cultures are called relapses. It is usually caused by a different bacteria or fungus. The morbidity and mortality rate of recurrence is higher than that of the initial attack.
Screening]
Although the “classic” clinical manifestations of the disease are no longer common and some signs and symptoms appear late in the course of the disease, coupled with the fact that patients have been treated with antibiotics and have technical limitations in bacteriologic testing, which make early diagnosis difficult, it is still recommended in principle that patients with heart valve disease, congenital cardiovascular malformations, or prosthetic valve replacements with an unexplained fever of up to 10 days’ duration should be examined. Patients with unexplained fever for more than 1 week should be suspected of the possibility of this disease, and blood cultures should be performed immediately, and the diagnosis of this disease should be considered if both anemia, peripheral embolic phenomena and murmurs are present. Patients with repeated short-term clinical use of antibiotics and recurrent fever, especially in the presence of valve murmurs, should be alerted to the possibility of this disease, and prompt echocardiography is helpful in diagnosing this disease. Positive blood cultures are of decisive diagnostic value and provide a basis for antibiotic selection.
The presence of this disease should be noted in unexplained anemia, intractable heart failure, stroke, paralysis, peripheral artery embolism, progressive obstruction of the prosthetic valve orifice, and displacement and avulsion of the valve. In patients with recurrent pneumonia, followed by hepatomegaly, mild jaundice and finally progressive renal failure, the possibility of right-sided cardiac infective endocarditis should be considered even if there is no heart murmur.
(a) Blood cultures are positive in about 75% to 85% of patients. Positive blood cultures are the most direct evidence for the diagnosis of infective endocarditis and also allow follow-up for the persistence of bacteremia. Pathogens are continuously disseminated from the flora into the blood and are continuous and variable in number. Two to three blood specimens should be taken within 1 to 2 h before the application of antibiotics in acute patients, and three to four blood specimens should be collected 24 h before the application of antibiotics in subacute cases. Patients who have previously applied antibiotics should have blood cultures drawn at least daily for a total of 3 d, with a view to improving the positive rate of blood cultures.
The time of blood collection is preferable to chills or sudden rise in body temperature, and each blood collection should be done by changing the part of the venipuncture, and the skin should be strictly disinfected. Each time to take 10-15ml of blood, in patients who have applied antibiotic treatment, the amount of blood should not be too much, the ratio of culture fluid to blood is at least about 10:1. Because too much antibiotics in the blood can not be diluted by the culture medium, affecting the growth of bacteria. Routinely should be made aerobic and anaerobic bacteria culture, in artificial valve replacement, a longer period of indwelling intravenous cannula, catheter or have drug addiction, fungal culture should be added. The observation time should be at least 2 weeks, and when the culture result is negative, it should be kept until 3 weeks, and more than 2 positive blood cultures are necessary to confirm the diagnosis. Venous blood cultures are usually done, and the rate of positive arterial blood cultures is not higher than venous blood. Rarely, bone marrow cultures may be positive in patients with negative blood cultures. Positive cultures should be tested for drug sensitivity to various antibiotics alone or in combination in order to guide treatment.
(b) General laboratory tests are performed to reduce red blood cells and hemoglobin, with the latter mostly around 6% to 10g%. Occasionally, hemolysis may be present. The white blood cell count may be normal or mildly increased in uncomplicated patients, and sometimes a left shift may be seen. The erythrocyte sedimentation rate is mostly increased. Proteinuria and microscopic hematuria may be seen in more than half of the patients. In cases of complicated acute glomerulonephritis, interstitial nephritis or large renal infarction, there may be carnituria, pusuria and an increase in blood urea nitrogen and creatinine. Enterococcal endocarditis often leads to enterococcal bacteriuria, as does Staphylococcus aureus endocarditis, so a urine culture may also be useful for diagnosis.
(iii) Electrocardiography is generally nonspecific. It may show characteristic changes in the presence of embolic myocardial infarction and pericarditis. Incomplete or complete atrioventricular block, or bundle branch block and premature ventricular beats may be seen in the presence of septal abscess or annular abscess. If an intracranial mycotic aneurysm ruptures, “neurogenic” T-wave changes may be seen.
(d) Radiological imaging is only useful for the diagnosis of complications such as heart failure and pulmonary infarction. When abnormal shaking or displacement of the valve is found in patients with prosthetic valve replacement, it indicates possible combined infective endocarditis.
Computerized tomography (CT) or spiral CT is diagnostic when a large periaortic valve abscess is suspected. However, the artifacts of the prosthetic valve and the pulsation of the heart affect its valuation of valve morphology, and its dependence on contrast and limited cross-sectional views limit its clinical use. Magnetic resonance imaging (MRI), which is not affected by prosthetic valve artifacts, can play an adjunctive role when aortic root abscesses cannot be excluded by 2-dimensional echocardiography; however, it is more expensive.
(v) Echocardiography can detect redundancies on valves, especially in infective endocarditis with positive blood cultures, and can detect the location, size, number, and morphology of redundancies. Transthoracic 2D echocardiography is valuable for the early diagnosis of biologic PVE and slightly less so for mechanical PVE. Because it shows the former valve morphology well, it is easy to detect redundancies on biologic valves (especially porcine valves), whereas redundancies on mechanical valves are difficult to identify because of the multiple and variable reflections of the echogenic echoes. In contrast, the mechanical flap is difficult to identify because of its multiple and variable reflections. It is sometimes difficult to identify sparse calcifications or pseudo-redundancies on the valve.
The recent development of transesophageal 2D echocardiography is significantly superior to transthoracic 2D echocardiography. 90% of cases can be detected, and even smaller flabby organisms of 1-1.5 mm in diameter can be detected. It is not affected by the echogenicity caused by mechanical flaps and is more suitable for emphysema, obesity, and thoracic deformities. Significantly improves the diagnostic rate. It can also detect the extent of valve destruction or perforation, rupture of tendon cords, mitral or tricuspid valves with fetters, infected aortic aneurysms and mitral valve aneurysms due to endothelial damage to the anterior mitral leaflet ventricular surface caused by infected aortic regurgitation, and various septic intracardiac complications, hairy aortic root or annular abscesses, septal abscesses, myocardial abscesses, and septic pericarditis. It also helps to determine the original cardiac lesion, and the assessment of the severity of valve regurgitation and left ventricular function can be used as a reference to judge the prognosis and determine the need for surgery.
(f) Cardiac catheterization and cardiovascular angiography are useful for diagnosing the original cardiac lesion, especially in combination with coronary artery disease, and also for evaluating the function of the valve. Some people have taken blood specimens through cardiac catheterization at the proximal and distal ends of the valve to determine the difference in bacterial counts and believe that the site of the infection can be determined. However, cardiac catheterization and cardiovascular angiography may cause embolism due to dislodgement of the redundant organisms, or cause serious arrhythmias and aggravate heart failure, which should be considered carefully and the indications should be strictly controlled.
(vii) Radionuclide 67Ga (crop) cardiac scan is useful for the diagnosis of inflammatory sites of endocarditis and myocardial abscess, but it takes 72h to show positive, and the sensitivity specificity is significantly worse than that of two-dimensional echocardiography, and there are more false negatives, so the clinical application is not very valuable.
(H) serum immunological examination subacute infective endocarditis disease up to 6 weeks, 50% rheumatoid factor positive, after antibiotic treatment, its potency can be rapidly decreased. Sometimes hypergammaglobulinemia or hypocomplementemia can occur, commonly in patients with concomitant glomerulonephritis, and the level of decline is often consistent with poor renal function. Circulating immune complex CIC is positive in about 90% of patients and is often above 100 μg/ml, which is higher than in septic patients without endocarditis and has differential diagnostic value, especially in those with negative blood cultures. However, it should be noted that CIC serum levels can also be greater than 100 μg/ml in patients with systemic lupus erythematosus, hepatitis B surface antigen-positive patients and other immune diseases.
Other tests include precipitating antibody assays, agglutinin reactions and complement binding tests in fungal infections. Staphylococcus aureus antibody assay for cytosolic acid, etc.
Treatment]
Early treatment can improve the cure rate, but before the application of antibiotic treatment should take enough blood culture, according to the severity of the disease delay antibiotic treatment for a few hours or even 1 to 2 days, does not affect the cure rate and prognosis of the disease. And clarifying the pathogen and using the most effective antibiotics is the most fundamental factor in curing the disease.
(a) Drug therapy is generally considered to choose larger doses of penicillins, streptomycins, cephalosporins and other bactericidal agents, which can penetrate the superfluous matrix of platelet-fibrin and kill bacteria to achieve the eradication of infection of the valve and reduce the risk of recurrence. Combinations of bacteriostatic and bactericidal agents are sometimes used with good results. The efficacy depends on the susceptibility of the causative organism to antibiotics, and if the blood culture is positive, the drug can be selected according to the drug sensitivity. As the bacteria are buried in the superfluous organisms and covered by fibrin and thrombus, high doses of antibiotics are needed to maintain an effective bactericidal concentration in the blood. When available, the minimum bactericidal concentration of antibiotics in the patient’s serum can be determined in a test tube, usually drawn 1 hour after administration, and then the antibiotics are given at the minimum bactericidal concentration determined at a serum dilution level of at least 1:8 of the bactericidal agent.
The course of treatment should also be long enough to strive for a cure, usually 4 to 6 weeks. In patients suspected of having the disease, penicillin G is given intravenously at 6-12 million u daily and combined with streptomycin at 1-2 g daily intramuscularly immediately after serial blood cultures are sent. If the fever does not subside after 3 days of treatment, the dose of penicillin G should be increased to 20 million u intravenously, which can be maintained for 6 weeks if the treatment is effective. When applying larger doses of penicillin G, attention should be paid to the concentration in the cerebrospinal fluid. Neurotoxic manifestations, such as myoclonus, hyperreflexia, convulsions and coma, can occur when it is too high. At this point, attention should be paid to differentiate from the neurological manifestations of the disease to avoid misdiagnosis as further development of the disease and increase the dose of antibiotics, resulting in death.
If the treatment is not effective, it is advisable to switch to other antibiotics, such as semi-synthetic penicillin. benzathine (oxacillin), amoxicillin (Aspoxicillin), piperacillin (oxypiperazine penicillin, piperacillin), etc., 6 to 12 g daily, given intravenously; cephalothin (cephalothin) 6 to 12 g/d or vancomycin (vacomycin), 2 to 3 g/d, etc. Later, if positive blood cultures are obtained, the type and dose of antibiotics can be adjusted appropriately according to the drug sensitivity of the bacteria. In order to increase the percentage of cure, intermittent intravenous or intramuscular injections are generally advocated, the latter causing local pain, which is often unacceptable to patients. Therefore, penicillin G potassium salt can also be given as a slow intravenous drip during the day (penicillin G potassium salt contains 1.5 mEq/L per 1 million u. When given in very high doses, one should be alert to the occurrence of hyperkalemia), and supplemented by intramuscular injection at night.
Penicillin G is still the first choice in cases caused by Streptococcus oxalis, and penicillin alone is sufficient in most patients. Penicillin is a cell wall inhibitor, and the combination of penicillin and aminoglycosides can enhance the entry of the latter into the cells. Penicillin is a cell wall inhibitor. Patients who are allergic to penicillin can use erythromycin, vancomycin or first generation cephalosporins. However, it is important to note that cephalosporins are contraindicated in patients with severe penicillin allergy, such as anaphylaxis, because they can cause cross-allergic reactions with penicillin (approximately 1).
Enterococcal endocarditis is less sensitive to penicillin G and requires 2 to 40 million u/d. Therefore, ampicillin 6 to 12 g/d or a combination of vancomycin and aminoglycoside antibiotics for 6 weeks is preferred.
Cephalosporins have poor effect on enterococci and cannot replace penicillin in them. Recently, some strains producing β-lactamase resistant to aminoglycosides have also been reported, and strains resistant to vancomycin have also emerged. Drugs such as ciprofloxacin (Ciprofloxacin), sulbactam-ampicillin (Sulbactam-Ampicillin) and tylenol (Imipenem) of the quinolone class are available.
Staphylococcal endocarditis, if non-penicillin-resistant strains, still use penicillin G treatment, 10-20 million u/d and gentamicin combination. First-generation cephalosporins, vancomycin, rifampicin (Riforpin) and various penicillin-resistant penicillins such as benzocillin (oxacillin) can be used for resistant strains.
Treatment should be carefully examined for metastatic lesions or abscesses that must be treated to avoid bacterial re-implantation from these lesions at the site of the cardiac lesion. Staphylococcus epidermidis has low invasive power but is ineffective against penicillin G. A combination of vancomycin, gentamicin, and rifampin is appropriate.
Endocarditis caused by gram-negative bacilli has a high mortality rate, but is less common as the causative agent of this disease. Generally, β-lactams and aminoglycosides are used in combination. The third generation cephalosporins can be used according to the drug sensitivity, such as cefoperazone (cefoperazone pioneer) 4-8g/d; cefotaxime (cefotaxime) 6-12g/d; ceftriaxone (ceftriaxone, bacteriophage) 2-4g/d. The combination of ampicillin and aminoglycosides can also be used.
For Pseudomonas aeruginosa, third generation cephalosporins can be used, among which ceftazidine is the best, 6g/d. Piperacillin and aminoglycosides can also be used together or polymyxin B 100mg/d, polymyxin E 150mg/d.
Serratia spp. can be used with oxypiperazine penicillin or ampicillin plus aminoglycosides. For anaerobic infections, 0.5% metronidazole (metronidazole) 1.5-2g/d in 3 intravenous drips or cefoxitin 4-8g/d. Pioneerbine (ineffective against weakly mimicking bacilli in the anaerobic genus) can also be used.
The mortality rate of fungal endocarditis is as high as 80% to 100%, and drug cure is extremely rare. Early surgical excision of the involved valve tissue, especially fungal PVE, during antifungal therapy should be performed, and postoperative antifungal therapy should be continued to provide a chance of cure. Drug therapy is still preferable to amphotericin B, starting at 0.1 mg/kg/d and gradually increasing to 1 mg/(kg?d) for a total dose of 1.5-3 g. Amphotericin B is toxic and can cause fever, headache, significant gastrointestinal reactions, localized thrombophlebitis, and renal impairment, as well as neurological and psychiatric changes. 5 -Flurocytosine (5-FC, flurocytosine) is a less toxic antifungal drug, which only has an antibacterial effect when used alone and is prone to resistance. Combined with dicloxacillin B, it can enhance the fungicidal effect, reduce the dosage of dicloxacillin B and reduce the resistance of 5-FC. The dosage of the latter is 150mg/(kg?d) intravenously.
Rickettsial endocarditis can be treated with tetracycline 2g/d given intravenously for 6 weeks.
For those with high clinical suspicion of the disease and repeatedly negative blood cultures, high-dose penicillin and aminoglycosides can be used empirically to treat enterococcal and Staphylococcus aureus infections for 2 weeks, while blood cultures and serological tests are performed to exclude infections caused by fungi, mycoplasma, and rickettsiae. If ineffective, switch to other bactericidal agents, such as vancomycin and cephalosporins.
In case of recurrence of infected endocarditis, it should be treated again and the course of treatment should be appropriately extended.
(b) Surgery In recent years, the development of surgical treatment has reduced the mortality rate of infective endocarditis, especially in those with significant heart failure.
The main surgical treatments for natural valve endocarditis are refractory heart failure; other infections with uncontrollable drugs, especially fungal and antibiotic-resistant Gram-negative bacillary endocarditis; multiple embolisms; and septic complications such as septic pericarditis, Varicella aneurysm (or rupture), perforation of the interventricular diaphragm, and myocardial abscess. When complete or high atrioventricular block is present, temporary artificial pacing may be given, and permanent pacing therapy may be given when necessary.
The death rate of prosthetic valve endocarditis is higher than that of natural valve endocarditis. The mortality rate of PVE treated with antibiotics alone is 60%, but the mortality rate can be reduced to about 40% with antibiotics and prosthetic valve reoperation. Therefore, once PVE is suspected, it is advisable to treat with at least two antibiotics after taking at least three blood cultures within a few hours. Most early stage PVE pathogens are highly invasive and early surgery is generally advocated. Most of the later stages of PVE are caused by streptococci, and internal treatment is preferred. The fungal PVE is treated with medical drugs only as an adjunct to emergency surgical revalvuloplasty, and early revalvuloplasty should be performed. Early surgical treatment of drug-resistant Gram-negative bacillus PVE is also advisable. Others, such as moderate or severe heart failure due to valve dysfunction, severe perivalvular leakage or tearing of the bioprosthetic valve and valve stenosis, and the appearance of new conduction block. Recalcitrant infections, recurrent peripheral embolism, should all be considered for replacement of the infected prosthetic valve.
Pharmacologic treatment of the vast majority of right-sided cardiac endocarditis is effective, while surgical treatment is generally not considered because the right ventricle is well tolerated to tricuspid and pulmonary valve insufficiency. Surgery is often required to remove or replace the tricuspid valve in cases of progressive heart failure and Pseudomonas aeruginosa and fungal infections where medical therapy is ineffective.
To reduce the rate of residual infection after surgery during active infection, vitamins should be used continuously for 4 to 6 weeks after surgery.