Infectious vegetations

Introduction The basic pathological change of infective endocarditis is the attachment of neoplasms composed of platelets, fibrin, red blood cells, white blood cells and infectious pathogens on the surface of the heart valve. Infective endocarditis refers to the inflammation of the heart valve or the lining of the ventricular wall caused by direct infection of bacteria, fungi and other microorganisms (such as viruses, rickettsia, chlamydia, spirochetes, etc.), which is different from Non-infectious endocarditis caused by rheumatic fever, rheumatoid, systemic lupus erythematosus, and the like. In the past, this disease was called bacterial endocarditis, which is not used because it is not comprehensive enough. Typical clinical manifestations of infective endocarditis include fever, murmur, anemia, embolism, skin lesions, splenomegaly, and blood culture positive.

Cause

Causes:

Often in the heart of the original disease, the number of people who have not had heart disease has increased in recent years, especially in patients who have received long-term intravenous therapy, intravenous anesthesia addiction, and suppression of immune function caused by drugs or diseases. Infective endocarditis after artificial valve replacement has also increased.

Endocarditis in the left heart mainly involves the aortic valve and the mitral valve, especially in mild to moderate closure. Endocarditis in the right heart is less common, mainly involving the tricuspid valve. In various congenital heart diseases, patent ductus arteriosus, ventricular septal defect, and tetralogy of Fallot occur most frequently. In a single valvular disease, bicuspid aortic stenosis is most likely to occur, and valve prolapse (aortic valve) The mitral valve is also susceptible to this disease. Hypertrophic obstructive cardiomyopathy, degenerative valvular disease, and coronary heart disease have also been reported in this disease.

Acute infective endocarditis is often caused by the invasion of purulent bacteria into the endocardium, which is caused by infection of pathogens with strong virulence. S. aureus accounts for more than 50%. Subacute infective endocarditis Before the application of antibiotics to the clinic, 80% were caused by non-hemolytic streptococcus, mainly infection with Streptococcus viridans. In recent years, due to the widespread use of broad-spectrum antibiotics, pathogenic bacteria have changed significantly. Almost all known pathogenic microorganisms can cause this disease. The same pathogen can produce an acute course of disease and a subacute course. And cases of rare drug-resistant microorganisms have increased in the past. The incidence of green staphylococcus in grass is decreasing, but it still dominates. The proportion of Staphylococcus aureus, Enterococcus, Staphylococcus epidermidis, Gram-negative bacteria or fungi is significantly increased. Anaerobic bacteria, actinomycetes, and Listeria are occasionally seen. A mixed infection of two bacteria was found. Fungi are particularly found in cardiac surgery and intravenous anesthetic addicts. Long-term use of antibiotics or hormones, immunosuppressive agents, intravenous catheters to high nutrient solutions can increase the chance of fungal infections. Among them, Candida, Aspergillus and Histoplasma are more common.

In the lesions of heart valve lesions, congenital cardiovascular malformations or acquired arteriovenous fistulas, there is an abnormal blood pressure gradient, causing strong jets of blood and eddy currents. The jet impact of blood flow damages the endothelium of the endocardium and exposes collagen to form a platelet-cellulose thrombus. The eddy current causes the bacteria to settle on the endocardium that is damaged at the proximal end of the low pressure chamber and where the blood is abnormally discharged. Although there are a few bacteria in the blood flow of normal people, the bacteremia caused by wound invasion from the mouth, nasopharynx, gums, examination operation or surgery is mostly temporary and is quickly eliminated by the body, which has little clinical significance. However, repeated temporary bacteremia causes the body to produce circulating antibodies, especially lectins, which can cause a small number of pathogens to aggregate into groups and easily adhere to platelet-cellulose thrombus to cause infection.

The common infection site of aortic regurgitation is on the left ventricular surface of the aortic valve and the mitral chord; the infection of the mitral regurgitation is on the atrial surface and the left atrium of the mitral valve; The defect is at the endometrial surface of the right ventricular septal defect and the ventricular surface of the pulmonary valve. However, when the defect area is large enough that there is no pressure gradient in the left and right ventricles or that pulmonary hypertension is combined to reduce the partial flow, the disease is less likely to occur. In congestive heart failure and atrial fibrillation, the disease is less likely to occur due to weaker blood ejection forces and eddy currents.

Some people think that it is the role of receptor attachment. Because some Gram-positive pathogens, such as Enterococcus, Staphylococcus aureus, Epidermis, etc., all have a surface component that reacts with receptors on the surface of endocardial cells. Causes inflammation of the intima.

Contaminated artificial valves, suture materials, instruments, and hands are important causes of artificial valve endocarditis. The pathogen enters the body from the infected chest wound, urinary tract and various arteriovenous intubation, tracheotomy, postoperative pneumonia, etc., and the phagocytosis is destroyed after the blood is transferred through the extracorporeal circulation, which weakens the body to the pathogen. The ability to clear is also one of the reasons.

Pathological changes

The basic pathological change of this disease is the attachment of neoplasms composed of platelets, fibrin, red blood cells, white blood cells and infectious pathogens on the surface of the heart valve. The latter can be extended to the chordae, papillary muscles and the intima of the ventricular wall. The endocardium under the neoplasm may have inflammatory reactions and focal necrosis. Later, the infected pathogen is engulfed by phagocytic cells, and the neoplasm is surrounded by fibrous tissue, which is mechanized, glassy or calcified, and finally epithelialized by the endothelium. However, the healing of the neoplasms in different parts of the heart varies, somewhere may be healed, and the inflammation at other places is active, and some may recur after healing, re-forming the lesion. When the lesion is severe, the heart valve can form deep ulcers and even perforation. Occasionally, the papillary muscles and the chordae tend to break.

The neoplasms of this disease are larger and more brittle than those produced by rheumatic endocarditis, and are easily broken into infected emboli. They are spread to the various parts of the body with large circulating blood flow, especially in the brain, spleen, kidney and limb arteries. More, causing an infarction or abscess in the corresponding organ. Embolization obstructs blood flow, or destroys the vessel wall, and cystic dilatation of the vessel wall forms a bacterial aneurysm, often a fatal complication. If the arteries of the brain nourish the blood vessels and cause aneurysms, they can suddenly rupture and cause death in the ventricles or subarachnoid space. Diffuse meningitis is more common than brain abscess.

The disease often has small vasculitis caused by micro-embolism or immune mechanism, such as skin and mucous membrane defects, bleeding under the nail, Osler knot and Janeway damage. Infected pathogens and in vivo produce corresponding antibodies to bind to immune complexes, deposited on the basement membrane of the glomerulus, causing focal glomerulonephritis or diffuse or membranous proliferative glomerulonephritis, which can cause kidney Functional failure.

an examination

Related inspection

Blood routine heart sound map examination blood and bone marrow bacteria culture heart blood vessel ultrasonography

Although the "classical" clinical manifestations of this disease are not very common, and some symptoms and signs appear in the late stages of the disease, and the patients have been restricted by antibiotics and bacteriological examination techniques, which makes early diagnosis difficult, but In principle, it is still advocated for patients with valvular heart disease, congenital cardiovascular malformation or artificial valve replacement, if there is unexplained fever for more than 1 week, the possibility of the disease should be suspected, and blood culture should be performed immediately, such as anemia. Peripheral embolism and murmurs should be considered, and the diagnosis of this disease should be considered. Repeated short-term use of antibiotics in clinical practice, often repeated fever, especially in patients with valve murmur, should be alert to the possibility of this disease, timely echocardiography, is very helpful in the diagnosis of this disease. Positive blood culture has decisive diagnostic value and provides a basis for antibiotic selection.

First, the main clinical manifestations and signs have the following aspects:

(1) Fever: the most common, the hot type is variable, the most irregular, can be intermittent or relaxation type, accompanied by chills and sweating. There may also be only low fever. The body temperature is mostly between 37.5 and 39 ° C, and can be as high as 40 ° C or higher. About 3% to 15% of patients with normal or lower body temperature, more common in elderly patients with embolism or fungal aneurysm rupture caused by cerebral hemorrhage or subarachnoid hemorrhage and severe heart failure, uremia. In addition, antibiotics, antipyretics, and hormones have not been diagnosed before the disease has been diagnosed.

(2) 70% to 90% of patients have progressive anemia, sometimes to the severity, and even the most prominent symptoms. Anemia causes general weakness, weakness and shortness of breath. Patients with longer durations often have generalized pain and may be caused by toxemia or embolism in various parts of the body. Joint pain, low back pain and myalgia are more common at onset, mainly involving the gastrocnemius and thigh muscles, tendons, wrists and other joints, but also multiple joint involvement. If there is a serious bone pain in the course of the disease, it should be considered that it may be caused by periostitis, subperiosteal hemorrhage or embolism, or embolization of the aneurysm.

(3) The clinical manifestations of elderly patients are more variable, and fever is often misdiagnosed as respiratory tract or other infections. Heart murmurs are often mistaken for elderly degenerative valvular disease. Some may have no fever or heart murmur, but manifest as nerves, mental changes, heart failure or hypotension. Easy to have complications of the nervous system and renal insufficiency.

(4) The main signs are the murmur of the original heart disease or the murmur of the original normal heart. Changes in the nature of the noise during the course of the disease are often due to anemia, tachycardia or other hemodynamic changes. About 15% of patients initially had no heart murmur, and there was a murmur during the treatment. A few patients did not have murmur until 2 to 3 months after treatment. Occasionally, there was no murmur after many years of healing. In subacute infective endocarditis, right heart valve damage is uncommon, 2/3 of the right heart endocarditis, especially those who invade the tricuspid valve, and the neoplasms proliferate in the endocardium of the ventricular wall. As well as aortic atherosclerotic plaque, there is no murmur, but the latter is rare.

(5) Skin and mucous membrane defects, linear bleeding under the nail bed, Osler knot, Janeway lesions and other skin lesions have decreased significantly in the past 30 years. The point is that the toxin acts on the capillaries to increase the fragility, rupture or bleeding, or due to embolism. The incidence rate is the highest, but it has dropped from 85% before applying antibiotics to 19% to 40%. It is more common in the orbital combined membrane, oral mucosa, chest and back of the hands and feet. It lasts for several days, reappears after disappearing, and its center can be whitish. However, microscopic embolism caused by cardiopulmonary bypass can also cause ocular submucous membrane hemorrhage. Therefore, some people think that the center is grayish white, which is more important than the yellow one. Systemic purpura can occur. The hemorrhage under the nail bed is characterized by a linear shape, and the distal end does not reach the front edge of the nail bed, and the pressure may be painful. The incidence of Osler knot has dropped from the past 50% to 10% to 20%, purple or red, slightly higher than the leather surface, smuggling is about 1 ~ 2mm, the larger one can reach 5 ~ 15mm, mostly occurs in the fingers or feet The palm of the toe end, the size of the fish or the sole of the foot may have tenderness, often lasting 4 to 5 days to subside. The Osler knot is not unique to this disease and can also occur in systemic lupus erythematosus, typhoid, and lymphoma. A small, painless hemorrhagic or erythematous lesion of 1 to 4 mm in diameter on the palm and sole of the foot is called Janeway lesion. The clubbing (toe) is now rare. Retinopathy has the most bleeding, is fan-shaped or round, may have a white center, and sometimes only a round white spot on the fundus is called the Roth point.

(6) The spleen is often mild to moderately swollen, soft and tender. The incidence of splenomegaly has been significantly reduced. Unexplained anemia, refractory heart failure, stroke, paralysis, peripheral arterial embolism, progressive obstruction of the artificial valve orifice, and valve displacement, avulsion, etc. should be noted whether the disease exists. In patients with recurrent pneumonia, followed by liver enlargement, mild jaundice and finally progressive renal failure, even if there is no heart murmur, the possibility of right heart infective endocarditis should be considered.

Second, the disease can be divided into two types:

(1) Acute infective endocarditis

Often occurring in the normal heart, endocarditis in the right heart that occurs in intravenous anesthetic addicts tends to be more acute. Pathogens are usually highly virulent bacteria such as Staphylococcus aureus or fungi. Onset is often sudden, accompanied by high fever, chills, systemic toxemia symptoms, often part of a serious systemic infection, the course of the disease is more acute and dangerous, easy to cover up the clinical symptoms of acute infective endocarditis, due to heart valves and chordae The sharp damage, in the short term, has a high-profile murmur or the original murmur property changes rapidly. It can often develop rapidly into acute congestive heart failure leading to death.

On the affected endocardium, especially fungal infections, large and fragile neoplasms can be attached. Exfoliated emboli can cause multiple embolisms and metastatic abscesses, including myocardial abscess, brain abscess and purulent meningitis. . If the embolus is from the right heart chamber of the infection, pneumonia, pulmonary embolism, and single or multiple lung abscesses may occur. The skin may have erythematous erythema and purpuric hemorrhagic damage. A small number of patients may have splenomegaly.

(two) subacute infective endocarditis

Most patients have slow onset and only have non-specific insidious symptoms such as general malaise, fatigue, low fever and weight loss. A small number of onsets begin with complications of the disease, such as embolism, unexplained stroke, progressive exacerbation of valvular heart disease, refractory heart failure, glomerulonephritis, and heart valve murmur after surgery.

[Special type]

(a) artificial valve infective endocarditis

In infective endocarditis complicated by cardiac surgery, the incidence of prosthetic valve endocarditis (PVE) accounts for about 2.1%, which is 2-3 times higher than that of other types of heart surgery. PVE after double valve replacement has a higher incidence of PVE than single valve replacement. The PVE of the aortic valve is higher than that of the mitral valve. This may be due to the longer time of aortic valve replacement and the pressure of the transaortic aneurysm. The difference is large and the local turbulence is related. For those who have had native valvular endocarditis before surgery, the chance of developing PVE after surgery is increased by a factor of five. The incidence of mechanical flaps and artificial bioprosthetic PVE was about 2.4%. The incidence of early PVE in mechanical flaps was higher than that in artificial bioprostheses. The mortality rate of PVE is high, about 50%. The early PVE (within 2 months after surgery) was higher than the late PVE (2 months after surgery). The former pathogen is mainly Staphylococcus, accounting for 40% to 50%, including Staphylococcus epidermidis and Staphylococcus aureus. Diphtheria-like bacilli, other Gram-negative bacilli, and mold are also common.

The incidence has decreased since prophylactic antibiotic treatment before surgery. Later PVE is similar to natural endocarditis. It is mainly caused by various streptococcus (mainly by Streptococcus mutans), Enterococcus, and Staphylococcus aureus. Staphylococcus epidermidis is more sensitive to antibiotics than Staphylococcus epidermidis of early PVE. Fungi (most commonly Candida albicans, followed by Aspergillus), Gram-negative bacilli, and diphtheria-like bacilli are not uncommon.

The clinical manifestations of artificial valve endocarditis are similar to those of natural valve endocarditis, but the sensitivity and specificity as a basis for diagnosis are not high. Postoperative bacteremia, indwelling of various intubations, thoracic surgery wounds, pericardial incision syndrome, post-perfusion syndrome, and anticoagulant therapy can cause fever, bleeding, and hematuria. More than 95% of patients have fever, white blood cell count increased by about 50%, anemia is common, but skin lesions rarely occur in early PVE. Most of the splenomegaly is seen in the late PVE. Sometimes the serum immune complex titer can be increased, rheumatoid factor can be positive, but the serological test negative can not exclude the presence of PVE.

About 50% of patients have reflux murmurs. Artificial bioprosthetic endocarditis mainly causes the destruction of the leaflets, resulting in a murmur of insufficiency, and rarely an annulus abscess. The infection of the mechanical valve mainly occurs at the attachment of the annulus, causing the suture of the annulus and the valve to detach and rupture, forming a paravalvular leak and a new closed dysfunction and hemolysis, which makes the anemia worse and the annulus diffuse. The infection even completely abolishes the artificial valve. When an annulus abscess is formed, it easily spreads to adjacent cardiac tissue, and complications similar to those of natural endocarditis occur. In the early stage of PVE, when the valve has no obvious damage, there is no noise, so the diagnosis cannot be delayed due to the lack of new noise.

A murmur that causes a narrowing of the valve when the neoplasm blocks the valve orifice. Systemic embolism can occur anywhere, and in fungal PVE (especially caused by Aspergillus), embolization may be the only clinical finding. Skin flaky hemorrhage is not diagnostic in early PVE, as it can also be seen after surgery through an artificial heart-lung machine. Other complications of PVE, like natural endocarditis, may also have cardiac insufficiency, embolism, myocardial abscess, and bacterial aneurysm. The artificial valve has a weakened sound intensity, and the X-ray fluoroscopy sees an abnormal swing and displacement of the artificial valve, the angle is greater than 7° to 10° and the stinson's sign caused by the annulus splitting. Two-dimensional echocardiography found that the presence of neoplasms is helpful in diagnosis. Blood culture is often positive. If the blood culture is negative for many times, be alert to the possibility of fungal or rickettsia infection and slow-growing diphtheria-like infection. PVE pathogens often come from hospitals, so they are easily resistant.

(two) staphylococcal endocarditis

Most of the onset of illness, the condition is sinister, so it is mostly acute, only a few are subacute. Usually caused by penicillin G-resistant Staphylococcus aureus. It is more likely to invade the normal heart, often causing severe and rapid valve damage, resulting in aortic and mitral regurgitation. The emergence of metastatic infections and abscesses in multiple organs and tissues is important in diagnosis.

(three) enterococcal endocarditis

More common in patients with prostate and genitourinary tract infections, it is highly destructive to heart valves, with more obvious murmurs, but often in subacute forms.

(four) fungal endocarditis

Due to the increased use of broad-spectrum antibiotics, hormones and immunosuppressive agents, long-term use of intravenous infusion, indwelling of blood vessels and intracardiac catheters, extensive development of open heart surgery, and increased number of intravenous anesthetic addicts in some countries, fungal heart The incidence of endometritis is gradually increasing, and about 50% occurs after cardiac surgery. The pathogens are mostly Candida, histoplasm, genus Aspergillus or sputum. Fungal endocarditis has a rapid onset, a few are more insidious, and the incidence of embolism is high. The sputum is large and brittle, and it is easy to fall off, causing embolization of larger arteries such as the femoral artery and the radial artery. Occurrence of right endocarditis can cause fungal pulmonary embolism. If the giant sputum occludes the valve orifice and forms a narrow stenosis, severe hemodynamic disturbance may occur. Fungal endocarditis can cause skin damage. For example, patients with histoplasmosis may have subcutaneous ulcers, damage to the oral cavity and nasal mucosa. If histological examination is performed, it often has important diagnostic value. Infection with Aspergillus can cause intravascular diffuse coagulation.

(5) Endocarditis involving the right heart

Seen from left to right shunt congenital heart disease and artificial tricuspid valve replacement, urinary tract infections and infectious abortion. Cardiac pacing, right heart catheterization, and normal childbirth can also be caused. In recent years, the incidence of endocardial inflammation in right heart has increased significantly in some countries due to the increase in intravenous anesthetic addicts, about 5% to 10%. Most drug addicts have no heart disease and may be associated with contamination of the drug, failure to follow aseptic procedures, and damage to the tricuspid valve by specific substances in the intravenous material. Most of the bacteria are Staphylococcus aureus, followed by fungi, yeast, Pseudomonas aeruginosa, pneumococcal, etc. Gram-negative bacilli can also be caused. Infective endocarditis on the right side involves the tricuspid valve, and a few involve the pulmonary valve. The neoplasm is mostly located in the tricuspid valve, right ventricular wall or pulmonary valve. The sputum biofracture causes lung inflammation, pulmonary artery branch septic arteritis, and bacterial pulmonary infarction. If the Staphylococcus aureus is caused, the infarction site can be converted into a lung abscess.

Because the clinical manifestations are mainly in the lungs, splenomegaly, hematuria and skin lesions are rare. Patients may have cough, sputum, hemoptysis, pleural inflammatory chest pain and shortness of breath. There may be a murmur of tricuspid regurgitation, because the pressure gradient between the right atrium and the right ventricle is small (except for those with structural heart disease and pulmonary hypertension), the tricuspid systolic murmur is short and very light, very Soft, easy to mix with respiratory noise or mistaken for bloody murmur, but increased intensity of noise when deep inhalation is highly suggestive of tricuspid regurgitation. In the case of pulmonary valve, the middle diastolic murmur caused by pulmonary regurgitation can be heard. Cardiac enlargement or right heart failure is not common. Chest X-ray showed nodular or fragmental inflammatory infiltration in both lungs, which can cause pleural effusion. Lung abscess or necrotizing pneumonia can also lead to pus. The most common cause of death for right heart endocarditis is pulmonary valve insufficiency and respiratory distress syndrome caused by recurrent septic pulmonary embolism. Uncontrolled sepsis, severe right heart failure, and simultaneous involvement of the left valve are rare causes of death. If early diagnosis, early application of antibiotics or surgery, timely treatment of complications, simple right heart infective endocarditis has a good prognosis.

(6) Recurrence and recurrence of infective endocarditis

Recurrence refers to infection signs or positive blood cultures within 6 months after the end of antibiotic treatment or during treatment, and the recurrence rate is about 5% to 8%. Early recurrence is more than 3 months. It may be due to the fact that the bacteria hidden in the sputum are not easy to kill or have a long course before treatment or the previous antibiotic treatment is insufficient, thus increasing the resistance of the bacteria and serious complications such as the brain, Embolization of the lungs. It is also possible that there is a double infection due to the application of broad-spectrum antibiotics.

After 6 months of initial onset, all cardiac manifestations and positive blood culture reproduction of infective endocarditis are referred to as recurrence. Usually caused by different bacteria or fungi. The recurrence rate is higher than that of the first-time person.

Differential diagnosis

Differential diagnosis of infectious neoplasms:

1. Due to the diverse clinical manifestations of this disease, it is often confused with other diseases. The main manifestations of fever and mild cardiac signs must be identified with typhoid fever, tuberculosis, upper respiratory tract infections, tumors, and collagen disease. On the basis of rheumatic heart disease, this disease occurs, and after a sufficient amount of antibiotic treatment, the fever does not retreat, heart failure does not improve, and the possibility of rheumatism should be suspected. At this time, you should pay attention to check the changes in the pericardium and myocardium, such as progressive enlargement of the heart with galloping, pericardial friction or pericardial effusion. But these two diseases can also exist at the same time. Fever, heart murmur, and embolization are sometimes associated with atrial myxoma.

2, the disease with neurological or psychiatric symptoms as the main manifestation, in the elderly should pay attention to cerebral thrombosis caused by cerebral arteriosclerosis, cerebral hemorrhage and mental changes.

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