Endocarditis is mainly an inflammation of the heart valves. There are two categories: infectious and non-infectious (e.g., rheumatic, lupus erythematosus, rheumatoid). Infectious endocarditis is the predominant clinical condition, mostly caused by bacterial infections, and is therefore also known as bacterial endocarditis.
Infective endocarditis is divided into acute and subacute depending on the basis of its pathogenesis and the virulence of the bacteria. However, because there are often individual differences between bacterial virulence and human resistance, the same bacteria can have different clinical differences in different patients, and in addition, in recent years, the widespread use of antibiotics, the clinical manifestations of the two, there is no obvious boundary, sometimes difficult to strictly distinguish.
Acute infective endocarditis is often caused by pathogenic bacteria such as Staphylococcus aureus, Streptococcus hemolyticus, Streptococcus pneumoniae, S. influenzae, S. pyogenes, and E. coli. These bacteria are more virulent, have a rapid onset, are severe, and are often secondary to infections at other sites as part of a systemic infection, such as meningitis, pneumonia, and thrombophlebitis, sometimes accompanied by metastatic septic lesions in other organs. It usually occurs in the normal heart.
Pathology Acute infective endocarditis, 50-60% occurs in normal heart valves. Valves and tendons may have ulcerated perforations, tendon fractures and large, brittle redundancies, which are shed as bacterial emboli, leading to embolism and migrating abscesses.
The clinical manifestations are mainly: ① septic manifestations, rapid onset and progression, with high fever, chills, malaise and other toxic symptoms. ② Skin bleeding spots and embolism phenomenon. ③ Cardiac manifestations, early mostly no murmur, individual onset of new murmur within a short period of time and quickly become high-pitched, rough, and the emergence of heart failure. Staphylococcal infection can be complicated by lung abscess, brain abscess and other migrating abscesses, manifested by cough, dyspnea, convulsions and hemiparesis. ⑤ Increased white blood cells, progressive anemia, and a high rate of multiple consecutive positive blood cultures.
Diagnosis and Differentiation
The diagnosis of acute infective endocarditis is mainly the clinical manifestations of sepsis, especially in the absence of heart murmurs. The disease is often masked by the primary infection and is easily missed, and for fever of more than one week, changes in cardiac auscultation, skin bleeding spots and embolic phenomena need to be noted. It is often differentiated from influenza, acute arthritis, acute septic meningitis, acute pyelonephritis, etc. In recent years, due to the progress of cardiac surgery and the widespread use of antibiotics, there is an increasing trend of atypical or specific types of infectious endocarditis, such as prosthetic valve replacement, hemodialysis or postoperative correction of precordial disease, all of which increase the chance of endocardial infection, and patients with postoperative fever should be alerted.
Treatment
The prognosis of this disease depends on the early or late treatment, the ability of antibiotics to control the primary bacteria, the degree of heart valve damage and the patient’s resistance. Staphylococcus aureus, Streptococcus hemolyticus, Diplococcus pneumoniae, Gram-negative bacilli, etc., due to the strong virulence of bacteria, can make the infected valve leaflet damage more quickly. If heart failure occurs during antibiotic treatment or the original heart failure is aggravated, new murmurs or murmurs with multiple changes appear If there is embolism, etc., it is a sign that the infection cannot be controlled, and a change of antibiotics should be considered. After strengthening supportive therapy and improving the general condition, early surgery is sought. If delayed too long, the condition may progressively deteriorate and the opportunity for surgery is often lost.
The specific details of antibiotic therapy are the same as in the section on subacute infective endocarditis.
Subacute infective endocarditis Subacute infective endocarditis is far more common and important than the acute form.
Etiology
Subacute infective endocarditis occurs in rheumatic heart valve disease, such as mitral and aortic valve insufficiency, and certain congenital heart diseases, such as ventricular septal defect, patent ductus arteriosus, and organic heart disease such as mitral aortic valve. Individuals also occur on the basis of the original heart disease, the pathogen is mostly conditional pathogens, such as Streptococcus straw green, Staphylococcus albicans, alkaline-producing bacteria and enterococci. A few of them are mycobacterial infections, among which Candida is the most common. Route of infection: Streptococcus gramineus infection is often associated with oral surgery, enterococcus often occurs after urinary tract surgery or abortion and delivery, staphylococcus, gram-negative bacillus, mycobacterial infection often occurs after intracardiac surgery.
Pathogenesis
Bacteria can enter the bloodstream during local oral surgery, abortion, delivery or urinary tract surgery, cardiac surgery or respiratory tract infections, and are mostly harmless due to the body’s defense mechanisms. However, when bacteria adhere to the heart valves or endocardium with existing lesions, there are local deposits of platelets and fibrin, which encircle the bacteria and form superfluous organisms, and phagocytes have difficulty in phagocytosis of bacteria.
Infective endocarditis has certain sites of predilection, mostly occurring at sites of blood flow impact or localized eddy flow, such as the atrial surface of mitral valve closure insufficiency, the ventricular surface of aortic valve closure insufficiency, the right ventricular surface of ventricular septal defect the endothelial surface of the pulmonary artery in arteriovenous catheterization, etc.
Subacute infective endocarditis has a chronic course, and the bacteria on the superfluous organisms are difficult to destroy and can survive for a long time, and migrating infections are less likely to occur because of the low virulence of the bacteria.
Pathology
The basic pathological changes are the formation of redundant organisms on the damaged heart valves or endocardium. The redundant organisms are composed of fibrin, platelets and leukocytes, in which bacteria are hidden.
The flap to which the superfluous organism is attached has an inflammatory reaction and focal necrosis, surrounded by lymphocytes, fibroblasts and giant cells. The necrotic cells are surrounded by new capillaries, connective tissue and granulation tissue. When the inflammation subsides, the flap becomes fibrotic and the surface is covered by endothelial cells, and it takes three months for complete healing in treated cases, and in untreated cases, healing is crossed with inflammatory reaction. In cases of precardiac disease and infective endocarditis, pulmonary embolism is a common complication. Local bacterial growth can cause ulceration or perforation of the valve leaflets, rupture of tendons and papillary muscles and bacterial aneurysms. Deposition of antigen-antibody complexes in the renal vascular bulb can lead to renal vascular bulb nephritis, due to immune response causing small arterial intimal hyperplasia, obstruction and small vessel perivasculitis, manifested as bruised spots on the skin and mucous membranes, occurring on the palmar surface at the end of the fingers and toes, slightly above the skin surface, with pressure pain, 5-15 mm in size, called Osler ( Osler’s nodules, and a few millimeters of purplish-red spots on the posterior palm and toes, called Janeway’s nodules.
Clinical presentation
Most cases have a slow onset with low-grade fever, malaise, and fatigue, while a few have a rapid onset with chills, high fever, or embolism, and some patients have a history of oral surgery, respiratory tract infection, miscarriage, or childbirth prior to onset.
I. Systemic infection
Fever is the most common, often of unknown origin for more than a week, irregular low fever, mostly between 37.5℃-39℃, but also intermittent or flaccid fever, accompanied by malaise, night sweats, progressive anemia splenomegaly, and pestle finger in the late stage.
II. Cardiac manifestations
Inherent signs of heart disease, the murmur is variable or new murmurs appear due to the growth or detachment of redundant organisms, destruction of valves and tendons. If the presence of endocarditis cannot be excluded even when there is no murmur, heart failure may occur in late stages. When the infection spreads to the atrioventricular bundle or ventricular septum, it can cause atrioventricular block and bundle branch conduction block. Arrhythmias are rare and may include premature beats or atrial fibrillation.
Embolic phenomena and vascular lesions
(A) Skin and mucous membrane lesions
Infected toxin acts on capillaries to increase their fragility and rupture bleeding, or caused by microembolism. Petechiae may appear in batches on the skin, alkaline conjunctiva, and oral mucosa of the extremities, and purple or red Osler nodules may appear slightly above the surface of the palm of the fingers and toes, or small nodular bleeding spots (Janewey nodules) may appear on the palm of the hand or foot without pressure pain.
(B) Cerebrovascular lesions
There may be several manifestations as follows.
(i) Meningoencephalitis Similar to tuberculous meningitis, with increased cerebrospinal fluid pressure, increased protein and white blood cell counts, and normal chloride or sugar quantification. Cerebral hemorrhage with persistent headache or meningeal irritation, caused by bacterial aneurysm rupture. ③ Cerebral embolism The patient is febrile and suddenly develops paralysis or blindness. (iv) Central retinal embolism may cause sudden blindness.
(iii) Renal embolism
It is the most common, accounting for about 1/2 of the cases, with carnal or microscopic hematuria. Severe renal insufficiency is often the result of antigen-antibody complexes deposited in the renal vascular bulb after bacterial infection, causing renal vascular bulb nephritis.
(iv) Pulmonary embolism
It is common in cases of congenital heart disease with infective endocarditis. The redundant organisms are mostly located on the endocardial surface of the right ventricle or pulmonary artery, with rapid onset, chest pain, dyspnea, coughing up blood, cyanosis or shock. If the infarct size is small, there may be no obvious symptoms.
In addition, there can be coronary embolism, which presents as an acute infarction, and splenic embolism with left upper abdominal pain or left quarter rib pain, with fever and local friction sounds. Mesenteric artery embolism, manifesting as acute abdomen, bloody stools, etc. Arterial embolism of the extremities may have pale chills in the embolized limbs, weakened or absent arterial pulses, and painful ischemia in the limbs.
Laboratory and other tests
I. Blood culture
Positive blood culture can confirm the diagnosis and provide the basis for choosing antibiotics. In order to provide a positive culture rate, the following points need to be noted: ① 4-6 consecutive cultures before antibiotic application. ② Each time the amount of blood drawn 10ml, while making aerobic and anaerobic culture. ③Culture time should be long, not less than three weeks. ④ positive culture results, drug sensitivity test should be done.
II. Blood picture
Progressive anemia, normal or increased white blood cell count.
III. Increased blood sedimentation
Urine routine
There is proteinuria and hematuria, and about 1/3 of advanced patients have renal insufficiency.
V. Echocardiography
There are redundant heart valves or endocardial wall, and abnormal manifestations of intrinsic heart disease.
Diagnosis and differential diagnosis
Early diagnosis mainly relies on raising awareness of the disease. Any patient with organic heart disease who has unexplained fever lasting for more than a week needs to be considered for the possibility of the disease. Blood culture and drug sensitivity test should be sent immediately and continuously. Positive blood cultures can confirm the diagnosis of the disease and its etiology. If the blood culture is repeatedly negative, the patient should be differentiated by rheumatic fever recurrence or left atrial mucinous neoplasm, or non-bacterial endocarditis. A heart murmur only, fever, and negative blood cultures also need to be differentiated from long-term febrile diseases such as tuberculosis, brucellosis, lymphoma, and liver abscess. Although the presence of hemorrhagic spots or emboli may be helpful in diagnosing the disease, most of them are in the more advanced stages of the disease.
Prognosis
The prognosis of the disease is related to the early or late treatment, the ability of antibiotics to control the pathogenic bacteria, the degree of damage to the heart valve, and the patient’s resistance. Postoperative prosthetic valve infections, particularly Gram-negative bacillary and mycobacterial infections, have the worst prognosis. Those with multiple recurrences have a poor prognosis.