Infectious Endocarditis (IE)- this is an infective, more often bacterial, polypose-ulcer damage to the valve apparatus of the heart and the closed endocardium, accompanied by the formation of vegetation and the development of valve deficiency due to the destruction of its sash, characterized by systemic damage to vessels and internal organs, as well as thromboembolic complications.
Epidemiology.The incidence of infectious endocarditis is an average of 30-40 cases per 100,000 population. Men sick in 2 - 3 times more often of women, among the diseases prevail their working age (20-50 years old). Distinguish primary EE., developing on the background of intact valves (in 30-40% of cases), and secondary IE, Developing against the background of previously altered valves and sublocked structures (congenital and acquired valve defects of the heart, prosthetic valves, mitral valve prolapse, post-infarction aneurysms, artificial vascular shunts, etc.).
In recent years, there has been a steady increase in the incidence of IE, which is associated with the widespread dissemination of invasive methods of examination and surgical treatment, the growth of drug addiction and the number of persons with immunodeficiency states.
The peculiarities of the "modern" infectious endocarditis include:
The increase in the frequency of the disease in the elderly and old age (more than 20% of cases).
Increasing the frequency of primary (on intact valves) Form IE.
The emergence of new forms of the disease - IE drug addicts, IE prosthetized valve, IE nodogenic (nosocomial) due to hemodialysis, infection of intravenous catheters, hormone therapy and chemotherapy.
Failure in infectious endocarditis, despite the emergence of new generations of antibiotics, remains at a high level - 24-30%, and in older people - more than 40%.
EtiologyIE is distinguished by a wide range of pathogens:
1. Samoa frequent cause Diseases are streptococci (up to 60 - 80% of all cases), among which the most common pathogen is considered green Streptococcus (at 30 - 40%). Factors contributing to the activation of streptococcus are purulent diseases and surgical interventions in the oral cavity and nasopharynx. Streptococcal endocardits are distinguished by a subacute flow.
In recent years, the etiological role has increased enterococcus Especially with EE in patients who have undergone weighting operations on the abdominal cavity, urological or gynecological operations. Enterococcal endocardits are distinguished by malignant current and resistance to most antibiotics.
2. In second place in frequency among etiological factors IE is located golden Staphylococcus (10 -27%), the invasion of which occurs against the background of surgical and cardiac surgical manipulations, at an injection drug addiction, against the background of osteomyelitis, abscesses of various localization. For staphylococcal endocardits, the acute flow and frequent damage to intact valves are characterized.
3. The most difficult to occur EE caused by gram-negative microflora (intestinal, sinic sticks, protea, microorganisms of the member group), developing more often in injection drug addicts and alcoholism persons.
4. Against the background of immunodeficiency states of various genesis, IE is developing mixed etiology, including pathogenic mushrooms, rickettsia, chlamydia, viruses and other infectious agents.
Thus, the most frequent entrance gate infection These are: Operational interventions and invasive procedures in the oral cavity, urinary sphere related to the opening of abscesses to various localization, heart surgery, including valve prosthetics, aorto-coronary shunting, long-term catheter penette in Vienna, frequent intravenous infusion, especially injecting addiction, Chronic hemodialysis.
Due to the frequent start of antibacterial therapy before studying the blood of patients with IE on sterility, it is not always possible to identify the causative agent of the disease. In 20 - 40% of patients, the etiology of the disease remains unknown, which makes it difficult to appoint adequate antibacterial therapy.
Pathogenesis.In the development of IE, the following pathogenetic mechanisms can be distinguished:
1. Transient bacteremiawhich can be observed with any surgical interventions on the abdominal organs, the urogenital system, on the heart, vessels, nasopharynx organs, during the extraction of the tooth. The source of bacteriamia can be purulent infections of various localization, invasive studies of internal organs (bladder catheterization, bronchoscopy, colonoscopy, etc.), as well as non-compliance with sterility in injections from drug addicts. Thus, short-term bacteremia is a frequent phenomenon that does not necessarily lead to the development of IE. For the occurrence of the disease, additional conditions are needed.
2. Endothelium damageit develops as a result of impact on endockard of high-speed and turbulent blood flows, due to metabolic violations of endocardium in elderly and senile people. In the presence of the original valve pathology, the risk of transformation of bacteremia in IE reaches 90% (according to M.A. Gurevich et al., 2001). Many invasive diagnostic and operational interventions are accompanied by damage to the endothelium and, it means a high risk of developing IE.
3 . In the zone of damaged endothelium, most often on the surface of the sash valves of the heart occurs platelet adhesion,their aggregation and formation of thrombocyte cloth thrombus with fibrin deposition. In the conditions of Bacteriamia, microorganisms from the blood stream are deposited on the microtrombach and form colonies. On top view, new portions of platelets and fibrin are layered on them, which cover microorganisms from the action of phagocytes and other anti-infectious protection factors. As a result, large polypo-shaped clusters of platelets, microorganisms and fibrin, which are called on the surface of the endothelium vegetations. Microorganisms in vegetation have favorable conditions for breeding and vital activity, which leads to the progression of the infectious process.
4. Weakening of the organism resistanceas a result of various external and internal factors, it is a prerequisite for the development of an infectious hearth in the heart under conditions of Bacteriamia.
5. As a result infectious destruction The flaps of the valve sash and the subcase structures occurs perforation of the sash, the separation of tendon threads, which leads to acute development of insufficiency of the affected valve.
6. Against the background of a pronounced local infectious destructive process in the body, general immunopathological reactions are naturally developing (inhibition of the T-system of lymphocytes and activation of the B-system, the formation of circulating immune complexes (CEC), the synthesis of autoantibodies to its own damaged tissues, etc.), which leads to immune process generalization.As a result of immunocomplex reactions, systemic vasculites are developed, glomerulonephritis, myocarditis, polyarthritis, etc.
7. For EE characteristic thromboembolic complications:infected thromboembols, which are particles of vegetation or destroyed valve, migrate through the arterial channel of a large or small circle of blood circulation - depending on the lesion of the endocarda of the left or right heart chambers, and form microabscesses of organs (brain, kidneys, spleen, lungs, etc.).
8. The progression of IE naturally leads to development cardiac and renal failure.
Patanatomy.The left heads of the heart are more affected - the aortic and mitral valves, with the drug addicts - mostly a three-rolled valve. Vegetations are revealed on endocardium, consisting of platelets, fibrin and colonies of microorganisms, perforation or separation of flaps, tearing tendon chord. Vegetations are more likely to occur during valve insufficiency than in the stenosis of the valve opening, and are located preferably on the atrial side of the mitral valve or on the ventricular side - aortic. Characterized by the micrones of vessels, abscesses of internal organs.
Classification IE
Clinico-morphological:
primary IE,
secondary IE.
By etiology:streptococcal, enterococcal, staphylococcal, protein, fungal, etc.
With the flow:
acute, durable less than 2 months,
subacute, durability for more than 2 months,
chronic recurrent flow.
Special forms of EE:
Hospital (nosocomial) IE:
IE prosthetized valve,
IE in persons with a pacemaker (ex),
IE in persons on program hemodialysis.
Ie at Narkomanov
IE in people of elderly and senile age
Clinical picture:
The modern clinical course of IE is distinguished by the predominance
subacute or atypical forms of the disease with an erased clinical symptom. Sometimes the disease is diagnosed only at the stage of acute destruction of the heart valves or the development of systemic immunopathological processes in the form of vasculitis, glomerulonephritis, etc.
When describing the IE clinic, domestic scientists (A.A. DEMIN, 2005) traditionally distinguish 3 pathogenetic stages of disease, characterized by clinical, laboratory and morphological indicators and treatment principles:
Infectious-toxic.
Immunovipal.
Dystrophic.
Complaints.The first symptoms usually appear in 1-2 2 weeks after the episode of Bacteremia. It - fever and intoxication. With a subacute, endocardite disease begins with a subfebrile temperature, which is accompanied by a common weakness, cognition, sweating, rapid fatigue, decreased appetite, heartbeat. During this period, the correct diagnosis is usually not installed. The symptoms arising as viral infection, myocarditis, tuberculosis intoxication, etc.
A few weeks later, a hectic or permanent fever is installed with a body temperature lifting up to 38 - 39 o and pronounced chills, night sweating, weight loss at 10 - 15 kg, headaches, arthralgia and Malgia. Cardiac complaints appear and progress: shortness of breath during exercise, pain in the heart, resistant tachycardia. Despite the severity of clinical symptoms, the diagnosis of IE in the absence of signs of the formed heart failure can not be installed yet. At this time, the decisive moment can be the detection of vegetation on the valves using echocardiography. In the development of the damage of the damaged valve, signs of levels or right-hand deficiency quickly appear, which is accompanied by characteristic physical and instrumental data, making the diagnosis of EE obvious. In the formation of heart defects against the background of perforation of valve valve and destruction of valve vegetations, thromboembolic complications often arise with the development of ischemic stroke, a silence infarct, kidney (at left-sided IE) and lungs (at right-sided IE), which is accompanied by characteristic complaints. For fungal Ia, thromboembolism in the artery of the limbs with the development of mycotic aneurysm or foot necrosis
In a later immunocamipal stage, complaints appear, testifying to the development of glomerulonephritis, hemorrhagic vasculitis, myocarditis, arthritis, etc.
Lookingrevealed pallor of skin With a grayish-yellowish tint (color "coffee with milk"), which is associated with the anemia characteristic of IE, involvement in the process of the liver and hemolysis of erythrocytes. The weight loss is rapidly developing. The characteristic changes of the end phalange of the fingers are detected in the form of "Drum sticks" and nails by type "Hour glasses", Emerging sometimes after 2 - 3 months of illness. On the skin of patients (on the front surface chest, on the limbs) may be observed petechial hemorrhagic rash (painless, not pale with pressing). Sometimes Petechia is localized at the transitional fold of the conjunctivities of the lower eyelid spots Lukina or on the mucous membrane of the oral cavity. In the center of small hemorrhages in the conjunctival and mucous membranes there is a characteristic zone of pale. Similar to appearance rota spots Defined on the retina of the eye in the eye study. In soles and palms of the patient may be observed painless red janeway spots diameter 1 - 4 mm. The appearance of linear hemorrhages under the nails of the fingers is possible. Characteristic nodes of Osler - painful reddish formations with a pea size, located in the skin and subcutaneous tissue on the palms and soles associated with the development of thrombovasculitis. Reveal positive symptoms Tie (Gekhta) I. sample RUME-LEDE-Konchalovskywhich indicate an increased fragility of small vessels due to vasculitis. When conducting samples, the cuff is superimposed on the shoulder to measure blood pressure and it creates a constant pressure equal to 100 mm Hg, for 5 minutes. With increased permeability of vessels or thrombocytopathy (decrease in platelet function), more than 10 patechs on an area of \u200b\u200ba limited diameter of 5 cm appear below.
In the study lymph nodes Lymphadenopathy is often detected.
When developing heart failure, detected exterior signs stagnant phenomena for a large or small circulation of blood circulation
(position orthop, cyanosis, swelling of legs, swelling of the cervical veins, etc.).
With thromboembolic complications, characteristic external signs are also identified: paralysis, paresa, signs of TEL, etc.
Cardiac manifestations of IE:
Under the acute course of the IE and the rapid destruction of the affected valve, an acute left left ventricular or right-hand deficiency with characteristic objective features is developing. The lesion of the aortic valve is observed in 55 - 65% of cases, the mitral valve - at 15-40%, the simultaneous lesion of the aortic and mitral valves - in 13%, the three-risk valve - in 1-5%, but among drug addicts, this localization is detected in 50% of patients. .
Percussion and auxual signs of valve defects during primary IE, the character of the pulse and hell mainly correspond to physical manifestations of rheumatic heart defects.
It is a complex diagnosis of IE, which has connected to already existing innate or rheumatic heart defects. With differential diagnosis, along with anamnesis and characteristic non-recorded signs of IE, the emergence of new or change in the earlier cardiac noise due to the formation of new heart defects is taken into account.
Change abdominal organsmanifested in increasing liver and splenomegaly (in 50% of patients) associated with generalized infection and frequent thromboembolic infarction of the spleen.
Complications of IE.:
Abscess fibrous rings valve and its destruction.
Diffuse myocarditis.
Heart failure, including acute during valve destruction.
Thromboembolism (in 35-65%) patients.
Miocardial abscess, septic infarction of lungs, spleen, brain.
Glomerulonephritis, leading to chronic renal failure.
Diagnostics:
1. A general blood testdetects leukocytosis with leukoformula shift to the left, an increase in ESP to 50-70 mm / hour, normal anemia due to oppression bone marrow. Establishing ESP is usually preserved 3-6 months.
2. Biochemical blood testrelaxes expressed disproteinemia due to the reduction of albumin and an increase in the content of α 2 and γ-globulins, the content of fibrinogen, sermukoid, is increased, a C-jet protein appears, positive sedimentary samples - forms, sulea, thymol. In 50% of patients, a rheumatoid factor is detected.
3. Sowing blood for sterilitymay appear to confirm the diagnosis of IE and the choice of adequate antibacterial therapy. To obtain reliable results, the blood fence must be carried out before the start of antibacterial therapy or after the short-term cancellation of antibiotics in compliance with all the ranges and antiseptic rules by puncture or artery. In the area of \u200b\u200bthe vessel puncture, double-handed skin treatment with antiseptic, palpate vein follows in sterile gloves, from veins take 5-10 ml venous blood In 2 bottles with nutritional environments and immediately send them to the laboratory.
With acute IE, blood is taken three times with an interval of 30 minutes at the height of the fever, with a subacute of IE, a three-year blood pressure is carried out within 24 hours. If after 2-3 days the growth of the flora is not recommended to produce sowing 2-3 times. With a positive result, the number of bacteria ranges from 1 to 200 per 1 ml of blood. Their sensitivity to antibiotics is determined.
4. Electrocardiographyit may identify signs of focal or diffuse myocarditis, thromboembolism in coronary arteries is accompanied by extracts of myocardial infarction, thromboembolism in the pulmonary artery (TEL) will be manifested by the ecg-signs of acute overload of the right ventricle.
5. Echocardiographyin many cases, it allows you to identify direct signs of IE - vegetation on the valves, if their dimensions exceed 2-3 mm, evaluate their shape, magnitude and mobility. There are also signs of breaking tendon chord, perforations of valve sesters, forming valve heart defects.
Cardiologist
Higher education:
Cardiologist
Kabardino-Balkarian State University. HM Berbekova, Faculty of Medicine (KBSU)
Education Level - Specialist
Additional education:
"Cardiology"
GOU "Institute of Improvement of Doctors" Ministry of Health and Social Development of Chuvashia
In the list cardiology diseases Includes infectious endocarditis. It is dangerous possible complications (myocarditis, kidney damage, lungs, liver, central nervous system). In the event of the development of this pathology, patients are mandatory to be hospitalized.
The endocardium is called the inner layer of the heart, which lifts the cavity of the atrial and ventricles. It is also formed by heart valves that take part in unidirectional blood movement. Infectious endocarditis is called inflammatory disease of the inner shell of infectious origin. This is not transmitted from one person to another type of heart pathology. The pathogens may be a variety of microorganisms (bacteria, viruses).
The level of morbidity in the world ranges from 3 to 10 cases per 100,000 people. The progression of endocarditis leads to the destruction of valves and impaired their functioning. The consequence of all this is the development of their insufficiency. Most often in the process involve aortic and mitral valves. The first is located between the left ventricle and the aorta, and the second - between the left hearts.
The main purpose of the valve apparatus is an obstacle to the reverse blood cast. This eliminates the overload of ventricles and atrial. In recent years, the number of patients with infectious myocarditis has increased. Causes - immunodeficiency, frequent heart surgery and the use of invasive treatment methods.
The disease can occur in a recurrent form. With this pathology, the percentage of fatal outcomes is high. Almost every third patient dies without due medical care. In 2015, this cardiac pathology was detected mainly in the young population aged 20 to 50 years. Often the disease develops from drug addicts and persons with reduced immunity. Less often inflammation of endocardia is observed in childhood.
The classification of infectious endocarditis is known not to everyone. It is divided according to the following signs:
Depending on the main cause of inflammation, primary and secondary endocarditis are isolated. They have a fundamental difference between themselves. In the primary form of endocarditis, inflammation develops against the background of sharp infectious states (sepsis, septicemia, septicopemia). In this case, the valves were originally not changed. Secondary endocarditis is a complication of another pathology. The disease can flow in acute, subacute and protracted form.
In the first case, the symptoms are worried about a person for no more than 2 months. The most common cause is sepsis. It takes very hard. Subacute endocarditis lasts more than 2 months. If complaints and signs of the lesion of the heart shell persist for a long time, then such an endocarditis is called a protracted one. Inflammation can only be limited to valve flaps or go beyond their limits. Highlight 3 clinical forms of the disease:
The toxic type of endocarditis has the following signs:
In the case of the progression of the pathological process, a dystrophic form of inflammation is developing. With it, irreversible changes are observed. The infectious-allergic form of endocarditis is characterized in that it leads to jade, hepatitis and other complications. There is another classification that is based on the activity of the inflammatory process. It allows you to judge the condition of the patient. According to it, the aligned and active endocardits distinguish.
The etiology of the infectious endocarditis knows only the doctor. The following causes of the lesion of the heart sheath and the valves of the microbes are distinguished:
Secondary infectious endocarditis develops mainly against the background of congenital heart defects and rheumatism. The impairment of hemodynamics leads to damage to the valve apparatus and the affection of the endocardium. This disease becomes the cause of heart failure and vasculitis. The pathogenesis of infectious endocarditis is based on adhesion (sticking) of microbes to endocardium and valves.
It is most often happening from drug addicts, alcoholics and older people. Risk factors include the use of drugs overwhelming immunity. The most frequent pathogens of endocarditis are staphylococci, streptococci, enterococci and fungi. Total known more than 120 types of microbes that can cause this heart pathology.
From this largely depends on the forecast for health. The highest rates of mortality are observed when infected with epidermal and gold streptococci. The share of fungal endocarditis accounts for up to 7% of all cases of illness. The highest activity of the inflammatory process is observed against the background of an infection caused by anaerobic microflora.
The new stage of the development of medicine entailed the appearance of diseases caused by the residence of a person in a hospital. It is often a nosocomial endocarditis. It develops within 48 hours after a person's arrival in the hospital. The endocarditis not related to hospitalization may arise at home. This is facilitated by hemodialysis, intravenous administration medicines, care for a sick person. Separately allocated repeated endocarditis, which develops after some time after the primary inflammation.
With infectious endocarditis, symptoms are determined by the following factors:
The sharp shape of the endocarditis caused by pathogenic stamps of staphylococcus flows. In this disease, the following symptoms are observed:
The manifestations of intoxication are the most permanent diagnostic sign. It is due to the presence of microbes and their toxins. The temperature in patients may be subfebrile or hectic. Frequent manifestation Endocarditis is shortness of breath. It is due to heart failure. Small blood vessels of patients become fragile.
It is manifested by multiple hemorrhages (petechias). They appear in the region of the clavicle, century, nails, mucous membranes. Specific symptom of endocarditis are company spots. They are hemorrhages in mesh shell eyes. Similar changes are detected at an ophthalmic examination.
The subacute infectious endocarditis is often manifested by the symptom of drum sticks and hourly glasses. Patients thicken the phalange of the fingers. Often on the skin appear nodules of the Osler. This is a sign of septic endocarditis. A distinctive feature of the disease is the development of complications in the early period.
In presentations on the infectious endocarditis of famous doctors, possible complications of this disease are always indicated. This pathology may lead to the following consequences:
With endocardium, the infection spreads through the body, leading to a violation of the function of all vital organs. The kidneys are very often amazed. The process involves predominantly the glomerular apparatus, which is responsible for filtering blood plasma. Glomerulonephritis develops. It is manifested by a decrease in diurea, high pressure and edema syndrome.
In 2015, many people died from renal pathology. Complications of infectious endocarditis include blood thickening and the formation of thrombus. The latter can cause inflammation of blood vessels and their blockage. With pulmonary artery thromboembolism, the likelihood of a lung infarction is high. This is a dangerous state due to the acute lack of oxygen.
The infarction is manifested by pain in the chest, shortness of breath, difficult to breathe. In the case of the tomb of the thrombus and the blockage of cerebral vessels they can develop ischemic stroke. It is manifested by a disorder of consciousness, a violation of speech and a motor function, weakness in the legs and arms, dizziness. Neurological complications include meningitis, strip paresis, brain abscess. If the therapy of the infectious endocarditis is not carried out, the development of secondary arterial hypertension is possible.
If the doctor has a presentation on endocarditis, he knows that against the background of this disease, the heart is suffering. In the absence of proper treatment, there is a risk of developing defects (deficiency of mitral and aortic valves), myocarditis and inflammation of the near-carrying bag. To the most dangerous consequences Endocarditis includes septic shock and acute respiratory failure. In case of late treatment of respiratory distress syndrome, mortality reaches 70%.
Diagnosis and treatment are conducted by a doctor. To reveal endocarditis in a patient, you need to hold a number of studies:
Consultation of several specialists (cardiologist, pulmonic, therapist, ophthalmologist) may be required. In case of suspected infectious endocarditis, the diagnosis necessarily includes heart ultrasound. This is the main and most informative method for assessing the condition of the heart chambers and valves. Echography is simple and percussive. In the latter case, the sensor is introduced through the esophagus.
During the ultrasound, the following changes are detected:
To establish the pathogen, a polymerase chain reaction can be carried out. The diagnosis of infectious endocarditis includes a survey, inspection, blood pressure and pulse, listen to lungs and hearts. In the process of auscultation, signs of valve deficiency are often detected. Pathological noise and weak heart tones are listened. During the damage to the liver and kidneys, biochemical blood biochemical changes change dramatically.
After the diagnosis is raised, proceed to treatment. The main documents that take into account the doctor, assigning medicines, is the history of the disease and an outpatient map. When the endocarditis is detected, hospitalization is shown. Therapy is combined. Next treatment is carried out:
There are various recommendations, but always with a given disease, systemic antimicrobial drugs are prescribed. Most often it is antibiotics. Pre-determined the type of bacteria. When revealing streptococci, antibiotic therapy is carried out within 4 weeks. Breaks do not. In the case of staphylococci selection, treatment of infectious endocarditis can be delayed for a month and a half.
The longest therapy requires inflammation due to anaerobic microflora. It is recommended to use modern antibiotics Wide spectrum. They need to be administered intravenously or intramuscularly. The most effective penicillins (benzylpenicillin, phenoxymethylpenicilline, ampicillin, amoxiclav). Penicillins are often combined with aminoglycosides.
Antibacterial treatment is terminated in normalization of temperature, negative results of microbiological research and normalization of blood and urine indicators. Recommendations for treatment are known to each doctor. According to the indications, anti-staphylococcal globulin is introduced. With infectious endocarditis, symptomatic therapy is carried out.
The following drug groups can be used:
Treatment recommendations include the reception of antiagregants and anticoagulants. This reduces the likelihood of thrombosis and vascular embolism. Any good lecture or presentation on the topic of endocarditis states that to eliminate the symptoms of intoxication requires massive infusion therapy.
Strong fever is an indication for the appointment of antipyretic drugs. With the damage to the heart, medications are often prescribed, reduced the load on the organ. Treatment recommendations include the use of systemic glucocorticoids (prednisone). With infectious endocarditance, treatment implies plasmapheresis.
A competent presentation or lecture on endocardite states that in severe cases of one drug treatment is not always enough. Operation is required when developing complications. Surgical treatment is planned, emergency and deferred. In the first case, the help is in the first 24 hours. The urgent surgery is carried out within a few days. Often, radical treatment is delayed.
Antibiotic therapy is performed. The urgent surgery is shown in heart failure, long, repeating fever and non-efficiency of drugs. Often, treatment recommendations include surgical intervention in order to prevent embolism. This is possible with large vegetation and high risk of thrombom education. Very often there is an intervention for the replacement of valves for artificial.
Endocarditis is one of the most dangerous cardiovascular diseases, so the forecast is not always favorable. In the case of acute inflammation without treatment, a person dies in 1-1.5 months from complications. In the elderly, the forecast is worse. In 10-15% of cases, acute endocarditis goes into chronic with periodic exacerbations.
Specific prevention of infectious endocarditis is absent. The transfer of infection from the patient to healthy does not occur, so contact with other people does not play roles in the development of this pathology. Any presentation on endocarditis includes prevention. To avoid damage to endocardium and valves, you need to adhere to the following recommendations:
Very often the heart is amazed against the background of sepsis. To avoid it, it is necessary to conduct a sanation of foci of infection and with the slightest complaints to contact the doctor. With the risk of infection, a short course of antibiotic therapy may be carried out in order to prevent. Thus, endocarditis is a dangerous heart pathology. When the first symptoms appear, you need to contact a cardiologist or therapist.
Rheumatism is an infectious-allergic disease, which is based on inflammation and disorganization of connective tissue. The main cause of rheumatism is considered to be beta-hemolytic streptococcus Group A. When first contact with this microorganism, the patient usually suffers from tonsillitis or pharyngitis ( in childhood). Without qualified medication treatment, the initial disease passes within 1 - 2 weeks. However, then the most dangerous phase occurs.
The human immune system begins to produce antibodies against the causative agent. In some cases, this reaction becomes excessively strong ( hypeergic immune response). In such patients, antibodies begin to attack connecting tissue cells ( mainly in the cardiovascular system). Such inflammation is called rheumatism.
With rheumatic endocarditis, the following heart structures are most often affected:
The most frequent pathogens of the bacterial endocarditis are:
An important feature of bacterial endocardits is the formation of so-called vegetations on valve flaps. Most often they arise in the left hearts. Vegetations are small accumulations of microorganisms attached to the sash. Usually, a small thrombus is formed at the first stage in the place of damage to the endocardium. Subsequently, it is precisely the first infection pathns that are attached. As they reproduce and enhance the inflammatory process of vegetation, it may increase. If they have a flat form and firmly attached to the sash, they are called immobile. Moving vegetations on the structure resemble polyps on the leg. They seem to hang on the flap of the valve and move depending on the blood current. Such vegetations are the most dangerous, as the separation of this education leads to its injection into the bloodstream and acute thrombosis. The separation of large rolling vegetations is quite frequent cause of serious complications and even death with infectious endocarditis. The severity of the consequences depends on what level the vessel thrombosis occurs.
Separately, it should be considered fibroplastic eosinophilic endocarditis Lefball. The reasons for its development are unknown. With a given disease, it is amazed predominantly trimming pericard, which distinguishes it from other disease options. It is assumed that in the development of endocarditis Lefball play a certain role of complex allergic reactions.
Infectious endocardits can be divided into two main groups:
The following patient groups are predisposed to the chronic course of the disease:
In chronic infectious endocardius, periods of remissions and relapses are usually observed. Remissions are improved patient's condition and the disappearance of sharp symptoms. During this period, patients are mainly observed signs of damage to valves, but the infectious focus in the heart is not liquidated. The relapse is called a sharp deterioration in the patient's condition associated with the activation of infection and the development of the acute inflammatory process. This flow is also observed with rheumatic endocarp.
In some countries, in addition to the sharp, subacute and chronic form of endocarditis, there is another abortive measure of the flow. It is characterized by rapid and persistent recovery ( without recurrence). Such an outcome is most favorable, since the valve apparatus of the heart does not have time to suffer due to inflammation. The abutient flow is observed in infectious and toxic endocardits, when the disease was diagnosed at an early stage, and timely treatment was started.
Rheumatic endocarditis has a somewhat different classification. It is not based on the duration of the disease ( because it is always a protracted), and on the nature of changes in cardiac valves. They allow you to estimate the intensity of the inflammatory process and assign the right treatment.
Rheumatic endocarditis is divided into four types:
With the endockarization of Lefefler distinguish the following steps:
Symptoms and signs of heart failure when various forms Endocarditis
Symptom or manifestation of the disease | Description of the symptom | The mechanism of appearance of symptom |
Dyspnea | Initially, shortness of breath appears in severe physical exertion. It is characterized in the inability to restore the normal respiratory rhythm. The patient can even start torn, as there is no stable air inflow into the lungs. Dyspnea lasts 1 - 2 minutes and stops after stopping the load. In the later stages, shortness of breath may occur and spontaneously, at rest. | Dyspnea with endocarditis can be due to several pathological mechanisms at once. With an active inflammatory process, the volume of cardiac cameras decreases somewhat. Accordingly, the heart cannot pump the same blood volume as before. There is a stagnation of blood in a small circulation circle ( in the lung vessels). Another reason for stagnation can be the battle of valve flaps or its narrowing. It does not allow blood to pass from one heart chamber to another in sufficient quantity, which also suffers from the pump function. Blood stagnation in the lungs violates gas exchange and the body lacks oxygen. The reflexively violates the rhythm of breathing and shortness of breath occurs. |
Heart pain | Heart pain pain is relatively rare for endocarditis symptom. They may occur in late stages of the disease during exercise or during stressful situations. | Most often, the pain is due to a violation of blood flow to the heart muscle. This is explained by the spasm or blockage of coronary vessels that feed myocardium. With endocarditance, these vessels may be clogged by fragments of vegetation on the valves. Moreover, inflammatory process In the area of \u200b\u200bthe aortic valve can contribute to the narrowing of the lumen coronary arterieswho originate near this place. |
Tachycardia (heartbeat) | The rapid heartbeat is characteristic practically for any forms of endocarditis. A distinctive feature It is that it is not associated with exercise and usually does not depend on body temperature, as it happens with other diseases. | Tachycardia with infectious endocardius can be explained by hitting microbial toxins and increasing body temperature ( in the early stages of the disease). In the later stages, the cardiac frequency increases reflex. So the body tries to compensate for cardiac insufficiency. |
Fingers in the form of "drum sticks" (drum fingers, hippocratic fingers) | This symptom may appear in the later stages of the disease ( more often with rheumatic heart defects). Fingers become narrower, and the last phalanx, on the contrary, expands. This symptom is not characteristic only for endocarditis. It meets with other heart disease, lungs and gastrointestinal tract (less frequent). | Thickening occurs due to the growth of the connective tissue between the nail plate and the bone. The unambiguous mechanism of this process has not yet been established. Nevertheless, the connection of this symptom with chronic tissue hypoxia is clearly traced ( lack of oxygen). |
Nails in the shape of watch windows | Nails expand and take more rounded shape. central part nail plate Raised, because of which the nail becomes like a dome. It is clearly noticeable if you ask the patient to compare the final phalanxies big fingers back side ( symptom of Shamrota). | This symptom usually develops in parallel with drum fingers. The mechanism of their occurrence is similar. The process affects all fingers. |
Pallor skin | The skin's pallor can appear with any form of endocarditis and at any stage. As a rule, it depends on the stage of heart failure. With a protracted course of the disease or with severe damage to the valves, not only the pallor may be observed, but even the formation ( akrcyanosis) The tip of the nose and fingers. | The skin's pallor is explained by the fact that the heart does not supply with tissues enough oxygen. The volume of pumped blood may fall due to the weakening of heart abbreviations, narrowing valves or thickening the walls of the heart ( the amount of heart chamber itself decreases). |
Fast fatiguability | Fast fatigue, like shortness of breath, appears in the first stages of the disease only during exercise. Over time, the patient can start tired strongly and from the usual everyday occupations. | This symptom is also explained by oxygen fasting fabrics. |
The following symptoms speak in favor of infectious endocarditis:
The absence or a minor increase in temperature (despite the acute infectious process) may be observed in the following groups of patients:
In patients with endocarditis, the following skin manifestations may be observed:
Rheumatic endocarditis is characterized by signs of lesion of cardiac valves. In the early stages, patients may not make complaints. Diagnose disease is possible only with a careful examination from a cardiologist or conducting laboratory research. In the later stages, the deformation of the valves leads to the emergence of symptoms of heart failure. Distinctive features It is the rheumatic process that sometimes is the defeat of other organs and systems. This disease is rarely limited only by cardiac manifestations. In this regard, patients often impose complaints that are not characteristic of endocarditis.
With rheumatic damage to the valves, symptoms of the defeat of the following organs and systems can be observed:
The following research methods are applied to the diagnosis of endocardits of any origin:
During the general inspection, the doctor collects data on illness in the following ways:
In general and biochemical blood tests in patients with endocarditis, you can detect the following changes:
Specific analyzes to confirm rheumatic inflammation are:
In urine analysis, there are usually no pronounced changes. With serious heart failure in the later stages of the disease, Oliguria may be observed ( reduced urine formation). It is explained by the weakening of the pumping function of the heart, because of which the pressure required for normal filtration is not supported in the kidneys. In rheumatism with the damage to the kidney tissue in the urine there may be traces of blood.
When taking blood for bacteriological sowing, followed by the following principles:
An alternative to bacteriological analysis is the conduct of serological tests. They determine the presence of antibodies in various microbes or directly microbial antigens are detected. The disadvantage of such a study is that there is no possibility to make an antibioticogram.
The following instrumental diagnostic methods have the greatest value at endocarbage:
Generally accepted criteria for the diagnosis of bacterial endocarditis
Large criteria | Small criteria |
In two of the three blood sampling, a typical endocarditis causative agent is revealed ( green Streptococcus, Golden Staphylococcus, Hacek Group Bacteria). | The presence of risk factors for infectious endocarditis ( congenital heart defects, artificial valves, drug use injecting, etc.). |
Bacteremia confirmed by blood tests with an interval of 12 hours. | Increase body temperature more than 38 degrees. |
Movable vegetations on echochegte or abscess fibrous valve ring. | Patechial rash or thrombosis of the arteries of internal organs. |
Pronounced valve failure ( also evaluated using Ehoche). | Detection of rheumatoid factor and other extraimedar signs of rheumatism. |
Positive analysis When sowing one of the three basic blood samples. |
One of the serious problems in the diagnosis of endocarditis is the identification of its root cause in the early stages of the disease. Doctors often have to decide whether they are dealing with infection or with rheumatic inflammation. The fact is that treatment in these two cases will be different. The correct diagnosis in the initial stages will allow to begin medical therapy earlier, which will prevent complications and eliminate the threat to the patient's life.
The main differences between the bacterial and rheumatic endocarditis
Symptom or diagnostic test | Infectious endocarditis | Rheumatic endocarditis |
Accompanying illnesses | Often develops after acute infectious diseases or simultaneously with them ( sinusitis, surgical interventions, gOOD INFECTION, pneumonia, etc.). | Can develop on the background chronic tonsillita Or after transferred scarletin. |
Fever | Temperature can rise to 38 - 40 degrees and change greatly during the day. | The temperature rarely exceeds 38 - 38.5 degrees and is not prone to quick drops. |
Symptoms accompanying fever | Often, a strong chill is observed, abundant sweating ( especially at night). | These symptoms are rarely observed. |
Embolia | There are quite often found. | Not characteristic, observed only against the background of serious rhythm violations. |
Symptom of "drum sticks" | For chronic flow Diseases fingers relatively quickly change the form. | The symptom appears only with pronounced valve defects. |
Typical changes in blood test | Anemia, thrombocytopenia ( lowering platelet levels), increased levels of leukocytes. | Anemia is rare. Leukocytosis is more characteristic than leukopenia. |
Bacteriological research | Repeated blood sown most often ( 70% of cases) give repeated positive results for the same microorganism. | Sowing blood does not reveal the pathogens. |
Changes on Ehocheg | Often it is possible to distinguish between vegetation on cardiac valve flaps. | Vegetations are not detected. |
Reaction to the use of antibiotics. | The patient's condition begins to improve already on 2 - 3 days of treatment. | There are no pronounced changes in the patient state. |
As a rule, neither one of the above symptoms or research is impossible to accurately determine the origin of the endocarditis. However, the complex assessment of the patient's condition and the comparison of all manifestations of the disease contribute to the setting of the correct diagnosis.
Depending on the type of illness and leading symptoms, treatment can be carried out in the rheumatological, infectious or cardiovascular branch. Consultation of the cardiologist is shown in any form of endocarditis. With this specialist, it is obligatory to coordinate the course of treatment.
Immediately the treatment of endocardits is largely determined by the disease stage and nature of the inflammatory process. The erroneous diagnosis often leads to incorrect treatment. Medical errors are recognized as the most common cause of chronic infectious endocardits.
The following methods are used in the treatment of endocarditis:
Treatment of acute infectious endocarditis involves taking antibiotics to destroy the causative agent of the disease. Antimicrobial preparations are prescribed after 1 - 2 hours after the admission of patients, immediately after taking blood to bacteriological analysis. Before receiving the results of this analysis ( usually a few days) The patient takes the drug chosen empirically. The main requirement for it is wide spectrum actions. After determining the specific pathogen, the corresponding drug is prescribed.
Antibiotics used in the treatment of bacterial endocarditis
Revealed pathogen | Recommended drugs | Dosage preparations and reception mode |
Green Streptococcus ( Streptococcus Viridans) | Bezylpenicillin | 2 - 3 million units of the drug 6 times a day intravenously ( v / B.) or intramuscularly ( v / M.). The course of treatment lasts 4 weeks. |
Ceftriaxon | 2 g 1 time per day in / in or per / m for 4 weeks. | |
Ampicillin | 2 g 4 - 6 times a day in / in or per / m for 4 weeks. | |
Gentamicin | 3 mg per 1 kg of body weight ( if the patient does not suffer obese). It is introduced in / in or per / m 1 - 3 times a day. The course of treatment is 4 weeks. | |
Amoxicillin / Clawulanic Acid | 1.2 - 2.4 g 3 - 4 times a day in / in or per / m for 4 weeks. | |
Golden Staphylococcus ( Staphylococcus aureus) | Oxacillin | 2 g 6 times a day in / in or per / m within 4 - 6 weeks. |
Cefasoline | 2 g 3 - 4 times a day in / in or per / m within 4 - 6 weeks. | |
Imipenem | 0.5 g 4 times a day in / in or per / m for 4 - 6 weeks. | |
Vancomycin | 1 g 2 times a day in / in within 4 - 6 weeks. | |
Linezolid | ||
Enterococci ( Enterococcus) | Bezylpenicillin | 4 - 5 million units of the drug 6 times a day in / c for 4 - 6 weeks. |
Ampicillin | ||
Gentamicin | ||
Pneumococcus ( Streptococcus Pneumoniae) | Linezolid | 0.6 g 2 times a day in / c for 4 - 6 weeks. |
Cefotaxim | 2 g 6 times a day in / c for 4 - 6 weeks. | |
Levofloxacin | 0.5 g 1 time per day in / c for 4 - 6 weeks. | |
Pathogens from the group Hacek. | Ceftriaxon | 2 g 1 time per day in / c for 4 - 6 weeks. |
Ampicillin | 2 g 6 times a day in / c for 4 - 6 weeks. | |
Gentamicin | 3 mg per 1 kg of body weight 1 - 3 times a day in / c for 4 - 6 weeks. | |
Sinnaya stick ( Pseudomonas Aeruginosa) | Ceftazidim | 2 g 2 - 3 times a day in / c for 4 - 6 weeks. |
Fungal infections | Amicacin | 0.5 g 2 times a day in / c for 4 - 6 weeks. |
Meropem | 1 g 3 times a day in / c for 4 - 6 weeks. | |
Amphotericin B. | 0.5 mg per 1 kg body weight per day in / in. | |
Flucitozin | 100 - 200 mg per 1 kg of body weight per day in / c. |
To end the course of treatment and cancellation of antibiotics, compliance with the following criteria:
Further treatment is aimed at eliminating the actual inflammatory process. This use glucocorticosteroid drugs. The standard treatment diagram includes prednisone 20 mg per day. The drug is accepted after breakfast in one sitting inside ( in the form of a tablet). Glucocorticosteroid drugs are used in order to bring down acute inflammation with other forms of endocarditis. The main purpose of their reception is to prevent the formation of heart defect.
In addition to the antimicrobial and anti-inflammatory treatment, aimed at the causes that cause endocarditis, patients often prescribe a number of cardiac drugs. They help restore the pumping function of the heart and struggle with the first signs of heart failure.
To maintain normal operation of the heart in patients with chronic endocarditis, the following groups of drugs are used:
Indications for surgical treatment of endocarditis are:
Sanitation of the infectious hearth with endocarditis consists of three stages:
In the case of bacterial endocarditis, even an open surgical sorry of the heart does not always guarantee the complete destruction of infection. Therefore, surgical treatment in no way implies the abolition of a medication course of treatment. It is only a supplement to achieve a faster effect and correction of irreversible violations.
An important element of prevention is proper nutrition. Diet with endocarditis is not very different from a diet with any other cardiovascular disease ( diet number 10 and 10a). These power modes are aimed at reducing the load on the heart and the prevention of atherosclerosis. The latter can lead to a narrowing of coronary arteries and deterioration of myocardial oxygen.
Diet number 10 recommends limiting salt eating ( no more than 5 g per day), fatty and sharp products, alcohol. All these products directly or indirectly increase the load on the heart muscle and exacerbate heart failure.
Patients who have endured endocarditis either undergoing treatment is recommended to use the following products:
The main consequences and complications of endocarditis are:
This problem can be solved by implanting the artificial valve of the heart. If you have completely cured endocarditis, destroying the valve, the forecast for such patients remains favorable.
If the thrombus was formed in the right ventricular departments, it falls into a small circle of blood circulation. Here he gets stuck in the vascular network of the lungs, disturbing gas exchange. Without urgent help, the patient quickly dies. Such a tombalization of the tomb is called pulmonary artery thromboembolism.
If the thrombus is formed in the left hearts, it enters a large circle of blood circulation. Here it can be stuck in almost any part of the body, causing the corresponding symptoms. When blocking the arteries of internal organs or brain almost always there is a danger to the patient's life. If the artery is clocked in the limb, it can lead to the death of fabrics and amputation.
The most often clomes from the left ventricle lead to the blockage of the following vessels:
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Endocarditis - a disease that affects the inner sheath of the heart, as well as aortic and heart valves. This serious, threatening pathology is characterized by rapid development, the danger of the embolus of blood vessels, internal vital organs and the development of immunopathological processes.
Endocardits are divided into infectious (bacterial) and noncommunicable. Although in the overwhelming majority of cases, endocardits are infectious in nature, there are pathologies developing as a reaction to metabolic changes in the framework of the immunopathological process or with mechanical damage to the heart.
Unconfecting endocardits include:
Almost always, the above-mentioned diseases are an indicator that the risk of developing infectious endocarditis (IE) in these cases is extremely high, namely, it represents the greatest danger to the life of the patient.
The disease occurs infrequently, but recently there has been a steady tendency to increase the development cases of IE, which is associated with increasing resistance (resistance) of bacterial microflora to antibiotics as a result of mutations. Another reason for the growth of the number of septic endocarditis is an increase in the number of people taking intravenously narcotic substances.
Most often pathogenic gram-positive microorganisms are most often pathogens: in most cases it is staphylococcus, streptococcal, enterococcal infections. It is much less likely to develop other microorganisms, among which gram-negative bacteria may be, rare atypical pathogens and fungal infections.
The lesion of the heart shell during IE occurs with bacteremia. The concept of "infectious endocarditis" is synonymous with such definitions as septic or bacterial endocarditis. Bacteremia (the presence of blood bacteria) is capable of developing under favorable conditions even after the most innocuous procedures.
Treatment with high risk of development of bacteriamia are:
Cardiologists allocate risk groups with endocardium inflammation prerequisites for which antimicrobial therapy is necessary for endocarditis prophylaxis.
The high risk group includes:
The following categories of patients are subject to moderate risk:
Less than other dangers of developing this disease are patients with the following diagnoses:
The period from the penetration of infection to the development of the IE clinic is different - from several days to several months. It depends on the virulence of the pathogen, the state immune system Patient and Hearts.
Inside the cavity of the heart, the causative agent settles on the valve flaps and begins to grow, while colonies of microorganisms (vegetation) are formed. In addition to microorganisms, there are red blood cells, leukocytes, thrombocytes, fibrin. As infection develops, the surface of the valves is deformed, forming a bug surface or ulcers with thrombotic overlay.
When the deformation reaches significant sizes, heart valves lose the ability to clog tightlyWhat leads to the development of hemodynamic disorders and the emergence of acute heart failure. This condition develops rapidly and carries the danger to the life of the patient. From the destroyed valve, destroyed pieces of flaps, fragments of colonies of microorganisms can be broken. With the blood current, they are spread over a small and large circulation of blood circulation, they can cause ischemia of important organs and, which is accompanied by various neurological disorders, paresses and paralysis and other serious complications.
When diagnosing a diagnosis, the doctor should formulate a refined diagnosis characterizing the main features inherent in this type of disease, which allows you to make a more accurate and detailed idea of \u200b\u200bthe course of the disease.
There are also several types of flow and severity of the inflammatory process, taking into account the initial characteristics of damaged valves.
In addition, the disease is classified for the following types:
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