Distinguish between primary and secondary pericarditis, which arises as a complication of pathological processes in the myocardium, lungs, pleura, esophagus and other organs.
Depending on the characteristics of the clinical course, acute and chronic pericarditis are distinguished.
ETIOLOGY AND PATHOGENESIS
Acute pericarditis
Acute inflammation of the pericardium is most often of tuberculous origin, and also occurs with collagenosis. In surgical practice, secondary pericarditis occurs more often, which occurs in severe inflammatory diseases of neighboring organs or sepsis. Much less often, trauma is the cause of acute pericarditis.
Acute pericarditis can be divided into dry (fibrinous) and effusion - serous and purulent.
Primary purulent pericarditis occurs as a result of infection of the pericardium during wounds (open wounds, operations), secondary - as a result of the introduction of infection by lymphogenous (pleural empyema, mediastinitis, subphrenic abscess, etc.) or hematogenous (influenza, typhoid, tonsillitis, erysipelas, osteomyelitis, septicopyemia and others) by.
Serous-fibrinous exudate first turns into purulent with putrefactive infection with gas bubbles. Purulent exudate accumulates mainly behind the cardiac and transverse sinuses. As the exudate increases, the lateral part of the pericardium also fills. The amount of exudate varies between 100 g and 1 liter. Purulent pericarditis can occur as a complication of mediastinitis, pleurisy, disintegrating tumors of the lungs and esophagus. Hematogenous pericarditis occurs with osteomyelitis, pneumococcal pneumonia, diphtheria, etc.
Chronic pericarditis
Distinguish between chronic exudative (effusion) and constrictive (squeezing) pericarditis.
Chronic exudative (effusion) pericarditis
The most common cause of the disease is rheumatism.
Usually chronic pericarditis is the outcome of acute exudative pericarditis, less often from the very beginning it has a chronic course.
Chronic effusion pericarditis is characterized by a sharp thickening of the parietal layer of the pericardium, which undergoes a connective tissue degeneration, fuses with the surrounding tissues, becomes rigid and does not subside after repeated removal of the exudate.
The most common causes are tuberculosis,
less often nonspecific infectious diseases; pericarditis can also develop after suffering a chest injury, which was accompanied by the formation of hemopericardium.
Often the cause of the disease remains unclear.
Constrictive pericarditis is the final (sclerotic) stage of previously transferred fibrinous, serous-fibrinous or purulent pericarditis. As a result of the transition of the process to the phase of productive chronic inflammation, a fibrinous change occurs in the parietal and visceral layers of the pericardium. They thicken, grow together, lose elasticity and often calcify, the pericardial cavity is obliterated. The leaves can reach a thickness of 1.5-2.0 cm or more, forming a thick connective tissue carapace, which, due to the progressive shrinking of fibrous tissue, squeezes the heart ("carapace heart"). Pericardial adhesions can evenly cover all parts of the heart or be localized only in the apex, atrioventricular groove or the mouth of the vena cava. Simultaneously with intrapericardial adhesions, adhesions of the pericardium with the surrounding tissues also occur, which leads to the development of cicatricial mediastinopericarditis.
Mediastinopericardial adhesions fix the pericardium to the mediastinal pleura, lungs, ribs, spine, which significantly complicates the work of the heart and leads to even greater compression of it.
Intra- and extrapericardial adhesions, undergoing permanent cicatricial changes, gradually squeeze the heart and the openings of the vena cava and prevent normal heart contractions. To a greater extent, with constrictive pericarditis, the relaxation of the heart in the diastole phase is disturbed. This leads to difficulty in blood flow to the right heart, increased venous pressure and symptoms of stagnation in the systemic circulation. In most cases, the course of constrictive pericarditis is progressive. The patient's condition gradually deteriorates and over time they become disabled. Secondary irreversible changes develop in the myocardium and parenchymal organs, and patients die from heart or liver failure.
CLINICAL PICTURE
Fibrinous ("dry") pericarditis
This pericarditis is characterized by fibrin deposits on the visceral and parietal layers of the pericardium.
The disease proceeds with a slight and short-term increase in body temperature, pain in the region of the heart, which intensifies with a deep breath; cough; moderate tachycardia and rapid breathing.
The main symptom of fibrinous pericarditis is pericardial friction murmur. The noise is rough in nature, synchronous with heartbeats, and intensifies when the patient bends forward. Unlike pleural murmurs, it does not disappear when the breath is held. On the phonocardiogram, pericardial friction noise is recorded in both phases of the cardiac cycle. On the electrocardiogram, an upward shift of the S-T interval in I and II standard and chest leads, deformation of the T wave, which indicate circulatory disorders in the subepicardial layers of the myocardium, are found. The outcome of the disease is favorable, but acute fibrinous pericarditis is often the initial stage of other forms of the disease.
Pericardial effusion
It is customary to refer to effusion pericarditis as serous pericarditis and purulent pericarditis.
Serous pericarditis, along with inflammatory changes in the visceral and parietal sheets, is characterized by the formation and accumulation of serous or serous-fibrinous exudate in the pericardial cavity.
The main symptoms of the disease are pain in the region of the heart and shortness of breath. The pains are acute, increasing in intensity, radiating to the back and shoulder area.
Because of the pain, the patient takes a forced anteriorly bent position. As a result of compression by the pericardial exudate of the esophagus, recurrent and phrenic nerves, difficulty in swallowing, hiccups, and hoarseness may occur. Examination reveals moderate cyanosis, swelling of the intercostal spaces in the heart. The apical impulse is weakened or not palpable. When a significant amount of effusion (over 300 ml) accumulates in the pericardium, an expansion of absolute cardiac dullness is noted. Heart sounds become muffled, pericardial rubbing may persist.
X-ray and ultrasound studies reveal the expansion of the shadow of the heart, the contours of which acquire a triangular or spherical shape, the accumulation of inflammatory fluid in the pericardial cavity, and a decrease in the mobility of the contours of the heart. On the electrocardiogram, as it accumulates, a decrease in the voltage of the QRS complex, a change in the ST interval and deformation of the T wave are determined. In laboratory studies, an increase in the number of neutrophilic leukocytes, an increase in ESR are found. The course of acute exudative, including serous, pericarditis is less favorable than fibrinous. With the rapid accumulation of a large amount of exudate in the pericardial cavity, a severe picture of cardiac tamponade may develop. Clinically, it is manifested by increasing tachycardia, a decrease in blood pressure, severe cyanosis, swelling of the cervical veins, and an enlarged liver.
Purulent pericarditis
The disease has the same manifestations as any other pericardial effusion. However, the course of purulent pericarditis is more severe. Symptoms of intoxication and severe circulatory disorders predominate. High temperature of an intermittent nature, a feeling of heaviness and pain in the heart region, tachycardia, shortness of breath, general weakness. Most often, purulent pericarditis is a complication of another underlying disease, which masks its clinical picture. An increase in purulent exudate causes symptoms of compression with cardiac abnormalities. Cyanosis, stagnation of blood in the veins of the neck and sometimes enlargement of the liver appear. Pulse is small, quickened, blood pressure drops. Pains appear in the epigastric region, often accompanied by peritonism.
Chronic pericarditis
The most common symptoms of the disease are shortness of breath, stitching pains in the region of the heart, and palpitations. When examining the patient, a slight cyanosis, moderate swelling of the face, neck, upper extremities, swelling of the cervical veins is noted. These symptoms occur after prolonged lying on the back. In this position, greater compression of the superior vena cava occurs. The apical impulse disappears or is weakened. Percussion determines a significant expansion of the area of heart dullness.
Heart sounds are muffled. The pulse in patients is usually quickened. Systemic arterial pressure is reduced, and venous pressure is increased. In some patients, an enlarged liver, a slight ascites is noted.
X-ray and ultrasound studies reveal a significant expansion of the shadow of the heart, a decrease in the amplitude of heart contractions. The electrocardiogram shows a decrease in the voltage of the ventricular complex. The course of the disease is remitting. Periods of deterioration are followed by periods of relative well-being.
Increased dullness of the heart, dull tones of rhythm disturbance, typical ECG, general septic phenomena indicate purulent pericarditis. Pericardial friction is sometimes heard. With a large amount of exudate, it is impossible to establish a heartbeat. For the purpose of differential diagnosis with other forms of pericarditis, diagnostic punctures of the pericardium are performed. The most expedient punctures of Larrey and Marfan. The puncture is performed from the epigastric region under the xiphoid process to the pericardium.
Constrictive (compressive) pericarditis
Patients complain of a feeling of compression in the region of the heart, shortness of breath, general weakness. On examination, moderate cyanosis, enlargement of the saphenous veins, an increase in the abdomen (ascites), and edema in the legs are noted. Often, retraction of the intercostal spaces during ventricular systole, expansion and pulsation of the veins of the neck, associated with the presence of extrapericardial adhesions in the patient, are detected. The pulse is usually of weak filling and tension, often paradoxical: on inhalation, the filling of the pulse decreases, and on exhalation, it increases. This indicates a sharp decrease in the diastolic filling of the right heart. Patients have atrial fibrillation. The borders of the heart, as a rule, are not expanded, the apical impulse is not defined. Heart sounds are muffled. No noise. The liver is congested, significantly enlarged. Ascites is determined in the abdominal cavity. Systemic blood pressure is lowered. Constrictive pericarditis is characterized by a persistent increase in venous pressure, the value of which can reach 300-400 mm of water column. In biochemical blood tests, a decrease in the content of total blood plasma protein to 20 g / l is determined.
On x-ray examination, the heart has the usual size and clear contours. The first arch along the right contour of the heart is enlarged due to the bulging of the superior vena cava. Often there are deposits of lime in the pericardium in the form of separate islands or a solid plate. With ultrasound Doppler cardiography and roentgenokymogram, a decrease in the amplitude of the teeth of the heart contractions is revealed; in the pleural cavities moderate effusion. On the electrocardiogram, a significant decrease in the voltage of all teeth is recorded, a negative T wave.
Ultrasound scanning of the heart reveals a different thickness of pericardial adhesions over different parts of the heart, areas of calcification in the thickness of the myocardium, atria and ventricles. Similar results are obtained with computed and magnetic resonance imaging. Constrictive pericarditis is characterized by the presence of signs of a decrease in the diastolic filling of the heart: a sharp and rapid decrease in intracardiac pressure at the beginning of diastole, followed by a rapid increase and the formation of a "plateau" at the level of 30-40 mm Hg. Art.
Differential diagnosis should be carried out with exudative pericarditis, heart defects, myocarditis and extracardiac diseases, accompanied by circulatory decompensation in a large circle (portal hypertension, mediastinal tumors).
TREATMENT
Acute pericarditis
In acute forms of the disease, in most cases, conservative treatment is carried out, analgesics and heart drugs, broad-spectrum antibiotics, oxygen therapy, and diuretics are prescribed. According to indications, specific and non-specific anti-inflammatory therapy is carried out. With purulent pericarditis and the threat of cardiac tamponade, pericardial punctures are performed in order to evacuate exudate and administer antibacterial drugs. Usually, the puncture of the pericardium is performed in the left costo-xiphoid angle. After infiltration anesthesia, the skin and soft tissues are pierced to a depth of 2.0-2.5 cm. The needle is advanced along the posterior edge of the sternum by 3-5 cm and the pericardium is reached. After puncturing the pericardium, the syringe plunger is slightly pulled out, controlling the contents. If repeated punctures are ineffective, pericardiotomy is performed: after resection of the seventh costal cartilage, the parietal layer of the pericardium is widely dissected; pus is aspirated, the pericardial cavity is washed and drained.
Even in cases of a favorable course of purulent pericarditis, a transition to a chronic form of the disease is often observed.
Chronic pericarditis
Treatment of chronic pericarditis is surgical. The operation of choice is subtotal pericardiectomy, which is performed from a longitudinal sternotomy. The operation consists in radical removal of the altered pericardium. To do this, the modified pericardial layers are separated from the left ventricle, the anterior surface of the heart and the right atrium. Isolation from the fusion of the aorta, pulmonary artery and the mouth of the hollow veins is mandatory. During the operation, care should be taken due to the possibility of injury to the myocardium and coronary arteries. In the area of adhesions with the coronary arteries, it is permissible to leave areas of the calcified pericardium in the form of isolated islets.
The positive effect of radical pericardiectomy occurs already in the immediate postoperative period. In the long term, 90% of operated patients return to normal work activities.
- infectious inflammation of the serous membrane of the heart, accompanied by the formation of purulent effusion in the pericardial sac. Purulent pericarditis occurs with severe symptoms of intoxication (chills, fever, torrential sweats, lack of appetite) and hemodynamic disturbances (shortness of breath, cyanosis, palpitations and pain in the heart). The diagnosis of purulent pericarditis is established by X-ray examination, echocardiography, pericardial puncture. Treatment for purulent pericarditis includes antibiotic therapy, pericardial drainage, or pericardiectomy.
Purulent pericarditis is a bacterial exudative pericarditis characterized by the accumulation of purulent exudate in the pericardial sac. Purulent pericarditis is often secondary in nature and complicates the course of a number of diseases in cardiology, pulmonology, gastroenterology, and traumatology. Purulent pericarditis is 7.4-8.8% of all pericarditis. Currently, the incidence of purulent pericarditis has significantly decreased, which is mainly associated with the widespread use of antibiotics. Meanwhile, the mortality rate for purulent pericarditis is extremely high.
With purulent pericarditis, exudate can fill the entire pericardial cavity, but more often it is enclosed in one or more sinuses. The amount of purulent exudate with pericarditis can range from 100 ml to 1 liter.
Causes of purulent pericarditis
Purulent pericarditis, as a rule, is secondary in nature and is a consequence of the spread of a primary infection of any localization. In most cases, purulent pericarditis develops in patients with pleural empyema, mediastinitis, pneumonia, lung abscess, subphrenic abscess, myocarditis, infective endocarditis. In these cases, there is a contact spread of the infection to the pericardium from adjacent anatomical regions.
Metastatic (hematogenous and lymphogenous) purulent pericarditis occurs in patients with osteomyelitis, peritonitis, erysipelas, sore throat, diphtheria, odontogenic phlegmon of the oral cavity, peritonsillar abscess, periodontal disease, soft tissue abscess, sepsis. With some viral infections (influenza, chickenpox, measles), a decrease in the body's immunobiological reactivity leads to the addition of a bacterial infection and the development of purulent pericarditis of a coccal nature.
Purulent pericarditis can be a complication of pericardial puncture, thoracic and cardiac surgery, gunshot and stab wounds to the heart. In the literature, there is information about the occurrence of bacterial pericarditis against the background of an abdominal aortic aneurysm of mycotic etiology, esophageal cancer, as a result of the Nissen fundoplication operation, gastric resection, etc.
The most common pathogenic causing purulent pericarditis remains Staphylococcus aureus (22–31% of cases). Less common are purulent pericarditis caused by streptococci, pneumococci, proteus, enterococcus, klebsiella, mycoplasma, tuberculosis microbacterium, gonococcus. Among the anaerobic pathogens, prevotella, peptostreptococcus, propionic bacteria, acne, etc. are detected.
Pathogenesis of purulent pericarditis
Pathomorphological changes in pericarditis pass through the stages of fibrinous, serous, and purulent inflammation. With moderate exudation, the absorption capacity of the pericardial sheets is preserved, therefore, changes in the pericardium are characterized by hyperemia, swelling and desquamation of the mesothelium, loss of fibrin between the pericardial sheets. When trying to separate the pericardium from the epicardium, fibrinous cords create the phenomenon of a "hairy" or "villous" heart.
With significantly pronounced exudative processes in the pericardial sac, serous effusion initially accumulates, containing fibrin flakes, desquamated mesothelium, and blood cells. When the contents of the pericardium are infected, at the stage of purulent pericarditis, pathogenic microorganisms, protozoa, fungi, etc. are additionally found in the effusion.
At the stage of organizing effusion and subsequent scarring, calcification and ossification of scar tissue may occur, which leads to immobilization of the heart. Cicatricial changes can affect not only the pericardium and epicardium, but sometimes the whole heart, spreading to the endocardium ("armored heart"). Scarring and calcification of the layers of the pericardium and epicardium limits the strength and amplitude of heart contractions; under these conditions, the pumping function of the heart is carried out only due to the movements of the interventricular septum (constrictive pericarditis).
Symptoms of purulent pericarditis
The predominant syndromes in the clinic of purulent pericarditis are intoxication and severe hemodynamic disturbances. The grave condition of patients is aggravated by manifestations of the primary focus of infection.
Almost all patients with purulent pericarditis have hectic fever, tremendous chills, general weakness, weakness, torrential sweats, and lack of appetite. As purulent exudate accumulates in the pericardial cavity, symptoms of cardiac dysfunction appear: cyanosis, shortness of breath, tachycardia, a feeling of heaviness and pain in the heart. Pain can radiate to the left arm, resembling a clinic for angina pectoris. The excruciating shortness of breath forces the patient with purulent pericarditis to take a half-sitting position, which makes breathing easier.
Compression syndrome caused by compression of blood vessels, trachea and esophagus manifests itself in swelling of the veins of the neck, coughing, and dysphagia. The obstruction of venous circulation is accompanied by a cooling of the skin of the head, neck, upper body, and upper extremities.
With purulent pericarditis, cardiac tamponade occurs early, characterized by arterial hypotension, an increase in venous pressure, the appearance of pressing pains in the heart, in the epigastric region, an increase and severe soreness of the liver, and a feeling of fear of death. With cardiac tamponade, a critical drop in cardiac output leads to cerebrovascular accident; in this case, only an urgently undertaken unloading of the pericardial cavity from exudate can save the patient's life. The incidence of cardiac tamponade with purulent pericarditis varies from 42 to 80%.
The outcome of purulent pericarditis may be adhesive or fibrous pericarditis, requiring pericardiectomy.
Diagnostics of the purulent pericarditis
Examination of a patient with purulent pericarditis reveals swelling of the superficial tissues of the precordial region, a network of venous collaterals on the chest, soreness in the epigastric region, and an enlarged liver. Auscultation reveals a pericardial friction noise, deafness of heart sounds; percussion is determined by an increase in cardiac dullness in the form of a triangle. The pulse is quickened, weak, blood pressure is reduced. Changes in the general blood test are characterized by signs of pronounced inflammation - neutrophilic leukocytosis, high ESR.
In chest X-ray, an intense triangular shadow in the heart region is determined, due to the filling of supraphrenic and anteroposterior turns of the pericardial cavity with pus.
An informative instrumental examination method for purulent pericarditis is echocardiography, which makes it possible to detect even a small amount of effusion in the pericardial cavity, to determine the signs of cardiac tamponade. With the help of echocardiography with a high degree of accuracy, it is possible to judge the purulent nature of the exudate by the presence of hyperechoic inclusions, flakes, suspension, intrapericardial cords, thickened pericardium. Of great importance in the diagnosis of purulent pericarditis are computed and magnetic resonance imaging of the heart.
The final diagnosis of purulent pericarditis is confirmed by puncture of the pericardium. In order to prevent heart injury, puncture is carried out under the control of ultrasound and electrocardiogram. In the process of pericardiocentesis, a thick, turbid exudate is obtained, containing many neutrophilic leukocytes, fibrin, protein, and often bacteria. To clarify the etiology of purulent pericarditis, a culture study of the effusion is performed.
Differential diagnosis of purulent pericarditis is carried out with left-sided exudative pleurisy and expansion of the borders of the heart.
Treatment of purulent pericarditis
Purulent pericarditis is treated in a specialized cardiac surgery hospital. In the acute phase, conservative measures are taken: antibiotics are prescribed, taking into account the sensitivity of the pathogen, symptomatic therapy is carried out (analgesics, heart drugs, diuretics, oxygen therapy).
Patients with purulent pericarditis undergo therapeutic punctures or percutaneous drainage of the pericardium in order to evacuate purulent effusion. Along with systemic antimicrobial therapy, intrapericardial administration of antibiotics and enzymes (urokinase, streptokinase) is carried out.
In the absence of an effect from the conservative management of purulent pericarditis, the issue of surgical drainage is resolved - pericardiotomy, which allows emptying the pericardial cavity from pus. In the presence of dense adhesions, localized purulent effusion, repeated cardiac tamponade, persistent infection, pericardiectomy is indicated.
Prediction and prevention of purulent pericarditis
In the absence of special treatment, purulent pericarditis in 100% of cases is fatal due to cardiac tamponade and intoxication. Drug treatment of purulent pericarditis is accompanied by the death of patients in 66-82% of cases. An integrated approach to the management of purulent pericarditis in a specialized cardiac surgery hospital can reduce mortality rates to 20-36%. In connection with the subsequent constrictive pericarditis, heart failure often develops in the future. Patients who have undergone purulent pericarditis require the supervision of a cardiologist and cardiac surgeon.
Prevention of purulent pericarditis requires the prevention and timely treatment of diseases complicated by inflammation of the pericardium (tonsillitis, purulent diseases of the lungs, pleura, mediastinum), adherence to surgical techniques for operations on the chest cavity, proper treatment of heart and pericardial wounds.
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Purulent pericarditis
Purulent pericarditis- the disease is mainly secondary, which complicates purulent pleurisy, mediastinitis, lung abscess, peritonitis, osteomyelitis, erysipelas, etc., as well as rheumatism, sore throat, gonorrhea, tuberculosis. It can be a complication of intra-thoracic operations, pericardial puncture.The causative agents of purulent pericarditis can be any pyogenic microorganisms, but more often it is staphylococcus, proteus, pneumococcus. Specific pericarditis can be caused by gonococcus, tuberculosis microbacteria, etc. Infection of the pericardium is possible by contact, lymphogenous and hematogenous pathways.
Pathological changes in the pericardium develop in a certain sequence. At first, the inflammation is non-suppurative, a transparent serous effusion is formed, which later becomes serous-fibrinous. Then the effusion can turn into purulent, purulent pericarditis develops. Due to the constant trauma of the inflamed pericardium, small blood vessels are damaged during contractions of the heart, the effusion can become hemorrhagic.
The myocardium is involved in the inflammatory process, its edema develops. When the inflammation is eliminated, the fibrin that has fallen on the pericardium is organized and intrapericardial adhesions, adherent pericarditis, armored heart are formed.
The clinical manifestations of purulent pericarditis are determined by serious disturbances in the work of the heart, caused by compression of it with pus and general intoxication.
With a small amount of inflammatory exudate in the heart shirt, there are usually no signs of compression of the heart; the accumulation of large amounts of exudate leads to the development of subjective and objective signs, palpitations, pain in the region of the heart, feelings of heart compression and fear. The pain often radiates to the left arm and is very similar to pain in angina pectoris. The pulse becomes weak, irregular, intermittent. Shortness of breath, cyanosis and swelling of the veins of the neck develop.
With further accumulation of fluid in the pericardial cavity, a cough appears, difficulty swallowing, which is associated with compression of the trachea and esophagus. Because of the painful shortness of breath, the patient takes a forced position, which makes breathing easier: he usually half-sits, the auxiliary respiratory muscles are involved in the act of inhalation, and the intercostal spaces are drawn in.
In connection with a sharp obstruction of the venous circulation, not only cyanosis is observed, but also a cooling of the upper body, neck, head.
Percussion noted an increase in cardiac dullness, which takes on a triangular shape, which is associated with the filling of the cavity of the cardiac sac and both supraphrenic and anterior-non-superior turns of it with exudate.
In the early stages of development of pericarditis, a pericardial friction noise is heard, which disappears after the accumulation of exudate in the heart bag. By this time, the deafness of the heart tones increases and becomes pronounced. The impulse is not defined or is detected inward from the left border of the cardiac dullness.
In addition to the listed signs associated with the accumulation of exudate in the heart shirt, symptoms caused by purulent intoxication are noted: high fever, often with chills, leukocytosis with a predominance of neutrophils, weakness, lack of appetite, etc.
X-ray examination determines an intense triangular shadow in the heart area, which confirms the accumulation of fluid in the heart bag.
Echocardiography allows you to determine the fluid in the pericardium, its volume, density, the presence of impurities, fibrin deposits on the inner surface of the pericardium and on the outer surface of the myocardium. Certain information is provided by an electrocardiographic study.
Puncture of the pericardium clarifies the diagnosis of purulent pericarditis.
With exudative pericarditis, fluid accumulates in the heart bag on the sides, especially on the left, behind and below the heart. The exudate deflects the heart anteriorly, it is tightly attached to the sternum and costal cartilage. In this regard, there is a significant risk of heart damage during puncture of the pericardium through the intercostal spaces, and with a small amount of effusion, the pleura, intrathoracic artery or vein can be damaged. Puncture under ultrasound control avoids complications.
Puncture according to Marfan is performed under local anesthesia. The needle is inserted at the base of the xiphoid process and advanced obliquely up the posterior surface of the sternum to the pericardium. Reverse movement of the syringe plunger determines the puncture of the pericardium and the presence of pus in the heart bag, which is removed. Puncture ends with the introduction of antibacterial drugs.
a - at the base of the xiphoid process; b - through the fifth intercostal space along the parasternal line
Puncture of the pericardium according to Marfan, if necessary, allows you to completely remove fluid from the heart bag and introduce a microirrigator.
With pericardial punctures, it should be remembered that the main amount of fluid in exudative pericarditis accumulates behind the heart in the lower parts of the cardiac sac, and the heart is always adjacent to the posterior surface of the sternum.
Based on clinical data, the results of X-ray examination and ultrasound, exudative pericarditis is diagnosed. Obtaining pus during puncture of the pericardium confirms the diagnosis of purulent pericarditis.
Purulent pericarditis must be differentiated with left-sided exudative pleurisy, which displaces the heart to the right, and with expansion of the heart. A significant role in differential diagnosis belongs to multi-axis X-ray examination, ultrasound. According to the indications, a trial puncture is done. With a history of expansion of the heart, there are indications of prolonged heart disease, leading to expansion of the heart.
Data of auscultation (muffled tones with pericarditis), X-ray examination, echocardiography are also important. In contrast to the expansion of the heart, with purulent pericarditis, symptoms of purulent intoxication are observed. With the expansion of the heart, the heart beat is determined along the outer border of dullness, with pericarditis it is not defined at all or is noted inward from the left border of dullness.
Treatment
In connection with the use of antibiotics, the treatment of purulent pericarditis has become more successful.Patients are given a semi-sitting position, complete rest is provided, oxygen therapy, antibiotic therapy are performed, and cardiac drugs are prescribed according to indications.
A test diagnostic puncture of the pericardium in case of receiving pus immediately turns into a therapeutic one, i.e. pus is completely removed from the pericardium and an antiseptic solution is injected through the same needle.
The lack of success after 3-4 therapeutic punctures of the pericardium raises the question of pericardiotomy. The operation allows you to completely empty the pericardium from pus, but is always fraught with the danger of secondary infection. Pericardiotomy is indicated only if conservative treatment is unsuccessful. The task of pericardiotomy is to ensure a constant outflow of pus through the lowest point of the heart bag.
Pericardiotomy
Intercostal approaches for opening and draining the pericardium in purulent pericarditis are not shown, since the narrowness of the operating field creates a risk of damage to the internal thoracic artery, vein or pleura, and in the postoperative period, adequate drainage is not provided. These disadvantages can be avoided by using approaches with resection of one or more ribs and opening the bursa in its lowest section.The operation can be performed under local infiltration anesthesia.
Kocher's method
An oblique skin incision 6-7 cm long is carried out from the middle of the sternum along the VI rib. The soft tissues are infiltrated with a solution of novocaine, the perichondrium is dissected and exfoliated along the incision, the wedge-shaped portion of the cartilage at the edge of the sternum is excised, the perichondrium is exfoliated along the posterior surface with a rasp, a portion of cartilage 3-4 cm long is resected. vessels.With a Kocher probe, the transverse muscle of the chest is carefully peeled off, which is loosely connected with the pericardium and is easily separated. The muscle is pushed outward along with the pleura. Two clamps capture the pericardium, bring it into the wound and open the cavity, aspirate pus, install a soft drainage tube to remove pus and administer antiseptics in the postoperative period. The drainage tube is fixed to the skin incision. The wound is sutured before drainage.
The Mints method is most widespread at the present time, since it provides the most favorable conditions for the drainage of both halves of the cardiac sac in case of purulent pericarditis.
The operation is performed under infiltration anesthesia.
An incision 7-8 cm long is made from the base of the xiphoid process of the sternum along the VII rib on the left. The perichondrium is exposed, dissected along the rib and separated from the cartilage, which is resected at an area of 5-6 cm. The posterior wall of the perichondrium is carefully dissected, the internal thoracic vessels are tied and transected.
Exfoliating soft tissues, the diaphragm is pushed backward and downward, and in the inner corner of the wound, the fatty tissue covering the pericardium is exposed. Having stratified the fiber, the pericardial cavity is punctured and the heart bag is opened through the needle, the pus is removed and then drained.
Postoperative treatment, including antibiotic therapy, is carried out according to the general rules.
Complications with purulent pericarditis can be observed in the course of its development (heart weakness, sepsis, etc.), as well as after healing due to scars and adhesions between the myocardium and pericardium, which sharply complicates the activity of the heart.
With purulent pericarditis, the prognosis is always serious. Despite the significant success of treatment, which made it possible to sharply reduce the immediate mortality, subsequently, in connection with adhesive pericarditis, severe cardiovascular failure often develops. All survivors of acute purulent pericarditis should be under dispensary supervision. When signs of compressive pericarditis appear, they should be referred for surgical treatment.
Prevention of purulent pericarditis consists in the timely and correct treatment of heart and pericardial wounds and in the prevention and successful treatment of diseases, the complication of which is purulent pericarditis (tonsillitis, purulent diseases of the lungs, mediastinum, pleura).
Heart abscess
Heart abscess is a rare form of purulent surgical infection. This is a limited accumulation of pus with morphological signs of an abscess localized in the thickness of the heart muscle, under the epicardium or in the fibrous tissues of the valve apparatus. The most common localization of abscesses is the fibrous ring of the aortic valve. Treatment methods for this type of cardiac pathology are presented in the works of Yu.L. Shevchenko.The causative agents of the infectious process in the heart are streptococcus, staphylococcus, proteus, etc., almost the entire spectrum of pyogenic microflora. Heart abscess is of secondary origin: the source of infection is bacterial vegetation on the heart valves and endocardium. The infection spreads by contact or by embolism in the coronary arteries.
The second place in importance and frequency among the causes of heart abscesses is occupied by infected artificial valves, pacemaker electrodes, ligature abscesses.
A less significant part of the sources of heart infection are purulent-inflammatory foci in neighboring tissues - in the pericardium, mediastinum. Microflora in such cases is spread by contact.
It is possible to spread the infection from distant purulent foci by a hematogenous route, as in septicopyemia.
Introduced blood clots with many virulent microorganisms cause inflammation of the surrounding tissues. The severity of the inflammatory reaction is determined not only by bacterial contamination, but also by circulatory disorders in the area of microthrombi. The inflammatory reaction is typical: serous tissue edema, leukocyte infiltration, accumulation of inflammatory mediators, cytokines, macrophage reaction.
The transition of inflammation from the serous phase to the destructive phase determines tissue necrosis under the influence of bacterial toxins, circulatory disorders due to microcirculation disorders, and the formation of microthrombi. Foci of destruction are surrounded by infiltrated tissues with the formation of a pyogenic capsule and the formation of granulations. This usually occurs in the first 2 weeks of abscess formation, and after 4-5 weeks a chronic abscess is formed. Heart abscesses are sometimes multiple, they are small - 1-1.5 cm, rarely reach a diameter of 4-5 cm.
Clinical manifestations and diagnosis
Heart abscesses do not have pathognomonic signs. The manifestations of the disease consist of general signs of purulent inflammation - fever, chills, signs of intoxication, leukocytosis, shift of the leukocyte count to the left, increased ESR, signs of heart failure, development of heart failure (tachycardia, arrhythmia, various types of heart murmurs).Consider changes in the physical manifestations of heart disease that existed before the appearance of signs of purulent inflammation, the addition of heart failure. Initial signs of a severe purulent disease are possible, followed by manifestations of heart failure. This condition of the patient allows only to suspect an abscess of the heart (purulent myocarditis).
A similar clinical picture, the course of the disease requires the use of special research methods. Ultrasound of the heart using esophageal sensors, MRI give certain information about changes in the heart, help to visualize the area of formed abscesses. In this regard, the resolution of CT is insufficient. The results of instrumental studies allow one or another to suspect a heart abscess.
With conservative therapy of heart abscess, mortality reaches 100%. Indications for surgery were formulated by Yu.L. Shevchenko and SA Matveev (1996): "With a sufficiently substantiated suspicion of abscess formation in the heart, there is an absolute indication for surgical treatment ...".
Treatment
Treatment of patients with heart abscess is carried out in cardiac surgery clinics. As a rule, due to the difficulty of diagnosis, patients receive massive empiric antibiotic therapy for a long time.The operation is performed in conditions of artificial circulation, a right-sided anterolateral approach is used because of the risk of developing purulent complications associated with sternotomy. Artificial blood circulation is used to sanitize the cavities of the heart, blood vessels; a daily dose of broad-spectrum antibiotics is added to the perfusate. Sanitation of purulent foci is carried out on an open heart by mechanical removal of pus, necrotic tissues, vegetation with washing purulent foci with a solution of antiseptics. Ultrasonic cavitation increases the efficiency of sanitation.
The prognosis for cardiac abscesses is always serious, postoperative mortality reaches 30%.
Pericarditis is an acute or chronic inflammation of the bursa pericardium.
Pericarditis is rarely observed as an independent nosology, usually it occurs as a complication of various non-infectious and infectious diseases, intoxications or injuries.
Etiology
In the development of pericarditis, a variety of infectious and non-infectious factors can be important, which can be divided into several groups (see classification by etiology).
Pathogenesis
Up to 1 liter of effusion can accumulate in the pericardial cavity in a short or long time. Fluid accumulation and decreased pericardial compliance due to abnormal effusion result in decreased ventricular filling during diastole. Consequently, diastolic pressure rises, which entails the appearance and growth of systemic venous congestion. In addition, the hydrostatic pressure in the capillaries becomes equal to the osmotic pressure, leading to the appearance of extravasation of blood plasma from the capillaries into the surrounding tissues, which manifests itself on the periphery by edema and ascites.
With pericarditis, pathological changes will be expressed mainly in the systemic circulation, while the small circle remains intact.
The rapid accumulation of fluid in the pericardial cavity causes a sharp increase in pressure in the ventricles, atria and veins, a drop in stroke output and blood pressure, and the development of a clinic for cardiac tamponade. In this case, severe tachycardia, shortness of breath, hypotension are observed, the filling of the pulse decreases. Determination of the paradoxical pulse is of decisive importance in the diagnosis of cardiac tamponade, when on inhalation the left parts of the heart become empty and the filling of the pulse decreases.
In cases of constrictive pericarditis, there is a gradual thickening and fusion of the pericardial sheets, relaxation of the heart in the diastole phase is limited, which leads to an increase in diastolic pressure in the ventricles, and then to an increase in venous pressure in the systemic circulation. These pathological changes lead to the development of disorders in the pulmonary circulation (dyspnea and orthopnea), and then to congestion in the large circle (peripheral edema, ascites, pleural effusion, hepatomegaly).
Classification
Etiological classification (EE Gogin, 1979).
1. Infectious:
1) rheumatic;
2) tuberculous;
3) bacterial (non-specific - coccal, including pneumonia and septic; specific - with typhoid fever, dysentery, cholera, brucellosis, anthrax, plague, tularemia);
4) caused by protozoa;
5) fungal (aspergillus, blastomycetes, coccidioidomycetes);
6) viral (Coxsackie viruses, adenoviruses, influenza viruses, parainfluenza, ECHO);
7) rickettsial.
2. Aseptic pericarditis:
1) allergic (the causes are serum sickness, drug allergy);
2) with diffuse connective tissue diseases (rheumatoid arthritis, systemic lupus erythematosus, rheumatism);
4) with malignant tumors (primary, metastatic);
5) traumatic, including postoperative (the reasons are pericardotomy, chest trauma);
6) ionizing radiation and X-rays (massive X-ray therapy);
7) postinfarction (episthenocardial myocardial infarction and postinfarction syndrome);
8) caused by metabolic disorders (with gout, amyloidosis, chronic renal failure with uremia, severe hypothyroidism);
9) caused by taking medications (novocainamide, cromolyn, hydralazine, heparin, indirect anticoagulants, glucocorticoids);
10) hypovitaminosis C.
3. Idiopathic pericarditis.
Clinical classification (Z.M. Volynsky).
1) dry (fibrinous);
2) exudative (effusion) - serous-fibrinous, hemorrhagic, purulent, putrid, cholesterol;
1) effusion;
2) adhesive:
a) asymptomatic;
b) with functional disorders of cardiac activity;
c) with lime deposition ("carapace heart");
d) with extrapericardial adhesions; 3) constrictive pericarditis.
Clinic and diagnostics
The symptomatology of pericarditis depends on various factors, including its type, the rate of accumulation of exudate in the pericardial cavity, the localization and prevalence of the adhesive process, etc.
In the acute phase of the underlying disease, fibrinous, or dry, pericarditis is usually noted. Over time, the symptoms change and dry pericarditis turns into effusion.
Dry pericarditis
sometimes does not show itself in anything.
However, some patients at the beginning of the development of the disease complain of dull (or aching), constant pain in the heart. More often the pains are of moderate intensity, but sometimes they are significantly pronounced and radiate to the neck, epigastrium, left shoulder blade and left arm, resembling an attack of angina pectoris. Less commonly, patients may complain of palpitations, shortness of breath, dry cough, general malaise, weakness, lethargy, chills.
A characteristic feature of pericardial pain is its dependence on breathing, movements, changes in body position. The patient spares himself, does not take deep breaths, but breathes often and shallowly. There may be a forced position on the right side.
On examination, pain is noted when pressing over the sternoclavicular joint and at the base of the xiphoid process, that is, in the places of the superficial location of the phrenic nerve.
At the initial examination of the patient, listening to the pericardial friction noise is of greatest importance for the diagnosis of dry pericarditis. At the height of pain, the noise of friction is gentle, short. However, over time, with an increase in the layer of fibrinous deposits on the surface of the inner layer of the pericardium, the pain gradually decreases, and the noise, on the contrary, becomes more coarse, audible over the entire region of the heart. In some cases, the friction noise can be short-term and can only be heard for a few hours. The friction murmur is always limited to the zone of absolute dullness of the heart or is localized in some part of it and is heard synchronously with the heartbeats.
An important diagnostic sign of pericardial friction noise in pericarditis is its poor conductance, as well as variability in time and often dependence on the phases of respiration. The frictional noise of the pericardium can increase when pressed by the head of the phonendoscope, as well as when the position of the patient's body changes.
Effusion (exudative) pericarditis
is, as a rule, the stage of development of the disease following dry pericarditis. Sometimes the accumulation of effusion in the pericardial cavity can occur, bypassing the stage of dry pericarditis. This is possible with rapidly beginning total pericarditis (allergic) and with primary chronic "cold" (tuberculous, tumor). With a slow accumulation of fluid in a significantly enlarged pericardial cavity, the sternocostal surface of the heart and its apex retain contact with the parietal leaf of the serous pericardium or are separated from it by a thin layer of fluid. In these cases, the rubbing noise of the pericardium disappears gradually. The apical impulse of the heart remains, but shifts upward from the lower and inwardly from the left border of cardiac dullness due to the accumulation of fluid in the pericardium.
As a result of a sharp movement of the heart in the systole phase, echocardiography is determined by the displacement of the mitral valve leaflets, which can be mistaken for prolapse. After removal of fluid from the pericardium, these changes disappear.
With effusions of a large volume, percussion is determined by the expansion of the boundaries of cardiac dullness in all directions: to the left in the lower sections to the anterior and even middle axillary line, in the II and III intercostal spaces - to the mid-clavicular line; to the right in the lower parts (V intercostal space) - to the right mid-clavicular line, in the II-IV intercostal spaces - somewhat less, but also lateral to the right parasternal line.
When viewed in the epigastric region, there may be swelling due to large effusion and enlargement of the liver. The boundaries of cardiac dullness change depending on the position of the patient's body: in the standing position, the zone of dullness in the II and III intercostal spaces decreases by 2-4 cm on each side, and in the lower intercostal spaces it expands by the same amount. Dullness over the region of the heart with exudative pericarditis is much more intense than usual.
Auscultation with pericardial effusion, heart sounds can remain clear and well audible even when a large amount of fluid accumulates in the pericardial cavity, but only if they are heard inwardly from the apical impulse; in other zones of dullness, heart sounds are sharply weakened.
The friction noise of the pericardium as the volume of fluid in the pericardial cavity increases, it can weaken and be heard only under certain conditions: when the patient's head is thrown back, while inhaling.
The late symptoms of exudative pericarditis include signs of compression of the mediastinal organs: compression by volumetric effusion of the trachea can cause persistent "barking" dry cough, compression of the esophagus leads to difficulty in swallowing.
In the absence of timely treatment of exudative pericarditis, cardiac tamponade gradually develops, manifested by circulatory disorders. Significant tachycardia develops, pulse filling decreases, and blood pressure also decreases. On examination, attention is drawn to the swelling of the peripheral and cervical veins in the absence of their pulsation. Pallor appears and grows with pronounced cyanosis of the nasolabial triangle. The liver enlarges and becomes painful on palpation. From the symptoms of stagnation in the systemic circulation, ascites first appears, and then edema in the lower extremities. The patient takes a forced position in bed: he sits, the body is tilted forward, rests his forehead on a pillow or kneels and presses his face and shoulders against the pillow. With the progression of cardiac tamponade, painful attacks of weakness appear, accompanied by a fear of death. The skin becomes covered with cold, sticky sweat, cyanosis grows, the limbs feel cold to the touch. Episodes of loss of consciousness may occur.
Purulent pericarditis
it can begin as serous-fibrinous, eventually turning into purulent, or immediately develops as purulent. Purulent pericarditis is very difficult due to severe intoxication and accumulation in the pericardial cavity of a large amount of pus (up to 3 liters). But sometimes the exudate is encased in one or more pericardial sinuses.
Gangrenous pericarditis
- the most severe of all types of pericarditis. The symptoms of severe intoxication come to the fore.
When examining a patient in a supine position in the area of cardiac dullness, a box sound is determined, and with an upright position in the lower part, the percussion sound is dull, and in the upper parts - tympanic.
Auscultation determines a large number of various noises - splash noise, the sound of a falling drop, "ringing a bell".
Allergic pericarditis
It is characterized by an acute onset with sharp pain in the region of the heart and a tendency to relapse. Occurs some time after exposure to a resolving factor (administration of serums or allergenic drugs). It usually proceeds in the form of myopericarditis with the formation of serous-fibrinous effusion. Skin rashes and other manifestations of drug disease or allergic conditions are characteristic.
Lupus pericarditis
More common in young women as a dry, exudative or adhesive process. As a rule, pleurisy and pneumonitis are simultaneously noted.
Pericarditis due to tumor
More often, the exudate is formed in large volume and is hemorrhagic in nature. In the exudate, during the study, up to 90% of all leukocytes are lymphocytes, conglomerates of tumor cells can be found.
Uremic pericarditis
It happens dry, serous-fibrinous or hemorrhagic. It is asymptomatic, not accompanied by pain in the region of the heart.
Xanthomatous (cholesterol) pericarditis
develops when the absorption capacity of the pericardium is sharply reduced. The effusion in the pericardial cavity contains lipoprotein complexes, the decomposition of which is significantly slowed down under these conditions. This leads to the formation of numerous crystals of cholesterol in the effusion. Xanthomatous pericarditis occurs regardless of the level of cholesterol in the blood, it lasts for a long time.
Adhesive (cohesive) pericarditis
have different clinical manifestations depending on the localization and prevalence of the adhesive process. The disease may be asymptomatic. In some patients, tolerance to increased physical activity decreases, pains in the region of the heart and circulatory disorders appear.
Often, with adhesive pericarditis, pain syndrome, severe shortness of breath, weakness, dry cough are observed, arising from changes in the condition of the heart, when changing the position of the body or at the beginning of movement, disappearing with continued load. Most often, pain that aggravates with physical exertion is associated with extrapericardial adhesions. They restrict inhalation and force the patient to maintain a certain posture for a long time.
Some signs of the adhesion process can be determined already during the external examination of the patient.
You can observe a negative cardiac impulse - the retraction of the apical impulse area in the systole phase (Sali-Chudnovsky symptom). During diastole, the retracted area makes a reverse jerk, similar to a strong apical impulse.
On palpation, chest tremor in the region of the heart may be detected, similar to protodiastolic "cat purr". Fusion of the pericardium with the anterior chest wall during the overgrowth of its cavity leads to an expansion of the boundaries of absolute and relative cardiac dullness. In patients with adhesions of the heart on the anterior or posterior surface, movements of only the upper ribs are visible in the act of breathing, the lower ribs are not involved in breathing. On examination, there is an asymmetry of the respiratory excursions of the chest.
Auscultation with adhesive pericarditis can sometimes determine a click tone in systole, similar to a bifurcation of the II tone. However, it is permanent, does not change depending on the respiratory phases and is poorly conducted. In addition, pleuropericardial murmurs are sometimes heard, more often in the II-III intercostal spaces on the left border of the heart or at the xiphoid process. The severity of the murmurs varies depending on the respiratory phases.
Tuberculous pericarditis
More often occurs in persons with a hyperergic tuberculosis process of another localization or who have had tuberculosis in the past. Pain in the region of the heart is rare. Patients are worried about low-grade fever, sweating at night, dry cough. The course of the disease is long. The effusion can be large without the development of cardiac tamponade.
Sometimes the effusion persists for years in a minimal inflammatory reaction - the so-called cold current. The myocardium is not involved in the process. Tuberculosis tests are of diagnostic value, and at a later date - radiologically detected areas of calcification of the pericardium.
Constrictive (compressive) pericarditis
has a number of characteristic clinical symptoms. More common in men aged 20-50 years.
The main clinical symptoms of compressive pericarditis are included in the so-called Beck triad: high venous pressure, ascites, "small quiet heart".
Patients complain of a constant feeling of discomfort in the abdomen, a feeling of bloating, heaviness, overflow. Venous pressure is determined above 250-300 mm of water. Art.
On external examination of the patient, signs of venous hypertension are visible: cyanosis of the cheeks, nasolabial triangle, hands, swelling of the face and neck, swelling of the neck veins that do not collapse with a deep breath, their visible pulsation. However, the peripheral veins are not dilated.
Clinically, there are 3 stages of development of chronic constrictive pericarditis: initial, severe and dystrophic.
In the initial stage, the patient notes weakness and shortness of breath when walking, swelling of the face, low tolerance to normal physical activity.
The dystrophic stage develops in the late stages of the disease due to late diagnosis of the disease and inadequate and untimely treatment. Patients develop severe asthenia.
With a rapid accumulation of effusion, a salt-free diet is prescribed, fluid intake is limited to 500-600 ml per day, with chronic pericarditis, diuretics are administered.
The patient is prohibited from physical activity, assigned to bed rest, a sparing diet, restriction of salt and fluid. Apply cardiac glycosides, diuretics.
Causes
- Infections:
- viruses (30-50%): Coxsackie, ECHO, Epstein-Barr, mumps, chickenpox, rubella, human immunodeficiency; cytomegalovirus, parvovirus B19;
- bacteria (5-10%): pneumococcus, staphylococcus, meningococcus, treponema, borrelia, chlamydia, mycobacterium tuberculosis;
- Mushrooms: candida, histoplasm;
- Parasites: amoeba, echinococcus;
- Acute MI (episthenocarditis pericarditis) (5-20%);
- Myocarditis (30%);
- Metabolic disorders: uremia, renal failure, myxedema (30%), cholesterol pericarditis;
- Neoplasms;
- Injuries: with direct or indirect damage to the pericardium;
- Systemic autoimmune diseases: acute rheumatic fever (20-50%); collagenoses: rheumatoid arthritis (30%), scleroderma (> 50%), systemic lupus erythematosus (30%);
- Autoimmune processes (damage): postinfarction syndrome, postpericardiotomy syndrome;
- Idiopathic (viral etiology has not been established) (3-50%).
Pericarditis can be acute (dry or exudative) or chronic (compressive or effusion). Acute pericarditis lasts less than 6 weeks, chronic pericarditis lasts more than 6 weeks.
The incidence of acute pericarditis ranges from 2 to 6% according to data - 1 per 1000 hospitalized. This indicates that pericarditis is often not diagnosed, although it often occurs with various pathologies. Conditions and complications of pericarditis, such as cardiac tamponade, constructive and purulent pericarditis, pose an immediate threat to the patient's life and require timely diagnosis and vigorous treatment.
Chronic compressive pericarditis can result from all causes of acute pericarditis. Common causes are tuberculosis or other infections: radiation, rheumatoid arthritis, trauma, and cardiac surgery.
Chronic pericardial effusion is usually caused by tuberculosis, a fungal infection. Tumor metastases - carcinomas (especially lung or breast), sarcomas (especially melanoma), leukemia, lymphoma - are common causes of large pericardial effusion in clinical practice. Tumor invasion is often complicated by serous or hemorrhagic effusion, which may be limited or diffuse, such as resulting in cardiac tamponade.
Acute pericarditis can be serous, fibrinous, hemorrhagic, or purulent. In this case, the process may involve the surface layers of the subepicardial areas of the myocardium. Pathological changes in pericarditis - acute inflammation, includes the presence of polymorphonuclear leukocytes, an increase in pericardial vascularization and fibrin deposition. Development of fibrous adhesions between the pericardium and epicardium, sternum and pleura is possible. The visceral pericardium responds to acute inflammation by accumulating fluid.
Symptoms
Clinical:
- chest pain: usually long-term (from several hours to several days), acute, retrosternal, can radiate to both shoulders, trapezius muscle, to the neck, increases with deep breathing (pleurisy may be misdiagnosed), with coughing, swallowing, depending on the position body (worse when lying on your back and decreases when sitting or lying on your stomach);
- other symptoms (shortness of breath, fever, malaise, myalgia, manifestations of the underlying disease).
Physical:
- pericardial friction noise (rough, hard, high-frequency two-component murmur, captures the systole of the atria and ventricles, is unstable; in 50% of cases, the third component of the noise is during the period of early diastolic filling of the ventricles);
- percussion increase in pericardial dullness (with effusion into the pericardial cavity);
- weakening of heart sounds;
- swelling of the cervical veins, paradoxical pulse with tamponade.
Instrumental:
- ECG changes (early changes - depression of the RO segment. Trough-like elevation of the TR segment without reciprocal depression in other leads and pathological O wave, changes in VT and T are dynamic, the T wave becomes negative);
- EchoCG (presence of effusion in the pericardial cavity);
- X-ray changes (increase in the size of the "heart shadow", smoothing of the waist of the heart, "pseudomitral" configuration of the heart, weakening of the pulsation of the "heart shadow" contour in the presence of effusion);
- changes in the jugular phlebogram (gentle Y-recession, steep X-recession) with pronounced effusion in the pericardial cavity.
Laboratory:
- tuberculin tests (for the diagnosis of tuberculosis);
- blood cultures (for the diagnosis of infective endocarditis);
- virological research;
- determination of antibodies to HIV infection;
- serological tests for mushrooms;
- determination of antinuclear antibodies, rheumatoid factor, increased ESR (for the diagnosis of SLE, rheumatoid arthritis);
- determination of antistreptolysin-0 (for the diagnosis of rheumatism);
- determination of cold antibodies (for the diagnosis of mycoplasma infection);
- determination of heterophilic antibodies (for the diagnosis of mononucleosis);
- determination of the level of thyroid hormones (for the diagnosis of hypothyroidism);
- determination of the level of creatinine (for the diagnosis of uremia).
Acute pericarditis Acute pericarditis can manifest as chest pain, shortness of breath, fever, pericardial rubbing, tamponade, ECG, and radiographic changes. The pain is localized in the precordial or sub-sternal region, radiating to the neck or left shoulder. The pain is variable in severity and is often worse when lying down, with coughing, deep breathing, swallowing, and decreases when sitting and bending forward. Pain in pericarditis should be distinguished from pain in pleurisy, myocardial infarction, and pulmonary infarction. Shortness of breath is usually associated with shallow breathing, occurs to reduce pain, as well as hyperthermia or large hydrothorax.
The pathognomonic sign of acute pericarditis is presystolic, systolic and diastolic murmurs, pericardial friction, reflecting the friction of the pericardial and endocardial surfaces. Its peculiarity is the frequent change of the auscultatory picture. The pericardial friction murmur differs from other heart murmurs in that: 1) it does not change during exercise, 2) it does not change at different breathing phases and position. Significant pericardial effusion can muffle heart sounds, increase cardiac dullness, and alter the size and shape of the heart.
In classic cases, acute pericarditis is characterized by a triad of clinical signs: chest pain, pericardial friction murmur, and variable ECG.
Sample Diagnosis Formulation
- Bacterial (staphylococcal) pericarditis, acute course, moderate severity of pericardial effusion, CH0 IIIА, diastolic variant, III FC.
- Chronic compressive (unknown etiology) pericarditis, progressive course, insignificant severity of pericardial effusion, CH0 IIB, diastolic variant, IV FC.
Diagnostics
- Collection of complaints and anamnesis: pain in the chest, behind the sternum or in the left precordial region, pain can radiate to the upper part of the trapezius muscle, be pleural or ischemic in nature, depending on the position of the body; there may be shortness of breath, paradoxical pulse.
- Clinical examination: during auscultation, pericardial murmur, weakened heart sounds, swelling of the cervical veins, a fall of ATC on inspiration by 12-15 mm. rt. Art.
- Blood pressure measurements.
- Central venous pressure measurements.
- Laboratory examination: general blood and urine tests, ALT, AST, bilirubin, creatinine, cholesterol, blood glucose, potassium, sodium, C-reactive protein, ASL-O, AG titers.
- 12-lead ECG:
- a concordant negative ST segment with a simultaneous lower bulge in the standard and chest leads with a transition to a high positive T wave;
- after 1 - 2 days, the ST interval descends below the isoline, protrudes upward, then returns to the isoelectric line for several days, despite further inflammatory process in the pericardium;
- the positive T wave is flattened and after 10-15 days it becomes two-phase or negative in those. leads in which the dynamics of the ST segment took place. In the future, the ECG returns to normal;
- there are no changes in the QRS complex.
- Echocardiography and Doppler study: thickening of the pleural layers, the presence of fluid.
- Radiography of the OGK: the image of the heart can vary from normal to the appearance of a "water bottle" silhouette, it is possible to reveal concomitant diseases of the lungs and organs of the mediastinum.
Daily research:
- Daily ECG monitoring;
- Puncture of the pericardium with cytological examination of the effusion;
- CT or MRI;
- CEC, lgMG, neutralizing or complement-binding antibodies to Coxsackie viruses of group B, ECHO, herpes in paired sera.
Prophylaxis
Acute pericarditis. The first step in the treatment of acute pericarditis is to determine the relationship of pericarditis with any concomitant pathology that requires specific treatment.
Non-specific therapy for pericarditis includes bed rest until pain and fever disappear, since activity can increase symptoms. All patients with pericarditis should be hospitalized for examination and observation of possible complications, including pericardial tamponade.
Pericardial pain is usually treated with nonsteroidal anti-inflammatory drugs. Severe pain syndrome resistant to NSAIDs for 48 hours is treated with corticosteroids and narcotic analgesics. In some cases, many months of treatment may be required. Given the side effects of long-term therapy with corticosteroids, they should be used in the treatment of pain syndrome only in these cases, using if necessary, in the future every other day or switching to treatment with non-steroidal drugs.
Antibiotics are used only for proven infectious genesis of pericarditis. Anxiety or insomnia may require benzodiazepines. Anticoagulants are contraindicated in pericarditis due to the risk of intrapericardial bleeding, up to the development of tamponade.
Pericarditis caused by a bacterial or fungal infection is treated with specific antimicrobial drugs. In postpericardiotomy syndrome, postinfarction pericarditis, antibiotics are not indicated. In case of rheumatic fever or other diseases of the connective tissue and damage to the pericardium in malignant tumors, treatment of the main process is required.
Uremic pericarditis are treated with hemodialysis and corticosteroids.
With effusion pericarditis pericardiocentesis is not performed until cardiac compression develops. The clinical significance of any pericardial effusion depends on: 1) the presence or absence of hemodynamic disturbances and 2) the presence and severity of concomitant pathology. Pericardiocentesis is indicated to reduce tamponade and if suppurative pericarditis is suspected. It should be used for diagnostic purposes if effusion and symptoms progress after 1–3 weeks of treatment.
Pericardiocentesis is needed with the rapid development of cardiac tamponade, a drop in blood pressure and the development of shock symptoms. Fluid from the pericardial cavity is evacuated by: 1) percutaneous pericardium using a needle and catheter through the subxiphoidal access, or 2) partial or extensive surgical pericardiectomy with thoracotomy. Manipulation should be performed in a catheterization laboratory under the control of an echocardiogram. It is necessary to monitor the ECG for the timely detection of cardiac arrhythmias arising from a possible puncture of the myocardium. Typically, right atrial pressure, pulmonary wedge pressure, and intrapericardial pressure are monitored. After removal of fluid during pericardiocentesis, the clinic is rapidly improving. Now it is a relatively safe procedure: if it is performed by an experienced operator, it has a risk of life-threatening complications of up to 5%.
Chronic pericarditis. Constrictive pericarditis is a progressive disease. Only a small number of patients can live for many years with a moderate increase in the jugular veins and peripheral edema against the background of restriction of sodium chloride, fluids and diuretics. With the development of supraventricular arrhythmias or systolic myocardial dysfunction, digoxin is indicated.
In most symptomatic patients, weakness, ascites, and peripheral edema progressively increase, which further leads to the development of cardiac cachexia. In this situation, the treatment of constrictive pericarditis is complete resection of the pericardium. The operation is not performed in the elderly, with severe liver dysfunction, severe pericardial calcification and heart dilatation. A significant improvement in the state of hemodynamics and a decrease in symptoms in some patients occurs immediately after the operation, in others it occurs gradually, over weeks or months.
