Practice EssentialsAcute pericarditis is an inflammation of the pericardium characterized by chest pain, pericardial friction rub, and serial ECG changes.

Signs and symptomsChest pain is the cardinal symptom of pericarditis, usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. Common associated signs and symptoms include low-grade intermittent fever, dyspnea/tachypnea (a frequent complaint and may be severe, with myocarditis, pericarditis, and cardiac tamponade), cough, and dysphagia. In tuberculous pericarditis, fever, night sweats, and weight loss are commonly noted (80%).

Specific causes of pericarditis include the following:

Idiopathic causesInfectious conditions, such as viral, bacterial, and tuberculous infectionsInflammatory disorders, such as RA, SLE, scleroderma, and rheumatic feverMetabolic disorders, such as renal failure, hypothyroidism, and hypercholesterolemiaCardiovascular disorders, such as acute MI, Dressler syndrome, and aortic dissectionMiscellaneous causes, such as iatrogenic, neoplasms, drugs, irradiation, cardiovascular procedures, and traumaSee Clinical Presentation for more detail.

DiagnosisInitial evaluation includes a clinical history and physical examination, ECG, echocardiography, chest radiography, and lab studies.

ECG can be diagnostic in acute pericarditis and typically shows ST elevation in all leads. The ratio of the amplitude of ST segment to the amplitude of the T wave in leads I, V4, V5, and V6 on electrocardiogram can be used to differentiate acute pericarditis (AP) from early repolarization (ER) and early repolarization of left ventricular hypertrophy (ERLVH), according to a recent study. When ST elevation was present in lead I, the ST/T ratio had the best predictive value for discriminating between AP, ER and ERLVH. The study involved 25 patients with AP, 27 with ER, and 28 with ERLVH.[1]

Echocardiography is particularly helpful if pericardial effusion is suspected on clinical or radiographic grounds, the illness lasts longer than 1 week, or myocarditis or purulent pericarditis is suspected.

A chest radiograph is only helpful for diagnosis in patients with effusions >250mL. Patients with small effusions (less than a few hundred milliliters) may present with a normal cardiac silhouette.

Lab tests may include CBC; serum electrolyte, blood urea nitrogen (BUN), and creatinine levels; erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels; and cardiac biomarker measurements, lactate dehydrogenase (LDH), and serum glutamic-oxaloacetic transaminase (SGOT; AST) levels.

See Workup for more detail.

ManagementTreatment for specific causes of pericarditis is directed according to the underlying cause. For patients with idiopathic or viral pericarditis, therapy is directed at symptom relief.

Pharmacologic treatment

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstay of therapy. These agents have a similar efficacy, with relief of chest pain in about 85-90% of patients within days of treatment. A full-dose NSAID should be used, and treatment should last 7-14 days.

Colchicine, alone or in combination with an NSAID, can be considered for patients with recurrent or continued symptoms beyond 14 days.[2]

Corticosteroids should not be used for initial treatment of pericarditis unless it is indicated for the underlying disease, the patients condition has no response to NSAIDs or colchicine, or both agents are contraindicated.

Surgical treatment

Surgical procedures for pericarditis include pericardiectomy, pericardiocentesis, pericardial window placement, and pericardiotomy.

Pericardiectomy is the most effective surgical procedure for managing large effusions, because it has the lowest associated risk of recurrent effusions. This procedure is used for constrictive pericarditis, effusive pericarditis, or recurrent pericarditis with multiple attacks, steroid dependence, and/or intolerance to other medical management.

Patients with effusions larger than 250 mL, effusions in which size increases despite intensive dialysis for 10-14 days, or effusions with evidence of tamponade are candidates for pericardiocentesis.

Pericardial window placement is used for effusive pericarditis therapy. In critically ill patients, a balloon catheter may be used to create a pericardial window, in which only 9 cm2 or less of pericardium is resected.

Consider subxiphoid pericardiotomy for large effusions that do not resolve. This procedure may be performed under local anesthesia and has a lower risk of complications than pericardiectomy.

See Treatment and Medication for more detail.

Image libraryThis 12-lead electrocardiogram is representative oThis 12-lead electrocardiogram is representative of pericarditis.BackgroundAcute pericarditis is an inflammation of the pericardium characterized by chest pain, pericardial friction rub, and serial electrocardiographic (ECG) changes (see an example of such an ECG below). Pericarditis and cardiac tamponade involve the potential space surrounding the heart or pericardium; pericarditis is one cause of fluid accumulation in this potential space, and cardiac tamponade is the hemodynamic result of fluid accumulation.

This 12-lead electrocardiogram is representative oThis 12-lead electrocardiogram is representative of pericarditis.For more information, see the the Medscape Reference articles Constrictive Pericarditis, Constrictive-Effusive Pericarditis, Pediatric Infective Pericarditis, and Imaging in Constrictive Pericarditis.

For patient education information, see the Cholesterol Center and Heart Center, as well as Pericarditis, Heart Attack, and Chest Pain.

AnatomyThe pericardium (pericardial complex) serves as a protective barrier from the spread of infection or inflammation from adjacent structures. It is composed of the parietal pericardium (an outer fibrous layer) and the visceral pericardium (an inner serous membrane made of a single layer of mesothelial cells). The fibrous pericardium is a flask-shaped, tough outer sac with attachments to the diaphragm, sternum, and costal cartilage. The visceral pericardium is thin, adjacent to the surface of the heart, and attached to the epicardial fat; it reflects back on itself to form the parietal pericardium.

The pericardium normally contains as much as 20-50 mL of an ultrafiltrate of plasma. Approximately 90-120 mL of additional pericardial fluid can accumulate in the pericardium without an increase in pressure. The capacity of the atria and ventricles to fill is mechanically compromised with further fluid accumulation, which can result in marked increases in pericardial pressure, eliciting reduced stroke volume, decreased cardiac output, and hypotension (cardiac tamponade physiology). The rapidity of fluid accumulation influences the hemodynamic effect. Drainage occurs via the thoracic duct and the right lymphatic duct into the right pleural space.

PathophysiologyPericardial physiology includes 3 main functions. First, through its mechanical function, the pericardium promotes cardiac efficiency by limiting acute dilation, maintaining ventricular compliance with preservation of the Starling curve, and distributing hydrostatic forces. The pericardium also creates a closed chamber with subatmospheric pressure that aids atrial filling and lowers transmural cardiac pressures. Second, through its membranous function, the pericardium shields the heart by reducing external friction and acting as a barrier against extension of infection and malignancy. Third, through its ligamentous function, the pericardium anatomically fixes the heart.

In most cases of acute pericarditis, the pericardium is acutely inflamed and has an infiltration of polymorphonuclear (PMN) leukocytes and pericardial vascularization. Often, the pericardium manifests a fibrinous reaction with exudates and adhesions. The pericardium may develop a serous or hemorrhagic effusion. A granulomatous pericarditis occurs with tuberculosis, fungal infections, rheumatoid arthritis (RA), and sarcoidosis.

Uremic pericarditis is thought to result from inflammation of the visceral and parietal layers of the pericardium by metabolic toxins that accumulate in the body owing to kidney failure. Other factors may be involved, however, because pericarditis also may occur in patients with chronic renal failure who are already receiving dialysis therapy.

The putative toxins suggested to precipitate uremic pericarditis when they accumulate are poorly characterized, but they may include urea, creatinine, methylguanidine, guanidinoacetate, parathyroid hormone, beta2-microglobulin, uric acid, and others. More than one toxin apparently may be involved, although considerable controversy surrounds this point.

The precise pathogenetic changes induced by these toxins when causing uremic pericarditis have not been elucidated, although a rough correlation with the degree and the duration of azotemia exists; the blood urea nitrogen (BUN) level is usually greater than 60 mg/dL (22 mmol/L). Uremic pericarditis may be associated with hemorrhagic or serous effusion, although considerable overlap exists. Hemorrhagic effusions are more common and result in part from uremia-induced platelet dysfunction.

Some authors distinguish between 2 types of pericarditis in patients with renal failure. One type is uremic pericarditis, which occurs in patients with uremia who have never received dialysis. The other type is dialysis-associated pericarditis, which occurs in patients who are already receiving dialysis. In the latter case, inadequate dialysis may usually be implicated, because aggressive dialysis often leads to resolution. Other causes of dialysis-associated pericarditis may include volume overload and bacterial or viral infections.

In an observational study that employed data from 88 maintenance hemodialysis patients, investigators found that intensive dialysis is the most effective treatment for dialysis-associated pericarditis in patients on dialysis who have diabetes and those who do not.[3] Following the intensification of hemodialysis, pericarditis improved in 85.1% of patients with diabetes and in 82.9% of those without diabetes. Among patients with diabetes, 85.1% survived without recurrence of pericarditis, 4.3% survived but did suffer recurrence, and 10.6% died, with similar outcomes recorded in the group without diabetes (87.8%, 4.9%, and 7.3%, respectively).[3]

EtiologyThis section will first briefly discuss acute pericarditis, chronic pericarditis, and cardiac tamponade; then, several specific entities that cause pericarditis will be briefly reviewed.

Acute pericarditisSerous pericarditis is usually caused by noninfectious inflammation such as occurs in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Fibrous adhesions rarely occur.

Fibrous and serofibrinous pericarditis represent the same basic process and are the most frequent type of pericarditis. Common causes include acute myocardial infarction (MI), postinfarction (including Dressler syndrome), uremia, radiation, RA, SLE, and trauma. Severe infections may also cause a fibrinous reaction, as does routine cardiac surgery.

Purulent or suppurative pericarditis due to causative organisms may arise from direct extension, hematogenous seeding, or lymphatic extension, or by direct introduction during cardiotomy. Immunosuppression facilitates this condition. Clinical features include fever, chills, and spiking temperatures. Constrictive pericarditis is a serious potential complication.

Hemorrhagic pericarditis involves blood mixed with a fibrinous or suppurative effusion, and it is most commonly caused by tuberculosis or direct neoplastic invasion. This condition can also occur in severe bacterial infections or in patients with a bleeding diathesis. Hemorrhagic pericarditis is common after cardiac surgery and may cause tamponade. The clinical significance is similar to suppurative pericarditis.

Until proven otherwise, caseation within the pericardial sac is tuberculous in origin. Untreated, caseous pericarditis is the most common antecedent to chronic constrictive pericarditis of a fibrocalcific nature.

Chronic pericarditisAdhesive mediastinopericarditis is a reaction that usually follows suppurative or caseous pericarditis, cardiac surgery, or irradiation. This condition is rarely caused by a simple fibrinous exudate. The pericardial potential space is obliterated, and adhesion of the external surface of the parietal layer to surrounding structures occurs. Clinically, systolic contraction of the ribcage and diaphragm and pulsus paradoxus may be observed. The increased workload may cause massive cardiac hypertrophy and dilatation, which can mimic an idiopathic cardiomyopathy.

Constrictive pericarditis is usually caused by suppurative, caseous, or hemorrhagic pericarditis. The heart may become encased in a 0.5-cmthick to 1-cmthick layer of scar or calcification (concretio cordis), resembling a plaster mold. Contrary to clinical findings in adhesive mediastinopericarditis, the heart cannot become hypertrophic or dilate because of insufficient space.

Imazio et al suggest that constrictive pericarditis is a rare complication of viral or idiopathic acute pericarditis (< 0.5%). However, it appears to be comparatively frequent for specific etiologies, especially bacterial.[4]

Cardiac tamponadeTamponade is more common in patients with malignant pericarditis. Effusions caused by tumors often progress to tamponade, eliciting bleeding in the pericardium. Blood accumulates more rapidly than a transudate or exudate and more commonly causes tamponade.

Identification of any pericardial fluid in the setting of penetrating injury to the thorax or upper abdomen requires aggressive resuscitation; penetrating cardiac injuries may occur, with hemopericardium as the most common feature. In acute massive hemopericardium, the time is insufficient for defibrination to occur. The hemopericardium organizes and may partially clot, resulting in a pericardial hematoma. The hematoma may appear echogenic instead of echo free.

Potential sources of iatrogenic cardiac perforation include central line placement, pacemaker insertion, cardiac catheterization, sternal bone marrow biopsies, and pericardiocentesis. The right atrium is the most common site of perforation from catheter placement. Perforation, as well as direct catheter infusion of fluids, can cause tamponade. In fact, a tamponade delay of hours to days has occurred secondary to catheter misplacement.

In one case report, tamponade was described as the first manifestation of dermatopolymyositis.[5]

Specific causes of pericarditis include the following and are briefly reviewed below:

Idiopathic causesInfectious conditions, such as viral, bacterial, and tuberculous infectionsInflammatory disorders, such as RA, SLE, scleroderma, and rheumatic feverMetabolic disorders, such as renal failure, hypothyroidism, and hypercholesterolemiaCardiovascular disorders, such as acute MI, Dressler syndrome, and aortic dissectionMiscellaneous causes, such as iatrogenic, neoplasms, drugs, irradiation, cardiovascular procedures, and traumaIdiopathic causesBetween 26% and 86% of cases of acute pericarditis are idiopathic in nature.[6] No clinical features distinguish idiopathic cases from viral pericarditis. It is likely that most idiopathic cases are undiagnosed viral infections. Seasonal peaks occur in spring and fall.

Chronic idiopathic pericarditis is defined as a pericardial effusion that persists more than 3 months without any apparent etiology. Pericardiocentesis alone results in resolution of large effusions; however, recurrence is common.

Viral infectionViral infection is the most common cause of acute pericarditis and accounts for 1-10% of cases. The disease is usually a short self-limited disease that lasts 1-3 weeks and can occur as seasonal epidemics, especially coxsackievirus B and influenza.

Causative viruses include coxsackievirus B,[7] echovirus, adenoviruses, influenza A and B viruses, enterovirus, mumps virus, Epstein-Barr virus, human immunodeficiency virus (HIV), herpes simplex virus (HSV) type 1, varicella-zoster virus (VZV), measles virus, parainfluenza virus (PIV) type 2, and respiratory syncytial virus (RSV), cytomegalovirus (CMV), and hepatitis viruses A, B, and C (HAV, HBV, HCV, respectively).

Patients may have associated myocarditis. Pericardial involvement is frequent in persons with HIV, but is usually an asymptomatic pericardial effusion of small volume. Individuals with advanced HIV infection develop pericardial involvement more frequently, with one study noting right atrial diastolic compression in 5% of cases involving advanced HIV infection.[8] Symptomatic pericarditis occurs in less than 1% of cases involving HIV, and its etiology can include the usual causes, opportunistic infection, Kaposi sarcoma, and HIV.

Bacterial infectionBacterial infections accounts for 1-8% of pericarditis cases and result from direct pulmonary extension, hematogenous spread, myocardial abscess or endocarditis, penetrating injury to chest wall from either trauma or surgery, or a subdiaphragmatic suppurative lesion. Purulent pericarditis may result from previous aseptic pericarditis, and a high percentage of patients develop constrictive pericarditis.

Organisms that have been isolated include gram-positive species such as Streptococcus pneumoniae and other Streptococcus species and Staphylococcus.[9] Isolated gram-negative species include Proteus, Escherichia coli, Pseudomonas, Klebsiella, Salmonella, Shigella, Neisseria meningitidis, and Haemophilus influenzae.

Less common organisms include Legionella, Nocardia, Actinobacillus, Rickettsia, Borrelia burgdorferi (Lyme borreliosis), Listeria, Leptospira, Chlamydophila psittaci, and Treponema pallidum (syphilis).

Anaerobes have also been isolated in 40% of patients in reviews of the pediatric population.

Previously, Pneumococcus was the predominant organism. However, in the antibiotic era, staphylococcal and gram-negative species have become more common. Most cases are now associated with thoracic surgery, renal disease, and immunosuppression.

Tuberculous infectionTuberculosis accounts for 4% of cases and should be considered in all instances of pericarditis without a rapid course, especially in high-risk groups, such as elderly patients in nursing homes and those with acquired immunodeficiency syndrome (AIDS).[10] Approximately 50% of affected patients develop constrictive pericarditis.

Fungal and parasitic infectionFungal organisms that may cause acute pericarditis include Histoplasma, Blastomyces, Coccidioides, Aspergillus, and Candida. Parasitic organisms include Entamoeba, Echinococcus, and Toxoplasma.

Rheumatoid arthritisPericarditis occurs predominantly in males with severely destructive and nodular RA. The pericardial involvement is usually clinically silent, with the diagnosis made in only 2% of adults and 6% of juveniles with RA. Rarely, pericarditis precedes the onset of RA. Autopsy studies show a pericarditis prevalence of 11-50%.

Systemic lupus erythematosus, scleroderma, sarcoidosisClinically evident pericarditis has been reported in 25% of patients with SLE and usually occurs in lupus flare-ups, but it may be the presenting manifestation. Autopsy series reveal pericardial involvement in 62% of lupus patients.

Pericarditis is recognized in 5-10% of patients with scleroderma, with a 70% autopsy prevalence. Pericardial effusions occur in 40% of patients with scleroderma and can be due to scleroderma, myocardial failure (restrictive cardiomyopathy), and renal failure. Restrictive cardiomyopathy and pericardial constriction can coexist. Usually, pulmonary hypertension, right heart failure, and systolic dysfunction occur.

Sarcoidosis may result in pericarditis, but this condition rarely causes cardiac tamponade or constrictive pericarditis

Rheumatic feverPericarditis in those with rheumatic fever occurs more commonly in lower socioeconomic groups and in children, often accompanying endocarditis and myocarditis, with a worse prognosis. Consider rheumatic fever as an etiology in any child with pericarditis. However, this disease is not a demonstrated cause of constrictive pericarditis.

In adults, pericarditis may not occur with myocardial or valvular involvement, and it is associated with a better prognosis. The pericarditis usually appears 7-10 days after the onset of fever and arthritis. Often, stage 1 electrocardiographic (ECG) findings are absent (see Electrocardiography).

Other inflammatory conditionsThe following conditions may also cause acute pericarditis:

Sjgren syndromeMixed connective-tissue diseaseReiter syndromeAnkylosing spondylitisInflammatory bowel diseaseWegener granulomatosisVasculitis (eg, giant cell arteritis, polyarteritis)PolymyositisBehet syndromeWhipple diseaseFamilial Mediterranean feverSerum sicknessRenal failureRichard Bright described uremic pericarditis in 1836. Since that classic description, this common complication of chronic renal failure has evolved from an ominous event heralding the terminal stages of disease to an event that, with early management, is likely to have a good outcome. Furthermore, advances in dialysis technology with early and timely management of chronic renal failure have dramatically reduced the prevalence of uremic pericarditis. Uremic pericarditis has a prevalence of 6-10% in patients with acute or chronic renal failure, and it continues to be associated with significant morbidity and occasional mortality.

Renal failure accounts for approximately 12% of cases of pericarditis. In the predialysis era, pericarditis developed in 35-50% of patients with uremia who had chronic renal failure and less commonly in those with acute renal failure. Death often followed in several weeks. With dialysis, the pericarditis incidence rate is less than 10%; however, this condition occurs after the onset of dialysis in 8-12% of cases.

Asymptomatic pericardial effusions can occur in 36-62% of patients with uremia who require dialysis; these effusions are often small to moderate in size and can occur secondary to volume overload. Pericardial effusions can lead to significant hemodynamic complications during routine dialysis. Moreover, the presence of a large pericardial effusion that persists for longer than 10 days after intensive dialysis has a high likelihood of causing tamponade.

HypothyroidismHypothyroidism accounts for as many as 4% of pericarditis cases. In fact, myocardial involvement is common, and pericardial involvement usually occurs with severe hypothyroidism. Patients may develop large pericardial effusions, but they rarely develop tamponade.

Cholesterol pericarditisCholesterol pericarditis, also called gold-paint pericarditis, is a complication of a chronic pericardial effusion exacerbated by cholesterol crystals. It usually presents with large effusions that are not hemodynamically important, and development of constriction is rare. Granulomatous pericarditis has been implicated in some cases.

Myocardial infarctionAfter a transmural infarction, a fibrinous pericardial exudate appears within 24 hours, begins to organize at 4-8 days, and completes organization at 4 weeks.[11, 12] Pericardial pain occurs less frequently than the friction rub, which is often detected on the second or third day after an acute MI but may be heard within 24 hours and as late as 10 days.

Before thrombolytic therapy, infarct-associated pericarditis ranges from 7% to 23% of cases. At autopsy in one study, almost all patients were noted to have localized fibrinous pericarditis overlying the area of infarction. With thrombolytic therapy and direct infarct angioplasty, the incidence of postMI-associated pericarditis has decreased to 5-8%.

Overall, pericardial involvement indicates a larger infarction, greater incidence of left ventricular dysfunction, and greater mortality. The pericarditis usually heals without consequence; effusions may occur, but they rarely lead to tamponade.

Dressler syndromeDressler syndrome is now considered rare. When pericarditis associated with Dressler syndrome does occur, it is usually observed 2-3 weeks after a myocardial infarction. Initially, the syndrome was described in as many as 4% of patients following and acute MI. Later studies suggested a much lower incidence. Dressler syndrome is rarely described with pulmonary embolism.

This syndrome may be a unique autoimmune-mediated phenomenon to myocardial antigens, or it may merely be an unrecognized postMI pericarditis. Patients may develop pulmonary infiltrates and large pericardial effusions.

Because of the risk of hemorrhagic pericarditis, anticoagulant therapy should be stopped in patients with Dressler syndrome.

Aortic dissection and Takotsubo cardiomyopathyAortic dissection accounts for 1% of cases of acute pericarditis, especially for cases with hemorrhage into the pericardium.

Takotsubo cardiomyopathy is a transient cardiac syndrome that involves left ventricular apical akinesis and mimics acute coronary syndrome.

NeoplasmMalignancy account for 5-17% of pericarditis cases; in patients presenting with acute pericarditis or pericardial effusion, 4-7% have an unsuspected malignancy. Primary neoplasm of the heart and pericardium is rare; most cases of neoplasm-related pericarditis are a result of metastatic disease. Autopsy studies have noted that approximately 10% of patients with cancer develop cardiac involvement, and it is often clinically silent. The neoplastic cells reach the pericardium through the bloodstream, through the lymphatic system, or via local growth.

Neoplastic disease, particularly advanced disease, is the most frequent cause of tamponade in the hospital. Occasionally, the tumor encases the heart and causes constrictive pericarditis rather than tamponade.

Pericardial mesothelioma and angiosarcoma are lethal malignancies with aggressive local spread that respond poorly to treatment. Infants and children can present with a teratoma in the pericardial space. These can often be successfully removed.

Lung cancer, including adenocarcinoma and squamous and small cell carcinoma, accounts for approximately 33% of cases; breast cancer accounts for 25%; leukemia and lymphoma, including Hodgkin and non-Hodgkin, account for 15% of cases; and malignant melanoma represents another 5%. Almost all other malignancies, except primary brain, comprise the rest of the cases. Kaposi sarcoma has also become a more prominent cause of neoplastic disease with the AIDS epidemic.

DrugsSome medications, including penicillin and cromolyn sodium, induce pericarditis through a hypersensitivity reaction. The anthracycline antineoplastic agents, such as doxorubicin and cyclophosphamide, have direct cardiac toxicity and can cause acute pericarditis and myocarditis.

Pericarditis can also develop from a drug-induced lupus syndrome caused by medications including procainamide, hydralazine, methyldopa, isoniazid, mesalazine, and reserpine. Methysergide causes constrictive pericarditis through mediastinal fibrosis. Dantrolene, phenytoin, and minoxidil produce pericarditis through an unknown mechanism.

Smallpox vaccination infrequently leads to myocarditis. In a review of a large vaccination program in the US military, approximately 12 per 100,000 vaccinated troops developed myopericarditis within 14 days of vaccination.[13, 14] Whether this was due to a direct viral cytopathic effect or an immune-mediated phenomenon is unclear.

IrradiationPericardial disease is the most common cardiac toxicity from radiation therapy. Others are coronary artery disease, conduction disturbance, and myocardial and valvular disease.[15] A high incidence of such toxicity occurs with high doses, especially those greater than 4000 rad.

Radiation pericarditis can present as acute pericarditis, with or without effusion; chronic constrictive pericarditis; or effusive-constrictive pericarditis.

Invasive cardiac proceduresElectrophysiologic studies, radiofrequency ablation, pacemaker implantation, and percutaneous coronary intervention are among several invasive cardiac procedures that can cause pericarditis.

Postpericardiotomy syndrome is similar to Dressler syndrome, except that postpericardiotomy syndrome occurs after cardiac surgery. Several series note an incidence rate of 10-40%; approximately 1% of patients with postpericardiotomy syndrome develop tamponade.

Pericardial effusions can occur in the absence of typical features of postpericardiotomy syndrome. In one study, 56% developed pericardial effusions early after cardiac surgery, without correlation to pericarditis or tamponade. The effusions were more common after heavy postoperative bleeding.

TraumaApproximately 1% of cases of acute pericarditis are caused by trauma, such as penetrating and nonpenetrating cardiac trauma. Also consider esophageal rupture or perforation and pancreatitis.

EpidemiologyEpidemiologic data on the incidence of acute pericarditis are lacking, likely because this condition is frequently inapparent clinically, despite its presence in numerous disorders. Lorell noted a diagnosis of acute pericarditis in approximately 1 per 1000 hospital admissions.[16] In addition, acute pericarditis comprises 1% of emergency room visits in patients with ST-segment elevation.[17] In fact, the reported incidence of acute pericardial tamponade is approximately 2% of penetrating trauma; however, this condition is rarely seen in blunt chest trauma.

Uremic pericarditis may occur in 6-10% of patients with advanced renal failure before initiation of dialysis. When patients with large effusions are studied, uremia may account for up to 20% of cases in some series. The widespread availability of dialysis has reduced the incidence of uremic pericarditis.

Malignant disease is the most common cause of pericardial effusion with tamponade in developed countries; However, tuberculosis should be considered in endemic areas.

Acute pericarditis is more common in men than in women. However, although this condition is more common in adults than in children, adolescents are more commonly affected than young adults. Nonetheless, Merce et al found no difference in etiology, clinical course, and prognosis between elderly and younger patients with moderate and large pericardial effusions.[18]

PrognosisThe prognosis in individuals with pericarditis depends on the etiology of this condition, as well as the presence of a pericardial effusion and/or tamponade. Idiopathic and viral etiologies usually have a self-limited course, without any risk of evolution toward constrictive pericarditis.[19, 20] Most postMI cases have a benign course; however, pericarditis is associated with larger infarcts, and therefore, overall long-term mortality may be increased.

Patients with scleroderma or children with rheumatic fever and pericarditis have a poor prognosis, and purulent, tuberculous, and neoplastic pericardial involvement have more complicated courses with worse outcomes. Purulent pericarditis is associated with a mortality rate nearing 100% for untreated persons and a mortality rate of 12-40% for treated patients. The mortality rate in tuberculous pericarditis approaches 50%.

Uremic pericarditis continues to be associated with significant morbidity and occasional mortality. Of patients with uremic pericarditis, 3-5% may develop hemorrhagic pericarditis.

For penetrating injuries, the prognosis depends heavily on the rapid identification of tamponade. Mortality may occur in 3-5% of cases resulting from cardiac tamponade or arrhythmias. Favorable factors include minor perforations, isolated right ventricular wounds, systolic blood pressure more than 50 mm Hg, and the presence of tamponade.Essentials practicPericardita acut este o inflamaie a pericardului caracterizata prin dureri in piept , freca frecare pericardic , i modificri ECG seriate .

Semne si simptomeDureri n piept este simptomul cardinal de pericardit , de obicei, precordiala sau retrosternala cu trimitere la marginea trapezului , gtul , umrul stng , sau brat . Semnele asociate comune si simptome includ febra intermitenta , dispnee / tahipnee ( o plngere frecvent i pot fi severe , cu miocardita , pericardita , i tamponad cardiac ) , tuse , si disfagie . n pericardita tuberculoas , febr , transpiraii nocturne , si pierderea in greutate sunt notate frecvent ( 80 % ) .

Cauzele specifice ale pericarditei includ urmtoarele :

idiopatica cauzeazCondiii infecioase , cum ar fi infeciile virale , bacteriene , i tuberculoasaAfectiuni inflamatorii , cum ar fi RA , LES , sclerodermia , si febra reumaticaTulburri metabolice , cum ar fi insuficien renal , hipotiroidism , i hipercolesterolemieTulburri cardiovasculare , cum ar fi IM acut , sindromul Dressler , i disectie aorticaCauze diverse , cum ar fi iatrogene , neoplasme , medicamente , iradiere , proceduri cardiovasculare , si traumeA se vedea tabloul clinic pentru mai multe detalii .

diagnosticEvaluarea iniial include un istoric clinic i examenul fizic , ECG , ecocardiografie , radiografia toracica , precum si studii de laborator .

ECG poate fi diagnostic n pericardita acuta si de obicei arata supradenivelare de segment ST n toate pistele . Raportul dintreamplitudinea segmentului ST laamplitudineaundei T n derivaiile I , V4 , V5 , V6 i pe electrocardiogram pot fi folosite pentru a diferenia pericardita acut ( AP ) din repolarizare precoce ( ER ) i repolarizare precoce a hipertrofiei ventriculare stngi ( ERLVH ) , potrivit unui studiu recent . Cnd supradenivelare de segment ST a fost prezent n conduc eu , raportul ST / T a avut cea mai bun valoare predictiva pentru discriminarea ntre AP , ER i ERLVH . Studiul a implicat 25 de pacienti cu AP , 27 cu ER , si 28 cu ERLVH . [ 1 ]

Ecocardiografia este deosebit de util n cazul n revrsatul pericardic este suspectat pe motive clinice sau radiografice , boala dureaza mai mult de 1 sptmn , sau miocardita sau pericardita purulenta este suspectat .

O radiografie toracica este util doar pentru diagnostic la pacienii cu revrsate > 250ml . Pacientii cu revrsate mici ( mai puin de cteva sute de mililitri ), se pot prezenta cu o silueta cardiac normal .

Testele de laborator pot include CBC , electrolii serice , ureei ( BUN ) , i nivelul creatininei , viteza de sedimentare a hematiilor ( VSH ) i ( CRP ) niveluri de proteine C - reactive , si masuratori biomarker cardiace , lactat dehidrogenaz ( LDH ) , i ser glutamic - oxaloacetic transaminazelor ( GOT , AST ) niveluri .

Vezi Reacia conduce pentru mai multe detalii .

administrareTratament pentru anumite cauze de pericardite este direcionat n funcie decauza. Pentru pacientii cu pericardita idiopatica sau virale , tratamentul este ndreptat la ameliorarea simptomelor .

tratament farmacologic

Medicamente antiinflamatoare nesteroidiene ( AINS ) sunt de temelie a tratamentului . Aceti ageni au o eficacitate similar , cu scutire de durere toracic n aproximativ 85-90 % dintre pacienti in termen de zile de tratament . Un AINS full - doza ar trebui s fie utilizat , iar tratamentul trebuie s dureze 7-14 zile .

Colchicina , singur sau n combinaie cu un AINS , pot fi luate n considerare pentru pacientii cu simptome recurente sau continuat mai mult de 14 zile. [ 2 ]

Corticosteroizii nu trebuie utilizat pentru tratamentul initial de pericardit dac nu este indicat pentru boala de baza , starea pacientului nu are nici un rspuns la AINS sau colchicin , sau ambele medicamente sunt contraindicate .

tratamentul chirurgical

Proceduri chirurgicale pentru pericardita includ Pericardiectomia , pericardiocenteza , plasarea pericardic fereastr , i pericardiotomy .

Pericardiectomia este procedura chirurgicala cel mai eficient pentru gestionarea colecii mari , deoarece are cel mai scazut risc asociat de efuziunilor recurente . Aceast procedur este folosit pentru pericardita constrictiva , pericardit exuberant , sau pericardit recurent cu mai multe atacuri , dependena de steroizi , i / sau intoleran la alte management medical .

Pacientii cu efuziuni mai mari de 250 ml , efuziuni n care dimensiunea crete , n ciuda dializa intensiv de 10-14 de zile , sau efuziuni cu dovezi de tamponare sunt candidati pentru pericardiocentez .

Plasarea pericardic fereastr este folosit pentru tratamentul pericardit exuberant . La pacienii n stare critic , un cateter cu balon poate fi utilizat pentru a crea o fereastr pericardic , n care numai 9 cm2 sau mai puin din pericard este rezecat .

Luai n considerare pericardiotomy subxiphoid pentru efuziuni mari care nu rezolva . Aceast procedur poate fi efectuat sub anestezie local i are un risc mai mic de complicatii decat Pericardiectomia .

A se vedea, de tratament si medicatie pentru mai multe detalii .

bibliotec de imaginiAcest electrocardiogram cu 12 derivaii este reprezentativ oAcest electrocardiogram cu 12 derivaii este reprezentativ de pericardit .fundalPericardita acut este o inflamaie a pericardului caracterizata prin dureri in piept , freca frecare pericardic , i electrocardiografice ( ECG ) schimbari de serie ( a se vedea un exemplu de astfel de ECG de mai jos ) . Pericardit i tamponad cardiac implice potenialul de spaiul din jurul inimii sau a pericardului , pericardita este o cauza de acumulare de lichid n acest spaiu potenial , i tamponad cardiac este rezultatul hemodinamice de acumulare de lichid .

Acest electrocardiogram cu 12 derivaii este reprezentativ oAcest electrocardiogram cu 12 derivaii este reprezentativ de pericardit .Pentru mai multe informaii , consultai Pericardita articolele referin Medscape constrictive , pericardit constrictiv - exuberant , Pericardita infecioas Pediatrica , i imagistic n pericardita constrictiv .

Pentru informaii educatia pacientului , consultai Centrul de colesterol i Heart Center , precum i pericardit, atac de cord, i dureri n piept.

anatomiePericard ( complex pericardic) serveste ca o bariera de protectie de la rspndirea de infecii sau inflamaii la structurile adiacente . Acesta este compus dinpericard parietale ( un strat fibros exterior ) ipericard viscerale ( o membrana interioara seros realizat dintr-un singur strat de celule mezoteliale ) . Pericardul fibros este un sac balon n form , dur exterior cu anexele la diafragma , stern , i cartilajul costal . Pericardul visceral este subire , adiacent lasuprafaainimii i este fixat degrsime epicardice ci reflect napoi pe ea nsi , pentru a formapericard parietal .

Pericardul conine n mod normal, la fel de mult ca 20-50 ml de o ultrafiltratul de plasm . Aproximativ 90-120 ml de lichid pericardic suplimentare se pot acumula n pericard , fr o cretere a tensiunii . Capacitatea de a atrii i ventricule pentru a umple este compromis mecanic cu acumulare de lichid , care poate duce la cresteri semnificative a tensiunii pericardic , provoca accident vascular cerebral volum redus , debit cardiac sczut , i hipotensiune arterial ( fiziologie tamponad cardiac ) . Rapiditatea acumularea de lichid influeneazefectul hemodinamice . Drenaj are loc prin intermediul canalului toracic i ductul limfatic drept n spaiul pleural dreapta .

FiziopatologiePericardic fiziologie include trei funcii principale . n primul rnd , prin funcia sa mecanic ,pericardul promoveaz eficiena cardiace prin limitarea dilatarea acut , meninnd respectarea ventricular cu meninereacurbei Starling , i distribuirea forelor hidrostatice . Pericard creeaz , de asemenea, o camer nchis cu presiune redus dect cea atmosferic , care ajuta umplerea atriala si scade presiunile cardiace transmurale . n al doilea rnd , prin funcia sa membranos , scuturile pericardinimii prin reducerea frecrii extern i acioneaz ca o barier mpotriva extinderii infeciei i malignitate . Al treilea rnd, prin funcia sa ligamentous ,pericardul fixeaz anatomicinima .

n cele mai multe cazuri de pericardita acuta , pericardul este acut inflamat i are o infiltrare de polimorfonucleare ( PMN ), leucocitelor si vascularizatie pericardic . De multe ori , pericardul manifesta o reacie fibrinoas cu exudate i adeziunilor . Pericardului poate dezvolta o efuziune seroas sau hemoragic . Un pericardita granulomatoasa apare cu tuberculoz, infecii fungice , artrita reumatoida ( RA ) , i sarcoidoza .

Pericardita uremic este gandit pentru a rezultat din inflamaie a straturilor viscerale i parietal ale pericardului de toxine metabolice care se acumuleaza in organism din cauza la insuficienta renala . Ali factori pot fi implicate , cu toate acestea , deoarece pericardita , de asemenea, poate aprea la pacienii cu insuficien renal cronic crora li se administreaz deja tratament de dializa .

Toxinele presupuse a sugerat s precipite pericardita uremic atunci cnd se acumuleaz sunt slab caracterizat , dar ele pot include uree , creatinina , methylguanidine , guanidinoacetate , hormon paratiroidian , beta2 - microglobulin , acid uric , i altele . Mai mult de o toxina aparent pot fi implicate , dei controverse nconjoar acest punct .

Schimbrile patogene precise induse de aceste toxine atunci cnd provoac pericardita uremic nu au fost elucidate , dei exist o corelaie dur cu gradul i durata azotemie ,ureei ( BUN ), nivelul este de obicei mai mare de 60 mg / dL ( 22 mmol / L ) . Pericardita uremic pot fi asociate cu efuziune hemoragic sau seros , dei se suprapun n mare exist . Effusions hemoragice sunt mult mai frecvente i rezultat n parte din disfunctii plachetare induse de uremie .

Unii autori disting ntre 2 tipuri de pericardita la pacienii cu insuficien renal . Un tip este pericardita uremic , care apare la pacientii cu uremie care nu au primit dializa . Cellalt tip este pericardita dializa - asociate , care apare la pacienii care primesc deja dializ . n acest din urm caz , dializa inadecvat poate fi, de obicei implicat , deoarece dializa agresiv duce adesea la rezoluie . Alte cauze de pericardit dializa asociate pot include suprancrcare de volum i infecii bacteriene sau virale .

ntr- un studiu observational care datele folosite la 88 de pacienti hemodializati de ntreinere , cercetatori au descoperit ca dializa intensiv este cel mai eficient tratament pentru pericardita dializa asociate la pacientii dializati care au diabet zaharat si cei care nu . [ 3 ] Ca urmare a intensificrii de hemodializa , pericardita mbuntit n 85,1 % dintre pacientii cu diabet zaharat i la 82,9 % din cei fara diabet . Printre pacientii cu diabet zaharat , 85,1 % au supravietuit fara reaparitia de pericardit , 4,3% au supravietuit , dar a suferit recurenta , i 10,6% au murit , cu rezultate similare nregistrate n grupul fr diabet zaharat ( 87,8 % , 4,9 % , i 7,3 % , respectiv ) . [ 3 ]

etiologieAceast seciune primul va discuta pe scurt pericardita acuta , pericardita cronica , i tamponad cardiac , apoi , mai multe entiti specifice care produc pericardita vor fi revizuite pe scurt .

pericardita acutPericardita seros este de obicei cauzata de inflamatia neinfectioasa , cum ar fi apare in poliartrita reumatoida ( RA ) i lupus eritematos sistemic ( LES ) . Aderente fibroase apar foarte rar .

Pericardit fibroase i serofibrinous reprezint acelai proces de baz i sunt cel mai frecvent tip de pericardit . Cauzele comune includ infarctul miocardic acut ( MI) , postinfarct ( inclusiv sindromul Dressler ) , uremie , radiatii , RA , LES , si trauma . Infeciile severe poate provoca , de asemenea, o reacie fibrinoas , la fel ca chirurgie cardiaca de rutina .

Pericardite purulente sau purulent , datorit organisme cauzali pot aprea de extensie directa , nsmnarea hematogene , sau extinderea limfatic , sau prin introducerea direct n timpul cardiotomy . Imunosupresie faciliteaz aceast condiie . Caracteristicile clinice includ febra , frisoane , i temperaturi spiking . Pericardita constrictiva este un potenial complicatie grava .

Hemoragic pericardita implic snge amestecat cu o efuziune fibrinoas sau purulent , i este cel mai frecvent cauzata de tuberculoza sau invazie neoplazic direct . Aceast condiie poate aprea , de asemenea, n infecii bacteriene severe sau la pacientii cu un Diatez hemoragic . Pericardita hemoragic este comun dupa interventii chirurgicale cardiace i poate provoca tamponada . Semnificaia clinic este similar cu pericardita purulent .

Pn la proba contrarie , caseation n interiorul sacului pericardic este tuberculoas de origine . Netratate , pericardita brnza este cel mai frecvent antecedente de pericardita constrictiva cronica de natur fibrocalcific .

pericardita cronicaMediastinopericarditis adeziv este o reacie care urmeaz , de obicei, pericardita purulent sau cazeoas , chirurgie cardiaca , sau de iradiere . Aceast condiie este foarte rar cauzata de un exudat simplu fibrinoas . Spaiu potenial pericardic este distrus , iar aderenasuprafeei exterioare astratului parietale la structurile din jur apare . Punct de vedere clinic , a tensiunii arteriale sistolice contracie a cutiei toracice i diafragma i paradoxal pulsului pot fi observate . A crescut volumul de munc poate duce la hipertrofie cardiaca masiv i dilatarea , care poate imita o cardiomiopatie idiopatica .

Pericardita constrictiva este de obicei cauzata de pericardita supurative , cazeoase , sau hemoragic . Inima poate fi integrate ntr-o 0,5 cm grosime de strat de 1 cm grosime de cicatrice sau calcifiere ( concretio CORDIS ) , care seamn cu un mulaj . Spre deosebire de rezultatele clinice n mediastinopericarditis adeziv , inima nu poate deveni hipertrofice sau se dilata din cauza spaiului insuficient .

Imazio et al sugereaza ca pericardita constrictiva este o complicatie rara de pericardita acuta virala sau idiopatica ( < 0,5 % ) . Cu toate acestea , se pare a fi relativ frecvent pentru etiologii specifice , n special bacteriene . [ 4 ]

tamponada cardiacTamponada este mai frecventa la pacientii cu pericardita maligne . Efuziuni cauzate de tumori de multe ori trece la tamponada , provoca sngerri n pericard . Snge se acumuleaz mai rapid dect un transudat sau exudat i mai frecvent provoaca tamponare .

Identificarea orice lichid pericardic n stabilirea de patrundere a prejudiciului a toracelui sau abdomenului superiornecesit resuscitare agresiv , se pot produce accidente cardiace penetrante , cu hemopericardium ca caracteristica cea mai comun. n hemopericardium acut masiv , timpul este insuficient pentru defibrination s apar . Hemopericardium organizeaz i poate parial cheag , rezultnd ntr- un hematom pericardic . Hematomul poate aprea echogenic n loc de ecou liber .

Surse poteniale de perforare cardiace iatrogen includ Amplasarea centrala linie , inserarea stimulator cardiac , cateterism cardiac , sternale biopsii de mduv osoas , i pericardiocentez . Atriul drept este site-ul cel mai frecvent de perforare de plasare cateter . Perforare , precum perfuzie cateter direct de fluide , poate provoca tamponare . De fapt , o ntrziere tamponare de ore sau zile a avut loc secundar la misplacement cateter .

ntr-un raport de caz , tamponare a fost descris ca fiind prima manifestare de dermatopolymyositis . [ 5 ]

Cauzele specifice ale pericardit includ urmtoarele i sunt analizate pe scurt mai jos :

idiopatica cauzeazCondiii infecioase , cum ar fi infeciile virale , bacteriene , i tuberculoasaAfectiuni inflamatorii , cum ar fi RA , LES , sclerodermia , si febra reumaticaTulburri metabolice , cum ar fi insuficien renal , hipotiroidism , i hipercolesterolemieTulburri cardiovasculare , cum ar fi IM acut , sindromul Dressler , i disectie aorticaCauze diverse , cum ar fi iatrogene , neoplasme , medicamente , iradiere , proceduri cardiovasculare , si traumeidiopatica cauzeazntre 26 % i 86 % din cazuri de pericardita acuta sunt idiopatice n natur . [ 6 ] Nu caracteristici clinice distinge cazuri idiopatic, de pericardit viral . Este posibil ca cele mai multe cazuri idiopatice sunt infecii virale nediagnosticate . Vrfuri sezoniere apar n primvara i toamna .

Idiopatic cronic pericardite este definit ca o efuziune pericardic care persist mai mult de 3 luni , fr nici o etiologie aparent . Pericardiocenteza singur duce la rezoluie de revrsate masive , cu toate acestea , recurenta este comuna .

Infecii viraleInfecie viral este cea mai frecventa cauza de pericardita acuta si conturi de 1-10 % din cazuri . Boala este , de obicei, o scurt boal auto-limitate , care dureaza 1-3 saptamani si poate aparea ca epidemii sezoniere , n special coxsackievirus B i gripa .

Virusuri cauzali includ coxsackievirus B , [ 7 ] echovirus , adenovirusuri , virusurilor gripale A si B , enterovirus , virusul urlian , virusul Epstein - Barr , virusul imunodeficientei umane ( HIV ) , virusul herpes simplex ( HSV ) tip 1 , virusul varicelo-zosterian ( VZV ) , virusul rujeolic , virusul paragripal ( PIV ) de tip 2 , i virusul respirator sinciial ( RSV ) , citomegalovirus ( CMV ) , i virusurile hepatitei A , B , i C ( HAV , HBV , HCV , respectiv ) .

Pacientii pot fi asociate miocardita . Implicarea pericardic este frecventa la persoanele cu HIV , dar este , de obicei, o efuziune pericardic asimptomatic de volum mic . Persoanele cu infecie HIV avansat dezvolta implicarea pericardic mai frecvent , cu un studiu menionat de compresie diastolice n atriul drept n 5 % din cazuri de infecie cu HIV avansat [ 8 ] pericardita simptomatic apare la mai puin de 1 % din cazurile de HIV , iar etiologia acesteia pot include . cauzele obinuite , infecii oportuniste, sarcom Kaposi , i HIV.

infectie bacterianaConturi de infecii bacteriene pentru 1-8 % din cazuri, pericardit i rezultatul de extindere pulmonar directe , hematogene rspndirea , abces miocardic sau endocardita , leziuni penetrante a peretelui toracic , fie de traumatisme sau interventii chirurgicale , sau o leziune supurative subdiafragmatic . Pericardita purulent pot rezulta din pericardita aseptice anterior , i un procent mare de pacienti dezvolta pericardita constrictive .

Organisme care au fost izolate include specii gram-pozitive , cum ar fi Streptococcus pneumoniae si alte specii Streptococcus i Staphylococcus . [ 9 ] specii gram -negative izolate includ Proteus , Escherichia coli , Pseudomonas , Klebsiella , Salmonella , Shigella , Neisseria meningitidis , i Haemophilus influenzae .

Organisme mai puin comune includ Legionella , Nocardia , Actinobacillus , Rickettsia , Borrelia burgdorferi ( Borelioza Lyme ) , Listeria , Leptospira , Chlamydophila psittaci , i Treponema pallidum ( sifilis ) .

Anaerobe au fost , de asemenea, izolat n 40 % dintre pacientii din comentarii de copii i adolesceni .

Anterior , Pneumococcus fostorganismului predominant . Cu toate acestea , n epoca antibiotic , specii de stafilococ i gram - negativ au devenit mai frecvente . Cele mai multe cazuri sunt n prezent asociate cu chirurgie toracica , boli renale , si imunosupresie .

infecie tuberculoasDe tuberculoz 4 % din cazuri, i ar trebui s fie luate n considerare n toate cazurile de pericardita , fr un curs rapid , n special n grupurile cu risc ridicat , cum ar fi pacienii vrstnici din azilurile de btrni i cei cu sindromul imunodeficienei dobndite ( SIDA ) . [ 10 ] Aproximativ 50 % dintre pacientii afectati dezvolta pericardita constrictive .

Infecii fungice i parazitareOrganisme fungice care pot determina pericardita acuta includ Histoplasma , Blastomyces , Coccidioides , Aspergillus i Candida . Organisme parazitare includ Entamoeba , Echinococcus , i Toxoplasma .

poliartrita reumatoidaPericardita apare predominant la barbati cu sever distructive i nodular RA . Implicarea pericardic este de obicei clinic tcut , cu diagnosticul fcut n doar 2 % dintre adulti si 6 % dintre minorii cu RA . Rareori , pericardita precede debutul RA . Studiile autopsiei arat o prevalen pericardita de 11-50 % .

Lupusul eritematos sistemic , sclerodermia , sarcoidozaClinic pericardita evident a fost raportata la 25 % dintre pacientii cu LES i apare de obicei n lupus flare -up-uri , dar poate fi o manifestare . Seria autopsie dezvluie implicarea pericardic n 62 % dintre pacientii cu lupus .

Pericardita este recunoscut n 5-10 % din pacientii cu sclerodermie , cu o prevalen de 70 % autopsie . Exsudat pericardic apar la 40 % dintre pacientii cu sclerodermie si poate fi din cauza unor defeciuni sclerodermie , miocardic ( cardiomiopatie restrictiv ) i insuficien renal . Cardiomiopatie restrictiv i constrictie pericardic pot coexista . De obicei , hipertensiune pulmonara , insuficienta cardiaca dreapta , i disfuncie sistolic apar .

Sarcoidoza poate duce la pericardita , dar aceast condiie rareori cauzeaza tamponad cardiac sau pericardita constrictiv

febr reumaticPericardita la cei cu febr reumatic apare mai frecvent la grupurile socio-economice mai mici i la copii , de multe ori nsoesc endocardita si miocardita , cu un prognostic mai rau . Luai n considerare febr reumatic ca o etiologie , n orice copil cu pericardit . Cu toate acestea , aceast boal nu este o cauz a demonstrat de pericardite constrictive .

La aduli , pericardite nu pot aprea cu implicarea miocardic sau valvulare , iar acesta este asociat cu un prognostic mai bun . Pericardita apare de obicei 7-10 zile de la debutul de febra si artrita . De multe ori , etapa 1 electrocardiografice ( ECG ), rezultatele sunt absente ( vezi Electrocardiograma ) .

Alte afectiuni inflamatoriiUrmtoarele condiii pot provoca , de asemenea, pericardita acuta :

sindromul SjgrenBoala mixt conjunctiv , tesutsindromul Reiterspondilita anchilozantaBoli inflamatorii intestinalegranulomatoza WegenerVasculit ( de exemplu , arterita cu celule gigant , poliarterita )polimiozitasindromul Behetboala WhippleFMFboala seruluiInsuficien renalRichard Bright descris pericardita uremic n 1836 . Din acel descrierea clasic , aceasta complicatie comuna de insuficienta renala cronica a evoluat de la un eveniment de ru augur anun fazele terminale ale bolii la un eveniment care , cu managementul devreme , este probabil s aib un rezultat bun . Mai mult , progresele n tehnologia de dializa cu managementul precoce i n timp util de insuficienta renala cronica au redus dramatic prevalenta de pericardit uremic . Pericardita uremic are o prevalenta de 6-10 % la pacienii cu insuficien renal acut sau cronic , i continu s fie asociate cu o morbiditate i mortalitate ocazional .

Conturile insuficien renal pentru aproximativ 12 % din cazuri de pericardit . n epoca predializai , pericardit dezvoltat n 35-50 % dintre pacientii cu uremie care au avut insuficien renal cronic i mai puin frecvent la cei cu insuficien renal acut . Moartea urmat de multe ori n cteva sptmni . Cu dializa , rata de inciden pericardita este mai mic de 10 % , cu toate acestea , aceast condiie apare dup debutul de dializ n 8-12 % din cazuri .

Exsudat pericardic asimptomatice pot aparea in 36-62 % din pacientii cu uremie care au nevoie de dializa , aceste colecii sunt de multe ori mici pana la moderate n dimensiune i poate s apar secundar de suprancrcare . Exsudat pericardic poate duce la complicatii hemodinamice semnificative n timpul dializei rutin . Mai mult dect att ,prezena unui revrsat pericardic mare, care persist pentru mai mult de 10 de zile dup dializ intensiv are o mare probabilitate de a provoca tamponare .

hipotiroidismulConturile Hipotiroidismul pentru ct mai multe ca 4 % din cazuri, pericardit . De fapt , implicarea miocardic este comun , iar implicarea pericardic apare, de obicei , cu hipotiroidism sever . Pacientii pot dezvolta exsudat pericardic mari , dar rareori dezvolta tamponada .

colesterol pericarditaPericardita colesterol , de asemenea, numit pericardit aur - vopsea , este o complicatie a unui revarsat pericardic cronic exacerbate de cristale de colesterol . Acesta se prezinta de obicei cu efuziuni mari, care nu sunt hemodinamic importante , i dezvoltarea de constrictie este rar . Pericardita granulomatoasa a fost implicata in unele cazuri .

infarct miocardicDup un infarct transmural , un exudat pericardic fibrinoas apare n 24 de ore , ncepe s se organizeze la 4-8 zile , si completeaza organizarea putin 4 saptamani . [ 11 , 12 ] durere pericardic se produce mai frecvent dect freca frecare , care este adesea detectate la a doua sau a treia zi dup un IM acut , dar poate fi auzit n 24 de ore i ct mai trziu de 10 zile.

nainte de terapia trombolitic , infarct asociate variaz de pericardit de la 7 % la 23 % din cazuri . La autopsie ntr-un studiu , aproape toi pacienii au fost observate de a avea pericardit fibrinoas localizate de deasupra zonei de infarct . Cu terapia trombolitic i direct infarctului angioplastie ,incidena post-IM -asociate pericardite a sczut la 5-8 % .

n general , implicarea pericardic indic un infarct mai mare , incidenta mai mare de disfunctie ventriculara stanga , si mortalitate mai mare . Pericardita , de obicei, se vindeca fara consecin , pot aprea efuziuni , dar ei rareori conduc la tamponada .

sindromul DresslerSindromul Dressler este acum considerate rare . Cnd pericardita asociata cu sindromul Dressler se produce , se observ , de obicei, 2-3 sptmni dup un infarct miocardic . Iniial , sindromul a fost descris n ct mai multe ca 4 % dintre pacienii care au urmat i de infarct miocardic acut . Studii ulterioare au sugerat o inciden mult mai mic . Sindromul Dressler este rareori descris cu embolie pulmonara .

Acest sindrom poate fi un fenomen autoimun mediat unic la antigeni miocardice , sau poate fi pur i simplu o nerecunoscut pericardite post-IM . Pacientii pot dezvolta infiltrate pulmonare i revrsate pericardice mari .

Din cauza riscului de pericardita hemoragic , tratamentul anticoagulant trebuie oprit la pacientii cu sindromul Dressler .

Disecie aortic i tsubo cardiomiopatieConturile disecie aortice de 1 % din cazurile de pericardit acut , n special pentru cazurile cu hemoragie npericard .

Tsubo cardiomiopatie este un sindrom cardiac tranzitoriu care implic ventriculului stng akinesis apical si imita sindrom coronarian acut .

neoplasmCont de tumori maligne de 5-17 % din cazuri, pericardit , la pacienii cu pericardit acut sau efuziunea pericardica , 4-7 % au o malignitate nebanuite . Neoplasm primar al inimii i pericardul este rar , cele mai multe cazuri de pericardit neoplasm - conexe sunt un rezultat al bolii metastatice . Studiile de autopsie au constatat c aproximativ 10 % dintre pacientii cu cancer dezvolta afectare cardiac , i este de multe ori punct de vedere clinic tcut . Celulele neoplazice ajungepericardului prin fluxul sanguin , prin sistemul limfatic , sau prin creterea local .

Boli neoplazice , boli deosebit de avansate , este cea mai frecventa cauza de tamponada n spital . Ocazional , tumora mbrac inima i provoac pericardita constrictiva , mai degrab dect tamponare .

Mezoteliom pericardic i angiosarcomul sunt tumori maligne letale cu rspndirea locale agresiv care raspund slab la tratament . Sugarii i copiii pot prezenta cu o teratoma n spaiul pericardic . Acestea pot fi de multe ori eliminate cu succes .

Cancer pulmonar , inclusiv adenocarcinom i carcinom cu celule scuamoase i mici , reprezint aproximativ 33 % din cazuri ; conturi de cancer de san de 25 % , leucemie i limfom , inclusiv Hodgkin i non - Hodgkin , cont pentru 15 % din cazuri , si melanomul malign reprezint o alt 5 % . Aproape toate celelalte boli maligne , cu excepia creierului primar , cuprindrestul cazurilor . Sarcom Kaposi a devenit , de asemenea, o cauz mai proeminent a bolii neoplazice cu epidemia de SIDA .

droguriUnele medicamente , inclusiv penicilina si sodiu cromolyn , induce pericardit , printr-o reacie de hipersensibilitate . Antraciclinei medicamente antineoplazice , cum ar fi doxorubicina si ciclofosfamida , au efect toxic cardiac direct i poate cauza pericardita acuta si miocardita .

Pericardita poate dezvolta , de asemenea, de la un sindrom lupus induse de droguri cauzate de medicamente , inclusiv procainamide , hydralazine , metildopa , izoniazida , mesalazina , i rezerpina . Metilsergida cauzeaza pericardita constrictive prin fibroza mediastinale . Dantrolen , fenitoina , i minoxidil produc pericardite , printr-un mecanism necunoscut .

Vaccinare variola rareori duce la miocardita . ntr-o analiz a unui program de vaccinare mare n armata SUA , aproximativ 12 la 100.000 de militari vaccinai dezvoltat myopericarditis n termen de 14 zile de la vaccinare [ 13 , 14 ] Dac acest lucru a fost din cauza unui efect citopatic viral direct sau un fenomen imun mediat este neclar . .

radiaiePericardit este toxicitatea cardiaca cele mai frecvente de radioterapie . Altele sunt boli coronariene , tulburri de conducere , i de boal miocardic i valvulara . [ 15 ] O inciden ridicat de astfel de toxicitate apare cu doze mari , n special cele mai mari de 4000 rad .

Pericardita radiatii poate prezenta ca pericardita acuta , cu sau fara efuziune , pericardita constrictive cronice , sau pericardita exuberant - constrictive .

Proceduri invazive cardiologiceStudiile electrofiziologice , ablatie radiofrecventa , implantare stimulator cardiac , si interventie coronariana percutanata sunt printre cele mai multe proceduri invazive cardiologice care pot provoca pericardit .

Sindromul Postpericardiotomy este similar cu sindromul Dressler , cu excepia faptului c sindromul postpericardiotomy apare dupa interventia chirurgicala cardiaca . Mai multe serii de remarcat o rata de incidenta de 10-40 % , aproximativ 1 % din pacientii cu sindrom postpericardiotomy dezvolta tamponada .

Exsudat pericardic poate aprea n absena de caracteristicile tipice ale sindromului postpericardiotomy . ntr-un studiu , 56 % au dezvoltat exsudat pericardic devreme dupa o interventie chirurgicala cardiaca , fr corelarea cu pericardita sau tamponad . Coleciile au fost mai frecvente dup sngerare post-operatorie grele .

traumaAproximativ 1 % din cazurile de pericardite acute sunt cauzate de traume , cum ar fi penetrarea i nonpenetrating traume cardiace . De asemenea, s ia n considerare ruptura esofagiana sau perforare i pancreatit .

EpidemiologieDatele epidemiologice privind incidena de pericardita acuta lipsesc , probabil c aceast condiie este frecvent asimptomatic clinic , n ciuda prezenei sale n numeroase afectiuni . Lorell remarcat o diagnosticul de pericardit acut la aproximativ 1 la 1000 de admitere spital . [ 16 ] n plus , pericardita acuta cuprinde 1 % din vizite de urgenta camera la pacientii cu supradenivelare de segment ST . [ 17 ] De fapt , incidena raportat de acute pericardic tamponada este de aproximativ 2 % din traumatism penetrant , cu toate acestea , aceast condiie este rar vzut n piept traumatism contondent .

Pericardita uremic pot s apar n 6-10 % din pacienii cu insuficien renal avansat nainte de iniierea de dializa . Cnd pacienii cu revrsate mari sunt studiate , uremie pot reprezenta pn la 20 % din cazuri, n unele serii . Disponibilitatea larg de dializa a redus incidenta de pericardit uremic .

Boli maligne este cea mai frecventa cauza de efuziune pericardic cu tamponada n rile dezvoltate , cu toate acestea , tuberculoza ar trebui s fie luate n considerare n zonele endemice .

Pericardita acut este mai frecvent la brbai dect la femei . Cu toate acestea , dei aceast condiie este mai frecventa la adulti decat la copii , adolescenti sunt mai frecvent afectate decat adultii tineri . Cu toate acestea , Merce et al constatat nici o diferen n etiologie , clinica , iar prognosticul ntre pacienii vrstnici i tineri cu exsudat pericardic moderate i mari . [ 18 ] prognozPrognosticul la persoanele cu pericardite depinde etiologia aceast condiie, precum i prezena unui pericardic efuziune i / sau tamponare. Idiopatic i etiologii virale au, de obicei, un curs de auto-limitate, fr nici un risc de evoluie spre pericardita constrictive [19, 20] Cele mai multe cazuri post-MI au o evolutie benigna,. Cu toate acestea, pericardita este asociat cu infarcte mari, i, prin urmare, n general lung termen mortalitatea poate fi crescut.

Pacientii cu sclerodermie sau copii cu febr reumatic i pericardita au un prognostic saraci, si implicarea pericardic purulent, tuberculoas, i neoplazice au cursuri mai complicate cu rezultate mai rau. Pericardita purulent este asociat cu o rata de mortalitate apropie de 100% pentru persoanele netratate i o rat a mortalitii de 12-40% pentru pacienii tratai. Rata mortalitii n pericardita tuberculoas se apropie de 50%.

Pericardite uremic continu s fie asociat cu o morbiditate i mortalitate ocazionale. Dintre pacientii cu pericardita uremic, 3-5% poate dezvolta pericardita hemoragic.

Pentru leziuni penetrante, prognosticul depinde foarte mult de identificarea rapid a tamponare. Mortalitatea pot aprea n 3-5% din cazuri rezult din tamponada cardiaca sau aritmii. Factori favorabili includ perforaii minore, izolate rni ventriculului drept, tensiunii arteriale sistolice mai mult de 50 mm Hg, i prezena de tamponare.