Acute pericarditis is an inflammation of the pericardium characterized by pericarditic chest pain, pericardial friction rub, and serial electrocardiographic (ECG) changes (eg, new widespread ST-elevation or PR depression; new/worsening pericardial effusion).[1, 2, 3, 4] The first and last stages of ECG changes are seen in the images below.
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Stage 1 electrocardiograph changes in a patient with acute pericarditis.
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Stage 4 electrocardiograph changes in the same patient as in the previous image, taken approximately 3 months after acute pericardial illness. The pat....
Signs and symptoms
Chest 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 causes
Infectious conditions, such as viral, bacterial, and tuberculous infections
Inflammatory disorders, such as RA, SLE, scleroderma, and rheumatic fever
Metabolic disorders, such as renal failure and hypothyroidism
Cardiovascular disorders, such as acute MI, Dressler syndrome, and aortic dissection
Miscellaneous causes, such as iatrogenic, neoplasms, drugs, irradiation, sarcoidosis, cardiovascular procedures, and trauma
See Presentation for more detail.
Diagnosis
Initial 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 diffuse ST elevation. 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.[5]
Echocardiography is indicated 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 helpful to exclude pulmonary conditions that may be responsible for or are associated with the cause of pericarditis (ie, cancer, infection, SLE, sarcoidosis, etc). It is not helpful for evaluating the presence of pericardial fluid, as patients with small effusions (less than a few hundred milliliters) may present with a normal cardiac silhouette; it is only helpful for diagnosing fluid in patients with effusions larger than 250 mL.
Laboratory 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. Serum titers for suspected infectious etiologies and testing for tuberculosis exposure (ie, PPD or interferon-gamma release assays) may be helpful.
See Workup for more detail.
Management
Treatment 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
Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) are the mainstays of therapy. NSAID 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 aspirin or an NSAID, can be considered as first-line therapy as an adjunct for patients with acute pericarditis, particularly to prevent recurrences.[3, 4]
Corticosteroids should not be used for initial treatment of pericarditis unless it is indicated for the underlying disease, the patient’s 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, 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.
Acute pericarditis is an inflammation of the pericardium characterized by pericarditic chest pain, pericardial friction rub, and serial electrocardiographic (ECG changes (eg, new widespread ST-elevation or PR depression; new/worsening pericardial effusion).[1, 2, 3] {ref4 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.
For more information, see the Medscape Drugs and Diseases articles Constrictive Pericarditis, Effusive-Constrictive-Pericarditis, Pediatric Infective Pericarditis, and Imaging in Constrictive Pericarditis.
For patient education information, see the Cholesterol Center and Heart Health Center, as well as Pericarditis, Heart Attack, and Chest Pain.
The 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 rapidly 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. With slow accumulation of fluid, the pericardium has time to stretch and accommodate the fluid increase so that hemodynamic compromise does not ensue. Drainage of the pericardium occurs via the thoracic duct and the right lymphatic duct into the right pleural space.
Pericardial physiology includes three main functions. First, through its mechanical function, the pericardium promotes cardiac efficiency by limiting acute cardiac 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. In recurrent pericarditis, the innate immune system appears to play a role in its pathogenesis.[6, 7]
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 underlying cause of pericarditis may be infectious or noninfectious.[1] In developed nations, although pericarditis is predominantly referred to as idiopathic, the most frequent causes are autoreactive/lymphocytic, malignant, and infectious.[6]
A retrospective study (2004-2014) that evaluated the etiology of acute pericarditis in 32 children found that the most common cause was infectious (34%), followed by inflammatory disorders (28%).[8] Staphylococcus aureus was the responsible agent in four of five cases of purulent pericarditis; all five patients also had concurrent infection of the soft tissue, bone, lung, or other. Other infectious agents included Histoplasma capsulatum, Mycoplasma pneumoniae, influenza A, and Enterovirus.[8]
This section will first briefly discuss acute pericarditis, chronic pericarditis, and cardiac tamponade; then, several specific entities that cause pericarditis will be briefly reviewed.
Acute pericarditis
Serous 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, 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 or trauma 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 pericarditis
Adhesive 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-cm–thick to 1-cm–thick 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.[9]
Cardiac tamponade
Tamponade 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.[10]
Specific causes of pericarditis include the following and are briefly reviewed below:
Idiopathic causes
Infectious conditions, such as viral, bacterial, and tuberculous infections
Inflammatory disorders, such as RA, SLE, scleroderma, and rheumatic fever
Metabolic disorders, such as renal failure, hypothyroidism, and hypercholesterolemia
Cardiovascular disorders, such as acute MI, Dressler syndrome, and aortic dissection
Miscellaneous causes, such as iatrogenic, neoplasms, drugs, irradiation, sarcoidosis, cardiovascular procedures, and trauma
Idiopathic causes
Between 26% and 86% of cases of acute pericarditis are idiopathic in nature.[11] 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.
More recently, there has been evidence that the innate immune system and autoinflammation contribute to acute and recurrent pericarditis.[6, 7]
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 infection
Viral 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,[12] 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.[13] 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 infection
Bacterial 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.[14] 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 infection
Tuberculosis 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).[15] Approximately 50% of affected patients develop constrictive pericarditis. On rare occasion, acute purulent pericarditis is caused by coinfection with Mycobacterium tuberculosis and S aureus, and this may be the first manifestation of infection with human immunodeficiency virus (HIV).[16]
Fungal and parasitic infection
Fungal organisms that may cause acute pericarditis include Histoplasma, Blastomyces, Coccidioides, Aspergillus, and Candida. Parasitic organisms include Entamoeba, Echinococcus, and Toxoplasma.
Uremia
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.[17] 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).[17]
Rheumatoid arthritis
Pericarditis 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%.
Clinically 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 fever
Pericarditis 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 conditions
The following conditions may also cause acute pericarditis:
Richard 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.
Hypothyroidism
Hypothyroidism 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 pericarditis
Cholesterol 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 infarction
After a transmural infarction, a fibrinous pericardial exudate appears within 24 hours, begins to organize at 4-8 days, and completes organization at 4 weeks.[18, 19] 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 post–MI-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 syndrome
Dressler 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 post–MI 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 cardiomyopathy
Aortic 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.
Neoplasm
Malignancy 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.
Drugs
Some 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.[20, 21] Whether this was due to a direct viral cytopathic effect or an immune-mediated phenomenon is unclear.
Irradiation
Pericardial disease is the most common cardiac toxicity from radiation therapy. Others are coronary artery disease, conduction disturbance, and myocardial and valvular disease.[22] 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 procedures
Electrophysiologic 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.
Trauma
Approximately 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.
Epidemiologic data on the incidence of acute pericarditis are lacking, likely because this condition is frequently inapparent clinically, despite its presence in numerous disorders. However, it appears to be the most common form of pericardial disease and a relatively common cause of chest pain.[1]
Lorell noted a diagnosis of acute pericarditis in approximately 1 per 1000 hospital admissions.[23] In addition, acute pericarditis comprises 1% of emergency room visits in patients with ST-segment elevation.[24] 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.[25]
The 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.[26, 27] Most post–MI cases have a benign course; however, pericarditis is associated with larger infarcts, and therefore, overall long-term mortality may be increased.
Poor prognostic factors include the following features at presentation[1, 3, 4] :
Temperature above 100.4ºF (38ºC)
Subacute disease course
Presence of a large pericardial effusion or tamponade
Unsuccessful therapy with aspirin or nonsteroidal anti-inflammatory agents after at least 1 week of therapy
Minor predictors of poor prognosis include the following[3, 4] :
Myopericarditis
Immunosuppression
Trauma
Oral anticoagulation therapy
Factors associated with the development of complicated pericarditis include the following[28] :
Early administration of high-dose corticosteroids
Lack of colchicine treatment
Elevated levels of high-sensitivity C-reactive protein
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.
Palpitations may be the presenting complaint, but chest pain is the cardinal symptom of pericarditis, usually precordial or retrosternal with referral to the trapezius ridge, neck, left shoulder, or arm. The quality of the pain is usually pleuritic, but it range from sharp, dull, aching, burning, or pressing, and the intensity varies from barely perceptible to severe. The pain is worse during inspiration, when lying flat, or during swallowing and with body motion, and it may be relieved by leaning forward while seated.
Common associated signs and symptoms include low-grade intermittent fever, dyspnea/tachypnea (a frequent complaint and may be severe with myocarditis, pericarditis, and tamponade), cough, and dysphagia. In tuberculous pericarditis, fever, night sweats, and weight loss were commonly noted (80%).
Children may present with abdominal pain.
Interestingly, symptomatic rheumatoid arthritis–pericardial disease tends to occur in patients with arthritis, pleuritis, and other complications who are already being treated with anti-inflammatory agents such as corticosteroids, gold, and antimalarial drugs.
In uremic patients, heart rates may be deceptively slow with tamponade, fever, and hypotension due to autonomic impairment. Symptoms of neoplastic pericarditis develop over days to weeks; dyspnea is common and is the most significant symptom.
Patients with cardiac tamponade may present subacutely with symptoms of anxiety, dyspnea, fatigue, or altered mental status. They may have a history of medical illnesses associated with pericardial involvement, particularly end-stage renal disease (ESRD).
A waxing and waning clinical picture may be present in intermittently decompressing tamponade, and traumatic tamponade may present with acute dyspnea or altered mental status.
Physical findings in acute pericarditis and cardiac tamponade are discussed in this section.
Acute pericarditis
A pericardial friction rub is pathognomonic for acute pericarditis; the rub has a scratching, grating sound similar to leather rubbing against leather. Serial examinations may be necessary for detection, as a friction rub may be transient from one hour to the next and is present in approximately 50% of cases.
Auscultation with the diaphragm of the stethoscope over the left lower sternal edge or apex during end expiration with the patient sitting up and leaning forward (or on hands and knees) allows the best detection of the rub and increases the likelihood of observing this finding.
More than 50% of pericardial friction rubs are triphasic: (1) An atrial systolic rub that precedes S1, (2) a ventricular systolic rub occurs between S1 and S2 and is coincident with the peak carotid pulse, and (3) an early diastolic rub occurs after S2 (usually the faintest).
The biphasic to-and-fro rub is less common (24%). It can occur with tachycardia and is due to summation of the atrial and early diastolic rub. Monophasic rubs (the ventricular systolic) are the least common but may occur in patients with atrial fibrillation.
Especially when the pericardial friction rub is monophasic, it can be mistaken for a systolic murmur. Pericardial rubs may be differentiated if the rub does not change with usual respiratory or positional maneuvers, if 3 components are present, and if the findings on the electrocardiograms are typical. That is, a friction rub has a changing character from heartbeat to heartbeat and with patient position changes. In addition, a friction rub is closer to the ear on auscultation than a murmur.
Other physical findings may include dyspnea/tachypnea, particularly in patients with sizable effusions, and Ewart sign (dullness and bronchial breathing between the tip of the left scapula and the vertebral column) Fever (usually low grade but occasionally reach 104°F [40°C]), cyanosis, and varying degrees of consciousness may also be present, as well as hepatomegaly and ascites. Tachycardia and cardiac arrhythmias, such as premature atrial and ventricular contractions, are occasionally present.
Cardiac tamponade
Cardiac tamponade is influenced by the volume and rate of fluid accumulation. The Beck triad (ie, hypotension; elevated systemic venous pressure, often with jugular venous distention; muffled heart sounds) may occur in affected patients, especially from sudden intrapericardial hemorrhage.
Pulsus paradoxus occurs in 70-80% of patients with pericardial tamponade and is measured by careful auscultation with a blood pressure cuff. The first sphygmomanometer reading is recorded at the point when the beats are audible during expiration and disappear with inspiration. The second reading is taken when each beat is audible during the entire respiratory cycle (ie, both inspiration and expiration).
A difference of more than 10 mm Hg defines pulsus paradoxus. This decrease is important in patients with more slowly developing tamponade, because they may lack findings of the Beck triad. If an associated hemorrhage is outside the pericardial sac, hypotension and tachycardia without elevated jugular venous distension may be found.
Pulsus paradoxus also occurs in patients with severe asthma, constrictive pericarditis, and severe congestive heart failure. See the image below.
View Image
Recording of aortic pressure showing pulsus paradoxus. During inspiration, systolic pressure declines 20 mm Hg. Courtesy of Zhi Zhou, MD.
The 2015 European Society of Cardiology (ESC) recommendations
Acute pericarditis (all class I, level C evidence)[3] :
Obtain electrocardiography (ECG), transthoracic echocardiography (TTE), and/or chest radiography in all individuals with suspected acute pericarditis.
Evaluate markers of inflammation (ie, C-reactive protein [CRP]) and myocardial injury (ie, creatine kinase [CK], troponin) when acute pericarditis is suspected.
Pericardial effusion (all level C evidence)[3]
Obtain TTE in all patients with suspected pericardial effusion (class I).
Obtain chest radiography in patients with suspected pericardial effusion or pleuropulmonary involvement (class I).
Evaluate markers of inflammation (ie, CRP) in patients with suspected pericardial effusion (class I).
Consider computed tomography (CT) scanning or cardiac magnetic resonance imaging (CMRI) when loculated pericardial effusion, pericardial thickening and masses, and associated chest abnormalities are suspected (class IIa).
Cardiac tamponade (all class I, level C evidence)[3]
Obtain echocardiography as the first imaging modality for suspected cardiac tamponade to evaluate the size, location, and degree of hemodynamic impact of the pericardial effusion.
Perform urgent pericardiocentesis (or cardiac surgery) for cardiac tamponade.
To guide timing of pericardiocentesis, a judicious clinical evaluation including echocardiographic findings is recommended.
Constrictive pericarditis (all class I, level C evidence)[3]
Obtain TTE and frontal and lateral chest radiographs in all patients with suspected constrictive pericarditis.
Obtain CT scanning and/or CMRI as second-level imaging to evaluate calcifications, pericardial thickness, and degree and extension of pericardial involvement.
Cardiac catheterization is indicated when noninvasive diagnostic methods do not provide a definitive diagnosis of constriction.
Viral pericarditis (all level C evidence)[3]
For a definitive diagnosis of viral pericarditis, perform a comprehensive workup comprising histologic, cytologic, immunohistologic, and molecular studies in pericardial fluid; consider peri-/epicardial biopsies (class IIa).
Avoid routine viral serology, except possibly for human immunodeficiency virus (HIV) and hepatitis C virus (HCV) (class III)
Tuberculous pericarditis and effusion
Consider diagnostic pericardiocentesis in all patients with suspected tuberculous pericarditis (class IIa, level C evidence).[3]
Purulent pericarditis (all class I, level C evidence)[3]
Perform urgent pericardiocentesis for the diagnosis of purulent pericarditis Send pericardial fluid for bacterial, fungal, and tuberculous studies, and draw blood for cultures.
Traumatic pericardial effusion and hemopericardium in aortic dissection
Obtain urgent TTE or CT scanning in individuals with a history of chest trauma and systemic arterial hypotension (class I, level B evidence).[3]
Neoplasm-associated pericarditis (all level B evidence)[3]
Perform pericardiocentesis for cardiac tamponade for symptomatic relief and diagnosis of malignant pericardial effusion, and obtain cytologic analysis of the pericardial fluid to confirm the diagnosis (both class I). Consider pericardiotomy when pericardiocentesis cannot be performed (class IIa).
Consider pericardial or epicardial biopsy to confirm the diagnosis of malignant pericardial disease (class IIa).
Consider tumor marker testing of pericardial fluid to differentiate between malignant and benign effusions (class IIa).
Sample diagnostic protocol
An example of a diagnostic workup protocol is as follows:
The initial evaluation includes a clinical history and physical examination; ECG; chest radiography, echocardiography, CT scanning, CMRI, positron-emission tomography (PET) scanning, or PET/CT scanning, as indicated; and initial laboratory work.[3, 4]
Consider thoracentesis with adenosine deaminase (to evaluate for tuberculosis) in addition to conventional studies in patients with a pleural effusion.
Pericardiocentesis should be performed on all patients with cardiac tamponade or suspected purulent pericarditis.
Other considerations
Tension pneumothorax may mimic cardiac tamponade. Trauma ultrasonography has limited this misdiagnosis.
If echocardiography is unavailable, placement of a central venous pressure (CVP) line may reveal increased right-sided pressures. CVP measurements more than 12-14 mm Hg are usually found in cardiac tamponade.
The diagnosis of rheumatoid arthritis (RA) pericarditis is suggested by serous or hemorrhagic pericardial fluid with a glucose level of less than 45 mg/dL, a white blood cell (WBC) count higher than 15,000/µL with cytoplasmic inclusion bodies, a protein level higher than 5 g/dL, a low total serum hemolytic complement (CH50), a high immunoglobulin G (IgG) level, and a high rheumatoid factor. Cholesterol levels may be high in the fluid of patients with RA who have nodules.
For pericarditis due to RA and other systemic autoimmune diseases, the European Society of Cardiology (ESC) 2004 guideline, and its 2015 update, on the diagnosis and management of pericardial diseases recommends intensified treatment of the underlying disease and symptomatic management.[3, 4, 32]
In patients with rheumatic fever pericarditis, the antistreptolysin O titer is usually greater than 400. Rarely is a large effusion present.
When evaluating for tuberculous pericarditis, the diagnostic yield for acid-fast bacilli (AFB) in pericardial fluid is fairly low (30-76%). Pericardial biopsy has a much better yield (approximately 100%). Elevated adenosine deaminase in pericardial fluid is useful for diagnosing tuberculosis; studies note greater than 90% sensitivity and specificity with levels higher than 50-70 U/L. Elevated interferon (IFN)-gamma levels in pericardial fluid are also indicative of tuberculous pericarditis.
In neoplastic pericarditis, the pericardial carcinoembryonic antigen (CEA) level is often elevated. Cytology findings are positive in 80-90% of breast and lung cancer cases, but the percentage is lower in other malignancies. Obstruction of the lymphatic drainage can cause the pericardial effusion to be more significant than the tumor mass.
The ESC 2004 guideline recommends pericardial drainage in all neoplastic pericarditis patients with large effusions because of the high recurrence rate (40-70%). Tetracyclines used as sclerosing agents control malignant pericardial effusion in roughly 85% of cases, but side effects and complications such as fever, chest pain, and atrial arrhythmias, are frequent.[32]
In patients with radiosensitive tumors, such as lymphomas and leukemias, the ESC 2004 guideline states that radiation therapy is very effective (93%) in controlling malignant pericardial effusion.[32]
Obtain a CBC count with a differential. Significant leukocytosis may be present with an either inflammatory or infective cause of pericarditis.
Also, determine prothrombin time/activated partial thromboplastin time (PT/aPTT) and, if abnormal, correct in order to lessen the chance of developing tamponade.
Serum electrolytes, BUN, creatinine
Determine serum electrolyte (ie, sodium, potassium, chloride, magnesium, calcium, phosphate) concentrations because of the increased risk of cardiac arrhythmias in patients with pericarditis. In addition, during dialysis, frequent monitoring of electrolytes is helpful to detect and treat hypokalemia and hypophosphatemia, especially in patients with dialysis-associated pericarditis.
Blood urea nitrogen (BUN) and creatinine levels can be measured to evaluate for uremia. These levels are often elevated with azotemia.
ESR and CRP
Erythrocyte sedimentation rate (ESR) and CRP levels are usually elevated in pericarditis. High-sensitivity CRP (hs-CRP) levels are elevated in 78% of cases of acute pericarditis. Thus, an elevated CRP level may confirm the diagnosis of acute pericarditis. A normal value does not exclude a diagnosis of acute pericarditis; in some patients, the hs-CRP increases later, supporting the use of serial testing in patients with an initial negative result. Most patients showed normalization of CRP level by 2 weeks and all patients by 4 weeks. Persistently elevated hs-CRP level was a marker for increased risk of reoccurrence. Serial monitoring of hs-CRP level weekly may be warranted to follow disease activity and guide the appropriate length of therapy, with continuation of treatment doses until the CRP level normalizes.[33]
Cardiac biomarkers
Evaluate cardiac biomarkers, such as creatine kinase and isoenzymes levels, as well as LDH and SGOT (AST) for associated myocarditis or myocardial infarction. Troponin I may be elevated in viral or idiopathic acute pericarditis.
In a study by Imazio and colleagues, an elevated troponin I level was found in 32% of patients with viral or idiopathic pericarditis.[34] In this study, the troponin I level was related to the extent of myocardial inflammation but was not a negative prognostic marker.[34] In a study by Machado et al, elevated troponin I levels were found to be associated with a significant increase in cardiac mortality in patients with myopericarditis compared with pericarditis only.[35]
Further laboratory workup may be clinically indicated, as follows:
Blood and/or viral cultures
Tuberculosis skin testing and/or tuberculin sputum testing for acid-fast bacilli (AFB) can be used if the illness exceeds 1 week duration. The ESC 2004 guideline also recommends obtaining mycobacterium culture or radiometric growth detection (eg, BACTEC-460), adenosine deaminase (ADA), interferon (IFN)-gamma, and pericardial lysozyme, in addition to polymerase chain reaction (PCR) analyses of tuberculosis.[32]
Antistreptolysin titer
Rheumatoid factor (RF), antinuclear antibody (ANA), and anti-DNA values, particularly if the illness is prolonged or severe
Thyroid function in patients with large pericardial effusion
The ESC 2004 guideline on the diagnosis and management of pericardial diseases recommends pericardial fluid or pericardial or epicardial biopsy analyses to confirm diagnosis of malignant pericardial disease. The guideline states that at least 3 cultures of pericardial fluid for aerobes and anaerobes, as well as blood cultures, are mandatory in cases of suspected bacterial infection.[32]
Chest radiography is not helpful in uncomplicated pericarditis. Patients with small effusions (less than a few hundred milliliters) may present with a normal cardiac silhouette. In one study, pleural effusions were seen in 33% of patients with pericarditis. Approximately 75% of the effusions were left-sided only.
A flask-shaped, enlarged cardiac silhouette may be the first indication of a large pericardial effusion (200-250 mL of fluid accumulation) or cardiac tamponade (see the following image). This occurs in patients with slow fluid accumulation, compared with a normal cardiac silhouette seen in patients with rapid accumulation and tamponade. Thus, the chronicity of the effusion may be suggested by the presence of a huge cardiac silhouette.
View Image
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardioc....
Go to Imaging in Constrictive Pericarditis for complete information on this topic.
Although transthoracic echocardiography remains the initial test of choice for detecting pericardial effusions and diagnosing tamponade, this study is limited in its capacity to reveal the entire pericardium and its operator dependence. Nonetheless, 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.
This study is helpful in quickly confirming the diagnosis, particularly if cardiac tamponade is suspected,[36] and it can also be used to evaluate for chamber size and ventricular dysfunction.
Go to Imaging in Constrictive Pericarditis for complete information on this topic.
Acute pericarditis
Any form of pericardial inflammation can induce pericardial effusion. It is important to note that the pericardium may have a normal appearance in pericarditis, without evidence of fluid accumulation.
M-mode is used to evaluate pericardial fluid and timing during the cardiac cycle; it demonstrates persistence of the echo-free space between the parietal pericardium and the epicardium during this cycle. Fluid is distributed from the posterobasal left ventricle apically and anteriorly, then laterally and posteriorly to the left atrium. Fluid adjacent to the right atrium is an early indicator of an effusion. Other causes of echo-free space that must be considered include pleural effusion, pericardial masses, and epicardial fat.
To a limited extent, an echocardiogram can characterize the effusion. Very small effusions are located posterior and inferior to the left ventricle. Moderate effusions extend toward the apex of the heart, and large effusions circumscribe the heart. Weitzman criteria define a moderate effusion as an echo-free pericardial space (anterior plus posterior) of 10-20 mm during diastole and a large effusion as an echo-free space more than 20 mm.
A “swinging heart” may be present with large effusions. This is characterized as counterclockwise rotational movement, which occurs in addition to the triangular movement of the heart, producing a dancelike motion.
Thin fibrous strands within the pericardial space can be seen in acute effusive pericarditis. Shaggy exudate may indicate a potentially difficult pericardiocentesis, but this finding is not diagnostic.
Echocardiographic studies have noted pericardial effusions in 50% of patients with rheumatoid arthritis (RA) with nodules and in only 15% of patients with RA without nodules. In patients with sarcoidosis, this study shows that pericardial involvement is present in 20% of cases; however, patients may not have significant myocardial infiltration.
An example of an echocardiographic image is shown below.
View Image
This ultrasonogram demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearan....
Cardiac tamponade
In the emergency department, there may be difficulty using the classic textbook ultrasonographic findings of tamponade, as the trauma patient is often tachycardic and the examination abbreviated. A dilated inferior vena cava (IVC) without inspiratory collapse (plethora) is highly suggestive of tamponade.
Computed tomography (CT) scanning provides anatomic details of the entire pericardium due to its capacity in providing a wide field of view. The normal thickness of the pericardium as measured by CT scanning is less than 2 mm; pericardial thickening is suggestive of acute pericarditis.[37]
Effusions are easily detected through different radiographic coefficients of fluid and the pericardium. Similarly, the nature of the effusion may be surmised, given the different attenuation coefficients for blood, exudate, chyle, and serous fluid. However, hemopericardium may be difficult to assess without intravenous contrast, because blood has the same radiodensity as myocardium.
Lazaros et al have suggested that CT quantification of epicardial fat volume (EFV) provides prognostic information in patients with acute pericarditis.[38] In their study comprising 50 patients, the investigators noted that patients who presented with chest pain had a lower EFV compared to those without chest pain, as well as found a strong positive correlation not only between EFV and pericardial effusion size but also EFV and the incidence of inpatient atrial fibrillation. At 18-month follow-up, those who developed constrictive, recurrent, or incessant pericarditis or had poor response to NSAIDs had a lower EFV.[38]
More recently, findings from a single-center retrospective study (2009-2016) that comprised data from all patients admitted for idiopathic acute pericarditis with pericardial effusion who underwent fluorodeoxyglucose (FDG)-positron emission tomography (PET)/CT (FDG-PET/CT) scanning (N = 23) found that pericardial FDG uptake at diagnosis was independently associated with pericarditis relapse.[39] In the follow-up period (median 7.6 months), a higher rate recurrence occurred individuals who had increased FDG-PET/CT pericardial uptake at diagnosis.[39]
An advantage of CT scanning over other imaging modalities includes its capacity to detect pericardial calcifications. Magnetic resonance imaging (MRI) can miss significant calcium deposits. The presence of any calcification is important in patients suspected of having constrictive pericarditis. CT scanning is also less operator dependent than ultrasonography.
Limitations of CT scanning include the need for contrast administration, patient exposure to ionizing radiation, and difficulty in differentiating fluid from thickened pericardium.
Go to Imaging in Constrictive Pericarditis for complete information on this topic.
Magnetic resonance imaging (MRI) can provide anatomic details of the pericardium and heart without ionizing contrast or radiation. The normal pericardium can be up to 4-mm thick.
This imaging modality is sensitive for detecting pericardial effusion and loculated pericardial effusion and thickening. Additionally, delayed enhancement of thickened pericardium after administration of contrast medium usually suggests active inflammation characteristic of acute pericarditis.[40]
Limitations to use of MRI include the need to gate the image acquisition. In addition, a high-quality MRI may need more than 250 regular heartbeats; thus, the examination may be limited in patients with arrhythmias.
Go to Imaging in Constrictive Pericarditis for complete information on this topic.
Electrocardiography (ECG) can be diagnostic in acute pericarditis and evolves in 4 stages. However, only 50% of patients with pericarditis experience all four stages.
An important ECG finding is PR-segment depression, which has been reported in as many as 80% of viral pericarditis cases.
Hooper et al described the clinical characteristics, assessment, and treatment of patients diagnosed with acute pericarditis in an emergency department (ED) by conducting a medical record review of patients with an ED diagnosis of pericarditis over a 5-year period. ST segment elevation was present in 69.3% of patients, and PR segment depression was present in 49.2% of patients.[41]
Electrical alternans is pathognomonic of cardiac tamponade and is characterized by alternating levels of ECG voltage of the P wave, QRS complex, and T waves. This is a result of the heart swinging in a large effusion.
Stage 1 ECG changes in pericarditis
Stage 1 accompanies the onset of acute pain and is the hallmark of acute pericarditis. ECG changes include diffuse concave upward ST elevation, except in leads aVR and V1 (usually depressed). T waves are upright in the leads with ST elevation, and the PR segment deviates opposite to P-wave polarity. See the image below.
View Image
Stage 1 electrocardiograph changes in a patient with acute pericarditis.
Stage 2 ECG changes in pericarditis
Stage 2 occurs several days later with the return of the ST segment to baseline, followed by flattening of the T waves.
Stage 3 ECG changes in pericarditis
T waves become inverted in stage 3 but without Q-wave formation.
Stage 4 ECG changes in pericarditis
Finally, in stage 4, the ECG returns to the prepericarditis baseline weeks to months after the initial onset (see the following image). The T-wave inversion may persist indefinitely in the chronic inflammation observed with tuberculosis, uremia, or neoplasm.
View Image
Stage 4 electrocardiograph changes in the same patient as in the previous image, taken approximately 3 months after acute pericardial illness. The pat....
Idiopathic pericarditis and ECG changes
ECGs often fail to demonstrate the diffuse ST- and T-wave elevations observed in idiopathic pericarditis because of the lack of penetration of inflammatory cells into the myocardium. In fact, the presence of these changes on ECG mandates a search for an alternative cause for pericarditis.
Inflammatory disorders and ECG changes
In patients with RA pericarditis, ECGs almost never demonstrate typical findings. In contrast, lupus pericarditis findings on ECG usually demonstrate typical changes of pericarditis.
In uremic patients with pericarditis, ECG commonly does not show the typical ST-T segment changes due to lack of inflammation; in hypothyroidism, low ECG voltage is often observed due to the presence of a large effusion.
Cardiovascular disorders and ECG changes
Regional ECG changes may be present in infarction-associated pericarditis. If the pericardial involvement is confined to the infarction zone, stage 1 ECG findings are often not seen. Positive T waves that last longer than 48 hours after an acute MI or premature reversal of inverted T waves may indicate pericardial involvement. An ST-segment–to–T-wave ratio of 0.25 or more in lead V6 helps distinguish acute pericarditis from early repolarization.
In Dressler syndrome, ECG findings may demonstrate diagnostic changes of acute pericarditis, especially if the ECG findings normalize after the infarction.
Pericardiocentesis under fluoroscopic guidance or echocardiography "is the gold standard for pericardial drainage and biopsy."[3, 4]
This procedure is relatively safe when guided by echocardiography, especially with large free anterior effusion. One study noted only 3 minor complications in 117 procedures with ultrasound guidance. Conversely, blind percutaneous pericardial puncture increases the risk of complication to 5-50% and should be performed only in an emergency. Complications include fatal cardiac laceration.
In a large study, diagnostic pericardiocentesis led to a diagnosis in only 6% of cases, versus 29% diagnosed with therapeutic pericardiocentesis. As such, pericardiocentesis should not be performed unless tamponade or suspected purulent pericarditis is present.
If a pericardiocentesis is performed for drainage, an indwelling catheter should be placed in the pericardial space for continued drainage over several days. If the catheter continues to drain a large amount, a more definitive procedure should be performed.
According to the ESC 2004 guideline on the diagnosis and management of pericardial disease, the diagnosis of viral pericarditis is impossible without the evaluation of pericardial effusion and/or pericardial/epicardial tissue, ideally by PCR or in-situ hybridization. Pericardial fluid obtained by percutaneous pericardiocentesis should undergo Gram, acid-fast, and fungal staining, and cultures of the pericardial and body fluids should be obtained.[32]
Traditional pericardiocentesis
The traditional approach is the subxiphoid technique. This technique avoids injury to the coronary arteries, as follows.
The chest is prepared with Betadine and a 16-gauge to 18-gauge needle is introduced between the xiphoid and the left subcostal margin.
The needle is directed toward the inferior tip of the left scapula with slow advancement and with aspiration.
If fluid is found, the needle is exchanged for a catheter over a guidewire. Fluid is removed via the catheter.
The catheter may be sutured in place for subsequent use. Alternatively, a 16-gauge to 18-gauge spinal needle may be used for one-time drainage.
Echocardiographically guided pericardiocentesis
Echocardiographically guided pericardiocentesis has evolved over the past 20 years and is now considered the procedure of choice for removal of pericardial fluid. This technique differs from traditional blind pericardiocentesis primarily in the site of needle entry, in which the left chest wall has become the preferred location for needle entry. The intended needle trajectory is investigated with echocardiography to confirm the optimal direction and depth for needle advancement. A 16-gauge needle (with poly-Teflon sheath) is advanced in a straight line without side-to-side manipulation. Needle position can be established via echocardiography while agitated sterile saline is injected.
Thus, the step-by-step approach for echocardiographically-guided pericardiocentesis is as follows:
Assess the size, distribution, and ideal needle entry site and trajectory with a 2.5-MHz to 5-MHz ultrasound transducer placed approximately 3-5 cm from the parasternal border. Locate the point where the effusion is closest to the transducer as well as an area of maximal pericardial fluid accumulation.
Assess or measure the distance from the skin to the pericardial space. The needle trajectory is established by the angle of the transducer. Keep this trajectory in mind during the procedure.
Use a sterile skin preparation such as povidone-iodine and, if readily available, a transparent sterile plastic sheet (one author recommends a 1030 Baxter drape) to allow imaging and a sterile field.
Place a sterile 16-gauge catheter on the predetermined location on the chest wall, avoiding the inferior rib margin. Advance in the predetermined direction, angle, and depth. Advance 2 mm further once fluid is obtained. Consider leaving the catheter in place after removing the needle. If needed, a guidewire can be advanced through the catheter.
The pericardial fluid should be analyzed for red blood cells (RBCs), total protein level, LDH level, adenosine deaminase activity, and culture (ordinary and Loewenstein media). Directly investigate for tuberculous bacilli and perform a cytologic study.
The fluid in purulent or suppurative pericarditis from is usually 400-500 mL in volume and shows a thin to creamy pus.
Findings in inflammatory disorders
The fluid in RA and SLE pericarditis demonstrates few polymorphonuclear neutrophils, lymphocytes, or histiocytes. The usual volume is 50-200 mL and accumulates slowly. Also found in SLE pericardial fluid is a high protein level, low-to-normal glucose level, low complement, and, possibly, a pH level of less than 7. In addition, fluid analysis reveals positive autoantibodies, such as ANA or anti–double-stranded DNA.
Pericardial fluid in scleroderma has a protein value greater than 5 g/dL and a low cell count, but it does not demonstrate the antibodies found in RA and SLE.
Findings in metabolic disorders
In uremic pericarditis, adhesions are present between the pericardial membranes, which are thickened, which frequently result in bloody effusions. In hypothyroidism, pericardial fluid is often straw colored with high protein and cholesterol levels and with few cells.
If tamponade recurs after pericardiocentesis, perform a pericardial biopsy with histologic and bacteriologic examinations of the pericardium. If significant clinical activity persists for 3 weeks after admission and without an etiologic diagnosis, some authors recommend pericardial biopsy.
Cardiac catherization is used for assessing pericarditis and tamponade. This procedure can evaluate constrictive pericarditis versus restrictive cardiomyopathy.
Oxygen and a cardiac monitor should be provided. Rule out other life-threatening causes of chest pain, such as myocardial infarction (MI) or aortic dissection. Evaluate for evidence of hemodynamic instability. Consider whether further management is safe to continue on an outpatient basis.
2015 European Society of Cardiology (ESC) recommendations
Outpatient versus inpatient treatment
The 2015 European Society of Cardiology (ESC) update of their 2004 guidelines on the diagnosis and management of pericardial diseases recommends managing patients considered to be low risk (no risk factors) on an outpatient basis, whereas those with at least one risk factor should be managed as inpatients (both class I, level B evidence).[3, 4] After 1 week, evaluate the clinical response to anti-inflammatory therapy (class I, level B evidence).[3]
Fever above 100.4°F (38°C), subacute onset, immunosuppression, trauma, oral anticoagulation therapy, aspirin or nonsteroidal anti-inflammatory drug (NSAID) treatment failure, myopericarditis, severe pericardial effusion, and cardiac tamponade are considered poor prognostic predictors.[3, 4, 42] Patients without these factors were treated on an outpatient basis without serious complications after a mean follow-up of 38 months.[42] Similar poor prognostic indicators were noted in a systematic review (fever of more than 100.4°F [38°C], subacute onset, unsuccessful NSAID therapy, large pericardial effusion or tamponade).[1]
Pericardial effusion (all class I, level C evidence)[3]
In patients with pericardial effusion, treat the underlying cause. In the setting of pericardial effusion and systemic inflammation, administer aspirin/NSAIDs/colchicine and treat pericarditis.
Cardiac tamponade (all level C evidence)[3]
Perform urgent pericardiocentesis or cardiac surgery for cardiac tamponade or for symptomatic moderate to large pericardial effusions refractory to medical therapy, as well as when an unknown bacterial or neoplastic etiology is suspected (class I).
To guide timing of pericardiocentesis, a judicious clinical evaluation including echocardiographic findings is recommended (class I).
Avoid vasodilators and diuretics in the presence of cardiac tamponade (class III).
Constrictive pericarditis (all level C evidence)[3]
Pericardiectomy is the treatment mainstay of chronic permanent constriction (class I). To prevent progression of constriction, administer medical therapy for specific pericarditis conditions (ie, tuberculous pericarditis) (class I).
Consider empiric anti-inflammatory therapy in the setting of transient or new diagnosis of constriction with concomitant evidence of pericardial inflammation (ie, elevated CRP or pericardial enhancement on computed tomography scan/cardiac magnetic resonance imaging) (class IIb).
Purulent pericarditis (all level C evidence)[3]
Perform effective pericardial drainage (class I).
Administer intravenous antibiotics (class I).
Consider subxiphoid pericardiotomy and pericardial cavity rinsing (class IIa).
Consider pericardiectomy for dense adhesions, loculated/thick purulent effusion, tamponade recurrence, persistent infection, and progression to constriction (class IIa).
Pericarditis in renal failure (all level C evidence)[3]
Consider dialysis in uremic pericarditis (class IIa).
Consider intensifying dialysis in the setting of pericarditis despite adequate dialysis (class IIa); when intensive dialysis is ineffective, consider systemic or intrapericardial NSAIDs and corticosteroids (class IIb).
Consider pericardial aspiration and/or drainage in the setting of nonresponse to dialysis (class IIb).
Colchicine is contraindicated in the setting of pericarditis and severe renal impairment (class III).
Traumatic pericardial effusion and hemopericardium in aortic dissection[3]
Perform immediate thoracotomy (class I, level B evidence), or consider pericardiocentesis as a bridge to thoracotomy (class IIb, level B evidence), in the setting of cardiac tamponade caused by penetrating heart and chest trauma.
In the setting of aortic dissection with hemopericardium, consider controlled pericardial drainage of very small amounts of the hemopericardium as a temporary stabilizing measure for maintenance of blood pressure at about 90 mmHg (class IIa, level C evidence).
Chylopericardium (all level C evidence)[3]
Consider pericardial drainage and parenteral nutrition in symptomatic or large uncontrolled effusion caused by chylopericardium (class IIa).
Consider surgical therapy for chylopericardium if conservative management does not reduce pericardial drainage and the course of the thoracic duct is identified (class IIa).
Consider octreotide therapy (100 μg subcutaneously [SC] three times daily for 2 weeks) (presumed mechanism of action: reduction in chyle production) (class IIb).
Other considerations
Avoid NSAIDs and corticosteroids in acute MI pericarditis, because they may interfere with ventricular healing, remodeling, or both.
Avoid corticosteroid therapy in viral pericarditis (class III, level C evidence).[3]
When cardiac irradiation is necessary, use radiation therapy methods that reduce the irradiation volume and the dose whenever possible (class I, level C evidence).[3]
For cases of complicated pericarditis, therapies targeting the inflammasome may result in more durable remission and resolution.[28]
Patients may require transfer to a hospital setting in which hemodialysis and cardiothoracic surgery are available.
For more information, see the Medscape Drugs and Diseases topics Constrictive Pericarditis, Constrictive-Effusive Pericarditis, and Pediatric Infective Pericarditis.
Patients with chest pain, regardless of etiology, should routinely be treated with oxygen and cardiac monitor.
Patients suspected of having pericarditis should have routine care as for patients with acute cardiac conditions. The initial prehospital care for suspected cardiac tamponade is the same as for any major trauma. The diagnosis may also be suspected based on the location of any penetrating wounds. The possibility of a tension pneumothorax should also be considered.
The emergency care of the patient centers on prompt diagnosis and treatment of potentially life-threatening entities. Thoracotomy and pericardiotomy may be required if the patient has rapid deterioration or cardiac arrest.
For acute pericarditis, the 2015 European Society of Cardiology (ESC) update of their 2004 guidelines on the diagnosis and management of pericardial diseases recommends the following (all class I, level A evidence)[3, 4] :
Aspirin (750-1000 mg) or nonsteroidal anti-inflammatory drugs (NSAIDs) (ibuprofen 600 mg), every 8 hours for 1-2 weeks, with gastric protection
First-line therapy as adjunct to aspirin or NSAID therapy: Colchicine 0.5 mg daily (weight < 70 kg) or twice daily (weight ≥70 kg) for 3 months
Consider low-dose corticosteroids in cases of acute pericarditis when aspirin/NSAIDs and colchicine are contraindicated or have failed, and when an infectious cause has been excluded, or when there is a specific indication (eg, autoimmune disease) (class IIa, level C evidence).[3] However, corticosteroids are not recommended as first-line therapy for acute pericarditis (class III, level C evidence).[3]
In the setting of recurrent pericarditis, the ESC recommends administering aspirin or NSAIDs at full doses, if tolerated, until symptomatic relief, with the addition of 6 months of colchicine (0.5 mg twice daily or 0.5 mg daily for those < 70 kg or intolerant to higher doses) (both class I, level A evidence).[3, 4] In select cases, colchicine therapy longer than 6 months should be considered based on clinical response (class IIA, level C evidence). In cases of corticosteroid-dependent recurrent pericarditis refractory to colchicine, consider agents such as intravenous immunoglobulin (IVIG), anakinra, and azathioprine (class IIA, level C evidence).
Pericarditis
Ideally, echocardiography should be readily available to determine the presence or absence of a pericardial effusion (see Echocardiography under Workup). If no pericardial effusion is noted, stable patients with presumptive viral pericarditis may be discharged with appropriate instructions and follow-up care.
If a large effusion is present, the stable patient may undergo a pericardiocentesis or placement of a pericardial window (see Surgical Care).
Cardiac tamponade
Treatment for this condition depends on the patient’s stability. Unstable patients require immediate treatment of the increase in pericardial pressure with pericardiocentesis (see Surgical Care). Removing as little as 30-50 mL may produce dramatic hemodynamic improvement.
Patients may have subacute tamponade (intermittently decompressing) and may benefit from decompression in the operating room with cardiothoracic care available to treat cardiac injuries.
The treatment for specific types of pericarditis are briefly discussed in this section.
Use serum levels of C-reactive protein (CRP) to guide treatment duration and assess clinical response (class IIa, level C evidence).[3]
Idiopathic pericarditis
Treatment for this condition is similar to viral pericarditis and includes anti-inflammatory drugs to control symptoms and inflammation.[43] Colchicine may prevent recurrent pericarditis resistant to aspirin or nonsteroidal anti-inflammatory agents (NSAIDs). Steroids are not administered initially as their use is associated with an increased incidence of recurrent pericarditis.
Infectious pericarditis
The treatment of viral pericarditis is based on the symptoms present, with observation for the development of tamponade. Treatment for bacterial pericarditis includes appropriate antibiotics for at least 4 weeks and drainage of pericardial fluid.
For fungal infection, the European Society of Cardiology (ESC) 2004 guideline recommends fluconazole, ketoconazole, itraconazole, amphotericin B, liposomal amphotericin B, or amphotericin B lipid complex for treatment of fungal infection. Corticosteroids and NSAIDs can be used to support the antifungal drug treatment.[32]
Intrapericardial fibrinolysis can be a useful treatment to assist with drainage of thick, loculated fluid, but open surgical drainage is preferred. Occasionally, patients require partial to total pericardiectomy.
Tubercular infection is managed with the usual antituberculous chemotherapy. The 2015 updated ESC guidelines recommend consideration of intrapericardial urokinase to reduce the risk of constriction in tuberculous effusive pericarditis (class IIb, level C evidence).[3]
Controversy exists regarding the use of steroids in the treatment of tuberculous pericarditis. The ESC 2004 guideline advises using corticosteroid therapy only in patients with secondary tuberculous pericarditis, and only as an adjunct to tuberculostatic treatment. A meta-analysis of patients with effusive and constrictive TBC pericarditis found that tuberculostatic treatment, combined with steroids, might be associated with fewer deaths, less frequent need for pericardiocentesis or pericardiectomy.[24]
The 2015 ESC updated guidelines indicate adjunctive steroids may be considered in human immunodeficiency virus (HIV)-negative TB pericarditis, but these agents should be avoided in HIV-associated TB (class IIb, level C evidence).[3] Regarding empiric anti-tuberculosis treatment in patients, ESC 2015 indicates the following (all level C evidence)[3] :
Endemic regions: Recommended for exudative pericardial effusion after other causes have been ruled out (class I)
Non-endemic regions: Not recommended in the absence of a diagnosis of tuberculous pericarditis after systematic investigation (class III)
In the setting of tuberculous pericardial constriction, 6 months of standard antituberculosis agents is recommended (class I, level C evidence).[3] If the patient's condition does not improve or deteriorates after 4-8 weeks of antituberculosis therapy, pericardiectomy is recommended. (class I, level C evidence).[3]
Use of adjunctive prednisolone in patients with acquired immunodeficiency syndrome (AIDS) may reduce mortality in this population.
Inflammatory pericarditis
Only symptomatic rheumatoid arthritis (RA) pericarditis should be treated. However, treat lupus pericarditis with anti-inflammatory agents and optimize systemic lupus erythematosus (SLE) treatment.
Rheumatic fever pericarditis resolves with anti-inflammatory treatment.
Metabolic pericarditis
The development of pericarditis in a patient with severe acute or chronic renal failure is an absolute indication for intensive dialysis. In most patients, relief of chest pain and reduction in the size of any effusion occurs within 1-2 weeks.
If no improvement is noted after 7-10 days or if the patient has hemodynamic instability, proceed with pericardiocentesis or pericardiectomy (see Surgical Care). The ESC 2004 guideline recommends pericardiocentesis for treating cardiac tamponade and large chronic effusions resistant to dialysis.[24] Intensive dialysis is beneficial to most patients with uremia who develop pericarditis before dialysis. Dialysis-induced pericarditis fails to respond to more intensive dialysis in 25-33% of patients.
Both hemodialysis and peritoneal dialysis are efficacious in the treatment of uremic pericarditis, though each technique has unique advantages and disadvantages. Hemodialysis may cause hypotension, which may be dangerous in the setting of tamponade. In addition, some physicians advocate heparin-free hemodialysis to reduce the risk of intrapericardial hemorrhage. Peritoneal dialysis may compromise respiratory function because of the effect of intraperitoneal fluid on the diaphragm.
In dialysis-associated pericarditis, an increased intensity of dialysis for 10-14 days is recommended. Close monitoring of fluid volume and electrolytes is mandatory to detect and correct hypophosphatemia and hypokalemia, which may occur with intensive dialysis. The response of dialysis-associated pericarditis is not predictable. In some instances, consider a switch to peritoneal dialysis if heparin-free dialysis cannot be performed.
NSAIDs and steroids may offer symptomatic relief but are not effective without dialysis. Indomethacin ameliorates fever, but it does not accelerate resolution of the effusion.
Early intervention with dialysis may prevent the development of uremic pericarditis. Maintenance of adequate dialysis therapy lessens the likelihood of a patient developing dialysis-associated pericarditis.
Treatment in hypothyroidism-associated pericarditis is hormone replacement.
The ESC 2004 guideline also recommends thyroid hormone therapy to decrease pericardial effusion.[32]
Cardiovascular pericarditis
Pericarditis does not contraindicate thrombolytic or anticoagulant therapy for an acute MI. However, anticoagulation should be discontinued if pericardial effusion develops or effusion size increases. Treatment is with aspirin.
In Dressler syndrome, anticoagulant therapy should be stopped because of the risk of hemorrhagic pericarditis. Treatment is with NSAIDs.
Miscellaneous conditions
Neoplasm-associated pericarditis
With neoplasm-associated pericarditis, initial treatment includes relief of tamponade, confirmation of the diagnosis, and systemic treatment of the neoplasm. Further treatment options include sclerosis of the pericardial space, instillation of chemotherapeutic agents into the pericardial space, local radiation, or pericardiectomy.[3, 44]
The ESC 2004 guideline and its 2015 update indicate that prevention of recurrences of neoplastic pericarditis may be achieved via intrapericardial instillation of sclerosing, cytotoxic agents, or immunomodulators.[3, 44] Intrapericardial treatment tailored to the type of tumor shows that administration of cisplatin is most effective in secondary lung cancer and intrapericardial instillation of thiotepa was more effective in breast cancer or pericardial metastases.[3, 45, 44]
The ESC 2004 guideline and its 2015 update states that treatment of cardiac tamponade is a class I indication for pericardiocentesis in the presence of neoplastic pericarditis.[3, 32] In suspected neoplastic pericardial effusion without tamponade, the following are recommended[32] :
Systemic antineoplastic treatment as baseline therapy
Pericardiocentesis to relieve symptoms and to confirm diagnosis
Intrapericardial instillation of cytostatic/sclerosing agent
Drug-induced pericarditis treatment includes stopping the administration of the offending agent and anti-inflammatory therapy as needed. Treatment is with aspirin or NSAIDs.
Colchicine is effective in the prevention of postpericardiotomy syndrome and may halve the risk of developing this syndrome when used following cardiac surgery.[46]
Imazio et al found evidence that in patients with acute pericarditis, colchicine, when added to conventional anti-inflammatory therapy, significantly reduced the rate of incessant or recurrent pericarditis.[47] In a trial of 240 adults with acute pericarditis randomly assigned to receive colchicine (n = 120) or placebo (n = 120) for 3 months in addition to conventional anti-inflammatory therapy with aspirin or ibuprofen, the primary study outcome of incessant or recurrent pericarditis occurred in 20 patients (16.7%) in the colchicine group and 45 patients (37.5%) in the placebo group. Colchicine reduced the rate of symptom persistence at 72 hours, the number of recurrences per patient, and the hospitalization rate. Furthermore, colchicine improved the remission rate at 1 week. Both groups had similar overall adverse effects and rates of study-drug discontinuation, and no serious adverse events were reported.[47]
Surgical procedures for pericarditis include pericardiectomy for constrictive pericarditis, as well as pericardiocentesis, pericardial window placement, or pericardiotomy to drain pericardial fluid.
Pericardiectomy
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.
Consider pericardiectomy for radiation-induced constrictive pericarditis, but with a worse outcome than when performed for constrictive pericarditis from other causes, because of coexisting myopathy (class IIa, level B evidence).[3]
Pericardiectomy requires general anesthesia and a thoracotomy; therefore, pericardiectomy should be considered only if pericardiotomy cannot be performed or has been unsuccessful.[48]
Studies demonstrate that failure rates are proportional to the amount of pericardium removed (ie, the more pericardium removed, the less likely the procedure will fail). In effusive pericarditis, the higher failure rate associated with a pericardial window procedure or partial pericardiectomy is likely secondary to the continued fluid production from the remaining pericardium, with sealing of the remaining pericardium to the heart.
The operative mortality rate was 14% in one series, with a range of 1% for New York Heart Association (NYHA) class 1-2, 10% for class 3, and 46% for class 4. The 5-year survival rate was 80% for class 3-4 and approximately 95% for 1-2.
As with pericardiocentesis, studies involving pericardiectomy note a greatly improved diagnostic yield if pericardial biopsy is performed as part of a therapeutic procedure. Diagnostic biopsies yielded 5%, whereas therapeutic biopsies were at 22-54%.
A study by Thompson et al indicated that complete pericardiectomy can produce good outcomes in properly selected pediatric patients with pericarditis.[49] The report involved 27 pediatric patients (mean age, 16.7 y), including 16 patients with inflammatory pericarditis and 11 with constrictive pericarditis. The median presurgical period of symptom duration for these patients was 1 year. Before the pericardiectomies were performed, 10 patients had been hospitalized for treatment of symptoms, 15 had undergone pericardiocentesis, and 3 had already undergone a partial pericardiectomy.[49]
The procedures in the above study consisted of complete pericardiectomy (21 patients), biventricular pericardiectomy (3 patients), and completion pericardiectomy (3 patients). The postoperative course was, for most of the patients, uneventful, although one patient with radiation-induced heart disease died of acute hepatic failure 155 days after undergoing pericardiectomy.[49] At follow-up (median period, 1 y), 89% of the patients had experienced complete symptom resolution.
Pericardiocentesis
People 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 (for the technique, see Pericardiocentesis under Workup).
The image below shows preprocedure and postprocedure images of a cardiac silhouette.
View Image
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardioc....
Pericardial window placement
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. This procedure is a modification of balloon valvuloplasty in which an uninflated balloon is passed inside the pericardial space, where it is opacified, inflated, and then pulled through the pericardium to create a window through which pericardial fluid drains into the peritoneal or pleural space.
Pericardial window placement is used for effusive pericarditis therapy. Some studies note the need for repeat operation in nearly 25% of patients who undergo the procedure at 2 years.
Consider the creation of a pericardial window via left minithoracotomy in the surgical management of malignant cardiac tamponade (class IIb, level B evidence).[3]
Pericardiotomy
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 compared with pericardiectomy.
The European Society of Cardiology (ESC) 2004 guideline recommends percutaneous balloon pericardiotomy, which creates a pleuro-pericardial direct communication, allowing for drainage of fluid into the pleural space.[32] In large malignant pericardial effusions and recurrent tamponade, it appears to be a safe and effective (90-97%) intervention.[32] Consider percutaneous balloon pericardiotomy to prevent recurrence of neoplastic pericardial effusions (class IIb, level B evidence).[3]
Post-cardiac injury syndromes (PCIS)
The 2015 ESC updated guidelines have the following recommendations for patients with PCIS[3] :
Administer anti-inflammatory therapy to speed up symptomatic remission and reduce recurrences (class I, level B evidence).
Aspirin is first line for anti-inflammatory therapy of post-myocardial infarction (MI) pericarditis, as well as for individuals receiving antiplatelet therapy (class I, level C evidence).
Consider adding colchicine to aspirin/NSAIDs to treat PCIS, as for treating acute pericarditis (class IIa, level B evidence).
To prevent postpericardiotomy syndrome, consider administering post-cardiac surgery colchicine using weight-adjusted doses (ie, ≤70 kg: 0.5 mg once daily; >70 kg: 0.5 mg twice daily) and without a loading dose, for 1 month, providing there are no contraindications and it is tolerated (class IIa, level A evidence).
Consider careful echocardiographic follow-up every 6-12 months after PCIS to exclude potential development of constrictive pericarditis, based on the patient's clinical features and symptoms (class IIa, level C evidence).
The following conditions are possible complications of acute pericarditis itself or treatment used in its management:
Recurrence in 15-32% of patients
Cardiac tamponade
Constrictive pericarditis. In addition, liver disease has been reported in asymptomatic constrictive pericarditis
Combination of effusive and constrictive pericarditis
Noncompressive effusion
Cardiac perforation with pericardiocentesis
Bronchopericardial fistula has been reported as a complication of multi–drug-resistant tuberculosis in a patient with human immunodeficiency virus (HIV) infection.[50]
Consult a cardiologist or internist for acute and idiopathic cases of pericarditis. In complicated cases (eg, tuberculous, traumatic pericardial injury, purulent uremic etiologies require multidisciplinary involvement) obtain consultations with a cardiologist, cardiac and/or trauma surgeon, and medical subspecialists (eg, infectious diseases specialist, nephrologist).
Consult with a cardiothoracic surgeon for all patients with large effusions. Development of tamponade is unpredictable, and it is important for the surgeon to be aware of the patient if an emergent procedure is necessary.
In patients with uremic or dialysis-associated pericarditis, carefully monitor the patient at follow-up hemodialysis visits for recurrence of signs or symptoms. Up to 15% of these patients may have recurrence of pericarditis.
Patients on dialysis require a daily diet restricted to 1.2 g/kg of protein, 2 g of sodium, and 2 g of potassium. Patients on peritoneal dialysis may require less stringent protein restriction.
Activity
Activity should be limited to avoid strenuous activities or trauma, which may increase the risk of hypotension or arrhythmias.
The 2015 ESC update of their 2004 guidelines recommends the following regarding activities in individuals with acute or recurrent pericarditis (both class IIa, level C evidence)[3] :
Non-athletes: Consider exercise restriction until symptomatic resolution and normalization of C-reactive protein (CRP), electrocardiography (ECG), and echocardiography.
Athletes: Consider at least 3 months of exercise restriction until symptomatic resolution and normalization of CRP, ECG, and echocardiography.
Treatment 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. 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. Ibuprofen has the advantage of few adverse effects and increased coronary flow. Indomethacin has a poor adverse effect profile and reduces coronary flow.
A full-dose NSAID should be used (aspirin, 2-4 g/d; ibuprofen 1200-1800 mg/d; indomethacin 75-150 mg/d); treatment should last at least 7-14 days. A full-dose NSAID should be maintained until normalization of the C-reactive protein (CRP) followed by gradual tapering of the drug for another 1-2 weeks to prevent early reoccurrence.[13]
Aspirin is recommended for treatment of pericarditis after ST-elevation myocardial infarction.
According to the 2004 ESC, corticosteroids can be used for refractory symptoms, but their use can delay myocardial infarction healing.[32]
Colchicine, in combination with an NSAID can be considered in the initial treatment to prevent recurrent pericarditis. Colchicine, alone or in combination with an NSAID, can be considered for patients with recurrent or continued symptoms beyond 14 days.
Several small studies have noted successful use of colchicine to prevent recurrence of acute pericarditis after failure of conventional treatment, especially in idiopathic cases.[51, 52, 53, 54] One report found marked improvement following corticosteroid therapy in a patient with refractory uremic pleuropericarditis.[45]
Corticosteroids should not be used for initial treatment of pericarditis unless it is indicated for the underlying disease, the patient’s condition has no response to NSAIDs or colchicine, or both agents are contraindicated.
Clinical Context:
Indomethacin is the classic treatment used in pericarditis and is often considered the first choice. This drug is rapidly absorbed, and it is metabolized in the liver by demethylation, deacetylation, and glucuronide conjugation. Although, indomethacin ameliorates fever, it does not accelerate resolution of effusion.
Clinical Context:
Ketorolac is used for the relief of mild to moderate pain and inflammation. This agent inhibits prostaglandin synthesis by decreasing the activity of the enzyme cyclooxygenase, which results in decreased formation of prostaglandin precursors.
Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Small studies have documented rapid relief of symptoms with 1-2 doses of ketorolac. Doses of more than 75 mg do not increase therapeutic effects; therefore, administer high doses with caution, and closely observe patient response.
Clinical Context:
Ibuprofen is usually the drug of choice for mild to moderate pain, if no contraindications exist. This drug inhibits inflammatory reactions and pain, probably by decreasing the activity of the enzyme cyclooxygenase, which results in decreased prostaglandin synthesis.
Clinical Context:
Ketoprofen is used to relieve mild to moderate pain and inflammation. Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease. Doses of more than 75 mg do not increase therapeutic effects; therefore, administer high doses with caution, and closely observe patient response.
Clinical Context:
Naproxen is indicated for the relief of mild to moderate pain. This agent acts by inhibiting inflammatory reactions and pain via decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
Because pericarditis is primarily due to inflammation, anti-inflammatory medications are considered the drugs of choice. These agents are effective for chest discomfort and underlying inflammation. However, although nonsteroidal-anti-inflammatory drugs (NSAIDs) may offer symptomatic relief, they are ineffective in uremic pericarditis absence of dialysis.
Clinical Context:
Colchicine is used for recurrent pericarditis. This agent acts by decreasing the leukocyte motility and phagocytosis observed in inflammatory responses.
Clinical Context:
Aspirin is used for pericarditis secondary to myocardial infarction. This drug inhibits prostaglandin synthesis and blocks prostaglandin synthetase action, which prevents formation of the platelet-aggregating thromboxane A2. Use caution in pregnant women, because full doses are unsafe during pregnancy.
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body's immune response to diverse stimuli. However, although corticosteroids may offer symptomatic relief, they are ineffective in uremic pericarditis in the absence of dialysis.
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effective treatment for dialysis-associated pericarditis?What is the role of rheumatoid arthritis (RA) in the etiology of acute pericarditis?What is the role of systemic lupus erythematosus (SLE) in the etiology of acute pericarditis?What is the role of scleroderma in the etiology of acute pericarditis?What is the role of sarcoidosis in the etiology of acute pericarditis?What is the role of rheumatic fever in the etiology of acute pericarditis?Which conditions may cause acute pericarditis?What is the role of renal failure in the etiology of pericarditis?What is the prevalence of pericarditis caused by renal failure?What is the role of pericardial effusions in the etiology of pericarditis?What is the role of hypothyroidism in the etiology of acute pericarditis?What is cholesterol pericarditis?What is the role of myocardial infarction (MI) in the etiology of acute pericarditis?What is the role of Dressler syndrome in the etiology of acute pericarditis?What is the prevalence of acute pericarditis caused by aortic dissection?What is the etiologic relationship between Takotsubo cardiomyopathy and acute pericarditis?What is the prevalence of malignancy in acute pericarditis?What is the role of neoplasms in the etiology of acute pericarditis?Which malignancies are associated with acute pericarditis?What is the prevalence of acute pericarditis caused by lung cancer?What is the role of medications in the etiology of acute pericarditis?What is the role of radiation therapy in the etiology of acute pericarditis?What is the role of invasive cardiac procedures in the etiology of acute pericarditis?What is the role of trauma in the etiology of acute pericarditis?What is the incidence of acute pericarditis?What is the incidence of uremic pericarditis?How common is malignant disease in acute pericarditis?How does the incidence of acute pericarditis vary by sex and age?What is the prognosis of acute pericarditis?What are poor prognostic factors in acute pericarditis?Which 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in the diagnosis of purulent or suppurative pericarditis?How is the pericardial fluid characterized in diagnosis of acute pericarditis with an underlying inflammatory disorder?How is the pericardial fluid characterized in diagnosis of uremic pericarditis?What is the role of pericardial biopsy in the diagnosis of acute pericarditis?What is the role of cardiac catheterization in the diagnosis of acute pericarditis?What is the initial treatment approach for acute pericarditis?What are other approach considerations in the treatment of acute MI pericarditis?What are the 2015 ESC recommendations for the treatment of pericarditis?What is included in the prehospital care of acute pericarditis?What are the 2015 ESC recommendations for the emergency care of pericarditis?What is included in the emergency department (ED) care of acute pericarditis?What is included in the emergency department (ED) care of cardiac tamponade?How is idiopathic pericarditis treated?How is viral pericarditis treated?How is fungal pericarditis treated?What is the role of intrapericardial fibrinolysis in the treatment of acute pericarditis?How is tubercular infection managed in pericarditis?What is the role of steroids in the treatment of tuberculous pericarditis?How is rheumatoid arthritis (RA) pericarditis treated?How is rheumatic fever pericarditis treated?When is dialysis indicated in the treatment of acute pericarditis?What is the role of hemodialysis and peritoneal dialysis in the treatment of acute pericarditis?What are the dialysis recommendations in the treatment of acute pericarditis?Which drugs are used to provide symptomatic relief in acute pericarditis?What measures may prevent uremic pericarditis?How is hypothyroidism-associated pericarditis treated?What are the European Society of Cardiology (ESC) treatment guidelines for metabolic pericarditis?What are the treatment options for cardiovascular pericarditis?What is the treatment for neoplasm-associated pericarditis?What are the European Society of Cardiology (ESC) guidelines for the prevention of recurrence of neoplastic pericarditis?What are the European Society of Cardiology (ESC) treatment guidelines for neoplastic pericardial effusion without tamponade?How is drug-induced pericarditis treated?What is the role of colchicine in the treatment of acute pericarditis?Which surgical interventions are used in the treatment of acute pericarditis?What is the role of pericardiectomy in the treatment of acute pericarditis?When is pericardiectomy indicated for the treatment of acute pericarditis?What factor increases the failure rates for pericardiectomy in the treatment of acute pericarditis?What is the operative mortality rate for pericardiectomy in the treatment of acute pericarditis?What are the 2015 ESC guidelines for the treatment of post-cardiac injury syndromes?What can increase the diagnostic yield for pericardiectomy in acute pericarditis?What is the prognosis of surgery for acute pericarditis?When is pericardiocentesis indicated for the treatment of acute pericarditis?What is the role of a balloon catheter in the treatment of acute pericarditis?What is the role of pericardial window placement in the treatment of acute pericarditis?What is the role of pericardiotomy in the treatment of acute pericarditis?What are possible complications of acute pericarditis or the treatments used in its management?Which specialist consultations are needed for the treatment of acute pericarditis?What are the dietary restrictions for patients with acute pericarditis?What are the activity restrictions for patients with acute pericarditis?What is the focus of treatment for acute pericarditis?How are NSAIDs used in the treatment of acute pericarditis?When is aspirin indicated in the treatment of acute pericarditis?What is the role of corticosteroids in the treatment of acute pericarditis?What is the role of colchicine in the treatment of acute pericarditis?When are corticosteroids indicated for the treatment of acute pericarditis?Which medications in the drug class Corticosteroids are used in the treatment of Acute Pericarditis?Which medications in the drug class Salicylates are used in the treatment of Acute Pericarditis?Which medications in the drug class Anti-inflammatory agents are used in the treatment of Acute Pericarditis?Which medications in the drug class Nonsteroidal anti-inflammatory drugs are used in the treatment of Acute Pericarditis?
Sean Spangler, MD, Cardiologist, William Beaumont Army Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Philip J Gentlesk, MD, Director, Cardiac Electrophysiology, Section of Cardiovascular Disease, Brooke Army Medical Center
Disclosure: Nothing to disclose.
Chief Editor
Terrence X O'Brien, MD, MS, FACC, Professor of Medicine/Cardiology, Director, Clinical Cardiovascular Research, Medical University of South Carolina College of Medicine; Director, Echocardiography Laboratory, Veterans Affairs Medical Center of Charleston
Disclosure: Nothing to disclose.
Acknowledgements
George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine
George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, and National Kidney Foundation
Disclosure: Nothing to disclose.
Vecihi Batuman, MD, FACP, FASN Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology
Disclosure: Nothing to disclose.
David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Steven J Compton, MD, FACC, FACP Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals
Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society
Disclosure: Nothing to disclose.
Christopher A Fly, MD Assistant Professor, Department of Emergency Medicine, Medical College of Georgia
Christopher A Fly, MD is a member of the following medical societies: American College of Emergency Physicians
Disclosure: Nothing to disclose.
Anupama Gowda, MBBS, MD Consulting Staff, Atlanta Nephrology Associates, PC
Disclosure: Nothing to disclose.
Eric L Legome, MD Chief, Department of Emergency Medicine, Kings County Hospital Center; Associate Professor, Department of Emergency Medicine, New York Medical College
Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences
James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research
Disclosure: Genzyme Honoraria Speaking and teaching
G Shawn Lynchard, MD Consulting Cardiologist, Medical Director of Cardiac Care Unit, Congestive Heart Failure Clinic, and ECG and Stress Testing Clinic, Brooke Army Medical Center
G Shawn Lynchard, MD is a member of the following medical societies: American College of Cardiology and American College of Physicians
Disclosure: Nothing to disclose.
Chike Magnus Nzerue, MD Associate Dean for Clinical Affairs, Vice-Chairman of Internal Medicine, Meharry Medical College
Chike Magnus Nzerue, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, and National Kidney Foundation
Disclosure: Nothing to disclose.
David A Peak, MD Assistant Residency Director of Harvard Affiliated Emergency Medicine Residency, Attending Physician, Massachusetts General Hospital; Consulting Staff, Department of Hyperbaric Medicine, Massachusetts Eye and Ear Infirmary
David A Peak, MD is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Medscape Salary Employment
Verena T Valley, MD Associate Professor, Director of Ultrasound, Department of Emergency Medicine, University of Mississippi School of Medicine; Consulting Staff, Department of Emergency Medicine, Singing River Hospital System, Singing River Hospital, and Ocean Springs Hospital
Verena T Valley, MD is a member of the following medical societies: American College of Emergency Physicians
Bach DS. 2015 ESC guidelines for pericardial disease. American College of Cardiology. Available at https://www.acc.org/latest-in-cardiology/ten-points-to-remember/2015/10/30/12/01/2015-esc-guidelines-for-the-diagnosis-and-management-of-pericardial-diseases. October 30, 2015; Accessed: April 2, 2019.
Stage 1 electrocardiograph changes in a patient with acute pericarditis.
Stage 4 electrocardiograph changes in the same patient as in the previous image, taken approximately 3 months after acute pericardial illness. The patient remained symptom free despite continued T-wave inversion.
Recording of aortic pressure showing pulsus paradoxus. During inspiration, systolic pressure declines 20 mm Hg. Courtesy of Zhi Zhou, MD.
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B). Courtesy of Zhi Zhou, MD.
This ultrasonogram demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearance). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. Part B courtesy of Wikimedia Commons/Patrick J Lynch and C Carl Jaffe.
Stage 1 electrocardiograph changes in a patient with acute pericarditis.
Stage 4 electrocardiograph changes in the same patient as in the previous image, taken approximately 3 months after acute pericardial illness. The patient remained symptom free despite continued T-wave inversion.
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B). Courtesy of Zhi Zhou, MD.
Stage 1 electrocardiograph changes in a patient with acute pericarditis.
Stage 4 electrocardiograph changes in the same patient as in the previous image, taken approximately 3 months after acute pericardial illness. The patient remained symptom free despite continued T-wave inversion.
Chest radiographs revealing markedly enlarged cardiac silhouette and normal-appearing lung parenchyma in prepericardiocentesis (A) and postpericardiocentesis (B). Courtesy of Zhi Zhou, MD.
Recording of aortic pressure showing pulsus paradoxus. During inspiration, systolic pressure declines 20 mm Hg. Courtesy of Zhi Zhou, MD.
This ultrasonogram demonstrates a normal subcostal 4-chamber view of the heart. The pericardium is brightly reflective (echogenic or white in appearance). LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle. Part B courtesy of Wikimedia Commons/Patrick J Lynch and C Carl Jaffe.
H&E stain, medium power magnification showing a rheumatoid nodule in rheumatoid pericarditis, composed of histiocytes and scattered multinucleated giant cells (lower right) surrounding necroinflammatory debris (upper left).
Pap stain, high power magnification of adenocarcinoma metastatic to the pericardium on pericardiocentesis with the red arrow showing a normal mesothelial cell and the black arrowhead showing adenocarcinoma.
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