INTRODUCTION — The pericardium is a fibroelastic sac made up of visceral and parietal layers separated by a (potential) space, the pericardial cavity. In healthy individuals, the pericardial cavity contains 15 to 50 mL of an ultrafiltrate of plasma.
Diseases of the pericardium present clinically in one of several ways:
●Acute and recurrent pericarditis
●Pericardial effusion without major hemodynamic compromise
Acute pericarditis refers to inflammation of the pericardial sac. The term myopericarditis, or perimyocarditis, is used for cases of acute pericarditis that also demonstrate myocardial inflammation; myopericarditis is used for cases with predominant pericarditis and normal ventricular function, and perimyocarditis is used for cases with predominant myocarditis and/or ventricular dysfunction (ie, new wall motion abnormalities or reduced left ventricular ejection fraction). (See "Myopericarditis".)
The treatment and prognosis of acute pericarditis will be reviewed here. The etiology, clinical presentation, and diagnostic evaluation of acute pericarditis and other pericardial disease processes are discussed separately. (See "Etiology of pericardial disease" and "Acute pericarditis: Clinical presentation and diagnosis" and "Recurrent pericarditis" and "Myopericarditis" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic evaluation" and "Diagnosis and treatment of pericardial effusion".)
TREATMENT — The therapy of acute pericarditis should be targeted as much as possible to the underlying etiology (table 1) [1-5]. However, in resource-abundant countries, most cases of acute pericarditis in immunocompetent patients are due to viral infection or are idiopathic; it is generally assumed that most cases of "idiopathic" pericarditis are viral in etiology. Because of the relatively benign course associated with the most common causes of pericarditis (>80 percent of cases), it is not necessary to search for the etiology in all patients. As such, most patients are treated for a presumptive viral cause with nonsteroidal antiinflammatory drugs (NSAIDs) and colchicine. (See "Pericardial disease associated with cancer: Clinical presentation and diagnosis" and "Tuberculous pericarditis" and "Purulent pericarditis".)
In acute viral or idiopathic pericarditis, no therapy has been rigorously proven to prevent serious sequelae, such as cardiac tamponade and constrictive pericarditis. Fortunately, however, these complications are rare [6,7]. (See "Constrictive pericarditis: Diagnostic evaluation" and "Cardiac tamponade".)
General approach to treatment — In the treatment of acute pericarditis, the goals of therapy are the relief of pain, resolution of inflammation (and, if present, pericardial effusion), and the prevention of recurrence. Our general approach to treatment is as follows (algorithm 1):
●Ambulatory versus inpatient treatment – Most low-risk patients with acute pericarditis can be managed effectively in an ambulatory setting, while high-risk patients should be admitted to initiate treatment and continue the diagnostic evaluation. (See 'Which patients require hospitalization?' below.)
●Activity restriction – Patients should be instructed to restrict strenuous physical activity until symptoms have resolved and biomarkers have normalized. (See 'Activity restriction' below.)
•For nearly all patients with acute idiopathic or viral pericarditis, we recommend combination therapy with colchicine plus NSAIDs. (See 'Nonsteroidal antiinflammatory drugs' below and 'Colchicine' below.)
•For patients with an identified cause other than viral infection, specific therapy appropriate to the underlying disorder is indicated.
•Glucocorticoids should be used for initial treatment of acute pericarditis only in patients with contraindications to NSAIDs (eg, renal failure or pregnancy at ≥20 weeks gestation), or for specific indications (eg, systemic inflammatory diseases), and should be used at the lowest effective dose. (See 'Glucocorticoids' below.)
●Tapering treatment – Following the resolution of symptoms, we taper the dose of the antiinflammatory agent weekly in an attempt to reduce the subsequent recurrence rate. Colchicine is continued for a total duration of three months. (See 'NSAID dosing' below and 'Glucocorticoid dosing' below and 'Colchicine dosing' below.)
●Refractory or recurrent symptoms – Most patients whose symptoms worsen or recur following the initial course of therapy can still be managed effectively with medical therapy alone, and outpatient management remains feasible in almost all cases. (See "Recurrent pericarditis".)
Which patients require hospitalization? — High-risk patients with acute pericarditis (algorithm 1) should be admitted to the hospital in order to initiate appropriate therapy and expedite a thorough initial evaluation. Conversely, patients with uncomplicated (ie, low-risk) acute pericarditis can usually be evaluated and sent home, with outpatient follow-up to assess the efficacy of treatment.
Features of acute pericarditis associated with a higher risk include [8,9]:
●Fever (>38°C [100.4°F])
●Subacute course (without acute onset of chest pain)
●Evidence suggesting cardiac tamponade (eg, hemodynamic compromise) (see "Cardiac tamponade")
●A large pericardial effusion (ie, an end-diastolic echo-free space of more than 20 mm)
●Immunosuppression and immunodepressed patients
●Anticoagulant use (eg, vitamin K antagonists [eg, warfarin] or novel oral anticoagulants)
●Failure to show clinical improvement following seven days of appropriately dosed NSAID and colchicine therapy
●Elevated cardiac troponin, which suggests myopericarditis/perimyocarditis
Patients with none of these high-risk features can be safely treated on an outpatient basis (algorithm 1). A full discussion of risk assessment and determining the need for hospitalization is presented separately. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Assessment of risk and need for hospitalization'.)
Activity restriction — Strenuous physical activity may trigger recurrence of symptoms; therefore, such activity should be avoided until symptom resolution and normalization of biomarkers. While there are little systematic data to guide recommendations on activity restriction, our experts' approach to activity restriction is consistent with the advice of professional societies :
●Noncompetitive athletes should restrict activity until the resolution of symptoms and normalization of biomarkers (this approach has been endorsed by the 2015 ESC guidelines) .
●Competitive athletes should not participate in competitive sports for at least three months following the resolution of symptoms and normalization of biomarkers, and should be re-evaluated by a clinician prior to resuming training and competition. In patients with milder symptoms which promptly resolve with treatment, a shorter period or activity restriction (a minimum of one month) may be reasonable on a case-by-case basis.
●In cases of myopericarditis or perimyocarditis, we recommend withdrawal from competitive sports for six months and return to play only after normalization of laboratory data (eg, markers of inflammation, electrocardiogram [ECG], and echocardiogram). (See "Myopericarditis", section on 'Treatment'.)
Nonsteroidal antiinflammatory drugs — For nearly all patients with acute idiopathic or viral pericarditis, we recommend NSAIDs (in combination with colchicine) as the initial treatment (algorithm 1). There are two approaches to determine the duration of NSAID therapy and the proper time to begin tapering treatment; long-term data demonstrating superiority of one method over the other are not available.
●Duration of treatment is based upon the resolution of symptoms, which usually occurs in two weeks or less, with tapering once the patient is symptom-free for at least 24 hours.
●Duration of treatment is based upon the resolution of symptoms and normalization of C-reactive protein (CRP). In this approach, CRP is assessed at presentation and then weekly, using the antiinflammatory dose of NSAIDs until complete resolution of symptoms (for at least 24 hours) and normalization of CRP, at which point tapering begins .
Failure to respond to aspirin or NSAID therapy within one week (defined as persistence of fever, pleuritic chest pain, a new pericardial effusion, or worsening of general illness) suggests that a cause other than idiopathic or viral pericarditis is present. In such instances, a thorough search for the etiology should be performed. To expedite the diagnostic evaluation and for symptom control, some patients may require admission to the hospital. The main causes to be ruled out include tuberculous or other bacterial forms of pericarditis, cancer (especially lung cancer, breast cancer, and lymphomas and leukemias), post-cardiac injury syndromes, and systemic inflammatory diseases. (See "Acute pericarditis: Clinical presentation and diagnosis", section on 'Establishing a definite etiology'.)
Based on the results of multiple cohort studies and one randomized study, treatment with an antiinflammatory dose of NSAIDs alone appears to be effective in approximately 70 to 80 percent of pericarditis cases presumed to be of viral or idiopathic origin [7,8,13]. Primary therapy has been the administration of oral NSAIDs, particularly ibuprofen or aspirin; ketorolac, a parenteral NSAID, is also effective (table 2) . NSAIDs (including aspirin) function to both reduce inflammation and relieve pain in most patients [7,8,13,15-17]. Despite these benefits, however, there is no evidence that NSAIDs alter the natural history of acute pericarditis.
In a series of 254 patients deemed to be at low risk who were treated with aspirin as outpatients, 98 percent of patients who responded to aspirin were presumed to have idiopathic or viral disease, while 2 percent of the patients who responded to aspirin were subsequently diagnosed with an autoimmune disorder . By contrast, among the patients who did not respond to aspirin after seven days, only 39 percent were deemed idiopathic, while 43 percent were diagnosed with an autoimmune disorder and 18 percent with tuberculous pericarditis. At follow-up, aspirin resistance was associated with significant increases in the rates of recurrent pericarditis (61 versus 10 percent) and constrictive pericarditis (9 versus 1 percent).
A theoretical concern is that the antiplatelet activity of aspirin (or another NSAID) might promote the development of a hemorrhagic pericardial effusion. However, such a relationship has never been convincingly established, and the risk-benefit ratio seems to favor the use of these drugs. (See 'Bleeding risk of NSAIDs combined with other antithrombotics' below.)
NSAID dosing — We agree with the 2015 ESC guidelines, which recommended the use of an NSAID for the treatment of acute pericarditis . One of the following NSAID regimens is commonly used (table 2):
●Ibuprofen – The ibuprofen dose is 600 to 800 mg three times per day (table 2). Following the resolution of symptoms, we taper the ibuprofen dose weekly in an attempt to reduce the subsequent recurrence rate [8,18].
●Aspirin – The aspirin dose is 650 to 1000 mg three times per day (table 2). Following the resolution of symptoms, we taper the aspirin dose weekly in an attempt to reduce the subsequent recurrence rate .
●Indomethacin – The indomethacin dose is 25 to 50 mg three times per day (table 2). Following the resolution of symptoms, we taper the indomethacin dose weekly in an attempt to reduce the subsequent recurrence rate [8,18]. Indomethacin is associated with more side effects, and it is usually considered for recurrences. (See "Recurrent pericarditis", section on 'NSAID or aspirin'.)
Any of the listed NSAIDs can be continued for days or weeks, if necessary, for recurrent or incessant attacks. (See "Recurrent pericarditis", section on 'NSAID or aspirin'.)
In symptomatic pericarditis occurring within days after an acute myocardial infarction, we suggest aspirin plus colchicine rather than another NSAID plus colchicine. The use of NSAIDs other than aspirin should be avoided, since antiinflammatory therapy may impair scar formation . Aspirin may also be the first choice in patients who require concomitant antiplatelet therapy for any reason. With either regimen, gastrointestinal protection should be provided. (See "Pericardial complications of myocardial infarction" and "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity" and 'Gastrointestinal protection' below.)
Gastrointestinal protection — NSAIDs can lead to gastrointestinal toxicity (ie, gastritis, ulcers, etc), particularly when used in high doses or for prolonged periods of time. In addition to high doses or prolonged periods of treatment, patient-related factors associated with a higher risk of gastrointestinal toxicity include:
●History of peptic ulcer disease
●Age greater than 65 years
●Concurrent use of aspirin, corticosteroids, or anticoagulants
Patients considered at risk of gastrointestinal toxicity related to NSAID treatment should be treated with NSAIDs for the shortest interval possible and receive concomitant gastroprotective therapy while taking NSAIDs. Proton pump inhibitors (eg, omeprazole, pantoprazole) are generally preferred for prevention of gastrointestinal toxicity due to their efficacy and favorable safety profile. (See "NSAIDs (including aspirin): Primary prevention of gastroduodenal toxicity".)
Bleeding risk of NSAIDs combined with other antithrombotics — In patients who require more than one antiplatelet or anticoagulant as therapy for an underlying condition, there is a greater risk of bleeding complications. On occasion, patients with acute pericarditis treated with NSAIDs may also have an indication for an additional antiplatelet or anticoagulant, in which case the overall risk of bleeding should be assessed. Because NSAIDs (especially aspirin) can impact the metabolism of vitamin K antagonists, patients will typically require close monitoring and dose adjustments for the duration of treatment for acute pericarditis. (See "Management of warfarin-associated bleeding or supratherapeutic INR", section on 'Mitigating bleeding risk' and "Biology of warfarin and modulators of INR control", section on 'Aspirin/NSAIDs'.)
In patients who require antiplatelet therapy for another indication (eg, following coronary stenting), there are no specific contraindications or additional risks of bleeding when NSAIDs are used during acute pericarditis. In this setting, however, aspirin is generally the first choice to treat pericarditis, but doses should be increased to reach antiinflammatory effects (from 100 to 300 mg to up to 650 to 1000 mg three times per day). (See 'NSAID dosing' above.)
Concomitant use of heparin and anticoagulant therapies is often perceived as a possible risk factor for the development of a worsening or hemorrhagic pericardial effusion that may result in cardiac tamponade, but the available evidence does not support this .
●An analysis of 453 consecutive cases of acute pericarditis did not show a higher risk of hemorrhagic effusion in patients on antithrombotics .
●In another study of 274 patients with acute pericarditis or myopericarditis, the use of heparin or other anticoagulants was not associated with an increased risk of cardiac tamponade (odds ratio [OR] 1.1, 95% CI 0.3-3.5) .
NSAIDs (including aspirin) alter the metabolism of vitamin K antagonists (eg, warfarin), thus enhancing the anticoagulant effect. Consequently, careful monitoring and frequent dose adjustment are needed. Additionally, consideration should be given to using alternative antiinflammatory options, such as glucocorticoids. Although glucocorticoids have the potential for fewer bleeding-related drug interactions in patients requiring both antiinflammatory drugs and chronic anticoagulation therapy, the potential benefits of reduced risk of bleeding should be weighed against potential side effects and a higher rate of recurrent pericarditis associated with glucocorticoids. Because of these glucocorticoid concerns, we generally prefer therapy with NSAIDs, with additional monitoring for drug interactions and bleeding complications. (See "Major side effects of systemic glucocorticoids".)
Colchicine — For all patients with acute idiopathic or viral pericarditis (algorithm 1), we recommend that colchicine be added to antiinflammatory therapy (either NSAIDs or glucocorticoids) (table 2) [11,23]. Additionally, colchicine is generally efficacious for pericarditis caused by systemic inflammatory diseases and post-cardiac injury syndromes. However, for patients with diagnosed bacterial pericarditis, colchicine has not been proven efficacious and, on the contrary, may theoretically impair the clearance of the infectious agent. Colchicine is also not proven to be efficacious in malignancy-related pericarditis and pericardial effusion.
Colchicine, when used as an adjunct to NSAID therapy, reduces symptoms, decreases the rate of recurrent pericarditis, and is generally well tolerated. The 2015 ESC guidelines concluded that the weight of evidence supported the efficacy of colchicine, alone or in combination with NSAIDs, in the treatment of acute pericarditis . Of note, colchicine is not approved for the prevention of recurrent pericarditis in North America and most European countries (as of 2019, it is approved for this indication in Italy and Austria), as such its use is off-label. (See "Recurrent pericarditis", section on 'Colchicine'.)
The efficacy of colchicine in the primary management of acute pericarditis has been evaluated in randomized trials:
●In the ICAP trial, a randomized, double-blind study of colchicine versus placebo in addition to standard antiinflammatory therapy for treatment of a first episode of acute pericarditis (77 percent idiopathic) in 240 patients, colchicine added to standard antiinflammatory therapy significantly reduced the risk of recurrence (17 versus 38 percent with antiinflammatory therapy alone; relative risk reduction 0.56, 95% CI 0.30-0.72) . In addition, colchicine added to antiinflammatory treatment resulted in significantly better rates of remission and fewer hospitalizations compared with antiinflammatory treatment alone. No serious adverse events were observed.
●In the open label COPE trial of 120 patients with a first episode of acute pericarditis (84 percent idiopathic), the recurrence rate of pericarditis within 18 months was significantly lower in the colchicine plus aspirin group (11 versus 32 percent with aspirin alone; number needed to treat to prevent one recurrence equals five) .
●In a later open-label trial in 110 patients with a first episode of acute idiopathic pericarditis, the addition of colchicine to conventional antiinflammatory treatment did not reduce the recurrence rate . However, the study has important limitations to be acknowledged (eg, probably underpowered to test colchicine efficacy, diagnostic criteria for pericarditis not consistent with 2015 ESC guidelines, and possible significant delay in the administration of colchicine from symptoms onset) that may limit its clinical applicability .
In the COPE and ICAP studies, adult patients were excluded if they had elevated levels of aminotransferases, creatinine, or troponin and liver diseases, myopathy, blood dyscrasias, or inflammatory bowel disease. Pregnant or lactating women were also excluded as well as patients with bacterial or neoplastic pericarditis.
The efficacy of colchicine in the treatment of pericarditis has also been assessed in several systematic reviews and meta-analyses (which include patients with both acute and recurrent pericarditis) [27-30]. In a 2014 systematic review and meta-analysis, which included four randomized, double-blind trials (564 patients) of colchicine for both initial and recurrent episodes of pericarditis, colchicine use was associated with a reduced risk of recurrent pericarditis at 18 months in patients being treated for acute (hazard ratio [HR] 0.40, 95% CI 0.27-0.61) or recurrent (HR 0.37, 95% CI 0.24-0.58) pericarditis . There was no significant increase in adverse effects related to colchicine therapy . (See "Recurrent pericarditis", section on 'Colchicine'.)
Colchicine dosing — The 0.5 mg dose of colchicine is not available in many countries, including the United States and Canada where 0.6 mg tablets are used empirically in place of 0.5 mg tablets.
Colchicine may be given with or without a loading dose. When a loading dose is chosen, the loading dose is typically 0.5 to 1 mg (or 0.6 to 1.2 mg) twice daily on day 1, depending upon the patient’s body weight.
The daily maintenance dose of colchicine is weight-based:
●Patients weighing ≥70 kg should receive 0.5 to 0.6 mg twice daily
●Patients weighing <70 kg should receive 0.5 to 0.6 mg once daily
Colchicine should be administered for a total of three months for patients with an initial episode of acute pericarditis. In ICAP, colchicine was given without a loading dose as 0.5 mg twice daily for three months for patients weighing >70 kg or 0.5 mg once daily for patients weighing ≤70 kg.
Colchicine side effects — Colchicine is typically well tolerated. Side effects, most commonly gastrointestinal (eg, diarrhea, nausea, vomiting), are uncommon at low doses (0.5 to 1.2 mg per day), even when given continuously over years. Less common (<1 percent) side effects include bone marrow suppression, hepatotoxicity, and myotoxicity. Chronic renal insufficiency leading to increased colchicine levels appears to be the major risk factor for side effects and other possible negative interactions. In addition, colchicine has drug interactions and altered metabolism in certain patient populations.
Glucocorticoids — Glucocorticoids should be used for initial treatment of acute pericarditis only in patients with contraindications to NSAIDs (eg, renal failure or pregnancy at ≥20 weeks gestation), or for specific indications (eg, systemic inflammatory diseases), and should be used at the lowest effective dose. The number of such patients requiring glucocorticoids should be quite low (10 percent or less), as illustrated in two studies by an almost 90 percent response rate to aspirin alone within seven days, with most of the nonresponders having an autoimmune disease or tuberculosis [8,13]. Glucocorticoids may also be used in the event of failed initial therapy with aspirin/NSAID plus colchicine, suggesting recurrent or refractory pericarditis. (See "Recurrent pericarditis".)
Limited data are available on the efficacy of glucocorticoid therapy for acute pericarditis, as such therapy is generally limited to patients with nonresponse or contraindications to NSAID use . Observational studies suggest that glucocorticoid therapy early in the course of the disease is more likely to be associated with recurrent episodes [13,31-33]. The best data come from the COPE trial of colchicine therapy in which glucocorticoids were given only when aspirin was contraindicated or not tolerated . Glucocorticoid use was a significant predictor of recurrence (OR 4.30, 95% CI 1.21-15.25). The same effect has been reported for patients with the first recurrence or multiple recurrences and may be due to promotion of viral replication [31,34-36]. In a subsequent systematic review which included two randomized trials comparing steroid therapy with standard NSAID therapy and one trial of low-dose versus high-dose steroid therapy (with or without other therapy with NSAIDs or colchicine), the administration of steroids was associated with a trend toward a higher rate of recurrent pericarditis (OR 7.50, 95% CI 0.62-90.65) .
In addition to concerns about the efficacy of glucocorticoid therapy as initial treatment of acute pericarditis, chronic use of systemic glucocorticoids is associated with a number of potentially significant side effects. As such, when glucocorticoids are required, they should be given at the lowest appropriate and effective dose. (See "Major side effects of systemic glucocorticoids".)
Glucocorticoid dosing — While NSAIDs and colchicine remain the preferred treatment options for acute pericarditis, a minority of patients will have refractory symptoms requiring treatment with systemic steroid therapy. There are conflicting data, mostly derived from observational studies, regarding the optimal dosing and tapering of steroid therapy when used to treat pericarditis.
Our approach to glucocorticoid dosing — For patients who require glucocorticoid therapy for acute pericarditis, we suggest the use of moderate initial dosing (eg, 0.2 to 0.5 mg/kg/day of prednisone) followed by a slow taper (table 2) rather than high doses with a rapid taper. We add colchicine during glucocorticoid therapy and continue colchicine for three months for initial cases of acute pericarditis and six months in recurrent cases. We introduce aspirin or another NSAID toward the end of tapering or in case of recurrences instead of increasing the dose of the glucocorticoids. (See "Recurrent pericarditis".)
Results from a study of patients with recurrent pericarditis suggest that lower glucocorticoid doses may also be feasible in acute pericarditis, although these populations differ. In an observational study, 100 patients with recurrent pericarditis were treated with glucocorticoids (51 with prednisone 1 mg/kg/day and 49 with prednisone 0.2 to 0.5 mg/kg/day) . After adjustment for potential confounders, only high doses of prednisone were associated with more side effects, recurrences, and hospitalizations (HR 3.61, 95% CI 1.96-6.63). In a systematic review of published studies on medical therapy for pericarditis, data from three observational studies of steroid treatment showed that steroid use was associated with a trend toward increased risk of recurrent pericarditis (OR 7.50, 95% CI 0.62-90.65) . However, low-dose steroids were superior to high-dose steroids for treatment failure or recurrent pericarditis (OR 0.29, 95% CI 0.13-0.66), rehospitalization for pericarditis (OR 0.19, 95% CI 0.06-0.63), and adverse effects (OR 0.07, 95% CI 0.01-0.54).
In our experience, rapid tapering of systemic glucocorticoids increases the risk of treatment failure and recurrence. Although high doses of glucocorticoids (eg, prednisone 1 mg/kg/day) have been recommended in the ESC guidelines, use of lower doses (eg, prednisone 0.2 to 0.5 mg/kg/day) may be equally efficacious . These lower doses may be useful in reducing the risk of steroid side effects, which have been reported in up to 25 percent of patients treated with high doses. (See "Major side effects of systemic glucocorticoids".)
We usually begin tapering glucocorticoids at two to four weeks after resolution of symptoms and CRP normalization. Each decrement in prednisone dose should proceed only if the patient is asymptomatic and CRP remains normalized, particularly for doses lower than 25 mg/day. A proposed tapering scheme follows:
●Daily dose >50 mg – Taper 10 mg/day every one to two weeks
●Daily dose 25 to 50 mg – Taper 5 to 10 mg/day every one to two weeks
●Daily dose 15 to 25 mg – Taper 2.5 mg/day every two to four weeks
●Daily dose <15 mg – Taper 1.25 to 2.5 mg/day every two to six weeks
Other approaches — The 2015 ESC guidelines recommended that systemic steroid therapy be restricted to patients with the following conditions :
●Patients with symptoms refractory to standard therapy
●Acute pericarditis due to connective tissue disease
The 2015 ESC guidelines recommend use of low to moderate doses of glucocorticoids (eg, prednisone 0.2 to 0.5 mg/kg/day) when indicated. In contrast to our suggestions, the ESC guidelines recommend rapid tapering to reduce the risk of systemic side effects [11,37]. In patients with a coexisting pericardial effusion, intrapericardial steroid administration is an option that limits systemic toxicity .
Adjunctive therapies — Most patients with uncomplicated low risk acute pericarditis are managed effectively with medical therapy alone. On occasion, however, patients may require adjunctive therapies for:
●In patients with persistent symptoms and elevated heart rate (eg, heart rate >70 to 75 beats per minute) despite full antiinflammatory therapies, adjunctive use of betablockers, if not contraindicated, can be helpful to improve symptom control by reducing heart rate and exacerbation of chest pain at higher heart rates .
●A moderate to large pericardial effusion, particularly if hemodynamically significant and causing cardiac tamponade or symptomatic and refractory to medical therapy.
●Suspicion of a neoplastic or bacterial etiology and moderate to large pericardial effusion.
●Frequent, highly symptomatic recurrences of acute pericarditis with pericardial effusion.
●Evidence of constrictive pericarditis (a late occurrence when present).
Percutaneous and surgical techniques may be considered for such patients.
Pericardial drainage — Prolonged catheter drainage of a pericardial effusion is an effective means of preventing fluid reaccumulation. The mechanism by which this occurs is probably more related to the obliteration of the pericardial space following inflammation provoked by the catheter, rather than fluid drainage itself. Catheter drainage may be required for several days, and the catheter should not be removed until drainage stops or is minimal. If significant drainage continues for more than three to four days, a pericardial window should be considered. The management of pericardial effusions with and without cardiac tamponade is discussed in detail separately. (See "Cardiac tamponade" and "Diagnosis and treatment of pericardial effusion", section on 'Treatment'.)
Pericardiectomy — Surgical removal of all or part of the pericardium is virtually never required for the treatment of acute pericarditis. The role of pericardiectomy in patients with recurrent pericarditis is discussed separately. (See "Recurrent pericarditis", section on 'Role of pericardiectomy'.)
Treatment in patients with chronic kidney disease — Treatment for pericarditis in patients with advanced chronic kidney disease involves initiation or intensification of dialysis when uremia is the underlying cause, along with selective use of NSAIDs, colchicine, and corticosteroids. Patients with uremic pericarditis who are not already receiving dialysis should initiate dialysis. In patients already receiving dialysis for over two months (dialysis-associated pericarditis), the dialysis prescription is usually intensified. However, the frequency of improvement in pericarditis in these patients is lower than in patients in whom dialysis was recently initiated, and medical therapies are often required. The approach to medical therapy is similar to patients without chronic kidney disease.
PROGNOSIS — Patients with acute idiopathic or viral pericarditis have a good long-term prognosis. Cardiac tamponade rarely occurs in patients with acute idiopathic pericarditis and is more common in patients with a specific underlying etiology such as malignancy, tuberculosis, or purulent pericarditis. Constrictive pericarditis may occur in approximately 1 percent of patients with acute idiopathic pericarditis and is also more common in patients with a specific etiology. (See "Constrictive pericarditis: Diagnostic evaluation".)
Approximately 15 to 30 percent of patients with idiopathic acute pericarditis who are not treated with colchicine develop either recurrent or incessant disease. Immune mechanisms appear to be of primary importance in the majority of cases, and the term "chronic autoreactive" pericarditis has been used. Risk factors for recurrent pericarditis include lack of response to NSAIDs, the need for corticosteroid therapy, and creation of a pericardial window. The pathogenesis, course, and treatment of recurrent pericarditis are discussed separately. (See "Recurrent pericarditis".)
Sex may also predict the likelihood of complications. In a series of 453 consecutive cases of acute pericarditis, women were at increased risk of complications (hazard ratio 1.65, 95% CI 1.08-2.52) . A possible explanation of this finding is the higher frequency of autoimmune etiologies (eg, connective tissue diseases) in women.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pericardial disease".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Pericarditis in adults (The Basics)")
●Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Indications for hospitalization – Patients with acute pericarditis with one or more high-risk markers (eg, fever, evidence of cardiac tamponade, immunosuppression, etc) should be admitted to the hospital in order to initiate appropriate therapy and expedite a thorough initial evaluation (algorithm 1). Conversely, patients with uncomplicated (ie, low-risk) acute pericarditis can usually be evaluated and sent home, with outpatient follow-up. (See 'Which patients require hospitalization?' above.)
•General regimen – For nearly all patients with acute idiopathic or viral pericarditis, we recommend combination therapy with a nonsteroidal antiinflammatory drug (NSAID) plus colchicine rather than an NSAIDs alone (Grade 1A). This is based upon a reduced rate of recurrent pericarditis and a low incidence of side effects with colchicine (table 2). We generally administer ibuprofen or aspirin plus colchicine. An acceptable alternative is indomethacin plus colchicine in cases that are poorly responsive to ibuprofen or aspirin. (See 'Nonsteroidal antiinflammatory drugs' above and 'Colchicine' above.)
•Following acute myocardial infarction – In patients with acute pericarditis occurring within days following a myocardial infarction (MI), we suggest aspirin plus colchicine (table 2) rather than another NSAID plus colchicine (Grade 2C). These patients already have an indication to use aspirin at lower doses. Moreover, other NSAIDs may interfere with healing and scar formation. Glucocorticoids and NSAIDs other than aspirin should generally be AVOIDED in patients with acute pericarditis following an acute MI, but may be considered in those with persistent pericardial effusion not responding to aspirin and colchicine and with evidence of constrictive physiology and organization. (See 'Nonsteroidal antiinflammatory drugs' above and "Pericardial complications of myocardial infarction", section on 'Management of PIP'.)
•For patients with NSAID contraindications or a specific indication for glucocorticoid therapy – Glucocorticoids are used for initial treatment of acute pericarditis only in patients with contraindications to NSAIDs (eg, renal failure or pregnancy at ≥20 weeks gestation), or for specific indications (eg, systemic inflammatory diseases), and should be used at the lowest effective dose. The latter recommendation results from the greater likelihood of recurrent pericarditis when glucocorticoid therapy is used early in the course of the disease, along with a number of potentially significant side effects of systemic glucocorticoid therapy. (See 'Glucocorticoids' above.)
For patients who require glucocorticoid therapy for acute pericarditis, we suggest the use of moderate initial dosing (eg, 0.2 to 0.5 mg/kg/day of prednisone) followed by a slow taper rather than high doses with a rapid taper (table 2) (Grade 2C). (See 'Our approach to glucocorticoid dosing' above.)
●Specific therapy – In cases of pericarditis due to identifiable causes other than viral infection (eg, bacterial infection or malignancy), management is focused upon the underlying disorder and, if necessary, drainage of an associated pericardial effusion. (See 'Adjunctive therapies' above and 'General approach to treatment' above.)
●Activity restriction – Strenuous physical activity may trigger recurrence of symptoms; therefore, such activity should be avoided until symptom resolution and normalization of biomarkers. (See 'Activity restriction' above.)
●Adjunctive therapies – Most patients with uncomplicated low risk acute pericarditis are managed effectively with medical therapy alone. Patients with one or more of the following clinical features may require adjunctive therapies such as pericardial drainage or pericardiectomy: a moderate or large pericardial effusion (particularly if hemodynamically significant and causing cardiac tamponade or suspicion of a neoplastic or bacterial etiology), frequent highly symptomatic recurrences of acute pericarditis with pericardial effusion, or the late development of constrictive pericarditis. Beta blockers may be considered for those with symptoms despite full antiinflammatory therapies and high heart rates (eg, heart rate >70 to 75 beats per minute at rest) to achieve better and faster control of symptoms.
●Prognosis – Patients with acute idiopathic or viral pericarditis generally have a good long-term prognosis. Cardiac tamponade and late constrictive pericarditis rarely occur in patients with acute idiopathic pericarditis. (See 'Prognosis' above.)
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