Acute Pericarditis - Treatment and Prognosis

18/7/23, 14:55 Acute pericarditis: Treatment and prognosis - UpToDate
Official reprint from UpToDate®

www.uptodate.com © 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Acute pericarditis: Treatment and prognosis

AUTHOR: Massimo Imazio, MD, FESC, FHFA
SECTION EDITOR: Martin M LeWinter, MD
DEPUTY EDITOR: Susan B Yeon, MD, JD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2023.

This topic last updated: Apr 18, 2022.
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
● Cardiac tamponade
● Constrictive pericarditis
● Effusive-constrictive pericarditis
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
https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 1/25
"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 malignancy" 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.)
● Initial treatment
• 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)
● Acute trauma
● 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 [10]:
● Noncompetitive athletes should restrict activity until the resolution of symptoms and
normalization of biomarkers (this approach has been endorsed by the 2015 ESC guidelines)
[11].
● 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'.)
Medical therapies
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 [12].

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) [14]. 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 [8]. 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 [11]. 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 [8].
● 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 [19]. 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 [20].
● An analysis of 453 consecutive cases of acute pericarditis did not show a higher risk of
hemorrhagic effusion in patients on antithrombotics [9].
● 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) [21].
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".)
There are no significant reported interactions between NSAIDs or other antiplatelet therapies
and colchicine [22].
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 [11]. 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) [24]. 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) [13].
● 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 [25]. 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 [26].

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 [28]. There was no significant increase
in adverse effects related to colchicine therapy [29]. (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 [25].
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 [13]. 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) [37].
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
https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_r… 10/25

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) [38]. 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) [37]. 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 [11]. 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 [11]:
● Patients with symptoms refractory to standard therapy

● Acute pericarditis due to connective tissue disease
● Uremic pericarditis
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 [11].
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 [39].
● 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) [9]. 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.)
● Initial antiinflammatory therapy ( algorithm 1) (see 'General approach to treatment'

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.)
Use of UpToDate is subject to the Terms of Use.
REFERENCES
1. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of

pericardial diseases. Circulation 2010; 121:916.
2. Imazio M, Brucato A, Derosa FG, et al. Aetiological diagnosis in acute and recurrent
pericarditis: when and how. J Cardiovasc Med (Hagerstown) 2009; 10:217.
3. Imazio M, Brucato A, Mayosi BM, et al. Medical therapy of pericardial diseases: part I:
idiopathic and infectious pericarditis. J Cardiovasc Med (Hagerstown) 2010; 11:712.
4. Imazio M, Brucato A, Mayosi BM, et al. Medical therapy of pericardial diseases: part II:
Noninfectious pericarditis, pericardial effusion and constrictive pericarditis. J Cardiovasc
Med (Hagerstown) 2010; 11:785.
5. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic
Review. JAMA 2015; 314:1498.
6. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a

prospective series of 231 consecutive patients. Am J Cardiol 1985; 56:623.
7. Zayas R, Anguita M, Torres F, et al. Incidence of specific etiology and role of methods for
specific etiologic diagnosis of primary acute pericarditis. Am J Cardiol 1995; 75:378.
8. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a

management program for outpatient therapy. J Am Coll Cardiol 2004; 43:1042.
9. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute pericarditis.

Circulation 2007; 115:2739.
10. Pelliccia A, Solberg EE, Papadakis M, et al. Recommendations for participation in
competitive and leisure time sport in athletes with cardiomyopathies, myocarditis, and

pericarditis: position statement of the Sport Cardiology Section of the European Association
of Preventive Cardiology (EAPC). Eur Heart J 2019; 40:19.
11. Adler Y, Charron P, Imazio M, et al. 2015 ESC Guidelines for the diagnosis and management
of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial
Diseases of the European Society of Cardiology (ESC)Endorsed by: The European Association
for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015; 36:2921.
12. Imazio M, Brucato A, Maestroni S, et al. Prevalence of C-reactive protein elevation and time
course of normalization in acute pericarditis: implications for the diagnosis, therapy, and
prognosis of pericarditis. Circulation 2011; 123:1092.
13. Imazio M, Bobbio M, Cecchi E, et al. Colchicine in addition to conventional therapy for acute
pericarditis: results of the COlchicine for acute PEricarditis (COPE) trial. Circulation 2005;
112:2012.
14. Arunasalam S, Siegel RJ. Rapid resolution of symptomatic acute pericarditis with ketorolac
tromethamine: a parenteral nonsteroidal antiinflammatory agent. Am Heart J 1993;
125:1455.
15. Spodick DH. Acute pericarditis: current concepts and practice. JAMA 2003; 289:1150.
16. McGinn JT, Rosati M, McGinn TG. Indomethacin in treatment of pericarditis. N Y State J Med
1970; 70:1783.
17. Berman J, Haffajee CI, Alpert JS. Therapy of symptomatic pericarditis after myocardial
infarction: retrospective and prospective studies of aspirin, indomethacin, prednisone, and
spontaneous resolution. Am Heart J 1981; 101:750.
18. Imazio M, Trinchero R. Clinical management of acute pericardial disease: a review of results
and outcomes. Ital Heart J 2004; 5:803.
19. Hammerman H, Alker KJ, Schoen FJ, Kloner RA. Morphologic and functional effects of
piroxicam on myocardial scar formation after coronary occlusion in dogs. Am J Cardiol 1984;
53:604.
20. Imazio M, Trinchero R. Triage and management of acute pericarditis. Int J Cardiol 2007;
118:286.
21. Imazio M, Cecchi E, Demichelis B, et al. Myopericarditis versus viral or idiopathic acute
pericarditis. Heart 2008; 94:498.
22. Imazio M, Brucato A, Trinchero R, et al. Colchicine for pericarditis: hype or hope? Eur Heart J
2009; 30:532.
23. Imazio M. Contemporary management of pericardial diseases. Curr Opin Cardiol 2012;
27:308.

24. Imazio M, Brucato A, Cemin R, et al. A randomized trial of colchicine for acute pericarditis. N
Engl J Med 2013; 369:1522.
25. Sambola A, Roca Luque I, Mercé J, et al. Colchicine Administered in the First Episode of
Acute Idiopathic Pericarditis: A Randomized Multicenter Open-label Study. Rev Esp Cardiol
(Engl Ed) 2019; 72:709.
26. Imazio M. Why Colchicine Should Continue To Be The First Line Therapy For Acute And
Recurrent Pericarditis. Rev Esp Cardiol (Engl Ed) 2019; 72:705.
27. Imazio M, Brucato A, Forno D, et al. Efficacy and safety of colchicine for pericarditis
prevention. Systematic review and meta-analysis. Heart 2012; 98:1078.
28. Alabed S, Cabello JB, Irving GJ, et al. Colchicine for pericarditis. Cochrane Database Syst Rev
2014; :CD010652.
29. Imazio M, Brucato A, Belli R, et al. Colchicine for the prevention of pericarditis: what we
know and what we do not know in 2014 - systematic review and meta-analysis. J Cardiovasc
Med (Hagerstown) 2014; 15:840.
30. Melendo-Viu M, Marchán-Lopez Á, Guarch CJ, et al. A systematic review and meta-analysis of
randomized controlled trials evaluating pharmacologic therapies for acute and recurrent
pericarditis. Trends Cardiovasc Med 2023; 33:319.
31. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004; 351:2195.
32. Shabetai R. Often neglected yet important: the pericardium and its diseases. Herz 2000;
25:717.
33. Imazio M, Demichelis B, Parrini I, et al. Recurrent pain without objective evidence of disease
in patients with previous idiopathic or viral acute pericarditis. Am J Cardiol 2004; 94:973.
34. Imazio M, Bobbio M, Cecchi E, et al. Colchicine as first-choice therapy for recurrent
pericarditis: results of the CORE (COlchicine for REcurrent pericarditis) trial. Arch Intern Med
2005; 165:1987.
35. Artom G, Koren-Morag N, Spodick DH, et al. Pretreatment with corticosteroids attenuates
the efficacy of colchicine in preventing recurrent pericarditis: a multi-centre all-case analysis.
Eur Heart J 2005; 26:723.
36. Imazio M, Demichelis B, Parrini I, et al. Management, risk factors, and outcomes in
recurrent pericarditis. Am J Cardiol 2005; 96:736.
37. Lotrionte M, Biondi-Zoccai G, Imazio M, et al. International collaborative systematic review
of controlled clinical trials on pharmacologic treatments for acute pericarditis and its
recurrences. Am Heart J 2010; 160:662.

38. Imazio M, Brucato A, Cumetti D, et al. Corticosteroids for recurrent pericarditis: high versus
low doses: a nonrandomized observation. Circulation 2008; 118:667.
39. Imazio M, Andreis A, Agosti A, et al. Usefulness of Beta-Blockers to Control Symptoms in
Patients With Pericarditis. Am J Cardiol 2021; 146:115.
Topic 15800 Version 40.0

GRAPHICS
Acute pericarditis etiologies: Data from published clinical studies with

unselected populations
Western Europe Africa

[1] [2]
(2007-2012) (1995-2001)
Idiopathic* 516 (55.0%) 32 (13.7%)
Specific etiology 417 (46.0%) 201 (86.3%)
Neoplastic ¶ 85 (8.9%) 22 (9.4%)
Tuberculosis ¶ 4 (<1.0%) 161 (69.5%)
Autoimmune etiologies ¶ 25 (2.6%) Δ 12 (5.2%)
Purulent ¶ 29 (3.0%) 5 (2.1%)
* Most idiopathic cases are likely viral.
¶ As a fraction of the entire sample.
Δ Autoimmune pericarditis can be caused by autoimmune disease or as a complication of myocardial

infarction (MI) or cardiac surgery. In this table, we only report pericarditis caused by autoimmune
disease, while the original paper (Gouriet et al) reports an additional 188 cases related to MI or
cardiac surgery.
Data from:
1. Gouriet F, Levy PY, Casalta JP, et al. Etiology of pericarditis in a prospective cohort of 1162 cases. Am J Med 2015;
128:784.
2. Reuter H, Burgess LJ, Louw VJ, et al. The management of tuberculous pericardial effusion: experience in 233
consecutive patients. Cardiovasc J S Afr 2007; 18:20.
Graphic 60949 Version 8.0

Initial treatment of acute pericarditis in adults
NSAIDs: nonsteroidal antiinflammatory drugs.
* NSAIDs are the preferred antiinflammatory for nearly all patients

with acute idiopathic or viral pericarditis. Glucocorticoids should be
used for initial treatment of acute pericarditis only in patients with
contraindications to NSAIDs or for specific indications (ie, systemic
inflammatory diseases, pregnancy, renal failure), and should be
used at the lowest effective dose. Refer to the UpToDate topic on
treatment of acute pericarditis for glucocorticoid dosing
information.
¶ Response to treatment includes improvement/resolution of

symptoms within 1 to 2 weeks of initiation of therapy and
normalization of C-reactive protein level (if measured).
Δ Refer to UpToDate content on recurrent/refractory pericarditis for

therapeutic approach to patients who are not showing clinical
improvement.

Drug therapy in acute and recurrent pericarditis for adult patients
Duration of initial
Antiinflammatory ¶
Drug or maintenance Tapering regimen
dose
dose*
First-line therapy for most patients: Δ
Aspirin ◊ 650 to 1000 mg orally 3 1 to 2 weeks Decrease dose by

times daily about 250 mg per week
or
Ibuprofen ◊ 600 to 800 mg orally 3 1 to 2 weeks Decrease dose by 200

§
times daily mg per week
or
Indomethacin ◊ 25 to 50 mg orally 3 1 to 2 weeks Decrease dose by 25

times daily mg per week
plus
Colchicine ¥ ‡ 0.5 to 0.6 mg orally 2 3 months (acute) Usually not tapered

times daily
6 months or more
(recurrent)
Second-line therapy (for refractory cases or patients with a contraindication to NSAID therapy):
Prednisone 0.2 to 0.5 mg/kg daily 2 to 4 weeks (acute or Gradual tapering over
recurrent † ) 2 to 3 months; refer to
UpToDate topic review
of treatment of acute
pericarditis, section on
glucocorticoids
plus
Colchicine ¥ ‡ 0.5 to 0.6 mg orally 2 3 months or more Usually not tapered

times daily (acute)
6 months or more
(recurrent)
Colchicine is generally
continued for 4 weeks
or more after
discontinuation of
glucocorticoid
Third-line therapy: Second-line therapy plus aspirin dosed as for first-line therapy
Fourth-line therapy: One of the following agents (or pericardiectomy)

Rilonacept Loading dose of 320 160 mg SC weekly for Slow taper over 3
mg delivered as 2 SC several months months or more
doses of 160 mg on the
same day at 2 different
sites
Anakinra 1 to 2 mg/kg SC daily Several months Slow taper over 3

(maximum dose 100 months or more
mg daily)
Azathioprine 1 mg/kg orally daily Several months Not tapered

increasing to 2 to 3
mg/kg daily (maximum
dose 150 mg daily)
IVIG 400 to 500 mg/kg IV 5 days (may repeat Not tapered

daily after 1 month)
NSAID: nonsteroidal antiinflammatory drug; SC: subcutaneous injection; IVIG: intravenous

immunoglobulin; IV: intravenous; CRP: C-reactive protein.
* This column describes the typical duration of full-dose therapy for symptom control. Except for
colchicine, the duration of full-dose therapy and subsequent tapering should be tailored according to
resolution of symptoms and normalization of markers of inflammation; refer to topic reviews for
approach.
¶ Tapering is begun once symptoms have resolved for at least 24 hours and CRP level has
normalized. Tapering is continued only if the patient remains asymptomatic with normal CRP levels.
Some clinicians taper more slowly than shown in the table by reducing the total daily dose (rather
than each individual dose) by the taper dose amount indicated.
Δ For patients treated with aspirin as an antiplatlet agent (including patients with peri-infarction
pericarditis), NSAIDs (such as ibuprofen and indomethacin) are avoided. Glucocorticoid therapy is
also avoided in patients with peri-infarction pericarditis. Refer to UpToDate content on pericardial
complications of myocardial infarction.
◊ Proton pump inhibitor (eg, omeprazole) gastrointestinal protection may be indicated.
§ Some patients may require ibuprofen every 6 hours (4 times daily), in which case the dose should
not exceed 600 mg every 6 hours.
¥ 0.5 mg colchicine is not available in the United States. It is widely available elsewhere.
‡ Colchicine dose should be reduced to 0.5 to 0.6 mg once daily in patients <70 kg. Refer to UpToDate
content on colchicine dosing for other indications for dosage reduction.
† Patients with acute pericarditis are generally treated with prednisone for a duration at the lower
end of this range, while patients with recurrent pericarditis are generally treated for a duration at the
upper end of this range.
Data from:
1. Lange RA, Hillis LD. Clinical practice. Acute pericarditis. N Engl J Med 2004; 351:2195.

2. Maisch B, Seferovic PM, Ristic AD, et al. Guidelines on the diagnosis and management of pericardial disease: The task
force on the diagnosis and management of pericardial disease of the European Society of Cardiology. European Heart
Journal 2004; 25:587.
3. Imazio M, Brucato A, Trinchero R, et al. Individualized therapy for pericarditis. Expert Rev Cardiovasc Ther 2009; 7:965.

Contributor Disclosures
Massimo Imazio, MD, FESC, FHFA Consultant/Advisory Boards: Kiniksa [Recurrent pericarditis]. All of the
relevant financial relationships listed have been mitigated. Martin M LeWinter,
MD Grant/Research/Clinical Trial Support: Kiniksa Pharmaceuticals [Pericarditis]. Consultant/Advisory
Boards: Kiniksa Pharmaceuticals [Pericarditis]. All of the relevant financial relationships listed have been
mitigated. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to
disclose.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.
Conflict of interest policy

Acute Pericarditis - Treatment and Prognosis

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Acute Pericarditis - Treatment and Prognosis

Uploaded by

Copyright:

Available Formats

18/7/23, 14:55 Acute pericarditis: Treatment and prognosis - UpToDate

Official reprint from UpToDate®

Acute pericarditis: Treatment and prognosis

Literature review current through: Jun 2023.

Diseases of the pericardium present clinically in one of several ways:

● Acute and recurrent pericarditis

● Activity restriction – Patients should be instructed to restrict strenuous physical activity

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 2/25

● Refractory or recurrent symptoms – Most patients whose symptoms worsen or recur

Which patients require hospitalization? — High-risk patients with acute pericarditis

Features of acute pericarditis associated with a higher risk include [8,9]:

● Fever (>38°C [100.4°F])

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 3/25

hospitalization is presented separately. (See "Acute pericarditis: Clinical presentation and

Activity restriction — Strenuous physical activity may trigger recurrence of symptoms;

● In cases of myopericarditis or perimyocarditis, we recommend withdrawal from

● Duration of treatment is based upon the resolution of symptoms and normalization of C-

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 4/25

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 5/25

In symptomatic pericarditis occurring within days after an acute myocardial infarction, we

Gastrointestinal protection — NSAIDs can lead to gastrointestinal toxicity (ie, gastritis,

● History of peptic ulcer disease

Patients considered at risk of gastrointestinal toxicity related to NSAID treatment should be

Bleeding risk of NSAIDs combined with other antithrombotics — In patients who

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 6/25

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 7/25

glucocorticoids) ( table 2) [11,23]. Additionally, colchicine is generally efficacious for

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 8/25

Colchicine dosing — The 0.5 mg dose of colchicine is not available in many countries,

The daily maintenance dose of colchicine is weight-based:

● Patients weighing ≥70 kg should receive 0.5 to 0.6 mg twice daily

Colchicine side effects — Colchicine is typically well tolerated. Side effects, most

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_re… 9/25

Glucocorticoids — Glucocorticoids should be used for initial treatment of acute pericarditis

Glucocorticoid dosing — While NSAIDs and colchicine remain the preferred treatment

Our approach to glucocorticoid dosing — For patients who require glucocorticoid

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_r… 10/25

● Daily dose >50 mg – Taper 10 mg/day every one to two weeks

Other approaches — The 2015 ESC guidelines recommended that systemic steroid

● Patients with symptoms refractory to standard therapy

● A moderate to large pericardial effusion, particularly if hemodynamically significant and

● 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

Pericardiectomy — Surgical removal of all or part of the pericardium is virtually never required

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_r… 12/25

Treatment in patients with chronic kidney disease — Treatment for pericarditis in patients

SOCIETY GUIDELINE LINKS

INFORMATION FOR PATIENTS

● Basics topics (see "Patient education: Pericarditis in adults (The Basics)")

SUMMARY AND RECOMMENDATIONS

● Initial antiinflammatory therapy ( algorithm 1) (see 'General approach to treatment'

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_r… 14/25

• Following acute myocardial infarction – In patients with acute pericarditis occurring

• For patients with NSAID contraindications or a specific indication for

● Activity restriction – Strenuous physical activity may trigger recurrence of symptoms;

https://www-uptodate-com.ez.urosario.edu.co/contents/acute-pericarditis-treatment-and-prognosis/print?search=acute pericarditis&source=search_r… 15/25

significant and causing cardiac tamponade or suspicion of a neoplastic or bacterial

Use of UpToDate is subject to the Terms of Use.

1. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of

6. Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J. Primary acute pericardial disease: a

8. Imazio M, Demichelis B, Parrini I, et al. Day-hospital treatment of acute pericarditis: a