Management of Pericardial Effusion and Acute Pericarditis During Pregnancy - UpToDate

23/2/24, 14:11 Management of pericardial effusion and acute pericarditis during pregnancy - UpToDate
Official reprint from UpToDate®

www.uptodate.com © 2024 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Management of pericardial effusion and acute

pericarditis during pregnancy
AUTHOR: Massimo Imazio, MD, FESC, FHFA
SECTION EDITORS: Martin M LeWinter, MD, Jae K Oh, MD
DEPUTY EDITOR: Susan B Yeon, MD, JD
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2024.

This topic last updated: Apr 19, 2022.
INTRODUCTION
Although diseases of the pericardium occur sporadically during pregnancy, there is no

evidence that pregnancy increases the susceptibility to pericardial diseases [1]. The
outcomes of pregnancies in women with pericardial disease are similar to those expected in
the general population. More complex cases may require a multidisciplinary approach
involving different subspecialties (eg, cardiology, internal medicine, maternal-fetal medicine,
and neonatology).
Limited data are available to guide the management of pericardial disease during
pregnancy. However, as with pregnancy in general, the major tenet of avoiding all
medications and interventions that are not absolutely necessary should be followed.
This topic will discuss the clinical features, diagnosis, and management of pericardial
effusion and acute (or recurrent) pericarditis during pregnancy. A broader discussion of
pericardial disease in the general population is presented separately. (See "Acute pericarditis:
Clinical presentation and diagnosis" and "Acute pericarditis: Treatment and prognosis" and
"Recurrent pericarditis" and "Pericardial effusion: Approach to diagnosis".)
PERICARDIAL EFFUSION
Fetal pericardial fluid — After 20 weeks of gestation, a small amount of pericardial fluid (<3
mm) can be detected in the normal fetus by fetal ultrasound [1,2]. Larger fetal pericardial
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/management-of-pericardial-effusion-and-acute-pericarditis-during-pregnancy/pr… 1/23
effusions should raise suspicion of disease conditions, such as nonimmune hydrops fetalis,
fetal hemolytic disease due maternal antibodies to Rh or other red cell antigens, structural
anomaly (eg, heart or diaphragm, teratoma), chromosomal abnormality, infection, or an
immunopathy [3,4]. Because of the limited distensibility of the fetal pericardial sac,
pathologic pericardial effusion may be the first sign of hydrops, detectable before the
appearance of ascites, pleural effusion, and soft tissue edema. (See "Nonimmune hydrops
fetalis", section on 'Fetal findings'.)
Maternal pericardial effusion
Epidemiology and clinical features — Pericardial effusion has been reported in the first
and second trimester in 15 to 20 percent of pregnancies and in approximately 40 percent of
pregnant women during the third trimester [5]. In general, these effusions are
asymptomatic, benign, transient, and resolve spontaneously without therapy. In the absence
of signs or symptoms of acute pericarditis or cardiac tamponade, neither diagnostic testing
(generally with echocardiography) nor specific treatment is required.
The following observations have been made regarding pericardial effusions in pregnancy:
● The effusion is usually small to moderate in size, with separation of the pericardial
layers of less than 10 mm. When sampled, these effusions are usually found to be a
transudate (hydropericardium) [5-8].
● Slightly elevated blood pressure and/or nonspecific ST-T changes have been reported in
association with pericardial effusion [6,7].
● The clinical examination and electrocardiogram (ECG) are generally normal.
● The pericardial effusion is usually transient and disappears within two months
following delivery [6].
● In the absence of signs or symptoms of acute pericarditis or cardiac tamponade,

treatment is not required [5-8]. (See "Acute pericarditis: Treatment and prognosis" and
"Cardiac tamponade".)
The signs and symptoms of cardiac tamponade may be masked during pregnancy due to the
physiologic increase in circulating blood volume. This may lead to a larger pericardial
effusion being present before signs or symptoms are detected.
Management and follow-up — For pregnant women who are identified as having a
moderate or large pericardial effusion that is not felt to require immediate drainage, serial
follow-up testing with echocardiography should be performed. Echocardiography
examination should include Doppler recording of mitral inflow velocities and hepatic vein
flow velocities as well as M-mode and 2D echocardiography to assess the hemodynamic
impact of pericardial effusion. In general, if the patient remains asymptomatic and

hemodynamically stable and the effusion is not increasing in size, we continue with serial
echocardiograms every three months until the pericardial effusion is decreasing in size or
resolved. For pregnant women with a small asymptomatic pericardial effusion, we repeat the
echocardiogram only if clinically indicated by signs or symptoms suggestive of possible
pericardial tamponade, as small pericardial effusions are usually benign and spontaneously
resolve.
ACUTE PERICARDITIS
Epidemiology and etiology — There are no published data on the frequency of acute
pericarditis in pregnancy. There is no evidence to suggest an incidence that is higher or
lower than in the general population. (See "Acute pericarditis: Clinical presentation and
diagnosis", section on 'Epidemiology'.)
As in the general population, idiopathic acute pericarditis is the most frequent final diagnosis
( table 1); the etiology is often presumed to be viral [9]. Infectious etiologies other than
viral are less common than in the general population. Tuberculous pericarditis should be
suspected especially in cases coming from endemic areas or in case of HIV infection [10,11].
(See "Etiology of pericardial disease".)
Clinical manifestations — Acute pericarditis can present in a variety of ways, depending on

the underlying etiology. Patients with an infectious etiology may present with signs and
symptoms of systemic infection such as fever and leukocytosis. Viral etiologies in particular
may be preceded by "flu-like" respiratory or gastrointestinal symptoms. Patients with a
known autoimmune disorder or malignancy may present with signs or symptoms specific to
their underlying disorder. (See "Acute pericarditis: Clinical presentation and diagnosis",
section on 'Clinical features'.)
The major clinical manifestations of acute pericarditis include [12]:
● Chest pain – Typically sharp and pleuritic, improved by sitting up and leaning forward.
● Pericardial friction rub – A superficial scratchy or squeaking sound best heard with the
diaphragm of the stethoscope over the left sternal border.
● ECG changes – New widespread ST elevation and/or PR depression.
● Pericardial effusion.
Diagnosis — The diagnosis of acute pericarditis is usually suspected based on a history of

characteristic pleuritic chest pain, and is confirmed if a pericardial friction rub, typical ECG
changes, or an effusion is present. Pericarditis should also be suspected in a patient with
persistent fever and pericardial effusion or new unexplained cardiomegaly [10]. Additional
testing, which typically includes blood work, chest radiography, electrocardiography, and
echocardiography, can support the diagnosis but is frequently normal or unrevealing. The
electrocardiogram is usually the first and one of the most helpful diagnostic tests in patients
with chest pain and suspected acute pericarditis. Because ST segment elevations in a patient
with chest pain may also be seen in patients with an acute coronary syndrome, careful
evaluation of all ECG findings is critical. Echocardiography is often normal, but it is an
essential part of the evaluation if there is evidence of an associated pericardial effusion
and/or signs of cardiac tamponade. (See "Acute pericarditis: Clinical presentation and
diagnosis", section on 'Diagnosis'.)
The diagnosis of acute pericarditis in pregnancy is made using the same criteria ( table 2)
as in the general population [10,13]. Echocardiography is the imaging method of choice for
diagnosis, evaluating the hemodynamic impact of pericardial fluid, absence of regional wall
motion (when STEMI is considered), guidance for pericardiocentesis when needed, and
follow-up [14].
Diagnostic radiographs of the chest, if indicated, produce almost no scatter to the fetus; any
radiation received would not result in a measurably increased risk, especially if the maternal
abdomen is shielded. However, in clinical practice, they are avoided in most cases.
Magnetic resonance imaging with gadolinium and nuclear isotope scans with gallium-67 are
generally avoided unless necessary to significantly improve diagnostic performance and
improve fetal or maternal outcome. (See "Diagnostic imaging in pregnant and lactating
patients".)
Determination of risk and need for hospitalization — Many clinicians admit all new cases
of acute pericarditis to the hospital, but this may not be necessary. A pregnant patient with
uncomplicated acute pericarditis can undergo initial evaluation in a same-day hospital facility
or clinic, although outpatient follow-up is required [15,16]. On the other hand, pregnant
patients with high-risk features are at increased risk of short-term complications and have a
higher likelihood of a specific disease, as is also the case in nonpregnant patients [15].
Hospital admission is indicated for high-risk patients to initiate appropriate therapy and a
thorough etiologic evaluation. (See "Acute pericarditis: Clinical presentation and diagnosis",
section on 'Assessment of risk and need for hospitalization'.)
Management — The management of pregnant women with acute pericarditis is similar to

that in the general population , with the notable exception that the impact of all therapies on
the fetus must be considered ( algorithm 1). General outcomes of pregnancy in patients
with pericarditis are good when the mothers are followed by a multidisciplinary team with
experience in the field [17-19].
In addition to activity restriction, the therapy of acute pericarditis should be targeted as

much as possible to the underlying etiology [20-24]. In patients with an identified cause
other than viral infection, specific therapy appropriate to the underlying disorder is indicated
( table 1). However, in resource-rich countries, most cases of acute pericarditis in
immunocompetent patients are idiopathic and considered to be most likely due to a viral
infection.
Because of the relatively benign course associated with the common causes of pericarditis
(>80 percent of cases), it is at not necessary to search for the etiology in all patients. As such,
most patients are initially treated for a presumptive viral cause with nonsteroidal
antiinflammatory drugs (NSAIDs), which can generally be continued until gestational week
20, as discussed below. (See 'NSAID therapy' below.)
Most patients with acute pericarditis can be managed effectively with medical therapy alone.
However, patients with a large pericardial effusion, a hemodynamically significant pericardial
effusion, a suspicion of a bacterial or neoplastic etiology, or evidence of constrictive
pericarditis should be evaluated for invasive therapies, such as pericardial drainage and/or
pericardiotomy (pericardial window). (See "Acute pericarditis: Treatment and prognosis",
section on 'Adjunctive therapies'.)
Activity restriction — Strenuous physical activity may trigger a recurrence of symptoms in

patients with acute (or recurrent) pericarditis; therefore, such activity should be avoided at
least until symptom resolution or preferably for two to three months following the cessation
of symptoms. The approach to reintroduction of physical activities is discussed separately.
(See "Acute pericarditis: Treatment and prognosis", section on 'Activity restriction'.)
Initial treatment — The general approach to the pharmacologic management of acute (or
recurrent) pericarditis during pregnancy ( algorithm 1) is somewhat similar to that for
nonpregnant individuals. Patients with a specific cause identified should have treatment
tailored to that specific etiology, while patients with idiopathic pericarditis should receive
antiinflammatory therapy, with the exception that colchicine is not used in pregnant patients.
(See 'Colchicine' below.)
● In patients with an identified cause other than viral or idiopathic disease, specific
therapy appropriate to the underlying disorder is indicated ( table 1).
● In acute viral or idiopathic pericarditis, the optimal approach to therapy varies before
and after gestational week 20 due to the impact of NSAIDs on the ductus arteriosus in
the second half of gestation ( algorithm 1).
• For pregnant women who are less than 20 weeks pregnant, we recommend NSAIDs,
either aspirin (500 to 750 mg every eight hours) or ibuprofen (600 to 800 mg every
eight hours). (See 'NSAID therapy' below.)
• For pregnant women at gestational week 20 week or greater, NSAIDs are

contraindicated and should not be started (or should be withdrawn if already in use).
In this population, glucocorticoids are the preferred therapy as they have not been
associated with congenital anomalies after the first trimester, and neonatal adrenal
suppression is rare. Generally, low to moderate glucocorticoid doses are used and
are sufficient to control the disease. Inducing maternal gestational diabetes is a
potential concern. (See "Acute pericarditis: Treatment and prognosis", section on
'Glucocorticoids'.)
As is true for the use of all drugs during pregnancy, treatment of acute pericarditis must
balance the benefits of therapy against the potential harm to the fetus. A list of common
antiinflammatory and immunosuppressive drugs used in the treatment of pericardial
diseases is provided ( table 3 and table 4).
One of the largest reports of pregnant women with pericarditis includes six cases (mean age
30 years, mean gestational age at delivery 38 weeks, and mean birth weight 2839 g), all with
an idiopathic etiology [25]. Four women were treated with aspirin 800 mg three times daily
with gradual tapering in three within 20 weeks of gestation. In one case, aspirin was
continued until delivery. All women were treated with prednisone at a low to moderate dose
(eg, 10 to 25 mg daily), in four cases during all the pregnancy and in two cases starting at the
third trimester. Five pregnancies (83 percent) were uneventful; HELLP syndrome developed in
the mother who was treated with aspirin until delivery. (See "HELLP syndrome (hemolysis,
elevated liver enzymes, and low platelets)".)
In another series, 21 pregnancies were evaluated in 14 women with a history of recurrent

idiopathic pericarditis (mean maternal age 31.5 years, mean gestational age 39.0 weeks)
[18]. Ten pregnancies were uneventful, three ended in spontaneous early abortion, and one
fetal death occurred at 19 weeks. Recurrences of pericarditis occurred in eight and were
treated by adding NSAIDs in two cases; in five cases the dose of corticosteroids was
increased, and in two cases aspirin was started/increased; paracetamol was always allowed.
Colchicine was used in two cases in the prospective cohort. HELLP syndrome occurred in one
patient, which resolved after delivery, and one patient experienced arterial hypertension and
elevated transaminase. All infants had a good outcome (mean birth weight 3114 g, 10
males). In the retrospective cohort, birth weight was significantly lower (2806 g versus 3320
g) when higher doses of corticosteroids (median dose respectively 10.0 mg versus 2.5 mg)
were used. Five recurrences of pericarditis occurred after delivery, easily treated with
standard therapy.
NSAID therapy — NSAIDs are not teratogenic and can be safely used during the first
trimester and the first part of the second trimester. After gestational week 20, all NSAIDs
(except aspirin at less than 100 mg/day) can cause constriction of the ductus arteriosus and
impair fetal renal function leading to oligohydramnios, and the risk seems to increase
dramatically after week 28. Thus, aspirin and other NSAIDs, excluding COX-2 inhibitors, can
be continued until the first part of the second trimester but should be withdrawn beginning
at 20 weeks of gestation [13]. Because there are insufficient safety data on selective COX-2
inhibitors, these medications should be avoided during pregnancy.
For pregnant women who are less than 20 weeks pregnant, we recommend NSAIDs rather
than glucocorticoids as the initial treatment. The 2015 European Society of Cardiology (ESC)
guidelines recommend high-dose aspirin (500 to 750 mg every eight hours) as the first
choice of therapy, although other NSAIDs are allowed [13]. There is no evidence that
ibuprofen is inferior to aspirin, and therefore it may also be used as first-line therapy. The
initial administration of an NSAID should be at a full dose (ie, "attack dose") every six to eight
hours to achieve better symptom control than with a lower dose ( table 5). The attack dose
is maintained empirically for one to two weeks or until complete symptom resolution.
Tapering should be considered following the attack dose in an attempt to reduce the
subsequent risk of recurrence. (See "Acute pericarditis: Treatment and prognosis", section on
'Nonsteroidal antiinflammatory drugs'.)
Glucocorticoid therapy — As glucocorticoids are not teratogenic (although there may

be a small increase in the risk of cleft palate when used in the first trimester), they are often
used in the setting of pericarditis during pregnancy, especially if the patient is refractory to
NSAIDs or is more than 20 weeks pregnant. In general, however, for patients who are less
than 20 weeks pregnant, aspirin or NSAIDs should be the initial treatment of choice [13]. (See
"Acute pericarditis: Treatment and prognosis", section on 'Glucocorticoids'.)
Our approach to glucocorticoid dosing has been endorsed by the 2015 ESC guidelines
favoring low to moderate doses ( table 5) [13]. In our experience, rapid tapering of
systemic glucocorticoids increases the risk of treatment failure and recurrence.
We usually begin tapering glucocorticoids at two to four weeks, after resolution of symptoms
and/or C-reactive protein normalization. Each decrement in prednisone dose should proceed
only if the patient is asymptomatic, particularly for doses lower than 25 mg/day. A proposed
tapering scheme follows:
● 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
Prednisone and prednisolone are metabolized by the placenta into inactive 11-keto forms,
and only 10 percent of the active drugs may reach the fetus [26]. Prednisone and
prednisolone appear to be reasonable therapies if used at low to medium doses (eg, 10 to 25
mg daily) and are reasonable choices when glucocorticoids are required [25]. Rarely,
maternal use of systemic glucocorticoids during first-trimester of pregnancy may lead to a
small increase in orofacial clefts, from approximately 1:1000 births in the general population
to a possible increase of three or four for every 1000 births [27]. A more extensive discussion
of the risks of glucocorticoid therapy during pregnancy is presented separately. (See "Safety
of rheumatic disease medication use during pregnancy and lactation", section on
'Glucocorticoids'.)
Colchicine — Use of colchicine during pregnancy and lactation should be discussed

with the mother if its use is important to control recurrent pericarditis or if it is indicated to
treat a specific condition (eg, familial Mediterranean fever) [19].
Breast feeding — Following delivery, breastfeeding infants may be exposed to the

medications if they are excreted into breast milk. Among the usual therapies prescribed for
acute pericarditis in pregnancy, aspirin has the greatest potential for harm in infants due to
the theoretical risk of Reye syndrome. (See "Acute toxic-metabolic encephalopathy in
children", section on 'Reye syndrome'.)
Most NSAIDs are excreted into human breast milk, although generally in very small
quantities. Several NSAIDs, including flufenamic acid, diclofenac, ibuprofen, indomethacin,
mefenamic acid, naproxen, and piroxicam are considered consistent with breastfeeding by
the American Academy of Pediatrics [28]. Aspirin (>100 mg/day) should be considered with
caution (and preferably avoided) because of potential adverse effects for the infant [13,28]. A
useful practice may be to postpone the NSAID dose until after breastfeeding in order to
reduce the infant's exposure, although the 2015 ESC guidelines state that aspirin is
"preferably avoided" during breastfeeding [13,17].
Breastfeeding is feasible during corticosteroid therapy, but should be postponed (four hours)
with doses >40 mg/day [17].
PLANNING FOR PREGNANCY
Women with recurrent pericarditis on therapy should be evaluated carefully prior to any
planned pregnancy. Pregnancy should be planned in a phase of disease quiescence. In
women with chronic recurrent pericarditis, pregnancy should be avoided during a period of
disease activity. (See "Recurrent pericarditis".)
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"
and "Society guideline links: Management of cardiovascular diseases during pregnancy".)
SUMMARY AND RECOMMENDATIONS
● Pericardial effusion has been reported in the first and second trimester in 15 to 20
percent of pregnancies and in approximately 40 percent of pregnant women during the
third trimester. In general, these effusions are asymptomatic, benign, transient, and
resolve spontaneously without therapy. In the absence of signs or symptoms of acute
pericarditis or cardiac tamponade, neither diagnostic testing (eg, follow-up
echocardiography) nor specific treatment is required. (See 'Epidemiology and clinical
features' above.)
● For pregnant women who are identified with a moderate or large pericardial effusion
that is not felt to require immediate drainage, serial follow-up testing with
echocardiography should be performed every three months until resolved. For
pregnant women with a small asymptomatic pericardial effusion, we repeat the
echocardiogram only if clinically indicated by signs or symptoms suggestive of possible
pericardial tamponade. (See 'Management and follow-up' above.)
● The diagnosis of acute pericarditis is usually suspected based on a history of

characteristic pleuritic chest pain and confirmed if a pericardial friction rub,
characteristic ECG, or pericardial effusion is present. Pericarditis should also be
suspected in a patient with persistent fever and pericardial effusion or new unexplained
cardiomegaly. The diagnosis of acute pericarditis in pregnancy is made using the same
criteria ( table 2) as in the general population. (See 'Clinical manifestations' above and
'Diagnosis' above.)
● The management of pregnant women with acute pericarditis is similar to that in the
general population ( algorithm 1), with the notable exception that the impact of all
medical therapies on the fetus must be considered. (See 'Management' above.)
• Strenuous physical activity may trigger recurrence of symptoms in patients with

acute (or recurrent) pericarditis; therefore, such activity should be avoided until
symptom resolution. (See "Acute pericarditis: Treatment and prognosis", section on
'Activity restriction'.)
• In patients with an identified cause other than viral or idiopathic disease, specific
therapy appropriate to the underlying disorder is indicated.
• For pregnant women who are less than 20 weeks pregnant, we suggest nonsteroidal
antiinflammatory drugs (NSAIDs) rather than glucocorticoids (Grade 2C). We use
aspirin (500 to 750 mg every eight hours) or ibuprofen (600 to 800 mg every eight
hours). (See 'NSAID therapy' above.)
• For pregnant women at gestational week 20 week or greater, NSAIDs are

contraindicated and should not be started (or should be withdrawn if already in use).
In this population, glucocorticoids are the preferred therapy, as their use during
pregnancy at low to moderate doses is considered reasonable. (See 'Glucocorticoid
therapy' above.)
• Use of colchicine during pregnancy and lactation should be discussed with the
mother if its use is important to control recurrent pericarditis or there is an
underlying disease to control (eg, familial Mediterranean fever). (See 'Colchicine'
above and "Management of familial Mediterranean fever", section on 'Pregnancy'.)
Use of UpToDate is subject to the Terms of Use.
REFERENCES
1. Spodick DH. Pericardial disorders during pregnancy. In: The pericardium: a comprehensi
ve textbook, Dekker, New York 1997. p.89.
2. Dizon-Townson DS, Dildy GA, Clark SL. A prospective evaluation of fetal pericardial fluid
in 506 second-trimester low-risk pregnancies. Obstet Gynecol 1997; 90:958.
3. Mohan MS, Patole SK. Isolated fetal pericardial effusion: case report and review of the
literature. Aust N Z J Obstet Gynaecol 2002; 42:216.
4. Kyeong KS, Won HS, Lee MY, et al. Clinical outcomes of prenatally diagnosed cases of
isolated and nonisolated pericardial effusion. Fetal Diagn Ther 2014; 36:320.
5. Abduljabbar HS, Marzouki KM, Zawawi TH, Khan AS. Pericardial effusion in normal
pregnant women. Acta Obstet Gynecol Scand 1991; 70:291.
6. Halphen C, Haiat R, Clément F, Michelon B. [Silent pericardial effusion in late pregnancy:

echocardiographic detection in the third trimester of pregnancy (author's transl)]. J
Gynecol Obstet Biol Reprod (Paris) 1982; 11:245.
7. Haiat R, Halphen C. Silent pericardial effusion in late pregnancy: a new entity. Cardiovasc
Intervent Radiol 1984; 7:267.
8. Enein M, Zina AA, Kassem M, el-Tabbakh G. Echocardiography of the pericardium in

pregnancy. Obstet Gynecol 1987; 69:851.
9. Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor prognosis of acute
pericarditis. Circulation 2007; 115:2739.
10. Imazio M, Trinchero R. Triage and management of acute pericarditis. Int J Cardiol 2007;
118:286.
11. Mayosi BM. Contemporary trends in the epidemiology and management of

cardiomyopathy and pericarditis in sub-Saharan Africa. Heart 2007; 93:1176.
https://www-uptodate-com.bibliotecavirtual.udla.edu.ec/contents/management-of-pericardial-effusion-and-acute-pericarditis-during-pregnancy/… 10/23
12. Troughton RW, Asher CR, Klein AL. Pericarditis. Lancet 2004; 363:717.
13. 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.
14. Tsang TS, Enriquez-Sarano M, Freeman WK, et al. Consecutive 1127 therapeutic
echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and
outcomes spanning 21 years. Mayo Clin Proc 2002; 77:429.
15. 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.
16. Imazio M, Trinchero R. Clinical management of acute pericardial disease: a review of
results and outcomes. Ital Heart J 2004; 5:803.
17. Østensen M, Khamashta M, Lockshin M, et al. Anti-inflammatory and

immunosuppressive drugs and reproduction. Arthritis Res Ther 2006; 8:209.
18. Brucato A, Pluymaekers N, Tombetti E, et al. Management of idiopathic recurrent

pericarditis during pregnancy. Int J Cardiol 2019; 282:60.
19. Serati L, Carnovale C, Maestroni S, et al. Management of acute and recurrent pericarditis
in pregnancy. Panminerva Med 2021; 63:276.
20. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of
pericardial diseases. Circulation 2010; 121:916.
21. 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.
22. 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.
23. 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.
24. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic

Review. JAMA 2015; 314:1498.
25. Brucato A, Imazio M, Curri S, et al. Medical treatment of pericarditis during pregnancy.
Int J Cardiol 2010; 144:413.
26. Beitins IZ, Bayard F, Ances IG, et al. The transplacental passage of prednisone and
prednisolone in pregnancy near term. J Pediatr 1972; 81:936.
27. Park-Wyllie L, Mazzotta P, Pastuszak A, et al. Birth defects after maternal exposure to
corticosteroids: prospective cohort study and meta-analysis of epidemiological studies.
Teratology 2000; 62:385.
28. https://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm (Accessed on July 01, 2016).

Topic 4934 Version 27.0
GRAPHICS
Acute pericarditis etiologies: Data from published clinical studies with

unselected populations
Western Europe Africa

(2007-2012) [1] (1995-2001) [2]
Idiopathic * 516 (55.3%) 32 (13.7%)
Specific etiology 417 (44.7%) 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 9.0
Diagnostic criteria for acute pericarditis and myopericarditis in the clinical

setting
Acute pericarditis (at least two criteria of four should be present)*:
1. Typical chest pain
2. Pericardial friction rub
3. Suggestive ECG changes (typically widespread ST segment elevation)
4. New or worsening pericardial effusion
Myopericarditis:
1. Definite diagnosis of acute pericarditis, PLUS
2. Suggestive symptoms (dyspnea, palpitations, or chest pain) and ECG abnormalities beyond
normal variants, not documented previously (ST/T abnormalities, supraventricular or ventricular
tachycardia or frequent ectopy, atrioventricular block), OR focal or diffuse depressed LV function of
uncertain age by an imaging study
3. Absence of evidence of any other cause
4. One of the following features: Evidence of elevated cardiac enzymes (creatine kinase-MB fraction,
or troponin I or T), OR new onset of focal or diffuse depressed LV function by an imaging study, OR
abnormal imaging consistent with myocarditis (MRI with gadolinium, gallium-67 scanning, anti-
myosin antibody scanning)
Case definitions for myopericarditis include:
Suspected myopericarditis: Criteria 1 plus 2 and 3
Probable myopericarditis: Criteria 1, 2, 3, and 4
Confirmed myopericarditis ¶ : Histopathologic evidence of myocarditis by endomyocardial biopsy o

on autopsy
ECG: electrocardiogram; LV: left ventricular; MRI: magnetic resonance imaging.
* Pericardial effusion confirms the clinical diagnosis, but its absence does not exclude it.
¶ In clinical practice, a confirmed diagnosis would require an endomyocardial biopsy that is not
warranted in self-limited cases with predominant pericarditis.
Reproduced with permission from: Imazio M, Trinchero R. Triage and management of acute pericarditis. Int J Cardiol 2006,
doi:10.1016/j.ijcard.2006.07.100. Copyright © 2006 Elsevier.
Algorithm for the initial management of acute pericarditis during pregnancy
NSAIDs: nonsteroidal anti-inflammatory drugs.
* Commonly used NSAID dosing regimens include:

Aspirin 500 to 750 mg every eight hours
Ibuprofen 600 to 800 mg every eight hours
NSAID dosing should be continued until asymptomatic, then tapered weekly.
¶ Unlike idiopathic acute pericarditis in non-pregnant patients, colchicine is not used in pregnant
patients due to unknown adverse effects and concerns about teratogenicity.
Δ Typical glucocorticoid dosing regimen is prednisone 25 mg daily until asymptomatic (usually less
than two to four weeks), then taper by 2.5 mg daily every two to four weeks.
Anti-inflammatory and immunosuppressive drugs potentially useful in the

treatment of pericardial disease
Potential
fetal- L
Pregnancy Transplacental
Drug Teratogenicity neonatal
category* passage
adverse o
effects
Aspirin (analgesic C (1st, 2nd T) Yes Yes No pattern of Un

dosed) and non- birth defects (no
D (3rd T)
selective NSAIDs established; can wit
be used safely as
during 1st and
2nd trimesters.
Use in late
pregnancy
avoided due to
concerns over
possible effects
on ductus
arteriosus and
renal function;
refer to topic
discussion. Rare
adverse reports
(eg, cardiac
defects,
gastroschisis,
low birth
weight) might
be exposure
related (all T).
Celecoxib C (1st, 2nd T) Expected Unknown Unknown. Un

(human) Interferes with
D (3rd T)
embryonic
Yes (animal)
development in
rats and rabbits.
Avoid during
pregnancy.
Short-acting D (1st T) Yes Yes May increase No

glucocorticoids risk of orofacial
C (2nd, 3rd
(prednisone, clefting (1st T)
T)
prednisolone, and restrict fetal
methylprednisolone) growth (all T).
Hypoadrenalism
may occur in
neonate. Most
data are
reassuring
when used at
low to medium
doses (ie, 10 to
20 mg orally per
day).
Colchicine C Yes No (human) Colchicine Un

should not be
Yes (animal)
used in
pregnancy
beyond
compelling
maternal
indication (ie,
FMF). It is
generally
tapered before
conception and
substituted with
aspirin and/or
low dose
prednisone.
Azathioprine D Yes No (human) Reports of Un

hematologic
Yes (animal)
abnormalities,
immune
impairment,
growth
restriction, and
prematurity
may be
exposure
related. May be
rarely used in
selected cases
in pregnancy.
Methotrexate X Yes Yes Spectrum De

defects include de
skull, facial int
feature, and im
limb anomalies rep
when exposed
during
organogenesis
(1st T). CNS
abnormalities
also reported.
Growth
retardation and
mortality may
be elevated in
2nd and 3rd T
exposure. Use
in pregnancy is
absolutely
contraindicated.
Cyclophosphamide D Yes Yes Skeletal, palate, Un

ocular, and limb
defects
associated with
exposure
during 1st T.
2nd and 3rd T
exposure
associated with
smaller risk of
malformations
but hematologic
abnormalities
and growth
restriction
reported may
be exposure
related. Use in
pregnancy is
absolutely
contraindicated.
Cyclosporine C Yes No Experience, Un

based on
limited case
reports, does
not establish an
increased risk of
birth defects.
Reports of
growth
restriction,
miscarriage,
and preterm
delivery may be
exposure
related. May be
rarely used in
selected cases
during
pregnancy.
Intravenous C Yes No Experience does Un

immunoglobulins not suggest an
(IVIG) increased risk of
congenital
anomalies or
other adverse
embryonic
effects. May be
rarely used in
selected cases
in pregnancy.
T: trimester of pregnancy; NSAID: nonsteroidal anti-inflammatory drug; FMF: familial Mediterranean

fever; CNS: central nervous system.
* Description of the US Food & Drug Administration (FDA) pregnancy risk categories is provided in a
separate table available in UpToDate. In 2015, US FDA began overseeing the phase-out of pregnancy
risk categories (A, B, C, D, and X ) from prescription drug labeling and began requiring information
from available human and animal studies of (1) known or potential maternal or fetal adverse
reactions, and (2) dose adjustments needed during pregnancy and the postpartum period. Additional
information is available at the US FDA website: Pregnancy and Lactation Labeling Final Rule.
Data from:
1. Briggs GG, Freeman RK. Drugs in pregnancy and lactation 10th ed. ©2015 Wolters Kluwer Health, Philadelphia PA.
2. United States FDA approved product information.
http://dailymed.nlm.nih.gov.bibliotecavirtual.udla.edu.ec/dailymed/index.cfm (Accessed November 25, 2014).
Food and Drug Administration pregnancy categories
Category Animal studies Human data Benefit may outweigh risk
A Negative* Studies ¶ negative Yes
B Negative Studies not done Yes
B Positive Δ Studies negative Yes
C Positive Studies not done Yes
C Not done Studies not done Yes
D Positive or negative Studies or reports positive Yes
X◊ Positive Studies or reports positive No
In 2015, the US Food & Drug Administration (FDA) began overseeing the phase-out of pregnancy risk
categories (A, B, C, D, and X) from prescription drug labeling and began requiring information from
available human and animal studies of (1) known or potential maternal or fetal adverse reactions, and
(2) dose adjustments needed during pregnancy and the postpartum period. Additional information is
available at the FDA website: Pregnancy and Lactation Labeling Final Rule.
* No teratogenicity demonstrated
¶ Adequate and well-controlled studies in pregnant women (Fed Reg 1979; 44:37461)
Δ Teratogenicity demonstrated
◊ Drug is contraindicated in pregnancy
Reproduced with permission from: Schatz M, Hoffman CP, Zeiger RS, et al. The course and management of asthma and
allergic diseases during pregnancy. In: Allergy: Principles and Practice, Middleton E, Reed CE, Ellis EF, et al (Eds), St. Louis,
Mosby, 1998. Copyright © 1998 Mosby.
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 2
recurrent † ) 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 NSAID 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 (includes ibuprofen, indomethacin, and aspirin); 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.

Management of Pericardial Effusion and Acute Pericarditis During Pregnancy - UpToDate

Uploaded by

Document Information

Original Title

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

Management of Pericardial Effusion and Acute Pericarditis During Pregnancy - UpToDate

Uploaded by

Copyright:

Available Formats

23/2/24, 14:11 Management of pericardial effusion and acute pericarditis during pregnancy - UpToDate

Official reprint from UpToDate®

Management of pericardial effusion and acute

Literature review current through: Jan 2024.

Although diseases of the pericardium occur sporadically during pregnancy, there is no

Maternal pericardial effusion

● The clinical examination and electrocardiogram (ECG) are generally normal.

● In the absence of signs or symptoms of acute pericarditis or cardiac tamponade,

impact of pericardial effusion. In general, if the patient remains asymptomatic and

Clinical manifestations — Acute pericarditis can present in a variety of ways, depending on

The major clinical manifestations of acute pericarditis include [12]:

● ECG changes – New widespread ST elevation and/or PR depression.

Diagnosis — The diagnosis of acute pericarditis is usually suspected based on a history of

Management — The management of pregnant women with acute pericarditis is similar to

In addition to activity restriction, the therapy of acute pericarditis should be targeted as

Activity restriction — Strenuous physical activity may trigger a recurrence of symptoms in

• For pregnant women at gestational week 20 week or greater, NSAIDs are

In another series, 21 pregnancies were evaluated in 14 women with a history of recurrent

Glucocorticoid therapy — As glucocorticoids are not teratogenic (although there may

● Daily dose 15 to 25 mg – Taper 2.5 mg/day every two to four weeks

Colchicine — Use of colchicine during pregnancy and lactation should be discussed

Breast feeding — Following delivery, breastfeeding infants may be exposed to the

PLANNING FOR PREGNANCY

SOCIETY GUIDELINE LINKS

SUMMARY AND RECOMMENDATIONS

● The diagnosis of acute pericarditis is usually suspected based on a history of

• Strenuous physical activity may trigger recurrence of symptoms in patients with

• For pregnant women at gestational week 20 week or greater, NSAIDs are

Use of UpToDate is subject to the Terms of Use.

6. Halphen C, Haiat R, Clément F, Michelon B. [Silent pericardial effusion in late pregnancy:

8. Enein M, Zina AA, Kassem M, el-Tabbakh G. Echocardiography of the pericardium in

11. Mayosi BM. Contemporary trends in the epidemiology and management of

17. Østensen M, Khamashta M, Lockshin M, et al. Anti-inflammatory and

18. Brucato A, Pluymaekers N, Tombetti E, et al. Management of idiopathic recurrent

24. Imazio M, Gaita F, LeWinter M. Evaluation and Treatment of Pericarditis: A Systematic

28. https://toxnet.nlm.nih.gov/newtoxnet/lactmed.htm (Accessed on July 01, 2016).

Acute pericarditis etiologies: Data from published clinical studies with

Western Europe Africa

Idiopathic * 516 (55.3%) 32 (13.7%)

Specific etiology 417 (44.7%) 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

Graphic 60949 Version 9.0

Diagnostic criteria for acute pericarditis and myopericarditis in the clinical

Acute pericarditis (at least two criteria of four should be present)*:

1. Typical chest pain

2. Pericardial friction rub

3. Suggestive ECG changes (typically widespread ST segment elevation)

4. New or worsening pericardial effusion

3. Absence of evidence of any other cause

Case definitions for myopericarditis include:

Suspected myopericarditis: Criteria 1 plus 2 and 3

Probable myopericarditis: Criteria 1, 2, 3, and 4

Confirmed myopericarditis ¶ : Histopathologic evidence of myocarditis by endomyocardial biopsy o

ECG: electrocardiogram; LV: left ventricular; MRI: magnetic resonance imaging.

Graphic 74376 Version 7.0

Algorithm for the initial management of acute pericarditis during pregnancy

NSAIDs: nonsteroidal anti-inflammatory drugs.