Post-Cardiac Injury Syndromes

Official reprint from UpToDate
www.uptodate.com 2016 UpToDate
Post-cardiac injury syndromes

Author: Brian D Hoit, MD
Section Editor: Martin M LeWinter, MD
Deputy Editor: Brian C Downey, MD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2016. | This topic last updated: Dec 10, 2015.
INTRODUCTION Pericarditis with or without a pericardial effusion resulting from injury of the
pericardium constitutes the post-cardiac injury syndrome. Postcardiac injury syndrome was first described
after myocardial infarction by Dressler in 1956 [1]. The principal conditions considered under this rubric
are:
Postmyocardial infarction syndrome
Postpericardiotomy syndrome
Posttraumatic pericarditis
The term "postpericardiotomy syndrome" was substituted for the previous "postcardiotomy syndrome"
after it was discovered that the syndrome can occur after the pericardium is opened even if no other
cardiac structures are involved (eg, after surgery for bronchogenic lung carcinoma). Furthermore, the
provoking cardiac injury may be surprisingly minor (eg, percutaneous coronary intervention, insertion of a
pacing lead, radiofrequency ablation) [2].
The clinical presentation, diagnostic evaluation, and treatment of post-cardiac injury syndromes will be
reviewed here. The clinical presentation, evaluation, and treatment of acute pericarditis, pericardial
effusion, cardiac tamponade, and constrictive pericarditis are discussed separately. (See "Etiology of
pericardial disease" and "Clinical presentation and diagnostic evaluation of acute pericarditis" and
"Treatment of acute pericarditis" and "Diagnosis and treatment of pericardial effusion" and "Cardiac
tamponade" and "Constrictive pericarditis".)
INCIDENCE While generally considered to occur infrequently, the incidence of post-cardiac injury
syndromes is not entirely clear. Studies performed in post-myocardial infarction (MI) patients in the era
prior to reperfusion reported different rates of post-cardiac injury syndrome, with one study estimating the
incidence at 3 percent of patients post-MI, while another report from the same era found almost no cases
[3,4]. Subsequently, the post-cardiac injury syndrome following MI appears to have largely disappeared in
the reperfusion era, perhaps due to a decrease in size of most MIs. In one cohort of 201 consecutive
patients with acute MI treated with fibrinolysis, only one patient developed post-cardiac injury syndrome,
and this patient had no evidence of reperfusion [5].
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The risk factors may be different for early (within seven days) versus late effusions and suspected postcardiac injury syndrome. This was illustrated in a registry of patients with significant pericardial effusions
after cardiothoracic surgery who underwent pericardiocentesis guided by echocardiography [6].
Anticoagulant therapy was a considered to be a contributing factor in the majority of early effusions (<7
days), while postpericardiotomy syndrome was an important contributing factor in approximately one-third
of effusions occurring after seven days.
ETIOLOGY 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.
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.
The post-cardiac injury syndrome, including posttraumatic pericarditis, appears to be initiated by the
combination of damage to mesothelial pericardial cells and blood in the pericardial space [7,8]. The initial
injury is thought to release cardiac antigens and stimulate an immune response. The immune complexes
that are generated are then deposited in the pericardium, pleura, and lungs, eliciting an inflammatory
response [8]. The following observations are compatible with this hypothesis:
The discrete latent period from cardiac injury to the clinical onset of post-cardiac injury syndrome.
Coexistent pleural effusion and/or pulmonary infiltrates in some cases.
Studies in patients undergoing cardiac surgery have found a statistically significant correlation
between the postoperative to preoperative ratios of antiactin and antimyosin antibodies and the
clinical occurrence of post-cardiac injury syndrome [9,10].
The generally excellent response to anti-inflammatory therapy, and occasional relapses after steroid
withdrawal [8].
The initial prospective study that identified immune complexes in the post-cardiac injury syndrome
compared children who did and did not develop a postpericardiotomy syndrome after cardiac surgery [11].
Those who developed postpericardiotomy syndrome had increased antimyocardial antibodies resulting
from myocardial injury. Several subsequent studies have demonstrated the presence of antimyocardial
antibodies in patients who develop the postpericardiotomy syndrome [9,10,12,13]. Antimyocardial
antibodies have also been discovered in the pleural fluid of one such patient [14]. However, the
significance of these antibodies and their relation to the severity of myocardial injury is unclear [12].
Support for antiheart antibodies being an epiphenomenon comes from a prospective study of 20 surgical
patients in whom serum was sampled for antiheart antibodies before and periodically after elective
coronary artery bypass surgery [13]. Antiheart antibodies were absent in all patients on the day before
surgery. Three patients developed postpericardiotomy syndrome. All were seronegative at the time of
diagnosis, but they became seropositive within the ensuing 14 days.
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The post-cardiac injury syndrome has also been described in children following orthotopic cardiac
transplant [15]. Because these children are immunosuppressed, it has been suggested this syndrome is
not always an autoimmune process.
CLINICAL FEATURES Patients who develop post-cardiac injury syndrome present with signs and
symptoms similar to those seen in patients with acute pericarditis and/or pericardial effusion in other
clinical settings. (See "Clinical presentation and diagnostic evaluation of acute pericarditis" and
"Diagnosis and treatment of pericardial effusion".)
In brief, the features of the post-cardiac injury syndrome include [7]:
Predisposition and latency
Prior injury to, or invasion of, the pericardium, myocardium, or both.
Latent period, typically weeks to months, between the injury and the development of pericarditis
or pericardial effusion. The latent period can be highly variable from patient to patient.
Signs, symptoms, and findings
Pleuritic chest pain and fever.
Leukocytosis and other markers of inflammation (eg, elevated erythrocyte sedimentation rate,
elevated C-reactive protein). (See 'Evaluation' below.)
Electrocardiographic changes (classically diffuse ST-segment elevation in association with PR
depression, although often absent or masked by other electrocardiogram [ECG] findings).
Pericardial and sometimes pleural effusion, with or without a pulmonary infiltrate. (See
'Evaluation' below.)
Treatment response
Responsiveness to nonsteroidal anti-inflammatory drugs, colchicine, and glucocorticoids. (See
'Treatment' below.)
Tendency for recurrence. (See 'Prognosis and follow-up' below.)
The presentation and clinical course of the postpericardiotomy syndrome is comparable to that of acute
pericarditis. In a cohort of 360 consecutive patients undergoing cardiac surgery, 54 patients (15 percent)
developed post-cardiac injury syndrome [16]. The most frequent signs and symptoms in patients who
developed post-cardiac injury syndrome in this cohort were pleuritic chest pain (56 percent) and fever (54
percent) [16]. Common findings on physical examination and diagnostic testing included [16]:
Pericardial effusion (89 percent), although cardiac tamponade was rare (2 percent)
Elevated C-reactive protein or erythrocyte sedimentation rate (74 percent)
Pericardial rub (32 percent)
Electrocardiographic changes (24 percent)
Physical examination may sometimes disclose a pericardial friction rub (movie 1). A mediastinal friction
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rub or "crunch" (a substernal, crunching, rasping sound that is synchronous with the heartbeat and
usually associated with palpable chest wall surgical emphysema) is frequently appreciated in the first few
days after cardiac surgery and is caused by surgical emphysema; it should be distinguished from a true
pericardial friction rub. (See "Auscultation of heart sounds", section on 'Pericardial friction rub and other
adventitious sounds'.)
Chylopericardium is a rare manifestation of post-cardiac injury syndrome. It tends to occur in children who
have had extensive surgical treatment for complex congenital malformations. However, any operation
involving dissection of the ascending aorta and the main pulmonary artery risks injury to the right efferent
lymphatic trunk and subsequent chylopericardium [17]. (See "Chylopericardium and cholesterol
pericarditis".)
EVALUATION The diagnostic evaluation of all patients with suspected post-cardiac injury syndrome
includes laboratory testing, a 12-lead electrocardiogram (ECG), a chest radiograph, and an
echocardiogram.
Laboratory testing Patients with suspected post-cardiac injury syndrome should have laboratory
testing including complete blood count (CBC), C-reactive protein (CRP), erythrocyte sedimentation rate
(ESR), and troponin. Most but not all patients will have an elevated white blood cell count and
inflammatory markers (CRP and ESR). There is little consensus on the need for serial or follow-up
studies, but most experts recheck inflammatory markers (CRP and ESR) following the resolution of
symptoms (typically within one to two weeks) to ensure that the inflammation is resolving prior to tapering
or discontinuing therapy. (See 'Prevention and treatment' below.)
Electrocardiogram A 12-lead ECG should be performed in all patients with suspected post-cardiac
injury syndrome, although it is difficult to make the diagnosis based on ECG findings alone. The ECG is
most often abnormal following a myocardial infarction or other forms of cardiac surgery, for a variety of
reasons (eg, ischemic ST segment or T wave changes, developing Q waves, post-operative epicardial
pacing, etc). However, when ECG changes suggestive of pericarditis are present (ie, diffuse ST-segment
elevation in association with PR depression) and represent a change from the patient's baseline ECG,
this is highly suggestive of post-cardiac injury syndrome. (See "Clinical presentation and diagnostic
evaluation of acute pericarditis", section on 'Electrocardiogram'.)
Chest radiograph Similar to the ECG, a chest radiograph should be performed in all patients with
suspected post-cardiac injury syndrome, although it is not possible to definitively make the diagnosis
based on radiographic findings alone. The chest radiograph in a patient who has developed a
postoperative pericardial effusion often reveals an increase in heart size (particularly when compared to a
baseline radiograph). When this is seen, the presence of an effusion should be promptly confirmed or
excluded by echocardiography. In a significant minority of patients, the chest radiograph also reveals a
pleural effusion, usually unilateral, although this may become apparent only on a subsequent film.
Pulmonary infiltrates are occasionally seen. (See "Pleural effusions following cardiac surgery".)
Echocardiogram All patients with suspected post-cardiac injury syndrome should be evaluated with
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echocardiography. In most instances, transthoracic echocardiography is satisfactory, but transesophageal

echocardiography may be required in patients with difficult or limited imaging windows (as can frequently
occur postoperatively) in whom the transthoracic study is non-diagnostic. The echocardiogram should
assess for the presence or absence of pericardial effusion, document the size of the effusion, and provide
echocardiographically-derived hemodynamic data, which may support or refute the presence of cardiac
tamponade. (See "Cardiac tamponade", section on 'Echocardiography'.)
Serial echocardiographic studies have shown that postoperative pericardial effusion following cardiac
surgery is considerably more common than is clinically obvious, occurring in as many as 85 percent of
patients [18]. The effusion is usually present by the second postoperative day but may not occur until day
10. In most cases, the effusion reaches its maximal size by about the tenth postoperative day followed by
gradual resolution. Because postoperative pericardial effusions are so common and most are benign,
there is no rationale for routine postoperative echocardiography in the absence of other clinical features
that suggest pericardial disease.
DIAGNOSIS The diagnosis of post-cardiac injury syndrome is typically suspected based upon the
characteristic clinical picture of pleuritic chest pain and fever in a patient with a myocardial infarction or
pericardial injury/invasion within the appropriate time frame (as early as one week to as late as three
months prior to symptoms). Abnormalities seen on laboratory testing (leukocytosis, elevated erythrocyte
sedimentation rate, elevated CRP), electrocardiogram (diffuse ST-segment elevation in association with
PR depression, although often absent and masked by other ECG findings), chest radiograph (increased
heart size, pleural effusion), and echocardiogram (pericardial effusion) are supportive, but none is specific
enough to definitively make the diagnosis. The combination of a pericardial friction rub and ECG findings
typical of pericarditis strongly supports the diagnosis, and the diagnosis is also strongly supported if an
echocardiogram reveals a pericardial effusion at a time when effusions are no longer routine.
DIFFERENTIAL DIAGNOSIS Post-cardiac injury syndrome should be distinguished from other clinical
conditions that result in fever and pleuritic chest pain. In most instances, post-cardiac injury syndrome
can be distinguished from other entities by the clinical scenario; however, in some instances, post-cardiac
injury syndrome can coexist with other pathology (eg, rib fractures or pneumothorax following chest
trauma, etc).
Pleuritis or pleuropericarditis (including infectious and noninfectious causes such as pneumonia and
malignancy) Infectious causes are typically associated with sputum production, while noninfectious
causes such as malignancy have other associated systemic symptoms (eg, weight loss, night
sweats, signs of the primary malignancy, etc). (See "Outpatient evaluation of the adult with chest
pain" and "Pneumococcal pneumonia in adults".)
Pulmonary embolism Patients will often have an associated risk for thromboembolism (eg, surgery,
immobility, malignancy) and are typically hypoxic. Pulmonary embolism is typically diagnosed when
filling defects are seen on computed tomography pulmonary angiography. The considerable overlap
in clinical presentation between post-cardiac injury syndrome and pulmonary embolism with
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associated pulmonary infarction often requires computed tomography (CT) angiography to

distinguish between the two entities. (See "Clinical presentation, evaluation, and diagnosis of the
adult with suspected acute pulmonary embolism".)
Blunt chest wall trauma Typically following an automobile accident, a fall from a significant height,
or other major trauma, this is often associated with hemothorax, pneumothorax, pulmonary
contusion, or fractures that can be identified on chest radiograph. (See "Initial evaluation and
management of blunt thoracic trauma in adults".)
Esophageal rupture (Boerhaave syndrome) Typically this occurs following vomiting, prolonged
coughing, childbirth, or weightlifting with straining. Free air within the mediastinum or peritoneum on
a chest radiograph is suggestive of esophageal rupture. (See "Boerhaave syndrome: Effort rupture of
the esophagus".)
Pneumothorax Primary pneumothorax typically occurs in younger patients (less than 40 years of
age), while secondary pneumothorax is typically iatrogenic (eg, following central venous catheter
placement or bronchoscopy) or traumatic (eg, rib fractures). In most instances this should be visible
on the chest radiograph. (See "Imaging of pneumothorax".)
Connective tissue disorders (eg, systemic lupus erythematosus) Typically patients have other signs
of systemic involvement by the connective tissue disorder (eg, musculoskeletal symptoms, rash,
kidney disease, etc). Laboratory testing for connective tissue disorders may be required to
differentiate this from other causes of pleuritis or pleuropericarditis. (See "Pericardial involvement in
systemic autoimmune diseases" and "Pulmonary manifestations of systemic lupus erythematosus in
adults".)
When the post-cardiac injury syndrome occurs after an acute myocardial infarction (MI), it is also known
as Dressler's syndrome [19]. This disorder must be distinguished from the pericarditis and/or effusion
which may occur early after a transmural MI as a result of involvement of the epicardial surface or rupture
of the free wall of the left ventricle [20]. The former is almost always benign, while the latter usually results
in rapid and severe hemodynamic compromise. Early pericardial complications typically occur two to four
days after MI, while post-MI cardiac injury syndrome occurs one week to as long as two to three months
after MI. (See "Pericardial complications of myocardial infarction", section on 'Peri-infarction pericarditis'.)
PREVENTION AND TREATMENT Colchicine has been demonstrated to significantly reduce the
incidence of post-cardiac injury syndrome following cardiac surgery [21,22]. We suggest the
administration of colchicine prophylactically following cardiac surgery in an effort to prevent the
development of postpericardiotomy syndrome. For patients who develop postpericardiotomy syndrome
following surgery, or for those who develop post-cardiac injury syndrome following a myocardial infarction
or trauma, anti-inflammatory agents are the treatment of choice. (See "Treatment of acute pericarditis".)
Prevention When administered prophylactically pre- or post-cardiac surgery, colchicine appears to
reduce the incidence of postpericardiotomy syndrome, whereas dexamethasone appears to have no
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protective effect [21-26].

Colchicine For most patients undergoing cardiac surgery, we suggest a 30-day course of
colchicine beginning one to three days following surgery (0.5 or 0.6 mg twice daily for patients 70 kg, 0.5
or 0.6 mg daily for those <70 kg) to reduce the risk of developing post-cardiac injury syndrome. Two
randomized, double-blind trials have evaluated colchicine for this patient population:
In the Colchicine for the Prevention of Post-pericardiotomy Syndrome (COPPS) study, 360 cardiac
surgery patients were randomly assigned on postoperative day three to colchicine (1 mg twice daily
on day 1, then 0.5 mg twice daily) or placebo administered for 30 days [21]. Colchicine significantly
reduced the occurrence of the primary endpoint of postpericardiotomy syndrome at 12 months (9
versus 21 percent with placebo, relative risk 0.42, 95% CI 0.24-0.73). The rate of side effects,
primarily related to gastrointestinal intolerance, was similar in the colchicine and placebo groups.
In the COPPS-2 trial, 360 cardiac surgery patients were randomly assigned to receive colchicine (0.5
mg twice daily for patients 70 kg, 0.5 mg daily for those <70 kg) or placebo beginning 48 to 72
hours prior to surgery and continued for one month postoperatively [25]. Colchicine significantly
reduced the occurrence of the primary endpoint-postpericardiotomy syndrome at three months (19
versus 29 percent with placebo; 10 percent absolute risk reduction, 95% CI 1.1-18.7; number needed
to treat [NNT] = 10 to prevent one case of postpericardiotomy syndrome). However, unlike in the
original COPPS trial, treatment with colchicine was associated with significantly more adverse
effects, primarily gastrointestinal (20 versus 12 percent with placebo; absolute difference 8 percent,
95% CI 0.76-15.9; number needed to harm = 12 to cause one additional adverse effect).
While colchicine has been shown in multiple studies to significantly reduce the incidence of post-cardiac
injury syndrome, the increase in adverse effects seen in the COPPS-2 trial is somewhat concerning. Our
suggested approach to prophylactic colchicine use in this population places a higher value on the
reduction in post-cardiac injury syndrome and its potential complications rather than the risk of
medication-related side effects. Patients who place a higher value on the avoidance of additional
medications and potential colchicine-related side effects may reasonably opt not to take colchicine, in
which case the treating clinician should emphasize with the patient the importance of early recognition of
potential symptoms and treatment should symptoms arise.
Glucocorticoids In contrast to colchicine, prophylactic glucocorticoid therapy in patients
undergoing cardiac surgery appears to have no beneficial effect on post-cardiac injury syndrome. In a
single-center post-hoc analysis of 822 patients from the DECS trial who underwent valvular surgery and
received a one-time intraoperative dose of 1 mg/kg of dexamethasone (421 patients) or placebo (401
patients), there was no significant difference in the development of postpericardiotomy syndrome (13.5
versus 15.5 percent with placebo; RR 0.88; 95% CI 0.63-1.22); moreover, the incidence of a complicated
postpericardiotomy syndrome (defined as the need to drain a pericardial or pleural effusion, or
rehospitalization for a recurrence) was similar (3.8 versus 3.2 percent, respectively; RR 1.17; 95% CI
0.57-2.41) [24].
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Treatment For patients who develop post-cardiac injury syndrome, first-line treatment consists of
nonsteroidal anti-inflammatory drugs (NSAIDs), usually in combination with colchicine, though there are
no randomized controlled trials of different dosing regimens. Either aspirin or a different NSAID (eg,
ibuprofen, naproxen, etc) may be tried as initial therapy if there are no contraindications. Colchicine may
also be effective in the treatment of post-cardiac injury syndrome, although there are limited data in this
setting.
NSAIDs As with acute pericarditis, NSAIDs are the primary treatment for all patients with postcardiac injury syndrome, with the duration of treatment and tapering of medication based upon the
persistence of symptoms. The 2015 European Society of Cardiology guidelines do not distinguish
between aspirin or other NSAIDs (usually ibuprofen) with respect to efficacy and suggest that drug
selection should be based on criteria other than efficacy (eg, likelihood of side effects, other aspirin
indications) [26]. Two commonly used regimens are [27]:
Aspirin The dose of aspirin should be 750 to 1000 mg every six to eight hours, with gradual
tapering of the total daily dose by 650 to 800 mg every week for a treatment period of three to four
weeks.
Ibuprofen The dose of ibuprofen should be 600 to 800 mg every six to eight hours, with gradual
tapering of the total daily dose by 400 to 800 mg every week for a treatment period of three to four
weeks.
In pericarditis associated with an acute myocardial infarction (MI), aspirin is preferred as nearly all
patients post-MI will require aspirin for secondary prevention purposes. Aspirin may also be the first
choice in patients who require concomitant antiplatelet therapy for any reason. (See "Pericardial
complications of myocardial infarction".)
With any aspirin or NSAID regimen, gastrointestinal protection should be provided. (See "NSAIDs
(including aspirin): Primary prevention of gastroduodenal toxicity".)
Colchicine Given its effectiveness in the treatment of other inflammatory pericardial disease states
(ie, acute pericarditis, recurrent pericarditis), colchicine may also be effective in the treatment of postcardiac injury syndrome, although there are limited data in this setting. In one single-center, retrospective
study of 239 patients with post-cardiac injury syndrome following cardiac surgery in which 51 patients (21
percent) received colchicine as part of their treatment, patients treated with the combination of colchicine
and an anti-inflammatory drug were less likely to require intervention (ie, pericardiocentesis, pericardial
window, pericardiectomy) for complications of post-cardiac injury syndrome (adjusted OR 0.43; 95% CI
0.20-0.90) [28]. The 2015 European Society of Cardiology guidelines support the routine use of colchicine
for the treatment of post-cardiac injury syndrome [26].
The routine use of colchicine does not appear useful in the treatment of asymptomatic postoperative
pericardial effusions [29]. In a double-blind randomized trial of 197 patients with asymptomatic moderate
to large-sized pericardial effusions at 7 to 30 days after surgery, both colchicine and placebo had similar
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effects on the effusion volume and the likelihood of late cardiac tamponade [30]. Similar findings were
reported in a randomized trial in 149 patients with asymptomatic pericardial effusions (mild to moderate in
size) identified by echocardiography three weeks after surgery, in which patients randomized to colchicine
had similar outcomes to patients who received placebo [29]. Based on these findings we do not use
colchicine in the treatment of asymptomatic postoperative pericardial effusions.
Treatment for refractory cases While NSAIDs and colchicine are the preferred treatment options
for post-cardiac injury syndrome, a minority of patients will have refractory symptoms requiring treatment
with systemic glucocorticoid therapy (usually in combination with colchicine). Once a specific cause of
pericarditis has been excluded, a course of glucocorticoids is generally effective. For patients who require
glucocorticoid therapy for refractory post-cardiac injury syndrome, we have a similar approach as used for
patients with recurrent acute pericarditis, with moderate initial doses of glucocorticoid (eg, 0.25 to 0.50
mg/kg/day of prednisone) followed by a slow taper rather than high doses with a rapid taper (table 1).
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 therapy in
patients with pericarditis is discussed separately. (See "Treatment of acute pericarditis", section on
'Approaches to glucocorticoid use' and "Recurrent pericarditis", section on 'Glucocorticoids'.)
Among patients with recurrent or persistent autoreactive pericarditis with effusion (not limited to postcardiac injury syndrome), pericardiocentesis with intrapericardial instillation of triamcinolone (300 mg/m2)
has been proposed as an alternative to systemic therapy to avoid systemic side effects [31]. As these
data are limited, this approach requires further investigation prior to widespread use. (See "Recurrent
pericarditis", section on 'Intrapericardial steroids'.)
PROGNOSIS AND FOLLOW-UP Although the prognosis of the post-cardiac injury syndrome is
relatively good for most patients, a recurrence rate of between 10 and 15 percent has been reported [7].
In addition, because of a small but distinct risk of developing constrictive pericarditis, longer-term followup for several years appears to be warranted [7]. The variable presentation and course of post-cardiac
injury syndrome requires significant individualization of the approach to follow-up. Our experts suggest
the following approach for a typical patient with post-cardiac injury syndrome:
Office follow-up with laboratory testing for inflammatory markers (C-reactive protein [CRP],
erythrocyte sedimentation rate [ESR]) at four weeks post-diagnosis.
If symptoms persist or inflammatory markers remain elevated at four weeks, close office-based
follow-up with repeat laboratory testing for inflammatory markers (CRP and ESR) every two to four
weeks until asymptomatic with improving markers of inflammation.
If symptoms resolved and inflammatory markers normalized (or trending toward normal), office
follow-up with laboratory testing for inflammatory markers (CRP and ESR) and echocardiography at
three months post-diagnosis.
Annual office follow-up for several years, with repeat echocardiography if any signs or symptoms or
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constrictive pericarditis. (See "Constrictive pericarditis".)

PERICARDIAL TRAUMA In addition to the post-cardiac syndrome that can arise following a
myocardial infarction or invasion of the pericardium during surgery, the pericardium is vulnerable to
traumatic injury. Pericardial injury may result from blunt trauma, as with steering wheel contact in an
automobile accident, or sharp trauma, such as that inflicted by a knife or bullet, and can result in one of
the following complications:
Acute tamponade due to cardiac trauma (pericardial injury syndrome, which is not immunemediated) (see "Cardiac tamponade")
Delayed tamponade, which may develop either slowly or rapidly after the passage of considerable
time (post-cardiac injury syndrome)
Constrictive pericarditis months or years later (see "Constrictive pericarditis")
Patients with acute injury may present either with shock due to acute blood loss or due to cardiac
tamponade [32]. The volume of blood responsible for tamponade in this setting is much smaller than that
of most pericardial effusions that develop more slowly, in which the pericardium can gradually expand and
more easily accommodate the increased volume (figure 1). Blood in the pericardial cavity may be
defibrinated by the lytic activity normally present in the pericardium, form a hematoma that may create
local cardiac compression, simulate a tumor, or cause the late development of constrictive pericarditis.
Patients with penetrating chest wounds may also develop delayed pericardial effusions and tamponade
[33]. (See "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial evaluation
and management of penetrating thoracic trauma in adults".)
Blunt trauma Blunt chest trauma is most commonly the result of an automobile accident but may also
occur due to falls, explosions, and crush injuries. (See "Initial evaluation and management of blunt
thoracic trauma in adults".)
In one study of 59 patients with blunt chest trauma requiring emergency surgical treatment, the cause
was an automobile or motorcycle accident in 85 percent [34]. An isolated pericardial rupture was present
in 29 percent, while 63 percent had rupture of one or more cardiac chambers. The diagnosis was made
by thoracotomy in all of the patients who arrived in cardiac arrest, while in those with vital signs present
on admission, the diagnosis was made by urgent thoracotomy, pericardial window, or during laparotomy.
The mortality rate was 76 percent overall and 52 percent in the group who arrived at the trauma center
with vital signs present.
Other traumatic lesions can mimic these findings. These include myocardial contusion of the right
ventricle, which results in hemodynamic abnormalities that develop over a few days, injury to a coronary
vessel, ventricular septal defect, pseudoaneurysm, and mitral valve injury [35,36]. Traumatic valve injury
associated with pericardial effusion after blunt injury in less critically ill patients can be identified by
echocardiography as well as hemodynamic evaluation at the time of pericardiocentesis [37]. (See "Acute
aortic regurgitation in adults" and "Acute mitral regurgitation in adults".)
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Severe blunt trauma, as with a fall from a considerable height, automobile accident, or other significant
injury, can rupture the pericardium, resulting in the potentially fatal complication of herniation of the heart.
This event should be suspected if the chest radiograph shows pneumothorax or air in the mediastinum
distributed between the heart and diaphragm [38].
Iatrogenic trauma All invasive cardiac procedures and therapies have the potential to cause trauma
to the pericardium, although some, such as transseptal catheterization of the left heart, pose a higher risk.
Examples of procedures associated with iatrogenic pericardial trauma include [39]:
Right heart and pulmonary artery catheterization
Central venous access of a hemodialysis catheter or parenteral feeding tube via the jugular or
subclavian vein
Penetration of the heart, a great vein, or the coronary sinus by pacemaker electrode leads or during
electrophysiology studies, endomyocardial biopsy, or valvuloplasty
Perforation of a coronary artery by catheters or guidewires placed during coronary interventions
Cardiac tamponade must be considered when, in one of the above settings, a patient develops
hypotension, particularly when associated with tachycardia, or in extreme cases with profound
bradycardia. If the patient is still in the invasive cardiac laboratory, pulsus paradoxus and disappearance
of cardiac pulsations by fluoroscopy can help to establish or exclude tamponade. When doubt remains,
echocardiography should be performed, a procedure that is also helpful in monitoring the results of
pericardiocentesis. (See "Cardiac tamponade" and "Pulsus paradoxus in pericardial disease" and
"Diagnosis and treatment of pericardial effusion", section on 'Echocardiography'.)
Echocardiographically-guided rescue pericardiocentesis may be the procedure of choice in patients with
acute tamponade resulting from a diagnostic or interventional catheter-based procedure. In a report of 88
such patients, this approach was the definitive therapy in 82 percent and was successful in 99 percent
[39]. There was a low rate of major complications (3 percent) or minor complications (2 percent), and no
deaths. Continued bleeding into the pericardial space requires blood transfusion and prompt surgical
closure of the bleeding site.
When shock occurs after an interventional procedure involving the coronary arteries, the problem is more
difficult and the operator must establish the cause quickly (eg, acute vessel closure or acute stent
thrombosis versus perforation of a coronary artery). The coronary angiograms obtained during the
therapeutic procedure should be reviewed since they may reveal contrast flowing from a coronary artery
into the pericardial cavity. This abnormality may not have been initially recognized when the operator's
attention was focused on the lesion being treated rather than distally where the wire can perforate a
vessel. Suspicion of perforation of a coronary artery calls for reinjection of the coronary artery if review of
the original arteriogram fails to show contrast medium outside the artery. (See "Clinical manifestations
and diagnosis of cardiogenic shock in acute myocardial infarction" and "Periprocedural complications of
percutaneous coronary intervention".)
INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The
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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 information: Pericarditis in adults (The Basics)")
Beyond the Basics topic (see "Patient information: Pericarditis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
Pericarditis with or without a pericardial effusion resulting from injury to the pericardium constitutes
the post-cardiac injury syndrome. The clinical conditions considered under these terms include
postmyocardial infarction syndrome, postpericardiotomy syndrome, and posttraumatic pericarditis.
The incidence of post-cardiac injury syndromes is not entirely clear, but it is relatively infrequent.
(See 'Introduction' above and 'Incidence' above.)
The post-cardiac injury syndrome appears to be initiated by the combination of damage to
mesothelial pericardial cells and blood in the pericardial space. The initial injury is thought to release
cardiac antigens and stimulate an immune response. The immune complexes that are generated
then deposit onto the pericardium, pleura, and lungs, eliciting an inflammatory response. (See
'Etiology' above.)
Patients who develop post-cardiac injury syndrome present with signs and symptoms similar to those
seen in patients with acute pericarditis and/or pericardial effusion in other clinical settings, such as
pleuritic chest pain, pericardial friction rub, fever, and leukocytosis. (See 'Clinical features' above.)
The diagnostic evaluation of all patients with suspected post-cardiac injury syndrome includes
laboratory testing, a 12-lead electrocardiogram (ECG), a chest radiograph, and an echocardiogram.
(See 'Evaluation' above.)
The diagnosis of post-cardiac injury syndrome is typically suspected based upon the characteristic
clinical picture of pleuritic chest pain and fever, pericardial friction rub, and typical ECG changes in a
patient with a myocardial infarction or pericardial injury/invasion within the appropriate time frame.
The presence of a pericardial effusion is confirmatory, but effusions are not always present. (See
'Diagnosis' above.)
Colchicine is the only therapy that has been demonstrated to significantly reduce the incidence of
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post-cardiac injury syndrome following cardiac surgery, but there are conflicting data suggesting that
colchicine use postoperatively may be associated with an increased number of adverse medicationrelated side effects. (See 'Prevention and treatment' above.)
For most patients undergoing cardiac surgery, we suggest a 30-day course of colchicine beginning
one to three days following surgery (0.5 mg twice daily for patients 70 kg, 0.5 mg daily for those <70
kg) (Grade 2B). Our approach places a higher value on the reduction in post-cardiac injury
syndrome and its potential complications than the risk of medication-related side effects. Patients
who place a higher value on the avoidance of additional medications and potential colchicine-related
side effects may reasonably opt not to take colchicine, in which case the treating clinician should
educate the patient regarding the potential symptoms of post-cardiac injury syndrome to promote
early recognition and treatment. (See 'Colchicine' above.)
Treatment of the post-cardiac injury syndrome is similar to other types of acute pericarditis. First-line
treatment consists of the combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and
colchicine, though there are no randomized controlled trials of different dosing regimens. Either
aspirin or a different NSAID (eg, ibuprofen, naproxen, etc) may be tried as initial therapy if there are
no contraindications. (See 'Treatment' above and "Treatment of acute pericarditis".)
The prognosis of the post-cardiac injury syndrome is relatively good for most patients, although 10 to
15 percent of patients will experience a recurrence. Patients require close office-based follow-up until
they are asymptomatic with normalized inflammatory markers. (See 'Prognosis and follow-up'
above.)
Pericardial trauma can result in acute cardiac tamponade, post-cardiac injury syndrome, and/or
constrictive pericarditis. Common causes of pericardial trauma include blunt trauma (eg, automobile
accidents), penetrating trauma (eg, stabbing or bullet wound), and iatrogenic trauma. (See
'Pericardial trauma' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. DRESSLER W. A post-myocardial infarction syndrome; preliminary report of a complication
resembling idiopathic, recurrent, benign pericarditis. J Am Med Assoc 1956; 160:1379.
2. Wessman DE, Stafford CM. The postcardiac injury syndrome: case report and review of the
literature. South Med J 2006; 99:309.
3. Welin L, Vedin A, Wilhelmsson C. Characteristics, prevalence, and prognosis of postmyocardial
infarction syndrome. Br Heart J 1983; 50:140.
4. Lichstein E, Arsura E, Hollander G, et al. Current incidence of postmyocardial infarction (Dressler's)
syndrome. Am J Cardiol 1982; 50:1269.
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5. Shahar A, Hod H, Barabash GM, et al. Disappearance of a syndrome: Dressler's syndrome in the
era of thrombolysis. Cardiology 1994; 85:255.
6. Tsang TS, Barnes ME, Hayes SN, et al. Clinical and echocardiographic characteristics of significant
pericardial effusions following cardiothoracic surgery and outcomes of echo-guided
pericardiocentesis for management: Mayo Clinic experience, 1979-1998. Chest 1999; 116:322.
7. Imazio M, Hoit BD. Post-cardiac injury syndromes. An emerging cause of pericardial diseases. Int J
Cardiol 2013; 168:648.
8. Khan AH. The postcardiac injury syndromes. Clin Cardiol 1992; 15:67.
9. De Scheerder I, De Buyzere M, Robbrecht J, et al. Postoperative immunological response against
contractile proteins after coronary bypass surgery. Br Heart J 1986; 56:440.
10. Nomura Y, Yoshinaga M, Haraguchi T, et al. Relationship between the degree of injury at operation
and the change in antimyosin antibody titer in the postpericardiotomy syndrome. Pediatr Cardiol
1994; 15:116.
11. Engle MA, Zabriskie JB, Senterfit LB, et al. Viral illness and the postpericardiotomy syndrome. A
prospective study in children. Circulation 1980; 62:1151.
12. Bartels C, Hnig R, Burger G, et al. The significance of anticardiolipin antibodies and anti-heart
muscle antibodies for the diagnosis of postpericardiotomy syndrome. Eur Heart J 1994; 15:1494.
13. Hoffman M, Fried M, Jabareen F, et al. Anti-heart antibodies in postpericardiotomy syndrome: cause
or epiphenomenon? A prospective, longitudinal pilot study. Autoimmunity 2002; 35:241.
14. Kim S, Sahn SA. Postcardiac injury syndrome. An immunologic pleural fluid analysis. Chest 1996;
109:570.
15. Cabalka AK, Rosenblatt HM, Towbin JA, et al. Postpericardiotomy syndrome in pediatric heart
transplant recipients. Immunologic characteristics. Tex Heart Inst J 1995; 22:170.
16. Imazio M, Brucato A, Rovere ME, et al. Contemporary features, risk factors, and prognosis of the
post-pericardiotomy syndrome. Am J Cardiol 2011; 108:1183.
17. Kan CD, Wang JN, Wu JM, Yang YJ. Isolated chylopericardium after intrapericardial procedures:
possible role of inadvertent right efferent lymphatic trunk injury. Tex Heart Inst J 2007; 34:82.
18. Weitzman LB, Tinker WP, Kronzon I, et al. The incidence and natural history of pericardial effusion
after cardiac surgery--an echocardiographic study. Circulation 1984; 69:506.
19. DRESSLER W. The post-myocardial-infarction syndrome: a report on forty-four cases. AMA Arch
Intern Med 1959; 103:28.
20. Khan AH. Pericarditis of myocardial infarction: review of the literature with case presentation. Am
Heart J 1975; 90:788.
21. Imazio M, Trinchero R, Brucato A, et al. COlchicine for the Prevention of the Post-pericardiotomy
Syndrome (COPPS): a multicentre, randomized, double-blind, placebo-controlled trial. Eur Heart J
2010; 31:2749.
22. Imazio M, Brucato A, Markel G, et al. Meta-analysis of randomized trials focusing on prevention of
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the postpericardiotomy syndrome. Am J Cardiol 2011; 108:575.

23. Finkelstein Y, Shemesh J, Mahlab K, et al. Colchicine for the prevention of postpericardiotomy
syndrome. Herz 2002; 27:791.
24. Bunge JJ, van Osch D, Dieleman JM, et al. Dexamethasone for the prevention of
postpericardiotomy syndrome: A DExamethasone for Cardiac Surgery substudy. Am Heart J 2014;
168:126.
25. Imazio M, Brucato A, Ferrazzi P, et al. Colchicine for prevention of postpericardiotomy syndrome
and postoperative atrial fibrillation: the COPPS-2 randomized clinical trial. JAMA 2014; 312:1016.
26. 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 CardioThoracic Surgery (EACTS). Eur Heart J 2015; 36:2921.
27. Imazio M, Spodick DH, Brucato A, et al. Controversial issues in the management of pericardial
diseases. Circulation 2010; 121:916.
28. Alraies MC, Al Jaroudi W, Shabrang C, et al. Clinical features associated with adverse events in
patients with post-pericardiotomy syndrome following cardiac surgery. Am J Cardiol 2014; 114:1426.
29. Izadi Amoli A, Bozorgi A, HajHossein Talasaz A, et al. Efficacy of colchicine versus placebo for the
treatment of pericardial effusion after open-heart surgery: A randomized, placebo-controlled trial.
Am Heart J 2015; 170:1195.
30. Meurin P, Lelay-Kubas S, Pierre B, et al. Colchicine for postoperative pericardial effusion: a
multicentre, double-blind, randomised controlled trial. Heart 2015; 101:1711.
31. Maisch B, Risti AD, Pankuweit S. Intrapericardial treatment of autoreactive pericardial effusion with
triamcinolone; the way to avoid side effects of systemic corticosteroid therapy. Eur Heart J 2002;
23:1503.
32. Trinkle JK, Toon RS, Franz JL, et al. Affairs of the wounded heart: penetrating cardiac wounds. J
Trauma 1979; 19:467.
33. Harris DG, Janson JT, Van Wyk J, et al. Delayed pericardial effusion following stab wounds to the
chest. Eur J Cardiothorac Surg 2003; 23:473.
34. Fulda G, Brathwaite CE, Rodriguez A, et al. Blunt traumatic rupture of the heart and pericardium: a
ten-year experience (1979-1989). J Trauma 1991; 31:167.
35. Ruder MA, Flaker GC, Alpert MA, Selmon MR. Right ventricular myocardial contusion simulating
constrictive pericardial disease. Am Heart J 1984; 108:1353.
36. Fallahnejad M, Kutty AC, Wallace HW. Secondary lesions of penetrating cardiac injuries: a frequent
complication. Ann Surg 1980; 191:228.
37. Shabetai R, Aravindakshan V, Danielson G, Bryant L. Traumatic hemopericardium with tricuspid
incompetence. J Thorac Cardiovasc Surg 1969; 57:294.
38. Roebuck EJ, Minford J. Traumatic rupture of the pericardium with herniation of the heart. Br J Radiol
1983; 56:585.
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39. Tsang TS, Freeman WK, Barnes ME, et al. Rescue echocardiographically guided pericardiocentesis
for cardiac perforation complicating catheter-based procedures. The Mayo Clinic experience. J Am
Coll Cardiol 1998; 32:1345.
Topic 4915 Version 17.0
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GRAPHICS
Drug therapy in acute and recurrent pericarditis for adult patients
Drug
Duration of
therapy*
(antiinflammatory
dose)
Anti-inflammatory
dose
Tapering*
For initial combination treatment of most patients:

Aspirin
650 to 1000 mg orally

three times daily
One to two weeks
Weekly decrease once

patient is symptom-free
and CRP has normalized

three times daily
One to two weeks

25 to 50 mg orally three
times daily
One to two weeks

0.5 to 0.6 mg orally two

times daily
Three months (acute)
Usually not tapered
OR
Ibuprofen
OR
Indomethacin
PLUS
Colchicine
Six months or longer

(recurrent)
For initial combination therapy of patients following myocardial infarction:

Aspirin

three times daily
One to two weeks


times daily
Three months (acute)
Usually not tapered
PLUS
Colchicine
Six months or longer

(recurrent)
For refractory cases or patients with a contraindication to NSAID therapy:

Prednisone
0.25 to 0.5 mg/kg/day
Two weeks (acute)

Two to four weeks
(recurrent)
Gradual tapering over

three months; refer to
UpToDate topic review
of treatment of acute
pericarditis, section on
glucocorticoids
PLUS
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Colchicine

times daily
Three months
Usually not tapered
CRP: C-reactive protein.

* Duration and tapering of therapy (except colchicine) should be tailored according to resolution of symptoms
and normalization of markers of inflammation; refer to topic reviews for approach.
Proton pump inhibitor (eg, omeprazole) gastrointestinal protection may be indicated.
Some patients may require ibuprofen every six hours (four times daily), in which case the dose should not
exceed 600 mg every six hours.
0.5 mg colchicine is not available in US. It is widely available elsewhere.
Colchicine dose should be reduced to 0.5 to 0.6 mg once daily in patients <70 kg.
The duration of colchicine therapy for recurrent or refractory pericarditis is at least six months.
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.
Graphic 56484 Version 12.0
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Pericardial pressure in acute and chronic tamponade
Volume curves recorded from data acquired during pericardiocentesis. Curve A (in
red) plots data from a patient with hyperacute tamponade that followed laceration
of a coronary artery during an angioplasty-stenting procedure. Note the extreme
elevation of pericardial pressure and that withdrawal of only 100 mL, half the
volume we could aspirate, lowered the pressure to 10 mmHg. Curve B (in blue)
plots data from a patient who had a history of prior pericarditis, assumed to be of
viral etiology. Subsequently he developed a chronic pericardial effusion that
reached at least 1500 mL in volume. At the time of presentation to our service,
the jugular venous pressure was 22 mmHg. Aspiration of 300 mL of pericardial
fluid reduced the pericardial pressure to 10 mmHg, and removing another 600 mL
achieved a nearly normal pericardial pressure. Aspiration of the remaining large
effusion did not affect pericardial pressure. The curves of cases of intermediate
acuity or chronicity would fall between these two extremes.
Courtesy of Ralph Shabetai, MD.
Graphic 75068 Version 2.0
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Contributor Disclosures
Brian D Hoit, MD Speaker's Bureau: Philips Medical [Heart valve disease (3D Transesophageal
echo)]. Martin M LeWinter, MD Nothing to disclose Brian C Downey, MD, FACC Nothing 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
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echocardiography. In most instances, transthoracic echocardiography is satisfactory, but transesophageal

associated pulmonary infarction often requires computed tomography (CT) angiography to

protective effect [21-26].

constrictive pericarditis. (See "Constrictive pericarditis".)

the postpericardiotomy syndrome. Am J Cardiol 2011; 108:575.

For initial combination treatment of most patients:

650 to 1000 mg orally

One to two weeks

Weekly decrease once

600 to 800 mg orally

One to two weeks

Weekly decrease once

One to two weeks

Weekly decrease once

0.5 to 0.6 mg orally two

Three months (acute)

Usually not tapered

Six months or longer

For initial combination therapy of patients following myocardial infarction:

650 to 1000 mg orally

One to two weeks

Weekly decrease once

0.5 to 0.6 mg orally two

Three months (acute)

Usually not tapered

Six months or longer

For refractory cases or patients with a contraindication to NSAID therapy:

0.25 to 0.5 mg/kg/day

Two weeks (acute)

Gradual tapering over

0.5 to 0.6 mg orally two

Usually not tapered

CRP: C-reactive protein.

Pericardial pressure in acute and chronic tamponade

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