INTRODUCTION — Pericarditis with or without a pericardial effusion resulting from injury of the pericardium constitutes the post-cardiac injury syndrome. The principal conditions considered under this rubric are:
●Post-myocardial infarction (MI) 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).
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 "Acute pericarditis: Clinical presentation and diagnosis" and "Acute pericarditis: Treatment and prognosis" and "Diagnosis and treatment of pericardial effusion" and "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic evaluation and management".)
INCIDENCE — Post-cardiac injury syndrome was first described after MI by Dressler in 1956 [1]. While generally considered to occur infrequently, the actual incidence of post-cardiac injury syndromes is uncertain.
●Studies performed in post-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 [2,3]. 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 [4].
●Among a cohort of 28,761 patients in Finland who underwent cardiothoracic surgery between 2005 and 2014, 493 patients (1.7 percent) developed post-cardiac injury syndrome requiring hospital admission or contributing to mortality [5]. The risk appeared higher in patients undergoing valvular or aortic surgery, compared with patients undergoing only coronary artery bypass grafting. However, in a much smaller cohort of 360 consecutive patients undergoing cardiac surgery, 54 patients (15 percent) developed post-cardiac injury syndrome [6].
ETIOLOGY AND PATHOPHYSIOLOGY — 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 antiinflammatory 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.
The risk factors may be different for early (within seven days) versus late effusions and suspected post-cardiac injury syndrome. This was illustrated in a registry of patients with significant pericardial effusions after cardiothoracic surgery who underwent pericardiocentesis guided by echocardiography [15]. Anticoagulant therapy was 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.
The post-cardiac injury syndrome has also been described in children following orthotopic cardiac transplant [16]. 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 "Acute pericarditis: Clinical presentation and diagnosis" 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 [ESR], elevated C-reactive protein). (See 'Evaluation' below.)
•Electrocardiographic (ECG) changes (classically diffuse ST-segment elevation in association with PR depression, although often absent or masked by other ECG findings) (waveform 1).
•Pericardial and sometimes pleural effusion, with or without a pulmonary infiltrate. (See 'Evaluation' below.)
●Treatment response
•Responsiveness to nonsteroidal antiinflammatory drugs (NSAIDs), 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. 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) [6]. Common findings on physical examination and diagnostic testing included [6]:
●Pericardial effusion (89 percent), although cardiac tamponade was rare (2 percent)
●Elevated C-reactive protein or ESR (74 percent)
●Pericardial rub (32 percent)
●ECG changes (24 percent)
Physical examination may sometimes disclose a pericardial friction rub (movie 1). A mediastinal friction 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 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 I or T. 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 usually abnormal following an MI and after various types of cardiac surgery for a variety of reasons (eg, ischemic ST segment or T wave changes, developing Q waves, various nonspecific ST-T abnormalities, postoperative 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 "Acute pericarditis: Clinical presentation and diagnosis", 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 is helpful in excluding other pathology (eg, pneumonia, pneumothorax, etc).
The chest radiograph in a patient who has developed a postoperative pericardial effusion often reveals an increase in heart size (particularly when compared with 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 "Evaluation and management of pleural effusions following cardiac surgery".)
Echocardiogram — All patients with suspected post-cardiac injury syndrome should be evaluated with 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 is used to determine the presence or absence of pericardial effusion, to quantify the size of an effusion, and to detect the various echocardiographic signs that are used to support or refute the presence of cardiac tamponade. (See "Cardiac tamponade", section on 'Echocardiography'.)
Multimodality imaging — Cardiac computed tomography (CCT) and cardiovascular magnetic resonance (CMR) imaging have important functions when echocardiographic imaging is suboptimal and in difficult cases by virtue of their ability to detect pericardial thickening, calcification, and effusions (CCT), and inflammation, edema, and characteristic hemodynamics (CMR) [18].
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 [19]. 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 approximately the 10th postoperative day and is 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 an MI 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 C-reactive protein), ECG (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 (non-trivial effusions are uncommon after 7 to 10 days postinjury).
DIFFERENTIAL DIAGNOSIS — Post-cardiac injury syndrome should be distinguished from other clinical conditions that result in fever and/or pleuritic chest pain. In most instances, post-cardiac injury syndrome can be distinguished from these 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 patients requiring hospitalization".)
●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 CT pulmonary angiography. The considerable overlap in clinical presentation between post-cardiac injury syndrome and pulmonary embolism with associated pulmonary infarction usually requires CT angiography to distinguish between the two entities. (See "Clinical presentation, evaluation, and diagnosis of the nonpregnant 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.
●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 MI, it is also known as Dressler's syndrome [20]. 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 [21]. 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 [22,23]. We suggest a 30-day course of colchicine prophylactically following cardiac surgery in an effort to prevent the development of postpericardiotomy syndrome. Colchicine should be started one and three days postsurgery, rather than preoperatively. For patients who develop postpericardiotomy syndrome following surgery, or for those who develop post-cardiac injury syndrome following an MI or trauma, antiinflammatory agents are the treatment of choice. (See "Acute pericarditis: Treatment and prognosis".)
Prevention — When administered prophylactically pre- or post-cardiac surgery, colchicine appears to reduce the incidence of postpericardiotomy syndrome, whereas dexamethasone appears to have no protective effect [22-27].
Colchicine — For most patients undergoing cardiac surgery, we suggest postoperative prophylactic treatment with colchicine rather than expectant management. We treat with 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). Our 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 opt to not use 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.
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 [22]. 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 [26]. 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. In particular, diarrhea, the main gastrointestinal side effect of colchicine, is very problematic in patients early after cardiac surgery; for this as well as other reasons, routine use of prophylactic colchicine does not appear to have been widely adopted.
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) [25].
Treatment — For patients who develop post-cardiac injury syndrome, first-line treatment consists of 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 (table 1), NSAIDs are the primary treatment for all patients with post-cardiac 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) [27]. Two commonly used regimens are [28]:
●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 750 to 1000 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 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 post-cardiac 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 antiinflammatory 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) [29]. The 2015 European Society of Cardiology guidelines support the routine use of colchicine for the treatment of post-cardiac injury syndrome [27].
The routine use of colchicine does not appear useful in the treatment of asymptomatic postoperative pericardial effusions [30]. 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 effects on the effusion volume and the likelihood of late cardiac tamponade [31]. 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 [30]. 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 other specific causes of pericarditis have been excluded (eg, infectious causes, etc), 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 optimal dosing and tapering of steroid therapy when used to treat pericarditis. Our approach to glucocorticoid therapy in patients with pericarditis is discussed in more detail separately. (See "Acute pericarditis: Treatment and prognosis", section on 'Glucocorticoid dosing' and "Recurrent pericarditis", section on 'Glucocorticoids'.)
Among patients with recurrent or persistent autoreactive pericarditis with effusion (not limited to post-cardiac 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 [32]. As these data are limited, this approach requires further investigation prior to widespread use. (See "Recurrent pericarditis", section on 'Intrapericardial steroids'.)
The role of interleukin 1 inhibitor (rilonacept or anakinra) for patients with recurrent pericarditis and an inflammatory phenotype is discussed separately. (See "Recurrent pericarditis", section on 'Our approach' and "Recurrent pericarditis", section on 'Interleukin 1 inhibitors'.)
Treatment options for recurrent pericarditis with a noninflammatory phenotype are discussed separately. (See "Recurrent pericarditis", section on 'Our approach' and "Recurrent pericarditis", section on 'Other immune therapy'.)
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 follow-up 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 postdiagnosis. Markers of inflammation that were elevated at the time of diagnosis should be trending toward more normal values following four weeks of therapy.
●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 are resolved and inflammatory markers have normalized (or trend toward normal), office follow-up with laboratory testing for inflammatory markers (CRP and ESR) and echocardiography at three months postdiagnosis.
●Annual office follow-up for several years, with repeat echocardiography if any signs or symptoms or constrictive pericarditis. (See "Constrictive pericarditis: Diagnostic evaluation and management".)
PERICARDIAL TRAUMA — In addition to the post-cardiac injury syndrome that can arise following an MI or invasion of the pericardium during surgery, the pericardium is vulnerable to traumatic injury, and patients may develop the post-cardiac injury syndrome following trauma. 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. In addition, late complications of trauma can complicate the clinical presentation. These include:
●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: Diagnostic evaluation and management".)
A post-cardiac injury syndrome may also occur after iatrogenic pericardial trauma (eg, associated with a percutaneous cardiac procedure such as percutaneous coronary intervention, insertion of a pacing or defibrillator lead, radiofrequency or cryoablation ablation, or percutaneous valvular procedures). In these instances, the provoking cardiac injury may be surprisingly minor.
The acute management of patients with traumatic chest injuries is discussed in detail elsewhere. (See "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial evaluation and management of penetrating thoracic trauma in adults" and "Initial evaluation and management of blunt cardiac injury".)
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: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)" and "Society guideline links: Pericardial disease".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topics (see "Patient education: Pericarditis in adults (The Basics)")
●Beyond the Basics topic (see "Patient education: Pericarditis (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition and incidence – 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 post-myocardial infarction (MI) 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.)
●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, such as pleuritic chest pain, pericardial friction rub (movie 1), fever, and leukocytosis. (See 'Clinical features' above.)
●Evaluation – The diagnostic evaluation of all patients with suspected post-cardiac injury syndrome includes laboratory testing, a 12-lead ECG, a chest radiograph, and an echocardiogram. (See 'Evaluation' above.)
●Diagnosis – 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 an MI 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.)
●Prevention – For most patients undergoing cardiac surgery, we suggest postoperative prophylactic treatment with colchicine rather than expectant management (Grade 2B). Colchicine is the only therapy that has been demonstrated to reduce post-cardiac injury syndrome following cardiac surgery. However, there are concerns about adverse effects, mainly diarrhea and other gastrointestinal complaints, that have limited adoption of colchicine in this setting. Side effects appear to be lower when colchicine is started postoperatively rather than preoperatively. We begin colchicine one to three days following surgery (0.5 mg twice daily for patients ≥70 kg, 0.5 mg daily for those <70 kg) and continue therapy for a 30-day course. (See 'Colchicine' above.)
●Treatment – Treatment of the post-cardiac injury syndrome is similar to other types of acute pericarditis (table 1). First-line treatment consists of the combination of nonsteroidal antiinflammatory 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 "Acute pericarditis: Treatment and prognosis".)
●Prognosis – 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.)
