Chest pain of acute onset carries a wide differential diagnosis, including several potentially life threatening causes. In this patient, the potential diagnoses include cardiac causes such as an acute coronary syndrome (ACS), aortic dissection and acute pericarditis, as well as non cardiac causes such as acute pulmonary embolism or pneumothorax. Points in favor of an ACS include the presence of diabetes and hypertension, which are risk factors for ischemic heart disease. However, the lack of a history of angina is against this diagnosis, as is the pleuritic nature of the chest pain. Aortic dissection is unlikely, as the pain is typically catastrophic in onset. In addition, many patients describe the pain as 'tearing' in nature, while there often are associated symptoms secondary to involvement of other organs (such as the nervous system). The pain of acute pericarditis is characteristically postural (as lying down causes the heart to rest upon the posterior pericardium, while bending forward relieves this), as in this patient. In addition, the presence of a pericardial friction rub is further supportive of this diagnosis. Acute pulmonary embolism has a wide clinical spectrum of presentation and cannot be definitively diagnosed or excluded clinically. However, the absence of risk factors such as immobilization, recent surgery or previous episodes of venous thrombosis is against this diagnosis. Pneumothorax is unlikely, as most patients manifest some degree of dyspnea, while the chest pain is typically sudden in onset. Thus, acute pericarditis is the probable clinical diagnosis. As this may be a manifestation of an underlying systemic disease, further clinical assessment in this regard is mandatory. Causes of acute pericarditis include viral and bacterial infections (e.g. tuberculosis), systemic autoimmune disease, malignancies and uremia. It is also important to keep in mind that acute pericarditis may occur secondary to an ACS or aortic dissection. Note that no etiological cause can be found in the majority of patients with acute pericarditis. Such cases are termed "idiopathic" acute pericarditis. The history of this patient is not suggestive of a recent infection, while no features suggestive of autoimmune disease are present. In addition, her normal renal functions exclude uremia. Thus, as no obvious etiology can be found, idiopathic acute pericarditis is the likely diagnosis. Further evaluation via a 12-lead ECG shows diffuse PR segment depressions and upwardly concave ST segment elevations, both of which are suggestive of acute pericarditis. Note that PR segment depression is almost pathognomonic of acute pericarditis as the only other cause is atrial ischemia, which is very rare. Her echocardiogram shows a mild pericardial effusion, which may be secondary to the pericarditis. In addition, the absence of wall motion abnormalities makes an ACS unlikely, while the normal appearing aorta makes a dissection unlikely (note however, that visualization of the whole thoracic aorta requires a trans-esophageal echocardiogram). The normal d-dimer assay excludes pulmonary embolism. Note that a troponin-T assay is of limited diagnostic value as a positive result may be caused by any one of acute pericarditis, ACS or pulmonary embolism, while a negative result does not rule out any of these diagnoses. Thus the final diagnosis is idiopathic acute pericarditis. Treatment with an NSAID will both relive pain and reduce inflammation. Thrombolysis and anticoagulation would be indicated in an ACS or pulmonary embolism. The small pericardial effusion does not require aspiration.
Acute pericarditis is a common disorder caused by inflammation of the pericardium and may occur in isolation, or as a manifestation of underlying systemic disease. While almost 90% of cases are idiopathic, the remainder are caused by a remarkably broad range of diseases. These include viral infections, bacterial infections such as tuberculosis, autoimmune disease, malignancies and uremia. In addition, acute pericarditis may occur following myocardial infarction or cardiac surgery. Note that two forms of pericarditis may be encountered following myocardial infarction. Pericarditis within the first 1 to 3 days after transmural infarction is believed to occur due to the interaction of the necrotic myocardium with the overlying pericardium. Pericarditis several weeks or months after infarction (also known as Dressler's syndrome) is believed to be due to an autoimmune reaction. Pericarditis which occurs following cardiac surgery is termed the 'post cardiomyotomy syndrome', and is believed to be similar in nature to Dressler's syndrome. The chest pain of acute pericarditis is typically sharp, retrosternal, worse with inspiration and upon lying supine, and relieved when sitting forward. Pain referred to the scapular ridge is highly suggestive of pericarditis, and possibly arises from irritation of the phrenic nerves. There may also be systemic signs such as a mild fever - although a high fever is unusual and suggests purulent bacterial pericarditis. Note however, that acute pericarditis may be clinically silent in certain patients. Examination may show a pericardial friction rub, which is a high-pitched, scratchy sound that can have between 1 to 3 components. While it is often assumed that the pericardial friction rub occurs from the inflamed parietal and visceral pericardial surfaces rubbing against each other, this finding may be also found in some patients with a pericardial effusion (which should keep the surfaces separate and also act as a lubricant). The ECG in acute pericarditis shows sequential changes. Initially, the typical findings are diffuse ST elevations in association with PR depressions (except in lead AvR, where ST depressions and PR elevations are expected). These subsequently normalize, following which widespread T-inversions develop, which themselves normalize later on. Note that the pericarditis following an acute myocardial infarction may be localized, with ST segment changes only evident in the affected leads. In addition, uremic pericarditis may show few or no ECG changes. Echocardiography usually demonstrates a pericardial effusion, while minimal elevation of troponins is common, possibly due to involvement of the adjacent myocardium by the inflammatory process. Laboratory investigations may show features of systemic inflammation, such as a neutrophil leukocytosis and elevated ESR and CRP. The principles of management are treatment of the pericardial inflammation, and treatment of the underlying cause, if present. NSAIDs are first line drugs, with treatment both alleviating pain and reducing inflammation. Note that NSAIDs other than Aspirin should be avoided in pericarditis following a myocardial infarction. Colchicine may be used as an adjunct to NSAID therapy. While systemic corticosteroids are highly effective in the treatment of acute pericarditis, cessation of treatment is associated with an increased incidence of relapse. Thus steroids should probably be considered only when treatment with NSAIDS and colchicine has failed. If cardiac tamponade occurs, or if purulent or malignant pericarditis is suspected pericardiocentesis (with or without pericardial biopsy) should be performed. In most patients, acute pericarditis is a mild and self-limiting disease, especially if idiopathic or due to viral causes. Predictors of a poor outcome include fever > 38 C, traumatic pericarditis, presence of a large pericardial effusion, symptoms developing over several weeks in association with immunosuppressed state, pericarditis in a patient receiving oral anticoagulants, and failure to respond to NSAIDs.