An apparently “isolated” pericardial effusion without pericarditis is another common pericardial syndrome that can be encountered in clinical practice. In physiologic condition, the pericardial space contains 10–50 mL of plasma ultrafiltrate (pericardial fluid) that lubricates the pericardial layers allowing cardiac chamber movements without attrition with the surrounding mediastinal structures [1].

An increased production, usually stimulated by an inflammatory process, or a reduced absorption (e.g. lymphatic obstruction by metastatic spread by lung cancer or pulmonary hypertension or increased filling pressure in heart failure), may be responsible for an increase of the amount of pericardial effusion that starts accumulating posteriorly and inferiorly according to gravity forces (thus a mild effusion is located in inferolateral position and close to the right atrium in four chamber view in transthoracic echocardiography with the patient supine on his/her left side), then as circumferential (moderate to large pericardial effusions) (Fig. 13.1). Thus a pericardial effusion can be defined as an abnormal accumulation of pericardial fluid that can be visualized by echocardiography (the first echocardiographic sign of very mild effusion is systo-diastolic separation on M-mode recordings, while a simple systolic separation may be considered physiologic) (Fig. 13.2) [1, 2].

A common semiquantitative assessment is performed measuring the largest telediastolic echo-free space in different echocardiographic views, including standard and off-axis views. If the size of the effusion is <10 mm, the pericardial effusion is mild; if between 10 and 20 mm, it is moderate; and if >20 mm, the effusion is large (Fig. 13.3) [1–4].

Pericardial effusions can be classified according to the onset (acute, subacute, chronic), the size (usually according to semiquantitative assessment), distribution (loculated and circumferential) and its composition (transudate, exudates, blood, air, etc.).

A practical classification of pericardial effusions is reported in Table 13.1.

An isolated pericardial effusion may be asymptomatic or has symptoms related to the underlying disease or related to the effusion itself, if moderate to large. Moreover, a pericardial effusion may be an isolated process, but often (50–60 % of cases), it is associated and related to a systemic or underlying disease [5, 6].

The speed of its accumulation is critical for the time course of symptoms. Since the pericardium is rather inelastic (as witnessed by a steep relationship between pressure and volume), a rapid accumulating pericardial effusion reaches the limit of pericardial starch very soon with low volumes, while a slowly accumulating fluid reaches the limit of pericardial stretch only for huge volumes as big as 1–2 L without the development of cardiac tamponade [1].

Classical reported symptoms include dyspnoea on exertion progressing to orthopnoea and/or fullness. Additional symptoms may be related to the compressive effect of pericardial effusions on surrounding structures and include nausea (diaphragm), dysphagia (oesophagus), hoarseness (recurrent laryngeal nerve), hiccups (phrenic nerve), cough, weakness, fatigue, anorexia and palpitations (related to the compressive effect of the pericardial fluid or reduced blood pressure) and sinus tachycardia. Additional features (e.g. fever) may be related to the underlying disease (e.g. infectious or systemic inflammatory diseases) more than the pericardial effusion itself [1, 5].

The aetiology of pericardial effusion is varied and reflects the potential complexity of the full aetiological spectrum of pericardial diseases including infectious and non-infectious causes.

The most common reported causes include infections (viral, especially tuberculosis that is the most common cause all over the world) [7, 8], cancer (especially lung and breast cancer, lymphomas and leukemias), systemic inflammatory diseases, post-cardiac injury syndromes (emerging cause in developing countries and related to the increased use of invasive cardiovascular interventions and ageing of the population), heart failure, pulmonary hypertension, hypothyroidism and renal failure (Table 13.2) [6, 9–12].