**2.1 Etiology**

Among the elderly, the spectrum of etiologies for pericardial effusion does not differ significantly from the rest of the population. The underlying cause of effusion can usually be inferred from the clinical picture. One study in 322 patients


**13**

**2.3 Diagnostics**

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

**2.2 Clinical presentation**

has reported around 60% of cases had a known cause of pericardial effusion [5]. A varying amount of effusion can be seen in other conditions such as malignancy (with or without direct pericardial involvement), renal failure, pregnancy, aortic or cardiac wall rupture, trauma, heart failure, cirrhosis of the liver, nephrotic syndrome, autoimmune diseases, radiation, etc. One study incorporated demographics in their review of pericarditis etiology by comparing a younger patient population (age 15–65, *n* = 221) to a geriatric population (age 66–88, *n* = 101) and found no statistically significant differences in the incidence of idiopathic (33 vs. 38%) versus neoplastic (14.4 vs. 10.8%) pericarditis or the incidence of tamponade (36 vs. 38.6%) [6]. The cause of effusion may also vary by geographical area and clinical setting. For example, effusions related to viral pericarditis or idiopathic pericarditis are more common in outpatient populations of the western world, whereas bacterial and tuberculous inflammation and effusion are more common in sub-Saharan Africa and the developing world. Effusions associated with uremic pericarditis or

According to one study with a mean participant age of 56, when determining the cause of moderate to severe pleural effusions, it is important to consider three major factors: (1) size of effusion; (2) presence of tamponade; and (3) inflammatory signs (defined as two or more from: fever >37°C, pericardial friction rub, characteristic chest pain, and diffuse ST-segment elevation). The presence of inflammatory signs was associated with acute idiopathic pericarditis (likelihood ratio = 5.4, P < 0.001), a large effusion without any inflammatory signs or tamponade was found to be associated with chronic idiopathic pericardial effusion (likelihood ratio = 20, P < 0.001), and the features of tamponade without inflammatory signs were associ-

The presentation of pericardial effusion varies according to the speed of accumulation, size of effusion, and etiology. The rate of fluid collection plays a critical role in clinical presentation as rapidly accumulating pericardial effusion causes a quick rise in intrapericardial pressure, which results in cardiac tamponade, while slowly accumulating fluid accommodates comparatively larger volume before signs of tamponade [2, 3]. The cases of isolated pericardial effusion can be asymptomatic or can have symptoms related to the underlying etiology or to the effusion itself. The classically reported symptom is dyspnea on exertion; however, the wide spectrum of symptoms related to compressive effect includes cough, weakness, fatigue, palpitations (from compressive effect of the pericardial fluid or reduced blood pressure), nausea (diaphragm), dysphagia (esophagus), hoarseness of voice (recurrent laryngeal nerve), etc. Patients may present with fever from underlying disease (infectious or systemic inflammatory disease), pleural effusion, ascites, or

malignancies are frequently found in hospital settings [3, 7].

ated with malignant effusions (likelihood ratio = 2.9, P < 0.01) [5].

hepatic dysfunction from long standing pericardial constriction [2, 8].

Physical examination may remain normal without any significant findings in patients with no hemodynamic compromise. Pulsus paradoxus is an inspiratory drop in systolic BP >10 mmHg due to the augmentation of right ventricular preload causing impaired left ventricular filling resulting in abnormal decrease in stroke volume [9] and is a phenomenon commonly seen with large pericardial effusion or cardiac tamponade. Pericardial friction rub is rarely heard but is a usual finding of pericarditis.

Upon clinical suspicion of pericardial effusion, the diagnostic approach should consider three major steps: (1) confirm the presence of effusion; (2)

#### **Table 1.** *Classification of pericardial effusion.*

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

*Inflammatory Heart Diseases*

effusion.

**2.1 Etiology**

production (i.e., any inflammatory condition) or from reduced fluid reabsorption (i.e., heart failure, pulmonary hypertension, and pericardial lymphatic obstruction). The fluid starts accumulating according to gravitational forces, initially in the posterior-inferior site then circumferentially resulting in moderate to large

Pericardial effusion can be classified based on various characteristics such as size (mild, moderate, and large), onset (acute, subacute, and chronic), distribution (localized or circumferential), composition (transudate, exudate, blood, or rarely gas from bacterial infections), and hemodynamic effects (without tamponade, with

The normal pericardium is made up of a high content of collagen fibers, which creates a relatively inelastic sac that contains the heart. The pressure-volume curve of the normal pericardium is a J-shaped curve, which allows a limited stretch of the pericardium in response to physiological events such as posture or volume status without significant change in the intrapericardial pressure; however, after reaching a certain intrapericardial volume, the intrapericardial pressure rises suddenly and can cause sudden systemic hemodynamic derangements. The rapid rate of the fluid collection also plays a role in the pressure-volume curve; a sudden rise in intrapericardial volume (such as with aortic dissection or trauma with hemopericardium) of 100–200 mL significantly raises the intrapericardial pressure, whereas the slow collection of fluid may allow the development of a large pericardial effusion (1–2 L)

Among the elderly, the spectrum of etiologies for pericardial effusion does not differ significantly from the rest of the population. The underlying cause of effusion can usually be inferred from the clinical picture. One study in 322 patients

> 10–20 mm—moderate More than 20 mm—large

>3 months—chronic

Circumferential

Tamponade effect effusive-constrictive

>1 week to <3 months—subacute

Non-infectious—transudate Hemopericardium—blood Pneumopericardium—air Chylopericardium—chylous

Size of fluid collection in TTE\* Less than 10 mm—mild

Onset of fluid collection <1 week—acute

Fluid composition Infectious—exudative

Hemodynamic effects No tamponade effect

Fluid distribution Localized

tamponade, effusive-constrictive) [2, 3]. (**Table 1**).

without signs of cardiac tamponade [3, 4].

**12**

*\**

**Table 1.**

*TTE, transthoracic echocardiography.*

*Classification of pericardial effusion.*

has reported around 60% of cases had a known cause of pericardial effusion [5]. A varying amount of effusion can be seen in other conditions such as malignancy (with or without direct pericardial involvement), renal failure, pregnancy, aortic or cardiac wall rupture, trauma, heart failure, cirrhosis of the liver, nephrotic syndrome, autoimmune diseases, radiation, etc. One study incorporated demographics in their review of pericarditis etiology by comparing a younger patient population (age 15–65, *n* = 221) to a geriatric population (age 66–88, *n* = 101) and found no statistically significant differences in the incidence of idiopathic (33 vs. 38%) versus neoplastic (14.4 vs. 10.8%) pericarditis or the incidence of tamponade (36 vs. 38.6%) [6]. The cause of effusion may also vary by geographical area and clinical setting. For example, effusions related to viral pericarditis or idiopathic pericarditis are more common in outpatient populations of the western world, whereas bacterial and tuberculous inflammation and effusion are more common in sub-Saharan Africa and the developing world. Effusions associated with uremic pericarditis or malignancies are frequently found in hospital settings [3, 7].

According to one study with a mean participant age of 56, when determining the cause of moderate to severe pleural effusions, it is important to consider three major factors: (1) size of effusion; (2) presence of tamponade; and (3) inflammatory signs (defined as two or more from: fever >37°C, pericardial friction rub, characteristic chest pain, and diffuse ST-segment elevation). The presence of inflammatory signs was associated with acute idiopathic pericarditis (likelihood ratio = 5.4, P < 0.001), a large effusion without any inflammatory signs or tamponade was found to be associated with chronic idiopathic pericardial effusion (likelihood ratio = 20, P < 0.001), and the features of tamponade without inflammatory signs were associated with malignant effusions (likelihood ratio = 2.9, P < 0.01) [5].

#### **2.2 Clinical presentation**

The presentation of pericardial effusion varies according to the speed of accumulation, size of effusion, and etiology. The rate of fluid collection plays a critical role in clinical presentation as rapidly accumulating pericardial effusion causes a quick rise in intrapericardial pressure, which results in cardiac tamponade, while slowly accumulating fluid accommodates comparatively larger volume before signs of tamponade [2, 3]. The cases of isolated pericardial effusion can be asymptomatic or can have symptoms related to the underlying etiology or to the effusion itself. The classically reported symptom is dyspnea on exertion; however, the wide spectrum of symptoms related to compressive effect includes cough, weakness, fatigue, palpitations (from compressive effect of the pericardial fluid or reduced blood pressure), nausea (diaphragm), dysphagia (esophagus), hoarseness of voice (recurrent laryngeal nerve), etc. Patients may present with fever from underlying disease (infectious or systemic inflammatory disease), pleural effusion, ascites, or hepatic dysfunction from long standing pericardial constriction [2, 8].

Physical examination may remain normal without any significant findings in patients with no hemodynamic compromise. Pulsus paradoxus is an inspiratory drop in systolic BP >10 mmHg due to the augmentation of right ventricular preload causing impaired left ventricular filling resulting in abnormal decrease in stroke volume [9] and is a phenomenon commonly seen with large pericardial effusion or cardiac tamponade. Pericardial friction rub is rarely heard but is a usual finding of pericarditis.

#### **2.3 Diagnostics**

Upon clinical suspicion of pericardial effusion, the diagnostic approach should consider three major steps: (1) confirm the presence of effusion; (2) assess the hemodynamic impact; and (3) effort to identify the underlying etiology. Transthoracic echocardiography (TTE) is recommended in all patients with suspected effusion as a class I, level C recommendation. Further imaging modalities such as computed tomography (CT) scan, cardiac magnetic resonance imaging (CMRI), pericardial fluid analysis, or biopsy can be considered in cases where loculated effusion, masses, or thickening of the pericardium are suspected. Basic diagnostic work up, including blood counts, chemistry, thyroid function tests, cardiac biomarkers, inflammatory markers such as C-reactive protein (CRP) and sedimentation rate (ESR), electrocardiogram (ECG), and chest X-ray, should be done [2, 10]. ECG findings in pericardial effusion include low QRS voltage and electrical alternans, a finding of large pericardial effusion or tamponade that is usually associated with sinus tachycardia.

TTE is recommended as the first modality to determine the hemodynamic significance of pericardial effusion and is highly sensitive and specific. The pericardial fluid appears as echo-lucent space between the pericardium and epicardium on TTE. The semi-quantitative assessment for largest echo-free space in echocardiographic views provides an assessment of severity. Mild pericardial effusion is considered <10 mm, moderate between 10 and 20 mm, and large effusion is any collection >20 mm. The collection of effusion follows gravity initially in the inferolateral position close to right atrium in the apical four chamber view with the patient in a supine-left lateral position. The pattern of collection changes to circumferential in the pericardium with increasing amount of fluid (**Figure 1**). After the development of a large amount of effusion, the heart can be seen swinging in the pericardial cavity, a finding that correlates with electrical alternans on ECG [2, 3, 11].

Cardiac CT and CMRI are useful imaging modalities for the evaluation of pericardial effusion and tamponade especially for more detailed assessment and the localization of the effusion and associated abnormalities in the mediastinum, lungs,

**15**

*Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

quick [2, 11].

infectious etiologies.

depicted in **Figure 2** [2, 3].

1.22–1.92; P < 0.0001, 31 months follow-up) [12].

**2.5 Prognosis**

**2.4 Treatment**

and adjacent structures. They are useful for the guidance of pericardiocentesis since loculated effusions or calcified pericardium can be identified. CMRI is superior to CT in differentiating fluids especially highly exudative fluid from thickened pericardium. CT detects a minimum amount of pericardial calcium and is relatively

Pericardial fluid analysis is often performed when the patient requires pericardiocentesis. Routine fluid studies include measuring fluid protein level, protein fluid/serum ratio, lactate dehydrogenase (LDH), LDH fluid/serum ratio, glucose, cell counts, and specific gravity. Fluid cytology and tumor markers (carcinoembryonic antigen, cancer antigen 19-9, adenosine deaminase, and interferon gamma) are useful measures in malignancy. Polymerase chain reaction and fluid cultures help in

For small-to-medium sized, asymptomatic pericardial effusion without signs of hemodynamic instability, regular outpatient follow-up with clinical examination and/or echocardiography should be preferred. Management of pericardial effusion with signs of inflammation (pericarditis) should follow the standard or treatment for pericarditis; however, in the absence of any inflammation, antiinflammatory drugs, such as nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and corticosteroids, are generally not effective. Such cases as well as cases with large effusion that failed empiric anti-inflammatory therapy would require pericardiocentesis. Recurrence of effusion is fairly common and further management options include pericardial window formation or pericardiectomy. A study comparing patients age 15–65 to a group of patients age 66–88 years showed elderly people had more persistence of effusion (6.3 vs. 14%; P < 0.05) but no statistically significant difference in mortality (24 vs. 30%) or evolution of cardiac constriction (4 vs. 2%) during median follow up time of 11 months [6]. There is no standard guideline available for elderly patients regarding pleural effusions; however, the expert consensus suggests adjusting the type and dosages of medications with special attention to drug interactions and renal function given the prevalence of polypharmacy and renal dysfunction in the geriatric population [2]. A proposed management algorithm for pericardial effusion of unknown origin is

The prognosis of pericardial effusion is related to its etiology and size. Moderate-to-large size effusions are more commonly associated with bacterial infection, systemic inflammatory disease, or malignancy. Idiopathic pericardial effusion has a good prognosis, but effusion related to bacteria, post-radiation, or pericardial injury has a higher rate of developing either early (cardiac tamponade) or late complications (constrictive pericarditis). Large effusion (>3 months) carries a 30–35% risk of progression to cardiac tamponade. The follow-up of pericardial effusion is mainly based on symptomatic evaluation with the follow-up of inflammatory biomarkers and echocardiography [3]. A recent meta-analysis regarding prognosis of pericardial effusion in an elderly population with mean age > 60 reported that pericardial effusion can be considered as a marker of severity of the underlying disease as evidenced by a higher hazard ratio (HR) in patients with pericardial effusion with myocardial infarction (HR 2.65, 95% CI: 1.4–4.99; P = 0.003, 15 months follow-up) versus those with chronic heart failure (HR 1.53, 95% CI:

**Figure 1.** *Large circumferential pericardial effusion.*

#### *Pericardial Diseases in Elderly Patients DOI: http://dx.doi.org/10.5772/intechopen.89473*

and adjacent structures. They are useful for the guidance of pericardiocentesis since loculated effusions or calcified pericardium can be identified. CMRI is superior to CT in differentiating fluids especially highly exudative fluid from thickened pericardium. CT detects a minimum amount of pericardial calcium and is relatively quick [2, 11].

Pericardial fluid analysis is often performed when the patient requires pericardiocentesis. Routine fluid studies include measuring fluid protein level, protein fluid/serum ratio, lactate dehydrogenase (LDH), LDH fluid/serum ratio, glucose, cell counts, and specific gravity. Fluid cytology and tumor markers (carcinoembryonic antigen, cancer antigen 19-9, adenosine deaminase, and interferon gamma) are useful measures in malignancy. Polymerase chain reaction and fluid cultures help in infectious etiologies.
