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emedicine.medscape.com eMedicine Specialties > Cardiology > Pericardial Disease Pericardial Effusion William J Strimel, DO,, Fellow, Cardiovascular Disease, Scott and White Memorial Hospital Ramin Assadi, MD, Fellow, Department of Cardiology, Loma Linda University; Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago; Abraham G Kocheril, MD, FACC, FACP,Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago Updated: Jun 30, 2010 Introduction Background Pericardial effusion defines the presence of an abnormal amount and/or character of fluid in the pericardial space. It can be caused by a variety of local and systemic disorders, or it may be idiopathic. Pericardial effusions can be acute or chronic, and the time course of development has a great impact on the patient's symptoms. Treatment varies, and is directed at both removal of the pericardial fluid and alleviation of the underlying cause, which usually is determined by a combination of fluid analysis and correlation with comorbid illnesses. Image is from a patient with malignant pericardial effusion. Note the "water- bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest film.

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Page 1: PERICARDIAL EFFUSION

 

emedicine.medscape.com 

eMedicine Specialties > Cardiology > Pericardial Disease

Pericardial EffusionWilliam J Strimel, DO,, Fellow, Cardiovascular Disease, Scott and White Memorial HospitalRamin Assadi, MD, Fellow, Department of Cardiology, Loma Linda University; Ali A Sovari, MD, Clinical and Research Fellow in Cardiovascular Medicine, Section of Cardiology, University of Illinois at Chicago; Abraham G Kocheril, MD, FACC, FACP,Professor of Medicine, Director of Clinical Electrophysiology, University of Illinois at Chicago

Updated: Jun 30, 2010

Introduction

Background

Pericardial effusion defines the presence of an abnormal amount and/or character of fluid in the pericardial space. It can be caused by a variety of local and systemic disorders, or it may be idiopathic. Pericardial effusions can be acute or chronic, and the time course of development has a great impact on the patient's symptoms. Treatment varies, and is directed at both removal of the pericardial fluid and alleviation of the underlying cause, which usually is determined by a combination of fluid analysis and correlation with comorbid illnesses.

Image is from a patient with malignant pericardial effusion. Note the "water-bottle"

appearance of the cardiac silhouette in the anteroposterior (AP) chest film.

Pathophysiology

Embryology

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In the human embryo, the pericardial cavity develops from the intraembryonic celom during the fourth week. The pericardial cavity initially communicates with the pleural and peritoneal cavities, but during normal development these are separated by the eighth week. Both the visceral and parietal pericardium are derived from the mesoderm, albeit from different parts of the embryo. The visceral pericardium develops from splanchnic mesoderm, as cells originating from the sinus venous spread out over the myocardium. The parietal pericardium derives from lateral mesoderm that covers and accompanies the developing pleuropericardial membrane, which will eventually separate the pleural and pericardial cavities. In healthy subjects, the pericardium covers the heart and great vessels, with the exception of only partially covering the left atrium.

Congenital absence of the pericardium can occur, and can be either partial or complete. It is often clinically silent, but can potentially lead to excessive cardiac motion (in the case of complete absence) causing vague chest pain or dyspnea, or, in case of partial absence with significant defects, strangulation of heart muscle and possible death.[1 ]

Physiology 

The pericardial space normally contains 15-50 mL of fluid, which serves as lubrication for the visceral and parietal layers of the pericardium. This fluid is thought to originate from the visceral pericardium and is essentially an ultrafiltrate of plasma. Total protein levels are generally low; however, the concentration of albumin is increased in pericardial fluid owing to its low molecular weight.

The pericardium and pericardial fluid provide important contributions to cardiac function.

The parietal pericardium contributes to resting diastolic pressure, and is responsible for most of this pressure in the right atrium and ventricle.

Through their ability to evenly distribute force across the heart, the pericardial structures assist in ensuring uniform contraction of the myocardium.

The normal pericardium can stretch to accommodate a small amount of fluid without significant change in intrapericardial pressure. However, once this pericardial reserve volume is surpassed, the pressure-volume curve becomes steep. With slow increases in volume, pericardial compliance can increase to lessen the increase in intrapericardial pressure.

Clinical manifestations of pericardial effusion are highly dependent upon the rate of accumulation of fluid in the pericardial sac. Rapid accumulation of pericardial fluid may cause elevated intrapericardial pressures with as little as 80 mL of fluid, while slowly progressing effusions can grow to 2 L without symptoms.

Understanding the properties of the pericardium can help predict changes within the heart under physiologic stress:

During hypervolemic states, the pericardium limits acute cardiac cavitary dilatation. By distributing forces across the heart, the pericardium plays a significant role in the

physiologic concept of ventricular interdependence, whereby changes in pressure, volume, and function in one ventricle influence the function of the other.

The pericardium plays a pivotal role in cardiac changes during inspiration. As the right atrium and ventricle fill during normal inspiration, the pericardium, by limiting the ability of these chambers to dilate, contributes to the bowing of the atrial and ventricular septums to the left. This reduces LV filling volumes, which lead to the drop in cardiac output. As intrapericardial pressures rise, this effect becomes pronounced, eventually leading to the finding of pulsus paradoxus (discussed below), heralding the development of pericardial tamponade.

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The cause of abnormal fluid production depends on the underlying etiology, but it is usually secondary to injury or insult to the pericardium (ie, pericarditis). Transudative fluids result from obstruction of fluid drainage, which occurs through lymphatic channels. Exudative fluids occur secondary to inflammatory, infectious, malignant, or autoimmune processes within the pericardium.

Frequency

United States

Few large studies have characterized the epidemiology of pericardial effusion; however, the available data consistently shows that they are more prevalent than clinically evident.

A higher incidence of pericardial effusion is associated with certain diseases.

Small pericardial effusions are often asymptomatic, and pericardial effusion has been found in 3.4% of subjects in general autopsy studies.

A wide variety of malignant neoplasms and hematologic malignancies can lead to pericardial effusion. Data on the prevalence varies, with some studies showing the presence of pericardial effusion as high as 21% in such patients. A large study by Bussani et al showed cardiac metastases (9.1%) and pericardial metastases (6.3%) in cases of death from all causes in individuals with an underlying carcinoma at autopsy.[2 ]Malignancies with the highest prevalence of pericardial effusion include lung (37% of malignant effusions), breast (22%), and leukemia/lymphoma (17%).

Patients with HIV, with or without AIDS, are also found to have increased prevalence of pericardial effusion.[3 ]Studies have shown the prevalence of pericardial effusion in these patients to range from 5-43%, depending on the inclusion criteria, with 13% having moderate-to-severe effusion. The incidence of pericardial effusion in patients infected with HIV has been estimated at 11%; however, whether highly active anti-retroviral therapy (HAART) has influenced this number is unknown.

Mortality/Morbidity

The mortality and morbidity of pericardial effusion is dependent upon etiology and comorbid conditions.

Idiopathic effusions are well tolerated in most patients. As many as 50% of patients with large, chronic effusions were asymptomatic during long-term follow-up.

Pericardial effusion is the primary or contributory cause of death in 86% of cancer patients with symptomatic effusions.

Survival rate for patients with HIV and symptomatic pericardial effusion is 36% at 6 months, 19% at 1 year.

Race

No consistent difference among races is reported in the literature. AIDS patients with pericardial effusion are more likely to be white.

Sex

No sexual predilection exists.

Age

Observed in all age groups

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Mean occurrence in fourth or fifth decades; earlier in patients with HIV[3 ]

Clinical

History

A patient with pericardial effusion may report the following symptoms:

Cardiovascularo Chest pain, pressure, discomfort: Characteristically, pericardial pain may be relieved

by sitting up and leaning forward and is intensified by lying supine.

o Light-headedness, syncope

o Palpitations

Respiratory

o Cough

o Dyspnea

o Hoarseness

Gastrointestinal

o Hiccoughs

Neurologic

o Anxiety

o Confusion

Physical

Upon examination, a patient with pericardial effusion may have the following signs:

Cardiovascularo Classic Beck triad of pericardial tamponade (hypotension, muffled heart sounds,

jugular venous distension).

o Pulsus paradoxus: Exaggeration of physiologic respiratory variation in systemic blood

pressure, defined as a decrease in systolic blood pressure of more than 10 mm Hg with inspiration, signaling falling cardiac output during inspiration.

o Pericardial friction rub: The most important physical sign of acute pericarditis may

have up to 3 components per cardiac cycle and is high-pitched, scratching, and grating. It can sometimes be elicited only when firm pressure with the diaphragm of the stethoscope is applied to the chest wall at the left lower sternal border. The pericardial friction rub is heard most frequently during expiration with the patient upright and leaning forward.

o Tachycardia

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o Hepatojugular reflux: This can be observed by applying pressure to the periumbilical

region. A rise in the jugular venous pressure (JVP) of greater than 3 cm H2 O for more than 30 seconds suggests elevated central venous pressure. Transient elevation in JVP may be normal.

Respiratory

o Tachypnea

o Decreased breath sounds (secondary to pleural effusions)[4 ]

o Ewart sign - Dullness to percussion beneath the angle of left scapula from

compression of the left lung by pericardial fluid

Gastrointestinal - Hepatosplenomegaly

Extremities

o Weakened peripheral pulses

o Edema

o Cyanosis

Causes

In up to 60% of cases, pericardial effusion is related to a known or suspected underlying process. Therefore, the diagnostic approach should give strong consideration to coexisting medical conditions.

Idiopathic: In many cases, the underlying cause is not identified. However, this often relates to the lack of extensive diagnostic evaluation.

Infectious

o HIV infection can lead to pericardial effusion through several mechanisms, including

the following:

Secondary bacterial infection

Opportunistic infection

Malignancy (Kaposi sarcoma, lymphoma)

"Capillary leak" syndrome, which is associated with effusions in other body cavities

o Viral: The most common cause of infectious pericarditis and myocarditis is viral.

Common etiologic organisms include coxsackievirus A and B, and hepatitis viruses.

o Pyogenic (pneumococci, streptococci, staphylococci, Neisseria, Legionella species)

o Tuberculous

o Fungal (histoplasmosis, coccidioidomycosis, Candida)

o Other infections (syphilitic, protozoal, parasitic)

Neoplasia

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o Neoplastic disease can involve the pericardium through the following mechanisms:

Direct extension from mediastinal structures or the cardiac chamber

Retrograde extension from the lymphatic system

Hematologic seeding

As mentioned previously, the most common cases of malignant effusion are lung, breast, lymphoma, and leukemia. However, patients with malignant melanoma or mesothelioma have a high prevalence of associated pericardial effusions.

Postoperative/postprocedural

o Pericardial effusions are common after cardiac surgery. In 122 consecutive patients

studied serially before and after cardiac surgery, effusions were present in 103 patients; most appeared by postoperative day 2, reached their maximum size by postoperative day 10, and usually resolved without sequelae within the first postoperative month. In a retrospective survey of more than 4,500 postoperative patients, only 48 were found to have moderate or large effusions by echocardiography; of those, 36 met diagnostic criteria for tamponade.[5 ]

o Use of preoperative anticoagulants, valve surgery, and female sex were all

associated with a higher prevalence of tamponade. Symptoms and physical findings of significant postoperative pericardial effusions are frequently nonspecific, and echocardiographic detection and echo-guided pericardiocentesis, when necessary, are safe and effective; prolonged catheter drainage reduces the recurrence rate.[6 ]

o Pericardial effusions in cardiac transplant patients are associated with an increased

prevalence of acute rejection.[7 ]

Other less common causes include the following:

o Uremia

o Myxedema

o Severe pulmonary hypertension

o Radiation therapy

o Acute myocardial infarction, including the complication of free wall rupture

o Aortic dissection, leading to hemorrhagic effusion in from leakage into pericardial sac

o Trauma

o Hyperlipidemia

o Chylopericardium

o Familial Mediterranean fever

o Whipple disease

o Hypersensitivity or autoimmune related

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Systemic lupus erythematosus [8 ]

Rheumatoid arthritis

Ankylosing spondylitis

Rheumatic fever

Scleroderma

Wegener granulomatosis

o Drug-associated (eg, procainamide, hydralazine, isoniazid, minoxidil, phenytoin,

anticoagulants, methysergide)

Differential Diagnoses

Cardiac Tamponade Pericarditis, Constrictive-Effusive

Cardiomyopathy, Dilated Pericarditis, Uremic

Myocardial Infarction Pulmonary Edema, Cardiogenic

Pericarditis, Acute Pulmonary Embolism

Pericarditis, Constrictive

Other Problems to Be Considered

Myocardial ischemia

Workup

Laboratory Studies

The extent to which pericardial effusions should be evaluated with fluid analysis remains an area of some debate. Initially, in a patient with a new pericardial effusion, the likelihood of myocarditis or pericarditis should be assessed, and the initial diagnostic evaluation should be directed toward these conditions. In general, all patients with pericardial tamponade, suspected purulent effusion, or poor prognostic indicators in the setting of pericarditis should undergo diagnostic pericardiocentesis. Those with recurrent effusions or large effusions that do not resolve with treatment of the underlying condition may also warrant fluid analysis.

The following lab studies may be performed in patients with suspected pericardial effusion.

Electrolytes - Metabolic abnormalities (eg, renal failure) CBC count with differential - Leukocytosis for evidence of infection, as well as cytopenias, as

signs of underlying chronic disease (eg, cancer, HIV)

Cardiac enzymes: Troponin level is frequently minimally elevated in acute pericarditis, usually in the absence of an elevated total creatine kinase level. Presumably, this is due to some involvement of the epicardium by the inflammatory process. Although the elevated troponin may lead to the misdiagnosis of acute pericarditis as a myocardial infarction, most patients with an elevated troponin and acute pericarditis have normal coronary angiograms. An elevated troponin level in acute pericarditis typically returns to normal within 1-2 weeks and is not associated with a worse prognosis.

Thyroid-stimulating hormone - Thyroid-stimulating hormone screen for hypothyroidism

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Rickettsial antibodies - If high index of suspicion of tick-borne disease

Rheumatoid factor, immunoglobulin complexes, antinuclear antibody test (ANA), and complement levels (which would be diminished) - In suspected rheumatologic causes

PPD and controls

Pericardial fluid analysis - Routine tests (these should be considered part of the standard pericardial fluid analysis)

o Lactic (acid) dehydrogenase (LDH), total protein - The Light criteria (for exudative

pleural effusion) found to be as reliable in distinguishing between exudative and transudative effusions

Total protein fluid-to-serum ratio >0.5

LDH fluid-to-serum ratio >0.6

LDH fluid level exceeds two thirds of upper-limit of normal serum level

o Other indicators suggestive of exudate - Specific gravity >1.015, total protein >3.0

mg/dL, LDH >300 U/dL, glucose fluid-to-serum ratio <1

o Cell count - Elevated leukocytes (ie, >10,000) with neutrophil predominance suggests

bacterial or rheumatic cause, although unreliable

o Gram stain - Specific but insensitive indicator of bacterial infection

o Cultures - Signals and identifies infectious etiology

o Fluid hematocrit for bloody aspirates - Hemorrhagic fluid hematocrits usually

significantly less than simultaneous peripheral blood hematocrits

Pericardial fluid - Special tests (these should be considered individually based on the pretest probability of the coexisting condition under concern)

o Viral cultures

o Adenosine deaminase; polymerase chain reaction (PCR); culture for tuberculosis;

smear for acid-fast bacilli in suspected tuberculosis infection, especially in patients with HIV

o A definite diagnosis of tuberculous pericarditis is based on the demonstration of

tubercle bacilli in pericardial fluid or on a histological section of the pericardium. Probable tuberculous pericarditis is based on the proof of tuberculosis elsewhere in a patient with otherwise unexplained pericarditis, a lymphocytic pericardial exudate with elevated adenosine deaminase levels, and/or appropriate response to a trial of antituberculosis chemotherapy.

Tumor markers: Elevated carcinoembryonic antigen (CEA) levels in pericardial fluid have a high specificity for malignant effusions.

Imaging Studies

Chest radiography

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Findings include enlarged cardiac silhouette (so-called water-bottle heart) and pericardial fat stripe.

Image is from a patient with malignant pericardial effusion. Note the "water-

bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest

film.

A third of patients have a coexisting pleural effusion. Radiography is unreliable in establishing or refuting diagnosis of pericardial effusion.

Echocardiography

Echocardiography is the imaging modality of choice for the diagnosis of pericardial effusion, as the test can be performed rapidly and in unstable patients. Most importantly, the contribution of pericardial effusion to overall cardiac enlargement and the relative roles of tamponade and myocardial dysfunction to altered hemodynamics can be evaluated with echocardiography.[9 ]

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Echocardiogram (parasternal, long axis) of a patient with a moderate pericardial

effusion.

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Subcostal view of an echocardiogram that shows a moderate-to-large amount of

pericardial effusion.

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This echocardiogram shows a large amount of pericardial effusion (identified by the

white arrows).

2-D echocardiographyo Pericardial effusion appears as an echo-free space between the visceral and parietal

pericardium. Early effusions tend to accumulate posteriorly owing to expandable posterior/lateral pericardium. Large effusions are characterized by excessive motion within the pericardial sac. Small effusions have an echo-free space of less than 10 mm, and are generally seen posteriorly. Moderate-sized effusions range from 10-20 mm and are circumferential, and greater than 20 mm indicates a large effusion. Fluid adjacent to the right atrium is an early sign of pericardial effusion.[10 ]

o Severe cases may be accompanied by diastolic collapse of the right atrium and right

ventricle (and in hypovolemic patients, the left atrium and left ventricle), signaling the onset of pericardial tamponade (see Cardiac Tamponade).

o

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This image is from a patient with malignant pericardial effusion. The

effusion is seen as an echo-free region to the right of the left ventricle

(LV).

M-mode echocardiographyo M-mode is adjunctive to 2D imaging for the detection of pericardial effusion. Effusions

can be classified using M-mode according to a system proposed by Horowitz, et al.[11 ]

Type A: No effusion

Type B: Separation of epicardium and pericardium

Type C1: Systolic and diastolic separation of pericardium

Type C2: Systolic and diastolic separation of pericardium, attenuated pericardial motion

Type D: Pronounced separation of pericardium and epicardium with large echo-free space

o In the parasternal long-axis view, discordant changes in right and left ventricular

cavity size can suggest pronounced interventricular dependence.

Doppler echocardiography

o Transmitral and transtricuspid inflow velocities should be interrogated to assess for

respiratory variation. Decreases in flow during inspiration (transmitral) or expiration (transtricuspid) should raise the suspicion of clinically significant interventricular dependence and tamponade physiology.

o Pulmonic vein inflow may show a decrease in early diastolic flow with

hemodynamically significant effusions. Hepatic vein diastolic flow reversal may also be seen.

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False-positive echocardiograms can occur in pleural effusions, pericardial thickening, increased epicardial fat tissue, atelectasis, and mediastinal lesions.

Epicardial fat tissue is more prominent anteriorly but may appear circumferentially, thus mimicking effusion. Fat is slightly echogenic and tends to move in concert with the heart, 2 characteristics that help distinguish it from an effusion, which is generally echolucent and motionless.[9 ]

In addition to its mimicry, pericardial fat accumulation is a source of bioactive molecules, is significantly associated with obesity-related insulin resistance, and may be a coronary risk factor.[12,13 ]

In patients with pericardial effusion, imaging from low to midposterior thorax can provide additional diagnostic echocardiographic images and should be used in patients in whom conventional images are technically difficult or require additional information.

Transesophageal echocardiography (TEE) 

TEE maintains all of the advantages of transthoracic echocardiography and is useful in characterizing loculated effusions. However, this may be difficult to perform in patients with symptomatic effusions due to hemodynamic instability, making the required sedation more difficult.

Intracardiac echocardiography (ICE)

ICE is generally reserved for the assessment of pericardial effusion in the setting of percutaneous interventional or electrophysiology procedure. Phased array ICE systems can perform both 2-D and Doppler interrogations.

Computed tomography

CT can potentially determine composition of fluid and may detect as little as 50 mL of fluid. CT can detect pericardial calcifications, which can be indicative of constrictive pericarditis.

CT results in fewer false-positive results than echocardiography.

CT can be problematic in patients who are unstable given the time required to transport to and from the scanner and perform the test.

Magnetic resonance imaging MRI can detect as little as 30 mL of pericardial fluid. May be able to distinguish hemorrhagic and no hemorrhagic fluids, as hemorrhagic fluids

have a high signal intensity on T-1 weighted images, whereas no hemorrhagic fluids have a low signal intensity.

Nodularity or irregularity of the pericardium seen on MRI may be indicative of a malignant effusion.

MRI is more difficult to perform than CT scan acutely, given the length of time the patient must remain in the scanner.

Both MRI and CT scan may be superior to echocardiography in detecting loculated pericardial effusions, especially when located anteriorly. Also, these modalities allow for greater visualization of the thoracic cavity and adjacent structures, and therefore may identify other abnormalities relating to the cause of the effusion.

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Other Tests

Electrocardiography 

Early in the course of acute pericarditis, the ECG typically displays diffuse ST elevation in association with PR depression. The ST elevation is usually present in all leads except for aVR, but postmyocardial infarction pericarditis, the changes may be more localized. Classically, the ECG changes of acute pericarditis evolve through 4 progressive stages:

o Stage I - Diffuse ST-segment elevation and PR-segment depression

o Stage II - Normalization of the ST and PR segments

o Stage III - Widespread T-wave inversions

o Stage IV - Normalization of the T waves

This electrocardiogram (ECG) is from a patient with malignant pericardial

effusion. The ECG shows diffuse low voltage, with a suggestion of electrical

alternans in the precordial leads.

Patients with uremic pericarditis frequently do not have the typical ECG abnormalities.

Procedures

Pericardiocentesiso This procedure is used for diagnostic as well as therapeutic purposes. Support for the

use of echocardiographic guidance is increasing, unless emergent treatment is required.

o Indications include impending hemodynamic compromise (ie, pericardial tamponade),

suspected infectious etiology, and uncertain etiology.

o Use of a needle that is at least 5 cm long, 16-gauge in diameter, and has a short

bevel can minimize the risk of complications and should allow for adequate pericardial drainage. A system allowing placement of a catheter over the needle is preferred.

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o Contrast echocardiography using agitated saline is useful in cases when bloody fluid

is aspirated to determine if the needle is in the ventricular cavity.

o Attaching an ECG electrode to the pericardiocentesis needle is also useful for

avoiding myocardial puncture. Electrical activity will be seen on the monitor when the needle comes into contact with atrial or ventricular myocardium. These changes may be delayed, however, and instill a false sense of security in needle placement; sense of touch and the findings on aspiration should guide the procedure, with the clinician ultimately relying on good clinical sense.

o Complications of pericardiocentesis include ventricular rupture, dysrhythmias,

pneumothorax, myocardial and/or coronary artery laceration, and infection.

o Recurrence rates within 90 days may be as high as 90% in patients with cancer.

Balloon pericardotomy

o A catheter is placed in the pericardial space under fluoroscopy, which, after inflation

of the balloon, creates a channel for passage of fluid into the pleural space, where reabsorption occurs more readily.

o This may be useful for recurrent effusions.

Pericardial sclerosis

o Several pericardial sclerosing agents have been used with varying success rates (eg,

tetracycline, doxycycline, cisplatin, 5-fluorouracil).

o The pericardial catheter may be left in place for repeat instillation if necessary until

the effusion resolves.

o Complications include intense pain, atrial dysrhythmias, fever, and infection.

o Success rates are reported as high as 91% at 30 days.

Pericardioscopy

o This procedure is not universally available.

o It may increase diagnostic sensitivity in cases of unexplained pericardial effusions. It

allows for visualization of pericardium and for pericardial biopsies.

CT-guided pericardiostomy

o Patients with effusions after cardiothoracic surgery often have limited

echocardiographic windows, loculated effusions, and may be on continued ventilatory support, all of which increase the difficulty of echo-guided pericardiocentesis.

o A report by Palmer et al suggests that, in postsurgical cases, CT-guided pericardial

drainage is safe and effective. The authors reported on 36 patients—33 who underwent major cardiothoracic surgery and 3 who were treated with minimally invasive procedures—whose symptomatic pericardial effusions were drained using CT-guided percutaneous placement of an indwelling pericardial catheter. There were no clinically significant complications associated with any of the placement procedures. Thirty-three patients experienced no symptom recurrence following catheter removal, although pericardial effusion did recur in the remaining 3 patients,

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requiring a repeat treatment. Comparing procedure costs, the authors determined that the CT-guided tube pericardiostomies cost 89% less than intraoperative pericardial window procedures would have. No significant procedure-cost differences were found between CT-guided and ultrasonographically guided tube pericardiostomies.[14 ]

Treatment

Medical Care

Initially, medical care of pericardial effusion is focused on determination of the underlying etiology.

Aspirin/nonsteroidal anti-inflammatory agents (NSAIDs)o Most acute idiopathic or viral pericarditis occurrences are self-limited and respond to

treatment with aspirin (650 mg q6h) or another NSAID.

o Aspirin may be the preferred nonsteroidal agent to treat pericarditis after myocardial

infarction because other NSAIDs may interfere with myocardial healing.

o Indomethacin should be avoided in patients who may have coronary artery disease.

o Meurin et al performed a multicenter, randomized, double-blind trial on the effect of

the NSAID diclofenac in reducing postoperative pericardial effusion volume. Diclofenac, 50 mg, or placebo twice daily for 14 days was given to 196 patients at high risk for tamponade because of pericardial effusion more than 7 days after cardiac surgery. The authors found that diclofenac was not effective at reducing the size of the effusion or preventing late cardiac tamponade.[15 ]

Colchicine: The routine use of colchicine is supported by results from the COlchicine for acute PEricarditis (COPE) trial. In this trial, 120 patients with a first episode of acute pericarditis (idiopathic, acute, postpericardiotomy syndrome, and connective tissue disease) entered a randomized, open-label trial comparing aspirin treatment alone with aspirin plus colchicine (1-2 mg for the first day followed by 0.5-1 mg/d for 3 mo). Colchicine reduced symptoms at 72 hours (11.7% vs 36.7%; P =0.03) and reduced recurrence at 18 months (10.7% vs 36.7%; P =0.004; 5 needed treatment). Colchicine was discontinued in 5 patients because of diarrhea. No other adverse events were noted. Importantly, none of the 120 patients developed cardiac tamponade or progressed to pericardial constriction.[16 ]

Steroids

o Steroid administration early in the course of acute pericarditis appears to be

associated with an increased incidence of relapse after tapering the steroids.

o In the COPE trial, steroid use was an independent risk factor for recurrence (odds

ratio=4.3). Also, an observational study strongly suggests that the use of steroids increases the probability of relapse in patients treated with colchicine.[16 ]

o Systemic steroids should be considered only in patients with recurrent pericarditis

unresponsive to NSAIDs and colchicine or as needed for treatment of an underlying inflammatory disease. If steroids are to be used, an effective dose (1-1.5 mg/kg of prednisone) should be given, and it should be continued for at least 1 month before slow tapering.

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o The intrapericardial administration of steroids has been reported to be effective in

acute pericarditis without producing the frequent reoccurrence of pericarditis that complicates the use of systemic steroids, but the invasive nature of this procedure limits its use.

Hemodynamic support

o Patients who have effusions with actual or threatened tamponade should be

considered to have a true or potential emergency. Most patients require pericardiocentesis to treat or prevent tamponade. However, treatment should be carefully individualized.

o Hemodynamic monitoring with a balloon flotation pulmonary artery catheter is useful,

especially in those with threatened or mild tamponade in whom a decision is made to defer pericardiocentesis. Hemodynamic monitoring is also helpful after pericardiocentesis to assess both reaccumulation and the presence of underlying constrictive disease. However, insertion of a pulmonary artery catheter should not be allowed to delay definitive therapy in critically ill patients.

o Intravenous fluid resuscitation may be helpful in cases of hemodynamic compromise.

o In patients with tamponade who are critically ill, intravenous positive inotropes

(dobutamine, dopamine) can be used but are of limited use and should not be allowed to substitute for or delay pericardiocentesis.

Antibiotics

o In patients with purulent pericarditis, urgent pericardial drainage combined with

intravenous antibacterial therapy (eg, vancomycin 1 g bid, ceftriaxone 1-2 g bid, and ciprofloxacin 400 mg/d) is mandatory. Irrigation with urokinase or streptokinase, using large catheters, may liquify the purulent exudate, but open surgical drainage is preferable.

o The initial treatment of tuberculous pericarditis should include isoniazid 300 mg/day,

rifampin 600 mg/day, pyrazinamide 15-30 mg/kg/day, and ethambutol 15-25 mg/kg/day. Prednisone 1-2 mg/kg/day is given for 5-7 days and progressively reduced to discontinuation in 6-8 weeks. Drug sensitivity testing is essential. Uncertainty remains whether adjunctive corticosteroids are effective in reducing mortality or progression to constriction. Surgical resection of the pericardium remains the appropriate treatment for constrictive pericarditis. The timing of surgical intervention is controversial, but many experts recommend a trial of medical therapy for noncalcific pericardial constriction and pericardiectomy in nonresponders after 4-8 weeks of antituberculosis chemotherapy.

Antineoplastic therapy (eg, systemic chemotherapy, radiation) in conjunction with pericardiocentesis has been shown to be effective in reducing recurrences of malignant effusions.

Corticosteroids and NSAIDs are helpful in patients with autoimmune conditions.

Surgical Care

Surgical care of pericardial effusion includes the following:

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Subxiphoid pericardial window with pericardiostomy[17 ]

o This procedure is associated with low morbidity, mortality, and recurrence rates, and

can be considered as a reasonable alternative diagnostic or treatment modality to pericardiocentesis in selected patients.

o It can be performed under local anesthesia. This is advantageous because general

anesthesia often leads to decreased sympathetic tone, resulting in hemodynamic collapse in patients with pericardial tamponade and shock.

o It may be less effective when effusion is loculated.

o One study indicated it may be safer and more effective at reducing recurrence rates

than pericardiocentesis. However, only patients who were hemodynamically unstable underwent pericardiocentesis, and no change in overall survival rate was observed.

Thoracotomy

o This should be reserved for patients in whom conservative approaches have failed.

o Thoracotomy allows for creation of a pleuropericardial window, which provides

greater visualization of pericardium.

o Thoracotomy requires general anesthesia and thus has higher morbidity and mortality

rates than the subxiphoid approach.

Video-assisted thoracic surgery[18 ]

o Video-assisted thoracic surgery (VATS) enables resection of a wider area of

pericardium than the subxiphoid approach without the morbidity of thoracotomy.

o The surgeon is able to create a pleuropericardial window and address concomitant

pleural pathology, which is especially common in patients with malignant effusions.

o One disadvantage of VATS is that it requires general anesthesia with single lung

ventilation, which may be difficult in otherwise seriously ill patients.

Median sternotomy

o This procedure is reserved for patients with constrictive pericarditis.

o Operative mortality rate is high (5-15%).

Consultations

A cardiologist should be involved in the care of patients with pericardial effusion. Cardiothoracic surgery may be required for recurrent or complicated cases (see Surgical

Care).

Medication

Autoimmune pericardial effusions may respond to treatment with anti-inflammatory medications. In general, selection of an agent depends on the severity of the patient's symptoms and the tolerability and adverse effect profiles of the medications.

Nonsteroidal anti-inflammatory drugs

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Are used mostly for patients with active, nonhemorrhagic pericarditis with or without pericardial effusion. NSAIDS have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action in pericarditis is not known, but NSAIDS may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Indomethacin (Indocin, Indometh)

Drug of choice in this class, although other NSAIDs (ie, ibuprofen, naproxen, aspirin) possess some efficacy. Used as initial therapy for mild-to–moderately severe inflammatory pericardial effusions.

Dosing

Adult

25-50 mg PO bid/tid75 mg SR PO bid; titrate to effectiveness; not to exceed 200 mg/d

Pediatric

1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d

Interactions

Aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity; may decrease effects of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; may increase phenytoin levels

Contraindications

Documented hypersensitivity; GI bleeding; renal insufficiency

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in third trimester; acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur (discontinue if persistent leukopenia, granulocytopenia, or thrombocytopenia)May mask signs and symptoms of infection

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

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Prednisone (Deltasone, Orasone, Sterapred)

Used for patients with severe inflammatory pericardial effusions or for those in whom initial treatment with NSAIDs has failed. Other agents may be used if adverse effect profile warrants; dosages should be determined by prednisone equivalents.

Dosing

Adult

5-60 mg/d PO qd or divided bid/qid; taper over 2 wk, as symptoms resolve, to 5-10 mg PO qd

Pediatric

4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk, as symptoms resolve

Interactions

Estrogens may decrease clearance; may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism (consider increasing maintenance dose); diuretics require monitoring for hypokalemia

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Abrupt discontinuation may cause adrenal crisis; adverse effects may include hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections

Anti-inflammatory Agent

These agents inhibit key factors involved in inflammatory reactions.

Colchicine

Alkaloid extract that inhibits microtubule formation. Has unique anti-inflammatory properties. Concentrates well in leukocytes and reduces neutrophilic chemotaxis and motility. Reduces release of lactic acid and proinflammatory enzymes. Inhibits release of histamine-containing granules from mast cells, which may be important in pathogenesis of elastic tissue changes found in anetoderma.

Use in autoimmune disease is primarily empiric, and mechanism of action in decreasing inflammation is not clear, nor is it truly an immunomodulating agent.

Dosing

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Adult

1-2 mg PO to start, then 0.5- 1 mg PO qd

Pediatric

<12 years: Not established>12 years: Administer as in adults

Interactions

Sympathomimetic agent toxicity and effect of CNS depressants are significantly increased with colchicine

Contraindications

Documented hypersensitivity; severe renal, hepatic, GI, or cardiac disorders; blood dyscrasias

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Risk of renal failure, hepatic failure, permanent hair loss, bone marrow suppression, numbness or tingling in hands and feet, disseminated intravascular coagulopathy, and decreased sperm count; dose-dependent GI upset is common

Follow-up

Further Inpatient Care

Patients with pericardial effusion who present with significant symptoms or cardiac tamponade require emergent treatment and admission to ICU.

The pericardial catheter (if placed) should be removed within 24-48 hours to avoid infection.

Symptomatic patients should remain hospitalized until definitive treatment is accomplished and/or symptoms have resolved.

Further Outpatient Care

Patients should be educated on symptoms of increasing pericardial effusion and should be evaluated whenever these symptoms begin to occur.

Indications for echocardiography after diagnosis include the following:

o A follow-up imaging study to evaluate for recurrence/constriction: Repeat studies may

be performed to answer specific clinical questions.

o The presence of large or rapidly accumulating effusions (to detect early signs of

tamponade)

Transfer

Symptomatic patients requiring treatment (who are surgical candidates) should receive care at an institution with cardiothoracic surgery capabilities.

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Complications

Pericardial tamponadeo Can lead to severe hemodynamic compromise and death.

o Heralded by equalization of diastolic filling pressures.

o Treat with expansion of intravascular volume (small amounts of crystalloids or

colloids may lead to improvement, especially in hypovolemic patients) and urgent pericardial drainage. Avoid positive-pressure ventilation if possible, as this decreases venous return and cardiac output. Vasopressor agents are of little clinical benefit.

Chronic pericardial effusion

o Effusions lasting longer than 6 months.

o Usually well tolerated.

Prognosis

Most patients with acute pericarditis recover without sequelae. Predictors of a worse outcome include the following: fever greater than 38°C, symptoms developing over several weeks in association with immunosuppressed state, traumatic pericarditis, pericarditis in a patient receiving oral anticoagulants, a large pericardial effusion (>20 mm echo-free space or evidence of tamponade), or failure to respond to NSAIDs. In a series of 300 patients with acute pericarditis, 254 (85%) did not have any of the high-risk characteristics and had no serious complications. Of these low-risk patients, 221 (87%) were managed as outpatients and the other 13% were hospitalized when they did not respond to aspirin.

Patients with symptomatic pericardial effusions from HIV/AIDS or cancer have high short-term mortality rates.

Miscellaneous

Medicolegal Pitfalls

Failure to consider pericardial effusion as a principal or secondary diagnosis may lead to rapid deterioration and death secondary to cardiac tamponade.

Patients with viral cardiomyopathy, especially in the acute setting, may have a similar presentation, with an enlarged heart on chest radiographs. Echocardiography readily distinguishes the difference between enlarged cardiac chambers and a pericardial effusion.

Multimedia

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Media file 1: Image is from a patient with malignant pericardial effusion. Note the

"water-bottle" appearance of the cardiac silhouette in the anteroposterior (AP) chest

film.

Media file 2: Echocardiogram (parasternal, long axis) of a patient with a moderate

pericardial effusion.

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Media file 3: This image is from a patient with malignant pericardial effusion. The

effusion is seen as an echo-free region to the right of the left ventricle (LV).

Media file 4: This electrocardiogram (ECG) is from a patient with malignant pericardial

effusion. The ECG shows diffuse low voltage, with a suggestion of electrical alternans in

the precordial leads.

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Media file 5: Subcostal view of an echocardiogram that shows a moderate-to-large

amount of pericardial effusion.

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Media file 6: This echocardiogram shows a large amount of pericardial effusion

(identified by the white arrows).

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